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PubMed1992

Use of a mouth gag instrument to facilitate bite block insertion and prevent finger and probe bites during transesophageal echocardiography.

Transesophageal echocardiography greatly enhances the examination of patients difficult to image transthoracically. While of low patient risk, a potential for harm from human bites to the echocardiography staff and to the transesophageal probe remains, particularly when dealing with uncooperative patients. This risk potential prompted implementation of additional anti-bite protection in our universal precautions policy beyond use of a standard mouth guard. A mouth gag instrument was modified by placing latex rubber tubing over the instrument blades. This instrument was inserted into the mouth and set in an open position giving the operator safe access for probe and mouth bite guard insertion. This technique improved access to the patient's mouth and visualization of probe insertion without the mouth bite guard. The mouth gag instrument provided an insertion of the transesophageal probe in impaired or otherwise uncooperative patients, which was safer for the patient, laboratory staff, and the probe itself.

Bites, Human↗

PubMed1993

ELISA detection of glycosaminoglycan (GAG)-linked proteoglycans in gingival crevicular fluid.

The purpose of this study was to develop an ELISA method to detect chondroitin sulfate isomer-linked proteoglycans in gingival crevicular fluid (GCF), and to elucidate the role played by the glycosaminoglycans (GAGs) in GCF during experimentally-induced periodontitis in dogs. Experimental periodontitis was induced by placement of a silk ligature below the gingival margin of the molar teeth in 3 mongrel dogs. GCF was collected using microcapillary tubes at 0, 7, 21 and 60 days after ligature placement. To compare with GAG in GCF, bovine nasal cartilage proteoglycan monomer, dog's serum and supernatant of homogenized gingival tissue were prepared. Combination of monoclonal antibodies, 3B3 and 9A2, and specific enzymatic digestion made possible the identification of chondroitin 4 sulfate (C4S), chondroitin 6 sulfate (C6S) and dermatan sulfate (DS). The ELISA method detected very small amount of chondroitin sulfate (CS) isomers (15-1000 ng/ml of bovine nasal cartilage proteoglycan). The ELISA value of CS isomers in GCF was lower than that of homogenized gingival tissue but higher than that of the serum. The ELISA value of C4S, C6S and DS, although fluctuating, increased in proportion to the severity of the inflammation.

Animals↗

PubMed1977

Feline leukemia virus: biochemical and immunological characterization of gag gene-coded structural proteins.

The major non-glycosylated structural proteins of feline leukemia virus have been isolated, and competition immunoassays have been developed for each. These proteins include the 27,000- to 30,000-molecular-weight major internal antigen designated p30, a 15,000-molecular-weight protein (p15), an acidic protein of 12,000 molecular weight (p12), and a highly basic 10,000-molecular-weight protein (p10). Immunologically and biochemically corresponding proteins of feline and murine leukemia viruses have been identified. and, on the basis of analogy to the known sequence of a prototype type C virus of mouse origin, the map order of the gag region of the feline type C viral genome has been tentatively deduced as NH2-p15-p12-p10-COOH. The demonstration of two feline leukemia virus gag gene-coded proteins, p15 and p12, expressed in the form of an uncleaved precursor in a mink cell line nonproductively transformed by feline sarcoma virus provides indirect support for the proposed sequence.

AKR murine leukemia virus↗

PubMed1978

Acquisition of oncogenicity by endogenous mouse type C viruses: effects of variations in env and gag genes.

