胎盘型谷胱甘肽S转移酶mRNA在大鼠肝癌癌前病变组织中的原位表达

应用原位杂交技术，观察了二乙基亚硝胺（ＤＥＮ）诱发大鼠肝癌前病变组织中胎盘型谷胱甘肽Ｓ转移酶（ＧＳＴ－Ｐ）ｍＲＮＡ的表达。结果显示，ＧＳＴ－ＰｍＲＮＡ主要在癌前病变肝组织中的变异灶及灶外卵圆形细胞内表达，且在变异灶间或和同一灶内阳性细胞间表达程度不尽一致，而正常肝、再生肝组织中未见其表达。提示在分子水平上变异灶细胞及卵圆型细胞可能成为实验性肝癌的癌前期细胞     

生长激素、肝细胞生长因子和烟酰胺对人胎胰岛细胞的增殖作用

目的研究生长激素(GH)，肝细胞生长因子(HGF)和烟酰胺(NIC)对体外培养的人胎胰岛细胞的增殖作用及其交互作用。方法采用La(2^7)正交设计法在体外培养的人胎胰岛细胞的各组中分别加入不同浓度及组合的GH，HGF和NIC，培养48h后，收集各孔细胞，DTZ染色，计数。结果GH，HGF和NIC均起主要作用，HGF和NIC的交互作用不可忽视，最佳的生长因子组合及适配浓度为GH(100ng／ml)HGF(25ng／ml)NIC(100mmol／L)。结论GH，HGF和NIC均能促进体外培养的胰岛细胞的增殖，且组合GH(100ng／ml)HGF(25ng／ml)NIC(100mmol／L)的作用最大。     

一氧化碳中毒迟发性脑病的临床预防

目的　探讨临床治疗措施对一氧化碳中毒迟发性脑病的预防。方法　将 130例一氧化碳中毒患者随机分为A、B、C 3组 ,A组采用纳络酮、低分子肝素、高压氧治疗 ;B组采用胞二磷胆碱、醒脑注射液、高压氧治疗 ;C组采用胞二磷胆碱、醒脑注射液治疗。结果　A组昏迷时间与B、C组对比 ,B组与C组对比 ,明显缩短 ,有显著性差异 (P <0 .0 5或P <0 .0 1) ;本组 130例患者中 ,共发生迟发性脑病15例 ,发生率为 11.5 % ,迟发性脑病发生率A组与B、C组对比 ,B组与C组对比 ,明显降低 ,有显著性差异 (P <0 .0 5或P <0 .0 1)。结论　选择有效的药物 ,及早应用高压氧和充足的疗程是迟发性脑病临床预防的关键。     

新生儿缺氧缺血性脑病的MRI表现

目的:探讨新生儿缺氧缺血性脑病(HIE)的MRI表现。材料和方法:对87例临床确诊为HIE的患儿行MRI扫描,并对其MRI表现进行分析。结果:87例HIE患儿中,74例(85.1%)可见皮层、皮层下及深部白质T1WI迂曲条状、点状高信号;69例(79.3%)显示基底节、丘脑T1WI异常高信号及内囊后肢高信号消失;62例(71.3%)出现弥漫性脑水肿;58例(66.7%)可见颅内出血,包括蛛网膜下腔出血、硬膜下出血、脑室内出血及脑实质出血;19例(21.8%)可见侧脑室周围白质软化;7例(8.0%)可见脑梗死。结论:MRI在HIE正确诊断和早期治疗中具有重要临床价值。     

急性胰腺炎恢复期并Wernicke脑病一例

患者男，34岁。大量饮酒后出现剑突下疼痛，伴恶心、发热，体温最高达38．5℃，发病3天入住当地医院治疗，诊断为“急性胰腺炎”。经禁食、胃肠减压、抑制胰酶分泌、抑酸、抗感染治疗，3天后疼痛明显减轻，血淀粉酶恢复正常、尿淀粉酶仍高于正常值。维持原治疗，治疗16天后，自觉上述症状消失后拔除胃管，但化验检查发现尿淀粉酶高（1294u／L），1天后再次留置胃管行胃肠减压，治疗33天后拔除胃管。出现头晕、恶心呕吐，呕吐物为胃内容物，予以“吗丁啉、思密达、多酶片”等药物对症治疗，效差。治疗38天后出现复视、视物不清、耳鸣，为进一步诊治，以“尿淀粉酶升高42天，呃逆1天，复视、乓鸣5天”为主诉入住我院。     

Fat-Derived Hormone Adiponectin Combined with FTY720 Significantly Improves Small-for-Size Fatty Liver Graft Survival

Owing to the discrepancy between organ donation and the demand for liver transplantation, expanding the liver donor pool is of vital importance. However, marginal liver grafts, such as small-for-size and/or fatty grafts, were associated with primary graft nonfunction or poor function. Therefore, novel combination therapies to rescue small-for-size fatty liver grafts should be investigated. In this study, we applied a combination therapy using a fat-derived hormone adiponectin (anti-steatosis) plus immunomodulator FTY720 (anti-inflammatory) in a rat liver transplantation model using small-for-size fatty liver grafts, and investigated the underlying protective mechanism such as anti-steatosis, intra-graft energy metabolism, hepatic microcirculatory changes, cell signaling cascades for survival, apoptosis and inflammation. The current study demonstrated that even a single treatment of adiponectin or FTY720 improved the 7-day graft survival from 0% to 62.5% (p = 0.001). The combination therapy significantly increased the 7-day graft survival rate to 100% by remarkable attenuation of graft steatosis and acute phase inflammatory response, significant activation of cell survival Akt pathway and maintenance of intra-graft adenosine triphosphate metabolism and improvement of hepatic microcirculation. In conclusion, the fat-derived hormone adiponectin combined with FTY720 might be a novel combination drug therapy for prevention of small-for-size fatty liver graft injury.     

