Thursday, August 13, 2015

IBM 併購 Merge Healthcare 快速建立智慧型醫療影像分析(雲端人工智慧) 領域

IBM「華生」進擊醫療影像分析領域 20150811 21:36 陳怡均 華爾街日報周二報導,IBM上周宣布收購醫療影像資訊服務業者Merge Healthcare,藉此取得大量資料提供人工智慧平台「華生」(Watson)學習,也意味藍色巨人向醫學影像分析領域跨出重要一步。Merge Healthcare的系統可協助醫師儲存和取得醫療影像,該公司的重要資產為300億張影像,包括X光、斷層掃描、核磁共振造影掃描,IBM想要利用這些資訊「訓練」華生軟體辨識癌症、心臟病等疾病,並期待推出相關服務協助醫師更有效診斷與治療病患。

Shares of International Business Machines Corporation (NYSE:IBM) moved down 0.68% in early trading session on Tuesday as it intended to buyout of Merge Healthcare Inc., which sells systems that help doctors store and access medical images, is a crucial move in its intension to put artificial intelligence to use in medicine. IBM declared $700 million deal previous week. Merge's crown jewels are 30 billion images, comprising X-rays, magnetic-resonance-imaging scans, computerized tomography that IBM plans to use to train its Watson software to recognize ailments like cancer and heart disease. IBM is betting that the similar technology that recognizes cats can recognize tumors and further signs of diseases. The nascent attempt could help IBM capture a larger slice of the $7.2 trillion spent internationally annually on health care. IBM's deal also could reform the $3 billion market for archiving medical images and breathe life into firms devoted to computer-driven interpretation of images. It underscores the value of such imagery, which typically is anonymzed and shared by hospitals for research purposes, as the software technique known as through learning becomes more prevalent in medicine.

IBM Acquires Merge Healthcare To Upgrade Watson Medical Capabilities By Ted Ranosa, Tech Times | August 8, 7:03  IBM Corp. announced that it has agreed to purchase medical image company Merge Healthcare Inc. for the price of $1 billion and combine it with the company's newly established health analytic's division that is powered by its Watson supercomputer. The technology company said that it plans to acquire images and data collected from Merge Healthcare's own medical imaging management system and combine them with IBM Watson's cloud-based health care computing program. Watson's system is designed to analyze large volumes of data, interpret complex questions stated in natural language and provide answers to these questions based on available evidence. The new agreement between IBM and Merge Healthcare will allow researchers and physicians to collate and examine various data such as the family and medical history of a patient, data on other patients with similar symptoms of illness and clinical studies, trials and findings. Brooks O'Neil, analyst for Dougherty and Co., stated that imaging is a vital aspect to effective diagnosis of illness and treatment. He added that it is increasingly important, however, to share images between health care providers to provide high-quality, cost-effective care. The deal with Merge Healthcare is part of IBM's efforts to aggressively expand in the sector of health care information technology. It is the technology company's third primary acquisition related to health since the launch of its Watson Health division in April. "Organically, we will continue to build and invest from a research perspective in core technologies," IBM Watson vice-president Stephen Gold said. "We will compliment and supplement that with acquisitions." With its latest acquisition of Merge Healthcare, IBM will gain access to 7,500 health care sites in the United States. The two companies said that shareholders of Merge Healthcare will receive $7.13 for each share based on a 31.8 percent premium to Wednesday's close. The medical image company shares were trading at $7.08 for each share by the afternoon, while shares owned by IBM experienced little change at $156.33 per share. "Merge is widely recognized for delivering market-leading imaging workflow and electronic data-capture solutions," Merge Healthcare CEO Justin Dearborn said. "Today's announcement is an exciting step forward for our employees and clients. Becoming a part of IBM will allow us to expand our global scale and deliver added value and insight to our clients through Watson's advanced analytic and cognitive computing capabilities."

