Current and Emerging Therapies for the Management of Functional GI disorders

2019年以来关于记忆的参考文献近年来，记忆研究领域得到了广泛的关注与深入研究。

本文旨在梳理2019年以来关于记忆的参考文献，总结其中的研究成果和趋势。

以下是一些重要的研究论文和书籍，它们为我们深入了解记忆的机制和应用提供了宝贵的参考。

一、记忆的机制和神经基础1.1 "Memory and the brain: what we know and what we don't" - David Glanzman（2019）这篇论文回顾了过去几十年内记忆研究的发展，并提出了记忆的理论模型。

作者通过对海蜗牛等模型动物的研究，揭示了记忆形成的分子、细胞和网络机制。

1.2 "The hippocampus as a cognitive map: oscillations and learning" - Gyorgy Buzsáki（2019）本文探讨了海马在认知地图构建和学习过程中的神经机制。

作者通过大脑电图记录和成像技术，详细阐述了海马的振荡活动与记忆编码之间的关系。

1.3 "Neuroepigenetic regulation of memory formation and impairment: multiple molecular mechanisms" - Isabelle Mansuy（2020）该研究综述了神经表观遗传学在记忆形成和损伤中的作用。

作者强调了DNA甲基化、组蛋白修饰以及非编码RNA等多种表观遗传调控机制对记忆过程的调控。

二、记忆的影响因素和应用2.1 "The influence of emotional valence on memory processing: a neuroimaging perspective" - Mara Mather（2019）该文论述了情绪价值对记忆处理的影响，并从神经影像学的角度探讨了情绪对海马、前额叶和杏仁核等结构的作用。

二型糖尿病文献综述范文英文回答：Type 2 Diabetes: A Comprehensive Literature Review.Abstract.Type 2 diabetes is a chronic metabolic disorder characterized by hyperglycemia and insulin resistance. It is a major public health concern, affecting millions of people worldwide. This literature review provides an overview of type 2 diabetes, including its epidemiology, pathophysiology, clinical presentation, diagnosis, and management. The review also discusses current research and emerging therapies for type 2 diabetes.Epidemiology.The prevalence of type 2 diabetes has increased dramatically over the past few decades. It is estimatedthat over 462 million people worldwide have type 2 diabetes, and this number is expected to rise to 700 million by 2045. Type 2 diabetes is more common in certain populations, such as individuals who are overweight or obese, have a family history of the disease, or are of certain ethnicities.Pathophysiology.Type 2 diabetes is primarily caused by insulin resistance. Insulin is a hormone produced by the pancreas that helps glucose enter cells. In type 2 diabetes, thebody becomes resistant to the effects of insulin, resulting in hyperglycemia. Over time, the pancreas may also lose its ability to produce enough insulin, further exacerbating the hyperglycemia.Clinical Presentation.The clinical presentation of type 2 diabetes varies widely. Some individuals may experience classic symptoms such as polyuria, polydipsia, and unexplained weight loss. Others may have no symptoms at all. Over time, uncontrolledtype 2 diabetes can lead to serious complications,including cardiovascular disease, kidney disease, and diabetic retinopathy.Diagnosis.The diagnosis of type 2 diabetes is based on blood glucose levels. A fasting blood glucose level of 126 mg/dL or higher on two separate occasions is diagnostic for type 2 diabetes. An oral glucose tolerance test may also be used to diagnose type 2 diabetes.Management.The management of type 2 diabetes involves lifestyle modifications and medication. Lifestyle modifications include weight loss, regular exercise, and a healthy diet. Medications for type 2 diabetes include oral medications such as metformin and sulfonylureas, and injectable medications such as insulin.Current Research and Emerging Therapies.Current research on type 2 diabetes focuses on developing new medications and therapies to improveglycemic control and prevent complications. Some promising emerging therapies include incretin-based therapies,sodium-glucose cotransporter-2 (SGLT2) inhibitors, and glucagon-like peptide-1 (GLP-1) receptor agonists.Conclusion.Type 2 diabetes is a major public health concern that affects millions of people worldwide. Understanding the epidemiology, pathophysiology, clinical presentation, diagnosis, and management of type 2 diabetes is crucial for healthcare professionals and patients alike. Ongoing research and the development of new therapies are essential for improving the lives of individuals with type 2 diabetes.中文回答：2型糖尿病，综合文献综述。

多发性硬化实验动物模型研究进展陈永妍;李林;张旗;尹琳琳【摘要】多发性硬化实验动物模型可模拟人类该病的不同类型或不同阶段,是研究该病病因和研发治疗药物的有效工具.【期刊名称】《基础医学与临床》【年(卷),期】2013(033)011【总页数】4页(P1500-1503)【关键词】多发性硬化;动物模型;自身免疫;髓鞘多肽;病毒;神经毒素【作者】陈永妍;李林;张旗;尹琳琳【作者单位】首都医科大学宣武医院药物研究室北京市老年病医疗研究中心神经变性病教育部重点实验室,北京100053;郑州大学药学院,河南郑州450001;首都医科大学宣武医院药物研究室北京市老年病医疗研究中心神经变性病教育部重点实验室,北京100053;郑州大学药学院,河南郑州450001;首都医科大学宣武医院药物研究室北京市老年病医疗研究中心神经变性病教育部重点实验室,北京100053【正文语种】中文【中图分类】R744.5+1多发性硬化(multiple sclerosis，MS)属中枢神经系统(central nervous system，CNS)炎性反应脱髓鞘疾病，是CNS脱髓鞘疾病的典型代表［1-2］。

目前多发性硬化的发病机制尚不明确，较为公认的学说是病原体侵入机体引发异常的自身免疫反应所致［3］。

由于神经组织取样的局限性，为了获得疾病不同方面的信息，采用动物模型模拟MS的病理改变和临床特征是十分必需和必要的。

1 髓鞘多肽片段诱导的MS动物模型实验性自身免疫性脑脊髓炎模型(experimentally allergic encephalomyelitis，EAE)是一种以特异性致敏的CD4+和CD8+T细胞介导为主的，以中枢神经系统内小血管周围出现单核细胞浸润及髓鞘脱失为特征的自身免疫疾病，是人类多发性硬化经典的实验动物模型［4］。

致脑炎物质能够诱发实验性自身免疫性脑脊髓炎模型(experimentally allergic encephalomyelitis，EAE)［5］，这些物质主要包括髓鞘碱性蛋白(myelin basic protei，MBP)、蛋白脂质蛋白(proteolipid protein，PLP)、髓磷脂少突胶质细胞糖蛋白(myelin oligodendrocyte glycop rotein，MOG)或合成的能够替代上述蛋白的多肽序列。

帕金森最新治疗方案引言帕金森病是一种逐渐丧失运动控制能力的神经系统疾病，给患者的生活带来了极大困扰。

由于帕金森病的复杂性和多样性，寻找最新的治疗方案成为医学界的关注焦点。

本文将介绍一些最新的帕金森病治疗方案，包括药物治疗、手术治疗和非药物治疗。

药物治疗多巴胺激动剂（DA）多巴胺激动剂是帕金森病药物治疗的基石之一。

通过补充丧失的多巴胺，多巴胺激动剂能够改善患者的运动症状。

最新研究发现，某些DA具有更长的作用时间和更稳定的效果，有效减少药物剂量和不良反应。

非多巴胺药物除了多巴胺激动剂外，还有一些非多巴胺药物也被用于帕金森病的治疗。

例如，脑嘧啶核苷酸（NRT）类药物可以通过增加神经细胞内的脑嘧啶核苷酸水平来改善运动功能。

此外，抗胆碱药物也可以用于治疗帕金森病患者的运动障碍。

基因治疗基因治疗是一种新兴的治疗帕金森病的方法。

最近的研究表明，通过基因治疗可以恢复患者丧失的多巴胺神经元，从而改善帕金森病的症状。

这种治疗方法还处于实验阶段，但已经显示出很大的潜力。

手术治疗深部脑刺激（DBS）深部脑刺激是一种常见的手术治疗方法，通过在脑部植入电极来改善帕金森病患者的运动症状。

最新的研究表明，通过精确定位和调整电极的刺激参数，可以获得更好的治疗效果和减少不良反应。

脑组织移植脑组织移植是一种试图恢复患者丧失的多巴胺神经元的手术治疗方法。

它涉及从供体脑中提取多巴胺神经元移植到患者的大脑中。

尽管这种方法在某些病例中取得了成功，但由于手术风险和供体限制，它还需要进一步研究和改进。

非药物治疗物理治疗物理治疗是一种辅助性的非药物治疗方法，以改善帕金森病患者的运动功能和生活质量。

最新的物理治疗方法包括平衡训练、抗阻力训练和大肌肉主动训练，旨在提高患者的运动能力和自主性。

艺术治疗艺术治疗作为一种创新的非药物治疗方法，被证明可以改善帕金森病患者的情绪和认知功能。

音乐疗法、舞蹈疗法和美术疗法等艺术治疗形式，通过激发患者的创造力和表达能力，提高患者的生活质量。

白介素4、10、12、13、IFN-γ、TGF-β在不同时期特应性皮炎病人血清中的变化李妍;徐薇;程海艳;孙晓丽;李邻峰【摘要】目的研究疾病发作期和缓解期特应性皮炎(atopic dermatitis,AD)病人血清中白细胞介素-4(interleukin-4,IL-4)、IL-10、IL-12、IL-13、干扰素-γ(interferon-γ,IFN-γ)、转化生长因子-β(transforming growth factor-β,TGF-β)等细胞因子的变化,探讨其在AD发病机制中的作用.方法收集疾病发作期AD病人79例,其中经治疗皮损缓解的AD病人(缓解组)40例,未缓解的AD病人(未缓解组)39例.采用酶联免疫吸附试验(enzyme-linked immunosorbent assay,ELISA)测定病人治疗前后血清中IL-4、IL-10、IL-12、IL-13、IFN-γ、TGF-β的浓度.结果缓解组AD病人治疗后血清中IL-4、IL-12、IL-13、IFN-y与治疗前相比,差异均有统计学意义(均P＜0.05).缓解组AD病人治疗后血清中IL-10、TGF-β与治疗前相比,差异无统计学意义(P＞0.05).未缓解组AD病人治疗后血清中IL-4、IL-10、IL-12、IL-13、IFN-γ、TGF-β与治疗前相比,差异均无统计学意义(P＞0.05).结论AD病人病情缓解时血清中IL-4、IL-13表达显著下调,IFN-γ和IL-12表达显著升高.%Objective To investigate the changes of interleukin-4(IL-4),IL-10,IL-12,IL-13,interferon-γ (IFN-γ) and transforming gro wth factor-β (TGF-β) in the serum of atopic dermatitis patients at different stages of the disease,and explore their significance.Methods Seventy-nine atopic dermatitis patients at acute stage were enrolled.There were 40 cases at remission stage(remission group,RG),and 39 cases were still at acute stage after treatment(acute group,AG).The serum levels of IL-4,IL-10,IL-12,IL-13,IFN-γ and TGF-β were detected by enzyme-linked immunosorbentassay (ELISA) before and after treatment.Results There were significant differences in the serum levels of IL-4,IL-12,IL-13 and IFN-γ before and after treatment in the remission group(P ＜0.05).There were no significant differences in the serum levels of IL-10,TGF-β before and after treatment in the remission group(P ＞ 0.05).There were no significant differences in the serum levels of IL-4,IL-10,IL-12,IL-13,IFN-γ and TGF-β before and after treatment in the acute group(P ＞ 0.05).Conclusion Lower expression of IL-4,IL-13,and higher expression of IFN-γ,IL-12 in serum at remission stage of atopic dermatitis.【期刊名称】《首都医科大学学报》【年(卷),期】2017(038)005【总页数】5页(P635-639)【关键词】特应性皮炎;辅助性T淋巴细胞;白细胞介素;干扰素-γ;转化生长因子-β【作者】李妍;徐薇;程海艳;孙晓丽;李邻峰【作者单位】首都医科大学附属北京友谊医院皮肤性病科,北京100050;首都医科大学附属北京友谊医院皮肤性病科,北京100050;首都医科大学附属北京友谊医院皮肤性病科,北京100050;首都医科大学附属北京友谊医院皮肤性病科,北京100050;首都医科大学附属北京友谊医院皮肤性病科,北京100050【正文语种】中文【中图分类】R758.23特应性皮炎(atopic dermatitis, AD)又名特应性湿疹等，是一种与遗传相关的慢性复发性瘙痒性皮肤病。

180·中国CT和MRI杂志　2024年3月 第22卷 第3期 总第173期【第一作者】路　阳，男，主治医师，主要研究方向：颅脑影像。

E-mail：****************【通讯作者】陆敏艳，女，副主任医师，主要研究方向：神经病学。

E-mail：****************·短篇报道·一例早期误诊为垂体腺瘤的垂体癌*路　阳1 戚志强2 陆敏艳2,*1.南京医科大学附属江苏盛泽医院放射科 (江苏 苏州 215228)2.南京医科大学附属江苏盛泽医院神经内科 (江苏 苏州 215228)【关键词】垂体腺瘤；垂体神经内分泌肿瘤；垂体癌【中图分类号】R736.4【文献标识码】D【基金项目】苏州市吴江区“临床医学专家团队”引进项目(WJYJTD201802) DOI:10.3969/j.issn.1672-5131.2024.03.055A Case of Pituitary Carcinoma Early Misdiagnosed as Pituitary Adenoma*LU Yang 1, QI Zhi-qiang 2, LU Min-yan 2,*.1.Department of Radiology, Jiangsu Shengze Hospital Affiliated to Nanjing Medical University,Suzhou 215228, Jiangsu Province, China2.Department of Neurology, Jiangsu Shengze Hospital Affiliated to Nanjing Medical University,Suzhou 215228, Jiangsu Province, ChinaKeywords: Pituitary Adenoma; Pituitary Neuroendocrine Tumor; Pituitary Carcinoma 垂体癌(PC)是一种极其罕见的恶性肿瘤，占所有垂体神经内分泌肿瘤(PitNETs)的0.1%-0.2%。

