经剑突下孔直接取石法在腹腔镜胆总管切开取石术中的应用

目的 探讨经剑突下孔直接取石法在腹腔镜胆总管切开取石术中的应用效果,并总结手术经验。方法 回顾性分析蚌埠市第一人民医院2014年11月-2018年4月86例胆总管结石患者的临床资料,其中男28例、女58例,年龄25~78(50.8±10.5)岁,均观察行腹腔镜手术,术中于胆总管切开后经剑突下孔直接取石。记录成功实施腹腔镜手术患者的手术时间、术中出血量、术后下床时间、术后排气时间、引流管拔除时间、术后住院时间、手术成功率及随访并发症,并总结技术经验。结果 成功完成腹腔镜下手术81例,成功率94.2%(81/86),其中1例因末端结石嵌顿难以取出,后经胆道镜下碎石取出。其余5例中,1例因胆囊十二指肠漏中转开放手术,4例因胆囊炎急性发作后三角区纤维化难以分离而中转开腹。81例成功手术者:手术时间为(80.2±18.6)min,术中出血量为 (20.0±3.0) mL,术后下床时间为(15.5±5.7)h,术后排气时间为(30.2±10.2)h,引流管拔除时间为术后(2.4±0.4)d,术后住院时间 (10.4±2.6) d。术后4~6周拔除T管;随访6~12个月,平均8.5个月,无术后胆漏、胆道狭窄、再发胆管结石等并发症。结论 经剑突下孔直接取石法使腹腔镜下胆总管切开取石术变得简单易行且安全,通过选择合适的患者,调整剑突下孔的位置、注意手术细节,改进手术流程,可减少了手术时间、创伤,并能取尽结石,获得满意的疗效。     

Expression of silencer of death domains and death-receptor-3 in normal human kidney and in rejecting renal transplants

We have previously reported the pattern of cellular expression of tumor necrosis factor receptors (TNFR) in human kidney and their altered expression in transplant rejection. We have extended our studies to examine the expression of Silencer of Death Domains (SODD), a protein that binds to the cytoplasmic portion of TNFR1 to inhibit signaling in the absence of ligand. In normal human kidney SODD is expressed in glomerular endothelial cells where it colocalizes with TNFR1. During acute rejection both SODD and TNFR1 are lost from glomeruli, but we found strong expression of SODD on the luminal surface of tubular epithelial cells. This occurs in the absence of detectable TNFR1 expression, suggesting that SODD could interact with other proteins at these sites. Several other members of the TNF superfamily, including Fas and death receptors (DR)-3, -4, and -5, also contain intracellular death domains, but SODD only interacts with the death domain of DR3. We therefore studied the expression of DR3 in human kidney, and report that this death receptor is up-regulated in renal tubular epithelial cells and endothelial cells of some interlobular arteries, in parallel with SODD, during acute transplant rejection. In less severe rejection episodes, DR3 and SODD were more focally induced, generally at sites of mononuclear cell infiltrates. In ischemic allografts, eg, with acute tubular necrosis but no cellular rejection, DR3 was induced on tubular epithelial cells and on glomerular endothelial cells. These data confirm that TNF receptor family members are expressed in a regulated manner during renal transplant rejection, and identify DR3 as a potential inducible mediator of tubular inflammation and injury.     

Stimulating capacity of fresh and cultured human leukaemic lymphoid and myeloid cells in `one-way'' mixed lymphocyte reaction

