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)

Puumala virus, a hantavirus belonging to the Bunyaviridae family, causes a human disease known as nephropathia epidemica, a mild form of hemorrhagic fever with renal syndrome. The implementation of effective decontamination procedures is critical in hantavirus research to minimize the risk of personnel exposure. This study investigated the efficacy of Clidox((R)), Dettol((R)), ethanol, Halamid-d((R)), peracetic acid, sodium hypochloride and Virkon((R))S for inactivating Puumala virus. A real-time quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was used to quantify Puumala virus before and after treatment with these products. Inactivation of Puumala virus was effective after 10min with all products except ethanol. Inactivation with absolute ethanol was effective only after 30min. Using the qRT-PCR method, this study has shown that the commercially available products Clidox((R)), Halamid-d((R)) and Virkon((R))S in particular represent a rapid and safe way to decontaminate surfaces with possible Puumala virus contamination. These products can be used in solutions of 1-2%, with contact times greater than 10min, for inactivating effectively Puumala virus.
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PMID:Evaluation of the efficacy of disinfectants against Puumala hantavirus by real-time RT-PCR. 1718 60

The mechanisms of teratogenic effects of ethanol in Japanese medaka embryogenesis were investigated by testing the hypothesis that ethanol or its metabolite ameliorates the expression of ethanol metabolizing enzymes. We have previously demonstrated that ethanol is unable to alter the expression pattern of alcohol dehydrogenase (ADH) mRNA, the first enzyme of ethanol metabolism, in medaka embryos during development. We, therefore, extended our investigation to aldehyde dehydrogenase (ALDH) system, the next enzyme of alcohol metabolic pathway. As the first step towards studying the regulation of Aldh mRNA expression by ethanol, we have cloned a cDNA by reverse transcriptase polymerase chain reaction (RT-PCR) from adult Japanese medaka (Oryzias latipes) liver representing the medaka ALDH9 gene product, with a coding region of 1515 nucleotides. The deduced amino acid sequences share 81.2% identity with cod liver betaine aldehyde dehydrogenase (BADH, EC 1.2.1.8), and 71.1% identity with human ALDH9A1 sequences. RT-PCR analysis further showed that in adults Aldh9 mRNA is constitutively expressed in all organs tested (brain, eye, gill, GI, heart, liver, kidney, muscle, skin, testis and ovary). Using semi-quantitative (rRT-PCR) and quantitative real time RT-PCR (qRT-PCR), we detected Aldh9 mRNA at all time points of development and the expression was lowest between approximately 1 and 8 h post-fertilization (hpf). Treatment of the embryos with ethanol for 48 h post-fertilization (hpf) attenuates (delayed) the expression of Aldh9 mRNA. This delayed expression of Aldh9 mRNA by ethanol may enhance acetaldehyde concentration in the embryo and induce teratogenesis during development.
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PMID:Ethanol attenuates Aldh9 mRNA expression in Japanese medaka (Oryzias latipes) embryogenesis. 1723 98

A practical sampling method for bursal tissue using ordinary paper for molecular diagnosis of infectious bursal disease (IBD) was established. IBD virus-infected bursa was directly smeared on chromatography paper, filter paper, or stationery copy paper and was then fixed with absolute ethanol, Tris-HCl-saturated phenol, or phenol:chloroform:isoamyl alcohol (25:24:1). Flinders Technology Associates (FTA) card, which is designed for the collection of biological samples for molecular detection, was also used. After storage at 37 C for up to 30 days, total RNA directly extracted from the tissue fixed on the papers and FTA card were subjected to reverse transcriptase-polymerase chain reaction (RT-PCR) for detection of IBD virus (IBDV) RNA. In addition, the ability of each chemical used in the fixation and the FTA card to inactivate IBDV was evaluated. Regardless of the paper quality, storage period, and fixation method, IBDV RNA was consistently detected in all of the samples. IBDV in the bursal tissue was inactivated with phenol but not with ethanol or the unknown chemicals in FTA card. These results show that ordinary papers sustain the viral RNA, as does FTA card, but phenol fixation is superior to FTA card in inactivating IBDV. The new sampling method using ordinary paper with phenol fixation is safe, inexpensive, simple, and easy, and is thus suitable for conducting a global survey of IBD even where laboratory resources are limited. This practical method should contribute to the control of IBD worldwide.
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PMID:A practical tissue sampling method using ordinary paper for molecular detection of infectious bursal disease virus RNA by RT-PCR. 1727 94

