严重感染患者发生感染性休克的危险因素分析

目的研究严重感染患者发生感染性休克的危险因素。方法选取北京协和医院加强医疗病房中5个月内连续收治的49例严重感染患者，记录其人口统计学资料、临床信息、血单核细胞人白细胞抗原DR（HLA-DR）、血二胺氧化酶（DAO）等指标，主要研究终点为住院病死率，对上述资料先进行单因素分析，在此基础上选择有统计学差异的变量进行多因素非条件Logistic回归分析。结果共有23例（46．9％）严重感染患者发生感染性休克。统计结果显示血培养阳性、HLA—DR降低、血小板计数下降和血DAO升高与感染性休克的发生有关；其中血培养阳性（OR=6．524，95％CI：1．364—31．206，P：0．019）、HLA—DR降低（OR=0．956，95％CI：0．920—0．993，P=0．020）和血DAO活性升高（OR=2．312，95％CI：1．162～4．600，P=0．017）是发生感染性休克的独立危险因素。结论伴有血培养阳性、HLA—DR降低和外周血DAO活性升高的严重感染患者发生感染性休克的风险较高。     

PACS的科学评估

通过介绍美国ECRI与KLAS的两次PACS评比,提出科学评估PACS优劣成败的原则,即在制定PACS的战略计划时,除了考虑体系结构、经费预算及实施方案外,还要包括投入产出分析,资本应急计划,资源利用战略以及质量控制与管理方案.PACS是医学影像诊断信息化的一项基础建设.其目的就是构建一个以比特流为载体(而不是以胶片为载体)的数字化医学影像诊断的网络平台或网络环境.它不是单一产品.多数情况下它也不仅仅是一个系统.实际上,PACS是一项信息化工程.因此,如何科学评估PACS建设的优劣成败至关重要.我国迄今尚无一个权威机构(包括政府机构、学术组织、行业协会……)对PACS进行过科学评估,甚至对评估标准也未有正式的文字共识,这不能不说是一大缺憾.而且,长此下去,对我国PACS的建设乃至医院信息化的建设都是不利的.     

Arsenic trioxide (As(2)O(3)) induces apoptosis through activation of Bax in hematopoietic cells

This study explores the roles of Bax and other Bcl-2 family members play in arsenic trioxide (As(2)O(3))-induced apoptosis. We showed that As(2)O(3) treatment triggered Bax conformational change and subsequent translocation from cytosol to mitochondria to form various multimeric homo-oligomers in IM-9 cells. On the other hand, human leukemic Jurkat cells deficient in Bax showed dramatically reduced apoptosis in response to As(2)O(3). Stable overexpression of Bcl-2 in IM-9 cells (IM-9/Bcl-2) inhibited As(2)O(3)-mediated Bax activation and apoptosis, and this inhibition could be partially averted by cell-permeable Bid-Bcl-2 homology (BH)3 peptide. Meanwhile, Bax conformational change and oligomerization induced by As(2)O(3) were not inhibited by the pancaspase inhibitor z-VAD-fmk, although Bid cleavage could be completely abolished. Bax activation by As(2)O(3) seemed to require stress-induced intracellular reactive oxygen species (ROS), since the ROS scavengers (N-acetyl-L-cysteine and lipoic acid) could completely block the conformational change and translocation of Bax from cytosol to mitochondria. These data suggest that As(2)O(3) might exert the cell killing in part by inducing Bax activation through a Bcl-2-suppressible pathway in hematopoietic cells that is caspase independent and intracellular ROS regulated.     

幽门螺杆菌粪便抗原诊断方法的系统评价

目的评价幽门螺杆菌(Hp)粪便抗原诊断Hp感染的价值。方法电子检索以中国生物医学文献数据库、中国生物医学期刊文献数据库、中国学术期刊全文数据库与中文科技期刊全文数据库为主进行文献检索,再根据已发表文献中的参考文献追溯进行手工检索。发表时间截止至2004年3月1日。按确定的纳入标准筛选文献,对纳入的文献进行质量评价,运用Coehrane协作网诊断与筛查小组推荐的SROC曲线法,以敏感性、特异性、准确性、阳性预测值、阴性预测值及似然比等指标行Meta分析。结果19篇文献、3123例符合纳入标准。Hp粪便抗原诊断Hp感染的敏感度及特异度为94％和93％。结论Hp粪便抗原诊断Hp感染简便、无创、准确度高。     

