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Biomedical subjects

L A Glasgow

Publications and source records attributed to L A Glasgow.

At least 19 recordsLinked to original sources
PubMed2002

Vortex-enhanced capture of airborne particulates.

The study reported here sought to exploit aeroelastically-generated vortices for enhanced capture of airborne particles by horizontal, flat plate collectors. Elastically-supported bluff bodies of different cross-sections were screened for suitable plunge (transverse) oscillation at air velocities ranging from about 1 to 10 m s(-1). Both "D" shapes and trapezoidal prisms proved to be particularly effective; the "D" provided an increase in particle capture of 64% relative to the undisturbed flow over a flat plate at a mean air speed of 1.5 m s(-1). At higher velocities, a "T" shaped cross-section (producing mainly torsional oscillation) was found to be extremely effective at increasing capture for airborne particles with a mean diameter of 8 microm. Dynamic pressure measurements made downstream from the oscillators revealed that the torsional oscillation of the "T" produced a flow with multiple periodicities, whereas the plunge oscillators produced a wake that was more sharply periodic. These results indicate that aeroelastically intensified vortices, generated at Reynolds numbers ranging from about 2300 to 5200, can significantly improve particle removal from air streams. Furthermore, the effect can be exploited in both internal (duct) and external (free) flows.

Air Movements↗
PubMed1993

A review of the effects of shear and interfacial phenomena on cell viability.

The shear sensitivity of animal and plant cells is a problem often encountered in large-scale cell culture. Such sensitivity varies with different cell lines and the severity of cellular damage may depend on both the magnitude and the duration of the shear stress. In a bioreactor, the shear susceptibility of cells depends on their response to hydrodynamic forces arising from fluid motions of particular scale. Cell damage may be induced by forces in the bulk liquid phase, but fluid motions associated with the gas-liquid interface are especially energetic. The detrimental effects of hydrodynamic forces are abated by the addition of some polymers, such as Pluronic F-68, methylcellulose, or serum; the exact mechanisms of protection are the subject of current research.

Animals↗
PubMed1984

Failure of interferon to inhibit plutonium-induced osteosarcomas in mice.

The injection of murine interferon three times weekly in dose levels of 1,250, 5,000, or 20,000 U produced no significant antitumor effect against primary 239Pu-induced osteosarcomas in C57BL/6J mice. The interferon treatment was begun 94 days after the plutonium injection, which is well before the radiographic or microscopic appearance of neoplasia, and was continued until the moribund state or death. The average radiation dose accumulated by the skeleton at the time of first treatment was approximately 300 rad. The largest dose of interferon studied, 20,000 U/injection, was approximately 3 X 10(6) U/m2 of body surface, or 10(6) U/kg body weight.

Animals↗
PubMed1983

Acyclovir treatment of experimental genital herpes simplex virus infections. I. Topical therapy of type 2 and type 1 infections of mice.

Intravaginal inoculation of mice with herpes simplex virus (HSV) provides a model infection of genital herpes to determine the effectiveness of potential antiviral agents. topical (intravaginal) treatment with 1% or 5% acyclovir (ACV) in an ointment of gel vehicle initiated 3, 6 or 24 h after inoculation with HSV type 2, significantly inhibited viral replication in the genital tract and usually reduced final mortality. Treatment with 5% ACV initiated 48 or 72 h after infection also reduced vaginal virus titers but did not alter final mortality. When mice were inoculated with HSV type 1 treatment with 5% ACV significantly reduced viral replication in the genital tract when begun as late as 72 h. In HSV-2 infected mice, treatment initiated 3 h but not 24 h after infection prevented the establishment of latent infection in sacral ganglie. These results suggest that topical ACV may be effective antiviral agent for primary genital herpes in humans.

Acyclovir↗
PubMed1983

Establishment and preliminary characterization of a cell line persistently infected with Newcastle disease virus.

A murine osteosarcoma (OGS) cell line was permanently infected with Newcastle disease virus (NDV). The presence of NDV in the subsequent passages was demonstrated by haemadsorption and by immunofluorescence. Compared to the uninfected OGS line the persistently infected cells had a slightly reduced growth rate and they had a reduced sensitivity to several viruses, shown by several different methods. Interferon sensitivity was considerably reduced in the OGS-NDV cells, both the antiviral activity and the cell multiplication inhibitory activity.