While altered activities in sensory neurons were noticed in neuropathic pain, caused by highly diverse insults to the peripheral nervous system, such as diabetes, alcohol ingestion, cancer chemotherapy and drugs used to treat AIDS, other infections and autoimmune diseases, as well as trauma, our understanding of how these various peripheral neuropathies manifest as altered neuronal activity is still rudimentary. The recent development of models of several of those neuropathies has, however, now made it possible to address their impact on primary afferent nociceptor function. We compared changes in mechanically-evoked C-fiber activity, in models of painful peripheral neuropathy induced by drinking ethanol (alcohol) or administering 2',3'-dideoxycytidine (ddC), a nucleoside reverse transcriptase inhibitor for AIDS therapy, two co-morbid conditions in which pain is thought to be mediated by different second messenger signaling pathways. In C-fiber afferents, ddC decreased conduction velocity. In contrast, alcohol but not ddC caused enhanced response to mechanical stimulation (i.e., decrease in threshold and increase in response to sustained threshold and supra-threshold stimulation) and changes in pattern of evoked activity (interspike interval and action potential variability analyses). These marked differences in primary afferent nociceptor function, in two different forms of neuropathy that produce mechanical hyperalgesia of similar magnitude, suggest that optimal treatment of neuropathic pain may differ depending on the nature of the causative insult to the peripheral nervous system, and emphasize the value of studying co-morbid conditions that produce painful peripheral neuropathy by different mechanisms.
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PMID:Mechanically-evoked C-fiber activity in painful alcohol and AIDS therapy neuropathy in the rat. 1731 57

Previous studies show that chronic alcohol abuse is an independent risk factor for acute lung injury (ALI) and impairs alveolar epithelial barrier function through glutathione depletion. However, the precise molecular structures that are damaged by chronic ethanol ingestion have not been identified. To test whether chronic ethanol ingestion impairs the alveolar epithelium barrier by tight junction protein deterioration and predisposes to ALI, this study determined the alterations in tight junction proteins occludin, zonula occludens (ZO)-1, and adherens junction protein E-cadherin in alveolar epithelium and observed the protective effect of glutamine (Gln) supplementation. Sixty Sprague-Dawley rats were assigned to control, ethanol (6 weeks' ethanol feeding), lipopolysaccharide ([LPS] 2 mg/kg, i.v.), ethanol plus LPS, ethanol plus Gln (0.3 g/kg, gavage daily), and ethanol plus Gln plus LPS groups. Treatment with both ethanol and LPS significantly increased bronchoalveolar epithelial permeability, and treatment with ethanol plus LPS further increased the permeability. Using immunofluorescence, immunoblotting, and reverse transcriptase-polymerase chain reaction, this study shows that treatment with both ethanol and LPS induced partial breakdown of membrane staining and decreased cytoplasm staining in alveolar epithelium and decreased the messenger RNA and protein expression of those molecules in alveolar epithelial cells. Treatment with ethanol plus LPS caused further deterioration. Moreover, Gln supplementation markedly attenuated the enhanced bronchoalveolar epithelial permeability and decreased messenger RNA and protein expression of those molecules induced by ethanol and ethanol plus LPS. These data suggest that chronic ethanol ingestion impairs the alveolar epithelial barrier function via occludin, ZO-1, and E-cadherin deterioration, and predisposes to ALI. Glutamine supplementation has protective effect.
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PMID:Effects of chronic ethanol ingestion on tight junction proteins and barrier function of alveolar epithelium in the rat. 1751 55