Several dual-tropic isolates derived from the thymuses of preleukemic or leukemic AKR mice and a more recrnt group of viruses generated by in vitro or in vivo passage of a poorly infectious endogenous virus of C3H mouse cells have been shown to be highly oncogenic. By analysis of the immunological properties of their gag gene-coded structural proteins, each of the AKR-derived isolates and two dual-tropic C3H-derived isolates were found to closely resemble AKR murine leukemia virus. In contrast, gag gene-coded proteins of two other leukemogenic isolates of C3H origin, including one ecotropic and one dual-tropic virus, were indistinguishable from those of Moloney murine leukemia virus. All of the oncogenic isolates, including those of AKR and C3H origin, were found to possess common envelope glycoprotein determinants of a unique class not shared by the nononcogenic ecotropic viruses from which they were derived. These findings support the possibility that oncogenic variants of endogenous ecotropic mouse type C viruses are derived by genetic recombination. This recombinational event appears to involve the acquisition, by different ecotropic viruses, of a common class of endogenous virus-coded envelope glycoprotein determinants which are presumably required, but not necessarily sufficient, for oncogenicity.

AKR murine leukemia virus↗

PubMed1979

In vitro, the major ribosome binding site on Rous sarcoma virus RNA does not contain the nucleotide sequence coding for the N-terminal amino acids of the gag gene product.

Ribosomes from the reticulocyte lysate bind strongly and mainly to a region located in the 5' end of the Rous sarcoma virus RNA molecule between residues 9 and 53. This binding involves the participation of initiator tRNA and is sensitive to inhibitors of initiation of protein synthesis such as 7-methyl-GMP and aurintricarboxylic acid. The nucleotide sequence of this ribosome binding site has been determined: it conatains a GUG codon centered at position 26 that is not in phase with any termination codon within the 5' end nucleotide sequence of the RNA that we have analyzed (101 residues). However, the predicted N-terminal amino acid sequence starting from this GUG codon (or even from any AUG or GUG codon in the 5' end of the RNA) does not coincide with that of the in vitro-synthesized product of the 5' end proximal gag gene. Nevertheless, inhibition of ribosome binding to this site is accompanied by an inhibition of the in vitro translation of the gag gene.

Amino Acid Sequence↗

PubMed1979

High-frequency recombination within the gag gene of Rous sarcoma virus.

We isolated 28 recombinants of Rous sarcoma virus at early (24 h) and late (7 days) times after infection. These recombinants were selected for wild type in the pol and src genes and analyzed for their env and gag phenotypes. We were unable to show strong linkage between any two markers, including two markers within a single gene (gag).

Animals↗

PubMed1982

Isolation and biochemical characterization of partially transformation-defective mutants of avian myelocytomatosis virus strain MC29: localization of the mutation to the myc domain of the 110,000-dalton gag-myc polyprotein.

Recently, we isolated three mutants of MC29 virus which, although able to transform fibroblasts with the same efficiency as wild-type MC29, were 100-fold less efficient at transforming macrophages. In this study we found that MC29-transformed quail producer cell line Q10 was able to generate these partially transformation defective mutants at a high frequency. Using tryptic peptide mapping, we determined that the smaller gag-myc polyproteins encoded by the transformation-defective viruses had lost myc-specific tryptic peptides. This suggested that the mutations which resulted in the transformation-defective viruses being inefficient at transforming macrophages were located in the v-myc sequence and thus directly implicated v-myc and the gag-myc polyprotein in transformation by MC29.

Animals↗

PubMed1988

Retroviral gag gene amber codon suppression is caused by an intrinsic cis-acting component of the viral mRNA.

In some type C retroviruses, translation of the pol gene appears to require translational suppression of the proximal gag amber codon. To identify the region of the viral nucleic acid responsible for synthesis of the pol gene products, a 300-base-pair DNA fragment containing the stop codon from a type C murine virus (AK virus) was inserted into the Escherichia coli lacZ gene such that the translational reading frame was maintained. Introduction of the resulting fusion gene into cells resulted in the suppression of the viral stop codon. As measured by beta-galactosidase production, suppression occurred at a frequency of approximately 10%. Suppression could occur in at least several vertebrate cell types and was not augmented by virus replication or the expression of viral gene products. This indicates that gag amber codon suppression does not require augmented levels of suppressor tRNA species.

Acetyltransferases↗

PubMed1988

Localization and footprinting of an enhancer within the avian sarcoma virus gag gene.

