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Among infectious diseases, viral infections are the leading cause of death worldwide, especially in the most low-income countries, particularly in young children. Most of the human viruses are all well characterized in terms of structure, life-cycle, tropism, and associated primary pathologies, but many of the pathogenetic mechanisms underlying their ability to cause acute infection, persist or reactivate in the host and cause chronic and/or degenerative damage, and still need to be fully clarified. At the same time, it seems necessary to develop novel therapeutic approaches and rationale, and possibly more potent antiviral compounds that are addressed to novel targets.
Medicine --- hRSV --- F gene --- G gene --- children --- respiratory diseases --- genotyping --- Saudi Arabia --- α chemokine receptor 4 --- β-chemokine receptor 5 --- human immunodeficiency virus --- monocyte-derived macrophages --- HPV --- sexually transmitted diseases (STDs) --- laboratory methods --- PCR --- genotypes --- surveillance --- epidemiology --- exopolysaccharides --- lactic acid bacteria --- human adenovirus type 5 --- antiviral activity --- cell cycle --- prevalence --- hepatitis B virus --- genotype --- bahrain --- sRAGE --- oxidative stress --- inflammation --- warts
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Among infectious diseases, viral infections are the leading cause of death worldwide, especially in the most low-income countries, particularly in young children. Most of the human viruses are all well characterized in terms of structure, life-cycle, tropism, and associated primary pathologies, but many of the pathogenetic mechanisms underlying their ability to cause acute infection, persist or reactivate in the host and cause chronic and/or degenerative damage, and still need to be fully clarified. At the same time, it seems necessary to develop novel therapeutic approaches and rationale, and possibly more potent antiviral compounds that are addressed to novel targets.
hRSV --- F gene --- G gene --- children --- respiratory diseases --- genotyping --- Saudi Arabia --- α chemokine receptor 4 --- β-chemokine receptor 5 --- human immunodeficiency virus --- monocyte-derived macrophages --- HPV --- sexually transmitted diseases (STDs) --- laboratory methods --- PCR --- genotypes --- surveillance --- epidemiology --- exopolysaccharides --- lactic acid bacteria --- human adenovirus type 5 --- antiviral activity --- cell cycle --- prevalence --- hepatitis B virus --- genotype --- bahrain --- sRAGE --- oxidative stress --- inflammation --- warts
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Dear Colleagues, When Hayflick and Moorhead coined the term “cellular senescence” (CS) almost 60 years ago, this phenomenon was understood as a mechanism, usually induced by activation of the DNA-repair machinery, to prevent uncontrolled proliferation. Meanwhile, additional beneficial roles for CS have been identified, such as embryonic development and wound healing. The senescence associated secretory phenotype (SASP) activated in most senescent cells (SC) signals to the immune system “come here and remove me”. In organisms with young and functional immune systems, occurring SC are usually detected and removed. If SC remain in the tissue expressing the SASP, this will cause not just a damaging local inflammation but can also induce remodeling and regeneration of the surrounding tissue as well as spreading of senescence. Old organisms show reduced regenerative potential and immune function which leads to accumulation of SC. Accordingly, accumulation of SC was observed in tissues of aged individuals, but importantly also in the context of age-related disorders, neurodegenerative, or cardiovascular diseases and others. Because of its detrimental effect of the surrounding tissue, accumulation of SC is not just a consequence, but can rather been understood as a major driver of aging. In line with this, recent studies described that removal of SC showed beneficial effects on healthspan and lifespan. This exciting research led to the discovery of “senolytics”, drugs which can kill SC. Given the heterogeneity of cell types that show senescence-like phenotypes, including heart muscle and post-mitotic neuronal cells, further research is required to unravel the molecular background that renders a cell type vulnerable to senesce. Additionally, it will be important to understand how senescence is cell type-specifically induced and which molecules serve as drug targets to prevent senescence and its spreading, or actively kill SC. This special issue will shed light on the molecular pathways of CS and inflammaging and on possible strategies to interfere with these processes. Dr. Markus Riessland Guest Editor
γH2AX --- Alzheimer’s disease --- DNA damage --- mild cognitive impairment --- senescence --- secreted protein acidic and rich in cysteine --- regeneration --- homeostasis --- cellular senescence --- biology of aging --- neurodegeneration --- brain --- geroscience --- senolytics --- tauopathy --- cancer --- stress response --- post-mitotic --- neuronal senescence --- amyotrophic lateral sclerosis --- senescence-associated secretory phenotype (SASP) --- cell-cycle --- melanoma --- pancreatic adenocarcinoma --- tumor infiltration --- chemotherapy resistance --- prostate --- inflammation --- AIM2 inflammasome --- POP3 --- n/a --- Alzheimer's disease
