Analysis of clinical features of 231 cases with pernicious placenta previa: A retrospective cohort study.

ABSTRACT: Pernicious placenta previa (PEPP) is a severe complication of late pregnancy, which might result in adverse maternal-fetal outcome. To explore the application value of placenta accreta score (PAS) for PEPP and its association with maternal-fetal outcome.In this retrospective cohort study, the clinical data of PEPP patients were analyzed. According to the ultrasonic PAS, patients were grouped into 3 groups: scores ≤5, a scores between 6 and 9, and scores ≥10. The clinical data, intraoperative and postoperative outcomes were collected. Receiver operating characteristic (ROC) curves were used to evaluate the performance of PAS in disease severity evaluation. Multivariate logistic and linear regression analysis were performed to assess associations of PAS with intraoperative and postoperative outcomes.A total of 231 patients were enrolled. There were significant differences in intraoperative, postoperative and neonatal outcomes, such as operation time, bladder repair, ICU admission, postoperative hospitalization days, operation complications, Apgar score of newborns in 1 minute and premature delivery among the 3 groups (all P < .05), while the worst outcomes were found in those with a score ≥ 10 (all P < .05). According to ROC curves, scores <5.5, between 5.5 and 7.5, and >7.5 indicated placenta accreta, placenta increta and placenta percreta, respectively. PAS was independently associated with longer time of operation, surgical complications, intraoperative bleeding volume, and postoperative hospitalization days (all P < .05).Placenta accreta score might help with PEPP subtype diagnosis and predict the maternal-fetal outcome of PEPP patients.

mAChRs activation induces epithelial-mesenchymal transition on lung epithelial cells.

BACKGROUND: Epithelial-mesenchymal transition (EMT) has been proposed as a mechanism in the progression of airway diseases and cancer. Here, we explored the role of acetylcholine (ACh) and the pathway involved in the process of EMT, as well as the effects of mAChRs antagonist. METHODS: Human lung epithelial cells were stimulated with carbachol, an analogue of ACh, and epithelial and mesenchymal marker proteins were evaluated using western blot and immunofluorescence analyses. RESULTS: Decreased E-cadherin expression and increased vimentin and α-SMA expression induced by TGF-ß1 in alveolar epithelial cell (A549) were significantly abrogated by the non-selective mAChR antagonist atropine and enhanced by the acetylcholinesterase inhibitor physostigmine. An EMT event also occurred in response to physostigmine alone. Furthermore, ChAT express and ACh release by A549 cells were enhanced by TGF-ß1. Interestingly, ACh analogue carbachol also induced EMT in A549 cells as well as in bronchial epithelial cells (16HBE) in a time- and concentration-dependent manner, the induction of carbachol was abrogated by selective antagonist of M1 (pirenzepine) and M3 (4-DAMP) mAChRs, but not by M2 (methoctramine) antagonist. Moreover, carbachol induced TGF-ß1 production from A549 cells concomitantly with the EMT process. Carbachol-induced EMT occurred through phosphorylation of Smad2/3 and ERK, which was inhibited by pirenzepine and 4-DAMP. CONCLUSIONS: Our findings for the first time indicated that mAChR activation, perhaps via M1 and M3 mAChR, induced lung epithelial cells to undergo EMT and provided insights into novel therapeutic strategies for airway diseases in which lung remodeling occurs.

A novel mutant allele specific amplification and electrochemiluminescence method for the detection of point mutation in clinical samples.

A novel mutant allele specific amplification (MASA) and electrochemiluminescence (ECL) method for point mutation detection is proposed. Briefly, the target gene was amplified by a biotinylated mutant specific sense primer and a Ru(bpy)(3)(2+) (TBR)-labeled universal antisense primer. Only the mutant allele can be selectively amplified by the mutant specific primer pair. Then, the MASA product was captured onto the streptavidinylated magnetic beads through biotin-streptavidin linkage and detected by measuring the ECL emission of TBR. The method was applied to detect a possible point mutation at codon 12 of K-ras oncogene in 30 colorectal cancer (CAC) clinical samples. The experimental results show that the method can detect K-ras mutant in a 5000-fold excess of wild-type allele. Furthermore, different kinds of mutations can be clearly discriminated. The point mutation was found in 15 (50%) out of 30 CAC samples. This novel MASA-ECL method could potentially become a sensitive, specific, simple, rapid and safe approach for point mutation detection.