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Case of chromosome 22q11.2 deletion syndrome in Russian family 俄罗斯家族22q11.2染色体缺失综合征1例
Pub Date : 2018-09-24 DOI: 10.15406/MOJI.2018.06.00208
Svetlana Deriabina, M. Bolkov, I. Tuzankina, E. Vlasova
Our Center for Clinical Immunology has been working in the sphere of primary immunodeficiencies (PID) for 30 years. Early diagnostics and management of PID patients is our priority.1,2 Followup of adults and children in our Center can be done as it has two main clinical bases Region Children Clinical Hospital No 1 and Region Clinical Hospital No 1 (Yekaterinburg, Ural region, Russia). Center also closely collaborates with the Institute of Immunology and Physiology of Russian Academy of Sciences and international organizations on PID jproject (collaboration with Professor L. Marodi, University of Debrecen) and Jeffrey Modell Foundation. There are 15 patients with chromosome 22q11.2 deletion (14 children and 1 adult) out of total number of 309 PID patients in our Center for Clinical Immunology. Thereby, the prospects for identifying these patients are wide. According to many reports, chromosome 22q11.2 deletion occurs 1: 3,000 6,000 live births, affecting both sexes equally.3,4 It has been reported that chromosome 22q11.2 deletion is found in 90% of the patients with disgorge phenotype, 70% of the patients with Velo-Cardio-Facial Syndrome (VCFS), and 15% of the patients with isolated conotruncal cardiac defect.5 Most of the patients were diagnosed by slightly and severely decreased immunity, facial defects, and heart anomalies and some patients had kidney abnormalities, hypoparathyroidism, hypothyroidism, and developmental retardation.6 Chromosome 22q11.2 deletion is mostly diagnosed in early childhood by pediatricians as a congenital disease so that the syndrome is difficult to diagnose in the late adulthood7‒9 In literature there are only a few works devoted to adult patients with chromosome 22q11.2 deletion syndrome.3,4,10‒12 This is due to low awareness of physicians and other specialists of chromosome 22q11.2 deletion syndrome as well as high variability of phenotypic manifestations of this syndrome and the presence of mild forms. Under our surveillance there is a family K, wherein two siblings and their mother have the chromosome 22q11.2 deletion syndrome. The purpose of this study is to analyze phenotypic manifestations in family members with chromosome 22q11.2 deletion syndrome. Methods
我们的临床免疫学中心已经在原发性免疫缺陷(PID)领域工作了30年。对PID患者的早期诊断和管理是我们的首要任务。1、2本中心有两个主要临床基地,可对成人和儿童进行随访,分别为第一地区儿童临床医院和第一地区临床医院(俄罗斯乌拉尔地区叶卡捷琳堡)。中心还与俄罗斯科学院免疫学和生理学研究所以及国际组织在PID jproject(与德布勒森大学L. Marodi教授合作)和Jeffrey Modell基金会密切合作。临床免疫学中心309例PID患者中,22q11.2染色体缺失15例(儿童14例,成人1例)。因此,识别这些患者的前景是广阔的。根据许多报道,22q11.2染色体缺失的发生率为每3000 000个活产婴儿中有1个,对两性的影响是平等的。3,4据报道,90%的呕吐表型患者、70%的Velo-Cardio-Facial Syndrome (VCFS)患者和15%的孤立性conotrunal心脏缺陷患者存在22q11.2染色体缺失多数患者表现为轻微或严重的免疫力下降、面部缺损、心脏异常,部分患者表现为肾脏异常、甲状旁腺功能减退、甲状腺功能减退、发育迟缓22q11.2染色体缺失多在儿童早期被儿科医生诊断为先天性疾病,因此该综合征在成年后期很难诊断。7 - 9在文献中,针对22q11.2染色体缺失综合征的成年患者的文献很少。3,4,10 - 12这是由于医生和其他专家对染色体22q11.2缺失综合征的认识较低,以及该综合征的表型表现的高度可变性和轻度形式的存在。在我们的监测下,有一个家庭K,其中两个兄弟姐妹和他们的母亲有染色体22q11.2缺失综合征。本研究旨在分析22q11.2染色体缺失综合征家族成员的表型表现。方法
