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Biomedical subjects

G H Tignor

Publications and source records attributed to G H Tignor.

At least 19 recordsLinked to original sources
PubMed1997

Device-specific sharps injury and usage rates: an analysis by hospital department.

BACKGROUND: Whether universal precautions training has reduced percutaneous sharps injuries is questioned. Prevention programs directed to specific problem areas are required to further reduce injury. Our purpose was to identify target areas. METHODS: Device-specific sharps injury rates per 100,000 devices purchased were determined by department at Yale New Haven Hospital (1993 to 1994). Usage per full-time equivalent was calculated by department. Rates were modelled using Poisson regression. RESULTS: Three epidemiologic patterns resulted: (1) injury rates were independent of usage (butterfly needles); (2) injury rates varied directly with usage (lancets); (3) injury rates varied inversely with usage (intravenous catheters, sutures, and scalpels). Device-specific usage and injury rates varied by department. Devices used little (9/full-time equivalent) but under difficult circumstances, such as intravenous catheters in pediatric patients, were associated with high injury rates (67.7/100,000). Devices, sometimes disassembled, such as blood collecting tubes, caused significantly more injury in departments where health care professionals work under time constraints, such as in the emergency department and nursing. Unconventional use of devices (Luer-Lok syringes and scalpels) resulted in higher rates of injury (nursing and laboratories). Building services appeared to be at risk for injury. CONCLUSIONS: With device-specific injury and usage rates by department, injury prevention programs can now focus on specific devices and departments.

Accidents, Occupational↗
PubMed1995

Characterization of a highly attenuated Japanese encephalitis virus generated from molecularly cloned cDNA.

Six recombinant Japanese encephalitis virus (JEV) isolates were recovered from infectious RNAs transcribed by T7 RNA polymerase from molecularly cloned cDNA templates. Three of the recombinant viruses had characteristics similar to the wild-type parent virus, JaOArS982. The other 3 recombinant viruses exhibited an attenuated phenotype in mice. An avirulent recombinant virus, IC47, was characterized and compared with the wild-type parent virus and a virulent recombinant virus, IC37. IC47 produced smaller plaques than parent or IC37 viruses and exhibited no viremia or neuroinvasion in young adult mice inoculated subcutaneously and no mortality when inoculated intracerebrally. IC47 was also immunogenic and protective in the murine model. The probable basis for attenuation, revealed by nucleotide sequence analysis, was a single amino acid substitution at position 138 (Glu to Lys) in the E protein.

Animals↗
PubMed1993

Ribavirin efficacy in an in vivo model of Crimean-Congo hemorrhagic fever virus (CCHF) infection.

After intraperitoneal (i.p.) infection of infant mice with CCHF virus, virus titers in liver remained significantly higher than in other organs except blood (serum). Within the liver, virus antigen was first found by immunofluorescence (IFA) in Kupffer cells followed by more extensive hepatic spread. Later, virus was found in other organs including brain and heart. Ribavirin treatment significantly reduced infant mouse mortality and extended the geometric mean time to death. Ribavirin treatment reduced CCHF virus growth in liver and significantly decreased, but did not prevent, viremia. Despite a substantial viremia, infection of other organs including brain and heart was not detected in ribavirin-treated mice. A hepatotropic virus subpopulation with less neurovirulence than the parent was isolated from liver of ribavirin-treated mice (single dose, 100 mg/kg). After serial passage in placebo-treated mice, the exclusive hepatotropism was lost.

Animals↗
PubMed1993

Evidence from the anti-idiotypic network that the acetylcholine receptor is a rabies virus receptor.

