Effect of Television Programming and Advertising on Alcohol Consumption in Normal Drinkers

The drinking behavior of 96 male normal drinking college students was assessed after they viewed a videotape of a popular prime-time television program complete with advertisements. Different versions of the videotape were used to evaluate the effects of a television program with and without alcohol scenes as crossed with the effects of three different types of advertisements (i.e., beer, nonalcoholic beverages and food). After viewing the videotape, the subjects, who were led to believe that they were participating in two separate and unrelated sets of experimental procedures, were asked to perform a taste rating of light beers, which actually provided an unobtrusive measure of their alcohol consumption. The results provided no support for the widely held assumption that drinking scenes in television programs or televised advertisements for alcoholic beverages precipitate increased drinking by viewers. This finding, however, must be considered in the context of the laboratory setting of the study, and thus may not generalize to real-life television viewing. Further research in this area is clearly needed, including an evaluation of the effects of television program content and advertisements on other populations (e.g., alcohol abusers)

The Reliability of Alcohol Abusers’ Self-Reports Of Drinking and Life Events That Occurred In the Distant Past

This study investigated the test-retest reliability of 69 alcohol abusers\u27 current reports about their past (approximately 8 years prior to interview) drinking behavior and life events. Drinking behavior was assessed by the Lifetime Drinking History (LDH) questionnaire and life events were assessed using the Recent Life Changes Questionnaire (RLCQ). Reliability coefficients for LDH variables were generally moderate to high (r = .52 to .81). Using empirical criteria, the diagnostic power of the two LDH interviews to classify correctly subjects as either having had or not having had a drinking problem was quite high. The reliability coefficient for the RLCQ was r = .85 and 91.7% of the identified events were reported in both interviews. Similarly high test-retest reliabilities and individual event agreement rates were obtained for the six homogeneous subscales of the RLCQ. Subjects were also asked why they had given inconsistent answers to life events questions in the two interviews. Inconsistencies often resulted from errors in the temporal placement of events or from misunderstanding items, rather than from failure to recall an event; this suggests that some sources of error in recalling life events can be reduced. It is concluded that alcohol abusers\u27 reports of drinking and life events occurring many years prior to the date of interview are generally reliable. This finding is consistent with previous studies showing high test-retest reliabilities for reports of recent drinking and related events

FGFR3IIIS: a novel soluble FGFR3 spliced variant that modulates growth is frequently expressed in tumour cells

Fibroblast growth factor receptor 3 (FGFR3) is one of four high-affinity tyrosine kinase receptors for the FGF family of ligands, frequently associated with growth arrest and induction of differentiation. The extracellular immunoglobulin (IgG)-like domains II and III are responsible for ligand binding; alternative usage of exons IIIb and IIIc of the Ig-like domain III determining the ligand-binding specificity of the receptor. By reverse transcriptase polymerase chain reaction (RT–PCR) a novel FGFR3IIIc variant FGFR3IIIS, expressed in a high proportion of tumours and tumour cell lines but rarely in normal tissues, has been identified. Unlike recently described nonsense transcripts of FGFR3, the coding region of FGFR3IIIS remains in-frame producing a novel protein. The protein product is coexpressed with FGFR3IIIc in the membrane and soluble cell fractions; expression in the soluble fraction is decreased after exposure to bFGF but not aFGF. Knockout of FGFR3IIIS using antisense has a growth-inhibitory effect in vitro, suggesting a dominant-negative function for FGFR3IIIS inhibiting FGFR3-induced growth arrest. In summary, alternative splicing of the FGFR3 Ig-domain III represents a mechanism for the generation of receptor diversity. FGFR3IIIS may regulate FGF and FGFR trafficking and function, possibly contributing to the development of a malignant phenotype

Evidence for long-range glycosyl transfer reactions in the gas phase

AbstractA long-range glycosyl transfer reaction was observed in the collision-induced dissociation Fourier transform (CID FT) mass spectra of benzylamine-labeled and 9-aminofluorene-labeled lacto-N-fucopentaose I (LNFP I) and lacto-N-difucohexaose I (LNDFH I). The transfer reaction was observed for the protonated molecules but not for the sodiated molecules. The long-range glycosyl transfer reaction involved preferentially one of the two L-fucose units in labeled LNDFH I. CID experiments with labeled LNFP I and labeled LNFP II determined the fucose with the greatest propensity for migration. Further experiments were performed to determine the final destination of the migrating fucose. Molecular modeling supported the experiments and reaction mechanisms are proposed

Transgenic Expression of Nonclassically Secreted FGF Suppresses Kidney Repair

FGF1 is a signal peptide-less nonclassically released growth factor that is involved in angiogenesis, tissue repair, inflammation, and carcinogenesis. The effects of nonclassical FGF export in vivo are not sufficiently studied. We produced transgenic mice expressing FGF1 in endothelial cells (EC), which allowed the detection of FGF1 export to the vasculature, and studied the efficiency of postischemic kidney repair in these animals. Although FGF1 transgenic mice had a normal phenotype with unperturbed kidney structure, they showed a severely inhibited kidney repair after unilateral ischemia/reperfusion. This was manifested by a strong decrease of postischemic kidney size and weight, whereas the undamaged contralateral kidney exhibited an enhanced compensatory size increase. In addition, the postischemic kidneys of transgenic mice were characterized by hyperplasia of interstitial cells, paucity of epithelial tubular structures, increase of the areas occupied by connective tissue, and neutrophil and macrophage infiltration. The continuous treatment of transgenic mice with the cell membrane stabilizer, taurine, inhibited nonclassical FGF1 export and significantly rescued postischemic kidney repair. It was also found that similar to EC, the transgenic expression of FGF1 in monocytes and macrophages suppresses kidney repair. We suggest that nonclassical export may be used as a target for the treatment of pathologies involving signal peptide-less FGFs