中国整合胃癌前病变临床管理指南

正确应对和处理胃癌前病变和癌前疾病,对降低胃癌发病率具有重大意义.本指南结合我国胃癌前病变和癌前疾病的发病和诊治现状,从定义和流行病学、诊断和分期、监测、治疗、疗效评价五个方面切入,中西医整合、多学科参与,共同提出针对性的诊治要点和策略,以期对此类疾病的临床规范诊治发挥指导作用,从而实现胃癌的有效二级预防.     

老年脊柱外科手术并发症

随着社会的发展和进步,人口老龄化的加快和寿命的延长,老年脊柱疾病患者和手术日渐增多。由于老年人的自然条件、代谢能力和机体的储备能力都在不断下降,并且大多合并有其他疾病,在手术中和手术后容易出现各种并发症和意外,严重影响手术治疗的效果及生活质量。因此,老年脊柱外科手术并发症越来越受到人们的关注。众多学者开始研究老年脊柱手术并发症的病因、预防措施和治疗手段,本文就此予以综述。     

24例糖尿病酮症酸中毒患者的急救与护理探讨

目的分析和探索糖尿病酮症酸中毒患者的急救和护理。方法选取该院2013年收治的24例糖尿病酮症酸中毒患者为研究对象,对其进行急救,纠正酮症酸中毒以及心理、饮食方面的护理,总结急救和护理体会。结果及时治疗和护理的患者,24例患者中,死亡1例,总成功率为95.83%。结论对于糖尿病酮症酸中毒患者,应及时诊断和治疗,同时给予其细致的护理和观察,可提高抢救成功率,减少病患和家庭的痛苦。     

心脑血管疾病的激光治疗及其功效

众所周知,无论是心脑血管疾病还是糖尿病等中老年性疾病,均有不同程度的脂代谢异常和高脂血症及高粘血症,高血脂和高血粘是引发心脑血管疾病的重要危险因素和早期表现;其直接损害是引起动脉粥样硬化和血栓形成。而动脉粥样硬化和血栓形成各种心脑血管疾病的罪魁祸首和中期主要病变;由于机体各器官组织都需要血液循环供血供氧,动脉粥样硬化和/或血栓形成均可使血管狭窄和血液循环不通畅,从而导致组织器官缺血缺氧。而缺血缺氧则是心脑血管疾病的主要临床表现和晚期特征。糖尿病是     

本期专栏组稿专家介绍

伍骥,空军总医院骨科丰任,临床医学博士,教授,主任医师,博士研究生和博士后导师,享受军队津贴。毕业于华西医科大学临床医学院,进修于美国脊柱外科教育和培训中心、日本北海道大学、倚兰阿姆斯特丹自由大学、法国和德国脊性外科和关节外科中心等。     

中国炎症性肠病消化内镜诊疗共识

炎症性肠病(inflammatory bowel disease,IBD),主要包括溃疡性结肠炎(ulcerative colitis,UC)和克罗恩病(Crohn disease,CD),是一种主要累及胃肠道的慢性、非特异性、复发性、炎症性疾病。近20余年来,虽然国内外学者对IBD的发生机制和临床诊疗进行了深入的研究,但是,IBD的具体病因和确切的发生机制目前仍然不清楚,也未发现能够治愈IBD的药物和方法。研究发现,IBD与高脂肪、高蛋白和高糖饮食等生活方式密切相关,多见于西欧和北美地区。既往中国IBD罕见,但近20年来,中国IBD发病率快速增长,以珠江三角洲地区和长江三角洲地区增长最快,可能与国人的饮食习惯、生活节奏、环境改变等有关。目前,IBD已经成为我国消化系统常见的疑难疾病之一,是消化系统疾病基础研究和临床诊疗的重点、热点和难点。     

中国慢性胃炎诊治指南（2022年，上海）撤回

慢性胃炎是常见病,认识其病因和临床表现,规范其诊断和治疗,以及预防其癌变一直为临床医师所重视。本指南在过去3次慢性胃炎诊治共识意见的基础上,参考国际上胃黏膜癌前病变处理指南等相关共识和指南,制定符合我国国情的慢性胃炎诊断和治疗指南,具有临床价值和可行性。本指南由中华医学会消化病学分会发起,中华医学会消化病学分会消化系统肿瘤协作组主要成员作为召集人和撰写者,遵循国际通用的指南制定原则和方法,在广泛征集消化内科和内科医师意见的基础上,针对有关慢性胃炎的九大类临床问题,有循证依据地给出53项推荐意见,旨在提高我国临床医师对慢性胃炎这一多发病的诊治管理水平。     

