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Early neonatal handling of rat pups produces dampened hypothalamic-pituitary-adrenal axis reactivity to stress in adult male offspring. However, less is known about whether there is a similar effect for females. Although, most studies of neonatal handling have examined subsequent effects during adulthood, adolescence is an important developmental stage for stress responsivity. To address these issues, the effect of neonatal handling on the endocrine stress response and brain activity of male and female rats was determined in response to acute restraint stress during adolescence. Consistent with previous findings in adult males, neonatal handling reduced restraint stress-induced hormone levels in adolescent males. However, in contrast, we found elevated plasma hormone concentrations in handled females. A gender-specific handling effect on brain activity was also evident, with significantly increased stress-induced activation of the posterior cingulate cortex of handled females, as measured by c-fos mRNA expression. The striking gender difference in the effect of early neonatal handling provides evidence that this must be considered as an important variable in subsequent stress responsivity induced by early manipulations.

Activation. --- Activity. --- Adolescence. --- Adult. --- Adulthood. --- Brain. --- C-fos. --- Cortex. --- Corticosterone. --- Endocrine. --- Expression. --- Female rats. --- Female. --- Females. --- Gender. --- Handling. --- Hormone. --- Hypothalamic-pituitary-adrenal axis. --- Hypothalamic-pituitary-adrenal. --- Level. --- Male. --- Males. --- Neonatal handling. --- Neonatal. --- Plasma. --- Posterior cingulate cortex. --- Pups. --- Rat. --- Rats. --- Reactivity. --- Response. --- Restraint stress. --- Restraint. --- Sex differences. --- Stress reactivity. --- Stress response. --- Stress-response. --- Stress. --- Striking.

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The present study aimed to determine whether the medial prefrontal cortex (mPFC) (prelimbic and infralimbic regions) is implicated in the integration of a stress response. Sprague-Dawely rats were implanted with telemetry probes and guide cannulae so that either muscimol or vehicle could be administered locally within the mPFC or dorsomedial hypothalamus (DMH). The heart rate and blood pressure of rats was continuously recorded as either muscimol or vehicle was administered centrally and rats were either exposed to restraint stress or left alone in their home cages. After the stress challenge, or equivalent period, rats that had received intra-mPFC injections were processed for immunohistochemical detection of Fos throughout the neuraxis. Bilateral microinjection of muscimol into the mPFC had no effect upon either baseline cardiovascular parameters or restraint stress-induced tachycardia or pressor responses whereas, in the DMH, pretreatment with muscimol attenuated the cardiovascular stress response. Analysis of Fos expression throughout the CNS of nonstressed rats showed no effect of muscimol injections into the mPFC on baseline expression in the nuclei examined. In contrast, rats that had received muscimol injections into their mPFC and were subsequently restrained exhibited an increase in the number of Fos-positive cells in the DMH, medial amygdala, and medial nucleus tractus solitarius as compared to vehicle-injected rats that experienced restraint stress. These results indicate that, during acute psychological stress, the mPFC does not modulate the cardiovascular system in rats but does inhibit specific subcortical nuclei to exert control over aspects of an integrated response to a stressor

Amygdala. --- Analysis. --- Blood pressure. --- Blood-pressure. --- Blood. --- C-fos expression. --- Cage. --- Cages. --- Cardiovascular system. --- Cardiovascular-system. --- Cardiovascular. --- Cingulate cortex. --- Control. --- Cortex. --- Dorsomedial hypothalamus. --- Excitotoxic lesions. --- Expression. --- Fos. --- Frontal-cortex. --- Heart rate. --- Heart-rate. --- Hypothalamus. --- Increase. --- Infralimbic cortex. --- Infralimbic. --- Injections. --- Medial amygdala. --- Medial prefrontal cortex. --- Microinjection. --- Norepinephrine release. --- Nucleus tractus solitarius. --- Nucleus-accumbens. --- Nucleus. --- Parameters. --- Prefrontal cortex. --- Prelimbic. --- Psychological stress. --- Rat. --- Rats. --- Response. --- Responses. --- Restraint stress. --- Restraint. --- Stress response. --- Stress-response. --- Stress. --- Stressor. --- System. --- Tachycardia. --- Telemetry. --- Time.

