视网膜缺血对兔视神经纤维损害的定量研究

目的：定量研究视网膜缺血对视神经的损害。方法：通过计算机图像分析定量测算视神经纤维数量；通过前房灌注平衡液，造成超高眼压，形成兔视网膜完全缺血模型，观察视神经纤维数量的变化。结果：正常兔眼平均视神经轴突数为１０９６０８±１４５６１（ｎ＝２２）；视网膜缺血眼视神经纤维数量明显减少（Ｐ〈０．００１）。结论：急性高眼压造成的视网膜缺血可使视神经节细胞及轴突的数量明显减少，应用计算机图像分析可定量检测这种     

固体废物处理和处置设施的选址

新建废物处理和处置设施的选址是一项综合性很强的工作，涉及自然环境，社会政治和经济、安全和技术等诸多方面，选址的主要目标通过一系列的选址技术的步骤来具体体现。     

小鼠肝损伤模型的建立及HSS对肝的保护作用的初探

从三周龄幼鼠制备了肝细胞再生刺激物质（Ｈｅｐａｔｉｃｒｅｇｅｎｅｒａｔｉｏｎｓｔｉｍｕｌａｔｉｎｇｓｕｂｓｔａｃｅ，ＨＳＳ）研究结果提示：注射ＣＣｌ４导致小鼠血清ＡＬＴ显著升高，ＡＳＴ也明显增高，表明ＣＣｌ４致小鼠急性肝损伤，而ＨＳＳ对肝损伤具有显著保护作用，为深入研究ＨＳＳ对肝保护作用机理、ＨＳＳ用于临床的可行性提供了基础。     

Ⅱ孔型房间隔缺损直视修补术后心律失常的临床观察

210例Ⅱ孔型房间隔缺损术后发生心律失常90例,14种类型,共292例次,其中,室上性占96%。30例需药物治疗,93%的患者出院时恢复正常。本文着重分析心律失常的特点,讨论影响因素及预防措施。     

头孢托仑酯随机双盲对照治疗细菌性感染临床评价

为评价头孢托仑酯（ＭＥ１２０７）治疗细菌性感染的有效性和安全性，采用随机双盲对照试验和开放试验方法共治疗８０例患者，其中ＭＥ１２０７（Ａ药）与头孢克肟（Ｂ药）随机双盲各治疗２０例（呼吸系统和泌尿系统各１０对），ＭＥ１２０７开放试验治疗４０例（呼吸系统２０例、泌尿系统１０例、皮肤软组织感染１０例）。每日４００ｍｇ，疗程７～１４ｄ。ＭＥ１２０７痊愈率和有效率在对照试验中为８０％和９５％，在开放试验中为７５％和９２．５％，总痊愈率为７６．７％，总有效率为９３．３％，细菌培养阳性率为１００％，细菌清除率在对照试验和开放试验中分别为９５％和９２．５％。纸片法药敏试验中ＭＥ１２０７敏感株百分率为１００％，与头孢哌酮相同，而优于头孢克肟和头孢克洛，明显优于阿莫西林（４８．８％）。ＭＥ１２０７６０例中６例出现不良反应，表现为消化道反应３例，转氨酶升高２例，凝血酶原时间延长１例。与对照药头孢克肟相比在痊愈率、有效率、细菌清除率及不良反应发生方面均无显著性差异（Ｐ＞０．０５）。ＭＥ１２０７在每日４００ｍｇ剂量下治疗轻、中度细菌感染安全、有效。     

血管周围脂肪与心血管疾病的研究进展

在人体中,存在着一种围绕着除脑血管外的所有心血管的脂肪组织,称为血管周围脂肪（perivascular adipose tissue,PVAT）。近年来,由于其位置及功能的特殊性,PVAT被视为一种不同于传统内脏脂肪的新型脂肪组织,可通过旁分泌、内分泌具有促进血管舒缩功能的脂肪因子,介导免疫炎症反应及脂肪细胞表型转换等途径,对心血管系统产生双面性的影响,包括在生理状态下对心血管的保护作用及病理状态下促心血管疾病（cardiovascular disease,CVD）发生的不良作用。而通过对PVAT的实验室及影像学检查与干预,有助于提高对心血管疾病的诊断能力、增加具有可行性的治疗手段。本文将叙述PVAT与经典脂肪类型的区别,其生理、病理情况下对心血管系统的影响及在心血管疾病诊疗中的作用。     

Macrophage activation and Fcgamma receptor-mediated signaling do not require expression of the SLP-76 and SLP-65 adaptors