Control of spermatogenesis in primate and prospect of male contraception

The present review is a summary of mechanisms of spermatogenesis in primates with emphasis on anti-spermatogenesis of testosterone (T), gossypol, and "testicular heat stress" for development of male contraception, Both FSH and testosterone stimulate all phases of spermatogenesis. FSH is capable of amplifying the population of the differential spermatogonia (B1, B2, B3 and B4) and controls the spermatogonia production rate, and, in synergy with testosterone, regulating spermatogenesis in adult monkeys. Pituitary FSH beta gene expression is governed by a feedback of Beta inhibin, which is a major component of the testicular negative feedback signals. Beta inhibin secreted by Sertoli cells is in turn inhibited by testosterone from Leydig cells under the control of LH. Disturbance of the normal interaction of pituitary FSH with Sertoli cell Beta inhibin is responsible for azoospermia or oligozoospermia induced by exogenous T. Three possible regimens of T, gossypol and "heat stress" have been suggested for male contraception. They act on different sites and stages of spermatogenesis in testis or sperm activity in epididymis. Apoptosis induced by testosterone occurs mainly at staged VII-VIII of spermatogenesis while that by testicular "heat stress" mostly occurs at stages I-IV and X-XII. Low dose of gossypol mainly influences the sperm activity in the epididymis although it also acts on testicular spermatids.     

Regulation of matrix metalloproteinases (MMPS) and their inhibitors (TIMPS) during mouse peri-implantation: role of nitric oxide

Nitric oxide (NO) is believed to play pivotal roles in embryo implantation. The purpose of this study was to investigate the effect of NO on matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs), as well as the mechanism of NO during mouse implantation. Nitric oxide synthase (NOS) inhibitor, L-NAME was administered with or without sodium nitroprusside (SNP), NO donor, into one uterine horn on day 3 of pregnancy, and the contralateral uterine horn served as the control. We collected the uteri on days 5, 6, and 7 of pregnancy and examined the mRNA expression of MMP-2, -9, and TIMP-1, -2, -3, as well as the activities of MMP-2 and -9 by using in situ hybridization and gelatin zymography, respectively. The results showed that, compared with the control, the expression of MMP-2 and -9 mRNAs was decreased in L-NAME-treated uteri during peri-implantation. Treatment of mice with L-NAME had slight effect on the expression of TIMP-1 mRNA on day 5 of pregnancy, and no effect on TIMP-2 mRNA expression during peri-implantation. However, the expression of TIMP-3 mRNA was increased. The gelatin zymography results indicated that the activity of MMP-9 was decreased during peri-implantation, but the activity of MMP-2 did not change significantly in these time points examined. The L-NAME-mediated effect on MMPs and TIMPs were significantly reversed when SNP was co-administered with L-NAME. These data suggest that inhibition of NO production regulates the gene expression of MMP-2, -9, and TIMP-3, together with the activity of MMP-9 during peri-implantation, which may have serious consequence on embryo implantation.     

VEGF, bFGF and their receptors at the fetal-maternal interface of the rhesus monkey

Placental development involves trophoblast outgrowth and a coordinated angiogenesis in the implantation site. In this study, expression of angiogenic factors, vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), VEGF receptors, kinase insert domain-containing region (KDR), and bFGF receptor Flg was characterized at the maternal-embryonic boundary of the rhesus monkey on Day 17, 19, 28 and 34 of pregnancy. Immunohistochemistry and in situ hybridization showed that VEGF mRNA and protein were both strongly expressed in the cytotrophoblast, the blood vessels and certain immunocytes. These sites were also immunopositive for KDR. In addition to the vascular endothelial cells and the vascular smooth muscle cells, the protein and mRNA for bFGF were also detected in cyto/syncytiotrophoblast bilayer, whereas the staining for Flg protein was mainly localized in the cytotrophoblast cells. The staining degree of VEGF and bFGF in the villi gradually decreased with the development of placenta. Strong expression of bFGF, Flg and KDR was also detected in the decidual cells. These data suggest that VEGF and bFGF may be involved in angiogenesis, cytotrophoblast proliferation and migration during early stage of placentation in the rhesus monkey.     