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Cellular Responses to Stress brings together a group of scientists who work on different but interrelated aspects of cellular stress responses. The book provides state-of-the-art information on the wide spectrum of ways in which cells can respond to different forms of stress induced by chemicals, oxidants, and DNA-damaging agents. Mechanisms are described that involve altered uptake and efflux of chemical agents, intracellular detoxification, and DNA damage responses. Many of these changes trigger a cascade of reactions mediated by stress-activated signaling pathways, which have the capacity to determine whether a cell will survive or die. The spectrum of topics covered in this book aims to provide a broad overview of our current knowledge of the different forms of adaptive response systems.It is hoped that this text will stimulate further research to establish the relative cellular role of specific response pathways and will enable us to gain a deeper understanding of the mechanisms that allow cells to live or die. This book will be valued by university researchers at all levels, industrial scientists in the pharmaceutical and biotechnology industries, and clinical researchers.Originally published in 1999.The Princeton Legacy Library uses the latest print-on-demand technology to again make available previously out-of-print books from the distinguished backlist of Princeton University Press. These editions preserve the original texts of these important books while presenting them in durable paperback and hardcover editions. The goal of the Princeton Legacy Library is to vastly increase access to the rich scholarly heritage found in the thousands of books published by Princeton University Press since its founding in 1905.

Stress (Physiology) --- Cell metabolism --- Cellular control mechanisms --- Cells --- Metabolism --- Regulation --- AMPK. --- ASK1. --- Actin. --- Activation. --- Angiogenesis. --- Antibody. --- Antigen. --- Apoptosis. --- Autoimmunity. --- Autophosphorylation. --- C-Fos. --- C-Jun N-terminal kinases. --- C-terminus. --- Cell Cycle Arrest. --- Cell Line, Transformed. --- Cell cycle. --- Cell membrane. --- Cell migration. --- Cell surface receptor. --- Cellular differentiation. --- Cellular stress response. --- Conformational change. --- Cytochrome P450. --- Cytokine receptor. --- Cytokine. --- Cytotoxicity. --- DNA-PKcs. --- Drug metabolism. --- Ectopic expression. --- Effector (biology). --- Endonuclease. --- Enzyme. --- Epidermal growth factor receptor. --- Epidermal growth factor. --- Extracellular signal–regulated kinases. --- Fibroblast growth factor. --- Gene expression. --- Gene therapy. --- Gene. --- Germinal center. --- Glutathione S-transferase. --- HMG-CoA reductase. --- Heat shock. --- Histidine kinase. --- Hormone-sensitive lipase. --- Hsp27. --- Immortalised cell line. --- Immunodeficiency. --- Immunoglobulins. --- Immunoprecipitation. --- In vitro. --- Inducer. --- Inflammation. --- Jurkat cells. --- Kinase. --- Lymphotoxin. --- Macrophage colony-stimulating factor. --- Mechanism of action. --- Mechanistic target of rapamycin. --- Metabolism. --- Mitogen-activated protein kinase kinase. --- Mitogen-activated protein kinase. --- Mitogen. --- Mitosis. --- Model organism. --- Neuropeptide. --- Neurotoxin. --- Osmotic shock. --- Oxidative phosphorylation. --- Oxidative stress. --- P38 mitogen-activated protein kinases. --- Pathogenesis. --- Peptide. --- Peroxidase. --- Phosphatase. --- Phosphoinositide 3-kinase. --- Phosphorylation cascade. --- Phosphorylation. --- Post-translational modification. --- Protease. --- Protein kinase. --- Protein phosphorylation. --- Protein synthesis inhibitor. --- Protein. --- Proteolysis. --- RNA interference. --- Receptor (biochemistry). --- Receptor tyrosine kinase. --- Repressor. --- Response element. --- Signal transduction. --- Ternary Complex Factors. --- Thrombin. --- Transcription factor. --- Transcriptional regulation. --- Transfection. --- Transposable element. --- Tumor necrosis factor superfamily. --- Turgor pressure. --- Vascular endothelial growth factor.

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The sensation of flavor reflects the complex integration of aroma, taste, texture, and chemesthetic (oral and nasal irritation cues) from a food or food component. Flavor is a major determinant of food palatability—the extent to which a food is accepted or rejected—and can profoundly influence diet selection, nutrition, and health. Despite recent progress, gaps in knowledge still remain regarding how taste and flavor cues are detected at the periphery, conveyed by the brainstem to higher cortical levels, and then interpreted as a conscious sensation. Taste signals are also projected to central feeding centers where they can regulate hunger and fullness. Individual differences in sensory perceptions are also well known and can arise from genetic variation, environmental causes, or a variety of metabolic diseases, such as obesity, metabolic syndrome, and cancer. Genetic taste/smell variation could predispose individuals to these same diseases. Recent findings have opened new avenues of inquiry, suggesting that fatty acids and carbohydrates may provide nutrient-specific signals informing the gut and brain of the nature of the ingested nutrients. This Special Issue, Taste, Nutrition, and Health, presents original research communications and comprehensive reviews on topics of broad interest to researchers and educators in sensory science, nutrition, physiology, public health, and health care.

