Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ninety-four institutionalized subjects (mean age 82.9 years; 13 men and 81 women) were assessed for serum dehydroepiandrosterone sulfate (DHEAS) levels. The mean value was 457 ng/ml (SD = 426) in this cross-sectional study. There was a significant decrease in DHEAS levels with age. There was no difference among demented patients with Alzheimer's disease (n = 46), other dementia cases (n = 16), and other individuals (n = 32). The subjects treated for arterial hypertension had significantly lower DHEAS levels. No correlation was found between DHEAS and cortisol values. After age adjustment, no association was observed between DHEAS and chronic diseases, medications, several biochemical or hematological parameters, or 3-year mortality.
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PMID:Dehydroepiandrosterone sulfate in a long-term care aged population. 858 91

Vascular dementia (VD) and Alzheimer's type dementia are two main causes of dementia in the aged. Considering historical backgrounds and ethnic differences, a simplified classification of VD is suggested. First, poststroke dementia of acute onset associated with an infarct that is large enough to impair general cognitive functions, or strategically located. Second, multi-infarct dementia that develops incrementally with increasing numbers of infarcts, and which should be classified as multiple cortical infarct dementia and multiple small infarctor lacunar dementia. Third, vascular dementia of the Binswanger type (VDBT). We compared two types of white matter lesions, periventricular hyperintensity (PVH) and confluent centrum semiovale hyperintensity (CCSH) in lacunar stroke patients with regard to the cerebral blood flow (CBF). In patients with PVH, there was a significant positive correlation between the dementia scores and the CBF in the parietal and temporal areas but not in the frontal area. In CCSH patients, there was a significant positive correlation in the frontal area but not in the parieto-temporal areas. Therefore, dementia in most patients with PVH may not be primarily related to the PVH, but may possibly be due to coexisting Alzheimer's type dementia, and dementia in most CCSH patients may be related to cerebrovascular disease. VDBT is unique clinically in its slowly progressive intellectual deterioration and pathologically in diffuse, confluent, and almost symmetrical white matter lesions. For the pathogenesis of VDBT, our studies suggest that hypertension, short-term variations in blood pressure, and a sustained nighttime elevation of blood pressure promote small vessel disease and cause ischemia of the cerebral white matter that is located in the end-fields of penetrating arteries; this leads to an imparied integrity of the blood-brain barrier and free radical generation, both of which may have important roles in producing diffuse white matter degeneration.
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PMID:[Problems in vascular dementia]. 864 89

Differential diagnosis of dementing diseases is very important to rule in the so-called treatable dementia. The new DSM-IV criteria for dementia include memory disturbances and one or more of aphasia, apraxia, or frontal lobe dysfunctions as essentials. Alzheimer disease requires, in addition, slowly progressive course and ruling out other brain or systemic diseases. Vascular dementia requires focal neurological or neuroimaging signs. Other diseases which cause dementia include chronic subdural hematoma, infection and brain tumor. CT or MRI can readily diagnose them if suspected and they may be treated. Systemic diseases associated with treatable dementia include electrolyte disturbances, hypothyroidism, vitamin deficiency, alcohol or drug intoxication, syphilis and HIV infection. Prevention of dementia seems to be the future problem as we could prevent cerebrovascular diseases by treating hypertension.
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PMID:[Clinical aspects of dementia]. 875 26

This study examined relationships between chronic stress and insulin/glucose in two groups of nondiabetics, M age = 69.4: spouse caregivers (CGs) of persons with Alzheimer's disease (n = 73) and age- and gender-matched spouses of nondemented controls (COs) (n = 69). Fasting insulin/glucose and psychological variables were assessed twice (Time 1, Time 2) over a 15-18 month period. CGs had significantly higher insulin levels at Times 1 and 2 than did COs even when obesity, exercise, gender, age, alcoholic drinks, hormone replacement therapy (HRT), lipids, and hypertension (HTN) were considered in the analyses. CGs generally reported significantly more psychological distress (higher burden, depression, hassles, and lower uplifts) than did COs at each time. Differences in psychological distress at Time 1 between CGs and COs did not mediate the insulin difference in the groups at Time 1, but differences in distress at Time 2 between CGs and COs did mediate their difference in insulin at Time 2. Although caregiver status was not associated with glucose at Time 1 or Time 2, psychological distress was positively associated with glucose at Time 2. Moreover, psychological distress at Time 1 was associated with higher glucose at Time 2 after controlling for glucose at Time 1. These data suggest that relationships between psychological and physiological distress exist both cross-sectionally and over time. These results may be important because higher insulin and glucose levels are associated with increased coronary risk and coronary heart disease.
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PMID:Psychological distress, caregiving, and metabolic variables. 880 5

