腹腔镜与传统腹横纹小切口手术治疗小儿腹股沟斜疝效果的比较

目的：比较腹腔镜与传统腹横纹小切口手术治疗小儿腹股沟斜疝的效果。方法回顾性分析安徽医科大学附属安庆医院小儿外科2011年9月—2013年3月收治456例小儿腹股沟斜疝患儿的临床资料,其中230例采用腹腔镜(腹腔镜组)手术治疗,226例采用腹横纹小切口(传统手术组)手术治疗,比较两种术式的疗效及并发症。结果腹腔镜组：术中发现62例(26.96%,62/230)合并对侧鞘状突未闭,同时行对侧疝囊高位结扎,全组无一例中转开腹;单侧手术时间(19.3±5.4)min,双侧手术时间(26.8±6.2)min;切口均I期愈合,无明显手术瘢痕;术后阴囊肿胀3例,无阴囊血肿和医源性隐睾病例;随访3~21个月,复发2例。传统手术组：单侧手术时间(20.8±6.5)min,双侧手术时间(28.6±7.8)min;患儿切口下有少量积液3例,切口感染1例,阴囊肿胀202例,阴囊血肿9例,医源性隐睾2例;随访3~21个月,复发4例,对侧新发7例。两组患儿单侧和双侧手术时间、切口感染率、医源性隐睾率、术后复发率比较,差异均无统计学意义(P值均>0.05);阴囊肿胀、阴囊血肿及对侧新发疝发生率比较,腹腔镜组均低于传统手术组,差异均有统计学意义(P值均<0.05)。结论腹腔镜与传统腹横纹小切口手术比较,具有切口美观,术后阴囊肿胀、血肿发生率低等优点,可同时发现并处理对侧隐匿性疝,术后对侧新发率低,是一种安全、可靠、有效的手术方式。     

腹腔镜与传统腹股沟切口手术治疗低位腹腔型隐睾效果比较

目的 比较腹腔镜与传统腹股沟切口手术治疗低位腹腔型隐睾的疗效。方法 回顾性分析2014年1月—2018年6月安徽医科大学附属安庆医院收治的小儿低位腹腔型隐睾116例(127侧)患儿的临床资料。患儿年龄8个月~7岁[(2.74±1.89)岁];右侧57例,左侧48例,双侧11例。116例患儿按手术方式不同分为传统手术组、腹腔镜组,对两组手术时间、术中出血量、术后并发症进行对比分析。结果 (1)腹腔镜组:均顺利完成手术,无一例中转开腹;术中发现13例合并对侧鞘状突未闭(19.40%),同时行对侧鞘状突高位结扎;单侧手术时间(53.62±4.44)min,术中出血量(6.57±1.05)mL;双侧手术时间(75.22±4.11)min,术中出血量(7.86±0.35)mL。所有患儿切口一期愈合,无明显手术瘢痕;术后阴囊血肿1例,予相应处理后好转。本组患儿术后随访3~24个月,平均15个月。随访期间所有患儿睾丸发育良好,无睾丸回缩或萎缩,无腹股沟疝及鞘膜积液发生。(2)传统手术组:均顺利完成手术,单侧手术时间(44.32±3.22)min,术中出血量(8.50±1.50)mL;双侧手术时间(68.70±5.16)min,术中出血量(10.23±0.71)mL。术后切口感染2例,阴囊血肿8例,均予相应处理后好转。患儿术后均获随访3~24个月,平均14个月。随访期间2例睾丸回缩至腹股沟区,2例睾丸萎缩,余病例睾丸血供良好,无睾丸萎缩或回缩;2例患儿因对侧新发腹股沟疝行腹腔镜疝囊高位结扎术。腹腔镜组术中出血量、并发症发生率低于传统手术组,但手术时间长于传统手术组,差异均有统计学意义(P值均＜0.05)。结论 腹腔镜手术治疗低位腹腔型隐睾,具有术中出血少、术后并发症少、切口美观等特点,术后睾丸回缩、睾丸萎缩等严重并发症减少,可作为手术治疗小儿低位腹腔型隐睾的常规术式。     

