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。     

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.     

Comparison Between Phenylephrine and Dopamine in Maintaining Cerebral Oxygen Saturation in Thoracic Surgery: A Randomized Controlled Trial

Fluid is usually restricted during thoracic surgery, and vasoactive agents are often administered to maintain blood pressure. One-lung ventilation (OLV) decreases arterial oxygenation; thus oxygen delivery to the brain can be decreased. In this study, we compared phenylephrine and dopamine with respect to maintaining cerebral oxygenation during OLV in major thoracic surgery.Sixty-three patients undergoing lobectomies were randomly assigned to the dopamine (D) or phenylephrine (P) group. The patients’ mean arterial pressure was maintained within 20% of baseline by a continuous infusion of dopamine or phenylephrine. Maintenance fluid was kept at 5 mL/kg/h. The depth of anesthesia was maintained with desflurane 1MAC and remifentanil infusion under bispectral index guidance. Regional cerebral oxygen saturation (rScO₂) and hemodynamic variables were recorded using near-infrared spectroscopy and esophageal cardiac Doppler.The rScO₂ was higher in the D group than the P group during OLV (OLV 60 min: 71 ± 6% vs 63 ± 12%; P = 0.03). The number of patients whose rScO₂ dropped more than 20% from baseline was 0 and 6 in the D and P groups, respectively (P = 0.02). The D group showed higher cardiac output, but lower mean arterial pressure than the P group (4.7 ± 1.0 vs 3.9 ± 1.2 L/min; 76.7 ± 8.1 vs 84.5 ± 7.5 mm Hg; P = 0.02, P = 0.02). Among the variables, age, hemoglobin concentration, and cardiac output were associated with rScO₂ by correlation analysis.Dopamine was superior to phenylephrine in maintaining cerebral oxygenation during OLV in thoracic surgery.     

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.     

关节镜下TightRope治疗后交叉韧带撕脱骨折

目的探讨关节镜下使用TightRope治疗后交叉韧带(PCL)撕脱骨折的技术应用和临床疗效。方法 12例膝关节PCL撕脱骨折患者在关节镜下使用TightRope固定PCL撕脱骨块。术后1周开始在支具保护下被动活动膝关节,术后10个月评估膝关节功能恢复情况。结果 12例患者均获随访,时间10～14个月,平均12.6个月,骨折均Ⅰ期愈合。1例屈膝受限15°,无伸膝受限;2例后抽屉试验(+)。Lysholm膝关节功能评分术前(45.6±6.3)分,术后10个月(87.8±4.8)分,差异有统计学意义(P 0.05)。结论关节镜下使用TightRope治疗PCL撕脱骨折固定可靠,操作相对简单,疗效满意。     

《金匮要略》痈脓辨治探讨

回顾《内经》相关理论，指出痈脓病机关键在于气血凝滞、经络阻塞、脏腑失和，可分期论治。总结《金匮要略》治疗痈脓的方法，认为痈脓应尽早治疗，防邪深入；并根据证情辨证使用清热解毒，活血消散；排除脓毒，泄浊于外等治法。对现代临床仍具实用价值。      

中性粒细胞与淋巴细胞比值对三阴性乳腺癌临床预后及与Ki - 67表达的影响

目的 探讨中性粒细胞与淋巴细胞比值（neutrophil to lymphocyte ratio，NLR）对三阴性乳腺癌的临床预后影响及与Ki - 67表达的关系。方法 回顾性分析2006年1月 - 2012年12月于我院乳腺外科住院治疗的134例三阴性乳腺癌患者。NLR最佳临床分界值采用ROC曲线确定，并依此分NLR＜2.64组和NLR≥2.64组。临床独立预后因素采用单因素和多因素Cox回归模型分析。术后生存时间和生存曲线比较采用Kaplan - Meier和log - rank方法。Ki - 67的表达采用免疫组织化学方法检测。结果 NLR是三阴性乳腺癌的独立预后因素，最佳临界值为2.64。NLR＜2.64组术后中位DFS为39.10月，中位OS为52.30月；NLR≥2.64组术后中位DFS为27.35月，中位OS为37.35月。2组术后DFS和OS比较，差异具有统计学意义（P＜0.05）。NLR低组伴Ki - 67表达阴性的三阴性患者术后中位DFS和OS生存时间显著高于其他情况。结论 NLR是三阴性乳腺癌的关键影响预后因素，具有重复性强、非侵袭性、方便实用等特性，可用于预测三阴性乳腺癌临床预后。     

互动式歌唱表演对轻中度阿尔茨海默病患者抑郁、精神行为和运动训练参与率的影响

目的 观察互动式歌唱表演对轻中度阿尔茨海默病（AD）患者抑郁、精神行为症状及运动训练参与率的影响。方法 选取符合入组条件≥60周岁AD患者63例，随机分为研究组（31例）和对照组（32例）。所有受试患者常规药物治疗及常规运动训练，对照组接受被动性音乐治疗，研究组接受以互动歌唱为主的主动性音乐治疗，1次/d，每次1小时，每周训练5天，持续干预6个月。于治疗前、治疗1个月后、治疗3个月后、治疗6个月后分别采用康奈尔痴呆抑郁量表（CSDD）评分、阿尔茨海默病病理行为（BEHAVE AD）评分、参与率进行评估。结果 治疗1个月、3个月后，研究组CSDD评分较治疗前均降低（P<0.05）；治疗6个月后，研究组患者CSDD评分较治疗前、治疗1个月、3个月后均显著降低（P<0.05），且与对照组比较差异有统计学意义（P<0.05）。治疗1个月、3个月后，研究组BEHAVE AD评分较治疗前均降低（P<0.05）；治疗6个月后，研究组患者BEHAVE AD评分较治疗前、治疗1个月、3个月后均显著降低（P<0.05），且与对照组比较差异有统计学意义（P<0.05）。治疗6个月后，两组运动训练参与率组间比较差异有统计学意义（P<0.05）。结论 互动式歌唱表演可能对改善轻中度AD患者的抑郁和精神行为症状有着积极的疗效，同时对提高受试者运动训练的参与率可能有着更积极的疗效。