Esophageal cancer is malignancy of the esophagus. There are various subtypes, primarily squamous cell cancer and adenocarcinoma. Squamous cell cancer arises from the cells that line the upper part of the esophagus. Adenocarcinoma arises from glandular cells that are present at the junction of the esophagus and stomach.[1] Esophageal tumors usually lead to dysphagia (difficulty swallowing), pain and other symptoms, and are diagnosed with biopsy. Small and localized tumors are treated surgically with curative intent. Larger tumors tend not to be operable and hence cannot be cured; their growth can still be delayed with chemotherapy, radiotherapy or a combination of the two. In some cases chemo- and radiotherapy can render these larger tumors operable. Prognosis depends on the extent of the disease and other medical problems, but is fairly poor.
Symptoms
Dysphagia (difficulty swallowing) is the first symptom in most patients. Odynophagia (painful swallowing) may be present. Fluids and soft foods are usually tolerated, while hard or bulky substances (such as bread or meat) cause much more difficulty. Substantial weight loss is characteristic as a result of poor nutrition and the active cancer. Pain, often of a burning nature, may be severe and worsened by swallowing, and can be spasmodic in character. An early sign may be an unusually husky or raspy voice.
The presence of the tumor may disrupt normal peristalsis (the organised swallowing reflex), leading to nausea and vomiting, regurgitation of food, coughing and an increased risk of aspiration pneumonia. The tumor surface may be fragile and bleed, causing hematemesis (vomiting up blood). Compression of local structures occurs in advanced disease, leading to such problems as upper airway obstruction and superior vena cava syndrome. Fistulas may develop between the esophagus and the trachea, increasing the pneumonia risk; this condition is usually heralded by cough, fever or aspiration.
If the disease has spread elsewhere, this may lead to symptoms related to this: liver metastasis could cause jaundice and ascites, lung metastasis could cause shortness of breath, pleural effusions, etc.
Causes and risk factors
Increased risk
Barrett's esophagus is considered to be a risk factor for esophageal adenocarcinoma.There are a number of risk factors for esophageal cancer.[2] Some subtypes of cancer are linked to particular risk factors:
Age. Most patients are over 60, and the median in US patients is 67.
Sex. It is more common in men.
Heredity. It is more likely in people who have close relatives with cancer.
Tobacco smoking and heavy alcohol use increase the risk, and together appear to increase the risk more than either individually.
Gastroesophageal reflux disease (GERD) and its resultant Barrett's esophagus increase esophageal cancer risk due to the chronic irritation of the mucosal lining (adenocarcinoma is more common in this condition, while all other risk factors predispose more for squamous cell carcinoma).
Human papillomavirus (HPV)[4]
Corrosive injury to esophagus by swallowing strong alkalines (lye) or acids.
Particular dietary substances, such as nitrosamine.
A medical history of other head and neck cancers increases the chance of developing a second cancer in the head and neck area, including esophageal cancer.
Plummer-Vinson syndrome (anemia and esophageal webbing)
Tylosis and Howel-Evans syndrome (hereditary thickening of the skin of the palms and soles).
Radiation therapy for other conditions in the mediastinum.
Celiac disease predisposes towards squamous cell carcinoma.
Obesity increases the risk of adenocarcinoma fourfold.[6] It is suspected that increased risk of reflux may be behind this association.[3][7]
Drinking large quantities of hot beverages, especially hot brewed teas[citation needed]
Alcohol consumption in individuals predisposed to alcohol flush reaction[8]
Achalasia[9]
Decreased risk
Risk appears to be less in patients using aspirin or related drugs (NSAIDs).[10]
The role of Helicobacter pylori in progression to esophageal adenocarcinoma is still uncertain, but, on the basis of population data, it may carry a protective effect.[11][12] It is postulated that H. pylori prevents chronic gastritis, which is a risk factor for reflux, which in turn is a risk factor for esophageal adenocarcinoma.[13]
According to the National Cancer Institute, "diets high in cruciferous (cabbage, broccoli, cauliflower) and green and yellow vegetables and fruits are associated with a decreased risk of esophageal cancer."[14]
Moderate coffee consumption is associated with a decreased risk.[15]
According to one Italian study of "diet surveys completed by 5,500 Italians"—a study which has raised debates questioning its claims among cancer researchers cited in news reports about it—eating pizza more than once a week appears "to be a favorable indicator of risk for digestive tract neoplasms in this population."[16]
[edit] Diagnosis
Endoscopy and radial endoscopic ultrasound images of submucosal tumour in mid-esophagus.[edit] Clinical evaluation
Although an occlusive tumor may be suspected on a barium swallow or barium meal, the diagnosis is best made with esophagogastroduodenoscopy (EGD, endoscopy); this involves the passing of a flexible tube down the esophagus and visualising the wall. Biopsies taken of suspicious lesions are then examined histologically for signs of malignancy.
Additional testing is usually performed to estimate the tumor stage. Computed tomography (CT) of the chest, abdomen and pelvis, can evaluate whether the cancer has spread to adjacent tissues or distant organs (especially liver and lymph nodes). The sensitivity of CT scan is limited by its ability to detect masses (e.g. enlarged lymph nodes or involved organs) generally larger than 1 cm. FDG-PET (positron emission tomography) scan is also being used to estimate whether enlarged masses are metabolically active, indicating faster-growing cells that might be expected in cancer. Esophageal endoscopic ultrasound (EUS) can provide staging information regarding the level of tumor invasion, and possible spread to regional lymph nodes.
The location of the tumor is generally measured by the distance from the teeth. The esophagus (25 cm or 10 inches long) is commonly divided into three parts for purposes of determining the location. Adenocarcinomas tend to occur distally and squamous cell carcinomas proximally, but the converse may also be the case.
[edit] Histopathology
Most tumors of the esophagus are malignant, only about 0.5% are benign. A very small proportion (under 10%) is leiomyoma (smooth muscle tumor) or gastrointestinal stromal tumor (GIST). Malignant tumors are generally adenocarcinomas, squamous cell carcinomas, and occasionally small-cell carcinomas. The latter share many properties with small-cell lung cancer, and are relatively sensitive to chemotherapy compared to the other types.
[edit] Classification
Esophageal cancers are typically carcinomas which arise from the epithelium, or surface lining, of the esophagus. Most esophageal cancers fall into one of two classes: squamous cell carcinomas, which are similar to head and neck cancer in their appearance and association with tobacco and alcohol consumption, and adenocarcinomas, which are often associated with a history of gastroesophageal reflux disease and Barrett's esophagus.
Treatment
Self-expandable metallic stents are used for the palliation of esophageal cancer.General approaches
Esophageal cancer affecting the lower esophageus. Insets show the tumor in more detail both before and after placement of a stent.The treatment is determined by the cellular type of cancer (adenocarcinoma or squamous cell carcinoma vs other types), the stage of the disease, the general condition of the patient and other diseases present. On the whole, adequate nutrition needs to be assured, and adequate dental care is vital.
If the patient cannot swallow at all, a stent may be inserted to keep the esophagus patent; stents may also assist in occluding fistulas. A nasogastric tube may be necessary to continue feeding while treatment for the tumor is given, and some patients require a gastrostomy (feeding hole in the skin that gives direct access to the stomach). The latter two are especially important if the patient tends to aspirate food or saliva into the airways, predisposing for aspiration pneumonia.
[edit] Tumor treatments
Surgery is possible if the disease is localised, which is the case in 20–30% of all patients. If the tumor is larger but localised, chemotherapy and/or radiotherapy may occasionally shrink the tumor to the extent that it becomes "operable"; however, this combination of treatments (referred to as neoadjuvant chemoradiation) is still somewhat controversial in most medical circles. Esophagectomy is the removal of a segment of the esophagus; as this shortens the length of the remaining esophagus, some other segment of the digestive tract (typically the stomach or part of the colon) is pulled up to the chest cavity and interposed.[17] If the tumor is unresectable or the patient is not fit for surgery, palliative esophageal stenting can allow the patient to tolerate soft diet.
Endoscopic Therapy for Localized Disease There is accumulating data that endoscopic therapy is a safe, less invasive, and effective therapy for very early esophageal cancer. The candidates for endoscopic therapy are Stage 1 patients with tumors invading into the lamina propria (T1 mucosal) or submucosa (T1 submucosal) that do not have regional or distant metastasis. Patients with carcinoma in-situ or high-grade dysplasia can also be treated with endoscopic therapy. Submucosa cancers with increased risk of nodal metastases may not be as amenable to curative therapy.
The two forms of endoscopic therapy that have been used for Stage 0 and I disease are endoscopic mucosal resection (EMR) and mucosal ablation using photodynamic therapy , Nd-YAG laser, or argon plasma coagulation.
EMR Endoscopic Mucosal Resection has been advocated for early cancers (that is, those that are superficial and confined to the mucosa only) and has been shown to be a less invasive, safe, and highly effective nonsurgical therapy for early squamous cell esophageal cancer. Preliminary reports also suggest its safety and efficacy for early adenocarcinoma arising in Barrett’s esophagus. The prognosis after treatment with endoscopic mucosal resection is comparable to surgical resection. This technique can be attempted in patients, without evidence of nodal or distant metastases, with differentiated tumors that are slightly raised and less than 2 cm in diameter, or in differentiated tumors that are ulcerated and less than 1 cm in diameter. The most commonly employed modalities of endoscopic mucosal resection include strip biopsy, double-snare polypectomy, resection with combined use of highly concentrated saline and epinephrine, and resection using a cap.
The strip biopsy method for endoscopic mucosal resection of esophageal cancer is performed with a double-channel endoscope equipped with grasping forceps and snare. After marking the lesion border with an electric coagulator, saline is injected into the submucosa below the lesion to separate the lesion from the muscle layer and to force its protrusion. The grasping forceps are passed through the snare loop. The mucosa surrounding the lesion is grasped, lifted, and strangulated and resected by electrocautery. The endoscopic double-snare polypectomy method is indicated for protruding lesions. Using a double-channel scope, the lesion is grasped and lifted by the first snare and strangulated with the second snare for complete resection.
Endoscopic resection with injection of concentrated saline and epinephrine is carried out using a double-channel scope. The lesion borders are marked with a coagulator. Highly concentrated saline and epinephrine are injected (15–20 ml) into the submucosal layer to swell the area containing the lesion and elucidate the markings. The mucosa outside the demarcated border is excised using a high-frequency scalpel to the depth of the submucosal layer. The resected mucosa is lifted and grasped with forceps, trapping and strangulating the lesion with a snare, and then resected by electrocautery.
A fourth method of endoscopic mucosal resection employs the use of a clear cap and prelooped snare inside the cap. After insertion, the cap is placed on the lesion and the mucosa containing the lesion is drawn up inside the cap by aspiration. The mucosa is caught by the snare and strangulated, and finally resected by electrocautery. This is called the "band and snare" or "suck and cut" technique. The resected specimen is retrieved and submitted for microscopic examination for determination of tumor invasion depth, resection margin, and possible vascular involvement. The resulting "ulcer" heals within 3 weeks.
Although most lesions treated in the esophagus have been early squamous cell cancers, endoscopic snare resection can also be used to debulk or completely treat polypoid dysplastic or malignant lesions in Barrett’s esophagus. In a preliminary report from Germany, EMR was performed as primary treatment or adjunctive therapy following photodynamic therapy for early adenocarcinomas in Barrett's esophagus. The "suck and cut" technique (with and without prior saline injection) was used as well as the "band and cut" technique. Although all tumors were resected without difficulty, 12.5% developed bleeding (which was managed successfully by endoscopic therapy). Eighty-one percent of the lesions were completely resected. The other lesions were also treated with other endoscopic techniques. While this report suggests it is feasible to completely resect local, circumscribed, early adenocarcinomas arising in Barrett's esophagus, the relative safety and efficacy of EMR in conjunction with photodynamic therapy is unknown.
The major complications of endoscopic mucosal resection include postoperative bleeding and perforation and stricture formation. During the procedure, an injection of 100,000 times diluted epinephrine into the muscular wall, along with high frequency coagulation or clipping can be applied to the bleeding point for hemostasis. It is important to administer acid-reducing medications to prevent postoperative hemorrhage. Perforation may be prevented with sufficient saline injection to raise the mucosa containing the lesion. The "non-lifting sign" and complaints of pain when the snare strangulates the lesion are contrainidications of EMR. When perforation is recognized immediately after a procedure, the perforation should be closed by clips. Surgery should be considered in cases of endoscopic closure failure. The incidence of complication range from 0–50% and squamous cell recurrence rates range from 0–8%.
Laser therapy is the use of high-intensity light to destroy tumor cells; it affects only the treated area. This is typically done if the cancer cannot be removed by surgery. The relief of a blockage can help to reduce dysphagia and pain. Photodynamic therapy (PDT), a type of laser therapy, involves the use of drugs that are absorbed by cancer cells; when exposed to a special light, the drugs become active and destroy the cancer cells.
Chemotherapy depends on the tumor type, but tends to be cisplatin-based (or carboplatin or oxaliplatin) every three weeks with fluorouracil (5-FU) either continuously or every three weeks. In more recent studies, addition of epirubicin (ECF) was better than other comparable regimens in advanced nonresectable cancer. Chemotherapy may be given after surgery (adjuvant, i.e. to reduce risk of recurrence), before surgery (neoadjuvant) or if surgery is not possible; in this case, cisplatin and 5-FU are used. Ongoing trials compare various combinations of chemotherapy; the phase II/III REAL-2 trial – for example – compares four regimens containing epirubicin and either cisplatin or oxaliplatin and either continuously infused fluorouracil or capecitabine.
Radiotherapy is given before, during or after chemotherapy or surgery, and sometimes on its own to control symptoms. In patients with localised disease but contraindications to surgery, "radical radiotherapy" may be used with curative intent.
Follow-up
Patients are followed up frequently after a treatment regimen has been completed. Frequently, other treatments are necessary to improve symptoms and maximize nutrition.
Prognosis