Animals↗
PubMed1982

Optimal treatment of herpes simplex virus encephalitis in mice with oral acyclovir.

The effect of oral or intraperitoneal administration of acyclovir was evaluated in four experimental models of herpes simplex virus (HSV) encephalitis in mice. Mice were inoculated with HSV-1 or HSV-2 intracerebrally or with HSV-2 intranasally, intraperitoneally, or intravaginally. With all four routes of inoculation, oral acyclovir therapy significantly reduced mortality when started as late as 72 to 96 hours after viral challenge. Intraperitoneal acyclovir was not effective in protecting mice inoculated intravaginally, but was effective if given 24 to 48 hours after intracerebral or intranasal challenge and as late as 96 hours after intraperitoneal infection. Oral acyclovir was more active than intraperitoneal treatment in all four model infections. Levels of acyclovir inhibitory for HSV in cell culture were maintained in plasma and brain tissue throughout oral treatment but lasted only three to six hours after each intraperitoneal treatment. These results suggest that acyclovir may be useful in treating serious HSV infections in humans.

Acyclovir↗
PubMed1982

Effect of acyclovir treatment on acute and chronic murine cytomegalovirus infection.

Murine cytomegalovirus (MCMV) is inhibited in vitro by 1 to 2 microM acyclovir. Therapy of a systemic MCMV infection in weanling mice with acyclovir was only minimally effective when drug was administered intraperitoneally, while oral administration by addition of acyclovir to the drinking water was highly efficacious in mice with disseminated MCMV. Effective therapy was characterized by reduction of virus titers in lung, liver, spleen, and kidney. In mice chronically infected with MCMV, treatment for 30 days with oral acyclovir eliminated or reduced virus titers in all target organs except the salivary gland. Therapeutic efficacy in this model infection using oral administration of acyclovir could be correlated with the achievement of acyclovir levels in the plasma of experimental animals two to 10 times greater than the mean inhibitory concentration for MCMV in vitro throughout treatment. The lack of efficacy observed when drug was administered intraperitoneally was associated with acyclovir levels exceeding 1 microM for one to three hours after each dose.

Acute Disease↗
PubMed1982

Anti-herpesvirus activity of adenine arabinoside analogues in tissue culture and a genital infection of mice and guinea pigs.

Four analogues of adenine arabinoside (ara-A) were compared for activity against herpes simplex virus (HSV) in tissue culture and in a genital infection of mice and guinea pigs. These analogues, 5'-monophosphate (ara-AMP), 5'-valerate ester (ara-AV), 2'3'-diacetate ester (ara-ADA), and 2',3',5'- triacetate ester (ara-ATA) have greater water and lipid solubility and resistance to deamination than ara-A. In mouse embryo fibroblast cells, similar viral inhibitory levels were noted with ara-A, AMP, and ara-Av, while ara-ADA and ara-ATA were 6-10 time less active. In mice infected intravaginally with HSV type 2 (HSV-2), intravaginal treatment with 10% concentrations of each of the compounds beginning 3 h after viral challenge, had no effect on infection rates, titers of virus in vaginal secretions, mortality rates or the mean day of death as compared with placebo-treated controls. In the HSV-2 genital infection of guinea pigs, treatment with 10% vaginal creams or placebo vehicle was initiated 6 or 24 h after viral inoculation. In animals treated at 6 h with ara-A, ara-AMP and ara-AV, there was complete inhibition of viral replication in the vaginal tract and development of external genital lesions. When treatment with these three drugs was delayed 24 h after infection, there was no effect on vaginal virus titers, but lesions severity was reduced by ara-A or ara-AMP therapy. Ara-ATA was ineffective whether begun at 6 or 24 h. The greater solubility in water and lipid as well as the resistance to deamination of ara-AMP and ara-AV did not appear to enhance their antiviral activity over that of ara-A. Additionally, ara-ADA and ara-ATA exhibited less activity both in tissue culture and in the experimental genital infections.

