Effective melatonin protection of burn-induced hepatic disorders in rats

We studied the effect of melatonin on morphological and functional disorders using serum markers of liver dysfunction such as cholinesterase and gamma glutamyl transpeptidase, hepatic protein content and malondialdehyde in a burned-rat model. Melatonin (10 mg/kg (?1), i.p) was administered immediately and then 12 h after 30% of total body surface area burns of male Wistar rats. The burns induced an increase of hepatic malondialdehyde levels by 166% (p<0.001), and also vascular congestion, leukocyte infiltration around the central veins, intracellular vacuolization, hepatic cell degeneration and apoptotic bodies (Councilman’s bodies). These changes were associated with significantly reduced serum cholinesterase (36%), gamma glutamyl transpeptidase (76%), hepatic proteins (52%) and serum albumin (37%) (p<0.001–0.0001). Treatment with melatonin reduced elevated hepatic malondialdehyde values by 50% (p<0.01). Melatonin restricted degenerative alteration in the hepatocytes: it protected the burninduced decrease of serum gamma glutamyl transpeptidase activity by 48% (p<0.01), hepatic proteins by 64% (p<0.01), and serum activity of cholinesterase as the only marker of liver damaged synthetic function by 57% (p<0.0001) but did not exert any significant influence on serum albumin concentration. Melatonin repaired the pathomorphological lesions and functional disorders. It could restore liver damage following thermal injury in humans.     

Molecular mechanisms associating oxidative stress with endothelial dysfunction in the development of various vascular complications in diabetes mellitus

Endothelial dysfunction plays a key role in the pathogenesis of microangiopathy and macroangiopathy in type 2 diabetes mellitus. The endothelial dysfunction is induced by some cell metabolism disorders which are implicated in the pathogenesis of micro- and macroangiopathies through the principal mediation of oxidative stress. The discussion focuses preferentially on the recently found molecular mechanisms of free radical generation and on the endothelial disorders resulting from some free-radical-induced abnormalities in the intracellular signal pathways. We specify the molecular targets in the vascular complication therapy of diabetes on the basis of evidence of association between oxidative stress, metabolic abnormalities and endothelial dysfunction.     

Reverse actin sliding triggers strong myosin binding that moves tropomyosin

Actin/myosin interactions in vertebrate striated muscles are believed to be regulated by the “steric blocking” mechanism whereby the binding of calcium to the troponin complex allows tropomyosin (TM) to change position on actin, acting as a molecular switch that blocks or allows myosin heads to interact with actin. Movement of TM during activation is initiated by interaction of Ca²⁺ with troponin, then completed by further displacement by strong binding cross-bridges. We report x-ray evidence that TM in insect flight muscle (IFM) moves in a manner consistent with the steric blocking mechanism. We find that both isometric contraction, at high [Ca²⁺], and stretch activation, at lower [Ca²⁺], develop similarly high x-ray intensities on the IFM fourth actin layer line because of TM movement, coinciding with x-ray signals of strong-binding cross-bridge attachment to helically favored “actin target zones.” Vanadate (Vi), a phosphate analog that inhibits active cross-bridge cycling, abolishes all active force in IFM, allowing high [Ca²⁺] to elicit initial TM movement without cross-bridge attachment or other changes from relaxed structure. However, when stretched in high [Ca²⁺], Vi-“paralyzed” fibers produce force substantially above passive response at pCa ~ 9, concurrent with full conversion from resting to active x-ray pattern, including x-ray signals of cross-bridge strong-binding and TM movement. This argues that myosin heads can be recruited as strong-binding “brakes” by backward-sliding, calcium-activated thin filaments, and are as effective in moving TM as actively force-producing cross-bridges. Such recruitment of myosin as brakes may be the major mechanism resisting extension during lengthening contractions.     

居住环境因素对出生缺陷影响的Meta分析

目的 探讨居住地附近存在污染源、孕期居室装修、室内饲养宠物这三种居住环境因素与出生缺陷的关系。方法 在线检索知网、万方和维普数据库,系统收集1977年1月1日—2018年7月30日间公开发表的关于中国出生缺陷影响因素的流行病学相关研究,根据严格的纳入排除标准筛选,对纳入的文献进行异质性检验和效应值合并,并对结果进行敏感性分析、发表偏倚检验及校正。结果 最终纳入21篇文献,采用随机效应模型计算居住地附近存在污染源、孕期居室装修、室内饲养宠物因素危险性的合并OR值分别为2.474(1.659~3.688)、2.149(1.807~555)、2.721(2.006~3.693)(校正后)。结论 居住地附近存在污染源、孕期居室装修、室内饲养宠物这三种居住环境因素会增加出生缺陷发生的风险。     