Aldea Pharmaceuticals 創辦人: 陳哲宏 (開發 aldehyde dehydrogenase enzyme ,ALDH 酒精代謝藥物)

Small molecule might help reduce cancer in at-risk population, study finds FEB 23 2015  Scientists have shown that small molecules can "hijack" enzyme function in mice, suggesting a possible preventive mechanism for alcohol-related cancers in an at-risk population. Researchers at the Stanford University School of Medicine have found that by changing the selectivity of an enzyme, a small molecule could potentially be used to decrease the likelihood of alcohol-related cancers in an at-risk population. Enzymes are enablers. They are highly specialized parts of cellular machinery tasked with bringing together molecules to make it easier for chemical reactions to happen. Sometimes enzymes are defective and malfunction, which can cause disease. In a study of mice, the researchers discovered a creative way to circumvent the problems caused by a defective enzyme. They used a small molecule to "hijack," or change the function of, another enzyme so that it mimicked and compensated for the function of the broken enzyme. "We found a molecule that can steer an enzyme to perform a new function," said Daria Mochly-Rosen, PhD, professor of chemical and systems biology, who is the senior author of a paper about the study. Che-Hong Chen, PhD, a senior research scientist, is lead author of the paper, which was published online Feb. 23 in the Proceedings of the National Academy of Sciences. Specifically, the researchers found that a small molecule could convert a particular enzyme from being ineffective at metabolizing alcohol-derived acetaldehyde to being very effective at the process. Although this molecule, Alda-89, is not suitable for use in humans because of its toxicity, enzyme hijacking is a promising new route for drug discovery, the researchers said. Finding other, safer molecules that can hijack enzymes could help prevent certain human cancers and is the current focus of the Mochly-Rosen laboratory. "What is novel about this study is using a small molecule to co-opt a related enzyme to help a broken one," said Daniel Erlanson, PhD, who has worked in the pharmaceutical industry for 17 years and is president and co-founder of Carmot Therapeutics, a biotechnology company. "This is a really clever way to address a genetic disorder that has not received much attention." Erlanson was not involved in the research.

Beware of beer — and yogurt  When most people and animals consume alcohol, the body digests it rapidly, within a few hours. One of the byproducts of alcohol metabolism is a chemical called acetylaldehyde. According to the World Health Organization, acetylaldehyde is a Group-1 carcinogen, which means there is a direct link between exposure and cancer.  For most people, acetylaldehyde is not a major health risk — though it can contribute to hangover symptoms — because an enzyme called ALDH2 quickly converts it to a harmless acid. But for some, acetylaldehyde is a big problem. This is a really clever way to address a genetic disorder that has not received much attention. These people lack a working version of ALDH2 because of a genetic mutation. ALDH2 deficiency is the most common genetic mutation in humans, affecting about 40 percent of East Asians — some 560 million people, or nearly 8 percent of the world's population. Without a working enzyme, the body cannot clear the toxic acetylaldehyde quickly. When people with the ALDH2 mutation consume moderate amounts of alcohol, they experience symptoms ranging from severe flushing of the skin, impaired functioning, headache, nausea and palpitations. People with defective ALDH2 enzyme are also at an increased risk for various alcohol-related cancers of the mouth, throat and upper gastrointestinal system. Among people who carry the mutation, nondrinkers are about twice as likely to develop such cancers, while heavy drinkers who also smoke are 100 times more likely. The ALDH2 mutation has also been linked with colorectal, lung and liver cancers, likely due to elevated acetaldehyde exposure. "Acetylaldehyde exposure does not just happen from drinking alcohol; it is also present in fermented foods like soy sauce and yogurt," Chen said, adding that he believes the danger of acetaldehyde toxicity is under-recognized and is a great public health risk for a large segment of the East Asian population.

From small molecules to mice  Another enzyme, ALDH3A1, contributes minimally to alcohol metabolism. But the researchers wanted to see if using a small molecule to hijack the function of ALDH3A1 could increase its role in the process. The researchers studied mice with and without the defective ALDH2 enzyme. They used computer models to visualize the shapes of ALDH2 and ALDH3A1. Both are aldehyde dehydrogenases, enzymes that detoxify aldehydes by converting them into acids. The researchers specifically focused on what the "active site" looked like for each enzyme. An enzyme's active site is like a keyhole: If a molecule fits into the active site, the enzyme changes shape in a way that makes a chemical reaction easier. The researchers compared the shapes of the active sites for ALDH2 and ALDH3A1 with a library of small-molecule structures. Molecules that looked like they would fit into the active sites were tested in mice for their ability to increase the activity of ALDH3A1. The most active compound for ALDH3A1 was a small molecule named Alda-89. Previously, the researchers had identified and studied another small molecule, Alda-1, that increases the activity of the ALDH2 enzyme. After being injected with alcohol, mice with and without defective ALDH2 were given just Alda-1, just Alda-89 or both small molecules together to see which combination changed the activity of ALDH3A1. Alda-1 was not effective by itself, but together with Alda-89 it boosted the clearance of toxic acetylaldehyde via ALDH3A1 in both groups of mice. "This really is a beautiful scientific study," Erlanson said. "It goes from very fundamental biochemistry and enzymology, onto structural biology and cell biology, and finishes with animal work. It is a tour de force."

