669 research outputs found
Environmental toxicity, redox signaling and lung inflammation:the role of glutathione
Glutathione (gamma-glutamyl-cysteinyl-glycine, GSH) is the most abundant intracellular antioxidant thiol and is central to redox defense during oxidative stress. GSH metabolism is tightly regulated and has been implicated in redox signaling and also in protection against environmental oxidant-mediated injury. Changes in the ratio of the reduced and disulfide form (GSH/GSSG) can affect signaling pathways that participate in a broad array of physiological responses from cell proliferation, autophagy and apoptosis to gene expression that involve H(2)O(2) as a second messenger. Oxidative stress due to oxidant/antioxidant imbalance and also due to environmental oxidants is an important component during inflammation and respiratory diseases such as chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, acute respiratory distress syndrome, and asthma. It is known to activate multiple stress kinase pathways and redox-sensitive transcription factors such as Nrf2, NF-kappaB and AP-1, which differentially regulate the genes for pro-inflammatory cytokines as well as the protective antioxidant genes. Understanding the regulatory mechanisms for the induction of antioxidants, such as GSH, versus pro-inflammatory mediators at sites of oxidant-directed injuries may allow for the development of novel therapies which will allow pharmacological manipulation of GSH synthesis during inflammation and oxidative injury. This article features the current knowledge about the role of GSH in redox signaling, GSH biosynthesis and particularly the regulation of transcription factor Nrf2 by GSH and downstream signaling during oxidative stress and inflammation in various pulmonary diseases. We also discussed the current therapeutic clinical trials using GSH and other thiol compounds, such as N-acetyl-l-cysteine, fudosteine, carbocysteine, erdosteine in environment-induced airways disease
Macrophage plasticity and polarization in tissue repair and remodelling
Mononuclear phagocyte plasticity includes the expression of functions related to the resolution of inflammation, tissue repair and remodelling, particularly when these cells are set in an M2 or an M2-like activation mode. Macrophages are credited with an essential role in remodelling during ontogenesis. In extraembryonic life, under homeostatic conditions, the macrophage trophic and remodelling functions are recapitulated in tissues such as bone, mammary gland, decidua and placenta. In pathology, macrophages are key components of tissue repair and remodelling that occur during wound healing, allergy, parasite infection and cancer. Interaction with cells bearing stem or progenitor cell properties is likely an important component of the role of macrophages in repair and remodelling. These properties of cells of the monocyte-macrophage lineage may represent a tool and a target for therapeutic exploitation
Biswas-Milovic model and its optical solitons
International Conference on Numerical Analysis and Applied Mathematics 2018, ICNAAM 2018 -- 13 September 2018 through 18 September 2018 -- -- 149843In this work, optical solitons are obtained for the Biswas - Milovic equation as a generalized model via the extended generalizing Riccati mapping method. This method reveals several optical solitons including traveling wave solutions. The found solutions are identified with two different forms including the hyperbolic functions, the rational functions and the trigonometric functions. Reliability of our solution is given graphical consequens. © 2019 Author(s)
Tumor Microenvironment and Myelomonocytic Cells
Tumor microenvironment represents an extremely dynamic niche shaped by the interplay of different cell types (e.g. tumor cells, stromal cells), their soluble products (e.g.cytokines, chemokines and growth factors) and varied physico-chemical conditions (e.g low oxygen concentration or hypoxia). Recent studies have identified myelomonocytic cells as key players in regulating the tumor microenvironment and hence, tumor progression in a variety of cancers. In view of these findings, the present book attemps to provide a comprehensive account of the diversity of tumor microenvironment across different cancers and how myelomonocytic cells have taken the center-stage in regulating this niche to direct cancer progression. A better understanding of the myelomonocytic cells and the mechanisms by which they regulate cancer progression will open new vistas in cancer therapeutics
Tumor Microenvironment and Myelomonocytic Cells
Tumor microenvironment represents an extremely dynamic niche shaped by the interplay of different cell types (e.g. tumor cells, stromal cells), their soluble products (e.g.cytokines, chemokines and growth factors) and varied physico-chemical conditions (e.g low oxygen concentration or hypoxia). Recent studies have identified myelomonocytic cells as key players in regulating the tumor microenvironment and hence, tumor progression in a variety of cancers. In view of these findings, the present book attemps to provide a comprehensive account of the diversity of tumor microenvironment across different cancers and how myelomonocytic cells have taken the center-stage in regulating this niche to direct cancer progression. A better understanding of the myelomonocytic cells and the mechanisms by which they regulate cancer progression will open new vistas in cancer therapeutics
On connections on principal bundles
AbstractA new construction of a universal connection was given in Biswas, Hurtubise and Stasheff (2012). The main aim here is to explain this construction. A theorem of Atiyah and Weil says that a holomorphic vector bundle E over a compact Riemann surface admits a holomorphic connection if and only if the degree of every direct summand of E is zero. In Azad and Biswas (2002), this criterion was generalized to principal bundles on compact Riemann surfaces. This criterion for principal bundles is also explained
Vascular Modulatory Functions of Macrophages
Monocytes/macrophages have long been regarded as important regulators of angiogenesis and vascular remodeling in both developmental and pathological processes. Historically, the ability of macrophages to promote vascular growth has been primarily attributed to their secretion of proangiogenic growth factors, like VEGFA, and matrix-remodeling enzymes, like metallo-proteinases. Recent studies have also suggested that physical contacts with endothelial cells are important to mediate some of the vascular modulatory functions of macrophages. In this review, we provide an account of the cellular and molecular mechanisms that underlie the involvement of macrophages in the regulation of vascular development and growth during angiogenesis, arteriogenesis, and lymphangiogenesis. Furthermore, we discuss the prospect of either inhibiting or enhancing the vascular modulatory functions of macrophages in disease conditions characterized by either excessive or insufficient tissue vascularizationUPDEPALM
Satellite-retrieved direct radiative forcing of aerosols over North-East India and adjoining areas: climatology and impact assessment
The article by J. Biswas et al. contained an update in affiliation of author Binita Pathak. The author would like to add another affiliation to her name. Her updated affiliations are the following
Correction: De Francesco et al. In Vitro Characterization of Canine Microfragmented Adipose Tissue Non-Enzymatically Extracted from the Thigh and Lumbar Regions. Animals 2021, 11, 3231
Reetuparna Biswas was not included as an author in the original publication [...
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