Fresh normal peripheral blood B lymphocytes possess a strong stimulating capacity while fresh thymus cells or fresh peripheral T lymphocytes possess a weak, but significant stimulating capacity on allogeneic lymphocytes in `one-way' mixed lymphocyte reaction. Fresh leukaemic T lymphoid cells from patients with T-cell ALL or T-cell CLL exert little or no stimulation on allogeneic lymphocytes. Fresh leukaemic B lymphoid cells from patients with B-cell CLL or B-cell HCL, on the other hand, exert a lesser stimulation on allogeneic lymphocytes, as compared to that of normal B lymphocytes. Leukaemic myeloblasts from patients with AML or Ph<sup>1</sup>(+) CML-BP exert significantly higher stimulation than leukaemic lymphoid cells in `one-way' mixed lymphocyte reaction (P<0.05). Cultured leukaemic T lymphoid cells (MOLT-4) possess no stimulating capacity, cultured leukaemic B lymphoid cells (BALM-2) possess a moderate degree of stimulating capacity and cultured leukaemic, possibly myeloid, cells (NALM-1 and K562) possess vigorous stimulation on allogeneic lymphocytes. The stimulating capacity of NALM-1 or K562 cells is significantly higher than that of BALM-2 cells (P<0.01 or P<0.05, respectively) and that of MOLT-4 cells (P<0.001). These observations suggest that the stimulating capacity of leukaemic T or B lymphoid cells may have been completely or partially lost during the process of leukaemogenesis. Since we do not have an opportunity to study the stimulating capacity of normal myeloblasts, it is not known whether the stimulating capacity of leukaemic myeloblasts, which is found to be very strong on allogeneic lymphocytes, may have been modified during the process of leukaemogenesis.     

外固定架治疗桡骨远端粉碎性骨折

目的总结桡骨远端粉碎性骨折的外固定架治疗疗效。方法从1995年～2003年采用外固定架治疗桡骨远端粉碎性骨折46例,并进行随访。结果治疗后均随访1年,术后按Dienst评分,优良率为83．3％。结论外固定架固定牢靠,可早期活动腕关节,是治疗桡骨远端粉碎性、开放性骨折的有效方法。     

Anti-HBV effects of CpG oligodeoxynucleotide-activated peripheral blood mononuclear cells from patients with chronic hepatitis B

Unmethylated CpG dinucleotides in bacterial DNA or synthetic oligodeoxynucleotides containing immunostimulatory CpG motifs (CpG ODN) are known as a potent Th1-like immune enhancer in vertebrates. Chronic hepatitis B is the immunocompromising condition. We therefore investigated the effects of CpG ODN on cultured cells from chronic hepatitis B patients and healthy controls. The inhibitory effects of CpG ODN on hepatitis B virus (HBV) were also studied. The secretion of IFN-alpha by CpG ODN-activated peripheral blood mononuclear cells (PBMCs) from chronic hepatitis B patients and healthy controls was significantly increased when compared with PBMCs alone or GpC ODN-stimulated PBMCs. After activation with CpG ODN, the IFN-alpha secretion by chronically HBV-infected patient PBMCs is less than that by healthy control PBMCs. Treatment of HepG2 2.2.15 cells with culture supernatants of PBMCs activated by CpG ODN can significantly suppress the secretion of HBsAg, HBeAg and HBV DNA as compared with that of PBMCs without CpG ODN activation under the same conditions. No inhibitory effect on the replication of HBV was found for CpG ODN treatment alone. Our results indicated that CpG ODN could efficiently enhance the immune response of chronic hepatitis B patients. Moreover, the CpG ODN-activated PBMCs from chronic hepatitis B patients were able to significantly inhibit HBV replication in vitro, suggesting that CpG ODN may be a potential immunoregulator against HBV infection in the future.     

原发性前列腺滑膜肉瘤临床病理分析

前列腺滑膜肉瘤罕见,1999年Iwasaki等[1]首次报道,至今仅检索到5例,其中原发4例[2-5]、转移1例[5].我们收集2例原发性前列腺滑膜肉瘤,对其临床表现、病理形态、免疫学表型及分子生物学特征进行分析,并探讨其诊断及鉴别诊断.     

徐州地区334例早产儿临床分析

目的探讨我院2006年334例早产儿,分析发生的危险因素,以总结提高产科早产预防、医疗水平,并提供研究参考。方法早产组334例与同期分娩的足月对照组334例分析比较,早产的临床相关因素及对围产儿的影响。结果胎膜早破,妊娠高血压综合征,前置胎盘,臀位,多胎妊娠是早产的重要因素。早产使新生儿窒息,围生儿死亡,低体重儿增加。结论早产使围产儿窒息和死亡率增加。加强早产预测可望降低早产的发生,提高围生医学质量。     

