1,720,992 research outputs found
Stress and Obesity as Risk Factors in Cardiovascular Diseases: A Neuroimmune Perspective
No full textObesity is now growing at an alarming rate reaching epidemic proportions worldwide thus increasing morbidity and mortality rates for chronic disease. But although we have ample information on the complications associated with obesity, precisely what causes obesity remains poorly understood. Some evidence attributes a major role to a low-grade chronic inflammatory state (neurogenic inflammation) induced in obesity by inflammatory mediators produced and secreted within the expanded activated adipocyte pool. Adipose tissue is an endocrine organ that secretes numerous adipose tissue-specific or enriched hormones, known as adipokines, cytokine-like molecules thought to play a pathogenic role in cardiovascular diseases. The imbalance between increased inflammatory stimuli and decreased anti-inflammatory mechanisms may depend on chronic stress. Hence the positive correlation found between stress, obesity and cardiovascular diseases. The chronic inflammatory state associated with insulin resistance and endothelial dysfunction is highly deleterious for vascular function. This review focuses on the proposed neuroimmunodulatory mechanisms linking chronic (psychological) stress, obesity and cardiovascular diseases
Stress-induced cytokines and neuronal dysfunction in Alzheimer's disease
No full textIncreasing evidence has been accumulating about the role of stress as an important challenge to the onset and progression of Alzheimer's disease (AD). The hippocampus, one of the areas of the brain damaged during AD, was the first brain region, besides the hypothalamus, to be recognized as a target of stress hormones, including cortisol, sympathetic and parasympathetic transmitters, cytokines, and metabolic hormones. The present review aims at summarizing neuroinflammatory mechanisms induced by stress, resulting in neuronal dysfunction and impaired neurogenesis. Lifestyle and environmental factors related to metabolic and inflammatory alterations observed in stressed subjects and thought to favor AD development and progression, as well as the possible ways of prevention, are discussed
Leptin,ghrelin and TNF-alpha before and after traditional Chinese diet and auricular acupuncture.
No full textAlzheimer's disease promotion by obesity: induced mechanisms-molecular links and perspectives.
Full text linkThe incidence of AD is increasing in parallel with the increase in life expectancy. At the same time the prevalence of metabolic syndrome and obesity is reaching epidemic proportions in western populations. Stress is one of the major inducers of visceral fat and obesity development, underlying accelerated aging processes. Adipose tissue is at present considered as an active endocrine organ, producing important mediators involved in metabolism regulation as well as in inflammatory mechanisms. Insulin and leptin resistance has been related to the dysregulation of energy balance and to the induction of a chronic inflammatory status which have been recognized as important cofactors in cognitive impairment and AD initiation and progression. The aim of this paper is to disclose the correlation between the onset and progression of AD and the stress-induced changes in lifestyle, leading to overnutrition and reduced physical activity, ending with metabolic syndrome and obesity. The involved molecular mechanisms will be briefly discussed, and advisable guide lines for the prevention of AD through lifestyle modifications will be proposed
Modification of lymphocyte subsets in patients with rhinoscleroma
No full textPURPOSE: Rhinoscleroma is a rare, chronic, granulomatous disorder of the upper airways. This disease presents some etiopathogenetic aspects that are not yet clear. Infection by Klebsiella rhinoscleromatis is fundamental for the onset of the disease, but it is impossible to reproduce rhinoscleroma experimentally only via infection with the bacteria both in man and in animals. Furthermore, this disease mainly affects blood-related people and occurs in certain geographic areas. In this context, we present a study that brings to light some of the quantitative abnormalities of the lymphocyte subsets. MATERIALS AND METHODS: The study group consisted of 5 patients with rhinoscleroma. The following parameters were studied for each patient: clinical manifestations, histologic examinations, number of leukocytes, lymphocytes, and lymphocyte subsets. RESULTS: In all patients, we noted the following: There was a relative reduction of the CD4+ cells, an absolute increase of the CD8+ cells, and an inversion of the CD4+/CD8+ ratio. There was an absolute increase of the CD56+ cells and cytotoxic cells that coexpress CD8+CD56+ antigens. There was a relative reduction of the CD3+ cells, and the CD19+ cells tended to show an ambiguous behavioral pattern. CONCLUSION: We believe that K. rhinoscleromatis does not play a major role in the etiopathogenesis of rhinoscleroma. However, we do believe that the anomalous behavior of the immune system can favor rhinoscleroma
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