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De plus en plus de chevaux présentant des pathologies abdominales sont dirigés vers des solutions chirurgicales. Cette procédure chirurgicale peut présenter un certain nombre de complications, dans certains cas cela est directement lié aux voies d’abord et se présentent sous forme de déhiscence de plaies ou d’hernies abdominales. D’autres fois , ces complications peuvent survenir dans la cavité abdominale et plus particulièrement au niveau de l’intestin, et ceci est représenté par l’iléus paralytique . Cette affection engendre des obstructions qui peuvent être à plusieurs localisations dans l’intestin et sont partielles ou totales. Elles sont responsables quelques fois d’un reflux, qui, lui-même, peut engendrer un ulcère gastrique. Les ulcères gastriques post-chirurgicaux observés ne sont pas seulement la conséquence de l’acte chirurgical en lui-même, mais sont la conséquence de l’ensemble de la procédure qui précède et succède à celle-ci : le transport, le changement d’alimentation, le stress, certaines molécules administrés peuvent avoir une influence concrète dans le développement de cette pathologie. Et de ce fait, un certain nombre de solutions peuvent être proposées pour limiter le développement de ces ulcères : cela passera tout d’abord par une bonne suspicion de leur apparition en sachant bien reconnaitre les signes cliniques et de bonnes méthodes de diagnostic. Mais aussi par la gestion préventive (gestion de l’alimentation, du transport, limiter le stress) et curative des lésions confirmées. More and more horses presenting abdominal pathologies are referred to surgical solutions. These surgical procedures can present a number of complications, sometimes this is directly related to the surgical approach, it can be wound dehiscence or abdominal hernia, other times, these complications can occur in the abdomen and specifically in the intestine and causes paralytics ileus. These conditions cause obstructions at different localizations and can be partial or total. Sometimes they are responsible for gastro-intestinal reflux, which can cause a gastric ulcer. The post-surgical gastric ulcers observed are not only the consequence of the surgical act itself, but are the consequences of the entire process which precedes and follows it: transport, change of diet, molecules administration can have an influence in the development of this pathology. And therefore, a certain number of solutions can be proposed in the surgical process to limit the development of these ulcers: this will first of all pass through a good suspicion, by knowing how to recognize the clinical signs, and good methods of diagnosis. But also, through preventive management (management of food, transport, limiting stress) and curative management with the confirmed ulcers.
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Drug metabolism/pharmacokinetics and drug interaction studies have been extensively carried out in order to secure the druggability and safety of new chemical entities throughout the development of new drugs. Recently, drug metabolism and transport by phase II drug metabolizing enzymes and drug transporters, respectively, as well as phase I drug metabolizing enzymes, have been studied. A combination of biochemical advances in the function and regulation of drug metabolizing enzymes and automated analytical technologies are revolutionizing drug metabolism research. There are also potential drug–drug interactions with co-administered drugs due to inhibition and/or induction of drug metabolic enzymes and drug transporters. In addition, drug interaction studies have been actively performed to develop substrate cocktails that do not interfere with each other and a simultaneous analytical method of substrate drugs and their metabolites using a tandem mass spectrometer. This Special Issue has the aim of highlighting current progress in drug metabolism/pharmacokinetics, drug interactions, and bioanalysis.