~（131）I内照射治疗对甲状腺功能亢进症患者血液成分的影响

目的探讨放射性131I治疗甲状腺功能亢进症（甲亢）时,辐射对患者血液成分的影响。方法利用全自动血液分析仪,对20例健康人、128例甲亢患者131I治疗前、治疗后7天及3个月血液成分进行检测并分析研究。结果131I治疗后7天血红蛋白测定、血小板计数显著降低（t=-40.177,t=-4.363,P〈0.01）;白细胞计数升高（t=4.281,P〈0.01）,其中粒细胞明显升高（t=10.114,P〈0.01）;淋巴细胞显著降低（t=6.667,P〈0.01）,其余检测项目与对照组比较均无明显差异;治疗后3个月患者血液成分所有检测项目与对照组比较均无明显差异。结论利用131I治疗甲亢时,辐射对患者血象有一过性轻微影响,随时间推移,血象各项指标均可恢复正常。     

利妥昔单抗联合CHOP方案治疗原发性乳腺非霍奇金淋巴瘤1例并文献复习

目的:提高临床医生对原发性乳腺非霍奇金淋巴瘤的认识,以期对本病有全面的认识,采取合适的治疗方法,提高患者的生存率。方法:报道1例乳腺非霍奇金淋巴瘤,观察R-CHOP方案疗效,并结合文献复习。结果:R-CHOP对该患者效果不理想。结论:乳腺非霍奇金淋巴瘤罕见,确诊依赖于病理活检及免疫组织化学。本病的治疗方案尚未统一,干细胞支持下的大剂量化疗可能是首选方案。     

Fragile X syndrome: clinical,cytogenetic and molecular screening among autism spectrum disorder children in Indonesia

Fragile X testing is a priority in the evaluation of autism spectrum disorders (ASD) cases because identification of the FMR1 mutation leads to new treatment options. This study is focused on determining the prevalence of the FMR1 gene mutation among ASD cases in Indonesia. DSM‐IV‐TR criteria were administered to diagnose ASD; symptom severity was classified using the Childhood Autism Rating Scale. Cytogenetic analysis, polymerase chain reaction, and Southern blot for FMR1 gene analysis were carried out to confirm the diagnosis of fragile X syndrome. The fragile X site and FMR1 full mutation allele were identified in 3 out of 65 (4.6%) and 4 out of 65 (6.15%) children aged 3–17 years (57 boys and 8 girls), respectively. The Fragile X laboratory workup is essential in the evaluation of patients with ASD. Molecular analysis is most accurate, while cytogenetic documentation of the fragile X site can also be useful if molecular testing is not available.     

32P玻璃微球血管栓塞内照射加局部灌注抗癌药对肺癌的治疗作用

目的: 探讨32P玻璃微球(phosphorus-32 glass microspheres,32P-GMS)经支气管动脉栓塞内照射治疗支气管肺癌的有效性和安全性. 方法: 经病理确诊的24例支气管肺癌患者均接受2个周期的全身化疗. 非小细胞肺癌(NSCLC)采用CAP方案化疗;小细胞肺癌(SCLC)采用EP方案化疗. 4 wk为一周期. 所有患者均于第8周后复查胸部CT,在证实其病灶变化不明显后行支气管动脉局部灌注化疗并以32P-GMS与超液化碘油的混悬液进行栓塞. 于第12周观察治疗前后胸部CT影像学改变、临床症状、副作用及介入并发症等发生率. 结果: 32P-GMS支气管动脉超选择性介入栓塞内照射术治疗肺癌疗效显著,完全缓解(CR) 5例(21%),部分缓解(PR) 15例(62%),稳定(SD) 3例(12%),进展(PD) 1例(4%),有效率(CR PR) 83%;除1例出现一过性脊髓缺血,经积极治疗后好转外,未见其他并发症. 结论: 全身化疗后序贯32P-GMS肿瘤血管支栓塞内照射加局部灌注化疗治疗支气管肺癌有较高的近期缓解率,患者耐受良好,是治疗肺癌安全、有效的方法之一.     

河北省保定市社区2型糖尿病糖化血红蛋白控制率的调查

目的 了解保定市社区2型糖尿病糖化血红蛋白(HbA1c)达标率及影响因素.方法 随机整群抽取保定市3个社区,应用横断面研究方法调查45岁以上居民中已经确诊的2型糖尿病患者HbA1c控制情况.结果 社区内糖尿病HbA1c达标者87例,占18.6％.经过百分率的趋势性检验,糖尿病并发大血管和微血管病变与HbA1c水平呈正趋势,随着HbA1c升高,大血管病变患病率和微血管病变患病率均增加(均P＜0.05).Logistic回归分析显示,治疗措施和对防治知识的了解程度是影响达标的主要因素.结论 社区糖尿病HbA1c控制达标率低,理解并接受胰岛素治疗可能是降低HbA1c的主要方式之一.