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In socially unstable groups of male laboratory mice, individuals may experience a chronic stress situation. Previous experiments have shown that the transfer of specific olfactory cues during cage cleaning, and the provision of nesting material decrease aggression and stress in group-housed male mice. In this study, the combined effect of these husbandry procedures were tested for their long-term effect on stress in groups of moderately aggressive (BALB/c) and severely aggressive (CD-1) male mice. The physiological and behavioural stress-related parameters used were body weight, food and water intake, spleen and thymus weight, adrenal tyrosine hydroxylase activity, urine corticosterone levels and behaviour in a cage emergence test. Long-term provision of nesting material and its transfer during cage cleaning was found to influence several stress-related physiological parameters. Mice housed in cages enriched with nesting material had lower urine corticosterone levels and heavier thymuses, and they consumed less food and water than standard-housed mice. Furthermore, marked differences were found between strains. CD-1 mice were less anxious in the cage emergence test, weighed more, ate and drank more, and had heavier thymuses but lighter spleens and lower corticosterone levels than BALB/c mice. We conclude that the long-term provision of nesting material, including the transfer of nesting material during cage cleaning, reduces stress and thereby enhances the welfare of laboratory mice
Activity. --- Adrenal tyrosine hydroxylase. --- Adrenal. --- Aggression. --- Aggressive-behavior. --- Aggressive. --- Behaviour. --- Body weight. --- Body-weight. --- Cage. --- Cages. --- Chronic stress. --- Cleaning. --- Corticosterone levels. --- Corticosterone. --- Cues. --- Enriched. --- Environmental enrichment. --- Experience. --- Experiment. --- Experiments. --- Food. --- Group. --- Husbandry. --- Inbred strains. --- Laboratory mice. --- Laboratory. --- Level. --- Long-term. --- Male dba/2j mice. --- Male laboratory mice. --- Male mice. --- Male-mice. --- Male. --- Mice. --- Modulation. --- Mouse. --- Nesting material. --- Olfactory cues. --- Olfactory. --- Parameters. --- Physiological. --- Provision. --- Rats. --- Stress. --- Test. --- Time. --- Tyrosine-hydroxylase. --- Tyrosine. --- Urine. --- Weight. --- Welfare.
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Environmental enrichment is intended to improve the welfare of laboratory animals. However, regarding male mice, numerous studies indicate an increase in aggressive behavior due to cage structuring. On the one hand, this might be a problem concerning animal welfare. On the other hand, enrichment is though to hamper environmental standardization and to increase variability of data. Furthermore, increasing fights, arousal, and/or injury in enriched housed animals might superimpose other (positive) environmental effects on behavior and physiology. Therefore, the present study investigated effects of environmental enrichment on behavioral, endocrinological, and immunological parameters in male mice of the docile inbred strain ABG. From weaning until day 77 +/- 3 of life, animals were kept in stable sibling groups of four under three different housing conditions: (A) nonstructured Makrolon type III laboratory cages ("standard housing" = S); (B) equivalent laboratory cages that were enriched with a box and scaffolding ("enriched housing" = E); and (C) spacious terrariums that were structured richly (" super-enriched housing"= SE). No differences in agonistic behavior, levels of plasma corticosterone (CORT), and activities of adrenal tyrosine hydroxylase (TH) existed among S-, E-, and SE-housed ABG males. Play behavior and general activity increased significantly with increasing enrichment. Concerning immunological parameters, males of both forms of enriched housing showed significantly lower percentages of CD4 and CD8 cells compared to S-housed mice. However, regarding the ratio of CD4/CD8 cells, IL-2, IL-4, IL-10, IFN-gamma, IgGI, and IgG2a, no significant housing-dependent differences were found. Enrichment did neither hamper standardization nor negatively influence the variability of physiological parameters. In summary, using a docile strain of mice revealed the positive effects of environmental enrichment also on male mice. The lack of adverse effects on behavior
