Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemorrhagic shock (HS) is a major cause of morbidity and mortality in trauma patients. The early growth response 1 (Egr-1) transcription factor is induced by a variety of cellular stresses, including hypoxia, and may function as a master switch to trigger the expression of numerous key inflammatory mediators. We hypothesized that HS would induce hepatic expression of Egr-1 and that Egr-1 upregulates the inflammatory response after HS. The Egr-1 mice and wild-type (WT) controls (n>or=5 for all groups) were subjected to HS alone or HS followed by resuscitation (HS/R). Other mice were subjected to a sham procedure which included general anesthesia and vessel cannulation but no shock (sham). After the HS, HS/R, or sham procedures, mice were euthanized for determination of serum concentrations of interleukin (IL) 6, IL-10, and alanine aminotransferase. Northern blot analysis was performed to evaluate Egr-1 messenger RNA (mRNA) expression. Liver whole cell lysates were evaluated for Egr-1 protein expression by Western blot analysis. Hepatic expression of IL-6, granulocyte colony-stimulating factor, and intracellular adhesion molecule 1 mRNA was determined by semiquantitative reverse transcriptase-polymerase chain reaction. The Egr-1 DNA binding was assessed using the electrophoretic mobility shift assay. Hemorrhagic shock results in a rapid and transient hepatic expression of Egr-1 mRNA in WT mice by 1 h, whereas protein and DNA binding activity was evident by 2.5 h. The Egr-1 mRNA expression diminished after 4 h of resuscitation, whereas Egr-1 protein expression and DNA binding activity persisted through resuscitation. The Egr-1 mice exhibited decreased levels of hepatic inflammatory mediators compared with WT controls with a decrease in hepatic mRNA levels of IL-6 by 42%, granulocyte colony-stimulating factor by 39%, and intracellular adhesion molecule 1 by 43%. Similarly, Egr-1 mice demonstrated a decreased systemic inflammatory response and hepatic injury after HS/R compared with their WT counterparts. Early growth response 1 is rapidly upregulated in the liver during and after resuscitation from HS. Our results showing a blunted inflammatory response in Egr-1 mice provides evidence that Egr-1 functions as a proximal signal transduction mechanism responding to shock by amplifying the systemic inflammatory response.
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PMID:Early growth response 1 mediates the systemic and hepatic inflammatory response initiated by hemorrhagic shock. 1722 90

The purpose of this study was to investigate the hepatoprotective effects of a fermented substance from Aspergillus phoenicis (FSAP) on chronic liver injuries induced by carbon tetrachloride (CCl(4)) in rats. CCl(4) (20%; 0.2 ml/100 g body weight) was given twice a week for 9 weeks, and the rats received FSAP throughout the whole experimental period. Plasma ALT and AST, spleen weight, and hepatic levels of lipid peroxidation and hydroxyproline were significantly lower in the rats treated with FSAP as compared to CCl(4) only. Liver pathology in the FSAP-treated rats was also improved. Real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR) analysis showed that FSAP treatment increased the expression of matrix metalloproteinase 13 and decreased the expression of methionine adenosyltransferase 2A, collagen (alpha1)(I), collagen (alpha1)(III), transforming growth factor-beta1, and tissue inhibitor of metalloproteinase 1. These results clearly indicate that FSAP partially reduced the liver fibrosis in rats induced by CCl(4).
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PMID:A fermented substance from Aspergillus phoenicis reduces liver fibrosis induced by carbon tetrachloride in rats. 1748 51

One of the hallmarks of cancer is limitless proliferative capacity, which is tightly associated with the ability to maintain telomeres. Over the last decade, the telomere biology of pediatric cancers has begun to be elucidated. Most pediatric leukemias and embryonal solid tumors activate the enzyme telomerase, a specialized reverse transcriptase that adds nucleotide repeats to telomeres. In general, high levels of tumor telomerase expression are associated with unfavorable outcome, although results vary according to tumor type. Some pediatric tumors, including osteosarcoma and glioblastoma multiforme, lack telomerase activity and maintain telomeres via a recombination-based mechanism called ALT (alternative lengthening of telomeres). Telomerase is a highly attractive therapeutic target for pediatric cancer because the enzyme plays a key role in conferring cellular immortality, is present in most tumors, and is relatively specific for cancer cells. Telomerase inhibitors have been evaluated in preclinical models of adult cancers, but few studies have been conducted on pediatric cancers. Further research is required to define how telomere biology can be used to clinical advantage in malignancies of childhood.
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PMID:Telomere biology of pediatric cancer. 1753 Apr 90

