Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q8NEX9 (reductase)
 26,410 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 27 children, 4-8 years old, with recurrent respiratory infections of the upper and lower respiratory tracts Isoprinosine (ISO) tablets were administered for 7-10 days at daily doses of 50-100 mg/kg. Clinical signs of acute respiratory disease, including temperature abnormalities and subjective complaints, subsided in a short time and the children showed no symptoms for periods ranging from several weeks to several months following the therapy. The children were selected for immunotherapy with ISO on the basis of their low levels of E-rosette forming cells in peripheral blood. Several immune function parameters assessed immediately after treatment with ISO and compared with those obtained before illness and ISO administration. Low levels of T-lymphocytes returned to normal after ISO therapy, B-lymphocyte relative and absolute numbers, however, were not affected by the treatment. Nor were any changes due to ISO found in immunoglobulins, complement components, beta 2-microglobulin and C-reactive protein. Moreover, ISO had no stimulative effect on spontaneous tetrazolium reductase activity of granulocytes but it showed a slight inhibition of their phagocytosis-associated metabolic activity.
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PMID:Immunorestoration in children with recurrent respiratory infections treated with isoprinosine. 244 56

After detection of a few clinical cases of methaemoglobinaemia (methb) in our NICU, a prospective clinical study was undertaken to determine the extent of the problem and to identify the causes. Consequently, during the following 8 months all haemoglobin tests included simultaneous measurements of methb on an OSM 3 hemoximeter (Radiometer): 8% (n = 33) of 415 neonates were found to be methb positive (defined as > or = 6% methb). Mean methb was 19% (range 6.5-45.5%). Maximum methb concentrations were found on day 4-31 postpartum (mean 12 days) and the number of days with a positive methb sample ranged from 1 to 18 days (mean 6 days). About 40% of the neonates born at 25-30 weeks of gestation and 60% with a birth weight < 1000 g were methb positive. Also, there was a negative correlation between the size of the methb positive concentration and gestational age (r = -0.38, p = 0.02). Measurements of C-reactive protein and leucocytes, NADH reductase, pH, Cl, nitrate and nitrite were carried out in methb positive patients. The tests were repeated 1 week after cessation of methb. The only significant difference was an increase in NADH reductase at the second measurement. Likewise, a wide range of clinical parameters were registered and they occurred with a higher frequency among the methb positive patients when compared with a methb negative control group matched with regard to gestational age and the closest possible birth weight. The mean birth weight of methb positive patients was 1170 g and that of negative controls 1380 g (p < 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Methaemoglobinaemia among neonates in a neonatal intensive care unit. 779 42

Clinical trials of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors or statin therapy demonstrate an improvement in cardiovascular end points and coronary stenosis. However, an improvement in cardiovascular end points and coronary stenosis is incompletely explained by the baseline or treated LDL cholesterol level. The beneficial effects of statins on clinical events may involve nonlipid mechanisms that modify endothelial function, smooth muscle cells, and monocyte-macrophage: vasomotor function, inflammatory responses, and plaque stability. Augmented bioactivity of NO by statin therapy either indirectly by its effect on lipoprotein levels and protection of LDL from oxidation, or directly by effects on NO synthesis and release, might account for enhancement of endothelium-dependent vasodilation. Recent experimental and animal studies have demonstrated that statins dose-dependently decrease smooth muscle cells migration and proliferation, independently of their ability to reduce plasma cholesterol. Moreover, statins are able to reduce the in vitro cholesterol accumulation in macrophages and expression of matrix metalloproteinase, resulting in plaque stability. These effects of statins were completely prevented by the addition of mevalonate and partially by all-trans farnesol and all-trans geranylgeraniol, confirming the specific role of isoprenoid metabolites, probably through prenylated proteins, in regulating these cellular events. Statins have been shown to prevent the activation of monocytes into macrophages, inhibit the production of pro-inflammatory cytokines, C-reactive protein, and cellular adhesion molecules. Statins decrease the adhesion of monocyte to endothelial cells. Accordingly, statins exert their cardiovascular benefits through a direct antiatherogenic properties in the arterial wall, beyond their effects on plasma lipids.
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PMID:Effects of statins on vascular wall: vasomotor function, inflammation, and plaque stability. 1097 15

