咖啡的好處很多

Coffee: The Original Wonder Drug?

July 24, 2012

Mental and Medical Benefits of Coffee:

Introduction
The best part of waking up...is reducing your risk of neurodegeneration. And depression, and cancer, and cardiovascular disease... It's becoming increasingly clear that coffee is more than just a morning routine. The body of data suggesting that the world's most widely used stimulant is beneficial in a variety of mental and medical conditions is growing at a staggering rate. A recent study published in the New England Journal of Medicinefound that coffee consumption lowered all-cause mortality by over 10% at 13-year follow-up.[1] Based primarily on recent Medscape Medical News coverage, the following slideshow reviews the potential medical and psychiatric benefits of coffee consumption.

Cardiovascular Disease      
It may seem counterintuitive: A substance known to increase blood pressure might actually be good for your cardiovascular system. Caffeine consumption can cause a short-lived increase in blood pressure – a major risk factor for cardiovascular disease (CVD) – and regular use has been linked to a longer-term increase. However, when caffeine is ingested via coffee, enduring blood pressure elevations are small and CVD risks may be balanced by protective properties. Coffee beans contain antioxidant compounds that reduce oxidation of low-density lipoprotein (LDL) cholesterol and coffee consumption has been associated with reduced concentrations of inflammatory markers.[2-7] Moderate coffee intake was associated with a lower risk for coronary heart disease as far out as 10 years,[3] and new data suggest that an average of 2 cups a day protects against heart failure.[8]

Cerebrovascular Disease and Stroke      
The vascular benefits of coffee are not lost on the brain. According to a 2011 meta-analysis, consuming between 1 and 6 cups a day reportedly cut stroke risk by 17%.[9] A 22% to 25% risk reduction was seen in a large sample of Swedish women followed for an average of 10 years.[10] And while coffee's impact on stroke risk in those with CVD is still in question, a meta-analysis presented at the European Meeting on Hypertension 2012 found that 1 to 3 cups a day may protect against ischemic stroke in the general population.[11]

Diabetes and Weight Loss      
Despite coffee's association with increased blood pressure, the steamy brew appears to benefit other aspects of so-called “metabolic syndrome,” the dangerous cluster of hypertension, hyperglycemia, abnormal lipid levels, and increased body fat. Numerous studies have linked regular coffee drinking with improved glucose metabolism, insulin secretion, and a significantly reduced risk for type 2 diabetes.[12-14] Preliminary data from an ongoing study also suggest that coffee consumption can promote weight loss. Overweight patients treated with unroasted coffee beans in supplement form lost an average of 17 pounds over 22 weeks. The study authors suspect that this effect may be due in part to coffee containing chlorogenic acid, a plant compound with antioxidant properties thought to reduce glucose absorption.[15]

Cancer
       With so many ingestibles thought to increase cancer risk – soda, grilled meat, all things pickled – at least we can rest easy when it comes to coffee (according to recent data, anyway). Evidence suggests that moderate to heavy coffee consumption can reduce the risk for numerous cancers, including endometrial (> 4 cups/day),[16]prostate (6 cups/day),[17] head and neck (4 cups/day),[18,19] basal cell carcinoma (> 3 cups/day),[20] and estrogen receptor-negativebreast cancer (> 5 cups/day).[21] The benefits are thought to be at least partially due to coffee's antioxidant and antimutagenic properties.[16,18]

Neurodegeneration      
It's clear that coffee temporarily affects cognition – try getting through morning rounds without a cup. But new research also links coffee with more enduring effects on cognitive well-being. A studypublished in the Journal of Alzheimer's Disease showed that patients with mild cognitive impairment and plasma caffeine levels of > 1200 ng/mL – courtesy of ~3 to 5 cups of coffee a day – avoided progression to dementia over the following 2 to 4 years. [22]Corresponding studies in mice suggest that caffeine suppresses enzymes involved in amyloid-beta production, while coffee consumption boosts G-CSF, interleukin-10, and interleukin-6 levels, cytokines thought to contribute to the reported benefits. Caffeinated coffee has long been thought to be neuroprotective in Parkinson disease (PD), and recent work found that variants in the glutamate-receptor gene GRIN2A affect PD risk in coffee drinkers.[23]Furthermore, data presented at this year's American Academy of Neurology Annual Meeting showed that 3 cups of coffee a day may prevent the formation of Lewy bodies, a signature preclinical pathologic finding in PD.[24] Despite the encouraging associations in neurodegenerative disease, caffeine intake has also been associated with accelerating age of onset of Huntington disease.[25]

Depression      
A 2011 study suggests that a boost in coffee consumption might also benefit our mental health[26]: Women who drank 2 to 3 cups of coffee per day had a 15% decreased risk for depression compared with those who drank less than 1 cup per week. A 20% decreased risk was seen in those who drank 4 cups or more per day. The short-term effect of coffee on mood may be due to altered serotonin and dopamine activity, whereas the mechanisms behind its potential long-term effects on mood may relate to its antioxidant and anti-inflammatory properties, factors that are thought to play a role in depressive illnesses.[26-29]

Liver Disease      
The liver might help break down coffee, but coffee might protect the liver (in some cases). Evidence suggests that coffee consumption slows disease progression in patients with alcoholic cirrhosis and hepatitis C and reduces the risk of developing hepatocellular carcinoma.[30-33] A 2012 study reported that coffee intake is associated with a lower risk for nonalcoholic fatty liver disease (NAFLD),[34] while other recent work found that coffee protects against liver fibrosis in those with already established NAFLD.[32]

But That's Not All...
A grab-bag of other research suggests that coffee intake may relieve dry-eye syndrome by increasing tear production,[35] reduce the risk for gout,[36] and potentially fight infection.[37] Coffee and hot tea consumption were found to be protective against one of the medical community's most concerning bugs, methicillin-resistantStaphylococcus aureus (MRSA).[37] While it remains unclear whether the beverages have systemic antimicrobial activity, study participants who reported any consumption of either were approximately half as likely to have MRSA in their nasal passages.

And Finally, the Risks
As is often the case, with the benefits come the risks, and coffee consumption certainly has negative medical and psychiatric effects to consider. Besides the aforementioned potential increase in blood pressure, coffee can incite or worsen anxiety, insomnia, and tremor and potentially elevate glaucoma risk.[38] Also, given the potential severity of symptoms, caffeine withdrawal syndrome is under consideration for inclusion in the forthcoming DSM-5.[39]
Additional research is necessary to better assess and balance the potential benefits and drawbacks of coffee consumption. But mounting evidence suggests that going back for a second cup might not necessarily be a bad decision.

References

1. Freedman ND, Park Y, Abnet CC, et al. Association of coffee drinking with total and cause-specific mortality. N Engl J Med. 2012;366:1891-1904. Abstract

2. Larsson SC, Orsini N. Coffee consumption and risk of stroke: a dose-response meta-analysis of prospective studies. Am J Epidemiol. 2011;174:993-1001. Abstract

3. Wu JN, Ho SC, Zhou C, et al. Coffee consumption and risk of coronary heart diseases: a meta-analysis of 21 prospective cohort studies. Int J Cardiol. 2009;137:216-225. Abstract

4. Natella F, Nardini M, Belelli F, et al. Coffee drinking induces incorporation of phenolic acids into LDL and increases the resistance of LDL to ex vivo oxidation in humans. Am J Clin Nutr. 2007;86:604-609. Abstract

5. Gómez-Ruiz JA, Leake DS, Ames JM. In vitro antioxidant activity of coffee compounds and their metabolites. J Agric Food Chem. 2007;55:6962-6969. Abstract

6. Nardini M, D'Aquino M, Tomassi G, et al. Inhibition of human low-density lipoprotein oxidation by caffeic acid and other hydroxycinnamic acid derivatives. Free Radic Biol Med. 1995;19:541-552. Abstract

7. Montagnana M, Favaloro EJ, Lippi G. Coffee intake and cardiovascular disease: virtue does not take center stage. Semin Thromb Hemost. 2012;38:164-177. Abstract

8. Mostofsky E, Rice MS, Levitan EB, Mittleman MA. Habitual coffee consumption and risk of heart failure: a doseresponse meta-analysis. Circ Heart Fail. 2012;DOI:10.1161/CIRCHEARTFAILURE.112.967299. http://circheartfailure.ahajournals.org

9. Larsson SC, Orsini N. Coffee consumption and risk of stroke: a dose-response meta-analysis of prospective studies. Am J Epidemiol. 2011;174:993-1001. Abstract

10. Larsson SC, Virtamo J, Wolk A. Coffee consumption and risk of stroke in women. Stroke. 2011;42:908-912. Abstract

11. D'Elia L, Cairella G, Garbagnati F, et al. Moderate coffee consumption is associated with lower risk of stroke: meta-analysis of prospective studies. J Hypertension. 2012;30 (e-Supplement A):e107.

12. Huxley R, Lee CM, Barzi F, et al. Coffee, decaffeinated coffee, and tea consumption in relation to incident type 2 diabetes mellitus: a systematic review with meta-analysis. Arch Intern Med. 2009;169:2053-2063. Abstract

13. Sartorelli DS, Fagherazzi G, Balkau B, et al. Differential effects of coffee on the risk of type 2 diabetes according to meal consumption in a French cohort of women: the E3N/EPIC cohort study. Am J Clin Nutr. 2010;91:1002-112.Abstract

14. Floegel A, Pischon T, Bermann MM, et al. Coffee consumption and risk of chronic disease in the European Prospective Investigation into Cancer and Nutrition (EPIC)Germany study. Am J Clin Nutr. 2012;95:901-908. Abstract

15. Vinson JA, Burnham B, Nagendran MV, et al. Randomized double-blind placebo-controlled crossover study to evaluate the efficacy and safety of a green coffee bean extract in overweight subjects. Program and abstracts of the 243rd American Chemical Society National Meeting and Exposition; March 25-29, 2012; San Diego, California. Abstract 92.

16. Je Y, Hankison SE, Tworoger SS, et al. A prospective cohort study of coffee consumption and risk of endometrial cancer over a 26-year follow-up. Cancer Epidemiol Biomarkers Prev. 2011;20:1-9.

17. Wilson KM, Kasperzyk JL, Rider JR, et al. Coffee consumption and prostate cancer risk and progression in the Health Professionals Follow-up Study. J Natl Cancer Inst. 2011;8;103:876-884.

18. Turati F, Galeone C, La Vecchia C, et al. Coffee and cancers of the upper digestive and respiratory tracts: meta-analyses of observational studies. Ann Oncol. 2011;22:536-544. Abstract

19. Galeone C, Tavani A, Pelucchi C, et al. Coffee and tea intake and risk of head and neck cancer: pooled analysis in the international head and neck cancer epidemiology consortium. Cancer Epidemiol Biomarkers Prev. 2010;19:1723-1736. Abstract

20. Song F, Qureshi AA, Han J. Increased caffeine intake is associated with reduced risk of Basal cell carcinoma of the skin. Cancer Res. 2012;72:3282-3289. Abstract

21. Li J, Seibold P, Chang-Claude J, et al. Coffee consumption modifies risk of estrogen-receptor negative breast cancer. Breast Cancer Res. 2011;13:R49.

22. Cao C, Loewenstein DA, Lin X, et al. High blood caffeine levels in MCI linked to lack of progression to dementia. J Alzheimer Dis. 2012;30:559-572.

23. Hamza TH, Chen H, Hill-Burns EM, et al. Genome-wide gene-environment study identifies glutamate receptor gene GRIN2A as a Parkinson's disease modifier gene via interaction with coffee. PLoS Genet. 2011;7: e1002237.

24. Ross W, Duda J, Abbott R, et al. Association of coffee caffeine consumption with brain Lewy pathology in the Honolulu-Asia Aging Study. Program and abstracts of the 64th Annual Meeting of the American Academy of Neurology; April 21-28, 2012; New Orleans, Louisiana. Abstract #S42.005.

