[爆卦]Smad 中文是什麼?優點缺點精華區懶人包

雖然這篇Smad 中文鄉民發文沒有被收入到精華區:在Smad 中文這個話題中,我們另外找到其它相關的精選爆讚文章

在 smad產品中有3篇Facebook貼文,粉絲數超過1萬的網紅JOHN YUYI,也在其Facebook貼文中提到, Interview with i-D CHINA talking about "SMAD" “社交网络焦虑”症 “people knows me through the internet....but I feel kip napped at the same time" “网络让无国界的...

 同時也有2部Youtube影片,追蹤數超過166萬的網紅瀬戸弘司 / Koji Seto,也在其Youtube影片中提到,本日、2021年3月2日 AM10時より、ソニーの新型シネマカメラ「FX3」の予約が開始されました。 <商品リンク> SONY FX3 ボディ ILME-FX3 | マップカメラ https://www.mapcamera.com/item/4548736123205 <ワイヤレスピンマイクに...

smad 在 Charis 姜姜? Instagram 的最佳解答

2020-11-22 13:16:11

#肉乾界的愛馬仕 真的有夠時髦🔥 #水根肉乾 從外到內都是精品等級! 60年職人手作肉乾,選用台灣純正豬肉 更是 #彰化十大伴手禮 之一 還研發全台第一款麻辣口味 #青花椒肉乾 採用江津九葉青花椒,香麻而不辣👍 這次體驗的輕奢品味組($1199元) 總共有三種口味 #青花椒肉乾 非常特別,是我的...

  • smad 在 JOHN YUYI Facebook 的最佳解答

    2017-10-09 14:28:06
    有 54 人按讚


    Interview with i-D CHINA
    talking about "SMAD" “社交网络焦虑”症

    “people knows me through the internet....but I feel kip napped at the same time"
    “网络让无国界的人们知道我......但同时我也觉得被他们绑架”

    "you wanna take a good picture on the beach to post on your social media, but you forgot to swim in the ocean"
    “你要拍一张海边美照发在网上,却忘了好好在海里游泳。“

    http://i-d.vice.cn/topic/yuyi%20john

  • smad 在 未來流通研究所 Facebook 的精選貼文

    2017-07-05 16:40:28
    有 10 人按讚


    #日本國內零售市場規模連續兩年衰退面臨險峻挑戰

    #貼近客製化服務與高度彈性成為實體零售轉型策略

    日本Bic Camera東京秋葉原新店「Bic Camera AKIBA」開張

    日本大型家電零售企業Bic Camera東京秋葉原新店「Bic Camera AKIBA」於上個月底開幕,在Yodobashi Camera、Edion、山田電機等眾多電器零售企業雲集的秋葉原區域,對於吸引國內消費者與境外旅客購物腳步較慢的Bic Camera,轉而將目標擴展至女性客戶族群,希望藉此打造出新的營收驅動基礎,並突破電腦家電銷售業績低迷的困境。

    Bic Camera AKIBA坐落於秋葉原中央大道,取代sofmap在秋葉原的旗艦店「秋葉原本館」。不同於Bic Camera過去的門市配置與經營模式,Bic Camera AKIBA一樓主要銷售日用品及日本特産,二層則以化粧品及美容家電為主,原本的主力銷售品項電腦與白色家電,則被配置在四樓以上進行展售,未來Bic Camera將持續開展新的店型,取代過去以家電銷售為主的門市經營。不過,根據日本經濟新聞報導,Bic Camera AKIBA 1號店開張當天仍多以外國遊客為主,亦有女性顧客對於店內商品陳列方式表達不滿。

    雖然Bic Camera是否能兼顧家電銷售本業與新興消費需求仍是未知數,但可以看出,從電器街到日本次文化發源地,再到訪日遊客爆買集中地,經歷了層層蛻變的秋葉原正迎來新一波的轉型浪潮。由於訪日遊客爆買風潮趨緩,旅客消費重心轉向追求精緻服務與特色商品,加上秋葉原鄰近區域重新開發,辦公區域擴充帶來較以往更多的女性顧客,使當地商家為吸引各年齡層消費者的爭奪日趨激烈。2016年,秋葉原開設了以女性為主要目標族群的動漫周邊商品店舖、以及女性專用的膠囊旅館,Laox秋葉原總店亦計劃於近期開設化粧品銷售專櫃,以吸引更多女性客戶。顯見零售企業與整體商圈經營為吸引消費者正積極各變其法,由過去高度標準化與集中化的優勢展店策略,走向貼近客製化服務需求、提供高度彈性服務的特色化商圈經營。

