Are women who have abortions different from those who do not? A secondary analysis of the 1990 national survey of sexual attitudes and lifestyles

Studies of women undergoing termination of a pregnancy are often used to make recommendations about family planning and health education policy. However, it is not clear how similar the women in these studies are to the general population of women of childbearing age. Our secondary analysis of the National Sexual Attitudes and Lifestyles Survey allowed us to test the hypothesis that women who have undergone an abortion are the same as those who have not (in terms of socio-demographic characteristics, lifestyles, and attitudes). Our findings show significant differences between these two groups of women, particularly regarding ethnicity, marital status, number of natural children, lifetime number of sexual partners, and attitudes to abortion. We conclude that family planning/reproductive health services and health education policies need to take these differences into account and that further research is required to explain why these differences arise.     

Short term reductions in cerebral muscarinic receptor concentration of the mouse after in vivo administration of cycloheximide

[³H]quinuclidinyl benzilate ([³H]QNB) was used to investigate the effects of administration of cycloheximide to mice on the concentration of muscarinic receptors in the cerebral cortex. A single subcutaneous (s.c.) injection of cycloheximide (3.5 mg/kg) reduced receptor concentration by 18% after an apparent latency of 1 hr. A single intraperitoneal (i.p.) injection of 3.5 mg/kg produced a 14% reduction in muscarinic receptor concentration 20 min after injection. After both s.c. and i.p. administration the effects of cycloheximide were reversible, dose-related and maximal at a dose of 3.5 mg/kg. The maximum reductions in receptor concentrations obtained were 13–18%. Multiple doses of cycloheximide did not produce greater falls in receptor concentration than single doses and did not prevent its return towards control levels. Treatment of mice for 10 days with cycloheximide reduced muscarinic receptor concentration to 71% of the control at 3 days after stopping administration; receptor levels returned to control values 35 days after the last dose of cycloheximide. Treatment of mice with cycloheximide had no effect on the affinity of [³H]QNB for the receptor and, in vitro, 10^?4M cycloheximide did not have any significant effect on the binding of the radiolabel.     

Transforming growth factor-β (TGF-β) activity in urine of patients with glomerulonephritis is related to their renal functional and structural changes

SUMMARY: Transforming growth factor-β (TGF-β) has been considered the principal cytokine involved in the pathogenesis of renal fibrosis. In the present study, we evaluated TGF-β activity in occasional samples from 22 normal individuals and 29 patients (11 with focal glomerulosclerosis, 11 with membranous nephropathy, five with Berger disease, one with type I membranoproliferative glomerulonephritis and one with postinfectious glomerulonephritis) using a CCL-64 mink lung cell growth inhibition assay.
A significantly increased urinary TGF-β activity (reported in relation to urine creatinine, Ucreat, and median) was observed in patients with glomerulonephritis compared with normal individuals ( P <0.01). the patients with Berger disease [median (Md) = 9.96/10 μg Ucreat.], membranous glomerulonephritis (Md = 7.23/10 μg Ucreat.) and focal glomerulosclerosis (Md = 16.6/10 μg Ucreat.) showed higher urinary TGF-β than normal individuals (Md = 1.09/10 μg Ucreat.) ( P <0.01). We found a positive correlation between the TGF-β activity in the urine of these patients and the incidence of segmental glomerulosclerosis ( r = 0.45, P <0.05) and their plasma creatinine levels ( r = 0.87, P <0.01). A negative correlation was observed between the TGF-β activity in the urine of these patients and their creatinine clearance ( r =−0.75, P <0.01).
Our data suggest that measurement of urinary TGF-β activity could be a useful non-invasive procedure for the evaluation of renal TGF-β production, permitting the assessment of prognosis and the evaluation of therapeutic efficacy in patients with renal disease.     

Effect of phenobarbitone pretreatment upon endothelium-dependent relaxation to acetylcholine in rat superior mesenteric arterial bed.

1. Pretreatment of rats for 5 days with phenobarbitone (80 mg kg-1 day-1) enhanced the potency enhanced the potency of acetylcholine in opposing noradrenaline-induced vasoconstriction in the isolated perfused superior mesenteric arterial bed; in 10 saline-pretreated control animals the ED50 was 14.0 +/- 3.9 ng whereas it was 3.23 +/- 1.00 ng in 10 phenobarbitone-pretreated animals. 2. In both saline- and phenobarbitone-pretreated rats acetylcholine was ineffective at opposing noradrenaline vasoconstriction after the mesentery had been perfused for 90s with a 0.3% solution of the detergent CHAPS in distilled water (to remove the endothelium), but pressor responses to noradrenaline were unaffected. 3. Pretreatment with phenobarbitone had no effect on the opposition by sodium nitroprusside of noradrenaline pressor responses. Also, the effects of nitroprusside were not affected by perfusion with CHAPS in either control or barbiturate-pretreated groups. 4. Inclusion of indomethacin (10 microM) in the perfusion fluid had no effect on the enhancement by phenobarbitone pretreatment of the endothelium-dependent opposition by acetylcholine of noradrenaline pressor responses; the ED50 values in the absence and presence of indomethacin were, respectively, 2.40 +/- 0.31 ng and 1.87 +/- 0.27 ng (n = 6). 5. The concentration of cytochrome P450 in the microsomal fraction obtained from the mesenteric preparation was increased from 204 +/- 32 (saline-pretreated; n = 7) to 784 +/- 249 pmol g-1 wet wt (n = 7) by the phenobarbitone pretreatment. 6. It is concluded that the increase in potency of acetylcholine as an endothelium-dependent vasodilator by phenobarbitone pretreatment is most probably at the level of the endothelium rather than the vascular smooth muscle.