Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peroxisome proliferator-activated receptors (PPARs) are transcription factors belonging to the nuclear receptor superfamily and form heterodimers with retinoid X receptor. To date, three PPARs isoforms have been isolated and termed alpha, beta (or delta), and gamma. Although PPAR gamma is expressed predominantly in adipose tissue and associated with adipocyte differentiation and glucose homeostasis, it has been recently demonstrated that PPAR gamma is present in a variety of cell types. Synthetic antidiabetic thiazolidinediones (TZDs) and natural prostaglandin D(2) (PGD(2)) metabolite, 15-deoxy-Delta(12, 14)-prostaglandin J(2) (15d-PGJ(2)), are well-known as ligands for PPAR gamma. After it has been reported that activation of PPAR gamma suppresses production of proinflammatory cytokines in activated macrophages, medical interest in PPAR gamma have grown and a huge research effort has been concentrated. PPAR gamma, is currently known to be implicated in various human chronic diseases such as diabetes mellitus, atherosclerosis, rheumatoid arthritis, inflammatory bowel disease, and Alzheimer's disease. Moreover, PPAR gamma ligands have potent tumor modulatory effects against colorectal, prostate, and breast cancers. Recent studies suggest that TZDs not only ameliorate insulin sensitivity but also have pleiotropic effects on many tissues and cell types. Although activation of PPAR gamma seems to have beneficial effects on atherosclerosis and heart failure, the mechanisms by which PPAR gamma ligands prevent the development of cardiovascular diseases are not fully understood. This review will focus on the latest developments in the PPAR gamma field and the roles of PPAR gamma-dependent pathway in cardiovascular diseases.
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PMID:Pleiotropic actions of PPAR gamma activators thiazolidinediones in cardiovascular diseases. 1532 Jul 43

Responsible locus for dementia in Parkinson disease (PD) was investigated. Serial 1,395 autopsy cases were studied for the combined pathology of PD and Alzheimer disease (AD). Following the one-year rule by the first Consensus Guidelines, definite AD pathology was quite rare in PD with dementia (PDD) but common in dementia with Lewy bodies (DLB) . Plaque-dominant senile changes apparently enhanced neocortical Lewy-body pathology in both the conditions. About the hypometabolism in the visual cortex of PDD, a 66-year old man presented with fluctuation in hallucination commensurate with fluctuating hypometabolism. Considering the paucity in pathological changes of the visual cortex, this hypometabolism may represent functional impairment in the fiber connection. Comparative pathological studies with PD and PDD were carried out. Only one case of a 48-year-old woman, who unexpectedly died of heart failure, was free from cognitive decline, and did not show limbic and neocortical involvement. Another case of a 75-year old man with MCI presented with the similar pathology. All other cases showed clinical documentation of cognitive impairment and limbic and neocortical pathological involvement. Thus, the combination of prospective clinical and radiological studies and retrospective pathological studies (dynamic neuropathology) may be essential to investigate a role of the basal-forebrain cholinergic system.
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PMID:[Parkinson disease with dementia--responsible locus for dementia]. 1565 3

Depression is an important but inadequately diagnosed mood disorder in elderly. Depressed elderly patients often have chronic concomitant diseases. This paper intended to determine the prevalence of depression and its relation with concomitant disorders and social status among the patients admitted to our geriatric unit. Seven hundred and eighty-nine females and 466 males admitted to our unit were examined for the presence of depression by using the geriatric depression scale (GDS) test. The presence of concomitant diseases was assessed. Depression was diagnosed in 273 patients (21.8%), 193 (70.7%) females and 80 (29.3%) males. Depressed patients suffered from a wide range of other diseases the number and prevalence of which were as follows: Alzheimer's disease (AD) (34; 12.5%), vascular dementia (27; 9.9%), hypertension (HT) (211; 77.3%), diabetes mellitus (DM) (64; 23.4%), osteoporosis (182; 66.7%), atherosclerotic coronary artery disease (CAD) (89; 32.6%), cardiac failure (23; 8.5%), bronchial asthma (8; 2.9%), chronic obstructive pulmonary disease (COPD) (25; 9.2%) and osteoarthritis (133; 48.8%). The correlation between depression and concomitant diseases was statistically significant in hypertensive, demented and osteoporotic patients, as determined in a large elderly population. Previous studies examined the correlation of depression with only one concomitant disease, while we performed the analysis on multiple correlations.
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PMID:Depression and concomitant diseases in a Turkish geriatric outpatient setting. 1581 64