In general, the prognosis of esophageal cancer is quite poor, because so many patients present with advanced disease: The overall five-year survival rate (5YSR) is less than 5%. Individualized prognosis depends largely on stage. Those with cancer restricted entirely to the esophageal mucosa have about an 80% 5YSR, but submucosal involvement brings this down to less than 50%. Extension into the muscularis propria (muscular layer of the esophageus) has meant a 20% 5YSR and extension to the structures adjacent to the esophagus results in a 7% 5YSR. Patients with distant metastases (who are not candidates for curative surgery) have a less than 3% 5YSR. Of all patients undergoing surgery with curative intent, the 5YSR is only about 25%.[citation needed] But these statistics are getting better, as more patients are getting diagnosis earlier because of the awareness of Barrett's Esophagus.
Epidemiology
Esophageal cancer is a relatively rare form of cancer, but some world areas have a markedly higher incidence than others: China, Iceland, India and Japan, as well as the United Kingdom, appear to have a higher incidence, as well as the region around the Caspian Sea.
The American Cancer Society estimates that during 2007, approximately 15,560 new esophageal cancer cases will be diagnosed in the United States.[20]
The esophageal cancer incidence and mortality rates for people of African-American descent have been higher than the rate for Caucasians.[21] According to the NCI, incidence of adenocarcinoma of the esophagus, which is associated with Barrett's esophagus, is rising in the United States. This type is more common in Caucasian men over the age of 60.
Multiple reports indicate that esophageal adenocarcinoma incidence has increased during the past 20 years, especially in non-Hispanic white men. Esophageal adenocarcinoma age-adjusted incidence increased in New Mexico from 1973 to 1997. This increase was found in non-Hispanic whites and Hispanics and became predominant in non-Hispanic whites.[
Saturday, October 31, 2009
Curry kills cancer cells
LONDON - A molecule found in a curry ingredient can kill esophageal cancer cells in the laboratory, suggesting it might be developed as an anti-cancer treatment, scientists said on Wednesday.
Researchers at the Cork Cancer Research Center in Ireland treated esophageal cancer cells with curcumin -- a chemical found in the spice turmeric, which gives curries a distinctive yellow color -- and found it started to kill cancer cells within 24 hours.
The cells also began to digest themselves, they said in a study published in the British Journal of Cancer.
Previous scientific studies have suggested curcumin can suppress tumors and that people who eat lots of curry may be less prone to the disease, although curcumin loses its anti-cancer attributes quickly when ingested.
But Sharon McKenna, lead author of the Irish study, said her study suggested a potential for scientists to develop curcumin as an anti-cancer drug to treat esophageal cancer.
Cancers of the esophagus kill more than 500,000 people across the world each year. The tumors are especially deadly, with five-year survival rates of just 12 to 31 percent.
McKenna said the study showed curcumin caused the cancer cells to die "using an unexpected system of cell messages."
Normally, faulty cells die by committing programed suicide, or apoptosis, which occurs when proteins called caspases are 'switched on' in cells, the researchers said.
But these cells showed no evidence of suicide, and the addition of a molecule that inhibits caspases and stops this "switch being flicked' made no difference to the number of cells that died, suggesting curcumin attacked the cancer cells using an alternative cell signaling system.
U.S. researchers said in 2007 they had found curcumin may help stimulate immune system cells in the Alzheimer's disease.
Researchers at the Cork Cancer Research Center in Ireland treated esophageal cancer cells with curcumin -- a chemical found in the spice turmeric, which gives curries a distinctive yellow color -- and found it started to kill cancer cells within 24 hours.
The cells also began to digest themselves, they said in a study published in the British Journal of Cancer.
Previous scientific studies have suggested curcumin can suppress tumors and that people who eat lots of curry may be less prone to the disease, although curcumin loses its anti-cancer attributes quickly when ingested.
But Sharon McKenna, lead author of the Irish study, said her study suggested a potential for scientists to develop curcumin as an anti-cancer drug to treat esophageal cancer.
Cancers of the esophagus kill more than 500,000 people across the world each year. The tumors are especially deadly, with five-year survival rates of just 12 to 31 percent.
McKenna said the study showed curcumin caused the cancer cells to die "using an unexpected system of cell messages."
Normally, faulty cells die by committing programed suicide, or apoptosis, which occurs when proteins called caspases are 'switched on' in cells, the researchers said.
But these cells showed no evidence of suicide, and the addition of a molecule that inhibits caspases and stops this "switch being flicked' made no difference to the number of cells that died, suggesting curcumin attacked the cancer cells using an alternative cell signaling system.
U.S. researchers said in 2007 they had found curcumin may help stimulate immune system cells in the Alzheimer's disease.
Monday, October 26, 2009
自信心的培养
自信心的培养，是素质教育的重要内容。美国哲学家爱默生说: “自信是导向成功的第一要诀。” 居里夫人也说：“自信是成功的基石。”
自信，就是自己相信自己。自信是一种积极的心理品质，是促使一个人向上奋进的内在动力,是一个人的人格支柱，是一切成功的基础。但是在教学中，经常会遇到这样一些学生，做什么事情，总对自己没有信心。
长期处于自卑、自怨的心理状态，使他们越来越不敢尝试新的事物，不敢主动与其他人交往，从而失去了很多学习和锻炼的机会，影响自身的发展，对自己越来越没有信心。甚至会自暴自弃、破罐子破摔。
如果孩子是个自信的人，那么他就能乐观进取，做事就能主动积极，勇于尝试，乐于接受各种挑战，更能走向成功。所以激发学生的自信，让他们抬起头来走路，毫不含糊地说“我能行”，是我们每一位教师和家长必需重视的问题。
自信，就是自己相信自己。自信是一种积极的心理品质，是促使一个人向上奋进的内在动力,是一个人的人格支柱，是一切成功的基础。但是在教学中，经常会遇到这样一些学生，做什么事情，总对自己没有信心。
长期处于自卑、自怨的心理状态，使他们越来越不敢尝试新的事物，不敢主动与其他人交往，从而失去了很多学习和锻炼的机会，影响自身的发展，对自己越来越没有信心。甚至会自暴自弃、破罐子破摔。
如果孩子是个自信的人，那么他就能乐观进取，做事就能主动积极，勇于尝试，乐于接受各种挑战，更能走向成功。所以激发学生的自信，让他们抬起头来走路，毫不含糊地说“我能行”，是我们每一位教师和家长必需重视的问题。
許下願望，實現夢想，成就美麗人生
記得幾年前過生日時許下的願望嗎？如果，你沒有許願，或根本忘了曾經許下的願望。那麼，讓我提醒你：趕快許願喔！並祝福你，美夢成真。
不一定要在過生日那天才能許願，當你有一個強烈的念頭，願意傾一生之力，去實現、去完成，這個時候就可以說出你的夢想，或許下你的願望。
只有努力作夢的人，才會對未來有美好的憧憬。也只有用心盼望的人，能夠享受「如願以償」的快樂。千萬不要害怕說出你的夢想，會被取笑。也不要顧慮：「萬一將來做不到，會很沒有面子！」。更不要擔心：「願望若沒有實現，多麼丟臉！」當你說出夢想、許下願望，親友們才知道要如何幫助你達成。
就算有人要說風涼話、扯後腿，他們這些心懷不軌的人，都會敗在你的決心中。別忘了，邪不勝正！只要你的決心夠堅定，只要你的付出夠盡力，所有的阻礙終將節節敗退。而你，最後一定會贏得夢想、實現願望。
保羅‧柯賀這位來自拉丁美洲的暢銷書作家，在他的作品「牧羊少年奇幻之旅〈原名：鍊金術士〉」一書中提到：「沒有一顆心會因為追求夢想而受傷。」、「當你真心渴望某樣東西時，整個宇宙都會聯合起來幫助你完成！」
我一直很喜歡伸手摘星，雖不一定能夠次次如願以償；但至少不會弄髒你的手！」這句座右銘。這至理名言，是通往夢想、實現願望途中，最有力道的心靈補給。
「對那麼好的成果，想都不敢想！」這話聽來若入不是謙虛，就是很沒有志氣。缺乏夢想、沒有願望的人生，真的很沒有意思。我不能說這樣的人生一定是黑白，但絕對沒有太豐富的色彩。你怎能指望一個對未來沒有任何期待的人，活得多麼精采？
實現願望，像在孵蛋。破殼而出之後，還會生生不息。
天下最可惜的是－只會作「白日夢」的人。光會用腦袋想、只用嘴巴說，對自己夢想的內容沒有信心，對實現願望的努力也做得很少。這種人的夢想或願望，講出來的時候，別說聽見的人會笑他，恐怕自己心裡也覺得十分可笑吧！
證嚴法師說：「願有多大，力就有多大」，人生有夢，有夢最美，希望與熱誠相隨，總有一天，我必將實現心中的夢想，美夢成真，成就美麗人生吧！朋友們。
不一定要在過生日那天才能許願，當你有一個強烈的念頭，願意傾一生之力，去實現、去完成，這個時候就可以說出你的夢想，或許下你的願望。
只有努力作夢的人，才會對未來有美好的憧憬。也只有用心盼望的人，能夠享受「如願以償」的快樂。千萬不要害怕說出你的夢想，會被取笑。也不要顧慮：「萬一將來做不到，會很沒有面子！」。更不要擔心：「願望若沒有實現，多麼丟臉！」當你說出夢想、許下願望，親友們才知道要如何幫助你達成。
就算有人要說風涼話、扯後腿，他們這些心懷不軌的人，都會敗在你的決心中。別忘了，邪不勝正！只要你的決心夠堅定，只要你的付出夠盡力，所有的阻礙終將節節敗退。而你，最後一定會贏得夢想、實現願望。
保羅‧柯賀這位來自拉丁美洲的暢銷書作家，在他的作品「牧羊少年奇幻之旅〈原名：鍊金術士〉」一書中提到：「沒有一顆心會因為追求夢想而受傷。」、「當你真心渴望某樣東西時，整個宇宙都會聯合起來幫助你完成！」
我一直很喜歡伸手摘星，雖不一定能夠次次如願以償；但至少不會弄髒你的手！」這句座右銘。這至理名言，是通往夢想、實現願望途中，最有力道的心靈補給。
「對那麼好的成果，想都不敢想！」這話聽來若入不是謙虛，就是很沒有志氣。缺乏夢想、沒有願望的人生，真的很沒有意思。我不能說這樣的人生一定是黑白，但絕對沒有太豐富的色彩。你怎能指望一個對未來沒有任何期待的人，活得多麼精采？
實現願望，像在孵蛋。破殼而出之後，還會生生不息。
天下最可惜的是－只會作「白日夢」的人。光會用腦袋想、只用嘴巴說，對自己夢想的內容沒有信心，對實現願望的努力也做得很少。這種人的夢想或願望，講出來的時候，別說聽見的人會笑他，恐怕自己心裡也覺得十分可笑吧！
證嚴法師說：「願有多大，力就有多大」，人生有夢，有夢最美，希望與熱誠相隨，總有一天，我必將實現心中的夢想，美夢成真，成就美麗人生吧！朋友們。
巫石吉﹕永遠有顆熱誠的心
拿破崙．希爾指出，若你能保持一顆熱誠之心，那是會給你帶來奇跡的。
一個濃霧之夜，當拿破崙．希爾和他母親從紐澤西乘船渡江到紐約的時候，母親歡叫道：「這是個多麼令人驚心動魄的情景啊！」
「有甚麼出奇的事情呢？」拿破崙．希爾問道。
母親依舊充滿熱情，「你看呀，那濃霧，那四周若隱若現的光，還有消失在霧中的船帶走了令人迷惑的燈光，那麼令人不可思議。」
或許是被母親的熱情所感染，拿破崙．希爾也著實感受到厚厚的白色中那種隱藏著的神秘，虛無及點上的迷惑。拿破崙．希爾那顆遲鈍的心得到一些新鮮血液的滲透，不再是沒有感覺的了。
母親注視著拿破崙．希爾，「我從沒有放棄過對你的忠告。無論以前的忠告你接受不接受，但這一刻的忠告你一定要聽，而且要永遠牢記。那就是：世界從來就有美麗和興奮的存在，她本身就是如此動人，令人神往，所以，你自己必須要對她敏感，永遠不要讓自己的感覺遲鈍，嗅覺不靈，永遠不要讓自己失去那份應有的熱情。」
一個人若只有一點點熱誠是遠不夠的，所以增強熱心是必須的。
那麼，怎樣才能增強熱誠呢？
（一）深入瞭解每個問題
多年來，拿破崙．希爾對於現代畫沒有一點好感。當經過一個內行的朋友開導以後，拿破崙．希爾才恍然大悟：「說實在的，有進一步的瞭解以後，他才發現它真的那麼有趣，那麼吸引人。」
（二）做事要充滿熱誠
你熱心不熱心或有沒有興趣，都會很自然地在你的行為上表現出來，沒有辦法隱瞞。
（三）培養「你很重要」的態度
每一個人，無論他在印度或在美國中西部或印地安那，無論他默默無聞還是身份顯赫，文明或野蠻，年輕或年老，都有成為重要人物的願望。這種願望是人類最強烈、最迫切的一種目標。
（四）強迫自己採取熱誠的行動
深入發掘你的題目，研究它、學習它、和它生活在一起，儘量搜集有關它的資料。這樣做下去就會不知不覺地使你變得更為熱忱。
（五）身體健康是產生熱誠的基礎
一個人如果行動充滿活力，他的精神和情感也會充滿了活力。
（六）說些鼓舞的話
拿破崙．希爾說得好，在做任何事前，來段精彩講話，以鼓舞自己，將會大有收益。
我在一篇文章中提到過：「優秀是一種習慣」，那是一種對於自己充分自信的熱誠，有了優秀的想法，才有可能產生更大的熱誠為你所用，進而有更大的能量去面對更大的挑戰。
麥克阿瑟將軍年輕時就有一種高貴的想法，決不受命運環境的安排，一定要能左右這個世界的熱誠與勇氣，果然，他不僅左右第二次世界大戰，如果不是當時美國杜魯門總統的阻撓，他還想趁勝追擊，把中國的共產黨整個徹底剷平呢！(
一個濃霧之夜，當拿破崙．希爾和他母親從紐澤西乘船渡江到紐約的時候，母親歡叫道：「這是個多麼令人驚心動魄的情景啊！」
「有甚麼出奇的事情呢？」拿破崙．希爾問道。
母親依舊充滿熱情，「你看呀，那濃霧，那四周若隱若現的光，還有消失在霧中的船帶走了令人迷惑的燈光，那麼令人不可思議。」
或許是被母親的熱情所感染，拿破崙．希爾也著實感受到厚厚的白色中那種隱藏著的神秘，虛無及點上的迷惑。拿破崙．希爾那顆遲鈍的心得到一些新鮮血液的滲透，不再是沒有感覺的了。
母親注視著拿破崙．希爾，「我從沒有放棄過對你的忠告。無論以前的忠告你接受不接受，但這一刻的忠告你一定要聽，而且要永遠牢記。那就是：世界從來就有美麗和興奮的存在，她本身就是如此動人，令人神往，所以，你自己必須要對她敏感，永遠不要讓自己的感覺遲鈍，嗅覺不靈，永遠不要讓自己失去那份應有的熱情。」
一個人若只有一點點熱誠是遠不夠的，所以增強熱心是必須的。
那麼，怎樣才能增強熱誠呢？
（一）深入瞭解每個問題
多年來，拿破崙．希爾對於現代畫沒有一點好感。當經過一個內行的朋友開導以後，拿破崙．希爾才恍然大悟：「說實在的，有進一步的瞭解以後，他才發現它真的那麼有趣，那麼吸引人。」
（二）做事要充滿熱誠
你熱心不熱心或有沒有興趣，都會很自然地在你的行為上表現出來，沒有辦法隱瞞。
（三）培養「你很重要」的態度
每一個人，無論他在印度或在美國中西部或印地安那，無論他默默無聞還是身份顯赫，文明或野蠻，年輕或年老，都有成為重要人物的願望。這種願望是人類最強烈、最迫切的一種目標。
（四）強迫自己採取熱誠的行動
深入發掘你的題目，研究它、學習它、和它生活在一起，儘量搜集有關它的資料。這樣做下去就會不知不覺地使你變得更為熱忱。
（五）身體健康是產生熱誠的基礎
一個人如果行動充滿活力，他的精神和情感也會充滿了活力。
（六）說些鼓舞的話
拿破崙．希爾說得好，在做任何事前，來段精彩講話，以鼓舞自己，將會大有收益。
我在一篇文章中提到過：「優秀是一種習慣」，那是一種對於自己充分自信的熱誠，有了優秀的想法，才有可能產生更大的熱誠為你所用，進而有更大的能量去面對更大的挑戰。
麥克阿瑟將軍年輕時就有一種高貴的想法，決不受命運環境的安排，一定要能左右這個世界的熱誠與勇氣，果然，他不僅左右第二次世界大戰，如果不是當時美國杜魯門總統的阻撓，他還想趁勝追擊，把中國的共產黨整個徹底剷平呢！(
巫石吉﹕逼自己成功
因為研究書法的關係，對於中國文字的來龍去脈有較多的認識，前些時候練習寫小篆，翻閱許慎的說文解字，意外的有了一些靈感與寫書的內容有關，便把這段想法述說出來：
有關「一口田」旁邊有神的保佑，是「福」至心靈的「福」字。
至於「一口田」上面加個屋頂，表示有房有田，是大「富」由天的「富」字。
但是「一口田」長了腳，要你行動，要你進取，去得到生活上的經濟需求，那就是富貴「逼」人的「逼」字。
上班的人，禮拜一早上不想去，還得去，因為生活逼。
唸書的學生，每天放學不想做功課，還得做，因為師長逼。
一個在家不入廚房的人，留學在外，居然燒得一手好菜，因為環境逼。
一個登山者，跳過一條他平常絕不敢跳的深溝，因為有隻野獸逼。
所幸世界上有「逼」這件事，我們才能超越自己，完成超人才做得到的事。而所謂的成功，是個「相對值」而非「絕對值」。你可以與昨天的自己比較，與一個月前的自己比較，與一年前的自己比較，但不管如何比較，出於自動自發、心甘情願才是朝成功路邁進的真實動力。
記得很小的時候，每天放學回家，家人總是問，「今天老師教了什麼呀？」
隨著年紀增長，這些話語越來越少聽到，現在的你，每天都會問自己「今天新學了些什麼東西嗎？」
哥倫布是憑著「信心」才發現新大陸，而不是憑著「航海圖」呀！我們也是一樣，必須有信心，才能夠做出一番事業，因為，「自信心，是一切成就的起點！」所以，許多棒球專家都同意──「得分總在二出局之後才開始！」只要不放棄信念與希望，再努力試試看，相信就一定會有峰迴路轉、起死回生的契機！
「再多一點努力，就多一點成功！」
聽過「百分之一百二十哲學」嗎？就是「百分百的努力」之後，還要加上「百分之二十的勉強」！只要付出更多，回收自然會更大！所以：
失敗的人──什麼都不做：
一般的人──只做這一點；
成功的人──多做一點點；
頂尖的人──再多做一點！
逼自己進步，只有超越自己，才有可能超越別人，老子說：「勝人者有力，自勝者強。」「勉力務之必有喜。」可見成功不全然是自動自發的想法，遇到困難，遇到挫折，學那些成功的人，多做一點點；向頂尖的人看齊，再多做一點！逼自己克服困難，堅忍圖強，這何嘗不是逼自己解決人生的問題，邁向成功之道！(
有關「一口田」旁邊有神的保佑，是「福」至心靈的「福」字。
至於「一口田」上面加個屋頂，表示有房有田，是大「富」由天的「富」字。
但是「一口田」長了腳，要你行動，要你進取，去得到生活上的經濟需求，那就是富貴「逼」人的「逼」字。
上班的人，禮拜一早上不想去，還得去，因為生活逼。
唸書的學生，每天放學不想做功課，還得做，因為師長逼。
一個在家不入廚房的人，留學在外，居然燒得一手好菜，因為環境逼。
一個登山者，跳過一條他平常絕不敢跳的深溝，因為有隻野獸逼。
所幸世界上有「逼」這件事，我們才能超越自己，完成超人才做得到的事。而所謂的成功，是個「相對值」而非「絕對值」。你可以與昨天的自己比較，與一個月前的自己比較，與一年前的自己比較，但不管如何比較，出於自動自發、心甘情願才是朝成功路邁進的真實動力。
記得很小的時候，每天放學回家，家人總是問，「今天老師教了什麼呀？」
隨著年紀增長，這些話語越來越少聽到，現在的你，每天都會問自己「今天新學了些什麼東西嗎？」
哥倫布是憑著「信心」才發現新大陸，而不是憑著「航海圖」呀！我們也是一樣，必須有信心，才能夠做出一番事業，因為，「自信心，是一切成就的起點！」所以，許多棒球專家都同意──「得分總在二出局之後才開始！」只要不放棄信念與希望，再努力試試看，相信就一定會有峰迴路轉、起死回生的契機！
「再多一點努力，就多一點成功！」
聽過「百分之一百二十哲學」嗎？就是「百分百的努力」之後，還要加上「百分之二十的勉強」！只要付出更多，回收自然會更大！所以：
失敗的人──什麼都不做：
一般的人──只做這一點；
成功的人──多做一點點；
頂尖的人──再多做一點！
逼自己進步，只有超越自己，才有可能超越別人，老子說：「勝人者有力，自勝者強。」「勉力務之必有喜。」可見成功不全然是自動自發的想法，遇到困難，遇到挫折，學那些成功的人，多做一點點；向頂尖的人看齊，再多做一點！逼自己克服困難，堅忍圖強，這何嘗不是逼自己解決人生的問題，邁向成功之道！(
巫石吉：自信心的培養法
你心裡想什麼，就會成為什麼。在大部分的時間裡，你會成為你所想像的你。征服畏懼、建立自信的最切實的方法，就是去做你害怕的事，直到獲得成功的經驗。建立自信的方法包括：
一、約束自己務必忍耐、等待、絶不灰心，告訴自己「我擁有創造優秀人生的能力！」
二、確信不久的將來，願望一定能實現，所以請每日花三十分鐘確實描繪自己成功後的面目。
三、信任自我暗示的偉大力量，所以請每日花十分鐘集中精神作自我暗示。有首詩十足表現出了自我暗示的卓越功能：
你想你會輸，你便會輸
你想你已無救，你便無救
你想你也許不會勝利，你便不會勝利
你想你將失敗，你便失敗
看看這個社會吧！成功永遠屬於將願望堅持到底的人
「心」決定一切，信願行。
你想你必勝利，你便勝利
你想奮發，你想向上，你便成為奮發向上的人
努力吧，重新起來！
強有力的人不一定勝利，敏覺、靈活的人也不一定成功
堅信「我能夠！」勝利便非你莫屬！
四、將自己的「目標」明確地寫在紙上，而後一步步秉持信心向前邁進。
五、利他無障礙，，因此禁絶自己建立利己性目標。任何成功都是因於眾人之力，所以首先便須為大眾著想。「成功不可建築在別人的痛苦上」，應有體貼之心，利他之心，利學生之心。每日大聲誦讀這些「誓言」，告訴自己：「我的信心很堅固，我必成功！」
六、向優秀的成功者學習經驗。
優秀的成功者都有一種氣味，全身上下充滿熱誠，活力充沛，相信擁有極佳的未來，只要妳願意累積好過人的學問與實力，往自己的興趣努力發揮，請教優秀的成功者成為妳的老師，隨時請益經驗與自己所走的方向正不正確，這樣才能擁有更大的想像空間。
七、將注意力集中在以下六個重要的成分：
（一）、身體安全：身體完全不受傷害的自由。
（二）、情緒安全感：沒有脅迫及恐懼。
（三）、個人識別：問「我是誰？」這個心靈feeling。
（四）、聯盟關係：一種歸屬感與向心力的feeling。
（五）、競爭力：感覺有能力與信心去面對未來挑戰的feeling。
（六）、使命感：感覺個人的生命有意義和目標，讓自己心靈儘量昇華到靈魂層次，如此，妳才有更大的宇宙能量為你所用。@(
一、約束自己務必忍耐、等待、絶不灰心，告訴自己「我擁有創造優秀人生的能力！」
二、確信不久的將來，願望一定能實現，所以請每日花三十分鐘確實描繪自己成功後的面目。
三、信任自我暗示的偉大力量，所以請每日花十分鐘集中精神作自我暗示。有首詩十足表現出了自我暗示的卓越功能：
你想你會輸，你便會輸
你想你已無救，你便無救
你想你也許不會勝利，你便不會勝利
你想你將失敗，你便失敗
看看這個社會吧！成功永遠屬於將願望堅持到底的人
「心」決定一切，信願行。
你想你必勝利，你便勝利
你想奮發，你想向上，你便成為奮發向上的人
努力吧，重新起來！
強有力的人不一定勝利，敏覺、靈活的人也不一定成功
堅信「我能夠！」勝利便非你莫屬！
四、將自己的「目標」明確地寫在紙上，而後一步步秉持信心向前邁進。
五、利他無障礙，，因此禁絶自己建立利己性目標。任何成功都是因於眾人之力，所以首先便須為大眾著想。「成功不可建築在別人的痛苦上」，應有體貼之心，利他之心，利學生之心。每日大聲誦讀這些「誓言」，告訴自己：「我的信心很堅固，我必成功！」
六、向優秀的成功者學習經驗。
優秀的成功者都有一種氣味，全身上下充滿熱誠，活力充沛，相信擁有極佳的未來，只要妳願意累積好過人的學問與實力，往自己的興趣努力發揮，請教優秀的成功者成為妳的老師，隨時請益經驗與自己所走的方向正不正確，這樣才能擁有更大的想像空間。
七、將注意力集中在以下六個重要的成分：
（一）、身體安全：身體完全不受傷害的自由。
（二）、情緒安全感：沒有脅迫及恐懼。
（三）、個人識別：問「我是誰？」這個心靈feeling。
（四）、聯盟關係：一種歸屬感與向心力的feeling。
（五）、競爭力：感覺有能力與信心去面對未來挑戰的feeling。
（六）、使命感：感覺個人的生命有意義和目標，讓自己心靈儘量昇華到靈魂層次，如此，妳才有更大的宇宙能量為你所用。@(
Sunday, October 25, 2009
如何保持积极的心态
01 记住，你的心态是你——而且只有你——惟一能完全掌 握的东西，练习控制你的心态，并且利用积极心态来导引它。
02 切断和你过去失败经验的所有关系，消除你脑海中和积极心态背道而驰的所有不良因素。
03 找出你一生中最希望得到的东西，并立即着手去得到它， 借着帮助他人得到同样好处的方法，去追寻你的目标，如此一来，你便可将多付出一点点的原则，应用到实际行动之中。
04 确定你需要的资源之后，便订定得到这些资源的计划，然而所订的计划必须不要太过度，也不要太不足，别认为自己要求得太少，记住：贪婪是使野心家失败的最主要因素。
05 培养每天说或做一些使他人感到舒服的话或事，你可以利用电话、明信片，或一些简单的善意动作达到此一目的。例如给他人一本励志的书，就是为他带来一些可使他的生命充满奇迹的东西。日行一善，可永远保持无忧无虑的心情。
06 使你自己了解打倒你的不是挫折，而是你面对挫折时所 抱的心态，训练自己在每一次不如意中，都能发现和挫折等值 积极面。
07 务必使自己养成精益求精的习惯，并以你的爱心和热情发挥你的这项习惯，如果能使这种习惯变成一种嗜好那是最好不过的了。如果不能的话，至少你应记住：懒散的心态，很快就会变成消极心态。
08 当你找不到解决问题的答案时，不妨帮助他人解决他的 问题，并从中找寻你所需要的答案。在你帮助他人解决问题的同时，你也正在洞察解放自己问题的方法。
09 每周阅读一次爱默生的“报酬随笔”，直到你能领悟其中 的道理为止。这本著作可使你确信，能从积极心态获得好处。彻底地“盘点”一次你的财产，你会发现你所拥有的最有价值舶财产就是健全的思想，有了它你就可以自己决定自己 的命运。和你曾经以不合理态度冒犯过的人联络，并向他致上最诚挚的歉意，这项任务愈困难，你就愈能在完成道歉时，摆脱调心的消极心态。
10 我们在这个世界上到底能占有多少空间，是和我们为他人利益所提供之服务的质与量，以及提供服务时所产生出的心态，成正比例的关系。
11 改掉你的坏习惯，连续一个月每天禁绝一项恶习，并在一周结束时反省一下成果。如果你需要顾问或帮助时，切勿让你的自尊心使你怯步。
12 要知道自怜是独立精神的毁灭者，请相信你自己才是惟 一可以随时依靠的人。
13 把你一生当中所发生的所有事件，都看作是激励你上进而发生的事件，因为只要你能给时间圆润你烦恼的机会的话， 即使是最悲伤的经验，也会为你带来最多的财产。
14 放弃想要控制别人的念头，在这个念头摧毁你之前先摧毁它，把你的精力转而用来控制你自己。把你的全部思想用来做你想做的事，而不要留半点思维空间给那些胡思乱想的念头。
15 借着在每天的祈祷中，加入感谢你己拥有的生活来调整你的思想，以使它为你带来你想要的东西和想处的环境。
16 向每天的生活索取合理的回报，而不要光等着回报跑到你的手中，你会因为得到许多你所希望的东西而感到惊讶——虽然你可能一直都没有察觉到。
17 以适合你生理和心理的方式生活，别浪费时间以免落于他人之后。
18 除非有人愿意以足够证据，证明他的建议具有一定的可靠性，否则别接受任何人的建议，你将会因谨慎而避免被误导，或被当成傻瓜。
19 务必了解人的力量并非全然来自物质而已。甘地领导他的人民争取自由所依靠的并非财富。 使自己多多活动以保持自己的健康状态，生理上的疾病很容易造成心理的失调，你身体应和你的思想一样保持活动，以维持积极的行动。增加自己的耐性，并以开阔的心胸包容所有事物，同时也应与不同种族和不同信仰的人多接触，学习接受他人的本性， 而不要一味地要求他人照着你的意思行事。
20 你应承认，“爱”是你生理和心理疾病的最佳药物，爱会改 变并且调适你体内的化学元素，以使它们有助于你表现出积 极心态，爱也会扩展你的包容力。接受爱的最好方法就是付出你自己的爱。
21 以相同或更多的价值回报给你好处的人。“报酬增加律” 最后还会给你带来好处，而且可能会为你带来所有你应得到 的东西的能力。
22 记住，当你付出之后，必然会得到等价或更高价的东西。抱着这种念头，可使你驱除对年老的恐惧。一个最好的例子 就是，年轻消逝，但换来的却是智慧。
23 你要相信你可以为所有的问题找到适当的解决方法，但 也要注意你所找到的解决方法，未必都是你想要的解决方法。参考别人的例子，提醒自己任何不利清况，都是可以克服的。虽然爱迪生只接受过三个月的正规教育，但他却是最伟大的发明家。虽然海伦·凯勒失去了视觉、听觉和说话能力， 但她却鼓舞了数万人。明确目标的力量必然胜过任何限制。对于善意的批评应采取接受的态度，而不应采取消极的 反应，接受学习他人如何看待你的机会，利用这种机会做一番反省，并找出应该改善的地方，别害怕批评，你应勇敢地 面对它。
24 和其他献身于成功原则的人组成智囊团，讨论你们的进 程，并从更宽广的经验中获取好处，务必以积极面作为基础进 行讨论。
25 分清楚愿望(Wishing)、希望(Hoping)、欲望(Desiring)以及强烈欲望(a burning Desire)与达到目标之间的差别，其中只有强烈的欲望会给你驱动力，而且只有积极心态才能供给产生驱动力所需的燃料。
26 避免任何具有负面意义的说话型态，尤其应根除吹毛求疵、闲言闲语或中伤他人名誉的行为，这些行为会使你的思想 朝向消极面发展。锻炼你的思想，使它能够导引你的命运朝着你希望的方向发展，把握住“报酬”信封里的每一项利益，并将它们据 为已有。随时随地都应表现出真实的自己，没有人会相信骗子的。相信无穷智慧的存在，它会使你产生为掌握思想和导引思想而奋斗所需要的所有力量。
27 相信你所拥有的解放自己并使自己具备自决意识的能力，并借着这种信心作为行事基础将它应用到工作上，现在就开始做!相信美国式的政府，可保证你为了追求明确目标所需要的自由和权利，必要时你应采取行动保护你的自由。信任和你共事的人，并承认如果和你共事的人不值得你 信任时，就表示你选错人了。
28 最后连续6个月每周阅读本章一次。6个月之后你将会 脱胎换骨。当你学会本章所要求的良好习惯并且调适好你的 思想之后，你的心态便会随时处于积极状态
02 切断和你过去失败经验的所有关系，消除你脑海中和积极心态背道而驰的所有不良因素。
03 找出你一生中最希望得到的东西，并立即着手去得到它， 借着帮助他人得到同样好处的方法，去追寻你的目标，如此一来，你便可将多付出一点点的原则，应用到实际行动之中。
04 确定你需要的资源之后，便订定得到这些资源的计划，然而所订的计划必须不要太过度，也不要太不足，别认为自己要求得太少，记住：贪婪是使野心家失败的最主要因素。
05 培养每天说或做一些使他人感到舒服的话或事，你可以利用电话、明信片，或一些简单的善意动作达到此一目的。例如给他人一本励志的书，就是为他带来一些可使他的生命充满奇迹的东西。日行一善，可永远保持无忧无虑的心情。
06 使你自己了解打倒你的不是挫折，而是你面对挫折时所 抱的心态，训练自己在每一次不如意中，都能发现和挫折等值 积极面。
07 务必使自己养成精益求精的习惯，并以你的爱心和热情发挥你的这项习惯，如果能使这种习惯变成一种嗜好那是最好不过的了。如果不能的话，至少你应记住：懒散的心态，很快就会变成消极心态。
08 当你找不到解决问题的答案时，不妨帮助他人解决他的 问题，并从中找寻你所需要的答案。在你帮助他人解决问题的同时，你也正在洞察解放自己问题的方法。
09 每周阅读一次爱默生的“报酬随笔”，直到你能领悟其中 的道理为止。这本著作可使你确信，能从积极心态获得好处。彻底地“盘点”一次你的财产，你会发现你所拥有的最有价值舶财产就是健全的思想，有了它你就可以自己决定自己 的命运。和你曾经以不合理态度冒犯过的人联络，并向他致上最诚挚的歉意，这项任务愈困难，你就愈能在完成道歉时，摆脱调心的消极心态。
10 我们在这个世界上到底能占有多少空间，是和我们为他人利益所提供之服务的质与量，以及提供服务时所产生出的心态，成正比例的关系。
11 改掉你的坏习惯，连续一个月每天禁绝一项恶习，并在一周结束时反省一下成果。如果你需要顾问或帮助时，切勿让你的自尊心使你怯步。
12 要知道自怜是独立精神的毁灭者，请相信你自己才是惟 一可以随时依靠的人。
13 把你一生当中所发生的所有事件，都看作是激励你上进而发生的事件，因为只要你能给时间圆润你烦恼的机会的话， 即使是最悲伤的经验，也会为你带来最多的财产。
14 放弃想要控制别人的念头，在这个念头摧毁你之前先摧毁它，把你的精力转而用来控制你自己。把你的全部思想用来做你想做的事，而不要留半点思维空间给那些胡思乱想的念头。
15 借着在每天的祈祷中，加入感谢你己拥有的生活来调整你的思想，以使它为你带来你想要的东西和想处的环境。
16 向每天的生活索取合理的回报，而不要光等着回报跑到你的手中，你会因为得到许多你所希望的东西而感到惊讶——虽然你可能一直都没有察觉到。
17 以适合你生理和心理的方式生活，别浪费时间以免落于他人之后。
18 除非有人愿意以足够证据，证明他的建议具有一定的可靠性，否则别接受任何人的建议，你将会因谨慎而避免被误导，或被当成傻瓜。
