Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to determine whether the development of myocardial infarction in different countries is associated with different risk factors, 240 male survivors, aged 40 or less, were studied in nine countries. In the seven centres in developed countries (Auckland, Melbourne, Los Angles/Atlanta, Cape Town, Tel Avic, Heidelberg, and Edinburgh) there was a high procedure of risk factors, particularly of hyperlipidaemia and cigarette smoking. The prevalence of hypertension, obesity, hyperglycaemia, and hyperuricaemia varied from centre to centre. Risk factors were less prevalent in Bombay and Singapore: the most common risks operating in Bombay seemed to be cigarette smoking and hyperglycaemia, while in Singpore cigarette smoking was the commonest. The mean age of the whole group was 35.4 years. Serum cholesterol levels of 7.25 mmol/l (280 mg/dl) or more were present in 25 per cent of all patients, serum triglyceride levels of 2.26 mmol/l )l200 mg/dl) or more in 35 per cent. 80 per cent of the patients were smokers, and 15 per cent were either for hypertension before myocardial infarction or had a raised blood pressure after myocardial infarction. Obesity was found in 19 per cent of all patients and serum uric acid levels over 0.5 mmol/l (8.5 mg/dl) in 17 per cent. 10 per cent of all patients were either treated for diabetes mellitus before myocardial infarction or showed an abnormal glucose tolerance after myocardial infarction. This collaborative study may help, by showing differences in the prevalence of risk factors, to indicate to each centre and to national and to international organizations, the direction for their future studies into the causation and prevention of myocardial infarction in young men.
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PMID:Myocardial infarction in young men. Study of risk factors in nine countries. 113 58

Stroke during sleep is an unexplored area of vascular neurology and its pathogenesis; clinical significance and prevention still remain uncertain. The aim of our study was to determine the epidemiological and clinical patterns of ischemic stroke occurring during sleep. Consecutive patients (n = 1822) with acute ischemic stroke recorded in the Tel Aviv Stroke Register were studied. Stroke during sleep was determined whenever focal neurological deficit was verified to have occurred while the patient had been asleep. The comparisons between patients with stroke during sleep and while awake were performed using the t test with Bonferroni correction and the chi(2) test for age, sex, vascular risk factors (i.e. ischemic heart disease, myocardial infarction, atrial fibrillation, arterial hypertension, hyperlipidemia, diabetes mellitus, peripheral vascular disease, smoking), vascular distribution (carotid versus vertebrobasilar) and severity of stroke (mild, moderate or severe). Data regarding the onset of stroke (during sleep or while awake) were available for 1,671 patients. A minority of strokes occurred during sleep (n = 311, 18.6%), and stroke during sleep was severer (chi(2) = 11.9, p < 0.002). No significant differences were found in terms of age, sex and vascular distribution between the two groups. None of the vascular risk factors was found to be more frequent in stroke during sleep. Strokes occurring during sleep were found to be severer than those with onset while awake. However, no specific clinical patterns of risk factor profiles could be identified in these patients. Hemodynamic factors may play an important role in the occurrence of stroke during sleep, and this issue should be further investigated.
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PMID:Stroke during sleep: epidemiological and clinical features. 1054 88

It is now accepted that the incidence of ischaemic stroke is significantly increased in the morning. Any attempts to prevent its occurrence must be based on determining the mechanisms, special risk factors and appropriate protective measures needed during this vulnerable period. We studied the epidemiological features of morning stroke and reviewed the records of 2312 consecutive patients recorded prospectively in the Tel Aviv Stroke Register. Information about time of stroke onset was obtained from the patient, family members or other observers. The study parameters of age, sex, vascular distribution (carotid versus vertebrobasilar), ischaemic heart disease, myocardial infarction, diabetes mellitus, arterial hypertension, smoking, hyperlipidaemia, stroke severity and recurrence were compared between patients with morning stroke and those with stroke occurring at other times. In 599 patients (34%) stroke occurred between 06:00 and 10:00 h. No evaluated parameter was found to be statistically different among the morning stroke patients compared with stroke occurring at other times (P < 0.2). Patients with arterial hypertension and ischaemic heart disease and male patients had a greater likelihood of stroke occurrence between 22:00 and 02:00 h (P < 0.05). Our data suggest that none of the common vascular risk factors could explain the morning peak of stroke occurrence. The next step in the quest for understanding the phenomenon of circadian variation is to identify other physiological factors and the effects of pharmacological agents in morning stroke protection.
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PMID:Are there any unique epidemiological and vascular risk factors for ischaemic strokes that occur in the morning hours? 1080 38

A 71-year-old man with acute myelogenous leukemia (AML, M2) developed signs of chest oppression, and was diagnosed as having acute myocardial infarction (AMI). At the same time, his leukemia relapsed in association with disseminated intravascular coagulation (DIC). The patient's risk factors for AMI were hyperlipidemia, hyperglycemia, and a history of smoking. Coronary angiography showed occlusion of the circumflex branch. Percutaneous transluminal angioplasty (PTCA) was performed successfully, followed by administration of heparin. After chemotherapy, the patient's DIC improved and a second remission was attained. When elderly patients with AML show evidence of DIC, we should be aware of AMI as a possible complication. PTCA is a safe operation for such patients.
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PMID:[Acute myelogenous leukemia associated with disseminated intravascular coagulation and acute myocardial infarction at relapse]. 1168 Sep 86

Citrus flavonoids are reported to be promising bioactive compounds against hyperlipidemia and lipid biosynthesis. However, the mechanism of the lipid lowering effect by flavonoids remains unknown. The present study examines the effect of some flavanones on the adipocytic conversion of the human preadipocyte cell line, AML-I. Among four structure-related flavanones including naringenin, naringenin-7-rhamnoglucoside (naringin), hesperetin, and hesperetin-7-rhamnoglucoside (hesperidin), the aglycones such as naringenin and hesperetin exhibited the growth arrest of AML-I cells. When the cells were examined by Annexin V-FITC staining method, it was noticed that growth arrest was induced by apoptotic cell death. In the study of apoptosis-related protein in the naringenin-treated cells, anti-apoptotic proteins such as p-Akt, NF-kappaB, and Bcl-2 were decreased, and pro-apoptotic protein Bad was accumulated by Western blot analysis. Interestingly, exposure of AML-I cells to naringenin or hesperetin during short-term cultures increased cytoplasmic lipid droplets by Sudan Black B staining. Furthermore, expression of fatty acid synthase (FAS) and peroxisome proliferator activated receptor (PPAR)-gamma was enhanced in naringenin-treated cells. These data suggest that apoptosis by flavanones does not inhibit the adipocytic conversion of AML-I preadipocytes. The result also indicates that adipocyte may not be a direct target for the lipid-lowering activity of the flavanones.
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PMID:Naringenin and hesperetin induce growth arrest, apoptosis, and cytoplasmic fat deposit in human preadipocytes. 1898 Mar 25