39例急性嵌顿性腹股沟疝的手术治疗分析

目的探讨无张力疝修补术治疗成人急性嵌顿性腹股沟疝的临床效果。方法回顾性分析我院2000年1月-2007年12月对39例急性嵌顿性腹股沟疝患者行无张力疝修补术的临床资料。结果39例手术过程均顺利,平均手术时间为60min。无切口感染和排斥反应,无术后死亡。术后疼痛4例,阴囊积液2例。全组病例术后随访6个月,未见复发。结论无张力疝修补术可以安全有效地用于急性嵌顿性腹股沟疝的患者。     

26例急性嵌顿性腹股沟疝的手术治疗

目的探讨无张力疝修补术治疗成人急性嵌顿性腹股沟疝的临床效果。方法回顾性分析我院2001年1月～2008年5月对26例急性嵌顿性腹股沟疝患者行无张力疝修补术的临床资料。结果26例手术过程均顺利,平均手术时间为60 min。无切口感染和排斥反应,无术后死亡。术后疼痛4例,阴囊积液2例。全组病例术后随访6个月,未见复发。结论无张力疝修补术可以安全有效地用于急性嵌顿性腹股沟疝的患者。     

对于腹股沟疝无张力修补术41例及腹股沟嵌顿疝修补术4例临床分析

目的探析腹股沟疝无张力修补术及腹股沟嵌顿疝修补术的临床治疗效果。方法将我院接收的45例腹股沟疝患者作为观察对象,分析总结腹股沟疝无张力修补术及腹股沟嵌顿疝修补术的临床效果。结果本组45例患者,有4例患者为急诊手术行腹股沟嵌顿疝修补术,41例患者行腹股沟疝无张力修补术,手术后有4例患者发生尿潴留,2例患者出现阴囊水肿,3例患者有伤口异物感,2例患者有切口哆开。所有患者均随访2~3个月,未见有复发病例。结论腹股沟疝无张力修补手术简单安全创伤小,手术后恢复快。复发率低,是较为理想的手术方式,值得临床应用和推广,腹股沟嵌顿疝急诊手术宜选用传统疝修补术。     

腹腔镜治疗成人嵌顿疝137例分析

目的 探讨腹腔镜在治疗嵌顿疝的作用.方法 回顾总结自2005年1月~2010年11月运用腹腔镜治疗嵌顿疝137例的临床经验.结果 全组137例嵌顿疝行腹腔镜疝修补术135例,中转开腹手术2例,全组无死亡病例.结论 腹腔镜治疗嵌顿疝是安全的,具有患者创伤少,恢复快,同时可探查腹腔其它的隐匿病变,如双侧疝、隐匿疝、闭袢梗阻坏死的肠段,同时治疗发现的隐匿病变.     

腹腔镜探查并修补腹股沟嵌顿疝在临床中的应用

目的：回顾分析28例腹股沟嵌顿疝患者行腹腔镜探查后如无肠管坏死行腹膜前疝修补术的体会,探讨腹腔镜探查及修补的应用技巧及价值。方法2010年10月~2012年10月对28例腹股沟嵌顿疝患者全部先行腹腔镜探查,再根据具体情况行相应的修补方式,对其相关临床资料进行回顾性分析。结果其中6例经腹腔镜探查后发现肠颜色发暗或坏死,随中转开腹,余22例行腹膜前疝修补术成功,术后腹腔镜1例发生阴囊血清肿,1例发生皮下气肿,开腹2例发生切口感染。随访1~2年无复发。结论熟练掌握腹腔镜探查及修补嵌顿疝的手术技巧,掌握好适应征,腹腔镜可以安全、有效的应用于嵌顿性腹股沟疝患者。     

