Association between Placental Thickness and Intraoperative Hemorrhage in Patients with Suspected Placenta Accreta Spectrum and Placenta Previa: A Retrospective Cohort Study

Background: Placenta accreta spectrum (PAS) can easily lead to life-threatening hemorrhage. However, the association between placental thickness (PT) and massive bleeding remains unclear. Thus, this study investigated the association between PT and massive bleeding to determine which patients with suspected PAS and placenta previa were more likely to experience intraoperative hemorrhage. Methods: This retrospective cohort study was conducted between January 2018 and December 2020 at a general tertiary care hospital in Chongqing, China. Covariates included demographic, clinical, and ultrasonographic characteristics. Logistic regression analysis was used to explore the association between PT and massive bleeding. A sensitivity analysis was conducted by detecting trends in the association between PT quartile and massive bleeding risk. Results: PT was associated with a risk of massive intraoperative bleeding. The sensitivity analysis yielded a similar result using the minimally adjusted model (p for trend = 0.001), and minimal changes were observed using the crude and fully adjusted models (p for trend = 0.001 and 0.037, respectively). The risk of major bleeding was significantly higher in the fourth quartile (Q4) versus first quartile (Q1) group (odds ratio = 2.26, p = 0.034). A linear relationship was observed between PT and the risk of massive bleeding. Conclusions: PT was independently and linearly associated with the risk of massive bleeding. The risk of intraoperative hemorrhage was significantly higher in the higher PT (Q4) than lower PT (Q1) group. Clinical Trial Registration: The study was registered at Chinese Clinical Trial Registry (https://www.chictr.org.cn), registration number: ChiCTR2100044798

Higher Soil Aggregate Stability in Subtropical Coniferous Plantations Than Natural Forests Due to Microbial and Aggregate Factors

Forest restoration and soil structure stabilization are the focus of forestry and ecology. However, the combined mechanisms of soil microorganisms and organic and inorganic aggregate binding agents on soil aggregation is unclear. In order to explore the effects of subtropical forest restoration types on soil aggregates and the underlying mechanisms, we collected soil samples from subtropical natural forests and coniferous and broad-leaved plantations that are commonly used for forest restoration. The mean weight diameter (MWD) of the soil aggregate was used to indicate the aggregates’ stability. The soil microbial diversity and structure, the organic and inorganic aggregate binding agents including the mycorrhizal density, the glomalin-related soil protein and the Fe and Al oxides were investigated. Results showed that the Shannon and Simpson indices of soil microbial communities in the coniferous plantations were both significantly higher than those in the natural forests. At the annual level, compared with the natural forests, the plantations decreased the proportion of 0.25–1 mm aggregates while the MWD significantly increased. The forest type also significantly affected the mycorrhizal density, the easily extractable glomalin-related soil proteins (EEG) and the Fe oxide. A variance decomposition analysis showed that soil microbial communities, organic and inorganic binding agents, and their interactions together contributed to the aggregates’ composition and stability by 75.07%. The MWD was positively correlated with the microbial diversity, mycorrhizal density and Fe oxide. We therefore suggest that the combined effects of the soil microbial communities and the organic (mycorrhizal density) and inorganic binding agents (Fe oxide) can be the main mechanisms of soil aggregation in the study area, resulting in a higher soil aggregate stability in the subtropical coniferous plantation than in the natural forest

High Frequency of AIFM1 Variants and Phenotype Progression of Auditory Neuropathy in a Chinese Population

To decipher the genotype-phenotype correlation of auditory neuropathy (AN) caused by AIFM1 variations, as well as the phenotype progression of these patients, exploring the potential molecular pathogenic mechanism of AN. A total of 36 families of individuals with AN (50 cases) with AIFM1 variations were recruited and identified by Sanger sequencing or next-generation sequencing; the participants included 30 patients from 16 reported families and 20 new cases. We found that AIFM1-positive cases accounted for 18.6% of late-onset AN cases. Of the 50 AN patients with AIFM1 variants, 45 were male and 5 were female. The hotspot variation of this gene was p.Leu344Phe, accounting for 36.1%. A total of 19 AIFM1 variants were reported in this study, including 7 novel ones. A follow-up study was performed on 30 previously reported AIFM1-positive subjects, 16 follow-up cases (53.3%) were included in this study, and follow-up periods were recorded from 1 to 23 years with average 9.75±9.89 years. There was no hearing threshold increase during the short-term follow-up period (1-10 years), but the low-frequency and high-frequency hearing thresholds showed a significant increase with the prolongation of follow-up time. The speech discrimination score progressed gradually and significantly along with the course of the disease and showed a more serious decline, which was disproportionately worse than the pure tone threshold. In addition to the X-linked recessive inheritance pattern, the X-linked dominant inheritance pattern is also observed in AIFM1-related AN and affects females. In conclusion, we confirmed that AIFM1 is the primary related gene among late-onset AN cases, and the most common recurrent variant is p.Leu344Phe. Except for the X-linked recessive inheritance pattern, the X-linked dominant inheritance pattern is another probability of AIFM1-related AN, with females affected. Phenotypical features of AIFM1-related AN suggested that auditory dyssynchrony progressively worsened over time

Fangchinoline Exerts Anticancer Effects on Colorectal Cancer by Inducing Autophagy via Regulation of the AMPK/mTOR/ULK1 Pathway

Autophagy has become a promising target for cancer therapy. Fangchinoline (Fan) has been shown to exert anticancer effects in some types of cancers. However, the anticancer effects on colorectal cancer (CRC) and the underlying mechanisms have never been elucidated. More specifically, regulation of autophagy in CRC by Fan has never been reported before. In the present study, Fan was found to induce apoptosis and autophagic flux in the CRC cell lines HT29 and HCT116, which was reflected by the enhanced levels of LC3-II protein and p62 degradation, and the increased formation of autophagosomes and puncta formation by LC3-II. Meanwhile, combination with the early-stage autophagy inhibitor 3-methyladenine (3-MA) but not the late-stage autophagy inhibitor chloroquine (CQ) further increased Fan-induced cell death, which suggested the cytoprotective function of autophagy induced by Fan in both HT29 and HCT116 cells. Moreover, Fan treatment demonstrated a dose- and time-dependent increase in the phosphorylation of AMPK and decrease in the phosphorylation of mammalian target of rapamycin (mTOR) and ULK1, leading to the activation of the AMPK/mTOR/ULK1 signaling pathway. Furthermore, in the HT29 xenograft model, Fan inhibited tumor growth in vivo. These results indicate that Fan inhibited CRC cell growth both in vitro and in vivo and revealed a new molecular mechanism involved in the anticancer effect of Fan on CRC, suggesting that Fan is a potent autophagy inducer and might be a promising anticancer agent