3起老人院诺如病毒胃肠炎暴发疫情分析

目的分析3起发生在老人院内的诺如病毒胃肠炎局部暴发疫情的流行特征,为今后预防类似事件的发生提供参考依据。方法收集2007年佛山市老人院诺如病毒胃肠炎暴发疫情现场流行病学调查报告．采用描述性流行病学方法对疫情调查处理情况进行分析。结果2007年佛山市共报告3起老人院诺如病毒胃肠炎暴发疫情,共发病56例,无死亡病例;疫情集中发生在2～3月份;每起疫情均从部分患者粪便标本中检测诺如病毒Ⅱ型核酸;3起疫情主要以人-人密切接触的途径传播。结论早发现、早报告、早处理疫情．以及日常加强院内卫生,强化护工的规范操作,是预防和控制诺如病毒胃肠炎在老人院发生的关键。     

我国诺如病毒急性胃肠炎散发病例流行病学系统性分析

目的系统评价诺如病毒急性胃肠炎散发病例在国内的流行现状。方法在万方、中国知网和PubMed数据库中, 检索2010年1月—2023年10月发表的关于国内诺如病毒急性胃肠炎散发病例的文献。筛选符合纳入和排除标准的文献, 采用Excel软件和SPSS20.0软件进行数据分析, 对我国诺如病毒急性胃肠炎散发病例的流行病学特征进行描述性分析。结果共纳入文献500篇, 涉及全国32个省份和地区, 急性胃肠炎患者784 486例, 共检测样本670 292份。分析结果显示, 近年我国诺如病毒急性胃肠炎流行株仍以GⅡ基因群为主, 不同时间基因型和流行株分布存在明显差异, GⅡ.4型是各年份主要基因型, GⅡ.4/2006b和GⅡ.4/Sydney₂012为主要流行株。诺如病毒感染性腹泻全年均有发生, 每年10—12月为感染高发期。诺如病毒感染在<5岁儿童中发病率最高, 其阳性率存在地域差异。结论散发性诺如病毒急性胃肠炎在我国仍以GⅡ基因群为主, 但流行株呈明显变异趋势, 对诺如病毒感染性腹泻的防控和有针对性的疫苗研发应考虑流行株变化及时间地域等因素。     

河北省卢龙地区2008-2009年5岁以下腹泻住院儿童中诺如病毒的检测和分型

目的 了解河北省卢龙地区2008 -2009年5岁以下住院儿童中诺如病毒的分子流行病学特征.方法 收集2008年10月至2009年8月325例5岁以下腹泻住院患儿粪便标本和流行病学资料,采用酶联免疫吸附试验( ELISA)检测轮状病毒抗原,利用多重RT-PCR方法检测诺如病毒,并对部分诺如病毒阳性株进行序列测定和系统进化分析.结果 诺如病毒的检出率为11.3％ (37/325),仅次于轮状病毒的检出率(48.6％),高于腺病毒(6.5％)和星状病毒(4.3％),主要感染2岁以下儿童,季节高峰在11月,系统进化分析表明诺如病毒流行优势株为GⅡ-4/2006b变异株,并发现一株未见报道的新型GⅡ-4变异株.结论 诺如病毒是引起2008 -2009年卢龙地区的急性胃肠炎的重要病原之一,GⅡ-4/2006b变异株仍是流行优势株,要进一步监测新型GⅡ-4变异株的流行.     

贵阳地区GⅡ.4型诺如病毒变异株的初步研究

目的 了解贵阳地区GⅡ.4型诺如病毒变异株的组成及其点突变.方法 监测2010年6-11月于贵阳地区哨点医院就诊的急性胃肠炎病例,收集粪便标本,采用荧光定量逆转录-聚合酶链反应(real-time RT-PCR)初步鉴定,随机选取部分GⅡ型诺如病毒阳性标本,采用一步法RT-PCR对其VP1基因区克隆及测序,基因序列与国内外流行的GⅡ.4型诺如病毒进行系统进化及氨基酸位点的突变分析.结果 检测标本426份,有267份(62.68％)GⅡ型诺如病毒阳性,测序获得了9份GⅡ.4型诺如病毒VP1基因组序列,贵州省2010年流行的GⅡ.4型诺如病毒包括2个变异株(GⅡ.42008a和GⅡ.4 2008b新型变异株),亚型组闻的VP1基因的同源性为95.90％ ～ 96.72％,亚型组内同源性为99.45％ ～ 100％,有2个氨基酸位点易发生突变.结论 贵阳地区2010年夏秋季急性胃肠炎以诺如病毒GⅡ型为主,并且变异株具有多样性.     