经脐单孔腹腔镜下手术治疗对嵌顿性腹股沟斜疝患儿的效果及血清 CRP、β-EP 水平的影响

目的:探讨经脐单孔腹腔镜下手术治疗嵌顿性腹股沟斜疝患儿的效果及对血清C反应蛋白(C-Reactive Protein,CRP)、β-内啡肽(Endorphin,β-EP)水平的影响.方法:回顾性分析2019年1月至2021年1月本院确诊的115例嵌顿性腹股沟斜疝患儿的临床资料,根据手术方式分为观察组(n=58)和对照组(n=57),分别采用腹腔镜疝囊高位结扎术以及开放手术进行治疗.记录两组患儿手术时间、术中出血量、下床时间、住院时间与并发症发生情况;分别于手术前后采用酶联免疫吸附试验法测定患者血清CRP、白细胞介素-6(Interleukin-6,IL-6)、肿瘤坏死因子-α(Tumor Necrosis Factor-α,TNF-α)及氧化应激指标,如β-EP、生长激素(Growth Hormone,GH)、总抗氧化能力(Total antioxidant capacity,T-AOC)水平.结果:观察组手术时间、术中出血量、下床时间、住院时间均短于对照组(P<0.05);手术后,观察组患儿CRP、IL-6、TNF-α及β-EP水平均低于对照组,GH、T-AOC均高于对照组(P<0.05).观察组并发症发生率明显低于对照组(P<0.05).结论:经脐单孔腹腔镜下手术治疗嵌顿性腹股沟斜疝患儿的效果较好,可促进患儿早期康复,降低血清CRP、β-EP水平及并发症发生风险.     

无张力疝修补术在腹股沟嵌顿疝中的应用（附21例报告）

目的探讨疝环充填式无张力疝修补术在腹股沟嵌顿疝中的临床应用价值。方法对我院2003年1月至2007年6月行疝环充填式无张力疝修补术治疗21例腹股沟嵌顿疝病人的临床资料进行回顾性分析。结果无术后死亡,术后疼痛2例,1例发生阴囊积液,手术全部成功完成,平均手术时间65min,病人术后2d可正常活动。随访6-18个月,未见复发病例。结论疝环充填式无张力疝修补术治疗腹股沟嵌顿疝具有安全、创伤小、恢复快的优点,临床效果满意。     

老年嵌顿性腹股沟斜疝的临床分析

目的 探讨老年人嵌顿性腹股沟斜疝的临床特点和治疗方法.方法 回顾47例老年人嵌顿性腹股沟斜疝患者的临床资料并进行分析讨论.结果 对47例患者全部进行术后随访,时间6个月～2年,无一例因手术死亡.术后有伤口不适感者6例,阴囊胀痛或有硬结者6例,给予热敷理疗3个月后治愈;未发生切口感染;给予疝修补术者未发生疝复发;未见肠梗阻、深静脉血栓等并发症.结论 对老年嵌顿性腹股沟斜疝患者的问诊和体格检查要耐心细致,避免漏诊误诊.对于大多数老年嵌顿性腹股沟斜疝给予疝修补术是可行的,对于无肠坏死者可行无张力疝修补术.     

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.     

'Very sore nights and days': the child's experience of illness in early modern England, c.1580-1720

Sick children were ubiquitous in early modern England, and yet they have received very little attention from historians. Taking the elusive perspective of the child, this article explores the physical, emotional, and spiritual experience of illness in England between approximately 1580 and 1720. What was it like being ill and suffering pain? How did the young respond emotionally to the anticipation of death? It is argued that children’s experiences were characterised by profound ambivalence: illness could be terrifying and distressing, but also a source of emotional and spiritual fulfilment and joy. This interpretation challenges the common assumption amongst medical historians that the experiences of early modern patients were utterly miserable. It also sheds light on children’s emotional feelings for their parents, a subject often overlooked in the historiography of childhood. The primary sources used in this article include diaries, autobiographies, letters, the biographies of pious children, printed possession cases, doctors’ casebooks, and theological treatises concerning the afterlife.