The COVID-19 epidemic and other notifiable infectious diseases in China

Many infection control measures have been implemented to prevent the spread of SARS-CoV-2 during COVID-19 pandemic. We aimed to investigate the impact of COVID-19 epidemic on the other notifiable infectious diseases in China, including respiratory infectious diseases, diseases transmitted through the digestive tract and animal-borne diseases. Compared with 2019, the overall decline rate of respiratory infectious diseases in 2020 is the highest (60–90%), and the diseases transmitted by the digestive tract and animal-borne diseases are similar at 20–30%. Both hepatitis and sexually transmitted diseases decreased significantly in February, and there were basically no significant changes in other months compared with previous years. The series of measures taken by China government to prevent the spread of SARS-CoV-2 are also very effective in preventing the spread of respiratory infectious diseases. But they also have a certain degree of prevention against notifiable infectious diseases spread by other routes.     

Cytokine imbalance in non-immunological chronic disease

Over the last decade, cytokine imbalances have been associated with a plethora of diseases. While the Th(1)/Th(2) paradigm is widely used to explain the pathogenesis of immunological diseases, the role of cytokine imbalances for non-immunological diseases is still incompletely defined. The major obstacle here is to assess the extent to which non-immunological diseases are influenced by inflammation. Non-immunological diseases cover the whole spectrum from those triggered by infection-as may be the case for Alzheimer's disease-to those where the immune system has no apparent impact at all. Examples of the latter are bone diseases, including post-menopausal osteoporosis and skeletal malformations. In between there are diseases such as intrinsic asthma and osteoarthritis where the impact of the immune system is unclear. Thus far, imbalances affecting tumour necrosis factor (TNF)-alpha and members of the interleukin (IL)-1 and the TGF superfamily have been found in association with all of these diseases. We speculate here that cytokine imbalance will be found in additional diseases and touch on the role in phylogeny of cytokines outside the immune system.     

The real place of infectious pathology in overall population morbidity

The statistical decrease of the proportion of infections in the structure of morbidity of the population reflects the existing classification of diseases when only acute diseases are classified with the group "infectious and parasitic diseases". The proportion of diseases caused by infective agents remains constantly high. According to WHO data, such diseases make up one-third of all diseases in the world. In Moscow the proportion of infectious diseases in all diseases registered among the inhabitants of this big city fluctuated within 36.1% and 49.7% during the period of 1926-1997.     

Diversity in autosomal-dominant diseases in the Russian population

Results of 20-year studies on the diversity of autosomal dominant (AD) diseases are summarized. The studies were carried out in six regions of Russia: Kirov, Kostroma, and Bryansk oblasts; Krasnodar krai; and Adygea and Marii El republics. A total of 1.5 million subjects from 44 raions (districts) were studied. In the populations studied, 144 AD diseases were found; the total number of affected persons was 1723. The prevalence rate in the region where the disease was found and the average prevalence rate in the total population studied were calculated for each disease. Only 11 AD diseases had prevalence rates of 1:50,000 or higher. About half of AD diseases (64) had a very low prevalence rate (1:861,408). However, most cases (about 70% of the affected persons) were accounted for by more frequent diseases. Forty-six diseases exhibited local accumulation. The AD mutation rate was estimated by direct calculation. This rate was 0.542 x 10(-6) per gamete per generation.     

Possible involvement of transglutaminase-catalyzed reactions in the physiopathology of neurodegenerative diseases

Transglutaminases are ubiquitous enzymes, which catalyze post-translational modifications of proteins. Recently, transglutaminases and tranglutaminase-catalyzed post-translational modification of proteins have been shown to be involved in the molecular mechanisms responsible for several human diseases. Transglutaminase activity has been hypothesized to be involved also in the pathogenetic mechanisms responsible for human neurodegenerative diseases. Neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, supranuclear palsy, Huntington’s disease and other polyglutamine diseases, are characterized in part by aberrant cerebral transglutaminase activity and by increased cross-linked proteins in affected brains. In this review, we focus on the possible molecular mechanisms by which transglutaminase activity could be involved in the pathogenesis of neurodegenerative diseases, and on the possible therapeutic effects of selective transglutaminase inhibitors for the cure of patients with diseases characterized by aberrant transglutaminase activity.     

药物作用靶点研究最新进展

通过对我国学者近2年在国内外发表的相关论文进行检索和整理,分类综述针对神经退行性疾病（如阿尔茨海默病、帕金森病等）、心血管疾病（如高血压、心律失常、心衰、冠心病、心肌梗死、动脉粥样硬化等）、脑血管疾病、代谢类疾病（如肥胖症、血脂异常、脂肪肝、糖尿病等）、感染性疾病（如艾滋病、流感、结核病等）、恶性肿瘤、自身免疫性疾病等多种疾病的药物作用靶点研究最新进展。     

Emerging and re-emerging bacterial diseases in India

There has been a remarkable progress in the prevention, control and even eradication of infectious diseases with improved hygiene and development of antimicrobials and vaccines. However, infectious diseases still remain a leading cause of global disease burden with high morbidity and mortality especially in the developing world. Furthermore, there have been threats of new diseases during the past three decades due to the evolution and adaptation of microbes and the re-emergence of old diseases due to the development of antimicrobial resistance and the capacity to spread to new geographic areas. The impact of the emerging and re-emerging diseases in India has been tremendous at socioeconomic and public health levels. Their control requires continuing surveillance, research and training, better diagnostic facilities and improved public health system. Emerging and reemerging zoonotic diseases, foodborne and waterborne diseases and diseases caused by multiresistant organisms constitute the major threats in India. This review of bacterial emerging and re-emerging diseases should be of critical importance to microbiologists, clinicians, public health personnel and policy makers in India.     

