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Biomedical subjects

M Bruns

Publications and source records attributed to M Bruns.

At least 37 records · Page 2Linked to original sources
PubMed1994

Intranasal sphenoethmoidectomy: an evolution of technique.

Intranasal sphenoethmoidectomy was originally used primarily for the provision of adequate drainage of acute and subacute bacterial sinusitis. However, the spectrum of inflammatory sinus disease has changed dramatically since the popularization of broad-spectrum antibiotics, and chronic hyperplastic rhinosinusitis has replaced acute sinusitis as the primary indication for ethmoidectomy. In such cases total or almost total disease removal is crucial to providing long-term drainage and ventilation. We describe several modifications of the Yankauer sphenoethmoidectomy technique that enable the sinus surgeon to provide clearance of disease and excellent drainage for all sinuses by complete marsupialization of the sphenoid, ethmoid, and maxillary sinuses. These modifications include (1) complete rather than partial removal of the middle turbinate, (2) extended middle meatal antrostomy with palatine bone resection to the pterygoid process with delineation of the inferior and medial orbital wall, and (3) introduction of operative endoscopes as adjunctive tools in areas inaccessible to conventional visualization. The current technique and results in nearly 2000 procedures are described.

Chronic Disease↗
PubMed1993

Decrease in peritonitis rate by integrated disconnect system in patients on continuous ambulatory peritoneal dialysis.

The prevention of peritonitis is of major concern for successful long-term continuous ambulatory peritoneal dialysis (CAPD) treatment. The effect of a Y-system on peritonitis incidence and patient morbidity was observed in a comparative, retrospective single-center analysis over a period of 5 years. The integrated disconnect system prolonged the peritonitis-free period from 1:11 patient-months, observed with the conventional system, to greater than 1:50 patient-months. The rate of hospitalization was reduced by 45%.

Humans↗
PubMed1990

Virus-specific delayed-type hypersensitivity (DTH). Cells mediating lymphocytic choriomeningitis virus-specific DTH reaction in mice.

We had previously shown that the local lymphocytic choriomeningitis virus-induced delayed-type hypersensitivity (DTH) reaction in mice consists of two well delineated phases that are mediated by CD8+ and CD4+ T lymphocytes, respectively. These findings have been confirmed and extended by showing that the first CD8+ cell-dependent part of the response was enhanced by either the presence of CD4+ cells or systemic treatment with IL-2 and that it developed in the absence of detectable numbers of mononuclear phagocytes, whereas the later CD4+ cell part required monocytes or related elements. Furthermore, in the DTH reaction that was elicited with noninfectious viral Ag in mice previously immunized by infection, only the CD4+ cells participated. Thus, the two phases of the lymphocytic choriomeningitis-viral DTH reaction are principally different, which has to be taken into account when trying to assess the relevance of DTH during this virus infection.

Animals↗
PubMed1990

Mode of replication of lymphocytic choriomeningitis virus in persistently infected cultivated mouse L cells.

During persistent infection of mouse L cells with strain Armstrong lymphocytic choriomeningitis virus, the latter undergoes characteristic changes, including loss of mouse pathogenicity and failure to form plaques on cultivated cells. We call this virus L(Arm) and have analyzed transcription and translation of its S-RNA, which codes for the viral nucleoprotein (NP) and the glycoprotein precursor (GP-C). In L(Arm) virus-infected L cells, S-RNA and genomic-sized viral complementary S-RNA (VC-S-RNA) were detected and, in addition, considerable quantities of shortened molecules of either species. The cells' content of NP was high, but they contained little GP-C; instead, a viral glycoprotein with MW 65,000 was present. We propose a hypothesis in which it is assumed that along the VC-S-RNA there is more than one recognition site for the viral RNA-dependent RNA polymerase, which leads to the generation of truncated forms of S-RNA, VC-S-RNA, and mRNA for GP-C; this, in turn, results in relative overproduction of NP and relative underproduction of GP-C as well as the emergence of a new form of viral glycoprotein.

Animals↗
PubMed1990

Effect of rimantadine on cytotoxic T lymphocyte responses and immunity to reinfection in mice infected with influenza A virus.

Administration of rimantadine to mice via drinking water, following a prophylactic dose, reduced lung virus titers by greater than 3 log10 plague-forming units (pfu)/ml but caused only marginal reductions in lung virus titers when therapy was started 8 h after exposure to virus. Mice given rimantadine prophylactically plus therapeutically were resistant to rechallenge with virus at a dose equivalent to that used for the primary infection (50 pfu/mouse) but not to a high dose (1 x 10(5) pfu/mouse). Virus-neutralizing-antibody titers were reduced only by rimantadine treatment, which included prophylaxis, whereas the cytotoxic T lymphocyte (CTL) response was depressed by treatment given with or without prophylaxis. Mice infected with rimantadine-resistant virus had no decrease in CTL or antibody responses when treated with rimantadine. Therefore, the depression in CTL and antibody responses associated with rimantadine treatment appears to be due to a decrease in the amount of viral antigen available or interference with viral antigen processing and not to nonspecific immunosuppressive effects.