According to the free radical theory, aging can be considered as a progressive, inevitable process partially related to the accumulation of oxidative damage into biomolecules -- nucleic acids, lipids, proteins or carbohydrates -- due to an imbalance between prooxidants and antioxidants in favor of the former. More recently also the pathogenesis of several diseases has been linked to a condition of oxidative stress. In this review we focus our attention on the evidence of oxidative stress in aging brain, some of the most important neurodegenerative diseases -- Alzheimer's disease (AD), mild cognitive impairment (MCI), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD) -- and in two common and highly disabling vascular pathologies--stroke and cardiac failure. Particular attention will be given to the current knowledge about the biomarkers of oxidative stress that can be possibly used to monitor their severity and outcome.
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PMID:Oxidative stress in brain aging, neurodegenerative and vascular diseases: an overview. 1618 38

Physical inactivity is the most important planetary reason for non-transmissible mortality. Technical developments have allowed a sedentary lifestyle. This causes health problems such as insulin resistance, atherosclerosis, heart failure and obesity. In addition, disturbances of bones and muscles as well as dementia of the Alzheimer type are associated with sedentarity. Assessing this risk factor and attempting to increase physical activity should be a very important part of any general practitioner's measures.
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PMID:[Sedentarity--sedentary lifestyle and physical activity]. 1621 5

Nearly 20 years after murine embryonic stem cells (mESC) were isolated, the first report of the derivation of human embryonic stem cells (hESC) in 1998 spawned the field of hESC research [Evans MJ, Kaufman MH, Establishment in culture of pluripotential cells from mouse embryos. Nature 1981; 292 (5819): 154-6; Thomson JA, Itskovitz-Eldor J, Shapiro SS, et al. Embryonic stem cell lines derived from human blastocysts. Science 1998; 282 (5391): 1145-7.]. Although this field is only in its infancy, hESC represent a theoretically inexhaustible source of precursor cells that could be differentiated into any cell type to treat degenerative, malignant, or genetic diseases, or injury due to inflammation, infection, and trauma. This pluripotent, endlessly dividing cell has been hailed as a possible means for treating diabetes, Parkinson's disease, Alzheimer's, spinal cord injury, heart failure, and bone marrow failure. But the regenerative medicine applications of embryonic stem cells are only one facet of hESC therapeutic potential. Human ESC are an invaluable research tool to study development, both normal and abnormal, and can serve as a platform to develop and test new therapies. In addition to discussing the therapeutic potential of hESC, this chapter will cover limitations to using hESC for replacement cell therapy, strategies to overcome these limitations, and alternative methods of deriving hESC.
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PMID:Therapeutic potential of embryonic stem cells. 1627 20

Voluntary physical activity and exercise training can favorably influence brain plasticity by facilitating neurogenerative, neuroadaptive, and neuroprotective processes. At least some of the processes are mediated by neurotrophic factors. Motor skill training and regular exercise enhance executive functions of cognition and some types of learning, including motor learning in the spinal cord. These adaptations in the central nervous system have implications for the prevention and treatment of obesity, cancer, depression, the decline in cognition associated with aging, and neurological disorders such as Parkinson's disease, Alzheimer's dementia, ischemic stroke, and head and spinal cord injury. Chronic voluntary physical activity also attenuates neural responses to stress in brain circuits responsible for regulating peripheral sympathetic activity, suggesting constraint on sympathetic responses to stress that could plausibly contribute to reductions in clinical disorders such as hypertension, heart failure, oxidative stress, and suppression of immunity. Mechanisms explaining these adaptations are not as yet known, but metabolic and neurochemical pathways among skeletal muscle, the spinal cord, and the brain offer plausible, testable mechanisms that might help explain effects of physical activity and exercise on the central nervous system.
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PMID:Neurobiology of exercise. 1664 3

