不同软组织衍射增强图像的比较研究

我们着重于衍射增强成像(DEI)中的图像及其衬度分析,确定不同组织类型对DEI成像的影响.利用北京同步辐射装置4W1A束线上的形貌与成像站获得三种软组织的衍射增强图像,采用像素-像素的"加"或"减"算法得到表观吸收图像和折射图像,并用衬度分析法对DEI中的峰位图像、表观吸收图像和折射图像的成像质量进行比较.结果显示:软组织的峰位图像与表观吸收图像的吸收衬度相近,但边界效应不及折射图像.不同软组织折射图像的折射衬度不完全相同,肺组织和肾组织的吸收衬度和折射衬度比较高,而肝脏组织的衬度比较低,说明衍射增强成像对改善肝脏组织的成像效果不够明显.因此,折射图像辨别能力强,更适合观察肺和肾等软组织的细微结构.     

正常及挫伤脊髓血管的三维直视化:同步辐射相衬成像

背景:同步辐射相位衬度成像凭借硬X射线光源的高准直、高相干等特性,其能大幅度提高对软骨细胞及微血管的空间分辨能力。目的:利用高空间分辨率同步辐射相衬成像技术观察大鼠正常及急性损伤脊髓的微血管的形态变化。方法:雄性SD大鼠分为2组:实验组以改良ALLEN’s打击法制作大鼠急性脊髓挫伤模型;伪手术组大鼠只行椎板减压术,不打击脊髓作为正常对照。术后第1天取正常及伤段脊髓标本经甲醛-水杨酸甲酯序贯处理48 h,标本于上海光源BL13W1硬X射线站进行扫描和成像。采集数据以利用VG Studio Max 2.1软件包进行3D图形重建及血管量化分析。结果与结论:相位衬度成像以特有的血管边缘增强效应直观呈现脊髓微血管形态,其结合CT技术(相衬断层成像)从三维视角对脊髓微血管进行直观成像,急性脊髓挫伤后神经组织的破坏伴随着严重的血管结构的损毁,组织损伤及血供的缺失在髓内由中央区向头、尾两侧呈梭性蔓延。三维血管量化数据显示脊髓挫伤后微血管数目及血管灌注容积急剧减少(P0.01)。结果表明无需血管造影的条件下,相衬断层成像可作为一种新的有潜力的超高分辨率可视化技术用于脊髓微血管3D结构成像及量化分析。     

基于相位衬度成像的小鼠肺肿瘤三维可视化研究

目的肿瘤的早期发现对患者意义重大。鉴于相位衬度成像对于如肺部这样的软组织成像效果显著,本文提出利用相位衬度成像技术,以微米尺度的空间分辨对肿瘤进行成像,并定量分析,早期发现肿瘤。方法在KM小鼠肺部原位接种人肺癌细胞,培育10d后取出肺组织,利用上海同步辐射光源进行相位衬度成像获取投影图像,拍摄结束后对样本进行切片、HE染色,并光学显微镜观察病理切片。然后利用滤波反投影对获取的投影图进行CT断层重建,并通过病理切片对比验证肿瘤位置,最后通过Amira软件进行三维模型的建立。结果重建出了清晰的三维模型,在模型上可以发现小肿瘤结节的存在,并测量得出该肿瘤体积为0．655mm3。结论相位衬度成像对软组织分辨率高,能发现体积较小的肿瘤．对肿瘤的早期发现有一定意义。     

基于X射线相位衬度成像技术的兔眼球血管重建

目的 利用X射线相位衬度成像技术构建兔眼血管网的三维可视化模型,观测兔眼虹膜血管的形态学特征。结果 用硫酸钡对新西兰白兔眼球血管进行造影,利用X射线相位衬度成像技术采集离体兔眼样本的高精度投影图像。图像经由滤波反投影法重建出断层图像,利用Amira 5.2.2软件进行三维重建。方法 高精度投影图像中眼球主干血管清晰连贯,能够观测到部分细小血管的分布及走向,可分辨的最小血管直径约为10 μm;CT扫描图像三维重建后得到兔眼血管网的三维模型,精确到虹膜动脉大环4级分支结构,最小血管直径可达40 μm。结论 利用X射线相位衬度成像技术可以比较清楚地观察到兔眼血管,并且能够在一定程度上构建出血管网的三维可视化模型,为眼球内血管血流动力学分析提供依据,对青光眼的临床研究具有参考价值。     

同步辐射在医学成像中的应用综述

同步辐射(synchrotron radiation,SR)作为一种具有优良特性的新型光源已引起大家的广泛关注,几乎成为多学科公用的一个先进的、不可替代的综合科技平台,尤其在医学成像方面,更是表现出强劲的生命力.本文拟从同步辐射血管造影、支气管成像、断层显像、相位衬度显像等多面阐述同步辐射在医学成像中的应用.     