Adamantane↗
PubMed1989

Efficacy of rimantadine hydrochloride in the treatment of influenza infection of mice.

Rimantadine HCl was assessed for its effect on influenza A virus titer in lungs of infected BALB/c mice. Rimantadine administered orally via drinking water, with and without an intraperitoneal prophylactic loading dose, was compared to intraperitoneal administration. Mice were infected with a non-lethal dose of influenza A/Port Chalmers/H3N2 virus and the pulmonary virus titers were determined at intervals over a 21 day period. Prophylactic treatment with rimantadine followed by oral administration resulted in up to a 4 log10 reduction in pulmonary virus titer. The oral doses given to the mice were comparable on a mg/kg/day basis to those recommended for treatment of human infections. Reductions in pulmonary virus titers also occurred after intraperitoneal rimantadine treatment which included a prophylactic dose, but the reductions in pulmonary virus titers were less striking and not consistent over the course of infection. There were no significant reductions in pulmonary virus titers by either route if treatment was started 8 h after exposure to virus.

Adamantane↗
PubMed1988

Host cell-dependent homologous interference in lymphocytic choriomeningitis virus infection.

The generation of virus progeny as well as transcription, translation, and replication of the viral small RNA (S-RNA), which codes for the nucleoprotein (NP) and the glycoprotein precursor (GPC), was followed in L and MDCK cells after infection with multiplicities (m.o.i.) ranging from 0.01 to 100. In L cells, the yields of both plaque-forming units and interfering particles varied inversely with the m.o.i. Northern blot analysis revealed that early after infection with high multiplicity NP-mRNA was present, but later few or no signals of any specificity were registered. After low m.o.i. the results were negative at 8 hr, but large quantities of mRNAs for NP and GPC as well as viral genomic S-RNA and genomic-sized complementary S-RNA had been synthesized at 48 hr. In MDCK cells, throughout the range of m.o.i. both entities attained lower levels and most were generated at m.o.i. one. The degree of hybridization correlated roughly with the quantity of infectious virus to which the cells had been exposed. In the cells of both lines the NP-mRNA corresponded to the synthesis of its translation product, but once produced, most of it appeared to be retained in the phosphorylated form. We assume that the homologous interference seen in L cells after infection with high m.o.i. results from a host-dependent inhibition of viral transcription and replication mediated by NP.

Animals↗
PubMed1988

Lymphocytic choriomeningitis virus. X. Demonstration of nucleoprotein on the surface of infected cells.

Of a total of 17 monoclonal antibodies (MAb) directed against structural proteins of the lymphocytic choriomeningitis (LCM) virus, 3 were specific for the viral nucleoprotein (p63) and attached to the plasma membrane of infected cells, as disclosed by the indirect immunofluorescence procedure and complement-mediated cytolysis. We had previously demonstrated that a portion of the nucleoprotein (p63E) was part of the envelope of the intact virion (M. Bruns, W. Zeller, H. Rohdewohld, and F. Lehmann-Grube (1986) Virology 151, 77-85), and we now show that after external iodination of virions followed by limited proteolysis the label was attached to the smallest peptide thus obtained. If purified nucleocapsids were labeled with 125I, digested as before, and incubated with an anti-p63 MAb that has the ability to bind the surface of the infected cell, a similarly small peptide was precipitated; an antibody specific for p63 but not recognizing it on the cell surface precipitated the largest peptide and failed to bring down the small one. We conclude that the epitopes complementary to a few of our anti-p63 MAb are represented on both the virion and the surface of virus-infected cells.

Antibodies, Monoclonal↗
PubMed1986

Lymphocytic choriomeningitis virus. IX. Properties of the nucleocapsid.

Nucleocapsids (NC) of lymphocytic choriomeningitis (LCM) virus were obtained by treatment of purified infectious virus with detergent and salt at high concentrations, followed by gradient centrifugation. NC thus prepared contained 31 S RNA, 23 S RNA, and a protein with an apparent mol wt 63,000 and an isoelectric point pH 5.7 (p63), assumed to be the nucleoprotein. We had previously observed that the intact LCM virus contained two kinds of protein with mol wt 63,000 separable by their isoelectric points which were pH 5.7 and 7.7, respectively. We now found that the latter component was removed from the NC together with the glycoproteins, and labeling studies revealed that it was closely associated with the viral envelope. We have named the protein with a mol wt of 63,000 and an isoelectric point pH 7.7 p63E (E for envelope). By limited proteolysis both viral components of mol wt 63,000 could not be distinguished, indicating that they are basically identical. It appears that p63E is the phosphorylated form of p63.

Capsid↗
PubMed1984

Lymphocytic choriomeningitis virus. VIII. Reciprocal formation of pseudotypes with vesicular stomatitis virus.