疏肝消脂颗粒剂治疗非酒精性脂肪性肝炎的临床疗效观察翟芬芬;孙虹;苏晓星;邢宇锋;童光东;周大桥;柳臻【摘要】目的:观察疏肝消脂颗粒剂治疗非酒精性脂肪性肝炎的临床疗效.方法:选择非酒精性脂肪性肝炎患者120例,随机分为治疗组(60例),对照组(60例),其中治疗组用疏肝消脂颗粒剂冲服,对照组用多烯磷脂酰胆碱胶囊治疗.两组患者治疗3个月,分别观察其临床症状和体征、肝功能、血脂等指标的变化情况.结果:两组患者临床症状皆能改善,治疗组疗效优于对照组;在改善肝功能、血脂方面,两组患者治疗后均较治疗前有明显改善,差异均有显著性意义(P＜0.05),治疗组疗效优于对照组,差异有显著性意义(P＜0.05).结论:疏肝消脂颗粒剂治疗非酒精性脂肪性肝炎的临床疗效确切,可改善患者临床症状和体征、降低肝功能及血脂指标,其疗效优于多烯磷脂酰胆碱胶囊.【期刊名称】《中西医结合肝病杂志》【年(卷),期】2014(024)002【总页数】3页(P78-79,82)【关键词】非酒精性脂肪性肝炎;多烯磷脂酰胆碱胶囊;肝功能;血脂【作者】翟芬芬;孙虹;苏晓星;邢宇锋;童光东;周大桥;柳臻【作者单位】深圳市福田区慢性病防治院,广东深圳,518033;深圳市福田区慢性病防治院,广东深圳,518033;深圳市福田区慢性病防治院,广东深圳,518033;深圳市中医院肝病科;深圳市中医院肝病科;深圳市中医院肝病科;深圳市中医院医务科【正文语种】中文非酒精性脂肪性肝炎 (nonalcoholic steatohepatitis，NASH)作为单纯性脂肪肝发展为肝纤维化的一个病理阶段，常见于肥胖、2型糖尿病、高脂血症等代谢综合征患者［1，2］。

近年来中医药治疗非酒精性脂肪性肝炎显示较好的疗效，我们在2012年10月至2013年10月运用疏肝消脂颗粒剂治疗非酒精性脂肪性肝炎患者，临床资料总结如下。

1 资料与方法1.1 一般资料 120例均为2012年10月-2013年10月在深圳市福田区慢性病防治院、深圳市中医院收治的非酒精性脂肪性肝炎患者，诊断均符合中华医学会肝脏病学分会脂肪肝和酒精性肝病学组2006年制定的《非酒精性脂肪性肝病诊疗指南》［3］。

《临床皮肤科杂志》投稿须知《临床皮肤科杂志》是皮肤性病科专业性期刊.主要读者对 3.4摘要:论著,大样本的皮肤病治疗及少见病,疑难病,首报病例报告需附中,英文摘要,综述,继续医学教育需附中文摘要. 论著的摘要采用结构式形式,应包括目的,方法,结果(应给出主要数据),结论4个要素.每一要素前要冠以相应的标题.要用第3人称的写法,不要使用"本文","作者"等作为主语.中文摘要字数在200字左右.英文摘要应与中文摘要一致,英文摘要也采用结构式形式书写.病例报告及综述等摘要可采用陈述式形式,不必按结构式书写.英文摘要前还应用英文列出文题,作者姓名(采用汉语拼音,所有作者姓名均应列出,姓的字母全部大写,名的首字母大写,双名中间加一短线),单位名称,所在城市, 邮政编码及国家. 3.5关键词:所有文章均需标引2—5个关键词.尽可能选用最新版《医学索引)(Index Medicus,美国国立医学图书馆)中的医学主题词表(MESH)中的词语,如最新版MeSH中尚无相应的词语,可采用"组配","上靠"或选用习用的自由词列出. 3.6层次序号:稿件中尽量减少层次,标题层次一律用阿拉伯数字连续编号.不同层次的数字间加下圆点相隔(即圆点加在象为广大的皮肤性病科医师和科研,医教人员.并兼顾相关学科的医药卫生和科研人员及基层医药卫生工作者.本刊的办刊宗旨是贯彻党和国家的卫生工作方针政策.遵循理论与实践相结合,普及与提高并重的方针,以临床为主.面向基层,以其实用性服务于广大读者.本刊对所有来稿均采用同行审稿的方式进行公平,公正的审定. 1本刊常设栏目彩色图谱,论著,病例报告,皮肤病治疗,调查报告,综述,论坛,继续医学教育,病例分析,组织病理分析和短篇临床经验交流等,欢迎大家投稿. 2对来稿的要求 2.1彩色图谱:除提供临床,病理照片及特殊检查照片外.应书写病史,体格检查,实验室检查,诊断,治疗,转归及该病简介, 也可就该病例结合文献进行讨论. 2.2继续医学教育及病例分析一般为约稿.也欢迎自由来稿.作者在撰写前最好与编辑部联系,并告知题目,以免重复.2.3论著:要求以结合临床为主,具有科学性,实用性,创新性.主题明确,重点突出,资料和数据可靠,准确,数据应有必要的统计学处理.论文要求文字精炼,通顺,层次清晰,标点符号正确. 2.4皮肤病治疗:病例数不能太少(一般不低于30例),设计合理,方法科学,尽可能设立对照,并说明对照的方法.有科学的评分标准及判愈标准,对治疗前后作对比的数据应做统计学处理,有不良反应观察及随访结果.尽量提供治疗前后的照片.欢迎大样本,多中心,观察仔细的皮肤病治疗稿件. 2.5病例报告:要求病例真实,病史完整,有具体就诊时间,检查项目齐全,诊断依据充分及具体诊治方法.有为明确诊断所需的临床,组织病理及特殊检查的照片.数字的右下角,最末数字后面不加标点.例如:第1级标题—— l;第2级标题——1.1;第3级标题——1.1.1.论著性文章中的"材料和方法","结果","讨论"各节标题为第1级标题,用1,2, 3标明.各节内再分层时,按层次还可再标注第2级及第3级标题,如1.1,1.1.1……,2.1,2.1.1……,在正文中的序号用①,②,③……表示.4医学名词及药物名称简化字以国务院1986年lO月15日重新公布的《简化字总表》为准,通常可以《新华字典》为依据.医学名词以1986年全国自然科学名词审定委员会已审定公布的《医学名词》(科学出版社出版)为准,暂未审定公布者以人民卫生出版社出版的《英汉医学词汇》为准.中文药物名称应使用1995年版《中华人民共和国药典》(法定药物)或卫生部药典委员会1996年编辑的《中国药品通用名称》(原名《药名词汇》)中的名称.英文药物名称则采用国际非专利药名,不用商品名. 5统计学要求在统计学方法中应明确交待进行数据处理时所采用的统计软件和统计学方法,例如:t检验,是组间还是配对.统计学符号按GB 3358—82《统计学名词及符号》的有关规定书写:①样本的算术平均数用英文小写元(中位数仍用2.6对来稿字数要求:论著,综述,讲座等字数不超过4 000字(包括中英文摘要及参考文献),无中英文摘要的论著不超过2000字,皮肤病治疗,病例报告原则上不超过1 500字.短篇临床经验交流600字左右. 3稿件书写格式3.1格式:文稿请按题目,作者,单位,中文摘要,关键词,英文摘要,关键词,正文,参考文献的顺序打印在A4纸上.并将行距设为1.5倍,便于编辑修改.3.2文题:尽量简单明了.能概括文章主题.中文文题一般不宜超过20个汉字,外文文题不宜超过10个实词.中文题名应避免使用不常见的缩略词,首字母缩写字,字符和代号. 3.3作者:作者姓名在文题下方自行按序排列,不排并列作者. 投稿时已确定的作者排列顺序,在编排时不再作改动.不同单位者,请在作者姓名的右上角用阿拉伯数字按序标注,然后在作者姓名下方注明其单位名称,省市和邮政编码,不同单位均应列出.作者中如有外籍作者,应征得其本人同意.并提供外籍作者同意该文在本刊发表的证明信函.M);②标准差用英文小写s;③标准误用英文小写&;④t 检验用英文小写t;⑤F检验用英文大写F;⑥卡方检验用希文小写x:;⑦相关系数用英文小写r;⑧自由度用希文小写1J;⑨概率用英文大写P;样本数用英文小写//,,以上符号均用斜体. 6图表凡用文字能表达清楚的内容,尽量不用表和图,如用表和图,文中不需要重复其数据,只要摘其主要内容即可,正文和图表尽量避免重复.图表的设计应简单,明了,正确,合理,有自明性.同一数据不需要同时用图和表重复表达.每幅图(表)均要万方数据I有图(表)序,仅1幅图(表)则只须写作图1或表1,并在其后列出图(表)题.为便于审稿,图表均应随文排,不要单列于文后. 本刊表格采用三线表,不用竖线.如遇有合计,平均或统计学处理行(如t值,P值等),则在这行上方可加一条分界线.表内数据要求同一指标,有效位数一致,并须核对无误.表内"空白"代应按引用的先后顺序在文后用表列出.参考文献的作者应列出前3名,超过3名者在其后加"等",或其他与之相应的文字.外文期刊名称按(Index Medicus))规定缩写.中文期刊用全称.每条期刊的参考文献均需著录年,卷,期,起止页.每_二条文献的题名后应在方括号内标出文献类型标识符,【JJ:期刊文章,[M1:专著, 【c】:论文,[R】:报告,【s]:标准,【q:汇编,[0L】:联机网络等. 举例: [1】1范卫新.朱文元.环孢索A促毛发生长机理的研究叨.临床皮肤科杂志,2000,29(5):255—257.(期刊中析出文献) [2】HolderRM,Young CM.New and emerging therapies for vitiligo表未测或无此项,"～"或"…"(因"一"可能与代表阴性反应相混.故用长线)代表未发现,"0"代表实测结果为零.尽可能列出统计分析结果,如t值,x:值,P值等.线条图横座标一般不超过7 ca,高宽比例约为5:7左右.以计算机绘制者应提供激光打印图样.图片应清晰,对比度好.临床照片力求皮损典型,清晰(色彩鲜明,色真,背景不宜杂乱.以蓝色或黑色为佳),病理照图片须注明染色方法和放大倍数. 所有图片需提供彩色冲洗照片并附图题及简要的图解.并在照片背面注明图的序号和上下方向. 7计量单位文章中的计量单位一律按1984年2月27日国务院颁布的《中华人民共和国法定计量单位》的规定书写.并以单位符号表示.使用中可参考中华医学会杂志社编辑的《法定计量单位在医学上的应用》(第3版).单位名称与单位符号不可混用.组[J】.Dermatol Clin,2000,18(I):79—89.(期刊中析出文献)[3】杨圉亮,王侠生.现代皮肤病学[M].上海:上海医科大学出版社,1996:244—258.(专著) [4】WilsonterBD.Dermatologie Lesions of thePenis[M‖Gillen W卜JY,Grayhack JT.Adult and Pediatric Utdogy.3rd ed.Louis:Mosby,1996:2043—2057.(专著中析出的文献) 10获基金稿件论文涉及的研究课题如系国家自然科学基金项目或省,部级以上课题,请在文稿首页脚注处注明,如"基金项目(课题):XXX基金资助项目(基金编号×x×)",并需附基金资助合单位符号只用一个"每"字,即只用一条相除号''/',如m酞驽/日(天)应写成m绯g·d).计量的数值一般在9.1一l 000范围内,如0.003 94项目任务批准件的复印件,以便论文提前发表.论文如获奖也请及时通知编辑部,并将获奖证书复印件及时寄至编辑部.1m可以改写为3.94mm.ll401Pa可改写为11.401kPa.血压计量单位采用kPa,但首次使用时应注明1mill Hg--0.1331修改稿及软盘经审稿后拟刊用的稿件请按退修单上提出kPa.时间天,小时,分,秒的单位符号应写为d,h,min,s. 8数字公历,世纪,年代,年,月,日,时刻和计数,计量均使用阿拉伯数字.年份须用全称.书写小数点前或后有4位和4位以上的数字应采用3位分节法.节与节之间空似格,不用千分撇分节法.如"3,824.6975"应写成"3824.697的退修意见一一复核,修改.为缩短刊出周期.减少再打印稿及校对错误.请将修改稿以word文件存人软盘,与原稿,修改稿一并寄回编辑部,同时在退修单上注明联系电话和(或)E—mail地址.修改稿如3个月不寄回,应通知编辑部,视为自动撤稿处理, 如再寄回时将重新按新投稿处理. 12来稿来稿须附作者单位推荐信.不允许一稿两投,不涉及保密,署名需无争议.软盘在初投稿时不必寄出,待文稿经最后修正后再与修改稿一并寄至编辑部.来稿一律文责自负,根据《著作权法》有关规定.本刊对采用稿件可做文字修改和删节.5".序数词,年份,页数,部队番号,仪表型号和标准号不分节.5位以上的数字,尾数零多的可改写为以万,亿作单位的数.如"245 000 000人"可改写为"2.45亿人或24 500万人".日期范围号用"一".其他数值范围号使用66 99号,单位相同的参数范围.只需写出后一个参数的单位,如1.23A～1.68A应写为1.23～1.68A.百分数的范围和偏差,13稿件经编辑部确定刊出后,在退修时将由作者亲笔签署论文专有使用权授权书,专有使用权归临床皮肤科杂志编辑部所有, 临床皮肤科杂志编辑部有权以电子版,光盘版等其他方式出版, 未经临床皮肤科杂志编辑部同意.该论文的任何部分不得转载他处.作者需按版面费通知上的要求支付文章,彩色及黑白照片的版而费.文章发表后,编辑部将酌致稿酬,同时赠第1作者当期杂志1册.编辑部所发放的稿酬已包括电子版,光盘版及各大数据库网上检索的稿酬. 14稿件请自留底稿,投稿时需附寄8.00元邮票,请勿邮汇现金.无论刊登与否均不退回原稿,如需退回照片,请在来稿时说明.凡收剑本刊来稿回执后3个月以上未收到本刊处理通知,可能仍在审阅中,作者如欲投其他刊物,请先与本刊联系,切勿一稿两投或一稿多投. 15来稿请寄"南京市广州路300号,《临床皮肤科杂志》编辑部"(邮政编码:210029),请勿将稿件寄给个人,以免遗失.前一个参数的百分号"%"不能省略.如10%一90%不要写成lO～90%,25.3%±0.1%不要写成25.3+0.1%,应写成(25.3+0.1)%,一系列数值的计量单位相同时.可仅在最末一个数字后面写出单位符号.如60,80,120 moll,不必写作60 moil,80 moll,120 moll.附带尺寸单位的数值相乖表示空间的.不要写成4 X3 2 Xcm3,或4X2 X 3cm,而应写成4 cmx2 cm x3 cm.9参考文献参考文献应尽量精选.以公开发表并亲自阅读过的文献为限.论著性文章的参考文献限于10条以内.综述限于20条以内.按GB 7714--2005(文后参考文献著录规则》采用顺序编码制著录,按照正文中引用的先后顺序,要在文中引用处右上角将序号用阿拉伯数字加方括号连续编码.引文如写出原著者. 序号应放在著者姓名的右上角.如未写出著者姓名,序号应放在引文之后.如参考文献作正文叙述的直接补语时,用与正文相同的字号数码与正文并排,不用角码标注.正文引用的参考文献均万方数据Ⅱ。

