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Saturday, November 15, 2014

楊泮池....英聽好不等於英文能力好

台、交大不看英聽 他校後悔採計 2014/11/07 【聯合報╱記者林秀姿/台北報導】 104學年度大考簡章今起發售,共66校、1802個系組參與招生,較去年增加39個系組。首度有152個系組將英聽成績列為門檻,只占8.4%。台大、交大都沒採計。部分採計英聽的頂大理工科系看到台大未採計,「深感後悔」,擔心招生因此受影響。 大考分發委員會表示,152個系組中,設A級「幾乎完全聽懂」門檻的有31個系組,B級「大致聽懂」有83個系組,C級「約略聽懂」有38個系組。彰化師大採計比率達52.17%,全台最高,其次是陽明大學44.44%、政大35.9%,採計的科系都超過全校科系1/3 大考分發會主任詹錢登分析,明年是採用英聽門檻首屆,不少學校還在觀望,態度比較保守,例如台大擔心數理優秀的學生因為英聽不好而無法入學,私校則擔心英聽門檻太高,學生不來登記。 詹錢登說,看到台大決定所有科系都不採計英聽,不少決定採計的學校都「很後悔」,尤其理工科系,多認為數理優異的學生,通常語文能力不強,一旦採計英聽,「登記分發的機會都沒有。」 台大不採計英聽據了解有三種考量。首先是台大校長楊泮池認為城鄉差距大,偏鄉學校英聽設備、資源都不足,不應設門檻;其次,繁星推薦、個人申請不少學生會附上多益、全民英檢成績,重視英文能力的科系足以參考;更重要的是英聽好不等於英文能力好。 明年大考重大的變革還包括,指考採計科目上限將由6科降為5科。 詹錢登表示,今年124個採計6科的系組中,明年共41個系組不採計物理,33個系組不採計國文,受影響最大為第三類組。第一類組則以不採計數學乙跟地理居多。 第三類組中,11所大學醫學系都將從原先採計6科降為5科。詹錢登表示,台大醫學系等10個醫學系都選擇放棄採計國文,中山醫學大學選擇不採計英文,但台大醫學系雖不採計國文,卻要求學測國文成績須達頂標。  

 

 

蔣丙煌: 黑心油是長久以來的事實 ???!!!

檢驗好毒!綠委控蓄意殺人 蔣丙煌認了:吃頂新油傷身 陳鈞凱 2014 11 06 11:07 記者陳鈞凱/台北報導 頂新黑心油檢驗報告昨曝光,不僅豬、牛油重金屬銅、鉛超標,牛油還有不應存在的鉻,毒透全身,民進黨立委劉建國今(6)天重提總統馬英九去年一番黑心食品「吃了不會傷身,但會傷心」言論,嘲諷總統就是長期吃這些油才「傷腦」,指頂新根本蓄意殺人;衛福部長蔣丙煌也首度直言,依檢驗結果,頂新油品的確傷身。 彰化檢方昨公布頂新屏東廠豬、牛油採樣檢驗報告,發現豬油和牛油的鉛含量超標高達7倍、4倍之多,牛油還有不應存在的鉻。鉛具神經毒性,長期大量暴露恐引發腦病變、周邊神經病變,導致智力、認知異常。 蔣丙煌上午赴立法院社會福利及衛生環境委員會進行專案報告,劉建國質詢時,一一點名,包括總統當初「傷心不傷身」、前食藥署長葉明功「食安燈號維持綠燈」的言論,如今都被檢驗報告狠狠打臉。 劉建國表示,總統、江揆都曾為架上的食品背書保障,根本是離譜的總統、惡質的院長,且頂新黑心油現在被證實這麼「毒」,這不是蓄意殺人,什麼才是蓄意殺人,他並追問蔣丙煌,吃頂新油到底傷不傷身? 蔣丙煌無奈表示,葉明功當時代表食藥署,言論衛福部得概括承受,他坦言,檢驗的是未經過精煉的原料油,但若依現在的報告來看,頂新油品「的確會傷身」;但蔣丙煌強調,目前連環爆的黑心油,是長久以來都有的事實,現在被「發現」處理,對未來民眾的食品安全是有保障的,衛福部也一定會落實源頭管理。  

 

檢舉 蔣丙煌/ 林奏延/ 姜郁美涉包庇頂新 !