25. Duru C. Caffeine is a modifier of age at onset in Huntington's disease. Program and abstracts of the 15th International Congress of Parkinson's Disease and Movement Disorders; June 5-9, 2011; Toronto, Ontario, Canada. Abstract 180.

26. Lucas M, Mirzaei F, Pan A, et al. Coffee, caffeine, and risk of depression among women. Arch Intern Med. 2011;171:1571-1578. Abstract

27. Pasco JA, Nicholson GC, Williams LJ, et al. Association of high-sensitivity C-reactive protein with de novo major depression. Br J Psychiatry. 2010;197:372-377. Abstract

28. Ng F, Berk M, Dean O, Bush AI. Oxidative stress in psychiatric disorders: evidence base and therapeutic implications. Int J Neuropsychopharmacol. 2008;11:851-876. Abstract

29. O'Connor A. Coffee drinking linked to less depression in women. New York Times. February 13, 2012. http://well.blogs.nytimes.com/2011/09/26/coffee-drinking-linked-to-less-depression-in-women/ Accessed January 11, 2012.

30. Molloy JW, Calcagno CJ, Williams CD, Jones FJ, Torres DM, Harrison SA. Association of coffee and caffeine consumption with fatty liver disease, nonalcoholic steatohepatitis, and degree of hepatic fibrosis. Hepatology. 2012;55:429-436. Abstract

31. Gallus S, Tavani A, Negri E, La Vecchia C. Does coffee protect against liver cirrhosis? Ann Epidemiol. 2002;12:202-205.

32. Molloy JW, Calcagno CJ, Williams CD, et al. Association of coffee and caffeine consumption with fatty liver disease, nonalcoholic steatohepatitis, and degree of hepatic fibrosis. Hepatology. 2012;55:429-436. Abstract

33. Modi AA, Feld JJ, Park Y, et al. Increased caffeine consumption is associated with reduced hepatic fibrosis. Hepatology. 2010;51:201-209. Abstract

34. Birerdinc A, Stepanova M, Pawloski L, Younossi M. Caffeine is protective in patients with non-alcoholic fatty liver disease. Aliment Pharmacol Ther. 2012;3576-82.

35. Arita R, Yanagi Y, Honda N, Maeda S, et al. Caffeine increases tear volume depending on polymorphisms within the adenosine A2a receptor gene and cytochrome P450 1A2. Ophthalmology. 2012;119:972-978. Abstract

36. Choi HK, Willett W, Curhan G. Coffee consumption and risk of incident gout in men: A prospective study. Arthritis Rheum. 2007;56:2049-2055. Abstract

37. Matheson EM, Mainous AG, Everett CJ, King DE. Tea and coffee consumption and MRSA nasal carriage. Ann Fam Med. 2011;9:299-304. Abstract

38. Pasquale L. Program and abstracts of the American Glaucoma Society 22nd Annual Meeting; March 1-4, 2012; New York, New York. Abstracts 23 and 83.

39. Compton WM, Budney AJ, Hasin D. New approaches to substance and related diagnoses in the DSM-5. Program and abstracts of the American Academy of Addiction Psychiatry (AAAP) 22nd Annual Meeting and Symposium; December 8-11, 2011; Scottsdale, Arizona. Workshop B2. Presented December 9, 2011.
Author
Bret Stetka, MD, Editorial Director, Medscape from WebMD
Reviewers
Henry R. Black, MD, Clinical Professor of Internal Medicine; Director, Hypertension Research, Center for the Prevention of Cardiovascular Disease, New York University School of Medicine, New York, New York

 

楸出 "台灣薄熙來"，特偵組主任(檢察總長)可以競選台灣總統

[不論媒體如何爆料，特偵組不立即啟動調查，就不可能知道真相! 沒有公平的法治就沒有真正的民主。楸出最上層的' "台灣薄熙來"，特偵組主任(檢察總長)可以競選台灣總統!]





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阿嬌任帳房？　吳敦義改口：幫忙看帳款 【19:06】**********


吳敦義今對外改口說，阿嬌只是來幫忙，看看帳款，這很正常。（本報資料照，記者詹朝陽攝）
〔本報訊〕前行政院秘書長林益世案，持續延燒至副總統吳敦義，吳的小姨子阿嬌，遭民進黨立委趙天麟指稱為吳敦義的「白毛套」、「帳房」。吳敦義今對外再改口，坦承阿嬌有在選舉時到總部幫忙，並指「選舉時，親人去參與、去看看帳，這很正常。」

*****吳：選舉時親人來總部幫忙很正常*****

　針對民進黨立委爆料指控阿嬌擔任「帳房」的角色，吳敦義昨日原表示，阿嬌只是家庭主婦，低調到不行，怎可能是帳房，請爆料的立委提出證據，不要含血噴人。不過今日吳敦義接受訪問時又改口表示：「選舉時，親人去幫忙看看帳是很正常的。」他表示83年、87年在選市長時，由於阿嬌是蔡令怡的妹妹，所以會到總部幫忙、做事情。

　自從阿嬌被外界爆料是吳敦義的「帳房」後，歷經4天以來吳的說詞閃爍，已有明顯程度上的差異。先是於19日時連聲「她絕對不是帳房，絕對不是」，明確表示沒有這回事，更拿出通聯紀錄證明；21日再連忙撇清阿嬌只是家庭主婦；到了今日又表示「只是幫忙看帳」。隨著吳「擠牙膏式」的問答，讓外界更啟疑竇。

*****前議員爆料　吳將阿嬌安插市府職缺*****

　前高雄市議員黃昭星今日也表示，吳敦義擔任高雄市長時，阿嬌在官邸擔任管家。但吳敦義卻將阿嬌的職務安插在「環保局機要」的職缺。然而阿嬌並未在環保局工作，4、5年來領著公家的薪水。

　對這種「有名無實」的職缺，黃昭星表示，當時有民進黨議員質詢提到此事，並要求政風單位調查。然而，政風單位卻未做任何處理，黃昭星認為這有瀆職的嫌疑。

*****官邸管家變公職　吳：是大嫂阿雪、一切合法*****

　對於是否有將阿嬌安插在市府的職務，吳敦義澄清當時並非是阿嬌，而是自己的大嫂「阿雪」。他表示，官舍本來就有一個幫忙做打掃、接電話等工作的人，而將她的名字放在環保局機總務科，這都是「很正常、合法的事情」。

*****洪智坤再po文　批吳第一時間都說謊*****

　昨天踢爆「1998年吳敦義選高雄市長的時候，阿嬌就是負責大筆請款的帳房工作」的民進黨中執委洪智坤，今晚又在他的臉書po文表示「Bingo…吳敦義的問題，就是第一時間都說謊。」洪智坤認為吳敦義今天承認阿嬌有在總部幫忙，應進一步說明幫什麼忙？如果是財務會計，那趙天麟說「阿嬌是帳房」，為什麼吳敦義要那麼緊張？他也表示「吳敦義無論說看看帳、算算帳、收收帳…啊不就是帳房?」。

　洪智坤補充說，1998年奉新潮流之命，負責南部立委、市議員候選人文宣，當時進駐在高雄。由於當時選舉產業的廠商並不多，藍、綠常共用一個印刷、噴畫廠商，他從廠商口中提過「阿嬌」的角色----廠商大筆的請款，都要到吳敦義總部找蔡令怡的妹妹「阿嬌」。


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吳敦義頻澄清　智庫：僅15.4%民眾相信 【18:22】**********


總統馬英九的滿意度仍然持續低迷。（圖／翻攝自《台灣智庫》）
〔本報訊〕前行政院秘書長林益世案涉貪案，重創馬政府的聲望，據《台灣智庫》發布最新民調指出，僅約20.8%的民眾認為國民黨是「清廉」的。此外，副總統吳敦義的廉潔近期不斷被外界質疑，也使得他不斷出面澄清，然而據民調顯示，僅15.4%的民眾相信吳的說法。

*****66.7%認為有更高層官員涉入*****

　台灣智庫今發表最新民調，分別於17、18日採用隨機抽樣的方式，完成1073份有效的樣本數。近來外界不斷質疑林益世案背後還有許多的「案外案」，據民調指出，高達73.4%的民眾認為馬政府還有其餘「未爆彈」，且66.7%的民眾認為有更高層級的官員涉入。

　近期吳敦義的小姨子「阿嬌」郝英嬌，不斷遭外界質疑是吳的「白手套」。吳敦義不斷為自己澄清，但顯然不被民眾接受。民調指出，僅15.4%的民眾相信他是清白的，卻有高達64.4%的民眾不相信他。

*****反貪英雄　特偵組、廉政署不如媒體*****

　此外，林益世涉貪案的偵辦進度也被大作文章，僅31.6%民眾認為特偵組是積極的。最後問到對台灣反貪貢獻最大的，竟然由媒體《壹週刊》獲得39.2%的民眾支持，其次才是特偵組，但也僅16.2%，被總統馬英九賦予重任的廉政署，僅3.3%民眾認可。

台灣前任總統的套房

[對台灣前任總統如此的待遇，只顯示KMT及其選民的水準。最野蠻的土匪也不過如此]

"〈星期專論〉1.3坪的總統套房"


◎王美琇

這是台灣卸任總統陳水扁先生的牢房。

四面都是牆，只有一扇窗戶可以透進一些陽光。窗戶對面牆上有個柵欄小窗，看守的警衛隨時會透過小窗察看室內動靜。牆的右下角有一個老鼠洞般的小缺口，是遞送牢飯的入口。

沒有人性的總統牢房

獄方說，這個牢房有一．八六坪。但阿扁總統說只有一．三坪，因為扣掉如廁的茅坑和茅坑旁的水桶雜物置放區。這就是卸任總統在台北監獄的「總統套房」，而且是雙人房。

他上廁所的地方不是蹲式或坐式馬桶，而是中間挖一個洞的茅坑。起床時，他必須蹲在茅坑上刷牙洗臉；洗澡時，他雙腳站立在茅坑兩邊，伸手舀起水桶的水往身上淋浴。茅坑的左上角有個監視器，廿四小時監看，如廁洗澡全都錄，無所遁形。

在扣掉茅坑和置物區後，僅存的空間必須兩人對分，所以每個人實際可以使用的面積是○．六坪。阿扁總統就是在○．六坪的空間裡，睡地板、蹲著吃飯、坐著讀書、趴在地上寫文章。水泥地上雖隔了一層薄薄的木板，但冬天的寒意依舊穿透木板直逼脊骨，他必須鋪上棉被才得以驅寒入眠。

扁訴說著牢獄生活，臉上掛著有點苦澀又無奈的笑容。他的額頭暗沉、臉色黑黑的，少了以前常見的容光煥發。我問他為什麼臉這麼黑？他說是太陽曬的。以前一天只有放封半小時，一個月前因為很多立委和醫生關心，所以獄方增加到每天一小時，因此就盡量曬太陽。

也因為有太多立委和國內外醫生的關切，終於在一個月前，獄方在他的牢房對面的空牢房放了一張桌椅，讓扁在坐了近四年的牢獄後，第一次可以「坐著」吃飯和寫字。但這張桌椅只有幾小時的使用時限，時間到就必須回到他的「總統套房」。

很多探監者問獄方為何不讓扁「下工」（到工廠工作）？因為一般犯人每天可以下工八小時。獄方說，安全問題他們無法負責。安全問題？是擔心扁在工廠搞組織、搞工運嗎？因為不能下工，所以扁除了每天一小時的放封時間外，其餘二十三小時都必須蹲在一．三坪的總統套房。

