MOF-Decorated Poly(tetrafluoroethylene) Membranes with Underwater Superoleophobicity for Extracting Osmotic Energy from Oily Wastewater Effluents.

Industrial processes generate huge volumes of oily saline wastewater. Instead of being sent to the drainage system immediately, extracting osmotic energy from these effluents represents a promising means to reuse these wastes and contributes to mitigate the ever-growing energy crisis. Herein, an MOF-decorated PTFE membrane is engineered to extract osmotic energy from oily wastewaters. Copper hydroxide nanowires (CHNs) are intertwined with polystyrenesulfonate sodium (PSS), deposited onto a poly(tetrafluoroethylene) (PTFE) membrane, and thereafter used as metal precursors to in situ generate HKUST-1 doped with negative charges. The resulting HKUST-1PSS@PTFE hybrid membrane possesses abundant angstrom-scale channels capable of transporting cations efficiently and features a hierarchically structured surface with underwater superoleophobicity. The energy conversion performance of the HKUST-1PSS3.5@PTFE membrane can reach an output power density of 6.21 W m-2 at a 50-fold NaCl gradient, which is superior to those of pristine PTFE membranes. Once exposed to oily saline wastewater, the HKUST-1PSS@PTFE membrane can exhibit an excellent oil-repellent ability, thus contributing to sustain its osmotic energy harvesting. This work may promote the development of antifouling osmotic energy harvesters with a long working life and pave the way to fully exploit oily wastewater effluents as valuable energy sources.

Structural Basis of Bifunctional CTP/dCTP Synthase.

The final step in the de novo synthesis of cytidine 5'-triphosphate (CTP) is catalyzed by CTP synthase (CTPS), which can form cytoophidia in all three domains of life. Recently, we have discovered that CTPS binds to ribonucleotides (NTPs) to form filaments, and have successfully resolved the structures of Drosophila melanogaster CTPS bound with NTPs. Previous biochemical studies have shown that CTPS can bind to deoxyribonucleotides (dNTPs) to produce 2'-deoxycytidine-5'-triphosphate (dCTP). However, the structural basis of CTPS binding to dNTPs is still unclear. In this study, we find that Drosophila CTPS can also form filaments with dNTPs. Using cryo-electron microscopy, we are able to resolve the structure of Drosophila melanogaster CTPS bound to dNTPs with a resolution of up to 2.7 Å. By combining these structural findings with biochemical analysis, we compare the binding and reaction characteristics of NTPs and dNTPs with CTPS. Our results indicate that the same enzyme can act bifunctionally as CTP/dCTP synthase in vitro, and provide a structural basis for these activities.

Effect of berberine combined with metformin on autophagy in polycystic ovary syndrome by regulating AMPK/AKT/mTOR pathway.

The pathologic mechanism of polycystic ovary syndrome (PCOS) is related to increased autophagy of granulosa cells. Both berberine and metformin have been shown to improve PCOS, but whether the combination of berberine and metformin can better improve PCOS by inhibiting autophagy remains unclear. PCOS models were constructed by injecting dehydroepiandrosterone into rats, and berberine, metformin or berberine combined with metformin was administered to rats after modeling. Rats' body weight and ovarian weight were measured before and after modeling. Histopathological examination of ovarian tissue and estrous cycle analysis of rats were performed. Insulin resistance, hormone levels, oxidative stress, and lipid metabolism in PCOS rats were assessed. Expression of the AMPK/AKT/mTOR pathway and autophagy-related proteins was analyzed by Western blot assays. Granulosa cells were isolated from rat ovarian tissue and identified by immunofluorescence staining followed by transmission electron microscopy analysis. Berberine combined with metformin reduced the body weight and ovarian weight of PCOS rats, increased the number of primordial and primary follicles, decreased the number of secondary and atretic follicles, normalized the estrous cycle, and improved insulin resistance, androgen biosynthesis, oxidative stress and lipid metabolism disorders, and increased estrogen production. In addition, berberine combined with metformin reduced the number of autophagosomes in granulosa cells, which may be related to AMPK/AKT/mTOR pathway activation, decreased Beclin1 and LC3II/LC3I levels, and increased p62 expression. Berberine combined with metformin could inhibit autophagy by activating the AMPK/AKT/mTOR pathway in PCOS, indicating that berberine combined with metformin is a potential treatment strategy for PCOS.