包庇頂新?北社告蔣丙煌等3人傷害罪 多個本土社團今(6)日前往監察院檢舉衛福部長蔣丙煌、前代理衛福部長林奏延與食藥署代理署長姜郁美3人包庇頂新。圖:邱珮文/ 新頭殼newtalk2014.11.06 邱珮文/台北報導 對於綠委踢爆衛福部早在10/9日得知大幸福出口為飼料油,卻拖了13天才要求頂新下架相關油品,多個本土社團今(6)天前往監察院檢舉衛福部長蔣丙煌、前代理衛福部長林奏延與食藥署代理署長姜郁美3人涉嫌包庇頂新。隨後更前往台北地檢署按鈴控告3人幫助詐欺、傷害罪,讓全民多吃2週噁油。 台灣北社社長張葉森表示,這3人明知頂新製油公司自越南進口油脂,僅能供飼料用油,不能製成食品用油,依法應於得知事實時,立即下架並查封違法食品。但是,3人早在10/9得知廠商違法,竟仍不作為,縱容廠商繼續銷售至10/22,有包庇之嫌,要求監察院與司法單位介入調查。 台灣北社律師陳達成則指出,檢警雖已開始偵辦黑心油案,但對象只針對黑心廠商。事實上,民眾更有興趣的是,一連串的食安風暴,如果沒有政府官員的包庇,要怎麼發生?因此這次行動,就是要司法、監察單位針對衛福部的官員進行調查。 代表永社的台大學生洪崇晏則質疑,食安問題接二連三發生,引起民眾恐慌,政府竟然沒有任何人出來負責。另外,包括高雄氣爆事件、洪仲丘案、323行政院衝突以來,也都沒有中央官員下台。他指出,台灣是責任政治,「做不好,就走人!」他們今天要求3人負起法律責任,更要用年底選舉,讓政府負起政治責任。 檢舉書中指出,衛福部長蔣丙煌、前代理衛福部長林奏延與食藥署代理署長姜郁美3人涉嫌包庇頂新,違反公務員服務法,要求監察院行使彈劾或糾舉權。 另外,張葉森也在刑事告訴狀中指出,自己在10/910/22之間曾食用有害人體、染頂心黑油的食品,他認為前述3人涉嫌以「不作為」的方式幫助頂新詐欺、傷害等罪,因此決定控告。  

早知頂新「油」問題還瞞? 林奏延、蔣丙煌全遭檢舉 ▲台灣北社、永社等團體6日上午到監察院具狀檢舉衛福部長蔣丙煌、次長林奏延等人。(圖/記者賴于榛攝) 記者賴于榛/台北報導 油安事件延燒引起民眾不滿,本土社團台灣北社、永社等團體6日上午到監察院具狀檢舉衛福部長蔣丙煌、次長林奏延等人早在10月初就得知頂新進口的越南油有問題,卻拖到月底才公布,危害人民健康。台灣北社法政組召集人、律師陳達成還直接指控,「如果沒有政府包庇、協助,這怎麼可能發生?」 民進黨立委段宜康曾指出,衛福部早於今年109日就得知頂新進口的越南油品全部有問題,卻遲至22日才要求下架,要求衛福部解釋;今日數個本土社團健康的油品,有違《公務員服務法》,要求監察院應視情節輕重,分別懲處。 台灣北社社長張葉森指出,衛福部應該保障人民健康,卻接連讓毒澱粉、大統混油、飼料油等事件發生,監察院應立案調查衛福部長蔣丙煌、曾擔任代理部長的次長林奏延,與食藥署代理署長姜郁美。陳達成則說,檢警目前都是調查黑心廠商,質疑政府難道沒有問題?「如果沒有政府包庇、協助,這怎麼可能發生?」表示也將前往北檢控告蔣丙煌、林奏延、姜郁美涉嫌以不作為方式幫助詐欺、傷害等罪。

