Prenatal alcohol exposure can result in a wide range of adverse health outcomes, including in some cases fetal alcohol spectrum disorder (FASD), a lifelong neurodevelopmental disorder. Thus, there is pressing need for effective interventions to prevent alcohol-exposed pregnancies (AEPs).

A systematic review was undertaken to provide an up-to-date analysis of the current prevention literature. PubMed, Embase, CINAHL, and PsycINFO were searched for relevant English-language articles published from 1970 onward. Studies were eligible for the current systematic review if the interventions included pregnant and postpartum women and/or their support networks to prevent AEPs and FASD. Outcomes of interest included alcohol consumption, knowledge, contraceptive use, neonatal outcomes, family well-being or functioning, economics, and healthcare utilization outcomes.

Thirty-four peer-reviewed studies met the inclusion criteria. Fifteen studies employed brief intervention (BI) methods, 6 used long-term/intensive stried variable results from available interventions to prevent alcohol use among pregnant and postpartum women. Preliminary evidence demonstrated that BIs may be effective among subgroups of pregnant women with higher initial alcohol consumption, those with partner involvement, and those who used alcohol and other substances concurrently. Some preliminary evidence relating to long-term interventions with pregnant women with polysubstance use emerged, specifically case management that not only focused on reduction in substance use, but also on addressing the complex interplay between health and social well-being of families. Overall, additional research is required to improve the effectiveness of preventative approaches during pregnancy and the postpartum period.Preclinical data suggests that protein and calorie restriction (PCR) might improve treatment tolerability without impairing antitumor efficacy. Therefore, we have studied the influence of PCR on irinotecan pharmacokinetics and toxicity. In this crossover trial, patients with liver metastases of solid tumors were included and randomized to treatment with irinotecan preceded by 5 days of PCR (~ 30% caloric and ~ 70% protein restriction) during the first cycle and a second cycle preceded by a normal diet or vice versa. Pharmacokinetic blood sampling and biopsies of both healthy liver and liver metastases were performed. The primary end point was the relative difference in geometric means for the active metabolite SN-38 concentration in healthy liver analyzed by a linear mixed model. No significant differences were seen in irinotecan (+ 16.8%, P = 0.22) and SN-38 (+ 9.8%, P = 0.48) concentrations between PCR and normal diet in healthy liver, as well as in liver metastases (irinotecan -38.8%, P = 0.05 and SN-38 -13.8%, P = 0.50). Selleckchem LMK-235 increased irinotecan plasma area under the curve from zero to 24 hours (AUC0-24h ) with 7.1% (P = 0.04) compared with normal diet, whereas the SN-38 plasma AUC0-24h increased with 50.3% (P less then 0.001). Grade ≥ 3 toxicity was not increased during PCR vs. #link# normal diet (P = 0.69). No difference was seen in neutropenia grade ≥ 3 (47% vs. 32% P = 0.38), diarrhea grade ≥ 3 (5% vs. 21% P = 0.25), and febrile neutropenia (5% vs. 16% P = 0.50) during PCR vs. normal diet. In conclusion, plasma SN-38 exposure increased dramatically after PCR, whereas toxicity did not change. PCR did not alter the irinotecan and SN-38 exposure in healthy liver and liver metastases. PCR might therefore potentially improve the therapeutic window in patients treated with irinotecan.

To evaluate whether the concentration of serum lactate during the diagnosis of postpartum hemorrhage (bleeding ≥500mL during labor or ≥1000mL during cesarean delivery) predicts severe hemorrhage (SPPH; blood loss ≥1500mL at end of labor or in the following 24h).

A prospective cohort pilot study was conducted of women with a vaginal or cesarean delivery from February 2018 to March 2019 who presented with bleeding ≥500mL measured by the gravimetric method in a reference hospital in San Luis Potosi, Mexico. Venous blood samples were taken for analysis of serum lactate. A receiver operating characteristic curve determined the serum lactate threshold value for SPPH and χ

test assessed the difference in serum lactate elevation between SPPH and non-SPPH groups. Lastly, the prognostic capacity between the thresholds was compared.

SPPH developed in 43.33% of the 30 women in the study group. The best prognostic threshold was 2.68mmol/L of serum lactate (odds ratio [OR] 17.88, 95% confidence interval [CI] 2.7-16.8, P<0.001); sensitivity was 0.85 (95% CI 0.55-0.98); specificity was 0.76 (95% CI 0.50-0.93).

Serum lactate may be a useful prognostic marker for SPPH, more studies are needed to validate these findings.

Serum lactate may be a useful prognostic marker for SPPH, more studies are needed to validate these findings.The plant hormone jasmonic acid (JA) is involved in the cold stress response, and the inducer of CBF expression 1 (ICE1)- C-repeat binding factor (CBF) regulatory cascade plays a key role in the regulation of cold stress tolerance. In this study, we showed that a novel B-box (BBX) protein MdBBX37 positively regulates JA-mediated cold-stress resistance in apple. We found that MdBBX37 bound to the MdCBF1 and MdCBF4 promoters to activate their transcription, and also interacted with MdICE1 to enhance the transcriptional activity of MdICE1 on MdCBF1, thus promoting its cold tolerance. Two JA signaling repressors, MdJAZ1 and MdJAZ2 (JAZ, JAZMONATE ZIM-DOMAIN), interacted with MdBBX37 to repress the transcriptional activity of MdBBX37 on MdCBF1 and MdCBF4, and also interfered with the interaction between MdBBX37 and MdICE1, thus negatively regulating JA-mediated cold tolerance. E3 ligase MdMIEL1 (MIEL1, MYB30-Interacting E3 Ligase1) reduced MdBBX37-improved cold resistance by mediating ubiquitination and degradation of the MdBBX37 protein. The data reveal that MIEL1 and JAZ proteins co-regulate JA-mediated cold stress tolerance through the BBX37-ICE1-CBF module in apple. These results will aid further examination of the post-translational modification of BBX proteins and the regulatory mechanism of JA-mediated cold stress tolerance.