Research & information: general --- Biology, life sciences --- Food & society --- acceptability --- food development --- sensory attributes --- CATA --- dietotherapy --- aromas --- linoleic acid --- gustation --- hedonic --- BDNF --- fat taste --- c-Fos --- Zif-268 --- Glut-1 --- sweeteners --- sugar reduction --- psychophysical dose-response --- sweetness growth rate --- sweetness potency --- cross-cultural --- food liking --- sensory --- questionnaire --- fMRI --- caffeine --- taste --- memory --- sensory evaluation --- tea --- EGCG --- hedonics --- sweet taste --- psychophysics --- nutrition --- diet --- threshold --- intensity --- liking --- sweetness --- taste test --- individual differences --- classification method --- taste perception --- umami --- carbohydrate --- sweet --- salt --- bitter --- physical activity --- basic tastes --- taste reception --- smell --- dysgeusia --- burning sensation --- halitosis --- saliva --- caries --- primary Sjögren’s syndrome --- non-SS sicca syndrome --- sweet liking --- fat liking --- e-cigarettes --- body mass index --- dietary behaviors --- tobacco --- cigarettes --- chronic smoking --- electrophysiological recording from human tongue --- fat perception --- CD36 --- PROP tasting --- grapefruit --- consumer --- naringin --- aroma --- color --- satiety --- tastants --- food intake --- intraduodenal infusion --- intraileal infusion --- overweight --- weight management --- Obesity --- eating behavior --- prebiotics --- microbiota --- sex differences --- biopsychosocial --- children --- brain imaging --- smell sensitivity --- olfaction --- staircase --- QUEST --- choice --- familiarity --- PROP --- food neophobia --- sensitivity to disgust --- sensitivity to punishment --- vegetables --- caffeinated beverages --- bitterness --- astringency --- taste preference questionnaire --- validation --- European children --- adolescents --- adults --- genetics --- food preferences --- heritability --- candidate gene --- GWAS --- adiposity --- polygenic risk score --- n/a --- primary Sjögren's syndrome

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In this Special Issue, we have published papers on the health-promoting effects of nutraceuticals from different sources, and their effects in different pathologies. Extracts from plants have been analyzed, for example, extracts from olive leaves, Mikania micrantha, the devil’s claw, raspberries and others, alongside marine phytoplankton, egg-yolk and marketed dietary supplements. The effects of these extracts and dietary supplements have been studied in diseases associated with obesity, and in diseases where inflammation pathways are involved. The effectiveness of resveratrol and curcumin to support the anticancer activity of cisplatin has also been reported, as well as the ability of devil’s claw root extract to stimulate the CB2 receptors in synoviocytes in osteoarthritis patients. The anti-oxidant effect of marine phytoplankton has been studied on muscle damage, both in humans and in an animal model, and the effects of the metabolite of antocianin were analyzed in a mouse model of amyotrophic lateral sclerosis. Finally, reviews on the use of lactoferrin, ω3 and ω6 and abscisic acid have been reported, in addition to the crosstalk between prostate cancer and microbiota inflammation. Although it is not yet possible to draw definitive conclusions on the use of nutraceuticals, several mechanisms of action for many of them have been further clarified.

Humanities --- Social interaction --- fertility --- ingredients --- male reproduction --- semen parameters --- supplements --- allithiamine --- garlic --- hyperglycaemia --- advanced glycation end-products --- cytokines --- abscisic acid --- prediabetes --- type 2 diabetes mellitus --- metabolic syndrome --- insulin resistance --- adipocyte browning --- AMP-activated protein kinase --- food supplement --- frambinone --- meal frequency --- open-field test --- elevated plus maze --- sensory motor gating --- pre-pulse inhibition --- c-Fos --- amyotrophic lateral sclerosis --- anti-inflammatory --- antioxidant --- phenolic acid --- neuroprotective --- neurodegeneration --- obesity --- overweight --- beta-glucans --- chitosan --- follow up study --- weight loss programs --- weight gain --- weight loss --- body weight changes --- phytoplankton --- antioxidants --- muscle damage --- muscle recovery --- muscle soreness --- Viburnum opulus --- phenolic compounds --- adipogenesis --- PPARγ --- lipase inhibition --- green tea --- epigallocatechin --- lipid profile --- high-fat diet --- fast food --- osteoarthritis --- nutraceuticals --- polyphenols --- volatile compounds --- β-caryophyllene --- eugenol --- FAAH --- cannabinoid receptors --- phospholipases --- lactoferrin --- bovine milk --- nutraceutical --- human health --- resveratrol --- curcumin --- cisplatin --- head and neck cancer --- cell cycle --- apoptosis --- prostate cancer --- microbiota --- nutraceutical compounds --- fecundation --- inflammation --- cytokine --- growth factors --- metabolomics --- lipidomics --- ω-3PUFAs --- ω-6PUFAs --- endocannabinoids --- CRC --- fatty acids --- Gymnema inodorum --- gymnemic acid --- Mikania micrantha --- anti-hypercholesterolemia --- steatosis --- olive leaf --- macrophages