Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 157 sera from adults and children with rheumatoid arthritis, rheumatic fever, myocarditis, neurodermite, bronchial asthma, wound infections, second degree obesity without symptoms of diabetes were examined. 60% of sera contained high concentrations of antibodies possessing cytotoxicity against thymus cells, but not against bone marrow cells. Sera of healthy children and adults contained no cytotoxic antibodies. Sera cytotoxic against mouse thymus cells inhibited the suppressing activity of mouse splenocytes in experiments on syngeneic transfer, reducing the ability of human lymphocytes to form T-RFC. The latter phenomenon is associated with the decline in the number of T-theophyllin-sensitive lymphocytes, known as T-suppressors.
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PMID:[Antilymphocyte antibodies in various human diseases as a factor of reduced functional activity of T-suppressors]. 294 95

157 sera from adults and children with rheumatoid arthritis, rheumatic fever, myocarditis, neurodermatitis, bronchial asthma, wound infections, second degree obesity without symptoms of diabetes were examined. 60% of sera contained high concentrations of antibodies possessing cytotoxicity against thymus cells, but not against bone marrow cells. Sera of healthy children and adults contained no cytotoxic antibodies. Sera cytotoxic against mouse thymus cells inhibited the suppressing activity of mouse splenocytes in experiments on syngeneic transfer, reducing the ability of human lymphocytes to form T-RFC. The latter phenomenon is associated with the decline in the number of T-theophylline-sensitive lymphocytes, known as T-suppressors.
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PMID:[Antilymphocytic antibodies in human diseases as a factor decreasing the functional activity of T-suppressors]. 294 28

Severe thyroid atrophy was found at the autopsy of a 39-year-old white woman who died of myocarditis, probably of viral etiology. Prolonged ingestion of thyroid hormone for the treatment of obesity appears to be the only plausible explanation for the atrophy, secondary to suppression of the pituitary thyrotrope.
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PMID:Severe thyroid atrophy due to prolonged ingestion of thyroid hormone for treatment of obesity. 670 2

The dynamics in schoolchildren's health status varies in time, as the incidence of some chronic diseases decreases and that of the others increases. As a result, the health status of schoolchildren has deteriorated due to a reduction in the number of healthy children and an increase in the number of chronic patients in the past 30 years. Nervous, immune (allergic), and blood diseases have become frequent. Chronic ENT diseases have been encountered more infrequently due to the noticeable reduction in the incidence rates of tonsillitis and otitis. The positive trend is that schoolchildren have no rheumatism, infective allergic myocarditis, chronic pneumonia and diffuse glomerulonephritis and that the prevalence of locomotor disorders, renal and metabolic (obesity) diseases is low. During school time, the health status of children slightly improves due to the lower incidence rates of chronic diseases and the higher proportion of healthy children, but it has remained still worse than it was 30 years ago. The formation of chronic diseases has been found to occur in health group II children, who have morphological and functional changes, in 50% of cases from the first to the sixth forms and in 20% of cases from the seventh to the tenth forms. The present-day children are characterized by a combination of abnormalities and functional disturbances. This all require active and timely prophylactic measures to block chronization at the premorbid stage. Lifestyle (to keep the hygienic school regime, to do exercises and to go in for sports), sociohygienic conditions and genetic factors have profound effects on the health status.
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PMID:[The health status dynamics of schoolchildren and the importance of biomedical factors in its development]. 768 98

Hypertension is the commonest cardiovascular disease in Africans occurring in more than 15% of the adult population in some studies. It occurs in the lower as much as in the higher socio-economic groups. Recent studies have confirmed earlier findings that essential hypertension in Africans is characterised by volume loading, low plasma renin activity, high salt taste threshold, high urinary sodium and low potassium excretion and high plasma aldosterone. The commonest complication of hypertension in Africans is congestive cardiac failure followed by cerebrovascular accidents. Coronary heart disease is rare. Even in the absence of overt heart failure and compounding factors like obesity, alcoholism, cigarette smoking, diabetes mellitus and myocarditis, evidence of abnormal left ventricular morphology and function is often present in newly diagnosed patients with moderate or severe hypertension. Response to monotherapy with beta-blockers or ACE inhibitors is usually poor but is good with thiazide diuretics or calcium channel blockers. The diuretics are an essential component of a two or three drug regime containing other classes of antihypertensive drugs. Cost of drugs is the most important determinant of compliance with drug treatment and consequently the likelihood of progression of the diseases to more severe forms in long term follow-up.
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PMID:Hypertension in Africa and effectiveness of its management with various classes of antihypertensive drugs and in different socio-economic and cultural environments. 826 3

