Human collagen sequence polypeptides mediated biomineralization and its molecular mechanism.

Biotechnology provides alternatives for regenerative medicine with more controllable functions. Herein, the polypeptides encoded with human collagen I amino-acid sequences were studied for the first time to modulate biomimetic hydroxyapatite (HAP). With a length of 50-100 nm and a width of 20-30 nm, the HAP crystal formed was plate-like. The interaction of the human collagen sequence polypeptide on the (001), (100), and (211) crystal faces of HAP crystal had been studied using Molecular Dynamics (MD) simulations, respectively. Based on MD simulations, van der Waals forces and hydrogen bonds are the main interactions between polypeptides and HAP through the -NH2, -CH2-, -OH, and -COOH, respectively. According to the calculated results, der Waals forces might be the main interaction. The human collagen sequence polypeptides exhibited the highest adsorption energy on the (001) plane of HAP, significantly higher than any of the adsorption energy on the (100) and (211) planes. Therefore, the growth of the (001) would be inhibited, which kept accurate with the result of images from the Transmission Electron Microscope (TEM). Study results provide a basis for rational designing of peptides with human collagen sequences to regenerate hard tissues.

Essential features of weak current for excellent enhancement of NOx reduction over monoatomic V-based catalyst.

Human society is facing increasingly serious problems of environmental pollution and energy shortage, and up to now, achieving high NH3-SCR activity at ultra-low temperatures (<150 °C) remains challenging for the V-based catalysts with V content below 2%. In this study, the monoatomic V-based catalyst under the weak current-assisted strategy can completely convert NOx into N2 at ultra-low temperature with V content of 1.36%, which shows the preeminent turnover frequencies (TOF145 °C = 1.97×10-3 s-1). The improvement of catalytic performance is mainly attributed to the enhancement catalysis of weak current (ECWC) rather than electric field, which significantly reduce the energy consumption of the catalytic system by more than 90%. The further mechanism research for the ECWC based on a series of weak current-assisted characterization means and DFT calculations confirms that migrated electrons mainly concentrate around the V single atoms and increase the proportion of antibonding orbitals, which make the V-O chemical bond weaker (electron scissors effect) and thus accelerate oxygen circulation. The novel current-assisted catalysis in the present work can potentially apply to other environmental and energy fields.

The phthalide compound tokinolide B from Angelica sinensis exerts anti-inflammatory effects through Nur77 binding.

BACKGROUND: Nur77, an orphan member of the nuclear receptor superfamily, regulates inflammatory diseases and is a therapeutic target for treating inflammation. Phthalides in Angelica sinensis exhibit anti-inflammatory activity. PURPOSE: This study aimed to screen compounds from A. sinensis phthalide extract that could exert anti-inflammatory activity by targeting Nur77. To provide new theoretical support for better elucidation of Chinese medicine targeting mitochondria to achieve multiple clinical efficacies. METHODS: The anti-inflammatory capacity of phthalides was assessed in tumor necrosis factor-alpha (TNF-α)-stimulated HepG2 cells using western blotting. The interaction between phthalides and Nur77 was verified by molecular docking, surface plasmon resonance, and cellular thermal shift assay. Co-immunoprecipitation, western blotting, and immunostaining were performed to determine the molecular mechanisms. The in vivo anti-inflammatory activity of the phthalides was evaluated in a lipopolysaccharide (LPS)/d-galactosamine (d-GalN)-induced acute hepatitis and liver injury mouse model of acute hepatitis and liver injury. Finally, the toxicity of phthalide toxicity was assessed in zebrafish experiments. RESULTS: Among the 27 phthalide compounds isolated from A. sinensis, tokinolide B (TB) showed the best Nur77 binding capacity and, the best anti-inflammatory activity, which was induced without apoptosis. In vivo and in vitro experiments showed that TB promoted Nur77 translocation from the nucleus to the mitochondria and interacted with tumor necrosis factor receptor-associated factor 2 (TRAF2) and sequestosome 1 (p62) to induce mitophagy for anti-inflammatory functions. TB substantially inhibited LPS/d-GalN-induced acute hepatitis and liver injury in mice. TB also exhibited significantly lower toxicity than celastrol in zebrafish experiments. CONCLUSION: These findings suggested that TB inhibits inflammation by promoting Nur77 interaction with TRAF2 and p62, thereby inducing mitophagy. These findings offer promising directions for developing novel anti-inflammatory agents, enhance the understanding of phthalide compounds, and highlight the therapeutic potential of traditional Chinese herbs.

Bone controls browning of white adipose tissue and protects from diet-induced obesity through Schnurri-3-regulated SLIT2 secretion.