In the current study, we examined the cytocompatibility of eight vinyl esters as candidate plasticizers for producing phthalate- and ethanol-free tissue conditioners. We measured the estrogenic activity and cytotoxicity of vinyl esters in human fibroblasts and keratinocytes using an E-screen assay and a mitochondrial dye conversion assay, respectively. We also assessed the cytotoxicity of three prototype materials and commercially available tissue conditioners on human fibroblasts grown in collagen gels. Finally, we measured the effects of these materials on the expression of cytokines in three-dimensional cultures by reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assays. None of the tested vinyl esters had estrogenic activity. Vinyl octanoate and vinyl pivalate were the least cytotoxic of the eight tested vinyl esters. In the same vein, a prototype tissue conditioner containing vinyl octanoate had equivalent or weaker cytotoxicity and induction of cytokine expression than conventional materials.
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PMID:Cytocompatibility of a tissue conditioner containing vinyl ester as a plasticizer. 1820 82

Escherichia coli contains a four-gene operon, pgaABCD, which encodes the proteins necessary for the synthesis of polymeric N-acetylglucosamine, or PGA. Poly-N-acetyl-glucosamine was first described in Staphylococcus aureus and Staphylococcus epidermidis and was found to have important roles in biofilm formation and immune evasion. PGA also plays a role in biofilm formation in E. coli, but its role in immune evasion has not been thoroughly studied. We previously reported that E. coli PGA cross-reacts with an opsonic-antibody raised against S. aureus PNAG and this is the basis for an ongoing investigation regarding the development of a vaccine against both pathogens. In this paper we investigated pga expression in wild type and csrA or nhaR deletion mutant strains during different growth phases and temperatures, and in response to chemical stimuli using a pga promoter-reporter fusion construct, real-time reverse transcriptase-PCR, immunoblotting, and biofilm assays. Expression of pga and polysaccharide synthesis were induced by glucose, NaCl, and ethanol, but only glucose augmented biofilm formation. The regulatory factor NhaR was required for NaCl-induced pga expression, whereas the effects of glucose and ethanol were independent of CsrA and NhaR.
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PMID:Effect of growth conditions on poly-N-acetylglucosamine expression and biofilm formation in Escherichia coli. 1844 67

Abacavir is a carbocyclic 2'-deoxyguanosine nucleoside reverse transcriptase inhibitor that is used as either a 600-mg once-daily or 300-mg twice-daily regimen exclusively in the treatment of HIV infection. Abacavir is rapidly absorbed after oral administration, with peak concentrations occurring 0.63-1 hour after dosing. The absolute bioavailability of abacavir is approximately 83%. Abacavir pharmacokinetics are linear and dose-proportional over the range of 300-1200 mg/day. To date, one study has assessed the steady-state pharmacokinetics of abacavir following a 600-mg once-daily regimen, and reported a geometric mean steady-state abacavir peak concentration of 3.85 microg/mL. Although this concentration is higher than the steady-state abacavir peak concentration reported following a 300-mg twice-daily regimen (0.88-3.19 microg/mL, depending on the study), the geometric mean steady-state abacavir exposure over 24 hours was similar following these regimens. Coadministration with food has no significant effect on abacavir exposure; therefore, abacavir may be administered with or without food.The apparent volume of distribution of abacavir after intravenous administration is approximately 0.86 +/- 0.15 L/kg, suggesting that abacavir is distributed to extravascular spaces. Binding to plasma proteins is about 50% and is independent of the plasma abacavir concentration. Abacavir is extensively metabolized by the liver; less than 2% is excreted as unchanged drug in the urine. Abacavir is primarily metabolized via two pathways, uridine diphosphate glucuronyltransferase and alcohol dehydrogenase, resulting in the inactive glucuronide metabolite (361W94, ~36% of the dose recovered in the urine) and the inactive carboxylate metabolite (2269W93, approximately 30% of the dose recovered in the urine). The remaining 15% of abacavir equivalents found in the urine are minor metabolites, each less than 2% of the total dose. Faecal elimination accounts for about 16% of the dose. The terminal elimination half-life of abacavir is approximately 1.5 hours. The antiviral effect of abacavir is due to its intracellular anabolite, carbovir-triphosphate (CBV-TP). When assessed by validated high-performance liquid chromatography electrospray ionization tandem mass spectrometry, CBV-TP has been shown to have a long elimination half-life (>20 hours), supporting once-daily dosing. The mean CBV-TP trough concentrations do not differ following abacavir 600-mg once-daily and 300-mg twice-daily regimens. Limited data are available for abacavir in subjects with renal dysfunction or hepatic impairment. Abacavir pharmacokinetics in HIV-infected subjects with end-stage renal disease were found to be no different from those observed in healthy adults; this finding was consistent with the kidney being a minor route of abacavir elimination. A study of abacavir pharmacokinetics in hepatically impaired adults (Child-Pugh score of 5-6) showed that the abacavir area under the plasma concentration-time curve and elimination half-life were 89% and 58% greater, respectively, suggesting that the daily dose of abacavir should be reduced in patients with mild hepatic impairment (Child-Pugh score of 5-6). Abacavir pharmacokinetics have not been studied in patients with higher Child-Pugh scores. Abacavir is not significantly metabolized by cytochrome P450 (CYP) enzymes, nor does it inhibit these enzymes. Therefore, clinically significant drug interactions between abacavir and drugs metabolized by CYP enzymes are unlikely. The potential for drug interactions is no different when abacavir is used as a once-daily regimen versus a twice-daily regimen. No clinically significant drug interactions have been observed between recommended doses of abacavir and lamivudine, zidovudine, alcohol (ethanol) or methadone.
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PMID:A review of the pharmacokinetics of abacavir. 1847 71

