GPR34-mediated sensing of lysophosphatidylserine released by apoptotic neutrophils activates type 3 innate lymphoid cells to mediate tissue repair

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皮质—网状—脊髓通路——HRP法结合溃变电镜法研究

用ＨＲＰ逆行标记法结合溃变电镜技术，观察了１２只大鼠的蓝斑，外侧网状核，中缝大核，巨细胞网状核在旁正中网状核中皮质纤维终末的超微结构及其与网状脊髓神经元的突触联系。损伤皮质感觉运动区的各例动物，均出现两种溃变型，电子致密型和微丝增生型。前者为皮质的主要溃变型，分布于各核；后者出现很少，只见于外侧网状核。电子致密型终扣有大小两种，大终扣少，有含圆形清亮型小泡，多形清亮型小泡，清亮型和颗粒型小泡并存的     

肾移植取肾方法的改进

报道了自1985年2月至今共摘取供肾132例,取得尸肾263只(1例独立肾),其中251只供肾用于临床。分侧切取肾38例,整块切肾41例,改进后整块切肾53例。文中着重介绍改进后的整块切取尸肾的手术方法,讨论了术式的优缺点。     

CYP1A1基因多态性与急性淋巴细胞白血病的关系

目的　探讨CYP1A1基因多态性与急性淋巴细胞白血病 (ALL)遗传易感性的关系。方法　应用PCR -RFLP、ASA技术 ,分析 78例ALL患者和 112例健康人CYP1A1基因多态性 ,比较ALL患者与对照组间频率差异。结果　ALL组CYP1A1MspI基因多态位点 ,各等位基因和基因型频率与对照组比较有显著性差异 (P <0 .0 5 ) ,其中等位基因m2使患ALL的危险度提高了 1.5 4倍 ,m1m2、m2m2基因型使患ALL的危险度分别提高了 2 .2 7倍和 2 .77倍 ;ALL组CYP1A1Ile-Val各等位基因和基因型频率与对照组比较无显著性差异 (P >0 .0 5 )。结论　CYP1A1MspI基因多态可能与ALL的发生有关。     

Effects of baclofen on transient neurons in the mudpuppy retina: electrogenic and network actions

1. Baclofen increases transient light responses of amacrine and ganglion cells despite acting as a classical inhibitory transmitter to both hyperpolarize and shunt these cells. 2. This effect seems to occur at the level of the inner retina and appears not to be due to an additional input from bipolar cells. 3. In some transient cells baclofen increases the total amplitude of the light response but does not change the peak potential of the light evoked EPSP. In these cells, the baclofen-induced enhancement can be accounted for by an increase in driving force of the excitatory postsynaptic potential (EPSP) resulting from the hyperpolarization. 4. However, in other cells the peak of the light response after baclofen application is greater, which cannot be accounted for by a change in driving force. This effect of baclofen can be mimicked by a blockers of gamma-aminobutyric acid (GABA) and glycine, suggesting that in these cells baclofen's enhancement is due in part to network effects resulting in a removal of sustained inhibition. 5. Therefore, the paradoxical effect of an inhibitory transmitter producing an enhancement of synaptic responses seems due to at least two mechanisms. 6. The results indicate that some transient cells receive significant tonic inhibition which limits their response amplitude in a push-pull type mechanism, but other cells are not under this inhibitory control process.     

数字化大鼠动脉血管系统三维模型的建立

采用含造影剂及显色剂的填充剂对成年SD大鼠动脉血管系统进行灌注,并借助数字X射线成像设备对灌注效果进行实时监测,通过断层解剖成像系统获取切削间距为100 μm的二维断面解剖数据集(图像分辨率为4917×3446×24 bit,共1 464张),最后利用Visual C 结合可视化工具包编程实现数据集的动脉分割及三维可视化,得到数字化SD大鼠动脉血管系统的三维模型.该模型能提供大鼠动脉血管系统的空间结构信息,为实验大鼠血管系统的研究提供了更为准确可靠的形态学参考.     