    根據2016年度日本零售業調查結果顯示,日本國內零售市場規模已連續兩年衰退,且電商蠶食實體門市業績的局勢亦更加顯著,實體零售企業正面臨險峻挑戰:銷售額排行前20大企業中,減收企業比例達50%。即使是日本零售龍頭永旺亦僅增收334億日元,排在第2位的柒和伊控股由於旗下百貨商場及超市銷售業績低迷,銷售額大幅衰退2,100億日元。三越伊勢丹控股等大型百貨商場營收成長亦相當黯淡。面對高度飽和的經營環境,日本實體零售業者開始積極革新,希望透過多元創新的門市型態與科技應用,支撐營收持續增長。

    例如日本全家超商選定住商混和區域推出結合餐飲與生鮮超市的創新店態,在醫院或高齡住宅周邊商圈則結合藥局進行複合式經營;日本最大連鎖藥妝商店松本清,亦鎖定銀座、有樂町等海外旅客觀光商圈,推出精選品項與免稅服務的白色松本清店型,成功吸引大量商流;而傳統物流業者亦跨出血汗企業形象,如佐川急便在東京車站、淺草及京都等觀光商圈,設立仿古江戶驛站形象營業所,提供遊客快速行李配送服務。可以想見未來依據商圈特徵與消費需求差異,日本零售產業將更積極跨出既有業態界線,結合親子照護、高齡友善場所、觀光特化等創新商業型態與主軸,蛻變出新的產業風貌。

    我國流通產業同樣面臨消費市場成長趨緩、高度飽和競爭等經營困境,業者亦積極以更多樣化與差異化的精緻服務,滿足多元消費需求。例如我國超商龍頭企業統一超推出「一店一特色」策略,希望打造300家特色門市,而全家超商亦宣告將於2020年前,與天和鮮物、大樹藥局、吉野家等企業跨業合作,設立400家不同種類的複合店型,以貼近商圈需求差異。相信未來因應我國旅遊、零售等服務業變革與超高齡化社會趨勢演進,零售、物流、電子商務等流通企業,將演變出更加豐富多元的經營型態,在提高企業本身商業價值與獲利能力的同時,亦做為推動地方商圈活絡與產業發展的重要角色。

    #新聞評析

    http://www.excite.co.jp/…/smad…/20170703/E1498797203678.html

  • smad 在 貓婆選物所 Facebook 的最佳貼文

    2015-08-23 19:07:45
    有 28 人按讚


    看過一些數據,一年中死於化療的數字比本身癌症還多。

    【美國終於承認手術或化療後癌細胞反而加速擴散】 - 路透社報道

    科學家一項最近研究發現,有些癌症患者在接受手術、化療或放療後,癌細胞反而加速擴散,造成這種現象的原因之一是人體一種名為TGF-be-ta物質。因此,控制TGF-be-ta物質在人體內的含量,才是治癒癌症的關鍵。

    來自美國田納西州範德比爾特大學的研究人員在老鼠身上試驗發現,患有乳腺癌的老鼠在服用化療物質“阿黴素”或接受放療後,體內的TGF-be-ta物質含量提高,刺激癌細胞向肺部轉移。而使用某種抗體抑制它們體內的TGF-be-ta含量則能夠遏制癌細胞擴散。

    參考連結:Inhibition of TGF-β with neutralizing antibodies prevents radiation-induced acceleration of metastatic cancer progression

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1838926/

    此前有科學家提出,動物體內的原發性腫瘤可能會抑制其他腫瘤生長,但一旦原發性腫瘤被從體內清除,其他被抑制腫瘤可能會就此瘋長。而科學此次研究顯示,TGF-be-ta就是這樣一種既能抑制腫瘤生長,也能刺激癌細胞擴散的物質。

    主持研究的卡洛斯.。啊特亞加博士補充說,可能還有其他物質與TGF-be-ta一樣對癌症的治療有類此的影響。他們希望通過對TGF-be-ta的研究得出更多結論。 以上訊息在10月8日的《參考訊息》報也有報導。

    看來主張手術或放化療治療癌症的人,良心終於被發現了。 人類自從3000年前發明瞭藥物以來,200年前發現了抗生素,人類的疾病就更複雜,更多,更難治。

    很多慢性病,免疫系統紊亂症,都與藥物和抗生素的濫用有很大的關係。人的耐藥性越強。人就更難戰勝病魔。而癌症自然也有它的天敵。眾所周知醫學界對癌症束手無策。

    醫學界奪命奪錢三招“手術、化療、放療”。目前醫學科技很發達,世界各國投入無數財力物力去研究醫學,但是卻對絕大多數的慢性疾病無能為力,這不能不說是個人類天大的笑話。