BACTEC MIGT960在结核分枝杆菌药物敏感性试验中的临床研究

目的 评价BACTEC MIGT960快速检测8种抗结核药物敏感性效果。方法 收集住院结核病人痰标本分离的结核分枝杆菌菌株,分别采用L-J比例法和MGIT960法进行药物敏感性检测,在完成一线4种药物的药敏检测后,选取对任何一种一线药物(异烟肼、利福平、链霉素和乙胺丁醇)耐药的菌株进行二线药物(卷曲霉素、卡那霉素、氧氟沙星和乙硫异烟胺)敏感性检测。从结果报告时间和符合率等方面进行评价。统计学分析采用kappa检验和t检验,P值为0.05。结果 对212株结核分枝杆菌临床分离株进行了4种一线药物的药物敏感性检测,随后,对耐任何一种一线药物的90株菌进行了4种二线药物的药物敏感性检测,以L-J比例法为金标准,MGIT 960法的准确度和Kappa值分别为:异烟肼96.0%和0.92,利福平99.0%和0.98,链霉素99.0%和0.97,乙胺丁醇96.0%和0.81,卷曲霉素100.0%和1.00,卡那霉素99.0%和0.85,氧氟沙星96.0%和0.88,乙硫异烟胺94.0%和0.73;完成一线/二线药物药敏试验的平均时间,MGIT 960为8.10和10d,L-J法则均为30d,两种方法培养时间的差异有统计学意义(P < 0.05)。结论 MGIT 960法与传统的L-J比例法药敏试验比较,具有符合率较好、检测时间明显缩短的特点,有利于临床及时有效合理化用药。     

心房颤动与炎症和氧化应激

许多证据表明心房颤动中存在炎症和氧化应激,炎症和氧化应激可导致心房重构,包括电重构和结构重构,提示炎症和氧化应激可能在心房颤动的发生和维持中起着一定作用。抗炎和抗氧化治疗可减少心房颤动的发生和复发,这为干预心房颤动的发生和复发提供了新思路。     

棘球蚴囊液,头节和囊壁抗原的二维电泳初步研究

本文采用二维电泳和银染色法对棘球蚴囊液、头节和囊壁抗原进行了初步研究。结果表明:三者分别显示多肽斑点111、116和123个,其中特异斑点74、67和60个,共有斑点37、49和63个。在共有斑点中,三者共有斑点7个;两者共有斑点在囊液和头节为8个,囊液和囊壁22个,头节和囊壁34个。本文对多肽斑点和抗原的关系作了讨论。本结果可望对抗原的纯化提供参考。     

Potential vertebrate reservoir hosts and invertebrate vectors of Anaplasma marginale and A. phagocytophilum in central Spain

Organisms in the genus Anaplasma are obligate intracellular pathogens that multiply in both vertebrate and invertebrate hosts. The type species, A. marginale, causes bovine anaplasmosis and only infects ticks and ruminants. A. phagocytophilum causes human and animal granulocytic anaplasmosis, and genetically closely related strains show a wide host range, including ticks, ruminants, rodents, equids, canids, birds, and humans. Recent reports demonstrated that A. marginale and A. phagocytophilum co-exist in geographic areas and that concurrent infections occur in ruminants and ticks. In this study, we characterized A. marginale and A. phagocytophilum infections in wild and domestic animals, and ticks collected in central Spain by serology, PCR, and sequence of 16S rRNA genotypes. Species tested included humans, cattle, dogs, rodents, Iberian red deer, European wild boar, birds, and ticks. Species of hematophagous Diptera were analyzed as potential mechanical vectors of Anaplasma spp. A. marginale was detected in tabanids, ticks, cattle, and deer, while A. phagocytophilum was detected in ticks, deer, cattle, and birds. Concurrent infections of the two Anaplasma were found in cattle and deer. These results illustrate the complexity of the epizootiology of A. marginale and A. phagocytophilum in regions where both pathogens co-exist and share common reservoir hosts and vectors. The increasing contact between wildlife, domestic animals, and human populations increases the risk of outbreaks of human and bovine anaplasmosis, and the difficulty of implementing surveillance and control measures.     