19 务必了解人的力量并非全然来自物质而已。甘地领导他的人民争取自由所依靠的并非财富。 使自己多多活动以保持自己的健康状态，生理上的疾病很容易造成心理的失调，你身体应和你的思想一样保持活动，以维持积极的行动。增加自己的耐性，并以开阔的心胸包容所有事物，同时也应与不同种族和不同信仰的人多接触，学习接受他人的本性， 而不要一味地要求他人照着你的意思行事。
20 你应承认，“爱”是你生理和心理疾病的最佳药物，爱会改 变并且调适你体内的化学元素，以使它们有助于你表现出积 极心态，爱也会扩展你的包容力。接受爱的最好方法就是付出你自己的爱。
21 以相同或更多的价值回报给你好处的人。“报酬增加律” 最后还会给你带来好处，而且可能会为你带来所有你应得到 的东西的能力。
22 记住，当你付出之后，必然会得到等价或更高价的东西。抱着这种念头，可使你驱除对年老的恐惧。一个最好的例子 就是，年轻消逝，但换来的却是智慧。
23 你要相信你可以为所有的问题找到适当的解决方法，但 也要注意你所找到的解决方法，未必都是你想要的解决方法。参考别人的例子，提醒自己任何不利清况，都是可以克服的。虽然爱迪生只接受过三个月的正规教育，但他却是最伟大的发明家。虽然海伦·凯勒失去了视觉、听觉和说话能力， 但她却鼓舞了数万人。明确目标的力量必然胜过任何限制。对于善意的批评应采取接受的态度，而不应采取消极的 反应，接受学习他人如何看待你的机会，利用这种机会做一番反省，并找出应该改善的地方，别害怕批评，你应勇敢地 面对它。
24 和其他献身于成功原则的人组成智囊团，讨论你们的进 程，并从更宽广的经验中获取好处，务必以积极面作为基础进 行讨论。
25 分清楚愿望(Wishing)、希望(Hoping)、欲望(Desiring)以及强烈欲望(a burning Desire)与达到目标之间的差别，其中只有强烈的欲望会给你驱动力，而且只有积极心态才能供给产生驱动力所需的燃料。
26 避免任何具有负面意义的说话型态，尤其应根除吹毛求疵、闲言闲语或中伤他人名誉的行为，这些行为会使你的思想 朝向消极面发展。锻炼你的思想，使它能够导引你的命运朝着你希望的方向发展，把握住“报酬”信封里的每一项利益，并将它们据 为已有。随时随地都应表现出真实的自己，没有人会相信骗子的。相信无穷智慧的存在，它会使你产生为掌握思想和导引思想而奋斗所需要的所有力量。
27 相信你所拥有的解放自己并使自己具备自决意识的能力，并借着这种信心作为行事基础将它应用到工作上，现在就开始做!相信美国式的政府，可保证你为了追求明确目标所需要的自由和权利，必要时你应采取行动保护你的自由。信任和你共事的人，并承认如果和你共事的人不值得你 信任时，就表示你选错人了。
28 最后连续6个月每周阅读本章一次。6个月之后你将会 脱胎换骨。当你学会本章所要求的良好习惯并且调适好你的 思想之后，你的心态便会随时处于积极状态
如何预防和调整自卑心理
1)童年教育：
自卑感是幼小时在家庭里就开始形成的，所以幼年期的教育非常重要。做父母的不应对子女寄以超过其实际可能的期望值，要客观地观察并承认子女的天赋条件。要着重培养其实际能力，因材施教，并设法让他感到心里踏实。成才需要坚定的毅力，应帮助孩子培养起良好的心理品格。
(2)化不利为有利：
自卑感既会使人羞怯退缩，也能使人奋发进取。某种意义上，自卑感是走向成功的踏板。发现它，承认它的存在，并设法弥补它，从而达到人生的目标。
(3)系列摆脱法：
若是自己不能胜任的事，不要立即强制去做，而是先从较容易人手、获得自信后，再做较为复杂的事，以便一步一步地实现目标。这叫做系列摆脱法。
(4)共鸣性理解：
对怀有自卑感的人，应摆脱孤立无援、独自苦恼的状态，将自己的困惑向周围人诉说，帮助分忧解愁，体谅、理解其苦恼心情，争取周围人及家属的“共鸣性理解”，对消除自卑感具有良好作用。
(5)行为矫正法：
要针对自己的弱点制订一个逐步训练的计划，并坚持不懈地执行。如争取在集会上发言，主动接触陌生人；可以预先拟就话题，演练对话，提高语言技巧及社交手段。也可观察一下周围的人，发觉别人也不像自己所认为的那样十全十美，对自己又并无歧视之意，也就不再“自惭形秽”了。
(6)集体心理治疗：
对于自卑感的克服，一般心理治疗中的说理开导、分析评价、讲授对策、鼓励劝慰等，都是用得上的。心理治疗时还把有同样经历的人组织成集体小组，相互慰藉，共同探讨，鼓励进取，消除自卑。对个人单独难以克服的自卑者，参加这类有组织的自助小组，开展自救心理治疗会有更多裨益。
(7)伴同心理障碍的治疗：
若有明显的焦虑、抑郁、失眠及自主神经功能失调，当求医辅用适当药物同时治疗。当自卑感伴同神经衰弱、抑郁症、心身疾病等时，最好短期住院治疗。
自卑感是幼小时在家庭里就开始形成的，所以幼年期的教育非常重要。做父母的不应对子女寄以超过其实际可能的期望值，要客观地观察并承认子女的天赋条件。要着重培养其实际能力，因材施教，并设法让他感到心里踏实。成才需要坚定的毅力，应帮助孩子培养起良好的心理品格。
(2)化不利为有利：
自卑感既会使人羞怯退缩，也能使人奋发进取。某种意义上，自卑感是走向成功的踏板。发现它，承认它的存在，并设法弥补它，从而达到人生的目标。
(3)系列摆脱法：
若是自己不能胜任的事，不要立即强制去做，而是先从较容易人手、获得自信后，再做较为复杂的事，以便一步一步地实现目标。这叫做系列摆脱法。
(4)共鸣性理解：
对怀有自卑感的人，应摆脱孤立无援、独自苦恼的状态，将自己的困惑向周围人诉说，帮助分忧解愁，体谅、理解其苦恼心情，争取周围人及家属的“共鸣性理解”，对消除自卑感具有良好作用。
(5)行为矫正法：
要针对自己的弱点制订一个逐步训练的计划，并坚持不懈地执行。如争取在集会上发言，主动接触陌生人；可以预先拟就话题，演练对话，提高语言技巧及社交手段。也可观察一下周围的人，发觉别人也不像自己所认为的那样十全十美，对自己又并无歧视之意，也就不再“自惭形秽”了。
(6)集体心理治疗：
对于自卑感的克服，一般心理治疗中的说理开导、分析评价、讲授对策、鼓励劝慰等，都是用得上的。心理治疗时还把有同样经历的人组织成集体小组，相互慰藉，共同探讨，鼓励进取，消除自卑。对个人单独难以克服的自卑者，参加这类有组织的自助小组，开展自救心理治疗会有更多裨益。
(7)伴同心理障碍的治疗：
若有明显的焦虑、抑郁、失眠及自主神经功能失调，当求医辅用适当药物同时治疗。当自卑感伴同神经衰弱、抑郁症、心身疾病等时，最好短期住院治疗。
自信心的培养
自信，就是对自己能够达到某种目标的乐观、充分估计。美国作家爱默生说：“自信是成功的第一秘诀。”可以说，拥有自信就拥有无限机会。那么如何增强自信呢？
增强自信的第一个方法：关注自己的优点。在纸上列下十个优点，不论是哪方面（细心、眼睛好看等等，多多益善），在从事各种活动时，想想这些优点，并告诉自己有什么优点。这样有助你提升从事这些活动的自信，这叫做“自信的蔓延效应”。这一效应对提升自信效果很好。
增强自信的第二个方法：与自信的人多接触。“近朱者赤，近墨者黑”这一点对增强自信同样有效。
增强自信的第三个方法：自我心理暗示，不断对自己进行正面心理强化，避免对自己进行负面强化。一旦自己有所进步（不论多小）就对自己说：“我能行！”、“我很棒！”、“我能做得更好！”等等，这将不断提升自己的信心。
增强自信的第四个方法：树立自信的外部形象。首先，保持整洁、得体的仪表，有利于增强一个人的自信；其次，举止自信，如行路目视前方等，刚开始可能不习惯，但过一段时间后就会有发自内心的自信；另外，注意锻炼、保持健美的体形对增强自信也很有帮助。
增强自信的第五个方法：.不可谦虚过度。谦虚是必要的，但不可过度，过分贬低自己对自信心的培养是极为不利的。
增强自信的第六个方法：学会微笑。微笑会增加幸福感，进而增强自信。
增强自信的第七个方法：扬长避短。在学习、生活、工作中，抓住机会展现自己的优势、特长，同时注意弥补自己的不足，不断进步，肯定能增强自信。
增强自信的第八个方法：阅读名人传记，因为很多知名人士成名前的自身资质、外部环境并不好，如果多看一些这方面的材料有助于提升自信心。
增强自信的第九个方法：做好充分准备。从事某项活动前如果能做好充分准备，那么，在从事这项活动时，必然较为自信，而且这利于顺利完成活动并增强整体自信心。
增强自信的第十个方法：给自己定恰当的目标，并且在目标达成后，定更高的目标。目标不能太高，否则不易达到，如果达不到，对自信心会有所破坏。
增强自信的第十一个方法：冒一次险。当你做了以前不敢做的事以后，你会发现：原来作这事并没有什么了不起！这对提升自信心很有帮助。
增强自信的第十二个方法：排除压力。过重的压力会使自己意志消沉，对自身产生怀疑，从而破坏自信心，学会排除压力对保持原有自信帮助很大。
增强自信的第十三个方法：做自己喜欢做的事。对自己喜欢做的事，因为比较投入，容易取得成功，继而产生成就感，这非常有利于自信心的提高。
增强自信的第十四个方法：保持健康。注意全面的营养、保证身体锻炼、保持快乐的心境，良好的生理、心理状况会使自己产生幸福感，进而产生自信心。
增强自信的第十五个方法：尽量依靠自己。有事尽量依靠自己解决，能不断激发自身的潜力，并且通过一次次的成功，不断提升自信水平。
自信是成功的第一要诀，有志于成才、成功的人请培养你的自信
增强自信的第一个方法：关注自己的优点。在纸上列下十个优点，不论是哪方面（细心、眼睛好看等等，多多益善），在从事各种活动时，想想这些优点，并告诉自己有什么优点。这样有助你提升从事这些活动的自信，这叫做“自信的蔓延效应”。这一效应对提升自信效果很好。
增强自信的第二个方法：与自信的人多接触。“近朱者赤，近墨者黑”这一点对增强自信同样有效。
增强自信的第三个方法：自我心理暗示，不断对自己进行正面心理强化，避免对自己进行负面强化。一旦自己有所进步（不论多小）就对自己说：“我能行！”、“我很棒！”、“我能做得更好！”等等，这将不断提升自己的信心。
增强自信的第四个方法：树立自信的外部形象。首先，保持整洁、得体的仪表，有利于增强一个人的自信；其次，举止自信，如行路目视前方等，刚开始可能不习惯，但过一段时间后就会有发自内心的自信；另外，注意锻炼、保持健美的体形对增强自信也很有帮助。
增强自信的第五个方法：.不可谦虚过度。谦虚是必要的，但不可过度，过分贬低自己对自信心的培养是极为不利的。
增强自信的第六个方法：学会微笑。微笑会增加幸福感，进而增强自信。
增强自信的第七个方法：扬长避短。在学习、生活、工作中，抓住机会展现自己的优势、特长，同时注意弥补自己的不足，不断进步，肯定能增强自信。
增强自信的第八个方法：阅读名人传记，因为很多知名人士成名前的自身资质、外部环境并不好，如果多看一些这方面的材料有助于提升自信心。
增强自信的第九个方法：做好充分准备。从事某项活动前如果能做好充分准备，那么，在从事这项活动时，必然较为自信，而且这利于顺利完成活动并增强整体自信心。
增强自信的第十个方法：给自己定恰当的目标，并且在目标达成后，定更高的目标。目标不能太高，否则不易达到，如果达不到，对自信心会有所破坏。
增强自信的第十一个方法：冒一次险。当你做了以前不敢做的事以后，你会发现：原来作这事并没有什么了不起！这对提升自信心很有帮助。
增强自信的第十二个方法：排除压力。过重的压力会使自己意志消沉，对自身产生怀疑，从而破坏自信心，学会排除压力对保持原有自信帮助很大。
增强自信的第十三个方法：做自己喜欢做的事。对自己喜欢做的事，因为比较投入，容易取得成功，继而产生成就感，这非常有利于自信心的提高。
增强自信的第十四个方法：保持健康。注意全面的营养、保证身体锻炼、保持快乐的心境，良好的生理、心理状况会使自己产生幸福感，进而产生自信心。
增强自信的第十五个方法：尽量依靠自己。有事尽量依靠自己解决，能不断激发自身的潜力，并且通过一次次的成功，不断提升自信水平。
自信是成功的第一要诀，有志于成才、成功的人请培养你的自信
怎样培养自信心
有一位名人说过：大人物与小人物的区别在于有没有意志力和自信心，只要具备了意志力和自信心，除了违反法律的事以外，世界上没有事能难倒你。
你在上数理化的课时，心里总是害怕，害怕什么呢？担心学不好，考试成绩不理想对不对？我觉得你最重要的是缺乏自信心。现在，你有必要克服上课时心里害怕的精神状态。
增 强自信心。缺乏自信心的人出现紧张的频率最高，你若自信心不强，做事情一定是唯唯诺诺，瞻前顾后甚至摇摆不定，没有准确的主意，也要果断的作决定，不要遇 事慌乱手足无措。要相信自己，不断鼓励自己“我行，我一定行，我会成功，我会做得比别人更优秀！”这样，你就会精神抖擞，从容不迫地应对考试和其他事情。 信心是学生的灵魂，信心也是学生考试成功的精神支柱。
自信心，是对自己的完全相信，但不是盲目相信，是对自己明确的认识和把握。相信自己，是因为自己做不到的事别人也一定做不到。
记得电影《英雄本色》中有一句台词是这样的“连你自己都没有信心，别人怎么去帮你。”很平常但很精彩。
美国著名心理学家基恩，小时候亲历过一件让他终生难忘的事，正是这件事使得基恩从自卑走向了自信，也正是这种自信，使他一步步走向成功。
有一次，他躲在公园的角落里偷偷看到几个白人小孩在快乐的玩儿，他羡慕他们，也很想与他们一道游戏，但他不敢，因为自己是一个黑人小孩，心里很自卑。
这时，一位卖气球的老人举着一大把气球进了公园，白人孩子一窝蜂地跑了过去，每人买了一个，高高兴兴地把气球放飞到空中去。
白人小孩走了以后，他才胆怯地走到老人面前，低声请求：“你可以卖一个气球给我吗？”老人慈祥地说：“当然。你要一个什么颜色的？” 他鼓起勇气说：“我要一个黑色的。”老人给了他一个黑色的气球。他接过气球，小手一松，黑气球慢慢地升上了天空……
老人一边眯着眼睛看着气球上升，一边用轻轻拍着他的后脑勺，说：“记住，气球能不能升起来，不是因为颜色，形状，而是气球内充满了氢气。一个人的成败不是因为种族和出身，关键是你内心有没有自信。”
可见自信心是一种多么重要的物质。
而 自信心的养成，除了外在环境的影响，更主要在于你是否养成了自我肯定的习惯。自我肯定，从心理学范围来说，主要途径就是“自我暗示”，每当你一件事，或说 一段话，无论事之大小，话之长短，“这件事我做得很好，”“这席话我说得很得体”，长期保持这种习惯，有一天你会发现，自己已能自信面对人生了。
另外一点，意志力也是需要加强锻炼和培养的。如果仅仅是因为学习成绩不太理想，心灰意冷，则是一种不明智的表现。意志力，不是爆发力，是一种韧性，无坚不摧的往往正是这种看似绵薄但后劲十足的持久力。
老 师上课时给我们讲过一个这样的故事：在一人自行车拍卖会上，每辆自行车都被一个小男孩儿以五法郎第一个喊价，却从不加价。拍卖师忍不住停下来问他，小男孩 儿说，他仅仅只有五法郎。拍卖会如常进行，小男孩儿总是第一个报价，但很快就被高于五法郎的价被别人买走。这样到了最后一辆车的时候，大家都似乎有些紧张 起来，这一辆比任何一辆都好。这时，小男孩儿更是以急切的声音报价五法郎，这次，再也没有人加价，问过几遍，拍卖师一槌定音，小男孩儿激动地用已捏出汗的 钱换来这辆车。而作为小男孩儿只有五法郎，他要得到自行车，惟一的办法就是以一种意志坚持，以一种耐心，再付出虔诚的努力……同样，学习仍然需要一种意志 力，着急是没有用的！
人的意志力和自信心，就像鸟的两个翅膀，自行车的两个车轮，只有在这两个方面不断强化自己，才能够飞翔，自由行驶。
怎样提升自信
找出自己美好的一面，走出自己的方格，这里有几项具体方法可供参考：
1.发现自己的优点。花一个钟头去发掘自己的优点，然后逐点用笔记下来。优点可分数类，如：个人专长所在，已做过什么有益有建设性的事，过去什么人如何称赞过自己，家人朋友对自己的关怀，受过的教育等等，你一定会发现自己许多优点，从而知道自己原来还不差。
2.找出榜样人物。在认识或不认识的人中，找一个你最羡慕、最敬仰，希望自己可以成为他（她）那样的人做你的人生楷模。这人是司马迁？居里夫人？还是姨 妈？不管是谁，他们一定有什么模仿之处，他们也一定用过功，受过挫折，付出代价，那么目前自己的一时失败，又算得了什么呢？
3.肯定自己的能力。每天找出3件自己做成功的事。不要把“成功”看成登上月球那么大的事，成功可以是顺利跟医生约了治疗时间，上班交通一路畅顺，处理的 文件档案没出一次错等等，日常生活工作都可以有“成功”与“挫折”之分，一日至少顺利地做了3件事，又怎能说“一事无成”、“一无是处”呢？知道能把事情 做好，等于对自己的能力的肯定，你可振作精神。
4.计算已做妥的事。计算自己做妥的事而不是检讨自己还有多少件事没有做。人还 没做的事永远多过已做妥的事，如果老想着这个没做，那个没做，便会愈想愈沮丧，真的会觉得自己能力低，无效率，大为失意。但已做妥的工作并列出来，可是长 长的一张单子啊，能力还真的高呢，能这样想，立刻便自信心大增，不会萎靡。
5.培养某方面兴趣。在自己的优点、专长、兴趣中， 找一样（刚刚开始时，一样就够了）来加以特别培养、发展，使之成为自己的专长。虽然还不是专家，但在小圈子中，一提到某件事，大家都公认非你莫属了，专长 不必太困难如弹钢琴，气功治病那么高深莫测，可以简单至做蛋糕、剪头发、游泳、看星星、记电影的中英文名称……什么都可以，有了专长，就有机会做主角，做 主角，自然神采飞扬！
6.发挥自己的外在美。发挥自己的外在美，即所谓人靠衣装。衣，固然指衣着，也指打扮，可以不必名牌，但一定 要不落伍、清洁、光鲜、明亮、顺眼，要做到这样，必须穿得出众、大方。尤其在自知情绪低落时，更要穿得鲜艳明丽些，还得加上化妆及新剪的头发，这样不但自 己的坏心情会因打扮而分散了注意力，表情也生动活泼些。
你在上数理化的课时，心里总是害怕，害怕什么呢？担心学不好，考试成绩不理想对不对？我觉得你最重要的是缺乏自信心。现在，你有必要克服上课时心里害怕的精神状态。
增 强自信心。缺乏自信心的人出现紧张的频率最高，你若自信心不强，做事情一定是唯唯诺诺，瞻前顾后甚至摇摆不定，没有准确的主意，也要果断的作决定，不要遇 事慌乱手足无措。要相信自己，不断鼓励自己“我行，我一定行，我会成功，我会做得比别人更优秀！”这样，你就会精神抖擞，从容不迫地应对考试和其他事情。 信心是学生的灵魂，信心也是学生考试成功的精神支柱。
自信心，是对自己的完全相信，但不是盲目相信，是对自己明确的认识和把握。相信自己，是因为自己做不到的事别人也一定做不到。
记得电影《英雄本色》中有一句台词是这样的“连你自己都没有信心，别人怎么去帮你。”很平常但很精彩。
美国著名心理学家基恩，小时候亲历过一件让他终生难忘的事，正是这件事使得基恩从自卑走向了自信，也正是这种自信，使他一步步走向成功。
有一次，他躲在公园的角落里偷偷看到几个白人小孩在快乐的玩儿，他羡慕他们，也很想与他们一道游戏，但他不敢，因为自己是一个黑人小孩，心里很自卑。
这时，一位卖气球的老人举着一大把气球进了公园，白人孩子一窝蜂地跑了过去，每人买了一个，高高兴兴地把气球放飞到空中去。
白人小孩走了以后，他才胆怯地走到老人面前，低声请求：“你可以卖一个气球给我吗？”老人慈祥地说：“当然。你要一个什么颜色的？” 他鼓起勇气说：“我要一个黑色的。”老人给了他一个黑色的气球。他接过气球，小手一松，黑气球慢慢地升上了天空……
老人一边眯着眼睛看着气球上升，一边用轻轻拍着他的后脑勺，说：“记住，气球能不能升起来，不是因为颜色，形状，而是气球内充满了氢气。一个人的成败不是因为种族和出身，关键是你内心有没有自信。”
可见自信心是一种多么重要的物质。
而 自信心的养成，除了外在环境的影响，更主要在于你是否养成了自我肯定的习惯。自我肯定，从心理学范围来说，主要途径就是“自我暗示”，每当你一件事，或说 一段话，无论事之大小，话之长短，“这件事我做得很好，”“这席话我说得很得体”，长期保持这种习惯，有一天你会发现，自己已能自信面对人生了。
另外一点，意志力也是需要加强锻炼和培养的。如果仅仅是因为学习成绩不太理想，心灰意冷，则是一种不明智的表现。意志力，不是爆发力，是一种韧性，无坚不摧的往往正是这种看似绵薄但后劲十足的持久力。
老 师上课时给我们讲过一个这样的故事：在一人自行车拍卖会上，每辆自行车都被一个小男孩儿以五法郎第一个喊价，却从不加价。拍卖师忍不住停下来问他，小男孩 儿说，他仅仅只有五法郎。拍卖会如常进行，小男孩儿总是第一个报价，但很快就被高于五法郎的价被别人买走。这样到了最后一辆车的时候，大家都似乎有些紧张 起来，这一辆比任何一辆都好。这时，小男孩儿更是以急切的声音报价五法郎，这次，再也没有人加价，问过几遍，拍卖师一槌定音，小男孩儿激动地用已捏出汗的 钱换来这辆车。而作为小男孩儿只有五法郎，他要得到自行车，惟一的办法就是以一种意志坚持，以一种耐心，再付出虔诚的努力……同样，学习仍然需要一种意志 力，着急是没有用的！
人的意志力和自信心，就像鸟的两个翅膀，自行车的两个车轮，只有在这两个方面不断强化自己，才能够飞翔，自由行驶。
怎样提升自信
找出自己美好的一面，走出自己的方格，这里有几项具体方法可供参考：
1.发现自己的优点。花一个钟头去发掘自己的优点，然后逐点用笔记下来。优点可分数类，如：个人专长所在，已做过什么有益有建设性的事，过去什么人如何称赞过自己，家人朋友对自己的关怀，受过的教育等等，你一定会发现自己许多优点，从而知道自己原来还不差。
2.找出榜样人物。在认识或不认识的人中，找一个你最羡慕、最敬仰，希望自己可以成为他（她）那样的人做你的人生楷模。这人是司马迁？居里夫人？还是姨 妈？不管是谁，他们一定有什么模仿之处，他们也一定用过功，受过挫折，付出代价，那么目前自己的一时失败，又算得了什么呢？
3.肯定自己的能力。每天找出3件自己做成功的事。不要把“成功”看成登上月球那么大的事，成功可以是顺利跟医生约了治疗时间，上班交通一路畅顺，处理的 文件档案没出一次错等等，日常生活工作都可以有“成功”与“挫折”之分，一日至少顺利地做了3件事，又怎能说“一事无成”、“一无是处”呢？知道能把事情 做好，等于对自己的能力的肯定，你可振作精神。
4.计算已做妥的事。计算自己做妥的事而不是检讨自己还有多少件事没有做。人还 没做的事永远多过已做妥的事，如果老想着这个没做，那个没做，便会愈想愈沮丧，真的会觉得自己能力低，无效率，大为失意。但已做妥的工作并列出来，可是长 长的一张单子啊，能力还真的高呢，能这样想，立刻便自信心大增，不会萎靡。
5.培养某方面兴趣。在自己的优点、专长、兴趣中， 找一样（刚刚开始时，一样就够了）来加以特别培养、发展，使之成为自己的专长。虽然还不是专家，但在小圈子中，一提到某件事，大家都公认非你莫属了，专长 不必太困难如弹钢琴，气功治病那么高深莫测，可以简单至做蛋糕、剪头发、游泳、看星星、记电影的中英文名称……什么都可以，有了专长，就有机会做主角，做 主角，自然神采飞扬！
6.发挥自己的外在美。发挥自己的外在美，即所谓人靠衣装。衣，固然指衣着，也指打扮，可以不必名牌，但一定 要不落伍、清洁、光鲜、明亮、顺眼，要做到这样，必须穿得出众、大方。尤其在自知情绪低落时，更要穿得鲜艳明丽些，还得加上化妆及新剪的头发，这样不但自 己的坏心情会因打扮而分散了注意力，表情也生动活泼些。
自信心的培养
你是否充分相信自己？是否具备从事任何活动的信心？这关系到你是否能适应社会，能否走向成功。对人影响最大的心理缺陷是不自信，社会越向前发展，缺乏自信的人就越不适应。你对自己 的自信水平是否了解，对下面的问题你是否同意，如果你的否定答案超过5个，说明你的自信度低， 易于嫉妒他人。
成就不是我的主要目标
对我来说，做一个谦和宽厚的胜利者与取胜同样重要。
我的成就是不言自明的。
他人的成功不会诋毁我的成功。
我所做的工作本身孕含着价值，我并不是为了奖赏而工作。
我有自己独特的、其他任何人不具备的优点。
失败不能影响我的真正价值。
我对自己的评价不受别人的观点左右。
我相信我有应付困难的能力。
我很少对自己有消极的想法。
我正在尽可能地充分利用我的才干与能力。
自信心的分析
自信心是相信自己成功，成才的心理素质，是对自身能力的科学估价。自信才能有主见，才能做出他人未做之事。 缺乏自信心，就会产成心理上的自我鄙视、自我否定、自我挫败。因此说自信是人生的关键。每个青年都应强化自信，受挫不气馁，失败不灰心，顺利不自负。适应社会，努力奋斗，实现自身价值。
经过前面的努力，自信的种子终于萌芽，但要破土而出还有一道难关要突破害羞。害羞与自信是息息相关的。
因为，如果一个人从来就没有失败过，那么他基本上是自信的，不害羞的。但是，人多少会遇到挫折，都会有失败的时候，而失败和挫折使人无法达到要求，人就会害羞。由此可见自信与害羞之间是此长彼消的关系，自信多一点害羞就少一点，反过来，自信少一点害羞就多一点。
在现实生活中我们也可以发现这样有趣的一个现象：自信的人几乎不害羞，害羞的人往往不自信。因此克服害羞对培养自信十分重要。
那么该如何克服害羞呢？可以试试以下几种方法：
1、 永远不要无缘无故把自己说得一无是处。也许你有做错事的时候，例如说错话，但这并不表示你是笨拙的，也许你有缺点，如小眼睛，但也没必要感觉自己目光短浅、丑陋。
2、了解自己的优点和缺点。找些小卡片，把它们分成两种颜色：一种代表优点，另一种代表缺点，每张卡片写一个优点或缺点。然后检验一下哪个优点还没发挥，怎么去发挥这个优点；哪个缺点是你可以不在乎且可以忽略的，把这些可以忽略的、不在乎的缺点丢掉。这样做你就不会过分保护自己；然后你会发现自己的优点比缺点多。这样做能使你集中发挥自己的优点，克服自己的缺点。
3、试着坐在人群的中心位置。害羞的人常喜欢舵在角落，免得引人注目。因为这样也就没有人注意到自己，因而证实了“没人关心自己”的想法。改掉这个习惯，让别人有机会注意你、关心你。
4、有话大声说。害羞的人说话都很小声，不妨把你的音调提高，你就会更加相信自己有权说话。
5、别人跟你讲话时，眼睛要看着对方，害羞的人常常忘了这一点。当然不必瞪着对方，但至少要让对方知道你是在倾听。
6、别人没有应答你的话时，要再重复一遍。不要替自己找理由说是别人对你的话不感兴趣。
7、别人打断你的话时，要继续把话说完。我们讲话时常会被打断，而害羞的人有时还会用动作来造成别人打断他的话，就好象那正是自己所期望的事。有时对方插话也表示他对你说的话很感兴趣，所以下次不要把中断谈话当作借口而逃处人群。
其实就这么简单正确看待自己，大声说话，看着对方，让别人注意自己……就象改变其它行为一样，刚开始时总觉得不好意思，觉得还是回到老样子舒服些。
这时你不妨先将一切担心往好的方面想，最重要的是不要在乎那些害怕心理，慢慢地就会发现自己变成了另外一个人。一般人总认为是有了勇气才去行动，恰恰相反，对害羞的人来说是有了行动才会有勇气。
因此，心动不如行动，只要去做，你就会变得越来越自信。
成就不是我的主要目标
对我来说，做一个谦和宽厚的胜利者与取胜同样重要。
我的成就是不言自明的。
他人的成功不会诋毁我的成功。
我所做的工作本身孕含着价值，我并不是为了奖赏而工作。
我有自己独特的、其他任何人不具备的优点。
失败不能影响我的真正价值。
我对自己的评价不受别人的观点左右。
我相信我有应付困难的能力。
我很少对自己有消极的想法。
我正在尽可能地充分利用我的才干与能力。
自信心的分析
自信心是相信自己成功，成才的心理素质，是对自身能力的科学估价。自信才能有主见，才能做出他人未做之事。 缺乏自信心，就会产成心理上的自我鄙视、自我否定、自我挫败。因此说自信是人生的关键。每个青年都应强化自信，受挫不气馁，失败不灰心，顺利不自负。适应社会，努力奋斗，实现自身价值。
经过前面的努力，自信的种子终于萌芽，但要破土而出还有一道难关要突破害羞。害羞与自信是息息相关的。
因为，如果一个人从来就没有失败过，那么他基本上是自信的，不害羞的。但是，人多少会遇到挫折，都会有失败的时候，而失败和挫折使人无法达到要求，人就会害羞。由此可见自信与害羞之间是此长彼消的关系，自信多一点害羞就少一点，反过来，自信少一点害羞就多一点。
在现实生活中我们也可以发现这样有趣的一个现象：自信的人几乎不害羞，害羞的人往往不自信。因此克服害羞对培养自信十分重要。
那么该如何克服害羞呢？可以试试以下几种方法：
1、 永远不要无缘无故把自己说得一无是处。也许你有做错事的时候，例如说错话，但这并不表示你是笨拙的，也许你有缺点，如小眼睛，但也没必要感觉自己目光短浅、丑陋。
2、了解自己的优点和缺点。找些小卡片，把它们分成两种颜色：一种代表优点，另一种代表缺点，每张卡片写一个优点或缺点。然后检验一下哪个优点还没发挥，怎么去发挥这个优点；哪个缺点是你可以不在乎且可以忽略的，把这些可以忽略的、不在乎的缺点丢掉。这样做你就不会过分保护自己；然后你会发现自己的优点比缺点多。这样做能使你集中发挥自己的优点，克服自己的缺点。
3、试着坐在人群的中心位置。害羞的人常喜欢舵在角落，免得引人注目。因为这样也就没有人注意到自己，因而证实了“没人关心自己”的想法。改掉这个习惯，让别人有机会注意你、关心你。
4、有话大声说。害羞的人说话都很小声，不妨把你的音调提高，你就会更加相信自己有权说话。
5、别人跟你讲话时，眼睛要看着对方，害羞的人常常忘了这一点。当然不必瞪着对方，但至少要让对方知道你是在倾听。
6、别人没有应答你的话时，要再重复一遍。不要替自己找理由说是别人对你的话不感兴趣。
7、别人打断你的话时，要继续把话说完。我们讲话时常会被打断，而害羞的人有时还会用动作来造成别人打断他的话，就好象那正是自己所期望的事。有时对方插话也表示他对你说的话很感兴趣，所以下次不要把中断谈话当作借口而逃处人群。
其实就这么简单正确看待自己，大声说话，看着对方，让别人注意自己……就象改变其它行为一样，刚开始时总觉得不好意思，觉得还是回到老样子舒服些。
这时你不妨先将一切担心往好的方面想，最重要的是不要在乎那些害怕心理，慢慢地就会发现自己变成了另外一个人。一般人总认为是有了勇气才去行动，恰恰相反，对害羞的人来说是有了行动才会有勇气。
因此，心动不如行动，只要去做，你就会变得越来越自信。
为啥坏同学都成了老板？
一次回老家与几位小学同学相聚，“忆往昔”之后，聊起了其他人现在的情况。谢老大自己办工厂，资产几百万元；大王二当包工头，在县城买了几套房；杨拐子从卖盒饭起家，如今在城里盘下两家大酒店；小王二靠跑运输起家，发展到拥有60多台大小车辆的运输公司。大家纷纷感慨：想当年，他们还抄我们的试卷，如今却个个都当老板。而我们这些当初成绩优异的好学生，多半拿着死工资，境遇一般。
为什么坏同学都当了老板？仔细琢磨了一阵子，我逐渐瞧出了点儿门道。
一是成绩差、调皮捣蛋的同学从小被批评惯了，练就了一副“刀枪不入”的厚脸皮。你的话越难听，他越是赔笑脸。和气生财，于是生意兴隆。那些学习成绩好、听话乖巧的同学，从小听惯了肯定赞扬，偶尔听到一句批评，恨不得找条地缝钻进去。你要他放下架子低三下四地去求人，还不如杀了他。有这个才能吗？
二是成绩差、调皮捣蛋的同学，由于经常惹祸，免不了受皮肉之苦。天长日久，能吃常人不能忍受之苦。就拿杨拐子来说，十几岁就跑到县城帮人卖盒饭，天不亮就起床，凌晨才休息。甘甜磨砺苦中来，终于发展到拥有两家大酒店的大老板。反观成绩好、听话乖巧的同学，从小被老师和家长捧着惯着，连体育课都不愿到操场去出身汗，就甭说让他去干这种掉皮掉肉的活儿了。
三是不怕挫折。从小就经历考试的失利，挫折对于他们来说就如同韭菜一样，割了长，长了割，已经感觉不到痛苦。拿大王二来说，最初学做泥瓦匠，靠卖苦力挣到一笔钱后开始当包工头，但第一笔买卖就赔了十几万元。大王二不气馁，借了几十万元继续干，终于东山再起。反观成绩好的同学，总想睡在成功簿上享受胜利的喜悦，偶遇挫折就快速爬上救生艇。
四是冒险精神，虽然每次恶作剧被发现后，都要受到严惩，但他们总也放不下那份快乐。因此，在每办一件事之前，他们想的是怎样获得快乐，而不是计算风险有多大。而成绩好、听话乖巧的同学，从小到大，生活轨迹都被老师和家长设计好了。哪怕你给他一个发财的机会，他也会想“贷了那么多款，万一失败了怎么办？”
五是为人仗义，敢“为朋友两肋插刀”。记得那年谢老大带我和小王二蹿进小桥边一户人家院里，将一树枇杷摘了个精光，结果被主人追到学校。面对主人和老师的“拷问”，谢老大将责任全揽到自己身上。最后，我和小王二免受了惩罚，当时我感激得眼泪都出来了。试想，员工一时不慎犯了错，老板能站在对方的立场考虑，为其减压，谁还不感恩戴德拼死效劳？而反观学习成绩好、听话乖巧的同学，从小到大，唯恐自己沾惹是非，这样的人如果当老板，只会天天与员工为敌，搞得员工人人自危，谁还有心思去工作？一旦企业遇到一点儿挫折或困难，员工便会卷铺盖走人。
为什么坏同学都当了老板？仔细琢磨了一阵子，我逐渐瞧出了点儿门道。
一是成绩差、调皮捣蛋的同学从小被批评惯了，练就了一副“刀枪不入”的厚脸皮。你的话越难听，他越是赔笑脸。和气生财，于是生意兴隆。那些学习成绩好、听话乖巧的同学，从小听惯了肯定赞扬，偶尔听到一句批评，恨不得找条地缝钻进去。你要他放下架子低三下四地去求人，还不如杀了他。有这个才能吗？
二是成绩差、调皮捣蛋的同学，由于经常惹祸，免不了受皮肉之苦。天长日久，能吃常人不能忍受之苦。就拿杨拐子来说，十几岁就跑到县城帮人卖盒饭，天不亮就起床，凌晨才休息。甘甜磨砺苦中来，终于发展到拥有两家大酒店的大老板。反观成绩好、听话乖巧的同学，从小被老师和家长捧着惯着，连体育课都不愿到操场去出身汗，就甭说让他去干这种掉皮掉肉的活儿了。
三是不怕挫折。从小就经历考试的失利，挫折对于他们来说就如同韭菜一样，割了长，长了割，已经感觉不到痛苦。拿大王二来说，最初学做泥瓦匠，靠卖苦力挣到一笔钱后开始当包工头，但第一笔买卖就赔了十几万元。大王二不气馁，借了几十万元继续干，终于东山再起。反观成绩好的同学，总想睡在成功簿上享受胜利的喜悦，偶遇挫折就快速爬上救生艇。
四是冒险精神，虽然每次恶作剧被发现后，都要受到严惩，但他们总也放不下那份快乐。因此，在每办一件事之前，他们想的是怎样获得快乐，而不是计算风险有多大。而成绩好、听话乖巧的同学，从小到大，生活轨迹都被老师和家长设计好了。哪怕你给他一个发财的机会，他也会想“贷了那么多款，万一失败了怎么办？”
五是为人仗义，敢“为朋友两肋插刀”。记得那年谢老大带我和小王二蹿进小桥边一户人家院里，将一树枇杷摘了个精光，结果被主人追到学校。面对主人和老师的“拷问”，谢老大将责任全揽到自己身上。最后，我和小王二免受了惩罚，当时我感激得眼泪都出来了。试想，员工一时不慎犯了错，老板能站在对方的立场考虑，为其减压，谁还不感恩戴德拼死效劳？而反观学习成绩好、听话乖巧的同学，从小到大，唯恐自己沾惹是非，这样的人如果当老板，只会天天与员工为敌，搞得员工人人自危，谁还有心思去工作？一旦企业遇到一点儿挫折或困难，员工便会卷铺盖走人。
Thursday, October 22, 2009
糸山英太郎是日本富豪
糸山英太郎愛錢、賺錢，翻滾股市、笑傲錢海的六十年傳奇
糸山英太郎是何許人也？
根據《富比士》雜誌的調查和報導，糸山英太郎是日本近二十年來唯一連續名列「世界富豪排行榜」前一百名左右的大亨，目前身價高達4,150億日圓，無任何負債。
糸山是日本大富翁佐佐木真太郎之子，佐佐木真太郎曾在西元一九六九年拿下全日本年所得第一名。糸山少年時身體孱弱，飽受欺負。「我一定要好好用功！」成績優異的糸山充滿鬥志，決心一路從貴族私立高中，到日本頂尖學府東京大學，好讓那些欺負他的人瞧瞧！
但是，當糸山在日本保守的一九六○年代，發覺母親並非父親明媒正取的妻子、自己是私生子時，產生了強烈的自卑感和憤世嫉俗的心理，於是放浪形骸、自甘墮落，打架、勒索、販賣色情照片，成為警察局的常客。最後，父親放棄他、母親離家出走，二十歲的系山走到人生的谷底，一貧如洗。
為了生活，糸山販賣中古高級進口車，開始發揮驚人的生意長才，一年內賣掉七十七輛車，為公司賺進四千萬日圓（現值數億日圓）。然而，在自立門戶之後，花錢如流水的糸山因週轉不靈，為了三十五萬日圓向父親低頭，賣身給父親，含淚從高爾夫球場桿弟重新做起。
這是一個機會！糸山憑著優異的才能，讓父親的新日本觀光集團突破重重瓶頸和困難，事業蒸蒸日上。之後，他甚至奪下了同父異母的兄長之位，登上集團經營者的寶座。同時，糸山還在股市嶄露頭角，於中山製鋼一役擊敗日本股市第一名手近藤幸夫，並且強攻乾汽船、單挑讀賣新聞，迫使業界大亨不支求和。後來，在三井礦山、大同氧氣、神戶電鐵等一連串的炒作戰中，他也大獲全勝，因而聲名大噪！
另外，糸山還投身政治界，三十二歲當選為日本最年輕的參議員，並且擔任過農林水產政務次長、自民黨副幹事長、參議員、國會外務委員會委員長等職務。「玩政治家比完藝妓更有趣！」糸山之父佐佐木真太郎曾如此說道。糸山從二十多歲就開始接觸政治人物，在政治界三十年，散財一百億，再加上善於經營與投資，三十歲即擁有數十億日圓的資產，四十歲便坐擁數百億日圓，不但絲毫不比他父親遜色，甚至可謂是政壇與商界中呼風喚雨的人物。
五十歲之後，糸山淡出政壇，專心經營事業、浸淫股海，身價高達數千億日圓。現年六十一歲的糸山，不僅是新日本觀光集團的老闆、湘南工科大學理事長兼校長，而且是新日鐵、野村證券的大股東，以及JAL日本航空的最大個人股東（擁有六千萬股以上）、三菱重工的最大個人股東。
二十年來，糸山獲得了「日本的巴菲特」、「稀世投資家」等美譽。他不碰自己不懂的股票，堅持逆勢操作的投資信念，精確掌握投資進出的時間，以過人的膽識和自信，讓他的資產安然度過網路科技泡沫化的股災，在全球一片不景氣聲中，仍然年年持續成長。此外，在事業經營方面，糸山也有他獨到之處，不但細心體察顧客的需求，而且大膽採取雙贏或三贏的同業或異業合作方式、不按牌理出牌的行銷策略，總是成果豐碩，令人拍案叫絕！
現今，糸山除了繼續在經營與投資上努力不懈之外，還決心把財富回饋社會，在非洲和亞洲設立醫院、成立援助基金與獎學金、設置「糸山經營塾」來培養「糸山學校」的企業家。
此外，糸山透過《賺錢哲學》一書，坦誠揭露他在金錢、股票、政治及黑白兩道中打滾的精采人生經驗，甚至毫無保留地公開他的致富訣竅，如「糸山賺錢法」、「糸山投資術」「糸山用錢法」等，讓大眾一覽他成功的祕密。
「賺錢有什麼錯？」「經營權是奪取的、不是讓與的！」「誰惹惱糸山，就收購誰的股票！」「營業員和技術線型絕不可信！」「不要和窮人交往。」糸山就是這樣一位充滿爭議的傳奇人物。
想要了解糸山英太郎，獲得他賺錢法則的真髓，就千萬不能錯過難得一見的《賺錢哲學》！
糸山英太郎是何許人也？
根據《富比士》雜誌的調查和報導，糸山英太郎是日本近二十年來唯一連續名列「世界富豪排行榜」前一百名左右的大亨，目前身價高達4,150億日圓，無任何負債。
糸山是日本大富翁佐佐木真太郎之子，佐佐木真太郎曾在西元一九六九年拿下全日本年所得第一名。糸山少年時身體孱弱，飽受欺負。「我一定要好好用功！」成績優異的糸山充滿鬥志，決心一路從貴族私立高中，到日本頂尖學府東京大學，好讓那些欺負他的人瞧瞧！
但是，當糸山在日本保守的一九六○年代，發覺母親並非父親明媒正取的妻子、自己是私生子時，產生了強烈的自卑感和憤世嫉俗的心理，於是放浪形骸、自甘墮落，打架、勒索、販賣色情照片，成為警察局的常客。最後，父親放棄他、母親離家出走，二十歲的系山走到人生的谷底，一貧如洗。
為了生活，糸山販賣中古高級進口車，開始發揮驚人的生意長才，一年內賣掉七十七輛車，為公司賺進四千萬日圓（現值數億日圓）。然而，在自立門戶之後，花錢如流水的糸山因週轉不靈，為了三十五萬日圓向父親低頭，賣身給父親，含淚從高爾夫球場桿弟重新做起。
這是一個機會！糸山憑著優異的才能，讓父親的新日本觀光集團突破重重瓶頸和困難，事業蒸蒸日上。之後，他甚至奪下了同父異母的兄長之位，登上集團經營者的寶座。同時，糸山還在股市嶄露頭角，於中山製鋼一役擊敗日本股市第一名手近藤幸夫，並且強攻乾汽船、單挑讀賣新聞，迫使業界大亨不支求和。後來，在三井礦山、大同氧氣、神戶電鐵等一連串的炒作戰中，他也大獲全勝，因而聲名大噪！
