隆突性皮纤维肉瘤23例临床分析

本文报告了我科1978～1990年间收治的降突性皮纤维肉瘤23例,均经组织学证实.治疗以手术切除为主,术后局部复发率为65.2%.无一例发生转移.切除不彻底是复发的主要原因.作者指出广泛切除是防止复发的主要措施,手术前后的放疗有可能减少复发.     

中国中原地区33555名妇女妇科疾病发生情况与五种因素关系的调查报告

自１９９２年３月至１９９４年５月，对中原地区４个省２０多个县（市）近２００个单位３３５５５名２０～７５岁的已婚妇女，进行妇科疾病发生情况与年龄、职业、文化、月经、孕产等五种因素关系的调查分析。在３３５５５名妇女中，患病者２２３７０人，总患病率为６６．６７％，查出妇科疾病４２种，计７６９７４例次。结果证明：以２５～３５岁年龄组发病率最高，其中以内生殖器炎症为主；职业以经商者发病率高，特别是性病患者高于其他职业者二倍以上；文化程度以小学、初中者发病率高，尤其宫颈炎更明显；月经情况：随着经前期紧张综合征的加重，更年期综合征发病率增高；孕产次数越多，患病率越高。本次调查未发现宫颈癌，进一步证明我国对妇女保健工作的关心和重视。     

Antithrombotic effect of beta,beta''-monochloromethylene diadenosine 5'',5"''-P1,P4-tetraphosphate.

The feasibility of using beta,beta'-monochloromethylene diadenosine 5',5"'-P1,P4-tetraphosphate (AppCHCl-ppA) as an antithrombotic agent was studied in a rabbit intracarotid cannula thrombosis model previously shown to be sensitive to antiplatelet agents. This analogue, having a P-C-P bridge in place of a P-O-P internucleoside linkage, has been found resistant to phosphodiesterase activity. Rabbits were infused with the dinucleotide at a dose of 50 mg per kg over a 2-hr period, at a controlled rate by pump. A 1-cm length of polyethylene cannula (1 mm i.d.) was tied into the carotid artery. Animals were stable under general anesthesia during the entire period of the experiment. In the control group, 16 of 20 animals formed clots, an incidence of 80%, whereas in the test animals, 6 of the 20 formed clots (30% incidence, P < 0.05). After preincubation of whole blood with 50 microM AppCHClppA at 37 degrees C for up to 3 hr, a consistent suppression of ADP-induced platelet aggregation was observed. The present study suggests that AppCHClppA may be useful as an antithrombotic agent in certain clinical situations, such as hemodialysis, arteriovenous shunts, and introduction of artificial heart valves. It may also possibly prevent extension of recent clots. The toxicity and metabolism of AppCHClppA have, however, yet to be explored.     

Transforming growth factor J3 type II receptor (TGFpRII) mutation in gastric lymphoma without mutator phenotype

A new mutation in the serine-threonine klnase domain of the transforming growth factor β type II receptor (TGFpRII) was found in a case of diffuse, B cell non-Hodgkin's lymphoma of the stomach. A mfssense mutation (ACA to GCA, Thr to Ala) was detected In exon 5, and a wild type allele was also present. This Is the first naturally occurring mutation in the klnase domain of this gene identified in human primary lymphoma. The replication error at three loci was negative, and the poly A tract of exon 3, which is frequently a target of mismatch repair genes, was intact. Malignant lymphoma of B cell origin in the stomach Is an addition to an expanding catalogue of tumors with TGFβRII alterations, and the biological sequelae of the change in the functional domain and the clinical characteristics of the patient in this study are intriguing.     