Transglutaminases in disease.

Transglutaminases (TGases) are enzymes that are widely used in many biological systems for generic tissue stabilization purposes. Mutations resulting in lost activity underlie several serious disorders. In addition, new evidence documents that they may also be aberrantly activated in tissues and cells and contribute to a variety of diseases, including neurodegenerative diseases such as Alzheimer's and Huntington's diseases. In these cases, the TGases appear to be a factor in the formation of inappropriate proteinaceous aggregates that may be cytotoxic. In other cases such as celiac disease, however, TGases are involved in the generation of autoantibodies. Further, in diseases such as progressive supranuclear palsy, Huntington's, Alzheimer's and Parkinson's diseases, the aberrant activation of TGases may be caused by oxidative stress and inflammation. This review will examine the role and activation of TGases in a variety of diseases.     

基因编辑动物模型在人类疾病研究中的应用

近年来,随着以CRISPR/Cas9为代表的多种CRISPR系统的开发和不断改进,基因编辑技术逐渐完善,并广泛应用于人类疾病动物模型的制备。基因编辑动物模型为人类疾病的发病机理、病理过程以及预防和治疗等方面的研究提供了重要的素材。目前,用于人类疾病研究的基因编辑动物模型主要有小鼠、大鼠为代表的啮齿类动物模型和以猪为代表的大动物模型。其中啮齿类动物在机体各方面与人类差别较大,且寿命短,无法对人类疾病的研究和治疗提供有效评估和长期追踪;而猪在生理学、解剖学、营养学和遗传学等各方面与人类更接近,是器官移植和人类疾病研究领域重要的动物模型。文中主要介绍了基因编辑动物模型在神经退行性疾病、肥厚心肌病、癌症、免疫缺陷类疾病和代谢性疾病等5种人类疾病研究中的应用情况,以期为人类疾病研究及相关动物模型的制备提供参考。     

磷脂酰肌醇3-激酶γ/δ与炎症相关疾病

磷脂酰肌醇3-激酶(PI3K)是一类脂质与蛋白激酶家族,其主要通过在磷脂酰肌醇的肌醇环三位进行磷酸化产生胞内重要的第二信使——磷脂酰肌醇-3,4,5-三磷酸(phosphatidyl inositol 3,4,5-trisphosphate,PIP3)而发挥作用.磷脂酰肌醇3-激酶γ/δ(PI3Kγ/δ)是I类PI3K家族中的成员,其主要表达于免疫相关细胞中,这2种PI3K亚型参与先天性与获得性免疫应答.因此,PI3Kγ/PI3Kδ被视为因免疫反应调控异常导致的炎症疾病的治疗药物靶点.目前,利用特异性抑制剂靶向干预PI3Kγ和/或PI3Kδ,成为炎症相关疾病治疗的新策略.本文简介了PI3Kγ与PI3Kδ在不同类型免疫细胞中的功能;并就采用小分子特异性抑制剂,靶向抑制PI3Kγ和/或PI3Kδ在各类炎症相关疾病中的治疗作用和效果进行综述.     

Microparticles in physiological and in pathological conditions

Chronic diseases pose a severe burden to modern National Health Systems. Individuals nowadays have a far more extended lifespan than in the past, but healthy living was only scantily extended. As much as longer life is desirable, it is saddened by chronic diseases and organ malfunctions. One contributor to these problems was recognized to be represented by microparticles (MPs). Our purpose is to better understand MPs, to contrast their ominous threat and possible clinical importance. For this intent we correlated MPs with thrombotic pathologies, hemophilia, malaria, diabetes, cardiovascular diseases, endothelial dysfunctions, pulmonary hypertension, ischemic stroke, pre-eclampsia, rheumatologic diseases-rheumatoid arthritis, polymyositis-dermatomyositis, angiogenesis and tumor progression-cancer; we listed the possibilities of using them to improve transfusion methods, as a marker for acute allograft rejection, in stem cell transplantation, as neuronal biomarkers, to understand gender-specific susceptibility for diseases and to improve vaccination methods and we presented some methods for the detection of MPs.     

Neurodegeneration in humans caused by prions.