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引用次数: 0
Microbial dysbiosis in allergic lower airway disease (asthma) 过敏性下气道疾病(哮喘)的微生物生态失调
Pub Date : 2018-09-18 DOI: 10.15406/MOJI.2018.06.00207
Ö. Özdemir
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引用次数: 1
Differential immune response generation in rats acutely exposed to hypobaric hypoxia and determination of susceptibility and tolerance 低压缺氧急性暴露大鼠的差异性免疫反应产生及其易感性和耐受性的测定
Pub Date : 2018-09-11 DOI: 10.15406/moji.2018.06.00206
Shweta, K. Mishra, H. Tanwar, Sudipta Ch, S. Singh, L. Ganju
Abbreviations DAMP: Damage-Associated Molecular Pattern; DCFH2-DA:2′,7′dichloro-dihydro-fluorescein diacetate; ELISA: Enzyme Linked Immunosorbent Assay; FACS: Fluorescenceactivated cell sorting; HIF1α: Hypoxia-inducible factor 1-alpha; iNOS: Inducible Nitric oxide Synthase; MFI: Median Fluorescence Intensity; NO: Nitric Oxide; ROS: Reactive Oxygen Species; TLR: Toll-like receptors; TNF-α: Tumor Necrosis Factor Alpha; CD18: Cluster of Differentiation 18.
缩写DAMP:损伤相关分子模式;DCFH2-DA:2′,7′二氯二氢荧光素二乙酸酯;ELISA:酶联免疫吸附测定法;FACS:荧光激活的细胞分选;HIF1α:缺氧诱导因子1α;iNOS:诱导型一氧化氮合酶;MFI:中值荧光强度;NO:一氧化氮;ROS:活性氧;TLR:Toll样受体;TNF-α:肿瘤坏死因子α;CD18:分化簇18。
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引用次数: 1
Clinical application of animal based extracellular matrix in hernioplasty 动物细胞外基质在疝修补术中的临床应用
Pub Date : 2018-08-28 DOI: 10.15406/MOJI.2018.06.00205
Raghuvanshi, D. Mohan, D. Gautam, S. Shivaraju, S. K. Maiti, Naveen Kumar
Biological scaffolds are composed of natural ECM (extracellular matrix) due to their origin from animal-based proteinous molecules; they have efficient in the potential of therapeutic applications. The ECM has full potential which increases constructive remodeling. The structural and functional molecules of ECM are capable to establish proper attachment or communication with an adjacent environment of healing area of injury. Their biocompatibility is responsible for positive signaling to recipient own matrix formation.1 The ECM degradation with the promotion of native matrix is another property which makes it an ideal biomaterial.2
生物支架由天然的细胞外基质(ECM)组成,因为它们来源于动物蛋白分子;它们具有有效的治疗应用潜力。ECM具有充分的潜力,可以增加建设性的重塑。ECM的结构和功能分子能够与损伤愈合区域的邻近环境建立适当的连接或通信。它们的生物相容性对受体自身基质的形成起着积极的信号作用在天然基质的促进下,ECM的降解是其成为理想生物材料的另一个特性
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引用次数: 1
Inflammatory response induced by resistance exercise 抵抗运动引起的炎症反应
Pub Date : 2018-08-14 DOI: 10.15406/MOJI.2018.06.00204
E. S. Vasconcelos
