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Biomedical subjects

S Louie

Publications and source records attributed to S Louie.

9 recordsLinked to original sources
PubMed1992

Interaction of nitrogen dioxide with human plasma. Antioxidant depletion and oxidative damage.

Nitrogen dioxide (NO2.) is often present in inhaled air and may be generated in vivo from nitric oxide. Exposure of human blood plasma to NO2. caused rapid losses of ascorbic acid, uric acid and protein thiol groups, as well as lipid peroxidation and depletions of alpha-tocopherol, bilirubin and ubiquinol-10. No increase in protein carbonyls was detected. Supplementation of plasma with ascorbate decreased the rates of lipid peroxidation, alpha-tocopherol depletion and loss of uric acid. Uric acid supplementation decreased rates of lipid peroxidation but not the loss of alpha-tocopherol. We conclude that ascorbic acid, protein -SH groups, uric acid and alpha-tocopherol may be important agents protecting against NO2. in vivo. If these antioxidants are depleted, peroxidation of lipids occurs and might contribute to the toxicity of NO2..

Adult↗
PubMed1978

Penetration of clindamycin into decubitus ulcers.

Forty tissue samples, primarily of skin and bone, were obtained from 29 patients undergoing excision of decubitus ulcers after intravenous injection of 600 mg of clindamycin. Antibiotic concentrations exceeded 2.5 mug/g in 80% of the samples. In 50% of the instances, tissue levels were greater than those simultaneously present in the serum.

Adolescent↗
PubMed1976

Antibodies in human sera to oncorna virus-like proteins from normal or leukemia marrow cell cultures.

Some human marrows in culture release particles with oncornavirus-like properties. This study was designed to examine the immunological properties of similar particles in human marrow culture supernates. Leukemic and nonleukemic marrows were cultured for 5-7 days in the presence of [14C]uridine and [3H]leucine or [3H]glucosamine. Labeled supernatant components banding in sucrose gradient densities of 1.20-1.24 g/ml were used as antigen in a double antibody immunoprecipitation assay. The assay was validated by end point titrations and competition with unlabeled antigen; purified myeloma proteins were used as negative controls. Cross-reactivity with mammalian oncornaviruses, as judged by competitive inhibition of precipitation by these viruses, was slight and at the border of the sensitivity of the method. Precipitated antigens analyzed by SDS polyacrylamide gel electrophoresis contained three distinct polypeptides of about 70,000, 45,000 and 30,000 mol wt; these comigrated with the gp 70, pg 45, and p 30 of a murine leukemia virus. Similar polypeptides were obtained from both leukemic and nonleukemic marrow culture supernates. As determined by the radioimmunoprecipitation assay, 32 of 45 leukemic sera (71%), 36 of 45 normal sera (80%), 15 of 19 sera from family contacts of leukemic patients (79%), 14 of 21 cord blood specimens (67%), and 21 of 23 sera (91%) from patients with systemic lupus erythematosus had detectable antibody activity.

Antibodies, Viral↗
PubMed1976

Immunity to C-type RNA viruses: antibody formation after natural or deliberate infection.

A combined virologic and immunologic study was done in mice that were either naturally or deliberately infected with C-type RNA viruses. In about 60% of B10. A mice, natural infection was accompanied by detectable anti-VEA antibodies in the serum. The absence of such antibodies was a reliable indicator of the absence of virus in B10 mice. Deliberately infected young adult B10 mice failed to eliminate the virus completely, despite high titers of anti-VEA antibodies. B10 mice exposed to B tropic viruses at birth made anti-VEA antibodies but failed to eliminate the virus. By contrast, some NIH Swiss mice exposed to N-tropic virus at birth made anti-VEA antibodies and eliminated the virus.

Animals↗
PubMed1975

Ecotropic leukemia viruses in congenic C57BL mice: natural dissemination by milk-borne infection.

The incidence of infectious murine leukemia virus (MuLV) in congenic-resistant C57BL mice was studied. No constant relationship between the incidence of MuLV and the H-2 complex was apparent. Two lines, B10 and B10.A, were examined in detail because the incidence of MuLV in B10 was low and the virus appeared relatively late in life, whereas B10.A animals had a relatively high incidence of infection by MuLV early in life. Further studies of B10.A mice revealed an almost universal concordance between the virologic status of the mother and her offspring. This was particularly evident when (B10 times B10.A)F1 animals were compared with (B10.A times B10)F1 mice: Although genetically identical, the incidence of MuLV in the latter was high, whereas in the former it was low. Transmission of MuLV by milk was proved by foster-nursing experiments; when the infants of MuLV-positive B10.A mothers were suckled on MuLV-negative B10.A mothers, they were free of MuLV. Milk-borne infection may account for the natural dissemination of MuLV among some inbred lines of mice.

Animals↗
PubMed1975

Splenocyte plaque assay for the detection of murine leukemia virus.

A modified XC assay for murine leukemia virus (MuLV) employing splenocytes taken directly from the animal is described. This modification can be more than 1000 times more sensitive than XC plaque assays employing tissue extracts. This technique should lend itself readily to the quantitation of infectious MuLV in defined populations of lymphoid cells.

Animals↗