No abstract

Fetal heart sound is an important part of fetal monitoring and has attracted extensive research and attention from scholars at home and abroad in recent years. The fetal heart rate, extracted from the fetal heart sound signal, is one of the important indicators that reflect the health of the fetus in the womb. In this study, a maternal-fetal Holter monitor based on f ECG technology was used to collect maternal heart rate, fetal heart rate, and uterine contractions signals, isolate the fetal heart rate, and design an algorithm to extract the fetal heart rate baseline, acceleration, variation, wake-up cycle, and nonlinear parameters. Using statistical methods to analyze the average value and range of various characteristic parameters of fetal heart rate under continuous long-term monitoring, the results show that the baseline has a downward trend from 10 o’clock in the night to 4 o’clock in the morning and is the lowest around 2 o’clock in the morning. The area and acceleration time were significantly higher than those in the suspicious group. However, there was no significant difference in the number of acceleration values between the two groups; the proportion of small mutations in the normal group was lower than that of the suspicious group and the proportion of medium mutations was higher than that of the suspicious group. There is no statistically significant difference in maternal age, gestational age at childbirth, pregnancy comorbidities, and complication rates in the five-level interpretation system of ACOG (2009), RCOG (2007), SOGC (2007), and the United States (2007). The difference of pregnancy and parity in various images was statistically significant, P  < 0.05. The second type of fetal heart rate monitoring images appeared in the highest among the diagnostic standards, and the difference in the second type of fetal heart rate monitoring images between the various diagnostic standards was statistically significant, P  ≤ 0.001.

Malignant ascites in peritoneal metastases is a lipid-enriched microenvironment and is frequently involved in the poor prognosis of epithelial ovarian cancer (EOC). However, the detailed mechanisms underlying ovarian cancer (OvCa) cells dictating their lipid metabolic activities in promoting tumor progression remain elusive. Here, we report that two critical fatty acid desaturases, stearoyl-CoA desaturase-1 (SCD1) and acyl-CoA 6-desaturase (FADS2), are aberrantly upregulated, accelerating lipid metabolic activities and tumor aggressiveness of ascites-derived OvCa cells. Lipidomic analysis revealed that the elevation of unsaturated fatty acids (UFAs) is positively associated with SCD1/FADS2 levels and the oncogenic capacities of OvCa cells. In contrast, pharmaceutical inhibition and genetic ablation of SCD1/FADS2 retarded tumor growth, suppressed cancer stem cell (CSC) formation and reduced platinum resistance in OvCa cells. Mechanistically, inhibition of SCD1/FADS2 directly downregulated GPX4 and the GSH/GSSG ratio, causing disruption of the cellular redox balance and subsequent iron-mediated lipid peroxidation in ascites-derived OvCa cells. Hence, combinational treatment with SCD1/FADS2 inhibitors and cisplatin synergistically repressed tumor cell dissemination, providing a promising chemotherapeutic strategy against EOC platinum resistance and peritoneal metastases.

This randomized clinical trial evaluates urinary retention, uterine contraction pain, depressive symptoms, and lactation after acupoint hot compress treatment in women during their early postpartum period.

Background. Although the Bushen Huoxue (BSHX) recipe is commonly used for the effective treatment of the prethrombotic state of recurrent abortions, its mechanism of action is unclear. In this article, we investigated the therapeutic effects of BSHX on anti-cardiolipin antibody (ACA) positive recurrent miscarriage mice and the molecular mechanism involved in the treatment of the prethrombotic state of ACA-positive recurrent miscarriages based on the PI3K-Akt signaling pathway, to provide a scientific basis for clinical practice. Methods. An ACA-positive recurrent miscarriage mouse model and normal pregnancy mouse model were adopted in this experiment. Seventy CBA/J female mice were induced to establish the ACA-positive recurrent model; the mice were mated with DBA/2 male mice. Of these mice, 50 became pregnant, which were randomly divided into a BSHX high-dose group (BH, 2.52 g/kg), BSHX medium-dose group (BM, 1.26 g/kg), BSHX low-dose group (BL, 0.63 g/kg), model group (M, distilled water), and an aspirin enteric-coated tablet group; each group had 10 mice. In addition, 16 CBA/J female mice were induced to establish the normal pregnant mouse model; the mice were mated with BALB/C male mice. Of these mice, 10 became pregnant, which were used as the blank control group (C) and received distilled water by gavage. Stillbirth and abortion rates were recorded for each group, and the uterine tissue, urine, and serum were collected. The serum expression levels of ACA, interleukin-6 (IL-6), progesterone ,estradiol, and endometrial histological changes were compared between the groups. Metabolomics was performed on the urine and uterine tissues of both groups using UHPLC-QTOF/MS, and the expression levels of PI3K, p-PI3K, AKT, and p-AKT proteins in the uterine tissues were detected using Western blot. Results. Compared with the model pregnancy group, the BSHX high-dose group, BSHX medium-dose group, and BSHX low-dose group all had a lower absorption rate of mouse embryos, improved uterine histopathological morphology, significantly reduced serum levels of ACA and IL-6, increased serum levels of progesterone and estradiol, and significantly upregulated uterine levels of p-AKT, PI3K, and p-PI3K proteins. The metabolomic results showed that the metabolic levels in the urine and uterine tissues were significantly altered in the mouse model of ACA-positive recurrent abortion. The results also suggested that the pathogenesis of ACA-positive recurrent abortion may be associated with metabolic pathways, such as pentose, glucuronide, lysine degradation, and steroid hormone biosynthesis. Conclusion. The BSHX recipe improved the uterine histopathological morphology of pregnant mice and promoted vascular formation in uterine tissues. The mechanisms involved the reduction in serum ACA and IL-6 levels, the increment in serumprogesterone and estradiol levels, the upregulation of the levels of p-AKT, PI3K, and p-PI3K proteins, and the activation of the PI3K-Akt signaling pathway. These data will be useful for effective drug research and development.