The effect of Nestorone on gonadotropic cells in pituitary of rats

The implant containing Nestorone is a promising long-acting contraceptive especially suitable for lactating women. In this study, two experiments were designed to observe the effect of Nestorone on the gonadotropic cells in pituitary of rats for analyzing its antiovulation mechanism. In the first experiment, the ED₅₀ of Nestorone on inhibiting ovulation was found to be 1.32 mg/kg. The serum luteinizing hormone (LH) levels were significantly lower 60 h after being treated with Nestorone at 8:30–9:00 a.m. on Day 2 (D2) of estrus. Image analysis showed that the average size of the LH cells in groups treated with Nestorone at 2 or 4 mg/kg was larger than that of the control. In the group treated with 4 mg/kg, most of gonadotropic cells were regular round in shape. And, abundant granules in cytoplasm were found in those cells, which indicated that the LH stored in cells was not released. In the second experiment, the rats were treated with Nestorone at 5 mg/kg at 11:30–12:00 a.m. on D2 of estrus. The normal or higher expression of LHβ mRNA in pituitary suggested that the synthesis of LH was not inhibited by the treatment with Nestorone. The expression of PR mRNA in pituitary was significantly lower than that of the control at 33 h after treatment. This might be a direct effect of Nestorone, since there were no differences in the serum E₂ and P₄ levels between the treated and the control group. It is concluded that Nestorone prevents ovulation through inhibition of LH secretion and it has no effect on synthesis of LH. Progesterone receptors in pituitary might be involved in this process, but further study is needed to gain more evidence.     

Essential role of the voltage-dependent anion channel (VDAC) in mitochondrial permeability transition pore opening and cytochrome c release induced by arsenic trioxide

The precise molecular mechanism underlying arsenic trioxide (As(2)O(3))-induced apoptosis is a subject of extensive study. Here, we show that clinically relevant doses of As(2)O(3) can induce typical apoptosis in IM-9, a multiple myeloma cell line, in a Bcl-2 inhibitable manner. We confirmed that As(2)O(3) directly induced cytochrome c (cyto c) release from isolated mouse liver mitochondria via the mitochondrial permeability transition pore, and we further identified the voltage-dependent anion channel (VDAC) as a biological target of As(2)O(3) responsible for eliciting cyto c release in apoptosis. First, pretreatment of the isolated mitochondria with an anti-VDAC antibody specifically prevented As(2)O(3)-induced cyto c release. Second, in proteoliposome experiments, VDAC by itself was sufficient to mediate As(2)O(3)-induced cyto c release, which could be specifically inhibited by Bcl-X(L). Third, As(2)O(3) induced mitochondria membrane potential (DeltaPsim) reduction and cyto c release only in the VDAC-expressing, but not in the VDAC-deficient yeast strain. Finally, we found that As(2)O(3) induced the increased expression and homodimerization of VDAC in IM-9 cells, but not in Bcl-2 overexpressing cells, suggesting that VDAC homodimerization could potentially determine its gating capacity to cyto c, and Bcl-2 blockage of VDAC homodimerization represents a novel mechanism for its inhibition of apoptosis.     

Cell adhesion on gaseous plasma modified poly-(L-lactide) surface under shear stress field

A series of gases were used for plasma treatment of poly-(L-lactide) (PLLA) under various conditions such as atmosphere, electric power, pressure and time. The NH(3) was preferably selected for modifying the surface of PLLA because it can obtain appropriate hydrophilicity and surface energy with high polar component compared to other gases. Subsequently, cells were seeded onto NH(3) modified surface and exposed to 29.5N/m(2) of shear stress field by means of a parallel plate flow chamber in order to get good insight into the influence of N-containing incorporation on cell retention, cell morphology, and cell shape factor. The results showed that cell retention on the modified PLLA was much higher than that on the unmodified one. The NH(3) plasma modified PLLA with high cell affinity and resistance to shear stress was gained. Surface hydrophilicity, surface energy with high polar component and N-containing groups may play an important role in enhancing cell resistance to shear stress. It revealed that the parallel plate flow chamber is an effective device for evaluating the effects of surface modification on the cell affinity of a material.