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Spontaneously stereotyping female and male bank voles were injected daily (except on days assigned for monitoring behaviour) during 3 weeks with placebo, the neurolepticum clozapine or the SSRI antidepressant citalopram. Clozapine blocks dopamine (DA) receptors and acts as a partial serotonin (5-HT) antagonist, while citalopram is a specific 5-HT agonist. Stereotypies in both sexes were left unaffected by clozapine treatment, but citalopram markedly reduced stereotypy levels in females. Animal stereotypies have been widely used in models to provide insight into the underlying pathophysiological processes in human mental disturbances. The present findings highlight the importance of examining sex as a significant variable in evaluating responses to pharmacotherapy, and the demonstrated effect of citalopram indicates that stereotyping female bank voles may be useful in new animal models for human anxiety and mood disorders.

5-ht. --- 5-ht2c. --- Animal model. --- Animal-model. --- Animal-models. --- Animal. --- Antidepressant. --- Anxiety. --- Bank vole. --- Bank voles. --- Behavior. --- Behaviour. --- Citalopram. --- Clozapine. --- Compulsive. --- Disorder. --- Dopamine. --- Female. --- Females. --- Human. --- Knockout mouse. --- Knockout. --- Level. --- Male. --- Model. --- Models. --- Mood disorders. --- Mood. --- Mouse. --- Neuroleptica. --- Obsessive-compulsive disorder. --- Ocd. --- Pharmacotherapy. --- Placebo. --- Receptor. --- Receptors. --- Response. --- Responses. --- Serotonin. --- Sex. --- Sexes. --- Ssri. --- Stereotypies. --- Stereotypy. --- Treatment. --- Vole. --- Voles.

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Phospholipases are a ubiquitous group of enzymes that hydrolyze ester bonds within membrane phospholipids. These enzymes serve multiple biological functions that go far beyond a mere membrane remodeling role in cellular homeostasis; they also play key functions in nutrient digestion and the regulated formation of bioactive lipids involved in cell signaling. It is to the latter function, critical to life, that this book is primarily concerned with. All the chapters are written by renowned experts in the area, and provide forefront information on the role phospholipases in a number of physiological and pathophysiological settings.

inhibitor --- metabolic stability --- α-methylation --- oxoesters --- phospholipase A2 --- adrenic acid --- arachidonic acid --- mass spectrometry --- lipid signaling --- inflammation --- monocytes/macrophages --- crotoxin --- snake venom --- lung impairment --- inflammatory response --- lipid mediators --- neuromuscular blocker --- lipidomics --- PAP-2 --- autotaxin --- lysophosphatidate --- G protein-coupled receptor --- PLA2G6 --- fatty liver --- phospholipid remodeling --- diet-induced obesity --- morbidly obesity --- choline and methionine deficiency --- glioblastoma --- sphingolipid --- sphingosine-1-phosphate --- sphingomyelinase --- sphingomyelin --- metastasis --- phosphatidic acid --- diacylglycerol --- lipin --- signaling --- cPLA2α --- psoriasis --- proliferation --- anti-inflammatory --- atherosclerosis --- phospholipases --- macrophages --- T cells --- lipins --- pancreatic islets --- β-cells --- insulin secretion --- glucose tolerance --- insulin resistance --- group VIA phospholipase A2 --- fatty acid --- knockout mouse --- lipid mediator --- lysophospholipid --- membrane --- phospholipid --- ceramide --- acidic sphingomyelinase --- neutral sphingomyelinase --- hepatocellular carcinoma --- alcoholic and nonalcoholic steatohepatitis --- preadipocytes --- prostaglandins --- adipokines --- cytokines --- EP receptors --- Group V phospholipase A2 --- lipids --- majeed syndrome --- LPIN2 --- LIPIN2 --- chronic non-bacterial osteomyelitis --- chronic recurrent multifocal osteomyelitis --- autoinflammatory --- inflammasome --- macrophage --- osteoclast --- n/a