The major cause of morbidity and mortality associated with coronary atherosclerosis is plaque rupture, which often results in one of the acute coronary syndromes: unstable angina, non-Q-wave myocardial infarction (MI), or Q-wave MI. Plaque rupture may be attributable to the thickness of the overlying fibrous cap; thinner plaques are more likely to rupture. It appears that the presence of inflammation is a significant contributor to rupture. Acute-phase treatments are highly efficacious, but secondary prevention, often overlooked, also is life-saving. Diet, exercise, and medications are the interventions available for secondary prevention. Four classes of medications--aspirin, beta blockers, angiotensin-converting enzyme (ACE) inhibitors, and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins)--are also used in this setting with a high degree of success in reducing mortality and morbidity. Numerous studies have demonstrated a 30-50% reduction in mortality with aspirin. The reduction in mortality achieved with beta blockers in studies of patients after myocardial infarction are 15-50%. ACE inhibitors significantly reduce the risk of death from myocardial infarction in patients with coronary artery disease with or without myocardial infarction. Statins are beneficial even in patients whose cholesterol level is low to normal. Patients who were discharged on a statin showed a 50% reduction in mortality over those who did not receive statin therapy independent of lipid level. C-reactive protein, a marker of inflammation, is predictive of mortality, as are age and ejection fraction. Statins may be anti-inflammatory in addition to their lipid-lowering effect. Secondary-prevention strategies such as case management, electronic discharge prompting, better communication between referring physicians and cardiologists, and patient education may also have positive effects on after-discharge morbidity and mortality.
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PMID:Post-hospitalization management of high-risk coronary patients. 1107 26

Management of acute coronary syndromes has been the focus of increased interest in recent years. This has come about with the recognition that the majority of patients who present to the hospital with chest pain have unstable angina or non-Q-wave myocardial infarction (MI). Further, sensitive biochemical markers of myocardial necrosis, such as troponin and creatine kinase, have improved early diagnosis. Markers of inflammation such as C-reactive protein (CRP), although not in wide clinical practice, may provide an early and important marker of prognosis. The current approach to management of acute coronary syndromes is careful risk stratification so as to select appropriate medical therapies and to guide the clinician to appropriate interventions such as angiography or percutaneous coronary intervention (PCI). Established therapies such as aspirin, heparin, intravenous nitrates, and, in selected patients, beta blockers or calcium antagonists, are being used concomitantly with, or are being supplanted by, newer therapies such as low-molecular-weight heparins and glycoprotein IIb/IIIa inhibitors. The role of hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins) in patients with acute coronary syndromes is being investigated and shows promise.
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PMID:Medical therapy of unstable angina and non-Q-wave myocardial infarction. 1108 46

Hypolipidaemic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (statin) treatment reduces cardiovascular risk and is also associated with the reduction of C-reactive protein (CRP) concentrations. However, there is scant data concerning the relationship between CRP and lipid changes during statin treatment. We studied 60 hypercholesterolaemic coronary patients who participated in the Treat to Target (3T) study comparing atorvastatin and simvastatin. Serum lipids and CRP (with a sensitive method) were measured before treatment at baseline and after 12 months of statin treatment. Low-density lipoprotein (LDL) cholesterol was substantially decreased and high-density lipoprotein (HDL) cholesterol increased during statin treatment. CRP decreased significantly (sign test P = 0.03) during treatment, and the changes of CRP were significantly associated with changes in HDL cholesterol (r = -0.45; P < 0.001) and apolipoprotein A1 (r = -0.40; P < 0.001) but not with changes in LDL cholesterol or triglycerides. The change in HDL cholesterol explained 20% of the change in CRP during statin treatment. The results are in line with previous suggestions that HDL has anti-inflammatory properties.
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PMID:Associations between change in C-reactive protein and serum lipids during statin treatment. 1112 36

Extensive trial evidence supports the use of hydroxy-methyl-glutaryl-CoA reductase inhibitors (HMG-CoA-RI; statins) in atherosclerotic disease. Statins can be divided into two broad groups: the 'natural' statins derived from a fungal metabolites, and synthetic compounds. Whether all statins have similar anti-atherosclerotic properties, or whether these actions are specific to the 'natural' statins, is controversial. This commentary reviews the differences between natural and synthetic statins with regard to lipid-lowering and non-lipid-lowering effects, including their action on the acute phase reactant C-reactive protein. Among the newer synthetic statins, fluvastatin has some positive end-point evidence while cerivastatin shares many biochemical properties with the 'natural' statins. Extensive clinical trial programmes are underway with both atorvastatin and cerivastatin. These trials will give a definitive answer to the question of whether synthetic statins are as equally efficacious as 'natural' statins in preventing atherosclerotic events.
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PMID:Synthetic statins: more data on newer lipid-lowering agents. 1146 49