扁的身心都出問題

寫到這裡，心裡有點酸楚。我試著閉上眼睛（也請你試著閉上眼睛）想像一下：如果把自己關在一個一．三坪、有馬桶作伴的浴室裡，我能夠忍受多久？……恐怕一小時我都無法忍受。可是你知道嗎？扁已經在這樣的空間生活近四年了。他沒有被關到發瘋，實在是奇蹟。

台大創傷外科柯文哲醫師說起探扁的故事。扁問柯醫師：「我能不能到長庚醫院檢查身體？」柯問他為什麼想去長庚？扁說：「我只有上次去桃園醫院就醫時有睡過床。我很想睡在床上。」聽了真是鼻酸。

因為長期監禁在幽閉狹小的空間，而且長時間趴在地上寫字，他在長庚醫院徹底檢查後，醫院的醫生和扁總統醫師團的醫師們，都異口同聲指出扁已經罹患多種疾病，包括：心臟冠狀動脈問題、高血脂症、攝護腺血塊、胃食道逆流、十二指腸前壁炎、直腸糜爛、左下肺葉塌陷、輸精管出血、關節炎、自主神經錯亂、創傷後壓力症候群、重鬱症等。

美國人權醫師團來探監後，其中一位醫師Ken Yoneda說：「我完全無法想像一個前總統會被關在生活狀況這麼差的牢裡。這種事情在美國絕不會發生。就算前總統尼克森犯法，也沒有坐過牢。」另一位醫師Joeseph Lin說：「扁的獄中環境非常不人道，除了診斷出的心臟和胃食道逆流等問題外，他有時會感到窒息，無法呼吸，感覺快要死掉。」

美國醫師團做出診斷結論：扁因為長期密閉監禁和壓力，有嚴重身心問題，必須立刻接受全面性治療和改善監獄環境，否則健康會持續惡化下去。

七月十二日，美國眾議員安德魯斯和龍格聯名提交一份名為「長期囚禁對台灣前總統陳水扁身心狀況的影響」報告書，給美國國會「湯姆．藍托斯人權委員會」。這份二十四頁的調查報告，敦促台灣總統馬英九基於人道考量，儘速讓陳水扁保外就醫。

全世界沒有任何民主國家，敢如此明目張膽惡整一個卸任總統，即使他有罪。不過也有很多人認為，扁案的審理過程，充滿太多違反正當法律程序的司法瑕疵。

總統職位，是國家尊嚴和榮譽的最高象徵。馬政府對待陳前總統的做法，不但是在踐踏總統名位、踐踏國家尊榮和民主價值，更是法西斯的惡質權力鬥爭︱︱利用國家機器把政敵鬥到你死我活為止。

文明的最低檢驗標準

結束探訪，和扁握手道別。走兩步，回頭看他，只見他揮揮手又摸摸膝蓋。想起他因為長期趴在地上寫字而出問題的手指和膝蓋關節。

心頭百感交集。大步走出台北監獄，耳邊輕輕響起柯文哲醫師的話：「讓阿扁病死在監獄裡，符合台灣社會的最大利益嗎？」

到底是什麼樣的政權，可以把一個卸任總統折磨到瀕臨瘋狂和垂死邊緣？到底是什麼樣的文明素養，可以讓一個民主國家的現任總統如此對待一個卸任總統？是這個現任總統馬英九先生太殘忍？還是台灣社會太冷酷無情？

台灣，是一個文明社會嗎？還是一個弱肉強食的原始森林？究竟什麼是文明？

有人說，文明的最低檢驗標準，是看你對待弱者的態度。更何況，他是被關出一身病的卸任總統。不是嗎？

心裡的疑惑、憤怒和苦悶揪成一團，融化在炎炎夏日的台北街頭。

（作者王美琇為專欄作家）

（備註：筆者擬將本文譯成英文，並與社團合作擴大社會連署，然後將連署文本和醫界連署一併寄給全世界重要媒體與人權組織，請其嚴重關切此案。

****************************************
"柯文哲︰扁被知覺虐待 淪次等囚犯"

〔記者林恕暉／台北報導〕台大創傷醫學部主任柯文哲最近在臉書指出，一般囚犯每天可以和獄友團體互動，前總統陳水扁卻以安全為由，幾乎整天被關在一．三坪的空間，這是醫學上的「知覺剝奪」虐待，變成「次等囚犯」。

替陳水扁看診的柯文哲前晚在臉書發表「扁案Ｑ＆Ａ」文章，柯文哲認為，一般囚犯每天可出去工作八小時，可以和獄友團體互動，晚上再回牢房睡覺，而不是以安全為理由，幾乎整天被關在一．三坪的空間，醫學上這是一種「知覺剝奪」的虐待，「因為他的特別，使他變成次等囚犯」。

柯文哲認為，讓前任總統躺在地上睡覺，趴在地上寫字，坐在地上吃飯，穿著囚衣，面目猥瑣，不管是洗澡上廁所，二十四小時監視器盯著，「說得出名字的國家都沒有發生過這種事」。

柯文哲說，「我最生氣的是你抗議，他就改一點，還當做施捨要你感激，我說給他一個桌椅，他就在牆上釘一個板子，讓你坐在地上寫。你再抗議，他就準備桌椅，每天一次讓你坐兩個小時，時間到了，叫你回去繼續坐在地上，你再抗議，那就一天桌椅坐兩次」，「真的不需要這樣！」

柯文哲指出，給所有受刑人一張床睡覺，這無關藍綠，台灣號稱「人權立國」，卻讓受刑人睡在地上，把人當人看待，是文明國家的起碼要求，現在受刑人都沒有健保，他希望受刑人都得到該有的醫療，「歧視和虐待不會使台灣社會更好」。

憂鬱症會導致血液中維他命D濃度降低

"Low Vitamin D a Result, Not a Cause, of Depression"

Megan Brooks
July 20, 2012 — Low serum vitamin D is linked to depression, but treating with high doses of the supplement does not appear to ease depressive symptoms, new research suggests.
A randomized controlled trial conducted by investigators from the Medical Clinic, University Hospital of North Norway, in Tromsø, showed that participants with low vitamin D levels had significantly higher depression scores than participants with high vitamin D levels (P < .05) but that high-dose vitamin D supplementation for 6 months had no significant effect on depressive symptom scores when compared with placebo.
"This implies that vitamin D deficiency is the result of depression and not the cause of depression," first author Marie Kjærgaard, PhD, told Medscape Medical News.
"The take-home message," she said, is that clinicians "should not try to treat depression with vitamin D, but they must be aware that this patient population is at risk of vitamin D deficiency."
The study was published online July 12 in the British Journal of Psychiatry.
Clear Negative Result
There have been a number of cross-sectional studies linking low vitamin D to depression, including 1 published in Mayo Clinic Proceedings in November 2011 and reported byMedscape Medical News at that time.
This study and others have fueled suggestions that vitamin D supplementation might help alleviate depressive symptoms. Yet "very few" randomized controlled trials (RCTs) have been done, Dr. Kjærgaard said, "and these have all been on selected populations [and] have shown diverging results. It has not yet been established if there is a causal relationship between vitamin D and depression," she added.
For the study, investigators recruited 334 healthy volunteers. At baseline, 230 had low serum 25-hydroxyvitamin D (25[OH]D) levels (< 55 nmol/L), and 114 had high 25(OH)D levels (> 70 nmol/L).
Participants with low vitamin D levels were randomly assigned to receive either placebo or 40,000 IU vitamin D3 per week for 6 months. Participants with high vitamin D levels served as nested controls.
Depressive symptoms were evaluated with the Beck Depression Inventory (BDI), Hospital Anxiety and Depression Scale (HADS), Seasonal Pattern Assessment Scale (SPAQ), and Montgomery-Åsberg Depression Rating Scale (MADRS).
There was no significant effect of vitamin D supplementation regardless of whether the data were analyzed per-protocol, as intention-to-treat, or when only participants with very low (< 25 nmol/L) and low (< 40 nmol/L) baseline vitamin D levels were included, the researchers say. Analyses stratified for sex, age, body mass index, and smoking status did not alter the results.
"Our study," said Dr. Kjærgaard, "is the first RCT on a general population with a clear negative result, indicating that there is no causal relationship." Nonetheless, "our study is only a small piece in the puzzle, and more studies most be performed to support our results."
Laura Tripkovic, RD, from the Institute of Biosciences and Medicine, University of Surrey in Guildford, United Kingdom, who was not involved in the study, agrees that more research is needed. In the meantime, "it's beneficial to maintain healthy levels of vitamin D, if not to prevent depression, then to most certainly help protect bone health," she toldMedscape Medical News.
The study was supported by a grant from the Northern Norway Regional Health Authority. The authors and Dr. Tripkovic have disclosed no relevant financial relationships.
Br J Psychiatry. Published online July 12, 2012

Low Vitamin D a Result, Not a Cause, of Depression
Megan Brooks
July 20, 2012 — Low serum vitamin D is linked to depression, but treating with high doses of the supplement does not appear to ease depressive symptoms, new research suggests.
A randomized controlled trial conducted by investigators from the Medical Clinic, University Hospital of North Norway, in Tromsø, showed that participants with low vitamin D levels had significantly higher depression scores than participants with high vitamin D levels (P < .05) but that high-dose vitamin D supplementation for 6 months had no significant effect on depressive symptom scores when compared with placebo.
"This implies that vitamin D deficiency is the result of depression and not the cause of depression," first author Marie Kjærgaard, PhD, told Medscape Medical News.
"The take-home message," she said, is that clinicians "should not try to treat depression with vitamin D, but they must be aware that this patient population is at risk of vitamin D deficiency."
The study was published online July 12 in the British Journal of Psychiatry.
Clear Negative Result
There have been a number of cross-sectional studies linking low vitamin D to depression, including 1 published in Mayo Clinic Proceedings in November 2011 and reported byMedscape Medical News at that time.
This study and others have fueled suggestions that vitamin D supplementation might help alleviate depressive symptoms. Yet "very few" randomized controlled trials (RCTs) have been done, Dr. Kjærgaard said, "and these have all been on selected populations [and] have shown diverging results. It has not yet been established if there is a causal relationship between vitamin D and depression," she added.
For the study, investigators recruited 334 healthy volunteers. At baseline, 230 had low serum 25-hydroxyvitamin D (25[OH]D) levels (< 55 nmol/L), and 114 had high 25(OH)D levels (> 70 nmol/L).
Participants with low vitamin D levels were randomly assigned to receive either placebo or 40,000 IU vitamin D3 per week for 6 months. Participants with high vitamin D levels served as nested controls.
Depressive symptoms were evaluated with the Beck Depression Inventory (BDI), Hospital Anxiety and Depression Scale (HADS), Seasonal Pattern Assessment Scale (SPAQ), and Montgomery-Åsberg Depression Rating Scale (MADRS).
There was no significant effect of vitamin D supplementation regardless of whether the data were analyzed per-protocol, as intention-to-treat, or when only participants with very low (< 25 nmol/L) and low (< 40 nmol/L) baseline vitamin D levels were included, the researchers say. Analyses stratified for sex, age, body mass index, and smoking status did not alter the results.
"Our study," said Dr. Kjærgaard, "is the first RCT on a general population with a clear negative result, indicating that there is no causal relationship." Nonetheless, "our study is only a small piece in the puzzle, and more studies most be performed to support our results."
Laura Tripkovic, RD, from the Institute of Biosciences and Medicine, University of Surrey in Guildford, United Kingdom, who was not involved in the study, agrees that more research is needed. In the meantime, "it's beneficial to maintain healthy levels of vitamin D, if not to prevent depression, then to most certainly help protect bone health," she toldMedscape Medical News.
The study was supported by a grant from the Northern Norway Regional Health Authority. The authors and Dr. Tripkovic have disclosed no relevant financial relationships.
Br J Psychiatry. Published online July 12, 2012