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Dear Colleagues, When Hayflick and Moorhead coined the term “cellular senescence” (CS) almost 60 years ago, this phenomenon was understood as a mechanism, usually induced by activation of the DNA-repair machinery, to prevent uncontrolled proliferation. Meanwhile, additional beneficial roles for CS have been identified, such as embryonic development and wound healing. The senescence associated secretory phenotype (SASP) activated in most senescent cells (SC) signals to the immune system “come here and remove me”. In organisms with young and functional immune systems, occurring SC are usually detected and removed. If SC remain in the tissue expressing the SASP, this will cause not just a damaging local inflammation but can also induce remodeling and regeneration of the surrounding tissue as well as spreading of senescence. Old organisms show reduced regenerative potential and immune function which leads to accumulation of SC. Accordingly, accumulation of SC was observed in tissues of aged individuals, but importantly also in the context of age-related disorders, neurodegenerative, or cardiovascular diseases and others. Because of its detrimental effect of the surrounding tissue, accumulation of SC is not just a consequence, but can rather been understood as a major driver of aging. In line with this, recent studies described that removal of SC showed beneficial effects on healthspan and lifespan. This exciting research led to the discovery of “senolytics”, drugs which can kill SC. Given the heterogeneity of cell types that show senescence-like phenotypes, including heart muscle and post-mitotic neuronal cells, further research is required to unravel the molecular background that renders a cell type vulnerable to senesce. Additionally, it will be important to understand how senescence is cell type-specifically induced and which molecules serve as drug targets to prevent senescence and its spreading, or actively kill SC. This special issue will shed light on the molecular pathways of CS and inflammaging and on possible strategies to interfere with these processes. Dr. Markus Riessland Guest Editor
Research & information: general --- Biology, life sciences --- γH2AX --- Alzheimer's disease --- DNA damage --- mild cognitive impairment --- senescence --- secreted protein acidic and rich in cysteine --- regeneration --- homeostasis --- cellular senescence --- biology of aging --- neurodegeneration --- brain --- geroscience --- senolytics --- tauopathy --- cancer --- stress response --- post-mitotic --- neuronal senescence --- amyotrophic lateral sclerosis --- senescence-associated secretory phenotype (SASP) --- cell-cycle --- melanoma --- pancreatic adenocarcinoma --- tumor infiltration --- chemotherapy resistance --- prostate --- inflammation --- AIM2 inflammasome --- POP3
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Among infectious diseases, viral infections are the leading cause of death worldwide, especially in the most low-income countries, particularly in young children. Most of the human viruses are all well characterized in terms of structure, life-cycle, tropism, and associated primary pathologies, but many of the pathogenetic mechanisms underlying their ability to cause acute infection, persist or reactivate in the host and cause chronic and/or degenerative damage, and still need to be fully clarified. At the same time, it seems necessary to develop novel therapeutic approaches and rationale, and possibly more potent antiviral compounds that are addressed to novel targets.
Medicine --- hRSV --- F gene --- G gene --- children --- respiratory diseases --- genotyping --- Saudi Arabia --- α chemokine receptor 4 --- β-chemokine receptor 5 --- human immunodeficiency virus --- monocyte-derived macrophages --- HPV --- sexually transmitted diseases (STDs) --- laboratory methods --- PCR --- genotypes --- surveillance --- epidemiology --- exopolysaccharides --- lactic acid bacteria --- human adenovirus type 5 --- antiviral activity --- cell cycle --- prevalence --- hepatitis B virus --- genotype --- bahrain --- sRAGE --- oxidative stress --- inflammation --- warts
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The present book on Molecular & Diagnostic Imaging and Treatment Strategies of ovarian cancer is one of two companion books with the second one being focused on Cell and Molecular Biology of Ovarian Cancer. Both books include new exciting aspects of ovarian cancer research with chapters written by experts in their respective fields who contributed their unique expertise in specific ovarian cancer research areas and include cell and molecular details that are important for the specific subtopics. Comprehensive and concise reviews are included of key topics in the field.