Conjoint transcriptomics and metabolomics analyses provide insights into the toxicity of acetamiprid to Lethenteron reissneri larvae.

The neonicotinoid pesticide acetamiprid has been widely used in agricultural pest control and was frequently detected in the water environment. There have been some studies of the toxic effects of acetamiprid on fish, but studies on aquatic lower vertebrates are still very limited. As a primitive jawless vertebrate, Lethenteron reissneri has a special position in evolution and is now listed as a national second level protected animal in China. The present study aimed to investigate the toxic effect of acetamiprid on the liver of L. reissneri larvae. A conjoint analysis of the transcriptomics and metabolomics was performed to determine the responses of L. reissneri larvae liver to acetamiprid at different concentrations (L for low concentration 25 mg/L and H for high concentration 100 mg/L). Even low concentrations of acetamiprid can cause significant liver damage to L. reissneri larvae in a short period. In omics analyses, 2141 differentially expressed genes (DEGs) and 183 differentially abundant metabolites (DAMs) were identified in the H/Control group, and 229 DEGs and 144 DAMs were identified in the L/C group. Correlation analyses revealed acetamiprid affected the metabolic pathways of L. reissneri larvae liver such as the glycerophospholipid metabolism and arachidonic acid metabolism. This study not only enriches the basis for understanding the toxic effect of acetamiprid exposure to L. reissneri larvae liver and provides more information on the breeding and conservation of L. reissneri, but also further causes attention on toxicity risk from acetamiprid to aquatic lower vertebrate species.

Corrigendum: Glutamatergic and GABAergic neurons in the preoptic area of the hypothalamus play key roles in menopausal hot flashes.

[This corrects the article DOI: 10.3389/fnagi.2022.993955.].

Association between dipeptidyl peptidase-4 inhibitor use and diabetic retinopathy: a systematic review and meta-analysis of real-world studies.

BACKGROUND: The purpose of this review was to examine if dipeptidyl peptidase-4 inhibitor (DPP4i) use affects the risk of diabetic retinopathy (DR). METHODS: Cohort studies published up to 20th July 2023 in the databases of PubMed, CENTRAL, Embase, Scopus, and Web of Science were searched. The adjusted effect size was pooled to calculate the odds ratio (OR). RESULTS: Seven studies were included. Meta-analysis showed that the use of DPP4i was not associated with any significant change in the risk of DR (OR: 0.86 95% CI: 0.70, 1.06 I2 = 78%). The pooled analysis also found that DPP4i use was not associated with any significant risk of progression of DR (OR: 0.87 95% CI: 0.47, 1.59 I2 = 86%). The results did not change during sensitivity analysis. CONCLUSION: Present evidence from a limited number of real-world studies shows that DPP4i may not affect the incidence and progression of DR. There is a need for further studies from different countries using accurate definitions of DR and its progression to validate the current results.

Lamprey--an excellent model for iron metabolism.