In living organisms a large number of enzymes are working in complicated networks to express various biological functions. In order to analyze such functions from various aspects, specific enzyme inhibitors are likely to become useful tools. They are also useful for the studies of reaction mechanisms and analysis of three-dimensional structures of enzymes. Moreover, they are of great value in elucidating disease processes and seem to have usefulness in treatment of various diseases. Searching for inhibitors in culture filtrate of microbes, we discovered many substances which specifically inhibit various enzymes such as endopeptidases, exopeptidases, glycosidases, lipases, an so forth. These inhibitors have low-molecular-weights and unique structures. We found significant activities of exopeptidases, alkaline phosphatases, esterases, and so forth, on surface membranes of various mammalian cells. Searching for specific inhibitors against these cell surface enzymes, we have discovered many interesting inhibitors. These inhibitors proved to bind to the cellular surface and to modify the functions of cells involved in immune responses. Thus the studies on these enzyme inhibitors may well afford important keys to understand various aspect of biological phenomena and diseases: inflammation, immune response, hypertension, hyperlipemia, diabetes, Alzheimer's disease, carcinogenesis, metastasis, viral infection, autoimmune diseases, and so forth. Because of their interesting pharmacological activities, some of the inhibitors are now under clinical evaluation for their uses as medical drugs. Enzyme inhibitors seems to propose a new promising field of science.
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PMID:[Screening, characterization and pharmaceutical and medical application of enzyme inhibitors from microbial origin with low-molecular-weight]. 883 Dec 59

Low blood pressure is reported in Down's syndrome (DS). To assess this and determine whether low pressure results from the disease or from long-term residence in hospital, we measured blood pressure with a random-zero sphygmomanometer in three groups of patients: 52 DS inpatients, 62 DS outpatients, and 60 outpatients with other forms of mental handicap. Relative to normal reference populations, blood pressure was low in both DS inpatients (systolic, score -33 mm Hg, P < .0001) and DS outpatients (-25 mm Hg, P < .0001). It was normal in non-DS outpatients (-4.0 mm Hg, P = .3). Blood pressure rose normally with age in the non-DS group but not in the DS group. We conclude that blood pressure is low in DS and that this is a feature of the disease rather than of the protected environment in which patients live. A mechanism related to trisomy 21 is likely, and there may be a link with Alzheimer's disease (AD) because blood pressure is also low in Alzheimer's and a high proportion of Ds patients develop this disease. If, as is likely, blood pressure is lowered in Alzheimer's by the neuropathy, the same neuropathy developing early in DS may also reduce blood pressure.
Hypertension 1996 Oct
PMID:Low blood pressure in Down's syndrome, A link with Alzheimer's disease? 884 80

Genetic and other defects leading to brain changes in Down syndrome, Alzheimer disease, amyotrophic lateral sclerosis, Huntington disease, Gaucher disease, hypertension and other disorders are rapidly being identified. If brain access were possible, new candidates for gene replacement therapy, antisense oligonucleotides, immune proteins or growth factors might be used for treating these disease (Lowenstein et al., 1994; Wielbo et al., 1995). Further, a number of drugs, peptides, antibodies and biological response modifiers have proven valuable in inhibiting malignant, infectious and other pathological processes in vitro, but are unlikely to be employed clinically because of their limited access to brain.
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PMID:Modulation of blood-brain barrier permeability. 886 35