An autopsy case of carbamazepine overdose with focal myocarditis is reported. The decedent was a 33-year-old female with a history of schizophrenia and bipolar disorder, who reportedly took 5-day dose of prescribed medications at around midnight. Although she stayed home following the direction of the physician, she was pronounced dead 8h after the intake. At autopsy she was obese, and her face was slightly swollen. The 420 g heart was free of coronary atherosclerosis, and the myocardium had no obvious scars. Both the left and right lungs were markedly congested and edematous. Strong congestion was also noted in the brain and visceral organs. Microscopic examination disclosed focal infiltration of inflammatory cells, most of which were lymphocytes, into the myocardium. In the toxicological analyses, carbamazepine concentration in the blood was 9.9 microg/ml, and other medications were below the toxic levels. It was considered that under the compromised cardiac function due to myocarditis presumably induced by some prescribed medications, and obesity, the carbamazepine overdose deteriorated her condition by triggering critical arrhythmia or congestive heart failure.
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PMID:A case of carbamazepine overdose with focal myocarditis. 1682 Mar 15

Obesity is an important risk factor for heart disease. Whether weight loss affects the severity of heart failure induced by viral myocarditis is a matter of debate. We hypothesized that weight loss could improve cardiac dysfunction by inducing cardiac expression of a cardioprotective cytokine, adiponectin. We examined the relationship between weight loss by food restriction and heart failure due to viral myocarditis in obese KKAy mice. We intraperitoneally injected encephalomyocarditis virus (500 plaque-forming units/mouse) into KKAy mice fed ad libitum as a control (CF) or 60% restriction of that eaten by ad libitum (RF). The 14-day survival rate was 0% in FF, whereas it was 23% in RF (P<0.01). Heart weight/body weight ratio in RF was lower than that in FF on day 5 after viral inoculation (P<0.05). Histological scores for myocardial necrosis and inflammation on day 5 were significantly lower in RF than in FF (P<0.05). Circulating adiponectin level on day 0 was significantly elevated in RF compared with that in FF (32+9 vs. 22+2 microg/mL, P<0.05). Comparative expression of cardiac adiponectin mRNA in RF was significantly higher than that in FF (5.1+0.3 vs. 1+0.2, P<0.05). Cardiac tumor necrosis factor-alpha (TNF-alpha) mRNA in RF was significantly decreased compared with that in FF on day 5 (P<0.05). Cardiac expression of nuclear factor kappa B was reduced and that of peroxisome proliferator-activated receptor gamma mRNA was increased in RF in comparison with FF on day 0. Cardiac adiponectin mRNA was negatively correlated with cardiac TNF-alpha mRNA (r=-0.555; P=0.0097). Weight loss improved the survival and myocardial damage in obese mice with viral myocarditis, with cardiac induction of adiponectin. The induction of adiponectin might provide benefit through a cardioprotective effect against acute heart failure due to viral myocarditis in obese subjects.
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PMID:Reduced-energy diet improves survival of obese KKAy mice with viral myocarditis: induction of cardiac adiponectin expression. 1727 7

The measurement of cardiac troponins (cTn) is of considerable usefulness in the diagnosis of acute coronary syndrome. Abnormal levels of serum cTn are occasionally found in patients who are not suffering a myocardial infarction. This may be observed in several well-known situations including pulmonary embolism, pericarditis, myocarditis, coronary vasospasm, sepsis, congestive heart failure, supraventricular tachycardia with hemodynamic compromise, re-nal insufficiency, and prolonged strenuous endurance exercise. Endogenous antibodies such as heterophile antibodies, rheumatoid factor, and other autoantibodies are known to interfere with the immunoassay measurements of many different analytes, including the widely used Abbot AxSYM cTnI analyzer. Other sources of circulating antibodies include immunotherapies, vaccinations, or blood transfusions that may interfere with these immunoassays as well. We examine the case of a 48-year-old man with a history of hypercholesterolemia and obesity who presented with chest pain and was found to have elevated Tn I levels on two separate occasions. Further work-up revealed that the Tn I levels were spuriously elevated because the patient's blood revealed a normal cTnI level when mixed with polyethylene glycol to inactivate any antibodies interfering with the cTnI assay.
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PMID:Falsely elevated cardiac troponin I levels. 1732 64