甲氨蝶呤联合大剂量阿糖胞苷治疗急性淋巴细胞白血病致短暂失明一例报告并文献复习阿糖胞苷是最有效的抗血液肿瘤药物之一，在急性淋巴细胞白血病诱导达到完全缓解的早期行中大剂量阿糖胞苷强化治疗，可显著提高患者的长期生存。

大剂量阿糖胞苷化疗过程中发生中枢神经毒性的概率约有10%，但出现失明的案例极其少见，现报道1例应用大剂量阿糖胞苷治疗后发生严重不良反应导致短暂性失明的病例，同时结合相关文献进行复习。

作者单位：230601 安徽合肥，安徽医科大学第二附属医院血液内科通信作者：翟志敏病例资料患者，女，25岁，妊娠35+周，因发热伴洗肉水样血尿3天于2014年4月6号入住安徽医科大学第一附属医院血液科，查体：贫血貌，皮肤黏膜无出血点，浅表淋巴结未及肿大，胸骨压痛阴性，肝脾肋下未及，既往史、家族史、传染病史无殊。

入院查血常规：WBC 115.90×109/L,HB 75g/L,PLT 12×109/L，骨髓细胞学：淋巴细胞极度增生，原始、幼稚淋巴细胞占69%，核畸形明显，诊断急性白血病骨髓象，免疫分型提示：有核细胞以原始细胞为主，表达CD34、HLA-DR、CD19、CD22、CD38、CD10，部分表达CD20，提示B急性淋巴细胞白血病（Pre-B可能），融合基因筛查：检出E2A/PBX1融合基因阳性，染色体：46，XX,（7），骨髓活检：急性淋巴细胞白血病继发骨髓纤维化，诊断为急性淋巴细胞白血病（Pre-B，伴E2A/PBX1，高危组）。

4月9号予以VP方案预处理，后复查血象提示血小板明显升高，请妇产科会诊后转科行子宫下段剖宫产+B-Lynch缝扎术+双侧输卵管结扎术，手术顺利，考虑需进一步治疗原发病再次转回血液科，于5月3号行VIP方案诱导化疗，化疗后复查骨髓细胞学提示原始细胞约8.5%，病情评估为部分缓解，于6-21再次行Hyper CVAD+MA方案化疗。

期间患者于6月9号出现头痛、视物模糊，行腰穿检出提示白血病中枢神经系统浸润，先后行6次腰穿鞘注术，后脑脊液未检出白血病细胞，7月29号复查骨髓细胞学提示ALL缓解期骨髓象，流式未检出白血病细胞，提示达到完全缓解。

