8周基础军训对入伍新兵红细胞及其相关指标的影响

目的探讨8周基础军训(basic military training,BMT)对入伍新兵血像中红细胞及其相关指标的影响,为指导科学的军事训练提供参考。方法数据来自新疆边防部队2015年度入伍的50名男性新兵,分别在BMT前后测定并记录受试新兵的红细胞计数、血红蛋白浓度及血清铁蛋白等。结果经过8周的BMT,新兵血液中血红蛋白浓度、红细胞计数及血清铁蛋白均显著下降(P0.05,P0.01)。结论 8周BMT可能导致入伍新兵发生运动性贫血,铁缺乏可能是其主要原因。     

基于医院信息系统的乳腺癌临床特征及中西医用药特征分析

目的 解析真实世界中乳腺恶性肿瘤患者的人群特征、诊断特征、中西医用药特征，为乳腺癌的临床防治提供参考。方法 采集2002年2月至2015年5月全国60家三级甲等医 院信息系统（Hospital Information System，HIS）中，出院诊断为“乳腺癌”的患者用药信息，采用SAS9.3统计软件，对人口学信息、诊断信息、医嘱用药信息等进行描述性分析。结果 39798例乳腺癌患者，平均年龄（50.93者，平均年龄）岁；多以门诊入院，入院病情以“一般”为主;合并疾病主要为高血压，骨肿瘤，联用西药以抑制肿瘤细胞增殖、治疗并发症、缓解放化疗不良反应为主；中医辨证以痰瘀互结证，气阴两虚证，肝气淤滞证，脾气亏虚证型最为常见，临床清热解毒剂、益气扶正剂，活血化瘀剂应用较多。结论 乳腺癌中西医结合治疗，联用药物广泛，临床治疗基本符合临床指南。     

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。     

颈椎后路单开门微型钢板内固定术治疗颈椎管狭窄症

目的:探讨颈椎后路单开门微型钢板内固定术治疗颈椎管狭窄症的临床疗效和安全性。方法:2017年3月至2019年3月收治25例颈椎管狭窄症患者。男15例,女10例。年龄33~68岁,中位数45岁。C3~C5狭窄16例,C3~C6狭窄9例。发育型狭窄18例,退行性狭窄7例。病程1~7年,中位数4年。均采用颈椎后路单开门微型钢板内固定术治疗。测定患者的颈椎曲度和活动度,采用视觉模拟量表(visual analogue scale,VAS)和Oswestry功能障碍指数(Oswestry disability index,ODI)量表评价颈肩部疼痛情况,采用日本骨科学会(Japanese Orthopedic Association,JOA)脊髓型颈椎病评分量表(17分法)评价颈髓功能,采用Odom评级标准评价整体疗效,记录并发症发生情况。结果:所有患者均随访至术后12个月。与术前相比,术后3个月时患者的颈椎曲度和活动度均增大(5.25°±3.05°,8.02°±3.13°,t=3.169,P=0.003;38.48°±13.60°,56.12°±12.90°,t=4.705,P=0.000),颈肩部疼痛VAS评分和ODI均减小[(7.69±0.53)分,(3.14±0.21)分,t=39.906,P=0.000;(21.75±5.48)分,(10.13±2.12)分,t=9.888,P=0.000]。患者术前及术后3个月、6个月、12个月的JOA评分比较,总体差异有统计学意义[(8.22±1.51)分,(14.75±3.32)分,(16.53±3.52)分,(16.78±3.66)分,F=41.001,P=0.000];术后3个月、6个月、12个月的JOA评分均高于术前(P=0.000;P=0.000;P=0.000)。术后12个月时,按照Odom评级标准评定,优12例、良10例、一般2例、差1例;疗效评定为差的1例患者,经非手术治疗后病情控制。1例患者术后出现背部疼痛,服用非甾体抗炎止痛药后疼痛缓解;均未出现吞咽困难、脊髓损伤、内固定松动等并发症。结论:采用颈椎后路单开门微型钢板内固定术治疗颈椎管狭窄症,能有效改善患者的颈椎曲度和活动度、减轻颈肩部疼痛症状、改善颈髓功能,总体疗效较好,而且具有较高的安全性。     

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.     

HIFα Regulates Developmental Myelination Independent of Autocrine Wnt Signaling

The developing CNS is exposed to physiological hypoxia, under which hypoxia-inducible factor α (HIFα) is stabilized and plays a crucial role in regulating neural development. The cellular and molecular mechanisms of HIFα in developmental myelination remain incompletely understood. A previous concept proposes that HIFα regulates CNS developmental myelination by activating the autocrine Wnt/β-catenin signaling in oligodendrocyte progenitor cells (OPCs). Here, by analyzing a battery of genetic mice of both sexes, we presented in vivo evidence supporting an alternative understanding of oligodendroglial HIFα-regulated developmental myelination. At the cellular level, we found that HIFα was required for developmental myelination by transiently controlling upstream OPC differentiation but not downstream oligodendrocyte maturation and that HIFα dysregulation in OPCs but not oligodendrocytes disturbed normal developmental myelination. We demonstrated that HIFα played a minor, if any, role in regulating canonical Wnt signaling in the oligodendroglial lineage or in the CNS. At the molecular level, blocking autocrine Wnt signaling did not affect HIFα-regulated OPC differentiation and myelination. We further identified HIFα–Sox9 regulatory axis as an underlying molecular mechanism in HIFα-regulated OPC differentiation. Our findings support a concept shift in our mechanistic understanding of HIFα-regulated CNS myelination from the previous Wnt-dependent view to a Wnt-independent one and unveil a previously unappreciated HIFα–Sox9 pathway in regulating OPC differentiation.SIGNIFICANCE STATEMENT Promoting disturbed developmental myelination is a promising option in treating diffuse white matter injury, previously called periventricular leukomalacia, a major form of brain injury affecting premature infants. In the developing CNS, hypoxia-inducible factor α (HIFα) is a key regulator that adapts neural cells to physiological and pathologic hypoxic cues. The role and mechanism of HIFα in oligodendroglial myelination, which is severely disturbed in preterm infants affected with diffuse white matter injury, is incompletely understood. Our findings presented here represent a concept shift in our mechanistic understanding of HIFα-regulated developmental myelination and suggest the potential of intervening with an oligodendroglial HIFα-mediated signaling pathway to mitigate disturbed myelination in premature white matter injury.