膀胱粘膜下层无细胞基质的研制

目的 探讨膀胱粘膜下层无细胞基质的制作与评价。方法 自膀胱解剖出膀胱粘膜下层，置于PBS、0．5％SDS、双蒸水中反复洗涤去除细胞，必要时加用胰蛋白酶消化。获得的细胞外基质采用HE、免疫组化、扫描电镜评价去细胞效果，细胞植入无细胞基质观察细胞能否粘附于该材料。结果 HE、免疫组化、扫描电镜均未见制备的材料中存在细胞及细胞碎片，体外细胞植入试验见细胞可粘附于材料并增殖。结论 采用本制备方法可以得到膀胱粘膜下层无细胞基质，有望为临床提供尿道下裂生物替代材料。     

Functional localization of epileptic foci in cats using manganeseenhanced MRI

Objective： To determine the encephalic region correlated with epilepsy by manganese-enhanced MRI （MEMRI） and determine the correlation of epilepsy with calcium overloading. Methods： The cats were divided into two groups. The first group underwent EEG examination and ethological observation. The second group underwent MEMRI measurement. Signal enhanced encephalic regions were sectioned. Results： The achievement ratio of convulsive cats intramusclelarly injected with PTZ was 80%. MEMRI showed diffuse signal enhancement in the cerebral cortex of the cats with generalized tonic-clonic convulsive seizures compared with control animals. The enhancement rate of frontal-parietal-occipital lobe was 34.6% and 22.9% in temporl lobe compared with the control groups. Signal enhancement on frontal-parietal lobe persisted for 24 h after epileptic seizures were induced. The neurons of enhanced encephalic regions showed obvious degeneration and necrosis. Conclusion： Seizures can be induced in cats by intramuscular injection of PTZ （55 mg/kg）. Frontal-parietal lobe is the correlated encephalic regions of epilepsy. MEMRI plays an important role in localizing and revealing pathogenesis of epileptic seizures.     

舌下含服米索前列醇配伍米非司酮在终止早孕中的应用

目的 :探讨舌下含服米索前列醇配伍米非司酮用于早孕流产的可行性、安全性及有效性。方法 :将孕周在 7wk内的孕妇随机分为舌下组、口服组各 12 0例。 2组均经米非司酮预治疗后 ,舌下组含服米索前列醇 2 0 0 μg ,1h后重复 ,总量不超过6 0 0 μg ;口服组单次口服米索前列醇 6 0 0 μg。 结果 :舌下组完全流产率比口服组高 ,清宫率比口服组低 (P均 <0 0 1) ,引 -流时间缩短 (P <0 0 1) ,阴道流血及药物不良反应两者无明显差异。结论 :舌下组终止早孕具有简便、有效 ,引 -流时间短等优点     

Selenium substituted axitinib reduces axitinib side effects and maintains its anti-renal tumor activity

Axitinib is a potent vascular endothelial growth factor receptor (VEGFR) inhibitor, which has a strong inhibitory effect on the three isoforms of VEGFR 1–3. Having strong therapeutic efficacy, its broad use is limited by its side effects such as hypertension, proteinuria, cardiovascular damage, and liver and kidney dysfunction. Selenium compounds are broadly reported to have a good protective effect on cardiovascular disease, inflammation, infection, and immune function. In this study, a selenium substitute of axitinib was synthesized, and its anti-renal cell carcinoma activity and side effects were investigated. The results of the study indicated that Se-axitinib had potent antitumor activity on renal cell carcinoma (RCC), alleviated vascular hyperpermeability, and also alleviated axitinib-related side effects including hypertension, liver dysfunction and kidney dysfunction significantly. Therefore, we suggest that Se-axitinib could be a solution to the severe side effects of VEGFR inhibitors and provide evidence to improve the outcome of RCC treatment.

Se-axitinib is a selenium substitution of sulfur in axitinib, which reduced the side effect of VEGFR inhibitors and maintained the potent anticancer activity of the original drug.     

PXR activation impairs hepatic glucose metabolism partly via inhibiting the HNF4α–GLUT2 pathway

Drug-induced hyperglycemia/diabetes is a global issue. Some drugs induce hyperglycemia by activating the pregnane X receptor (PXR), but the mechanism is unclear. Here, we report that PXR activation induces hyperglycemia by impairing hepatic glucose metabolism due to inhibition of the hepatocyte nuclear factor 4-alpha (HNF4α)‒glucose transporter 2 (GLUT2) pathway. The PXR agonists atorvastatin and rifampicin significantly downregulated GLUT2 and HNF4α expression, and impaired glucose uptake and utilization in HepG2 cells. Overexpression of PXR downregulated GLUT2 and HNF4α expression, while silencing PXR upregulated HNF4α and GLUT2 expression. Silencing HNF4α decreased GLUT2 expression, while overexpressing HNF4α increased GLUT2 expression and glucose uptake. Silencing PXR or overexpressing HNF4α reversed the atorvastatin-induced decrease in GLUT2 expression and glucose uptake. In human primary hepatocytes, atorvastatin downregulated GLUT2 and HNF4α mRNA expression, which could be attenuated by silencing PXR. Silencing HNF4α downregulated GLUT2 mRNA expression. These findings were reproduced with mouse primary hepatocytes. Hnf4α plasmid increased Slc2a2 promoter activity. Hnf4α silencing or pregnenolone-16α-carbonitrile (PCN) suppressed the Slc2a2 promoter activity by decreasing HNF4α recruitment to the Slc2a2 promoter. Liver-specific Hnf4α deletion and PCN impaired glucose tolerance and hepatic glucose uptake, and decreased the expression of hepatic HNF4α and GLUT2. In conclusion, PXR activation impaired hepatic glucose metabolism partly by inhibiting the HNF4α‒GLUT2 pathway. These results highlight the molecular mechanisms by which PXR activators induce hyperglycemia/diabetes.Key words: Pregnane X receptor, Hepatocyte nuclear factor 4-alpha, Glucose transporter 2, Hepatic glucose uptake, Diabetes, Drug-induced hyperglycemia     

