Objective Compare changes in pelvic organ prolapse (POP) from 36-38 weeks of gestation to 1 year postpartum after unlaboured cesarean delivery(UCD)and trial of labour (TOL).Design Prospective observational cohort study.Setting Wenzhou Third People's Hospital, Wenzhou, Zhejiang, China.Population Nulliparous women undergoing UCD or TOL.Methods Pelvic organ prolapse was assessed at 36-38 weeks of gestation, then at 6 weeks, 6 months and 1 year postpartum, using the Pelvic Organ Prolapse Quantification (POPQ) system.Main outcome measures Postpartum POP status in UCD and TOL determined by POPQ measurements over time.Results Points Aa (Ba) determined the final stage assignment in most cases. Stage II POP was present in 35% and 37% of women in UCD and TOL at 36-38 weeks of gestation. After delivery, the likelihood of stage II POP declined during the first year postpartum in the whole cohort. The TOL group was much less likely to recover from stage II POP compared with the UCD group (odds ratio 0.04, 95% confidence interval 0.01-0.18) after adjustment for POP status at 36-38 weeks of gestation, age, firsttrimester body mass index, newborn birthweight, educational level, gravidity and smoking status. With the exception of age, education and gravidity, these covariates were also independent predictors of postpartum POP.Conclusion Factors unique to labour and delivery lead to sustained pelvic floor relaxation postpartum. Pelvic organ prolapse at 36-38 weeks of gestation, and higher first-trimester body mass index also appear to predict long-term POP. Further investigation into mechanisms leading to persistent or progressive POP after TOL are warranted. In addition, caution is needed in generalising the findings due to the single-centre design.Keywords Caesarean delivery, pelvic organ prolapse, pelvic organ prolapse quantification, pelvic organ support, postpartum, trial of labour.
The toxicity of exposure to polycyclic aromatic hydrocarbons (PAHs) or phytoestrogen is relatively well characterized. However, the toxicity of combined exposure to PAHs and phytoestrogen is not well investigated. In the present study, benzo(a)pyrene (B(a)P) and benzo(k)fluorathene (B(k)F), genistein, along with 17β-estradiol (E2), were investigated for their single and combined developmental toxicity using zebrafish embryos as model system. We demonstrated that two representative PAHs, both B(a)P (≥1 μM) and B(k)F (≥10 μM), can cause significant malformation and mortality in developing zebrafish embryos. The toxicity effect of B(a)P was in general higher than that of B(k)F. Developmental exposure to high level of genistein (>20 μM) or E2 (>10 μM), also caused significant malformation and mortality in zebrafish larvae at 120 hours post fertilization (hpf). However, different toxic effects were observed for the combined exposure to PAHs and phytoestrogen in zebrafish. Lower doses of genistein (1 and 10 μM) and E2 (0.1 and 1 μM), when used in combination with high concentration of B(a)P (1 μM) or B(k)F (20 μM), can significantly suppress the toxicity effect of B(a)P and B(k)F in developing zebrafish embryos. The beneficial effect of genistein may be due to the inhibition of cytochrome P450 enzymes via directly interacting with aryl-hydrocarbon receptor (AhR) pathway, or disturbing the AhR pathway through interacting with estrogen receptor pathway.
In this study, we developed a serum and urine metabolomic method based on gas chromatography-mass spectrometry (GC-MS) combination with biomedical results to evaluate the effect of vitamin E treatment on methomyl poisoning rats. The rats were divided into three groups: the control group, methomyl poisoning group, and vitamin E treatment group. Partial least squares discriminate analysis (PLS-DA) showed that methomyl poisoning induced metabolic perturbations. Compared to the control group, based on the urinary metabolomics data, the level of ribitol, l-proline, xylitol, hydrocinnamic acid, 11-cis-octadecenoic acid, octadecanoic acid, and hexadecanoic acid of methomyl poisoning group increased, while the level of 2,3,4-trihydroxybutyric acid, ethanimidic acid, pantothenic acid, and retinoic acid decreased. Vitamin E pretreatment effectively normalized the levels of metabolites in rat urine in vitamin E treatment group. There was no significant difference in rat plasma metabolomic data after acute methomyl poisoning. The results indicate that metabolomic method based on GC-MS may be useful to elucidate the vitamin E treatment for methomyl poisoning.
In embryonal rhabdomyosarcoma (ERMS) and generally in sarcomas, the role of wild-type and loss or gain of function TP53 mutations remains largely undefined. Eliminating mutant or restoring wild-type p53 is challenging; nevertheless, understanding TP53 effects on tumorigenesis remains central to realizing better treatment outcomes. In ERMS, >70% of patients retain wild-type TP53, yet TP53 mutations when present in tumors are associated with poor prognosis. Employing a kRASG12D-driven ERMS tumor model and newly generated tp53 null (tp53-/-) zebrafish, we define both wild-type and patient-specific TP53 mutant effects on tumorigenesis. We demonstrate that tp53 is a major suppressor of tumor initiation, where tp53 loss expands tumors initiation from <35% to >97% of animals. Next, characterizing three patient-specific mutants finds that TP53C176F partially retains wild-type p53 apoptotic activity that can be exploited, while the TP53P153Δ and TP53Y220C mutants define two structural mutations that predispose to head musculature ERMS.
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