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Preventive Measures for Corona Virus Considering Different Perspectives in Indian Conditions
Published in Suman Lata Tripathi, Kanav Dhir, Deepika Ghai, Shashikant Patil, Health Informatics and Technological Solutions for Coronavirus (COVID-19), 2021
Saumyadip Hazra, Abhimanyu Kumar, Souvik Ganguli, Sahil Virk
Deficiency of vitamin D may increase autoimmunity. Autoimmunity is the condition when the body of the organism starts immunizing against its own healthy cells and tissues. Vitamin D promotes calcium homeostasis and bone health. It also enhances absorption of calcium in small intestine. When antibiotics were not invented, vitamin D unknowingly treated several infections. The patients were told to sit in sunlight. Significant reduction in the amount of vitamin D has been observed with ageing process, which means there is insufficient vitamin D supply when a person gets older [11]. Also, the older individual is more prone to corona virus and hence there are more chances that the people with less proportion of vitamin D are more susceptible to have infection from the new corona virus. In Indonesia, 780 people who died of COVID-19 had vitamin D below the normal levels [12].
Hematopoietic Stem Cell Biology
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Animal models have been helpful in better understanding the biology of both hematopoietic stem cells (HSC) and autoimmunity. Autoimmunity is caused by a complex interplay of genetic and environmental factors. Spontaneous animal models of autoimmunity result from germ-line mutations; these include the lpr/lpr mouse as a model for arthritis and vasculitis,1 the NOD (nonobese diabetic) mouse for diabetes, and the NZB/W mouse for systemic lupus erythematosus.2 Although studies of murine susceptibility genes are likely to provide insights into the genetic mechanisms involved in the human predisposition to autoimmunity, these models differ significantly from most cases of human autoimmune disease. Spontaneous animal models with germ-line mutations virtually always develop autoimmunity, while only a fraction of individuals who harbor susceptibility genes develop autoimmunity; there are rare exceptions to this, such as patients with the autoimmune lymphoproliferative syndrome (ALPS), who, like lpr/lpr mice, inherit loss-of-function mutations of the Fas gene (refer to Chapter 17).3,4 Induced animal models of autoimmunity focus on the role of environmental factors in the development of autoimmunity.2 These animal models more closely approximate most cases of human autoimmunity, and have the advantage over spontaneous models in that the onset and progression of the disease can be controlled (refer to Chapters 29 and 30).
Application of Data Mining Techniques in Autoimmune Diseases Research and Treatment
Published in Shampa Sen, Leonid Datta, Sayak Mitra, Machine Learning and IoT, 2018
Sweta Bhattacharya, Sombuddha Sengupta
Autoimmunity is a situation in which the immune system goes off-course, resulting in an inappropriate response to self elements or self antigens.1 Earlier, it was proposed that the self reactive lymphocytes were screened and eliminated from the body, preventing an autoimmune response. However, later studies have shown that not all T-cells and B-cells that have the potential to target self antigens are successfully removed. This leads to a situation where the “army is fighting against the king.” The damage induced to cells and organs may be due to the antibodies or the T cells of the body. Some common autoimmune diseases have been listed in Table 7.1.
A comprehensive summary of disease variants implicated in metal allergy
Published in Journal of Toxicology and Environmental Health, Part B, 2022
In addition to metallosis, other potential forms of systemic ASIA have been associated with allergenic metals (Kagan et al. 2020). In one patient, implantation of metal plates led to development of delayed-type hypersensitivity to molybdenum. In subsequent months, symptoms of systemic lupus erythematosus (SLE) began to emerge, suggesting that sensitization to the metal may have been a trigger for the development of autoimmunity in this patient (Federmann et al. 1994). This observation is consistent with knowledge that the occurrence of type IV hypersensitivity to metals is elevated in patients with SLE. A similar trend is also evident amongst patients afflicted with similar autoimmune conditions, such as rheumatoid arthritis, chronic fatigue syndrome, and Sjogren’s syndrome (Bjørklund, Dadar, and Aaseth 2018; Geier and Geier 2021; Stejskal, Reynolds, and Bjørklund 2015; Sterzl et al. 1999). Allergic reactivity to Ni, Au, and Hg are often implicated in these cases (Bjørklund, Dadar, and Aaseth 2018; Loyo et al. 2012).
Systems toxicology approach explores target-pathway relationship and adverse health impacts of ubiquitous environmental pollutant bisphenol A
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Manigandan Nagarajan, Gobichettipalayam Balasubramaniam Maadurshni, Jeganathan Manivannan
The PPI network obtained from STRING database revealed a well-connected network among BPA targets. In addition, hub proteins of the predicted BPA targets are known to play vital roles in cellular signaling and physiology. In this regard, one of the hub protein, the nuclear receptor co-repressor 1 (NCoR1) has been implicated in transcriptional repression and embryonic organ development and along with its partner, histone deacetylase 3, modulates histone acetylation and gene transcription through binding the promoter regions of myeloid-differentiation genes (Wan et al. 2019). Further, the signal transducers and activators of transcription (STATs) are a family of transcription factors that regulate cell proliferation, differentiation, apoptosis, immune and inflammatory responses and angiogenesis (Xiong et al. 2014). STAT3 plays a key role in vertebrate development and mature tissue function including control of immunity, where mutations in human STAT3 gene is associated with diseases such as immunodeficiency, autoimmunity and cancer (Hillmer et al. 2016). Moreover, both MAPK1 and MAPK3 (also known as ERK2 and ERK1, respectively) are members of the mitogen-activated protein kinase family and its signaling pathways regulate a wide variety of cellular processes, including proliferation, differentiation, apoptosis and stress responses (Guo et al. 2020).
Regeneration of annulus fibrosus tissue using a DAFM/PECUU-blended electrospun scaffold
Published in Journal of Biomaterials Science, Polymer Edition, 2020
Chen Liu, Liang Xiao, Yu Zhang, Quanlai Zhao, Hongguang Xu
Decellularized matrix is fabricated by removing cellular components in tissues, whereas mainly preserving ECM by chemical, enzymatic, or mechanical methods. It not only significantly reduces autoimmunity, but also maintains the original biological function of the tissue [10]. At the same time, decellularized matrix has good biocompatibility and biodegradability, which is conducive to cell adhesion, expansion, and differentiation [11,12]. It has been widely used in tissue engineering of bone, cartilage, skin, bladder, blood vessels, heart, liver, and lung [13–20]. Therefore, we chose to investigate whether PECUU and decellularized AF matrix (DAFM) can be effectively combined to prepare scaffolds that can simulate the mechanical properties and composition of actual AF tissue.