管病研究,2022,20(6):481-485.[2]㊀中国心血管健康与疾病报告编写组.中国心血管健康与疾病报告2021概要[J].中国循环杂志,2022,37(6):553-578.[3]㊀魏峰,张松林,张玉顺,等.心力衰竭生物学标志物的临床意义及研究进展[J].重庆医科大学学报,2018,43(3): 311-315.[4]㊀Werhahn SM,Becker C,Mende M,et al.NT-proBNP as amarker for atrial fibrillation and heart failure in four observa-tional outpatient trials[J].ESC Heart Fail,2022,9(1):100-109.[5]㊀Givertz MM,Postmus D,Hillege HL,et al.Renal functiontrajectories and clinical outcomes in acute heart failure[J].Circ Heart Fail,2014,7(1):59-67.[6]㊀Anand IS,Gupta P.Anemia and iron deficiency in heart fail-ure:current concepts and emerging therapies[J].Circula-tion,2018,138(1):80-98.[7]㊀中华医学会心血管病学分会,心力衰竭学组,中国医师学会心力衰竭委员会,等.中国心力衰竭诊断和治疗指南2018[J].中华心血管病杂志,2018,46(10):760-789.[8]㊀Almeida AG.NT-proBNP and myocardial fibrosis:the invisi-ble link between health and disease[J].Am Coll Cardiol, 2017,70(25):3110-3112.[9]㊀国家心血管病医疗质量控制中心专家委员会心力衰竭专家工作组.2020中国心力衰竭医疗质量控制报告[J].中国循环杂志,2021,36(3):221-237.[10]㊀于舟淇,杨巍.心肾综合征病理生理机制及治疗研究的进展[J].心血管康复医学杂志,2021,30(5):606-609.[11]㊀李榕,王亮,钱豪英,等.肌酐作为生物标志物在疾病诊断及药物评价方面的研究进展[J].药物评价研究,2021,44(9):2007-2012.[12]㊀曲巍,付强.贫血对老年慢性心力衰竭患者预后的影响[J].武警后勤学院学报(医学版),2015,24(1):31-33.[13]㊀Senni M,Lopez-Sendon J,Cohen-Solal A,et al.Vericiguatand NT-proBNP in patients with heart failure with reducedejection fraction:analyses from the VICTORIA trial[J].ESC Heart Fail,2022,9(6):3791-3803. [14]㊀An Y,Wang Q,Wang H,et al.Clinical significance ofsFRP5,RBP-4and NT-proBNP in patients with chronicheart failure[J].Am Transl Res,2021,13(6):6305-6311.[15]㊀Losito A,Nunzi E,Pittavini L,et al.Cardiovascular morbid-ity and long term mortality associated with in hospital smallincreases of serum creatinine[J].Nephrol,2018,31(1):71-77.[16]㊀梁德贤,李庆军,陈康荣.慢性充血性心力衰竭患者贫血患病率与心功能的关系及血红蛋白对预后的影响[J].黑龙江医学,2015,39(7):739-741.[17]㊀Oremus M,Don-Wauchope A,McKelvie R,et al.BNP andNT-proBNP as prognostic markers in persons with chronicstable heart failure[J].Heart Fail Rev,2014,19(4):471-505.[18]㊀Zhang S,Hu Y,Zhou L,et al.Correlations between serumintact parathyroid hormone(PTH)and N-terminal-pro-brain natriuretic peptide levels in elderly patients with chro-nic heart failure(CHF)[J].Arch Gerontol Geriatr,2015,60(2):359-365.ʌ文章编号ɔ1006-6233(2023)10-1649-06血清HMGB1与COPD急性加重期患者炎性指标肺功能参数之间的相关性唐文君1,㊀曾㊀珠1,㊀杨㊀帆2,㊀肖㊀玮1(1.成都中医药大学附属医院呼吸内科,㊀四川㊀成都㊀6100722.成都医学院第一附属医院呼吸与危重医学科,㊀四川㊀成都㊀610500)ʌ摘㊀要ɔ目的:分析血清高迁移率族蛋白1(HMGB1)与急性加重期慢性阻塞性肺疾病(AECOPD)患者炎性指标㊁肺功能参数之间的相关性㊂方法:从2020年1月至2022年6月到我院就诊的AECOPD 患者中选取104例纳入AECOPD组;从就诊的稳定期慢性阻塞性肺疾病(COPD)患者中选取104例纳入COPD组;从同期健康体检者中选取104例那纳入健康对照组㊂比较各组入院时的外周血相关指标[HMGB1㊁缺氧诱导因子1α(HIF-1α)㊁白细胞计数(WBC)]水平㊁血清炎性因子[白细胞介素-6(IL-6)㊁C反应蛋白(CRP)㊁降钙素原(PCT)]水平及肺功能参数[6min步行距离(6MWD)㊁肺动脉压㊁二氧化碳分压(PaCO2)㊁氧分压(PaO2)];分析血清HMGB1与上述炎性指标及肺功能参数的关系㊂结果:三组入院时的血清HMGB1㊁HIF-1α㊁IL-6㊁CRP㊁PCT水平及WBC均表现为AECOPD组>COPD组>健康㊃9461㊃ʌ基金项目ɔ四川省科学技术厅项目,(编号:2022YFS0423);成都市科学技术局项目,(编号:2021-YF05-02035-SN)对照组,组间比较差异有统计学意义(P<0.05)㊂三组入院时的6MWD值及PaO2水平均表现为AECO-PD组<COPD组<健康对照组,组间比较差异有统计学意义(P<0.05)㊂三组入院时的肺动脉压㊁PaCO2水平均表现为AECOPD组>COPD组>健康对照组,组间比较差异有统计学意义(P<0.05)㊂Pearson相关性分析显示,AECOPD患者入院时的血清HMGB1水平与IL-6㊁CRP㊁肺动脉压水平呈正相关(r分别=0.566㊁0.287㊁0.230,P均<0.05),与PaO2水平呈负相关(r=-0.212,P<0.05)㊂结论:与稳定期COPD及健康体检者相较,AECOPD患者的血清HMGB1水平异常升高,且与IL-6㊁CRP㊁肺动脉压㊁PaO2水平密切相关㊂ʌ关键词ɔ㊀慢性阻塞性肺疾病;㊀急性加重期;㊀血清高迁移率族蛋白1;㊀肺功能;㊀相关性ʌ文献标识码ɔ㊀A㊀㊀㊀㊀㊀ʌdoiɔ10.3969/j.issn.1006-6233.2023.10.012Correlation between Serum HMGB1and Inflammatory Indicators and Lung Function Parameters in Patients with Acute Exacerbation of COPDTANG Wenjun,ZENG Zhu,et al(The Affiliated Hospital of Chengdu University of Traditional Chinese Medicine,Sichuan Chengdu610072,China)ʌAbstractɔObjective:To analyze the correlation of serum high mobility group protein1(HMGB1)with inflammatory indicators and pulmonary function parameters in patients with acute exacerbation of chronic ob-structive pulmonary disease(AECOPD).Methods:A total of104patients with AECOPD who were treated in the hospital from January2020to June2022were selected and included in AECOPD group,and another104 patients with stable chronic obstructive pulmonary disease(COPD)were enrolled as COPD group.104health-y subjects with physical examination during the same time period were included in healthy control group.The levels of peripheral blood related indicators[HMGB1,hypoxia-inducible factor-1α(HIF-1α),white blood cell count(WBC)]and serum inflammatory factors[interleukin-6(IL-6),C-reactive protein(CRP), procalcitonin(PCT)]and pulmonary function parameters[6-minute walk distance(6MWD),pulmonary ar-tery pressure,partial pressure of carbon dioxide(PaCO2),partial pressure of oxygen(PaO2)]were com-pared among the groups at admission.The relationship between serum HMGB1and the above inflammatory in-dicators and pulmonary function parameters was analyzed.Results:The levels of serum HMGB1,HIF-1α, IL-6,CRP,PCT and WBC in the three groups at admission were manifested as AECOPD group>COPD group >healthy control group(P<0.05).The6MWD and PaO2at admission were shown as AECOPD group<COPD group<healthy control group(P<0.05).The pulmonary artery pressure and PaCO2of the three groups at ad-mission showed AECOPD group>COPD group>healthy control group(P<0.05).Pearson correlation analysis showed that serum HMGB1level at admission was positively correlated with IL-6,CRP and pulmonary artery pressure in patients with AECOPD(r=0.566,0.287,0.230,all P<0.05),and was negatively correlated with PaO2(r=-0.212,P<0.05).Conclusion:Compared with patients with stable COPD and healthy sub-jects,serum HMGB1level in patients with AECOPD is abnormally increased,and serum HMGB1is closely related to IL-6,CRP,pulmonary artery pressure and PaO2.ʌKey wordsɔ㊀Chronic obstructive pulmonary disease;㊀Acute exacerbation;㊀Serum high mobility group protein1;㊀Pulmonary function;㊀Correlation㊀㊀慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是一种不可逆的肺功能损伤,患者以呼吸气流受限为特征,主要表现为胸闷㊁气短㊁咳痰等症状㊂抽烟㊁职业性粉尘接触㊁感染等均是引发COPD的相关因素㊂近年来随着空气污染的加重,COPD的发病率呈升高趋势㊂调查显示,COPD及相关疾病已成为世界第3大死因,至2060年可造成超540万人次死亡[1]㊂急性加重期COPD(acute exacerbation of chronic obstructive pulmonary disease,AECOPD)指呼吸道症状急性加重超过日常变异水平且需改变治疗方案,该病㊃0561㊃可诱发心血管疾病及呼吸衰竭等并发症,导致死亡㊂因此,探究AECOPD的致病机制,监测疾病进展,是改善患者预后的重要环节㊂血清高迁移率族蛋白1(highmobility group protein1,HMGB1)是与损伤相关的高度保守核蛋白,在多种肺泡细胞中表达,参与细胞的分化㊁转移㊁免疫应答等过程,其血清水平升高可能与肺部感染加重密切相关[2],但关于其与白细胞介素-6 (interleukin-6,IL-6)㊁C反应蛋白(C-reactive protein, CRP)等炎性因子水平及肺功能参数的关系还需更多临床支持㊂本研究选取同期到我院就诊的AECOPD㊁COPD患者及健康体检者为受试对象,获得如下报道㊂1㊀资料与方法1.1㊀临床资料:从2020年1月至2022年6月到我院就诊的AECOPD患者中选取104例纳入AECOPD组;从就诊的稳定期COPD患者中选取104例纳入COPD 组;从同期健康体检者中选取104例纳入健康对照组㊂AECOPD组患者中男61例,女43例;年龄50~81岁,平均(65.52ʃ8.21)岁㊂COPD组患者中男68例,女36例;年龄52~80岁,平均(66.10ʃ9.33)岁㊂健康对照组受试者中男59例,女45例;年龄49~78岁,平均(64.85ʃ8.24)岁㊂比较三组间一般资料比较差异均无统计学意义(P>0.05)㊂纳入标准:①AECOPD组㊁COPD组患者经临床诊疗确诊符合‘慢性阻塞性肺疾病基层诊疗指南(2018年)“[3]中相关诊断标准: COPD诊断:慢性咳嗽㊁咳痰㊁呼吸困难;有危险因素暴露史;肺功能检查吸入支气管扩张剂后第1秒用力呼气容积(forced expiratory volume in one second,FEV1)/用力肺活量(forced vital capacit,FVC)<0.7,排除其他疾病㊂AECOPD诊断:COPD患者出现气促加重㊁痰量增加㊁痰变脓性中2项即可确诊㊂②所有受试者入组前3个月未服用过免疫抑制剂㊁激素等影响本研究检测指标水平的药物;③所有受试者自愿参加本研究,签署知情同意书㊂排除标准:①需行机械通气或于重症监护室治疗者;②合并严重感染㊁血液系统疾病㊁自身免疫病㊁恶性肿瘤者;③心㊁肝㊁肾功能不全者;④近半年内重大外科手术史者;⑤患有先天性肺病㊁支气管扩张等其他肺部疾病者;⑥肢体运动功能障碍,无法完成6min步行距离(6-minute walk distance,6MWD)测定者㊂健康对照组均为本院健康体检者,且排除AECO-PD㊁COPD及其他呼吸系统疾病诊断,其余排除标准同AECOPD组㊁COPD组㊂本研究符合赫尔辛基人体试验标准,经医院伦理委员会批准㊂1.2㊀方㊀法1.2.1㊀血液生化指标检测:采患者入院24h清晨空腹静脉血4mL,采用Eppendorf5425离心机以3500r/ min,室温下离心10min,离心半径6cm,收集上清液于-80ħ冰箱保存备用㊂采用全自动生化分析仪(日立7600)及ELISA法测定血清HMGB1㊁IL-6㊁CRP㊁降钙素原(procalcitonin,PCT)水平;采用放射免疫法测定血清缺氧诱导因子1α(hypoxia-inducible factor-1α,HIF -1α)水平;相关试剂盒购自上海科艾博生物技术有限公司,所有操作均由专业检验科人员严格按照试剂盒说明进行㊂血常规检查测定白细胞计数(white blood cell count,WBC)㊂1.2.2㊀肺功能参数测定:采用6MWD测定患者活动量,患者测定前休息30min,而后在标有长度的医院走廊内行走,记录其6min步行距离,中途允许停歇㊂留取患者入院24h内的桡/股动脉血,采用全自动血气分析仪(罗氏cobas-b-123)测定二氧化碳分压(partial pressure of carbon dioxide,PaCO2)㊁氧分压(partial pres-sure of oxygen,PaO2)水平㊂采用彩色多普勒超声心动图(GE Vivid7-BT06)测定收缩期肺动脉压力㊂1.3㊀统计学方法:采用SPSS22.0进行数据处理分析,血清HMGB1㊁IL-6水平等计量资料以均数ʃ标准差( x ʃs)表示,三组间比较采用单因素方差分析,两两比较LSD-t检验;性别等计数资料以n(%)表示,采用χ2检验;采用Pearson相关分析血清HMGB1水平与炎性指标及肺功能参数的关系;以P<0.05表示差异或相关性有统计学意义㊂2㊀结㊀果2.1㊀三组入院时的外周血相关指标水平比较:三组入院时的血清HMGB1㊁HIF-1α水平及WBC差异有统计学意义(P<0.05),且AECOPD组>COPD组>健康对照组(P<0.05),见表1㊂表1㊀三组入院时的外周血相关指标水平比较( xʃs)组别例数HMGB1(μg/L)HIF-1α(ng/L)WBC(ˑ109L-1) AECOPD组104135.72ʃ26.37∗#202.30ʃ16.25∗#9.63ʃ0.58∗# COPD组104105.46ʃ20.15∗168.37ʃ13.62∗7.82ʃ0.61∗㊃1561㊃健康对照组10468.14ʃ10.3272.58ʃ12.41 6.94ʃ0.63F 295.9902339.429530.942P<0.001<0.001<0.001㊀㊀注:与健康对照组比较,∗P<0.017;与COPD 组比较,#P<0.0172.2㊀三组入院时的血清炎性因子水平比较:三组血清IL -6㊁CRP ㊁PCT 水平差异有统计学意义(P <0.05),且AECOPD 组>COPD 组>健康对照组(P<0.05),见表2㊂表2㊀三组入院时的血清炎性因子水平比较( xʃs)组别例数IL -6(pg /mL )CRP (mg /L )PCT (ng /mL )AECOPD 组10476.25ʃ6.04∗#32.35ʃ4.02∗#9.54ʃ1.20∗#COPD 组10451.38ʃ5.63∗25.17ʃ3.58∗7.61ʃ1.15∗健康对照组1045.78ʃ0.89 1.65ʃ0.390.85ʃ0.10F 5778.1532762.0722343.303P<0.001<0.001<0.001㊀㊀注:与健康对照组比较,∗P<0.017;与COPD 组比较,#P<0.0172.3㊀三组入院时的肺功能参数比较:三组入院时的6MWD 值及PaO 2水平差异有统计学意义(P <0.05),且AECOPD 组<COPD 组<健康对照组(P <0.05)㊂三组入院时的肺动脉压㊁PaCO 2水平差异有统计学意义(P<0.05),且AECOPD 组>COPD 组>健康对照组(P <0.05),见表3㊂表3㊀三组入院时的肺功能参数比较( xʃs)组别例数6MWD (m )肺动脉压(mmHg )PaCO 2(mmHg )PaO 2(mmHg )AECOPD 组104242.39ʃ22.62∗#50.20ʃ9.41∗#65.03ʃ6.42∗#69.50ʃ7.25∗#COPD 组104314.58ʃ26.73∗32.58ʃ8.29∗59.51ʃ6.53∗82.37ʃ6.46∗健康对照组104397.30ʃ35.899.92ʃ0.5333.12ʃ3.4597.32ʃ1.01F 745.613807.434947.661634.541P<0.001<0.001<0.001<0.001㊀㊀注:与健康对照组比较,∗P<0.017;与COPD 组比较,#P<0.0172.4㊀AECOPD 患者入院时血清HMGB1水平与炎性因子㊁肺功能参数等指标的相关性:Pearson 相关分析显示,AECOPD 患者入院时的血清HMGB1水平与IL -6㊁CRP ㊁肺动脉压水平呈正相关(P <0.05),与PaO 2水平呈负相关(P<0.05),见表4㊂表4㊀血清HMGB1水平与炎性因子肺功能参数等指标的相关性指标统计值HIF -1αWBC IL -6CRP PCT 6MWD 肺动脉压PaCO 2PaO 2HMGB1r0.1210.1860.5660.2870.132-0.1240.2300.131-0.212P 0.2220.059<0.0010.0030.1820.2100.0190.1840.0273㊀讨㊀论COPD 目前已成为全球公共卫生问题,其炎细胞㊃2561㊃浸润可累及内分泌系统㊁骨骼系统等多种组织,若不及时治疗病情加重,则诱发AECOPD㊂AECOPD患者短期内可出现呼吸困难加重,痰量增多,咳嗽加剧等症状,临床死亡率高㊂目前AECOPD的致病机制尚未完全明确,但关于机体炎性因子过度分泌对肺组织结构的破坏作用已形成共识㊂HMGB1主要来源有2种,一种由单核巨噬细胞㊁单核细胞等炎性细胞主动分泌,另一种由坏死细胞被动分泌,可扩大组织炎症级联反应,在多种疾病进展中发挥作用㊂此前Pouwels等经小鼠实验表明HMGB1与白细胞介素-37(IL-37)激活可诱导急性肺损伤,抑制肺泡上皮修复[4]㊂本研究显示AECOPD患者的血清HMGB1水平较COPD患者及健康受试者异常升高,且与IL-6㊁CRP㊁肺动脉压㊁PaO2水平显著相关,这为呼吸系统疾病的临床诊疗提供新方向㊂本研究中三组血清HMGB1㊁HIF-1α㊁IL-6㊁CRP㊁PCT及外周血WBC水平,AECOPD组>COPD组>健康对照组㊂说明上述炎性指标在COPD患者病情严重程度评估方面具有一定指导意义㊂IL-6作为一种多功能细胞因子,主要由单核巨噬细胞㊁T淋巴细胞合成释放,参与机体免疫调节,加剧炎性损伤㊂有报道称血清IL-6水平升高是COPD急性加重的预测指标,AECO-PD组患者的IL-6水平高于COPD稳定期及健康对照组㊂PCT主要由肺组织神经内分泌细胞及甲状腺髓质C细胞分泌,通常状态下血浆水平稳定,当机体出现细菌㊁真菌等感染时水平明显升高[5]㊂CRP是机体较为敏感的急性期时项蛋白,可激活补体,增强吞噬作用,以清除病原微生物㊂一项回顾性分析显示血清PCT㊁CRP可辅助诊断COPD合并Ⅱ型呼吸衰竭患者预后,与肺部CT联合诊断的效能为0.835[6]㊂Francis等[7]证明给予AECOPD住院患者CRP水平监测指导可有效反映患者病情状况,降低治疗过程中的抗生素用量㊂核蛋白HIF-1α普遍存在于哺乳动物细胞,缺氧状态下其降解作用得到抑制,与β亚基结合形成HIF,参与细胞核内基因转录[8]㊂贺孟君等[9]报道AECOPD患者血清HIF-1α高于正常水平,与肺功能密切相关,这为本研究提供理论支持㊂比较各组肺功能参数,结果显示三组6MWD值及PaO2水平:AECOPD组<COPD组<健康对照组,三组肺动脉压㊁PaCO2水平:AECOPD组>COPD组>健康对照组㊂肺动脉压升高可提示肺部炎症损伤,肺部血管平滑肌细胞增殖,血管内皮损伤均可提高血管阻力,形成肺动脉高压㊂Kovacs等[10]回顾性分析142例COPD 患者的临床资料,发现肺动脉高压严重程度是影响患者预后的相关因素㊂血氧PaCO2㊁PaO2水平是反映肺通气功能的重要指标㊂相关研究显示COPD合并呼吸衰竭患者的PaO2水平较低,PaCO2水平较高,且与细胞因子水平密切相关[11]㊂进一步分析血清HMGB1水平与炎性指标及肺功能参数的关系,显示HMGB1与IL-6㊁CRP㊁肺动脉压呈正相关,与PaO2水平呈负相关㊂表明HMGB1水平是评估COPD发生发展重要指标㊂近期一项非随机队列研究发现COPD患者HMGB1㊁IL-6㊁肿瘤坏死因子α(tumor necrosis fctor-alpha,TNF-α)及HIF-1α与肺动脉压呈正相关,与FEV1/FVC呈负相关㊂还有研究显示COPD患者痰液中HMGB1㊁IL-37㊁热应激蛋白(Heatstressproteins,HSP70)水平与S100A8蛋白浓度呈负相关[12]㊂综上所述,AECOPD患者的血清HMGB1水平异常升高,与IL-6㊁CRP㊁肺动脉压呈正相关,与PaO2水平呈负相关,这为AECOPD的临床诊断及预后评估提供新思路㊂ʌ参考文献ɔ[1]㊀中华医学会呼吸病学分会慢性阻塞性肺疾病学组,中国医师协会呼吸医师分会慢性阻塞性肺疾病工作委员会.慢性阻塞性肺疾病诊治指南(2021年修订版)[J].中华结核和呼吸杂志,2021,44(3):170-205.[2]㊀Yang K,Fan M,Wang X,et ctate promotes macrophageHMGB1lactylation,acetylation,and exosomal release inpolymicrobial sepsis[J].Cell Death Differ,2022,29(1):133 -146.[3]㊀中华医学会,中华医学会杂志社,中华医学会全科医学分会,等.慢性阻塞性肺疾病基层诊疗指南(2018年)[J].中华全科医师杂志,2018,17(11):15.[4]㊀Pouwels SD,Hesse L,Wu X,et al.LL-37and HMGB1in-duce alveolar damage and reduce lung tissue regeneration viaRAGE[J].Am J Physiol Lung Cell Mol Physiol,2021,321(4):641-652.[5]㊀Lin SH,He YP,Lian JJ,et al.Procalcitonin kinetics to guidesequential invasive-noninvasive mechanical ventilation wea-ning in patients with acute exacerbation of chronic obstructivepulmonary disease and respiratory failure:procalcitonin's ad-junct role[J].Libyan Med,2021,16(1):1961382. [6]㊀邓爱兵,宋健,王静,等.肺CT联合降钙素原㊁C反应蛋白检测对COPDⅡ型呼吸衰竭疗效㊁预后评估的临床价值[J].临床和实验医学杂志,2021,20(2):161-165. [7]㊀Francis NA,Gillespie D,White P,et al.C-reactive proteinpoint-of-care testing for safely reducing antibiotics for acuteexacerbations of chronic obstructive pulmonary disease:thePACE RCT[J].Health Technol Assess,2020,24(15):1-㊃3561㊃108.[8]㊀Shukla SD,Walters EH,Simpson JL,et al.Hypoxia-induc-ible factor and bacterial infections in chronic obstructive pul-monary disease[J].Respirology,2020,25(1):53-63. [9]㊀贺孟君,张家艳,李燕舞,等.血清SDC-1㊁HIF-1α㊁PGRN与AECOPD患者肺功能及预后恢复的相关性分析[J].标记免疫分析与临床,2021,28(6):977-982. [10]㊀Kovacs G,Avian A,Bachmaier G,et al.Severe pulmonaryhypertension in COPD:impact on survival and diagnosticapproach[J].Chest,2022,162(1):202-212.[11]㊀傅正,苏晋豫,白志余.PaO2㊁PaCO2㊁SaO2对呼吸衰竭病人病情发生发展的影响[J].内蒙古医科大学学报,2020,42(6):623-625.[12]㊀Huang X,Tan X,Liang Y,et al.Differential DAMP releasewas observed in the sputum of COPD,asthma and asthma-COPD overlap(ACO)patients[J].Sci Rep,2019,9(1):19241.ʌ文章编号ɔ1006-6233(2023)10-1654-06CT引导下经皮穿刺肺活检诊断非小细胞肺癌准确率及其影响因素分析刘㊀阳,㊀岳孟超(四川省巴中市中心医院放射科,㊀四川㊀巴中㊀636000)ʌ摘㊀要ɔ目的:探讨CT引导下经皮穿刺肺活检(PTNB)诊断非小细胞肺癌(NSCLC)准确率及其影响因素㊂方法:选取2020年5月至2022年5月在本院就诊的98例NSCLC患者为研究对象,均行PT-NB并以术后病理检查结果为金标准,统计PTNB诊断NSCLC结果,分析PTNB诊断NSCLC准确率的影响因素㊂结果:PTNB诊断NSCLC准确率为87.76(86/98),其中,诊断腺癌㊁鳞癌㊁大细胞癌㊁腺鳞癌的准确率分别为91.53%(54/59)㊁93.94(31/33)㊁0.00%(0/2)㊁25.00%(1/4)㊂单因素分析结果显示,诊断准确组和诊断不准确组在性别㊁年龄㊁是否合并钙化㊁穿刺活检组织大小㊁穿刺次数比较,差异无统计学意义(P>0.05);在病灶位置㊁病灶长径㊁病灶与胸壁的距离㊁是否合并坏死㊁穿刺深度比较,差异有统计学意义(P<0.05);多因素分析结果显示,病灶位置为下叶㊁病灶长径<2cm㊁病灶与胸壁的距离<2cm㊁合并坏死是影响PTNB诊断NSCLC准确率的独立危险因素㊂结论:PTNB应用于NSCLC,诊断腺癌和鳞癌的价值较高,诊断大细胞癌和腺鳞癌准确率偏低,影响PTNB诊断NSCLC准确率的独立危险因素有病灶位置为下叶㊁病灶长径<2cm㊁病灶与胸壁的距离<2cm㊁合并坏死,针对性采取措施,有利于提高诊断准确率㊂ʌ关键词ɔ㊀CT引导下经皮穿刺肺活检;㊀非小细胞肺癌;㊀准确率;㊀影响因素ʌ文献标识码ɔ㊀A㊀㊀㊀㊀㊀ʌdoiɔ10.3969/j.issn.1006-6233.2023.10.013Diagnostic Accuracy of CT-Guided Percutaneous Transthoracic NeedleBiopsy for Non-Small Cell Lung Cancer and Its Influencing FactorsLIU Yang,YUE Mengchao(Bazhong Central Hospital,Sichuan Bazhong636000,China)ʌAbstractɔObjective:To explore the diagnostic accuracy of CT-guided percutaneous transthoracic nee-dle biopsy(PTNB)for non-small cell lung cancer(NSCLC)and its influencing factors.Methods:A total of 98patients with NSCLC treated in the hospital were enrolled as the research subjects between May2020and May2022.All underwent PTNB.Taking the results of postoperative pathological examination as the golden standard,diagnostic results of PTNB for NSCLC were statistically analyzed,and the influencing factors of di-agnostic accuracy were analyzed.Results:The diagnostic accuracy of PTNB for NSCLC was87.76%(86/ 98),and the accuracy rates of adenocarcinoma,squamous cell carcinoma,large cell carcinoma and adeno-squamous carcinoma were91.53%(54/59),93.94%(31/33),0.00%(0/2)and25.00%(1/4),re-㊃4561㊃ʌ基金项目ɔ四川省医学科研青年创新课题,(编号:Q15010)。