Role of mercury toxicity in hypertension, cardiovascular disease, and stroke

Mercury has a high affinity for sulfhydryl groups, inactivating numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (N-acetyl-L-cysteine, alpha-lipoic acid, L-glutathione), with subsequent decreased oxidant defense and increased oxidative stress. Mercury binds to metallothionein and substitute for zinc, copper, and other trace metals, reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in adenosine triphosphate, depletion of glutathione, and increased lipid peroxidation. Increased oxidative stress and reduced oxidative defense are common. Selenium and fish containing omega-3 fatty acids antagonize mercury toxicity. The overall vascular effects of mercury include increased oxidative stress and inflammation, reduced oxidative defense, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, and immune and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, coronary heart disease, myocardial infarction, cardiac arrhythmias, reduced heart rate variability, increased carotid intima-media thickness and carotid artery obstruction, cerebrovascular accident, generalized atherosclerosis, and renal dysfunction, insufficiency, and proteinuria. Pathological, biochemical, and functional medicine correlations are significant and logical. Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury inactivates catecholaminei-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to mercury-induced heavy metal toxicity. Mercury toxicity should be evaluated in any patient with hypertension, coronary heart disease, cerebral vascular disease, cerebrovascular accident, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, and serum should be performed.     

Evolution of genome-phenome diversity under environmental stress

The genomic era revolutionized evolutionary biology. The enigma of genotypic-phenotypic diversity and biodiversity evolution of genes, genomes, phenomes, and biomes, reviewed here, was central in the research program of the Institute of Evolution, University of Haifa, since 1975. We explored the following questions. (i) How much of the genomic and phenomic diversity in nature is adaptive and processed by natural selection? (ii) What is the origin and evolution of adaptation and speciation processes under spatiotemporal variables and stressful macrogeographic and microgeographic environments? We advanced ecological genetics into ecological genomics and analyzed globally ecological, demographic, and life history variables in 1,200 diverse species across life, thousands of populations, and tens of thousands of individuals tested mostly for allozyme and partly for DNA diversity. Likewise, we tested thermal, chemical, climatic, and biotic stresses in several model organisms. Recently, we introduced genetic maps and quantitative trait loci to elucidate the genetic basis of adaptation and speciation. The genome-phenome holistic model was deciphered by the global regressive, progressive, and convergent evolution of subterranean mammals. Our results indicate abundant genotypic and phenotypic diversity in nature. The organization and evolution of molecular and organismal diversity in nature at global, regional, and local scales are nonrandom and structured; display regularities across life; and are positively correlated with, and partly predictable by, abiotic and biotic environmental heterogeneity and stress. Biodiversity evolution, even in small isolated populations, is primarily driven by natural selection, including diversifying, balancing, cyclical, and purifying selective regimes, interacting with, but ultimately overriding, the effects of mutation, migration, and stochasticity.     

Identification and distribution of New World Leishmania species characterized by serodeme analysis using monoclonal antibodies