Low Vitamin D a Result, Not a Cause, of Depression
Megan Brooks
July 20, 2012 — Low serum vitamin D is linked to depression, but treating with high doses of the supplement does not appear to ease depressive symptoms, new research suggests.
A randomized controlled trial conducted by investigators from the Medical Clinic, University Hospital of North Norway, in Tromsø, showed that participants with low vitamin D levels had significantly higher depression scores than participants with high vitamin D levels (P < .05) but that high-dose vitamin D supplementation for 6 months had no significant effect on depressive symptom scores when compared with placebo.
"This implies that vitamin D deficiency is the result of depression and not the cause of depression," first author Marie Kjærgaard, PhD, told Medscape Medical News.
"The take-home message," she said, is that clinicians "should not try to treat depression with vitamin D, but they must be aware that this patient population is at risk of vitamin D deficiency."
The study was published online July 12 in the British Journal of Psychiatry.
Clear Negative Result
There have been a number of cross-sectional studies linking low vitamin D to depression, including 1 published in Mayo Clinic Proceedings in November 2011 and reported byMedscape Medical News at that time.
This study and others have fueled suggestions that vitamin D supplementation might help alleviate depressive symptoms. Yet "very few" randomized controlled trials (RCTs) have been done, Dr. Kjærgaard said, "and these have all been on selected populations [and] have shown diverging results. It has not yet been established if there is a causal relationship between vitamin D and depression," she added.
For the study, investigators recruited 334 healthy volunteers. At baseline, 230 had low serum 25-hydroxyvitamin D (25[OH]D) levels (< 55 nmol/L), and 114 had high 25(OH)D levels (> 70 nmol/L).
Participants with low vitamin D levels were randomly assigned to receive either placebo or 40,000 IU vitamin D3 per week for 6 months. Participants with high vitamin D levels served as nested controls.
Depressive symptoms were evaluated with the Beck Depression Inventory (BDI), Hospital Anxiety and Depression Scale (HADS), Seasonal Pattern Assessment Scale (SPAQ), and Montgomery-Åsberg Depression Rating Scale (MADRS).
There was no significant effect of vitamin D supplementation regardless of whether the data were analyzed per-protocol, as intention-to-treat, or when only participants with very low (< 25 nmol/L) and low (< 40 nmol/L) baseline vitamin D levels were included, the researchers say. Analyses stratified for sex, age, body mass index, and smoking status did not alter the results.
"Our study," said Dr. Kjærgaard, "is the first RCT on a general population with a clear negative result, indicating that there is no causal relationship." Nonetheless, "our study is only a small piece in the puzzle, and more studies most be performed to support our results."
Laura Tripkovic, RD, from the Institute of Biosciences and Medicine, University of Surrey in Guildford, United Kingdom, who was not involved in the study, agrees that more research is needed. In the meantime, "it's beneficial to maintain healthy levels of vitamin D, if not to prevent depression, then to most certainly help protect bone health," she toldMedscape Medical News.
The study was supported by a grant from the Northern Norway Regional Health Authority. The authors and Dr. Tripkovic have disclosed no relevant financial relationships.
Br J Psychiatry. Published online July 12, 2012

美國國土安全部改正對台灣的稱呼

For Immediate Release
Washington, D.C. — July 20, 2012
Contact: (202) 547-3686

DHS AGREES TO DROP “CHINA (TAIWAN)” REFERENCE FROM I-94 DOCUMENTS AND GLOBAL ENTRY PROGRAM AT URGING OF REP. HOWARD BERMAN

WASHINGTON (July 20, 2012) — Responding to a recent letter from Congressman Howard Berman (D-CA), ranking member of the House Committee on Foreign Affairs, the U.S. Department of Homeland Security (DHS) this week announced its decision to correct references to Taiwan on Form I-94 documents issued to Taiwanese visitors entering the United States, and during the application process of the Global Entry Program.

On June 19, 2012 Berman wrote to DHS Secretary Janet Napolitano asking that I-94 documents issued by Customs and Border Protection (CBP) to Taiwanese visitors entering the United States list their country of citizenship as Taiwan, rather than “China (Taiwan).” The letter noted: “It has been a long-standing U.S. policy that the U.S. government refers to Taiwan as ‘Taiwan.’ This designation is employed by the Department of State, the Department of Defense and other federal agencies.”

In a letter to Berman dated July 17, 2012, Assistant Commissioner Michael Yeager of CBP’s Office of Congressional Affairs stated: “CBP has looked into and corrected this matter. Henceforth, persons presenting Taiwanese passports will have their country of citizenship listed and recorded as "Taiwan" on their respective Form I-94 and the Global Entry Program application process will refer to "Taiwan."

The issue was brought to FAPA’s attention by members in New York who discovered that their Taiwanese relatives were issued Form I-94 documents that referred to their country of citizenship as “China (Taiwan)” when crossing over the Canadian border into the United States at Niagara Falls. Other FAPA members found their country of birth listed as “Taiwan (Province of China)” when applying to CBP’s Global Entry Program in Orlando, FL.

In a press release, Berman thanked CBP for recognizing that a correction needed to be made, saying: “This is about fairness and today is a victory for the entire Taiwanese community.” He added: “It is an indignity to force Taiwanese citizens to list anything other than Taiwan on their U.S. entry documents, and together we righted this unfortunate wrong.”

On April 30, 2012, Rep. Howard Berman also wrote to California Secretary of State Debra L. Bowen, urging her to correct the reference to Taiwan as "Taiwan, Province of China” in the state’s online voter registration system. The state of California fixed the problem within the week, enabling Taiwanese Americans in California to list their country of birth as "Taiwan" when registering to vote.

In 1994, Rep. Berman was the primary force behind legislation allowing for Taiwanese Americans to list "Taiwan" in their American passports instead of "China."

FAPA President Mark Kao, PhD states: “We are very grateful for Congressman Berman’s steadfast efforts over the past 20 years to ensure that the official U.S. policy regarding Taiwan’s name is faithfully applied by all U.S. government agencies.” Dr. Kao concludes: “He has safeguarded the dignity and identity of Taiwanese Americans and of the people of Taiwan.”


"美國國土安全部同意回應柏曼議員之呼籲，修正I-94入境卡及「全球自動通關計畫」上對台灣的錯誤稱謂"

華府訊─美國國土安全局於本週宣佈決議修改發給入境美國之台灣旅客的I-94入境卡及「全球自動通關計畫」中對台灣的錯誤稱謂，以回應日前眾議院外交事務委員會副主席─加州共和黨眾議員柏曼（Howard Berman）日前之要求信函。

柏曼議員於六月十九日致函國土安全部部長拿坡莉塔諾（Janet Napolitano），要求該部轄下「海關及邊境保衛局」（CBP）發給入境美國之台灣旅客的I-94入境卡上需將其國籍列為「台灣」而非「中國台灣」。該信函中表示：「美國政府長久以來的政策一直將台灣稱之為『台灣』。美國國務院、國防部，及其他聯邦機構皆沿用此稱謂原則。」

該局「國會事務處」助理處長葉格（Michael Yeager）於七月十七日回函柏曼議員：「本局已調查並修正台灣國籍。此後，簽發予持台灣護照人士之I-94入境卡上所註明之國籍將列為『台灣』。『全球自動通關計畫』之申請手續中亦會將其註明為『台灣』。」

此事源起於台灣人公共事務會紐約分會會員之親屬從加拿大尼加拉瀑布入境美國時，赫見其I-94入境卡上將台灣列為「中國台灣」。另有其他會員在佛州奧蘭多申請CBP之「全球自動通關計畫」時發現該系統將其出生地列為「中國台灣省」。

在一新聞稿中，柏曼議員向CBP致意，感謝該局同意修正該錯誤。柏曼議員談道：「此事關公平原則。今天是整個台灣人社區的勝利。」他並表示：「強迫台灣國民必須在入境美國之文件上將其國籍列為『台灣』以外之稱謂都是有辱尊嚴的。今天我們一起改正了這項錯誤。」

柏曼議員曾於今年四月三十日致函加州州務卿包雯（Debra L. Bowen），呼籲其更正加州選舉註冊系統上將台灣列為「中國台灣省」之錯誤。加州當局於一週內即修正該錯誤，讓當地台美人得以將其出生地列為「台灣」。

早於1994年，柏曼眾議員便已是推動立法允許台美人在其美國護照上將出生地列為「台灣」而非「中國」的強力推手。

台灣人公共事務會會長高龍榮博士表示：「我們很感謝柏曼議員過去二十多年來的堅定，努力確保各美國政府機構有確實執行美國對台的稱謂原則。他保障了台美人和台灣人的尊嚴和認同。」

使用長髮劑Propecia可能失去男性性功能 !!

For Some Men, Propecia's Sexual Side Effects May Be Long-lasting

• (ABC News)

  
  

Kevin Malley was almost 30, and he was starting to lose his hair. He went to his doctor to see if there was a way to keep from going bald, and his doctor prescribed Propecia.

"I looked young for my age, so I wanted to hold off my hair loss for a little bit," Malley said. "I didn't plan on taking Propecia for more than a year."

Malley started taking the drug in May 2011, and by October he was completely impotent and had no sex drive whatsoever. His body changed, even his genitals shrank, and he slipped into a mental fog that he just couldn't clear. His doctor told him the side effects would go away if he stopped taking the drug, so he did. But nothing changed.

"I kept expecting the side effects to go away, but they did not, they only got worse," he said.

Malley is not alone: A new study published today in the Journal of Sexual Medicine suggests that for some men, the sexual side effects of Propecia may last for months to years, even after they stop taking the drug.

Researchers from George Washington University interviewed 54 men under age 40 who reported side effects for three months or more after taking Propecia, also called finasteride, to treat their hair loss. None of the men reported having any sexual, medical or psychiatric problems before they took the drug. Some of the men took the drug for a few weeks, others took it for years, but all of them reported side effects such as erectile dysfunction, decreased sexual drive, problems with orgasms, shrinking and painful genitals, even some neurological problems, such as depression, anxiety and mental fogginess.

For 96 percent of the men, the sexual problems lasted for more than a year after they stopped taking the drug.

"Our findings make me suspicious that this drug may have done permanent damage to these men," said Dr. Michael Irwig, the author of the study. "The chances that they will improve? I think it's lower and lower the longer they have these side effects."

Irwig cautions that it's possible that only men who were the most affected by the drug participated in the study. Because he recruited his study participants through an online forum called PropeciaHelp, a group for men who have experienced persistent sexual side effects from the drug, he said the study may not have included men who have fewer or less pervasive side effects.

FDA, Merck Know of Drug's Side Effects

Finasteride works by blocking the conversion of testosterone into a more potent form, called DHT, which contributes to hair loss. It was originally developed in 1992 by drug giant Merck as a treatment for enlarged prostates and sold as the drug Proscar.

Propecia was approved by the U.S. Food and Drug Administration in 1997, and at that time Merck noted that a few men reported sexual side effects during clinical trials of the drug. On its website, the agency said those side effects were resolved when patients stopped taking the drug.

But the agency received more than 400 reports over 13 years from consumers reporting sexual dysfunction, and nearly 60 men reported that those side effects lasted longer than three months after the men stopped the medication. In 2011, the FDA mandated a label change for Propecia and Proscar, warning that some patients reported erectile dysfunction that lasted after patients stopped taking it; in April, the agency updated the label to include reports of libido, ejaculation and orgasm disorders.

In a statement, Merck said no evidence has proved a causal relationship between Propecia and long-lasting sexual dysfunction.

"Merck believes that Propecia (finasteride) has demonstrated safety and efficacy profiles and that the product labeling appropriately describes the benefits and risks of the drug to help inform prescribing," the company wrote in the statement.

But researchers say many physicians who prescribe finasteride are likely not aware that the side effects of the drug may haunt patients for years.

"These things just get handed out left and right for any urinary symptoms," said Dr. Ryan Terlecki, an assistant professor of urology at Wake Forest School of Medicine, who has prescribed Proscar for some of his patients with enlarged prostates.