Homocysteine is a sulfur amino acid whose metabolism stands at the intersection of 2 pathways: remethylation, which requires folic acid and B-12 coenzymes, and transsulfuration, which requires pyridoxal-5'-phosphate, the B-6 coenzyme. Data from several studies suggest that mild elevations of homocysteine in plasma are a risk factor for occlusive vascular disease. In the Framingham studies we have shown that plasma total homocysteine concentration is inversely related to the intake and plasma levels of folate and vitamin B-6 as well as vitamin B-12 plasma levels. Almost two-thirds of the prevalence of high homocysteine is attributable to low vitamin status or intake. Elevated homocysteine concentrations in plasma are a risk factor for prevalence of extracranial carotid artery stenosis of at least 25% in both men and women. Prospectively elevated plasma homocysteine is associated with increased total and CVD mortality, increased incidence of stroke, increased incidence of dementia and Alzheimer's disease, increased incidence of bone fracture, and higher prevalence of chronic heart failure. This multitude of relationships between elevated plasma total homocysteine and diseases that afflict the elderly point to the existence of a common denominator that may be responsible for these diseases. Whether this denominator is homocysteine itself or whether homocysteine is merely a marker remains to be determined.
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PMID:The many facets of hyperhomocysteinemia: studies from the Framingham cohorts. 1670 47

The increase in average life expectancy is resulting in an increasing prevalence of major invalidating illnesses, such as cardiovascular disease and dementia. Congestive heart failure (CHF) is a chronic, progressive disease representing the advanced stage of cardiac illnesses. Cognitive impairment is known to be a frequent feature of CHF patients. The epidemiologic pictures of mild cognitive impairment (MCI), Alzheimer's disease (AD) and CHF are predicted to worsen with the demographic expansion of the elderly population. Nevertheless, there has been little structured research on cognitive impairment in patients with CHF. This is unfortunate not only because CHF is the leading cause of hospitalization in the elderly and a leading cause of disability and death, but also for important clinical and socioeconomic implications including those related to comorbidity in advanced age and the need to early detect factors which may precipitate the conversion of MCI to AD. In this review, several aspects of the role of CHF in cognitive impairment are evaluated. Owing to the lack of studies focusing on CHF in AD, the pathophysiology of cardiac failure in cognitive impairment is addressed in light of possible preventive strategies against the onset of AD. These include prevention of oxygen radical and peroxynitrite production, supplementation of nitric oxide (NO) donors, as well as the achievement of an adequate antioxidant supply, better if obtained with a targeted and individualized nutritional approach. A systematic neuropsychologic testing of older patients with heart failure is to identify those with early cognitive impairment and promptly establish traditional therapies such as angiotensin converting enzyme (ACE) inhibitors, digoxin or beta-blockers. The neuropsychologic assessment in CHF patients is also fundamental to disclose conditions potentially favoring the onset of cognitive impairment such as depression. Finally, management schemes should include exercise training programs as well as patient and caregiver education.
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PMID:Congestive heart failure and Alzheimer's disease. 1694 9

Moderate hyperhomocysteinemia (HHCY) is a risk factor for cardiovascular (CVD) and neurodegenerative diseases, osteoporotic fractures and complications during pregnancy. Elderly persons have a high prevalence of HHCY. Vitamin deficiency is by far the most common cause of HHCY. Retrospective and prospective studies emphasize a causal relationship between HHCY and the CVD risk. Some vitamin intervention trials, however, did not lower the risk of CVD. From power calculation one can conclude that these trials may not involve sufficient numbers of patients to assure statistically valid conclusions. Re-analysis of the VISP study (excluding renal failure and vitamin B12 status tampering factors), however, detected a 21% decrease in the risk of stroke. This number has been confirmed by results from the HOPE 2 vitamin intervention trial. Folic acid enrichment of grain products in the US and Canada has led to a significant decline of stroke mortality, since 1998 annually 12900 fewer stroke deaths in the US and 2800 fewer stroke deaths in Canada. Despite negative results from secondary prevention trials regarding the CVD risk reduction there is convincing evidence about the effectiveness of B-vitamin supplementation in lowering the stroke risk. The overall decline in stroke risk calculated in meta-analysis from prospective studies and found in intervention trials is around 20%. Additionally, HHCY was recently linked to the occurrence and severity of chronic heart failure. HHCY is also a risk factor for osteoporotic fractures and vitamin treatment lowered the fracture risk significantly. Furthermore, there is a correlation between HHCY and cognitive disorders or Alzheimer's disease. HHCY is a predictive parameter for the decline in cognitive function. Hypomethylation is among the central mechanisms through which HHCY acts cytotoxically. HHCY and low folate are causal factors for pregnancy complications. In addition to the recommended folate supplementation, vitamin B12 supplementation could further decrease pregnancy complications. Determination of homocysteine plasma concentration should be part of the individual risk profile, especially for elderly subjects who are at risk for CVD, neurodegenerative diseases or osteoporotic fractures.
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PMID:Significance of hyperhomocysteinemia. 1695 35


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