BackgroundMany Americans diagnosed with colon cancer do not receive indicated chemotherapy. Certain unmarried women may be particularly disadvantaged. A 3-way interaction of the multiplicative disadvantages of being an unmarried and inadequately insured woman living in poverty was explored.MethodsCalifornia registry data were analyzed for 2,319 women diagnosed with stage II to IV colon cancer between 1996 and 2000 and followed until 2014. Socioeconomic data from the 2000 census classified neighborhoods as high poverty (≥30% of households poor), middle (5–29%) or low poverty (<5% poor). Primary health insurance was private, Medicare, Medicaid or none. Comparisons of chemotherapy rates used standardized rate ratios (RR). We respectively used logistic and Cox regression models to assess chemotherapy and survival.ResultsA statistically significant 3-way marital status by health insurance by poverty interaction effect on chemotherapy receipt was observed. Chemotherapy rates did not differ between unmarried (39.0%) and married (39.7%) women who lived in lower poverty neighborhoods and were privately insured. But unmarried women (27.3%) were 26% less likely to receive chemotherapy than were married women (37.1%, RR = 0.74, 95% CI 0.58, 0.95) who lived in high poverty neighborhoods and were publicly insured or uninsured. When this interaction and the main effects of health insurance, poverty and chemotherapy were accounted for, survival did not differ by marital status.ConclusionsThe multiplicative barrier to colon cancer care that results from being inadequately insured and living in poverty is worse for unmarried than married women. Poverty is more prevalent among unmarried women and they have fewer assets so they are probably less able to absorb the indirect and direct, but uncovered, costs of colon cancer care. There seem to be structural inequities related to the institutions of marriage, work and health care that particularly disadvantage unmarried women that policy makers ought to be cognizant of as future reforms of the American health care system are considered.

Trypsin enhancement of parainfluenza-3 virus infectivity in HEp-2 cells was demonstrated. A substantial enhancement of infectivity was observed when cell cultures were exposed to trypsin during the adsorption period or when subcultured with trypsin late in the eclipse phase. Time-course studies on virus development indicated that treatment of cells with puromycin or cycloheximide for 1 h postinfection markedly inhibited the synthesis of infectious virus. However, this inhibitory effect could be reversed by the removal of drug and subsequent subculture of trypsinized cells.

SUMMARYThe addition of either isatin-fl-thiosemicarbazone (IBT) or its N-methyl derivative effectively inhibited the multiplication of various isolates of infectious bovine rhinotracheitis virus. Treatment of infected cultures with IBT early or late in the log. phase of replication markedly suppressed the production of infectious virus, indicating that the drug inhibits virus maturation. The time course of formation of infectious virus and of synthesis of viral DNA and viral protein was determined with the inhibitors FUdR and cycloheximide, respectively. In radioisotope experiments, IBT inhibited the incorporation of label into both RNA and DNA at a fairly early stage of the virus growth cycle.