Chronic morphine treatment inhibits oxytocin release from the supraoptic nucleus slices of rats

Effect of chronic morphine treatment on oxytocin (OT) release from the long term-cultured organotypic slice of the supraoptic nucleus (SON) was investigated using radioimmunoassay. The co-localization of oxytocin and mu-opioid receptor in neurons within the SON was observed with the double-labeled methods of in situ hybridization combined with immunohistochemistry. After exposure to morphine for 6days, the OT levels in culture media were significantly decreased. Naloxone caused much greater release of OT in chronic morphine treatment group than in controls. Naloxone has no effect after acute morphine treatment. 90% of OT-ir (immunoreactive) neurons expressed mu-opioid receptor mRNA in the SON and 45% of the neurons that expressed mu-opioid receptor mRNAs were OT-ir neurons. These results indicated that the neurons within SON could develop dependence on morphine in vitro, and these effects might be exerted via mu-opioid receptor in oxytocin neurons of the SON.     

Vascular endothelial growth factor receptor signaling is required for cardiac valve formation in zebrafish.

Vascular endothelial growth factor-receptors (VEGF-Rs) are pivotal regulators of vascular development, but a specific role for these receptors in the formation of heart valves has not been identified. We took advantage of small molecule inhibitors of VEGF-R signaling and showed that blocking VEGF-R signaling with receptor selective tyrosine kinase inhibitors, PTK 787 and AAC 787, from 17-21 hr post-fertilization (hpf) in zebrafish embryos resulted in a functional and structural defect in cardiac valve development. Regurgitation of blood between the two chambers of the heart, as well as a loss of cell-restricted expression of the valve differentiation markers notch 1b and bone morphogenetic protein-4 (bmp-4), was readily apparent in treated embryos. In addition, microangiography revealed a loss of a definitive atrioventricular constriction in treated embryos. Taken together, these data demonstrate a novel function for VEGF-Rs in the endocardial endothelium of the developing cardiac valve.     

Arthrobacter scleromae sp. nov. isolated from human clinical specimens

A gram-positive, coryneform bacterium was isolated from swollen scleromata of a dermatosis patient. An analysis of its phenotypic, chemotaxonomic, and genotypic characteristics showed that this bacterium is closely associated with Arthrobacter oxydans and Arthrobacter polychromogenes but that it belongs to a distinct species, for which the name Arthrobacter scleromae sp. nov. is proposed.     

髋臼CT图像轮廓跟踪方法

目的为重建和测量髋臼的解剖结构,需要大量地读取CT图像的信息,以获得髋臼轮廓的坐标值。方法本研究采用直方图阈值图像分割、kirsh边缘提取法获得髋臼的二值化轮廓图像。轮廓坐标的提取应用了“迷宫”边缘跟踪算法。结果本方法可大量、快捷、正确的提取图像轮廓信息。     

Cell cycle dependent intracellular distribution of two spliced isoforms of TCP/ILF3 proteins

TCP80 is an approximately 80kDa mammalian cytoplasmic protein that binds to a set of mRNAs and inhibits their translation in vitro and ex vivo. This protein has high sequence similarity to interleukin-2 enhancer-binding factors (NF90/ILF3) and the M-phase phosphoprotein (MPP4)/DRBP76. A 110kDa immunologic isoform of TCP80/NF90/MPP4/DRBP76, termed TCP110, also is present in cytoplasm and nuclei of many types of cells. A cDNA sequence coding for TCP110 was derived by 5(')RACE. The TCP110 sequence is identical to ILF3. The gene coding for TCP110/ILF3 mapped to human chromosome 19 and the gene organization was analyzed using TCP80 and TCP110/ILF3 cDNA sequences. The TCP/ILF3 gene spans >34.8kb and contains 21 exons. At least one alternatively spliced product involving exons 19-21 exists and predicts the formation of either TCP80 or TCP110/ILF3. However, the functional relationships of TCP80 and TCP110/ILF3 required elucidation. The metabolic turnover rates and subcellular distribution of TCP80 and TCP110/ILF3 during the cell cycle showed TCP80 to be relatively stable (t(1/2)=5 days) in the cytoplasmic compartment. In comparison, TCP110/ILF3 migrated between the cytoplasmic and nuclear compartments during the cell cycle. The TCP110 C-terminal segment contains an additional nuclear localizing signal that plays a role in its nuclear translocation. This study indicates that the multiple cellular functions, i.e., translation control, interleukin-2 enhancer binding, or cell division, of TCP/ILF3 are fulfilled by alternatively spliced isoforms.     

