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1.xlsx我有潛在基因毒性雜質(zhì)結構，需要做下軟件分析，最好可以提供PDF報告，感激。   [更多]

重性抑郁障礙（MDD）是一種使人衰弱的精神障礙，在美國約有20000000流行病例。然而不同的抗抑郁藥可用于治療不同的抑郁癥，，約50%的抑郁癥患者的初始治療結果不理想。最近有證據表明，在發(fā)病的幾個(gè)小時(shí)內氯胺酮給藥治療難治性抑郁癥已經(jīng)顯著(zhù)有所改善。勃林格殷格翰公司尋找氯胺酮在人體中反應和持續的抗抑郁作用的機理。 Boehringer Ingelheim Challenge: Understanding the Antidepressant Effect of Ketamine TAGS: Nature, Chemistry, Life Sciences, Ideation AWARD: $21,000 USD | DEADLINE: 1/15/15 | ACTIVE SOLVERS: 20 | POSTED: 12/15/14 1. The Challenge and qualification for the award Major depressive disorder (MDD) is a debilitating psychiatric disorder with about 20 million prevalent cases in the United States. Various antidepressants are available for treatment of patients suffering from MDD, however, about 50% of MDD patients do not respond adequately to initial treatments. Recent evidence shows that ketamine administered to patients with treatment resistant depression has resulted in marked improvement within hours of treatment. Boehringer Ingelheim (the Seeker) desires a working hypothesis for ketamine’s mechanism of action and sustained antidepressant effect. The submitted solutions will be considered for the award. There will be a guaranteed award for at least one submitted solution. The total payout will be $21,000, with at least one award being no smaller than $12,000 and no award being smaller than $3,000. 2. Additional application for Research Funding In addition to consideration for the award for the submitted Solutions, Solvers with appropriate qualifications and expertise having access to a suitable research laboratory and equipment can apply for research funding (“Research Funding”) to execute a research plan that is proposed in the Solution. The requested funding should not exceed a funding period of 2 years and a total budget of $200,000. The selection of candidates for Research Funding will be conducted after completion of this Challenge, and will require the submission of additional information. The decision to fund research will be at the discretion of the Seeker.   [更多]

求購部分化藥LD50和NOEL數據，且發(fā)給我來(lái)源的截圖。1維生素B2片2呋喃妥因腸溶片3雙氯芬酸鈉腸溶片4谷維素片5復方氨酚烷胺片6對乙酰氨基酚片7維D2磷酸氫鈣片8三合鈣咀嚼片   [更多]

1、動(dòng)物：最好為大鼠或小鼠； 2、藥品：口服的固體制劑（片劑、膠囊劑、顆粒劑都可以）； 3、一整套項目研發(fā)資料，可將公司名稱(chēng)、關(guān)鍵技術(shù)數據打碼，資料主要用于個(gè)人學(xué)習藥物代謝動(dòng)力學(xué)的研究方法和思路，不作商業(yè)用途。   [更多]

