Vascular cell adhesion molecule-1 modulation by tumor necrosis factor in experimental allergic encephalomyelitis

Anti-tumor necrosis factor (TNF) antibodies inhibit passively transferred experimental allergic encephalomyelitis (EAE) in SJL mice. The possibility that this occurs through interference in TNF's upregulation of endothelial cell adhesion molecules was investigated. Expression of both vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) on spinal cord vessels increased during EAE. The upregulation of VCAM-1 was markedly reduced or prevented by anti-TNF treatment. Leukocytic infiltration was 15-fold lower in anti-TNF-treated than diseased animals. Spinal cord endothelial expression of VCAM-1, though not ICAM-1 or fibronectin, positively correlated with the extent of T cell, B cell or monocyte infiltration in each animal.     

旋毛虫幼虫分泌物抗原在小鼠体内诱生肿瘤细胞毒因子的研究

本文应用Ｌ９２９细胞杀伤法，对注射旋毛虫肌肉期幼虫分泌物（Ｌ１ＥＳ）的小鼠血清进行了检测，发现Ｌ１ＥＳ对已注射卡介苗（ＢＣＧ）或感染旋毛虫的小鼠，均能诱生肿瘤细胞毒因子（ＴＣＦ），而正常对照鼠则不能发生，表明Ｌ１ＥＳ诱生ＴＣＦ需要首先激活巨噬细胞（Ｍφ）这一基本条件。将Ｌ１ＥＳ置３７℃、１ｈ，５６℃、３０ｍｉｎ或１００℃、２ｍｉｎ处理后，其诱生ＴＣＦ的能力均明显高于对照组（Ｐ＜０．０５）。Ｌ１ＥＳ     

Characterization of dihydropyridine binding sites in the rat brain: hypertension and age-dependent modulation of [H](+)-PN 200-110 binding

The properties of [³H]dihydropyridine (DHP), nitrendipine and (+)-PN 200-110, binding to rat cerebral membranes were investigated. In normotensive Wistar-Kyoto (WKY) adult rats, the highest densities of [³H]DHP binding sites were found in the hippocampus. Frontal cerebral cortex and hypothalamus had intermediate levels and no specific binding of [³H]DHP and [¹²⁵I]iodipine could be detected in the brainstem membranes and more precisely in the nucleus tractus solitarius and in the locus coeruleus. Changes in the maximal number of DHP binding sites (B_max) were observed in spontaneously hypertensive rats (SHR) and in old Sprague-Dawley rats. In adult SHR, there was a significant increase in theB_max values of [³H](+)-PN 200-110 binding in the hippocampus when compared to the values obtained in WKY. There was no difference in theB_max values between young (3 weeks) prehypertensive SHR and age-matched WKY. In senescent (26 months) Sprague-Dawley rats, theB_max values of [³H](+)-PN 200-110 binding were significantly reduced (30%) in the frontal cerebral cortex and the hippocampus, as compared with the number of DHP binding sites found in mature Sprague-Dawley rats (15 weeks).     

小鼠足容积的活体和离体测量

本实验建立小鼠足容积测量方法学并提供小鼠足容积的生理数值，为进一步研究实验性皮肤癌发生的免疫机制打下基础．根据毛细管放大原理，使用自制的小鼠足容积测量仪测量３５１只昆明种小鼠左右足容积，发现左右足容积几乎相等．另对１５０只小鼠左右足进行３６９次重复测量，发现合格测量超过９７％．不同体重小鼠足生长曲线研究表明，随着体重的增加，小鼠足容积渐趋于一定值，表明生长停止．并且体重２５ｇ以上小鼠活体离体足容积差接近一定值，这提示大龄小鼠足血管张力和容积基本恒定．     

大肠癌组织中免疫抑制因子和病理分期关系的探讨

本文观察16例大肠癌病人的癌组织培养上清液对人T细胞的增殖,ZL—2产生的影响和病理Dukes分期的关系,发现癌组织的TDSF对T细胞的增殖有显著抑制作用,对ZL—2的产生抑制作用不明显,对T细胞增殖率在DukesA与B期,其值与对照有显著差异(0.01P<0.05).在C期有非常显著差异(P<0.01).说明大肠癌组织确实分泌有能造成宿主免疫功能下降的抑制物质.且免疫作用不是通过ZL—2环节发生.     

NSCLC患者血清肿瘤标志物水平与肿瘤骨转移之间关系的研究

目的:探讨非小细胞肺癌患者治疗前血清肿瘤标志物水平与肿瘤骨转移之间的相关性。材料和方法:受检患者58名治疗前均行血清Cy21-1、SCC、NSE、CEA和CA15-3测定和SPECT全身骨显像。结果:血清Cy21-1和CA15-3水平与全身骨显像结果相关。(P<0.05),血清SCC,NSE及CEA水平则无相关(P>0.05)。结论:血清中Cy21-1和CA15-3升高水平与肿瘤骨转移之间存在正相关关系,尤以Cy21-1为著。     

4例着色于皮病伴发鳞状细胞癌临床病理分析

目的：探讨着色干皮病（xeroderma pigmentosum，XP）伴发鳞状细胞癌（squamous cell careinoma，SCC）的临床病理特点。方法：采用组织病理学方法对1993年～2004年间收集的XP伴发SCC患者进行分析。结果：4例中，男性1例，女性3例。发病年龄最小1岁，最大4岁，平均2．5岁。并发肿瘤年龄，最小7岁，最大18岁，平均12．8岁。其中有明确近亲婚配者2例（50％）。4例患者临床症状及病理结果均典型。结论：XP为常染色体隐性遗传性皮肤病，是一种癌前病变，以早年并发恶性肿瘤为其特征，其中以鳞状细胞癌和基底细胞癌最为常见。与皮肤损害和紫外线损伤程度密切相关。     

Differences in a K current in schwann cells from normal and neurofibromatosis-infected damselfish

Patch clamp techniques were used to study whole cell ionic currents in Schwann cells (SC) from a tropical marine fish, the bicolor damselfish, Pomacentrus partitus. The bicolor damselfish is affected by a disease termed damselfish neurofibromatosis (DNF), being developed as an animal model of neurofibromatosis-type 1 (NF1) in humans. NF1 affects SC, fibroblasts, and perineurial cells. The sole depolarization-activated ionic current present in cultured SC from normal fish peripheral nerve and from neurofibromas of fish with induced or spontaneously occurring DNF was an inactivating K⁺ current (K current), with a strong dependence on the Nernst potential for K⁺. This K current activated at depolarizations to -40 mV and above and inactivated during a maintained test pulse (0.2-1 s), but inactivation was significantly greater in tumored SC. Both currents were inhibited by 4-aminopyridine (K_d ? 1 mM) and by dendrotoxin (15 μM) but were insensitive to extracellular tetraethyammonium (≤ 150 mM), indicating that the whole cell currents were similar pharmacologically. The currents could be distinguished on the basis of their sensitivity to depolarized holding potential, with normal cells less sensitive. Half-inactivation of the current was -32 mV in normal cells and -38 mV in tumored cells. Inactivation curves constructed from the average normalized current for many SC were significantly different in normal and tumored cells. When the depolarized holding potential was maintained between test depolarizations, greater voltage-dependent inactivation in tumored cells was apparent. Normal cells maintained an average of 36% of peak current at a holding voltage of ?40 mV, while in tumored cells this average was 12%, a significant difference. © 1994 Wiley-Liss, Inc.