Our study shows that environments heavily polluted with antibiotics contain novel multiresistance plasmids transferrable to E. coli.
BACKGROUND: The long-term effects of 1 or 2 consecutive obstetrical anal sphincter injuries on bowel continence are still inadequately investigated, and published results remain contradictory. OBJECTIVE: This study aimed to present detailed descriptive measures of the current bowel incontinence 20 years after the first birth in women who had 2 vaginal deliveries with and without sphincter injuries. STUDY DESIGN: Birth register data were used prospectively and linked to information from a questionnaire survey about current symptoms. Women with 2 singleton vaginal births, from 1992 to 1998, and no further births were retrieved and surveyed by the Swedish Medical Birth Register and Statistics Sweden in 2015. A simple random sample of 11,000 women was drawn from a source cohort of 64,687 women. The cumulative effect was studied in all women with a repeat sphincter injury from 1987 to 2000. Postal and web-based questionnaires were used. The study population consisted of 6760 women with no sphincter injury, 357 with 1 sphincter injury, and 324 women with 2 sphincter injuries. Women with 2 deliveries without sphincter injuries aged 40 to 60 years as reference, were compared with those of women that sustained 1 or 2 consecutive sphincter injuries. Here, third-and fourth-degree perineal tears were presented as 1 group. Fecal incontinence was defined as current involuntary leakage of solid or liquid stool, with and without concomitant leakage of gas. The Fisher exact test and the Mann-Whitney U test were used to compare the results of the 2 groups. The trend was analyzed using the Mantel-Haenszel statistics. Logistic regression models obtained the estimated age-related probability of fecal incontinence components. RESULTS: The risk of sphincter injury at first delivery was 3.9%, and the risk of a repeat sphincter injury was 10.0% (odds ratio, 2.70; 95% confidence interval, 1.80e4.07). The overall prevalence of fecal incontinence in women without sphincter injuries was 11.7%, which doubled to 23.8% (odds ratio, 2.27; 95% confidence interval, 1.75e2.94) in those with 1 sphincter injury and more than tripled to 36.1% (odds ratio, 3.97; 95% confidence interval, 3.11e5.07) after 2 sphincter injuries (trend P<.0001). The proportion of women with severe fecal incontinence increased 3-fold and 5-fold from 1.8% after no obstetrical anal sphincter injury to 5.4% (95% confidence interval, 3.3e8.2) and 9.0% (95% confidence interval, 6.1e12.6) after 1 or 2 obstetrical anal sphincter injuries, respectively (trend P<.0001). In women without sphincter injuries, the estimated probability of fecal incontinence increased from 7.0% at the age of 40 years to 19.8% at the age of 60 years. In contrast, in women with 1 or 2 sphincter injuries, the estimated probability of fecal incontinence increased from 26.1% and 33.3%, respectively, at the age of 40 years to 36.8% and 48.8% at the age of 60 years. The prevalence of fecal incontinence increased after 52 years of age in women with 1 or 2 sphincter injuries. The dominant types of leakage in women...
A method has been developed for the quantitative determination of haloperidol in brain and other tissues. Such determinations have been made after acute and chronic administration of haloperidol to Sprague-Dawley rats. Different regions of the brain including the striatum, the limbic forebrain and the cerebellum have been analyzed separately. The haloperidol effects on Dopa formation have been studied in the same tissue samples. The stimulation of prolactin secretion via blockade of hypothalamic dopaminergic mechanisms and behavioural effects of the drug have been evaluated in parallel experiments. The elimination of haloperidol from brain tissue is a multiphasic process. The fourth phase of elimination is the slowest with a half life of 4 days. No strict correlation was found between serum and brain concentrations of haloperidol. Both after acute and chronic administration there exists apparently a saturating dose above which the brain concentration of the drug increases very little. The dose seems to coincide with that beyond which little increase in Dopa formation is observed. A pharmacokinetic analysis suggests an element of saturable binding or transfer of haloperidol to brain tissue. This mechanism is not preferentially localized to areas of brain rich in dopaminergic synapses. A good correlation was found between the haloperidol concentration in the brain on the one hand and its effects on behaviour, on serum prolactin values and on Dopa formation on the other.
Liver fatty acid-binding protein (LFABP) is an abundant protein in hepatocytes that binds most of the long chain fatty acids present in the cytosol. It is suggested to be of importance for fatty acid uptake and utilization in the hepatocyte. In the present study, the effects of bovine GH (bGH) and other hormones on the expression of LFABP and its messenger RNA (mRNA) were studied in hypophysectomized rats and in vitro using primary cultures of rat hepatocytes. One injection of bGH increased LFABP mRNA levels about 5-fold after 6 h, but there was no effect of this treatment on LFABP levels. However, 7 days of bGH treatment increased both LFABP mRNA and LFABP protein levels 2- to 5-fold. Female rats had higher levels of LFABP than male rats. Hypophysectomy of female rats, but not that of male rats, decreased LFABP levels markedly. Treatment of hypophysectomized rats with bGH for 7 days as two daily injections or as a continuous infusion increased LFABP levels to a similar degree. This finding indicates that the sex difference in the expression of LFABP is not regulated by the sexually dimorphic secretory pattern of GH. Neither insulin nor insulin-like growth factor I treatment of hypophysectomized rats for 6-7 days had any effect on LFABP mRNA or LFABP levels. In vitro, bGH dose-dependently increased the expression of LFABP mRNA, but only in the presence of insulin. Insulin alone had a marked dose-dependent effect on LFABP mRNA levels and was of importance for maintaining the expression of LFABP mRNA during the culture. Incubation with bGH increased LFABP mRNA levels within 3 h. GH had no effect on LFABP mRNA levels in the presence of actinomycin D, indicating a transcriptional effect of GH. Incubation with glucagon in vitro decreased LFABP mRNA levels markedly, indicating that glucagon, in contrast to GH, has an effect opposite that of insulin on LFABP mRNA expression. It is concluded that GH is an important regulator of LFABP in vivo and in vitro. In contrast to the effect of GH on insulin-like growth factor I mRNA, the presence of insulin was a prerequisite for the effect of GH on LFABP mRNA expression in vitro. The results emphasize the role of GH in the regulation of hepatic fatty acid metabolism.
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