金線(xiàn)蓮13大類(lèi)含量及作用 金線(xiàn)蓮的化學(xué)成分與含量中具有重要藥理活性的物質(zhì)主要為： 黃酮類(lèi)化合物（槲皮素、異鼠李素)： 黃酮類(lèi)化合物是一類(lèi)存在于自然界的、具有2-苯基色原酮（flavone）結構的化合物。它們分子中有一個(gè)酮式羰基，第一位上的氧原子具堿性，能與強酸成鹽，其羥基衍生物多具黃色，故又稱(chēng)黃堿素或黃酮。黃酮類(lèi)化合物在植物體中通常與糖結合成苷類(lèi)，小部分以游離態(tài)（苷元）的形式存在。絕大多數植物體內都含有黃酮類(lèi)化合物，它在植物的生長(cháng)、發(fā)育、開(kāi)花、結果以及抗菌防病等方起著(zhù)重要的作用。 甾體類(lèi)化合物（24～異丙烯基膽甾醇、開(kāi)唇蘭甾醇、麥角甾醇、豆甾醇、菜油甾醇、β-谷甾醇等）： 化學(xué)結構中都具有甾體母核，即它的基本碳架具有一個(gè)“環(huán)戊烷并多氫菲”的母核和三個(gè)側鏈。這類(lèi)成分的甾體母核上，都在C3有羥基，并可和糖結合成苷，而C17側鏈上育顯著(zhù)差別，根據C17鏈不同可以分為膽酸類(lèi)、強心苷、甾醇和昆蟲(chóng)變態(tài)激素、C21甾體類(lèi)、甾體皂苷和甾體生物堿等。甾體化合物廣泛存在于動(dòng)植物體內，許多具有各種生物活性，它們的應用非常廣泛，有些被采用治療疾病或發(fā)展生產(chǎn)，如治療過(guò)敏性疾病的氫化可的松、避孕藥黃體酮、利尿劑安體舒通、合成甾體激素的薯蕷皂甙元、強心作用的狄戈辛、蟾毒甙等都是甾體化合物。 三萜類(lèi)化合物（木栓酮、琥珀酸、香豆酸、阿魏酸、胡蘿卜苷、棕櫚酸、齊墩果酸、熊果酸）： 大部分為30個(gè)碳原子，少部分含27個(gè)碳原子的萜類(lèi)化合物。三萜類(lèi)成分（又叫靈芝酸）在自然界分布很廣，鯊魚(yú)油、甘草、五味子的有效成分中都有三萜類(lèi)物質(zhì)。靈芝三萜類(lèi)成分有五環(huán)萜和四環(huán)三萜兩類(lèi)，按分子所含碳原子數可分為C30、C27、C24三大類(lèi)，根據其所含功能團和不同的側鏈，還可分成7種基本骨架。 多糖： 由15個(gè)分子的單糖所組成的大分子的糖叫多糖。由幾種多糖組成的多糖，叫復合多糖。多糖是細胞的組成，又是細胞功能的重要基石，尤其能對免疫功能起到重要的調節作用，免疫多糖對免疫的調節是高效，無(wú)毒副作用的，而且作用點(diǎn)包括細胞免疫和體液免疫，作用點(diǎn)是全面、雙向的，當免疫力低下時(shí)免疫多糖能提升，當免疫功能過(guò)高時(shí)能加以調節，使之正?；?，并且通過(guò)神經(jīng)－內分泌－免疫網(wǎng)絡(luò )達到免疫的自穩和平衡。因此免疫多糖是當今世界公認的優(yōu)良免疫調節劑。 低聚糖： 低聚糖集營(yíng)養、保健、食療于一體，廣泛應用于食品、保健品、飲料、醫藥、飼料添加劑等領(lǐng)域。它是替代蔗糖的新型功能性糖源，是面向二十一世紀“未來(lái)型”新一代功效食品。是一種具有廣泛適用范圍和應用前景的新產(chǎn)品，近年來(lái)國際上頗為流行。美國、日本、歐洲等地均有規?；a(chǎn)，我國低聚糖的開(kāi)發(fā)和應用起于90年代中期，近幾年發(fā)展迅猛。 還原糖： 還原糖是指具有還原性的糖類(lèi)。在糖類(lèi)中，分子中含有游離醛基或酮基的單糖和含有游離醛基的二糖都具有還原性。還原性糖包括葡萄糖、果糖、半乳糖、乳糖、麥芽糖等。 生物堿： 生物堿是存在于自然界（主要為植物，但有的也存在于動(dòng)物）中的一類(lèi)含氮的堿性有機化合物，有似堿的性質(zhì)，所以過(guò)去又稱(chēng)為贗堿。大多數有復雜的環(huán)狀結構，氮素多包含在環(huán)內，有顯著(zhù)的生物活性，是中草藥中重要的有效成分之一。具有光學(xué)活性。有些不含堿性而來(lái)源于植物的含氮有機化合物，有明顯的生物活性，故仍包括在生物堿的范圍內。而有些來(lái)源于天然的含氮有機化合物，如某些維生素、氨基酸、肽類(lèi)，習慣上又不屬于“生物堿\"。 強心甙類(lèi)： (Glycosides) 甙，又稱(chēng)配糖體或苷，是由糖或糖的衍生物（如糖醛酸）的半縮醛羥基與另一非糖物質(zhì)中的羥基以縮醛鍵（甙鍵）脫水縮合而成的環(huán)狀縮醛衍生物。水解后能生成糖與非糖化合物，非糖部分稱(chēng)為甙元（Ag1ycone），通常有酚類(lèi)、蒽醌類(lèi)、黃酮類(lèi)等化合物。 酯類(lèi)： 酸（羧酸或無(wú)機含氧酸）與醇起反應生成的一類(lèi)有機化合物叫做酯。 分子通式為R-COO-R'（R可以是烴基，也可以是氫原子，R'不能為氫原子，否則就是羧基） 酯的官能團是-COO-，飽和一元酯的通式為CnH2nO2(n≥2，n為正整數)。 ?；撬幔? ?；撬幔═aurine）又稱(chēng)β-氨基乙磺酸，最早由牛黃中分離出來(lái)，故得名。純品為無(wú)色或白色斜狀晶體，無(wú)臭，?；撬峄瘜W(xué)性質(zhì)穩定，不溶于乙醚等有機溶劑，是一種含硫的非蛋白氨基酸，在體內以游離狀態(tài)存在，不參與體內蛋白的生物合成。?；撬犭m然不參與蛋白質(zhì)合成，但它卻與胱氨酸、半胱氨酸的代謝密切相關(guān)。人體合成?；撬岬陌腚装彼醽喠蛩狒让福–SAD）活性較低，主要依靠攝取食物中的?；撬醽?lái)滿(mǎn)足機體需要。 多種氨基酸： 氨基酸（amino   [更多]