Five hundred thirty stocks of Leishmania isolated from human and domestic and wild reservoir hosts, representing a wide geographic distribution of endemic foci of American cutaneous (ACL) and visceral leishmaniases (AVL) were characterized and identified at species and/or subspecies levels based on their reactivity to a cross-panel of specific monoclonal antibodies using a radioimmune binding assay. This study confirms and extends our preliminary results on the high specificity of some of these monoclonals for the L. braziliensis, L. mexicana, and L. donovani complexes. This study also demonstrates the relative stability of these molecular markers and the general usefulness of the method for parasite identification. Two hundred ninety-two of 420 isolates of ACL were classified as members of the L. braziliensis complex. Two hundred twenty-seven were L. b. braziliensis; these showed the widest geographical distribution (Brazil: Amazonas, Bahia, Ceara, Espirito Santo, Goias, Minas Gerais, Para, Paraiba, Rio de Janeiro, and Sao Paulo; Honduras: Santa Barbara and Yoko; Peru: Ancash, Piura, and Ucayali; and Venezuela: Cojedes, Distrito Federal, Lara, Portuguesa, Vale Hondo, Yaracuy, and Zulia). Forty-one stocks were identified as L. b. guyanensis (from North Brazil: Amazonas, Amapa, Para, and Rondonia). Twenty-one stocks were identified as L. b. panamensis (from Costa Rica: Alajuela, Guanacasten, Limon, Puntarenas, and San Jose; and Honduras: El Paraiso, and Olancho). Out of 128 isolates classified as members of the L. mexicana complex, 74 were differentiated as L. m. amazonensis (from Bolivia; Brazil: Amazonas, Bahia, Ceara, Goias, Maranhao, Mato Grosso do Norte, and Para; Peru: Pasco Forest and Van Humboldt; and Venezuela: Carabobo, Guarico, and Merida). Forty-four stocks were identified as L. m. venezuelensis (from Venezuela: Lara). Six stocks were L. m. mexicana (from Belize; and Mexico: Campeche [corrected] and Quintana Roo, Yucatan). One hundred ten isolates from AVL were identified as L. donovani chagasi (from Brazil: Bahia, Ceara, Maranhao, Minas Gerais, Mato Grosso do Sul, Piaui, Rio de Janeiro, and Sergipe; and Honduras: Valle). The implications of these results with respect to both the clinical and epidemiological data (including the detection of seven unusual characterized stocks) are discussed.     

神经肽在不同证候H22肝癌小鼠肾上腺组织的表达特征

[目的]揭示神经肽在不同证候肝癌小鼠肾上腺组织的基因表达特征。[方法]采用实验小鼠及其标准化四诊及辨证方法,以及GeneChip Mouse Exon 1．0 ST Array等技术,检测H22肝癌小鼠早期邪毒壅盛证和气虚证、中期阳气虚证、中晚期气阴阳虚证共3阶段4个证候肾上腺基因表达的差异,重点关注40个确切的神经肽基因在证候间的表达。[结果]在正常与肝癌小鼠肾上腺中,40个神经肽基因表达呈现3种情形：①生长激素（GH）、催乳素（PRL）、生长介素（SM）,神经肽Y（NPY）、缩胆囊肽（CCK）,阿黑皮素原（POMC）、脑啡肽（ENK）等为高表达基因;②垂体腺苷酸环化酶激活肽（PACAP）、卵泡刺激素（FSH）、促黄体生成激素（LH）、促甲状腺激素（TSH）、生长抑素（SS）、生长激素释放激素（GHRH）、神经降压肽（NT）、胰高血糖素样肽（GLP）、胰多肽（PP）、中间叶促皮质样肽（CLIP）、催产素（OT）、肾上腺髓质素（ADM）、P物质（SP）、K物质（SK）、8睡眠诱导肽（DSIP）、甘丙肽（Gal）、血管紧张素Ⅱ（AT-Ⅱ）和血管紧张素原（ATG）等为低表达量基因;③促性腺激素释放激素（GnRH）、胎盘生乳素（PL）、促甲状腺释放激素（TRH）、促皮质激素释放激素（CRH）、血管活性肽（VIP）、胃泌素释放肽（GRP）、神经肽K（NPK）、强啡肽（DYN）、血管加压素（AVP）、降钙素基因相关肽（CGRP）、胰岛淀粉样多肽（IAPP）、尾加压素Ⅱ（UⅡ）、内皮素（ET）、脑钠素（BNP）和心钠素（ANP）等神经肽基因不表达。就证候而言,与正常组比较,总体趋势为下调的基因多,上调的基因少,其中,邪毒壅盛证的LH、ET上调,气虚证中GH和POMC下调,阳气虚证和气阴阳虚证ATG和Gal上调;而FSH在各虚证中均下调,PACAP、CCK、NT基因在各个证候中均显著下调近10倍。[结论]神经肽基因在小?     

