教育性公益講演的通知_{生老病死的秘密 - 從科學的觀點切入}[2013-10-26-WD6]

教育性公益講演的通知_{生老病死的秘密 - 從科學的觀點切入}[2012-10-26-WD5]

教育性公益講演的通知_{生老病死的秘密 - 從科學的觀點切入}

演講的題目:
生老病死的秘密 - 從科學的觀點切入
The Secret of Life and Death – A Scientific Approach

引言人的姓名:
余儀呈 醫師先生, 芝山診所, 台北市士林區天母生活圈, 前台北榮民總醫院 家庭醫學科 主治醫師

主講人的姓名:
湯偉晉 先生, 總經理, 湯生科技股份有限公司
國際扶輪3520地區台北永康扶輪社推薦的主講人

演講當天的日期和時間:
西元 2012-10-26 星期六 下午2點~下午4點

地點:
芝山生活家 (芝山診所的舊址)

芝山生活家的電話:
(02) 2836-9493 (星期一公休)

芝山生活家的地址:
台北市德行東路203巷2號

備註:
因為座位有限，所以如果您想參加，請務必事先預約報名。謝謝！

New test for mysterious metabolic diseases developed at Stanford/Packard [2009](IR91); FNKWs{glutathione, Stanford university}

New test for mysterious metabolic diseases developed at Stanford/Packard [2009](IR91); FNKWs{glutathione, Stanford university}

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New test for mysterious metabolic diseases developed at Stanford/Packard [2009](IR91); FNKWs{glutathione, Stanford university}

http://med.stanford.edu/news_releases/2009/february/enns.html
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FEB. 9, 2009

PRINT MEDIA CONTACT
Erin Digitale | Tel (650) 724-9175
digitale@stanford.edu        BROADCAST MEDIA CONTACT
Robert Dicks | Tel (650) 497-8364
rdicks@lpch.org      
New test for mysterious metabolic diseases developed at Stanford/Packard
  4 212
BY ERIN DIGITALE

Related News

» Metabolic disorder found treatable, researcher says
» New Packard laboratory speeds diagnosis, treatment of genetic defects
STANFORD, Calif. —Scientists at Stanford University School of Medicine have devised a much-needed way to monitor and find treatments for a mysterious and devastating group of metabolic diseases that arise from mutations in cells' fuel-burning mechanism.

Mitochondrial disorders can cause organ failure, seizures, stroke-like episodes and premature death. The diseases—more than three dozen in total—arise from genetic errors of the mitochondria, the cell structures that process oxygen and turn food molecules into useable energy. Mitochondrial disorders affect one in 4,000 kids and one in 8,500 adults. They are difficult to diagnose, and no treatments or cures exist.

But that could soon change. A team at Stanford and Lucile Packard Children's Hospital has discovered a biological marker they can use to monitor the diseases. The finding will enable researchers to hunt for treatments and help physicians check patients' status before health crises erupt. The research was published online Feb. 9 in the Proceedings of the National Academy of Sciences.

"When a car engine doesn't work right, it smokes," said senior study author Greg Enns, MB, ChB, who is professor of pediatrics at Stanford University School of Medicine and director of the biochemical genetics program at Packard. "What we looked for is, in essence, biochemical smoke."

Like a car engine, when mitochondria are not burning fuel cleanly, they kick out nasty gunk. Defective mitochondria produce large quantities of oxygen free radicals—highly reactive molecules that damage DNA and cell structures. Comparing patients who have a mitochondrial disorder with healthy people in the control group, Enns' team searched for signs that free radicals overtax patients' natural antioxidant defense systems. And they found it.

"Even when these patients are coming into the clinic looking pretty healthy, they have evidence of extra metabolic stress," Enns said, noting the findings were surprising because none of the patients were in the midst of a health crisis such as organ failure when blood samples were taken. It is the first time such signs have been uniformly shown in the blood of patients across a wide range of mitochondrial disorders, he added.

The team saw that levels of glutathione, the body's primary antioxidant, were significantly reduced in white blood cells from the 20 mitochondrial disease patients in the study. The observation means patients' antioxidant defenses were indeed depleted. Glutathione was also diminished in nine patients with organic acidemias, another group of metabolic diseases that researchers think may be associated with aberrant mitochondrial function.