Cell cycle. --- Molecular biology. --- Cancer research. --- Radiology. --- Oncology . --- Cell Cycle Analysis. --- Molecular Medicine. --- Cancer Research. --- Diagnostic Radiology. --- Oncology. --- Tumors --- Radiological physics --- Physics --- Radiation --- Cancer research --- Molecular biochemistry --- Molecular biophysics --- Biochemistry --- Biophysics --- Biomolecules --- Systems biology --- Mitotic cycle --- Nuclear cycle (Cytology) --- Biological rhythms --- Ovaries --- Cancer. --- Càncer d'ovari --- Diagnòstic --- Terapèutica --- Teràpia --- Tractament (Medicina) --- Tractament de les malalties --- Medicina clínica --- Al·lopatia (Terapèutica) --- Antipirètics --- Cateterisme --- Dietoteràpia --- Fisioteràpia --- Fórmules magistrals --- Hormonoteràpia --- Immunoteràpia --- Injeccions intraarticulars --- Intubació --- Ioga --- Logopèdia --- Medicina alternativa --- Nutrició --- Quimioteràpia --- Radiologia intervencionista --- Terapèutica dental --- Terapèutica fisiològica --- Teràpia genètica --- Teràpia intravenosa --- Teràpia respiratòria --- Terapèutica veterinària --- Tractament pal·liatiu --- Ús terapèutic --- Diagnosi --- Diagnòstic físic --- Examen mèdic (Diagnòstic) --- Exploració médica (Diagnòstic) --- Exploració clínica (Diagnòstic) --- Cribratge --- Diagnòstic d'infermeria --- Diagnòstic diferencial --- Diagnòstic dual --- Diagnòstic molecular --- Diagnòstic prenatal --- Diagnòstic quirúrgic --- Diagnòstic per la imatge --- Electrodiagnòstic --- Entrevista clínica --- Examen físic --- Isòtops radioactius en diagnòstic mèdic --- Monitoratge de pacients --- Proves funcionals (Medicina) --- Patologia --- Pronòstic mèdic --- Símptomes --- Càncer d'ovaris --- Càncer
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Dear Colleagues, When Hayflick and Moorhead coined the term “cellular senescence” (CS) almost 60 years ago, this phenomenon was understood as a mechanism, usually induced by activation of the DNA-repair machinery, to prevent uncontrolled proliferation. Meanwhile, additional beneficial roles for CS have been identified, such as embryonic development and wound healing. The senescence associated secretory phenotype (SASP) activated in most senescent cells (SC) signals to the immune system “come here and remove me”. In organisms with young and functional immune systems, occurring SC are usually detected and removed. If SC remain in the tissue expressing the SASP, this will cause not just a damaging local inflammation but can also induce remodeling and regeneration of the surrounding tissue as well as spreading of senescence. Old organisms show reduced regenerative potential and immune function which leads to accumulation of SC. Accordingly, accumulation of SC was observed in tissues of aged individuals, but importantly also in the context of age-related disorders, neurodegenerative, or cardiovascular diseases and others. Because of its detrimental effect of the surrounding tissue, accumulation of SC is not just a consequence, but can rather been understood as a major driver of aging. In line with this, recent studies described that removal of SC showed beneficial effects on healthspan and lifespan. This exciting research led to the discovery of “senolytics”, drugs which can kill SC. Given the heterogeneity of cell types that show senescence-like phenotypes, including heart muscle and post-mitotic neuronal cells, further research is required to unravel the molecular background that renders a cell type vulnerable to senesce. Additionally, it will be important to understand how senescence is cell type-specifically induced and which molecules serve as drug targets to prevent senescence and its spreading, or actively kill SC. This special issue will shed light on the molecular pathways of CS and inflammaging and on possible strategies to interfere with these processes. Dr. Markus Riessland Guest Editor
Research & information: general --- Biology, life sciences --- γH2AX --- Alzheimer’s disease --- DNA damage --- mild cognitive impairment --- senescence --- secreted protein acidic and rich in cysteine --- regeneration --- homeostasis --- cellular senescence --- biology of aging --- neurodegeneration --- brain --- geroscience --- senolytics --- tauopathy --- cancer --- stress response --- post-mitotic --- neuronal senescence --- amyotrophic lateral sclerosis --- senescence-associated secretory phenotype (SASP) --- cell-cycle --- melanoma --- pancreatic adenocarcinoma --- tumor infiltration --- chemotherapy resistance --- prostate --- inflammation --- AIM2 inflammasome --- POP3 --- n/a --- Alzheimer's disease
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Brucellosis, caused by the facultative intracellular bacteria Brucella species, is one the most prevalent zoonosis worldwide. • The articles described in this book report several aspects of host-Brucella interactions. • The findings described here will help to advance in the comprehension of bacterial pathogenesis and contribute to the future development of drugs or vaccines to control brucellosis.
