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Biomedical subjects

B Gold

Publications and source records attributed to B Gold.

128 records · Page 8Linked to original sources

Cefuroxime: mechanisms of action, antimicrobial activity, pharmacokinetics, clinical applications, adverse reactions and therapeutic indications.

Cefuroxime is a second generation cephalosporin with a broad antimicrobial activity against both Gram-positive and Gram-negative organisms. It has excellent in vitro activity against staphylococcal strains, streptococcal strains (other than enterococci), N. gonorrhoeae, H. influenzae and N. meningitidis. It also has excellent in vitro activity against members of the Enterobacteriaceae with the exception of Serratia and indole-positive Proteus. Ps. aeruginosa and B. fragilis are resistant. Cefuroxime is relatively free of serious side effects. It is metabolically stable, and most of it is excreted unchanged in the urine. Three fourths of it are distributed in the extravascular compartment. Blood levels exceed the in vitro minimum inhibitory concentrations for many important gram negative pathogens. Clinical studies have shown cefuroxime to be effective therapy for infections of soft tissue, respiratory tract, urinary tract, genital tract (caused by N. gonorrhoeae) and the central nervous system. Superinfections with Ps. aeruginosa and enterococcal strains may present a problem. In spite of excellent diffusion into bone and joint tissues, the available clinical data are too limited to make a recommendation for its use in bone and joint infections.

Adolescent↗

Inhibition of ultraviolet light induced skin carcinogenesis in SKH-1 mice by apigenin, a plant flavonoid.

Apigenin, a widely distributed plant flavonoid, was previously found to inhibit chemically induced ornithine decarboxylase (ODC) activity and skin tumor promotion. The purpose of the present research was to determine if apigenin is effective in the prevention of ultraviolet-B light (UVB) induced skin carcinogenesis. Further studies ascertained if apigenin would be expected to absorb UVB light in a manner to prevent DNA damage in a cell free system. ODC activity was induced with 0.45 J/cm2 ultraviolet A and B (UVA/B) light. Apigenin (5 mumoles/200 microliters DMSO:acetone, 1:9) treatment from 12 hours before until 1 hour following UVA/B exposure was effective in inhibition (25-45% inhibition) of ODC activity measured at 28 hours following UVA/B exposure. Mouse skin carcinogenesis was induced by exposure to a total dose of 40 J/cm2 UVB over 11 weeks. Treatment with 10 mumoles apigenin in 200 microliters DMSO:acetone (1:9) prior to each UVB exposure resulted in reduction in cancer incidence (52% inhibition) and an increase in tumor free survival in comparison with control mice (P < 0.01). Apigenin (0-100 microM) did not prevent the in vitro production of photoproducts in salmon sperm DNA suggesting that apigenin did not inhibit UVA/B induced ODC activity or UVB induced skin carcinogenesis by simply absorbing ultraviolet light or decreasing DNA damage.

Animals↗