腎近端小管是腎單位的一部分(腎臟的功能部件)，是人體高專(zhuān)屬性參與重吸收和排泄各種物質(zhì)（包括鹽和礦物質(zhì)）的器官，鹽和礦物質(zhì)的重吸收對身體是非常重要的，否則會(huì )失去在尿液中。此外，腎近端小管對許多藥物的處理也是至關(guān)重要的，所謂的外源性物質(zhì),來(lái)自外面的身體和環(huán)境(如許多人造物質(zhì),包括潛在的毒素)。然而,沒(méi)有好的體外模型可以描述和模仿腎近端小管的功能。建立腎近端小管一個(gè)有力的模型是非常必要的，特別是在腎近端小管在藥物的相互影響方面有至關(guān)重要的作用，因為它是會(huì )由于藥物毒性和藥物之間的作用而非常容易受到傷害導致腎臟疾病。在體外開(kāi)發(fā)腎近端小管模型的系統可以幫助填補腎臟疾病研究中藥物毒性和藥物處理方面的一些空白。 具體看 https://www.innocentive.com/ar/challenge/9933749 The proximal tubule, a part of the kidney nephron (the functional unit of the kidney), has highly specialized properties to do with the salvage and excretion of various compounds, salts and minerals that are very important to the body and would otherwise be lost in the urine. In addition, the proximal tubule is essential for the handling of many drugs and so-called xenobiotics that come from outside the body and from the environment (e.g., many artificial substances, including potential toxins). However, there are no good human models in vitro that can recapitulate and reproduce the function of the proximal tubule. A robust model for the proximal tubule is needed, especially since the proximal tubule has an essential role in drug clearance, because it is highly susceptible to damage in many kidney diseases, and it is also a target for drug-drug interactions and drug toxicity. Development of a proximal tubule model system in vitro could help to address some of the gaps in laboratory models for the study of kidney disease, toxicity, and drug handling. AstraZeneca is seeking innovative approaches to developing a model system of the proximal tubule in vitro. Ideally, the model should incorporate a self-contained microphysiological unit in which biologically appropriate media, fluid flow, and shear stress can be modulated to reproduce the properties of the proximal tubule in vivo and ultimately recapitulate the structural and cellular conditions necessary for integrated proximal tubular function. This is an ideation challenge and only requires a written solution. Source: InnoCentive Challenge ID:   [更多]

