Anti-inflammatory cembranoids from the soft corals Sinularia querciformis and Sinularia granosa

Four new cembranoids, querciformolides A-D (1-4), along with two known cembranoids, 7 and 8, have been isolated from the soft coral Sinularia querciformis. Furthermore, chemical investigation of Sinularia granosa has afforded three new cembranoids, querciformolide B (2) and granosolides A (5) and B (6). The structures of the new metabolites were elucidated on the basis of extensive spectroscopic methods, and that of 2 was further confirmed by X-ray diffraction analysis. The absolute configurations of 1 and 2 were determined by a modified Mosher's method. Among these metabolites, 2-6 are rarely found cembranoids possessing a tetrahydrofuran moiety with a 4,7-ether linkage; in addition, 1 is the first epsilon-lactone cembrane found that possesses a tetrahydropyran moiety with a 4,8-ether linkage. None of these compounds were found to be cytotoxic toward a limited panel of cancer cell lines. However, compounds 3, 7, and 8 significantly inhibited the accumulation of the pro-inflammatory iNOS and COX-2 proteins in LPS-stimulated RAW264.7 macrophage cells.     

Maleimide and maleic anhydride derivatives from the mycelia of Antrodia cinnamomea and their nitric oxide inhibitory activities in macrophages

On cultivation of the fungus Antrodia cinnamomea (BCRC 36799) on a medium, the mycelium was extracted and evaluated for nitric oxide (NO) inhibitory activity. Bioactivity-directed fractionation led to the isolation of two new maleimide derivatives, antrocinnamomins A (1) and B (2), and two new maleic anhydride derivatives, antrocinnamomins C (3) and D (4), along with three known compounds, 3-isobutyl-4-[4-(3-methyl-2-butenyloxy)phenyl]furan-2,5-dione (5), 3-isobutyl-4-[4-(3-methyl-2-butenyloxy)phenyl]-1H-pyrrole-2,5-dione (6), and 3-isobutyl-4-[4-(3-methyl-2-butenyloxy)phenyl]-1H-pyrrol-1-ol-2,5-dione (7). Structural elucidation of compounds 1-4 was carried out by spectroscopic data. Compound 1 displayed significant inhibitory effect on nitric oxide (NO) production.     

Mining Health Social Media with Sentiment Analysis

With the rapid development of the Internet, more and more users utilize health communities (known as forums) to find health-related information, share their medical stories and experiences, or interact with other people in the communities. In this paper, we propose a framework to analyze the user-generated contents in a health community. The proposed framework contains three phases. First, we extract medical terms, including conditions, symptoms, treatments, effectiveness and side effects to form a virtual document for each question in the community. Next, we modify Latent Dirichlet Allocation (LDA) by adding a weighted scheme, called conLDA, to cluster virtual documents with similar medical term distributions into a conditional topic (C-topic). Finally, we analyze the clustered C-topics by sentiment polarities, and physiological and psychological sentiment. The experiment results show that conLDA outperforms the original LDA, and can cluster relevant medical terms and relevant questions together. The C-topics clustered by conLDA are more thematic than those clustered by the original LDA. The results of sentiment analysis may provide a quick reference and valuable insights for patients, caregivers and doctors.     

高糖对体外培养兔视网膜Müller细胞AQP4表达的影响

目的：观察体外培养兔视网膜Müller细胞在高糖条件下水通道蛋白-4（AQP4）表达的变化。方法：采用体外培养的兔视网膜Müller 细胞,分为正常对照组及高糖组（葡萄糖浓度：30、40和50 mmol•L^-1）,分别培养1、3和5 d;采用免疫细胞化学、流式细胞术及RT-PCR方法对Müller 细胞AQP4的表达情况进行检测。结果：高糖组Müller 细胞AQP4表达的绿色荧光明显弱于正常对照组（P<0.01）;流式细胞仪检测中波峰位置明显提前,AQP4表达强度较对照组明显减弱（P<0.01）,且随着葡萄糖浓度的增高和作用时间的延长,AQP4表达强度逐渐减弱;血糖浓度50 mmol•L^-1培养3 d时,RT-PCR半定量分析显示,AQP4 mRNA的表达比对照组明显降低（P<0.01）。结论：高糖能降低视网膜Müller细胞AQP4的表达,且随着葡萄糖浓度的增高和作用时间的延长,AQP4的表达强度也逐渐减弱;高糖时AQP4的表达下降可能是机体对糖尿病视网膜病变的一种保护性反应。     

Endovascular stenting for nutcracker syndrome

Nutcracker syndrome (NCS) is a rare pathology manifested by pain or hematuria in males and females alike. It can be easily overlooked, and should be considered in young men or women with symptoms of extended duration. We present a case of a 54-year-old female with chronic lower abdominal pain radiating to the left thigh of 4 years in duration. Computed tomography (CT) eventually revealed engorged left renal, gonadal, and uterine veins due to compression between the superior mesenteric artery (SMA) and the abdominal aorta, consistent with NCS. After a successful endovascular stenting and a 6-month period of antiplatelet and anticoagulant therapy, the patient returned to stable health. NCS, while rare, should be suspected in patients of both sexes with persistent pain or hematuria.     

Factors influencing the acceleration of human factor XIa inactivation by antithrombin III

Controversy exists in the literature concerning the potentiating effect of heparin on the inactivation rate of factor XIa by antithrombin III (AT III) in both purified systems and in plasma. We have analyzed the factors that could influence this reaction and found that ionic strength of the medium, as well as the type and concentration of the heparin preparations accounted for the major discrepancies in the literature. At I = 0.43 N, a preparation of bovine lung heparin at 1 U/mL did not augment the inactivation rate of factor XIa by inhibitors in plasma or by purified AT III. However, when ionic strength was decreased, a progressive increase in the potentiating effect was observed, reaching 6.5-fold at I = 0.15 N. At saturating concentrations of heparin, which results in the formation of 100% AT III-heparin complex, (greater than ten-fold molar excess over AT III) in purified systems, all heparin preparations (porcine, bovine, low molecular weight [LMW], and high affinity) yielded an approximately 30-fold augmentation of the factor XIa inactivation rate. However, when heparin was less than saturating, we observed that various heparin preparations affected the AT III-induced inactivation of factor XIa to different degrees even though they exhibited the same inhibitory activity (1 U/mL) against thrombin. This variation resulted from differences in the number of AT III binding sites in each heparin preparation, despite a similar Kd for each. Addition of high molecular weight kininogen (HK) to AT III-heparin complexes did not enhance their ability to inhibit factor XIa, and high concentrations of HK decreased the inactivation rate. A high therapeutic dose of heparin only permits the formation of 2.5% to 16.5% of the AT III-heparin complexes that can be achieved at saturation. We observed that 1 U/mL heparin (bovine lung heparin) (high therapeutic concentration) in virtually undiluted plasma only accelerated the inactivation rate of factor XIa (in the absence of other active enzymes) less than two-fold. These new observations further support our previous conclusion that therapeutic levels of heparin have little to no influence on the inactivation rate of factor XIa in plasma.