The future is a subject of endless fascination and speculation.As we look ahead,its natural to wonder what lies in store for us.The future is shaped by a myriad of factors, including technological advancements,social changes,and environmental shifts.Here are some perspectives on what the future might hold based on current trends and emerging ideas.Technological Innovations:The rapid pace of technology is set to continue,with artificial intelligence,machine learning,and automation becoming more integrated into our daily lives.This could lead to significant improvements in efficiency and convenience,but also raises questions about job displacement and the ethical implications of AI decisionmaking.Environmental Challenges:Climate change is one of the most pressing issues facing the future.We may see more severe weather events,rising sea levels,and shifts in ecosystems.The response to these challenges will likely involve a combination of mitigation strategies,such as reducing greenhouse gas emissions,and adaptation measures,like building more resilient infrastructure.Social Dynamics:Society is evolving,with increasing diversity and a growing emphasis on inclusivity and equality.The future may see a continued push for social justice,as well as the rise of new social movements that address emerging concerns.Healthcare Advancements:Medical science is on the brink of breakthroughs that could revolutionize healthcare. Personalized medicine,stem cell therapies,and gene editing technologies like CRISPR have the potential to cure diseases that are currently untreatable and to enhance human health in unprecedented ways.Education Transformation:The way we learn and educate may also change dramatically.With the rise of online learning platforms and digital resources,education could become more accessible and personalized.This shift could democratize learning and allow for more flexible and diverse educational paths.Economic Shifts:The global economy is likely to undergo significant changes,with emerging markets playing a more prominent role and the potential for new economic models that prioritize sustainability and social welfare over pure profit.Space Exploration:The future may also see humans establishing a more permanent presence in space.With missions to Mars and the potential for lunar bases,space exploration could become a more regular endeavor,opening up new frontiers for scientific discovery and even colonization.Cultural Evolution:As the world becomes more interconnected,we can expect a blending of cultures and the emergence of new cultural forms.This could lead to a richer,more diverse global culture, but also challenges in maintaining cultural identity and heritage.Privacy and Security:With the increasing amount of personal data being collected and stored,the future will likely see ongoing debates about privacy,surveillance,and the security of our digital lives.Urbanization:As more people move to cities,urban areas will continue to grow and evolve.This could lead to innovative solutions for housing,transportation,and resource management,but also challenges related to overcrowding and infrastructure.In conclusion,the future is a canvas of possibilities,painted with the brushstrokes of our present actions and decisions.While its impossible to predict with certainty what the future will look like,we can make educated guesses based on current trends and the direction in which society is moving.By considering these perspectives,we can better prepare for and shape the future we want to see.。

非感染性葡萄膜炎的系统治疗进展张雨晴; 邵毅; 周琼【期刊名称】《《国际眼科杂志》》【年(卷),期】2019(019)012【总页数】3页(P2045-2047)【关键词】非感染性葡萄膜炎; 系统治疗; 糖皮质激素; 免疫抑制剂; 生物制剂; 进展【作者】张雨晴; 邵毅; 周琼【作者单位】330000 中国江西省南昌市南昌大学第一附属医院眼科【正文语种】中文0引言炎症性眼病，如葡萄膜炎和巩膜炎，是全世界失明和视力损害的重要原因[1-4]，其中以葡萄膜炎最多见。

葡萄膜炎是累及葡萄膜、视网膜、视网膜血管以及玻璃体的一组炎症性眼病，临床症状主要有视力下降、眼红、眼痛、畏光、流泪、飞蚊症等[5]。

由于其主要影响青壮年，治疗棘手，易于反复发作，治疗不及时或处理不当易导致盲目，因此受到全球眼科学界的重视。

葡萄膜炎主要包括感染性葡萄膜炎和非感染性葡萄膜炎两大类。

当患者出现葡萄膜炎时，需要确定病因以指导研究和治疗[6]。

感染性葡萄膜炎常见的病原体有弓形虫、弓蛔虫、结核、梅毒、病毒、细菌和真菌等，通常需要特异性药物治疗，早期诊断和正确的治疗后，患者视力预后较好。

而非感染性葡萄膜炎因其病因复杂、发病率高等导致预后常不理想。

1非感染性葡萄膜炎在发达国家，非感染性葡萄膜炎占所有导致失明病例原因的10%～15%[7]。

导致患者视力丧失的常见原因有囊样黄斑水肿(cystic macular edema，CME)、继发性白内障、高眼压(high ocular pressure，HOP)和玻璃体混浊(vitreous opacity，VO)[8]。

动物实验和部分临床试验数据支持T细胞在葡萄膜炎发展中的关键作用[9-23]。

在环境和多基因影响的背景下，非感染性葡萄膜炎的发病机制被认为是免疫系统内调节和炎症机制之间的不平衡[24]。

非感染性葡萄膜炎被认为是由T细胞介导的自身免疫性炎症反应。

在发病时外周血中的白细胞介素(interleukin，IL)、干扰素(interferon，IFN)等细胞因子作用活跃，它们被发现与非感染性葡萄膜炎的发生、发展、静止密切相关。

西比灵治疗偏头痛的经颅多普勒研究齐永乐;孟红旗【摘要】目的评价西比灵治疗偏头痛的疗效及治疗前后的经颅多普勒改变.方法88例偏头痛患者随机分为治疗组和对照组,西比灵组予西比灵5mg,qn,两组均连续服药4周为1个疗程,2个疗程时间间隔3天,2个疗程后评定疗效,并在治疗前后有经颅多普勒(TCD)检测大脑前动脉(ACA)、大脑中动脉(MCA)、大脑后动脉(PCA)及基底动脉(BA)的血流速度.结果西比灵组头痛消失时间随每次发作而缩短,与对照组比较有显著性差异(P>0.01);治疗组治疗后,平均流速明显降低,与治疗前比较有非常显著性差异(P<0.01);对照组无显著性差异(P<0.05).结论西比灵能改善脑血流的供应,为偏头痛的治疗提供了依据.【期刊名称】《佛山科学技术学院学报（自然科学版）》【年(卷),期】2010(028)003【总页数】4页(P79-82)【关键词】西比灵;偏头痛;多普勒;血流速度【作者】齐永乐;孟红旗【作者单位】河南省三门峡市第三人民医院,内一科,河南,三门峡,472143;佛山科学技术学院,医学系,广东,佛山,528000【正文语种】中文【中图分类】R453偏头痛是一种反复发作的一侧搏动性头痛及神经功能障碍,是一种顽固难治、发病率较高的常见病[1]。