Terlecki said the findings about long-term side effects from the drug are alarming, but more research will likely be needed before doctors can know for sure that the symptoms are completely attributed to the drug.

"There are so many things that go into the male erectile response," he said. "You have to be very careful before you attribute it to one cause or another."

Men Report Neurological Side Effects, Too

Malley said before he took Propecia, he was a normal, ambitious guy. He was engaged and worked as a public health researcher at a university in Las Vegas.

"Before, I would get up at eight in the morning, go to work, go to school, go to the gym, come home, have sex with my girlfriend. I had a lot of ambition, I had career goals," he said. "Now basically I just sit in my room all day and don't talk to anyone."

His fiancée broke off their engagement, and Malley had to resign from his job because of his persistent cognitive symptoms. He has sought treatment for these side effects, but doctors told him there's nothing they can do for him. He said he is angry that no one told him that the drug might change his life so dramatically.

"Even if the side effects are rare, that doesn't mean that I should not have been warned. I did have a life before this," he said.

Steven Rossello, 29, said his doctor made no mention of the potential for any sort of side effects from finasteride when he prescribed it to treat Rossello's hair loss in 2010.

"That's what really makes me really mad. He never mentioned any side effects, not to mention that they last forever," Rossello said.

But after four months of taking Propecia, Rossello said he began suffering anxiety and crippling depression, along with the drug's sexual side effects, and decided to stop taking the drug.

But his symptoms only got worse. He was demoted from his job as an investigator for the Department of Homeland Security in Texas after his symptoms were evaluated by a psychiatrist, who pronounced him unfit for duty. Rossello said the psychiatrist was unfamiliar with the neurological side effects of Propecia.

Abdulmaged Traish, a professor of biochemistry and urology at Boston University School of Medicine, said scientists are just beginning to investigate finasteride's effects on the brain and nervous system.

"We are just beginning to venture in that direction. It might be in the next five to 10 years that we may find there's more to this story than we know now," Traish said.

He said he would not advise men to take this drug to treat a cosmetic problem like hair loss.

"Why take that chance? Telling the risks of the drug is fine, but most physicians don't sit and take the time to explain to their patients the possible effects of these drugs."

On its website, the FDA said only 36 of 945 men who took Propecia in clinical trials reported any adverse sexual side effects. Irwig agrees that the number of men who will experience these long-lasting side effects is relatively small, likely around 3 percent of all men who take the drug.

"But because the medication is prescribed so commonly, it's still a lot of people, likely several thousand men around the world," he said.

And currently, doctors have no way of knowing which patients will suffer the long-term side effects. Irvig said it's possible that an unknown genetic factor drives how individual men respond to the drug.

Both Malley and Rosello were not involved in Irwig's study, but they are two of many men who have joined class-action lawsuits against Merck over the side effects of Propecia. In May, Malley camped out in front of Merck's headquarters in New Jersey for a week, staging a hunger strike to protest the company's response to Propecia's side effects. A representative came out to deliver a letter to him, detailing how he could report his symptoms to the company.

Malley has a simple message for men who might consider taking Propecia for their hair loss.

"Stay away from it at all costs," he said.

 

 

 

 

multibiomarker disease activity blood test

Study Validates RA Disease Activity Biomarker Blood Test

Janis C. Kelly

July 10, 2012 — A blood test measuring 12 biomarkers for rheumatoid arthritis (RA), designed to complement standard clinical assessment, accurately discriminated both American College of Rheumatology criteria (ACR50) responses and Disease Activity Score 28–C-reactive protein (DAS28-CRP) improvement in patients with RA, according to data from a validation study. However, after reviewing the study, published online June 26 in Arthritis Care & Research, some experts think further validation of the test is necessary.

Lead author Jeffrey R. Curtis, MD, codirector of the University of Alabama at Birmingham Center for Education and Research on Therapeutics, told Medscape Medical News, "This study establishes validity of the multibiomarker disease activity (MBDA) blood test [Vectra DA, Crescendo Bioscience] with regard to DAS28-CRP in both seropositive and seronegative RA patients, and showed that changes in MBDA score at 6 to 12 weeks or even earlier could discriminate ACR50 response."

Dr. Curtis and colleagues emphasize that because the MBDA score reflects the activity of underlying biological pathways and does not include physical examination, it should be viewed as complementary to, not a replacement for, clinical assessment.

The 12 biomarkers used in the MBDA test were selected from a list of 396 candidates. The test algorithm combines the levels of interleukin 6, tumor necrosis factor receptor superfamily member 1A, vascular cell adhesion molecule 1, epidermal growth factor, vascular endothelial growth factor A, human cartilage glycoprotein 39, matrix metalloproteinases 1 and 3, CRP, serum amyloid A, leptin, and resistin to generate a MBDA score between 1 and 100. The researchers tested the MBDA score for criterion validity (the ability to measure disease activity), discriminant validity (sensitivity to changes in disease activity), face validity (credibility and relevance), content validity (comprehensiveness in measuring components of health status), and construct validity (relationship to outcomes such as damage and disability).

They used association with the DAS28-CRP to establish criterion validity and association with changes in DAS28-CRP and with clinical responses to establish discriminant validity.

The investigators selected patients (n = 512) and samples from 3 cohorts: the Index for Rheumatoid Arthritis Measurement (InFoRM) study, the Brigham and Women's Hospital Rheumatoid Arthritis Sequential Study (BRASS) Registry, and the Leiden Early Arthritis cohort.

They found that the MBDA score was associated with clinical disease activity in both seropositive and seronegative patients. MBDA thresholds were 29 for low/moderate disease activity and 44 for moderate/high disease activity. Furthermore, their analyses showed that changes in the MBDA score could differentiate clinical responders from nonresponders.

The authors conclude, "These results demonstrate a significant association between the MBDA score and the DAS28-CRP in heterogeneous groups of RA patients with diversity in autoantibody status, disease activity, and RA therapy receiving care in multiple clinical centers. The MBDA score was able to consistently distinguish patients in different categories of clinical disease activity. Our results provide evidence of criterion validity for the MBDA test by demonstrating significant association with D28-CRP and other validated disease activity measures."

Further Validation Needed

Some experts, however, are more cautious. After reviewing the study for Medscape Medical News, Karel Pavelka, MD, director of the Institute of Rheumatology at Charles University, Prague, Czech Republic, said "The whole concept [of the multibiomarker disease activity test] is very interesting. The study was very well performed. However, MBDA needs further validation." Dr. Pavelka's current work involves maximizing outcomes in patients with RA who have inadequate responses to disease-modifying antirheumatic drugs.

Dr. Curtis said that additional validation studies are ongoing, including tests of whether using the MBDA test as an adjunct to clinical assessment improves patient outcomes. He suggested that potential applications might include ability to predict flare, to know when to repeat intermittent drugs such as rituximab, to predict future radiographic joint damage to decide whether to change or add new treatments, to assess long-term longitudinal response, to make early prediction of longer response, or as a proxy for subclinical synovitis.

Crescendo Bioscience ran the InFoRM clinical study, is a contributor to the BRASS study, and carried out the biomarker analysis in this study. Dr. Curtis has served as a consultant for Crescendo Bioscience and receives research support from Amgen, UCB, CORRONA, Genentech, Centocor, Pfizer, and Crescendo Bioscience. Dr. Pavelka has disclosed no relevant financial relationships.

Arthritis Care Res. Published online June 26, 2012

Risk of infections in rheum. arthritis pts treated with tocilizumab.

Rheumatology (Oxford). 2012; 51(5):852-7 (ISSN: 1462-0332)

Lang VR ; Englbrecht M ; Rech J ; Nüsslein H ; Manger K ; Schuch F ; Tony HP ; Fleck M ; Manger B ; Schett G ; Zwerina J
Department of Internal Medicine 3, University of Erlangen-Nuremberg, Krankenhausstrasse 12, 91054 Erlangen, Germany.

OBJECTIVES: To investigate the occurrence and risk factors for infections in RA patients treated with tocilizumab.

METHODS: A cohort of all RA patients (n = 112) starting tocilizumab therapy between October 2008 and March 2010 in Northern Bavaria was screened for infections. Mild/moderate and severe infections were recorded. Multivariate logistic regression analysis was used to define risk factors for infection.

RESULTS: Overall, 26 patients developed infections [23.2%; 58.0/100 patient-years (py)], 18 of them were mild to moderate (16.1%, 40.1/100 py) and 8 were severe (17.9/100 py). Concomitant use of LEF and prednisone, high disease activity and previous therapy with rituximab were associated with the occurrence of mild/moderate infections. Severe infections were related to longer disease duration, exposure to more than three previous DMARDs and concomitant therapy with proton-pump inhibitors.

CONCLUSION: The rate of infection in RA patients treated with tocilizumab in clinical practice is higher than in the clinical trial populations. Increased attention should especially be given to patients with longer disease duration, previous exposure to multiple DMARDs, i.e. previous exposure to rituximab and those receiving concomitant LEF, prednisone or proton-pump inhibitor treatment.

Delamanid for multidrug-resistant pulmonary tuberculosis

N Engl J Med. 2012; 366(23):2151-60 (ISSN: 1533-4406)

Gler MT ; Skripconoka V ; Sanchez-Garavito E ; Xiao H ; Cabrera-Rivero JL ; Vargas-Vasquez DE ; Gao M ; Awad M ; Park SK ; Shim TS ; Suh GY ; Danilovits M ; Ogata H ; Kurve A ; Chang J ; Suzuki K ; Tupasi T ; Koh WJ ; Seaworth B ; Geiter LJ ; Wells CD
Makati Medical Center, Manila, Philippines.

BACKGROUND: Delamanid (OPC-67683), a nitro-dihydro-imidazooxazole derivative, is a new antituberculosis medication that inhibits mycolic acid synthesis and has shown potent in vitro and in vivo activity against drug-resistant strains of Mycobacterium tuberculosis.

METHODS: In this randomized, placebo-controlled, multinational clinical trial, we assigned 481 patients (nearly all of whom were negative for the human immunodeficiency virus) with pulmonary multidrug-resistant tuberculosis to receive delamanid, at a dose of 100 mg twice daily (161 patients) or 200 mg twice daily (160 patients), or placebo (160 patients) for 2 months in combination with a background drug regimen developed according to World Health Organization guidelines. Sputum cultures were assessed weekly with the use of both liquid broth and solid medium; sputum-culture conversion was defined as a series of five or more consecutive cultures that were negative for growth of M. tuberculosis. The primary efficacy end point was the proportion of patients with sputum-culture conversion in liquid broth medium at 2 months.

RESULTS: Among patients who received a background drug regimen plus 100 mg of delamanid twice daily, 45.4% had sputum-culture conversion in liquid broth at 2 months, as compared with 29.6% of patients who received a background drug regimen plus placebo (P=0.008). Likewise, as compared with the placebo group, the group that received the background drug regimen plus 200 mg of delamanid twice daily had a higher proportion of patients with sputum-culture conversion (41.9%, P=0.04). The findings were similar with assessment of sputum-culture conversion in solid medium. Most adverse events were mild to moderate in severity and were evenly distributed across groups. Although no clinical events due to QT prolongation on electrocardiography were observed, QT prolongation was reported significantly more frequently in the groups that received delamanid.

CONCLUSIONS: Delamanid was associated with an increase in sputum-culture conversion at 2 months among patients with multidrug-resistant tuberculosis. This finding suggests that delamanid could enhance treatment options for multidrug-resistant tuberculosis. (Funded by Otsuka Pharmaceutical Development and Commercialization; ClinicalTrials.gov number, NCT00685360.).