human liver microsomes --- alcohol addiction --- UGT --- ultra-high-pressure liquid chromatography --- adalimumab --- procainamide --- LC-MS/MS --- DA-9805 --- paeonol --- LC-QTOF-MS/MS --- YRA-1909 --- chlorogenic acid --- immunoprecipitation --- Eurycoma longifolia --- CYP --- caffeic acid --- rat --- pharmaceutical excipient --- Korean red ginseng extract --- Stauntonia hexaphylla leaf extract --- bioanalysis --- HPLC-MS/MS --- B6 --- eurycomanone --- bioavailability --- drying technology --- GB3 --- diclofenac --- 129-Glatm1Kul/J --- aglycone --- caffeic acid O-glucuronides --- organic anion transporting polypeptide --- protein precipitation --- metabolic stability --- Fabry disease --- biopharmaceuticals --- imperatorin --- neochlorogenic acid --- gastric ulcer --- saikosaponin a --- hair --- anthraquinone --- acetyl tributyl citrate --- pharmacokinetics --- brain distribution --- mematine --- ethyl glucuronide --- pharmacokinetic --- loxoprofen --- liquid chromatography-quadrupole TOF MS --- glucuronidation --- esomeprazole --- metformin --- cytochrome P450 --- glycoside --- AUDIT score --- protein stability --- efficacy --- LC-HR/MS --- cryptochlorogenic acid --- aceclofenac --- drug interaction --- liquid chromatography-tandem mass spectrometry --- Osthenol --- plasma --- N-acetylprocainamide --- diabetes --- Drugs --- Metabolism. --- Drug metabolism --- Pharmacokinetics
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The plant-derived polyphenol curcumin has been used in promoting health and combating disease for thousands of years. Its therapeutic effects have been successfully utilized in Ayurvedic and Traditional Chinese Medicine in order to treat inflammatory diseases. Current results from modern biomolecular research reveal the modulatory effects of curcumin on a variety of signal transduction pathways associated with inflammation and cancer. In this context, curcumin’s antioxidant, anti-inflammatory, anti-tumorigenic, and even anti-metastatic activities are discussed. On the cellular level, the reduced activity of several transcription factors (such as NFkB or AP-1) and the suppression of inflammatory cytokines, matrix degrading enzymes, metastasis related genes and even microRNAs are reported. On functional levels, these molecular effects translate into reduced proliferative, invasive, and metastatic capacity, as well as induced tumor cell apoptosis. All these effects have been observed not only in vitro but also in animal models. In combination with anti-neoplastic drugs like Taxol, kinase inhibitors, and radiation therapy, curcumin potentiates the drugs’ therapeutic power and can protect against undesired side effects. Natural plant-derived compounds like curcumin have one significant advantage: They do not usually cause side effects. This feature qualifies curcumin for primary prevention in healthy persons with a predisposition to cancer, arteriosclerosis, or chronic inflammatory diseases. Nonetheless, curcumin is considered safe, although potential toxic effects stemming from high dosages, long-term intake, and pharmacological interactions with other compounds have yet to be assessed. This Special Issue examines in detail and updates current research on the molecular targets, protective effects, and modes of action of natural plant-derived compounds and their roles in the prevention and treatment of human diseases.
minerals --- cancer treatment --- chitosan --- n/a --- neurodegeneration --- antioxidant activity --- senescence --- tumor proliferation --- nanoparticles --- antimicrobial agents --- oxidative metabolites --- drug discovery --- Akt/mTOR signaling --- micronutrients --- ulcerative colitis --- transmission electron microscopy --- metabolic reprogramming --- curcumin --- death receptor --- chaperone-mediated autophagy --- wound healing --- brain ischemia --- autophagy --- Alzheimer’s disease --- genes --- transthyretin --- inflammatory bowel disease --- cellular pathway --- centrifugal partition chromatography --- nutrition --- amyloid --- Curcuma longa --- protein aggregation --- supportive care --- IL-17 --- senolytics --- complementary medicine --- macronutrients --- structure activity relationship --- gastroprotection --- Zingiberaceae --- anti-inflamation --- TLC bioautography --- microbiota --- glioblastoma multiforme --- amyloidosis --- SHMT2 --- antioxidants --- silica --- apoptosis --- reflux esophagitis --- gastric ulcer --- TLC-MS --- anti-cancer --- anticancer --- ImageJ --- anti-tumor --- delivery system --- wound --- Helicobacter pylori --- direct protein binding --- protein misfolding --- tumor growth --- diet --- Crohn’s disease --- hydrostatic counter-current chromatography --- ageing --- renal cell cancer --- gastric cancer --- amino-acids --- STAT3 --- mechanism of action --- inflamm-aging --- mitophagy --- necrotizing enterocolitis --- cell cycling --- vitamins --- turmeric tuber --- cancer --- tau protein --- Alzheimer's disease --- Crohn's disease
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Dyslipidemia, and particularly hypercholesterolemia, remains a main cardiovascular disease risk factor, partly reversible with the improvement of life-style, including dietary, habits. Even when a pharmacological treatment is begun, dietary support to lipid-lowering is always desired. This book will provide a selection of new evidence on the possible lipid-lowering effects of some dietary and medicinal plant components, reporting some interesting reviews, experimental data and results from clinical trials. The book is adapted for experts in nutrition but also for all scientists involved in cardiovascular disease prevention.