If the shoe fits  Chen described hijacking an enzyme with a small molecule as similar to figuring out how to modify a pair of shoes that are too loose. "You could stuff a piece of newspaper inside the shoes to make them fit better," Chen said. "The piece of newspaper has to be there in order to create a better fit." The too-big shoe is the ALDH3A1 enzyme, acetaldehyde is the foot, and the piece of newspaper is Alda-89. When the small molecule bound to the active site of ALDH3A1, the enzyme was altered in such a way that enabled it to more effectively metabolize acetylealdehyde in laboratory mice that had defective ALDH2 activity. Mochly-Rosen, who is also the George D. Smith Professor in Translational Medicine, and Chen founded ALDEA Pharmaceuticals, a company that focuses on drug discovery of aldehyde dehydrogenase activator molecules. Mochly-Rosen holds stock in the company but otherwise is not involved with it; Chen holds stock and is a scientific adviser to the company. The other co-author of the paper is Leslie Cruz, PhD, former postdoctoral scholar at Stanford. The study was supported by the National Institutes of Health (grants AAA11147 and T32CA09151). Information about Stanford's Department of Chemical and Systems Biology, which also supported the work, is available at http://chemsysbio.stanford.edu.

About ALDEA Pharmaceuticals It is developing a number of small-molecule modulators of the aldehyde dehydrogenase enzyme (ALDH) superfamily. This proprietary scientific approach was originally discovered by Stanford University researchers and exclusively licensed to Aldea. With its ALDH platform, ALDEA has the unique opportunity to pursue novel targets across multiple therapeutics areas to address significant unmet medical needs.

Pipeline Aldea Pharmaceuticals is developing a platform of novel drugs called Aldehyde Dehydrogenase Activators (or ALDAs). The first drug candidate, Alda-1, was licensed from Stanford University. Through our medicinal chemistry efforts Aldea's scientists have generated improved second and third generation compounds. The therapeutic potential of ALDAs has been demonstrated in a number of models of human disease. Data regarding ALDAs have been published in a number of top tier scientific journals including Science, Nature Structural & Molecular Biology, and Science Translational Medicine. Aldea plans to file an IND on its lead candidate in 2014. A phase 1/2 acute alcohol challenge study in healthy volunteers is planned as a proof of concept for Aldea's therapeutic approach. More specifically, successful activation of ALDH2 will provide support for pursuit of studies in acute alcohol toxicity and orphan indications such as Fanconi Anemia.

(2015, PNAS) 陳哲宏..... 每天2杯紅酒 罹癌率高50倍 (缺乏ALDH2基因缺乏)

基因缺陷 台灣人不是喝酒咖 20150812 04:10 陳瑄喻/台北報導 台灣人最不能喝!美國史丹佛大學醫學院研究指出,近半台灣人體內基因缺乏乙醛去氫酶(ALDH2 Deficiency),比例全球最高,以致純酒精(乙醛)無法代謝,若每天2杯紅酒,罹患頭頸癌和食道癌的比率就比正常人高50倍。酒精進入人體後,會先由乙醇去氫酶(ADH)代謝成乙醛,再透過ALDH2代謝為醋酸,由於乙醛被列為一級致癌物,若無ALDH2協助代謝,長期累積於人體,將會提高癌症的發生率。台北醫學大學昨與史丹佛大學合辦《第一屆台灣─史丹佛ALDH2基因與人類疾病研討會》,會中美國史丹福大學醫學院高級研究員陳哲宏針對華人喝酒臉紅和口腔、食道癌的風險及保健進行演講。陳哲宏說,史丹佛研究指出,大陸有35%的民眾體內基因缺乏ALDH2,日本為30%、韓國20%,但比起這些國家,台灣卻高達47%的民眾缺乏ALDH2,是全球比率最高的國家。