We have developed idiotype-anti-idiotype monoclonal antibodies that provide evidence for rabies virus binding to the acetylcholine receptor (AChR). Hybridoma cell lines 7.12 and 7.25 resulted after fusion of NS-1 myeloma cells with spleen cells from a BALB/c mouse immunized with rabies virus strain CVS. Antibody 7.12 reacted with viral glycoprotein and neutralized virus infectivity in vivo. It also neutralized infectivity in vitro when PC12 cells, which express neuronal AChR, but not CER cells or neuroblastoma cells (clone N18), which have no AChR, were used. Antibody 7.25 reacted with nucleocapsid protein. Anti-idiotypic monoclonal antibody B9 was produced from fusion of NS-1 cells with spleen cells from a mouse immunized with 7.12 Fab. In an enzyme-linked immunosorbent assay and immunoprecipitation, B9 reacted with 7.12, polyclonal rabies virus immune dog serum, and purified AChR. The binding of B9 to 7.12 and immune dog serum was inhibited by AChR. B9 also inhibited the binding of 7.12 to rabies virus both in vitro and in vivo. Indirect immunofluorescence revealed that B9 reacted at neuromuscular junctions of mouse tissue. B9 also reacted in indirect immunofluorescence with distinct neurons in mouse and monkey brain tissue as well as with PC12 cells. B9 staining of neuronal elements in brain tissue of rabies virus-infected mice was greatly reduced. Rabies virus inhibited the binding of B9 to PC12 cells. Mice immunized with B9 developed low-titer rabies virus-neutralizing antibody. These mice were protected from lethal intramuscular rabies virus challenge. In contrast, anti-idiotypic antibody raised against nucleocapsid antibody 7.25 did not react with AChR.

Animals↗
PubMed1992

Chemotherapeutic prevention of complications caused by vaccinia virus-vectored immunogen.

Vaccinia virus strains and constructs differ greatly in the number of PFUs required to produce tail lesions in the vaccinia virus mouse model. The pathogenesis of lesion formation appeared to involve virus spread from an initial focus in specific cells surrounding hair follicles to other concentrated areas of the dermis and finally, at the time of lesion development, to the epidermis. Antivirals that suppressed tail lesions, to a greater or lesser degree, included ara A, ribavirin, rifampicin, adenosine N'-oxide, and selected analogues. Immunomodulators, including ampligen and recombinant interferon, suppressed lesions at very low doses. Spread of virus infection from the dermis to the epidermis was inhibited as determined by immunofluorescence. These studies in the tail lesion model have suggested drugs that could be tested further in primate models of vaccinia virus infection. In addition, these studies provide additional data on a model that may be a useful adjunct in safety testing of recombinant vaccinia virus vaccines.

Adjuvants, Immunologic↗
PubMed1985

Rabies virus binding to cellular membranes measured by enzyme immunoassay.

The binding of rabies virus to cellular membranes was measured using an enzyme-linked immunosorbent assay (ELISA). Virus binding to membranes adsorbed to the wells of microtiter plates was detected with rabies virus antibody and alkaline phosphatase-linked second antibody. The greatest degree of binding was to myotube, neuroblastoma, and salivary gland membranes; intermediate levels occurred in striated muscle and nerve membranes; and low levels of binding were found in other membranes, including those of most parenchymal organs. Binding of rabies virus to myotube membranes was saturable, dependent on pH (with an optimum of pH 6.0), facilitated by the divalent cations Ca++, Mn++, and Mg++, and was temperature dependent. Binding was greatly reduced by inactivation of virus with beta-propiolactone or treatment of virus with trypsin. In embryonic chick myotubes, total acetylcholine receptor content and acetylcholinesterase activity undergo marked changes during development, first increasing and then decreasing at the time of hatching. Binding of rabies virus followed a similar pattern, indicating that the virus may interact with the acetylcholine receptor or other surface molecules undergoing similar developmental changes.

Acetylcholinesterase↗
PubMed1985

Rabies virus binding at neuromuscular junctions.