In the body human, there are around 640 skeletal muscles which together account for ~38% of total body mass for men and 30% for women.1 Skeletal muscle is crucial in precise movement and your functional unit cell (muscle fibre) has a vigorous regenerative capacity, with rapid reestablishment (by 3 weeks) of full power occurring even after severe damage that causes widespread myofibre necrosis.2 Exercise-induced muscle damage (EIMD) in humans frequently occurs after unaccustomed exercise, particularly if the exercise involves a large amount of eccentric contractions. There are three types of muscle actions: concentric, eccentric and isometric. The eccentric actions occur during the lowering phase of any weightlifting exercise and are defined as muscle actions at the places where the muscle lengthens because the contraction force is less than the resistive force.3 Initial resistance exercise stress affects muscle homeostasis promoting changes in muscle morphology, loss of sarcomeric structural proteins (e.g. desmin and dystrophin), muscle fibre segmental necrosis, alterations in connective tissue, in T-tubules and sarcoplasmic reticulum.4,5 Muscle damage is commonly defined by disruption of the extracellular matrix, basal lamina, and sarcolemma as well as damage within the muscle fiber to the contractile and cytoskeletal proteins. Sarcolemma disruption is confirmed by an increase in blood-borne levels of intramuscular proteins such as creatine kinase (CK), which in turn has been linked to production of an inflammatory response.6 The severity of the inflammation depends on the type, duration and intensity of exercise. Moreover, exercise with eccentric contractions will cause more damage and inflammation than concentric exercise of equal intensity and duration.7 In addition, regular exercise is beneficial to up regulating defense mechanisms against oxidative stress and to increased resistance against infection and a lower risk of appearance of disease. The aim in this review was to focus attention in inflammatory process caused by muscle damage after resistance exercises and, in addition, show the benefits of regular intensity exercise against oxidative stress, infections and some diseases.
在人体中,大约有640块骨骼肌,男性和女性分别占总体重的38%和30%。1骨骼肌对精确运动至关重要,你的功能单位细胞(肌肉纤维)具有强大的再生能力,即使在严重损伤导致广泛的肌原纤维坏死后,也会迅速(3周)恢复全力。2人类运动诱发的肌肉损伤(EIMD)经常发生在不习惯的运动后,尤其是在运动涉及大量偏心收缩的情况下。有三种类型的肌肉动作:同心、偏心和等长。偏心动作发生在任何举重运动的下降阶段,被定义为肌肉因收缩力小于阻力而变长的地方的肌肉动作。3初始阻力运动压力影响肌肉稳态,促进肌肉形态的变化,肌肉结构蛋白(如结蛋白和肌营养不良蛋白)的损失,肌肉纤维节段性坏死,结缔组织、T小管和肌浆网的改变。4,5肌肉损伤通常定义为细胞外基质、基底层和肌膜的破坏,以及肌肉纤维内对收缩蛋白和细胞骨架蛋白的损伤。肌内肌内蛋白(如肌酸激酶(CK))的血液传播水平增加,进而与炎症反应的产生有关。6炎症的严重程度取决于运动的类型、持续时间和强度。此外,与同等强度和持续时间的同心运动相比,有偏心收缩的运动会造成更多的损伤和炎症。7此外,定期运动有利于增强对氧化应激的防御机制,增强对感染的抵抗力,降低患病风险。这篇综述的目的是关注抵抗运动后肌肉损伤引起的炎症过程,此外,还展示了定期高强度运动对氧化应激、感染和某些疾病的益处。
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引用次数: 3
Does the immune system of plant and animal kingdoms share any pathways or mechanisms of action in phytotherapy 植物和动物的免疫系统在植物治疗中是否有共同的途径或机制
Pub Date : 2018-08-13 DOI: 10.15406/moji.2018.06.00203
D. Beghelli
