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Biomedical subjects

N A Hynes

Publications and source records attributed to N A Hynes.

7 recordsLinked to original sources
PubMed1994

Prolonged clinical latency and survival of macaques given a whole inactivated simian immunodeficiency virus vaccine.

Simian immunodeficiency virus (SIV) infection of macaques is a useful and relevant model for evaluating candidate human immunodeficiency virus (HIV) vaccines. One important feature of this model is that SIV vaccines can be evaluated for their ability to prevent infection as well as to prevent or delay the onset of AIDS. In the present study, a group of macaques was vaccinated with whole inactivated SIV and challenged with peripheral blood mononuclear cells from an SIV-infected macaque. This challenge represented a rigorous and realistic test of the immunization protocol. All macaques became infected after challenge; however, immunized animals survived significantly longer (P < .03) than naive controls. These data suggest that similar vaccines administered to humans at risk for HIV-1 infection might delay or prevent AIDS even if the vaccine failed to prevent infection.

AIDS Vaccines↗
PubMed1989

An outbreak of influenza A/Taiwan/1/86 (H1N1) infections at a naval base and its association with airplane travel.

In late October 1986, an outbreak of influenza-like illness was detected at the Naval Air Station in Key West, Florida. Between October 10 and November 7, 1986, 60 active duty personnel reported experiencing a respiratory illness characterized by fever, cough, sore throat, and myalgia. Influenza A/Taiwan/1/86 (H1N1) virus was recovered from three symptomatic patients. Forty-one (68%) of 60 case-patients belonged to a 114-person squadron that had traveled to Puerto Rico for a temporary assignment from October 17-28, 1986. Among squadron members, the attack rate for persons previously vaccinated with the 1986-1987 trivalent influenza vaccine and for those unvaccinated was the same (37%). Transmission of infection among squadron personnel appeared to have commenced in Key West and continued in a barracks in Puerto Rico and aboard two DC-9 aircraft that transported the squadron back to Key West on October 28. There was no evidence that the outbreak spread to the surrounding civilian communities in Puerto Rico or Key West. This was the first reported outbreak of respiratory illness due to influenza A/Taiwan/1/86 (H1N1) in the continental United States in the 1986-1987 influenza season.

Adult↗
PubMed1984

Pathogenesis of skin lesions caused by sulfur mustard.

Sulfur mustard (SM) (di-2-chlorethyl sulfide), used for chemical warfare in World War I, is a highly reactive radiomimetic alkylating agent. When applied to the skin of rabbits and guinea pigs, it produced vascular leakage, leukocyte infiltration, and slow death of basal epidermal cells. Thirty to sixty minutes after exposure to SM, injury to the superficial microvasculature (beneath the SM application site) was detected by measuring vascular leakage with Evans blue dye and also with horseradish peroxidase. At this same time, injury to the superficial fibroblasts was observed ultrastructurally; and an unexpectedly high percentage of basophils was found among the early infiltrating granulocytes. At 2 to 4 hr, the vascular leakage ceased, and had resumed by 8 hr in a more diffuse form. At this time, the basal epidermal cells showed pyknotic nuclei, an increase in their lysosomal enzymes (observed histochemically), and autophagic vacuoles (observed ultrastructurally). Leukocyte infiltration was marked, consisting mostly of heterophils (PMN) with a reduced percentage of basophils. During the next 24 to 72 hr, the entire inflammatory reaction reached its peak; and a superficial, crust-covered ulcer developed. Then, over the next 10 days, the lesion gradually subsided with concomitant repair and healing. Glucocorticosteroids decreased the early edematous phase, but did not affect the rate of healing. These findings suggest that the skin response to sulfur mustard has an immediate and a delayed phase. The immediate phase, i.e., within the first hour, was characterized by injury to the superficial fibroblasts and to the endothelium of superficial capillaries and venules, possibly because of direct damage to their cell membranes. At this time, a restricted vascular leakage and a selective granulocyte infiltration containing many basophils occurred. The delayed phase, which became evident after 8 hr, was characterized by the death of basal epidermal cells, probably because of DNA damage. This phase was accompanied by generalized vascular leakage, by massive heterophil immigration, and eventually by ulceration.

Acid Phosphatase↗
PubMed1983

Improved techniques using Giemsa stained glycol methacrylate tissue sections to quantitate basophils and other leukocytes in inflammatory skin lesions.

Improved techniques were developed for processing inflammatory skin lesions in glycol methacrylate (JB-4, Polysciences, Inc.) and for quantitating their leukocyte infiltrates by light microscopy: (1) fixation of entire pelts from rabbits, guinea pigs, rats and mice bearing multiple lesions eliminated artifacts due to biopsy and produced uniformly oriented skin sections; (2) adding dimethylsulfoxide and hydrogen peroxide to the Karnovsky-type fixative increased the rate and effectiveness of fixation; (3) the presence of glycerol in the infiltrating methacrylate and the polymerized plastic block improved the sectionability of skin and other tissues; (4) coating slides with JB-4 Solution A prevented detachment of specimens; (5) Giemsa staining at a carefully selected pH provided optimal differentiation of leukocytes from the several species examined, including man. These techniques, which allowed an accurate histologic assessment of inflammatory skin lesions, were especially valuable for quantitating basophils.

Animals↗
PubMedDate not supplied

Tick-borne tularemia. An outbreak of lymphadenopathy in children.

Between June 1 and July 15, 1984, twenty persons with glandular tularemia were identified on the Lower Brule and Crow Creek Indian reservations in South Dakota. The median age of the patients was 6 years (range, 2 to 20 years). The clinical illness was mild, consisting of fever, headache, and lymphadenopathy. All lymphadenopathy was in the head and neck area. Dermacentor variabilis ticks were identified as the vector. Although the mild clinical illness suggested Francisella tularensis, type B, was the agent, both type A and type B strains of F tularensis were isolated from ticks collected from dogs in the area. Tularemia is generally thought to be a severe systemic illness in North America. This outbreak illustrates that it can be a mild disease and that both type A and type B strains can be tick-borne and coexist in the same ecosystem.

Adolescent↗