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)

To investigate the presence of infectious agents in human atherosclerotic arterial tissues. Atherosclerotic plaques were removed from 128 patients undergoing carotid endarterectomy or other bypass procedures for occlusive disease, and from twenty normal arterial wall samples, obtained from transplant donors with no history of diabetes, hypertension, smoking, or hyperlipidemia. Using the polymerase chain reaction (PCR) or reverse transcription-PCR, these samples were analyzed for the presence of Chlamydia pneumoniae, cytomegalovirus, enterovirus, adenovirus, herpes simplex viruses types 1 and 2, and Epstein-Barr virus. The amplicons were then sequenced, and phylogenetic analyses were performed. Enteroviral RNA was found in 22 of 128 atherosclerotic vascular lesions (17.2%), and C. pneumoniae and cytomegalovirus were each found in 2 samples (1.6%). In contrast, adenovirus, herpes simplex viruses, and Epstein-Barr virus were not identified in any of the atherosclerotic samples. Enterovirus was detected in 6/24 (25.0%) aortas, 7/33 (21.2%) carotid arteries, 6/40 (15.0%) femoral arteries, and 3/31 (9.7%) radial arteries of patients with chronic renal failure. There were no infectious agents detected in any of the control specimens. Using phylogenetic analysis, the enterovirus isolates were clustered into 3 groups, arranged as echovirus 9 and coxsackieviruses B1 and B3. Enteroviral RNA was detected in 17.2% of atherosclerotic plaques, but was not observed in any of the control specimens. This suggests a connection between enteroviral infection and atherosclerosis. These findings differ from those of other studies, which found more frequent incidence of C. pneumoniae and cytomegalovirus infection in atherosclerotic plaques.
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PMID:Detection of enterovirus, cytomegalovirus, and Chlamydia pneumoniae in atheromas. 1565 Jun 86

It is assumed that various infectious agents play direct or indirect roles in the pathogenesis of atherosclerosis which is accepted as a chronic inflammatory phenomenon. However, the data obtained from different studies are contradictory. The aim of this study was to investigate the roles of herpes virus group [Herpes simplex virus (HSV), Epstein-Barr virus (EBV), Cytomegalovirus (CMV)] and hepatitis A virus (HAV) which are debated in terms of their impact in the pathogenesis of coronary arterial diseases. For this purpose, atherome plaque samples collected from 28 patients (23 were male; age range: 43-74 years) with atherosclerotic heart disease and vein samples from 22 control patients (19 were male; age range: 37-85 years) who had vascular diseases other than atherosclerosis, were investigated by means of the presence of nucleic acids of the above mentioned viruses by real-time polymerase chain reaction (PCR). Besides, classical cardiovascular risk factors (hypertension, hyperlipidemia, hypercholestrolemia, diabetes mellitus, smoking habits, gender, age and familial background) were questioned in both patient and control groups. As a result, no positivity were detected for nucleic acids of HSV type 1 and 2, EBV and HAV, whereas CMV-DNA was found positive in three of 28 (10.7%) atheromateous plaques (viral loads were 21, 188 and 288 copies/mg). Amongst 22 vascular samples from controls, two (9.1%) yielded positive results for EBV-DNA (viral loads were 5 and 10 copies/mg), while the other samples were found negative for nucleic acids of HSV type 1 and 2, CMV and HAV. The evaluation of the known risk factors for atherosclerosis revealed that, the difference between the presence of hypertension and hyperlipidemia which are the major risk factors, was statistically important (p < 0.05) in patient group (64% and 50%, respectively) and control group (32% and 23%, respectively). In conclusion, the hypothesis concerning the possible relationship between these viral agents and the progression of atherosclerosis, have not been supported by our data which are similar to the results obtained from various other studies. Actually, further studies are needed to clarify such direct or indirect roles of infectious agents in the pathogenesis of coronary arterial diseases.
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PMID:[Investigation of herpes group and hepatitis A virus nucleic acids in the atherome plaque samples of patients with coronary arterial disease]. 1817 72

We evaluated the efficacy and safety of immunosuppressive regimens containing a mammalian target of rapamycin (mTOR) inhibitor with tacrolimus (TAC) minimization therapy in solid organ transplant recipients. A PubMed search was conducted using the terms (mTOR OR sirolimus OR everolimus) AND tacrolimus AND renal AND (low OR reduced OR reduction OR minimization) AND transplant*; limited to title/abstract and English-language articles published from January 1, 2003, through January 28, 2013. Twenty-one relevant studies of TAC minimization therapy were identified and evaluated in the context of known concerns associated with immunosuppressive therapy. Review of these studies suggests that immunosuppressive regimens including an mTOR inhibitor and TAC minimization therapy better preserve renal function versus standard-dose TAC, without significant changes in patient survival or graft rejection rates. Among patients treated with an mTOR inhibitor plus TAC minimization therapy in 12 randomized controlled trials (n=856 kidney, n=190 heart, n=108 lung, n=719 liver patients), reported rates of infection (BK, cytomegalovirus, or Epstein-Barr virus) and malignancy were low (0% to 7%). Other adverse events were more commonly reported including dyslipidemia/hyperlipidemia in up to two thirds of patients, new-onset diabetes mellitus in up to 38%, wound complications in up to 22%, and hypertension in up to 17%.
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PMID:Review of combination therapy with mTOR inhibitors and tacrolimus minimization after transplantation. 2393 18

The objective of the present study was to investigate the role of blood glucose, lipid metabolism, body mass index (BMI), C-reactive protein (CRP) as well as an interleukin (IL)-17/IL-35 imbalance in the pathogenesis of concurrent gestational diabetes mellitus (GDM) and preeclampsia (PE) (DPE). The mRNA expression of forkhead box protein 3 (FoxP3), IL-35 [including Epstein-Barr virus-induced gene 3 (EBI3) and P35 subunits] and IL-17 in the peripheral blood mononuclear cells of patients with DPE (n=30), GDM (n=33), PE (n=33) and normal pregnancy (n=33) were determined by reverse transcription-quantitative polymerase chain reaction. The serum levels of IL-35, IL-17 and CRP were analyzed using ELISA. Serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL) and fasting blood glucose (FBG) were also detected. The levels of low-density lipoprotein (LDL) were calculated using the Friedewald formula. Body weight and height were determined in order to calculate the BMI. It was observed that the levels of FBG were markedly elevated in patients with GDM, PE and DPE. In addition, significantly higher serum TG, TC, LDL and very LDL were detected in patients with GDM, PE and DPE compared with those in subjects with normal pregnancies. By contrast, the concentration of HDL was lower in the patient groups. In addition, higher BMI values were identified in patients with GDM, PE and DPE. A decreased expression of FoxP3, P35 and EBI3 mRNA, and an elevated expression of IL-17 in PBMCs was detected in patients with GDM, PE and DPE. In addition, higher serum levels of IL-17 and CRP, as well as lower levels of IL-35, were observed. Furthermore, in patients with DPE, positive correlations of diastolic blood pressure with IL-17 levels, BMI and TG, as well as IL-17 levels with BMI and proteinuria were identified. In conclusion, the present study indicated that abnormal maternal lipids, hyperglycemia, high BMI, high CRP and IL-17/IL-35 imbalance may have a role in the pathophysiology of DPE. Therefore, pregnant women and clinicians should be made aware that maternal hyperlipidaemia, hyperglycemia, high BMI, high CRP levels and IL-17/IL-35 imbalance may lead to DPE.
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PMID:Maternal lipids, BMI and IL-17/IL-35 imbalance in concurrent gestational diabetes mellitus and preeclampsia. 2997 66