北京市春季诺如病毒性腹泻流行病学及病原学调查

目的 探讨北京市春季诺如病毒性腹泻的流行病学规律及病原学特点.方法 对2007年1月至4月北京市各级各类医院报告的451例病毒性腹泻病例采集便标本,应用ELISA方法进行诺如病毒抗原检测.应用逆转录聚合酶链反应进行RNA检测,对9例阳性标本的PCR产物进行克降测序.结果 ELISA检测诺如病毒阳性166例,阳性率35.48%.166例病人主要集中在1月、2月,以20～29岁年龄组最多,男性多于女性,城区多于郊区.但在病毒性腹泻病例中,诺如病毒阳性率分布无时间、人群和空间差异.该9株病毒均为GⅡ/4型诺如病毒变异株,组内核苷酸同源性为97.0%～99.6%.系统发生树表明北京地Ⅸ的流行株与同时期世界上流行的诺如病毒株属于同一型别的GⅡ/4变异株.结论 北京市春季诺如病毒性腹泻主要山GⅡ/4变异株引起,与同期世界上流行株有共同的来源,各人群均存在感染的风险,应该加强相应的预防控制措施,并有必要在围外发生流行时建立预警机制.     

一起诺如病毒感染性腹泻暴发疫情流行病学调查

目的了解一起诺如病毒感染性腹泻暴发的特点和流行原因，探讨暴发疫情调查处理的经验，为制定防治对策提供科学依据。方法对开平市月山镇一起诺如病毒暴发疫情用流行病学方法进行分析。结果该镇水井片11月25日至12月5日共发生感染性腹泻238例，罹患率4．18％；患者各年龄组均有发病，青壮年居多；患者大多呈腹泻、呕吐等胃肠炎症状，病情较轻；对搜索到的575户2347人进行发病聚集性分析，发现有明显的家庭聚集性；不同村委会发病差异有统计学意义。部分病人粪便标本经检测诺如病毒阳性。疫情经加强饮用水消毒、病人隔离治疗、开展爱国卫生运动和健康教育等综合措施后得到控制。结论本起暴发疫情由诺如病毒感染引起，供水系统受到一过性污染是引起水源性暴发的主要原因。加强饮用水的消毒与管理，开展健康教育是控制疫情的关键。     

北京市东城区2013-2015年诺如病毒感染聚集性疫情流行病学特征分析

目的 对2013-2015年北京市东城区诺如病毒感染聚集性疫情的流行病学特征和病原学特征进行分析.方法 采取面对面问卷调查的方式,对2013年1月至2015年12月北京市东城区报告的诺如病毒感染聚集性疫情开展流行病学调查,描述性分析疫情流行病学特征;采集病例及环境标本进行诺如病毒实时荧光PCR检测和基因序列分析,掌握疫情病原学特征.结果 2013-2015年共报告20起聚集性疫情,每起疫情发病人数在8-78例之间,罹患率在6.3-61.5％之间.三年报告起数呈逐年递增趋势,34月和10-12月报告17起,占总起数的85.0％.疫情主要发生在小学、幼儿园、集体单位和医院病房.采集患者便标本、密接便标本和环境涂抹标本260份,检出诺如病毒GⅡ型核酸阳性122份,阳性率为46.9％.对14起疫情的阳性标本基因序列分析结果:GⅡ.17型6起,GⅡ.6型3起,GⅡ.4Sydney-2012型2起,GⅡ.2、GⅡ.3、GⅡ.7型各1起.结论 2013-2015年北京市东城区诺如病毒聚集性疫情春季和秋冬季高发,应加强学校和托幼机构疫情的监测,加强集体单位食堂员工以及医院护理人员的监测与管理.     