A great deal of secondary, or covariable, information is often collected during the course of large-scale clinical trials. This information typically includes demographic and anthropometric data but often also includes more elaborate laboratory-based measures that might be used to screen for adverse reactions to the preventive agent or treatment being tested. This information can be and often is used to identify individuals or, more likely, subgroups of individuals who appear to respond better (or worse) to the compound of relevance. Such heterogeneity in response is to be expected, since the basic biological constitution of individuals differs widely and since it is well known from simple pharmacokinetic assays that such differences can affect drug responses. Since genes influence the biological constitution of individuals, it is easy to argue that genetic differences between individuals could explain differential responsiveness to certain drugs, as pharmacogeneticists have suggested for years. In this article, it is argued that by collecting relevant genetic data on participants in large-scale clinical trials as though these data merely provided additional covariables, one might not only be in a position to identify responders and nonresponders to the compound being tested but could also be in a position to address fundamental questions about the nature and pathogenesis of the disease for which the compound was designed. Although we exemplify this simple argument by referring to antihypertensive compounds and research, this reference is made merely for reasons of convenience, since there are numerous compounds designed expressly for the prevention and treatment of hypertension, but rather few for Alzheimer disease. It is hoped that by adopting some of the guidelines and principles outlined herein, better and more appropriate compounds for the prevention and treatment of Alzheimer disease will be tested and ultimately made available to the patients for whom they work best.
Alzheimer Dis Assoc Disord 1996
PMID:The use of genetic information in large-scale clinical trials: applications to Alzheimer research. 887 85

This two-stage epidemiologic study was to investigate the prevalence and types of dementia among elderly people in the Saa-Min district of Kaohsiung City in Taiwan. In stage one, the Chinese Mini-Mental Status Examination (CMMSE) and Blessed Dementia Rating Scale were employed. In stage two, a comprehensive neurobehavioral examination and neuropsychologic tests were administered by neurologists and neuropsychologists. Dementia was defined by DSM-III-R criteria. The National Institute of Neurological and Communication Disorders and Stroke-Alzheimer's Disease and Related Disorders Association guidelines for Alzheimer's disease (AD) and the National Institute of Neurological Disorder and Stroke-Association international pour la Recherche et l'Enseignement en Neurosciences criteria for vascular dementia (VaD) were applied. A total of 1,016 randomly selected elderly people participated in phase one: 131 people with CMMSE below cutoff values participated in phase two, of whom 45 were confirmed to have a form of dementia. The prevalence of dementia in this sample was 4.4% (3.2% in men and 5.8% in women): 2.0% for those 65 to 74 years old, 8.3% for those 75 to 84 and 24.4% for those > or = 85 years old; 6.0% for those who were illiterate, 3.3% for those who attended grade-school; and 2.8% for those who finished junior-high-school. AD (22 cases, 48.9%) was the most common cause of dementia, followed by VaD (11 cases, 24.4%) and mixed dementia (MIX: 5 cases, 11.1%). Old age and being female were significant high risk factors for AD. Medical history indicated that stroke and hypertension were significant risk factors for VaD. A relatively high prevalence of dementia was observed in this study, probably because we assessed neurobehavior in great detail. Although AD was the leading cause of dementia in the present population sample. VaD and MIX also comprised an important proportion, reflecting the high prevalence of stroke in Taiwan. Older women had high risk for AD, not for VaD; and those with a history of stroke and hypertension had high risk for VaD, not for AD.
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PMID:Prevalence of dementia in an urban area in taiwan. 896 73

Deposits of amyloid beta-peptide (A beta) in senile plaques and cerebral blood vessels is the prominent feature of Alzheimer's disease (AD), regardless of genetic predisposition. The cellular origin of cerebral deposits of A beta or its precise role in the neurodegenerative process has not been established. Recently we demonstrated a novel action of beta-amyloid on blood vessels--vasoactivity and endothelial damage through superoxide radicals. Since endothelial dysfunction is associated with vascular degenerative diseases, we examined the direct action of A beta on endothelial cells in culture. Cells treated with A beta displayed characteristics of necrotic cell death which was prevented by the free radical scavenging enzyme superoxide dismutase. Stimulation of endothelial nitric oxide (NO) production by the calcium ionophore, A23187, or bradykinin was inhibited by beta-amyloid. We conclude that an imbalance of NO and oxygen radicals may mediate the A beta-induced endothelial damage on endothelial cells in culture and may also contribute to a variety of pathophysiological conditions associated with aging: hypertension, cerebral ischemia, vasospasm, or stroke.
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PMID:beta-amyloid-induced endothelial necrosis and inhibition of nitric oxide production. 902 96


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