Activity. --- Adrenal tyrosine hydroxylase. --- Adrenal. --- Adrenocortical system. --- Adrenomedullary system. --- Aggression. --- Aggressive-behavior. --- Aggressive. --- Agonistic. --- Animal welfare. --- Animal-welfare. --- Animal. --- Animals. --- Arousal. --- Behavior. --- Boxes. --- Cage enrichment. --- Cage. --- Cages. --- Cell surface antigens. --- Corticosterone. --- Cytokines. --- Enriched. --- Enrichment. --- Environmental enrichment. --- Fight. --- Group. --- Housing condition. --- Housing conditions. --- Housing. --- Immune system. --- Immunoglobulins. --- Increase. --- Injuries. --- Injury. --- Kept. --- Laboratory animals. --- Laboratory cages. --- Laboratory-animals. --- Laboratory. --- Level. --- Life. --- Male laboratory mice. --- Male mice. --- Male-mice. --- Male. --- Males. --- Mice. --- Mus-musculus mammalia. --- Parameters. --- Physiological. --- Physiology. --- Plasma corticosterone. --- Plasma-corticosterone. --- Plasma. --- Play. --- Rats. --- Rattus-norvegicus. --- Social stress. --- Standardization. --- Stress. --- Time. --- Tyrosine-hydroxylase. --- Tyrosine. --- Variability of experimental results. --- Variability. --- Weaning. --- Welfare. --- Wild house mice.
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Ubiquitination is a biological process mediated by ubiquitin itself, the E1 ubiquitin-activating enzyme, E2 ubiquitin-conjugating enzyme, E3 ubiquitin ligase, and deubiquitinating enzyme, respectively. Currently, these multiple biological steps are revealed to participate in various life phenomena, such as cell proliferation, regulation of cell surface proteins expression, and mitochondrial function, which are profoundly related to human health and diseases. Although clinical applications targeting ubiquitination are still limited compared to those directed toward kinase systems such as tyrosine kinases, multiple enzymatic consequences should be future therapeutic implications. This Special Issue of IJMS entitled “Ubiquitination in Health and Disease” successfully published15 distinguished manuscripts, with a total of 66 international authors and. This book provides the latest and most useful information for researchers and scientists in this field.
Humanities --- Social interaction --- deubiquitinase --- degradation --- therapeutic target --- cancer --- hematopoiesis --- hematopoietic stem cells --- immune response --- regulation of gene expression --- ubiquitin system --- genetic diseases --- ubiquitin ligase --- deubiquitinases --- monoubiquitin signaling --- vesicular trafficking --- protein complex formation --- inflammation --- inhibitor --- innate immune --- interferon --- LUBAC --- NF-κB --- ubiquitin --- Parkinson’s disease --- dopa-responsive dystonia --- tyrosine hydroxylase --- α-synuclein --- fatty acid-binding protein 3 --- ubiquitination --- proteasomal degradation --- ubiquitin-proteasome system --- mitochondria --- E3 ubiquitin ligase --- MITOL/MARCH5 --- salt-sensitive hypertension --- Nedd4L/Nedd4-2 --- epithelial sodium channel --- aldosterone sensitive distal nephron --- excitation-transcription coupling --- RNF183 --- RNF186 --- RNF182 --- RNF152 --- RING finger --- mTOR --- endoplasmic reticulum stress --- osmotic stress --- ubiquitin code --- virus infection --- virus-host interaction --- tau protein --- semisynthesis --- disulfide-coupling --- polyubiquitin --- fibrils --- aggregation --- neurodegeneration --- deubiquitination --- inhibitors --- protein quality control --- proteolysis --- protein stabilization --- regulatory T cells --- mesenchymal stem cell --- cortical bone derived stem cell --- myocardial infarction --- blood pressure --- renal salt reabsorption --- vascular function --- ubiquitin proteasome system --- ubiquitin–proteasome pathway --- cilia --- ciliogenesis --- differentiation --- proliferation --- ciliopathy --- E3s --- DUBs --- UPS --- neurodegenerative disease --- immune-related diseases
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Ubiquitination is a biological process mediated by ubiquitin itself, the E1 ubiquitin-activating enzyme, E2 ubiquitin-conjugating enzyme, E3 ubiquitin ligase, and deubiquitinating enzyme, respectively. Currently, these multiple biological steps are revealed to participate in various life phenomena, such as cell proliferation, regulation of cell surface proteins expression, and mitochondrial function, which are profoundly related to human health and diseases. Although clinical applications targeting ubiquitination are still limited compared to those directed toward kinase systems such as tyrosine kinases, multiple enzymatic consequences should be future therapeutic implications. This Special Issue of IJMS entitled “Ubiquitination in Health and Disease” successfully published15 distinguished manuscripts, with a total of 66 international authors and. This book provides the latest and most useful information for researchers and scientists in this field.