The question arises from the need to understand why the use of phytotherapy may modulate the immune responses even in the animal kingdom as reported by some authors.1 In fact, even if the traditional use of herbal medicine products may guarantee efficacy, for very few medical plants scientific data on mechanisms of action are available.2 The term Phytotherapy, derived from the Greek words ‘Phyto’ and ‘therapy’, was introduced into science by the French physician Henri Leclerc (1870-1955) and indicates the therapy practiced with medicaments of vegetable origin. A study conducted by the World Health Organization had reported that about 80% of world’s population relies on traditional medicine. The history of phytotherapy is very old and was presumably one of the first therapeutic methods undertaken by man. Already in ancient times (since the Egyptian and Mesopotamian era), mankind was so fascinated by the therapeutic action of plants that for centuries magical and divine properties were attributed to them. Later on, humans have learnt by experience and observations how to use plants correctly and since the nineteenth century the empirical use of plants has been brought back within the boundaries of rationality and scientific rigor. But in what way has man been using these plants for millenia? These ‘preparations’ of vegetable origin have always been used through essentially three administration routes: at a lesser extent, by local applications or fumigation, otherwise mainly by ingestion. The administration of herbal medicine products through the oral route may represent a crucial point, as we will discuss below, to explain the efficacy of the traditional medicine. Therefore, the text found in the work On Aliment: “In food excellent medication, in food bad medication, bad and good relatively”,3 nowadays attributed to the Hellenistic period, but in Antiquity (by Galenus in particular) erroneously associated with Hippocrates, brings us back to why mankind at some point has started to ingest plants or their fruits, roots and leaves in order to find in them not only nourishment and gratification, but also a therapeutic remedy for its illnesses. Indeed, the idea of using plants as medicine treatment was probably born from fortuitous observations or from the experiences that many plants used in nutrition could also prove to be toxic or poisonous or, better, able to improve disorders. However, also Hippocrates from Cos (around 460 BC-around 375 BC), the father of Western modern medicine, knowing that food was closely linked to health and disease, applied dietetic measures for the benefit of the sick.4 According to the World Health Organization (WHO), every vegetable that contains, in one or more of its organs, pharmacologically active substances deserves the name of a medicinal plant. The pharmacognosy studies have evidenced that the set of these pharmacologically active molecules, called phytocomplexes, have the ability to work in synergy with all compone