PreMedline Identifier:22670901

旅日台僑終獲正名為台灣---台灣正名運動始委

　　等了40年，旅日台灣僑胞們終於護得「正名」。日本政府從今天(9日)起，開始執行修正後的新入國管理法，同意讓過去在外國人登錄證國籍欄上寫為「中國」的台灣僑民，可以更正為「台灣」，一大早就有台灣僑民趕來換證。他們說，等這個「台灣」，已經等了快50年了。

　　今天一早7點鐘，位在日本東京品川港南的入國管理局前，76歲的「台生報」發行人連根藤就等在門口，希望儘早拿到寫著「台灣」的新身分證。

　　連根藤說，他等了近50年，終於在今天等到自己真正的國籍寫著「台灣」了。雖然是遲來的喜悅，但是仍舊很讓人欣慰。

　　將「台灣」人的國籍寫成「中國」，是台灣與日本斷交的1972年時，北京主張一個「中國」，台灣當時也自稱是「中國」，因此台灣人在日本被當作「中國」人登記，一晃就是近半個世紀。

　　這個現象在台灣的本土意識抬頭之後，才開始受到注意。但是日本政府基於法令規定，以及經常要看北京的臉色，一直無視於台灣僑民「正名」的要求。

　　歷代的駐日代表都努力要促成日本政府的「正名」，但是一直都沒有能夠辦到。三年前，在馮寄台擔任駐日代表時，在日本朝野政黨的協助下，才總算在國會修正了入管法令，將「國籍」欄改變成「國籍／地域」欄，名正言順的讓台灣人得以登錄「台灣」。




台灣正名運動


维基百科，自由的百科全书

台灣正名運動，早年是由台灣的泛綠陣營及旅居外國的台灣人所倡議的運動，被認為是台灣本土化運動之一，運動於2002年5月11日正式啟動，所以這個運動又稱511台灣正名運動，由前總統李登輝擔任總召集人。而2002年亦被參與者視為這個運動的啟蒙年。民主進步黨政府於2000年首度執政後，將多數運動的內涵加以實踐，並於2006-2008年間到達高峰。泛綠「正名運動」的重點在區別「臺灣」與「中國」的關係。

由於正名運動的目標為去除所有表示本國代表「中國」的名稱，因此多數內涵與中國國民黨的政綱及認同本質有落差，引發在野的泛藍政治人物與其支持者強烈反對，認為是斬斷「臺灣」和「中華民國」與「中國」的關係。正名運動除了去蔣化之外，亦包括駐外機構名稱與在居住國之身分。

目录
[隐藏] 1 正名意涵
2 正名事件
3 原住民族的正名運動
4 問題
5 参考文献


[编辑] 正名意涵

「正名運動」顧名思義就是把「不正確的名稱改正」，但「正確名稱」是一主觀字眼。泛綠人士認為「中國」已經被中共及其支持者宣傳成只有在中國大陸的中華人民共和國，世界大多數國家均承認中華人民共和國為「中國唯一合法政府」，所以在臺灣的所有政府機關公司行號名稱不應有「中國」相關字眼，「正確名稱」應該有「臺灣」或相關名稱。

泛綠人士的觀點被泛藍人士所反對的原因在泛藍人士不認為「中國」專指「中華人民共和國」，中華人民共和國不代表包含臺灣的「全中國」，在臺灣的「中華民國」也可以是「中國」，所以不認為名稱裡有「中國」是錯誤名稱。

[编辑] 正名事件
2003年起在中華民國護照封面加註臺灣英文「TAIWAN」，原規劃加註「ISSUED IN TAIWAN」，此改變確實減少台灣人在各國海關遇到的麻煩，獲得許多外僑的稱許，但也引起中國民族主義者的反感。

從2003年起在國中、國小學生使用的國編教科書方面中表記首都在台北市（參見中華民國首都），而1997年起國中生所使用的介紹台灣的地理、歷史、公民的教科書「認識台灣」則被視為正名運動先驅。

2004年起，政府官方所印製的地圖「中華民國全圖」不再加上政府並未實際統治的中國大陸。

2004年，民進黨籍立法委員蔡同榮指出，軍中的國防部總機叫「江蘇一號」、「上海總機」、陸軍十軍團叫「湖南總機」等稱號，不是打電話到大陸，因此沒有必要採用大陸地名當各軍事單位總機名稱。因此他在9月提案，要求國防部在年底前，將總機名稱代號「去中國化」。2005年元旦起，國防部所屬軍中總機代號，將改以區域代碼取代。[1]

2005年7月30日，總統府及其網站上的名稱變更為「中華民國（台灣）總統府」，之後其他政府部門及駐外大使館也紛紛仿照。2008年馬英九擔任中華民國總統後，政府及駐外大使館網站中文名稱不再加上「（台灣）」，但英文名稱保留加註「(Taiwan)」。

2005年8月31日，《中華中藥典》更名為《台灣傳統藥典》

2006年1月，行政院新聞局出版的《光華雜誌》（Sinorama）改名《台灣光華雜誌》（Taiwan Panorama）[2]。

2007年1月29日，政府修改歷史教科書內容，將中國史和台灣史分開，並把「我國」、「本國」、「大陸」改稱「中國」。

2007年2月12日，中華郵政更名為「台灣郵政」，中國石油股份有限公司更名為「台灣中油股份有限公司」，中國造船股份有限公司更名為台灣國際造船股份有限公司。但郵局更名涉及修法，立法院內泛藍居半數所以未能通過。2008年8月1日馬英九執政後改回中華郵政。

2007年2月28日，台灣郵政發行的228國家紀念館開館紀念郵票上以「臺灣 TAIWAN」取代「中華民國郵票 REPUBLIC OF CHINA」標記。2008年8月1日改回「中華民國郵票」，英文則加註「REPUBLIC OF CHINA (TAIWAN)」。

2012年7月9日，日本政府廢除向來的外國人登錄證，實施對旅居日本外籍人士的管理新制，旅日臺灣人的居留卡國籍欄正名記載為「臺灣」，而非「中國」。[3]日本「李登輝之友會」事務局長柚原正敬表示，這是長年以來日本友台人士與台僑不斷為「台灣正名」運動打拚，而引起日本國會議員重視並修法的結果，日本政府把「台灣是台灣，中國是中國」弄清楚，對在日台灣人的權益非常重要。他說，2003年台灣在護照上加註「TAIWAN」字眼，是日本將台灣人的國籍正名為「台灣」的最大原動力。[4][5]


[编辑] 原住民族的正名運動

另外，由於台灣經過近四百年來不同政權的治理及漢族文化思潮的影響，造成許多原本原住民地名被改為與統治者有關的名稱。因此在台灣原住民運動興起之後，不少地名也被「正名」為原住民地名。例如1988年嘉義縣「吳鳳鄉」正名為「阿里山鄉」、1992年屏東縣「三地鄉」正名為「三地門鄉」，以及2007年高雄縣「三民鄉」正名為「那瑪夏鄉」，並於2008年1月1日正式揭牌使用[6]。此外南投縣的「仁愛鄉」也有醞釀正名為「霧社鄉」之議以及花蓮縣的「秀林鄉」也有醞釀正名為「太魯閣鄉」之議。

[编辑] 問題

民進黨政府曾要求民營企業如中國鋼鐵公司等等應當予以改名；但企業內部則認為這類行動往往因為企業名稱沿用已久，並且在國際上已經具有一定規模，全面更名不但可能影響商譽，更名所耗費的成本亦被企業內部視為難以負擔。

而中華郵政的正名，也遭到工會的大規模抵制。民進黨政府也曾要求國立中正大學、中國醫藥大學、中國文化大學、中華大學等9所大學改名，但遭到學校的反對而沒有成功。

宣稱「台灣是中華人民共和國的一部份」的中華人民共和國政府，將台灣所進行的這項運動視為「促進台灣獨立」，並以對台灣行使武力為威脅，試圖阻止藉由正名推動獨立的進行。而在台灣境內，希望中華民國延續為「中國」主權代表的泛藍黨派全力反對正名運動。

[编辑] 参考文献

1.^ 臺軍方追隨「去中國化」 元旦起總機刪大陸地名
2.^ 關於台灣光華 [2010-06-15].
3.^ 等了40年 旅日台僑終獲正名為「台灣人」, 中央廣播電臺 Radio Taiwan International, 2012/7/9
4.^ 等了40年 旅日台僑國籍改回台灣, 自由時報, 2012/7/10
5.^ 旅日台僑 國籍正名台灣／40年遲來正義 還在日台灣人一個公道, 自由時報, 2012/7/10
6.^ 7席鄉代一致通過 三民鄉正名那瑪夏鄉《自由電子報》，2007年12月11日

呂秀蓮訪談--回憶馬英九的校園間諜活動

How a Harvard
rivalry changed Taiwan

Farah stockman

THIS STORY APPEARED IN

July
03, 2012|Farah Stockman

TAIPEI, Taiwan

‘I was educated to be patriotic — to be a proud Chinese,”
Annette Lu says as she sits imperiously in her spacious office in a skyscraper
in Taipei.

Her aging face looms like a white powdered moon over her
glittering black suit. She has just held a press conference, blasting Taiwan’s
president, Ma Ying-jeou.

She settles into a chair with a cup of green tea and
tells me the story of her life — how her studies in the United States in the
1960s and ’70s transformed her from an obedient student into one of Taiwan’s
most outspoken opposition figures.

Since then, she has survived an assassination attempt,
five years imprisonment, and — after free elections finally came — eight years
as vice president. She doesn’t show it to me, but I know that under her
clothes, there is a scar from a bullet wound near her knee.

I listen intently, because this is the story of how
democracy came to the tiny island of Taiwan, and how it might one day take root
on mainland China. Talk to Lu long enough, and democracy starts to feel
downright inevitable — destined to bloom as soon as the 150,000 Chinese
students in America drift back home.

But the story that led me to Lu is a different one. A
juicier one, about her bitter rivalry with President Ma, which began three
deacades ago, at Harvard Law School.

Lu starts at the beginning. She was born on Taiwan, the
daughter of a local shopkeeper who used to read the newspaper aloud to her,
sparking her interest in politics. Back then, Taiwan was an authoritarian
state, ruled by Kuomintang (or KMT) party, which had once governed all of
China. When the communists swept across China in 1949, KMT stalwarts fled to
Taiwan. But they never gave up their dream of retaking China. Every move they
made was preparation for driving the communists out.

They banned the local languages spoken by the island
people. Families that lived on Taiwan for generations were forced to speak like
people did on the mainland. Anybody who dared suggest that the KMT stop
focusing on defeating the communists — and instead improve life for Taiwanese —
was considered a traitor.

Lu believed all the KMT propaganda when she was a child.
Then she got a fellowship to study at the University of Illinois. She arrived

in the late 1960s, just as feminist ideas were spreading in America. By the
time she returned to Taiwan in 1971, she was an ardent activist, full of
passionate views about how far Taiwan was lagging in economic development and
human freedom.

She started a domestic violence hotline and a feminist
coffee shop. But the KMT was watching her. She discovered that one of her
hotline volunteers and the manager at the coffee house were both government
spies.

“I felt so frustrated,” she says.

But she was also making a name for herself. Renowned
China expert Jerome Cohen convinced her to take a fellowship at Harvard Law
School. In the bowels of Harvard’s libraries, she found documents that enabled
her to write a history of Taiwan — not as a renegade province of China, but as
a nation in its own right. That was the beginning of Lu’s outspoken calls for
formal independence from China. She smuggled her subversive book into Taiwan by
photographing each page and sending the rolls of undeveloped film.

But just as Lu geared up her activism,
a new PhD student arrived at Harvard Law School: Ma Ying-jeou, who was born on
mainland China to a senior KMT party official. Ma’s father was so dedicated to
the dream of reunifying with China that, after his death, a slogan about it was
written on the urn that held his ashes.

