莪术油明胶微球栓塞犬肝动脉的病理改变

目的观察莪术油明胶微球栓塞Beagle犬肝动脉后的病理改变,为临床实验提供依据.方法 Beagle犬随机分为生理盐水组(10ml/kg)、空白微球组(15mg/kg)、莪术油微球低剂量组(7.5mg/kg)和莪术油微球高剂量组(15mg/kg),每4周经肝动脉给药1次,连续给药3次,停药后观察4周.观察肝病理组织学改变.结果明胶微球肝动脉栓塞可致肝组织不可逆性损伤,高剂量组广泛全小叶坏死,低剂量组灶性坏死,空白微球组改变类似高剂量组,生理盐水组未见肝组织损伤.结论莪术油微球重复经Beagle犬肝动脉给药,可因肝动脉栓塞造成肝脏不可逆性缺血坏死.     

咽喉康胶囊(内容物)Beagle犬180天长期毒性试验

咽喉康胶囊(内容物)1250.0、625.0、312.5mg/kg(大、中、小)三个剂量,经Beagle犬连续180天口服给药和停药恢复期观察30天。 给药后各剂量组动物均未见异常。体重增长,备组给药180天与药前第2次自身体重比较,均有非常显著差异(P<0.01),平均体重增长大剂量4.02kg,中     

阿霉素纳米微粒经动脉给药对兔肝肿瘤的疗效观察

目的 观察阿霉素纳米微粒经动脉给药对免肝肿瘤的疗效.方法 将阿霉素纳米微粒(小粒径脂质体与毫微粒)与碘油制成乳剂,建立兔肝VX-2移植癌改良模型并随机分为六组,经肝动脉分别注入生理盐水(NS)、碘油(Lipi)、游离丝裂霉素(ADM,2mg/kg)、游离阿霉素加空白纳米微粒(ADM+NP,2mg/kg)、阿霉素纳米微粒组(NADM,2mg/kg)与阿霉素纳米微粒-碘油乳剂(Lip-NADM,2mg/kg).结果 经Lip-NADM治疗的兔生存期显著延长(P<0.01),与其它各组相比对肿瘤生长的抑制更为明显(P<0.01),肿瘤坏死更广泛,更彻底.结论 与其它各组相比,Lip-NADM经动脉给药具有更好的疗效.     

黄藤素注射液Beagle犬静脉给药毒性观察

目的：采用Beagle犬一次静脉滴注黄藤素注射液．观察其对试验动物所产生的急性毒性反应和死亡情况．为黄藤素注射液临床用药途径提供参考。方法：用近似致死剂量法(ALD)，选择3只健康6月龄Beagle犬，根据黄藤素注射液小鼠静脉注射给药急性毒性试验结果．按50％剂量递增．计算出剂量递增序列，在剂量序列范围内间隔一个剂最给一只动物。1号动物25．0mg/kg体重．2号动物50．0mg/kg体重．3号动物100．0mg/kg体重，     

国产DHAQ(Mitoxantrone)对兔的长期毒性试验

健康成年日本大耳白兔60只,随机分成DHAQ高剂量组(D高组,0.18mg/kg/d)、低剂量组(D低组,O.09mg/kg/d)和生理盐水组,连续静脉注射给药18天,处死半数动物,余下者停药继续观察25天,比较动物给药前、给药期及停药后的一般状况、各项生理、生化指标并作病理组织学检查。结果发现D高组给药一周后食欲普遍下降、活动减少、消     

狗肝菜多糖减轻D-氨基半乳糖与脂多糖诱导的大鼠急性肝损伤

目的:观察壮药狗肝菜多糖对D-氨基半乳糖(D-GalN)及脂多糖(LPS)所致大鼠急性重症肝炎的影响。方法:将48只雄性Wistar大鼠随机分成模型、狗肝菜多糖高、低剂量和对照组;狗肝菜多糖高剂量组(300mg·kg-1)、低剂量组(150mg·kg-1)在造模前灌胃给药6d,其它各组用生理盐水对照;末次给药后1h除对照组外均在腹腔内注射D-GalN(500mg.kg-1)和LPS(20μg/kg)建立大鼠急性重症肝炎模型,对照组用生理盐水对照。于6h、12h分别观察并计算各组动物死亡率;存活动物于6h行眶后静脉窦采血用于检测血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、肿瘤坏死因子α(TNF-α)、白介素1β(IL-1β);12h摘除眼球采血用于检测血清ALT、AST、TNF-α、IL-1β和一氧化氮(NO);分光光度法检测血清ALT、AST、NO含量,ELISA法检测血清TNF-α、IL-1β水平。12h后全部处死存活动物,肝组织切片观察肝脏病理形态学变化。结果:6h各组动物均存活;与模型组相比,狗肝菜处理组12h死亡率明显低于模型组。模型组血清ALT、AST活力和TNF-α、IL-1β、NO水平均升高,狗肝菜多糖高、低剂量组血清指标均明显低于模型组。模型肝组织大片坏死、淤血,狗肝菜多糖高、低剂量组组织损伤程度明显降低,以高剂量组效果最佳。结论:狗肝菜多糖能减轻D-GalN/LPS诱导的肝损伤,可能通过降低炎性介质TNF-α、IL-1β和NO的水平发挥作用。     

