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Biomedical subjects

J Sowinski

Publications and source records attributed to J Sowinski.

At least 37 records · Page 2Linked to original sources
PubMed1992

The clinical effect of a dentifrice containing triclosan and a copolymer in a sodium fluoride/silica base on plaque formation and gingivitis: a six-month clinical study.

A six-month, double-blind clinical study was entered into by three hundred twenty-five (325) male and female adult subjects to assess the efficacy of a dentifrice containing 0.3% triclosan (Irgacare MP, Ciba-Geigy Corp.) and 2.0% of a copolymer of methoxyethylene and maleic acid (Gantrez, ISP Corp.) on supragingival plaque formation and gingivitis, compared to a placebo dentifrice over a six-month period. Each dentifrice, the triclosan and the placebo, contained 0.243% sodium fluoride in a silica base. Only those subjects who were free of periodontal disease (no pockets > 4 mm), demonstrated a level of at least mild gingivitis (modified Loe-Silness score > or = 1.0) and had a modified Quigley-Hein Plaque Index score of > or = 1.5 were admitted into the study. Baseline plaque and gingivitis scores were used to stratify the subjects into two balanced groups. A thorough oral prophylaxis was administered to all subjects. They were then assigned either the triclosan/copolymer dentifrice or the placebo dentifrice to use for the next six months. Evaluation for gingivitis and supragingival plaque formation was made after three and six months. Evaluations made after six (6) months demonstrated a 17.0% statistically significant (at the 99% level of confidence) reduction in supragingival plaque formation was provided by the triclosan/copolymer dentifrice, compared to the placebo dentifrice. An 18.6% statistically significant (at the 99% level of confidence) reduction in plaque formation on the tooth surfaces with the highest plaque formation was provided by the triclosan/copolymer dentifrice, compared to the placebo dentifrice.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Uptake of human recombinant tissue-type plasminogen activator by rat hepatocytes in vivo: an electron microscope autoradiographic study.

The hepatic uptake of recombinant human tissue-type plasminogen activator (tPA) has been studied by electron microscope autoradiography (EMARG) of serial hepatic biopsies taken from anaesthetized, laparotomized rats following intravenous injection of 125I labeled tPA. Serial blood samples showed both radiolabel and biologic activity to be eliminated from circulation with an initial half-life of approximately two minutes. Grain half-distance distribution profiles and grain density analysis showed that the para-sinusoidal region of the hepatic parenchymal cell is the only site in the liver to concentrate radiolabeled tPA after intravenous injection. These data support the hypothesis that the parenchymal cell is the principal cell responsible for hepatic clearance of tPA from circulation and suggest that receptor mediated endocytosis may be the mechanism of cellular uptake.

Animals↗
PubMed1989

2H(d

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Journal Article↗
PubMed1988

1H(d

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Journal Article↗
PubMed1987

The mechanism of acute cytotoxicity of triethylphosphine gold(I) complexes. I. Characterization of triethylphosphine gold chloride-induced biochemical and morphological changes in isolated hepatocytes.

Triethylphosphine gold complexes are effective therapeutic agents used for the treatment of rheumatoid arthritis. Many of those molecules are also highly cytotoxic in vitro and can inhibit DNA and protein synthesis. Preliminary experiments have indicated that triethylphosphine gold chloride (TEPAu) may induce the peroxidative decomposition of cellular membrane lipids. The purpose of these investigations therefore was to evaluate the role of lipid peroxidation in the mechanism of acute cytotoxicity of a gold(I) coordination complex, TEPAu, and to examine the early morphological and biochemical changes induced by TEPAu in suspensions of freshly isolated rat hepatocytes. TEPAu caused a rapid loss of cell viability at concentrations above 25 microM which was significantly different from that of control by 60 min and complete by 180 min of incubation. TEPAu also depleted cells of reduced glutathione (GSH) and increased the formation of malondialdehyde (MDA) by 60 min. Incubation of cells with either of the antioxidants, N,N'-diphenyl-p-phenylenediamine (DPPD) or promethazine blocked the formation of MDA but did not alter the time course of cell death or GSH depletion induced by TEPAu. TEPAu also caused a decrease in cellular NADPH and NADH by 10 min. Electron microscopy of hepatocytes exposed to TEPAu revealed early (5 min) formation of flocculent electron-dense precipitates within condensed mitochondria. These changes characteristically preceded cell death. Energy-dispersive electron-probe microanalysis indicated that the electron-dense precipitates did not contain detectable amounts of gold. TEPAu also caused a concentration-dependent decrease in cellular ATP and oxygen consumption in isolated rat hepatocytes. These data suggest that lipid peroxidation, as indicated by the formation of MDA, is probably not a major mechanism by which triethylphosphine gold complexes lethally injure cells. These data, therefore, suggest that mitochondria may be target organelles in TEPAu-induced toxicity to isolated rat hepatocytes.

