农村妇女避孕方法使用及其影响因素分析

本文使用的数据来源于1986年在江苏省进行的“农村已婚育龄妇女使用避孕方法的变异”的调查。本次调查的目的是对已婚育龄妇女避孕方法使用的类型及动力学进行综合研究。调查的数据表明,江苏农村已婚育龄妇女的避孕率为85%,其中,宫内节育器和女性绝育术为最普遍使用的方法。在使用避孕方法的妇女中,宫内节育器和女性绝育术的使用比例分别为46.6%和36.4%。妇女对正在使用的避孕方法的评价和希望使用新方法的意愿都存在着差别。从这些差别的分析中不难看出,面对广大育龄妇女的避孕要求,我们应提供较为先进的避孕方法的信息及咨询服务,从而扩大避孕方法的可选择范围,避免一些方法的错误使用,提高使用者的满意程度。     

Autogenous tissue reconstruction in the management of aortoiliofemoral graft infection

Management of infected prosthetic arterial grafts remains a challenging clinical problem. Revascularization following removal of the infected arterial prosthesis is frequently necessary and usually achieved using remote extraanatomic bypasses. We present three cases where complete removal of the infected prosthesis was followed by autogenous reconstruction using reversed saphenous vein, endarterectomized segments of superficial femoral artery, or endarterectomy of the native occluded vessels. Eradication of the infection was seen in all three patients. The reconstructions have remained patent in the three patients with follow-up from four months to three years. Percutaneous balloon dilation was successful in the management of a distal limb stenosis in one patients. Autogenous vascular reconstruction following removal of infected prosthetic vascular grafts remains a viable alternative in the treatment of difficult, selected cases of infected arterial prosthesis. It is probably an underutilized alternative, when one considers that the surgical techniques employed are familiar to vascular surgeons. Cure of the infection and prepreservation of critical vascular beds can both be achieved with autogenous tissue, either in situ or from remote areas. Available percutaneous techniques may play an important role in maintaining durability of these reconstructions.Presented at the Annual Meeting of the Peripheral Vascular Surgery Society, New York, New York, June 17, 1989.     

头孢拉定及其胶囊剂中有关物质检查方法的探讨

目的:对头孢拉定原料及制剂的有关物质检查方法进行探讨.方法:对现行版药典中的头孢拉定及其制剂的有关物质检查方法进行比较和实验观察.结论:可用<中国药典>中检查拉定原料有关物质的方法对胶囊剂进行检查,并认为有必要增加此项目.同时建议对原料有关物质检查项中杂质对照的点样方法进行修改.     

Role of DNA Methylation on the Expression of the Anthracycline Metabolizing Enzyme AKR7A2 in Human Heart

The intracardiac synthesis of anthracycline alcohol metabolites by aldo–keto reductases (AKRs) contributes to the pathogenesis of anthracycline-related cardiotoxicity. AKR7A2 is the most abundant anthracycline reductase in hearts from donors with and without Down syndrome (DS), and its expression varies between individuals (≈tenfold). We investigated whether DNA methylation impacts AKR7A2 expression in hearts from donors with (n = 11) and without DS (n = 30). Linear models were used to test for associations between methylation status and cardiac AKR7A2 expression. In hearts from donors without DS, DNA methylation status at CpG site ?865 correlated with AKR7A2 mRNA (Pearson’s regression coefficient, r = ?0.4051, P = 0.0264) and AKR7A2 protein expression (r = ?0.5818, P = 0.0071). In heart tissue from donors with DS, DNA methylation status at CpG site ?232 correlated with AKR7A2 protein expression (r = 0.8659, P = 0.0025). Multiple linear regression modeling revealed that methylation at several CpG sites is associated with the synthesis of cardiotoxic daunorubicinol. AKR7A2 methylation status in lymphoblastoid cell lines from donors with and without DS was examined to explore potential parallelisms between cardiac tissue and lymphoid cells. These results suggest that DNA methylation impacts AKR7A2 expression and the synthesis of cardiotoxic daunorubicinol.     

Molecular basis of Tank-binding kinase 1 activation by transautophosphorylation

Tank-binding kinase (TBK)1 plays a central role in innate immunity: it serves as an integrator of multiple signals induced by receptor-mediated pathogen detection and as a modulator of IFN levels. Efforts to better understand the biology of this key immunological factor have intensified recently as growing evidence implicates aberrant TBK1 activity in a variety of autoimmune diseases and cancers. Nevertheless, key molecular details of TBK1 regulation and substrate selection remain unanswered. Here, structures of phosphorylated and unphosphorylated human TBK1 kinase and ubiquitin-like domains, combined with biochemical studies, indicate a molecular mechanism of activation via transautophosphorylation. These TBK1 structures are consistent with the tripartite architecture observed recently for the related kinase IKKβ, but domain contributions toward target recognition appear to differ for the two enzymes. In particular, both TBK1 autoactivation and substrate specificity are likely driven by signal-dependent colocalization events.     

Small molecule antagonist reveals seizure-induced mediation of neuronal injury by prostaglandin E2 receptor subtype EP2

With interest waning in the use of cyclooxygenase-2 (COX-2) inhibitors for inflammatory disease, prostaglandin receptors provide alternative targets for the treatment of COX-2-mediated pathological conditions in both the periphery and the central nervous system. Activation of prostaglandin E2 receptor (PGE(2)) subtype EP2 promotes inflammation and is just beginning to be explored as a therapeutic target. To better understand physiological and pathological functions of the prostaglandin EP2 receptor, we developed a suite of small molecules with a 3-aryl-acrylamide scaffold as selective EP2 antagonists. The 12 most potent compounds displayed competitive antagonism of the human EP2 receptor with K(B) 2-20 nM in Schild regression analysis and 268- to 4,730-fold selectivity over the prostaglandin EP4 receptor. A brain-permeant compound completely suppressed the up-regulation of COX-2 mRNA in rat cultured microglia by EP2 activation and significantly reduced neuronal injury in hippocampus when administered in mice beginning 1 h after termination of pilocarpine-induced status epilepticus. The salutary actions of this novel group of antagonists raise the possibility that selective block of EP2 signaling via small molecules can be an innovative therapeutic strategy for inflammation-related brain injury.