Large numbers of VSV (LCMV) pseudotypes with the genomes of vesicular stomatitis virus (VSV) and the coat proteins of lymphocytic choriomeningitis virus (LCMV) were produced by infecting L cells first with LCMV and subsequently with VSV, the latter in the presence of tunicamycin. Separation by gradient centrifugation from the concomitantly produced LCMV genotypes, followed by polyacrylamide gel electrophoresis (PAGE), failed to reveal measurable quantities of the one glycoprotein ("G") of VSV. By serologic analysis it could be shown that anti-VSV antibody still attached, although with low efficiency. VSV (LCMV) retained its infectivity during purification. Reversal of the sequence of infection under otherwise identical conditions led to the formation of LCMV (VSV) pseudotypes. When separated from VSV genotypes, PAGE did not disclose glycoproteins of LCMV, and serologic analysis failed to detect attachment of anti-LCM virus antibody. LCMV (VSV) lost its infectivity during purification.

Animals↗
PubMed1984

Lymphocytic choriomeningitis virus. VII. Structural alterations of the virion by treatment with proteolytic enzymes without loss of infectivity.

Treatment of lymphocytic choriomeningitis virus with proteolytic enzymes, hyaluronidase, and phospholipase C increased infectious titres. Biochemical analysis of bromelain- and trypsin-treated virus revealed that infectivity was high in spite of the decrease to low or undetectable levels of all viral glycoproteins as well as partial degradation of the nucleoprotein.

Antigens, Viral↗
PubMed1983

Lymphocytic choriomeningitis virus. VI. Isolation of a glycoprotein mediating neutralization.

A structural glycoprotein of lymphocytic choriomeningitis virus was obtained in pure form by immunoaffinity chromatography using a monoclonal antibody with high neutralizing activity. It blocked neutralization of viral infectivity by antibody and in polyacrylamide gel electrophoresis it migrated with an apparent molecular weight of 44 X 10(3). We conclude that the isolated material is identical with the previously described gp44 (GP-1).

Animals↗
PubMed1983

Lymphocytic choriomeningitis virus. IV. Electron microscopic investigation of the virion.

The structure of lymphocytic choriomeningitis virus (LCM virus) was investigated by a variety of conventional as well as novel electron microscopic procedures. Thin sections of infected cells revealed the characteristic arenavirus entities whose interiors contain ribosome-like granules but look otherwise empty. In contrast, most thin-sectioned virus particles from infectious cell culture fluid, both untreated and highly purified with little loss of initial infectivity, appeared to be filled with rather homogeneous cores. Cores rather than granules were also found in positively contrasted whole and thin-sectioned virus particles. We favor the explanation that the sandy grains, which have given this group of viruses its name, are altered cores that happen to look like ribosomes. However, the alternative cannot yet be excluded, namely, that LCM virus-infected cells produce two types of particles, of which only the core-containing ones represent virions.

Lymphocytic choriomeningitis virus↗
PubMed1983

Lymphocytic choriomeningitis virus. V. Proposed structural arrangement of proteins in the virion.

Previous work by M.J. Buchmeier and his colleagues and by our group has led to the conclusion that the lymphocytic choriomeningitis (LCM) virus contains seven distinct structural proteins, which we have named p200, gp85, p77, p63, gp60, gp44, and gp35. Their arrangement in the virion has now been analysed by establishing nearest-neighbour relationships with a homobifunctional crosslinker, by performing polyacrylamide gel electrophoresis in parallel under reducing and non-reducing conditions, and by determining the proteins that are covalently bound to viral lipids. A hypothetical model of the virion of LCM virus is proposed. Its envelope is assumed to consist of a membranous layer composed of gp60 and lipids and two types of spikes with either gp85 or gp44 as tips and gp35 as bases. The last-mentioned glycoprotein also appears to be complexed with p63, the main protein component of the nucleocapsid, and this in turn was found to be spatially associated with p200. Probably p77 is also an internal component, but a more exact position cannot yet be assigned to this protein.

Cross-Linking Reagents↗
PubMed1983

Lymphocytic choriomeningitis virus. III. Structural proteins of the virion.

Analysis of radioactively labelled and highly purified infectious lymphocytic choriomeningitis (LCM) virus by polyacrylamide gel electrophoresis (PAGE) revealed 12 components which, according to their apparent molecular weight and glycosylation status, were designated as p19, p25, p26, gp35, p38, gp44, gp60, p63, p77, gp85, gp130, and p200. As shown by immunoprecipitation, they all bound to rabbit anti-LCM virus antibodies. Three proteins, namely gp35 (= 'GP-2'), gp44 (= 'GP-1') and p63 (= 'NP'), had previously been described by others as major constituents of the virion. Our results confirm this and suggest that gp60, p77, gp85, and p200 are further distinct structural proteins. In contrast, p25 and p38 appear to be cleavage or degradation products of p63; p19 and p26 seem to belong to gp60, which could be the monomeric form of a dimer, gp130. Peptide mapping by limited proteolysis revealed considerable overlapping of amino acid sequences among the major glycoproteins with one peptide being common to all. From the results of PAGE performed after external labelling of intact virions, we conclude that gp44, gp60, and gp85 (but not gp35) form the surface of the virus envelope. Analytical isoelectric focusing under non-reducing conditions has shown that the major glycoproteins appeared to consist of several components with different isoelectric points.

Electrophoresis, Polyacrylamide Gel↗