beta-glucan --- fiber --- lipid profile --- cholesterol --- intestinal function --- green tea --- epigallocatechin gallate --- chitosan --- microspheres --- Eudragit --- metabolic diseases --- LCD score --- CHNS --- dyslipidemia --- dietary factor --- plant based --- animal based --- Chinese adults --- nutraceuticals --- PCSK9 --- SREBP --- HNF1α --- berberine --- metabolic syndrome --- plant extracts --- natural antioxidant --- polyphenols --- bergamot --- blackcurrant --- liver steatosis --- ovariectomized --- phytoestrogen --- vitamin B12 --- healthy --- Saudi Arabia --- serum cholesterol --- serum triglycerides --- serum low density lipoprotein --- serum high density lipoprotein --- dietary intake --- lifestyle --- black raspberry --- excessive choline --- TMAO --- hypercholesterolemia --- hepatic inflammation --- review --- CVD --- cardiovascular health --- dietary fats --- dietary fiber --- phytosterols --- plant-based diet --- dietary pattern --- sustainability --- propolis --- formononetin --- gastric ulcer --- rats --- Chrysanthemum morifolium Ramat leaves --- obesity --- lipidomics --- liquid chromatography tandem mass spectrometry --- phospholipid --- sphingolipid --- monacolins --- LDL-cholesterol --- red yeast rice --- clinical trial --- endothelial function --- alpha-linolenic acid --- flaxseed --- lipids --- omega-3 --- walnuts --- type 2 diabetes mellitus --- glibenclamide --- omega-3 fatty acids --- high fat diet --- transcription factors --- streptozotocin --- Armolipid Plus® --- nutraceutical --- supplementation --- blood pressure --- fasting plasma glucose --- n/a
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Dyslipidemia, and particularly hypercholesterolemia, remains a main cardiovascular disease risk factor, partly reversible with the improvement of life-style, including dietary, habits. Even when a pharmacological treatment is begun, dietary support to lipid-lowering is always desired. This book will provide a selection of new evidence on the possible lipid-lowering effects of some dietary and medicinal plant components, reporting some interesting reviews, experimental data and results from clinical trials. The book is adapted for experts in nutrition but also for all scientists involved in cardiovascular disease prevention.
Public health & preventive medicine --- beta-glucan --- fiber --- lipid profile --- cholesterol --- intestinal function --- green tea --- epigallocatechin gallate --- chitosan --- microspheres --- Eudragit --- metabolic diseases --- LCD score --- CHNS --- dyslipidemia --- dietary factor --- plant based --- animal based --- Chinese adults --- nutraceuticals --- PCSK9 --- SREBP --- HNF1α --- berberine --- metabolic syndrome --- plant extracts --- natural antioxidant --- polyphenols --- bergamot --- blackcurrant --- liver steatosis --- ovariectomized --- phytoestrogen --- vitamin B12 --- healthy --- Saudi Arabia --- serum cholesterol --- serum triglycerides --- serum low density lipoprotein --- serum high density lipoprotein --- dietary intake --- lifestyle --- black raspberry --- excessive choline --- TMAO --- hypercholesterolemia --- hepatic inflammation --- review --- CVD --- cardiovascular health --- dietary fats --- dietary fiber --- phytosterols --- plant-based diet --- dietary pattern --- sustainability --- propolis --- formononetin --- gastric ulcer --- rats --- Chrysanthemum morifolium Ramat leaves --- obesity --- lipidomics --- liquid chromatography tandem mass spectrometry --- phospholipid --- sphingolipid --- monacolins --- LDL-cholesterol --- red yeast rice --- clinical trial --- endothelial function --- alpha-linolenic acid --- flaxseed --- lipids --- omega-3 --- walnuts --- type 2 diabetes mellitus --- glibenclamide --- omega-3 fatty acids --- high fat diet --- transcription factors --- streptozotocin --- Armolipid Plus® --- nutraceutical --- supplementation --- blood pressure --- fasting plasma glucose --- beta-glucan --- fiber --- lipid profile --- cholesterol --- intestinal function --- green tea --- epigallocatechin gallate --- chitosan --- microspheres --- Eudragit --- metabolic diseases --- LCD score --- CHNS --- dyslipidemia --- dietary factor --- plant based --- animal based --- Chinese adults --- nutraceuticals --- PCSK9 --- SREBP --- HNF1α --- berberine --- metabolic syndrome --- plant extracts --- natural antioxidant --- polyphenols --- bergamot --- blackcurrant --- liver steatosis --- ovariectomized --- phytoestrogen --- vitamin B12 --- healthy --- Saudi Arabia --- serum cholesterol --- serum triglycerides --- serum low density lipoprotein --- serum high density lipoprotein --- dietary intake --- lifestyle --- black raspberry --- excessive choline --- TMAO --- hypercholesterolemia --- hepatic inflammation --- review --- CVD --- cardiovascular health --- dietary fats --- dietary fiber --- phytosterols --- plant-based diet --- dietary pattern --- sustainability --- propolis --- formononetin --- gastric ulcer --- rats --- Chrysanthemum morifolium Ramat leaves --- obesity --- lipidomics --- liquid chromatography tandem mass spectrometry --- phospholipid --- sphingolipid --- monacolins --- LDL-cholesterol --- red yeast rice --- clinical trial --- endothelial function --- alpha-linolenic acid --- flaxseed --- lipids --- omega-3 --- walnuts --- type 2 diabetes mellitus --- glibenclamide --- omega-3 fatty acids --- high fat diet --- transcription factors --- streptozotocin --- Armolipid Plus® --- nutraceutical --- supplementation --- blood pressure --- fasting plasma glucose
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Mitogen-activated protein kinases (MAPK) are a large family of enzymes that function as signal transducers to regulate a diverse range of physiological responses. However, signaling via extracellular signal-regulated kinase (ERK), c-Jun amino terminal kinase (JNK), and p38 MAPK also underpin many disease processes. This Special Issue provides new insights into how MAPK signaling contributes to specific pathological processes across a range of conditions, including disorders of lung development, type 2 diabetes, proliferative skin diseases, cardiovascular diseases, and neurological diseases.
Research & information: general --- Biology, life sciences --- Rabdosia inflexa --- inflammation --- gastric ulcer --- cytokines --- MAPK --- NF-κB --- extracellular signal-regulated kinases 1/2 --- hyperoxia --- bronchopulmonary dysplasia --- HPAECs --- angiogenesis --- cell cycle --- SIRT1 --- oxidative stress --- psoriasis --- antimicrobial peptide --- cecropin A --- tight junction protein --- MEK/ERK signaling --- porcine intestinal epithelial cell --- extracellular signal-regulated kinase 5 (ERK5) --- Kv4.2 --- PC12 cells --- infantile myofibromatosis --- receptor tyrosine kinases --- platelet-derived growth factor receptor --- protein kinase inhibitors --- sunitinib --- erlotinib --- FR180204 --- U0126 --- targeted therapy --- apoptosis --- ERK1/2 --- JNKs --- mitochondrial dysfunction --- neurodegeneration --- neuro-inflammation --- p38 MAPKs --- Parkinson's disease --- mitogen-activated protein kinases (MAPKs) --- MAPK kinetics --- osteoclast differentiation --- bone remodeling --- DAPK --- ERK --- p38 --- JNK --- mitogen-activated protein kinase pathway (MAPK pathway) --- protein tyrosine phosphatase interacting protein 51 (PTPIP51) --- protein-protein interaction (PPI) --- cancer signaling --- SR --- CR --- Compatibility --- T2DM --- metabolic profiling --- MAPK/PI3K/Akt signaling pathway --- reactive oxygen species --- PTPN6 --- SRC --- DOK4 --- MKK4 --- MKK7 --- p53 --- DUSP1 --- SIRT2 --- atherosclerosis --- aortic valve sclerosis --- aortic valve stenosis --- naphthalimide-metal complex conjugates --- N-heterocyclic carbene --- mitochondria --- ROS --- p38 MAPK --- cancer --- FGF-induced signaling --- FRS2 --- phosphorylation --- downregulation --- Rabdosia inflexa --- inflammation --- gastric ulcer --- cytokines --- MAPK --- NF-κB --- extracellular signal-regulated kinases 1/2 --- hyperoxia --- bronchopulmonary dysplasia --- HPAECs --- angiogenesis --- cell cycle --- SIRT1 --- oxidative stress --- psoriasis --- antimicrobial peptide --- cecropin A --- tight junction protein --- MEK/ERK signaling --- porcine intestinal epithelial cell --- extracellular signal-regulated kinase 5 (ERK5) --- Kv4.2 --- PC12 cells --- infantile myofibromatosis --- receptor tyrosine kinases --- platelet-derived growth factor receptor --- protein kinase inhibitors --- sunitinib --- erlotinib --- FR180204 --- U0126 --- targeted therapy --- apoptosis --- ERK1/2 --- JNKs --- mitochondrial dysfunction --- neurodegeneration --- neuro-inflammation --- p38 MAPKs --- Parkinson's disease --- mitogen-activated protein kinases (MAPKs) --- MAPK kinetics --- osteoclast differentiation --- bone remodeling --- DAPK --- ERK --- p38 --- JNK --- mitogen-activated protein kinase pathway (MAPK pathway) --- protein tyrosine phosphatase interacting protein 51 (PTPIP51) --- protein-protein interaction (PPI) --- cancer signaling --- SR --- CR --- Compatibility --- T2DM --- metabolic profiling --- MAPK/PI3K/Akt signaling pathway --- reactive oxygen species --- PTPN6 --- SRC --- DOK4 --- MKK4 --- MKK7 --- p53 --- DUSP1 --- SIRT2 --- atherosclerosis --- aortic valve sclerosis --- aortic valve stenosis --- naphthalimide-metal complex conjugates --- N-heterocyclic carbene --- mitochondria --- ROS --- p38 MAPK --- cancer --- FGF-induced signaling --- FRS2 --- phosphorylation --- downregulation
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Mitogen-activated protein kinases (MAPK) are a large family of enzymes that function as signal transducers to regulate a diverse range of physiological responses. However, signaling via extracellular signal-regulated kinase (ERK), c-Jun amino terminal kinase (JNK), and p38 MAPK also underpin many disease processes. This Special Issue provides new insights into how MAPK signaling contributes to specific pathological processes across a range of conditions, including disorders of lung development, type 2 diabetes, proliferative skin diseases, cardiovascular diseases, and neurological diseases.
Rabdosia inflexa --- inflammation --- gastric ulcer --- cytokines --- MAPK --- NF-κB --- extracellular signal-regulated kinases 1/2 --- hyperoxia --- bronchopulmonary dysplasia --- HPAECs --- angiogenesis --- cell cycle --- SIRT1 --- oxidative stress --- psoriasis --- antimicrobial peptide --- cecropin A --- tight junction protein --- MEK/ERK signaling --- porcine intestinal epithelial cell --- extracellular signal-regulated kinase 5 (ERK5) --- Kv4.2 --- PC12 cells --- infantile myofibromatosis --- receptor tyrosine kinases --- platelet-derived growth factor receptor --- protein kinase inhibitors --- sunitinib --- erlotinib --- FR180204 --- U0126 --- targeted therapy --- apoptosis --- ERK1/2 --- JNKs --- mitochondrial dysfunction --- neurodegeneration --- neuro-inflammation --- p38 MAPKs --- Parkinson’s disease --- mitogen-activated protein kinases (MAPKs) --- MAPK kinetics --- osteoclast differentiation --- bone remodeling --- DAPK --- ERK --- p38 --- JNK --- mitogen-activated protein kinase pathway (MAPK pathway) --- protein tyrosine phosphatase interacting protein 51 (PTPIP51) --- protein-protein interaction (PPI) --- cancer signaling --- SR --- CR --- Compatibility --- T2DM --- metabolic profiling --- MAPK/PI3K/Akt signaling pathway --- reactive oxygen species --- PTPN6 --- SRC --- DOK4 --- MKK4 --- MKK7 --- p53 --- DUSP1 --- SIRT2 --- atherosclerosis --- aortic valve sclerosis --- aortic valve stenosis --- naphthalimide-metal complex conjugates --- N-heterocyclic carbene --- mitochondria --- ROS --- p38 MAPK --- cancer --- FGF-induced signaling --- FRS2 --- phosphorylation --- downregulation --- n/a --- Parkinson's disease
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