原住民 沒這個問題 為何台灣人的體內基因缺乏ALDH2?陳哲宏指出,主要ALDH2缺乏症多出現在沿海地區漢人民族身上,因此像是中國大陸、日韓等國民眾都有這類基因缺陷,但台灣原住民就沒有缺乏。

罹癌比率 高出50「一些不合適的建議,反而提高民眾健康風險。」陳哲宏指出,常有醫師拿著美國心臟協會的建議,提醒民眾每天可小酌12杯紅酒,降低心血管疾病風險,但這項建議僅適合歐美民眾,並不適合缺乏ALDH2的亞洲人。陳哲宏舉例,體內缺乏ALDH2的民眾,若每天攝取14克純酒精(相當於2杯紅酒),罹患頭頸癌和食道癌的比率就比正常人高50倍,相當驚人。

20分鐘 自我檢測 陳哲宏說,目前史丹佛大學醫學院研究團隊正研發ALDH2活化劑,已篩選30萬種化學物質後發現有一種化合物(Alda)可以刺激人體內的ALDH2,目前正在第一期臨床實驗,預計510年後可望上市。如何自我檢測是否體內基因缺乏ALDH2?陳哲宏說,除了透過做基因檢測外,亦可將濃度較高的烈酒,倒在OK繃上,再貼到上手臂內側,經過20分鐘後,若皮膚出現紅色斑塊,體內就是缺乏ALDH2。記者實際測驗,原本喝酒就會臉紅的程小姐以及喝酒不會臉紅的廖小姐,使用這項檢驗方法實測,發現程小姐的手臂在短短10分鐘內就出現紅色斑塊,而廖小姐則都毫無反應,顯示這項檢驗方法既簡單又準確。

Che-Hong Chen, Ph.D. Senior Research Scientist  Che-Hong, a molecular biologist and geneticist, has been working with Prof. Daria Mochly-Rosen's laboratory at Stanford University for the past 21 years. Che-Hong's early research includes the characterization of the first intra-cellular receptor for protein kinase C and its protein-protein interaction with other signaling molecules. Che-Hong also studied the role of ethanol-mediated cardioprotection against ischemia-reperfusion injuries. His research demonstrated that acute ethanol protects the heart from ischemic events by mimicking cardiac preconditioning. Several protein kinase C substrates involved in this ethanol-induced protective mechanism have been identified in his research; among them is an important detoxifying enzyme aldehyde dehydrogenase (ALDH). More recently, Che-Hong has been focusing on the function of ALDH multi-gene family and its association with human diseases. By high throughput screening of small molecule libraries, Che-Hong pioneered the discovery of a class of novel enzyme activators and inhibitors of aldehyde dehydrogenase (Aldas & Aldis). Many of the 19 human ALDH isoyzmes and their mutations have been implicated in diseases caused by the accumulation of toxic aldehdyes and oxidative stress. Aldas have been shown to be effective in enhancing cell's detoxifying capacity both in vitro and in vivo. The discovery of Aldas & Aldis as a unique class of enzyme modulators carries a great potential for drug development for a wide range of human diseases. Che-Hong's current research focuses on the isolation and characterization of ALDH isozyme-specific modulators and the understanding of the basic molecular interaction between ALDH and these small molecules. In addition to the study of enzyme deficiency in ALDH, Che-Hong is also interested in applying what has learned from the ALDH project to another common human metabolic enzyme deficiency of glucose-6-phosphate dehydrogenase (G6PD).

