犬空肠动脉栓塞安全性的实验研究

目的通过超选择性插管人犬空肠动脉分支后用聚乙烯醇（polybvinyl alcohol particles,PVA）颗粒栓塞,观察肠壁缺血坏死程度和范围,探讨其安全性。方法44只犬随机分为A、B两组。A组（22只）：空肠动脉二级分支水平远端栓塞;B组（22只）：空肠末级动脉弓前一级分支水平栓塞。分别注入大小为150-250μm（A1组6只,B1组6只）、355～500μm（A2组8只,B2组8只）和710—1000μm（A3组8只,B3组8只）PVA颗粒。少量、缓慢、间断推注PVA,血流停滞时即停止。术后3、7、14d,处死犬取出空肠行大体及病理学观察。结果栓塞技术成功率为95．5％。PVA颗粒量为5．10mg。注入150～250μm、355～500μm、710～1000μmPVA颗粒肠坏死的发生率分别为：81．8％（9／11）、40．0％（6／15）、25．0％（4／16）,组间差异具有统计学意义（P〈0．05）。A、B两组发生肠坏死的发生率分别为61．9％（13／21）、28．6％（6／21）,组间差异有统计学意义（P〈0．001）。结论在同一栓塞水平下,PVA颗粒越小则越易发生肠坏死。最佳的栓塞水平在末级动脉弓前一级分支水平,PVA颗粒大小应选择710～1000μm。     

明胶海绵粉末栓塞犬髂内动脉

背景：明胶海绵已成为骶骨肿瘤术前栓塞的首选材料,但针对小颗粒明胶海绵对栓塞效果及栓塞后并发症的影响未见明确报道。 目的：观察小颗粒明胶海绵栓塞犬双侧髂内动脉后手术出血量变化和并发症情况。 方法：用直径为50-150 μm明胶海绵粉末对15只犬行双侧髂内及骶正中动脉栓塞,分别于栓塞后1,2,3 d模拟骶骨肿瘤手术测量出血量变化;病理观察栓塞区膀胱、直肠、臀部肌及坐骨神经变化。 结果与结论：栓塞后第3天出血量高于第1,2天(P < 0.05),栓塞后第1天与第2天出血量差异无显著性意义(P > 0.05)。在运用直径为50-150 μm明胶海绵粉末栓塞犬双侧髂内及骶正中动脉时,最小动脉是50 μm的微动脉,但主要集中在100-200 μm小动脉,数字减影血管造影下显示栓塞双侧髂内及骶正中动脉近端血管级别为其一级分支,此时犬盆腔脏器组织无明显变化。     

大鼠血管新生内膜形成过程中NF-κB的活化和ICAM-1及COX-2表达的变化

目的：探讨大鼠血管内膜增生过程中NF-κB活化与内膜炎性增生的相互关系。方法:Western blotting分析血管壁中NF-κB p65、IκBα及其下游炎性基因ICAM-1和COX-2的表达；用免疫沉淀分析检测NF-κB p65的苏氨酸磷酸化。结果:内皮剥脱后，血管总蛋白与核蛋白中p65的含量于术后7 d达峰值；术后21 d下降但仍高于0、1 d组；但胞浆p65含量无明显变化。p65苏氨酸磷酸化水平与NF-κB核转位成负相关关系。IκBα于术后1 d表现出一过性降低，术后14 d开始回升，21 d接近正常组水平；与此相反，ICAM-1和COX-2的表达于内皮剥脱后升高，至14 d时达峰值，21 d时表达量下降但仍高于正常组。结论:血管内皮剥脱诱导的内膜增生过程中伴有持续的NF-κB p65活化和炎性因子的表达。     

MTX微囊行肝动脉末梢栓塞的动物实验

目的 对含甲氨喋呤正常人体白蛋白微囊（MTX－HAS－MC）经动脉肝动脉灌注栓塞后的体内药物动力学过程及微肿在肝动脉内的栓塞方式，栓塞水平，降解时限等进行了研究。方法 选择健康杂种狗，肝动脉插管，分别注入含10％MTX白蛋白微囊及单纯MTX（溶于生理盐水）。定时测定肝组织，下腔静脉血药药物浓度及行肝组织病检，比较二者差异。结果 组织形态学观察发现实验组微囊大多呈单行串珠样排列栓塞肝微动脉或肝毛细动脉（窦前水平），多数在肝小动脉内以微囊为中心形成血栓。术后20天的标本内仍可见到完整无损的微囊检塞在位。动态检测肝组织，下腔静脉血药物浓度。实验组肝、血药物浓度一时程相差1．33－5．70倍；对照组肝、血药物浓度相差不大。微囊组肝药浓度始终高于相应的对照组肝药浓度，随着时间的推延，由1．3倍－28倍。微囊组的药物消除半衰期远远长过对照组，两者在肝内相差2．8倍，在下腔静脉血内相差3．6倍。结论 微囊为血管末梢栓塞剂，在体内其裂解时限超过20天。微囊栓塞阻断末梢血供，大量药物浓集于肝组织中，并可经微囊不断裂缓缓解，使肝内持续保持一定的药物浓度。以上作用对肝癌治疗有积极意义。     

