基于复小波域非线性扩散的超声图像去噪

超声图像易受斑点噪声的干扰,限制了其在医学诊断中的进一步应用。提出了一种将双树复小波变换(DT-CWT)与非线性扩散相结合的超声图像去噪方法。首先,对图像进行双树复小波分解;然后,高频部分和低频部分分别采用自适应对比度扩散和全变差扩散,最后重构图像。给出了实验结果,并与小波阈值收缩和全变差扩散结合的方法、基于小波和基于多小波的非线性扩散方法的图像去噪效果进行了比较。结果表明,本文提出的方法去噪效果更为优越:不但抑制噪声的能力更强,而且能够更好地保留超声图像原有的边缘和纹理特征。     

基于小波软阈值滤波的医学图像去噪

目的:为了更好的去除DR医学图像噪声.方法:通过分析其噪声来源,在小波去噪的基础上进行改进.引入方差不变性变换来调整原始图像的噪声模型为高斯噪声模型.图像分解为不同频率的不同子带的小波系数,分别进行不同阈值的滤波.结果:与普通的全局小波去噪方法相比,该方法不但可以保留图像的边缘信息,而且能提高去噪后图像的峰值信噪比.结论:用此方法处理DR图像在噪声去除、细节质量及骨骼锐化等方面比传统的高斯滤波及小波全局阈值滤波等方法效果要好.     

一种基于模糊均差和小波变换的医学图像去噪方法

小波阈值萎缩法能够有效地去除图像中的噪声,去噪阈值直接影响去噪的效果,而噪声标准差在去噪阈值的确定中起着至关重要的作用。针对医学图像的特点、基于寻找更合适的噪声标准差估计方法,本研究提出了一种新的利用模糊均差代替普通标准方差估计噪声标准差的方法。在各层小波分解的低频图像中利用模糊积分估计噪声标准差,然后确定每一层去噪阈值,进行图像去噪。试验结果表明,本研究算法在去除噪声的同时也较好地保持了图像的细节。     

基于小波阈值法的脉搏波去噪算法

目的消除可穿戴式脉搏波监测设备在连续测量中由于运动造成的运动伪差,保证设备准确性和稳定性。方法通过选取合适的小波基、小波最大分解层数、阈值函数和阈值方法,对脉搏波信号进行小波阈值处理,提出了一种基于小波阈值法去除脉搏波噪声的算法。并针对在脉搏波信号采集过程中出现的基线漂移、工频干扰和运动伪差,与加窗傅里叶变换去噪后的结果进行对比。结果在信噪比、均方差和平滑度等关键指标上,小波阈值法的效果更优。利用db9小波基对脉搏波信号进行6层小波分解,设置启发式阈值所得到的处理效果最好。结论该算法能够有效抑制工频干扰和运动干扰,使信噪比提高22 dB,均方差接近于0,且平滑度降为原来的11%,实现脉搏波信号采集中干扰的有效去除。     

医学设备远程监控图像变换尺度精准去噪方法

目的 为了提高医学设备远程监控图像的去噪效果,针对去噪准确度较差和去噪时间较长的问题,设计一种医学设备远程监控图像变换尺度精准去噪方法。方法 首先建立噪声的变化曲线模型,评估出噪声高等级区域进行针对性的降噪;然后采用小波算法去除图像冗余像素点,引入变换尺度阈值,优化医学设备远程监控图像去噪过程;最后采用去除模糊边缘法分割未成像图片,二次提取模糊图像中的主要像素,实现医学设备远程监控图像变换尺度精准去噪。结果 信息熵值高于21 H,处理过的图像较为清晰,图像信噪比高于21 dB,去噪时间低于4 min。结论 针对医学设备远程监控图像中具有多尺度特征的噪声,采用图像变换尺度精准去噪方法可以有效去除噪声,满足医学领域的实际去噪需求。     

小波变换的阈值选取及其在细胞图像去噪中的应用

阈值的选择是小波去噪的关键技术之一,但软硬阈值各有其缺陷.本文分析了自适应阈值的优点,进而提出逐点噪声方差法在去噪方面有更强的优势.仿真结果表明:采用自适应闭值并结合具有更强自适应性的逐点噪声方差法不仅能提高医学图像的峰值信噪比,还能有效地降低由传统阈值所带来的方块效应.     