 

 

基亞 重生二部曲­_德必碁(海滄) 葉金川、康照洲站台 (再建基亞IVD成功模式)

基亞廈門檢驗試劑廠 本周營運【聯合晚報╱記者徐睦鈞/台北報導】

2014.11.12 04:47 pm上櫃生技股基亞(3176)今宣布,100%持有的子公司德必碁生物科技(廈門),位於廈門海滄生物醫藥港的檢驗試劑廠,本周開始營運。隨著基亞在檢驗試劑研發上的深耕,該公司董事長張世忠表示,未來在中國大陸的布局,除了感染性疾病外,將逐步擴展至各式體外檢測領域及傳統的抗原抗體檢測、腫瘤基因檢測等個人化醫療,市場範圍將更為寬廣。2014/11/12 聯合晚報】

基亞廈門檢驗試劑廠開始營運2014-11-12 聯合晚報 記者徐睦鈞╱即時報導  上櫃生技股基亞(3176)今宣布,100%持有之子公司德必碁生物科技 (廈門),位於廈門海滄生物醫藥港之檢驗試劑廠,於本周舉行開業典禮,開始營運。現場出席的台灣貴賓包含宣明智、葉金川、康照洲等台灣科技界及醫藥界先進;廈門當地則有福建省及廈門市等當地省市行政、衛生官員、銀行行長等出席。基亞繼2012年出售上海浩源予美國Perkin Elmer公司實現投資獲利後,經過兩年的評估與準備,重新選定廈門海滄區的生物醫藥港,重啟大中華區的生產及銷售布局。隨著基亞在檢驗試劑研發上的深耕,該公司董事長張世忠表示,未來在中國大陸的布局,除了感染性疾病外,將逐步擴展至各式體外檢測領域及傳統的抗原抗體檢測、腫瘤基因檢測等個人化醫療,市場範圍將更為寬廣。張世忠說,廈門海滄特區提供租金補助、研發獎勵、租稅獎勵等多項吸引廠商進駐的優惠條件。基亞生技赴海滄投資計畫於201311月業經投審會核准。

基亞廈門子公司 啟動營運 【經濟日報╱記者黃文奇╱即時報導】2014.11.10 06:48 pm 基亞生技(3176)今日宣布,公司100%持有之子公司德必碁生物科技,位於廈門海滄生物醫藥港之檢驗試劑廠,正式開始營運。基亞今日舉行子公司德必碁開幕典禮,出席者包括宣捷生技董事長宣明智、前衛生署長葉金川、前食品藥物管理局局長康照洲等;另外,大陸出席官員則包含福建省藥監處副處長黃凌鴻、廈門市促投局局長等當地省市行政、衛生官員、銀行行長等。基亞表示,公司繼2012年出售上海浩源予美國Perkin Elmer公司實現投資獲利後,經過兩年的評估與準備,重新選定廈門海滄區的生物醫藥港,重啓大中華區的生產及銷售佈局。隨著基亞在檢驗試劑研發上的深耕,未來在中國大陸的佈局,除了感染性疾病外,將逐步擴展至各式體外檢測領域及傳統的抗原抗體檢測、腫瘤基因檢測等個人化醫療,市場範圍將更為寬廣。此外,廈門海滄特區提供租金補助、研發奬勵、租稅奬勵等多項吸引廠商進駐的優惠條件。2014/11/10 經濟日報】 

 

JAKAVI(捷可衛 Ruxolitinib) 禿頭人 新希望 ?!