Quiet and reserved, Ma set out to learn as much as he
could about China. He took Cohen’s classes on the Chinese legal system and
wrote his thesis on oil in the South China sea.

He became Lu’s nemesis. She felt he was watching
everything she did and reporting back to the KMT.

When she organized a protest in Boston against the arrest
of democracy activists in Taiwan, Lu says Ma photographed her from across the
street.

When she invited a prominent dissident from Taiwan to
Harvard to speak, Lu says Ma tipped off the KMT, which blocked him from getting
on his flight.

As the struggle for democracy heated up in Taiwan, Lu
went back home, with Cohen’s blessing.

“You are nobody here, but you might become somebody at
home,” she says he told her. Then he added, half-joking: “If you get arrested,
we’ll try to bail you out.”

A year later, after she gave a speech at a rally, she was
thrown in prison. She passed the time writing novels on toilet paper. Even when
she was struck with debilitating cancer, the government refused to let her out.

“The KMT hated me a lot,” she says.

Ironically, it was Ma — her enemy at Harvard — who
eventually set her free.

After Harvard, he worked at a bank in Boston and then
became an interpreter for Taiwan’s president, Chiang Ching-kuo, the son of
longtime KMT leader Chiang Kai-shek.

Ma had been raised on KMT party ideology. But Harvard had
exposed him to democracy. Five years after Lu’s arrest, Professor Cohen
traveled to Taiwan and pressed Ma, a rising star in the KMT, about why his
former classmate was in prison. Apparently embarrassed, Ma had Lu moved to a
hospital. He and Cohen visited her there. It was an emotional reunion. Lu
recalls Cohen wiping away tears when he saw her lying emaciated on the hospital
cot. She says he told her: “I never should have encouraged you to go back.”

A week later, she was freed from jail.

“In that regard, I owe President Ma,” she tells me.

But she was still forced to stay at home, under house
arrest — until the KMT allowed her to take another fellowship at Harvard. She was
living in Cambridge in 1987, when the KMT decided that democracy was the
future, and announced an end to martial law.

Lu and her fellow activists were pardoned. They formed
the largest opposition party. Lu was elected to parliament and eventually
became Taiwan’s vice president in the country’s first peaceful transition of
power.

“We proved that democracy can be achieved peacefully,” Lu
says.

Today, Taiwan is teeming with creative energy. Its
coffers are bulging with foreign reserves. Dueling political views duke it out
in the newspapers.

But Lu’s time in office was not a big success. Her
platform, which advocated officially breaking with the mainland, outraged China
at every turn. US officials worried that her calls for independence would drag
the United States — Taiwan’s protector — into a war with China.

After eight years — and a string of corruption scandals —
the KMT won the presidency back in a landslide. Their victorious candidate?
None other than the indefatigable Ma Ying-jeou.

President Ma ushered in a new era of friendly relations
with China. He negotiated a flurry of agreements to ease mail service, air
travel, and trade. Nowadays, 90 planes fly each week between Taipei and
Shanghai. Nearly 2 million Chinese tourists visited Taiwan last year.

“This is a real breakthrough,” Cohen, mentor to both Ma
and Lu, told me. Cohen is so proud of what his former student has accomplished
that he believes one day Ma should be considered for a Nobel Prize.

But avoiding a war might not be Ma’s biggest legacy. As
Chinese visitors flock to Taipei, they bring back descriptions of Taiwan’s
vibrant, free society, just as Ma and Lu did when they came from America.

“Over the long run, by word of mouth, it will spread,”
says Chong-Pin Lin, professor of international relations at TamKang University.
“Eventually China will ask the question: If the Taiwanese can, why can’t we?”

So Taiwan’s tourist industry just might take down
communism, succeeding where its army failed.

But activists like Lu worry that Ma’s cozy relationship
to China is a plot to take away Taiwan’s democracy and independence.

She grumbles about how the national museums and temples
are always packed with Chinese tourists now. “I never go to those places
anymore,” she tells me, twisting her mouth as if she sucked on a lemon.

Instead, Lu spends her time protesting Ma at rallies
where activists hold up signs that read: “We don’t want China.” After he was
elected for a second term, she held a press conference to announce a long list
of demands. One was that Ma appoint advisers from the opposition, like herself.

“Do you think he will listen?” I ask her.

She frowns at the very thought of him.

Then she says: “Probably not.”

Farah Stockman can be reached at fstockman@globe.com.
Follow her on Twitter @fstockman.

 

Linsanity 經典賽 youtubes

看個夠!

起碼，在看這林書豪籃球 youtubes 的時候可以忘卻 KMT集團  被揭露的驚人欺騙貪汙、無恥的顛倒是非、愚弄百姓，及(部分)民眾的奴性及愚蠢。

http://www.taiwanus.net/news/press/2012/201206162334391210.htm

 

破繭而出運動員 林書豪獲獎

中央社- 2012年07月12日 下午13:18

 

• 

（中央社記者吳協昌洛杉磯11日專電）2012年度體育卓越表現獎（ESPY）今天舉行頒獎典禮，第1個獎項就是年度「破繭而出運動員獎」，毫無意外，美國職籃NBA台裔球員林書豪順利獲獎，他致詞時感謝父母及隊友。

入圍年度破繭而出運動員獎的除了林書豪之外，還有今年帶領肯塔基大學贏得NCAA男籃賽冠軍的戴維斯（Anthony Davis）、貝勒大學美式足球好手葛瑞芬三世（Robert Griffin）、NFL新英格蘭愛國者隊葛隆柯斯基（Rob Gronkowski）與美國足球女將摩根（Alex Morgan）。

巧合的是，主辦單位安排的頒獎人正是今年剛轉到美式足球NFL紐約噴射機隊四分衛提博（Tim Tebow），似乎也早早暗示林書豪將是年度破繭而出運動員獎的得主。

林書豪在致詞時表示，能參加ESPY獎感到很開心，他尤其要感謝他的父母，同時也對他在紐約尼克隊的隊友致謝，更重要的是，他認為紐約是座偉大的城市，尤其是紐約的球迷，他要與紐約的球迷共同擁抱這座獎。

毫無疑問，林書豪出席ESPY頒獎典禮，也是頒獎典禮上最受矚目的球星，即使在頒發最佳比賽獎項時，頒獎人還開玩笑的說，「得獎人是林書豪，喔，這不可能」，引來全場大笑。

林書豪隨後在接受採訪時指出，即使在「林來瘋」結束之後，紐約球迷對他還是十分支持，能有這麼支持他的球迷，他覺得非常榮幸，也很酷。

NBA自由球員今天開始簽約，林書豪的去向也頗受矚目。林書豪表示，他在休士頓待了兩個星期，也看了他們的訓練營，他很享受在那裡的日子，不過現在就是只能等，看有什麼事情會發生。

對於即將在8月返回台灣與造訪大陸，林書豪坦言非常期待這次的行程，迫不及待想見到球迷，他說，「他們持續在臉書與推特上很酷的留言，也一直支持我」。1010711

（中央社記者吳協昌洛杉磯11日專電）2012年ESPY今天舉行頒獎典禮，第1個獎項就是年度「破繭而出運動員」獎，毫無意外，美國職籃NBA台裔球員林書豪順利獲獎，林書豪在致詞時也感謝他的父母及隊友。1010711

原來是這群水兵仔

原來是這群水兵仔 2012-07-05

◎ 毛清芬 一九七二年台灣少棒隊再度取得遠東代表權將遠赴威廉斯波特參賽，消息傳來，美國東岸的台灣同鄉振奮不已。一九六九年和一九七一年台灣同鄉前往加油，高舉「台灣隊加油」、「Team of Taiwan, Not Team of China」等標語以及由小飛機拖行的「台灣獨立萬歲 Go Go Taiwan」大標語，發生與國民黨人士衝突事件，此次亦聽聞國民黨將派出在麻州波士頓附近受訓的「水兵仔」來挑釁。 比賽當日除了二、三百名台灣同鄉遠來為台灣隊加油，約有二、三十位同鄉並沒坐在觀眾席上，大家攜家帶眷坐在棒球場外圍的斜坡上。幾位男生拉開布條。沒想到一群年輕小伙子們，應該就是「水兵仔」，六、七十名就緊站在拿著布條的同鄉旁，隨著賽事的進行愈趨愈近，他們手中所持的旗桿竟然是包著白布的不鏽鋼，顯然是為打架而來，威脅為台灣隊加油的台灣同鄉。 在賽事結束的那刻，離我十多公尺的左上方一陣混亂，已發生肢體衝突，我奔下斜坡朝向唯一在那裡一動也不動的美國警察大叫「You don’t see that they’re fighting?」沒想到，此刻二、三位面目猙獰的男生馬上圍住我，逼近我的臉咆哮著：「你先生是不是台獨？你先生是不是台獨？」在這一場混亂中，一架直昇機在頭上盤旋，降落在打群架中央，那一群水兵仔們馬上作鳥獸散。 四十年後七月一日中時電子報「歷史街道，潛艦的故事」中出現汪希苓大名，艦長關振清說「未料國民黨事後卻來函獎勵海軍愛國情操，揚威海外。」原來這群來棒打台灣同鄉就是由他們設計的。 （台灣獨立建國聯盟盟員）

文章題目： 歷史街道 潛艦的故事－赴美受訓接潛艦 海軍打群架 文章連結： http://news.chinatimes.com/politics/11050202/112012070100327.html 文章菁華： 　一九七二年世界少棒賽，中華少棒隊取得遠東區代表權，將赴美爭奪冠軍，在美國受訓的海軍弟兄獲悉，立刻向海軍學校爭取到現場觀賽，未料卻在球場和台獨人士打群架，轟動一時，艦長關振清回憶笑說：「不知當時在現場的人，有沒有現在民進黨檯面上的元老？」 　關振清說，當時校方見我國官兵離鄉背井受訓五個月，成績不錯，但沒有休閒動體，生活格外苦悶，因此同意撥錢派車。八月廿三日，全體官兵天未亮就分乘二部巴士，從New London直奔賓州威廉波特。 　汪希苓武官深知有些主張台獨的異議人士會到場抗議滋事，因此交代弟兄千萬別加入混戰，否則恐影響接艦計畫。 　廿六日，緊張的冠軍戰登場，關振清說，觀眾席擠滿僑胞、留學生，都來為中華小將加油。開賽前，球場一角果然出現十餘位蒙面客，手持木棍，高舉加油旗幟及台獨標語。比賽中，雙方相安無事，中華隊最終六比○力克美國北區隊，現場人士激情歡呼。 　在僑胞一片愛國口號聲中，幾名愛國留學生步步逼近台獨人士，意圖撕毀台獨標語，雙方先是一陣謾罵，接著演變成肢體衝突毆鬥，雙方陷入混戰。 　當時一位復興航運大副恰巧夥同船員來看球，見留學生打不過台獨人士，衝上前助陣，偏偏手無寸鐵，屈居劣勢，情急之下高喊：「海軍怎麼見死不救！」這一喊，激起官兵同仇敵愾之心，把事前告誡全拋諸腦後，一擁上前大打群架，扯下台獨標語，撕毀焚燒，在現場的警察眼看若再坐視不管，恐鬧出人命，大鳴警笛驅離雙方，還出動直升機運送傷者。 　關振清說，當時滲透在受訓官兵內的「細胞」將海軍打群架一事密報回國，海軍總部開會時嚴峻訓斥，未料國民黨部事後卻來函獎勵海軍「愛國情操」揚威海外，才讓這起事件落幕。

三十二年來最重要的細菌發現

The Medscape Awards in Infectious Diseases: Bacterium

1980-2012

John G. Bartlett, MD

Posted: 06/01/2012

The Medscape Awards in Infectious Diseases is a new series that will honor the greatest achievements in the field of infectious diseases during 1980-2012. John G. Bartlett, MD, Professor of Medicine, Johns Hopkins University School of Medicine, identified 8 key categories for these infectious disease awards. Within each category are several candidates for the honor of "greatest achievement." Readers will be asked to select the candidate that they believe is most worthy of this title, and then Dr. Bartlett will reveal his personal choice and the reasons for that choice. Obviously, the process will have an element of subjectivity, and opinions will differ. The goal is to credit great achievements, learn from those achievements, and pass these lessons down to succeeding generations.