A second finding gave the researchers a big hint about where to hunt for treatments. Patients taking antioxidant supplements did not have depleted glutathione, they found. Scientists have long suspected antioxidants such as vitamin C and vitamin E might help patients with mitochondrial disease or organic acidemias, and doctors sometimes suggest the supplements to their patients. But no one has been able to test whether they work.

"As a clinician, one of the most frustrating things has been not being sure if supplements are doing any good," said Enns. "Now we're able to take a baseline blood reading and see 'before' and 'after' snapshots."

William Craigen, MD, PhD, the director of the metabolic clinic at Texas Children's Hospital, called this finding "the beginning of insight into the mechanisms of mitochondrial disease." Craigen, who is also medical director for the mitochondrial diagnostic lab at Baylor College of Medicine, was not involved in the Stanford study. "This new research provides an opportunity to start treating a heterogeneous group of diseases in a single fashion, with a simple and easy-to-administer treatment, potentially improving patients' long-term outcomes," he added.

Glutathione measurements could also help diagnose patients, Enns said, by giving physicians a clear indication that something is awry in the mitochondria. Genetic and molecular tests have already led to increases in the number of diagnoses, but the diagnosis is still difficult to pin down.

The method Enns' team used to measure glutathione, called high-dimensional flow cytometry, has limitations: it requires very fresh blood samples, uses expensive equipment only available in research labs, and provides relative rather than absolute glutathione measurements. Now that the team knows what metabolic change to look for, they're working to develop a more broadly applicable measurement technique.

And glutathione measurements could help scientists unravel other disease mysteries, too. "You name the disease, you can postulate mitochondrial involvement," Enns said. "It's been proposed for everything from poor vision to hearing loss, kidney disease, liver disease, autism spectrum disorders, diabetes, Alzheimer disease, cancers. Our work could lead to research on therapies for a broad range of disorders."

Enns collaborated with research associate Kondala Atkuri, PhD; associate professor of pathology Tina Cowan, PhD; professor emeritus of genetics Leonard Herzenberg, PhD; and research professor of genetics Leonore Herzenberg, PhD, who is also a member of the Stanford Cancer Center. The Herzenbergs have a financial interest in BioAdvantex, a company whose dietary supplement, PharmaNAC, is intended to increase glutathione levels. The study was funded by grants from the United Mitochondrial Disease Foundation, the Lucile Packard Children's Hospital Pediatric Health Research Fund and the Arline and Pete Harman Scholarship.

# # #
   

The Stanford University School of Medicine consistently ranks among the nation's top 10 medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.
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教育性公益講演的通知_{生老病死的秘密 - 從科學的觀點切入}[2013-06-29-WD6]

教育性公益講演的通知_{生老病死的秘密 - 從科學的觀點切入}[2013-06-29-WD6]

教育性公益講演的通知_{生老病死的秘密 - 從科學的觀點切入}

演講的題目:
生老病死的秘密 - 從科學的觀點切入
The Secret of Life and Death – A Scientific Approach

引言人的姓名:
余儀呈 醫師先生, 芝山診所, 台北市士林區天母生活圈, 前台北榮民總醫院 家庭醫學科 主治醫師

主講人的姓名:
湯偉晉 先生, 總經理, 湯生科技股份有限公司
國際扶輪3520地區台北永康扶輪社推薦的主講人

演講當天的日期和時間:
西元 2013-06-29 星期六 下午2點~下午4點

地點:
芝山生活家 (芝山診所的舊址)

芝山生活家的電話:
(02) 2836-9493 (星期一公休)

芝山生活家的地址:
台北市德行東路203巷2號

備註:
因為座位有限，所以如果您想參加，請務必事先預約報名。謝謝！

長期接觸染劑 28歲美髮師卵巢退化 [2013-02-23]