Phage-displayed mimotopes recognizing a biologically active anti-HIV-1 gp120 murine monoclonal antibody

Antibody-dependent cellular cytotoxicity (ADCC) is a host defense mechanism in which Fc receptor-bearing effector cells in combination with antigen-specific antibodies recognize and kill antigen-expressing target cells. The authors previously described a murine monoclonal antibody (MAb-ID6) that mediated ADCC activity against HIV-infected cells. It was demonstrated that the specificity of MAb-ID6 maps to the first 204 amino acids of gp120; however, the exact epitope was not identified. In the present work, by screening phage display libraries with MAb-ID6, the authors have mapped the corresponding epitope to amino acids 86-100 (HIV-1 gp120 sequence). This epitope lies within the C1 region of gp120 and is highly conserved among all subtypes and circulating recombinant forms of HIV-1. Thus, these phage mimotopes of C1 may serve as components of a vaccine for the induction of gp120-specific antibodies mimicking MAb-ID6.     

Bone-specific antibodies in sera from patients with celiac disease: characterization and implications in osteoporosis

Osteopenia and osteoporosis are well-known complications detected in celiac disease patients with still obscure pathogenesis. In the present study we investigated the presence of circulating anti-bone autoantibodies in patients with celiac disease and explored their role in the associated bone disease. We evaluated serum samples from 33 patients at the time of diagnosis and from 20 of them after treatment. Sera from patients with inflammatory bowel disease (n = 9), nonceliac osteoporotic (n = 18), and healthy individuals (n = 10) were used as controls. The presence of IgA specific anti-bone antibodies was first investigated using indirect immunofluorescence on cryosections of fetal rat tibia (20-day pregnancy). Furthermore, samples were homogenized and total tissue extracts were subjected to Western blot analysis to confirm immunoreactivity. At diagnosis, sera from 51.5% (17/33) of celiac patients had antibodies that recognized antigenic structures in chondrocytes and the extracellular matrix along mature cartilage, bone interface, and perichondrium of fetal rat bone. Among controls, only two osteoporotic patients showed very low titles of anti-bone autoantibodies. The immunostaining was localized in areas where an active mineralization process occurred and was similar to the distribution of the native bone tissue transglutaminase. The frequency of patients with positive baseline titers of anti-bone antibodies diminished significantly after treatment (P = 0.048). Western blot assays confirmed the presence of autoantibodies in sera from patients with a positive immunofluorescence staining. Autoantibodies recognized a major protein band on tissue extracts with a molecular weight of 77–80 kDa, which could be displaced when sera were preadsorbed with human recombinant tissue transglutaminase. We provide original evidence that patients with celiac disease have IgA-type circulating autoantibodies against intra- and extracellular structures of fetal rat tibia. Our findings suggest that these antibodies recognize bone tissue transglutaminase as the autoantigen, and based on the localization of the immunoreactivity we speculate that they might have an active role in the pathophysiology of celiac disease-associated bone complications.     

Genetic Conservation of Hemagglutinin Gene of H9 Influenza Virus in Chicken Population in Mainland China

The hemagglutinin (HA) genes of 12 H9N2 influenza virus strains isolated from chickens in Mainland China during the period 1995–2002 were genetically analyzed. All the isolates possessed the same amino acid motif -R-S-S-R/G-L- at the cleavage site of HA. Except for the conserved amino acids, as is the case in the other avian influenza viruses, located in the receptor binding site, all of the 12 isolates possessed N at amino acid position 183; A, T, or V at position 190; K at position 137, whereas the representative strains of the other lineage (except Dk/HK/Y280/97-like lineage) virus of H9N2 viruses had H, E, and R at these positions respectively. These could be considered as the partial molecular markers of the H9 viruses isolated from chickens in Mainland China. Phylogenetic analyses showed HA genes of these isolates belonged to that of A/duck/Hong Kong/Y280/97-like virus lineage. No A/quail/Hong Kong/Gl/97-like virus was found in chicken, population since the outbreak of H9N2 influenza in Mainland China in 1992. The available evidence indicates that HA genes of H9 influenza virus circulating in Mainland China during the past years were well conserved.