This series will include the major discoveries or achievements since 1980 in the following categories:

1. Bacterium
2. Virus
3. Vaccine
4. Antiviral agent
5. Antibacterial agent
6. The infectious disease most likely to be the second eliminated from Earth
7. Consumer award
8. Demon award

Category: Bacterium

Candidates for the Most Important Discovery of a New Bacterium: 1980-2012

Questions answered incorrectly will be highlighted.

What do you believe was the most important discovery of a new bacterium during the time period 1980-2012?

1982: Borrelia burgdorferi (Lyme disease)

1982: Escherichia coli O157:H7 (hemorrhagic colitis)

1983: Helicobacter pylori (peptic ulcer disease)

1986: Chlamydia pneumoniae (atypical pneumonia)

1999: Bartonella henselae (cat-scratch disease)

2000: Tropheryma whipplei (Whipple disease)

2000: Methicillin-resistant Staphylococcus aureus (USA 300 strain)

2000: Clostridium difficile NAP-1 strain (C difficile epidemic)

Other: If not listed here, tell us about your choice in the Discussion

The Most Important Discovery of a New Bacterium (1980-2012)

My choice for the greatest achievement in the discovery of a new bacterium is Helicobacter pylori. The story of this organism and its etiologic roles in peptic ulcer disease and gastric cancer is a prime example of a relationship that was long suspected but resisted bitterly by the medical establishment, with eventual victory and a Nobel Prize.

Early history relevant to the role of H pylori in peptic ulcer disease includes the 1868 recommendation by Kussmaul to use bismuth agents to treat peptic ulcer disease, although the antibacterial properties of bismuth were yet to be discovered.¹ In 1939, A. Stone Freedberg reported H pylori in the human stomach but abandoned this research when he was ordered to move on to other subjects.^2,3 Barry Marshall later speculated that Freedberg would have won the Nobel Prize for his discovery in 1951 if his mentor had allowed him to continue his work.⁴ In 1964, John Lykoudis⁵ recommended antibiotic treatment for peptic ulcer disease at a meeting of the Medico-Surgical Society of Greece, but the manuscript was rejected and Lykoudis was subsequently fined 4000 drachmas for administering this treatment.

The roles of Robin Warren (Figure 1) and Barry Marshall (Figure 2) in the discovery of H pylori began in 1981, when Dr. Marshall, a young gastroenterologist, joined Dr. Warren, a pathologist, in the Royal Perth Hospital in Australia.⁶

Figure 1. Dr. Robin Warren, self-portrait. Used with permission.

Figure 2. Dr. Barry Marshall. Courtesy of The Office of the Nobel Laureates, University of Western Australia, Perth.

Dr. Warren had observed the bacterium in gastric biopsies and autopsies, and Dr. Marshall advocated antibiotic therapy, which proved successful.⁶ Despite the early successes of these 2 eventual Nobel laureates, the road they traveled was not always smooth. Marshall and Warren reported "unidentified curved bacilli on gastric epithelium in active chronic gastritis" in The Lancet in 1983⁷ and a more comprehensive description of this association based on a review of 100 gastric biopsies in 1984.⁸ The field of gastroenterology, however, was not ready for this challenge to long-held beliefs about peptic ulcer disease and its treatment.

The backlash was brutal.¹ Dr. Larry Altman, medical correspondent for The New York Times, who reported these results, later wrote, "I have never seen the medical community more defensive or critical of a story."⁹ I spoke with Dr. Altman about these events, and to this day, he recalls that "this was the review that got me the most heat for misleading the public" (Personal communication. May 16, 2012).

To defend his thesis, in 1984 Marshall intentionally drank cultured H pylori and developed gastric symptoms, which were relieved with antibiotics.¹⁰ Another health professional who was similarly frustrated by the rejection of the theory of an association between H pylori and gastritis leading to peptic ulcer disease also consumed the putative agent. Multiple gastric biopsies before and after ingestion nicely demonstrated the resulting disease; however, Marshall's colleague was less fortunate because antibiotics were unsuccessful in eradicating his disease, and he had debilitating symptoms for 3 years.^11,12

My experience with this disease was brief but telling. In 1986, I was invited to present a summary of the science of a bacterial cause of peptic ulcer disease at the annual meeting of the American Gastroenterology Association in San Francisco. I reviewed the data and submitted my abstract, but was somewhat shocked by the response from those who had invited me because they insisted on an editorial rebuttal. Their concern was that some attendees listening to my talk "might actually believe a bacterial cause." The "Editor's Note" for the program read:

Dr. Bartlett has summarized results from a number of reports dealing with gastric campylobacter-like organisms (GCLO) and gastritis. While intriguing, these reports (most of which are letters or abstracts) have done no more than call attention to an association between gastritis and GCLO. What remains completely unsettled, in our opinion, is whether GCLO are the cause of gastritis or present as a result of gastritis (ie, organisms colonize only in the presence of inflamed mucosa of some other etiology).

Despite this relatively rude treatment of an invited guest, I braced for the encounter and showed slides of the gastric biopsies from before and after self-ingestion of H pylori by Arthur Morris.¹¹ I then placed a glass of water (that I claimed to have seeded with H pylori but which was actually plain water) on the podium and invited skeptics to drink after my presentation. There were skeptical comments, but no one drank from the chalice.

It is not possible to identify a specific data set or a particular report that changed conventional teaching about peptic ulcer disease to a recognition that it was a bacterial infection rather than a consequence of gastric acidity. The period between 1987 and 1990 was particularly important because during this time, antibiotics to eradicate H pylori resulted in high rates of cure and prevention of relapses.¹³ Subsequent work implicated H pylori as a cause of gastric cancer¹⁴ and gastric lymphoma.¹⁵

The citation at the presentation of the Nobel Prize in 2005 is particularly important in terms of recognizing the importance of both the pathogen and the disease it causes:

Against prevailing dogmas, you [Drs. Warren and Marshall] discovered that one of the most common and important diseases of mankind, peptic ulcer disease, is caused by a bacterial infection of the stomach. Your discovery has meant that this frequently chronic and disabling condition can now be permanently cured by antibiotics, to the benefit of millions of patients. Your pioneering work has also stimulated research all around the world to better understand the link between chronic infections and diseases such as cancer.

The rationale for this selection as the most important discovery of a bacterium and its role in human disease is based on several observations that contribute to the weight of H pylori as an important and unusual pathogen.

• It is one of the most common infections, on the basis of serology studies that imply not simply colonization but an immune response to microbial infection. Most serologic studies show prevalence rates of 20%-90%; which vary substantially by age (with rates greater than 50% in persons older than 50 years) and by social class or national patterns of hygiene.¹⁶ In the United States, approximately 30% of people are colonized with H pylori, and colonization persists unless the person takes antibiotics directed against H pylori.
• H pylori is the major cause of peptic ulcer disease, which affects 15%-20% of those colonized or approximately 10% of the population at a cost of approximately $3.4 billion per year for healthcare in the United States.¹⁷
• H pylori is an unusual infection because it causes a chronic inflammatory response without the usual findings to suggest infection, such as elevation of C-reactive protein level, erythrocyte sedimentation rate, or procalcitonin level.¹⁸ As a traditional infectious disease model, H pylori violates all the rules.
• H pylori is a recognized carcinogen, presumably by its association with chronic inflammation (chronic gastritis).¹⁴ Thus, it is the only bacterium listed as a class 1 carcinogen,¹⁹ and it is also implicated in gastric lymphoma.¹⁵

The long battle to legitimize H pylori as a human pathogen was the classic example of the difficulty our profession has with unconventional theories. For this and the other reasons cited above, the discovery of H pylori receives my vote for the greatest achievement in discovery of a bacterium in the past 30 years.

Timeline: Historical Highlights -- Gastric Ulcer as a Chronic Bacterial Infection Caused by Helicobacter pylori Infection

1586: First report of gastric ulceration.¹

1825: Classic description of gastric function based on observations in a patient with a war wound that resulted in a gastric-cutaneous fistula.²

1857: Symptoms of peptic ulcer disease reported in detail.³

1881: Billroth provides the first report of upper gastrointestinal endoscopy.⁴

1906: Spirochetes reported in gastric biopsy specimens.⁵

1910: Peptic ulcer was attributed to gastric acid,⁶ and antacids became standard treatment.

1915: The "Sippy diet" is reported, using milk and cream throughout the day and much of the night.⁷ This became a favored therapy for the next 6 decades.

1924: Urease activity reported in human stomachs.⁸ This was thought to be generated from gastric mucosal cells because the stomach was thought to be sterile.

1966: Report of the gastric histamine receptor,⁹ and the first report of H₂-receptor therapy followed quickly.¹⁰

1973: The proton pump was described¹¹; this was immediately followed by proton pump inhibitor treatment.¹²

1975: Spirochetes and chronic gastritis are shown on gastroscopy in 80% of patients with gastric ulcers.¹³

1979: Robin Warren detected bacteria growing in gastric biopsy specimens, but the findings were apparently uninteresting to fellow pathologists. Two years later he met Barry Marshall, a young gastroenterologist, and the men spent the next 7 years studying what is now known as H pylori.

1983: Warren and Marshall report on bacteria associated with gastritis and peptic ulcer disease from their initial collaboration.¹⁴

1984: The seminal report¹⁵ from the Warren/Marshall collaboration showed the association of curved bacteria in the lesions of patients with chronic antral gastritis and ulcers.

Some of the observations in the seminal report are interesting, convincing, and even compelling, because the investigators found typical spiral or curved bacteria in antral specimens from 58 of 100 patients who underwent endoscopy with gastric biopsy.

We found a close association between pyloric campylobacter and antral gastritis. When polymorphonucleocytes (PMNs) infiltrated the mucosa, the bacteria were almost always present (38/40). In the absence of inflammation they were rare (2/31), suggesting they are not commensals. We know of no other disease state where, in the absence of complicating factors such as ulceration, bacteria and PMNs are so intimately related without the bacteria being pathogenic.

Conventional wisdom at the time was that the stomach is normally sterile owing to the acid environment, but the investigators opined that the bacteria were not in gastric fluid but rather on gastric cells.

1985: Self-inoculation experiment by Dr. Marshall was reported.¹⁶ This was a failed attempt to satisfy the Koch postulates because the result was gastritis, but he never developed a gastric ulcer.

1987: Eradication of H pylori shown to be associated with long-term cure of duodenal ulcer.^17,18

1987: Report of the urea breath test.¹⁹

1987: The antibacterial activity of bismuth against H pylori is reported.²⁰

1989: Campylobacter pylori is renamed Helicobacter pylori.^21,22

1994: H pylori is named a grade 1 ("definite") carcinogen.²³

1994: H pylori is implicated as the cause of gastric non-Hodgkin lymphoma.²⁴

1994: A National Institutes of Health consensus report endorses antibacterial therapy for peptic ulcer disease.²⁵

1997: Management guidelines for peptic ulcer disease recommend antibacterial treatment for the first time.²⁶

2005: The Nobel Prize is awarded to Drs. Barry Marshal and Robin Warren.

References

1. Donati M. Demedica historia mirabilt. Mantuae per fr. Osanam, Lib. IV, Cap iii:1586;196.
2. Beaumont W. A case of wounded stomach. Med Record. 1825;8:14-9, 840.
3. Brinton W. On the Pathology, Symptoms, and Treatment of the Stomach. With an Appendix of Cases. London: Churchill Livingston; 1857.
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