Administration, Topical↗
PubMed1982

Enhanced susceptibility of mice infected with murine cytomegalovirus to intranasal challenge with Escherichia coli: pathogenesis and altered inflammatory response.

Three-week-old mice inoculated intraperitoneally with murine cytomegalovirus (MCMV) and then challenged intranasally with Escherichia coli strain K1 demonstrated enhanced mortality (70%-90%) as compared with control animals infected with either pathogen alone (0-20%, P less than 0.05). Mortality was greatest when animals were challenged with E. coli on days 1 or 3 after MCMV inoculation. On day 3 of infection with MCMV, clearance of E. coli from blood and tissues was impaired, and there was a decreased inflammatory response to an E. coli-inoculated sponge implanted subcutaneously (geometric mean of 830 leukocytes in sponge fluid/mm3 in MCMV-infected animals vs. 8,510 leukocytes/mm3 in controls, P less than 0.01). On days 1 and 3 of MCMV infection, decreased leukocyte counts in sponge fluid correlated with increased levels of bacteremia (P less than 0.05). These results indicate that MCMV enhances susceptibility to an intranasal challenge with E. coli. A decrease in the inflammatory response may be one mechanism by which MCMV increases susceptibility to bacterial infections.

Animals↗
PubMed1982

Failure of 2-deoxy-D-glucose in the treatment of experimental cutaneous and genital infections due to herpes simplex virus.

The effectiveness of 2-deoxy-D-glucose (2-DG) was evaluated in the treatment of cutaneous infections with herpes simplex virus type 1 (HSV-1) in mice and genital infections with HSV type 2 (HSV-2) in mice and guinea pigs. Groups of mice were inoculated in the lumbosacral or orofacial area with HSV-1 and treated topically three times a day with 0.2% or 0.5% 2-DG solution beginning 3 hr after inoculation. No effect on skin lesions, mortality, or latency was observed. Mice were inoculated intravaginally with HSV-2 and treated intravaginally three times a day with 0.2%-5% 2-DG in solution or suspended in miconazole nitrate cream beginning 6 hr, 24 hr, or 48 hr after inoculation. Replication of HSV-2 in the vagina and final mortality were not affected. Guinea pigs were infected intravaginally with HSV-2 and treated both intravaginally and topically on the external genitalia four times a day with 1% or 5% 2-DG in miconazole nitrate cream. Treatment initiated just prior to development of lesions (on day 3 after inoculation) did not alter vaginal virus replication, lesion development and severity, or virus titers in lesions.

Administration, Topical↗
PubMed1982

Production of alpha and gamma interferons by spleen cells from cytomegalovirus-infected mice.

Antigen-induced lymphocyte proliferation and the production of a murine immune or type II interferon (MuIFN-gamma) by spleen cells in vitro were used to examine the cellular immune response to a cytomegalovirus infection of mice. Lymphocyte blastogenesis was induced by interaction with cytomegalovirus-infected mouse embryo fibroblasts in spleen cells from mice infected at least 6 days previously with cytomegalovirus. The peak of the blastogenic response occurred after 72 hr in culture with antigen. MuIFN was detected in cultures of cytomegalovirus-infected mouse embryo fibroblasts and spleen cells from both normal and infected mice. The MuIFN produced by spleen cells from normal or infected mice early during the course of the infection (days 1 to 2) was predominantly viral or type I interferon (MuIFN-alpha). Peak titers of MuIFN-alpha were present 24 to 48 h after exposure to antigen in vitro and before the peak of the blastogenic response. In contrast, spleen cells from mice infected at least 6 days previously produced both MuIFN-alpha and MuIFN-gamma in culture with the infected mouse fibroblasts. MuIFN-alpha was present early in the culture, before peak blastogenic activity. Peak levels of MuIFN-gamma were detected as lymphocyte blastogenic activity subsided. These results indicate that the cellular immune system of the murine host is capable of responding to cytomegalovirus infection, the afferent limb by antigen recognition and the efferent limb by the production of the lymphokine MuIFN-gamma.

Animals↗
PubMed1981

Effect of interferon on cyclic adenosine monophosphate levels in cells.