我院神经科自2003年1月～2007年5月诊治的门诊病人,应用西比灵,对88例偏头痛患者进行对照学研究,疗效显著,并在治疗前后进行TCD 检测,现报道如下。

1 对象与方法1.1 对象笔者诊治门诊病人88例,其中男48例,女40例,。

随机分为2组,治疗组44例中,年龄22～55岁,平均38.50岁;2病程最短1年,最长8.5年,平均4.6年。

对照组44例在年龄、性别及病程方面比较,经i 2及t检验,无显著性差异(P＞0.05),具有可比性。

1.2 诊断标准参照国际头痛学会(ISH)头痛分类委员会制定的诊断标准[2]。

［３０］ＧＵＯＹＰ，ＤＵＬＸ．Ｓｔｕｄｙｏｎｔｈｅｐｒｅｄｉｃｔｉｖｅｅｆｆｅｃｔｏｆｔｕｍｏｒｍａｒｋ ｅｒｓｏｎｌｙｍｐｈｎｏｄｅｍｅｔａｓｔａｓｉｓｉｎｐａｔｉｅｎｔｓｗｉｔｈｉｎｔｒａｈｅｐａｔｉｃｃｈｏｌａｎｇｉｏｃａｒｃｉｎｏｍａ［Ｊ］．ＧｕｉｚｈｏｕＭｅｄＪ，２０１９，４３（１２）：１８６３－１８６６．（ｉｎＣｈｉｎｅｓｅ）郭育鹏，杜立学．肿瘤标志物对肝内胆管细胞癌患者发生淋巴结转移的预测效果研究［Ｊ］．贵州医药，２０１９，４３（１２）：１８６３－１８６６．［３１］ＪＥＯＮＧＳ，ＬＵＯＧ，ＷＡＮＧＺＨ，ｅｔａｌ．ＩｍｐａｃｔｏｆｖｉｒａｌｈｅｐａｔｉｔｉｓＢｓｔａｔｕｓｏｎｏｕｔｃｏｍｅｓｏｆｉｎｔｒａｈｅｐａｔｉｃｃｈｏｌａｎｇｉｏｃａｒｃｉｎｏｍａ：Ａｍｅｔａ－ａｎａｌｙｓｉｓ［Ｊ］．ＨｅｐａｔｏｌＩｎｔ，２０１８，１２（４）：３３０－３３８．［３２］ＪＵＴＲＩＣＺ，ＪＯＨＮＳＴＯＮＷＣ，ＨＯＥＮＨＭ，ｅｔａｌ．Ｉｍｐａｃｔｏｆｌｙｍｐｈｎｏｄｅｓｔａｔｕｓｉｎｐａｔｉｅｎｔｓｗｉｔｈｉｎｔｒａｈｅｐａｔｉｃｃｈｏｌａｎｇｉｏｃａｒｃｉｎｏｍａｔｒｅａｔｅｄｂｙｍａｊｏｒｈｅｐａｔｅｃｔｏｍｙ：Ａｒｅｖｉｅｗｏｆｔｈｅｎａｔｉｏｎａｌｃａｎｃｅｒｄａｔａｂａｓｅ［Ｊ］．ＨＰＢ（Ｏｘｆｏｒｄ），２０１６，１８（１）：７９－８７．［３３］ＶＩＴＡＬＥＡ，ＭＯＵＳＴＡＦＡＭ，ＳＰＯＬＶＥＲＡＴＯＧ，ｅｔａｌ．Ｄｅｆｉｎｉｎｇｔｈｅｐｏｓｓｉｂｌｅｔｈｅｒａｐｅｕｔｉｃｂｅｎｅｆｉｔｏｆｌｙｍｐｈａｄｅｎｅｃｔｏｍｙａｍｏｎｇｐａｔｉｅｎｔｓｕｎｄｅｒｇｏｉｎｇｈｅｐａｔｉｃｒｅｓｅｃｔｉｏｎｆｏｒｉｎｔｒａｈｅｐａｔｉｃｃｈｏｌａｎ ｇｉｏｃａｒｃｉｎｏｍａ［Ｊ］．ＪＳｕｒｇＯｎｃｏｌ，２０１６，１１３（６）：６８５－６９１．［３４］ＬＵＷ，ＴＡＮＧＺＨ，ＱＵＡＮＺＷ．Ｖｉｅｗｐｏｉｎｔｏｆｓｙｓｔｅｍａｔｉｃｌｙｍｐｈ ａｄｅｎｅｃｔｏｍｙｆｏｒｉｎｔｒａｈｅｐａｔｉｃｃｈｏｌａｎｇｉｏｃａｒｃｉｎｏｍａｐａｔｉｅｎｔｓ［Ｊ］．ＣｈｉｎＪＳｕｒｇ，２０１９，５７（４）：２４７－２５２．（ｉｎＣｈｉｎｅｓｅ）陆巍，汤朝晖，全志伟．肝内胆管癌淋巴结相关问题的探讨［Ｊ］．中华外科杂志，２０１９，５７（４）：２４７－２５２．［３５］ＲＡＨＮＥＭＡＩ－ＡＺＡＲＡＡ，ＷＥＩＳＢＲＯＤＡＢ，ＤＩＬＬＨＯＦＦＭ，ｅｔａｌ．Ｉｎｔｒａｈｅｐａｔｉｃｃｈｏｌａｎｇｉｏｃａｒｃｉｎｏｍａ：Ｃｕｒｒｅｎｔｍａｎａｇｅｍｅｎｔａｎｄｅｍｅｒｇｉｎｇｔｈｅｒａｐｉｅｓ［Ｊ］．ＥｘｐｅｒｔＲｅｖＧａｓｔｒｏｅｎｔｅｒｏｌＨｅｐａｔｏｌ，２０１７，１１（５）：４３９－４４９．［３６］ＮＡＫＡＮＯＭ，ＡＲＩＩＺＵＭＩＳＩ，ＹＡＭＡＭＯＴＯＭ．Ｉｎｔｒａｈｅｐａｔｉｃｃｈｏｌａｎ ｇｉｏｃａｒｃｉｎｏｍａ［Ｊ］．ＳｅｍｉｎＤｉａｇｎＰａｔｈｏｌ，２０１７，３４（２）：１６０－１６６．［３７］ＬＥＥＡＪ，ＣＨＵＮＹＳ．Ｉｎｔｒａｈｅｐａｔｉｃｃｈｏｌａｎｇｉｏｃａｒｃｉｎｏｍａ：ＴｈｅＡＪＣＣ／ＵＩＣＣ８ｔｈｅｄｉｔｉｏｎｕｐｄａｔｅｓ［Ｊ］．ＣｈｉｎＣｌｉｎＯｎｃｏｌ，２０１８，７（５）：５２．［３８］ＭＯＲＩＮＥＹ，ＳＨＩＭＡＤＡＭ．Ｔｈｅｖａｌｕｅｏｆｓｙｓｔｅｍａｔｉｃｌｙｍｐｈｎｏｄｅｄｉｓｓｅｃｔｉｏｎｆｏｒｉｎｔｒａｈｅｐａｔｉｃｃｈｏｌａｎｇｉｏｃａｒｃｉｎｏｍａｆｒｏｍｔｈｅｖｉｅｗｐｏｉｎｔｏｆｌｉｖｅｒｌｙｍｐｈａｔｉｃｓ［Ｊ］．ＪＧａｓｔｒｏｅｎｔｅｒｏｌ，２０１５，５０（９）：９１３－９２７．引证本文：ＺＨＡＮＧＨＹ，ＪＵＭＧ，ＸＵＦ．Ｃｕｒｒｅｎｔｓｔａｔｕｓａｎｄｐｒｏｓｐｅｃｔｏｆｐｒｏｐｈｙｌａｃｔｉｃｌｙｍｐｈｎｏｄｅｄｉｓｓｅｃｔｉｏｎｆｏｒｉｎｔｒａｈｅｐａｔｉｃｃｈｏｌａｎｇｉｏｃａｒｃｉｎｏｍａ［Ｊ］．ＪＣｌｉｎＨｅｐａｔｏｌ，２０２０，３６（９）：２１０３－２１０６．（ｉｎＣｈｉｎｅｓｅ）张荷月，鞠明光，徐锋．肝内胆管癌预防性清扫淋巴结现状与前景［Ｊ］．临床肝胆病杂志，２０２０，３６（９）：２１０３－２１０６．（本文编辑：刘晓红）·国外期刊精品文章简介·替诺福韦相比恩替卡韦可显著改善ＨＢＶ相关肝细胞癌患者肝切除术后复发 【据Ｈｅｐａｔｏｌｏｇｙ２０２０年４月报道】题：替诺福韦与恩替卡韦对ＨＢＶ相关肝细胞癌肝切除术后复发的影响（作者ＣｈｏｉＪ等）替诺福韦（ＴＤＦ）和恩替卡韦（ＥＴＶ）均为目前慢性乙型肝炎（ＣＨＢ）临床指南中的一线治疗药物，有较高的抗病毒疗效和较低的耐药性。

巨大无功能肾上腺皮质癌1例报道并文献复习李鹏;杨庆【期刊名称】《重庆医学》【年(卷),期】2017(046)030【总页数】2页(P4316-4317)【作者】李鹏;杨庆【作者单位】解放军第一五三中心医院泌尿外科,郑州450014;第二军医大学附属长海医院泌尿外科,上海200003;第二军医大学附属长海医院泌尿外科,上海200003【正文语种】中文【中图分类】R699.3肾上腺皮质癌临床鲜见，其中无功能者更为罕见，该类肾上腺皮质癌缺乏特异性的临床症状，其早期确诊困难、手术治疗难度大、预后较差。

解放军第一五三中心医院于2015年10月收治右侧巨大肾上腺皮质癌1例，肿瘤最长径约23 cm，成功实施右肾上腺肿瘤切除术。

本文通过该病例资料结合文献复习对肾上腺皮质癌的诊断和治疗做简要讨论。

患者，男，19岁，以“右侧腰腹部疼痛6周”为主诉于2015年10月10日入院。

患者入院前6周无明显诱因出现右侧腰腹部持续性胀痛，无放射痛，无血压异常波动，无消化道症状及排尿异常。

入院查体：右上腹隆起，可触及一体积约13cm×10 cm大小的包块，形态欠规则，内界达腹正中线，外界达右侧腋前线，下界达肋缘下6 cm，上界不可触及，质地偏硬，活动度差，轻度压痛，余腹部无压痛、反跳痛。

实验室检查：血常规提示轻度贫血（Hb 105 g/L），肝肾功能、电解质均正常，甲胎蛋白、糖类抗原125、糖类抗原19-9、癌胚抗原水平均正常；血皮质醇、促肾上腺皮质激素、醛固酮及儿茶酚胺均正常。

腹部彩超：于右侧肝肾间隙见17.0 cm×14.3 cm×11.6 cm实性非均质性肿块，边界于肝脏分界欠清，内呈分叶状，彩色多普勒超声（CDFI）可见少量血流信号，肝肾均被肿块挤压。

肾动静脉CT增强造影：右侧肾上腺区见巨大软组织肿块影，边界欠清晰，大小约16 cm×12 cm，该肿块部分由腹腔干旁起源于腹主动脉供血，周围肝脏、右侧肾脏、下腔静脉及右肾静脉受压，增强后病灶中度不均匀强化。

海洋中丰富的生物资源、矿产资源、化学资源和动力资源是人类不可或缺的资源宝库，与人类的生存和发展密切相关。

主题语境：海洋探索篇幅：297词建议用时：6分钟The meaning of ocean exploration 海洋探索的意义江西孙朝岚1Despite the fact that the oceancovers approximately 70%of Earth s sur⁃face and plays a critical role in support⁃ing life on our planet,from the air we breathe and the food we eat to weather and climate patterns,our understanding of the ocean remains limited.2Ocean exploration is about making discoveries,searching for things that are unusualand unexpected.As the first step in the scientific process,the observations and documenta­tion of biological,chemical,physical,geological,and archaeological aspects of the ocean gained from exploration set the stage for future research and decision­making.3Through ocean exploration,we collect data and information needed to address bothcurrent and emerging (新兴的)science and management needs.Ocean exploration helps to ensure that ocean resources are not just managed,but managed in a sustainable way,sothose resources are around for future generations to enjoy.4Unlocking the mysteries of ocean ecosystems can reveal new sources for medical therapies and vaccines,food,and rmation from ocean exploration can help us understand how we are affecting and being affected by changes in Earth s environment,in­cluding changes in weather and climate.Insights from ocean exploration can help us better understand and respond to earthquakes,tsunamis,and other damage.5The challenges met while exploring the ocean can provide the impetus(动力)for new technologies and engineering innovations that can be applied in other situations,allowing us to respond more effectively in the face of an ocean crisis,such as an oil spill.And,ocean exploration can improve ocean literacy and inspire young people to seek critical careers in science,technology,engineering,and mathematics.6Humans naturally have desire for knowledge and quest for adventure.And if all of these examples don t provide enough reasons to explore the ocean,well,ocean exploration is also just cool.ReadingCheckInference 1.What s the function of the first paragraph?A.To introduce the topic of the text.B.To stress the ocean plays a role in our life.C.To tell us we know a little about the ocean.D.To help us know the importance of the ocean. Inference 2.In which part of a magazine can we read the text?A.Health.B.Economy.cation.D.Travel.Detail 3.What can we know about ocean exploration from the text?A.It can provide us with new technologies.B.It can help us find new sources for medicine.C.It helps us better avoid and respond to disasters.D.It inspires people to seek critical careers in science.LanguageStudyⅠ.Difficult sentence in the textDespite the fact that the ocean covers approximately70%of Earth s surface and plays a critical role in supporting life on our planet,from the air we breathe and the food we eat to weather and climate patterns,our understanding of the ocean remains limited.尽管海洋覆盖了地球表面约70%的面积，从我们呼吸的空气、吃的食物到天气和气候模式，海洋在维持地球上的生命方面发挥着至关重要的作用，但我们对海洋的了解仍然有限。

抑郁症患者负性情绪刺激注意偏向的眼动指标分析汪敏【摘要】目的探讨抑郁症患者负性情绪刺激注意偏向的眼动特征。

方法选取抑郁症患者53例为抑郁组,无抑郁症状患者44例为对照组,以中国情绪面孔系统(CAFPS)为刺激材料，比较被试执行过程中的眼动指标(首视点定向偏向分数、首视点注视时间、注视总时间偏向分数),并以“分组情况”和“呈现时间”为因素，对首视点定向偏向分数和注视总时间偏向分数进行效应分析。