deubiquitinase --- degradation --- therapeutic target --- cancer --- hematopoiesis --- hematopoietic stem cells --- immune response --- regulation of gene expression --- ubiquitin system --- genetic diseases --- ubiquitin ligase --- deubiquitinases --- monoubiquitin signaling --- vesicular trafficking --- protein complex formation --- inflammation --- inhibitor --- innate immune --- interferon --- LUBAC --- NF-κB --- ubiquitin --- Parkinson’s disease --- dopa-responsive dystonia --- tyrosine hydroxylase --- α-synuclein --- fatty acid-binding protein 3 --- ubiquitination --- proteasomal degradation --- ubiquitin-proteasome system --- mitochondria --- E3 ubiquitin ligase --- MITOL/MARCH5 --- salt-sensitive hypertension --- Nedd4L/Nedd4-2 --- epithelial sodium channel --- aldosterone sensitive distal nephron --- excitation-transcription coupling --- RNF183 --- RNF186 --- RNF182 --- RNF152 --- RING finger --- mTOR --- endoplasmic reticulum stress --- osmotic stress --- ubiquitin code --- virus infection --- virus-host interaction --- tau protein --- semisynthesis --- disulfide-coupling --- polyubiquitin --- fibrils --- aggregation --- neurodegeneration --- deubiquitination --- inhibitors --- protein quality control --- proteolysis --- protein stabilization --- regulatory T cells --- mesenchymal stem cell --- cortical bone derived stem cell --- myocardial infarction --- blood pressure --- renal salt reabsorption --- vascular function --- ubiquitin proteasome system --- ubiquitin–proteasome pathway --- cilia --- ciliogenesis --- differentiation --- proliferation --- ciliopathy --- E3s --- DUBs --- UPS --- neurodegenerative disease --- immune-related diseases
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Ubiquitination is a biological process mediated by ubiquitin itself, the E1 ubiquitin-activating enzyme, E2 ubiquitin-conjugating enzyme, E3 ubiquitin ligase, and deubiquitinating enzyme, respectively. Currently, these multiple biological steps are revealed to participate in various life phenomena, such as cell proliferation, regulation of cell surface proteins expression, and mitochondrial function, which are profoundly related to human health and diseases. Although clinical applications targeting ubiquitination are still limited compared to those directed toward kinase systems such as tyrosine kinases, multiple enzymatic consequences should be future therapeutic implications. This Special Issue of IJMS entitled “Ubiquitination in Health and Disease” successfully published15 distinguished manuscripts, with a total of 66 international authors and. This book provides the latest and most useful information for researchers and scientists in this field.