南京地区婴幼儿杯状病毒感染的分子流行病学研究

目的了解南京地区婴幼儿杯状病毒腹泻的感染状况、临床表现以及分子流行病学特征。方法采集2010年7月至2011年6月南京医科大学附属南京儿童医院5岁以下腹泻患儿粪便标本及儿童保健中心健康婴幼儿粪便标本各428份。采用反转录-聚合酶链反应（RT—PCR）检测杯状病毒,测序确定其基因型别。结果428份腹泻样本中有63份为杯状病毒阳性,检出率为14．72％。其中诺如病毒GⅡ型58例,未检出诺如病毒GI型,札如病毒5例,以诺如病毒GⅡ-42006b型为主要流行株。428份健康对照组标本杯状病毒检出19例,诺如病毒6例,札如病毒11例,2例为诺如病毒GⅡ型和札如病毒混合感染。结论南京地区婴幼儿中存在不同基因型杯状病毒感染,流行毒株以GⅡ-2006b为主。     

感染性腹泻疫情中诺如病毒的分子流行病学分析

目的 研究感染性腹泻疫情中诺如病毒的分子流行病学特点.方法 对2008-2010年湖州地区的感染性腹泻疫情标本共119份进行诺如病毒核酸检测,并选取部分阳性扩增产物经序列测定分析诺如病毒的基因型.结果 119份感染性腹泻标本荧光定量PCR检测阳性50份,其中GⅠ型9份,GⅡ型35份,GⅠ和GⅡ混合感染6份.对12份PCR扩增阳性产物进行序列分析显示：5株GⅠ型诺如病毒毒株分属于GⅠ/2和GⅠ/3两种基因型;7株GⅡ型诺如病毒毒株中除1株属于新基因型GⅡb外,其余6株均属于GⅡ/4基因型.结论 诺如病毒是引起湖州地区感染性腹泻疫情最重要的病原菌之一,且湖州地区的诺如病毒存在很高的遗传多样性,同时也存在基因型别的差异.     

南京地区婴幼儿杯状病毒感染的分子流行病学研究

目的 了解南京地区婴幼儿杯状病毒腹泻的感染状况、临床表现以及分子流行病学特征.方法 采集2010年7月至2011年6月南京医科大学附属南京儿童医院5岁以下腹泻患儿粪便标本及儿童保健中心健康婴幼儿粪便标本各428份.采用反转录-聚合酶链反应( RT-PCR)检测杯状病毒,测序确定其基因型别.结果 428份腹泻样本中有63份为杯状病毒阳性,检出率为14.72％.其中诺如病毒GⅡ型58例,未检出诺如病毒GⅠ型,札如病毒5例,以诺如病毒GⅡ-4 2006b型为主要流行株.428份健康对照组标本杯状病毒检出19例,诺如病毒6例,札如病毒11例,2例为诺如病毒GⅡ型和札如病毒混合感染.结论 南京地区婴幼儿中存在不同基因型杯状病毒感染,流行毒株以GⅡ.2006b为主.     

Renal dysplasia and asplenia in two sibs

A family is reported in which two sibs, one male and the other female, both died within 24 hours of birth with enlarged polycystic kidneys. Postmortem histology in the second child showed gross renal dysplasia. In both children the pancreas was enlarged, nodular and cystic but the liver appeared macroscopically normal. In the second child, histological examination confirmed pancreatic fibrosis with cystic dilation of ducts, but showed portal fibrosis with bile duct proliferation in the liver.
This combination of findings is very reminiscent of those in a girl and her brother reported by Ivemark et al. (1959). The children reported here also showed absence or hypoplasia of the spleen, cardiac anomalies and other features of the Ivemark syndrome (Ivemark 1955), a quite different, usually sporadic, congenital disorder. It is suggested that the children described here have a distinct lethal congenital disorder, probably inherited in an autosomal recessive manner.     