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Dear colleagues, This Special Issue, “Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches”, focuses on the pathophysiology of endothelial dysfunction, new biomarkers for endothelial dysfunction related to cardiovascular disorders or tumors, and novel therapeutic approaches for endothelial dysfunctions. Vascular endothelium is an active tissue and plays a crucial role in the maintenance of vascular homeostasis. Chronic exposure to risk factors, such as hypertension, high cholesterolemia, or oxidative stress, induces endothelial dysfunctions and results in a loss of endothelial integrity, smooth muscle cell proliferation, and macrophage recruitment. The pathophysiology of endothelial dysfunction (ED) is complex and multi-factorial factors are involved, such as oxidative stress or chronic inflammation. The primary prevention of cardiovascular risk factors and endothelial dysfunctions, as well as the early detection of or molecular imaging techniques for endothelial dysfunction, helps to prevent the development of cardiovascular disorders. Novel therapeutic approaches or drug delivery systems for endothelial dysfunctions have had promising beneficial effects in preclinical or clinical levels by affecting the progression of atherosclerotic changes, tumor angiogenesis, and host–immune reactions near tumor environments.

Technology: general issues --- Biotechnology --- endothelial cells --- oxidative stress --- inflammageing --- endothelial dysfunction --- aldehyde dehydrogenase-2 --- cardiovascular disease --- neurovascular disease --- vascular inflammation --- APE1/Ref-1 --- cardiovascular diseases --- subcellular localization --- serological biomarkers --- atherosclerosis --- aerobic exercise --- PCSK9 --- LOX-1 --- insulin resistance --- macrophage polarity --- serum γ-glutamyltransferase --- essential hypertension --- cardiovascular risk factors --- angiogenesis --- nargenicin A1 --- compound 9 --- VEGF --- VEGFR2 --- HIF-1α --- electronegative low-density lipoprotein --- LDL(-) --- L5 LDL --- oxidized LDL --- oxLDL --- ADMA --- arginine --- arginine paradox --- BH4 --- blood pressure --- COVID-19 --- dietary supplements --- endothelium --- eNOS uncoupling --- heart failure --- hypertension --- L-arginine --- myocardial infarction --- NADPH --- nitric oxide --- peripheral artery disease --- ApoE knockout mouse --- atorvastatin --- VCAM-1 --- galectin-3 --- neutrophil/lymphocyte ratio --- electronegative LDL --- LDL(−) --- lectin-like oxLDL receptor-1 --- dyslipidemia --- chronic venous insufficiency --- prolyl oligopeptidase (POP) --- inflammation --- endothelial disfunction --- lung disease --- endothelial to mesenchymal transition --- pulmonary hypertension --- pulmonary fibrosis --- metformin --- diabetes --- CV risk --- hyperglycemia --- glycated lipoproteins --- glycated LDL --- glycated HDL --- endothelial cell dysfunction --- molecular mechanisms --- epigenetic factors --- therapeutic approaches --- vasoactive factors --- EndoMT --- TGF-β --- epigenetics --- endothelial cell --- glycolysis --- metabolism --- pathological angiogenesis --- tumor microenvironment --- MRI (magnetic resonance imaging) --- high-fat diets --- plaque burden --- low-level laser therapy --- phototherapy --- vascular disease --- healing --- ischemia --- vascular calcification --- chronic kidney disease --- CKD --- uremic toxins --- hyperphosphatemia --- vascular smooth muscle cells --- VSMCs --- macrophages --- endothelial cells --- oxidative stress --- inflammageing --- endothelial dysfunction --- aldehyde dehydrogenase-2 --- cardiovascular disease --- neurovascular disease --- vascular inflammation --- APE1/Ref-1 --- cardiovascular diseases --- subcellular localization --- serological biomarkers --- atherosclerosis --- aerobic exercise --- PCSK9 --- LOX-1 --- insulin resistance --- macrophage polarity --- serum γ-glutamyltransferase --- essential hypertension --- cardiovascular risk factors --- angiogenesis --- nargenicin A1 --- compound 9 --- VEGF --- VEGFR2 --- HIF-1α --- electronegative low-density lipoprotein --- LDL(-) --- L5 LDL --- oxidized LDL --- oxLDL --- ADMA --- arginine --- arginine paradox --- BH4 --- blood pressure --- COVID-19 --- dietary supplements --- endothelium --- eNOS uncoupling --- heart failure --- hypertension --- L-arginine --- myocardial infarction --- NADPH --- nitric oxide --- peripheral artery disease --- ApoE knockout mouse --- atorvastatin --- VCAM-1 --- galectin-3 --- neutrophil/lymphocyte ratio --- electronegative LDL --- LDL(−) --- lectin-like oxLDL receptor-1 --- dyslipidemia --- chronic venous insufficiency --- prolyl oligopeptidase (POP) --- inflammation --- endothelial disfunction --- lung disease --- endothelial to mesenchymal transition --- pulmonary hypertension --- pulmonary fibrosis --- metformin --- diabetes --- CV risk --- hyperglycemia --- glycated lipoproteins --- glycated LDL --- glycated HDL --- endothelial cell dysfunction --- molecular mechanisms --- epigenetic factors --- therapeutic approaches --- vasoactive factors --- EndoMT --- TGF-β --- epigenetics --- endothelial cell --- glycolysis --- metabolism --- pathological angiogenesis --- tumor microenvironment --- MRI (magnetic resonance imaging) --- high-fat diets --- plaque burden --- low-level laser therapy --- phototherapy --- vascular disease --- healing --- ischemia --- vascular calcification --- chronic kidney disease --- CKD --- uremic toxins --- hyperphosphatemia --- vascular smooth muscle cells --- VSMCs --- macrophages