Morphological, immunocytochemical, biochemical, and immunological techniques have been used to describe rabies virus binding to a sub-cellular unit and molecular complex at the neuromuscular junction (NMJ). Early after infection in vivo, virus antigen and virus particles were found by immunofluorescence, electron microscopy and immunoelectron microscopy in regions of high density acetylcholine receptors (AChR) at NMJs. One monoclonal antibody (alpha-Mab) to the alpha subunit of the AChR blocked attachment of radio-labeled rabies virus to cultured muscle cells bearing high density patches of AChR. A sub-cellular structure, resembling an array of AChR monomers, bound both rabies virus antigens and alpha-Mab. By immunoblotting with electrophoretically transferred motor endplate proteins, rabies virus proteins and alpha-Mab bound to two proteins of 43 000 and 110 000 daltons. A rabies virus glycoprotein antibody detected virus antigen bound to the 110 000 dalton protein. An auto-immune (anti-idiotypic) response followed immunization of mice with rabies virus glycoprotein antigen; the antibody was directed to the 110 000 dalton protein. This auto-antibody altered the kinetics of neutralization by rabies virus antibody and induced the formation of rabies virus antibody after inoculation of mice. These results define, at the neuromuscular junction, a rabies virus receptor which may be part of the acetylcholine receptor complex.

Animals↗
PubMed1983

Immunoelectron microscopic localization of rabies virus antigen in central nervous system and peripheral tissue using low-temperature embedding and protein A-gold.

A protein A-gold technique was used in conjunction with low temperature embedding to visualize ultrastructurally mature virions and sites of viral replication in the brains of rabies virus-infected mice after peripheral inoculation of virus. The association of viral profiles and gold particles with synaptic membranes, microtubules and rough endoplasmic reticulum suggested a mechanism of rabies virus transport within the central nervous system. Early interactions of inflammatory cells with the virus inoculum were characterized by phagocytosis by non-degranulating neutrophils and mononuclear cells.

Animals↗
PubMed1982

Is the acetylcholine receptor a rabies virus receptor?

Rabies virus was found on mouse diaphragms and on cultured chick myotubes in a distribution coinciding with that of the acetylcholine receptor. Treatment of the myotubes with alpha-bungarotoxin and d-tubocurarine before the addition of the virus reduced the number of myotubes that became infected with rabies virus. These findings together suggest that acetylcholine receptors may serve as receptors for rabies virus. The binding of virus to acetylcholine receptors, which are present in high density at the neuromuscular junction, would provide a mechanism whereby the virus could be locally concentrated at sites in proximity to peripheral nerves facilitating subsequent uptake and transfer to the central nervous system.

Acetylcholine↗
PubMed1981

Entry of rabies virus into the peripheral nerves of mice.

Young adult mice were inoculated in the hind limb with rabies virus or Sindbis virus. Rabies 1820B virus antigen was detected in leg sections by immuno-fluorescence at 1 h post-inoculation at sites comparable in form and distribution to cholinesterase-positive sites, which represent motor end-plates (MEPs). Sites which were rabies virus antigen-positive by immunofluorescence were also cholinesterase- positive on double-stained slides. Rabies CVS virus detected by autoradiography was similarly distributed at 6 h post-inoculation. Uptake of rabies virus at motor nerve endings was confirmed by the detection of rabies antigen by immunofluorescence in ventral horn cells in the spinal cord at 20 h post-inoculation before involvement of dorsal root ganglia. Rabies virus antigen could not be detected at MEPs if the virus had been inactivated by beta propiolactone or mixed with antibody prior to injection or if the sciatic nerve had been cut 7 days earlier, similarly treated groups of mice survived for the observation period of 6 weeks. Rabies virus antigen was found at MEPs in mice given antibody 24 h before virus injection, but virus antigen was not found in the spinal cord, and mice similarly treated survived. Sindbis virus strain Ar86, which like rabies virus is neurotropic in adult mice, was also found at MEPs and in peripheral nerves by autoradiography at 6 h post-inoculation. In contrast to results with rabies virus-infected mice, stimulation of the sciatic nerve for the first hour post-inoculation prevented mortality. Sindbis virus strain Ar339, which is not neurotropic in adult mice, could not be detected at MEP's by immunofluorescence or autoradiography and mice injected with virus survived. The results presented here suggest that rabies virus and perhaps other neurotropic viruses can use the motor axon terminal at the neuromuscular junction as a site of entry into the nervous system.