Pharmacological recruitment of aldehyde dehydrogenase 3A1 (ALDH3A1) to assist ALDH2 in acetaldehyde and ethanol metabolism in vivo. Proc Natl Acad Sci U S A. 2015 Mar 10;112(10):3074-9. Chen CH, Cruz LA, Mochly-Rosen D. Correcting a genetic mutation that leads to a loss of function has been a challenge. One such mutation is in aldehyde dehydrogenase 2 (ALDH2), denoted ALDH2*2. This mutation is present in  0.6 billion East Asians and results in accumulation of toxic acetaldehyde after consumption of ethanol. To temporarily increase metabolism of acetaldehyde in vivo, we describe an approach in which a pharmacologic agent recruited another ALDH to metabolize acetaldehyde. We focused on ALDH3A1, which is enriched in the upper aerodigestive track, and identified Alda-89 as a small molecule that enables ALDH3A1 to metabolize acetaldehyde. When given together with the ALDH2-specific activator, Alda-1, Alda-89 reduced acetaldehyde-induced behavioral impairment by causing a rapid reduction in blood ethanol and acetaldehyde levels after acute ethanol intoxication in both wild-type and ALDH2-deficient, ALDH2*1/*2, heterozygotic knock-in mice. The use of a pharmacologic agent to recruit an enzyme to metabolize a substrate that it usually does not metabolize may represent a novel means to temporarily increase elimination of toxic agents in vivo.

(慈濟) 高瑞和/ 楊國梁… 捐髓破4000例

慈濟骨髓幹細胞中心 突破4000 2015-08-12 02:00:17 聯合報 記者徐庭揚/花蓮報導 慈濟骨髓幹細胞中心在今年8月突破4000例。花蓮慈濟醫院長高瑞和指出,22年來,從早期的困難重重到現在全家人陪伴捐贈,從骨髓幹細胞捐贈的成長速度,顯見骨髓捐贈的正確觀念日漸普及,且周邊血捐贈的推廣也是一大助力。慈濟骨髓幹細胞中心已是世界上重要的骨髓資料庫,捐髓大愛跨越種族、膚色的藩籬,已有29個國家病友受惠。中心主任楊國梁表示,從第1位捐贈者到第500名捐贈者歷經87個月,從第500名到第1000名捐贈者歷經3年,從第1000名到第2000名捐贈者歷經310個月,從第2000名到第4000名捐贈者歷經510個月,人數不斷成長。今年8月至今共有11位捐贈者,其中來自台中市的大學生余欣倫,參加驗血活動不到1年,就成功配對,她覺得不可思議也很幸運。她說,只要將心比心,想到有個人正等待她的造血幹細胞救人,她就變得勇敢,她也希望病人恢復健康後,成為一個凡事將心比心的人。年紀超過50歲的張四福,是較年長的捐贈者,這次抽取周邊血,太太和女兒全程陪伴,張四福表示,去年是外甥捐贈周邊血,今年輪到他,很感恩。來自北部的方志豪14年前參加驗血活動,在6月份接獲配對通知,8月完成捐贈。方志豪說,希望受贈者的親朋可以參加驗血活動,因為不知道什麼時候才可幫助到人,所以要更積極參與。

瑞士Actelion 攜手 大昌華嘉 戰略布局亞洲肺動脈高血壓(PAH)市場!

大昌華嘉與歐洲最大的生物醫藥企業簽訂協議 推動亞洲業務增長15811日美通社(亞洲專注於亞洲地區並處於領先地位的市場拓展服務公司大昌華嘉宣佈,已與總部設於瑞士的全球生物醫藥企業 Actelion 有限公司的聯繫公司 Actelion 製藥新加坡有限公司簽訂協議,推動亞洲業務增長 雙方的協議初步包括治療多種類別肺動脈高血壓(PAH)病人的處方藥物 Tracleer®。這款藥物目前正待在香港、馬來西亞和新加坡完成產品註冊程序,大昌華嘉和 Actelion 其後更可能會將合作範圍擴大至口服內皮素接受器拮抗劑 Opsumit® (macitentan)Opsumit 201311月開始已於美國有售,現正於世界各地多個市場接受監管機構審核。Actelion 製藥澳洲有限公司太平洋區副總裁 Simon Eade 表示:「大昌華嘉是可靠的合作夥伴,有助我們在增長迅速的亞洲市場發展業務。我們深信大昌華嘉會致力提供達國際最高水平的優質服務,並且遵守最嚴格的合規標準,協助我們處理所有營運工作。大昌華嘉在亞洲擁有豐富的監管合規經驗,如今成為我們在亞洲的單一聯絡點,可謂十分方便,可簡化多個市場之間的合作事務。」大昌華嘉醫藥保健部主管 Andrew Frye 表示:「大昌華嘉雄踞優勢,可提供強大的供應鏈支援,並且引領 Actelion 完成繁複的監管批核程序,以支援 Actelion 旗下產品的商業化工作。Actelion 與大昌華嘉合作之後,可專注於本身的核心實力,同時令未來業務發展更順利。」這次與 Actelion 簽訂協議,將可進一步鞏固大昌華嘉在亞洲的市場地位。