基于Bayesian估计的小波自适应阈值方法对图像进行去噪处理的研究

利用Bayesian估计的小波自适应阈值方法对图像进行去噪处理。通过高斯滤波和小波变换的三种方法(传统的硬阈值、传统的软阈值去噪、基于Bayesian估计的自适应阈值去噪)分别同时对加不同标准差σ的Rician噪声信号进行消噪处理,对比验证高斯滤波和传统小波阈值去噪的优劣,以及新的Bayesian估计自适应阈值小波去噪在磁共振成像(magnetic resonance imaging,MRI)图像信号去噪方面的优越性。小波去噪后的信号信噪比比高斯滤波去噪后信号的信噪比高,且均方根误差要低。采用基于Bayesian估计的自适应阈值小波去噪方法比采用的高斯滤波保留了更多有用信号,优化后的氧摄取分数(oxygen extraction fraction,OEF)值有一定程度增大,使结果更接近正电子发射型计算机断层显像(positron emission computed tomography,PET)测量金标准。成功完成信号和噪声分离优化,将一种新的基于Baysian估计的自适应小波阈值去噪应用到了功能核磁共振成像的降噪分析上,取得了不错的效果。     

基于全卷积神经网络的低剂量CT去噪算法

针对低剂量医学CT图像因减少辐射剂量而引入大量噪声，导致图像质量显著下降的问题，提出一种基于残差注意力机制和自适应特征融合的低剂量CT图像去噪算法，该算法使用全卷积神经网络来完成低剂量CT图像去噪。在网络框架中引入残差注意力机制和选择性内核特征融合模块，以过滤噪声信息，提取有效特征并自适应地融合图像特征，避免重建过程中的细节损失，提高图像质量，使去噪后的图像在感知上更接近原始图像。定性和定量实验表明，与现有的算法相比，在真实的临床数据集上，所提出的算法能够有效地抑制噪声，并恢复低剂量CT图像中更详细的纹理。与低剂量CT图像相比，所提出的算法将峰值信噪比提高14.94%，结构相似度提高4.68%，均方根误差降低40.11%，可以满足医学成像的诊断要求。     

基于树状小波的超声医学图像阈值函数降噪

针对超声医学图像中存在特有的斑点噪声,利用树状小波分解比传统小波分解精度高的特点,将超声医学图像进行树状小波分解,然后分别采用硬阈值、软阈值和半软阈值函数三种方法进行降噪处理.结果表明半软阈值函数方法是较优阈值函数方法,可以有效地降低原图像的斑点噪声并保留图像细节.     

DR image de-noising and acceleration based on recursive cycle pinning contourlet transformation

目的 数字化X线摄影(digital radiography,DR)图像中的高斯噪声对图像质量影响大,消除此类噪声有利于提高图像质量以辅助医生做出正确的诊断.方法 为抑制DR图像的高斯噪声,首先采用递归循环平移与Contourlet变换结合的(recursive cycle spinning Contourlet transform,RCSCT)方法变换分解DR图像,接着采用连续的二元软阈值函数处理变换系数防止系数被过度扼杀,然后基于CUDA(compute unified device architecture,计算统一设备架构)平台对去噪方法加速.结果 该方法提高了去噪后的图像峰值信噪比,有效抑制了伪吉布斯现象,保留了更多的图像细节信息,并且加速处理后运算耗时较短.结论 本文方法比小波变换和Contourlet变换在保留视觉细节信息方面效果更优,算法耗时少,实用性好.     

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.