另外，糸山還投身政治界，三十二歲當選為日本最年輕的參議員，並且擔任過農林水產政務次長、自民黨副幹事長、參議員、國會外務委員會委員長等職務。「玩政治家比完藝妓更有趣！」糸山之父佐佐木真太郎曾如此說道。糸山從二十多歲就開始接觸政治人物，在政治界三十年，散財一百億，再加上善於經營與投資，三十歲即擁有數十億日圓的資產，四十歲便坐擁數百億日圓，不但絲毫不比他父親遜色，甚至可謂是政壇與商界中呼風喚雨的人物。
五十歲之後，糸山淡出政壇，專心經營事業、浸淫股海，身價高達數千億日圓。現年六十一歲的糸山，不僅是新日本觀光集團的老闆、湘南工科大學理事長兼校長，而且是新日鐵、野村證券的大股東，以及JAL日本航空的最大個人股東（擁有六千萬股以上）、三菱重工的最大個人股東。
二十年來，糸山獲得了「日本的巴菲特」、「稀世投資家」等美譽。他不碰自己不懂的股票，堅持逆勢操作的投資信念，精確掌握投資進出的時間，以過人的膽識和自信，讓他的資產安然度過網路科技泡沫化的股災，在全球一片不景氣聲中，仍然年年持續成長。此外，在事業經營方面，糸山也有他獨到之處，不但細心體察顧客的需求，而且大膽採取雙贏或三贏的同業或異業合作方式、不按牌理出牌的行銷策略，總是成果豐碩，令人拍案叫絕！
現今，糸山除了繼續在經營與投資上努力不懈之外，還決心把財富回饋社會，在非洲和亞洲設立醫院、成立援助基金與獎學金、設置「糸山經營塾」來培養「糸山學校」的企業家。
此外，糸山透過《賺錢哲學》一書，坦誠揭露他在金錢、股票、政治及黑白兩道中打滾的精采人生經驗，甚至毫無保留地公開他的致富訣竅，如「糸山賺錢法」、「糸山投資術」「糸山用錢法」等，讓大眾一覽他成功的祕密。
「賺錢有什麼錯？」「經營權是奪取的、不是讓與的！」「誰惹惱糸山，就收購誰的股票！」「營業員和技術線型絕不可信！」「不要和窮人交往。」糸山就是這樣一位充滿爭議的傳奇人物。
想要了解糸山英太郎，獲得他賺錢法則的真髓，就千萬不能錯過難得一見的《賺錢哲學》！
别和穷人交往 日本富豪的投资哲学
系山英太郎，毕业于日本大学经济系，年轻时创下日本进口车销售纪录，在股票市场上也收获甚丰，被誉为“日本巴菲特”。他在30岁即拥有几十亿资产，经营18家公司，是日本航空最大股东，三菱重工最大个人股东，更是惟一连续10年登上《福布斯》“全球亿万富翁排行榜”的日本人。他在32岁投身政治，曾任前首相中曾根康弘秘书，1996年，他退出政坛，返回商界。
作为一位传奇式的日本富豪，系山先生的成功背后是其独到的投资理念和强烈的个性特征。
首先，系山认为社会所有动态都关系到投资活动，因此，他对资讯的关注到了偏执的地步，在任何情况下，都积极观察和掌握资讯。
比较极端的一个例子是他曾在2001年和2002年两度公开表示别和穷人交往，因为与穷人交往无法获得有价值的信息。与“没有钱的穷人”交往不仅会陷入老是自掏腰包的境地，而且，其中的很多人也缺乏有益于人的资讯，毫无利他的价值。不过，系山也特别强调了他乐于和年轻人交流，因为他们拥有许多他所不知道的资讯，使其能在闲聊中获得不同的资讯。因此，他认为与年轻人交流的花费其实是很便宜的投资，换句话说，即使是在与别人交往时，他也在计算着投资效果。
其次，系山对股票投资非常专注。他认为操作股票就必须要付出全部的时间、体力以及耐性，特别要一心一意做股票。他投资股票30多年，坚持自己一贯的反市场操作原则，丝毫不动摇。在100个投资者有99个看到股票下跌而慌了手脚拼命抛售股票时，我坚持买进，反之，则全面抛售。
系山坚信当其倾注100%的热忱，毫无杂念，认真努力的投入到当下所做的事情时，则不论遇到什么情况，将来一定能成功，也就能顺利克服事情操作过程中的困难和不愉快。
第三，系山不仅信奉“终身学习”而且身体力行，勇于挑战新事物，愿意了解未知的世界。碰到不懂的事情，他不仅不会搁着不管，反而会拼命去寻求解答。在年龄渐长之后，他就请老师从“电脑能做什么”开始学习，3个月后就成立了自己的网络，发表个人对时事问题的看法。
综合而言，在所有这些鲜明的个性中，系山的“忍耐”最终为其成功铺平了道路。他即使身处逆境，甚至在贫困潦倒时，都相信明天会成功。当股价不断下跌遭受极为惨重的投资损失时，还坚持忍耐，不放弃斗志。
或许，系山对未来生活的设想最好的诠释了系山以前的成功。他计划在自己60岁以后的20年里，把赚来的钱投资在他认为需要的地方，或许是慈善事业，或许是其他事业，将以自己多年积累的丰富的人生阅历，及一路走来所培养的感觉和经验，全心全力用自己的方式来回馈世界。
作为一位传奇式的日本富豪，系山先生的成功背后是其独到的投资理念和强烈的个性特征。
首先，系山认为社会所有动态都关系到投资活动，因此，他对资讯的关注到了偏执的地步，在任何情况下，都积极观察和掌握资讯。
比较极端的一个例子是他曾在2001年和2002年两度公开表示别和穷人交往，因为与穷人交往无法获得有价值的信息。与“没有钱的穷人”交往不仅会陷入老是自掏腰包的境地，而且，其中的很多人也缺乏有益于人的资讯，毫无利他的价值。不过，系山也特别强调了他乐于和年轻人交流，因为他们拥有许多他所不知道的资讯，使其能在闲聊中获得不同的资讯。因此，他认为与年轻人交流的花费其实是很便宜的投资，换句话说，即使是在与别人交往时，他也在计算着投资效果。
其次，系山对股票投资非常专注。他认为操作股票就必须要付出全部的时间、体力以及耐性，特别要一心一意做股票。他投资股票30多年，坚持自己一贯的反市场操作原则，丝毫不动摇。在100个投资者有99个看到股票下跌而慌了手脚拼命抛售股票时，我坚持买进，反之，则全面抛售。
系山坚信当其倾注100%的热忱，毫无杂念，认真努力的投入到当下所做的事情时，则不论遇到什么情况，将来一定能成功，也就能顺利克服事情操作过程中的困难和不愉快。
第三，系山不仅信奉“终身学习”而且身体力行，勇于挑战新事物，愿意了解未知的世界。碰到不懂的事情，他不仅不会搁着不管，反而会拼命去寻求解答。在年龄渐长之后，他就请老师从“电脑能做什么”开始学习，3个月后就成立了自己的网络，发表个人对时事问题的看法。
综合而言，在所有这些鲜明的个性中，系山的“忍耐”最终为其成功铺平了道路。他即使身处逆境，甚至在贫困潦倒时，都相信明天会成功。当股价不断下跌遭受极为惨重的投资损失时，还坚持忍耐，不放弃斗志。
或许，系山对未来生活的设想最好的诠释了系山以前的成功。他计划在自己60岁以后的20年里，把赚来的钱投资在他认为需要的地方，或许是慈善事业，或许是其他事业，将以自己多年积累的丰富的人生阅历，及一路走来所培养的感觉和经验，全心全力用自己的方式来回馈世界。
系山英太郎
系山英太郎，一位在日本政商界呼风唤雨的显赫人物，26岁时当上了前首相中曾根的秘书；30岁即拥有了几十亿的资产；32岁成为日本历史上最年轻的参议员；1996年退回商界成为日本首富之一；他从被金钱玩弄到把金钱驯服得服服帖帖；他崇尚“利益至上交往法”，提倡“赚了钱不要挥霍”、“至死都不要被时代淘汰”、“勇于挑战新事物”、“以忍耐为重，善于使不利局面为我所用”、“拓展人脉，成为一个爱人、受人信赖的人”。2004年《福布斯》杂志全球富豪排行榜上显示，系山英太郎个人净资产49亿美元，排行第86位。他赚钱的秘诀耐人寻味……
系山英太郎，1942年6月4日生于东京，日本大学经济系毕业。年轻时创下日本进口车销售纪录，在股票市场上收获甚丰，名留日本证券史。系山英太郎被誉为“日本巴菲特”的投资大师，他白手起家，凭自己的能力得到了父亲的赏识，30岁即拥有几十亿资产，经营18家公司，是JAL（日本航空）最大股东，三菱重工最大个人股东，个人投资4150亿日元，是惟一连续10年登上《福布斯》“全球亿万富翁排行榜”的日本人，一个在日本泡沫经济和全球不景气中仍然保持财富增值的魔法资本家。此外，他32岁投身政治，成为日本历史上最年轻的参议员，曾任前首相中曾根康弘秘书，在日本政商界呼风唤雨，1996年，他退出政坛，返回商界。
系山英太郎身世可以说得上是从地狱到天堂：
他是被拒之门外的私生子，父亲曾是60年代的日本首富。
少年时期打架、勒索、贩卖黄色照片，是小流氓头目和警察局的常客。
20岁，把客户的订金挥霍一空，不得已卖身还债。
30岁，谁惹恼系山，就收购谁的股票。
40岁，没有所谓争议的竞选，决不辞去议员的职务。
50岁，证券经纪人和技术图表根本不可信。
60岁，立志散财，把智慧和财富贡献给全世界。
从富豪出生到卖身还债
其父佐佐木真太郎是1969年的日本首富。系山英太郎能成为日本大财主，凭的却是个人的才干和奋斗。其发家之道与其父相去甚远，系山英太郎是股海的大赢家，其父则靠高尔夫球场发迹，对股票嗤之以鼻。
系山英太郎最初显露商业才华，是在他当二手车推销员的时候。当时他月薪才2万日元，而一年之内他卖掉77辆车，创下该行业的最高记录，令公司获利4000多万。不过当他此后另立门户的时候，却因周转不灵而节节亏损。最后他不得不向父亲借钱。父亲拒绝了他的要求，对他说：“如果你愿意卖身给我，我可以给你35万，但今后你要对我言听计从。”系山英太郎无奈，只好成了其父麾下的一名球童。
塞翁失马，焉知非福。系山英太郎却在高尔夫这个行业里再次发挥才干。正如他所说，“将打架战术用在商业对手上”。在帮父亲开发高尔夫球场时，他针锋相对地与对手打拼，非把对手弄垮不可。在围绕日本职业高尔夫球协会会长一职的争斗上，系山英太郎与“乾汽船”的董事长乾丰彦干上了。为了吞并“乾汽船”，系山英太郎连续多日大笔购进“乾汽船”的股票，短时间内买下800万股，远远超过对方手上的250万股，迫使乾丰彦不得不上门向他求饶。
系山英太郎投资股市手法独特，从不相信操作员和曲线图，坚持逆势入市的投资理念。最典型的例子莫过于与日本股市的风云人物近藤信男的比拼上。近藤信男在大笔抛售丰田汽车等股票上令对手战栗不已，最终却败在系山英太郎这个小字辈手下。此外，系山英太郎在三井矿山、神户电铁等一连串的炒作上也大获全胜，被舆论誉为“日本的巴菲特”。
日本前首相秘书
在20岁到30岁的10年中，系山英太郎已拥有数十亿日元的资产。此后他一边继续股票投资和生意运作，一边投身从政。26岁时，他当了前首相中曾根的秘书。32岁那年，系山英太郎成为日本史上最年轻的参议员。
1983年当选众议员，先后任建设政务次官、国会对策副委员长、众议院运作委员会理事、众议院外务委员会委员长等职。1996年退出政界，回任新日本观光集团各企业社长兼会长，并任湘南工科大学校长。同时身兼三菱重工最大股东及日本航空最大股东。设立了塞席尔经济合作援助基金、斯里兰卡福祉合作援助基金、柬埔寨医院设立基金等，积极贡献国际。著有《怪物商法》《向太阳挑战》《日本青年革命》等。也是百万畅销的作家。
在政坛上，系山英太郎敢于直言。时至今天，他仍不时在其个人网页上针砭时弊。对小泉执意出兵伊拉克，系山英太郎在文章里痛陈利弊，“这场战争的正义性很值得质疑”。他指出，日美同盟虽然重要，但决不能拿国民的生命当儿戏。
如今，系山英太郎全身心投入到他钟爱的商海，他已悉数购进其父的10个高尔夫球场，成为新日本观光股份公司董事长兼社长，身价年年增长，在日本富豪中排行第三；同时，他还非常热衷教育事业，担任湘南工科理事长和上海复旦大学顾问教授等职；此外，他还推出多本畅销书，传授他的投资理念。他宣布，今后将是他回馈社会的时候。“很多人问我赚这么多钱干什么？我想，在今后的20年里，我准备将钱投资到我认为需要的地方，或许是慈善事业，或许是教育，或许是其他,或许因此还会继续赚钱，但我会凭我的知识和经验，全身心回馈社会！”
赚钱哲学
有着不凡经历的他，谈起自己的赚钱哲学时，自然有相当的哲理和独到见解之处——
独门投资术
“我投资股票30多年，一贯以反市场操作为原则。当100个投资人有99个看到股票下跌而慌了手脚，拼命抛售股票的时候，我就买进；反之，就抛出。不过，我投资股票的钱不会一次用完，而是先投资1／3或者1／2,剩下的钱留待股票下跌时摊平运用，赚到15%或者20%就脱手。 ”
“我做股票时就专心做股票，吃饭时专心在食物上，睡觉时就好好睡觉。我总是倾注100%的热忱，认真投入当下所做的事情，毫无杂念，尽力而为，剩下的就‘尽人事，听天命’。困苦悲惨的童年使我充满斗志，并立志不做游手好闲的穷光蛋，要勤奋努力誓做有钱人。因此，我不论遇到什么情况，都相信将来必然成功，不愉快的事立刻抛诸脑后。到最后，我从被金钱玩弄于股掌之上到驯服它，使它服服帖帖。 ”
“我关注社会的所有动态，因为它们都关系到我的投资活动。换句话说，只要没有特别的事情，我每天都窝在房间里，面对股票，努力赚钱。即使外出，我也积极观察和掌握资讯。操作股票，就必须付出这样的时间、体力以及耐性。我想一般人可能做不到吧。然而，若只是单单看着股票上涨就高兴，下跌就消沉是无法根据股票赚钱的。”
利益至上交往法
“我在2001年秋天和2002年春天，两度针对全日本经营者举办研习会，在研习会上，我开宗明义地表示：‘别和穷人交往。’ ”
穷人有两种。一种是字面上所指的“没有钱的穷人”，跟这种人交往，只会陷入老是自掏腰包的境地。如果想要存钱，就必须节省这种不必要的花费。想找人一起吃饭、喝酒，找比自己有钱的人作伴当然更为明智。在这个世界上，有些人喜欢身边围绕着没钱的人，享受他们的阿谀奉承。但是穷人只是向钱低头而已，不论你曾经给过他们多少好处，当你没钱时，这些人就会忘记你曾经施与的恩惠，两脚开溜而去。
人际关系本来就是施与受的关系，如果只有施当然只有损失。而另一种穷人不只是没钱，也缺乏有益于人的资讯和娱乐别人的才能，毫无利他的价值。虽然我说“别和穷人交往”，但如果哪个没钱的人有值得我们请客的价值，那么即使他再穷，我也乐意和他交往。尤其是年轻人，他们拥有许多我不知道的资讯，花钱在他们身上绝对不会浪费。我从与他们交游闲聊中得到的资讯，往往成为生意上的灵感。由此看来，为他们花钱其实是很便宜的投资。也就是说，我与别人交往时，经常在瞬间计算着投资效果。
该享受怎样的生活
“事实上我是个不花钱的人，因为我根本没有“赚钱了就要挥霍”的想法。当我打着系山的名号外出应酬时，不得不去一流的酒店，但是平时我自己吃饭，都是很随便的。当然更加没有兴趣购买什么高级名牌服饰，平时生活比较简朴。不过，我愿意在车子上花大钱，汽车之外的奢侈就是游艇。当我在股市赚到钱高兴得合不拢嘴时，我耗资30亿元买下一艘游艇，这是一艘豪华游轮的四层楼大船，我搭乘这个船环游了世界3趟，充分享受了航海的乐趣。”
制胜的法宝
“我很喜欢“终身学习”这句话，碰到不懂的事情，我不会搁着不管，反而会拼命去寻求解答。我就是通过推销外国汽车而领悟销售技巧，我通过学习，开动脑筋，利用银行达到一石三鸟的赚钱招术。虽然在我的投资生涯里百战百胜，不过每天都有10亿日元上下的资金在我的账上进出，股市的风云变幻让我亦喜亦忧，但我认为善于学习是我制胜的法宝。只要准确把握时代脉搏，即便是“无偿服务”也能够赚大钱。年龄渐长之后，我至死都不愿意被时代淘汰，3年前，我请老师从“电脑能做什么”开始教我，3个月后，我成立了自己的网络，发表我个人对时事问题的看法。我打心底认为，学会电脑真好，我的世界一下子拓展开来，收集资讯也变得轻松方便。 终身学习。从今以后，我仍要继续发动我这老迈的躯体，勇于挑战新的事物，了解未知的世界。”
赚钱的秘诀
常常有人问我：“对您来说，赚钱是什么？”
首先，以“忍耐”为重，面包和烧酒，陪伴我度过困窘到极点的20岁生日，同时也让我充分见识了金钱威力的“青春时代”。所以，即使身处逆境或贫困深渊，也要相信明天就会成功，这样才会坚韧不拔。例如，当股价不断下跌，你遭受极为惨重的损失，甚至想要自杀时，你也必须忍耐，不可放弃斗志。投资股票时，“只有一股也是股东”这一信念支撑我挑起中山制钢股票大户战。从政时，“就算你揍我、踹我，我也决不辞去议员的职务”。如果工作得不到预期的成果，我也要把痛苦当作经验而忍耐下来，相信总有一天能够雪耻报仇，从不幸中努力向上爬。而且要将计就计，善于使不利的局面为我所用。其次，“信”。这里不是指成为一个宗教家向穷人化缘讨钱，而是认识许多能够互相帮助的人，以拓展人脉。如果能够成为爱许多人，也受许多人信赖的人物，事业自然兴盛，大家都能够赚钱。
那么，赚钱的目的是什么呢？赚钱是门永无止境的学问，那些不让别人赚钱的有钱人不可原谅。光知道要钱，乱作一团的人际关系、派系关系，我30年间撒在政界的钱近百亿，我不认为有钱之后就要过奢侈的生活。忍耐，努力，认真工作，成为一个爱人、受人信赖的人，事业自然会兴盛。接下来的目标就是“挑战新的事物”。就我目前的情况来看，在赚钱累积财富方面，我的成绩相当优异，即便现今经济不景气，我的资产还是一直增加。
或许，也可以说我已经打胜了人生这一仗。
60岁以后的20年，我打算把赚来的钱投资在我认为需要的地方，或许是慈善事业，或许是其他事业。我将以一路走来所培养的感觉和经验，全心全力用自己的方式来回馈世界。
系山英太郎，1942年6月4日生于东京，日本大学经济系毕业。年轻时创下日本进口车销售纪录，在股票市场上收获甚丰，名留日本证券史。系山英太郎被誉为“日本巴菲特”的投资大师，他白手起家，凭自己的能力得到了父亲的赏识，30岁即拥有几十亿资产，经营18家公司，是JAL（日本航空）最大股东，三菱重工最大个人股东，个人投资4150亿日元，是惟一连续10年登上《福布斯》“全球亿万富翁排行榜”的日本人，一个在日本泡沫经济和全球不景气中仍然保持财富增值的魔法资本家。此外，他32岁投身政治，成为日本历史上最年轻的参议员，曾任前首相中曾根康弘秘书，在日本政商界呼风唤雨，1996年，他退出政坛，返回商界。
系山英太郎身世可以说得上是从地狱到天堂：
他是被拒之门外的私生子，父亲曾是60年代的日本首富。
少年时期打架、勒索、贩卖黄色照片，是小流氓头目和警察局的常客。
20岁，把客户的订金挥霍一空，不得已卖身还债。
30岁，谁惹恼系山，就收购谁的股票。
40岁，没有所谓争议的竞选，决不辞去议员的职务。
50岁，证券经纪人和技术图表根本不可信。
60岁，立志散财，把智慧和财富贡献给全世界。
从富豪出生到卖身还债
其父佐佐木真太郎是1969年的日本首富。系山英太郎能成为日本大财主，凭的却是个人的才干和奋斗。其发家之道与其父相去甚远，系山英太郎是股海的大赢家，其父则靠高尔夫球场发迹，对股票嗤之以鼻。
系山英太郎最初显露商业才华，是在他当二手车推销员的时候。当时他月薪才2万日元，而一年之内他卖掉77辆车，创下该行业的最高记录，令公司获利4000多万。不过当他此后另立门户的时候，却因周转不灵而节节亏损。最后他不得不向父亲借钱。父亲拒绝了他的要求，对他说：“如果你愿意卖身给我，我可以给你35万，但今后你要对我言听计从。”系山英太郎无奈，只好成了其父麾下的一名球童。
塞翁失马，焉知非福。系山英太郎却在高尔夫这个行业里再次发挥才干。正如他所说，“将打架战术用在商业对手上”。在帮父亲开发高尔夫球场时，他针锋相对地与对手打拼，非把对手弄垮不可。在围绕日本职业高尔夫球协会会长一职的争斗上，系山英太郎与“乾汽船”的董事长乾丰彦干上了。为了吞并“乾汽船”，系山英太郎连续多日大笔购进“乾汽船”的股票，短时间内买下800万股，远远超过对方手上的250万股，迫使乾丰彦不得不上门向他求饶。
系山英太郎投资股市手法独特，从不相信操作员和曲线图，坚持逆势入市的投资理念。最典型的例子莫过于与日本股市的风云人物近藤信男的比拼上。近藤信男在大笔抛售丰田汽车等股票上令对手战栗不已，最终却败在系山英太郎这个小字辈手下。此外，系山英太郎在三井矿山、神户电铁等一连串的炒作上也大获全胜，被舆论誉为“日本的巴菲特”。
日本前首相秘书
在20岁到30岁的10年中，系山英太郎已拥有数十亿日元的资产。此后他一边继续股票投资和生意运作，一边投身从政。26岁时，他当了前首相中曾根的秘书。32岁那年，系山英太郎成为日本史上最年轻的参议员。
1983年当选众议员，先后任建设政务次官、国会对策副委员长、众议院运作委员会理事、众议院外务委员会委员长等职。1996年退出政界，回任新日本观光集团各企业社长兼会长，并任湘南工科大学校长。同时身兼三菱重工最大股东及日本航空最大股东。设立了塞席尔经济合作援助基金、斯里兰卡福祉合作援助基金、柬埔寨医院设立基金等，积极贡献国际。著有《怪物商法》《向太阳挑战》《日本青年革命》等。也是百万畅销的作家。
在政坛上，系山英太郎敢于直言。时至今天，他仍不时在其个人网页上针砭时弊。对小泉执意出兵伊拉克，系山英太郎在文章里痛陈利弊，“这场战争的正义性很值得质疑”。他指出，日美同盟虽然重要，但决不能拿国民的生命当儿戏。
如今，系山英太郎全身心投入到他钟爱的商海，他已悉数购进其父的10个高尔夫球场，成为新日本观光股份公司董事长兼社长，身价年年增长，在日本富豪中排行第三；同时，他还非常热衷教育事业，担任湘南工科理事长和上海复旦大学顾问教授等职；此外，他还推出多本畅销书，传授他的投资理念。他宣布，今后将是他回馈社会的时候。“很多人问我赚这么多钱干什么？我想，在今后的20年里，我准备将钱投资到我认为需要的地方，或许是慈善事业，或许是教育，或许是其他,或许因此还会继续赚钱，但我会凭我的知识和经验，全身心回馈社会！”
赚钱哲学
有着不凡经历的他，谈起自己的赚钱哲学时，自然有相当的哲理和独到见解之处——
独门投资术
“我投资股票30多年，一贯以反市场操作为原则。当100个投资人有99个看到股票下跌而慌了手脚，拼命抛售股票的时候，我就买进；反之，就抛出。不过，我投资股票的钱不会一次用完，而是先投资1／3或者1／2,剩下的钱留待股票下跌时摊平运用，赚到15%或者20%就脱手。 ”
“我做股票时就专心做股票，吃饭时专心在食物上，睡觉时就好好睡觉。我总是倾注100%的热忱，认真投入当下所做的事情，毫无杂念，尽力而为，剩下的就‘尽人事，听天命’。困苦悲惨的童年使我充满斗志，并立志不做游手好闲的穷光蛋，要勤奋努力誓做有钱人。因此，我不论遇到什么情况，都相信将来必然成功，不愉快的事立刻抛诸脑后。到最后，我从被金钱玩弄于股掌之上到驯服它，使它服服帖帖。 ”
“我关注社会的所有动态，因为它们都关系到我的投资活动。换句话说，只要没有特别的事情，我每天都窝在房间里，面对股票，努力赚钱。即使外出，我也积极观察和掌握资讯。操作股票，就必须付出这样的时间、体力以及耐性。我想一般人可能做不到吧。然而，若只是单单看着股票上涨就高兴，下跌就消沉是无法根据股票赚钱的。”
利益至上交往法
“我在2001年秋天和2002年春天，两度针对全日本经营者举办研习会，在研习会上，我开宗明义地表示：‘别和穷人交往。’ ”
穷人有两种。一种是字面上所指的“没有钱的穷人”，跟这种人交往，只会陷入老是自掏腰包的境地。如果想要存钱，就必须节省这种不必要的花费。想找人一起吃饭、喝酒，找比自己有钱的人作伴当然更为明智。在这个世界上，有些人喜欢身边围绕着没钱的人，享受他们的阿谀奉承。但是穷人只是向钱低头而已，不论你曾经给过他们多少好处，当你没钱时，这些人就会忘记你曾经施与的恩惠，两脚开溜而去。
人际关系本来就是施与受的关系，如果只有施当然只有损失。而另一种穷人不只是没钱，也缺乏有益于人的资讯和娱乐别人的才能，毫无利他的价值。虽然我说“别和穷人交往”，但如果哪个没钱的人有值得我们请客的价值，那么即使他再穷，我也乐意和他交往。尤其是年轻人，他们拥有许多我不知道的资讯，花钱在他们身上绝对不会浪费。我从与他们交游闲聊中得到的资讯，往往成为生意上的灵感。由此看来，为他们花钱其实是很便宜的投资。也就是说，我与别人交往时，经常在瞬间计算着投资效果。
该享受怎样的生活
“事实上我是个不花钱的人，因为我根本没有“赚钱了就要挥霍”的想法。当我打着系山的名号外出应酬时，不得不去一流的酒店，但是平时我自己吃饭，都是很随便的。当然更加没有兴趣购买什么高级名牌服饰，平时生活比较简朴。不过，我愿意在车子上花大钱，汽车之外的奢侈就是游艇。当我在股市赚到钱高兴得合不拢嘴时，我耗资30亿元买下一艘游艇，这是一艘豪华游轮的四层楼大船，我搭乘这个船环游了世界3趟，充分享受了航海的乐趣。”
制胜的法宝
“我很喜欢“终身学习”这句话，碰到不懂的事情，我不会搁着不管，反而会拼命去寻求解答。我就是通过推销外国汽车而领悟销售技巧，我通过学习，开动脑筋，利用银行达到一石三鸟的赚钱招术。虽然在我的投资生涯里百战百胜，不过每天都有10亿日元上下的资金在我的账上进出，股市的风云变幻让我亦喜亦忧，但我认为善于学习是我制胜的法宝。只要准确把握时代脉搏，即便是“无偿服务”也能够赚大钱。年龄渐长之后，我至死都不愿意被时代淘汰，3年前，我请老师从“电脑能做什么”开始教我，3个月后，我成立了自己的网络，发表我个人对时事问题的看法。我打心底认为，学会电脑真好，我的世界一下子拓展开来，收集资讯也变得轻松方便。 终身学习。从今以后，我仍要继续发动我这老迈的躯体，勇于挑战新的事物，了解未知的世界。”
赚钱的秘诀
常常有人问我：“对您来说，赚钱是什么？”
首先，以“忍耐”为重，面包和烧酒，陪伴我度过困窘到极点的20岁生日，同时也让我充分见识了金钱威力的“青春时代”。所以，即使身处逆境或贫困深渊，也要相信明天就会成功，这样才会坚韧不拔。例如，当股价不断下跌，你遭受极为惨重的损失，甚至想要自杀时，你也必须忍耐，不可放弃斗志。投资股票时，“只有一股也是股东”这一信念支撑我挑起中山制钢股票大户战。从政时，“就算你揍我、踹我，我也决不辞去议员的职务”。如果工作得不到预期的成果，我也要把痛苦当作经验而忍耐下来，相信总有一天能够雪耻报仇，从不幸中努力向上爬。而且要将计就计，善于使不利的局面为我所用。其次，“信”。这里不是指成为一个宗教家向穷人化缘讨钱，而是认识许多能够互相帮助的人，以拓展人脉。如果能够成为爱许多人，也受许多人信赖的人物，事业自然兴盛，大家都能够赚钱。
那么，赚钱的目的是什么呢？赚钱是门永无止境的学问，那些不让别人赚钱的有钱人不可原谅。光知道要钱，乱作一团的人际关系、派系关系，我30年间撒在政界的钱近百亿，我不认为有钱之后就要过奢侈的生活。忍耐，努力，认真工作，成为一个爱人、受人信赖的人，事业自然会兴盛。接下来的目标就是“挑战新的事物”。就我目前的情况来看，在赚钱累积财富方面，我的成绩相当优异，即便现今经济不景气，我的资产还是一直增加。
或许，也可以说我已经打胜了人生这一仗。
60岁以后的20年，我打算把赚来的钱投资在我认为需要的地方，或许是慈善事业，或许是其他事业。我将以一路走来所培养的感觉和经验，全心全力用自己的方式来回馈世界。
系山英太郎：抓住赚钱的机会，你不理财，财不理你！
我的独门投资术
我投资股票30多年，一贯以反市场操作为原则。当100个投资人有99个看到股票下跌而慌了手脚，拼命抛售股票的时候，我就买进；反之，就抛出。不过，我投资股票的钱不会一次用完，而是先投资1／3或者1／2,剩下的钱留待股票下跌时摊平运用，赚到15%或者20%就脱手。
我做股票时就专心做股票，吃饭时专心在食物上，睡觉时就好好睡觉。我总是倾注100%的热忱，认真投入当下所做的事情，毫无杂念，尽力而为，剩下的就“尽人事，听天命”。不论遇到什么情况，我都相信将来必然成功，不愉快的事立刻抛诸脑后。
我关注社会的所有动态，因为它们都关系到我的投资活动。换句话说，只要没有特别的事情，我每天都窝在房间里，面对股票，努力赚钱。即使外出，我也积极观察和掌握资讯。操作股票，就必须付出这样的时间、体力以及耐性。我想一般人可能做不到吧。然而，若只是单单看着股票上涨就高兴，下跌就消沉是无法根据股票赚钱的。
我的利益至上交往法
我在2001年秋天和2002年春天，两度针对全日本经营者举办研习会，在研习会上，我开宗明义地表示：“别和穷人交往。”
穷人有两种。一种是字面上所指的“没有钱的穷人”，跟这种人交往，只会陷入老是自掏腰包的境地。如果想要存钱，就必须节省这种不必要的花费。想找人一起吃饭、喝酒，找比自己有钱的人作伴当然更为明智。在这个世界上，有些人喜欢身边围绕着没钱的人，享受他们的阿谀奉承。但是穷人只是向钱低头而已，不论你曾经给过他们多少好处，当你没钱时，这些人就会忘记你曾经施与的恩惠，两脚开溜而去。
人际关系本来就是施与受的关系，如果只有施当然只有损失。而另一种穷人不只是没钱，也缺乏有益于人的资讯和娱乐别人的才能，毫无利他的价值。虽然我说“别和穷人交往”，但如果哪个没钱的人有值得我们请客的价值，那么即使他再穷，我也乐意和他交往。尤其是年轻人，他们拥有许多我不知道的资讯，花钱在他们身上绝对不会浪费。我从与他们交游闲聊中得到的资讯，往往成为生意上的灵感。由此看来，为他们花钱其实是很便宜的投资。也就是说，我与别人交往时，经常在瞬间计算着投资效果。
该享受怎样的生活？
事实上我是个不花钱的人，因为我根本没有“赚钱了就要挥霍”的想法。当我打着系山的名号外出应酬时，不得不去一流的酒店，但是平时我自己吃饭，都是很随便的。当然更加没有兴趣购买什么高级名牌服饰，平时生活比较简朴。不过，我愿意在车子上花大钱，汽车之外的奢侈就是游艇。当我在股市赚到钱高兴得合不拢嘴时，我耗资30亿元买下一艘游艇，这是一艘豪华游轮的四层楼大船，我搭乘这个船环游了世界3趟，充分享受了航海的乐趣。
赚钱的最大秘诀
常常有人问我：“对您来说，赚钱是什么？”
首先，以“忍耐”为重。就是即使身处逆境或贫困深渊，也要相信明天就会成功而坚忍不拔。例如，当股价不断下跌，你遭受极为惨重的损失，甚至想要自杀时，你也必须忍耐，不可放弃斗志。如果工作得不到预期的成果，也要把痛苦当作经验而忍耐下来，相信总有一天能够雪耻报仇，从不幸中努力向上爬。其次，“信”。这里不是指成为一个宗教家向穷人化缘讨钱，而是认识许多能够互相帮助的人，以拓展人脉。如果能够成为爱许多人，也受许多人信赖的人物，事业自然兴盛，大家都能够赚钱。
那么，赚钱的目的是什么呢？我不认为有钱之后就要过奢侈的生活。忍耐，努力，认真工作，成为一个爱人、受人信赖的人，事业自然会兴盛。接下来的目标就是“挑战新的事物”。就我目前的情况来看,在赚钱累积财富方面，我的成绩相当优异，即便现今经济不景气，我的资产还是一直增加。
或许，也可以说我已经打胜了人生这一仗。
60岁以后的20年，我打算把赚来的钱投资在我认为需要的地方，或许是慈善事业，或许是其他事业。我将以一路走来所培养的感觉和经验，全心全力用自己的方式来回馈世界。
终身学习拼命求解答
我很喜欢“终身学习”这句话，碰到不懂的事情，我不会搁着不管，反而会拼命去寻求解答。年龄渐长之后，我至死都不愿意被时代淘汰。3年前，我请老师从“电脑能做什么”开始教我，3个月后，我成立了自己的网络，发表我个人对时事问题的看法。我打心底认为，学会电脑真好，我的世界一下子拓展开来，收集资讯也变得轻松方便。
终身学习。从今以后，我仍要继续发动我这老迈的躯体，勇于挑战新的事物，了解未知的世界。
我投资股票30多年，一贯以反市场操作为原则。当100个投资人有99个看到股票下跌而慌了手脚，拼命抛售股票的时候，我就买进；反之，就抛出。不过，我投资股票的钱不会一次用完，而是先投资1／3或者1／2,剩下的钱留待股票下跌时摊平运用，赚到15%或者20%就脱手。
我做股票时就专心做股票，吃饭时专心在食物上，睡觉时就好好睡觉。我总是倾注100%的热忱，认真投入当下所做的事情，毫无杂念，尽力而为，剩下的就“尽人事，听天命”。不论遇到什么情况，我都相信将来必然成功，不愉快的事立刻抛诸脑后。
我关注社会的所有动态，因为它们都关系到我的投资活动。换句话说，只要没有特别的事情，我每天都窝在房间里，面对股票，努力赚钱。即使外出，我也积极观察和掌握资讯。操作股票，就必须付出这样的时间、体力以及耐性。我想一般人可能做不到吧。然而，若只是单单看着股票上涨就高兴，下跌就消沉是无法根据股票赚钱的。
我的利益至上交往法
我在2001年秋天和2002年春天，两度针对全日本经营者举办研习会，在研习会上，我开宗明义地表示：“别和穷人交往。”
穷人有两种。一种是字面上所指的“没有钱的穷人”，跟这种人交往，只会陷入老是自掏腰包的境地。如果想要存钱，就必须节省这种不必要的花费。想找人一起吃饭、喝酒，找比自己有钱的人作伴当然更为明智。在这个世界上，有些人喜欢身边围绕着没钱的人，享受他们的阿谀奉承。但是穷人只是向钱低头而已，不论你曾经给过他们多少好处，当你没钱时，这些人就会忘记你曾经施与的恩惠，两脚开溜而去。
人际关系本来就是施与受的关系，如果只有施当然只有损失。而另一种穷人不只是没钱，也缺乏有益于人的资讯和娱乐别人的才能，毫无利他的价值。虽然我说“别和穷人交往”，但如果哪个没钱的人有值得我们请客的价值，那么即使他再穷，我也乐意和他交往。尤其是年轻人，他们拥有许多我不知道的资讯，花钱在他们身上绝对不会浪费。我从与他们交游闲聊中得到的资讯，往往成为生意上的灵感。由此看来，为他们花钱其实是很便宜的投资。也就是说，我与别人交往时，经常在瞬间计算着投资效果。
该享受怎样的生活？
事实上我是个不花钱的人，因为我根本没有“赚钱了就要挥霍”的想法。当我打着系山的名号外出应酬时，不得不去一流的酒店，但是平时我自己吃饭，都是很随便的。当然更加没有兴趣购买什么高级名牌服饰，平时生活比较简朴。不过，我愿意在车子上花大钱，汽车之外的奢侈就是游艇。当我在股市赚到钱高兴得合不拢嘴时，我耗资30亿元买下一艘游艇，这是一艘豪华游轮的四层楼大船，我搭乘这个船环游了世界3趟，充分享受了航海的乐趣。
赚钱的最大秘诀
常常有人问我：“对您来说，赚钱是什么？”
首先，以“忍耐”为重。就是即使身处逆境或贫困深渊，也要相信明天就会成功而坚忍不拔。例如，当股价不断下跌，你遭受极为惨重的损失，甚至想要自杀时，你也必须忍耐，不可放弃斗志。如果工作得不到预期的成果，也要把痛苦当作经验而忍耐下来，相信总有一天能够雪耻报仇，从不幸中努力向上爬。其次，“信”。这里不是指成为一个宗教家向穷人化缘讨钱，而是认识许多能够互相帮助的人，以拓展人脉。如果能够成为爱许多人，也受许多人信赖的人物，事业自然兴盛，大家都能够赚钱。
那么，赚钱的目的是什么呢？我不认为有钱之后就要过奢侈的生活。忍耐，努力，认真工作，成为一个爱人、受人信赖的人，事业自然会兴盛。接下来的目标就是“挑战新的事物”。就我目前的情况来看,在赚钱累积财富方面，我的成绩相当优异，即便现今经济不景气，我的资产还是一直增加。
或许，也可以说我已经打胜了人生这一仗。
60岁以后的20年，我打算把赚来的钱投资在我认为需要的地方，或许是慈善事业，或许是其他事业。我将以一路走来所培养的感觉和经验，全心全力用自己的方式来回馈世界。
终身学习拼命求解答
我很喜欢“终身学习”这句话，碰到不懂的事情，我不会搁着不管，反而会拼命去寻求解答。年龄渐长之后，我至死都不愿意被时代淘汰。3年前，我请老师从“电脑能做什么”开始教我，3个月后，我成立了自己的网络，发表我个人对时事问题的看法。我打心底认为，学会电脑真好，我的世界一下子拓展开来，收集资讯也变得轻松方便。
终身学习。从今以后，我仍要继续发动我这老迈的躯体，勇于挑战新的事物，了解未知的世界。
Wednesday, October 21, 2009
Out of Energy?
See nine things that zap your vitality and how to get it back
It's 3 p.m.--do you know where your energy's gone? You probably expect to feel that late-afternoon drag, but you don't always have to. Turns out, some of your regular habits may be sneakily zapping your zip. Fix some or all of these energy stealers, and you just may be feeling brighter this afternoon.
Energy Zapper #1: Being Addicted to E-mail
Isn't being wired to the hilt--e-mail, voice mail, IM, BlackBerry--supposed to boost productivity, freeing up your energy? More often, the opposite is true. If you continually halt what you're doing to answer e-mail, check voice mail, and attend to a thousand other beeps and blips, your attention becomes diluted, which leaves you feeling depleted.
There are two things going on here, says John Salerno, MD, a New York City family physician and director of the Salerno Center for Complementary Medicine. "The brain needs a lot of physical and mental energy to multitask, which gets drained," he says. And continually redirecting your attention from the BlackBerry to other stimuli siphons more energy and distracts your brain further.
Energy Fix
Switch off electronic gadgets during your most productive work hours, which for most people tend to be in the morning, says Laura Stack, author of The Exhaustion Cure. As for e-mail, try to limit yourself to checking it once every hour, instead of hopping to whenever it beeps. (Hint: Turn off the beep sound.) If something pops into your mind that you need to remember--call back your mom, e-mail the soccer coach about the snack schedule--write it down and take care of it later.
Energy Zapper #2: Visual Clutter
We may be used to living in enclosed spaces with lots of stuff--a refrigerator door packed with artwork, a countertop laden with mail, a desk that's little more than a shifting pile of folders and paper--but it's not how we're meant to live, says Dr. Salerno. "Clutter signals disorder, which makes us anxious. Our brains sense that anxiety."
Energy Fix