The aims of this study were to investigate the viral differences among lamivudine-resistant hepatitis B virus (HBV) genotypes B and C in vivo. Fifty-three patients carrying lamivudine-resistant HBV were enrolled in this study. HBV genotypes, Levels of alanine aminotransferase (ALT), HBV DNA levels were monitored during therapy. The polymerase and precore/core promoter genes were amplified by polymerase chain reaction and their products were sequenced directly. Among 53 patients resistant HBV genotypes B and C accounted for 41.50% and 58.50%, respectively. The occurrence of reverse transcriptase rt204I mutants was lower in genotype B (36.36%) than that in genotype C (87.10%), whereas rt204V mutants was higher in genotype B (63.64%) than that in genotype C (12.90%). The occurrence of precore mutation (nt1896A) was higher in genotype B (77.27%) than that in genotype C (32.26%). Serum HBV DNA levels after emergence of lamivudine resistance were higher in genotype C (7.71 +/- 0.80 Log copies/mL) compared with genotype B (6.97 +/- 0.77 Log copies/mL). Multivariate analysis identified pretreatment HBV DNA levels, HBeAg status and HBV genotype as independent factors associated with a shorter time to lamivudine resistance(P = 0.035, P = 0.006 and P = 0.001, respectively). Multivariate analysis showed that HBV genotype (P = 0.004) and pretreatment ALT levels (P = 0.01) was independently associated with YMDD mutational patterns. The results showed that the YMDD mutational patterns, precore mutation and serum HBV DNA levels differ between lamivudine-resistant HBV genotypes B and C in vivo. It is valuable for treatment of lamivudine-resistant HBV in clinic.
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PMID:Differences of YMDD mutational patterns, precore/core promoter mutations, serum HBV DNA levels in lamivudine-resistant hepatitis B genotypes B and C. 1792 12

Anti-HAV IgM positive serum samples from acute phase hepatitis A patients from various areas in Turkey were tested for viral RNA by RT-PCR (reverse transcriptase polymerase chain reaction), using primer pairs from two different regions of the HAV genome. The PCR products amplified from both genomic regions underwent phylogenetic analyses. A comparison of the regions showed the same genotyping results, and the RT-PCR-2 in the 5'NCR demonstrated greater sensitivity compared to RT-PCR-1 in the VP1-P2A region. The majority of the isolates belonged to genotype IB and are related closely to each other; however, two isolates related even more strongly to the HAV HM175 strain. Two (n = 37) RT-PCR positive sera were classified under genotype IA. A surprising finding emerged for the mean levels of serum transaminases AST and ALT: higher levels were found in patients under 10 years of age compared to older patients. Anti-HAV IgM levels were determined quantitatively and, in addition, the HAV-RNA genome equivalents were ascertained by real time RT-PCR. No evidence was found for an association between viral load and the higher transaminase levels in the younger group.
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PMID:Acute hepatitis A virus infection in Turkey. 1836 Aug 91

GB virus C (GBV-C) infection is frequent in patients infected with the human immunodeficiency virus (HIV) due to similar transmission routes of these viruses. The aim of this study was to determine the rate of infection and genotypic characteristics of GBV-C in this population. The presence of GBV-C RNA was determined in serum samples of 106 patients infected with HIV by reverse transcriptase-nested polymerase chain reaction. GBV-C genotypes were determined by direct sequencing. Hepatitis B surface antigen (HBsAg), hepatitis B surface antibody (anti-HBs), hepatitis C antibody (anti-HCV), alanine aminotransferase (ALT) levels, HIV viral load and CD4(+) count were also tested in all patients. The overall prevalence of GBV-C infection was 11.3% in HIV patients. There was no significant difference between patients with and without GBV-C infection regarding age, sex, route of transmission, viral load, ALT levels, HBV and HCV co-infection and treatment with antiretroviral drugs. 66.7% of patients with GBV-C had a CD4(+) count > or = 200 and 33.3% had a CD4(+) count < 200 cells/mm(3). Phylogenetic analysis revealed that all GBV-C isolates were genotype 2, and classified as subtype 2a. GBV-C infection is relatively common in patients infected with HIV. The prevailing GBV-C genotype 2a in this study group concurred with reports from other parts of the Middle East.
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PMID:Frequency and genotype of GB virus C among Iranian patients infected with HIV. 1881 33

This study focuses on the prevalence of hepatitis G virus (GBV-C/HGV) in hemodialysis patients and blood donors in Denizli (located at Aegean region of Turkey). A total of 100 patients (mean age: 56.8 +/- 13.3 years; 46 female) receiving hemodialysis and 100 blood donors (mean age: 31.3 +/- 8.1 years; 8 female) were included in the study. The presence of GBV-C/HGV RNA was determined in all patients by reverse transcriptase-PCR and the presence of GBV-C/HGV anti-E2 antibodies was determined by a commercial enzyme immunoassay (Diagnostic Automation, INC). Viral RNA positivity was determined in 14 (14%) of the hemodialysis patients and 2 (2%) of the blood donors, the difference being statistically significant (p < 0.05). GBV-C/HGV anti-E2 antibodies were detected in 1 (1%) of the hemodialysis patients and 3 (3%) of the blood donors. Anti-E2 positive patient also revealed positive result for viral RNA. There was no statistically significant difference between the two groups in terms of anti-E2 positivity. The prevalence of GBV-C/HGV was 14% in hemodialysis patients and 5% in blood donors (p < 0.05). There was no significant difference in terms of duration of hemodialysis, serum ALT levels, age or gender between GBV-C/HGV positive and negative hemodialysis patients. In conclusion, since hemodialysis patients are at an increased risk of parenteral transmission, they have significantly higher GBV-C/HGV viremia rates and prevalence when compared to blood donors. However, the prevalence of GBV-C/HGV and coexistence between GBV-C/HGV and hepatitis C virus have been decreasing in our region owing to increased hygienic precautions in hemodialysis units, avoidance of unnecessary blood transfusions and more widespread use of erythropoietin.
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PMID:[Investigation of hepatitis G virus prevalence in hemodialysis patients and blood donors in Denizli, Turkey]. 1914 83