After 500 million years of evolution, lamprey is in a natural environment characterized by low temperature and high iron content, and its unique adaptive evolution mode has developed its organizational structure and life mechanism in the process of metamorphosis, which provides a new direction for people to further study the origin and evolution of life. Iron is one of the essential nutrients for the human body and plays an important role in metabolic processes, but when exceeded, it can lead to iron toxicity. For example, the serum iron concentration of pre-metamorphosis larvae is 149 times that of normal males, and the iron content in the liver of juveniles is about 2-3 times that of normal humans. Lamprey has a complete biochemical system to tolerate high concentrations of free iron in the body, and high expression of important genes for iron homeostasis, such as transferrin, ferritin heavy chain, superoxide dismutase, etc., improves iron transport, iron storage and antioxidant capacity. Lamprey has an IRE/IRP regulatory system, which is an important protection mechanism for lamprey to adapt to the high iron content environment in the organization. In addition, lampreys gradually form oral glands during metamorphosis and development, which become the unique iron metabolism organs of lampreys. In this review, we mainly summarize the distribution of iron in various tissues of lamprey and the potential mechanism of adapting to the content of iron in the body, so as to provide a theoretical basis for the subsequent search for the molecular mechanism of iron metabolism.

Lamprey VDAC2: Suppressing hydrogen peroxide-induced 293T cell apoptosis by downregulating BAK expression.

The voltage-dependent anion channel 2 (VDAC2) is the abundant protein in the outer mitochondrial membrane. Opening VDAC2 pores leads to the induction of mitochondrial energy and material transport, facilitating interaction with various mitochondrial proteins implicated in essential processes such as cell apoptosis and proliferation. To investigate the VDAC2 in lower vertebrates, we identified Lr-VDAC2, a homologue of VDAC2 found in lamprey (Lethenteron reissneri), sharing a sequence identity of greater than 50 % with its counterparts. Phylogenetic analysis revealed that the position of Lr-VDAC2 aligns with the lamprey phylogeny, indicating its evolutionary relationship within the species. The Lr-VDAC2 protein was primarily located in the mitochondria of lamprey cells. The expression of the Lr-VDAC2 protein was elevated in high energy-demanding tissues, such as the gills, muscles, and myocardial tissue in normal lampreys. Lr-VDAC2 suppressed H2O2 (hydrogen peroxide)-induced 293 T cell apoptosis by reducing the expression levels of Caspase 3, Caspase 9, and Cyt C (cytochrome c). Further research into the mechanism indicated that the Lr-VDAC2 protein inhibited the pro-apoptotic activity of BAK (Bcl-2 antagonist/killer) protein by downregulating its expression at the protein translational level, thus exerting an anti-apoptotic function similar to the role of VDAC2 in humans.

Oxidative stress plays an important role in the central regulatory mechanism of orofacial hyperalgesia under low estrogen conditions.

Hyperalgesia occurs in the orofacial region of rats when estrogen levels are low, although the specific mechanism needs to be investigated further. Furthermore, oxidative stress plays an important role in the transmission of pain signals. This study aimed to explore the role of oxidative stress in orofacial hyperalgesia under low estrogen conditions. We firstly found an imbalance between oxidative and antioxidant capacity within the spinal trigeminal subnucleus caudalis (SP5C) of rats after ovariectomy (OVX), resulting in oxidative stress and then a decrease in the orofacial pain threshold. To investigate the mechanism by which oxidative stress occurs, we used virus as a tool to silence or overexpress the excitatory amino acid transporter 3 (EAAT3) gene. Further investigation revealed that the regulation of glutathione (GSH) and reactive oxygen species (ROS) can be achieved by regulating EAAT3, which in turn impacts the occurrence of oxidative stress. In summary, our findings suggest that reduced expression of EAAT3 within the SP5C of rats in the low estrogen state may decrease GSH content and increase ROS levels, resulting in oxidative stress and ultimately lead to orofacial hyperalgesia. This suggests that antioxidants could be a potential therapeutic direction for orofacial hyperalgesia under low estrogen conditions, though more research is needed to understand its mechanism.

PANoptosis and Autophagy-Related Molecular Signature and Immune Landscape in Ulcerative Colitis: Integrated Analysis and Experimental Validation.