姜黄素衍生物B06对2型糖尿病大鼠肝脏的保护作用

 目的:研究姜黄素衍生物B06对2型糖尿病大鼠肝脏的保护作用及机制。方法:雄性SD大鼠35只，随机均分成5组：正常对照组、高脂组、高脂治疗组、糖尿病组和糖尿病治疗组。采用高脂饮食加链脲佐菌素诱导2型糖尿病大鼠模型。高脂治疗组及糖尿病治疗组用0.2 mg· kg-1·d-1B06灌胃8周。治疗结束后用光镜和透射电镜观察大鼠肝组织的形态学改变，并用Western blotting方法检测肝脏AMP活化蛋白激酶α（AMPKα）和磷酸化AMPKα（p-AMPKα）蛋白的表达。结果:高脂组及糖尿病组大鼠肝脏显示肝细胞脂肪变性、坏死，炎症细胞浸润，纤维组织增生，2型糖尿病大鼠和高脂血症大鼠肝脏组织p-AMPKα表达降低；经B06干预后，糖尿病大鼠和高脂血症大鼠肝脏的形态学损害明显得到改善，且肝脏组织p-AMPKα的表达水平升高（P<0.05）。结论:B06对2型糖尿病大鼠的肝脏具有保护作用,可能与其上调肝脏p-AMPKα蛋白表达有关。     

大鼠肾间质的形态学研究

应用光镜、电镜技术对大鼠肾间质的形态进行了观察.描述了皮、髓质中间质形态学特点,间质细胞的分型及超微结构特点,各型间质细胞的分布.同时应用体视学方法对皮质和髓质各段的间质体积分数进行了测算.     

微焦点类同轴X射线相衬成像实验及相位恢复重建

目的:基于微焦点X射线源,进行相衬成像实验和相位信息提取。方法:根据Fresnel-Kirchhoff衍射理论,考虑空间相干性与时间相干性的影响,对连续X射线相衬成像的一般公式进行推导。根据从含有相位信息和吸收信息的图片里提取纯相位信息的方法,通过MATLAB对相衬图片进行处理。结果:实验一,对塑料吸管进行相衬成像,通过改变探测器与样品之间的距离,得到比传统X射线成像更清晰、放大且能够突出边界信息的图像;实验二,在电压分别为45 kVp和70 kVp的情况下得到硼硅酸盐玻璃的相衬图像,然后通过相位恢复重建得到含有纯相位信息的相衬图像。结论:对于轻元素物质,微焦点类同轴X射线相衬成像比传统X射线相衬成像的分辨率高、图像衬度好;相位信息提取技术将会大大促进微焦点类同轴X射线相衬成像技术在普通实验室应用和医学肿瘤检测等方面的应用进展。     

硬X射线相衬成像在裸鼠肿瘤成像方面的研究

传统x射线对软组织的成像是目前的技术弱点.硬x射线是用x射线穿过物体后,x射线的相位改变作为成像因子,它对软组织有较好的成像效果.本课题用硬x射线成像对肝肿瘤组织和胃肿瘤组织进行成像.将25 μl HCT-8人结肠癌细胞移植在裸鼠肝脏上,分别在3 d、4 d、5 d和6 d处死裸鼠,取出肝脏.用同样的方法培养裸鼠早期胃肿瘤,并在3 d和4 d后取出裸鼠胃.对标本进行硬x射线的成像方法即类同轴全息法成像.硬x射线可以对裸鼠肝肿瘤和胃肿瘤进行成像,并且图像分辨率在微米数量级,培养6 d的肝肿瘤可见肿瘤组织.也可清晰观察到3 d和4 d的胃肿瘤.硬x射线成像原理是一个用相位改变因子成像的模式,它的成像对微小物体有着微米级的图像分辨率,是影像学从宏观成像到微观成像的关键,对发现早期的病变组织有明显的优势.     

兔膝关节神经支选择性切断后对关节软骨的影响

目的观察兔膝关节神经支选择性切断后关节软骨形态学变化。方法在外科显微镜下选择性切断兔膝关节神经支,术后4、8、16周取材,肉眼观察兔膝关节大体结构,组织切片HE染色,光镜下观察关节软骨组织结构,应用显微电脑测量软件测量关节软骨厚度。结果对照组兔膝关节软骨表面光滑,软骨细胞呈四层结构排列,软骨细胞为圆形或椭圆形,表层呈梭形。实验组兔膝关节软骨组织结构未见明显改变,软骨厚度与对照组比较差异无统计学意义(P0.05)。结论选择性切断兔膝关节神经支对关节软骨组织结构无明显影响,膝关节局部去神经化术治疗具有可行性。     

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.