基质金属蛋白酶1与冠状动脉粥样硬化斑块破裂的关系

目的 探讨冠状动脉粥样硬化斑块破裂与基质金属蛋白酶１（ＭＭＰ－１）的关系,以及不稳定斑块中ＭＭＰ－１的来源。方法 收集２０例死于急性心肌梗死、１０例有不稳定心绞痛史,以及１２例有稳定心绞痛史的尸体解剖病例共４２例,从冠状动脉各分支取材,常规病理检查、部分节段行ＭＭＰ－１、平滑肌肌动蛋白、ＣＤ６８、ＣＤ４５ＲＯ和ＣＤ２０洒色。结果 在急性心肌梗死及不稳定心绞痛病例中,均见有斑块破裂伴血栓形成,而在稳     

基于敏感性定理的EIT重构算法仿真研究

为了研究性能更好的EIT图像重构算法，我们对基于敏感性定理的EIT图像重构算法进行了计算机仿真研究，并与几种常用图像重构算法进行比较，提出对基于敏感性定理的EIT图像重构算法的改进措施。     

饮酒对小鼠睾丸生精小管一氧化氮合酶、增殖细胞核抗原表达及细胞凋亡影响的研究

目的　探讨酒精对小鼠睾丸的组织结构、内皮型一氧化氮合酶 (eNOS)、增殖细胞核抗原 (PCNA)及细胞凋亡的影响。　方法　用 5 %、10 %及 15 % 3种不同浓度的酒精作用于 2 2d龄小鼠 ,取睾丸做石蜡切片、HE染色 ;用免疫组织化学方法检测睾丸eNOS、细胞增殖的变化 ;TUNEL法检测细胞凋亡的变化 ,并进行统计学分析。　结果　随着酒精浓度的增大 ,睾丸组织结构发生明显改变 ,生精小管的直径逐渐减小 ,eNOS阳性细胞面积密度逐渐增大 ,单位面积内PCNA阳性细胞和凋亡细胞数目增加 ,高浓度酒精组与其他组差异极显著 (P <0 0 1)。　结论　酒精可使生精小管的直径变小 ,eNOS及PCNA表达增强 ,凋亡细胞增加并随酒精浓度的增大而变化加重。这可能是过量饮酒导致生精细胞减少 ,生殖能力降低的重要因素。     

Functional morphology and physiological properties of bronchopulmonary C-fiber afferents

Nonmyelinated (C-) fibers represent the majority of vagal afferents innervating the airways and lung, and play an important role in regulating the respiratory and cardiovascular functions under both normal and abnormal physiologic conditions. Studies of the relationship between the conduction velocities of the vagal afferents and their sensitivities to capsaicin and other chemical irritants reveal that C-fibers are the primary type of chemosensitive afferents in the rat lung. Furthermore, a distinct sensitivity to capsaicin and a weak response to lung inflation are the defining characteristics of these afferents. In cultured rat nodose and jugular ganglion neurons, capsaicin-sensitive cells were identified by measurement of the capsaicin-evoked calcium transients using the Fura-2-based ratiometric imaging technique. The percentage of capsaicin-sensitive neurons gradually decreases as the cell diameter increases. However, the capsaicin-sensitive neurons cannot be precisely identified solely on the basis of the cell size. Anandamide, an endogenous cannabinoid released from leukocytes and epithelial cells, consistently evokes a stimulatory effect on pulmonary C-fiber endings by activating vanilloid receptor type 1 (VR1). The discharge pattern of pulmonary C-fibers evoked by anandamide closely resembles that produced by a much lower ( approximately 1/600) dose of capsaicin in the same fibers. Whether anandamide acts as a potential endogenous ligand to VR1 at the C-fiber terminals is unclear, and the physiological role of VR1 in modulating the transduction properties of these afferents also remains to be determined.     

Substance P potentiates 5-HT3 receptor-mediated current in rat trigeminal ganglion neurons

The present study aimed to investigate the interaction between the coexistent SP receptor and 5-HT3 receptor in trigeminal ganglion (TG) neurons using whole-cell patch clamp technique. The majority of the neurons examined responded to 5-HT with an inward current (I5-HT) (78.2%, 79/101) that could be blocked by 5-HT3 receptor antagonist, ICS-205,930. The I5-HT was potentiated by preapplication of SP (10(-10) to 10(-8) M) in most 5-HT-sensitive cells(78.5%, 62/79). Coapplication of SP and GR-82334, antagonist of NK1 receptor, had no enhancing effect on I5-HT. The concentration-response curves for 5-HT with and without SP preapplication show that: (1) the threshold 5-HT concentrations with and without SP preapplication are basically the same, while SP preapplication increased the maximal value of I5-HT by 38.0% of its control; (2) the EC50 values of the curves with and without SP pretreatment are very close, i.e. 1.89 x 10(-5) M and 2.08 x 10(-5) M (P > 0.1; n = 9), respectively. Intracellular dialysis of GDP-beta-S, a non-hydrolyzable GDP analog, and GF-109203X, a selective protein kinase C inhibitor, removed the SP potentiation of I5-HT. These results may offer a clue to understanding the mechanism underlying the generation and/or regulation of peripheral pain caused by tissue damage inflammation, etc.