The skeleton has been suggested to function as an endocrine organ controlling whole organism energy balance, however the mediators of this effect and their molecular links remain unclear. Here, utilizing Schnurri-3-/- (Shn3-/-) mice with augmented osteoblast activity, we show Shn3-/-mice display resistance against diet-induced obesity and enhanced white adipose tissue (WAT) browning. Conditional deletion of Shn3 in osteoblasts but not adipocytes recapitulates lean phenotype of Shn3-/-mice, indicating this phenotype is driven by skeleton. We further demonstrate osteoblasts lacking Shn3 can secrete cytokines to promote WAT browning. Among them, we identify a C-terminal fragment of SLIT2 (SLIT2-C), primarily secreted by osteoblasts, as a Shn3-regulated osteokine that mediates WAT browning. Lastly, AAV-mediated Shn3 silencing phenocopies the lean phenotype and augmented glucose metabolism. Altogether, our findings establish a novel bone-fat signaling axis via SHN3 regulated SLIT2-C production in osteoblasts, offering a potential therapeutic target to address both osteoporosis and metabolic syndrome.

Dual-/multi-organelle-targeted AIE probes associated with oxidative stress for biomedical applications.

In situ monitoring of biological processes between different organelles upon oxidative stress is one of the most important research hotspots. Fluorescence imaging is especially suitable for biomedical applications due to its distinct advantages of high spatiotemporal resolution, high sensitivity, non-invasiveness, and in situ monitoring capabilities. However, most fluorescent probes can only achieve light-up imaging of single organelles, thus the combined use of two or more probes is usually required for monitoring biological processes between organelles, which can suffer from tedious staining and washing procedures, increased cytotoxicity and poor photostability. Exogenetic oxidants can affect broad-spectrum subcellular organelles, which are not conducive to in situ monitoring of biological processes between specific organelles. To tackle these challenges, a series of dual-/multi-organelle-targeted aggregation-induced emission (AIE) probes associated with oxidative stress have been designed and developed in the past few years. Herein, the recent progress of these AIE probes is summarized in biomedical applications, such as apoptosis monitoring, interplay between organelles, microenvironmental changes of organelles, organelle morphology tracking, precise cancer therapy, and so forth. Moreover, the further outlook for dual-/multi-organelle-targeted AIE probes is discussed, aiming to promote innovative research in biomedical applications.

Penfluridol regulates p62 / Keap1 / Nrf2 signaling pathway to induce ferroptosis in osteosarcoma cells.

The cure rate for patients with osteosarcoma (OS) has stagnated over the past few decades. Penfluridol, a first-generation antipsychotic, has demonstrated to prevent lung and esophageal malignancies from proliferation and metastasis. However, the effect of penfluridol on OS and its underlying molecular mechanism remains unclear. This study revealed that penfluridol effectively inhibited cell proliferation and migration, and induced G2/M phase arrest in OS cells. In addition, penfluridol treatment was found to increased reactive oxygen species (ROS) levels in OS cells. Combined with the RNA-Seq results, the anti-OS effect of penfluridol was hypothesized to be attributed to the induction of ferroptosis. Western blot results showed that penfluridol promoted intracellular Fe2+ concentration, membrane lipid peroxidation, and decreased intracellular GSH level to induce ferroptosis. Further studies showed that p62/Keap1/Nrf2 signaling pathway was implicated in penfluridol-induced ferroptosis in OS cells. Overexpression of p62 effectively reversed penfluridol-induced ferroptosis. In vivo, penfluridol effectively inhibited proliferation and prolonged survival in xenograft tumor model. Therefore, penfluridol is a promising drug targeting OS in the future.

PPAR-γ/NF-kB/AQP3 axis in M2 macrophage orchestrates lung adenocarcinoma progression by upregulating IL-6.

Aquaporin 3 (AQP3), which is mostly expressed in pulmonary epithelial cells, was linked to lung adenocarcinoma (LUAD). However, the underlying functions and mechanisms of AQP3 in the tumor microenvironment (TME) of LUAD have not been elucidated. Single-cell RNA sequencing (scRNA-seq) was used to study the composition, lineage, and functional states of TME-infiltrating immune cells and discover AQP3-expressing subpopulations in five LUAD patients. Then the identifications of its function on TME were examined in vitro and in vivo. AQP3 was associated with TNM stages and lymph node metastasis of LUAD patients. We classified inter- and intra-tumor diversity of LUAD into twelve subpopulations using scRNA-seq analyses. The analysis showed AQP3 was mainly enriched in subpopulations of M2 macrophages. Importantly, mechanistic investigations indicated that AQP3 promoted M2 macrophage polarization by the PPAR-γ/NF-κB axis, which affected tumor growth and migration via modulating IL-6 production. Mixed subcutaneous transplanted tumor mice and Aqp3 knockout mice models were further utilized, and revealed that AQP3 played a critical role in mediating M2 macrophage polarization, modulating glucose metabolism in tumors, and regulating both upstream and downstream pathways. Overall, our study demonstrated that AQP3 could regulate the proliferation, migration, and glycometabolism of tumor cells by modulating M2 macrophages polarization through the PPAR-γ/NF-κB axis and IL-6/IL-6R signaling pathway, providing new insight into the early detection and potential therapeutic target of LUAD.