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長期接觸染劑 28歲美髮師卵巢退化

http://video.chinatimes.com/video-cate-cnt.aspx?cid=6&nid=98218

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長期接觸染劑 28歲美髮師卵巢退化

2013-02-22

中視新聞》彰化一位從事美髮業10年的28歲女性，她因為突然停經到醫院檢查。結果醫生發現，她的卵巢功能居然是像48歲的女性一樣沒有辦法生育。醫生判斷，有可能是因為她長期接觸染髮、洗髮的有機溶劑，結果造成了這種情況。

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氯仿中毒，glutathione (穀胱甘肽) depletion (耗盡), 台北榮總 [2013-01-29](IR91)

氯仿中毒，glutathione (穀胱甘肽) depletion (耗盡), 台北榮總 [2013-01-29](IR91)

Source:
http://www.pcc.vghtpe.gov.tw/old/docms/50123.htm

氯仿(chloroform)中毒

長庚醫院 張玉龍醫師

簡介

近來台北榮總毒物中心接到數名氯仿中毒的個案。氯仿(chloroform, trichloromethane, ChCl3)自西元1847年起，曾被用於吸入性麻醉劑用途；然因其肝毒性較大，自西元1912年後，即不建議用於醫療用途。氯仿在工業上，可被用於樹脂、橡膠製造之溶劑、黏著劑、穀物燻蒸除蟲劑。在實驗室中則常用以萃取DNA, RNA及脂肪。氯仿乃一無色可揮發性液體，聞起來似乙醚味，嚐起來帶點甜味，具X光不透性。

歷年個案統計

根據台北榮總毒物諮詢中心之統計，自民國75年起至87年6月止，共有20個個案。其中男、女各半，中毒者年齡由9歲至76歲不等。其中服食氯仿自殺者有5位，這其中有1人因服食較大量而死亡；有6人係誤將氯仿當成開水服食，這6人症狀大多為噁心、嘔吐、上腹痛及喉嚨不適；另有6人係皮膚不小心接觸氯仿，大多數僅產生輕微灼熱感，但其中有一人引起接觸性皮膚炎，另一人則引起化學性肝炎。有2人係於工作時吸入氯仿，導致呼吸困難、噁心、頭痛及全身無力；尚有一人因氯彷不慎濺及眼睛，導致眼部灼熱疼痛。

作用機轉

氯仿進入體內後迅速被吸收，且快速分布於體內各組織尤其是脂肪組織，主要以其代謝物二氧化碳經由肺部排出。

氯仿(三氯甲烷)經由肝臟之p450酵素系統形CCL3OH，其後再分解成鹽酸和有毒的光氣COCL2 (phosgene)。光氣隨即和水作用釋出二氧化碳及形成氯離子Cl-。氯離子則和肝臟的glutathione (穀胱甘肽) 作用形成最終產物。當氯仿吸收量過多時，可導致體內的glutathione (穀胱甘肽) 量缺乏，而導致肝、腎之傷害。

臨床症狀

氯仿可經由吸入、口服或皮膚接觸而致中毒。氯仿係一刺激劑，對中樞神經系統及心臟系統會產生抑制作用，並可對肝、腎造成毒性。文獻上曾有人攝食10cc即導致昏迷、死亡。
五官：對眼睛可造成灼熱疼痛、結膜炎及角膜傷害。常導致口乾及喉嚨不適。
心臟血管系統：過量可致心律不整而致死，血壓降低。
呼吸系統：可產生呼吸抑制、吸入性肺炎或肺水腫。
神經系統：頭痛、全身無力、意識不清。
胃腸症狀：噁心、嘔吐及上腹疼痛。
肝、腎毒性：于食入10至48小時內，即可導致肝細胞壞死。且可致腎功能變差，甚至腎衰竭。
血液方面：可致溶血、白血球上升及凝血時間prothrombin降低(PT延長)。
皮膚：產生刺激感、灼傷或皮膚壞死。
治療