Liver regeneration in acute severe liver impairment: a clinicopathological correlation study.

BACKGROUND: Although normally quiescent, the adult mammalian liver possesses a great capacity to regenerate after different types of injury. Major players in the regeneration process are mature residual cells, including hepatocytes, cholangiocytes and stromal cells. However, if the regenerative capacity of mature cells is impaired, hepatic progenitor cells (HPCs) are activated and expand into the liver parenchyma. Upon transit amplification, the progenitor cells generate new hepatocytes and biliary cells to restore liver homeostasis. AIMS/METHODS: To study the relationship between different histopathological parameters as well as their correlations with clinical parameters and outcome, we examined liver specimens from 74 patients with acute or subacute severe liver impairment by immunohistochemistry for CK7/CK19 (evaluation of HPCs activation/differentiation), Mib1(Ki 67)/P21 (evaluation of proliferative activity/proliferation arrest of hepatocytes) and hematoxylin and eosin (evaluation of hepatocyte loss). RESULTS: Of the 74 patients, 32% survived without transplantation, 14% died without transplantation and 54% were transplanted. Our results show that a threshold of 50% loss of hepatocytes, associated with significant decrease in the proliferative activity of remaining mature hepatocytes, is needed for extensive hepatic progenitor cell activation. Such activation is a sign of disease severity and occurs early (within 1 week) in the disease course. However, development of intermediate hepatocytes, suggesting HPCs differentiation towards mature hepatocytes, takes at least 1 week's time. We found a positive correlation between histopathological parameters (percentage hepatocyte loss, number of proliferating hepatocytes and number of HPCs) and clinical parameters of liver impairment such as model for end stage liver diseases (MELD). Surviving patients compared with those who either died or were transplanted had significantly less hepatocyte loss, less HPCs activation and more mature hepatocyte proliferative activity. Hepatocyte proliferative activity and degree of hepatocyte loss were the most important independent histopathological parameters in predicting outcome. CONCLUSION: Liver biopsy can provide important additional information in a patient with severe acute liver impairment.     

Incretin mimetics as a novel therapeutic option for hepatic steatosis.

BACKGROUND: Fat accumulation in the liver or non-alcoholic fatty liver disease (NAFLD) is regarded as a key pathogenic factor and component of the metabolic syndrome. It was reported that administration of the incretin mimetic exenatide reversed hepatic steatosis in an obese mouse model. We had the opportunity to study the effect of additional exenatide administration on liver fat content in a patient with type 2 diabetes. CASE REPORT: A 59-year-old male with poorly controlled type 2 diabetes was treated with exenatide in addition to metformin monotherapy. Following 44 weeks of exenatide therapy, mean the liver fat measured by liver spectroscopy declined from 15.8% to 4.3%. This dramatic decrease in liver fat was accompanied by significant beneficial changes in several cardiovascular disease risk factors and improvement of all liver enzymes, in particular alanine aminotransferase, the most important marker of liver steatosis. CONCLUSION: This case report suggests that the incretin mimetic exenatide decreases hepatic fat accumulation and may play a role in the future treatment of NAFLD, and the associated insulin resistance and cardiovascular risk factors in an ever-growing high-risk population.     

急性一氧化碳中毒后迟发性脑病患者血清白介素水平的变化及其临床意义

目的 探讨急性一氧化碳（CO）中毒后迟发性脑病（DEACMP）患者血清白介素（IL）水平变化及其临床意义。方法 采用酶联免疫吸附法检测34例DEACMP患者治疗前、后血中IL-2、4、6的水平，并与30名健康人和30例急性CO中毒（ACMP）患者进行比较。结果 （1）DEACMP组治疗后血中IL-2、4、6的含量显著高于治疗前（均P〈0．01），但仍显著低于ACMP组和健康对照组（均P〈0．01）；（2）ACMP组血IL-2、4、6的含量明显高于健康对照组（均P〈0．01）。结论 DEACMP的发生与神经免疫病理损伤有关，血中IL-2、4、6的水平可以反映DEACMP患者机体的免疫状态。     

影响肝外伤手术死亡的危险因素分析

目的分析影响肝外伤手术死亡的危险因素,探讨其临床意义。方法根据AAST和ISS标准,回顾性分析90例肝外伤手术病例,对影响手术死亡的危险因素进行单因素比较和Logistic回归分析。结果死亡15例,其中Ⅲ级2例、Ⅳ级4例、Ⅴ级9例,总体手术死亡率17%。Ⅳ~Ⅴ级肝外伤手术方式的单因素比较提示:清创性肝切除术的相对危险度是0.73;而规则性肝切除术、肝静脉或肝后下腔静脉修补术相对危险度分别是1.32、1.52。Logistic回归分析提示:ISS分会和术中失血量是影响手术死亡率的2个独立因素。结论ISS分值、术中失出血量和手术方式是影响肝外伤手术死亡的3个重要因素,娴熟的手术技能和合理的手术方式可以减少术中出血量和降低手术死亡率。