Do your best to clear visual clutter, so when you look around, your eyes can "rest" rather than dart from mess to mess, says Janice Ash, organization expert and owner of I Declutter!. Instead of layering papers on a bulletin board, leave a small border of space around them. Clear the front of the fridge of all but the most current kids' artwork, and make a habit of leaving the kitchen counter stuff-free before bed each night.
Energy Zapper #3: Being Bored
Ever sat around for an hour or more not tackling a chore or work because it's just so darned monotonous? Mental foot-dragging, boredom and lack of motivation are draining, says Dr. Salerno. "Put simply, we like to see results, and getting things done gives us a mental energy boost." So avoiding tasks deprives you of that high.
Energy Fix
Find a partner for encouragement--a friend, a coworker--and call or e-mail to enlist her in a time challenge. "Say, ‘I'll check back in with you in an hour, and we'll see if we've gotten these reports/ organizing chores done.'" Or promise yourself motivational rewards for completing the task at hand, suggests Dr. Salerno.
Energy Zapper #4: Poor Posture
You already know that not sitting or standing straight is bad for your body. But all that hunching over a computer screen or cradling a phone on your shoulder wreaks havoc on your energy level, too, says Pia Martin, a San Diego health and wellness chiropractor. "When you sit for long periods, you tend to slump forward, leading to rounded shoulders and a tilted lower spine. Your muscles contract, and blood flow is impaired," which limits the amount of oxygen to your brain.
Energy Fix
Sit up straight! Your legs should be at right angles to the floor, your arms at right angles to your keyboard. Be conscious of keeping your shoulders down, not up near your ears. Adjust your computer screen so your eyes gaze at the middle of it. And don't just sit there--if you have to, set a timer to go off hourly to remind you to get up, stretch and get a drink of water. When you get back to your desk, do a quick posture check: Shoulders down! (Reboot your posture with these tips.)
Energy Zapper #5: Toxic Indoor Air
Humming copy machines. Cleaning products. Dry-cleaning chemicals. Synthetic carpeting. Even the desks in your office may be contributing to the load of toxins you breathe each day, because all of them release chemicals into the air. "No one knows for sure how much harm these cause to our bodies, but they do build up over time, and can drain your energy by potentially interfering with thyroid function and overloading the body's detox system," says Frank Lipman, MD, a New York City physician and author of Spent: End Exhaustion and Feel Great Again. (Reduce your exposure to chemical toxins.)
Energy Fix
Get outside. If you're feeling tired, go out for 10 minutes to breathe fresh air. Indoors, cultivate houseplants, which are remarkably good at absorbing toxins. And don't wear shoes inside the house--you're dragging not just dirt indoors on your soles, but pesticides and other harmful chemicals too.
Energy Zapper #6: Eating Too Much at Once
Consuming a big meal is always something that will cause a dip in energy later, but that effect is most noticeable in the afternoon because the slump happens at that reach-for-coffee-or-sugar hour: 3 p.m. Here's what happens: You fill up on a carb- and calorie-rich lunch and, as nutrients are absorbed by your body, excess glucose is dumped into your bloodstream, and your body releases insulin to process all that sugar. "A better idea is to spread out what and how you eat throughout the day to keep energy levels steady," says Gloria Tsang, RD, founder of the nutrition website HealthCastle.com.
Energy Fix
Eat every four hours, instead of the usual six. To reform lunch, "try to brownbag more often than eating out," says Tsang. It's a fact that if you buy takeout or dine in a restaurant, you're likely to eat more. Four hours after lunch, have a snack. If you're going to eat dinner a couple of hours later, keep the snack small, such as half a turkey sandwich, or a yogurt and some crackers. Other ideas: Drink liquids (water, tea) all day. "Dehydration makes you tired, too," says Tsang. If you usually have coffee right after lunch, try it a little later in the afternoon and make it a latte. The caffeine's an obvious pick-me-up, but the little bit of fat and protein in the milk gives you a snack-like boost. (Increase your energy with a smarter lunch.)
Energy Zapper #7: Living in Artificial Light
Our natural body rhythms are keyed to the rising and setting of the sun, says Carol Ash, DO, medical director of Sleep for Life, a sleep-disorder clinic in Somerset, New Jersey. When you open your eyes in the morning and get your first glimpse of sunlight, your brain receives a signal that helps it set its sleep-wake clock for the day. Similarly, seeing sunlight during the day gives your brain a boost. So if you are awake before the sun, and/or don't see much sun all day, your body is experiencing something a lot like jet lag.
Energy Fix
Instead of hitting the coffee cart when you're flagging, hit the sidewalk--the combination of physical exercise and a shot of sunlight will energize you. You don't need much: "A 10- to 20-minute walk in the sunshine will give you a boost," says Dr. Ash.
Energy Zapper #8: Listening to Negative Nellies
You may be upbeat, but it can be exhausting to listen to complainers all day long, whether it's the fellow mom who calls to trash-talk the neighbors or the coworker who never has a positive word to say. It's not your imagination: A 2006 study at Chicago's Northwestern University found that people forced to listen to "high-maintenance" colleagues became frustrated and unfocused, and suffered a decline in the quality of their work.
Energy Fix
Insulate yourself as best you can. If a coworker loves to enumerate her complaints, cut her off with a firm but polite "I really have to get this finished," then smile and get to work. She'll get the message. If it's your own negative thoughts that drag you down, train yourself to banish them by listing, daily, the things you're grateful for, so you can pull out that list when the negative stuff intrudes.
Energy Zapper #9: Holding a Grudge
It takes a surprising amount of energy to remember whom you have a grudge against, and to continually update the faults, missteps and things you're mad about. "Resentment is a huge drain physically as well as mentally," says Dr. Lipman. "Anger, resentment, grudges--all of these emotions are toxic, and we hang on to them in our bodies especially in tense, tired muscles."
Energy Fix
It takes practice, but try to forgive old mistakes. An easy way to start is to simply be aware of the times negative thoughts about others creep into your mind, says Dr. Lipman. "Think of others as flawed humans, which we all are," which makes it easier to forgive-and free up energy.
It's 3 p.m.--do you know where your energy's gone? You probably expect to feel that late-afternoon drag, but you don't always have to. Turns out, some of your regular habits may be sneakily zapping your zip. Fix some or all of these energy stealers, and you just may be feeling brighter this afternoon.
Energy Zapper #1: Being Addicted to E-mail
Isn't being wired to the hilt--e-mail, voice mail, IM, BlackBerry--supposed to boost productivity, freeing up your energy? More often, the opposite is true. If you continually halt what you're doing to answer e-mail, check voice mail, and attend to a thousand other beeps and blips, your attention becomes diluted, which leaves you feeling depleted.
There are two things going on here, says John Salerno, MD, a New York City family physician and director of the Salerno Center for Complementary Medicine. "The brain needs a lot of physical and mental energy to multitask, which gets drained," he says. And continually redirecting your attention from the BlackBerry to other stimuli siphons more energy and distracts your brain further.
Energy Fix
Switch off electronic gadgets during your most productive work hours, which for most people tend to be in the morning, says Laura Stack, author of The Exhaustion Cure. As for e-mail, try to limit yourself to checking it once every hour, instead of hopping to whenever it beeps. (Hint: Turn off the beep sound.) If something pops into your mind that you need to remember--call back your mom, e-mail the soccer coach about the snack schedule--write it down and take care of it later.
Energy Zapper #2: Visual Clutter
We may be used to living in enclosed spaces with lots of stuff--a refrigerator door packed with artwork, a countertop laden with mail, a desk that's little more than a shifting pile of folders and paper--but it's not how we're meant to live, says Dr. Salerno. "Clutter signals disorder, which makes us anxious. Our brains sense that anxiety."
Energy Fix
Do your best to clear visual clutter, so when you look around, your eyes can "rest" rather than dart from mess to mess, says Janice Ash, organization expert and owner of I Declutter!. Instead of layering papers on a bulletin board, leave a small border of space around them. Clear the front of the fridge of all but the most current kids' artwork, and make a habit of leaving the kitchen counter stuff-free before bed each night.
Energy Zapper #3: Being Bored
Ever sat around for an hour or more not tackling a chore or work because it's just so darned monotonous? Mental foot-dragging, boredom and lack of motivation are draining, says Dr. Salerno. "Put simply, we like to see results, and getting things done gives us a mental energy boost." So avoiding tasks deprives you of that high.
Energy Fix
Find a partner for encouragement--a friend, a coworker--and call or e-mail to enlist her in a time challenge. "Say, ‘I'll check back in with you in an hour, and we'll see if we've gotten these reports/ organizing chores done.'" Or promise yourself motivational rewards for completing the task at hand, suggests Dr. Salerno.
Energy Zapper #4: Poor Posture
You already know that not sitting or standing straight is bad for your body. But all that hunching over a computer screen or cradling a phone on your shoulder wreaks havoc on your energy level, too, says Pia Martin, a San Diego health and wellness chiropractor. "When you sit for long periods, you tend to slump forward, leading to rounded shoulders and a tilted lower spine. Your muscles contract, and blood flow is impaired," which limits the amount of oxygen to your brain.
Energy Fix
Sit up straight! Your legs should be at right angles to the floor, your arms at right angles to your keyboard. Be conscious of keeping your shoulders down, not up near your ears. Adjust your computer screen so your eyes gaze at the middle of it. And don't just sit there--if you have to, set a timer to go off hourly to remind you to get up, stretch and get a drink of water. When you get back to your desk, do a quick posture check: Shoulders down! (Reboot your posture with these tips.)
Energy Zapper #5: Toxic Indoor Air
Humming copy machines. Cleaning products. Dry-cleaning chemicals. Synthetic carpeting. Even the desks in your office may be contributing to the load of toxins you breathe each day, because all of them release chemicals into the air. "No one knows for sure how much harm these cause to our bodies, but they do build up over time, and can drain your energy by potentially interfering with thyroid function and overloading the body's detox system," says Frank Lipman, MD, a New York City physician and author of Spent: End Exhaustion and Feel Great Again. (Reduce your exposure to chemical toxins.)
Energy Fix
Get outside. If you're feeling tired, go out for 10 minutes to breathe fresh air. Indoors, cultivate houseplants, which are remarkably good at absorbing toxins. And don't wear shoes inside the house--you're dragging not just dirt indoors on your soles, but pesticides and other harmful chemicals too.
Energy Zapper #6: Eating Too Much at Once
Consuming a big meal is always something that will cause a dip in energy later, but that effect is most noticeable in the afternoon because the slump happens at that reach-for-coffee-or-sugar hour: 3 p.m. Here's what happens: You fill up on a carb- and calorie-rich lunch and, as nutrients are absorbed by your body, excess glucose is dumped into your bloodstream, and your body releases insulin to process all that sugar. "A better idea is to spread out what and how you eat throughout the day to keep energy levels steady," says Gloria Tsang, RD, founder of the nutrition website HealthCastle.com.
Energy Fix
Eat every four hours, instead of the usual six. To reform lunch, "try to brownbag more often than eating out," says Tsang. It's a fact that if you buy takeout or dine in a restaurant, you're likely to eat more. Four hours after lunch, have a snack. If you're going to eat dinner a couple of hours later, keep the snack small, such as half a turkey sandwich, or a yogurt and some crackers. Other ideas: Drink liquids (water, tea) all day. "Dehydration makes you tired, too," says Tsang. If you usually have coffee right after lunch, try it a little later in the afternoon and make it a latte. The caffeine's an obvious pick-me-up, but the little bit of fat and protein in the milk gives you a snack-like boost. (Increase your energy with a smarter lunch.)
Energy Zapper #7: Living in Artificial Light
Our natural body rhythms are keyed to the rising and setting of the sun, says Carol Ash, DO, medical director of Sleep for Life, a sleep-disorder clinic in Somerset, New Jersey. When you open your eyes in the morning and get your first glimpse of sunlight, your brain receives a signal that helps it set its sleep-wake clock for the day. Similarly, seeing sunlight during the day gives your brain a boost. So if you are awake before the sun, and/or don't see much sun all day, your body is experiencing something a lot like jet lag.
Energy Fix
Instead of hitting the coffee cart when you're flagging, hit the sidewalk--the combination of physical exercise and a shot of sunlight will energize you. You don't need much: "A 10- to 20-minute walk in the sunshine will give you a boost," says Dr. Ash.
Energy Zapper #8: Listening to Negative Nellies
You may be upbeat, but it can be exhausting to listen to complainers all day long, whether it's the fellow mom who calls to trash-talk the neighbors or the coworker who never has a positive word to say. It's not your imagination: A 2006 study at Chicago's Northwestern University found that people forced to listen to "high-maintenance" colleagues became frustrated and unfocused, and suffered a decline in the quality of their work.
Energy Fix
Insulate yourself as best you can. If a coworker loves to enumerate her complaints, cut her off with a firm but polite "I really have to get this finished," then smile and get to work. She'll get the message. If it's your own negative thoughts that drag you down, train yourself to banish them by listing, daily, the things you're grateful for, so you can pull out that list when the negative stuff intrudes.
Energy Zapper #9: Holding a Grudge
It takes a surprising amount of energy to remember whom you have a grudge against, and to continually update the faults, missteps and things you're mad about. "Resentment is a huge drain physically as well as mentally," says Dr. Lipman. "Anger, resentment, grudges--all of these emotions are toxic, and we hang on to them in our bodies especially in tense, tired muscles."
Energy Fix
It takes practice, but try to forgive old mistakes. An easy way to start is to simply be aware of the times negative thoughts about others creep into your mind, says Dr. Lipman. "Think of others as flawed humans, which we all are," which makes it easier to forgive-and free up energy.
Tuesday, October 20, 2009
玩欧洲轮盘的一种平均下注法
我们在这里讲的是欧洲轮盘的一种游戏策略,欧洲轮盘的介绍可以在博球通的游戏介绍里看到.
轮盘平均下注法相对来说风险比较小，是说每次的下注额固定，回报也固定。赌的是每把压注你的命中概率为2/3，也就是在36个数字中压24个数字左右。你选择的24个数字的选取则根据当前轮盘的历史数据，选择出现概率最大的24个数字或者数字所在的区间。这里的第一和第二中方式都是平注法，以希望在多次的压注过程中对庄家取得领先。
如果根据数学家的计算,欧洲轮盘出现零的赌场优势是百分之二点七，即是每玩一百元，按照概率算你会输去二点七元，如果是双零的桌子,赌场优势更会激增近一倍至百分之五点二,即是每玩一百元，按照概率算你会输去五点二元,因此选择单零的桌子对于你的赢利是有一倍的保证。
在运用这个策略的时候,我们要先统计轮盘出现的前36次结果，看1~12，13~24，25~36出现的次数来比较结果。
这里大家要记住一点，如果0和00出现次数累计超过一次的话，请大家换个桌子玩。
如果某两个区间出现次数明显多过另一个区间的话（如1~12出20次，13~24出18次，25~36出8次）：
那么我们的机会来了,准备200元作为本金，跟着我们的下注策略来吧!
1~12 压注 40元，13~24压注40元，观察最近出的红黑走向，判别为红压5元在9、12的split，否则压8、11的split，然后压5元在2、3、5、6的对角线（基于前面出现数字中没有1、4出现过，但有3、6出现）。
始终保持outside和inside对比40/5＝8的倍数，因为有超过2/3的赢钱概率，所以这样的情况下是可以赢钱的。准备200元可以保持两次不超过4/38的连续输钱概率。压注总额90元，每次赢30元，回报率非常可观，每次inside的split的压注要考虑红黑走向，然后以36次压注为一个基本压注周期
但是有两个情况是要及时退出的,不要恋战,任何一个周期没有赢利则退出，0出现两次以上也退出。
如果运气很好，累计赢得10次周期当积累到500元时，区间压注80元，另外inside压注各10元，总额180，400就可以保证连续两次失误也可以保证不输钱。这时候每次赢60元。
如果继续能总次数赢得10次，累计为1100元时，大家可以考虑离开桌子了。或者期望当晚利润2000元。采用区间160元，inside各20元的跳注法。此法连续两次全输的总金额为720元。所以380元为止损位，还有近200利润，切记切记。
这个策略的优点是不太需要统计历史数据，大家可以保持好的心态来玩,也不必过于紧张.心态平和自然能赢.
最后要点:单0的桌子是最佳选择,由于双0的概率大,所以不必在那样的桌子上使用此方法.