Actelion 有限公司簡介 Actelion 有限公司是領先的生物醫藥企業,專注於發掘、發展和在市場上推出創新的藥物,以治療在醫療上有殷切需求的疾病。Actelion在肺動脈高血壓(PAH)的範疇節節領先,公司治療 PAH 的方式涵蓋 PAH 所有領域,由世界衛生組織第二級至第四級症狀均有涉及,提供口服、吸氣和靜脈注射藥物。Actelion 的治療方式雖然並非於所有國家提供,但已獲得不少衛生監管機構批准,適用於多種專門疾病,包括第一型高雪氏症、尼曼匹克症C型、硬皮症患者的手指潰瘍,以及蕈狀肉芽腫皮膚T細胞淋巴瘤。Actelion 1997年終創立,如今擁有超過2,400位專業人員,業務涵蓋全球所有主要市場,包括歐洲、美國、日本、中國、俄羅斯和墨西哥,公司總部設於瑞士阿爾斯維爾/巴塞爾。Actelion 的股票現於瑞士證交所買賣(股票代號:ATLN),而且是瑞士藍籌股票指數SMI (瑞士市場指數SMI®)的成份股。所有商標均按照法律受到保障。

大昌華嘉簡介 大昌華嘉是一家專注於亞洲地區,在市場拓展服務領域處於領先地位的集團。正如「市場拓展服務」一詞所述,大昌華嘉致力於協助其他公司和品牌拓展當前市場或新興市場業務。大昌華嘉20123月在瑞士證交所公開發行上市,是一家總部位於瑞士蘇黎世的全球性企業。大昌華嘉在全球35個國家設有750個營運據點—其中720個分佈於亞洲地區,擁有超過27,600名專業員工。大昌華嘉於2014年的營收淨額為98億瑞士法郎。大昌華嘉於2015年慶祝150週年紀念,本身為一家富有傳統的瑞士企業,在亞洲經營的歷史源遠流長,早已扎根於亞太區多個市場,與當地社群和商界緊密聯繫。大昌華嘉醫藥保健部是頂尖的市場拓展服務供應商,專門服務有意於亞洲發展業務的醫療保健公司,為其提供度身訂造的解決方案,從產品註冊、市場進入研究,到進口、清關、市場推廣及銷售,以至傳統物流、發出單據及現金收款等服務,一應俱全。大昌華嘉醫藥保健品部亦提供處方藥品、保健消費品、非處方藥品及醫療器材等產品。醫藥保健品部業務覆蓋14個國家,於150個地點經營,專業員工約9,200人,服務逾150,000名顧客。2014年,該部門的淨銷售額約為45億瑞士法郎。

東宇生技 新總經理 吳靜翊

東宇生技:本公司董事會通過總經理任命 鉅亨網/鉅亨網新聞中心-20150812 上午11:20 第七條 第61.董事會決議日:104/08/112.變動人員職稱(請輸入〝董事長〞或〝總經理〞):總經理3.舊任者姓名及簡歷:不適用4.新任者姓名及簡歷:吳靜翊5.異動原因:董事會任命6.新任生效日期:104/08/117.其他應敘明事項:

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杏國新藥:公告本公司財務主管異動案 鉅亨網/鉅亨網新聞中心-20150811 下午16:08 第二條 第81.人員變動別(請輸入發言人、代理發言人、重要營運主管之名稱、財務主管、會計主管、研發主管、內部稽核主管或訴訟及非訟代理人):財務主管2.發生變動日期:104/08/113.舊任者姓名、級職及簡歷:葉明4.新任者姓名、級職及簡歷:陳蒨慧5.異動情形(請輸入「辭職」、「職務調整」、「資遣」、「退休」、「死亡」、「新任」或「解任」):職務調整6.異動原因:職務調整7.生效日期:104/08/118.新任者聯絡電話:(02)2764-08269.其他應敘明事項:

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