目的 分析甲状腺结节内不同类型的钙化,探讨其与甲状腺良恶性疾病的关系及微小钙化、粗大钙化、环状钙化等的诊断价值.方法 收集230例甲状腺结节患者的术前超声及术后病理资料,根据钙化类型分组,分析钙化与甲状腺良恶性结节的相关性及其诊断价值.结果 钙化组尤其是微小钙化组的恶性率明显高于其他各组,环状钙化组恶性率低于其他各组,而粗大钙化组对比环状钙化组及无钙化组恶性率无统计学差异,微小钙化诊断恶性结节的敏感性、特异性分别为48.6％、92.4％.结论 钙化对提示恶性结节意义重大,尤其是微小钙化更是密切相关,环状钙化对提示良性结节意义较大,而粗大钙化及无钙化对良恶性结节提示意义不大.

Elevated intracellular Ca(2+) content is implicated in ethanol-induced hepatocyte apoptosis and necrosis. Extracellular Ca(2+) influx has been suggested to play a role in this process. However, the exact Ca(2+)-permeable channel involved in the plasma membrane is still unclear. This study investigated the role of store-operated calcium entry (SOCE) in ethanol-induced cytosolic free Ca(2+) concentrations ([Ca(2+)](i)) increase and hepatotoxicity. Ethanol (25-800mM) dose-dependently increased [Ca(2+)](i) content and hepatocyte damage in HepG2 cells. 2-aminoethoxydiphenyl borate (2-APB), the proved efficient antagonist of SOCs, dose-dependently suppressed the ethanol (200nM)-increased [Ca(2+)](i) content and protected against ethanol-induced viability loss and transaminase leakage. Exposure to 200mM ethanol for 24h significantly upregulated the mRNA and protein expression of calcium release-activated calcium channel protein 1 (CRACM1, Orai1) and stromal interaction molecule 1 (STIM1), the two main molecular constituents of SOCs, which was sustained for at least 72h. In addition, small interfering RNA knockdown of STIM1 attenuated the ethanol-increased [Ca(2+)](i) content and hepatotoxicity. Taken together, these data indicate that the Ca(2+) channel of SOCE may be involved in the pathogenesis of ethanol-induced intracellular Ca(2+) elevation and consequent hepatocyte damage.

Objective To study the potential correlation between inhibited proteasome activity and occurrence and development of endoplasmic reticulum stress(ERS) in alcoholic liver disease(ALD).Methods HepG2 cells were treated with ethanol to establish an in vitro model of ALD,and then treated with betulinic acid or with both ethanol and betulinic acid.MRNA expression of glucose regulation protein 78(GRP78),an ERS marker,was detected.Also,proteasome activity and intracellular triglyceride(TG) content in different groups were detected.Results Ethanol inhibited activity of proteasome,with increases of GRP78 mRNA expression and intracellular TG content.Betulinic acid promoted proteasome activity with reductions of GRP78 mRNA level and TG content.Correlation analysis revealed a negative relativity between proteasome activity and expression of GRP78 mRNA,while the GRP78 mRNA level and intracellular TG content had positive relativity.Conclusion Ethanol can inhibit proteasome activity,thus inducing ERS,while betulinic acid can promote proteasome activity,thus reducing ERS.Proteasome activity and ERS have some negative relativity,and the latter aggravates the pathogenesis of ALD.

Objective: To interview the role of CGRP to hepatic microcirculation in acute liver injury induced by coneanavalin A(Con A). Methods: Sixty Kunming rats were divided into three groups randomly(n=20), acute liver injury was established by injection with 20 mg/kg Con A through the tail vein. A saline control group was established by injection with saline. In CGRP-administered group, CGRP was given to rats 30 min before Con A injected. Ten mice in each group were used to observe the average liver blood flow volume and concentration by laser-doppler flow-instrument, and the other ten rats were observed the hepatic microcirculation velocity in vivo by an inverted microscope. Liver damage was assessed by histological evaluation after the rat had been killed. Results: Compared to the injury group, the average liver blood flow volume and velocity were significantly increased in CGRP-administered group, meanwhile, the pathological injury was markedly alleviated, whereas the blood concentration was almost the same. Conclusion: CGRP can decrease the dysfunction of hepatic microcirculation by means of improving the tissue perfusion, and alleviate the pathological damage during acute liver injury.