Animals↗
PubMed1985

Organic hydroperoxide-induced lipid peroxidation and cell death in isolated hepatocytes.

Organic hydroperoxides such as tert-butyl hydroperoxide (TBHP) are cytotoxic to suspensions of isolated hepatocytes. The exact mechanism of toxicity is unknown but may involve peroxidation of cellular lipids, alkylation of cellular macromolecules, or alterations in cellular calcium homeostasis. These studies were designed to examine lipid peroxidation as a mechanism of organic hydroperoxide-induced cell death. Hepatocytes isolated from mice were more susceptible to the cytotoxic effects of TBHP than were rat hepatocytes. TBHP-induced cell death was preceded by malondialdehyde formation which was also greater in mouse than rat hepatocytes. Species differences in lipid peroxidation were due to intrinsic properties of hepatocyte membranes as lipids isolated from mouse liver and peroxidized with iron/ascorbate formed approximately eightfold more malondialdehyde than lipids isolated from rat liver. Initiation of lipid peroxidation in mouse and rat hepatocytes with iron/ascorbate caused the formation of malondialdehyde equal to that seen with TBHP and a slight depletion of cellular GSH. As with TBHP, malondialdehyde formation induced by iron/ascorbate was greater in mouse than in rat hepatocytes. However, iron/ascorbate had no effect on hepatocyte viability or morphology from either species. Furthermore, TBHP-induced malondialdehyde and ethane formation in isolated rat hepatocytes were completely blocked by promethazine whereas cell toxicity was altered only slightly. Therefore, these data do not support a role for lipid peroxidation in the acute cytotoxicity of TBHP to suspensions of isolated rat hepatocytes.

Animals↗
PubMed1979

An ultrastructural study of epididymal mouse spermatozoa binding to zonae pellucidae in vitro: sequential relationship to the acrosome reaction.

Mouse sperm bind to the zona pellucida of the egg prior to penetration of the zona and entry into the perivitelline space. The question then arises: when does the acrosome reaction occur relative to these processes? An ultrastructural study of mouse epididymal sperm bound to the surface of the zona and in the privitelline space was undertaken to clarify this point. Cumulus-free mouse eggs were inseminated in either a complete defined culture medium capable of supporting in vitro fertilization or in Tris/NaCl buffer containing Ca+2. Both media support sperm binding to the zona to the same extent; binding is complete in 15 minutes. Unbound sperm were removed by a step gradient density centrifugation to yield a preparation of eggs with sperm firmly bound. All sperm in the perivitelline space had undergone the acrosome reaction. Sperm bound at the surface of the zonae pellucidae of eggs recovered at ten minutes after insemination all had intact acrosomes. At 40 minutes after insemination, half of the sperm were intact; the other half were in the initial stages of the acrosome reaction. At 90 minutes after insemination, 12% of the sperm had undergone the full acrosome reaction and were starting to penetrate the zona; of the balance, half were in various stages of the acrosome reaction, while half were still intact. These findings support the hypothesis that the sequence of the early reactions leading to fertilization in the mouse is: intact sperm binding to zona; acrosome reaction at the zona surface; penetration of the zona.

Acrosome↗