Transgenic mice that express human equilibrative nucleoside transporter subtype 1 (hENT1) under the control of a neuron-specific enolase promoter have been generated. Southern blot and PCR revealed the presence of the transgene in five founder mice. Mice from each founder line were examined by reverse transcriptase (RT)-PCR and found to express hENT1 in RNA isolated from whole brain, cerebral cortex, striatum, hippocampus, and cerebellum but not liver, kidney, heart, lung or skeletal muscle. Cortical synaptosomes prepared from transgenic mice had significantly increased [(3)H]adenosine uptake and [(3)H]nitrobenzylthioinosine binding, relative to samples from wild-type mice. In behavioral tests, transgenic mice had altered responses to caffeine and ethanol, two drugs that inhibit and enhance, respectively, adenosine receptor activity. Caffeine-induced locomotor stimulation was attenuated whereas the hypnotic effect of ethanol was enhanced in transgenic mice. Caffeine was more potent in inhibiting ethanol-induced motor incoordination in wild-type than in transgenic mice. No differences in expression of mouse genes for adenosine receptors, nucleoside transporters, or purine metabolizing enzymes were detected by RT-PCR analyses. These data indicate that expression of hENT1 in neurons does not trigger adaptive changes in expression of adenosine-related genes. Instead, hENT1 expression affects dynamic changes in endogenous adenosine levels, as revealed by altered behavioral responses to drugs that affect adenosine receptor signalling.
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PMID:Transgenic expression of human equilibrative nucleoside transporter 1 in mouse neurons. 1922 1

It was recently shown that, as in yeast, alcohols selectively increase the hemolytic properties of certain staphylococci strains. This phenomenon has been called 'microbial alcohol-conferred hemolysis'(MACH). Here we present the changes in gene expression by Staphylococcus aureus 8325-4, in response to ethanol. Ethanol upregulated the expression of multiple toxins and increase the pathogen potential of S. aureus strain 8325-4. Ethanol also increased the level of genes considered necessary for production and viability of biofilm, such as: icaAD, sdrDE, pyr, and ure. Increased urease activity appeared to be an important factor in the ethanol response along with macromolecule repair mechanisms. Oxidative-stress responses, such as increased expression of sodA1, sodA2 and upregulation of zinc-containing alcohol dehydrogenase, alcohol-acetaldehyde dehydrogenase (adhE) and two aldehyde dehydrogenases (aldA1, aldA2), which can generate more reducing power, were also induced. Upregulation of fatty acid metabolism appears to be important in enabling the bacteria to handle excess amounts of ethanol which ultimately may lead to synthesis of lytic lypids. The patterns of regulation were confirmed by quantitive reverse transcriptase PCR (QRT-PCR). These results, taken together, suggest that exposure to ethanol increases pathogenic traits and induce oxidative-stress responses.
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PMID:Global gene expression in Staphylococcus aureus following exposure to alcohol. 1990 May 30


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