轮盘平均下注法相对来说风险比较小，是说每次的下注额固定，回报也固定。赌的是每把压注你的命中概率为2/3，也就是在36个数字中压24个数字左右。你选择的24个数字的选取则根据当前轮盘的历史数据，选择出现概率最大的24个数字或者数字所在的区间。这里的第一和第二中方式都是平注法，以希望在多次的压注过程中对庄家取得领先。
如果根据数学家的计算,欧洲轮盘出现零的赌场优势是百分之二点七，即是每玩一百元，按照概率算你会输去二点七元，如果是双零的桌子,赌场优势更会激增近一倍至百分之五点二,即是每玩一百元，按照概率算你会输去五点二元,因此选择单零的桌子对于你的赢利是有一倍的保证。
在运用这个策略的时候,我们要先统计轮盘出现的前36次结果，看1~12，13~24，25~36出现的次数来比较结果。
这里大家要记住一点，如果0和00出现次数累计超过一次的话，请大家换个桌子玩。
如果某两个区间出现次数明显多过另一个区间的话（如1~12出20次，13~24出18次，25~36出8次）：
那么我们的机会来了,准备200元作为本金，跟着我们的下注策略来吧!
1~12 压注 40元，13~24压注40元，观察最近出的红黑走向，判别为红压5元在9、12的split，否则压8、11的split，然后压5元在2、3、5、6的对角线（基于前面出现数字中没有1、4出现过，但有3、6出现）。
始终保持outside和inside对比40/5＝8的倍数，因为有超过2/3的赢钱概率，所以这样的情况下是可以赢钱的。准备200元可以保持两次不超过4/38的连续输钱概率。压注总额90元，每次赢30元，回报率非常可观，每次inside的split的压注要考虑红黑走向，然后以36次压注为一个基本压注周期
但是有两个情况是要及时退出的,不要恋战,任何一个周期没有赢利则退出，0出现两次以上也退出。
如果运气很好，累计赢得10次周期当积累到500元时，区间压注80元，另外inside压注各10元，总额180，400就可以保证连续两次失误也可以保证不输钱。这时候每次赢60元。
如果继续能总次数赢得10次，累计为1100元时，大家可以考虑离开桌子了。或者期望当晚利润2000元。采用区间160元，inside各20元的跳注法。此法连续两次全输的总金额为720元。所以380元为止损位，还有近200利润，切记切记。
这个策略的优点是不太需要统计历史数据，大家可以保持好的心态来玩,也不必过于紧张.心态平和自然能赢.
最后要点:单0的桌子是最佳选择,由于双0的概率大,所以不必在那样的桌子上使用此方法.
Tuesday, October 13, 2009
让你回味一生的凡人语录
1、一个人有生就有死，但只要你活着，就要以最好的方式活下去。
2、当我们失去的时候，才知道自己曾经拥有。
3、记住该记住的，忘记该忘记的。改变能改变的，接受不能改变的。
4、眼泪的存在，是为了证明悲伤不是一场幻觉。
5、妈妈说过没有人值得你为他哭，唯一值得你为他哭的那个人，永远都不会让你为他哭。
6、两人相爱时，渴求无限甜蜜的吻，但为何在争吵时，却要用接吻的嘴互相伤害呢？
7、幸福像掉到沙发下面的一粒纽扣――你专心找，怎么也找不到，等你淡忘了，它自己就滚出来了。
8、眼泪的温度有530℃，只是因为外面的世界太冷，流出来的时候才会降到53℃。
9、宠和爱是不同的两件事，宠可以没有交流，而爱则不能。
10、人生试题一共有四道题目：学业、事业、婚姻、家庭。平均分高才能及格，切莫花太多的时间和精 力 在任一题目上。
11、鱼说：你看不见我的眼中的泪，因为我在水里；水说：我能感受到你的泪，因为你在我心里。
12、人生在世，应该这样，在芬芳别人的同时美丽自己。
13、只需一分钟就可以碰到一个人，一小时喜欢上一个人，一天爱上一个人，但需要花尽一生的时间去忘掉一个人。
14、发光并非太阳的专利，你也可以发光。
15、人只要不失去方向，就不会失去自己！人生重要的不是所站的位置，而是所朝的方向。
16、每一件事都要用多方面的角度来看它。
17、理想的路总是为有信心的人预备着。
18、快乐要懂得分享，才能加倍的快乐。这也是三峡在线之所以总是在"盘点生活，分享经典"的理由。
19、抱最大的希望，为最大的努力，做最坏的打算。
20、生活中若没有朋友，就像生活中没有阳光一样。
21、一个人有生就有死，但只要你活着，就要以最好的方式活下去。
22、要做的事情总找得出时间和机会，不要做的事情总找得出借口。
23、令人不能自拔的，除了牙齿还有爱情。
24、爱情就像一双袜子，越是瞧起来不顺眼的袜子，越有可能永远陪在你身边，越是喜欢的漂亮袜子经常会少一只。
25、我们缺少的不是机会，而是在机会面前将自己重新归零的勇气。
26、微小的幸福就在身边，容易满足就是天堂。
27、没有人因水的平淡而厌倦饮水，也没有人因生活的平淡而摒弃生活。
28、思恋一个人的滋味就像喝了一大杯冰水，然后用很长很长的时间流成热泪。
29、得不到你所爱的，就爱你所得的。
30、日出东海落西山，愁也一天，喜也一天；遇事不钻角尖，人也舒坦，心也舒
31、失因为贪――说真的，老实人很少上当。
32、当你能飞的时候就不要放弃飞；当你能梦的时候就不要放弃梦；当你能爱的时候就不要放弃爱。
33、家！甜蜜的家！天下最美好的莫过于家。
34、如果敌人让你生气，那说明你还没有胜他的把握。如果朋友让你生气，那说明你仍然在意他的友情。
35、有些事情本身我们无法控制，只好控制自己。
36、聪明人是快乐的，自以为聪明的才烦恼。帮助别人减轻三分烦恼，自己就会享受七分快乐。
37、流言造成伤害至少需要两个人――你的敌人诋毁你，你的朋友转告你。
38、美好的生命应该充满期待、惊喜和感激。
39、最快乐的人并不是一切东西都是最好的，但他们会充分享受自己已有的东西。
40、自己要先看得起自己，别人才会看得起你。
41、假如一千个人从我身边踏过的，我也能听出你的脚步声，因为999个人的脚是踏在地上，只有你的脚步声是踏在我的心上。
42、生命太过短暂，今天放弃了明天不一定能得到。
43、每天告诉自己一次：我真的很不错。
44、要铭记在心：每天都是一年中最美好的日子。
45、爱的力量大到可以使人忘记一切，却又小到连一粒嫉妒的沙石也不能容纳。
46、爱一个人而那个人不爱你是很让人难受的，但更痛苦的是，爱一个人，却永远都没勇气告诉他。
47、后悔是一种耗费精神的情绪。后悔是比损失更大的损失，比错误更大的错误，所以请不要后悔。
48、每个人都有潜在的能量，只是很容易：被习惯所掩盖，被时间所迷离，被惰性所消磨。
49、能冲刷一切的除了眼泪，就是时间，以时间来推移感情，时间越长，冲突越淡，仿佛不断稀释的茶。
50、有勇气并不表示恐惧不存在，而是敢面对恐惧、克服恐惧。
51、生气是拿别人做错的事来惩罚自己。
52、人若软弱就是自己最大的敌人；人若勇敢就是自己最好的朋友。
53、要纠正别人之前，先反省自己有没有犯错。
54、少一点预设的期待，那份对人的关怀会更自在。
55、最好的朋友是你们静坐在游廊上，一句话也不说，当你们各自走开的时候，仍感到你们经历了一场十分精彩的对话。
56、人的价值，在遭受诱惑的一瞬间被决定。
57、有理想在的地方，地狱就是天堂。有希望在的地方，痛苦也成欢乐。
58、人总是珍惜未得到的，而遗忘了所拥有的。
59、用最少的悔恨面对过去。用最少的浪费面对现在。用最多的梦面对未来。
60、青春一经典当即永不再赎。
61、爱情是以微笑开始，以吻生长，以泪结束。
62、得意时应善待他人，因为你失意时会需要他们。
63、所有的胜利，与征服自己的胜利比起来，都是微不足道。所有的失败，与失去自己的失败比起来，更是微不足道。
64、一千个人就有一千种生存方式和生活道路，要想改变一些事情，首先得把自己给找回来。
65、在这个尘世上，虽然有不少寒冷，不少黑暗，但只要人与人之间多些信任，多些关爱，那么，就会增加许多阳光。
66、假如我不能，我一定要；假如我一定要，我就一定能。
67、一个能从别人的观念来看事情，能了解别人心灵活动的人，永远不必为自己的前途担心。
68、把你的脸迎向阳光，那就不会有阴影。
69、真正的爱，应该超越生命的长度、心灵的宽度、灵魂的深度。
70、你以为最酸的感觉是吃醋吗？不是的，最酸溜溜的感觉是没权吃醋，根本就轮不到你吃醋，那就是最酸最酸的。
71、死亡教会人一切，如同考试之后公布的结果――虽然恍然大悟，但为时晚矣！
72、你是你的敌人，只有你才能打倒你；你是你的上帝，只有你才能拯救你。
73、上帝从不埋怨人们的愚昧，人们却埋怨上帝的不公平。
74、世界上有两种人：索取者和给予者。前者也许能吃得更好，但后者绝对能睡得更香。
75、上帝从不埋怨人们的愚昧，人们却埋怨上帝的不公平。
76、要让事情改变，先改变我自己；要让事情变得更好，先让自己变得更好。
77、人要有三平心态：平和、平稳、平衡。对自己要从容，对朋友要宽容，对很多事情要包容，这样才能活的比较开心。
78、不要对挫折叹气，姑且把这一切看成是在你成大事之前，必须经受的准备工作。
79、每一个人都拥有生命，但并非每个人都懂得生命，乃至于珍惜生命。不了解生命的人，生命对他来说，是一种惩罚。
80、请你用慈悲心和温和的态度，把你的不满与委屈说出来，别人就容易接受。
81、你出生的时候，你哭着，周围的人笑着；在生命的尽头，你笑着，而周围的人在哭着。
82、伟人之所以伟大，是因为他与别人共处逆境时，别人失去了信心，他却下决心实现自己的目标。
83、你要包容那些意见跟你不同的人，这样子日子比较好过。你要是一直想改变他，那样子你会很痛苦。要学学怎样忍受他才是。你要学学怎样包容他才是。
84、良心是每一个人最公正的审判官，你骗得了别人，却永远骗不了你自己的良心。
85、什么时候也不要放弃希望，越是险恶的环境越要燃起希望的意志。
86、积极的人在每一次忧患中都看到一个机会，而消极的人则在每个机会都看到某种忧患。
87、许多人企求着生活的完美结局，殊不知美根本不在结局，而在于追求的过程。
88、定期去检查身体吧，别等最后别人送你去。三峡在线真诚提醒你。
89、影响我们人生的绝不仅仅是环境，其实是心态在控制-个人的行动和思想。同时，心态也决定了一个人的视野、事业和成就，甚至-生。
90、健康源于心，积极心态像太阳，照到哪里哪里亮；消极心态像病毒，传到哪里哪遭殃
91、第一个青春是上帝给的；第二个的青春是靠自己努力的。
92、也许有些人很可恶，有些人很卑鄙。而当我设身为他想象的时候，我才知道：他比我还可怜。所以请原谅所有你见过的人，好人或者坏人。
93、一句无心的话也许会点燃纠纷，一句残酷的话也许会毁掉生命，一句及时的话也许会消释紧张，一句知心的话也许会愈合伤口、挽救他人。
94、生命――-就是一个逐渐支出和利用时间的过程。一旦丧失了时间，生命也就走到了尽头。
95、没有口水与汗水，就没有成功的泪水。
96、世上并没有用来鼓励工作努力的赏赐，所有的赏赐都只是被用来奖励工作成果的。
97、当你感到悲哀痛苦时，最好是去学些什么东西。学习会使你永远立于不败之地。
98、世界上只有一样东西是任何人都不能抢走的，那就是智慧。
99、如果你希望成功，以恒心为良友，以经验为参谋，以小心为兄弟，以希望为哨兵。
100、一切伟大的行动和思想，都有一个微不足道的开始。
2、当我们失去的时候，才知道自己曾经拥有。
3、记住该记住的，忘记该忘记的。改变能改变的，接受不能改变的。
4、眼泪的存在，是为了证明悲伤不是一场幻觉。
5、妈妈说过没有人值得你为他哭，唯一值得你为他哭的那个人，永远都不会让你为他哭。
6、两人相爱时，渴求无限甜蜜的吻，但为何在争吵时，却要用接吻的嘴互相伤害呢？
7、幸福像掉到沙发下面的一粒纽扣――你专心找，怎么也找不到，等你淡忘了，它自己就滚出来了。
8、眼泪的温度有530℃，只是因为外面的世界太冷，流出来的时候才会降到53℃。
9、宠和爱是不同的两件事，宠可以没有交流，而爱则不能。
10、人生试题一共有四道题目：学业、事业、婚姻、家庭。平均分高才能及格，切莫花太多的时间和精 力 在任一题目上。
11、鱼说：你看不见我的眼中的泪，因为我在水里；水说：我能感受到你的泪，因为你在我心里。
12、人生在世，应该这样，在芬芳别人的同时美丽自己。
13、只需一分钟就可以碰到一个人，一小时喜欢上一个人，一天爱上一个人，但需要花尽一生的时间去忘掉一个人。
14、发光并非太阳的专利，你也可以发光。
15、人只要不失去方向，就不会失去自己！人生重要的不是所站的位置，而是所朝的方向。
16、每一件事都要用多方面的角度来看它。
17、理想的路总是为有信心的人预备着。
18、快乐要懂得分享，才能加倍的快乐。这也是三峡在线之所以总是在"盘点生活，分享经典"的理由。
19、抱最大的希望，为最大的努力，做最坏的打算。
20、生活中若没有朋友，就像生活中没有阳光一样。
21、一个人有生就有死，但只要你活着，就要以最好的方式活下去。
22、要做的事情总找得出时间和机会，不要做的事情总找得出借口。
23、令人不能自拔的，除了牙齿还有爱情。
24、爱情就像一双袜子，越是瞧起来不顺眼的袜子，越有可能永远陪在你身边，越是喜欢的漂亮袜子经常会少一只。
25、我们缺少的不是机会，而是在机会面前将自己重新归零的勇气。
26、微小的幸福就在身边，容易满足就是天堂。
27、没有人因水的平淡而厌倦饮水，也没有人因生活的平淡而摒弃生活。
28、思恋一个人的滋味就像喝了一大杯冰水，然后用很长很长的时间流成热泪。
29、得不到你所爱的，就爱你所得的。
30、日出东海落西山，愁也一天，喜也一天；遇事不钻角尖，人也舒坦，心也舒
31、失因为贪――说真的，老实人很少上当。
32、当你能飞的时候就不要放弃飞；当你能梦的时候就不要放弃梦；当你能爱的时候就不要放弃爱。
33、家！甜蜜的家！天下最美好的莫过于家。
34、如果敌人让你生气，那说明你还没有胜他的把握。如果朋友让你生气，那说明你仍然在意他的友情。
35、有些事情本身我们无法控制，只好控制自己。
36、聪明人是快乐的，自以为聪明的才烦恼。帮助别人减轻三分烦恼，自己就会享受七分快乐。
37、流言造成伤害至少需要两个人――你的敌人诋毁你，你的朋友转告你。
38、美好的生命应该充满期待、惊喜和感激。
39、最快乐的人并不是一切东西都是最好的，但他们会充分享受自己已有的东西。
40、自己要先看得起自己，别人才会看得起你。
41、假如一千个人从我身边踏过的，我也能听出你的脚步声，因为999个人的脚是踏在地上，只有你的脚步声是踏在我的心上。
42、生命太过短暂，今天放弃了明天不一定能得到。
43、每天告诉自己一次：我真的很不错。
44、要铭记在心：每天都是一年中最美好的日子。
45、爱的力量大到可以使人忘记一切，却又小到连一粒嫉妒的沙石也不能容纳。
46、爱一个人而那个人不爱你是很让人难受的，但更痛苦的是，爱一个人，却永远都没勇气告诉他。
47、后悔是一种耗费精神的情绪。后悔是比损失更大的损失，比错误更大的错误，所以请不要后悔。
48、每个人都有潜在的能量，只是很容易：被习惯所掩盖，被时间所迷离，被惰性所消磨。
49、能冲刷一切的除了眼泪，就是时间，以时间来推移感情，时间越长，冲突越淡，仿佛不断稀释的茶。
50、有勇气并不表示恐惧不存在，而是敢面对恐惧、克服恐惧。
51、生气是拿别人做错的事来惩罚自己。
52、人若软弱就是自己最大的敌人；人若勇敢就是自己最好的朋友。
53、要纠正别人之前，先反省自己有没有犯错。
54、少一点预设的期待，那份对人的关怀会更自在。
55、最好的朋友是你们静坐在游廊上，一句话也不说，当你们各自走开的时候，仍感到你们经历了一场十分精彩的对话。
56、人的价值，在遭受诱惑的一瞬间被决定。
57、有理想在的地方，地狱就是天堂。有希望在的地方，痛苦也成欢乐。
58、人总是珍惜未得到的，而遗忘了所拥有的。
59、用最少的悔恨面对过去。用最少的浪费面对现在。用最多的梦面对未来。
60、青春一经典当即永不再赎。
61、爱情是以微笑开始，以吻生长，以泪结束。
62、得意时应善待他人，因为你失意时会需要他们。
63、所有的胜利，与征服自己的胜利比起来，都是微不足道。所有的失败，与失去自己的失败比起来，更是微不足道。
64、一千个人就有一千种生存方式和生活道路，要想改变一些事情，首先得把自己给找回来。
65、在这个尘世上，虽然有不少寒冷，不少黑暗，但只要人与人之间多些信任，多些关爱，那么，就会增加许多阳光。
66、假如我不能，我一定要；假如我一定要，我就一定能。
67、一个能从别人的观念来看事情，能了解别人心灵活动的人，永远不必为自己的前途担心。
68、把你的脸迎向阳光，那就不会有阴影。
69、真正的爱，应该超越生命的长度、心灵的宽度、灵魂的深度。
70、你以为最酸的感觉是吃醋吗？不是的，最酸溜溜的感觉是没权吃醋，根本就轮不到你吃醋，那就是最酸最酸的。
71、死亡教会人一切，如同考试之后公布的结果――虽然恍然大悟，但为时晚矣！
72、你是你的敌人，只有你才能打倒你；你是你的上帝，只有你才能拯救你。
73、上帝从不埋怨人们的愚昧，人们却埋怨上帝的不公平。
74、世界上有两种人：索取者和给予者。前者也许能吃得更好，但后者绝对能睡得更香。
75、上帝从不埋怨人们的愚昧，人们却埋怨上帝的不公平。
76、要让事情改变，先改变我自己；要让事情变得更好，先让自己变得更好。
77、人要有三平心态：平和、平稳、平衡。对自己要从容，对朋友要宽容，对很多事情要包容，这样才能活的比较开心。
78、不要对挫折叹气，姑且把这一切看成是在你成大事之前，必须经受的准备工作。
79、每一个人都拥有生命，但并非每个人都懂得生命，乃至于珍惜生命。不了解生命的人，生命对他来说，是一种惩罚。
80、请你用慈悲心和温和的态度，把你的不满与委屈说出来，别人就容易接受。
81、你出生的时候，你哭着，周围的人笑着；在生命的尽头，你笑着，而周围的人在哭着。
82、伟人之所以伟大，是因为他与别人共处逆境时，别人失去了信心，他却下决心实现自己的目标。
83、你要包容那些意见跟你不同的人，这样子日子比较好过。你要是一直想改变他，那样子你会很痛苦。要学学怎样忍受他才是。你要学学怎样包容他才是。
84、良心是每一个人最公正的审判官，你骗得了别人，却永远骗不了你自己的良心。
85、什么时候也不要放弃希望，越是险恶的环境越要燃起希望的意志。
86、积极的人在每一次忧患中都看到一个机会，而消极的人则在每个机会都看到某种忧患。
87、许多人企求着生活的完美结局，殊不知美根本不在结局，而在于追求的过程。
88、定期去检查身体吧，别等最后别人送你去。三峡在线真诚提醒你。
89、影响我们人生的绝不仅仅是环境，其实是心态在控制-个人的行动和思想。同时，心态也决定了一个人的视野、事业和成就，甚至-生。
90、健康源于心，积极心态像太阳，照到哪里哪里亮；消极心态像病毒，传到哪里哪遭殃
91、第一个青春是上帝给的；第二个的青春是靠自己努力的。
92、也许有些人很可恶，有些人很卑鄙。而当我设身为他想象的时候，我才知道：他比我还可怜。所以请原谅所有你见过的人，好人或者坏人。
93、一句无心的话也许会点燃纠纷，一句残酷的话也许会毁掉生命，一句及时的话也许会消释紧张，一句知心的话也许会愈合伤口、挽救他人。
94、生命――-就是一个逐渐支出和利用时间的过程。一旦丧失了时间，生命也就走到了尽头。
95、没有口水与汗水，就没有成功的泪水。
96、世上并没有用来鼓励工作努力的赏赐，所有的赏赐都只是被用来奖励工作成果的。
97、当你感到悲哀痛苦时，最好是去学些什么东西。学习会使你永远立于不败之地。
98、世界上只有一样东西是任何人都不能抢走的，那就是智慧。
99、如果你希望成功，以恒心为良友，以经验为参谋，以小心为兄弟，以希望为哨兵。
100、一切伟大的行动和思想，都有一个微不足道的开始。
一个人凭什么自信呢？
有人说，自信来源于成功的暗示，也就是说，某项重任或创新一旦成功了，这个人就会自信。然而，此话虽不无道理，却仍未道出自信的根本依据。一个人在做某件事，尤其是在担当重任或大胆创新的时候，就需要自信，也应当自信，而不是只有在成功之后才能自信。美文如果你觉得自己不够聪明、能干和美丽，往往是因为你把自己和别人相比较的缘故，或者是把现实中的自己和理想中的模式相比较的结果。人们常常是看到别人怎么美好和幸运，总希望那些美好和幸运能被自己所拥有，却很少想到完全可以通过努力来改变自己，使自己变得更加聪明、能干和美丽，再塑一个全新的自我。
"认识自我"这句镌刻在古希腊戴尔菲城那座神庙里惟一的碑铭，犹如一把千年不熄的火炬，表达了人类与生俱来的内在要求和至高无上的思考命题。尼采曾说："聪明的人只要能认识自己，便什么也不会失去。"如今，随着社会的不断发展，人们对于自我的认识，也进入了一个突破性的新阶段。事实上，每个人都有巨大的潜能，每个人都有自己独特的个性和长处，每个人都可以选择自己的目标，并通过不懈的努力去争取属于自己的成功。
认识自我，是我们每个人自信的基础与依据。即使你处境不利，遇事不顺，但只要你赖以自信的巨大潜能和独特个性及优势依然存在，你就可以坚信：我能行，我能成功。一个人在自己的生活经历中，在自己所处的社会境遇中，能否真正认识自我、肯定自我，如何塑造自我形象，如何把握自我发展，如何抉择积极或消极的自我意识，将在很大程度上影响或决定着一个人的前程与命运。换句话说，你可能渺小而平庸，也可能美好而杰出，这在很大程度上取决于你的自我意识究竟如何，取决于你是否能够拥有真正的自信。
请记住，认识自我，你就是一座金矿，拥有自信、自主、自爱，你就一定能够在自己的人生中展出现应有的风采。
"认识自我"这句镌刻在古希腊戴尔菲城那座神庙里惟一的碑铭，犹如一把千年不熄的火炬，表达了人类与生俱来的内在要求和至高无上的思考命题。尼采曾说："聪明的人只要能认识自己，便什么也不会失去。"如今，随着社会的不断发展，人们对于自我的认识，也进入了一个突破性的新阶段。事实上，每个人都有巨大的潜能，每个人都有自己独特的个性和长处，每个人都可以选择自己的目标，并通过不懈的努力去争取属于自己的成功。
认识自我，是我们每个人自信的基础与依据。即使你处境不利，遇事不顺，但只要你赖以自信的巨大潜能和独特个性及优势依然存在，你就可以坚信：我能行，我能成功。一个人在自己的生活经历中，在自己所处的社会境遇中，能否真正认识自我、肯定自我，如何塑造自我形象，如何把握自我发展，如何抉择积极或消极的自我意识，将在很大程度上影响或决定着一个人的前程与命运。换句话说，你可能渺小而平庸，也可能美好而杰出，这在很大程度上取决于你的自我意识究竟如何，取决于你是否能够拥有真正的自信。
请记住，认识自我，你就是一座金矿，拥有自信、自主、自爱，你就一定能够在自己的人生中展出现应有的风采。
欣赏自己
也许你想成为太阳，可你却只是一颗星辰；
也许你想成为大树，可你却只是一株小草；
也许你想成为大河，可你却只是一泓山泉；
于是，你很自卑。
很自卑的你总是感叹命运；其实，你不必这样，欣赏别人的时候，总是都好；审视自己的时候，总是很糟。和别人一样，你也有一片风景，也有空气，也有阳光，也有寒来暑往，甚至有别人未曾拥有的一朵小花，一阵虫鸣……
做不了太阳，就做星辰，在自己的星座发热发光。
做不了大树，就做小草，让绿色装点希望。
做不了伟人，就做实在的自我，做最好的自己。
不必总是欣赏别人，也欣赏一下自己吧！你会发现，天空一样高远，大地一样宽广，平凡的你也有着自己美丽的风景！
超越自我，只有靠你自己。
也许你想成为大树，可你却只是一株小草；
也许你想成为大河，可你却只是一泓山泉；
于是，你很自卑。
很自卑的你总是感叹命运；其实，你不必这样，欣赏别人的时候，总是都好；审视自己的时候，总是很糟。和别人一样，你也有一片风景，也有空气，也有阳光，也有寒来暑往，甚至有别人未曾拥有的一朵小花，一阵虫鸣……
做不了太阳，就做星辰，在自己的星座发热发光。
做不了大树，就做小草，让绿色装点希望。
做不了伟人，就做实在的自我，做最好的自己。
不必总是欣赏别人，也欣赏一下自己吧！你会发现，天空一样高远，大地一样宽广，平凡的你也有着自己美丽的风景！
超越自我，只有靠你自己。
Sunday, October 11, 2009
Selecting a gym membership with swimming pool
Due to work and studies commitments, I have become rather unhealthy, as I sit on the chair for long hours without knowing and moving. Hence, I decided to look for a gym membership that would best serve my needs.
Basically, I would need a gym membership that is near my workplace or home that comes with a swimming pool. I intend to spend 45 minutes to an hour each time.
My budget is only $40 monthly.
One reputable gym got back to me and offered me a promotion: 36 months of gym membership (all gym access with pool at Suntec) and 6 months free, together with 3 complimentary sessions of workout with a personal trainer. It costs an average of $48 monthly. The only drawback is that I have to commit for 3 years at one go and the pool at Suntec is quite far (though within walking distance) from the gym.
Another gym membership costs roughly twice the price but there is no “lock in” period. It also comes with an integrated pool beside the gym but is too far from my workplace. Besides, it is way above my budget.
Registration fees were waived for the above 2 gyms.
I enquired on the SAFRA (Energy First) gym package and was appalled that it costs almost $60 per month after registration fees and monthly fees were factored in. If you have been to SAFRA gyms, you know it is only a slight tad better than the community sports centre ones.
The SAFRA membership was given by my company and we sometimes conduct our meetings there. My only impression of the facilities and environment is “minimalist” theme and a heaven for teenage kids. The bowling allies and pool centres are remembered to be packed with teenagers in the afternoons. However for less than $4 a month membership and an additional 7% off caltex petrol, I do not expect the sky.
After much consideration, I decided to go for the cheapo and convenient way of signing up for my community centre gym instead. It costs me a mere $10 monthly and comes with a treadmill and a few weights machine. It is only a 5 minutes walk from my home and this translates to savings on car parking and time. I will go for a swim in SAFRA clubs twice a week (which is free for members) and hit the treadmill twice in my community centre for 45 minutes. The drawbacks are it can be rather crowded in the evening and some people there can be boorish and vulgar. Not recommended for ladies though!
Hence my total cost for the healthy lifestyle cost a mere $18 a month inclusive of parking fees. Not bad for 4 workout sessions a week. The good thing of spending way below my initial budget is that I do not feel pressurised to go the gym or pool as my “sunk costs” are low. Even if I reduce the frequency of the exercises by 50%, I do not feel wasteful as I got a pretty good DIY hybrid deal.
Healthy lifestyle, here I come!
Basically, I would need a gym membership that is near my workplace or home that comes with a swimming pool. I intend to spend 45 minutes to an hour each time.
My budget is only $40 monthly.
One reputable gym got back to me and offered me a promotion: 36 months of gym membership (all gym access with pool at Suntec) and 6 months free, together with 3 complimentary sessions of workout with a personal trainer. It costs an average of $48 monthly. The only drawback is that I have to commit for 3 years at one go and the pool at Suntec is quite far (though within walking distance) from the gym.
Another gym membership costs roughly twice the price but there is no “lock in” period. It also comes with an integrated pool beside the gym but is too far from my workplace. Besides, it is way above my budget.
Registration fees were waived for the above 2 gyms.
I enquired on the SAFRA (Energy First) gym package and was appalled that it costs almost $60 per month after registration fees and monthly fees were factored in. If you have been to SAFRA gyms, you know it is only a slight tad better than the community sports centre ones.
The SAFRA membership was given by my company and we sometimes conduct our meetings there. My only impression of the facilities and environment is “minimalist” theme and a heaven for teenage kids. The bowling allies and pool centres are remembered to be packed with teenagers in the afternoons. However for less than $4 a month membership and an additional 7% off caltex petrol, I do not expect the sky.
After much consideration, I decided to go for the cheapo and convenient way of signing up for my community centre gym instead. It costs me a mere $10 monthly and comes with a treadmill and a few weights machine. It is only a 5 minutes walk from my home and this translates to savings on car parking and time. I will go for a swim in SAFRA clubs twice a week (which is free for members) and hit the treadmill twice in my community centre for 45 minutes. The drawbacks are it can be rather crowded in the evening and some people there can be boorish and vulgar. Not recommended for ladies though!
Hence my total cost for the healthy lifestyle cost a mere $18 a month inclusive of parking fees. Not bad for 4 workout sessions a week. The good thing of spending way below my initial budget is that I do not feel pressurised to go the gym or pool as my “sunk costs” are low. Even if I reduce the frequency of the exercises by 50%, I do not feel wasteful as I got a pretty good DIY hybrid deal.
Healthy lifestyle, here I come!
