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)

A study was undertaken to assess the etiology, optimal diagnostic method, and incidence of healing of perianal ulcers in HIV-seropositive men. Between March 1990 and December 1991, 26 HIV-seropositive homosexual or bisexual males were referred with perianal ulcerations. According to CDC criteria, three (12 percent) were Class II, six (23 percent) were Class III, and 17 (65 percent) were Class IV. Eighteen patients had one ulcer, five had two ulcers, and two had three ulcers. In one patient the ulcer was circumanal. Patients with superficial erosions were not included. Biopsies were obtained in 23 patients for routine microscopy, HIV, cytomegalovirus, herpes simplex virus, and acid-fast bacilli. Biopsy revealed an immunoblastic lymphoma in one patient. A comparison of microscopy and culture results revealed culture to be more helpful in determining the etiology of these ulcers. Medical treatment included reverse transcriptase inhibitors (zidovudine, dideoxyinosine, and dideoxycytosine), oral and topical Zovirax (Burroughs Wellcome, Research Triangle Park, NC), ganciclovir, and oral broad-spectrum antibiotics. Surgical treatment included lateral internal sphincterotomy in three patients and seton placement in one patient. Follow-up for at least four weeks was obtained in 22 patients. Overall, healing occurred in 15 patients (68 percent): three (20 percent) were Class II, four (27 percent) were Class III, and eight (53 percent) were Class IV. Healing occurred in all four patients who underwent surgical treatment. In conclusion, aggressive diagnostic maneuvers allow the use of both medical and conservative surgical measures to successfully treat the majority of perianal ulcers in this patient population.
Dis Colon Rectum 1993 Mar
PMID:Is aggressive management of perianal ulcers in homosexual HIV-seropositive men justified? 844 27

To elucidate which of the seven transcriptionally active genes of the carcinoembryonic antigen (CEA) subfamily are expressed in human colon, we first examined mRNA expression using reverse transcriptase PCR. The result showed the CEA, nonspecific crossreacting antigen 50/90 (NCA), biliary glycoprotein (BGP), and carcinoembryonic antigen gene family member 2 (CGM2) mRNAs were expressed in the colon. To determine the cellular sources of these members within normal colonic mucosa, in situ hybridization and immunocytochemistry were then performed. CEA and NCA mRNAs were clearly detectable in the cytoplasm of columnar and goblet cells at the free luminal surface and the upper crypts with low hybridization in the mid crypt and the crypt base. In contrast, BGP and CGM2 mRNAs were restricted only to columnar cells at the upper third of the crypts and the luminal surface. Colon epithelium expression of CEA, NCA, BGP and CGM2 coincided with that of corresponding mRNAs. Ultrastructurally, CEA, NCA, BGP and CGM2 were localized mainly to the apical surface glycocalyx, the fuzzy coat, of columnar cells. Interestingly, these molecules were localized in different microdomains within the fuzzy coat. Furthermore, BGP was highly expressed in the fuzzy coat of cryptal caveolated cells. As integral components of the fuzzy coat, CEA, NCA, BGP and CGM2 can hardly function as intercellular adhesion molecules; they possibly play an important role in epithelial-microbial interactions.
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PMID:Four carcinoembryonic antigen subfamily members, CEA, NCA, BGP and CGM2, selectively expressed in the normal human colonic epithelium, are integral components of the fuzzy coat. 1043 21

We recently demonstrated that the pattern recognition receptors (PRRs) toll-like receptor 2 (TLR2), TLR4, and CD14 are expressed in mouse colonic epithelium in a compartmentalized manner. Here we report the localization of TLR5, the receptor for bacterial flagellin, and its distinctive down-regulation during experimental colitis. Guts from normal BALB/c mice and those with dextran sodium sulfate (DSS)-induced colitis were compared. Each gut was divided into seven segments (stomach, small intestine [three parts], and colon [three parts]), and epithelial cells and crypt units were collected by scraping and EDTA treatment, respectively. Northern blotting showed that TLR5 mRNA was preferentially expressed in the epithelium of the proximal colon in normal mice. Laser capture microdissection coupled to reverse transcriptase PCR confirmed this localization. TLR5 protein expression reflected mRNA expression, as evidenced by Western blotting. In mice with acute colitis, inflammation occurred mainly in the distal colon. Interestingly, while TLR2, TLR4, and CD14 were up-regulated in the inflamed colon, TLR5 was down-regulated at both the mRNA and protein levels. Decreased TLR5 expression was more evident during chronic colitis. Additional in vitro studies using a mouse cell line, Colon-26, showed that gamma interferon (IFN-gamma) time- and dose-dependently down-regulates TLR5. In conclusion, epithelial cells, mainly in the proximal colon, constitutively express TLR5. TLR5 expression is down-regulated in vivo during acute and chronic DSS-induced colitis, in contrast to the expression of TLR2, TLR4, and CD14. The mechanism governing TLR5 regulation may therefore differ from that controlling other PRRs. Finally, IFN-gamma may be involved in down-regulating TLR5 expression.
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PMID:Epithelial toll-like receptor 5 is constitutively localized in the mouse cecum and exhibits distinctive down-regulation during experimental colitis. 1642 10

We report production of a monoclonal antibody against the hRRM2 subunit of ribonucleotide reductase and immunohistochemistry (IHC) staining of human cancer tissues available in paraffin block. BALB/c mice were immunized with purified hRRM2 protein, and splenocytes from these mice were fused with mice myeloma cell lines by using standard hybridoma production techniques. Resulting hybridomas producing anti-hRRM2 antibodies were screened by enzyme-linked immunosorbent assay (ELISA). The specificity was determined by limiting serial dilutions. Clones were chosen for antibody production based on their activities on paraffin-embedded human tissues. They were then isotyped and shown to produce immunoglobulin M (IgM) antibodies against hRRM2. Using these antibodies, we performed Western blot on oropharyngeal KB cancer cell lines and immunohistochemistry staining of available paraffin-embedded cancer tissues. Interestingly, cancer tissues stained positive with the anti-hRRM2 antibody but not normal tissues. Colon, stomach, liver, lung, pancreatic, and breast cancer had the strongest staining. No staining was identified on astrocytoma, mesothelioma, or myeloma. Our findings were validated with data from reverse transcriptase-polymerase chain reaction (RT-PCR) demonstrating overexpression of hRRM2 in breast cancer tissues compared to matched noncancer tissues. We propose that IHC with this monoclonal anti-hRRM2 antibody may be useful for ribonucleotide reductase research and as a biomarker for tumorgenesis.
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PMID:Production of a monoclonal antibody against the hRRM2 subunit of ribonucleotide reductase and immunohistochemistry study of human cancer tissues. 1704 81