正如一些作者所报道的,这个问题源于需要理解为什么植物疗法的使用即使在动物界也可以调节免疫反应。1事实上,即使传统的草药产品使用可以保证疗效,但对于极少数的药用植物来说,关于作用机制的科学数据是可用的。2,源自希腊语单词“Phyto”和“therapy”,由法国医生Henri Leclerc(1870-1955)引入科学,表示用蔬菜来源的药物进行的治疗。世界卫生组织进行的一项研究报告称,世界上约80%的人口依赖传统医学。植物疗法的历史非常悠久,可能是人类最早采用的治疗方法之一。早在古代(自埃及和美索不达米亚时代以来),人类就对植物的治疗作用如此着迷,以至于几个世纪以来,植物都具有神奇和神圣的特性。后来,人类通过经验和观察学会了如何正确使用植物,自19世纪以来,植物的经验使用已经回到了理性和科学严谨的范围内。但几千年来,人类一直以何种方式使用这些植物?这些蔬菜来源的“制剂”通常主要通过三种给药途径使用:在较小程度上,通过局部应用或熏蒸,否则主要通过摄入。通过口服途径给药草药产品可能是解释传统药物疗效的一个关键点,我们将在下文中进行讨论。因此,在《活着》一书中发现的文本:“在食物中,药物很好,在食物中药物很差,相对来说,坏和好”,3如今被认为是希腊化时期,但在《古代》(尤其是加勒努斯)中,错误地将其与希波克拉底联系在一起,这让我们回到了为什么人类在某个时候开始摄入植物或其果实,为了在根和叶中找到营养和满足,而且是治疗疾病的药物。事实上,使用植物作为药物治疗的想法可能源于偶然的观察,或者源于许多用于营养的植物也可能被证明是有毒或有毒的,或者更好的是,能够改善疾病的经验。然而,西方现代医学之父科斯(约公元前460年至公元前375年)的希波克拉底也知道食物与健康和疾病密切相关,因此采取了有益于病人的饮食措施。4根据世界卫生组织(世界卫生组织)的说法,药理活性物质是名副其实的药用植物。生药学研究证明,这些具有药理活性的分子,称为植物复合物,具有与所有成分协同作用的能力。植物复合物代表了药用植物的整体药理学单元。大多数发挥治疗作用的天然植物复合物,一旦摄入,就表现出抗氧化剂(从而降低自由基水平)、抗炎分子(从而降低慢性炎症疾病的风险)、抗癌,抗微生物和免疫调节剂。1植物和动物等活生物体可以被视为生物合成的实验室,不仅必须满足自身需求,还必须提供自身防御。因此,上述植物复合物可能代表一组甚至是为了保护植物生命本身而开发的分子。事实上,植物和动物都不断受到环境病原体的攻击,这些病原体通过进入这些生物体来寻找生存机会。
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引用次数: 0
New insight into potential role of inflammatory factors in the pathogenesis of vitiligo 炎症因子在白癜风发病机制中潜在作用的新认识
Pub Date : 2018-07-25 DOI: 10.15406/moji.2018.06.00202
R. Ghaderi
Vitiligo is an autoimmune disorder which causes skin depigmentation along with disorder in pro-inflammatory cytokines like INF-γ & TNF and so leads to dysfunction of melanocytes.1 Depigmentation in these areas occurs with progressive disappearance of melanocytes from basal layer of skin.2 The most common form of vitiligo disease is uniform amelanocytic macules or patches surrounded by normal skin. The color of lesions is usually milky or white. The macules are seen round, oval or linear and usually have convex and hyperpigmented margins.1‒3
白癜风是一种自身免疫性疾病,它会导致皮肤色素沉着,并伴有促炎细胞因子如INF-γ和TNF的紊乱,从而导致黑色素细胞功能障碍随着皮肤基底层黑色素细胞的逐渐消失,这些区域发生色素沉着白癜风疾病最常见的形式是被正常皮肤包围的均匀的无色素斑点或斑块。病变的颜色通常为乳白色或白色。斑圆形、卵圆形或线状,通常有凸缘和色素沉着
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引用次数: 0
Functional medicine–new concept or really what primary care physicians do 功能医学,新概念或者说是初级保健医生的工作
Pub Date : 2018-07-02 DOI: 10.15406/moji.2018.06.00221
N. Bradshaw
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引用次数: 0
Awareness about hypertension in biotechnology students 生物技术专业学生对高血压的认识
Pub Date : 2018-06-26 DOI: 10.15406/moji.2018.06.00220
M. Batool, M. Qadir
Hypertension can be regarded as one of the most important causes of morbidity worldwide. It is actually due to elevation in the blood pressure levels which is the result of rise in diastolic and systolic pressures. A survey was carried out in the form of questionnaires among biotechnology students. The resultant percentage of both males and females was enough to conclude that the students were truly aware about the causes of the disease.