戴维斯在线认知问卷在538名医学生中的试用

目的:建立戴维斯在线认知问卷中文版,并测试其信度和效度。方法:538名学生完成了戴维斯在线认知问卷,统计分析量表的信度和效度,并进行验证性因子分析。结果:戴维斯在线认知问卷中文版内部一致性系数为0.937,重测信度为0.905;验证性因子分析表明,各条目对4个一阶因子的标准负荷系数在0.423~0.814之间,4个一阶因子对上一级潜在因子的标准负荷系数在0.741~0.971之间;整体模式的适配度指标均符合心理测量学要求(RMSEA=0.012,GFI=0.943,NFI=0.931,CFI=0.994)。结论:戴维斯在线认知问卷中文版具有良好的信度和效度,可以作为一种较好的网络成瘾程度评价工具在我国青少年中使用。     

Enhanced responses of the anterior cingulate cortex neurones to colonic distension in viscerally hypersensitive rats

The anterior cingulate cortex (ACC) is critically involved in processing the affective component of pain sensation. Visceral hypersensitivity is a characteristic of irritable bowel syndrome. Electrophysiological activity of the ACC with regard to visceral sensitization has not been characterized. Single ACC neuronal activities in response to colorectal distension (CRD) were recorded in control, sham-treated rats and viscerally hypersensitive (EA) rats (induced by chicken egg albumin injection, i.p ). The ACC neurones of controls failed to respond to 10 or 30 mmHg CRD; only 22% were activated by 50 mmHg CRD. Among the latter, 16.4% exhibited an excitatory response to CRD and were labelled 'CRD-excited' neurones. In contrast, CRD (10, 30 and 50 mmHg) markedly increased ACC neuronal responses of EA rats (10%, 28% and 47%, respectively). CRD produced greater pressure-dependent increases in ACC spike firing rates in EA rats compared with controls. Splanchnicectomy combined with pelvic nerve section abolished ACC responses to CRD in EA rats. Spontaneous activity in CRD-excited ACC neurones was significantly higher in EA rats than in controls. CRD-excited ACC neurones in control and EA rats (7 of 16 (42%) and 8 of 20 (40%), respectively) were activated by transcutaneous electrical and thermal stimuli. However, ACC neuronal activity evoked by noxious cutaneous stimuli did not change significantly in EA rats. This study identifies CRD-responsive neurones in the ACC and establishes for the first time that persistence of a heightened visceral afferent nociceptive input to the ACC induces ACC sensitization, characterized by increased spontaneous activity of CRD-excited neurones, decreased CRD pressure threshold, and increased response magnitude. Enhanced ACC nociceptive transmission in viscerally hypersensitive rats is restricted to visceral afferent input.     

Compartmentalized transgene expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) in mouse lung enhances allergic airways inflammation

To investigate the role of GM-CSF in asthmatic airways inflammation, we have targeted GM-CSF transgene to the airway cells in a mouse model of ovalbumin (OVA)-induced allergic airways inflammation, a model in which there is marked induction of endogenous IL-5 and IL-4 but not GM-CSF. Following intranasal delivery of a replication-deficient adenoviral gene transfer vector (Ad), transgene expression was found localized primarily to the respiratory epithelial cells. Intranasal delivery of 0.03 × 10⁹ plaque-forming units (PFU) of AdGM-CSF into naive BALB/c mice resulted in prolonged and compartmentalized release of GM-CSF transgene protein with a peak concentration of ≈ 80 pg/ml detected in bronchoalveolar lavage fluid (BALF) at day 7, but little in serum. These levels of local GM-CSF expression per se resulted in no eosinophilia and only a minimum of tissue inflammatory responses in the lung of naive mice, similar to those induced by the control vector. However, such GM-CSF expression in the airways of OVA-sensitized mice resulted in a much greater and sustained accumulation of various inflammatory cell types, most noticeably eosinophils, both in BALF and airway tissues for 15–21 days post-OVA aerosol challenge, at which times airways inflammation had largely resolved in control mice. While the levels of IL-5 and IL-4 in BALF and the rate of eosinophil apoptosis were found similar between different treatments, there was an increased number of proliferative leucocytes in the lung receiving GM-CSF gene transfer. Our results thus provide direct experimental evidence that GM-CSF can significantly contribute to the development of allergic airways inflammation through potentiating and prolonging inflammatory infiltration induced by cytokines such as IL-5 and IL-4.