督脉灸联合香砂养胃丸治疗脾虚泄泻的临床观察

目的观察督脉灸联合香砂养胃丸治疗脾虚泄泻的临床疗效。方法将2018年3月—2019年3月在东营市垦利县人民医院确诊为脾虚泄泻的90例患者,按照随机数字表法分为对照组和观察组各45例。对照组采用香砂养胃丸治疗,观察组采用香砂养胃丸联合督脉灸治疗。两组治疗1个疗程后观察并比较疗效以及治疗前后各项中医证候积分变化情况。结果治疗后观察组总有效率为88.89%,高于对照组的57.87%,观察组各项中医证候积分均降低且低于对照组,两组各项指标差异均具有统计学意义(P<0.05)。结论督脉灸联合香砂养胃丸治疗脾虚泄泻疗效显著,能够有效改善患者临床症状。     

Deferoxamine promotes recovery of traumatic spinal cord injury by inhibiting ferroptosis

Ferroptosis is an iron-dependent novel cell death pathway. Deferoxamine, a ferroptosis inhibitor, has been reported to promote spinal cord injury repair. It has yet to be clarified whether ferroptosis inhibition represents the mechanism of action of Deferoxamine on spinal cord injury recovery. A rat model of Deferoxamine at thoracic 10 segment was established using a modified Allen's method. Ninety 8-week-old female Wistar rats were used. Rats in the Deferoxamine group were intraperitoneally injected with 100 mg/kg Deferoxamine 30 minutes before injury. Simultaneously, the Sham and Deferoxamine groups served as controls. Drug administration was conducted for 7 consecutive days. The results were as follows:(1) Electron microscopy revealed shrunken mitochondria in the spinal cord injury group.(2) The Basso, Beattie and Bresnahan locomotor rating score showed that recovery of the hindlimb was remarkably better in the Deferoxamine group than in the spinal cord injury group.(3) The iron concentration was lower in the Deferoxamine group than in the spinal cord injury group after injury.(4) Western blot assay revealed that, compared with the spinal cord injury group, GPX4, xCT, and glutathione expression was markedly increased in the Deferoxamine group.(5) Real-time polymerase chain reaction revealed that, compared with the Deferoxamine group, mRNA levels of ferroptosis-related genes Acyl-CoA synthetase family member 2(ACSF2) and iron-responsive element-binding protein 2(IREB2) were up-regulated in the Deferoxamine group.(6) Deferoxamine increased survival of neurons and inhibited gliosis. These findings confirm that Deferoxamine can repair spinal cord injury by inhibiting ferroptosis. Targeting ferroptosis is therefore a promising therapeutic approach for spinal cord injury.     

热疗对肿瘤免疫微环境中免疫细胞及免疫相关细胞因子的影响

随着对肿瘤热疗和肿瘤免疫微环境(TIME)的深入研究,近年来热疗对TIME的作用越来越受到学者们的重视。本文就目前国内外研究进展,对热疗与TIME中几类主要免疫细胞和免疫相关细胞因子的影响及作用机制作一综述。全面而透彻的了解热疗对TIME的调控作用,有助于为肿瘤治疗提供新的思路和方法。     

产前超声诊断胎儿右房异构一例

本文报道产前超声诊断胎儿右房异构一例。孕妇孕24周产前超声检查发现胎儿左位心合并复杂心血管畸形(右心室双出口、房室间隔缺损、肺动脉发育不良、双侧上腔静脉、心下型完全型肺静脉异位引流)、胃泡位于腹腔右侧、中位肝、可疑无脾、腹主动脉与下腔静脉位于脊柱左侧、双侧支气管呈右侧支气管对称形态,综合考虑右房异构可能。引产后经尸体解剖证实脾脏发育不良、右房异构。右房异构常合并复杂心血管畸形,因此产前超声发现复杂心血管畸形时,应警惕右房异构的可能。右房异构病死率极高,产前诊断具有重要意义。     

Sodium butyrate prevents radiation-induced cognitive impairment by restoring pCREB/BDNF expression

Sodium butyrate is a histone deacetylase inhibitor that affects various types of brain damages. To investigate the effects of sodium butyrate on hippocampal dysfunction that occurs after whole-brain irradiation in animal models and the effect of sodium butyrate on radiation exposure-induced cognitive impairments,adult C57BL/6 mice were intraperitoneally treated with 0.6 g/kg sodium butyrate before exposure to 10 Gy cranial irradiation. Cognitive impairment in adult C57BL/6 mice was evaluated via an object recognition test 30 days after irradiation. We also detected the expression levels of neurogenic cell markers(doublecortin)and phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor. Radiation-exposed mice had decreased cognitive function and hippocampal doublecortin and phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor expression. Sodium butyrate pretreatment reversed these changes. These findings suggest that sodium butyrate can improve radiation-induced cognitive dysfunction through inhibiting the decrease in hippocampal phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor expression. The study procedures were approved by the Institutional Animal Care and Use Committee of Korea Institute of Radiological Medical Sciences(approval No. KIRAMS16-0002) on December 30, 2016.