阿斯利康提出需求：在大多數的慢性腎臟疾病的情況下有關(guān)腎小球濾過(guò)屏障功能受損的研究。缺少良好的腎小球體外模型，就不能在細胞學(xué)和病理學(xué)的范疇詳細理解腎小球的功能。 阿斯利康正在尋找方法來(lái)開(kāi)發(fā)一個(gè)腎小球模型系統。理想情況下,體外模型應該包含一個(gè)獨立的微型藥學(xué)單元，有適當的介質(zhì)，流體流動(dòng)和所受壓力?？梢哉{整模擬體內黏膜所需條件屬性，最終建立形成一個(gè)功能腎小球濾過(guò)屏障。 具體看下面內容： https://www.innocentive.com/ar/challenge/9933748The majority of all cases of chronic kidney disease, a key research area within AstraZeneca, originate in the glomerulus when filtration barrier function is compromised. However, a detailed cellular understanding of the functioning and pathology of the glomerulus has been limited by the lack of good in vitro models of glomerular function. AstraZeneca is looking for approaches to develop a glomerular model system. Ideally, the in vitro model should incorporate a self-contained microphysiological unit where biologically appropriate media, fluid flow and shear stress can be modulated to simulate in vivo properties that will ultimately recapitulate the conditions necessary for endothelial and podocyte cell types to form a functional glomerular filtration barrier. This is an ideation challenge and only requires a written solution. Source: InnoCentive Challenge ID: 9933748 Challenge Overview The majority of all cases of chronic kidney disease, a key research area within AstraZeneca, originate in the glomerulus when filtration barrier is compromised. The coordinated efforts of the podocytes and endothelium together with their underlying basement membrane establish the glomerular filtration barrier and injury to these cells can lead to loss of kidney function. There are currently no human in vitro models that mimic a functional or diseased glomerulus. Development of a human glomerular filtration barrier biomimetic system will thus address gaps in in vitro models for simulating human kidney disease, toxicity and DMPK. We are looking for innovative approaches to developing a glomerular model that incorporates a self-contained microphysiological unit, ideally including podocytes, the endothelium, and   [更多]

藥物代謝酶的過(guò)程中，肝臟是主要負責將藥物基質(zhì)脂溶性化合物轉化為水溶性代謝物，可以很容易地通過(guò)腎臟排泄的。偶爾，這些代謝產(chǎn)物也會(huì )不恰當地和血蛋白結合，從而導致藥物的不良反應。阿斯利康希望尋找一種定量測定共價(jià)結合細胞蛋白質(zhì)的新方法。具體的鏈接請看下面： https://www.innocentive.com/ar/challenge/9933662 AWARD: $25,000 USD | DEADLINE: 3/16/15 | ACTIVE SOLVERS: 74 | POSTED: 1/16/15 Drug metabolism is the enzymatic process by which the body modifies pharmaceutical substrates. The liver is primarily responsible for reactions which convert lipid-soluble compounds into water-soluble metabolites that can easily be excreted by the kidney. Occasionally, these metabolites exhibit chemically reactivity towards host proteins, leading to inappropriate binding that may result in adverse drug reactions. AstraZeneca desires an innovative approach for the quantitative measurement of covalent binding to cellular proteins. This Challenge requires only a written proposal. Source: InnoCentive Challenge ID: 9933662 Challenge Overview When new medicines are introduced to the market, not only does the drug need to have a proven therapeutic benefit, but it also must possess an acceptable safety profile. To this end, drug development focuses on minimizing adverse drug reactions (ADRs) and idiosyncratic drug toxicities. ADRs are a major complication of drug therapy and come as a result of drug accumulation and/or the formation of chemically reactive metabolites (CRMs). Formation of CRMs within a cell poses an undesirable chemical liability and for this reason, AstraZeneca desires an innovative approach for the quantitative measurement of covalent binding of metabolites to cellular proteins. ABOUT THE SEEKER AstraZeneca is a global, research-based, biopharmaceutical company with a focus on five key therapeutic areas: 1) cardiovascular & metabolic diseases, 2) oncology, 3) respiratory, inflammation & autoimmunity, 4) neuroscience, and 5) infection. As an innovation-driven, research organization, AstraZeneca recognizes that great ideas come from many sources. Open innovation is an   [更多]