Background: Ulcerative colitis (UC) is an autoimmune inflammatory disorder of the gastrointestinal tract. Programmed cell death (PCD), including PANoptosis and autophagy, plays roles in inflammation and immunity. This study aimed to investigate the molecular signature and immune landscape of the PANoptosis- and autophagy-related differentially expressed genes (DEGs) in UC. Methods: Analyzing UC dataset GSE206285 yielded DEGs. Differentially expressed PANoptosis- and autophagy-related genes were identified using DEGs and relevant gene collections. Functional and pathway enrichment analyses were conducted. A protein-protein interaction (PPI) network was established to identify hub genes. TRRUST database predicted transcription factors (TFs), pivotal miRNAs, and drugs interacting with hub genes. Immune infiltration analysis, UC-associated single-cell sequencing data analysis, and construction of a competing endogenous RNA (ceRNA) network for hub genes were conducted. Machine learning identified key candidate genes, evaluated for diagnostic value via receiver operating characteristic (ROC) curves. A UC mice model verified expression of key candidate genes. Results: Identifying ten PANoptosis-related hub DEGs and four autophagy-related hub DEGs associated them with cell chemotaxis, wound healing and positive MAPK cascade regulation. Immune infiltration analysis revealed increased immunocyte infiltration in UC patients, with hub genes closely linked to various immune cell infiltrations. Machine learning identified five key candidate genes, TIMP1, TIMP2, TIMP3, IL6, and CCL2, with strong diagnostic performance. At the single-cell level, these genes exhibited high expression in inflammatory fibroblasts (IAFs). They showed significant expression differences in the colon mucosa of both UC patients and UC mice model. Conclusion: This study identified and validated novel molecular signatures associated with PANoptosis and autophagy in UC, potentially influencing immune dysregulation and wound healing, thus opening avenues for future research and therapeutic interventions.

Centrosymmetry-Breaking Morphotropic Phase Boundary: A Pathway to Highly Sensitive and Strong Pressure-Responsive Nonlinear Optical Switches.

The quest for high-performance piezoelectric materials has been synonymous with the pursuit of the morphotropic phase boundary (MPB), yet the full potential of MPBs remains largely untapped outside of the realm of ferroelectrics. In this study, we reveal a new class of MPB by creating continuous molecular-based solid solutions between centro- and noncentrosymmetric compounds, exemplified by (tert-butylammonium)1-x(tert-amylammonium)xFeCl4 (0 ≤ x ≤ 1), where the MPB is formed due to disorder of molecular cations. Near the MPB, we discovered an exceptionally sensitive nonlinear optical material in the centrosymmetric phase, capable of activation at pressures as low as 0.12-0.27 GPa, and producing tunable second-harmonic generation (SHG) signals from zero to 18.8 times that of KH2PO4 (KDP). Meanwhile, synchrotron diffraction experiments have unveiled a third competing phase (P212121) appearing at low pressure, forming a triple-phase point near the MPB, thereby providing insight into the mechanism underpinning the nonlinear optical (NLO) switch behavior. These findings highlight the opportunity to harness exceptional physical properties in symmetry-breaking solid solution systems by strategically designing novel MPBs.

CPEB1 induces autophagy and promotes apoptosis in ovarian granulosa cells of polycystic ovary syndrome.

Inflammatory damage in ovarian granulosa cells (GCs) is a key mechanism in polycystic ovary syndrome (PCOS), cytoplasmic polyadenylation element binding protein-1 (CPEB1) is important in inflammatory regulation, however, its role in PCOS is unclear. We aim to research the mechanism of CPEB1 in ovarian GCs in PCOS using dehydroepiandrosterone (DHEA)-induced PCOS rat models and testosterone-incubated GC models. The pathophysiology in PCOS rats was analyzed. Quantitative-realtime-PCR, TUNEL, immunohistochemistry, and Western blot were applied for quantification. Additionally, cell counting kit-8, flow cytometry, immunofluorescence, Western blot, and Monodansylcadaverine staining were performed. We found that PCOS rat models exhibited a disrupted estrus cycle, elevated serum levels of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH), increased LH/FSH ratio, and heightened ovarian index. Furthermore, reduced corpus luteum and increased follicular cysts were observed in ovarian tissue. In ovarian tissue, autophagy and apoptosis were activated and CPEB1 was overexpressed. In vitro, CPEB1 overexpression inhibited cell viability and sirtuin-1 (SIRT1), activated tumor necrosis factor-α, and interleukin-6 levels, as well as apoptosis and autophagy; however, CPEB1 knockdown had the opposite effect. In conclusion, overexpression of CPEB1 activated autophagy and apoptosis of ovarian GCs in PCOS.