A cis-acting regulatory element within the gag gene of avian retroviruses has been localized by deletion analysis, and sites of protein interaction have been studied by DNase I footprinting. Unidirectional deletions were made from both the 5' and 3' ends of a 656-base-pair fragment of the gag gene of Fujinami sarcoma virus. These deletion mutants were tested for enhancer activity in a chloramphenicol acetyltransferase transient expression assay. A sharp 5' boundary for enhancer activity was observed between 776 and 786 nucleotides downstream from the transcription initiation site. In contrast, deletion from the 3' side resulted in a gradual loss of enhancer activity, reaching a near basal level of activity by nucleotide 868. Internal deletion of 76 nucleotides just downstream of the 5' boundary abolished enhancement. Mutagenesis of a consensus enhancer core sequence (GTGGTTTG) showed that this sequence was not necessary for enhancer activity in our transient assays. DNase I footprinting with both a highly purified enhancer-binding protein from rat liver (EBP20) and a partially purified chicken liver nuclear extract showed specific protection of nucleotides 813 to 872 within the localized enhancer region. Footprinting of unidirectional deletion mutants that had lost activity indicated that this binding was not sufficient to confer enhancement.

Animals↗

PubMed1992

Induction of erythropoietin responsiveness in murine hematopoietic cells by the gag-myb-ets-containing ME26 virus.

ME26 virus, which was generated by inserting the coding region of the acute avian leukemia-inducing virus E26 into a murine retrovirus vector, encodes a 135-kDa gag-myb-ets fusion protein. Amphotropic murine leukemia virus pseudotypes of ME26 virus induce a high incidence of erythroleukemia 2 to 4 months after injection into newborn NFS/N mice. Spleen cells from the majority of these mice proliferate to high levels in the presence of the erythroid hormone erythropoietin (Epo) and can easily be established as permanent Epo-dependent cell lines. The cell lines contain multiple copies of ME26 viral DNA and express viral message and protein. An Epo receptor mRNA of normal size can be detected in these cells, and binding studies reveal a single class of lower-affinity Epo receptor with an affinity for Epo that is in the range of that previously reported for erythroid cells. The ME26 virus-induced Epo-dependent cell lines, however, appear more immature than previously described erythroid cell lines and more closely resemble early hematopoietic precursor cells, suggesting that the virus may be activating the Epo receptor in hematopoietic cells that do not normally express it. Consistent with this idea, we are able to infect an interleukin-3-dependent myeloid cell line, FDC-P2, with ME26 virus and convert it to Epo dependence. The ME26 virus-infected FDC-P2 cells, even before growth on Epo, showed a large increase in the amount of Epo receptor mRNA. However, no ME26 viral integrations can be detected adjacent to the Epo receptor gene, indicating that the virus is not activating the Epo receptor gene by promoter/enhancer insertion. Our results are more consistent with the hypothesis that the gag-myb-ets-encoded viral fusion protein, which is known to bind DNA, is directly or indirectly activating the expression of the Epo receptor gene in these cells.

Animals↗

PubMed2006

Relative dominance of Gag p24-specific cytotoxic T lymphocytes is associated with human immunodeficiency virus control.

Conflicting data on the role of total virus- and protein-specific cytotoxic-T-lymphocyte (CTL) responses in the control of human immunodeficiency virus (HIV) disease progression exist. We present data generated from a Peruvian cohort of untreated, clade B-infected subjects, demonstrating that the proportion of Gag-specific, and in particular p24-reactive, CTL responses among the total virus-specific CTL activity is associated with individuals' CD4 counts and viral loads. Analyses in a second cohort in the United States confirm these findings and point towards a dominant role of Gag-specific immunity in effective control of HIV infection, providing important guidance for HIV vaccine development.

CD4 Lymphocyte Count↗

PubMed2003

GAG BioScience GmbH.