Research & information: general --- Recombinant vaccine --- divalent vaccine --- brucellosis --- Omp25 --- L7/L12 --- Brucella abortus 544 --- ST2 receptor --- Brucella abortus --- oral infection --- human endometrial cells --- internalization --- intracellular replication --- decidualization --- chemokines --- macrophages --- Brucella --- HSC --- MHC --- IL-10 --- cell cycle --- (p)ppGpp --- rsh --- neurobrucellosis --- platelets --- brain microvascular endothelial cells --- endothelial cells --- adhesins --- Ig-like domain --- monomeric autotransporters --- trimeric autotransporters --- extracellular matrix --- polar localization --- virulence factors --- vaccine candidates --- fibronectin --- canonical inflammasome --- non-canonical inflammasome --- NLR --- pyroptosis --- ASC --- caspase-11 --- caspase-1 --- IL-1β --- gDNA --- replication niche --- reservoir --- persistence --- survival --- chronic infection --- n/a
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Brucellosis, caused by the facultative intracellular bacteria Brucella species, is one the most prevalent zoonosis worldwide. • The articles described in this book report several aspects of host-Brucella interactions. • The findings described here will help to advance in the comprehension of bacterial pathogenesis and contribute to the future development of drugs or vaccines to control brucellosis.
Recombinant vaccine --- divalent vaccine --- brucellosis --- Omp25 --- L7/L12 --- Brucella abortus 544 --- ST2 receptor --- Brucella abortus --- oral infection --- human endometrial cells --- internalization --- intracellular replication --- decidualization --- chemokines --- macrophages --- Brucella --- HSC --- MHC --- IL-10 --- cell cycle --- (p)ppGpp --- rsh --- neurobrucellosis --- platelets --- brain microvascular endothelial cells --- endothelial cells --- adhesins --- Ig-like domain --- monomeric autotransporters --- trimeric autotransporters --- extracellular matrix --- polar localization --- virulence factors --- vaccine candidates --- fibronectin --- canonical inflammasome --- non-canonical inflammasome --- NLR --- pyroptosis --- ASC --- caspase-11 --- caspase-1 --- IL-1β --- gDNA --- replication niche --- reservoir --- persistence --- survival --- chronic infection --- n/a
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Marine natural products are characterized by high chemical diversity, biochemical specificity, and other molecular properties that make them favorable as lead structures for drug discovery. In this field, one of the main problems is often the reduced natural availability of isolated substances, which can complicate both the structural characterization and possible future developments. For these reasons, the study of bioactive marine metabolites should rely on the development of chemical synthesis and synthetic strategies aimed at the preparation of pure compounds and analogs both for structural confirmation and/or for the large-scale preparation necessary for future applications. Moreover, natural products can be a crucial starting point for the preparation of molecules structurally inspired by the latter, opening the path to new classes of biologically active compounds with pharmacological potential. This book collects original research articles regarding synthetic strategies for secondary marine metabolites and/or analogs that favor applications of these molecules and/or solve structural challenges common in the field of natural substances.
organic synthesis --- meroterpenoids --- thiazinoquinones --- antiproliferative activity --- G0/G1 cell-cycle arrest --- cytostatic --- solid tumor cell lines --- alkylglycerol (AKG) --- ricinoleic acid (RA) --- antimicrobial activity --- structure–activity relationship (SAR) studies --- antibiotics (gentamicin --- tetracycline --- ciprofloxacin and ampicillin) --- marine-inspired --- breast cancer --- bis-indoles --- synthesis --- apoptosis --- carbohydrates --- polysaccharides --- semi-synthesis --- sulfation --- glycosylation --- fucose --- fucosylated chondroitin sulfate --- marine natural product --- largazole --- HDAC inhibitors --- modification --- fluoro olefin --- total synthesis --- natural product --- 7-deazapurine nucleoside --- disaccharide nucleoside --- tubercidin --- aureol --- tetracyclic meroterpenoids --- natural products synthesis --- labdane scaffold --- bioactive diterpenes --- sclareolide --- structure-activity relationships --- TRPV4 channel --- amides/esters --- COVID-19 --- SARS-CoV-2 --- lipophilic iminosugars --- polymer-supported triphenyl phosphine --- cholesterol --- antibacterial iminosugars --- n/a --- structure-activity relationship (SAR) studies
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