The number one cause of mortality in the US is cardiovascular related disease. Future predictions do not see a reduction in this rate especially with the continued rise in obesity [P. Poirier, et al., Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss, Arterioscler Thromb Vasc Biol. 26(5), (2006) 968-976.; K. Obunai, S. Jani, G.D. Dangas, Cardiovascular morbidity and mortality of the metabolic syndrome, Med.Clin. North Am., 91(6), (2007) 1169-1184]. Even so, potential molecular therapeutic targets for cardiac gene delivery are in no short supply thanks to continuing advances in molecular cardiology. However, efficient and safe delivery remains a bottleneck in clinical gene therapy [O.J. Muller, H.A. Katus, R. Bekeredjian, Targeting the heart with gene therapy-optimized gene delivery methods, Cardiovasc Res, 73(3), (2007) 453-462]. Viral vectors are looked upon favorably for their high transduction efficiency, although their ability to elicit toxic immune responses remains [C.F. McTiernan, et al., Myocarditis following adeno-associated viral gene expression of human soluble TNF receptor (TNFRII-Fc) in baboon hearts, Gene Ther, 14(23), (2007) 1613-1622]. However, this high transduction does not necessarily translate into improved efficacy [X. Hao, et al., Myocardial angiogenesis after plasmid or adenoviral VEGF-A(165) gene transfer in rat myocardial infarction model, Cardiovasc Res., 73(3), (2007) 481-487]. Naked DNA remains the preferred method of DNA delivery to cardiac myocardium and has been explored extensively in clinical trials. The results from these trials have demonstrated efficacy in regard to secondary end-points of reduced symptomatology and perfusion, but have failed to establish significant angiogenesis or an increase in myocardial function [P.B. Shah, D.W. Losordo, Non-viral vectors for gene therapy: clinical trials in cardiovascular disease, Adv Genet, 54, (2005) 339-361]. This may be due in part to reduced transfection efficiency but can also be attributed to use of suboptimal candidate genes. Currently, polymeric non-viral gene delivery to cardiac myocardium remains underrepresented. In the past decade several advances in non-viral vector development has demonstrated increased transfection efficiency [O.J. Muller, H.A. Katus, R. Bekeredjian, Targeting the heart with gene therapy-optimized gene delivery methods, Cardiovasc Res, 73(3), (2007) 453-462]. Of these polymers, those that employ lipid modifications to improve transfection or target cardiovascular tissues have proven themselves to be extremely beneficial. Water-soluble lipopolymer (WSLP) consists of a low molecular weight branched PEI (1800) and cholesterol. The cholesterol moiety adds extra condensation by forming stable micellular complexes and was later employed for myocardial gene therapy to exploit the high expression of lipoprotein lipase found within cardiac tissue. Use of WSLP to deliver hypoxia-responsive driven expression of hVEGF to ischemic rabbit myocardium has proven to provide for even better expression in cardiovascular cells than Terplex and has demonstrated a significant reduction in infarct size (13+/-4%, p<0.001) over constitutive VEGF expression (32+/-7%, p=0.007) and sham-injected controls (48+/-7%). A significant reduction in apoptotic values and an increase in capillary growth were also seen in surrounding tissue. Recently, investigations have begun using bioreducible polymers made of poly(amido polyethylenimines) (SS-PAEI). SS-PAEIs breakdown within the cytoplasm through inherent redox mechanisms and provide for high transfection efficiencies (upwards to 60% in cardiovascular cell types) with little to no demonstrable toxicity. In vivo transfections in normoxic and hypoxic rabbit myocardium have proven to exceed those results of WSLP transfections by 2-5 fold [L.V. Christensen, et al., Reducible poly(amido ethylenediamine) for hypoxia-inducible VEGF delivery, J Control Release, 118(2), (2007) 254-261]. This new breed of polymer(s) may allow for decreased doses and use of new molecular mechanisms not previously available due to low transfection efficiencies. Little development has been seen in the use of new gene agents for treatment of myocardial ischemia and infarction. Current treatment consists of using mitogenic factors, described decades earlier, alone or in combination to spur angiogenesis or modulating intracellular Ca2+ homeostasis through SERCA2a but to date, failed to demonstrate clinical efficacy. Recent data suggests that axonal guidance cues also act on vasculature neo-genesis and provide a new means of investigation for treatment.
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PMID:Novel polymer carriers and gene constructs for treatment of myocardial ischemia and infarction. 1866 30

Toll-like receptors (TLRs) form a large family of pattern recognition receptors with at least 11 members in human and 13 in mouse. TLRs recognize a wide variety of microbial components and potential host-derived agonists that have emerged as key mediators of innate immunity. TLR signaling also plays an important role in the activation of the adaptive immune system by inducing proinflammatory cytokines and upregulating costimulatory molecules of antigen presenting cells. The dysregulation of TLR signaling may cause autoimmunity. This review discusses the contribution of TLR signaling to the initiation and progression of autoimmune diseases, such as rheumatoid arthritis, experimental autoimmune encephalitis, myocarditis, hepatitis, kidney disease, systemic lupus erythematosus, diabetes, obesity, and experimental autoimmune uveitis as well as aging. The involvement of TLR signaling in the pathogenesis of autoimmune diseases may provide novel targets for the development of therapeutics.
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PMID:The critical role of Toll-like receptor signaling pathways in the induction and progression of autoimmune diseases. 1935 17


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