Humanities --- Social interaction --- deubiquitinase --- degradation --- therapeutic target --- cancer --- hematopoiesis --- hematopoietic stem cells --- immune response --- regulation of gene expression --- ubiquitin system --- genetic diseases --- ubiquitin ligase --- deubiquitinases --- monoubiquitin signaling --- vesicular trafficking --- protein complex formation --- inflammation --- inhibitor --- innate immune --- interferon --- LUBAC --- NF-κB --- ubiquitin --- Parkinson’s disease --- dopa-responsive dystonia --- tyrosine hydroxylase --- α-synuclein --- fatty acid-binding protein 3 --- ubiquitination --- proteasomal degradation --- ubiquitin-proteasome system --- mitochondria --- E3 ubiquitin ligase --- MITOL/MARCH5 --- salt-sensitive hypertension --- Nedd4L/Nedd4-2 --- epithelial sodium channel --- aldosterone sensitive distal nephron --- excitation-transcription coupling --- RNF183 --- RNF186 --- RNF182 --- RNF152 --- RING finger --- mTOR --- endoplasmic reticulum stress --- osmotic stress --- ubiquitin code --- virus infection --- virus-host interaction --- tau protein --- semisynthesis --- disulfide-coupling --- polyubiquitin --- fibrils --- aggregation --- neurodegeneration --- deubiquitination --- inhibitors --- protein quality control --- proteolysis --- protein stabilization --- regulatory T cells --- mesenchymal stem cell --- cortical bone derived stem cell --- myocardial infarction --- blood pressure --- renal salt reabsorption --- vascular function --- ubiquitin proteasome system --- ubiquitin–proteasome pathway --- cilia --- ciliogenesis --- differentiation --- proliferation --- ciliopathy --- E3s --- DUBs --- UPS --- neurodegenerative disease --- immune-related diseases
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This book outlines some new advances in genetics, clinical evaluation, localization, therapy (newly including immunotherapy) of pheochromocytoma and paraganglioma including their metastatic counterparts. Well-known and experienced clinicians and scientists contributed to this book to include some novel approaches to these tumors. This book will serve to various health care professionals from different subspecialties, but mainly oncologists, endocrinologists, endocrine surgeons, pediatricians, and radiologists. This book shows that the field of pheochromocytoma/paraganglioma is evolving and a significant progress has been made in last 5 years requiring that health care professionals and scientists will learns new information and implement it in their clinical practice or scientific work, respectively. This book should not be missed by anybody who is focusing on neuroendocrine tumors, their newest evaluation and treatment.
polycythemia --- peptide receptor radiotherapy --- n/a --- vasculogenesis --- catecholamines --- neuroendocrine --- GTV --- adaptive immunity --- therapy resistance --- histology --- transgenic mice --- cryoablation --- spheroids --- energy metabolism --- somatostatinoma --- angiogenesis --- pheochromocytoma --- SDHD --- percutaneous ethanol injection --- metanephrines --- SDHB --- global longitudinal strain --- mutation --- normetanephrines --- catecholamine --- PASS --- PGL --- 177Lu-DOTATATE --- chromosomal alteration --- speckle-tracking echocardiography --- lL-6 --- dog --- percutaneous ablation --- stem-like tumor cells --- EPAS1 --- neural crest --- fluorescence imaging --- neutrophil --- xenograft --- inflammation --- head and neck --- weighted standard deviation --- FGF21 --- calorimetry --- HIF --- average real variability --- next-generation sequencing --- adrenocortical carcinoma --- carotid body --- hypoxia-inducible factor --- paraganglioma --- succinate dehydrogenase --- blood pressure variability --- arrhythmia --- mortality --- NF1 --- toll-like receptor --- GAPP --- NET --- subclinical systolic dysfunction --- pheochromocytoma and paraganglioma --- PET-CT --- pan-cancer analysis --- mouse pheochromocytoma cells --- innate immunity --- neurogenesis --- neuroendocrine tumor --- obesity --- hypotension --- hypoxia --- CNV detection --- 18F-FDOPA --- comparative genomics --- adrenomedullary function --- PCC --- pathogen-associated molecular patterns --- adrenal tumor --- radiotherapy --- 11C-hydroxy-ephedrine --- radiofrequency ablation --- PPGL --- minimally invasive procedure --- sporadic --- diabetes mellitus --- adrenal incidentaloma --- germline mutation --- immunotherapy --- VHL --- immunohistochemistry --- metastatic OR malignant pheochromocytoma --- erythropoietin --- postoperative --- targeted therapy --- PRRT --- metastatic --- mitochondria --- T cell --- TCA cycle --- meta-analysis --- pseudohypoxia --- ectopic secretion --- radiosensitization --- chromogranin A --- hereditary --- hypertension --- PET --- phosphorylation tyrosine hydroxylase
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