双眼外直肌后徙术与常规疗法治疗斜视临床疗效比较

目的:比较双眼外直肌后徙术与常规疗法治疗斜视的临床疗效。方法:选取2016年6月-2017年6月笔者医院收治的128例斜视患者,按治疗方式不同分成对照组和研究组,每组各64例。其中对照组患者行常规单眼外直肌后徙联合内直肌缩短术(R&R),研究组患者行双眼外直肌后徙术(BLR-rec)。术后对患者随访1年,观察术后眼位正位率、欠矫率、过矫率,视觉功能恢复情况以及并发症发生率。结果:研究组患者正位率为89.06%高于对照组的68.75%,差异有统计学意义(P<0.05)。术前,对照组和研究组患者视近度、视远度和平均斜视度比较,两组患者融合功能和立体视功能占比比较,差异均无统计学意义(P>0.05)。术后,两组患者的斜视度较治疗前均出现了明显下降(P<0.05),且研究组治疗后斜视度下降幅度明显大于对照组(P<0.05);两组患者视觉功能恢复率均明显增加(P<0.05),且研究组恢复率明显大于对照组(P<0.05)。研究组并发症发生率明显低于对照组(P<0.05)。结论:双眼外直肌后徙术较单眼外直肌后徙联合内直肌缩短术有更好地临床效果,且安全性更高,值得临床推广。     

“龙虎交战”针法针刺八脉交会穴对偏头痛患者头痛天数及血清CGRP表达的影响＊

目的 观察“龙虎交战”针法针刺八脉交会穴对无先兆偏头痛（Migraine without aura，MO）患者头痛天数及外周血降钙素基因相关肽（Calcitonin gene related peptide，CGRP）表达水平的影响。方法 按照头痛程度将90例MO受试者区层随机分为治疗Ⅰ组、治疗Ⅱ组和对照组各30例。治疗Ⅰ组施以“龙虎交战”针法针刺八脉交会穴（外关和足临泣），治疗Ⅱ组施以平补平泻针法针刺八脉交会穴（外关和足临泣），对照组施以平补平泻针法针刺非经非穴点，每次留针30分钟，5次/周，共治疗20次。于治疗前、治疗结束4周后的随访分别记录三组患者头痛天数的变化情况以判定疗效，并采集患者治疗前、治疗结束4周后随访的肘部静脉血用ELISA法检测血清中的CGRP含量的变化。结果 ①各组治疗前患者的头痛天数无显著差异（Ｐ > 0.05），治疗Ⅰ组、治疗Ⅱ组和对照组治疗结束4周后随访的头痛天数较治疗前均显著降低（Ｐ < 0.05）；治疗Ⅰ组头痛天数的降低显著优于治疗Ⅱ组和对照组（Ｐ < 0.001），治疗Ⅱ组头痛天数的降低显著优于对照组（Ｐ < 0.05）；②3组治疗前CGRP的表达无显著差异，治疗Ⅰ组、治疗Ⅱ组治疗结束4周后随访CGRP的表达较治疗前均显著下降（Ｐ < 0.001），对照组治疗结束4周后随访CGRP的表达较治疗前差异无显著性（Ｐ > 0.05）；治疗Ⅰ组CGRP治疗结束4周随访的表达较治疗Ⅱ组和对照组均显著下降（Ｐ < 0.01），治疗Ⅱ组CGRP的表达较对照组显著下降（P < 0.01）。结论 ①八脉交会穴施以“龙虎交战”针法针刺能明显改善MO患者的头痛天数，同时降低MO患者血清CGRP的表达水平，这可能是针刺八脉交会穴治疗MO的机制之一；②非经非穴点的针刺效应无持续性，而八脉交会穴的针刺效应具有持续性；③八脉交会穴可以充分发挥复式针刺手法的治疗效应，提示我们在临床上治疗疾病时不仅要注意腧穴配伍，恰当的针刺手法更是提高临床疗效、事半功倍的关键。     