明胶海绵在肺结核咯血动脉栓塞中的应用

背景：目前国内用于支气管动脉栓塞的栓塞剂材料主要有明胶海绵、PVA颗粒、藻酸钠微球、弹簧圈等。 目的：分析总结明胶海绵应用于动脉栓塞治疗肺咯血治疗效果。 方法：以“肺咯血、栓塞、肺结核、明胶海绵”为中文关键词,以：“Hemoptysis 、Embolization 、Tuberculosis、 Gelfoam” 为英文关键词,采用计算机检索中国期刊全文数据库、维普数据库(1995-01/2011-05)相关文章。纳入明胶海绵栓塞法治疗肺结核咯血等相关的文章,排除重复研究或Meta分析类文章。 结果与结论：共入选17篇文章进入结果分析。综述了明胶海绵在肺结核咯血动脉栓塞中的应用。包括明胶海绵栓塞剂的介绍,动脉栓塞术止血技术以及用明胶海绵动脉栓塞治疗肺咯血治疗效果及不足等方面的研究内容。高压高温处理后的明胶海绵作为栓塞剂治疗肺咯血,不仅临床疗效满意而且非常经济,适合目前中国的国情。     

超选择肾动脉栓塞治疗外伤性肾出血的临床应用

目的:探讨DSA下超选择肾动脉插管栓塞治疗肾损伤出血的临床应用价值.方法:28例外伤性肾脏出血患者,采用Seldinger's技术,先行肾动脉DSA造影.明确肾动脉主干或/和其分支损伤的部位及程度,在超滑导丝引导下超选择插管至出血动脉部位应用金属弹簧圈或明胶海绵颗粒进行栓塞治疗.结果:28例患者经DSA肾动脉造影后均能明确肾动脉出血的部位,经超选择插管金属弹簧圈或明胶海绵颗粒栓塞后均能有效止血,栓塞后造影显示出血动脉闭塞,造影剂外溢征象消失,术后1～3 d肉眼血尿消失.结论:DSA下超选择肾动脉插管栓塞治疗肾出血创伤小、疗效好、并发症少,而且能最大限度的保护肾功能,是治疗外伤性肾出血的一种安全、快捷、有效的方法.     

MTX微囊行肝动脉末梢栓塞的动物实验

目的对含甲氨喋呤正常人体白蛋白微囊(MTX-HAS-MC)经动物肝动脉灌注栓塞后的体内药物动力学过程及微囊在肝动脉内的栓塞方式,栓塞水平,降解时限等进行了研究.方法选择健康杂种狗,肝动脉插管,分别注入含10%MTX白蛋白微囊及单纯MTX(溶于生理盐水).定时测定肝组织,下腔静脉血药药物浓度及行肝组织病检,比较二者差异.结果组织形态学观察发现实验组微囊大多呈单行串珠样排列栓塞肝微动脉或肝毛细动脉(窦前水平),多数在肝小动脉内以微囊为中心形成血栓.术后20天的标本内仍可见到完整无损的微囊检塞在位.动态检测肝组织,下腔静脉血药物浓度.实验组肝、血药物浓度一时程相差1.33～5.70倍;对照组肝、血药物浓度相差不大.微囊组肝药浓度始终高于相应的对照组肝药浓度,随着时间的推延,由1.3倍～28倍.微囊组的药物消除半衰期远远长过对照组,两者在肝内相差2.8倍,在下腔静脉血内相差3.6倍.结论微囊为血管末梢栓塞剂,在体内其裂解时限超过20天.微囊栓塞阻断末梢血供,大量药物浓集于肝组织中,并可经微囊不断裂解缓解,使肝内持续保持一定的药物浓度.以上作用对肝癌治疗有积极意义.     