Completion of the human genome project led to an explosion in available genomic information. Single nucleotide polymorphisms (SNPs) have emerged as a versatile and powerful tool for genotyping almost all variant species. The unique technological platform developed by GAG BioScience is exclusively based on SNP detection and allows genotyping of up to 60,000 samples per day. An analysis robot, a mass spectrometer and a database form a practically self-controlled analysis and documentation system that achieves high-throughput rates of samples with absolute precision. By using a Laboratory Information and Management System, up to 150 million genotypes can be simultaneously retrieved and stored. In cooperation with a partner, GAG BioScience develops new and powerful tools for further data analysis.

Animals↗

PubMed1996

Beta-thalassemia (beta 90 GAG-->TAG): genetic diagnosis by allele-specific polymerase chain reaction and estimation of mutant mRNA expression by reverse transcription polymerase chain reaction.

Genetic diagnosis of a family of beta-thalassemia (beta 90 GAG-->TAG) was carried out by allele-specific polymerase chain reaction (AS-PCR). The proband, her daughter and granddaughter were proved to be heterozygotes of normal and mutant alleles. As some nonsense mutations express a decreased amount of MrNAs, we determined the expression level of the mutant mRNA of beta-thalassemia (beta 90 GAG-->TAG), by application of a combination method of reverse transcription PCR (RT-PCR) and dot-blot hybridization with allele-specific oligonucleotides. The mutant mRNA was not markedly reduced. In conclusion, 1) individuals with the mutant beta-globin gene were diagnosed successfully by AS-PCR, and 2) a significant amount of the mutant beta-globin mRNA was synthesized.

Alleles↗

PubMed1994

Effects of Title X "gag rule" upon women's attitudes towards their healthcare providers.

79 women were randomly assigned to conditions in which they received pregnancy counseling including abortion information or excluding abortion information (with or without a reminder of the "gag rule"). Subjects not given abortion information viewed their caregivers as more biased, less competent, less empathetic, and holding anti-abortion views compared to those receiving such information. Those not given abortion information but reminded of the "gag rule" viewed their caregivers with relative dislike and mistrust.

Abortion, Legal↗

PubMed1993

[Adhesion of calcium oxalate crystal to Madin-Darby canine kidney cells: quantitative determination and effects of glycosaminoglycans (GAG) and cell injuries on adhesion].

The present investigation was designed to study adhesion of calcium oxalate crystals on the surface of intact MDCK cells quantitatively, and to estimate the effects of glycosaminoglycans (GAGs) and cell injuries on these adhesions. Calcium oxalate monohydrate (COM) crystals adhere to the cell surface by an active force, and the attachment is in a time and concentration dependency with plateau. Pre-treatments with low concentration of GAGs (chondroitin sulphate C, hyaluronic acid, heparan sulphate, heparin and sodium pentosan polysulphate) produce significant reductions of the adhesion. There are significant decreases of the adhesions with pre-treatments of Triton-X100, 0.1 N HCl and gentamicin. These phenomena might be induced by some alterations of cell surface structures or characters. The current quantitative system on MDCK cells should serve as a useful model for the investigations of interactions with crystals and tubular cells. Our studies may also support the hypothesis of attachment of microcrystals to the cellular membrane, which is one of the most important and the earliest process of the pathophysiology of kidney stone.

Animals↗

PubMed1992

The "gag rule" revisited: physicians as abortion gatekeepers.