结果抑郁组首视点定向偏向分数和总注视时间偏向分数均高于对照组(均P <0.05)。

“分组情况”与“呈现时间”对首视点定向偏向的主效应明显(P<0.05),交互效应差异无统计学意义(P> 0.05)；“分组情况”与“呈现时间”对总注视时间定向偏向主效应明显(P<0.05),交互效应差异无统计学意义(P> 0.05),“呈现时间”对总注视时间定向偏向效应高于“分组情况”(P<0.05)。

结论抑郁症患者对负性情绪刺激存在注意偏向情况，偏向自刺激开始随即发生，反应时长更久,可进一步加剧注意偏向发生。

【关键词】抑郁症;注意偏向;眼动doi:10.3969^.issn,1671-0800.2021.02.022【中图分类号】R749.4【文献标志码】A【文章编号】1671-0800(2021)02-0189-03认知决定情感反应与行为表现，而情绪与行为又反作用于认知。

信息获取过程中，情绪性信息更能吸引注意，并占用注意资源，引起情绪信息注意偏向叫抑郁症患者在信息摄取、加工、形成认知过程中，更容易向与自己心境一致的方向产生偏倚，这种偏倚是从摄取信息之初的注意偏倚开始的叫抑郁患者对负性刺激注意的偏向,正性刺激注意远离；这种警觉-逃避模式，使抑郁情绪表现趋于慢性化％本研究基于动眼技术，对抑郁症患者负性情绪刺激注意的定向、维持方面情况进行分析，旨在为抑郁症患者注意改善提供依据。

报道如下。

1资料与方法1.1一般资料选取杭州市第七人民医院心身科收治的抑郁症患者53例，均符合:(1)美国精神障碍诊断与统计手册(DSM-IV)中抑郁症诊断标准叫⑵视力或矫正视力正常，无其他不利完成眼动实验的眼部病变；(3)右利手，具备正常感知及语言沟通能力;(4)无严重躯体残疾、重病卧床或极度虚弱,不能配合研究者;(5)患者及家属知情同意。

Medical, Surgical, and Endoscopic Management of Gastroesophageal Reflux DiseaseDeron J Tessier, MDIntroductionGastroesophageal reflux disease (GERD) is one of the most common gastrointestinal diseases facing society today. In the US alone, more than 19 million people have the disease. Approximately 20% of US adults have one episode of GERD in a week, with about 7% reporting significant daily heartburn symptoms requiring some type of treatment.1 Medical treatments for GERD, both prescription and over the counter, cost approximately $19 billion per year in the US. Fortunately the majority of GERD symptoms are minor and self-limiting; however, complications, including esophagitis, Barrett syndrome, and adenocarcinoma, are on the rise in W estern countries, suggesting that GERD does not have a benign course in all patients. The term nonerosive reflux disease (NERD) has been used to describe the majority of patients that have a benign, uncomplicated disease course. This group has GERD symptoms without evidence of esophagitis on endoscopy.The clinical management of GERD has evolved rapidly since the early 1990s with the introduction of potent medications as well as less invasive surgical techniques to help treat patients with medically refractory disease. Novel medications to help prevent transient lower esophageal sphincter relaxations (tLESRs) are being developed and may be added to the armamentarium.2 Additionally, endoscopic therapies have gained some support, though long-term data suggest that these techniques are not durable. This article reviews the pathophysiology, presentation, workup, treatment, and emerging therapies for GERD with an emphasis on surgical management and outcomes to help primary care physicians have a better understanding of the role of surgery in this complex disease.TerminologyThe classification of GERD has been confusing because of numerous definitions based on symptomatic, physiologic, and/or diagnostic criteria. In simplistic terms, GERD refers to the pathologic reflux of gastric contents into the esophagus through the gastroesophageal junction. This refluxate can be acidic, neutral, or basic (bile). It can be gas, liquid, semisolid, or a combination. The operative term in this definition is pathologic, in that belching and vomiting would not be considered pathologic because they are typically isolated events. Previously GERD was defined as a reflux event resulting in a decrease in pH of <4, several centimeters above the gastroesophageal junction. With introduction of impedance testing (see below), this definition will likely be abandoned as our knowledge of nonacid reflux comes into focus.PathophysiologyThe normal anatomy of the gastroesophageal junction allows for relaxation of the lower esophageal sphincter (LES) as a bolus of food approaches the distal esophagus. Once the bolus is passed into the stomach, the LES contracts and remains a zone of high pressure until another bolus is swallowed. In patients with GERD, the tLESR is not coordinated with a swallow and can occur spontaneously, allowing for gastric contents to reflux into the distal esophagus. Additionally, the tLESR lasts several seconds in healthy patients, but in those with GERD, it can last more than ten seconds, resulting in significant gastric reflux. Studies have also shown that patients with pathologic GERD have more frequent tLESRs than healthy people do.3 Why this occurs in some people and not others is currently under investigation.In healthy people, the LES has a baseline pressure preventing the reflux of gastric contents into the esophagus. In patients with GERD, the baseline LES pressure is lower, which increases the likelihood of reflux events. This is worse in patients who tend to eat a large meal, which increases the intragastric pressure more than that of the LES, resulting in GERD. Esophageal body dysmotility does not directly result in GERD; however; if a patient has poor esophageal emptying, this can result in delayed clearance of esophageal contents when a reflux event occurs.4 The longer a refluxate is allowed to come in contact with the esophageal mucosa, the more damage it can produce. Similarly, delayed gastric emptying is known to increase the transit time of gastric contents into the duodenum. Stasis of gastric contents in the stomach of patients with gastroparesis who also have tLESR, LES hypotension, or both may result in more frequent and prolonged GERD events. Finally, a hiatal hernia is strongly associated with GERD most likely caused by a breakdown in the LES mechanism, resulting in decreased LES pressure.Risk factors for GERD are numerous, and each likely plays some role in increasing the frequency and length of tLESR (Table 1). Obesity, for instance, is known to be a risk factor for increased reflux, and tLESR is likely due to larger meals, which result in gastric distention, increased acid production, increased intra-abdominal pressure from larger girth, or increased relaxation due to higher levels of certain hormones (eg, estrogen) that stimulate tLESR.5 Foods and beverages known to either relax the LES or irritate the distal esophagus include citrus drinks, spicy food, caffeinated beverages (tea, cola, coffee), chocolate, and peppermint. Patients who eat large fatty meals will also have worse symptoms most likely because of increased acid production with associated decreased LES pressure. Medications known to exacerbate GERD by decreasing the LES pressure include calcium-channel blockers, theophylline, meperidine, some oral contraceptives, and nitrates.PresentationThe presentation of GERD is fairly characteristic, with the majority of patients treating their condition before they come to clinical attention. The most common presentation is a burning pain arising from the epigastrium and radiating retrosternally to the throat and neck. Meals (especially those containing some of the already-described foods), recumbency, and bending over worsen the symptoms, whereas antacids, milk, and sitting or standing up relieve the symptoms. Patients report acidic fluid coming up to the mouth and at times the sensation that solid material is coming back up. Frank vomiting is rare in uncomplicated GERD and should raise suspicion for another underlying disease. It is not uncommon for patients to present with chest pain; however, all patients deserve an appropriate cardiac workup before their chest pain is attributed to GERD.6 Globus is another symptom usually associated with GERD. D y sphagia, weight loss, and hematemesis are part of the ―alarm symptoms‖ and require a more aggressive workup to rule out peptic or malignant stricture, ulcerative esophagitis, and other causes of acute upper gastrointestinal bleeding that may or may not be related to GERD.Extraesophageal manifestations of GERD have been widely studied and debated. Chronic reflux–associated cough, laryngitis, asthma, and dental erosions have all been found to be associated with GERD. Other proposed extraesophageal manifestations of GERD include pharyngitis, sinusitis, idiopathic pulmonary fibrosis, and recurrent otitis media.7EvaluationThe mainstay in diagnosing GERD involves six-week trial of empiric therapy with a proton pump inhibitor (PPI). Patients should be reassessed after the trial to determine improvement. If symptoms have decreased, then no further workup is required and patients may continue taking the PPI either continuously or intermittently as needed. If, however, the patient’s disease responds inadequately, then f urther testing is necessary. The next step is to perform esophagogastroduodenoscopy (EGD). This strategy has been found to adequately diagnose GERD with a sensitivity of 75% and a specificity of 80%.8 It allows EGD to be reserved for those patients with persistent and refractory symptoms who are more likely to have a disease other than GERD. Some notable exceptions to this strategy include patients with alarm symptoms who are likely to have a more serious lesion, patients older than age 55 years who may have a higher risk of a serious lesion, and patients taking esophagotoxic medications such as nonsteroidal anti-inflammatory drugs and bisphosphonates who may have a complication related to their medication.9If patients’ disease responds minimally or not at all to PPIs and they undergo EGD and no abnormality is found to explain their symptoms, then the workup should be directed at the differential for dyspepsia (Table 2).As already mentioned, EGD is the standard clinical test for GERD and an important test in patients with alarm symptoms.9 It is highly sensitive and specific for esophagitis and complications of GERD such as ulcerative disease. EGD allows the ability to determine the exact extent of mucosal injury and is capable of performing biopsy if necessary. EGD allows identification of Barrett esophagus because of the characteristic salmon color of the mucosa on endoscopy, and biopsy allows pathologic staging.Ambulatory pH monitoring is the most sensitive test for acid reflux, but it does not detect nonacidic reflux events. The standard test requires placement of a nasal pH probe that monitors esophageal pH for 24 hours while the patient resumes his or her usual diet and activities. The patient then documents activities andesophageal symptoms either in a diary or with an external monitoring system. At the completion of the study, the patient’s symptoms are correlated with the pH monitorin g results and several criteria are used to determine the extent of the patient’s reflux disease.10,11 This test should be used only to confirm acid reflux if surgery is anticipated or to optimize medical treatment in patients with continued symptoms while taking PPIs. If surgery is anticipated, then the study should be performed while the patient has discontinued PPI therapy to allow documentation of the exact severity of acid reflux. If patients continue taking their PPI, then the study may produce false negative results. If surgery is not anticipated but the clinician would like to determine whether the patient’s medical treatment is optimum, then the study should be performed while the patient is still taking a PPI to determine whether the patient is having asymptomatic acidic reflux. Newer technology allows for a small pH probe to be placed 6 cm above the gastroesophageal junction, which then sends signals to an external monitoring system.12 This allows both for more comfort for the patient and for longer monitoring times (48 hours).A barium esophagram can be ordered to evaluate a patient with suspected GERD; it may demonstrate a GERD episode, detect esophageal mucosal injury, and identify a sliding or paraesophageal hernia. It may also exclude complications of GERD, such as esophagitis, stricture, ulcers, and adenocarcinoma. EGD has largely replaced the barium esophagram as a diagnostic test in GERD because of its higher sensitivity and ability to obtain tissue for diagnosis. The best use of a barium esophagram is in patients presenting with dysphagia, because the test has a better sensitivity than other tests for diagnosing Schatzki rings, webs, diverticula, and strictures.Although acid reflux is what most clinicians think causes GERD, recent evidence has shown that nonacidic reflux may be just as detrimental to the esophageal mucosa. Bile in duodenogastroesophageal reflux has been associated with Barrett esophagus.13 Monitoring of bile levels by using a miniature fiberoptic probe (such as the Bilitech device from Medtronic, Minneapolis, MN, US) can be performed on an outpatient basis. This test is not widely available, however, and should be interpreted by someone experienced in its use. Impedance monitoring is another emerging technology that is currently being evaluated to determine nonacidic reflux events.14,15 A special probe is placed nasally and used to detect changes in the electrical conductance of the intraluminal contents of the esophagus. This allows the physician to determine what substance (liquid, solid, gas) is passing through the esophagus as well as which direction it is going (antegrade or retrograde). For instance, swallowed liquid will cause an antegrade decrease in impedance, whereas liquid reflux produces a retrograde decrease in impedance regardless of pH. Several small studies have shown, through impedance monitoring, that in GERD that does not respond to PPIs, the underlying process is nonacidic GERD.14 Again, this technology is not widely available and requires experienced clinicians to meaningfully interpret the results before making recommendations for treatment. Esophageal manometry is an important test to perform especially in those patients with abnormal esophageal complaints or those patients desiring surgical intervention for GERD.16 In patients with atypical GERD symptoms that are refractory to PPIs, manometry may help diagnose achalasia, esophageal spasm, or other esophageal motility disorders. In patients desiring surgery, manometry should be performed to document normal peristalsis before fundoplication.TreatmentOverviewThe goals for treatment of GERD are to resolve symptoms, heal esophagitis and ulcers, and prevent complications such as stricture, Barrett esophagus, and bleeding. Strictures are known to occur in 0.1% of patients and occur most often in males, whites, and older patients. Barrett esophagus occurs as a complication of GERD and is characterized by the replacement of the distal squamous esophageal mucosa with intestinal metaplasia.17 Barrett esophagus is uncommonly found in patients younger than age 50 but is found in up to 2% of patients older than age 50 who are referred for endoscopy. The etiology of Barrett esophagus is unknown, but the most popular theory suggests that it is the mucosa’s attempt to adapt to the long-term reflux of gastric contents. Although esophagitis without the changes of Barrett disease is not associated with esophageal adenocarcinoma, patients with changes from Barrett disease have a 1% per year risk of developing adenocarcinoma.Medical and surgical therapies have varying success rates. Reports of study results favoring each modality have been widely published and touted by their proponents. It is more likely that medical, surgical, and potentially endoscopic therapies all play a role in the management of GERD; the following discussion will help primary care physicians and gastroenterologists decide which modality is best for a particular patient.Lifestyle and Dietary ModificationsMinor GERD symptoms can be initially treated with simple lifestyle and dietary modifications. Elevating the head of the bed (at least six inches) can help prevent nighttime symptoms. Additionally, avoiding late-night snacks and eating small dinners can help treat minor nighttime symptoms. Avoiding clothes that fit tightly around the mid-abdomen may help occasional symptoms as well. Avoidance of foods that increase reflux events or are caustic to the esophageal mucosa, as mentioned earlier, can help reduce symptoms. Weight loss can produce dramatic results in some patients; however, patients overweight for a long time have a high rate of weight regain and subsequent recurrence of GERD symptoms. Smoking and alcohol use should be reduced or ideally completely stopped. Although stress has not been shown to increase the frequency of GERD events, patients’ perception of GERD is increased during high stress events. Patients should be encouraged to avoid stressful situations at either work or home. Because GERD seems to be a progressive disease, it is likely that many patients will require medical therapy at some point.Medical TherapyAntacids and Proton Pump InhibitorsTraditionally, many patients have self-medicated with over-the-counter antacids before they seek medical attention. Antacids are generally quick and effective for intermittent symptoms. H2-blockers were the first medical treatment for GERD that showed substantial improvement over antacids for the chronic GERD. H2-blockers have also made their way into self-medication, with the general public being able to buy them over the counter. The limitations of H2-blockers include twice-daily dosing and limited response in moderate esophagitis (75%). PPIs have become the preferred medical therapy for erosive esophagitis because they produce a higher rate of response (80%–95%).18PPIs, which act by blocking the hydrogen potassium adenosine triphosphatase, are typically given only once a day. Side effects are minimal and include diarrhea and headaches. PPIs have been shown to be both safe and effective, even when taken for long periods. Chronic PPI therapy has been associated with smallreductions in vitamin B12 levels because of decreases in protein-bound vitamin B12 absorption. There has been an association of chronic PPI use with an increase in community-acquired pneumonias and Clostridium difficile infection.19 PPIs are not meant for patients with intermittent GERD, as the medications can take several hours to take effect.Once patients have had symptom remission for more than two or three months, a trial of tapering their dosage can be attempted. Patients taking PPIs twice daily should taper to once daily, whereas patients taking PPIs once daily can switch to twice-daily H2-blockers. Patients taking H2-blockers can have their dose tapered in a similar manner. If a patient is found to have erosive esophagitis, then that patient should be monitored with endoscopy during the tapering phase to determine if remission is occurring at the mucosal level as well as the symptomatic level. The majority of patients taking PPIs for esophagitis will require long-term—if not lifetime—therapy with the lowest dose of either PPIs or H2-blockers. Acute cessation of PPI therapy should be avoided, as there is a rebound hypersecretion of acid when the medication is abruptly stopped.Limitations of Medical TherapyAlthough PPIs have been found to be both safe and effective for GERD, current studies suggest that in approximately 30% of patients, the disease responds incompletely or, in some cases, not at all to therapy.20 Mechanisms of failure include poor compliance, visceral hypersensitivity, duodenogastroesophageal reflux, nonacid reflux disease, delayed gastric emptying, PPI resistance, and poor bioavailability. Additionally, in patients with psychologic disorders and concomitant bowel disorders, PPI therapy may fail. These patients will likely benefit more from treatment of their underlying psychologic and bowel disorders. In patients with erosive esophagitis, there is a small group of patients whose esophagitis heals but who continue to have significant symptoms (27%).21 Additionally, 80% of patients with erosive esophagitis have a relapse of their symptoms within 6 to 12 months after cessation of medical therapy. In a large review of published study results, the overall relapse rate of erosive esophagitis in patients treated with PPIs was 22% and in those treated with H2-blockers was 58%.20Surgical TherapyTechniquesGERD has been treated surgically since the early 1950s, with the most common procedure being the Nissen fundoplication. O ther procedures include the Hill, Belsey, and Toupet repairs. A complete review of all of these techniques and their outcomes is beyond the scope of this review. Unless otherwise stated, the data presented here are from studies of the Nissen fundoplication.In the era of open antireflux operations, symptom response rates of 80% to 90% were commonly reported. Many patients, however, did not undergo surgical intervention because of the high morbidity of the procedure. With the introduction of laparoscopic techniques, there was an exponential growth in the number of antireflux operations despite no clear evidence of its superiority. Recent long-term studies have confirmed that laparoscopic fundoplication is not only as effective as open surgery but also results in fewer incisional hernias, shorter hospital stays, less pain, quicker return to work, and fewer defective wraps atfollow-up endoscopy.22 Laparoscopic fundoplication has fallen out of favor as a primary treatment for GERD since the introduction of more potent medical therapy.Although medical therapy is the first-line therapy for GERD, there are still select indications for surgical treatment (Table 3). Because GERD is a chronic condition that is due to a mechanical failure of the antireflux mechanism and because current medical treatment is directed only at the suppression of acid, there is concern about the effectiveness of long-term medical therapy. As mentioned earlier, current data show that not all GERD is due to acid reflux. Alkaline reflux likely contributes to esophagitis and possibly Barrett esophagus. Because GERD is a chronic condition, most patients will require intermittent if not lifetime therapy. The expense, the psychologic burden of a lifetime of medical therapy, and the uncertainty of the long-term effects of a lifetime of medical therapy should be addressed with all patients considering long-term medication use.Patients who are averse to surgery and get excellent results with medications can be monitored safely. If patients have any uncertainty about taking medications and would like to explore surgical options, they should be referred to an experienced esophageal surgeon. This is especially true for young patients who face taking medications for 30 to 50 years, especially if they get excellent results with medications. These are the ideal candidates for antireflux surgery, with success rates approaching 90% in experienced hands.23 The opposite is true for patients who have limited life expectancy; these patients are best suited for medical treatment.Other patients who should be evaluated for surgical therapy include those in whom medical management has failed, those with complications of GERD (eg, esophagitis not responding to medical therapy, Barrett esophagus, stricture), and those with medical complications attributable to a large hiatal hernia, such as bleeding and dysphagia. Those patients with atypical symptoms of GERD such as asthma, hoarseness, cough, noncardiac chest pain, and recurrent aspiration pneumonia may also benefit from surgery. It is very important that a complete workup, including a 24-hour pH study, be performed in these patients to confirm acid reflux.Patients who are evaluated by their primary care providers and desire surgical intervention should be referred to an experienced esophageal surgeon. The appropriate workup in these cases begins with EGD to evaluate for esophageal complications and rule out gastric or duodenal causes for the symptoms. If EGD produces normal findings, then a 24-hour pH study while the patient is not taking medications should be performed to document acid reflux. If EGD shows esophagitis, a pH study is not mandatory. Before surgery, a motility study is paramount to evaluate the contractility of the patient’s esophagus. If this shows weak peristalsis, then a partial wrap may be the best option for the patient. Some surgeons will also obtain upper gastrointestinal swallow studies. This is helpful only if the patient has an associated hiatal hernia to determine the size of the hernia and length of the esophagus. If findings for all of the above studies are normal but the patient still has significant symptoms, then consideration should be made to referring these patients to an institution with impedance testing or testing with a Bilitech probe to evaluate for nonacid reflux disease.Surgical OutcomesResults of laparoscopic Nissen fundoplication have been excellent in experienced hands. Conversion rates to open surgery are <5% and typically occur early in a surgeon’s experience. Patients undergoing this procedure typically spend one night in the hospital, although some studies have reported excellent results with same-day procedures. Common complaints immediately after fundoplication include early satiety (84%), bloating and flatulence (61%), and dysphagia (32%). At examination three months after surgery, however, no patients complain of early satiety, 3% have bloating, and <1% have dysphagia. Patients with continued dysphagia after three months should undergo a contrast study to determine whether the wrap has slipped, which is the usual cause for this problem (80%).24Long-term studies have shown that when patients are properly selected for surgery and undergo fundoplication by experienced surgeons, the results are excellent. Patients can expect a remission rate >90%, with no need for medical therapy.23 Patients who do require some medication will usually require doses that are lower and less frequent than their preoperative dose. Long-term quality-of-life studies have shown that up to 95% of patients rate their surgery outcomes as either good or excellent and would undergo the surgery again.25 The results for those who undergo open surgery are equivalent. The laparoscopic technique does result in lower perioperative morbidity, making it the current gold standard.Endoscopic TherapySeveral endoscopic therapies have recently been developed as an alternative to surgical treatment of medically refractory GERD. The most widely studied include the Stretta device (Curon Medical, Inc, Fremont, CA), the EndoCinch suturing system (CR Bard, Inc, Murray Hill, NJ), the Enteryx system, and thePlicator (NDO Surgical, Inc, Mansfield, MA). Each of these procedures works by improving the mechanical barrier of the LES. The results from these endoscopic therapies have been generally disappointing and have limited widespread application.26 Although it is thought that these are relatively benign procedures, this is not the case. Indeed, the Enteryx system was voluntarily withdrawn from the market because of several deaths directly related to the procedure. The other techniques are typically done on an outpatient basis, but chest pain, dysphagia, and vomiting are some of the most common, albeit rare, complaints. Endoscopic therapies have not gained widespread application, and many experts from both surgical and gastroenterology fields believe that they are still experimental.ConclusionGERD is a progressive, lifelong disease that can severely limit up to 20% of patients who have it, despite optimal medical therapy. Primary care clinicians should not assume that patients are satisfied with their medical therapy for GERD and should refer appropriate candidates to discuss surgical therapy. Laparoscopic Nissen fundoplication has proven safe and effective in long-term studies when performed by experienced esophageal surgeons. Endoscopic therapies hold out the promise of decreased morbidity and increased efficacy that has yet to be realized and thus should be limited to specialized centers under supervised protocols.Disclosure StatementThe author(s) have no conflicts of interest to disclose.AcknowledgmentKatharine O’Moore-Klopf, ELS, of KOK Edit provided editorial assist ance.References1. Liu JJ, Saltzman JR. Management of gastroesophageal reflux disease. South Med J 2006 Jul;99(7):735–41.2. Richter JE. Novel medical therapies for gast roesophageal reflux beyond proton pump inhibit ors.Gastroent erol Clin North Am 2002 Dec;31(4 Suppl):S111–6.3. Dodds WJ, Dent J, Hogan WJ, et al. Mechanisms of gast roesophageal reflux disease in patients with refluxesophagitis. N Engl J Med 1982 Dec 16;307(25):1547–52.4. Achem AC, Achem SR, St ark ME, et al. F ailure of esophageal perist alsis in older patients: association wit hesophageal acid exposure. Am J Gast roent erol 2003 Jan;98(1):35–9.5. Murray L, Johnst on B, Lane A, et al. Relationship between body mass and gastro-oesophageal refluxsymptoms: The Bristol Helicobacter Project. Int J Epidemiol 2003 Aug;32(4):645–50.6. Faybush EM, Fass R. Gastroesophageal reflux disease in noncardiac chest pain. Gastroent erol Clin North Am2004 Mar;33(1):41–54.7. Richter JE. The many manifestations of gastroesophageal reflux disease: pre sent ation, evaluation, andtreat ment. Gastroent erol Clin N Am 2007 Sep;36(3):577–99, vii-ix.8. Fass R, Fennert y MB, Ofman JJ, et al. The clinical and economic value of a short course of omeprazole inpatients with noncardiac chest pain. Gastroenterology 1998 Jul;115(1):42–9.。

