Titrated Misoprostol Versus Dinoprostone for Labor Induction

Background: Misoprostol is as effective as dinoprostone for labor induction with low cost and temperature stability.Aim: This study designed to compare titrated misoprostol regarding its safety and efficacy with dinoprostone for induction of labor.Subjects and Methods: Women with a single pregnancy, above 37 weeks’ gestation, cephalic presentation, modified Bishop’s score <8, and not in labor with reassuring fetal heart rate, admitted for labor induction enrolled in this randomized controlled study. Studied women were randomized into; Group I: received oral misoprostol titrated in sterile water (200 μg tablet was dissolved in 200 ml sterile water [1 μg/ml]), starting dose of 20 μg misoprostol required, given every 2 h, and stopped if adequate contractions obtained and Group II: received vaginal dinoprostone tablet maximum two doses followed by augmentation of labor by oxytocin ± amniotomy if there is no uterine contractions after two doses of dinoprostone. In Group I, if the contractions were inadequate after two doses of oral titrated misoprostol (20 μg [20 ml]), the starting dose increased to 40 μg (40 ml), escalating the dose from 5 to 10 ml (45–50 μg), and 20 ml (60 μg) maximum ± amniotomy. If the uterine contractions were adequate, the next dose of misoprostol or dinoprostone was omitted. Statistical analysis done using Student’s t‑test for quantitative data and Chi‑square test for qualitative data.Results: Induction‑to‑delivery time was significantly longer in misoprostol than dinoprostone group (975 vs. 670 min, respectively), (P = 0.01). About 20.2% (21/104) of women in misoprostol group did not deliver vaginally within 24 h compared to 7.4% (8/108) in dinoprostone group (significant difference, P = 0.01). Augmentation of labor was significantly high in dinoprostone (37.96% [41/108]) compared to misoprostol group (10.6% [11/104]) (P < 0.01).Conclusion: Titrated misoprostol for induction of labor seems to be associated with significantly longer induction‑to‑delivery time, low incidence of vaginal birth within 24 h, and less need for augmentation of labor compared to vaginal dinoprostone.KEY WORDS: Dinoprostone, labor induction, titrated misoprosto

Docosahexaenoic Acid in Combination with Dietary Energy Restriction for Reducing the Risk of Obesity Related Breast Cancer

There is strong evidence that obesity poses a significant risk factor for postmenopausal breast cancer. There are multiple mechanisms by which obesity can predispose to breast cancer, prominent among which is the creation of a pro-inflammatory milieu systemically in the visceral and subcutaneous tissue, as well as locally in the breast. Although dietary intervention studies have shown in general a favorable effect on biomarkers of breast cancer risk, it is still unclear whether losing excess weight will lower the risk. In this manuscript, we will review the evidence that omega-3 fatty acids, and among them docosahexaenoic acid (DHA) in particular, may reduce the risk of obesity related breast cancer primarily because of their pleotropic effects which target many of the systemic and local oncogenic pathways activated by excess weight. We will also review the evidence indicating that intentional weight loss (IWL) induced by dietary energy restriction (DER) will augment the tumor protective effect of DHA because of its complementary mechanisms of action and its ability to reverse the obesity-induced alterations in fatty acid metabolism predisposing to carcinogenesis. We believe that the combination of DER and DHA is a promising safe and effective intervention for reducing obesity-related breast cancer risk which needs to be validated in appropriately designed prospective, randomized clinical trials

Inhibition of human cytochrome P450-catalyzed oxidations of xenobiotics and procarcinogens by synthetic organoselenium compounds

The effects of synthetic chemopreventive organoselenium compounds 1,2-, 1,3-, and 1,4-phenylenebis(methylene)selenocyanate (o-, m-, and p-XSC, respectively), benzyl selenocyanate (BSC), and dibenzyl diselenide (DDS) and inorganic sodium selenite on the oxidation of xenobiotics and procarcinogens by human cytochrome P450 (P450 or CYP) enzymes were determined in vitro. Spectral studies showed that BSC and three XSC compounds (but not sodium selenite or DDS) induced type II difference spectrum when added to the suspension of liver microsomes isolated from β-naphthoflavone-treated rats, with m-XSC being the most potent in inducing spectral interactions with P450 enzymes; m-XSC also produced a type II spectral change with human liver microsomes. o-, m-, and p-XSC inhibited 7-ethoxyresorufin O-deethylation catalyzed by human liver microsomes when added at concentrations below 1 μM levels, but BSC and DDS were less effective. All of these compounds inhibited the oxidation of model substrates for human P450s to varying extents. We studied the effects of these compounds on the activation of procarcinogens by recombinant human CYP1A1, 1A2, and 1B1 enzymes using Salmonella typhimurium NM2009 tester strain for the detection of DNA damage. The three XSCs were found to be very potent inhibitors of metabolic activation of 3-amino-1,4- dimethyl-5H-pyrido[4,3-b]indole, 2-amino-3,5-dimethylimidazo[4,5- f]quinoline, and 2-aminoanthracene, catalyzed by CYP1A1, 1A2, and 1B1, respectively. The potency of inhibition of m-XSC on CYP1B1-dependent activation of 2-aminoanthracene was compatible to those of α-naphthoflavone. These inhibitory actions may, in part, account for the mechanisms responsible for cancer prevention by organoselenium compounds in laboratory animals