In this article, I explore this failure [of the therapeutic exception as a compromise device in federal abortion counseling regulations] with an eye toward its broader lessons about the social uses of medical discretion and the difficulty of achieving an abortion compromise in America. I begin by examining the legal underpinning beneath the widespread belief that the "gag rule" imposed a near-absolute ban on discussion of the abortion option. This conventional wisdom, I conclude, collapses on careful inspection. It fails utterly to account for the strong support to be found in the Title X regulations and their larger legal context for a therapeutic exception unconstrained by administrative or judicial definition. Next, I observe that this legal unboundedness would have empowered Title X clinic physicians (and perhaps others who do counseling) to exercise broad discretion over abortion access, under the rubric of medical indication.... By so doing, however, physicians would have become abortion gatekeepers. This would have raised difficult ethical and clinical questions about the extent to which medical judgment should be allowed to incorporate (and shield) socially-disputed moral choices. I briefly consider some of these questions, along with the countervailing appeal of preserving a measure of intimate freedom under medical cover. I then conclude by positing some connections between the moral infirmities of medical gatekeeping and the political failure of the therapeutic exception. I suggest, in essence, that this failure was ensured by a strong resonance between the exception's moral infirmities and the fears of the medical leaders, pro-choice activists, and abortion opponents who framed the public debate over the "gag rule." The potential breadth of the therapeutic exception went unrecognized and unexplored because professional and popular understanding of the abortion counseling regulations was molded by the activists who framed the debate...

Abortion, Induced↗

PubMedDate not supplied

Wound healing mediator production by human dermal fibroblasts grown within a collagen-GAG matrix for skin repair in humans.

Cell and tissue therapy applications in humans are being used increasingly, particularly for tissue repair. Several reconstructed skin models have been proposed. Wound healing involves overlapping steps of inflammation, cell migration and proliferation, neovascularisation, extracellular matrix production and remodelling. This is regulated by numerous cytokines and other soluble mediators. We have prepared dermal substitutes (DS) consisting of a collagen-GAG, three-dimensional matrix colonized by human dermal fibroblasts (HDF), isolated by skin explant or enzymatic digestion of the skin for potential therapeutic use in humans. To test the functionality of these DS, we measured (ELISA) the stimulatory effect on HDF in the matrix, of serial dilutions of human serum (HS) on the production of wound healing mediators: interleukin-8 (IL-8), vascular endothelial growth factor (VEGF), keratinocyte growth factor (KGF) and tissue inhibitor of metalloproteinase-1 (TIMP-1). We observed: 1). a stimulatory effect of HS on HDF production of the different mediators tested, with a dose-dependent effect in the case of IL-8 and VEGF. 2). A matrix-potentiating effect on the production of the different mediators by HDF. 3). A decrease in the production of IL-8 and VEGF when HDF isolated by enzymatic digestion was used to colonize the matrix as compared with HDF isolated by skin explant. We conclude: 1). that the production by HDF, in a collagen-GAG matrix, of mediators involved in cutaneous wound healing is decreased when HDF are isolated by enzymatic skin digestion rather than by skin explant. 2). That measurement of the production of cytokines or other mediators could be a useful quality control to test the functionality of tissue-engineered DS for tissue repair therapy in humans and more generally of cells prepared for cell therapy.

Adult↗

PubMed2003

Serologic evidence of infection with ehrlichiae and spotted fever group rickettsiae among residents of Gag Island, Indonesia.

The causative agents of scrub and murine typhus are considered endemic to Indonesia. However, the presence of spotted fever group rickettsiae and ehrlichiae have not been previously described in this country. During an investigation of arthropod-borne diseases on Gag Island, located northwest of the island of New Guinea in eastern Indonesia, the prevalence of antibody to the etiologic agents of monocytic ehrlichiosis, spotted fever rickettsiosis, and scrub and murine typhus were determined. Analysis of 55 blood samples from residents of Gag Island showed seroreactivity to antigen preparations of Ehrlichia chaffeensis (7 of 48, 14.6%), two spotted fever group rickettsiae: Rickettsia rickettsii (5 of 48, 10.4%) and R. conorii (10 of 49, 20.4%), Orientia tsutsugamushi (5 of 53, 9.4%), and R. typhi (1 of 48, 2.1% [by an indirect immunofluorescence assay] and 1 of 50, 2.0% [by an enzyme-linked immunosorbent assay]). These results show serologic evidence of infection with ehrlichiae and spotted fever group rickettsiae for the first time in Indonesia in a location where the prevalence of antibody to O. tsutsugamushi and R. typhi was lower.

Antibodies, Bacterial↗