Inflammation is involved in the initiation and progression of atherosclerosis and the development of atherosclerotic events. Understanding of the molecular basis of inflammation has led to the identification of markers that may be important new targets in atherothrombotic disease. Inflammatory markers, such as cell adhesion molecules, cytokines, and high-sensitivity C-reactive protein, have been shown to predict future cardiovascular events in individuals with and without established disease. 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, or statins, inhibit the synthesis of cholesterol and have been demonstrated to reduce cardiovascular morbidity and mortality. Recently, statins have been shown to modulate several of the mechanisms of inflammation in atherosclerosis in vitro and in vivo, including reduction of inflammatory markers in clinical trials. In this article, we briefly review the biology, epidemiology, and clinical trial data on the effects of statins on some of the more promising inflammatory markers.
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PMID:Statins and inflammatory markers. 1177 21

Estrogen replacement therapy (ERT) is claimed to reduce cardiovascular mortality by about 50% in postmenopausal women. This improvement is caused by favorable changes in lipid and lipoproteins metabolism, however, it also increases the incidence of the endometrial hyperplasia. Addition of progestin to ERT, referred to as hormone replacement therapy (HRT), has been shown to successively reduce this risk to the endometrium. Unfortunately, it has an adverse effect on high-density lipoprotein cholesterol (HDLC) concentration, thus compromising the benefits of ERT. Therefore the issue here whether HRT given alone and/or concomitantly with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (lovastatin) could exert any significant additional favorable effect on the lipid profile in bilaterally ovariectomized female rats. Sixty female Wistar rats were ovariectomized and treated with ERT (0.625 mg kg (-1)estradiol, E (2), IM every 2 weeks), HRT (estradiol plus progesterone, E (2)+ P, 0.625 mg kg (-1)estradiol and 5 mg progesterone kg (-1) respectively, IM every 2 weeks), and lovastatin (20 mg kg (-1)day (-1)orally) plus HRT (L + HRT) for 6 weeks. Blood aliquots were collected for serum and plasma separation. Serum vitamin E and plasma levels of C-reactive protein (CRP), nitric oxide (NO), lipid profile, and the susceptibility of non-HDLC to oxidation were determined. Moreover, thoracic aortas were dissected and directed for measurement of its lipid peroxide and NO contents. Treatment of ovariectomized rats with HRT showed a significant decrease ( P< 0.0001) in HDLC concentration compared to the group treated alone with ERT and increase ( P< 0.0001) in CRP levels compared to ovariectomized rats. HDLC and CRP are two powerful and significant predictors for increased cardiovascular risk in postmenopausal women. Addition of lovastatin as a complementary therapy to HRT revealed a significant 27% increment in HDLC and 48% decrement in CRP concentrations. Moreover, it significantly increased vitamin E, each of plasma and tissue content of NO and decreased atherogenic indexes (TC/HDLC, LDLC/HDLC), aortic lipid peroxide and susceptibility of non-HDLC to oxidation. In conclusion, this current study demonstrated that lovastatin together with continuous combined HRT seems to be more effective in the secondary prevention of coronary heart disease not only due to lipid lowering properties but also related to several other additive effects such as modification of endothelial function and inflammatory responses.
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PMID:A novel concept to preserve the beneficial effects of hormone replacement therapy in bilaterally female ovariectomized rats: role of lovastatin therapy. 1188 11

Inflammation-related processes play a key role the current etiologic model of atherosclerosis and its acute complications. Recent evidence suggests that blood-based biomarkers that reflect systemic inflammation may contribute to our ability to predict future risk of cardiovascular disease. Global markers of inflammation, such as C-reactive protein and fibrinogen, have been well studied as potential cardiovascular risk factors. A variety of additional markers that reflect various elements of the complex systems governing inflammation, including proinflammatory and antiinflammatory cytokines, mediators of cellular adhesion, and matrix degradation enzymes, are also worthy of study. Although many previous studies have examined the relation of inflammation to myocardial infarction, emerging evidence suggests that other cardiovascular phenotypes such as ischemic stroke and early-stage atherosclerosis may also be related to inflammation. Further elucidating the role of inflammation in cardiovascular disease may lead to the identification of new targets for preventive or therapeutic interventions. In addition, markers of inflammation may be useful as a means to predict or monitor an individual's response to currently available cardiovascular therapies, such as aspirin or HMG coenzyme A reductase inhibitors, that may act via antiinflammatory mechanisms.
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PMID:Systemic inflammation as a cardiovascular disease risk factor and as a potential target for drug therapy. 1197 14


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