Tailoring competitive adsorption sites of hydroxide ion to enhance urea oxidation-assisted hydrogen production.

Alloys with bimetallic electron modulation effect are promising catalysts for the electrooxidation of urea. However, the side reaction oxygen evolution reaction (OER) originating from the competitive adsorption of OH- and urea severely limited the urea oxidation reaction (UOR) activity on the alloy catalysts. This work successfully constructs the defect-rich NiCo alloy with lattice strain (PMo-NiCo/NF) by rapid pyrolysis and co-doping. By taking advantage of the compressive strain, the d-band center of NiCo is shifted downward, inhibiting OH- from adsorbing on the NiCo site and avoiding the detrimental OER. Meanwhile, the oxygenophilic P/Mo tailored specific adsorption sites to adsorb OH- preferentially, which further released the NiCo sites to ensure the enriched adsorption of urea, thus improving the UOR efficiency. As a result, PMo-NiCo/NF only requires 1.27 V and -57 mV to drive a current density of ±10 mA cm-2 for UOR and hydrogen evolution reaction (HER), respectively. With the guidance of this work, reactant competing adsorption sites could be tailored for effective electrocatalytic performance.

LncRNA SNHG12 promotes cell proliferation and inhibits apoptosis of granulosa cells in polycystic ovarian syndrome by sponging miR-129 and miR-125b.

BACKGROUND: Polycystic ovarian syndrome (PCOS) is the most common endocrine disease in women of childbearing age which is often associated with abnormal proliferation or apoptosis of granulosa cells (GCs). Studies proved that long non-coding RNA SNHG12 (lncRNA SNHG12) is significantly increased in ovarian cancer and cervical cancer patients and cells. The inhibition of lncRNA SNHG12 restrains the proliferation, migration, and invasion in tumor cells. OBJECTIVE: This study explores the role of lncRNA SNHG12 in the apoptosis of GCs in PCOS and the underlying regulated mechanism. METHODS: In this study, the injection of dehydroepiandrosterone (DHEA) successfully induced the PCOS model in SD rats. The human granulosa-like tumor cell line KGN was incubated with insulin to assess the effects of lncRNA SNHG12 on GC proliferation and apoptosis. RESULTS: Overexpression of lncRNA SNHG12 influenced the body weight, ovary weight, gonadal hormone, and pathological changes, restrained the expressions of microRNA (miR)-129 and miR-125b, while downregulation of lncRNA SNHG12 exerted the opposite effects in PCOS rats. After silencing lncRNA SNHG12 in cells, the cell viability and proliferation were lessened whereas apoptosis of cells was increased. A loss-of-functions test was implemented by co-transfecting miR-129 and miR-125b inhibitors into lncRNA SNHG12-knocking down cells to analyze the effects on cell viability and apoptosis. Next, the existence of binding sites of SNHG12 and miR-129/miR-125b was proved based on the pull-down assay. CONCLUSION: lncRNA SNHG12 might be a potential regulatory factor for the development of PCOS by sponging miR-129 and miR-125b in GCs.

Agglomeration inhibition engineering of nickel-cobalt alloys by a sacrificial template for efficient urea electrolysis.