BOOKS

Book reviewed in this article: Molecular and Cellular Aspects of Erythropoietin and Erythropoiesis. NATO AS1 Series: Cell Biology, vol. 8, ed. Rich IN. Progress in Clinical and Biological Research, volume 251. Developmental Control of Globin Gene Expression, eds. Blood Transfusion in Clinical Medicine. Eighth edition, eds. Molliaon PL, Engelfriet CP & Contreras M. Immunobiology of Cancer and AIDS. Etiology, diagnosis and management, eds. Nieburgs HE & Bekesi JG. Thalassemia: Pathophysiology and Management. Part B, eds. Fucharoen S, Rowley PT & Paul NW. Atlas of Blood Cells. Function and Pathology, eds. Zucker-Franklin D, Greaves MF, Grossi CE & Marmont AM. Edi. Ermes, Milano. Genotypic, phenotypic and functional aspects of hematopoiesis, eds. Grignani F, Martelli MF & Mason DY. Recent Advances and Future Directions in Bone Marrow Transplantation. Experimental Hematology Today -1987, eds. Chronic Lymphocytic Leukemia, eds. Polliack A & Catovsky D. Harwood Biological Response Modifiers and Cancer Therapy, ed. Chiao JW. Human Retroviruses, Cancer, and AIDS. Approaches to prevention and therapy.     

双氢青蒿素抗日本血吸虫作用的体内实验观察

目的观察不同发育阶段日本血吸虫对双氢青蒿素的敏感性,探索双氢青蒿素抗日本血吸虫的效果。方法采用尾蚴腹部贴片法感染小鼠,每鼠感染日本血吸虫尾蚴40条;在血吸虫不同发育阶段灌服用药,于感染后50 d解剖小鼠,收集成虫,计算减虫率和减雌率。①在小鼠感染后2 h,3、5、7、10、14、18、21、28 d和35 d灌服双氢青蒿素（300 mg/kg）,观察双氢青蒿素对不同发育阶段血吸虫的作用效果。②以不同剂量双氢青蒿素分别给感染后7 d或35 d的小鼠用药,观察双氢青蒿素抗日本血吸虫作用的量-效关系。③以不同药物剂量分别在感染后第7天和第35天给药（共2次）,观察双氢青蒿素对日本血吸虫的作用效果。结果300 mg/kg双氢青蒿素一次灌服用药对7 d龄童虫和35 d龄成虫有明显杀灭作用,减虫率分别为64.81%和60.47%,减雌率分别为73.81%和90.48%。以200、300、400 mg/kg和600 mg/kg双氢青蒿素治疗感染后7 d小鼠,减虫率分别为46.84%、60.63%、59.55%和60.21%,减雌率分别为59.73%、72.29%、72.58%和76.61%;治疗感染后35 d小鼠,减虫率分别为47.23%、62.33%、76.31%和83.63%,减雌率分别为59.73%、89.36%、89.65%和93.96%;在感染后第7天和第35天共治疗2次,减虫率分别为58.16%、82.66%、83.42%和83.79%,减雌率分别为68.69%、90.43%、93.74%和94.63%。结论双氢青蒿素具有一定的抗日本血吸虫作用,对7 d童虫和35 d成虫较为敏感。     

Functions of the fibrinolytic system in human Ito cells and its control by basic fibroblast and platelet-derived growth factor

During liver fibrogenesis, hepatic stellate cells (HSC) proliferate and migrate under the influence of growth factors, including platelet-derived growth factor (PDGF) and basic-fibroblast growth factor (b-FGF). The plasminogen activation system regulates extracellular matrix (ECM) catabolism and cell movement. We evaluated the expression and biological functions of the plasminogen activation system in human HSC and its interaction with PDGF and b-FGF. Urokinase-plasminogen activator receptors (u-PAR) were measured by radioligand binding, cell cross-linking, immunoassay, and RNAse protection assay. u-PA and plasminogen activator inhibitors (PAIs) expression and activities were analyzed by zymography, immunoassay, and RNase protection assay. Cell migration and proliferation, studied in Boyden chambers and by microscopic counting, were evaluated after the addition of PDGF, b-FGF, and blockade with anti-u-PA, anti-u-PAR antibodies, and antisense oligodeoxynucleotides (aODN) against u-PAR mRNA. We have shown that HSC produce u-PAR, u-PA, and PAI-1. PDGF and b-FGF up-regulate u-PA and u-PAR, but not PAI-1, and exogenous addition of u-PA stimulates HSC proliferation, chemotaxis, and chemoinvasion. Inhibition of u-PA/u-PAR with antibodies against u-PA or u-PAR and with u-PAR aODN inhibit the proliferative, chemotactic, and chemoinvasive activity of PDGF and b-FGF. These findings indicate that u-PA and u-PAR are required for the mitogenic and chemoinvasive activity of PDGF and b-FGF on HSC.