Bone marrow drug could treat alopecia  Patients treated for alopecia with ruxolitinib responded well"Alopecia sufferers given new treatment hope with repurposed drug," The Guardian reports. Alopecia is a type of autoimmune condition where the body's own immune cells start to attack the hair follicles for an unknown reason, leading to hair loss. This new research actually involved two phases, one involving mice and one involving humans. The researchers identified the specific type of immune cell (CD8+NKG2D+ T cells) that is involved in this autoimmune process, and identified the signalling pathways that stimulate the activity of these cells. The researchers then demonstrated that using molecular treatments to block these signalling pathways was effective in preventing and reversing the disease process in mice genetically engineered to develop alopecia. These findings in mice were followed by promising results in three people with moderate to severe alopecia. These people were treated with ruxolitinib, which is currently licensed in the UK to treat certain bone marrow disorders. All three patients demonstrated "near-complete hair regrowth" after three to five months of treatment. This promising research is in very early stages. Ruxolitinib has been tested in only three people with alopecia, which is far too small a number to make any solid conclusions about the effectiveness or the safety of this treatment in people with alopecia. The safety and efficacy would need to be tested in many further studies involving larger numbers of people, and it would also need to be tested against other currently used treatments for alopecia, such as steroids.

Where did the story come from? The study was carried out by researchers from Columbia University in New York. The study received various sources of financial support including US Public Health Service National Institutes of Health, the Columbia University Skin Disease Research Center, the Locks of Love Foundation and the Alopecia Areata Initiative. The study was published in the peer-reviewed scientific journal Nature Medicine. The media gives varied reports of this study. The Mail in particular is overly premature, as the current study is a very long way away in terms of research steps before knowing whether there could be a new "standard treatment for the condition". Also, references to a "baldness pill" are potentially misleading as they could lead people to think that this treatment, or similar, would be effective against the most common type of baldness, male pattern baldness.

What kind of research was this? This was a laboratory and mouse study that aimed to examine the cellular processes that cause alopecia and to try and investigate a treatment to reverse the process. Alopecia is a condition where body hair falls out, ranging from just a patch of hair on the head to the entire body hair. It is understood to be a type of autoimmune condition where the body's own immune cells start to attack the hair follicles. Causes are not completely understood, with associations with stress and genetics speculated. Unfortunately, although various treatments may be tried (most commonly corticosteroids) there is currently no cure for alopecia. The autoimmune process is thought to be driven by T lymphocyte cells (a type of white blood cell). Previous laboratory studies in mouse and human models have shown that transfer of T cells can cause the disease. However, effective treatments are said to be limited by a lack of understanding of the key T cell inflammatory pathways in alopecia. The researchers had previously identified a particular subset of T cells (CD8+NKG2D+ T cells) surrounding hair follicles in alopecia, as well as identifying certain signalling molecules that seem to stimulate them. In this study, the researchers aimed to further investigate the role of these specific T cells using a group of mice genetically engineered to spontaneously develop alopecia, and also human skin samples.