Studies in the past decades have shown that active hepatitis B virus (HBV) replication is the key driver of liver injury and disease progression, and thus sustained viral suppression is of paramount importance in the management of chronic HBV infection. The nucleos(t)ide analogues lamivudine, adefovir, entecavir, telbivudine and tenofovir are potent inhibitors of HBV polymerase/reverse transcriptase activity and are highly effective in the suppression of HBV replication, but rarely eliminate the virus. Long-term therapy is usually required to achieve sustained hepatitis B e antigen seroconversion, HBV DNA suppression, ALT normalization and fibrosis reversal. Maintained long-term therapy has been demonstrated to significantly lower the rate of hepatic decompensation and development of cirrhosis or hepatocellular carcinoma. However, drug resistance is a serious risk on prolonged nucleos(t)ide analogue therapy, and this poses a critical challenge. Prevention and proper management of drug resistance are crucial to ensure long-term success.
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PMID:Nucleos(t)ide analogues for hepatitis B virus: strategies for long-term success. 1918 68

The aims of the study were to investigate the efficacy of rescue therapy with lamivudine (LAM) and adefovir (ADV) combination for 6 months followed by ADV monotherapy in lamivudine-resistant chronic hepatitis B (LAM-R CHB) patients, and to analyze the frequency of ADV resistance mutant development in such patients. A total of 170 consecutive LAM-R CHB patients (male/female: 130/40, mean age: 42.9+/-13.4 years) with viral breakthrough under LAM therapy were analyzed. A total of 68 had HBeAg-positive. Patients received rescue therapy with LAM [100 mg (qd)]+ADV [10 mg (qd)] for 6 months after which LAM was discontinued. HBV-DNA was assessed with the HBV-DNA 3.0 bDNA assay. ADV-resistant mutations were identified by sequencing the reverse transcriptase region. The median duration of rescue therapy was 24 months. Cumulative probability of becoming HBV-DNA undetectable was 33.8%, 59.6% and 68.2% after 24, 48 and 96 weeks of treatment, respectively. These figures were 43.2%, 58.0% and 73.1% for ALT normalization. Among 68 HBeAg-positive CHB patients, 10 patients had an e-antigen seroconversion. Low baseline HBV-DNA level (<10(7) copies/mL) was a significant predictor of response to ADV treatment (P<0.01). Cumulative probability of ADV resistance was 1.2%, 15.1% and 37.3% at 12, 24 and 36 months of therapy, respectively. By multivariate analysis, baseline high viral load and primary nonresponse to treatment at week 24 predicted ADV resistance. The data indicate that a time limited add-on strategy does not provide benefit over the switch strategy with respect emergence of ADV resistant mutants in LAM-R CHB patients.
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PMID:A short course of add-on adefovir dipivoxil treatment in lamivudine-resistant chronic hepatitis B patients. 1922 42

In hepatitis C virus (HCV) infection, the Th1-type immune response is involved in liver injury. A predominance of immunosuppressive regulatory T cells (Treg) is hypothesized in patients with persistently normal alanine aminotransferase (PNALT). Our aim was to clarify the role of Treg in the pathogenesis of PNALT. Fifteen chronically HCV-infected patients with PNALT, 21 with elevated ALT (CH) and 19 healthy subjects (HS) were enrolled. We determined naturally-occurring Treg (N-Treg) as CD4+CD25high+FOXP3+ T cells. The expression of FOXP3 and CTLA4 in CD4+CD25high+ cells was quantified by real-time reverse transcriptase-polymerase chain reaction. Bulk or CD25-depleted CD4+ T cells cultured with HCV-NS5 loaded dendritic cells were assayed for their proliferation and cytokine release. We examined CD127-CD25-FOXP3+ cells as distinct subsets other than CD25+ N-Treg. The frequencies of N-Treg in patients were significantly higher than those in HS. The FOXP3 and CTLA4 transcripts were higher in PNALT than those in CH. The depletion of CD25+ cells enhanced HCV-specific T cell responses, showing that co-existing CD25+ cells are suppressive. Such inhibitory capacity was more potent in PNALT. The frequency of CD4+CD127-CD25-FOXP3+ cells was higher in CH than those in PNALT. Treg are more abundant in HCV-infected patients, and their suppressor ability is more potent in patients with PNALT than in those with active hepatitis.
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PMID:Enhanced ability of regulatory T cells in chronic hepatitis C patients with persistently normal alanine aminotransferase levels than those with active hepatitis. 1948 78


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