ROCK I及TGF-β1在慢性血栓栓塞性肺动脉高压大鼠肺小动脉的表达

目的：观察Rho激酶（ROCK I）及转化生长因子β1（TGF—β1）在慢性血栓栓塞性肺动脉高压大鼠肺小动脉表达的动态变化。方法：雄性Wistar大鼠64只，随机分为8组，每组8只：初始对照组、栓塞3d组、1周组、2周组、4周组、8周组、12周组、终末对照组。采血制备血栓，颈静脉注入，2周后第2次栓塞，全程腹腔注射氨甲环酸。达实验设定日期后，测各组大鼠平均肺动脉压（mPAP）、肺动脉相对中膜厚度（PAMT）、管壁面积／管总面积（WA／TA）、右室肥厚指数（RVHI），原位杂交检测ROCK I mRNA表达，免疫组化检测TGF—β1蛋白表达。结果：栓塞4周组至12周组大鼠随时间延长mPAP明显增高（均P〈0．01）；PAMT、WA／TA在4周后随时间延长显著增高（4周组P〈0．05，8周、12周组P〈0．01）；8周后RVHI较对照组明显增高（8周组P〈0．05，12周组P〈0．01）；栓塞后ROCK I mRNA原位杂交染色强度随时间延长出现增高趋势（3d组至2周组P〈0．05，4周组至12周组P〈0．01），TGF—β1蛋白免疫组化染色强度随时间延长出现增高趋势（1周组、2周组P〈0．05，4周组至12周组P〈0．01）。相关分析表明，ROCK I mRNA及TGF—β1蛋白与mPAP、RVHI及血管重构指标均呈正相关（均P〈0．01）；ROCKImRNA与TGF—β1蛋白表达呈正相关（r=0．612，P〈0．01）。结论：ROCKI和TGF—β1均可能参与慢性血栓栓塞性肺动脉高压、肺血管重构的病理生理过程，此过程中Rho／Rho激酶信号通路可能是TGF—β1发挥生物学效应的重要途径之一。     

成年小鼠缺血性脑卒中后病理及行为功能的变化

文题释义：大脑中动脉末端闭塞模型：该模型最先由TAMURA等在大鼠上开发出来，即开颅手术找到大脑中动脉皮质分支并对其进行结扎或电凝，可以引起稳定的局灶性皮质梗死，在很好模拟人类卒中病理状态的同时死亡率较低。但这种手术方式对手术人员的技术以及设备有较高要求，并且需要后期评估才能确定造模成功与否。缺血性脑卒中：脑卒中分缺血性和出血性脑卒中，缺血性卒中是由于脑的供血动脉狭窄或闭塞，造成脑组织缺血、缺氧性坏死，是中国致死和致残的主要原因。 背景：大鼠大脑中动脉末端闭塞模型可以引起稳定的局灶性皮质梗死，在很好模拟人类卒中病理状态的同时死亡率较低，但对手术人员的技术以及设备有较高要求，并且需要后期评估才能确定造模成功与否。 目的：建立有效稳定简便的缺血性小鼠脑卒中模型；揭示小鼠脑卒中后梗死区及周围区域的病理变化；探索小鼠脑卒中后的行为学改变。 方法：对小鼠末端大脑中动脉进行永久电凝结扎，24 h后用TTC染色明确该模型梗死范围并统计该模型的成功概率；对小鼠大脑中动脉末端闭塞模型后不同时间点(1，3，7，10，14 d)的脑组织切片进行苏木精-伊红染色，观察缺血坏死区的体积在不同时间点的改变；进行胶质纤维酸性蛋白、Iba-1免疫组织化学染色，检测模型小鼠脑损伤后胶质反应及炎症反应变化；最后应用网格足部错误试验和圆柱体试验评价小鼠卒中后感觉运动功能的缺失情况。结果与结论：①大脑中动脉末端闭塞模型导致局灶性皮质梗死且该新模型死亡率仅9%，成功率达87%；②梗死区域主要位于M1/S1/S2区，梗死范围在闭塞10 d时趋于稳定；③脑卒中后3 d时炎症反应达到高峰，14 d时损伤区周围形成稳定星形胶质瘢痕；④局灶性皮质梗死后小鼠对侧肢体出现明显的感觉及运动的缺失；⑤结果表明，卒中后实验小鼠立即出现感觉及运动功能缺失，且持续至卒中后12周；实验建立的大脑中动脉末端闭塞模型稳定、可靠，梗死范围明确，适合缺血性脑卒中的研究。 ORCID: 0000-0002-5489-3807(梁彦峰) 中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程     

Neuroform支架结合Matrix Ⅱ弹簧圈栓塞颅内宽颈动脉瘤

目的探讨Neuroform支架植入结合MatrixⅡ弹簧圈栓塞治疗颅内宽颈动脉瘤的疗效、技术要点、安全性并发症防治。方法对诊断颅内宽颈动脉瘤6例的病人，其中大脑前动脉瘤1例，后交通动脉瘤2例，眼动脉瘤1冽，大脑中动脉分又部动脉瘤1例，基底动脉顶端1例，4例先行Neuroform支架瘤颈成形，将微导管通过支架网眼矬入动脉瘤内，填塞弹簧圈；2例先置入微导管于动脉瘤内，再释放支架后栓塞。术后3～6个月随访4例。结果所有病例栓塞操作均顺利完成，无手术并发症；其中致密填塞4例，部分致密填塞2例，术后病人均恢复良好，4例短期随访无再出血及血栓栓塞症状发生。结论Neuroform支架结合MatrixⅡ弹簧圈治疗颅内宽颈动脉瘤安全、有效。     

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.     

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.     

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.     

'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.