Schizophrenia in a North Swedish geographical isolate, 1900–1977. Epidemiology, genetics and biochemistry

Over 200 schizophrenic patients belonging to three major and interrelated pedigree complexes have been investigated over the past 30 years in a North Swedish geographically isolated population, presently numbering about 6,000. An intensive investigation of a number of biochemical correlates and genetic markers in a few selected families belonging to one of the major pedigrees has indicated new strategies for the current research program.
Schizophrenia, as defined operationally, is significantly associated with decreased activities of two enzymes (1) blood platelet monoamine oxidase, (2) plasma dopamine-β-hydroxylase, and (3) with the genetic marker Gc² (group specific antigen). Both enzymes are subject to genetic variation. A positive score for linkage between schizophrenia and low plasma DBH activity has been calculated, but, so far, available data are insufficient for discrimination between linkage and partial contribution of genetically controlled low plasma DBH to the pathogenesis of the disease. Alternatively, both mechanisms could be involved.
As a model for continued research, schizophrenia is explained as based on a double dominant-recessive genotype (Aabb), representing a vulnerability which in about 50 % of cases develops into clinical schizophrenia. It is suggested that the dominant mutation (A) operates on or affects MAO activity, and that the recessive genotype (bb) is instrumental in low variates of DBH activity and very likely such variates within the normal range of physiological variation. Moreover, it is suggested that the combined effects of MAO- and DBH-reduced efficiency on the metabolism of e.g. dopamine could be an essential pathogenic mechanism for the schizophrenic illness which is segregating in this population.     

What will studies of Fulani individuals naturally exposed to malaria teach us about protective immunity to malaria?

There are an estimated over 200 million yearly cases of malaria worldwide. Despite concerted international effort to combat the disease, it still causes approximately half a million deaths every year, the majority of which are young children with Plasmodium falciparum infection in sub-Saharan Africa. Successes are largely attributed to malaria prevention strategies, such as insecticide-treated mosquito nets and indoor spraying, as well as improved access to existing treatments. One important hurdle to new approaches for the treatment and prevention of malaria is our limited understanding of the biology of Plasmodium infection and its complex interaction with the immune system of its human host. Therefore, the elimination of malaria in Africa not only relies on existing tools to reduce malaria burden, but also requires fundamental research to develop innovative approaches. Here, we summarize our discoveries from investigations of ethnic groups of West Africa who have different susceptibility to malaria.     

The universal muscular chain reaction,muscle spasm,Torsions, ruptures and extravasations. Chameleons of pathology and some manifestations of simple muscular disorders

Most bodily functions require the coordinated actions of complementary and supplementary paired muscle groups. Where this essential muscular cooperation is lacking, hollow organs may burst and others become literally screwed up, giving rise to many similar spastic diseases such as Torticollis, Twisted ovarian cyst, Torsion of the Testis, Volvulus of the intestines, Varicose Veins, Megacolon, Aortamegaly, Scoliosis, Erb's Palsy, Peyronie's Disease, Main-en-Griffe, Undescended Foot (Pes Cavus), Talipes, Strabismus. Spasm is “panenepidemic” and unclassified examples of Torsion Dystonia and Dyskinesia really are as common as debt and taxes.     

The dominant diseases of modernized societies as omega-3 essential fatty acid deficiency syndrome: Substrate beriberi

About 1900, modern food selection and processing caused widespread $\text{epidemics}$ of the B vitamin deficiency diseases of beriberi and pellagra which, for genetic reasons, often expressed as different diseases ranging from bowel and heart disease to dermatoses and psychoses. But the B vitamins merely help convert essential fatty acids (EFA) into the prostaglandin (PG) tissue regulators and it now turns out that, through hydrogenation, milling and selection of w3-poor southern foods, we have also been systematically depleting, by as much as 90%, a newly discovered trace Nordic EFA (w3) of special importance to primates and sole precursor of the PG3(4) series, even as a concurrent fiber deficiency increases body demand for EFA. Since substrate EFA is processed by many B vitamin catalysts, an EFA deficiency will mimic a $\text{panh}$ypovitaminosis B, i.e., a mixture of $\text{substrate}$ beriberi and $\text{substrate}$ pellagra resembling vitamin beriberi and pellagra but exhibiting as even more diverse $\text{endemic}$ disease. This would consitute a second stage of the Modern Malnutrition and explain why some workers now hold the dominant diseases of modermized societies to be new, nutritionally based, pellagraform yet lipid-related and to range, once again, from heart disease to psychosis. It is an assumption that our dominant diseases are unrelated to each other or are merely revealed by our diagnostic acumen and therapeutic success; and that hydrogenating millions of tons of food oils annually, to destroy the rancidity producing w3-EFA, is safe for $\text{primates}$. Extensive beriberiform disease is reported here in 32 typical cases taken from medical practice which responds strikingly to linseed oil supplements (60% w3-EFA) in confirmation of identical results in Capuchins.     