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Dear colleagues, This Special Issue, “Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches”, focuses on the pathophysiology of endothelial dysfunction, new biomarkers for endothelial dysfunction related to cardiovascular disorders or tumors, and novel therapeutic approaches for endothelial dysfunctions. Vascular endothelium is an active tissue and plays a crucial role in the maintenance of vascular homeostasis. Chronic exposure to risk factors, such as hypertension, high cholesterolemia, or oxidative stress, induces endothelial dysfunctions and results in a loss of endothelial integrity, smooth muscle cell proliferation, and macrophage recruitment. The pathophysiology of endothelial dysfunction (ED) is complex and multi-factorial factors are involved, such as oxidative stress or chronic inflammation. The primary prevention of cardiovascular risk factors and endothelial dysfunctions, as well as the early detection of or molecular imaging techniques for endothelial dysfunction, helps to prevent the development of cardiovascular disorders. Novel therapeutic approaches or drug delivery systems for endothelial dysfunctions have had promising beneficial effects in preclinical or clinical levels by affecting the progression of atherosclerotic changes, tumor angiogenesis, and host–immune reactions near tumor environments.

endothelial cells --- oxidative stress --- inflammageing --- endothelial dysfunction --- aldehyde dehydrogenase-2 --- cardiovascular disease --- neurovascular disease --- vascular inflammation --- APE1/Ref-1 --- cardiovascular diseases --- subcellular localization --- serological biomarkers --- atherosclerosis --- aerobic exercise --- PCSK9 --- LOX-1 --- insulin resistance --- macrophage polarity --- serum γ-glutamyltransferase --- essential hypertension --- cardiovascular risk factors --- angiogenesis --- nargenicin A1 --- compound 9 --- VEGF --- VEGFR2 --- HIF-1α --- electronegative low-density lipoprotein --- LDL(–) --- L5 LDL --- oxidized LDL --- oxLDL --- ADMA --- arginine --- arginine paradox --- BH4 --- blood pressure --- COVID-19 --- dietary supplements --- endothelium --- eNOS uncoupling --- heart failure --- hypertension --- L-arginine --- myocardial infarction --- NADPH --- nitric oxide --- peripheral artery disease --- ApoE knockout mouse --- atorvastatin --- VCAM-1 --- galectin-3 --- neutrophil/lymphocyte ratio --- electronegative LDL --- LDL(−) --- lectin-like oxLDL receptor-1 --- dyslipidemia --- chronic venous insufficiency --- prolyl oligopeptidase (POP) --- inflammation --- endothelial disfunction --- lung disease --- endothelial to mesenchymal transition --- pulmonary hypertension --- pulmonary fibrosis --- metformin --- diabetes --- CV risk --- hyperglycemia --- glycated lipoproteins --- glycated LDL --- glycated HDL --- endothelial cell dysfunction --- molecular mechanisms --- epigenetic factors --- therapeutic approaches --- vasoactive factors --- EndoMT --- TGF-β --- epigenetics --- endothelial cell --- glycolysis --- metabolism --- pathological angiogenesis --- tumor microenvironment --- MRI (magnetic resonance imaging) --- high-fat diets --- plaque burden --- low-level laser therapy --- phototherapy --- vascular disease --- healing --- ischemia --- vascular calcification --- chronic kidney disease --- CKD --- uremic toxins --- hyperphosphatemia --- vascular smooth muscle cells --- VSMCs --- macrophages --- n/a --- LDL(-)