將患者移除暴露源，且依其症狀來治療。
皮膚接觸：脫去受沾染之衣服，並用水沖洗。
眼睛接觸：用大量清水沖洗眼睛至少15分鐘。
口服：避免催吐。若剛食入，可考慮洗胃及給予活性碳治療，惟須注意呼吸道之保護，避免吸入性肺炎。口服致命劑量就成人來說，約每公斤0.5至5公克。
吸入性傷害：移至新鮮空氣處，監測呼吸情形，若有呼吸不適，則給予100%氧氣。
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Inflammatory Response and Oxidate Stress in the Degeneration of Dopamine Neurons in Parkinson's Disease [2003](IR91)_P01.png

Inflammatory Response and Oxidate Stress in the Degeneration of Dopamine Neurons in Parkinson's Disease [2003](IR91)_P01.png

Glutathione (穀胱甘肽) deficiency (缺乏，不足，短缺) in the epithelial lining fluid of the lower respiratory tract in idiopathic pulmonary fibrosis (肺纖維化). [1989](IR91)

Glutathione deficiency in the epithelial lining fluid of the lower respiratory tract in idiopathic pulmonary fibrosis.

Glutathione (穀胱甘肽) deficiency (缺乏，不足，短缺) in the epithelial lining fluid of the lower respiratory tract in idiopathic pulmonary fibrosis (肺纖維化). [1989](IR91)

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Glutathione (穀胱甘肽) deficiency (缺乏，不足，短缺) in the epithelial lining fluid of the lower respiratory tract in idiopathic pulmonary fibrosis (肺纖維化). [1989](IR91)

http://www.ncbi.nlm.nih.gov/pubmed/2913886
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Am Rev Respir Dis. 1989 Feb;139(2):370-2.

Glutathione deficiency (缺乏，不足，短缺) in the epithelial lining fluid of the lower respiratory tract in idiopathic pulmonary fibrosis (肺纖維化).

Cantin AM, Hubbard RC, Crystal RG.
Source
Pulmonary Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892.

Abstract
Glutathione (L-gamma-glutamyl-L-cysteinyl-glycine, GSH), a sulfhydryl-containing tripeptide produced by most mammalian cells, is an efficient scavenger of toxic oxidants, including hydrogen peroxide, an oxidant that plays a major role in the oxidant burden placed on the epithelial surface of the lower respiratory tract in chronic inflammatory states. GSH is present in the epithelial lining fluid of the normal lower respiratory tract, where it is thought to play a major role in providing antioxidant (抗氧化劑) protection to the epithelial cells. In this regard, we hypothesized that the lower respiratory tract of patients with IPF may be chronically depleted (耗盡) of this antioxidant (抗氧化劑), thus leading to an increased susceptibility of lung epithelial cells to oxidant injury. To evaluate this concept, the concentration of glutathione was determined in the epithelial lining fluid of the lower respiratory tract of 15 patients with IPF and compared to that of 19 normal subjects. Strikingly, whereas ELF glutathione concentrations were high in normal subjects (429 +/- 34 microM), a fourfold decrease was found in patients with IPF (97 +/- 18 microM, p less than 0.001). In the context of the known oxidant burden present in the lower respiratory tract of patients with IPF, these observations of a "GSH deficiency" in IPF ELF suggest that there is a marked oxidant-antioxidant (抗氧化劑) imbalance at the alveolar surface of these persons, thus increasing the susceptibility to the severe epithelial cell damage characteristic of this disease.

PMID: 2913886 [PubMed - indexed for MEDLINE]
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Glutathione deficiency in the epithelial lining fluid of the lower respiratory tract in idiopathic pulmonary fibrosis.

http://www.ncbi.nlm.nih.gov/pubmed/2913886

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Am Rev Respir Dis. 1989 Feb;139(2):370-2.
Glutathione deficiency in the epithelial lining fluid of the lower respiratory tract in idiopathic pulmonary fibrosis.
Cantin AM, Hubbard RC, Crystal RG.
Source
Pulmonary Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892.