注射用头孢他啶舒巴坦钠Beagle犬长毒试验

注射用头孢他啶 /舒巴坦钠 2 .4 g/kg、1 .2g/kg、0 .6 g/kg(大、中、小 )三个剂量 ,采用 0 .9%生理盐水注射液稀释 ,按 1 0ml/kg体积 (等体积不等浓度 ) ,经Beagle犬连续 32天静脉滴注 ,停药后恢复期观察 2 6天。　　三剂量组均顺利完成全程试验。其中大、中剂量组静脉滴注时 ,个别犬均出现过不同程度烦燥不安或流涎、恶心、呕吐现象 ,呕吐物为食物。中剂量组较大剂量组恶心呕吐症状轻 ,给药完毕症状消失。个别犬双耳、腹部等皮肤出现不同程度的发红 ,精神状态无异常。小剂量和对照组 ( 0 .9%生理盐水注射液 )均无明显异常。停药观察 2 6…     

红景天甙减轻大鼠酒精性肝损伤

目的:探讨红景天甙对大鼠酒精性肝损伤的作用及其可能机制。方法:将100只SD大鼠随机分为5组:对照组、模型组、联苯双酯滴丸组及红景天甙低剂量(20 mg/kg)和高剂量(40 mg/kg)组,除空白组给予生理盐水外,其余各组均给予56%乙醇灌胃,建立酒精性肝损伤大鼠动物模型,给药组同时予以相应药物灌胃,于末次给药后12 h采血,处死动物后取出肝脏,采用全自动生化仪测定血清甘油三酯(TG)、丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)水平,苏木素-伊红(HE)染色观察肝组织病理学改变,试剂盒测定肝组织中丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性,ELISA法测定各组大鼠血清中肿瘤坏死因子α(TNF-α)和核因子κB(NF-κB)水平,Western blot法和RT-PCR测定肝组织TNF-α和NF-κB的蛋白和mRNA表达。结果:与模型组比较,红景天甙高、低剂量组肝组织损伤程度明显减轻;红景天甙对酒精性肝损伤大鼠血清TG、ALT及AST水平均具有明显抑制作用(P0.05),并可降低肝组织MDA含量,增强肝组织SOD活性(P0.05);红景天甙各剂量组大鼠血清TNF-α和NF-κB含量降低(P0.05)。结论:红景天甙能够改善大鼠酒精性肝损伤病理变化,减轻肝组织炎症反应,增加抗氧化酶的活性,降低脂质过氧化,该作用可能与调节NF-κB介导的炎症反应有关。     

海藻酸钠微球与明胶海绵栓塞肺结核大咯血的效果比较:143例分析

背景:在诸多治疗方案中,介入栓塞肺结核大咯血的疗效最明确、显著。而多种栓堵材料也随之而出现,从传统的明胶海绵、聚乙烯醇颗粒,到目前应用广泛的微弹簧圈、海藻酸钠微球栓塞剂,疗效各不相同。目的:比较海藻酸钠微球与明胶海绵支气管动脉内栓塞治疗肺结核大咯血的疗效。方法:143例肺结核大咯血患者,根据栓塞材料不同分为明胶组与海藻酸钠微球组。先行选择性支气管动脉插管造影,再做超选择支气管动脉插管,最后注入栓塞材料栓塞末梢支气管动脉。结果与结论:明胶组共栓塞靶血管92支,44例(58.7%)患者栓塞后即刻止血,总有效率为81.3%。随访2年,复发12例(25.3%)。海藻酸钠微球组共栓塞靶血管83支,60例(89.1%)患者栓塞后即刻止血,总有效率为92.6%。随访2年,复发5例(7.8%)。两组比较,海藻酸钠微球组即刻止血效果显著优于明胶组(P0.05),治愈率显著高于明胶组(P0.05);海藻酸钠微球组复发率显著低于明胶组(P0.05);海藻酸钠微球组总有效率显著高于明胶组(P0.05)。并发症的发生率两组差异无显著性意义(P0.05)。结果提示,海藻酸钠微球支气管动脉栓塞治疗肺结核大咯血安全、有效,复发率低,值得临床推广应用。     

二氢槲皮素与二氢杨梅素的抗肿瘤活性对比

目的:研究二氢槲皮素和二氢杨梅素对H22 荷瘤小鼠抑瘤作用。方法:建立小鼠H22 移植性肿瘤模型(除空白外)。造模24 h 后分成6 组:模型组,阳性对照组(环磷酰胺25 mg/ kg),二氢槲皮素和二氢杨梅素高、低剂量组(30、10 mg/kg),除阳性对照组腹腔给药,其余各组均灌胃给药,测定其对H22 荷瘤小鼠抑瘤率、免疫器官指数、生化指标和细胞因子含量的影响,并通过HE 染色,观察瘤组织内坏死程度。结果:二氢槲皮素和二氢杨梅素高、低剂量组(30 mg/ kg、10 mg/ kg)均对肿瘤具有一定抑制作用,且均可提高H22 荷瘤小鼠胸腺指数和脾指数,其中二氢槲皮素高剂量组(30 mg/ kg)抑瘤效果最佳,其抑瘤率为58.8%。二氢槲皮素和二氢杨梅素高、低剂量组均可升高H22 荷瘤小鼠细胞因子白细胞介素鄄2(IL-2)和肿瘤坏死因子 (TNF)的水平,升高超氧化物歧化酶(SOD)的水平,降低丙二醛(MDA)水平。此外,二氢槲皮素和二氢杨梅素高、低剂量组对H22 荷瘤小鼠肝肾功能没有毒理作用。结论:二氢槲皮素和二氢杨梅素高、低剂量组均对肿瘤具有一定抑制作用,其中二氢槲皮素组的作用较明显,且呈剂量依赖性,其作用机制可能与增强抗氧化能力、提高机体免疫功能和升高细胞因子水平有关。     

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.