Saturday, October 10, 2009
Helicobacter pylori
Helicobacter pylori is a Gram-negative, microaerophilic bacterium that can inhabit various areas of the stomach and duodenum. It causes a chronic low-level inflammation of the stomach lining and is strongly linked to the development of duodenal and gastric ulcers and stomach cancer. Over 80% of individuals infected with the bacterium are asymptomatic.
The bacterium was initially named Campylobacter pyloridis, then renamed C. pylori (pylori = genitive of pylorus) to correct a Latin grammar error. When 16S rRNA gene sequencing and other research showed in 1989 that the bacterium did not belong in the genus Campylobacter, it was placed in its own genus, Helicobacter. The genus derived from the Ancient Greek hělix/έλιξ "spiral" or "coil".[1] The specific epithet pylōri means "of the pylorus" or pyloric valve (the circular opening leading from the stomach into the duodenum), from the Ancient Greek word πυλωρός, which means gatekeeper.[1]
More than 50% of the world's population harbour H. pylori in their upper gastrointestinal tract. Infection is more prevalent in developing countries, and incidence is decreasing in western countries. The route of transmission is unknown, although it is known individuals typically become infected in childhood. H. pylori's helix shape (from which the generic name is derived) is thought to have evolved to penetrate the mucoid lining of the stomach.[2][3]
Microbiology
Scanning electron micrograph of H. pyloriH. pylori is a helix-shaped Gram-negative bacterium, about 3 micrometres long with a diameter of about 0.5 micrometres. It is microaerophilic; that is, it requires oxygen, but at lower concentration than is found in the atmosphere. It contains a hydrogenase which can be used to obtain energy by oxidizing molecular hydrogen (H2) that is produced by intestinal bacteria.[4] It produces oxidase, catalase, and urease. It is capable of forming biofilms[5] and can convert from spiral to a possibly viable but nonculturable coccoid form,[6] both likely to favor its survival and be factors in the epidemiology of the bacterium. The coccoid form can adhere to gastric epithelial cells in vitro.[7]
H. pylori possesses five major outer membrane protein (OMP) families.[8] The largest family includes known and putative adhesins. The other four families include porins, iron transporters, flagellum-associated proteins and proteins of unknown function. Like other typical Gram-negative bacteria, the outer membrane of H. pylori consists of phospholipids and lipopolysaccharide (LPS). The O antigen of LPS may be fucosylated and mimic Lewis blood group antigens found on the gastric epithelium.[8] The outer membrane also contains cholesterol glucosides, which are found in few other bacteria.[8] H. pylori has 4–6 flagella; all gastric and enterohepatic Helicobacter species are highly motile due to flagella.[9] The characteristic sheathed flagellar filaments of helicobacters are composed of two copolymerized flagellins, FlaA and FlaB.[10]
Genome
H. pylori consists of a large diversity of strains, and the genomes of three have been completely sequenced.[11][12][13][14][15] The genome of the strain "26695" consists of about 1.7 million base pairs, with some 1,550 genes. The two sequenced strains show large genetic differences, with up to 6% of the nucleotides differing.
Study of the H. pylori genome is centered on attempts to understand pathogenesis, the ability of this organism to cause disease. Approximately 29% of the loci are in the "pathogenesis" category of the genome database. Both sequenced strains have an approximately 40 kb-long Cag pathogenicity island (a common gene sequence believed responsible for pathogenesis) that contains over 40 genes. This pathogenicity island is usually absent from H. pylori strains isolated from humans who are carriers of H. pylori but remain asymptomatic.[16]
The cagA gene codes for one of the major H. pylori virulence proteins. Bacterial strains that have the cagA gene are associated with an ability to cause ulcers.[17] The cagA gene codes for a relatively long (1186 amino acid) protein. The cag pathogenicity island (PAI) has about 30 genes, part of which code for a complex type IV secretion system. The low GC content of the cag PAI relative to the rest of the helicobacter genome suggests that the island was acquired by horizontal transfer from another bacterial species.
Pathophysiology
Molecular model of H. pylori urease enzymeTo colonize the stomach H. pylori must survive the acidic pH of the lumen and burrow into the mucus to reach its niche, close to the stomach's epithelial cell layer. The bacterium has flagella and moves through the stomach lumen and drills into the mucoid lining of the stomach.[18] Many bacteria can be found deep in the mucus, which is continuously secreted by mucous cells and removed on the luminal side. To avoid being carried into the lumen, H. pylori senses the pH gradient within the mucus layer by chemotaxis and swims away from the acidic contents of the lumen towards the more neutral pH environment of the epithelial cell surface.[19] H. pylori is also found on the inner surface of the stomach epithelial cells and occasionally inside epithelial cells.[20] It produces adhesins which bind to membrane-associated lipids and carbohydrates and help it adhere to epithelial cells. For example, the adhesin BabA binds to the Lewis b antigen displayed on the surface of stomach epithelial cells.[21] H. pylori produces large amounts of the enzyme urease, molecules of which are localized inside and outside of the bacterium. Urease breaks down urea (which is normally secreted into the stomach) to carbon dioxide and ammonia (ammonia is converted into the ammonium ion by taking hydrogen from water upon its breakdown into hydrogen and hydroxyl ions. Hydroxyl ions then react with carbon dioxide, producing bicarbonate which neutralizes gastric acid). The survival of H. pylori in the acidic stomach is dependent on urease, and it would eventually die without the enzyme. The ammonia that is produced is toxic to the epithelial cells, and, along with the other products of H. pylori—including protease, vacuolating cytotoxin A (VacA), and certain phospholipases—damages those cells.[22]
Colonization of the stomach by H. pylori results in chronic gastritis, an inflammation of the stomach lining. The severity of the inflammation is likely to underlie H. pylori-related diseases.[23] Duodenal and stomach ulcers result when the consequences of inflammation allow the acid and pepsin in the stomach lumen to overwhelm the mechanisms that protect the stomach and duodenal mucosa from these caustic substances. The type of ulcer that develops depends on the location of chronic gastritis, which occurs at the site of H. pylori colonization.[24] The acidity within the stomach lumen affects the colonization pattern of H. pylori and therefore ultimately determines whether a duodenal or gastric ulcer will form. In people producing large amounts of acid, H. pylori colonizes the antrum of the stomach to avoid the acid-secreting parietal cells located in the corpus (main body) of the stomach.[8] The inflammatory response to the bacteria induces G cells in the antrum to secrete the hormone gastrin, which travels through the bloodstream to the corpus.[25] Gastrin stimulates the parietal cells in the corpus to secrete even more acid into the stomach lumen. Chronically increased gastrin levels eventually cause the number of parietal cells to also increase, further escalating the amount of acid secreted.[26] The increased acid load damages the duodenum, and ulceration may eventually result. In contrast, gastric ulcers are often associated with normal or reduced gastric acid production, suggesting that the mechanisms that protect the gastric mucosa are defective.[26] In these patients H. pylori can also colonize the corpus of the stomach, where the acid-secreting parietal cells are located. However chronic inflammation induced by the bacteria causes further reduction of acid production and, eventually, atrophy of the stomach lining, which may lead to gastric ulcer and increases the risk for stomach cancer.[27]
About 50-70% of H. pylori strains in Western countries carry the cag pathogenicity island (cag PAI).[28] Western patients infected with strains carrying the cag PAI have a stronger inflammatory response in the stomach and are at a greater risk of developing peptic ulcers or stomach cancer than those infected with strains lacking the island.[8] Following attachment of H. pylori to stomach epithelial cells the type IV secretion system expressed by the cag PAI "injects" the inflammatory inducing agent peptidoglycan from their own cell wall into the epithelial cells. The injected peptidoglycan is recognized by the cytoplasmic immune sensor Nod1, which then stimulates expression of cytokines that promote inflammation.[29]
The type IV secretion apparatus also injects the cag PAI-encoded protein CagA into the stomach's epithelial cells, where it disrupts the cytoskeleton, adherence to adjacent cells, intracellular signaling, cell polarity and other cellular activities.[30] Once inside the cell the CagA protein is phosphorylated on tyrosine residues by a host cell membrane-associated tyrosine kinase. Pathogenic strains of H. pylori have been shown to activate the epidermal growth factor receptor (EGFR), a membrane protein with a tyrosine kinase domain. Activation of the EGFR by H. pylori is associated with altered signal transduction and gene expression in host epithelial cells that may contribute to pathogenesis. It has also been suggested that a c-terminal region of the CagA protein (amino acids 873–1002) can regulate host cell gene transcription independent of protein tyrosine phosphorylation.[16][17] There is a great deal of diversity between strains of H. pylori, and the strain with which one is infected is predictive of the outcome.
Two related mechanisms by which H. pylori could promote cancer are under investigation. One mechanism involves the enhanced production of free radicals near H. pylori and an increased rate of host cell mutation. The other proposed mechanism has been called a "perigenetic pathway"[31] and involves enhancement of the transformed host cell phenotype by means of alterations in cell proteins such as adhesion proteins. It has been proposed that H. pylori induces inflammation and locally high levels of TNF-α and/or interleukin 6. According to the proposed perigenetic mechanism, inflammation-associated signaling molecules such as TNF-α can alter gastric epithelial cell adhesion and lead to the dispersion and migration of mutated epithelial cells without the need for additional mutations in tumor suppressor genes such as genes that code for cell adhesion proteins.[32]
Diagnosis
H. pylori colonized on the surface of regenerative epithelium (image from Warthin-Starry's silver stain)Diagnosis of infection is usually made by checking for dyspeptic symptoms and by tests which can indicate H. pylori infection. One can test noninvasively for H. pylori infection with a blood antibody test, stool antigen test, or with the carbon urea breath test (in which the patient drinks 14C- or 13C-labelled urea, which the bacterium metabolizes, producing labelled carbon dioxide that can be detected in the breath).[33] However, the most reliable method for detecting H. pylori infection is a biopsy check during endoscopy with a rapid urease test, histological examination, and microbial culture. There is also a urine ELISA test with a 96% sensitivity and 79% specificity. None of the test methods is completely failsafe. Even biopsy is dependent on the location of the biopsy. Blood antibody tests, for example, range from 76% to 84% sensitivity. Some drugs can affect H. pylori urease activity and give false negatives with the urea-based tests.
Prevention
H. pylori is a major cause of diseases of the upper gastrointestinal tract. Eradication of the infection in individuals will improve symptoms including dyspepsia, gastritis and peptic ulcers, and may prevent gastric cancer. Rising antimicrobial resistance increases the need for a prevention strategy for the bacteria.[35] There have been extensive vaccine studies in mouse models, which have shown promising results.[36] Researchers are studying different adjuvants, antigens, and routes of immunization to ascertain the most appropriate system of immune protection, with most of the research only recently moving from animal to human trials.
An intramuscular vaccine against H. pylori infection is undergoing Phase I clinical trials and has shown an antibody response against the bacterium. Its clinical usefulness requires further study.[38]
Studies have recently been published suggesting that H. pylori activity could be suppressed via dietary methods.
A Japanese study published April 1, 2009 in the journal Cancer Prevention Research found that eating as little as 2.5 ounces of broccoli sprouts daily for two months reduces the number of colonies of H. pylori bacteria in the stomach by 40% in mice and humans. This treatment also seems to help by enhancing the protection of the gastric mucosa against H. pylori, but is relatively ineffective on related gastric cancers. The previous infection returned within two months after broccoli sprouts were removed from the diet, so an ongoing inclusion in the diet is best for continued protection from H. pylori.[39]
Also, a Korean study published on June 28, 2008 in the journal Korean Journal of Microbiology and Biotechnology found that kimchi contains a bacterium strain "showing strong antagonistic activity against H. pylori." The bacterium strain isolated from kimchi, designated Lb. plantarum NO1, was found to reduce the urease activity of H. pylori by 40-60% and suppress the latter bacteria's binding to human gastric cancer cell line by more than 33%.
Treatment
Once H. pylori is detected in patients with a peptic ulcer, the normal procedure is to eradicate it and allow the ulcer to heal. The standard first-line therapy is a one week triple therapy consisting of a proton pump inhibitor such as omeprazole and the antibiotics clarithromycin and amoxicillin.[41] Variations of the triple therapy have been developed over the years, such as using a different proton pump inhibitor, as with pantoprazole or rabeprazole, or replacing amoxicillin with metronidazole for people who are allergic to penicillin.[42] Such a therapy has revolutionized the treatment of peptic ulcers and has made a cure to the disease possible; previously the only option was symptom control using antacids, H2-antagonists or proton pump inhibitors alone.
An increasing number of infected individuals are found to harbour antibiotic-resistant bacteria. This results in initial treatment failure and requires additional rounds of antibiotic therapy or alternative strategies such as a quadruple therapy, which adds a bismuth colloid.[45][46][47] For the treatment of clarithromycin-resistant strains of H. pylori the use of levofloxacin as part of the therapy has been suggested.[48][49]
Some practitioners of "functional medicine" use herbal formulas to treat Helicobacter pylori infection and claim a great rate of success. However, there are no peer-reviewed clinical studies that provide evidence of the effectiveness of herbal formulas, though many remedies are offered.
Prognosis
H. pylori colonizes the stomach and induces chronic gastritis, a long-lasting inflammation of the stomach. The bacterium persists in the stomach for decades in most people. Most individuals infected by H. pylori will never experience clinical symptoms despite having chronic gastritis. Approximately 10-20% of those colonized by H. pylori will ultimately develop gastric and duodenal ulcers.[8] H. pylori infection is also associated with a 1-2% lifetime risk of stomach cancer and a less than 1% risk of gastric MALT lymphoma.[8]
It is widely believed that in the absence of treatment, H. pylori infection—once established in its gastric niche—persists for life.[3] In the elderly, however, it is likely infection can disappear as the stomach's mucosa becomes increasingly atrophic and inhospitable to colonization. The proportion of acute infections that persist is not known, but several studies that followed the natural history in populations have reported apparent spontaneous elimination.[50][51]
While H. pylori has been disappearing from the stomach of humans, the incidence of the related disorders acid reflux disease, Barrett's esophagus, and esophageal cancer have been rising dramatically.[52] In 1996, Martin J. Blaser advanced the hypothesis that H. pylori has a beneficial effect: by regulating the acidity of the stomach contents, it lowers the impact of regurgitation of gastric acid into the esophagus.[25][52] The hypothesis is not universally accepted as several randomized controlled trials failed to demonstrate worsening of acid reflux disease symptoms following eradication of H. pylori.[53][54] Nevertheless, Blaser has refined his view to assert that H. pylori is a member of the normal flora of the stomach.[55] He postulates that the changes in gastric physiology caused by the loss of H. pylori account for the recent increase in incidence of several diseases, including type 2 diabetes, obesity, and asthma.[55][56] His group has recently shown that H. pylori colonization is associated with a lower incidence of childhood asthma.[57]
Epidemiology
At least half the world's population are infected by the bacterium, making it the most widespread infection in the world.[58] Actual infection rates vary from nation to nation; the Third World has much higher infection rates than the West (Western Europe, North America, Australasia), where rates are estimated to be around 25%.[58] Infections are usually acquired in early childhood in all countries.[8] However, the infection rate of children in developing nations is higher than in industrialized nations, probably due to poor sanitary conditions. In developed nations it is currently uncommon to find infected children, but the percentage of infected people increases with age, with about 50% infected for those over the age of 60 compared with around 10% between 18 and 30 years.[58] The higher prevalence among the elderly reflects higher infection rates when they were children rather than infection at later ages.[8] Prevalence appears to be higher in African-American and Hispanic populations, although this is likely related to socioeconomic rather than racial factors.[59][60] The lower rate of infection in the West is largely attributed to higher hygiene standards and widespread use of antibiotics. Despite high rates of infection in certain areas of the world, the overall frequency of H. pylori infection is declining.[61] However, antibiotic resistance is appearing in H. pylori; there are already many metronidazole- and clarithromycin-resistant strains in most parts of the world.
H. pylori is contagious, although the exact route of transmission is not known.[63][64] Person-to-person transmission by either the oral-oral or fecal-oral route is most likely.[3] Consistent with these transmission routes, the bacteria have been isolated from feces, saliva and dental plaque of some infected people.[3] Transmission occurs mainly within families in developed nations yet can also be acquired from the community in developing countries.[65] H. pylori may also be transmitted orally by means of fecal matter through the ingestion of waste-tainted water, so a hygienic environment could help decrease the risk of H. pylori infection.
History
See also: Timeline of peptic ulcer disease and Helicobacter pylori
Helicobacter pylori (H.pylori for short) was first discovered in the stomachs of patients with gastritis & stomach ulcers nearly 25 years ago by Dr Barry J. Marshall and Dr J. Robin Warren of Perth, Western Australia. At the time (1982/83) the conventional thinking was that no bacterium can live in the human stomach as the stomach produced extensive amounts of acid which was similar in strength to the acid found in a car-battery. Marshall & Warren literally “re-wrote” the text-books with reference to what causes gastritis & gastric ulcers. In recognition of their very important discovery, they were Awarded the 2005 Nobel Prize for Medicine & Physiology. German scientists found spiral-shaped bacteria in the lining of the human stomach in 1875, but they were unable to culture it and the results were eventually forgotten.[52] The Italian researcher Giulio Bizzozero described similarly shaped bacteria living in the acidic environment of the stomach of dogs in 1893.[66] Professor Walery Jaworski of the Jagiellonian University in Kraków investigated sediments of gastric washings obtained from humans in 1899. Among some rod-like bacteria, he also found bacteria with a characteristic spiral shape, which he called Vibrio rugula. He was the first to suggest a possible role of this organism in the pathogenesis of gastric diseases. This work was included in the Handbook of Gastric Diseases, but it had little impact as it was written in Polish.[67] Several small studies conducted in the early 1900s demonstrated the presence of curved rods in the stomach of many patients with peptic ulcers and stomach cancer.[68] However interest in the bacteria waned when an American study published in 1954 failed to observe the bacteria in 1180 stomach biopsies.
Interest in understanding the role of bacteria in stomach diseases was rekindled in the 1970s with the visualization of bacteria in the stomach of gastric ulcer patients.[70] The bacterium had also been observed in 1979 by Australian pathologist Robin Warren, who did further research on it with Australian physician Barry Marshall beginning in 1981. After numerous unsuccessful attempts at culturing the bacteria from the stomach, they finally succeeded in visualizing colonies in 1982 when they unintentionally left their Petri dishes incubating for 5 days over the Easter weekend. In their original paper, Warren and Marshall contended that most stomach ulcers and gastritis were caused by infection by this bacterium and not by stress or spicy food as had been assumed before.
Although there was some skepticism initially, within several years, numerous research groups verified the association of H. pylori with gastritis and to a lesser extent ulcers.[72] To demonstrate that H. pylori caused gastritis and was not merely a bystander, Marshall drank a beaker of H. pylori. He became ill several days later with nausea and vomiting. An endoscopy ten days after inoculation revealed signs of gastritis and the presence of H. pylori. These results suggested that H. pylori was the causative agent of gastritis. Marshall and Warren went on to show that antibiotics are effective in the treatment of many cases of gastritis. In 1987 the Sydney gastroenterologist Thomas Borody invented the first triple therapy for the treatment of duodenal ulcers.[73] In 1994, the National Institutes of Health (USA) published an opinion stating that most recurrent duodenal and gastric ulcers were caused by H. pylori and recommended that antibiotics be included in the treatment regimen.[74] Warren and Marshall were awarded the Nobel Prize in Medicine in 2005 for their work on H. pylori.
Recent research states that genetic diversity in H. pylori decreases with geographic distance from East Africa, the birthplace of modern humans. Using the genetic diversity data, the researchers have created simulations that indicate the bacteria seems to have spread from East Africa around 58,000 years ago. Their results indicate modern humans were already infected by H. pylori before their migrations out of Africa, remaining associated with human hosts since that time.
The bacterium was initially named Campylobacter pyloridis, then renamed C. pylori (pylori = genitive of pylorus) to correct a Latin grammar error. When 16S rRNA gene sequencing and other research showed in 1989 that the bacterium did not belong in the genus Campylobacter, it was placed in its own genus, Helicobacter. The genus derived from the Ancient Greek hělix/έλιξ "spiral" or "coil".[1] The specific epithet pylōri means "of the pylorus" or pyloric valve (the circular opening leading from the stomach into the duodenum), from the Ancient Greek word πυλωρός, which means gatekeeper.[1]
More than 50% of the world's population harbour H. pylori in their upper gastrointestinal tract. Infection is more prevalent in developing countries, and incidence is decreasing in western countries. The route of transmission is unknown, although it is known individuals typically become infected in childhood. H. pylori's helix shape (from which the generic name is derived) is thought to have evolved to penetrate the mucoid lining of the stomach.[2][3]
Microbiology
Scanning electron micrograph of H. pyloriH. pylori is a helix-shaped Gram-negative bacterium, about 3 micrometres long with a diameter of about 0.5 micrometres. It is microaerophilic; that is, it requires oxygen, but at lower concentration than is found in the atmosphere. It contains a hydrogenase which can be used to obtain energy by oxidizing molecular hydrogen (H2) that is produced by intestinal bacteria.[4] It produces oxidase, catalase, and urease. It is capable of forming biofilms[5] and can convert from spiral to a possibly viable but nonculturable coccoid form,[6] both likely to favor its survival and be factors in the epidemiology of the bacterium. The coccoid form can adhere to gastric epithelial cells in vitro.[7]
H. pylori possesses five major outer membrane protein (OMP) families.[8] The largest family includes known and putative adhesins. The other four families include porins, iron transporters, flagellum-associated proteins and proteins of unknown function. Like other typical Gram-negative bacteria, the outer membrane of H. pylori consists of phospholipids and lipopolysaccharide (LPS). The O antigen of LPS may be fucosylated and mimic Lewis blood group antigens found on the gastric epithelium.[8] The outer membrane also contains cholesterol glucosides, which are found in few other bacteria.[8] H. pylori has 4–6 flagella; all gastric and enterohepatic Helicobacter species are highly motile due to flagella.[9] The characteristic sheathed flagellar filaments of helicobacters are composed of two copolymerized flagellins, FlaA and FlaB.[10]
Genome
H. pylori consists of a large diversity of strains, and the genomes of three have been completely sequenced.[11][12][13][14][15] The genome of the strain "26695" consists of about 1.7 million base pairs, with some 1,550 genes. The two sequenced strains show large genetic differences, with up to 6% of the nucleotides differing.
Study of the H. pylori genome is centered on attempts to understand pathogenesis, the ability of this organism to cause disease. Approximately 29% of the loci are in the "pathogenesis" category of the genome database. Both sequenced strains have an approximately 40 kb-long Cag pathogenicity island (a common gene sequence believed responsible for pathogenesis) that contains over 40 genes. This pathogenicity island is usually absent from H. pylori strains isolated from humans who are carriers of H. pylori but remain asymptomatic.[16]
The cagA gene codes for one of the major H. pylori virulence proteins. Bacterial strains that have the cagA gene are associated with an ability to cause ulcers.[17] The cagA gene codes for a relatively long (1186 amino acid) protein. The cag pathogenicity island (PAI) has about 30 genes, part of which code for a complex type IV secretion system. The low GC content of the cag PAI relative to the rest of the helicobacter genome suggests that the island was acquired by horizontal transfer from another bacterial species.
Pathophysiology
Molecular model of H. pylori urease enzymeTo colonize the stomach H. pylori must survive the acidic pH of the lumen and burrow into the mucus to reach its niche, close to the stomach's epithelial cell layer. The bacterium has flagella and moves through the stomach lumen and drills into the mucoid lining of the stomach.[18] Many bacteria can be found deep in the mucus, which is continuously secreted by mucous cells and removed on the luminal side. To avoid being carried into the lumen, H. pylori senses the pH gradient within the mucus layer by chemotaxis and swims away from the acidic contents of the lumen towards the more neutral pH environment of the epithelial cell surface.[19] H. pylori is also found on the inner surface of the stomach epithelial cells and occasionally inside epithelial cells.[20] It produces adhesins which bind to membrane-associated lipids and carbohydrates and help it adhere to epithelial cells. For example, the adhesin BabA binds to the Lewis b antigen displayed on the surface of stomach epithelial cells.[21] H. pylori produces large amounts of the enzyme urease, molecules of which are localized inside and outside of the bacterium. Urease breaks down urea (which is normally secreted into the stomach) to carbon dioxide and ammonia (ammonia is converted into the ammonium ion by taking hydrogen from water upon its breakdown into hydrogen and hydroxyl ions. Hydroxyl ions then react with carbon dioxide, producing bicarbonate which neutralizes gastric acid). The survival of H. pylori in the acidic stomach is dependent on urease, and it would eventually die without the enzyme. The ammonia that is produced is toxic to the epithelial cells, and, along with the other products of H. pylori—including protease, vacuolating cytotoxin A (VacA), and certain phospholipases—damages those cells.[22]
Colonization of the stomach by H. pylori results in chronic gastritis, an inflammation of the stomach lining. The severity of the inflammation is likely to underlie H. pylori-related diseases.[23] Duodenal and stomach ulcers result when the consequences of inflammation allow the acid and pepsin in the stomach lumen to overwhelm the mechanisms that protect the stomach and duodenal mucosa from these caustic substances. The type of ulcer that develops depends on the location of chronic gastritis, which occurs at the site of H. pylori colonization.[24] The acidity within the stomach lumen affects the colonization pattern of H. pylori and therefore ultimately determines whether a duodenal or gastric ulcer will form. In people producing large amounts of acid, H. pylori colonizes the antrum of the stomach to avoid the acid-secreting parietal cells located in the corpus (main body) of the stomach.[8] The inflammatory response to the bacteria induces G cells in the antrum to secrete the hormone gastrin, which travels through the bloodstream to the corpus.[25] Gastrin stimulates the parietal cells in the corpus to secrete even more acid into the stomach lumen. Chronically increased gastrin levels eventually cause the number of parietal cells to also increase, further escalating the amount of acid secreted.[26] The increased acid load damages the duodenum, and ulceration may eventually result. In contrast, gastric ulcers are often associated with normal or reduced gastric acid production, suggesting that the mechanisms that protect the gastric mucosa are defective.[26] In these patients H. pylori can also colonize the corpus of the stomach, where the acid-secreting parietal cells are located. However chronic inflammation induced by the bacteria causes further reduction of acid production and, eventually, atrophy of the stomach lining, which may lead to gastric ulcer and increases the risk for stomach cancer.[27]
About 50-70% of H. pylori strains in Western countries carry the cag pathogenicity island (cag PAI).[28] Western patients infected with strains carrying the cag PAI have a stronger inflammatory response in the stomach and are at a greater risk of developing peptic ulcers or stomach cancer than those infected with strains lacking the island.[8] Following attachment of H. pylori to stomach epithelial cells the type IV secretion system expressed by the cag PAI "injects" the inflammatory inducing agent peptidoglycan from their own cell wall into the epithelial cells. The injected peptidoglycan is recognized by the cytoplasmic immune sensor Nod1, which then stimulates expression of cytokines that promote inflammation.[29]
The type IV secretion apparatus also injects the cag PAI-encoded protein CagA into the stomach's epithelial cells, where it disrupts the cytoskeleton, adherence to adjacent cells, intracellular signaling, cell polarity and other cellular activities.[30] Once inside the cell the CagA protein is phosphorylated on tyrosine residues by a host cell membrane-associated tyrosine kinase. Pathogenic strains of H. pylori have been shown to activate the epidermal growth factor receptor (EGFR), a membrane protein with a tyrosine kinase domain. Activation of the EGFR by H. pylori is associated with altered signal transduction and gene expression in host epithelial cells that may contribute to pathogenesis. It has also been suggested that a c-terminal region of the CagA protein (amino acids 873–1002) can regulate host cell gene transcription independent of protein tyrosine phosphorylation.[16][17] There is a great deal of diversity between strains of H. pylori, and the strain with which one is infected is predictive of the outcome.
Two related mechanisms by which H. pylori could promote cancer are under investigation. One mechanism involves the enhanced production of free radicals near H. pylori and an increased rate of host cell mutation. The other proposed mechanism has been called a "perigenetic pathway"[31] and involves enhancement of the transformed host cell phenotype by means of alterations in cell proteins such as adhesion proteins. It has been proposed that H. pylori induces inflammation and locally high levels of TNF-α and/or interleukin 6. According to the proposed perigenetic mechanism, inflammation-associated signaling molecules such as TNF-α can alter gastric epithelial cell adhesion and lead to the dispersion and migration of mutated epithelial cells without the need for additional mutations in tumor suppressor genes such as genes that code for cell adhesion proteins.[32]
Diagnosis
H. pylori colonized on the surface of regenerative epithelium (image from Warthin-Starry's silver stain)Diagnosis of infection is usually made by checking for dyspeptic symptoms and by tests which can indicate H. pylori infection. One can test noninvasively for H. pylori infection with a blood antibody test, stool antigen test, or with the carbon urea breath test (in which the patient drinks 14C- or 13C-labelled urea, which the bacterium metabolizes, producing labelled carbon dioxide that can be detected in the breath).[33] However, the most reliable method for detecting H. pylori infection is a biopsy check during endoscopy with a rapid urease test, histological examination, and microbial culture. There is also a urine ELISA test with a 96% sensitivity and 79% specificity. None of the test methods is completely failsafe. Even biopsy is dependent on the location of the biopsy. Blood antibody tests, for example, range from 76% to 84% sensitivity. Some drugs can affect H. pylori urease activity and give false negatives with the urea-based tests.
Prevention
H. pylori is a major cause of diseases of the upper gastrointestinal tract. Eradication of the infection in individuals will improve symptoms including dyspepsia, gastritis and peptic ulcers, and may prevent gastric cancer. Rising antimicrobial resistance increases the need for a prevention strategy for the bacteria.[35] There have been extensive vaccine studies in mouse models, which have shown promising results.[36] Researchers are studying different adjuvants, antigens, and routes of immunization to ascertain the most appropriate system of immune protection, with most of the research only recently moving from animal to human trials.
An intramuscular vaccine against H. pylori infection is undergoing Phase I clinical trials and has shown an antibody response against the bacterium. Its clinical usefulness requires further study.[38]
Studies have recently been published suggesting that H. pylori activity could be suppressed via dietary methods.
A Japanese study published April 1, 2009 in the journal Cancer Prevention Research found that eating as little as 2.5 ounces of broccoli sprouts daily for two months reduces the number of colonies of H. pylori bacteria in the stomach by 40% in mice and humans. This treatment also seems to help by enhancing the protection of the gastric mucosa against H. pylori, but is relatively ineffective on related gastric cancers. The previous infection returned within two months after broccoli sprouts were removed from the diet, so an ongoing inclusion in the diet is best for continued protection from H. pylori.[39]
Also, a Korean study published on June 28, 2008 in the journal Korean Journal of Microbiology and Biotechnology found that kimchi contains a bacterium strain "showing strong antagonistic activity against H. pylori." The bacterium strain isolated from kimchi, designated Lb. plantarum NO1, was found to reduce the urease activity of H. pylori by 40-60% and suppress the latter bacteria's binding to human gastric cancer cell line by more than 33%.