Abstract
Glutathione (L-gamma-glutamyl-L-cysteinyl-glycine, GSH), a sulfhydryl-containing tripeptide produced by most mammalian cells, is an efficient scavenger of toxic oxidants, including hydrogen peroxide, an oxidant that plays a major role in the oxidant burden placed on the epithelial surface of the lower respiratory tract in chronic inflammatory states. GSH is present in the epithelial lining fluid of the normal lower respiratory tract, where it is thought to play a major role in providing antioxidant (抗氧化劑) protection to the epithelial cells. In this regard, we hypothesized that the lower respiratory tract of patients with IPF may be chronically depleted (耗盡) of this antioxidant (抗氧化劑), thus leading to an increased susceptibility of lung epithelial cells to oxidant injury. To evaluate this concept, the concentration of glutathione was determined in the epithelial lining fluid of the lower respiratory tract of 15 patients with IPF and compared to that of 19 normal subjects. Strikingly, whereas ELF glutathione concentrations were high in normal subjects (429 +/- 34 microM), a fourfold decrease was found in patients with IPF (97 +/- 18 microM, p less than 0.001). In the context of the known oxidant burden present in the lower respiratory tract of patients with IPF, these observations of a "GSH deficiency" in IPF ELF suggest that there is a marked oxidant-antioxidant (抗氧化劑) imbalance at the alveolar surface of these persons, thus increasing the susceptibility to the severe epithelial cell damage characteristic of this disease.

PMID: 2913886 [PubMed - indexed for MEDLINE]
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Deficiency of alveolar fluid glutathione in patients with sepsis and the adult respiratory distress syndrome (成人呼吸窘迫症候群). [1991](IR91)

Deficiency of alveolar fluid glutathione in patients with sepsis and the adult respiratory distress syndrome (成人呼吸窘迫症候群). [1991](IR91)

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Deficiency of alveolar fluid glutathione in patients with sepsis and the adult respiratory distress syndrome (成人呼吸窘迫症候群). [1991](IR91)

http://www.ncbi.nlm.nih.gov/pubmed/1935300

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Chest. 1991 Nov;100(5):1397-403.

Deficiency of alveolar fluid glutathione in patients with sepsis and the adult respiratory distress syndrome (成人呼吸窘迫症候群).

Pacht ER, Timerman AP, Lykens MG, Merola AJ.

Source
Department of Internal Medicine, Ohio State University, Columbus.

Abstract
The adult respiratory distress syndrome (成人呼吸窘迫症候群) (ARDS) is a devastating clinical illness characterized by refractory hypoxemia and high-permeability pulmonary edema. Reactive oxygen species such as hydrogen peroxide (過氧化氫) and hypochlorous acid (次氯酸) may play a key role in the pathogenesis of the acute lung injury. Glutathione (GSH) (穀胱甘肽) is a tripeptide (三肽, i.e. 三種胺基酸連在一起) that is able to react with and effectively neutralize oxidants such as hydrogen peroxide (過氧化氫) and hypochlorous acid (次氯酸). The present study found that the alveolar epithelial lining fluid of patients with ARDS was deficient in total GSH compared to normal subjects (21.7 mumols +/- 7.8 mumols vs 91.8 mumols +/- 14.5 mumols; p = 0.002). In addition, if GSH was measured in unconcentrated bronchoalveolar lavage (BAL) fluid and indexed to total BAL protein, there was also a deficiency in patients with ARDS compared to normal subjects (0.004 +/- 0.003 nmol of GSH per microgram of total protein vs 0.026 +/- 0.005 nmol of GSH per microgram of total protein; p = 0.002). Since patients with ARDS are subjected to an increased burden of oxidants in the alveolar fluid, principally released by recruited neutrophils, this deficiency of GSH may predispose (使容易...) these patients to enhanced lung cell injury (肺細胞損傷).

PMID: 1935300 [PubMed - indexed for MEDLINE]
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TitleOrKeywordIsNotProvidedYet
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adult respiratory distress syndrome
成人呼吸窘迫症候群
adult respiratory distress syndrome (成人呼吸窘迫症候群)(ARDS)

acute respiratory distress syndrome
acute respiratory distress syndrome (ARDS)
急性呼吸窘迫症候群
acute respiratory distress syndrome (ARDS)(急性呼吸窘迫症候群)

呼吸, acute respiratory distress syndrome

肺炎併發急性呼吸窘迫症與敗血性休克
肺炎併發急性呼吸窘迫症與敗血性休克

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