What did the research involve? First of all the researchers examined skin biopsies from genetically engineered mice that had developed alopecia to confirm that these specific CD8+NKG2D+ T cells were infiltrating the hair follicles. They confirmed that there was an increase in numbers of these specific T cells, increase in total number of cells, and also noticed that there was an increase in growth of lymph nodes in the skin. They found that the type of T cell infiltrating the skin and infiltrating the lymph nodes was the same. They examined the genetic profile of these T cells from the lymph nodes. They then looked into the role of these specific T cells in disease development by transferring these specific T cells, or overall cells from the lymph nodes, into thus far healthy genetically engineered mice that had not yet developed alopecia. This was in order to confirm that the CD8+NKG2D+ T cells were the dominant cell type involved in the development of the disease and were sufficient to cause the disease. The researchers then examined the gene activity in skin samples from the genetically engineered mice, and from humans with alopecia. They identified several genes that were overexpressed around the areas of alopecia, as well as several signalling molecules that are drivers of this abnormal T cell activity, including interleukins 2 and 15, and interferon gamma. The researchers therefore then wanted to see whether using drug treatments that could block these signalling molecules would prevent disease development. To do this they grafted skin from mice that had developed alopecia on to the backs of mice who had not yet developed the condition. They then tested the effectiveness of drug treatments that can block the signalling molecules to see if they could prevent or reverse the disease. Finally, they followed their results in mice with tests in three people with alopecia. What were the basic results? When currently healthy mice were grafted with the skin of mice who had developed alopecia, 95-100% of them developed alopecia within 6 to 10 weeks. Giving antibodies to neutralise interferon gamma at the time of grafting prevented alopecia development. Giving antibodies to block interleukins 2 and 15 had a similar effect. However, though the researchers could prevent development if given at the same time, none were able to reverse the process if given after alopecia had developed. They then investigated whether they could block other signalling molecules that are involved in the downstream pathway from interferon gamma (called JAK proteins). Ruxolitinib (currently licensed in the UK to treat certain bone marrow disorders) is a molecule that blocks JAK1/2 proteins. Tofacitinib is another molecular treatment (not currently licensed for any condition in the UK) that blocks another (JAK3). When these two treatments were given at the same time the alopecia skin samples were grafted on to the healthy mice, the mice no longer developed alopecia. The researchers then tested whether giving tofacitinib seven weeks after grafting could reverse alopecia. Treatment did result in "substantial hair regrowth" all over the body and reduced numbers of T cells, which persisted for a few months after stopping treatment. They also tested whether these two JAK inhibitor treatments were effective when topically applied (rubbed into the skin on the back) instead of given by mouth, and found that they were, with hair regrowth occurring within 12 weeks. The human tests involved three people with moderate to severe alopecia who were given 20mg of ruxolitinib by mouth twice daily. All three people demonstrated "near-complete hair regrowth" within three to five months of treatment. No information on whether these people developed side effects was provided in the study.

How did the researchers interpret the results? The researchers conclude that their results demonstrate that CD8+NKG2D+ T cells are the dominant cell type involved in the disease process of alopecia. They say that "the clinical response of a small number of patients with alopecia to treatment with the JAK1/2 inhibitor ruxolitinib suggests future clinical evaluation of this compound or other JAK protein inhibitors currently in clinical development is warranted".

Conclusion This is valuable laboratory research that identifies the specific type of immune cell (CD8+NKG2D+ T cells) that is involved in the disease process of alopecia. It further identifies several signalling molecules that are drivers of this T cell activity. The researchers then demonstrate that giving two molecular treatments to block the signalling molecules – ruxolitinib (currently licensed in the UK to treat certain bone marrow disorders) and tofacitinib (not currently licensed for any condition in the UK) – were effective in preventing and reversing the disease process in mice with alopecia. These findings in mice were followed by promising results in three people with moderate to severe alopecia who were treated with ruxolitinib. All three patients demonstrated "near-complete hair regrowth" after three to five months of ruxolitinib treatment. These are promising results into the study of potential treatments for this devastating autoimmune condition, which currently has no cure. However, it is important to realise that this research is in the very early stages. So far ruxolitinib treatment has been tested in only three people with alopecia, which is far too small a number to make any solid conclusions about the effectiveness or the safety of this treatment in people with alopecia. This drug is currently not licensed for use in this condition. It would need to go through many further clinical trial stages in larger numbers of people with alopecia. It would also need to be tested for safety and efficacy against other currently used treatments for alopecia, such as steroids. Overall there is some way to go before we could know whether ruxolitinib holds real promise as a treatment for alopecia.

 

JAKAVI(捷可衛 Ruxolitinib) 利用血小板數量 調整劑量 !

(診斷骨髓纖維化 Primary myelofibrosis can begin with a blood picture suggestive of Polycythemia Vera or CML/ Most patients have moderate to severe anemia/ Eventually the patient develops thrombocytopenia/ The peripheral smear appears markedly abnormal/ Red cell abnormality includes bizarre shapes (teardrop-shaped RBCs on a peripheral smear). Nucleated erythroid precursors are seen in the peripheral blood/ Immature white cells are also seen and basophils are increased /Dry tap on bone marrow aspiration/ Reticulin or collagen fibrosis in bone marrow biopsy.