Hypo- und Hypermagnesämie aus kardiologischer Sicht

Zusammenfassung Eine Reihe pathologischer Zustände bedingen Magnesiummangel. Zustände mit Hypermagnesämie sind ebenfalls bekannt, doch wesentlich seltener. Für den Kardiologen beachtenswert ist, daß unter Therapie mit bestimmten Diuretica bei Herzinsuffizienz, bei Herzinfarkt, Kardiomyopathie, Digitalisintoxikation und bestimmten Herzrhythmusstörungen Hypomagnesämie beobachtet wurde. Leider kann in der klinischen Routine nur ein extracelluläres Magnesiumdefizit durch Serumbestimmungen gemessen werden; über Magnesiummangel einzelner Organe kann nichts ausgesagt werden. Hinweise für Magnesiummangel geben aber neben der Messung des Serumspiegels Anamnese, klinischer Befund, bestimmte EKG-Veränderungen wie auch evtl. Hypokalämie, ein Zustand, bei dem sich oft — besonders bei Aldosteronismus — parallele Veränderungen zeigten.Tierexperimente deuten darauf hin, daß infarktähnliche Läsionen unter Magnesiummangel entstehen, doch ob Herzinfarkt beim Menschen durch Magnesiummangel ausgelöst werden kann, ist noch ungeklärt. In Leichenherzen zeigte sich im Infarktgebiet neben Calciumakkumulation signifikanter Magnesiumverlust, wobei unklar blieb, ob sich Ursache oder Folge des Infarktes widerspiegelten. Falls ein ursächlicher Zusammenhang besteht, ist er im Myokardstoffwechsel selbst zu suchen, wie bei der Alkoholkardiomyopathie, wo myokardialer Magnesiummangel zumindest als pathogenetischer Teilfaktor anerkannt wird. Andererseits versucht man aber auch Beziehungen zwischen Atherosklerose, Blutgerinnung und Hypomagnesämie herzustellen, in der Meinung, daß Magnesiummangel auch über den coronaren Pathomechanismus des Herzinfarktes wirken könnte. Sicher scheint, daß gewisse EKG-Veränderungen und Herzrhythmusstörungen durch einen irritierten Magnesiumhaushalt bedingt sein können, da sie bei Gabe bzw. Entzug von Magnesium verschwinden. Daß Magnesiummangel die Glykosidtoleranz verringert, wird tierexperimentell bestätigt. Unter Hypomagnesämie bewirkt Acetylstrophanthidin eher und länger Rhythmusstörungen als ohne, außerdem lassen diese sich durch Magnesiumgaben eliminieren. Da in gewissen Fällen spontane und digitalisinduzierte Herzrythmusstörungen durch Magnesiuminjektionen beseitigt wurden, scheint Magnesium als Therapeuticum angebracht. Einsatz verschiedener Magnesiumsalze bei Angina pectoris, degenerativen Herzerkrankungen und Herzinsuffizienz ohne geprüften und offensichtlich gestörten Magnesiumhaushalt ist fragwürdig, weil keine eindeutigen klinischen Erfolgsbeweise vorliegen. Immerhin mag es aber larvierte, durch Serumbestimmungen nicht erfaßbare Mangelzustände geben. Allgemein erscheint es aus kardiologischer Sicht ratsam, den Magnesiumhaushalt zu überwachen und in entsprechenden Fällen auszugleichen, um möglichen Myokardläsionen oder fatalen Herzrhythmusstörungen entgegenzuwirken.     

