报告从政策环境、市场行情、厂商动态、科技研发、国际资讯、行业数据、分析评论等几个方面对医药行业进行了分析评论。

报告从医药行业事件分析、竞争环境、竞争对手、行业数据等几个方面进行了分析评论。

《每日经济新闻》9月17日报道，为进一步推动我国医药产业结构调整和转型升级，以及推动药品注册审批制度改革进入深水区，近日国家食药监总局发布第一批过度重复药品品种目录。 食药监总局通过全面筛查国内已上市药品和正在申报注册药品，遴选出相同活性成分、相同给药途径药品批准文号数量在500个以上的34个品种和相同活性成分、相同给药途径药品注册申请数量在50个以上的16个品种。这批过度重复药品已经有大量企业生产或正在申报投产，市场需求已经饱和或者接近饱和。同时，食药监总局提醒社会投资方和相关企业，注意评估研发风险，慎重进行投资经营决策，更好地引导药品合理申报，避免市场药品同水平重复，防止研发投入风险。

医疗器械是指单独或者组合使用于人体的食品设备、器具、材料或者其他物品，包括所需要的软件，其作用于人体体表及体内不是用药理学，免疫学或者代谢的手段获得。医疗器械行业是知识密集、资金密集、多学科交叉的高科技产业，是国家制造业和高科技尖端水平的标志之一。

双氯芬酸(Diclofenac)又称双氯灭痛，为一新型强效灭酸型非甾体类抗炎解热镇痛药，其解热、镇痛、消炎作用显著，不良反应较少，主要用于治疗风湿和类风湿性关节炎、神经炎、红斑狼疮、癌症和手术及创伤后疼痛以及各种原因引起的发热。目前，双氯芬酸已成为全球最畅销的解热镇痛消炎药物之一，除被收入到中国药典外，还被收入到美国、英国、日本等多个国家药典以及欧洲药典中。 近年来，双氯芬酸国内外市场销售不断上升，预计后市仍有较大发展潜力。

报告从医药行业事件分析、竞争环境、竞争对手、行业数据等几个方面进行了分析评论。

Biometrics is a technology that helps identify individuals on the basis of their physical or behavioral patterns. It involves the verification and identification of physiological traits such as fingerprints, face recognition, DNA, palm print, hand geometry, and iris recognition; and behavioral traits such as keystroke patterns and speech pattern/voice recognition.

Almost 50of all ER+ breast tumors will not respond to endocrine therapy. Resistance to endocrine therapy remains a significant clinical problem and advanced ER+ breast cancer is largely an incurable disease. Endocrine manipulation in sensitive cells can result in the induction of cell death through autophagy and/or apoptosis. We have recently obtained data implicating the unfolded protein response (UPR) as induced by the splicing of X-box binding protein-1 (XBP1) in the regulation of endocrine responsiveness in breast cancer cells. UPR is a key component of the endoplasmic reticulum stress response and has not previously been implicated in endocrine responsiveness. We hypothesize that XBP1(S) is a key regulator of breast cancer cell fate, acting through its regulation of UPR, BCL2, and BCL2:BECN1 heterodimers, and their subsequent effects on autophagy and apoptosis. We will determine how XBP1(S) affects cell fate, evaluating the role of an induction of UPR that activates a prosurvival autophagy. In endocrine sensitive cells, autophagy should persist and become a cell death mechanism that can also initiate apoptosis. In resistant cells, basal autophagy should represent a survival mechanism to deal with the loss of autocrine and other growth factor signaling that accompanies endocrine therapy. We will explore the mechanistic role of XBP1(S) and its integrated signaling through UPR and BCL2 to regulate cell fate in both endocrine sensitive and resistant cells.

The goal of this work is to increase the availability of critical mouse models of human muscular dystrophy (MD) for both hypothesis testing and preclinical therapy development. Our multi-disciplinary team from The Jackson Laboratory (JAX) and the Children s National Medical Center (CNMC) has expertise in MD, repository management, mouse models, and preclinical testing. At JAX, Drs. Lutz and Cox have established the MD Repository (Aim1) to leverage JAX s considerable expertise and infrastructure to maintain and distribute MD mouse and information resources to the scientific community. In Aim 2 we are developing novel DMD transgenic mice, which model patients receiving successful exon-skipping therapies. We propose to address the fundamental, but often overlooked question related to the functionality of resulting Dystrophin molecules containing in-frame deletions that are expected to arise by successful treatment of patient mutations. Our transgenic experiments will model the best-case-scenario outcome for AO-mediated therapy in which one assumes that a particular compound is capable of 100effective exon-skipping to restore the reading frame. In Aim 3, we are generating congenic mdx mice to better model the symptoms of the human disease and to identify genetic modifiers that can alter disease onset and severity. In Aim 4, Dr. Nagaraju at CNMC is carrying out preclinical studies with three promising therapeutic compounds (GW501516, AICAR and Dantrolene) using key models developed at JAX. Overall, this program will greatly expand the accessibility and availability of mouse model resources for MD translational research and therapeutic development.