諾華ruxolitinib (Rx) - Jakafi for Myelofibrosis  Kinase inhibitor indicated for treatment of patients with intermediate or high-risk myelofibrosis, including primary myelofibrosis, post-polycythemia vera myelofibrosis and post-essential thrombocythemia myelofibrosis

Initial dose (platelet count >200 x10^9/L): 20 mg PO q12hr

Initial dose (platelet count 100-200 x10^9/L): 15 mg PO q12hr

Initial dose (platelet count 50 to <100 x10^9/L): 5 mg PO q12hr

Titrate dose based on response; not to exceed 25 mg PO q12hr

 

JAKAVI(捷可衛 Ruxolitinib) 諾華 台灣上市 首部曲 (骨髓纖維化) !!

全新口服標靶藥物可降低死亡率達5 成功縮小脾臟達3一位骨髓纖維化病患脾臟長期腫大造成壓迫,無法自行站立行走、嚴重影響日常生活,食慾一蹶不振,長期下來由於苦無藥物可醫治,最後轉為急性血癌而過世。第一個針對骨髓纖維化研發的口服標靶藥物-捷可衛JAKAVI(Ruxolitinib)於今年9月獲得衛生福利部核准上市,較傳統治療方式可降低死亡風險達52%,有效縮減脾臟體積達35%,幫助台灣骨髓纖維化患者重拾美好人生,延長存活率。台北馬偕醫院血液暨腫瘤科主治醫師張明志說明,骨髓纖維化(Myelofibrosis,簡稱MF)是一種罕見的造血功能紊亂疾病,即骨髓已被纖維化,造血細胞沒有辦法在骨髓裡生長,所以必須轉換到其他組織如脾臟及肝臟扛起部份造血責任,造成這類病患最常出現脾臟腫大後引起的內臟壓迫症狀,疾病進展更甚者可轉型為急性白血病危及性命。根據統計,每10萬人當中,就有0.5~1人患有骨髓纖維化3,好發年齡為50~803,且男女性的病發機率相等,患者大多會產生骨髓結疤(纖維化)、脾臟腫大,以及相關併發症狀如疲憊、失眠、發燒、盜汗、皮膚搔癢、骨痛、腹部不適與體重下滑等,嚴重影響生活品質與工作表現。罹患骨髓纖維化的患者早期沒有明顯症狀、不易確診,病患多因貧血及血小板持續減少就醫檢查後才發現是骨髓纖維化。張明志醫師表示一直以來都沒有專門的治療藥物,骨髓移植是此病唯一的治癒方式,但是成功機率低,更會引起多種併發症,造成病患存活率低。嘉義長庚醫院內科部副主任陳志丞醫師表示,由於骨髓纖維化被認定與JAK1JAK2訊息傳導途徑失調有關,目前有全新口服標靶治療藥物-捷可衛JAKAVI(Ruxolitinib)獲衛福部核准上市,藉著抑制JAK1JAK2有效治療骨髓纖維化,核准之適應症為:"適用於治療International Working Group (IWG) Consensus Criteria中度風險-2或高風險之骨髓纖維化,包括原發性骨髓纖維化、真性紅血球增多症後骨髓纖維化或血小板增多症後骨髓纖維化"。根據兩項共超過500位患者、為期3年的臨床試驗(COMFORT-III)證實捷可衛JAKAVI(Ruxolitinib)能降低死亡風險達52%,且超過4成的受試者在半年內有效縮減脾臟體積達35%以上,並大幅改善骨髓纖維化相關症狀如食慾低落、疲憊、失眠、發燒、盜汗、體重下滑、搔癢、肌肉和骨骼疼痛、活動力降低等症狀。骨髓纖維化為一慢性病程,陳志丞醫師指出,曾有患者由於早期無明顯症狀而忽略治療,再加上之前沒有標靶藥物可以治療,最後引發併發症過世;臨床觀察也有一位70多歲骨髓纖維化的病患脾臟長期腫大,症狀最嚴重時腫大至20公分、無法行走,甚至連站立都有困難,三餐常常只吃了兩口就沒有胃口,半年內體重從50公斤下降至44公斤,疲倦、失眠、盜汗等症狀接踵而至,而服用新藥後兩周內脾臟即有效縮減5成,三個月後外觀已幾乎看不見脾臟腫大的症狀,現在已能自行下田工作且精神狀態良好。醫師提醒,早期若能妥善治療,可有效縮減脾臟大小,改善食慾與行動能力,換來良好的生活品質,也不須因為失眠或疲倦等症狀而影響工作表現。