抑制細胞外神經(jīng)信號的作用可以通過(guò)抑制受體或去除配位體來(lái)產(chǎn)生。我們需要一個(gè)實(shí)例或證據來(lái)證明抑制受體和損耗配體是怎么阻斷信號的，比如可以變構小分子或大分子或競爭性抑制。具體看下面鏈接： https://www.innocentive.com/ar/challenge/9933720 AWARD: $20,000 USD | DEADLINE: 2/25/15 | ACTIVE SOLVERS: 19 | POSTED: 1/26/15 Inhibition of extracellular signaling can occur through an inhibition of a receptor or removal of a ligand. What evidence is there that one method of inhibition is more efficient or efficacious than the other at blocking signaling? The Seeker is specifically looking for well-supported examples of receptor/ligand inhibition where both methods of inhibition exist. This Challenge requires only a written proposal. Source: InnoCentive Challenge ID: 9933720 Challenge Overview Inhibition of extracellular neuronal signaling can occur through the inhibition of a receptor or removal of a ligand. What evidence is there (or lack of) that one method of inhibition (inhibition of the receptor versus depletion of the ligand) is more efficient or efficacious than the other at blocking signaling? Inhibition can be allosteric or competitive, small molecule or large molecule. The Seeker is specifically looking for well-supported examples of receptor/ligand inhibition where both methods of inhibition exist. Submissions to this Challenge must be received by 11:59 PM (US Eastern Time) on February 25, 2015. Late submissions will not be considered.   [更多]

單人中標 賞金分配： $ 50,000 截止日期：計2015年1月12日 已有提案：57 件 發(fā)布時(shí)間：2014年11月6日 已選0個(gè)，還需要1個(gè)。 具體要求： 與年齡相關(guān)的黃斑變性（AMD）是造成50歲以上人的視力喪失的主要原因。黃斑變性會(huì )造成視網(wǎng)膜的中央點(diǎn)損害，并模糊，最后會(huì )使一個(gè)或兩個(gè)眼睛發(fā)展到失明。雖然AMD已有少量模型存在，但并沒(méi)有充分闡明疾病的病理，而且也不適合于徹底深入地篩選和開(kāi)發(fā)藥物。年齡相關(guān)性黃斑變性（AMD）被認為是由遺傳和環(huán)境因素來(lái)觸發(fā)一種復雜而且異質(zhì)性疾病。正如它的名字所示的，隨著(zhù)年齡的增長(cháng)AMD發(fā)病率增加，據估計，在美國，大約有800萬(wàn)55周歲以上的人具有中期或后期的疾病。 AMD出現的第一癥狀為黃斑色素的改變和被稱(chēng)為玻璃疣的視網(wǎng)膜下沉積物。疾病進(jìn)一步發(fā)展可能導致視網(wǎng)膜色素上皮（RPE）細胞和光感受器細胞或新血管的血管滲透，出血和疤痕。光感受器細胞和視網(wǎng)膜色素上皮細胞之間的相互作用對于正常的視力功能是必不可少的。這一懸賞只需要一個(gè)書(shū)面建議。 以下幾條信息必須同時(shí)滿(mǎn)足: 1. 必須在2015年1月12日下午11時(shí)59分（美國東部時(shí)間）收到，逾期的投標概不受理。只需要提案人一個(gè)書(shū)面建議提交。解決方領(lǐng)取獎金的同時(shí)，必須將其獨有的知識產(chǎn)權（IP）的權利轉讓給舉辦方。 2.這個(gè)懸賞任務(wù)是必須尋找一種新的，臨床前模型，描述光感受器細胞和視網(wǎng)膜色素上皮細胞之間的相互作用，在長(cháng)期生理分化中對視力的影響，以方便對最近出現的新興療法進(jìn)行療效評價(jià)。 3、在這個(gè)網(wǎng)站投稿：Preclinical Models of Age-Related Macular Degeneration | InnoCentive Challenge https://www.innocentive.com/ar/challenge/9933641   [更多]