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T Nass

Publications and source records attributed to T Nass.

5 recordsLinked to original sources
PubMed2005

Comparison of antibody- and cell-mediated immune responses after intramuscular hepatitis C immunizations of BALB/c mice.

Current treatments for hepatitis C infection have limited efficacy, and there is no vaccine available. The goal of this study was to compare the immune response to several immunization combinations against hepatitis C virus (HCV). Six groups of mice were immunized at weeks 0, 4, and 8 with different combinations of a candidate HCV vaccine consisting of 100 microg recombinant HCV core/E1/E2 (rHCV) DNA plasmid and/or 25 microg rHCV polyprotein and 50 microL Montanide ISA- 51. Four weeks after the last injection, all groups of mice were sacrificed and blood samples and spleens were collected for measuring the levels of specific HCV antibodies (total IgG, IgG1, and IgG2a). Cell proliferation and intracellular interferon-gamma were also measured. Among the groups of immunized mice, only the mice immunized with rHCV DNA plasmid, rHCV polyprotein, and montanide (group D) and mice immunized with rHCV polyprotein and montanide (group F) demonstrated a significant increase in the total IgG titer after immunization. IgG1 was the predominant antibody detected in both groups D and F. No IgG2a was detected in any of the groups. Proliferation assays demonstrated that splenocytes from group D and group C (rHCV DNA primed/rHCV polyprotein boost) developed significant anti-HCV proliferative responses. The combination of an rHCV DNA plasmid, rHCV polyprotein, and montanide induced a high antibody titer with a predominance of IgG1 antibodies and recognized the major neutralization epitopes in HVR1. In contrast, group C did not show an increase in anti-HCV antibodies, but did show a proliferative response.

Adjuvants, Immunologic↗
PubMed1996

Migration of the fungal pathogen Candida albicans across endothelial monolayers.

Migration of the fungal pathogen Candida albicans across the endothelial cell layer is considered a prerequisite for the invasion of multiple organs occurring in systemic candidiasis. We developed an experimental system in which C. albicans migrates from a luminal compartment across a monolayer of bovine aortic endothelial cells on a porous filter support to an abluminal compartment. In this system, a C. albicans wild-type strain (ATCC 10261) traverses the endothelial monolayer in a time-, glucose-, and cell concentration-dependent manner. A mutant derivative unable to grow and form hyphae (SGY-243) migrates at a reduced rate. Concomitant to transendothelial migration, the permeability of the endothelial monolayer for dextran diffusion markers is significantly increased. This increase in transendothelial exchange occurs before fungal cells are detectable in the abluminal compartment and is time, glucose, and cell concentration dependent. A mutant strain (hOG301) unable to interact with endothelial cells does not alter endothelial permeability. Thus, transendothelial migration of C. albicans is able to damage the barrier function of an endothelial monolayer. Our experimental system, which reflects key stages of transendothelial migration of C. albicans including adherence and passage across endothelial cells and the extracellular matrix, may be a useful model for comparisons of transendothelial migration characteristics of Candida strains.

Animals↗
PubMed1984

The effects of naloxone on hot flashes and gonadotropin secretion in postmenopausal women.

Hot flashes have a close temporal relationship with the initiation of LH pulses, suggesting that factors stimulating gonadotropin release are involved in the mechanism of this disturbance. It has been reported that the opiate antagonist naloxone acutely blocked subjective hot flashes, a seemingly paradoxical effect, since the use of this agent in premenopausal women increases the magnitude and frequency of LH pulses. We, therefore, studied the effects of naloxone in 16 postmenopausal women with frequent hot flashes using continuous recordings of finger temperature and skin resistance as objective indices of flushing and perspiration, respectively. After baseline recordings, the subjects were randomized into equal groups, and the recordings were repeated during 8-h infusion of either saline or naloxone (22 micrograms/min). Serum gonadotropin levels were measured at 15-min intervals before and during the last 4 h of the infusion. Naloxone did not change the rate of objectively measured hot flashes, mean serum LH or FSH levels, or the frequencies or amplitudes of gonadotropin pulses. These data suggest that there is a very low input of endogenous opiates on gonadotropin secretion in postmenopausal women and that opioid peptides do not play a role in the initiation of the postmenopausal hot flash.

Aged↗