针刺对实验性脑缺血作用机理的研究进展

缺血性脑血管疾病是一个非常复杂的病理生理过程 ,是多种机制共同作用的结果。本文从针刺对实验性脑缺血在脑组织形态学改变、血液流变学、脑微循环等方面的研究进展作一综述。     

^60Coγ射线全身照射后大鼠空肠亮脑啡肽的变化

应用免疫细胞化学(ICC)和放射免疫分析(RIA)方法观察了大鼠4、25Gy~(60)Coγ射线照射后24,48和,72h空肠亮脑啡肽(L-ENK)样免疫反应性神经的分布和L-ENK含量的变化。结果:4Gy照射后24h以及25Gy照射后24,48和72h光镜下见空肠L-ENK样免疫反应性神经的分布密度稍有增加,4Gy照射后24h以及25Gy照射后24,48和72h空肠L-ENK含量分别为29.81±0.84pg/mg,34.96±4.38pg/mg,40.71±3.62pg/mg和38.93±2.31pg/mg,与正常对照组(18.26±1.95pg/mg)相比明显升高(P<9.01)。     

Involvement of ERK, p38 and NF-kappaB signal transduction in regulation of TLR2, TLR4 and TLR9 gene expression induced by lipopolysaccharide in mouse dendritic cells

Toll-like receptors (TLR) are sentinel receptors capable of recognizing pathogen-associated molecule patterns (PAMP) such as lipopolysaccharide (LPS) and CpG-containing oligonucleotides (CpG ODN). TLR2 and TLR4 are major receptors for Gram-positive and Gram-negative bacterial cell wall components, respectively. TLR9 is necessary for CpG signalling. LPS or CpG ODN can activate immature dendritic cells (DC) and induce DC maturation characterized by production of cytokines, up-regulation of co-stimulatory molecules, and increased ability to activate T cells. However, little is known regarding the regulation of TLR gene expression in mouse DC. In this study, we investigated the regulation of TLR2, TLR4 and TLR9 gene expression by LPS in murine immature DC. TLR2, TLR4 and TLR9 mRNA were up-regulated following LPS stimulation. The up-regulation of TLR9 expression coincided with significantly increased production of tumour necrosis factor-alpha induced by LPS plus CpG ODN. While inhibition of extracellular signal-related kinase and NF-kappaB activation suppressed the up-regulation of the expression of TLR2, TLR4 and TLR9 mRNA, inhibition of p38 kinase prevented the up-regulation of TLR2 and TLR4 mRNA expression but enhanced the up-regulation of TLR9 expression. These results demonstrated that TLR2, TLR4 and TLR9 gene expression was differently regulated by LPS in mouse immature DC. Up-regulation of TLR2, TLR4 and TLR9 expression by LPS might promote the overall responses of DC to bacteria and help to explain the synergy between LPS and other bacterial products in the induction of cytokine production.     

Inhibitory effect of ketamine on phosphorylation of the extracellular signal-regulated kinase1/2 following brain ischemia and reperfusion in rats with hyperglycemia

To determine if the inhibitory effects of ketamine on the extracellular signal-regulated kinase (ERK) 1/2 are involved in reduction of the hyperglycemia-exaggerated cerebral ischemic lesion, rats with normoglycemia, hyperglycemia, or hyperglycemia supplemented with ketamine were subjected to 15 min of forebrain ischemia, and then, reperfusion for 0.5, 1, and 3h. Phosphorylation of ERK1/2 in the brain tissues was assessed by immunohistochemistry and Western blot analysis. In rats with normoglycemia, we demonstrated a moderate increase of the ERK1/2 phosphorylation in the cingulum cortex and hippocampus CA3 following an ischemic intervention. It quickly dropped to control levels after reperfusion for 0.5h. In rats with hyperglycemia, however, the increase of the ERK1/2 phosphorylation in these areas was significantly higher in all animals reperfused. The neuronal death, detected by the TdT-mediated-dUTP nick end labeling assays, was found in the cingulum cortex (5.23+/-2.34, per high power feild) and hippocampus CA3 areas (6.29+/-3.68, per 1mm(2)) in hyperglycemic group after reperfusion for 3h. With ketamine treatment, the ERK1/2 phosphorylation in cingulum cortex and hippocampus CA1 and CA3 areas was found to be the same as that in normoglycemia rats. Our results suggest that hyperglycemia may increase the ischemic insult through modulation of the signal transduction pathways involving ERK1/2. The inhibitory effects of ketamine on the hyperglycemia-activated ERK1/2 phosphorylation are probably through inhibition of the N-methyl d-aspartate-mediated calcium influx, which subsequently reduce the hyperglycemia-exaggerated cerebral damage.