Designing efficient non-precious metal-based catalysts for urea oxidation reaction (UOR) is essential for achieving energy-saving hydrogen production and the treatment of wastewater containing ammonia. In this study, sodium dodecyl sulfate (SDS) is employed as a sacrificial template to synthesize NiCo alloy nanowires (NiCo(SDS)/CC), and the instinct formation mechanism is investigated. It is found that SDS can inhibit the Ostwald ripening during hydrothermal and calcination processes, which could release abundant active cobalt, thereby modulating the electronic structure to promote the catalytic reaction. Moreover, SDS as a sacrificial template can induce the deposition of metal atoms and increase the specific surface area of the catalyst, providing abundant active sites to accelerate the reaction kinetics. As expected, the NiCo(SDS)/CC exhibits good activity for both UOR and hydrogen evolution reactions (HER) and it requires only 1.31 V and -86 mV to obtain a current density of ±10 mA cm-2, respectively. This work provides a new strategy for reducing the agglomeration of transition metals to design high-performance composite catalysts for urea oxidation.

Gut microbiota and its metabolic products in acute respiratory distress syndrome.

The prevalence rate of acute respiratory distress syndrome (ARDS) is estimated at approximately 10% in critically ill patients worldwide, with the mortality rate ranging from 17% to 39%. Currently, ARDS mortality is usually higher in patients with COVID-19, giving another challenge for ARDS treatment. However, the treatment efficacy for ARDS is far from satisfactory. The relationship between the gut microbiota and ARDS has been substantiated by relevant scientific studies. ARDS not only changes the distribution of gut microbiota, but also influences intestinal mucosal barrier through the alteration of gut microbiota. The modulation of gut microbiota can impact the onset and progression of ARDS by triggering dysfunctions in inflammatory response and immune cells, oxidative stress, cell apoptosis, autophagy, pyroptosis, and ferroptosis mechanisms. Meanwhile, ARDS may also influence the distribution of metabolic products of gut microbiota. In this review, we focus on the impact of ARDS on gut microbiota and how the alteration of gut microbiota further influences the immune function, cellular functions and related signaling pathways during ARDS. The roles of gut microbiota-derived metabolites in the development and occurrence of ARDS are also discussed.

Superstructured Optoionic Heterojunctions for Promoting Ion Pumping Inspired by Photoreceptor Cells.

Photoreceptor cells of vertebrates feature ultrastructural membranes interspersed with abundant photosensitive ion pumps to boost signal generation and realize high gain in dim light. In light of this, superstructured optoionic heterojunctions (SSOHs) with cation-selective nanochannels are developed for manipulating photo-driven ion pumping. A template-directed bottom-up strategy is adopted to sequentially assemble graphene oxide (GO) and PEDOT:PSS into heterogeneous membranes with sculptured superstructures, which feature programmable variation in membrane topography and contain a donor-acceptor interface capable of maintaining electron-hole separation upon photoillumination. Such elaborate design endows SSOHs with a much higher magnitude of photo-driven ion flux against a concentration gradient in contrast to conventional optoionic membranes with planar configuration. This can be ascribed to the buildup of an enhanced transmembrane potential owing to the effective separation of photogenerated carriers at the heterojunction interface and the increase of energy input from photoillumination due to a synergistic effect of reflection reduction, broad-angle absorption, and wide-waveband absorption. This work unlocks the significance of membrane topographies in photo-driven transmembrane transportation and proposes such a universal prototype that could be extended to other optoionic membranes to develop high-performance artificial ion pumps for energy conversion and sensing.

OAS Deep Q-Learning-Based Fast and Smooth Control Method for Traffic Signal Transition in Urban Arterial Tidal Lanes.