高血压可以被认为是世界范围内最重要的发病原因之一。实际上,这是由于舒张压和收缩压升高导致的血压水平升高。以问卷调查的形式对生物技术学生进行了调查。由此得出的男女比例足以得出结论,即学生们真正了解疾病的原因。
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引用次数: 10
Interplay of vitamin D with T regulatory cells (FOXP3+Treg) and thymic stromal lymphopoietin (TSLP) in children with atopic diseases 儿童特应性疾病中维生素D与T调节细胞(FOXP3+Treg)和胸腺基质淋巴生成素(TSLP)的相互作用
Pub Date : 2018-06-15 DOI: 10.15406/MOJI.2018.06.00201
Anil Chauhan, Meenu Singh, A. Agarwal, N. Sachdeva, S. Attri
In recent years, vitamin D has been postulated as a risk factor for asthma and evidence suggests a connection between vitamin D deficiency with allergy and asthma. There is also an association between the dysregulated immune response marked by an increase in FOXP3+ and IL-10 T-regulatory (Treg) cells with the inflammatory processes of asthma.1 Severe asthma was associated with lower vitamin D levels in one of the observational study.2 An in vitro study noted an increase in the synthesis of IL-10 from Treg and dendritic cells was seen in the presence of exogenous vitamin D.3 In cultured steroid resistance T cells, vitamin D restored the immunosuppressive ability of dexamethasone.4 Low vitamin D levels, i.e. serum 25-OHD3 less than 30ng/ml as insufficient and less than 20ng/ml as deficient, have been positively correlated with atopic diseases.5 there is negative correlation between asthma exacerbation and vitamin D levels.6 The inverse association between serum vitamin D levels and need for corticosteroid use in patients with asthma has also been observed.7 Decreased expression of FOXP3 (Forkhead boxP3) is associated with increased exacerbation of asthma and steroid sensitivity, and decreased formation, production and differentiation of FOXP3+Treg cells.8‒10 Upregulated expression of FOXP3+Treg cells by vitamin D supplementation reverses steroid resistance.11‒12 In what? Furthermore, increased expression of FOXP3+Treg cells in allergen specific immunotherapy correlated with higher serum vitamin D levels.13 Vitamin D potentiates the efficacy of allergen immunotherapy by increasing the anti-inflammatory cytokines (IL10 and TGF-beta) response in an animal model of OVA challenged and sensitized BALB/C mice.14 The association of TSLP with vitamin D and % FOXP3+Treg cells is yet to be fully explored. It has been observed that when 16 human bronchial epithelial celllines were exposed to 50 and 500nM of vitamin D, inactive 25-OHD3 is converted to active 1,25 D3 and there is increase in TSLP mRNA and protein expression levels.15‒16 In our previous report, we showed that higher concentrations of TSLP and IL-33 correlate negatively with Treg cells in children with asthma.17 Until now, no study has demonstrated an association of vitamin D levels with TSLP and T regulatory cells in children with atopic disease.
近年来,维生素D被认为是哮喘的危险因素,有证据表明维生素D缺乏与过敏和哮喘之间存在联系。以FOXP3+和IL-10 T调节(Treg)细胞增加为标志的失调免疫反应与哮喘的炎症过程之间也存在关联。1在一项观察性研究中,严重哮喘与维生素D水平降低有关。2一项体外研究注意到,在存在外源性维生素D.3在培养的类固醇抗性T细胞中,维生素D恢复了地塞米松的免疫抑制能力。4低维生素D水平,即血清25-OHD3低于30ng/ml为不足,低于20ng/ml为缺乏,与特应性疾病呈正相关。5哮喘恶化与维生素D水平呈负相关。6还观察到哮喘患者血清维生素D水平与皮质类固醇使用需求之间的负相关。7 FOXP3(Forkhead boxP3)表达减少与哮喘恶化和类固醇敏感性增加相关,以及FOXP3+Treg细胞的形成、产生和分化减少。8-10补充维生素D上调FOXP3+Treg细胞的表达可逆转类固醇耐药性。11-12在什么情况下?此外过敏原特异性免疫疗法中FOXP3+Treg细胞表达增加与血清维生素D水平升高相关。13维生素D通过在OVA激发和致敏的BALB/C小鼠的动物模型中增加抗炎细胞因子(IL10和TGF-β)反应来增强过敏原免疫疗法的疗效有待充分探索。已经观察到,当16个人类支气管上皮细胞系暴露于50和500nM的维生素D时,非活性的25-OHD3转化为活性的1,25 D3,TSLP mRNA和蛋白质表达水平增加。15-16在我们之前的报告中,我们发现较高浓度的TSLP和IL-33与哮喘儿童的Treg细胞呈负相关。17直到现在,没有研究表明在患有特应性疾病的儿童中维生素D水平与TSLP和T调节细胞有关。
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引用次数: 1
期刊
MOJ immunology
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