Treatment
Once H. pylori is detected in patients with a peptic ulcer, the normal procedure is to eradicate it and allow the ulcer to heal. The standard first-line therapy is a one week triple therapy consisting of a proton pump inhibitor such as omeprazole and the antibiotics clarithromycin and amoxicillin.[41] Variations of the triple therapy have been developed over the years, such as using a different proton pump inhibitor, as with pantoprazole or rabeprazole, or replacing amoxicillin with metronidazole for people who are allergic to penicillin.[42] Such a therapy has revolutionized the treatment of peptic ulcers and has made a cure to the disease possible; previously the only option was symptom control using antacids, H2-antagonists or proton pump inhibitors alone.
An increasing number of infected individuals are found to harbour antibiotic-resistant bacteria. This results in initial treatment failure and requires additional rounds of antibiotic therapy or alternative strategies such as a quadruple therapy, which adds a bismuth colloid.[45][46][47] For the treatment of clarithromycin-resistant strains of H. pylori the use of levofloxacin as part of the therapy has been suggested.[48][49]
Some practitioners of "functional medicine" use herbal formulas to treat Helicobacter pylori infection and claim a great rate of success. However, there are no peer-reviewed clinical studies that provide evidence of the effectiveness of herbal formulas, though many remedies are offered.
Prognosis
H. pylori colonizes the stomach and induces chronic gastritis, a long-lasting inflammation of the stomach. The bacterium persists in the stomach for decades in most people. Most individuals infected by H. pylori will never experience clinical symptoms despite having chronic gastritis. Approximately 10-20% of those colonized by H. pylori will ultimately develop gastric and duodenal ulcers.[8] H. pylori infection is also associated with a 1-2% lifetime risk of stomach cancer and a less than 1% risk of gastric MALT lymphoma.[8]
It is widely believed that in the absence of treatment, H. pylori infection—once established in its gastric niche—persists for life.[3] In the elderly, however, it is likely infection can disappear as the stomach's mucosa becomes increasingly atrophic and inhospitable to colonization. The proportion of acute infections that persist is not known, but several studies that followed the natural history in populations have reported apparent spontaneous elimination.[50][51]
While H. pylori has been disappearing from the stomach of humans, the incidence of the related disorders acid reflux disease, Barrett's esophagus, and esophageal cancer have been rising dramatically.[52] In 1996, Martin J. Blaser advanced the hypothesis that H. pylori has a beneficial effect: by regulating the acidity of the stomach contents, it lowers the impact of regurgitation of gastric acid into the esophagus.[25][52] The hypothesis is not universally accepted as several randomized controlled trials failed to demonstrate worsening of acid reflux disease symptoms following eradication of H. pylori.[53][54] Nevertheless, Blaser has refined his view to assert that H. pylori is a member of the normal flora of the stomach.[55] He postulates that the changes in gastric physiology caused by the loss of H. pylori account for the recent increase in incidence of several diseases, including type 2 diabetes, obesity, and asthma.[55][56] His group has recently shown that H. pylori colonization is associated with a lower incidence of childhood asthma.[57]
Epidemiology
At least half the world's population are infected by the bacterium, making it the most widespread infection in the world.[58] Actual infection rates vary from nation to nation; the Third World has much higher infection rates than the West (Western Europe, North America, Australasia), where rates are estimated to be around 25%.[58] Infections are usually acquired in early childhood in all countries.[8] However, the infection rate of children in developing nations is higher than in industrialized nations, probably due to poor sanitary conditions. In developed nations it is currently uncommon to find infected children, but the percentage of infected people increases with age, with about 50% infected for those over the age of 60 compared with around 10% between 18 and 30 years.[58] The higher prevalence among the elderly reflects higher infection rates when they were children rather than infection at later ages.[8] Prevalence appears to be higher in African-American and Hispanic populations, although this is likely related to socioeconomic rather than racial factors.[59][60] The lower rate of infection in the West is largely attributed to higher hygiene standards and widespread use of antibiotics. Despite high rates of infection in certain areas of the world, the overall frequency of H. pylori infection is declining.[61] However, antibiotic resistance is appearing in H. pylori; there are already many metronidazole- and clarithromycin-resistant strains in most parts of the world.
H. pylori is contagious, although the exact route of transmission is not known.[63][64] Person-to-person transmission by either the oral-oral or fecal-oral route is most likely.[3] Consistent with these transmission routes, the bacteria have been isolated from feces, saliva and dental plaque of some infected people.[3] Transmission occurs mainly within families in developed nations yet can also be acquired from the community in developing countries.[65] H. pylori may also be transmitted orally by means of fecal matter through the ingestion of waste-tainted water, so a hygienic environment could help decrease the risk of H. pylori infection.
History
See also: Timeline of peptic ulcer disease and Helicobacter pylori
Helicobacter pylori (H.pylori for short) was first discovered in the stomachs of patients with gastritis & stomach ulcers nearly 25 years ago by Dr Barry J. Marshall and Dr J. Robin Warren of Perth, Western Australia. At the time (1982/83) the conventional thinking was that no bacterium can live in the human stomach as the stomach produced extensive amounts of acid which was similar in strength to the acid found in a car-battery. Marshall & Warren literally “re-wrote” the text-books with reference to what causes gastritis & gastric ulcers. In recognition of their very important discovery, they were Awarded the 2005 Nobel Prize for Medicine & Physiology. German scientists found spiral-shaped bacteria in the lining of the human stomach in 1875, but they were unable to culture it and the results were eventually forgotten.[52] The Italian researcher Giulio Bizzozero described similarly shaped bacteria living in the acidic environment of the stomach of dogs in 1893.[66] Professor Walery Jaworski of the Jagiellonian University in Kraków investigated sediments of gastric washings obtained from humans in 1899. Among some rod-like bacteria, he also found bacteria with a characteristic spiral shape, which he called Vibrio rugula. He was the first to suggest a possible role of this organism in the pathogenesis of gastric diseases. This work was included in the Handbook of Gastric Diseases, but it had little impact as it was written in Polish.[67] Several small studies conducted in the early 1900s demonstrated the presence of curved rods in the stomach of many patients with peptic ulcers and stomach cancer.[68] However interest in the bacteria waned when an American study published in 1954 failed to observe the bacteria in 1180 stomach biopsies.
Interest in understanding the role of bacteria in stomach diseases was rekindled in the 1970s with the visualization of bacteria in the stomach of gastric ulcer patients.[70] The bacterium had also been observed in 1979 by Australian pathologist Robin Warren, who did further research on it with Australian physician Barry Marshall beginning in 1981. After numerous unsuccessful attempts at culturing the bacteria from the stomach, they finally succeeded in visualizing colonies in 1982 when they unintentionally left their Petri dishes incubating for 5 days over the Easter weekend. In their original paper, Warren and Marshall contended that most stomach ulcers and gastritis were caused by infection by this bacterium and not by stress or spicy food as had been assumed before.
Although there was some skepticism initially, within several years, numerous research groups verified the association of H. pylori with gastritis and to a lesser extent ulcers.[72] To demonstrate that H. pylori caused gastritis and was not merely a bystander, Marshall drank a beaker of H. pylori. He became ill several days later with nausea and vomiting. An endoscopy ten days after inoculation revealed signs of gastritis and the presence of H. pylori. These results suggested that H. pylori was the causative agent of gastritis. Marshall and Warren went on to show that antibiotics are effective in the treatment of many cases of gastritis. In 1987 the Sydney gastroenterologist Thomas Borody invented the first triple therapy for the treatment of duodenal ulcers.[73] In 1994, the National Institutes of Health (USA) published an opinion stating that most recurrent duodenal and gastric ulcers were caused by H. pylori and recommended that antibiotics be included in the treatment regimen.[74] Warren and Marshall were awarded the Nobel Prize in Medicine in 2005 for their work on H. pylori.
Recent research states that genetic diversity in H. pylori decreases with geographic distance from East Africa, the birthplace of modern humans. Using the genetic diversity data, the researchers have created simulations that indicate the bacteria seems to have spread from East Africa around 58,000 years ago. Their results indicate modern humans were already infected by H. pylori before their migrations out of Africa, remaining associated with human hosts since that time.
Barrett's esophagus
Barrett's esophagus (British English: oesophagus) (sometimes called Barrett's syndrome, CELLO, columnar epithelium lined lower esophagus and colloquially referred to as Barrett's) refers to an abnormal change (metaplasia) in the cells of the lower end of the esophagus thought to be caused by damage from chronic acid exposure, or reflux esophagitis.[1] The normal lining of the esophagus (squamous epithelium) is replaced by an intestinal-type lining (columnar epithelium).
Barrett's esophagus is found in 5-15% of patients who seek medical care for heartburn (gastroesophageal reflux disease, GERD), although a large subgroup of patients with Barrett's esophagus do not have symptoms.[2] It is considered to be a premalignant condition because it is associated with an increased risk of esophageal cancer (more specifically, adenocarcinoma) of about 0.5% per patient-year.[3][2] Diagnosis of Barrett's esophagus requires endoscopy (more specifically, esophagogastroduodenoscopy, a procedure in which a small tube with a camera at the top is used to look at the esophagus, stomach and first part of the bowels) and biopsy (taking small tissue samples which are analysed using microscopy). The progression from Barrett's esophagus to esophageal cancer is divided into non-dysplastic changes, low-grade and high-grade dysplasia (abnormal cell maturation associated with a risk of progression to cancer) and frank carcinoma. In high-grade dysplasia, the risk of developing cancer might be at 10% per patient-year or greater.[2]
Many professional medical societies propose endoscopic screening of patients with GERD and endoscopic surveillance of patients with Barrett's esophagus, although little direct evidence supports this practice, which is common in many developed countries.[2] Treatment options for high-grade dysplasia include surgical removal of the esophagus (esophagectomy) or endoscopic treatments such as endoscopic mucosal resection or ablation (destruction). Currently, there is no intervention that has been shown to prevent the development of Barrett's esophagus or its progression to esophageal cancer.[2]
The condition is named after Norman Barrett (1903–1979) who described the condition in 1957.[4]
Contents [hide]
1 Causes and symptoms
2 Pathology
3 Treatment
4 Additional images
5 References
6 External links
[edit] Causes and symptoms
Barrett's esophagus is caused by gastroesophageal reflux disease, GERD (UK: GORD), which allows the stomach's contents to damage the cells lining the lower esophagus. Researchers are unable to predict which heartburn sufferers will develop Barrett's esophagus. While there is no relationship between the severity of heartburn and the development of Barrett's esophagus, there is a relationship between chronic heartburn and the development of Barrett's esophagus. Sometimes people with Barrett's esophagus will have no heartburn symptoms at all. In rare cases, damage to the esophagus may be caused by swallowing a corrosive substance such as lye.
The change from normal to premalignant cells that indicates Barrett's esophagus does not cause any particular symptoms. However, warning signs that should not be ignored include:
frequent and longstanding heartburn
trouble swallowing (dysphagia)
vomiting blood
pain under the breastbone where the esophagus meets the stomach
unintentional weight loss because eating is painful
[edit] Pathology
Micrograph of Barrett's esophagus (left of image) and normal stratified squamous epithelium (right of image). Alcian blue stain.
High magnification micrograph of Barrett's esophagus showing the characteristic goblet cells. Alcian blue stain.Barrett's esophagus is marked by the presence of columnar epithelia in the lower esophagus, replacing the normal squamous cell epithelium—an example of metaplasia. The secretory columnar epithelium may be more able to withstand the erosive action of the gastric secretions; however, this metaplasia confers an increased risk of adenocarcinoma.[5]
The metaplastic columnar cells may be of two types: gastric (similar to those in the stomach, which is NOT technically Barrett's esophagus) or colonic (similar to cells in the intestines). A biopsy of the affected area will often contain a mixture of the two. Colonic-type metaplasia is the type of metaplasia associated with risk of malignancy in genetically susceptible people.
The metaplasia of Barrett's esophagus is grossly visible through a gastroscope, but biopsy specimens must be examined under a microscope to determine whether cells are gastric or colonic in nature. Colonic metaplasia is usually identified by finding goblet cells in the epithelium and is necessary for the true diagnosis of Barrett's.
There are many histologic mimics of Barrett's esophagus (i.e. goblet cells occurring in the transitional epithelium of normal esophageal submucosal gland ducts, "pseudogoblet cells" in which abundant foveolar (gastric) type mucin simulates the acid mucin true goblet cells). Assessment of relationship to submucosal glands and transitional-type epithelium with examination of multiple levels through the tissue may allow the pathologist to reliably distinguish between goblet cells of submucosal gland ducts and true Barrett's esophagus (specialized columnar metaplasia). Use of the histochemical stain Alcian blue pH 2.5 is also frequently used to distinguish true intestinal-type mucins from their histologic mimics. Recently, immunohistochemical analysis with antibodies to CDX-2 (specific for mid and hindgut intestinal derivation) has also been utilized to identify true intestinal-type metaplastic cells. It has been shown that the protein AGR2 is elevated in Barrett's esophagus,[6] and can be used as a biomarker for distinguishing Barrett's epithelium from normal esophageal epithelium.[7]
After the initial diagnosis of Barrett's esophagus is rendered, affected persons undergo annual surveillance to detect changes that indicate higher risk to progression to cancer: development of dysplasia. There is considerable variability in assessment for dysplasia among pathologists. Recently, gastroenterology and GI pathology societies have recommended that any diagnosis of high grade dysplasia in Barrett's be confirmed by at least two fellowship trained GI pathologists prior to definitive treatment for patients.
[edit] Treatment
The risk of malignancy is highest in the U.S. in Caucasian men > 50 years of age with > 5 years of symptoms. It is unusual for African-American men to develop adenocarcinoma of the esophagus, the cancer associated with Barrett's. Current recommendations include routine endoscopy and biopsy (looking for dysplastic changes). If two endoscopies and biopsy sessions performed within 12 months are negative for dysplasia then surveillance can be performed every 3 years while the underlying reflux is controlled with proton pump inhibitor drugs in combination with measures to prevent reflux. For patients found to have low grade or high grade dysplasia close observation and repeat endoscopy and biopsies are indicated and the patient should be followed closely by a gastroenterologist.
Proton pump inhibitor drugs have not yet been proven to prevent esophageal cancer. Laser treatment is used in severe dysplasia, while overt malignancy may require surgery, radiation therapy, or systemic chemotherapy. Additionally, a recent 5-year random-controlled trial has shown that photodynamic therapy using photofrin is statistically more effective in eliminating dysplastic growth areas than sole use of a proton pump inhibitor.[8]There is presently no reliable way to determine which patients with Barrett's esophagus will go on to develop esophageal cancer, although a recent study found that the detection of three different genetic abnormalities were associated with as much as a 79% chance of developing cancer in 6 years.[9]
Endoscopic mucosal resection (EMR) has also been evaluated as a management technique.[10] Additionally an operation known as a Nissen fundoplication can reduce the reflux of acid from the stomach into the esophagus.[11]
In a variety of studies, non-steroidal anti-inflammatory drugs (NSAIDS), like aspirin, have shown evidence of preventing esophageal cancer in Barrett's esophagus patients.[12][13] However, none of these studies have been randomized, placebo controlled trials, which are considered the gold standard for evaluating a medical intervention. In addition, the best dose of NSAIDs for cancer prevention is not yet known.
[edit] Additional images
Micrograph of Barrett's esophagus. Alcian blue stain.
[edit] References
^ Stein H, Siewert J (1993). "Barrett's esophagus: pathogenesis, epidemiology, functional abnormalities, malignant degeneration, and surgical management". Dysphagia 8 (3): 276–88. doi:10.1007/BF01354551. PMID 8359051.
^ a b c d e Shaheen NJ, Richter JE (March 2009). "Barrett's oesophagus". Lancet 373 (9666): 850–61. doi:10.1016/S0140-6736(09)60487-6. PMID 19269522.
^ Koppert L, Wijnhoven B, van Dekken H, Tilanus H, Dinjens W (2005). "The molecular biology of esophageal adenocarcinoma". J Surg Oncol 92 (3): 169–90. doi:10.1002/jso.20359. PMID 16299787.
^ Barrett N (1957). "The lower esophagus lined by columnar epithelium". Surgery 41 (6): 881–94. PMID 13442856.
^ Fléjou J (2005). "Barrett's oesophagus: from metaplasia to dysplasia and cancer". Gut 54 Suppl 1: i6–12. doi:10.1136/gut.2004.041525. PMID 15711008.
^ Elizabeth Pohler, Ashley L. Craig, James Cotton, Laura Lawrie, John F. Dillon, Pete Ross, Neil Kernohan and Ted R. Hupp (2004). "The Barrett’s Antigen Anterior Gradient-2 Silences the p53 Transcriptional Response to DNA Damage". Molecular and Cellular Proteomics 3: 534–547. doi:10.1074/mcp.M300089-MCP200. PMID 14967811.
^ Murray E, McKenna EO, Burch LR, Dillon J, Langridge-Smith P, Kolch W, Pitt A, Hupp TR (2007). "Microarray-formatted clinical biomarker assay development using peptide aptamers to anterior gradient-2". Biochemistry 46: 13742–51. doi:10.1021/bi7008739. PMID 17994709.
^ Overholt BF, Wang KK, Burdick JS, et al. (2007). "Five-year efficacy and safety of photodynamic therapy with Photofrin in Barrett's high-grade dysplasia.". Gastrointestinal endoscopy 66 (3): 460–8. doi:10.1016/j.gie.2006.12.037. PMID 17643436.
^ Galipeau P, Li X, Blount PL, Maley CC, Sanchez CA Odze RD, Ayub K, Rabinovitch PS, Vaughan TV, Reid BJ (2007). "NSAIDs modulate CDKN2A, TP53, and DNA content risk for progression to esophageal adenocarcinoma". PLoS Medicine 4 (2): e67. doi:10.1371/journal.pmed.0040067. PMID 17326708.
^ Reshamwala P, Darwin P (2006). "Endoscopic management of early gastric cancer". Curr Opin Gastroenterol 22 (5): 541–5. doi:10.1097/01.mog.0000239870.04457.80. PMID 16891887.
^ Abbas A, Deschamps C, Cassivi SD, et al. (2004). "The role of laparoscopic fundoplication in Barrett’s esophagus". Annals of Thoracic Surgery 77 (2): 393–396. doi:10.1016/S0003-4975(03)01352-3. PMID 14759403.
^ Corley DA, Kerlikowske K, Verma R, Buffler P (2003). "Protective association of aspirin/NSAIDs and esophageal cancer: a systematic review and meta-analysis.". Gastroenterology 124: 47–56. doi:10.1053/gast.2003.50008. PMID 12512029.
^ Vaughan TL, Dong LM, Blount PL, Ayub K, Odze RD, Sanchez, CA, Rabinovitch PS, Reid BJ (2005). "Non-steroidal anti-inflammatory drugs and risk of neoplastic progression in Barrett's oesophagus: a prospective study". Lancet Oncol 6: 945–52. doi:10.1016/S1470-2045(05)70431-9. PMID 16321762.
[edit] External links
Barrett's Esophagus at National Institute of Diabetes and Digestive and Kidney Diseases (NIDDKD)
Barrett's Info a peer-reviewed web site of information on Barrett's esophagus and its clinical management.
Barrett's Esophagus at Johns Hopkins University
Barrett's Esophagus Video Overview and Barrett's Esophagus Health Information at Mayo Clinic
Barrett's Oesophagus Campaign Originally The Barrett's Oesophagus Foundation, the UK charity committed to research into prevention of adenocarcinoma of the esophagus
Barrett's esophagus is found in 5-15% of patients who seek medical care for heartburn (gastroesophageal reflux disease, GERD), although a large subgroup of patients with Barrett's esophagus do not have symptoms.[2] It is considered to be a premalignant condition because it is associated with an increased risk of esophageal cancer (more specifically, adenocarcinoma) of about 0.5% per patient-year.[3][2] Diagnosis of Barrett's esophagus requires endoscopy (more specifically, esophagogastroduodenoscopy, a procedure in which a small tube with a camera at the top is used to look at the esophagus, stomach and first part of the bowels) and biopsy (taking small tissue samples which are analysed using microscopy). The progression from Barrett's esophagus to esophageal cancer is divided into non-dysplastic changes, low-grade and high-grade dysplasia (abnormal cell maturation associated with a risk of progression to cancer) and frank carcinoma. In high-grade dysplasia, the risk of developing cancer might be at 10% per patient-year or greater.[2]
Many professional medical societies propose endoscopic screening of patients with GERD and endoscopic surveillance of patients with Barrett's esophagus, although little direct evidence supports this practice, which is common in many developed countries.[2] Treatment options for high-grade dysplasia include surgical removal of the esophagus (esophagectomy) or endoscopic treatments such as endoscopic mucosal resection or ablation (destruction). Currently, there is no intervention that has been shown to prevent the development of Barrett's esophagus or its progression to esophageal cancer.[2]
The condition is named after Norman Barrett (1903–1979) who described the condition in 1957.[4]
Contents [hide]
1 Causes and symptoms
2 Pathology
3 Treatment
4 Additional images
5 References
6 External links
[edit] Causes and symptoms
Barrett's esophagus is caused by gastroesophageal reflux disease, GERD (UK: GORD), which allows the stomach's contents to damage the cells lining the lower esophagus. Researchers are unable to predict which heartburn sufferers will develop Barrett's esophagus. While there is no relationship between the severity of heartburn and the development of Barrett's esophagus, there is a relationship between chronic heartburn and the development of Barrett's esophagus. Sometimes people with Barrett's esophagus will have no heartburn symptoms at all. In rare cases, damage to the esophagus may be caused by swallowing a corrosive substance such as lye.
The change from normal to premalignant cells that indicates Barrett's esophagus does not cause any particular symptoms. However, warning signs that should not be ignored include:
frequent and longstanding heartburn
trouble swallowing (dysphagia)
vomiting blood
pain under the breastbone where the esophagus meets the stomach
unintentional weight loss because eating is painful
[edit] Pathology
Micrograph of Barrett's esophagus (left of image) and normal stratified squamous epithelium (right of image). Alcian blue stain.
High magnification micrograph of Barrett's esophagus showing the characteristic goblet cells. Alcian blue stain.Barrett's esophagus is marked by the presence of columnar epithelia in the lower esophagus, replacing the normal squamous cell epithelium—an example of metaplasia. The secretory columnar epithelium may be more able to withstand the erosive action of the gastric secretions; however, this metaplasia confers an increased risk of adenocarcinoma.[5]
The metaplastic columnar cells may be of two types: gastric (similar to those in the stomach, which is NOT technically Barrett's esophagus) or colonic (similar to cells in the intestines). A biopsy of the affected area will often contain a mixture of the two. Colonic-type metaplasia is the type of metaplasia associated with risk of malignancy in genetically susceptible people.
The metaplasia of Barrett's esophagus is grossly visible through a gastroscope, but biopsy specimens must be examined under a microscope to determine whether cells are gastric or colonic in nature. Colonic metaplasia is usually identified by finding goblet cells in the epithelium and is necessary for the true diagnosis of Barrett's.
There are many histologic mimics of Barrett's esophagus (i.e. goblet cells occurring in the transitional epithelium of normal esophageal submucosal gland ducts, "pseudogoblet cells" in which abundant foveolar (gastric) type mucin simulates the acid mucin true goblet cells). Assessment of relationship to submucosal glands and transitional-type epithelium with examination of multiple levels through the tissue may allow the pathologist to reliably distinguish between goblet cells of submucosal gland ducts and true Barrett's esophagus (specialized columnar metaplasia). Use of the histochemical stain Alcian blue pH 2.5 is also frequently used to distinguish true intestinal-type mucins from their histologic mimics. Recently, immunohistochemical analysis with antibodies to CDX-2 (specific for mid and hindgut intestinal derivation) has also been utilized to identify true intestinal-type metaplastic cells. It has been shown that the protein AGR2 is elevated in Barrett's esophagus,[6] and can be used as a biomarker for distinguishing Barrett's epithelium from normal esophageal epithelium.[7]
After the initial diagnosis of Barrett's esophagus is rendered, affected persons undergo annual surveillance to detect changes that indicate higher risk to progression to cancer: development of dysplasia. There is considerable variability in assessment for dysplasia among pathologists. Recently, gastroenterology and GI pathology societies have recommended that any diagnosis of high grade dysplasia in Barrett's be confirmed by at least two fellowship trained GI pathologists prior to definitive treatment for patients.
[edit] Treatment
The risk of malignancy is highest in the U.S. in Caucasian men > 50 years of age with > 5 years of symptoms. It is unusual for African-American men to develop adenocarcinoma of the esophagus, the cancer associated with Barrett's. Current recommendations include routine endoscopy and biopsy (looking for dysplastic changes). If two endoscopies and biopsy sessions performed within 12 months are negative for dysplasia then surveillance can be performed every 3 years while the underlying reflux is controlled with proton pump inhibitor drugs in combination with measures to prevent reflux. For patients found to have low grade or high grade dysplasia close observation and repeat endoscopy and biopsies are indicated and the patient should be followed closely by a gastroenterologist.
Proton pump inhibitor drugs have not yet been proven to prevent esophageal cancer. Laser treatment is used in severe dysplasia, while overt malignancy may require surgery, radiation therapy, or systemic chemotherapy. Additionally, a recent 5-year random-controlled trial has shown that photodynamic therapy using photofrin is statistically more effective in eliminating dysplastic growth areas than sole use of a proton pump inhibitor.[8]There is presently no reliable way to determine which patients with Barrett's esophagus will go on to develop esophageal cancer, although a recent study found that the detection of three different genetic abnormalities were associated with as much as a 79% chance of developing cancer in 6 years.[9]
Endoscopic mucosal resection (EMR) has also been evaluated as a management technique.[10] Additionally an operation known as a Nissen fundoplication can reduce the reflux of acid from the stomach into the esophagus.[11]
In a variety of studies, non-steroidal anti-inflammatory drugs (NSAIDS), like aspirin, have shown evidence of preventing esophageal cancer in Barrett's esophagus patients.[12][13] However, none of these studies have been randomized, placebo controlled trials, which are considered the gold standard for evaluating a medical intervention. In addition, the best dose of NSAIDs for cancer prevention is not yet known.
[edit] Additional images
Micrograph of Barrett's esophagus. Alcian blue stain.
[edit] References
^ Stein H, Siewert J (1993). "Barrett's esophagus: pathogenesis, epidemiology, functional abnormalities, malignant degeneration, and surgical management". Dysphagia 8 (3): 276–88. doi:10.1007/BF01354551. PMID 8359051.
^ a b c d e Shaheen NJ, Richter JE (March 2009). "Barrett's oesophagus". Lancet 373 (9666): 850–61. doi:10.1016/S0140-6736(09)60487-6. PMID 19269522.
^ Koppert L, Wijnhoven B, van Dekken H, Tilanus H, Dinjens W (2005). "The molecular biology of esophageal adenocarcinoma". J Surg Oncol 92 (3): 169–90. doi:10.1002/jso.20359. PMID 16299787.
^ Barrett N (1957). "The lower esophagus lined by columnar epithelium". Surgery 41 (6): 881–94. PMID 13442856.
^ Fléjou J (2005). "Barrett's oesophagus: from metaplasia to dysplasia and cancer". Gut 54 Suppl 1: i6–12. doi:10.1136/gut.2004.041525. PMID 15711008.
^ Elizabeth Pohler, Ashley L. Craig, James Cotton, Laura Lawrie, John F. Dillon, Pete Ross, Neil Kernohan and Ted R. Hupp (2004). "The Barrett’s Antigen Anterior Gradient-2 Silences the p53 Transcriptional Response to DNA Damage". Molecular and Cellular Proteomics 3: 534–547. doi:10.1074/mcp.M300089-MCP200. PMID 14967811.
^ Murray E, McKenna EO, Burch LR, Dillon J, Langridge-Smith P, Kolch W, Pitt A, Hupp TR (2007). "Microarray-formatted clinical biomarker assay development using peptide aptamers to anterior gradient-2". Biochemistry 46: 13742–51. doi:10.1021/bi7008739. PMID 17994709.
^ Overholt BF, Wang KK, Burdick JS, et al. (2007). "Five-year efficacy and safety of photodynamic therapy with Photofrin in Barrett's high-grade dysplasia.". Gastrointestinal endoscopy 66 (3): 460–8. doi:10.1016/j.gie.2006.12.037. PMID 17643436.
^ Galipeau P, Li X, Blount PL, Maley CC, Sanchez CA Odze RD, Ayub K, Rabinovitch PS, Vaughan TV, Reid BJ (2007). "NSAIDs modulate CDKN2A, TP53, and DNA content risk for progression to esophageal adenocarcinoma". PLoS Medicine 4 (2): e67. doi:10.1371/journal.pmed.0040067. PMID 17326708.
^ Reshamwala P, Darwin P (2006). "Endoscopic management of early gastric cancer". Curr Opin Gastroenterol 22 (5): 541–5. doi:10.1097/01.mog.0000239870.04457.80. PMID 16891887.
^ Abbas A, Deschamps C, Cassivi SD, et al. (2004). "The role of laparoscopic fundoplication in Barrett’s esophagus". Annals of Thoracic Surgery 77 (2): 393–396. doi:10.1016/S0003-4975(03)01352-3. PMID 14759403.
^ Corley DA, Kerlikowske K, Verma R, Buffler P (2003). "Protective association of aspirin/NSAIDs and esophageal cancer: a systematic review and meta-analysis.". Gastroenterology 124: 47–56. doi:10.1053/gast.2003.50008. PMID 12512029.
^ Vaughan TL, Dong LM, Blount PL, Ayub K, Odze RD, Sanchez, CA, Rabinovitch PS, Reid BJ (2005). "Non-steroidal anti-inflammatory drugs and risk of neoplastic progression in Barrett's oesophagus: a prospective study". Lancet Oncol 6: 945–52. doi:10.1016/S1470-2045(05)70431-9. PMID 16321762.
[edit] External links
Barrett's Esophagus at National Institute of Diabetes and Digestive and Kidney Diseases (NIDDKD)
Barrett's Info a peer-reviewed web site of information on Barrett's esophagus and its clinical management.
Barrett's Esophagus at Johns Hopkins University
Barrett's Esophagus Video Overview and Barrett's Esophagus Health Information at Mayo Clinic
Barrett's Oesophagus Campaign Originally The Barrett's Oesophagus Foundation, the UK charity committed to research into prevention of adenocarcinoma of the esophagus
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