Prion diseases include kuru, Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker disease, and fatal familial insomnia of humans as well as scrapie and bovine spongiform encephalopathy of animals. For many years, the prion diseases were thought to be caused by viruses despite evidence to the contrary. The unique characteristic common to all of these disorders, whether sporadic, dominantly inherited, or acquired by infection, is that they involve aberrant metabolism of the prion protein. In many cases, the cellular prion protein is converted into the scrapie variant by a process after translation that involves a conformational change. Often the human prion diseases are transmissible experimentally to animals, and all of the inherited prion diseases segregate with prion protein gene mutations.     

Analysis of mutations in leu tRNA gene in patients of heart diseases

Cardiovascular diseases (CVD) are the leading cause of death all over the world. Beside general risk factors, there are some genetic factors which lead to cardiovascular diseases. Various nuclear DNA mutation and also mitochondrial DNA mutations have been related with cardiovascular diseases. In the present study, a total of 21 samples were collected from different families residing in district Dir. DNA was extracted from buccal epithelial cells using saliva. The mitochondrial tRNA leu (MT TL1) gene was amplified by PCR and 10 samples of different families were sequenced. The sequence was aligned with revised Cambridge Reference Sequence (rCRS) accession # NC-012920.1. It is concluded that cardiovascular diseases in our subjects are not due to mutation in the mitochondrial leucine tRNA gene. However, a large population of subjects with cardiovascular diseases needs to be studied and whole mitochondrial DNA is needed to be sequenced in the subjects with CVD. This will give an idea about the probable DNA marker which can be used to prevent loses due to these diseases at a very early stages.     

BAFF在自身免疫性疾病方面的研究进展

自身免疫性疾病的特征是B细胞耐受丧失,B细胞激活因子（B cell activating factor belonging to theTNF family,BAFF）通过与受体结合,对B细胞的增殖、存活起重要作用。BAFF转基因小鼠易出现自身免疫性疾病。因此,拮抗或抑制BAFF的表达可能是治疗自身免疫性疾病的靶点。本文主要对BAFF在自身免疫性疾病方面的研究进展进行综述。     

Neglected Fungal Diseases in Sub-Saharan Africa: A Call to Action

Despite the considerable morbidity and mortality associated with fungal diseases in sub-Saharan Africa, it is notable that these diseases have been omitted from an expanded list of neglected tropical diseases. Inextricably tied together with HIV/AIDS and tuberculosis in sub-Saharan Africa, important fungal diseases such as cryptococcal meningitis and Pneumocystis jirovecii pneumonia (PCP) manifest as relatively common and deadly AIDS-defining opportunistic infections, often masked by and comorbid with tuberculosis. Others, such as mycetoma, which manifest as a debilitating and deforming illness primarily affecting rural adults, directly affect the socioeconomic productivity of rural communities. Lack of adequate diagnostic tests makes identifying the true disease burden due to fungal diseases difficult. To highlight the devastating impact of fungal diseases on the health and socioeconomic circumstances of sub-Saharan Africa’s poorest people and to increase the profile of efforts to control and prevent these diseases, we propose that the following fungal diseases be added to the list of neglected tropical diseases: cryptococcal meningitis, PCP, mycetoma, histoplasmosis, sporotrichosis, and blastomycosis. By outlining the prevalence, distribution, and disease burden of these fungal diseases in sub-Saharan Africa in this review, we hope to provide information to prioritize strategies for detection, control, and prevention of the neglected fungal diseases.     

Anti-O-phosphotyrosine antibodies in human sera

Antibodies reactive with O-phosphotyrosine (PTYR) were detected in 60 out of 621 inpatients, with high frequencies in hematologic and lung malignancies, hepatic diseases, cerebrovascular diseases, and autoimmune diseases. Affinity-purified antibodies proved capable of recognizing PTYR-containing proteins in a human carcinoma cell line, A431, both by immunofluorescent staining and by immunoaffinity chromatography, but had no detectable affinity for phosphorylated serine or threonine, or for the nucleotides tested. In these respects, the antibodies observed in human sera were indistinguishable from anti-PTYR antibodies raised experimentally in rabbits or mice.     

Nuclear bodies in neurodegenerative disease

Neurodegenerative diseases are characterized by a relentlessly progressive loss of the functional and structural integrity of the central nervous system. In many cases, these diseases arise sporadically and the causes are unknown. The abnormal aggregation of protein within the cytoplasm or the nucleus of brain cells represents a unifying pathological feature of these diseases. There is increasing evidence for nuclear dysfunction in neurodegenerative diseases. How this relates to protein aggregation in the context of "cause and effect" remains to be determined in most cases. Co-ordinated nuclear function is predicated on the activity of distinct nuclear subdomains, or nuclear bodies, each responsible for a specific function. If nuclear dysfunction represents an important etiopathological feature in neurodegenerative disease, then this should be reflected by functional and/or morphological alterations in this nuclear compartmentalization. For most neurodegenerative diseases, evidence for nuclear dysfunction, with attendant consequences for nuclear architecture, is only beginning to emerge. In this review, I will discuss neurodegenerative diseases in the context of nuclear dysfunction and, more specifically, alterations in nuclear bodies. Although research in this field is in its infancy, identifying alterations in the nucleus in neurodegenerative disease has potentially profound implications for elucidating the pathogenesis of these disorders.