自然流产模型小鼠绒毛滋养层细胞凋亡及相关调控蛋白的表达

目的探讨自然流产模型小鼠绒毛滋养层细胞凋亡异常与自然流产的关系。方法建立正常妊娠模型CBAXBALB/c和自然流产模型CBAXDBA/2。采用DNA缺口原位末端标记技术(TUNEL)测定两组模型孕13 d绒毛滋养层细胞凋亡情况;免疫组织化学SABC法测定两组模型孕13 d绒毛组织Bcl-2、Bax、Fas、FasL 4种凋亡调控蛋白的表达,并以MBIS-2000医用彩色病理图像免疫组织化学测量系统对其表达进行半定量分析,结果用平均灰度值表示。结果自然流产模型小鼠绒毛滋养层细胞凋亡指数明显高于正常妊娠模型(P<0.01)。Bax表达亦高于正常妊娠模型(P<0.05);FasL表达低于正常妊娠模型(P<0.01);Fas和Bcl-2表达两组无明显差异。结论早孕期绒毛滋养层细胞凋亡异常是自然流产机制之一,Bcl-2/Bax,Fas/FasL途径可能是诱导早孕期绒毛滋养层细胞凋亡的重要因素。     

Culture Medium Modulates Proinflammatory Conditions of Human Pancreatic Islets Before Transplantation

A portion of transplanted islets is lost during engraftment as a result of stressful events, involving hypoxia and production of proinflammatory molecules by islets. Two of these molecules (monocyte chemoattractant protein-1, CCL2/MCP-1 and tissue factor, TF) are directly correlated with reduced graft function. We evaluated which factors reduce islet proinflammatory conditions. In particular the effects of different culture media supplemented with proteins or antioxidant agents on CCL2/MCP-1 and TF human islet release were evaluated. We observed that human islets after culture in final wash culture medium (FW) significantly decreased CCL2/MCP-1 release and TF production compared with CMRL and M199. These effects were independent from the type of protein added to the media (human serum, human albumin, fetal calf serum). Glutathione in FW further decreased CCL2/MCP-1 in a dose-dependent manner. Culture conditions can modulate the proinflammatory state of islets, and could be used in clinical islet transplantation to reduce inflammation during engraftment.     

Monocyte adhesion molecule expression in interstitial inflammation in patients with renal failure.

BACKGROUND: Patients with renal failure have an increased susceptibility to infections. We therefore studied the recruitment of monocytes and their expression of adhesion molecules CD11b and CD62L at the site of interstitial inflammation in patients with renal failure. Furthermore, we studied if the capacity of monocytes to up-regulate CD11b in interstitial inflammation was determined by the interstitial concentration of chemotactic factors. METHODS: Three intensities of interstitial inflammation (0, intermediate and intense) were established in skin blister chambers. Leukocyte count, CD11b/CD62L expression, monocyte chemotactic protein-1 (MCP-1) and blister activity in terms of CD11b mobilization were determined. RESULTS: The CD62L expression on monocytes was lower in the peripheral circulation in patients with renal failure compared with healthy subjects (P<0.005 and P<0.001). At the site of interstitial inflammation patients had a higher expression of CD62L (intermediate, P<0.05; intense, P<0.005). Furthermore, monocytes from patients had an impaired capacity to mobilize CD11b both in the peripheral circulation (P<0.005) and at the intermediate and intense sites of interstitial inflammation (P<0.005 and P<0.001, respectively) compared with cells collected from healthy subjects. We incubated monocytes in blister exudates, in order to explore whether this phenomenon is caused by cellular factors and/or to the interstitial concentration of chemotactic mediators. The expression of CD11b on monocytes from healthy blood donors incubated in blister exudates from either patients or healthy subjects in vitro was similar. The interstitial concentration of MCP-1 at the site of intermediate inflammation was significantly lower in patients with renal failure compared with the corresponding blister exudate collected from healthy subjects (P<0.05), but no differences were observed at the site of intense inflammation. Furthermore, neutralizing the action of MCP-1 in blister exudates with monoclonal antibodies did not have any impact on monocyte CD11b expression following incubation in blister exudates. CONCLUSION: These studies indicate that the impaired capacity of monocytes to mobilize CD11b at the site of inflammation in patients with renal failure is more dependent on constitutive cellular factors than the concentration of CD11b mobilizing factors in the interstitium.     

Effects of bombesin and gastrin-releasing peptide on memory processing

We have previously shown that feeding mice immediately following training enhances memory retention and that one of the gastrointestinal hormones released during a meal, cholecystokinin, also enhances retention after peripheral administration. In the studies reported here we demonstrate that another gastrointestinal peptide, gastrin-releasing peptide (GRP), enhances retention after peripheral administration, as does its amphibian counterpart, bombesin. GRP_14–27 had the same effect as the intact peptide, while GRP_1–16 was ineffective at enhancing retention. The dose-response curves showed a characteristic inverted U-shape with high doses of both GRP and bombesin being amnestic. The effect of both peptides was time-dependent and both reversed amnesia induced by the anticholinergic, scopolamine. I.c.v. administration of the peptides required higher doses to produce an effect on memory retention. suggesting that the effect was mediated predominantly through a peripheral mechanism. Doses of the peptides that enhanced memory retention after peripheral administration failed to increase serum glucose, suggesting that glucose modulation was not the mechanism by which GRP and bombesin modulate memory processing. Vagotomy inhibited the memory-enhancing effects of both GRP and bombesin, suggesting that these peptides produced their effect by stimulating ascending vagal pathways. These studies, together with our previous study with cholecystokinin, suggest the existence of a gastrointestinal hormonal system, which is activated by the passage of food through the intestine, that enhances memory retention.     