Gastroduodenal intussusception caused by gastric gastrointestinal stromal tumor in adults: a case report and literature review

Intussusception mostly occurs in childhood and is rare in adults. Although intussusception can occur in any part of the gastrointestinal tract, gastroduodenal intussusception caused by a gastric tumor is relatively uncommon in clinical practice. A PubMed search identified 24 published cases of gastroduodenal intussusception caused by gastric gastrointestinal stromal tumor (GIST); however, it is possible that we missed other cases not included in PubMed. Here we report a case of gastroduodenal intussusception caused by gastric GIST in an 85-year-old man. He came to the hospital because of recurrent black stools. Plain computed tomography (CT) scan indicated a mass in the gastric antrum, with slight enhancement in the arterial phase on enhanced CT scan. He was diagnosed with GIST. In addition, images indicated that the mass overlapped into the duodenum, and gastroduodenal intussusception was thus considered. Gastroscopy showed a huge mass in the gastric body. According to the gastroscopy and CT results, gastroduodenal intussusception caused by a gastric tumor was considered. The patient underwent complete surgical removal, which revealed a mass originating from the gastric antrum and overlapping into the duodenum. The postoperative pathological diagnosis was intermediate-risk gastric GIST. The patient was followed up for 4 months without tumor recurrence.     

男男性行为者艾滋病暴露前预防用药性行为去抑制化情况

目的：了解男男性行为者（men who have sex with men,MSM）在参加暴露前预防用药（pre-exposure prophylaxis,PrEP）临床试验中是否存在性行为去抑制化现象及其影响因素。方法：采用非概率抽样法招募并筛选出108名MSM,随机分为77名服用药物组和31名空白对照组,第12、24、36、48周进行临床随访和问卷调查,问卷调查主要包括社会人口学特征,艾滋病相关知识、态度和行为等相关情况。采用单因素和多因素的广义估计方程分析MSM在参与PrEP中是否存在性行为去抑制化现象及其影响因素。结果：药物服用组MSM在参与PrEP的第12、24、36、48周的性伴个数中位数分别为1（0,6）、1（0,6）、1（0,10）、1（0,3）、1（0,3）,高危性行为次数中位数分别为1（0,26）、1.5（0,8）、1（0,12）、1（0,9）、2（0,30）;空白对照组性伴个数中位数分别为1（0,21）、1（0,2）、1（0,3）、1（0,3）、1（0,3）,高危性行为次数中位数分别为1（0,9）、1（0,6）、0.5（0,15）、0（0,10）、1（0,10）;多因素广义估计方程分析发现MSM在参与PrEP过程中性伴个数及高危性行为次数均没有发生改变（Z=-0.24,P=0.811;Z=0.93,P=0.355）,性行为方式为“1”和“0.5”的较性行为方式为“0”的拥有更多的性伴（Z=2.47,P=0.014;Z=2.24,P=0.025）;发生过商业性行为的MSM较没有发生过的拥有较少的性伴和高危性行为（Z=-2.82,P=0.005;Z=-2.28,P=0.023）;已婚较离异MSM发生较少的高危性行为次数（Z=-2.34,P=0.019）。结论：本研究中暂未发现PrEP中存在性行为去抑制化现象,性行为方式为“1”和“0.5”的MSM拥有较多性伴,是后期随访中的重点管理人群。还需进一步加强对艾滋病相关知识的科普。     

儿童屈光不正与立体视觉

目的探讨儿童屈光不正对立体视觉的影响。方法采用颜少明等《立体视觉检查图》对60例正常儿童及115例矫正视力正常的屈光不正患儿进行立体视阈值检查并进行统计学处理。结果远视眼立体视阈值明显高于正常组及近视眼组（P＜0．005），且随屈光度增高而增高，随发生年龄增高而降低，近视眼组与正常组之间无差异（P＞0．05）。近视眼之间戴眼镜前后立体视阈值无显著性，而远视眼戴镜后立体视阈值明显下降（P＜0．005）。结论屈光不正对立体视功能影响是由于视力下降引起。提示及早发现屈光不正，及时预防、矫正屈光不正性弱视，对保证立体视功能的正常发育具有重要意义     

麻痹性斜视183例临床分析

目的:探讨近年来麻痹性斜视的病因、麻痹肌分布和对视功能的影响。方法:对我院2009-03/2012-03住院行斜视矫正术的183例麻痹性斜视患者的病历资料进行回顾性研究。结果:先天性麻痹性斜视占80.87%,后天性麻痹性斜视占19.13%;原因不明者最多(77.60%),其次为外伤(14.21%)。垂直斜视中上斜肌麻痹占81.19%,下直肌麻痹占8.26%,上直肌麻痹占6.88%,下斜肌麻痹占2.29%,双上转肌麻痹占0.92%,双下转肌麻痹占0.46%。水平斜视中外直肌麻痹占54.17%,内直肌麻痹占45.83%。166例患者术前进行同视机检查,有双眼视功能患者占28.92%。结论:麻痹性斜视病因复杂,眼外肌中上斜肌最常累及,对双眼视功能有明显的影响,应尽早进行手术治疗。