不同高压氧治疗时机与预防一氧化碳中毒迟发性脑病相关性分析

目的:探讨不同高压氧治疗时机与预防急性一氧化碳中毒迟发性脑病的关系.方法:132例急性一氧化碳中毒患者依据高压氧治疗时机分为2组,在通风、吸氧、内给氧、胞二磷胆碱应用等常规治疗基础上,治疗组66例于一氧化碳中毒12 h内行高压氧治疗,对照组66例于一氧化碳中毒12 h后行高压氧治疗,观察2纽迟发性脑病发生率.结果:治疗组迟发牲脑病发生率(3.0%)低于对照组(21.2%)(P<0.05).结论:早期行高压氧治疗急性一氧化碳中毒,可有效降低迟发性脑病发生率.     

高压氧治疗与一氧化碳中毒迟发性脑病的关系

目的探讨高压氧治疗的次数与急性一氧化碳中毒迟发性脑病的发生机率。方法对246例中重度急性一氧化碳中毒患者行常规药物加高压氧治疗，观察分析其疗效及随访结果。结果所有患者均在治疗3天后症状明显改善，1周后临床痊愈。但随访3个月发现，中度中毒患者182例行高压氧治疗5—10次，无一例发生迟发性脑病；64例重度中毒患者中，34例行高压氧治疗10次后，有9例于发病的第13天～25天发生迟发性脑病；其余30例行20次高压氧治疗，无迟发性脑病的发生。结论对中度急性一氧化碳中毒患者常规药物加高压氧治疗5—10次，基本避免迟发性脑病的发生；对重度患者行20次高压氧治疗有可能预防迟发性脑病的发生。     

地塞米松联合肠溶阿司匹林预防一氧化碳中毒迟发脑病疗效观察

目的 观察地塞米松联合肠溶阿司匹林预防中重度一氧化碳中毒迟发脑病的临床疗效.方法 将100例中重度一氧化碳中毒患者随机分为治疗组(对照组治疗基础上加用地塞米松联合肠溶阿司匹林)和对照组(常规高压氧、防治脑水肿、脑保护治疗),观察患者一氧化碳中毒后第5天、10天、20天、30天、45天、60天.判断是否出现一氧化碳中毒迟发性脑病.结果 治疗组50例,出现迟发脑病4例,占8%;对照组50例,出现迟发脑病12例,占24%.两组比较差异有统计学意义(P<0.05).结论 地塞米松联合肠溶阿司匹林治疗中重度一氧化碳中毒,使其迟发脑病发生率较对照组明显降低,取得显著预防效应.     

急性一氧化碳中毒致迟发性脑病的临床相关因素及CT研究

目的研究急性一氧化碳中毒致迟发性脑病的临床相关因素及CT特征,探讨年龄、急性期昏迷时间、中毒程度及高压氧治疗时间等临床相关因素与迟发性脑病发生的关系,了解CT在急性一氧化碳中毒后病情判定、预测迟发性脑病发生中的应用价值。方法对154例急性一氧化碳中毒患者进行临床观察,并行CT检查,随诊2个月。结果急性一氧化碳中毒后迟发性脑病发生与年龄、昏迷时间长短、中毒后高压氧治疗时间有密切关系;迟发性脑病组患者的CT异常率高于无迟发性脑病组患者,且CT异常率与中毒程度呈平行关系。结论急性一氧化碳中毒后通过分析观察患者的临床相关因素、CT表现对预测迟发性脑病的发生有重要的参考价值。     

高压氧联合地塞米松治疗一氧化碳中毒后迟发性脑病疗效观察

目的:探讨高压氧联合地塞米松治疗一氧化碳中毒后迟发性脑病的疗效及对认知功能的影响.方法:选取2017年9月至2019年9月收治的46例一氧化碳中毒后迟发性脑病患者,采用随机数字表法分为对照组和观察组,各23例.对照组给予高压氧治疗,观察组给予地塞米松联合高压氧治疗.比较两组临床疗效,治疗前后认知功能、血清肌酸激酶(CK...     