Animals↗
PubMed1981

Improved method for trypsin digestion of Paraplast sections before immunofluorescence staining.

Formalin-fixed, Paraplast-embedded tissue sections mounted on subbed slides were digested with crude trypsin in modified Sorensen phosphate buffer containing sodium fluoride before immunofluorescence staining. This method prevented detachment of sections from slides during processing, thereby permitting immunofluorescence and histological examinations of adjacent serial sections.

Animals↗
PubMed1980

Host cell receptors for two strains of Sindbis virus.

Experiments were performed to determine whether neuronal cells have different numbers of receptors for a neurovirulent and an avirulent strain of the same virus and whether neurotropic strains of different viruses share the same cellular receptors. Attempts were also made to characterize the receptors for the two strains of Sindbis virus on viable cells by studying their enzyme sensitivity. The number of cellular receptors available for Sindbis virus attachment to several cell lines was determined by saturation studies using two virus strains differing in their pathogenicity for adult mice. Cultured neuronal cells had 1.3 x 10(6) receptors for a neurovirulent strain (SaAr86) and only 5 x 10(4) for the avirulent prototype strain (EgAr339) of Sindbis virus. A refractory Lepidopteran cell type possessed 1 x 10(5) surface receptors for the neurovirulent variant while the average number of receptors on five permissive cell types was 1.5 x 10(6). Cellular receptors for the two strains of Sindbis virus on rat glioma cells were found to be distinct. The cellular receptors for EgAr339 on viable mammalian cells were sensitive to proteolytic cleavage, while those on living mosquito cells were insensitive to proteases, phospholipases and neuraminidase. The receptors for the neurovirulent variant on three mammalian cell types were less sensitive to enzymatic inactivation than those for the avirulent counterpart. After cleavage, the receptors for EgAr339 reappeared rapidly at 37 degrees and 4 degrees C, apparently in the absence of cellular synthesis.

Aedes↗
PubMed1980

Close relationship of Crimean hemorrhagic fever-Congo (CHF-C) virus strains by neutralizing antibody assays.

Strains of Crimean hemorrhagic fever-Congo (CHF-C) virus originating in widely separated points representing diverse zoogeograhiczl and ecological areas were compared by a neutralization of fluorescent foci of infection-test, in an attempt to determine whether antigenic differences could be detected among the strains. Minor differences were found which could be confirmed by reciprocal kinetic neutralization tests with one-injection immune sera if the results were analyzed by linear regression. However, CHF-C virus strains cannot be reliably subdivided into geographic variants on the basis of the minor antigenic variations observed. In this apparent paucity of antigenic diversity over its wide distribution, CHF-C virus differs from other arboviruses with similar or even lesser distribution.

Animals↗
PubMed1977

Isolation and assay of rabies serogroup viruses in CER cells.

Infection of CER cell cultures with field strains of rabies virus, ranging from 0 to 5 mouse brain passages, was detected by immunoflurescence within 2-4 days after infection. A fluorescent focus assay for measuring infectivity of seven rabies serogroup viruses was rapid and reproducible. Rabies field strians and other rabies serogroup viruses also induced cytopathic effect, usually on initial passage. The hemadsorption-negative (HAD-) plaque test in BSC-1 cells was successfully applied to laboratory-adapted rabies strains. HAD- test attempts were unsuccessful with CER cells and with field isolates of rabies virus in both cell lines. CER cells are heteroploid and are antigenically related to BHK-21 cells by fluorsecent antibody tests.

Antigens, Viral↗