Demand-avoid-withdraw processes in adolescent dating aggression.

We conducted an observational study of a collection of interactive processes known as "demand-withdraw" in relation to adolescent dating aggression. Couples (N = 209) aged 14-18 years participated in a challenging observational laboratory assessment to measure demands (i.e.

Expression of beta-1,4-galactosyltransferase gene during 3T3 cell growth.

The beta-1,4-galactosyltransferase (GT; EC 2.4.1.

Cell-cycle-specific and serum-dependent expression of gamma-actin mRNA in Swiss mouse 3T3 cells.

We isolated cDNA clones that represent genes whose expression is enhanced when resting Swiss mouse 3T3 cells are stimulated to proliferate with serum. Two clones (designated pME1 and pMR6) were analyzed further. A partial sequence analysis of the pME1 insert DNA indicated that it contained a 104-base-pair stretch with extensive homology to the 3' untranslated region of gamma actin.

Interferon alters intracellular transport of vesicular stomatitis virus glycoprotein.

Double-label immunofluorescence staining studies in virus-infected subclone 11 of LB cells indicated that almost all of the vesicular stomatitis virus (VSV) glycoprotein (G) was plasma membrane-associated during the logarithmic phase of virus replication. In contrast, treatment with interferon (IFN) resulted in inhibition of VSV-G transport, so that almost all of the G remained associated with the Golgi complex (GC) at comparable times after infection. In both IFN-treated and control cells, G was resistant to treatment with the enzyme endo-beta-N-acetylglucosamine H (endo H) indicating that the bulk of the G had reached the trans compartment of the GC.

Tunicamycin enhances virus replication and inhibits antiviral activity of interferon in mice: correlation with natural killer cells.

Earlier we reported that tunicamycin (TM) treatment enhances Semliki Forest virus (SFV) and encephalomyocarditis virus (EMCV) replication in Swiss mice. Interferon (IFN) mediated antiviral protection was also inhibited in mice treated with TM. The in vitro natural killer (NK) cell reactivity of mice was significantly decreased after in vivo administration of TM; however, TM treatment did not affect the response of the same cells to mitogens.

Potentiation of thermal injury in mouse cells by interferon.

Mouse cells, when exposed to high temperature (43 degrees), shut off overall protein synthesis and continue to synthesize "heat shock proteins". Such heat shocked cells, upon reincubation at 37 degrees C, recover and proliferate. However, when mouse cells are pretreated with mouse interferon (IFN) and then exposed to 43 degrees, more than 99% of the cell population fail to recover.