保定地区首次证实为流行性出血热疫源地

保定地区1934年首次经血清学证实有EHF病例发生,并从疫区鼠类中查到EHF抗原,其阳性率分别为:褐家鼠4.85%,黑线姬鼠1.95%,大仓鼠0.79%,小家鼠0.51%,褐家鼠可能是我区的主要传染源。疫区健康人群血清EHF抗体阳性率为1.37%,女性显著高于男性。     

Structure-acute toxicity relationship of aromatic hydrocarbons in mice

The structure-acute toxicity relationship of aromatic hydrocarbons was examined in mice. In all test compounds, the acute toxicity was determined under 2 conditions: control LD₅₀ (LD₅₀-cont) and carbon tetrachloride (CCl₄)-pretreated LD₅₀ (LD₅₀-CCl₄). The CCl₄-pretreatment was done in order to evaluate the toxic potency of compound itself without the influence of metabolism. Both log (1/LD₅₀-cont) and log (1/LD₅₀-CCl₄) were functions of the log P, n-octanol/water partition coefficient, i.e., log (1/LD₅₀-cont) = 0.080 log P − 1.532 and log (1/LD₅₀-CCl₄) = −0.040(log P)² + 0.157 log P − 1.373. Both equations were statistically significant (P < 0.01). The ratio of LD₅₀-cont/LD₅₀-CCl₄ indicated that metabolic activation is more evident in hydrophobic compounds than in hydrophilic compounds. The results suggest that hydrophobicity of the aromatic hydrocarbons plays an important role in determining their acute toxicity.     

乌苯美司体外对人单核细胞功能的活化作用

观察了国产乌苯美司（乌比美克）体外对人单核细胞功能的影响：①０．０１￣１００μｇ／ｍｌ乌苯美司能直接诱导人单核细胞生成ＩＬ－１；②经０．１μｇ／ｍｌ乌苯美司作用４ｈ后，人单核细胞即开始分泌ＩＬ－１，２４ｈ达到高峰，以后逐渐下降；③经１０￣１００μｇ／ｍｌ乌苯美司预处理，单核细胞可促进ＮＫ细胞活性，而经０．０１￣０．１μｇ／ｍｌ乌苯美司处理，单核细胞则抑制ＮＫ细胞活性。     

芪胆通痹汤治疗类风湿性关节炎作用机理的实验研究

目的　研究芪胆通痹汤对大鼠Ⅱ型胶原类风湿性关节炎 (RA)模型的作用机理 ,观察“清少阳、益肝肾”治法的疗效。方法　免疫学实验方法。结果　该方能有效减轻大鼠局部足肿胀程度及降低炎症组织中前列腺素 (PGE2 )含量 (P <0 0 1) ,并且具有镇痛作用 ;能显著抑制DNFB所致的小鼠DTH反应 (P <0 0 1)、抑制DTH小鼠脾脏T细胞增殖 (P <0 0 1) ,血清在 1∶2比例稀释下能显著抑制脾细胞IL 2的分泌 (P <0 0 1)。结论　芪胆通痹汤能有效缓解RA症状 ,并通过抑制Ⅳ型免疫变态反应治疗RA。     

An in vitro study of nonadrenergic-noncholinergic activity on the cavernous tissue of mouse

The relaxant effects of electrical field stimulation (EFS) and exogenously applied acetylcholine (ACh) or acidified NaNO₂ (a-NaNO₂) were investigated in the isolated mouse corpus cavernosum precontracted with phenylephrine hydrochloride (PE). Tetrodotoxin (TTX) blocked the relaxant effects of EFS completely, whereas it had no effect on the responses to ACh or a-NaNO₂. Guanethidine and indomethacin failed to affect the electrically or ACh-induced relaxations. Atropine completely blocked the effect of ACh; however, it caused a slight reduction in the relaxation evoked by EFS.N ^G- Nitro-l-arginine (l-NOARG) reduced the effects of EFS and ACh significantly, but it was ineffective on the relaxations induced by a-NaNO₂. The inhibitory action ofl-NOARG was partly restored byl-arginine, but not byd-arginine. Methylene blue (MB) and hydroxocobalamin (HC) exhibited significant inhibition on the relaxations evoked by EFS, ACh and a-NaNO₂. Hydroquinone (HQ) reduced relaxation due to a-NaNO₂, but did not affect that of EFS and ACh. Our findings suggest that EFS-induced relaxations of mouse cavernosal tissue are mediated by a transmitter which probably resembles an organic nitrate.     

Purification of rabbit, rat and mouse protein C with the use of monoclonal antibody to human protein C, PC01

Ca(++)-dependent monoclonal antibody specific to gamma-carboxyglutamic acid (Gla) domain of protein C was produced. It did not cross-react to the other vitamin K-dependent plasma proteins but to protein C of the other species. Using this monoclonal antibody, PC01, rabbit (170 micrograms), rat (60 micrograms) and mouse (40 micrograms) protein Cs were isolated from 100 ml of their plasma by affinity chromatography. All of these protein Cs were two chain form linked by disulfide bond as well as human protein C and activated by thrombin-thrombomodulin complex. Rat and mouse protein Cs showed similar characters to human protein C. On the other hand rabbit protein C had different M(r) of heavy and light chains and showed lower anticoagulant activity compared with human protein C.