    1、成年人每人每天都有3000-6000個癌細胞產生(由於基因突變而讓正常細胞變成癌細胞,基因突變原因很多,化學藥物,肉類,動物荷爾蒙、空氣汙染等等)。

    2、但人每一天誕生的癌細胞幾乎都被人體自身自然殺手細胞(NK細胞)殺滅了。所以不是人人都會患上癌症.當免疫系統下降,也就是自然殺手細胞弱了,癌細胞就佔上風。久而久之5-10年以上就會得到癌症.如果我們能讓癌症病人身體裡的自然殺手細胞變強,恢復活力,對付癌症是簡單的事。

    所以癌症病人只能靠自己也就是自身免疫細胞-自然殺手細胞(NK細胞)來對付癌症。
      
    3、讓自然殺手細胞(NK細胞)恢復活力的唯一途徑是營養70%、心情10%、運動10%、休息10%(世界衛生組織的健康的四大基石)。

    4、只要有充足的營養,自然細胞就能恢復到以前的活力來殺滅癌細胞。(這個世界一物降一物,但一物應該是人體的細胞而不是藥物,也不是植物,更不是動物。人的免疫細胞是可以對付世界上所有的病毒和細菌,比如非典病毒,艾滋病毒,埃博拉病毒,流感病毒,關鍵是人的免疫細胞要足夠的強。例外:但人的免疫細胞沒有辦法對付毒藥。

    5、醫學上常規不得已用藥物和化療、放療、電療方法,除了把癌細胞部分殺滅外,反而把正常的大量的自然殺手細胞殺滅.醫學界奪命奪錢三招“手術、化療、放療”!所以手術藥物和化療放療有時能減輕病人的痛苦同時反而加速癌症病人的死亡.

    6、為什麼國內的癌症研究者都是研究藥物如何殺滅癌細胞(治標)。為什麼不能研究讓人體內的自然殺手細胞增強來殺滅癌細胞呢(治本)?只有0.5%的經過化療放療的病人能活過超過5年!!

    7、世界上最好的醫生是自己的免疫系統、免疫細胞,而不是醫生和藥物!!只有本人的免疫系統(自然殺手免疫細胞)才能殺滅癌細胞。可是藥物和化放療卻會快速讓人的免疫系統下降。

    8、請癌症病人去新華書店購買《營養免疫學》陳昭妃癌症研究博士著,《不要讓不懂營養學的醫生殺了你》雷.D.斯全德醫學博士著。《別讓醫生殺了你》, 《食物是最好的醫生》,《醫生對你隱瞞了什麼》...等最新學科書籍。但是闡述得最完整最好的還是《營養免疫學》這本書。
      
    9 四大基石裡的休息和運動促使免疫力提高。晚上安靜下來睡覺的時候,是人體內免疫細胞正在大量修復身體破損的細胞的時候,所以晚上也是最需要休息和營養的時候。
      
    10、偶然我們在報上看到有些極少數癌症病人得了癌症不治,反而過了幾年後身體的癌症症狀全無,經檢測沒有癌細胞的存在.這是因為這個癌症病人平常的飲食心情運動休息讓體內的自然殺手細胞得到增強來殺滅癌細胞.也就是自愈力了——自已治病的能力。治癌不能靠高科技,而只能靠自然的力量、自身的力量。

    Inhibition of TGF-β with neutralizing antibodies prevents radiation-induced acceleration of metastatic cancer progression

    Abstract
    We investigated whether TGF-β induced by anticancer therapies accelerates tumor progression. Using the MMTV/PyVmT transgenic model of metastatic breast cancer, we show that administration of ionizing radiation or doxorubicin caused increased circulating levels of TGF-β1 as well as increased circulating tumor cells and lung metastases. These effects were abrogated by administration of a neutralizing pan–TGF-β antibody. Circulating polyomavirus middle T antigen–expressing tumor cells did not grow ex vivo in the presence of the TGF-β antibody, suggesting autocrine TGF-β is a survival signal in these cells. Radiation failed to enhance lung metastases in mice bearing tumors that lack the type II TGF-β receptor, suggesting that the increase in metastases was due, at least in part, to a direct effect of TGF-β on the cancer cells. These data implicate TGF-β induced by anticancer therapy as a prometastatic signal in tumor cells and provide a rationale for the simultaneous use of these therapies in combination with TGF-β inhibitors.