 

彰基 張正雄: 真性紅血球增多症(Polycythemia Vera)轉化成骨髓纖維化(myelofibrosis)

新型口服標靶藥 骨髓纖維化治療契機 20141107 04:10 陳瑄喻/台北報導 一名70歲婦人起初感覺腹部腫脹、食慾不振,瘦到30幾公斤,行動力逐漸減弱,從過去能夠自行赴診至後來需由兒子攙扶陪同,經抽血與骨髓檢查後,才發現她原本罹患的真性紅血球增多症(Polycythemia Vera,簡稱PV),已轉化成罕見的造血功能紊亂疾病骨髓纖維化(myelofibrosis,簡稱MF 彰化基督教醫院暨血液腫瘤科主治醫師張正雄(圖)表示,骨髓纖維化是骨髓無法正常造血的病症,根據統計,每10萬人當中,就有0.51人患有骨髓纖維化,推算台灣約有100200人有這樣的罕見疾病,但過去沒有專門的診治方式,只能給予輔助性的緩解治療,無法有效改善病症,嚴重者甚至可能演變為急性白血病。 張正雄分享,後來這位70歲婦人服用新標靶藥物,治療效果良好,約2個星期後,脾臟已從肋骨下緣10公分縮小至摸不到的大小,不但貧血、體重減輕與食慾不振等相關症狀明顯好轉,一個月後體重恢復為原本的40幾公斤,病患的生活品質也大幅獲得改善。 張正雄強調,第一個針對骨髓纖維化研發的口服標靶藥物今年9月獲得衛福部許可上市,可有效治療骨髓纖維化,核准之適應症為是適用於治療International Working GroupIWGConsensus Criteria中度風險或高風險的骨髓纖維化,包括原發性骨髓纖維化、真性紅血球增多症後骨髓纖維化或血小板增多症後骨髓纖維化。臨床研究發現,新的口服標靶藥物可有效降低52%死亡風險,有效縮減35%脾臟體積,並大幅改善相關症狀。 罹患骨髓纖維化的患者早期會出現貧血、皮膚癢、食慾不振而體重減輕等不明顯的症狀,不易確診,隨著貧血愈來愈嚴重及脾臟腫脹明顯、疼痛,赴醫院檢查後才發現罹患骨髓纖維化。張正雄呼籲,病患如果有相關症狀,應盡速就醫檢查治療,換來良好的生活品質並延長生命。  

 

 