To address traffic flow fluctuations caused by changes in traffic signal control schemes on tidal lanes and maintain smooth traffic operations, this paper proposes a method for controlling traffic signal transitions on tidal lanes. Firstly, the proposed method includes designing an intersection overlap phase scheme based on the traffic flow conflict matrix in the tidal lane scenario and a fast and smooth transition method for key intersections based on the flow ratio. The aim of the control is to equalize average queue lengths and minimize average vehicle delays for different flow directions at the intersection. This study also analyses various tidal lane scenarios based on the different opening states of the tidal lanes at related intersections. The transitions of phase offsets are emphasized after a comprehensive analysis of transition time and smoothing characteristics. In addition, this paper proposes a coordinated method for tidal lanes to optimize the phase offset at arterial intersections for smooth and rapid transitions. The method uses Deep Q-Learning, a reinforcement learning algorithm for optimal action selection (OSA), to develop an adaptive traffic signal transition control and enhance its efficiency. Finally, a simulation experiment using a traffic control interface is presented to validate the proposed approach. This study shows that this method leads to smoother and faster traffic signal transitions across different tidal lane scenarios compared to the conventional method. Implementing this solution can benefit intersection groups by reducing traffic delays, improving traffic efficiency, and decreasing air pollution caused by congestion.

YAP represses intestinal inflammation through epigenetic silencing of JMJD3.

BACKGROUND: Epigenetics plays an important role in the pathogenesis of inflammatory bowel disease (IBD). Some studies have reported that YAP is involved in inflammatory response and can regulate target genes through epigenetic modifications. JMJD3, a histone H3K27me3 demethylase, is associated with some inflammatory diseases. In this study, we investigated the role of YAP in the development of IBD and the underlying epigenetic mechanisms. RESULTS: YAP expression was significantly increased in both in vitro and in vivo colitis models as well as in patients with IBD. Epithelial-specific knockout of YAP aggravates disease progression in dextran sodium sulfate (DSS)-induced murine colitis. In the TNF-α-activated cellular inflammation model, YAP knockdown significantly increased JMJD3 expression. Coimmunoprecipitation experiments showed that YAP and EZH2 bind to each other, and chromatin immunoprecipitation-PCR (ChIP-PCR) assay indicated that silencing of YAP or EZH2 decreases H3K27me3 enrichment on the promoter of JMJD3. Finally, administration of the JMJD3 pharmacological inhibitor GSK-J4 alleviated the progression of DSS-induced murine colitis. CONCLUSION: Our findings elucidate an epigenetic mechanism by which YAP inhibits the inflammatory response in colitis through epigenetic silencing of JMJD3 by recruiting EZH2.

Prediction Model of Adverse Pregnancy Outcome in Pre-Eclampsia Based on Logistic Regression and Random Forest Algorithm.

Aim: To construct a prediction model for adverse pregnancy outcomes of preeclampsia (PE). Thus assisting clinicians to identify high-risk patients. Provide guidance for treatment intervention. Methods: A retrospective study was conducted on 319 PE patients admitted to the Huzhou Maternal and Child Health Hospital from April 2021 to December 2022, The patients were divided into an adverse group (93 cases) and a non-adverse group (226 cases) based on whether they had adverse pregnancy outcomes after admission. Collect clinical data from patients, using a single factor analysis to screen statistically significant indicators as input variables, the outcome of the analysis is dependent on the incidence of PE adverse pregnancy outcomes. Divide patients into training and testing sets in a 7:3 ratio, Logistic regression model and random forest model were constructed respectively. Evaluate the predictive performance of two statistical models. Results: Among the 319 PE patients included 93 had adverse pregnancy outcomes after admission. Among them, Age (OR: 1.702, 95%CI: 1.069~2.710), small gestational age (OR: 0.757,95%CI: 0.607~0.945), more clinical symptoms (OR: 3.618, 95%CI: 1.682~7.783), high 24 h proteinuria (OR: 2.532, 95%CI: 1.290~4.968), low PLT index (OR: 0.616, 95%CI: 0.419~0.906), high AST index (OR: 1.554, 95%CI: 1.012~2.387), high D-Dimer index (OR:1.966, 95%CI: 1.183~3.267) were the influencing factors of adverse pregnancy outcomes in PE patients. The test set found that the random forest model was superior to the Logistic regression model in predicting the risk of adverse pregnancy outcomes in PE patients. Conclusions: The random forest model has good stability in predicting the risk of adverse pregnancy outcomes in PE, and its prediction efficiency is better than the Logistic regression model.