下颌前移矫治器治疗OSAHS的研究石瑛琦;王培军;陈萍;史雅绒【摘要】有大量研究证实,口腔矫治器可有效治疗阻塞性睡眠呼吸暂停综合征(OSAHS).其中下颌前移矫治器具有成本低,无创伤,患者易接受等优势,在临床中最为常见.使用下颌前移矫治器治疗过程中,应注重全面的追踪随访及监测,减少副反应,提高临床疗效.本文针对的下颌前移矫治器作用机制、临床效果、副作用等方面进行综述.【期刊名称】《医学信息》【年(卷),期】2019(032)011【总页数】3页(P39-41)【关键词】下颌前移矫治器;阻塞性睡眠呼吸暂停低通气综合征;口腔矫治器【作者】石瑛琦;王培军;陈萍;史雅绒【作者单位】哈尔滨医科大学附属第二医院口腔正畸科,黑龙江哈尔滨 150001;哈尔滨医科大学附属第二医院口腔正畸科,黑龙江哈尔滨 150001;哈尔滨医科大学附属第二医院口腔正畸科,黑龙江哈尔滨 150001;哈尔滨医科大学附属第二医院口腔正畸科,黑龙江哈尔滨 150001【正文语种】中文【中图分类】R766阻塞性睡眠呼吸暂停低通气综合征（obstructive sleep apnoea hypopnoeasyndrome，OSAHS）是一种间歇性上气道狭窄坍塌进而导致血氧下降和睡眠紊乱中断的常见疾病。

持续正压通气（continuous positive airway pressure，CPAP）是治疗OSAHS 的首选方法，但患者耐受性和依从性不佳使其临床疗效降低[1]。

近年来，口腔矫治器，尤其是下颌前移矫治器（mandibular advancement devices，MAD）作为CPAP的替代治疗手段取得很好疗效[2]，同时具有舒适，价格低廉等优势。

本文就MAD 的发展历史、作用机制、疗效、副作用等方面做一综述总结。

1 OSAHS流行病学调查显示，我国OSAHS 患病率约为4%[3]。

OSAHS 发病机制包括解剖结构异常，咽部肌肉舒张功能失调，肺容量降低等，上呼吸道坍塌是导致临床症状的源头因素。