基于VTK的肝组织CT断层图像三维重建

目的利用可视化开发包（VTK）将计算机断层扫描（cT）图像合成三维立体图像,以利于更好地制定肝癌患者的治疗方案。方法建立基于VC6．0平台上的VTK可视开发环境,获取患者的DICOM格式的CT图像,采用VTKfilter滤波器和拉普拉斯锐化模板对图像进行滤波、增强等预处理,利用光线投影Ray—Casting算法对图像进行三维重建。结果该方法可生成效果较好的三维图像,其分辨率较高,图像重建速度快,且可进行切割、旋转、缩放等功能。结论基于VTK的光线投影算法可用于对人肝组织的三维重建,有利于医生直观地观察病变组织的形状和位置,为诊断和治疗提供依据。     

基于区域生长法的冠状动脉三维分割

根据图像序列,对患者冠状动脉进行三维重建,有利于医生对冠脉病变部位做出准确诊断。首先利用光线透射法（ray casting method）并结合ITK和VTK函数库对CT扫描图像序列进行三维重建,得到胸腔三维模型,之后利用区域生长法（region growing method）进行冠状动脉三维分割,实现冠脉模型的重建任务。实验结果表明,本文算法可以成功的提取出冠状动脉的主要分支。结合VTK和ITK函数库,计算机可以有效地实现胸腔三维模型的重建以及冠状动脉的分割工作,对医生直观的了解冠状动脉的解剖结构及冠心病的临床诊断有重要意义。     

基于区域生长法的三维心血管模型的分割

目的医学图像能够反映人体各组织的生理或病理性的结构信息和功能信息,根据图像序列,对患者心血管组织进行三维重建,可以方便医生对血管的病灶部位做出准确诊断。本文将区域生长法(region growing method,RGM)在二维图像的基础上用于三维,并比较RGM的3种子方法对心血管模型进行三维分割的效果。方法结合VTK(Visualization Toolkit)与ITK(Insight Segmentation and Registration Toolkit)函式库,首先利用光线投射法(ray casting,RC)对患者的CT扫描图像序列进行三维重建,得到患者胸腔三维模型;之后分别利用区域生长法中连通阈值、置信连接和邻域连接3种算法进行三维分割处理,得到患者心血管模型的仿真结果。结果三维重建仿真技术,具有直观重现心血管造影序列所描述的人体胸腔部位各组织的可能性;3种分割算法的比较显示,邻域连接法相比于其他两种算法,模型的解剖结构信息丢失程度较大,血管树的分支数目及管径也明显偏小。结论使用VTK与ITK函式库,通过光线投射法的体绘制技术和区域生长法的图像分割技术,可以建立患者的心血管模型;区域生长法中的连通阈值和置信连接算法,对结果的细节保留程度最大。     

基于CT数据的医学图像处理系统设计

基于医学DICOM序列图像数据,利用Insight Segmentation and Registration Toolkit和Visualization Toolkit工具包对图像数据进行处理,实现图像的读取、滤波和调窗等预处理。对不同目标区域分别采用区域生长法和水平集法进行分割,实现面绘制的体素级重建方法绘制和体绘制的光线投影法绘制,构建出目标模型的三维模型。以QT和VS2013为平台,设计图像处理系统,完成图像的读取、预处理、二维分割、三维重建和人机交互等功能。系统可提供方便、快捷的操作,构建逼真的三维模型,对目标区域准确定位、快速诊断,提高医护人员的工作效率。     

基于滑动块的深度卷积神经网络乳腺X线摄影图像肿块分割算法

目的:提出一种基于滑动块的深度卷积神经网络局部分类、整图乳腺肿块分割的算法,为临床诊断提供有效的肿块形态特征。方法:首先通过区域生长算法和膨胀算法提取患者乳腺区域,并进行数据归一化操作。为了得到每一个像素位置上的诊断信息,在图像的对应位置中滑动提取肿块类及非肿块类图像块,根据卷积神经网络提取其中的纹理信息并对图像块进行分类。通过整合图像块的预测分类结果,进行由粗到细的肿块分割,获得乳腺整图中像素级别的肿块分割。结果:通过比较先进的深度卷积神经网络模型,本文算法滑动块分类结果DenseNet模型下准确率达到96.71%,乳腺X线摄影图像全图肿块分割结果F1-score最优为83.49%。结论:本算法可以分割出乳腺X线摄影图像中的肿块,为后续的乳腺病灶诊断提供可靠的基础。     

乳腺X线图像肿块分割

乳腺肿块分割是乳腺癌计算机辅助诊断(CAD)检测和识别系统中关键的一步.由于乳腺肿块与背景相互交叠、边界不清晰、乳房密度不均匀,使得其分割比较困难.本文基于区域增长算法,研究了利用乳腺肿块自身特征得到最优分割阈值的方法,从而提出一种对乳腺X线图像肿块快速、有效的分割方法.实验结果表明该方法在保证肿块针状化特征情况下,拥有较好的分割效果.     