穿戴式医疗: 英特尔/ Covidien/ 三星/ 飞利浦/ 谷歌/ 九安医疗

 医疗与IT融合步伐加快 作者:RFID世界网收录 来源:中国证券报  2014-11-14 09:39:20  摘要:作为智能医疗器械中的代表,穿戴式设备这两年来赚足了风头。越来越多的IT和医药巨头都对可穿戴式设备领域表现出浓厚兴趣,除了加强自身的科技研发,收购行动也愈演愈烈。作为智能医疗器械中的代表,穿戴式设备这两年来赚足了风头。越来越多的IT和医药巨头都对可穿戴式设备领域表现出浓厚兴趣,除了加强自身的科技研发,收购行动也愈演愈烈。今年3月,英特尔公司1亿美元收购健康监测佩戴表商Basis Science。后者的主打产品是健康跟踪设备,包括内置心率检测仪、运动强度检测仪以及体温表温度计等。英特尔借此并购进入可穿戴移动监测产品的芯片领域。5月,爱尔兰的外科手术设备生产商Covidien收购了可穿戴设备公司Zephyr TechnologyZephyr推出的移动产品BioPatch是经过FDA认可的产品,可为临床监测提供专业的记录数据。同月,三星发布了可穿戴医疗保健平台Simband三星将这款名为Simband的健身腕带称作一款"调查式设备",可以将传感器和其他电子元件与软件和服务相融合,从而创造出未来的数字健康技术。此外,包括飞利浦和谷歌在内的医疗设备巨头也投入了大笔资金用于可穿戴式医疗设备的研发。业内人士认为,可穿戴式设备将颠覆传统的医疗领域,开启医疗细分领域的智能化。可穿戴式医疗设备可以持续地跟踪患者的后续情况,医生据此可动态评价药物的疗效,及时跟踪患者的康复进展情况,发现其潜在的风险因素。以心脏病监测为例,一次心电图难以捕捉到有效的诊断依据,可穿戴式的设备可以很方便帮助患者监测并记录心电数据,能够及时发现常规心电图不易发现的心率失常和心肌缺血,是临床分析病情的重要依据。九安医疗Ihealth的无线动态心电图监测,通过其所收集的数据送达云端,医生可以轻松访问这些数据。高血压是严重威胁生命健康的心血管疾病。借助可穿戴式医疗设备可以24小时动态地监测用户的血压数据,向医生提供不同时段的血压数据信息。MIT2009年就开发出了能长时间连续测量的"可穿戴式血压计",能够24小时连续测量血压。传统的血糖检测是通过监控餐后或空腹血糖,但是餐后或空腹血糖的测定,只反映患者的某一具体时间的血糖水平。而可穿戴式医疗设备可以实施动态血糖监测,可以更好掌握血糖的变化,帮助患者及时发现问题,并且降低糖尿病并发症的风险。目前谷歌正在研发测血糖的隐形眼镜,可以衡量佩戴者眼泪中的葡萄糖水平,有效地帮助糖尿病人监控血糖水平。

 

 

全球跨業 醫療物聯網 蓄勢待發

蔡清彥:物聯網時代 抓緊三機會 鉅亨網新聞中心 (來源:聯合報系/udndata.com) 2014-10-21 08:47  工研院董事長蔡清彥昨(20)日表示,在後個人電腦(PC)時代產業遊戲規則重組,台廠過去錯失兩個良機,而今在物聯網的時代則迎來三大機會,透過硬體創新驅動,機會將集中在雲端運算、即時通訊與巨量資料服務方面。 蔡清彥昨日在玉山資通訊科技論壇表示,觀察20052013年,台廠面對典範轉移錯失兩大良機。第一在習慣於Wintel的個人電腦模式,未即時抓到智慧終端契機;第二則在網際網路及行動網路崛起,雖有蕃薯藤、PchomeKKbox等,但皆未走出台灣市場,反而是阿里巴巴等率先崛起 蔡清彥指出,當物聯網時代來臨,隨全球4G布建完成、感應器、App、產業領域知識建置到位等,台廠面對硬體驅動創新,加上系統整合與服務連結將帶動雲端運算、即時通訊與巨量資料服務創新事業的新機會,並影響人類生活。 中磊總經理王煒說,物聯網兩大前提在「雲」與「端」,應用服務則讓使用者從虛擬世界回到現實世界,「誰付錢」是商業模式能否續存的考驗。 台灣半導體產業協會理事長暨鈺創董事長盧超群則表示,台灣半導體產業已是世界第一,產值今年將突破2兆元,當物聯網時代來臨,所有新開發智慧電子裝置都需要台灣夥伴,可以說硬體製造是台廠的最強項。 中華電信董事長蔡力行指出,就電信商角度,裝置聯網的數量膨脹與行動通訊技術演進,帶動市場需求。 遠傳總經理李彬指出,電信業最大挑戰在「提升用戶使用經驗」,在物聯網時代,要能成功則有賴電信通訊服務整合,製造後還需要搭配貼近客戶的通訊服務。 【經濟日報╱記者尹慧中/台北報導】