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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular diseases caused 2.3 million deaths in India in the year 1990; this is projected to double by the year 2020. Hypertension is directly responsible for 57% of all stroke deaths and 24% of all coronary heart disease deaths in India. Indian urban population studies in the mid-1950s used older WHO guidelines for diagnosis (BP > or =160 and/or 95 mmHg) and reported hypertension prevalence of 1.2-4.0%. Subsequent studies report steadily increasing prevalence from 5% in 1960s to 12-15% in 1990s. Hypertension prevalence is lower in the rural Indian population, although there has been a steady increase over time here as well. Recent studies using revised criteria (BP > or =140 and/or 90 mmHg) have shown a high prevalence of hypertension among urban adults: men 30%, women 33% in Jaipur (1995), men 44%, women 45% in Mumbai (1999), men 31%, women 36% in Thiruvananthapuram (2000), 14% in Chennai (2001), and men 36%, women 37% in Jaipur (2002). Among the rural populations, hypertension prevalence is men 24%, women 17% in Rajasthan (1994). Hypertension diagnosed by multiple examinations has been reported in 27% male and 28% female executives in Mumbai (2000) and 4.5% rural subjects in Haryana (1999). There is a strong correlation between changing lifestyle factors and increase in hypertension in India. The nature of genetic contribution and gene-environment interaction in accelerating the hypertension epidemic in India needs more studies. Pooling of epidemiological studies shows that hypertension is present in 25% urban and 10% rural subjects in India. At an underestimate, there are 31.5 million hypertensives in rural and 34 million in urban populations. A total of 70% of these would be Stage I hypertension (systolic BP 140-159 and/or diastolic BP 90-99 mmHg). Recent reports show that borderline hypertension (systolic BP 130-139 and/or diastolic BP 85-89 mmHg) and Stage I hypertension carry a significant cardiovascular risk and there is a need to reduce this blood pressure. Population-based cost-effective hypertension control strategies should be developed.
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PMID:Trends in hypertension epidemiology in India. 1473 Mar 20

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an autosomal dominant vascular encephalopathy that has been mainly reported in Europe and the United States. Recently, this disease has been reported in Japan and the increasing number of reported cases has been attracting attention. Currently, the clinical diagnosis of CADASIL is based on the satisfaction of the following conditions: (1) development of the condition at a relatively young age (40-50 years), (2) no risk for stroke, (3) repeated attacks of lacunar infarction with gradual progression to pseudobulbar paralysis and dementia (migraine, emotional disturbance, cerebral infarction, and dementia in 30%, 20%, 85%, and 30-90% of patients, respectively), and (4) family members with similar symptoms (autosomal dominant inheritance). The diagnosis is also established on the basis of the following findings of imaging and laboratory studies: the presence of (1) leukoaraiosis and multiple small infarcts in the bilateral deep white matter, basal ganglia, thalamus, and pons revealed by MRI; (2) granular osmiophilic material (GOM) around the vascular smooth muscles in the brain, skeletal muscle, peripheral nerves, and skin demonstrated by electron microscopy; and (3) Notch3 mutations revealed by DNA analysis. Characteristics of CADASIL patients in Japan: Between 1997 and 2008, 38 CADASIL families have been reported in Japan. The age at onset of local neurological symptoms ranged from 15 to 71 years (mean 42. 3 +/- 11.4 years). All patients except one with borderline hypertension were normotensive or hypotensive. Out of 45 patients, 18 (40%) had migraine; 37 (82.2%) had repeated cerebral ischemic attacks including transient ischemic attacks (TIA); and 22 (48.9%), including borderline cases, had intellectual impairment. Nine of 38 patients (23.7%) had pseudobulbar paralysis. The retinal arteries were narrowed in 4 of 16 patients. The patients were distributed nationwide. Mutations in exon 4 have been reported in 22 of 31 families (71%). It is expected that an increase in the number of reported cases will lead to the discovery of other mutations associated with this condition. The mechanism of development of CADASIL due to Notch3 mutations is still unknown. However, a recent study has revealed that the Notch3 ectodomain is a major component of GOM. On binding to its ligand, Notch3 normally undergoes proteolytic cleavage, resulting in the clearance of the extracellular domain. However, in CADASIL, it accumulates as GOM and potentially inhibit the normal metabolism of smooth muscle cells.
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PMID:[CADASIL]. 1906 56


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