    Go to:
    Introduction
    TGF-β is both a tumor suppressor and a tumor promoter. The TGF-β ligands bind to cognate serine/threonine kinase transmembrane receptors, which in turn phosphorylate and activate the Smad family of signal transducers. Once activated, Smad2 and Smad3 associate with Smad4 and translocate to the nucleus, where they regulate the transcription of genes involved in cell cycle arrest and apoptosis (1), essential for the tumor suppressor role of the TGF-βs. Indeed, loss or attenuation of TGF-β signaling in epithelial cells and stroma is permissive for epithelial cell transformation (2, 3). On the other hand, introduction of dominant-negative TGF-β receptors into metastatic cancer cells has been shown to inhibit epithelial-to-mesenchymal transdifferentiation, motility, invasiveness, and survival, supporting the tumor promoter role in TGF-β in fully transformed cells (reviewed in ref. 4). Most carcinomas retain TGF-β receptors but attenuate or lose the Smad-dependent antimitogenic effect while, in some cases, gaining prometastatic abilities in response to TGF-β. In addition, excess production and/or activation of TGF-β by cancer cells can contribute to tumor progression by paracrine mechanisms involving modulation of the tumor microenvironment (2, 5, 6). These data have provided a rationale in favor of blockade of autocrine/paracrine TGF-β signaling in human cancers with a therapeutic intent.

    In addition to Smads, TGF-β can stimulate several transforming signaling pathways (7). TGF-β has previously been shown to protect transformed cells from apoptosis (8–10). One possible mechanism for this cellular response is TGF-β–induced activation of PI3K and its target, the serine-threonine kinase Akt (11, 12), a signaling program associated with resistance to anticancer drugs. Some tumors resistant to conventional anticancer chemotherapy overexpress TGF-βs (13, 14), and inhibitors of TGF-β have been shown to reverse this resistance (15). In addition, overexpression of TGF-β ligands have been reported in most cancers, and high levels of these in tumor tissues and/or serum are associated with early metastatic recurrences and/or poor patient outcome (16–21).

    In transgenic models of breast cancer, TGF-β signaling enhances the metastatic progression of established mammary tumors induced by oncogenes such as Neu/ErbB2 or polyomavirus middle T antigen (PyVmT) (22–24). Furthermore, in transgenic mice expressing the PyVmT oncogene under the control of the MMTV/LTR mammary promoter, conditional induction of active TGF-β1 for as little as 2 weeks increases lung metastases by more than 10-fold (10). Some anticancer therapies have been shown to induce TGF-β systemically or in situ (25–28). Therefore, we speculated that in tumors resistant to anticancer therapies or in resistant subpopulations within those tumors, treatment-induced TGF-β would provide a survival signal to cancer cells potentially accelerating tumor progression immediately after therapy. Using the MMTV/PyVmT transgenic model of metastatic breast cancer, we show here that administration of ionizing radiation or doxorubicin caused increased circulating levels of TGF-β1 as well as increased circulating tumor cells and lung metastases. These effects were abrogated by administration of a neutralizing pan–TGF-β antibody. Radiation did not increase lung metastases in mice bearing tumors that lack the type II TGF-β receptor (TβRII). These data implicate TGF-β induced by anticancer therapy as a prometastatic signal in tumors and thus provide a rationale for the simultaneous use of these therapies in combination with TGF-β inhibitors.

    Go to:
    Results
    Thoracic radiation and chemotherapy increase circulating TGF-β1.

    We administered 10 Gy to the thoraxes or pelvises of 8-week-old FVB virgin female mice. Blood was collected 24 hours after irradiation. We observed an approximate 2-fold increase in plasma TGF-β1 in irradiated mice over controls regardless of the site of radiation (thorax, P = 0.03; pelvis, P = 0.02; Figure Figure1A),1A), while TGF-β2 levels did not change (data not shown). Similar results were obtained in 8-week-old MMTV/PyVmT transgenic mice and in nontransgenic mice transplanted with MMTV/PyVmT tumor cells stably transfected with a luciferase expression vector (P = 0.015 and P = 0.007, respectively, versus controls; Figure Figure1B).1B). Levels of TGF-β1 remained higher than controls 7 days after radiation (data not shown). To expand these results to other anticancer therapies, we examined the effect of the DNA-intercalating agent and topoisomerase II inhibitor doxorubicin (Adriamycin). Transgenic mice were treated 3 times with doxorubicin (5 mg/kg i.p.) at 21-day intervals starting at week 8. In plasma collected on week 15, TGF-β1 was also elevated 2-fold compared with untreated mice (P = 0.009; Figure Figure1C),1C), whereas TGF-β2 levels remained constant. To measure activated TGF-β1 in the lung tissue harvested 5 weeks after radiation, we used a TGF-β1 bioassay that uses mink lung epithelial cells stably expressing a plasminogen activator inhibitor–1/luciferase reporter (PAI-1/luciferase reporter) (29). Tissue lysates from irradiated mouse lungs induced a 2-fold increase in active TGF-β1 compared with nonirradiated lung tissue lysates (P = 0.0008; Figure Figure1D). 1D).

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