Treatment of murine and human cells with homologous interferon (IFN) resulted in an elevation of the cellular cyclic adenosine monophosphate (cAMP) levels in a time- and dose-dependent manner. A similar elevation of cAMP levels could be produced by treatment of cells with isoproterenol, prostaglandin or methylxanthine. However, these agents did not produce an antiviral state. Pretreatment with an inhibitor of adenyl cyclase, N-ethylmaleimide, prevented the effect of IFN on cAMP levels, but did not influence tis antiviral activity.

Alprostadil↗
PubMed1981

A comparison of phosphonoacetic acid and phosphonoformic acid activity in genital herpes simplex virus type 1 and type 2 infections of mice.

The activity of phosphonoacetic acid (PAA) and phosphonoformic acid (PFA) against four strains of herpes simplex virus type 1 (HSV-1) and four strains of HSV-2 were compared in tissue culture and in a murine model of genital herpes. In mouse embryo fibroblast cells, both drugs were three-fold more active against the HSV-1 strains than against the HSV-2 strains. In contrast, in the animal model infections, PAA appeared to be more active against the HSV-2 strains, while PFA was equally effective against both HSV types. In mice infected intravaginally with HSV-2 and treated with intravaginal 5% PAA, none of the treated mice became infected, replication of virus in the genital tract was completely inhibited, none of the infected mice died from encephalitis, and latent infection in lumbosacral ganglia of surviving animals was completely prevented. In HSV-1 genital infection treated with PAA, 20-60% of mice became infected, replication of virus in the genital tract was strikingly reduced, none of the infected mice died, and latent infection was completely prevented. In both HSV-2 and HSV-1 genital infections, 20-70% of animals treated with 8% PFA became infected, growth of virus in the genital tract was reduced significantly but not completely suppressed, mortality was variably altered, and there was a trend towards reduction in the frequently of latent infection. These results indicate that HSV-1 strains are more sensitive to PAA and PFA in tissue culture, but the HSV-2 strains are generally more amenable to therapy in the murine model of genital herpes. Although PAA appeared to be more active that PFA in the genital infection, both drugs significantly altered the course of the infection. Since dermal toxicity associated with PAA precludes its use in humans and since PFA is already undergoing trials in patients with recurrent herpes labialis, the current results suggest that topical PFA deserved further evaluation in the treatment of mucocutaneous HSV infections, including genital herpes.

Animals↗
PubMed1981

Differences in neurovirulence among isolates of Herpes simplex virus types 1 and 2 in mice using four routes of infection.

Differences in neurovirulence between herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) were investigated using recent clinical isolates and laboratory-passaged strains in intravaginal, intranasal, intraperitoneal, and intracerebral infections of mice. The HSV-2 isolates caused higher death rates in all four infections. No differences in death rate were observed between recent and passaged isolates of either HSV-1 or HSV-2. After intravaginal inoculation, HSV-1 isolates replicated to higher titers in the vaginal mucosa, but HSV-2 isolates produced a higher death rate and a greater frequency of latent infection in lumbosacral ganglia of surviving animals. After intranasal inoculation, HSV-2 isolates again produced a higher death rate, but the frequency of latent infection in trigeminal ganglia was higher with HSV-1 isolates. The data suggest that the HSV-2 isolates have an enhanced capacity to enter and replicate in the central nervous system of mice but that latency is influenced by both virus type and route of inoculation.

Animals↗
PubMed1981

Effect of interferon administration on pulmonary osteogenic sarcomas in an experimental murine model.

The iv inoculation of a suspension of osteogenic sarcoma cells induced metastatic tumor nodules in the lungs of C57BL/6 mice. The administration of 50,000-100,000 U of interferon daily for 7 days strikingly reduced the tumor mass in the lung and the number of tumor nodules present in histopathologic sections when the interferon treatment was initiated immediately after tumor cell inoculation. In some animals the development of any detectable metastatic lesion was completely prevented. Extending the therapy form 7 days to 21 days failed to improve the protective effect. Interferon therapy delayed until 7 days after tumor cell inoculation had no effect. These findings indicate the effectiveness of exogenous interferon in this murine osteogenic sarcoma model when interferon treatment is initiated within 1 hour of tumor cell inoculation, but not when it is delayed until tumor nodules are established in the lungs.

Animals↗