自血穴位注射疗法联合马来酸茚达特罗治疗老年稳定期慢性阻塞性肺疾病的临床分析

目的探讨自血穴位注射疗法联合马来酸茚达特罗治疗老年稳定期慢性阻塞性肺疾病(COPD)的临床疗效及其对患者炎性因子、免疫功能及肺功能的影响。 方法将2015年5月至2016年5月我院收治的86例老年缓解期COPD患者分为观察组与对照组。对照组给予马来酸茚达特罗治疗，观察组在对照组治疗基础上另给予自血穴位注射疗法。治疗12周后，评价2组临床疗效。治疗前及治疗12周后，分别检测2组患者肺功能指标(FEV₁、FVC与PEF)，炎性因子(IL-8、α1-AT、IL-6及TNF-α)，免疫功能指标(IgG、IgA、CD3^＋及CD4^＋)水平。治疗期间，对2组患者的不良反应进行密切观察。 结果治疗后二组患者各项检测指标均优于治疗前。治疗12周后，观察组总有效率为90.7%，明显高于对照组的72.1%(P<0.05)。治疗12周后，观察组FEV₁、FVC与PEF等肺功能指标，IgG、IgA、CD3^＋及CD4^＋等免疫功能指标水平均明显高于对照组(P<0.05)，而IL-8、α1-AT、IL-6及TNF-α含量分别为(23.23±3.87)ng/L、(3.43±0.41)g/L、(52.25±5.38)ng/L及(43.12±3.98)ng/L，改善程度均明显优于对照组(P<0.05)。治疗期间，2组患者均未出现严重不良反应。 结论自血穴位注射疗法联合马来酸茚达特罗治疗老年稳定期COPD疗效确切，可有效改善患者炎症水平，值得进行深入研究。     

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.     

郑州市三甲医院急诊科护士道德困境与职业倦怠的现状及相关性研究

目的 调查郑州市三甲医院急诊科护士的道德困境与职业倦怠的现状,并分析两者之间的相关性。方法 采用便利抽样法选取郑州市5所三甲医院的228名急诊科护士作为研究对象,采用一般资料调查表、中文版护士道德困境量表、护士职业倦怠量表对其进行问卷调查。结果 郑州市三甲医院急诊科护士道德困境总分为(49.41±13.35)分,职业倦怠总分为(63.51±17.25)分。单因素分析显示,不同学历、工作年限的急诊护士的道德困境得分比较,差异均有统计学意义(F=4.830,P=0.015; F=6.302,P=0.001);不同年龄急诊护士的职业倦怠得分比较,差异有统计学意义 (F=8.328,P=0.005),急诊科护士道德困境与职业倦怠呈正关性(r=0.412,P<0.05)。结论 郑州市三甲医院急诊科护士的道德困境与职业倦怠普遍存在,护士的道德困境与职业倦怠呈正相关。     

Necroptotic TNFα-Syndecan 4-TNFα Vicious Cycle as a Therapeutic Target for Preventing Temporomandibular Joint Osteoarthritis

Temporomandibular joint osteoarthritis (TMJOA) is a chronic degenerative disease for which the underlying mechanism still remains unclear. Compared with apoptosis and autophagy, necroptosis causes greater harm to tissue homeostasis by releasing damage-associated molecular patterns (DAMPs). However, the role of necroptosis and downstream key DAMPs in TMJOA is unknown. Here, rodent models of TMJOA were established by the unilateral anterior crossbite (UAC). Transmission electron microscopy (TEM) and immunohistochemistry of receptor interacting protein kinase 3 (RIPK3)/phosphorylation of mixed lineage kinase domain-like protein (pMLKL) were conducted to evaluate the occurrence of necroptosis in vivo. The therapeutic effects of blocking necroptosis were achieved by intra-articularly injecting RIPK3 or MLKL inhibitors and using RIPK3 or MLKL knockout mice. In vitro necroptosis of condylar chondrocyte was induced by combination of tumor necrosis factor alpha (TNFα), second mitochondria-derived activator of caspases (SMAC) mimetics and carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]- fluoromethylketone (z-VAD-fmk). The possible DAMPs released by necroptotic chondrocytes were screened by quantitative proteomics and blocked by specific antibody. Translucent cytosol, swollen organelles, and ruptured cell membranes, features of necroptosis, were frequently manifested in chondrocytes at the early stage of condylar cartilage degeneration in TMJOA, which was accompanied by upregulation of RIPK3/pMLKL. Inhibiting or knocking out RIPK3/MLKL significantly prevented cartilage degeneration. DAMPs released by necroptotic condylar chondrocytes, such as syndecan 4 (SDC4) and heat shock protein 90 (HSP90), were verified. Furthermore, blocking the function of SDC4 significantly attenuated the expression of TNFα in cartilage and synovium, and accordingly increased cartilage thickness and reduced synovial inflammation. Thus, the necroptotic vicious cycle of TNFα-SDC4-TNFα contributes to cartilage degeneration and synovitis, and can serve as a potential therapeutic target for treating TMJOA. © 2022 American Society for Bone and Mineral Research (ASBMR).     

Growth Hormone Induces Recurrence of Infantile Hemangiomas After Apparent Involution: Evidence of Growth Hormone Receptors in Infantile Hemangioma

Infantile hemangiomas (IHs) are the most common benign tumor of infancy, characterized by a natural history of early proliferation in the first months of life to eventual involution during childhood, often with residual fibrofatty tissue. Once involution has been achieved, IHs do not typically recur. We present two cases of exogenous growth hormone therapy resulting in the recurrence of IHs in late childhood, supported by radiological, immunohistochemical, in vitro, and in vivo evidence.