基于Matlab GUI的脑胶质瘤三维显示辅助诊断系统的设计

针对脑科医生对二维脑部图像通过想象建立起三维空间的立体结构缺乏直观性与准确性的缺陷,设计了基于Matlab GUI的脑胶质瘤三维显示辅助诊断系统软件。软件具有读取MRI原始数据、对脑部MRI图像的预处理、图像插值放大、图像分割和三维重建等功能。通过该软件,可以对脑部MRI图像进行合适的预处理,提取出脑部肿瘤组织区域,三维重建可以凸显肿瘤区域的位置、形状和大小。该软件界面友好,使用方便,为临床医生诊断脑胶质瘤与确定治疗区域提供了参考。     

新型乳腺磁共振增强图像肿瘤区域的自动分割模型

乳腺磁共振增强图像上,乳腺癌主要有肿块型和非肿块型两种强化方式。由于乳腺肿瘤区域相对较小,肿块型和非肿块型之间形态学差异大,非肿块型自身差异性复杂,因而很难精确分割出乳腺肿瘤区域。针对这些问题,提出一套新颖的粗检测细分割的深度学习模型(YOLOv2+SegNet)。该模型在精准分割之前,首先运用YOLOv2网络在乳腺可能的肿瘤区域进行粗检测,从而得到大致可能的肿瘤区域;接下来在粗检测的基础上,针对检测到可能的肿瘤区域,运用SegNet网络进行精细分割,从而实现算法最优的性能。为了验证YOLOv2+SegNet模型的有效性,从医院采集的数据集中选取560张乳腺MRI增强图像作为训练和测试(其中训练和测试集分别为415张和145张乳腺MRI数据)。在实验的过程中,运用YOLOv2+SegNet模型,分别对乳腺肿块型、非肿块型、肿块和非肿块混合型3类MRI数据进行肿瘤区域自动分割的实验。实验结果表明:YOLOv2+SegNet模型和SegNet网络分割结果的Dice系数相比有约10%的提升,与传统的C-V模型、模糊C均值聚类、光谱映射主动轮廓模型以及深度模型U-net、DeepLab相比有更为明显的提升。     

一种基于小波变换的乳腺X线图肿块分割方法

目的：乳腺癌的早期诊断和治疗是能够降低乳腺癌患者死亡率的有效途径。通过乳腺X线图像观察乳腺状况是目前乳腺癌普查的首选影像方法。随着图像处理技术的高速发展,计算机辅助检测技术在乳腺癌的检测方面起到越来越重要的作用。方法：本文首先利用图像处理领域的形态学处理、区域增长等相关知识,对乳腺X线图像进行预处理操作,去除图像中所包含的干扰信息。之后提出一种对图像的灰度直方图进行小波变换,并根据其小波变换的模极大值点确定图像分割阈值的方法对乳腺X线图像中的疑似肿块区域进行粗分割。在通过粗分割过程获得乳腺肿块的大致位置信息之后,再利用区域增长的方法获得肿块的边缘信息。结果：本文选取MIAS乳腺图像数据库中的65幅图像作为测试图像,保证每幅图像至少包含一个乳腺肿块。利用本文所提方法对这65幅图像进行实验,并将实验结果与该数据库中的专家标注信息作对比,实验结果为当采用db40的小波系数时的检出率为95．5％。结论：本文所述方法能够有效地分割出乳腺X线图中的肿块区域,并且有较高的检出率,具有进一步研究和应用的价值。     

基于视觉感知信息的乳腺钼靶肿块检测分析与自动提取

医生的视觉感知信息与影像诊断联系紧密,如何有效利用该信息以提高医学影像辅助诊断中的决策准确性,是一个具有前沿性和实际临床价值的研究课题。针对医生临床诊断时其视觉感知行为的分析和利用,探讨医生读片时单纯的视觉注视信息在多大程度上反映肿块位置（可检测性）,以及如何利用视觉注视信息提取病灶。首先,用眼动仪采集医生读片时的注视点序列,每个注视点包括该点在钼靶影像中的相对位置、注视点停留时间和瞳孔直径等3个视觉特征,然后基于这些特征对注视点序列进行聚类分析,根据关注度评价找出医生浏览影像时的若干“关注点”位置,并对比分析其与肿块位置的关系,以评价“命中率”;以关注点为引导,利用区域生长和水平集方法对肿块病灶进行提取。利用DDSM数据库和浙江省肿瘤医院数据库的75张钼靶影像进行初步实验。将关注点数限制在4个以内时,肿块病灶命中率为58.49%,同时所有命中肿块中被完整提取的占70.97%。结果表明,医生视觉注意信息对肿块位置的反应有一定作用,有助于理解感知反馈提高诊断精度的内在机理。     

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.