金纳多、奥拉西坦联合高压氧治疗急性一氧化碳中毒迟发性脑病的疗效观察

目的 观察金纳多、奥拉西坦联合高压氧治疗一氧化碳中毒后迟发性脑病的临床疗效.方法 将32例一氧化碳中毒后迟发性脑病患者随机分为治疗组及对照组,每组16例.治疗组在高压氧等常规治疗基础上加用金纳多70 mg/次,1次/d,奥拉西坦3.0g/次,1次/d,对照组给予高压氧等常规治疗,治疗30 d.治疗前后检测简易精神状态检查表(MMSE)、事件相关电位P300潜伏期的变化.结果 与对照组比较,治疗组MMSE评分显著增高(P均＜0.05),P300潜伏期明显缩短(P＜0.05),未增加不良反应.结论 金纳多、奥拉西坦联合高压氧治疗一氧化碳中毒后迟发性脑病疗效好,值得临床推广.     

一氧化碳中毒与迟发性脑病的高压氧治疗

目的：观察高压氧治疗急性一氧化碳中毒与迟发性脑病的效果。方法：对129例急性一氧化碳中毒，19例迟发性脑病患者在药物治疗同时加用高压氧治疗。结果：通过高压氧治疗患者的症状、体征、脑电图的改善和治愈率明显提高。结论：对一氧化碳中毒迟发性脑病患者，重在预防，我们认为由昏迷转清醒，决不等于高压氧治疗结束，应多阶段、长疗程高压氧综合治疗，避免和减少迟发性脑病的发生。     

急性一氧化碳中毒后迟发性脑病临床分析

目的 分析急性一氧化碳中毒后迟发性脑病的临床特点.方法 选择2009年1月至2011年1月安阳地区医院收治的64例急性一氧化碳中毒迟发性脑病患者为研究对象,记为观察组;选择同期64例一氧化碳中毒后未发生迟发性脑病患者作对照,记为对照组,对比两组患者临床症状及特点.结果 与对照组相比,观察组患者年龄较大、合并症多、昏迷时间长、高压氧疗时间短且晚,恢复期多有精神刺激性表现.结论 迟发性脑病多发于高龄急性一氧化碳中毒患者,临床给予及早、有效的高压氧治疗可显著降低急性一氧化碳中毒后迟发性脑病的发生率.     

高压氧治疗迟发性脑病17例临床疗效分析

1993年3月至2000年6月我院收治急性一氧化碳中毒434例,发生迟发性脑病4例,占0.92%,收住外院一氧化碳中毒未行高压氧治疗发生迟发性脑病13例.17例患者均住院接受高压氧和药物治疗,现将临床疗效分析如下.……     

急性一氧化碳中毒迟发性脑病行高压氧治疗的护理

目的探讨加强对急性一氧化碳中毒迟发性脑病行高压氧治疗的护理效果。方法对39例急性一氧化碳中毒迟发性脑病行高压氧治疗患者,在常规改善微循环、营养神经等治疗的基础上结合心理、安全、康复等针对性的护理。结果39例急性一氧化碳中毒迟发型脑病的患者中,33例治愈,4例好转,2例转院治疗,治愈率89．1％。结论通过加强对患者的针对性护理是治疗成功的关键,强调做好护理工作可以提高高压氧治疗效果,使患者早日康复。     