The Src-homology 2 domain-containing, leukocyte-specific phosphoprotein of 76 kDa (SLP-76) is a hematopoietic adaptor that plays a central role during immunoreceptor-mediated activation of T lymphocytes and mast cells and collagen receptor-induced activation of platelets. Despite similar levels of expression in macrophages, SLP-76 is not required for Fc receptor for immunoglobulin G (IgG; FcgammaR)-mediated activation. We hypothesized that the related adaptor SLP-65, which is also expressed in macrophages, may compensate for the loss of SLP-76 during FcgammaR-mediated signaling and functional events. To address this hypothesis, we examined bone marrow-derived macrophages (BMM) from wild-type (WT) mice or mice lacking both of these adaptors. Contrary to our expectations, SLP-76(-/-) SLP-65(-/-) BMM demonstrated normal FcgammaR-mediated activation, including internalization of Ig-coated sheep red blood cells and production of reactive oxygen intermediates. FcgammaR-induced biochemical events were normal in SLP-76(-/-) SLP-65(-/-) BMM, including phosphorylation of phospholipase C and the extracellular signaling-regulated kinases 1 and 2. To determine whether macrophages functioned normally in vivo, we infected WT and SLP-76(-/-) SLP-65(-/-) mice with sublethal doses of Listeria monocytogenes (LM), a bacterium against which the initial host defense is provided by activated macrophages. WT and SLP-76(-/-) SLP-65(-/-) mice survived acute, low-dose infection and showed no difference in the number of liver or spleen LM colony-forming units, a measure of the total body burden of this organism. Taken together, these data suggest that neither SLP-76 nor SLP-65 is required during FcgammaR-dependent signaling and functional events in macrophages.     

鼻咽癌旁上皮细胞核DNA含量分析

应用显微分光光度计测定15例鼻咽癌19处癌旁病变的上皮细胞核DNA含量并与浸润癌相比较。中、重度异型增生上皮细胞核DI及超过2.5c细胞的百分数处于单纯增生+轻度异型增生与浸润癌之间,3组DI及超过2.5c细胞的百分数差异显著。中、重度异型增生以非整倍体为主,其细胞核DNA含量组方图相似于浸润癌。从细胞核DNA含量角度来看,中、重度异型增生是重要的癌前病变。     

Congenital clubfoot in Europe: A population‐based study

We aimed to assess prevalence, birth outcome, associated anomalies and prenatal diagnosis of congenital clubfoot in Europe using data from the EUROCAT network, and to validate the recording of congenital clubfoot as a major congenital anomaly by EUROCAT registries. Cases of congenital clubfoot were included from 18 EUROCAT registries covering more than 4.8 million births in 1995–2011. Cases without chromosomal anomalies born during 2005–2009, were randomly selected for validation using a questionnaire on diagnostic details and treatment. There was 5,458 congenital clubfoot cases of which 5,056 (93%) were liveborn infants. Total prevalence of congenital clubfoot was 1.13 per 1,000 births (95% CI 1.10–1.16). Prevalence of congenital clubfoot without chromosomal anomaly was 1.08 per 1,000 births (95% CI 1.05–1.11) and prevalence of isolated congenital clubfoot was 0.92 per 1,000 births (95% CI 0.90–0.95), both with decreasing trends over time and large variations in prevalence by registry. The majority of cases were isolated congenital clubfoot (82%) and 11% had associated major congenital anomalies. Prenatal detection rate of isolated congenital clubfoot was 22% and increased over time. Among 301 validated congenital clubfoot cases, diagnosis was confirmed for 286 (95%). In conclusion, this large population‐based study found a decreasing trend of congenital clubfoot in Europe after 1999–2002, an increasing prenatal detection rate, and a high standard of coding of congenital clubfoot in EUROCAT.     

Site-specific mutagenicity of stereochemically defined 1,N2-deoxyguanosine adducts of trans-4-hydroxynonenal in mammalian cells

Trans-4-hydroxynonenal (HNE) is a toxic compound produced endogenously during lipid peroxidation. HNE is a potent electrophile that is reactive with both proteins and nucleic acids. HNE preferentially reacts with deoxyguanosine to form four stereoisomeric HNE-deoxyguanosine (HNE-dG) adducts: (6R, 8S, 11R), (6S, 8R, 11S), (6R, 8S, 11S), and (6S, 8R, 11R). These adducts were synthesized into 12-mer oligodeoxynucleotides, inserted into a DNA shuttle vector and evaluated for the ability of each stereoisomer to induce mutagenesis when replicated through mammalian cells. The resultant mutagenicity of these adducts was related to their stereochemistry, in that two of the HNE-dG adducts, (6R, 8S, 11R) and (6S, 8R, 11S), were significantly more mutagenic than the (6R, 8S, 11S) and (6S, 8R, 11R) HNE-dG adducts. These data conclusively demonstrate that HNE-derived DNA adducts can be mutagenic in mammalian cells and their ability to cause mutations is dictated by their stereochemistry.