Environmental risk factors and their role in the management of atopic dermatitis

Introduction: The etiology of atopic dermatitis (AD) is multifactorial with interaction between genetics, immune and environmental factors.

Areas covered: We review the role of prenatal exposures, irritants and pruritogens, pathogens, climate factors, including temperature, humidity, ultraviolet radiation, outdoor and indoor air pollutants, tobacco smoke exposure, water hardness, urban vs. rural living, diet, breastfeeding, probiotics and prebiotics on AD.

Expert commentary: The increased global prevalence of AD cannot be attributed to genetics alone, suggesting that evolving environmental exposures may trigger and/or flare disease in predisposed individuals. There is a complex interplay between different environmental factors, including individual use of personal care products and exposure to climate, pollution, food and other exogenous factors. Understanding these complex risk factors is crucial to developing targeted interventions to prevent the disease in millions. Moreover, patients require counseling on optimal regimens for minimization of exposure to irritants and pruritogens and other harmful exposures.     

Class II HLA in Georgia Caucasus Tbilisi Georgians and their Mediterranean ancestry: The Usko Mediterranean languages

Georgia (or Sakartvelo in its own language) is a South Caucasus Mts. country with its easternmost part is enigmatically named Iberia, like the Iberian Peninsula, which may refer to rivers “Kura” and “Ebro” or their valleys respectively. Most of their inhabitants speak Georgian which is included within Dene-Caucasian group and Usko-Mediterranean subgroup of languages. The latter includes Basque, Berber, ancient Iberian-Tartessian, Etruscan, Hittite, Minoan Lineal A and others. In the present paper, HLA class II -DRB1 and -DQB1 alleles has been studied and extended haplotypes calculated. Most frequent haplotypes are also of Mediterranean origin (i. e.: (A*02-B*51)-DRB1*11:01-DQB1*03:01, (A*02-B*51)-DRB1*13:01-DQB1*06:03, or (A*24-B*35)-DRB1*01:01-DQB1*05:01) and DA genetic distances show that closest world populations to Georgians are Mediterraneans. Georgians also show common extended haplotypes ((A*02-B*51)-DRB1*11:01-DQB1*03:01, (A*02-B*13)-DRB1*07:01-DQB1*02:01 and (A*03-B*35)-DRB1*11:01-DQB1*03:01) with Svan people, a secluded population in North Georgia mountains. We can conclude that Georgians belong to a very old Mediterranean substratum according to both linguistics (Usko Mediterranean languages) and HLA genetics.     

HLA genes in Amerindians from Mexico San Vicente Tancuayalab Teenek/Huastecos

Huastecos or Teenek Amerindians are presently living at North East Mexico (San Luis Potosi State). They have probably one of the most ancient culture of Mexico and Central America together with Mayas and Olmec groups with which also show close relationships. Proximity to Atlantic Ocean/Mexican Gulf originated that Spaniards had very early contact with them at about 1519 CE or before. In the present paper we have aimed to study HLA gene profile which may be useful for HLA and disease epidemiology and transplant programs in Teeneks. HLA-DRB1*04:07, -DRB1*14:06 and -DRB1*04:11 have been found in high frequency like in other Amerindian groups. High frequency typical Amerindians HLA extended haplotypes have been found, such as A*02-B*35-DRB1*04:07-DQB1*03:02; A*68-B*39-DRB1*04:07-DQB1*03:02 and A*02-B*39-DRB1*04:07-DQB1*03:02; also new haplotypes have been described, like A*02-B*52-DRB1*04:11-DQB1*03:02, A*68-B*35-DRB1*14:02-DQB1*03:01 and A*68-B*40-DRB1*16:02-DQB1*03:01. Genetic proximity is observed not only to linguistically close Mayans, but also to Mazatecans, Mixtecans and Zapotecans, who speak an altogether different languages; it shows once more that genes and languages do not correlate. This population was greatly diminished after European contact between 1500 and 1600 years CE; in fact, North and South America First Inhabitants population was brought from 80 down to 8 million people because of diseases (i.e.: measles, smallpox or influenza), slavery and war.