Fibrinogen and fibrin structure and functions

Fibrinogen molecules are comprised of two sets of disulfide-bridged Aalpha-, Bbeta-, and gamma-chains. Each molecule contains two outer D domains connected to a central E domain by a coiled-coil segment. Fibrin is formed after thrombin cleavage of fibrinopeptide A (FPA) from fibrinogen Aalpha-chains, thus initiating fibrin polymerization. Double-stranded fibrils form through end-to-middle domain (D:E) associations, and concomitant lateral fibril associations and branching create a clot network. Fibrin assembly facilitates intermolecular antiparallel C-terminal alignment of gamma-chain pairs, which are then covalently 'cross-linked' by factor XIII ('plasma protransglutaminase') or XIIIa to form 'gamma-dimers'. In addition to its primary role of providing scaffolding for the intravascular thrombus and also accounting for important clot viscoelastic properties, fibrin(ogen) participates in other biologic functions involving unique binding sites, some of which become exposed as a consequence of fibrin formation. This review provides details about fibrinogen and fibrin structure, and correlates this information with biological functions that include: (i) suppression of plasma factor XIII-mediated cross-linking activity in blood by binding the factor XIII A2B2 complex. (ii) Non-substrate thrombin binding to fibrin, termed antithrombin I (AT-I), which down-regulates thrombin generation in clotting blood. (iii) Tissue-type plasminogen activator (tPA)-stimulated plasminogen activation by fibrin that results from formation of a ternary tPA-plasminogen-fibrin complex. Binding of inhibitors such as alpha2-antiplasmin, plasminogen activator inhibitor-2, lipoprotein(a), or histidine-rich glycoprotein, impairs plasminogen activation. (iv) Enhanced interactions with the extracellular matrix by binding of fibronectin to fibrin(ogen). (v) Molecular and cellular interactions of fibrin beta15-42. This sequence binds to heparin and mediates platelet and endothelial cell spreading, fibroblast proliferation, and capillary tube formation. Interactions between beta15-42 and vascular endothelial (VE)-cadherin, an endothelial cell receptor, also promote capillary tube formation and angiogenesis. These activities are enhanced by binding of growth factors like fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), and cytokines like interleukin (IL)-1. (vi) Fibrinogen binding to the platelet alpha(IIb)beta3 receptor, which is important for incorporating platelets into a developing thrombus. (vii) Leukocyte binding to fibrin(ogen) via integrin alpha(M)beta2 (Mac-1), which is a high affinity receptor on stimulated monocytes and neutrophils.     

Migraine and genetic and acquired vasculopathies

It is remarkable that migraine is a prominent part of the phenotype of several genetic vasculopathies, including cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL), retinal vasculopathy with cerebral leukodystrophy (RVCL) and hereditary infantile hemiparessis, retinal arteriolar tortuosity and leukoencephalopahty (HIHRATL). The mechanisms by which these genetic vasculopathies give rise to migraine are still unclear. Common genetic susceptibility, increased susceptibility to cortical spreading depression (CSD) and vascular endothelial dysfunction are among the possible explanations. The relation between migraine and acquired vasculopathies such as ischaemic stroke and coronary heart disease has long been established, further supporting a role of the (cerebral) blood vessels in migraine. This review focuses on genetic and acquired vasculopathies associated with migraine. We speculate how genetic and acquired vascular mechanisms might be involved in migraine.     

创伤高血糖与感染和MODS早期诊断和干预

本文详细介绍了创伤后血糖应激适度理论,以及高血糖与感染和多器官功能不全综合征的关系;提出涉及胰岛B细胞功能不全的MODS实验诊断新方案和极化液个体化干预新措施,可早期发现创伤MODS、降低感染率及MODS发生率和病死率。     

腹膜后纤维化与肾积水发生关系的临床研究

目的：探讨腹膜后纤维化（RPF）导致肾积水的原因及诊治经验。方法：回顾分析2004年1月—2010年12月24例腹膜后纤维化致肾积水患者的诊治资料。结果：（1）RPF患者常见首发症状为腰背痛或腹痛（69.2%）;（2）红细胞沉降率（ESR）增快和血清IgG4升高最常见。超声检查仅提示上尿路积水。RPF的静脉肾盂造影（IVP）和CT尿路成像（CTU）表现具有特征性。IVP肾盂输尿管显影不良时,CTU能较清晰的显示上尿路影像。CT扫描发现腹膜后软组织肿块9例（37.5%）,优于超声检查;（3）输尿管松解和腹腔化手术治疗22例;行肾切除术1例;行输尿管置双J管术1例。最终确诊为继发性RPF8例,其中4例为术前诊断,3例为术中腹膜后软组织肿块冷冻活检证实,1例为术后病理证实;（4）特发性RPF手术后肾积水均获长期缓解,而继发性RPF的预后取决于原发疾病及其治疗方案。结论：影像学检查是诊断RPF的重要手段,CTU优于超声检查和IVP。输尿管松解和腹腔化手术可以使特发性RPF输尿管梗阻得到长期的缓解,术中对肿块进行冷冻活检有助于鉴别特发性和继发性RPF,及时调整治疗方案。     

Telemedicine and teleradiology technologies and applications

Summary. Telemedicine and teleradiology hold the key for improving future health care delivery. In this paper we first review current communication and computer technologies used in telemedicine and teleradiology. Five examples in teleradiology applications are given including hospital-integrated picture archiving and communication systems, tele-neuro-imaging, telemammography, university consortium teleradiology service, and teleradiology for second opinion. Parameters important to teleradiology applications like costs, image quality, system reliability, and turn around time are considered. Data security is discussed, including patient confidentiality and image authenticity-which will be a major issue in future teleradiology applications.     

Physician and Nurse Practitioner Teamwork and Job Satisfaction: Gender and Profession

Designing interprofessional primary care teams composed of physicians and nurse practitioners (NPs) is a national priority. We assessed how profession and gender affect teamwork and job satisfaction among primary care physicians and NPs by using survey data from 186 physicians and 398 NPs practicing in New York State. Our regression models show profession (NP vs physician) moderates the associations of gender with teamwork and job satisfaction. Among NPs, men had higher job satisfaction than women. Among physicians, women had higher job satisfaction than men. Our results can benefit interprofessional primary care teams to optimize their professional and gender mix.     

探讨儿童慢性顽固性咳嗽与支原体感染的关系及临床治疗观察

目的探讨儿童慢性顽固性咳嗽与肺炎支原体（MP）感染的关系及临床疗效观察。方法采用回顾性研究方法对于现将2005年3月至2008年3月在我院的55例确诊慢性顽固性咳嗽患儿,主要表现为肺炎支原体感染为临床特点进行分析,并进一步临床治疗研究。结果①临床特点：在55例确诊慢性咳嗽的患儿中,以慢性顽固性咳嗽为主要症状。58％（32／55）的病例无肺部体征;②外周血：85％（47／55）的病例外周血变化不大,WBC（4—10）×10 9／L之间,嗜酸性粒细胞增多;③特别检查：47．27％（26／55）肺炎支原体IgM（MP—IgM）抗体阳性,83．64％（46／55）PeR技术检测肺炎支原体特异性DNA;④X光报告为多种形式。结论肺炎支原体（MP）感染是引起儿童慢性顽固性咳嗽的病因之一,对儿童慢性咳嗽,特别是顽固性咳嗽的诊治中应更加重视。     

Acetaminophen and acetylcysteine dose and duration: Past,present and future

Abstract

Acetylcysteine has been utilized successfully in the treatment of acetaminophen overdose since the 1970s. Although prospective trials as to efficacy and safety of acetylcysteine were conducted, there were no randomized controlled trials. This commentary addresses the reasons for this, and the background to choice of dose of acetylcysteine utilized in the oral and IV dosing regimens. Nomograms to predict possible hepatotoxicity based upon time of ingestion of acetaminophen were developed from a relatively arbitrary definition of toxicity as an aspartate aminotransferase/alanine aminotransferase (ALT/AST) greater than 1000 IU/L. While these have proved generally useful, patients still continue to develop hepatic damage after acetaminophen overdose, particularly if they present late after ingestion. The optimum management of these patients remains unclear, and one area of uncertainty is the dose and duration of acetylcysteine in various circumstances. This article discusses the issues that need to be elucidated to better target changes in acetylcysteine dose. The potential for measurements of other markers to improve treatment selection is the subject of further research.     

妊娠合并血小板减少症与心、肝、肾脏器损伤

目的探讨妊娠合并血小板减少症伴随重要脏器的损伤情况。方法前瞻性研究我院及北华大学附属医院2004年10月至2005年5月妊娠合并血小板减少症的临床资料，对41例妊娠合并血小板减少症者尿素氮（BUN）、肌酐（CREA）、谷丙转氨酶（ALT）、乳酸脱氢酶（LDH）的测定及妊娠期高血压疾病与血小板计数（PLT），血小板平均体积（MPV）和血小板体积分布宽度（PDW）参数的测定进行对比分析。结果妊娠合并血小板减少症患者心、肝、肾等重要脏器均有不同程度的改变，且随着血小板计数降低，损害程度加剧，差异具有显著性（P〈0．01）。妊娠期高血压疾病，随着疾病程度的加重，血小板计数较正常孕妇明显减少，MPV、PDW明显升高，有显著性差异（P〈0．01）。结论血小板参数是判断疾病的重要参考指标，肝、肾、心脏器损伤程度与血小板计数具有相关性。