Effect of TiO2 and CaO Addition on the Crystallization and Flexural Strength of Novel Leucite Glass-Ceramics.

The aim of this study was to investigate the effects of TiO2/CaO addition on the crystallization and flexural strength of leucite glass-ceramics (GC). Synthesis of translucent and high strength GCs is important for the development of aesthetic and durable dental restorations. To achieve this, experimental aluminosilicate glasses (1-3 mol% TiO2 and CaO (B1, B2, B3)) were melted in a furnace to produce glasses. Glasses were ball milled, screened and heat treated via crystallization heat treatments, and characterized using XRD, differential scanning calorimetry, dilatometry, SEM and biaxial flexural strength (BFS). Increasing nucleation hold time (1-3 h) led to a reduction in crystallite number for B2 and B3 GC, and significant differences in leucite crystal size at differing nucleation holds within and across test groups (p < 0.05). A high area fraction of leucite crystals (55.1-60.8%) was found in the GC, with no matrix microcracking. Changes in the crystal morphology were found with higher TiO2/CaO addition. Mean BFS of the GC were 211.2-234.8 MPa, with significantly higher Weibull modulus (m = 18.9) for B3 GC. Novel glass compositions enriched with TiO2/CaO led to crystallization of leucite GC of high aspect ratio, with high BFS and reliability. The study's findings suggest a potential high performance translucent leucite GC for use in the construction of dental restorations.

Prenatal exposure to PM2.5 and childhood body mass index growth trajectories from birth to 6 years old.

This study aimed to determine the relationships between prenatal PM2.5 exposure and childhood growth trajectories during the first 6 years of life. A total of 47,625 pairs of mothers and children were recruited from a prospective birth cohort conducted between 2011 and 2013 in Wuhan, China, and followed for 6 years. We used the group-based trajectory models to classify the population into three trajectory groups: slow growth (n = 13,671, 28.7%), normal growth (n = 29,736, 62.4%), and rapid growth (n = 4218, 8.9%). Multinomial logistic regression models were used to determine the associations of prenatal PM2.5 exposure and childhood growth trajectories. Compared to normal growth trajectory, increased PM2.5 exposure in trimester 1, trimester 2 and the entire pregnancy showed significant associations with an increased risk of the slow growth trajectory but reduced the risk for the rapid growth trajectory, significant association of prenatal PM2.5 exposure with rapid growth trajectory was only observed in the trimester 3. Stratified analyses displayed relatively stronger associations among those mothers with maternal age over 35 years, pre-pregnancy BMI ≥ 25 kg/m2, and previous delivery experience. Prenatal exposure to PM2.5, particularly during the midpoint period of pregnancy, was more likely to have a slow growth trajectory and a lower risk of rapid growth trajectory. Maternal age, pre-pregnancy BMI, and previous delivery experience might modify these associations.

Hydrous Molybdenum Oxide Coating of Zinc Metal Anode via the Facile Electrodeposition Strategy and Its Performance Improvement Mechanisms for Aqueous Zinc-Ion Batteries.

Aqueous zinc-ion batteries (ZIBs) are widely recognized as highly promising energy storage devices because of their inherent characteristics, including superior safety, affordability, eco-friendliness, and various other benefits. However, the significant corrosion of the zinc metal anode, side reactions occurring between the anode and electrolyte, and the formation of zinc dendrites significantly hinder the practical utilization of ZIBs. Herein, we utilized an electrodeposition method to apply a unique hydrous molybdenum oxide (HMoOx) layer onto the surface of the zinc metal anode, aiming to mitigate its corrosion and side reactions during the process of zinc deposition and stripping. In addition, the HMoOx layer not only improved the hydrophilicity of the zinc anode, but also adjusted the migration of Zn2+, thus facilitating the uniform deposition of Zn2+ to reduce dendrite formation. A symmetrical cell with the HMoOx-Zn anode displayed reduced-voltage hysteresis (80 mV at 2.5 mA/cm2) and outstanding cycle stability after 3000 cycles, surpassing the performance of the uncoated Zn anode. Moreover, the HMoOx-Zn anode coupled with a γ-MnO2 cathode created a considerably more stable rechargeable full battery compared to the bare Zn anode. The HMoOx-Zn||γ-MnO2 full cell also displayed excellent cycling stability with a charge/discharge-specific capacity of 129/133 mAh g-1 after 300 cycles. In summary, this research offers a straightforward and advantageous approach that can significantly contribute to the future advancements in rechargeable ZIBs.

Intensified bioleaching of a spent Co-Mo catalyst through the addition of extracellular polymeric substances (EPSs) and its mechanism exploration.

The extraction and recovery of valuable metals from various spent catalysts via bioleaching represents a green, low-carbon and eco-friendly process. However, the pulp density of spent catalysts is usually 1.0% or lower owing to their toxicity, denoting low process capacity and poor practical potential. In this study, an intensified bioleaching strategy was used for the first time to promote the release efficiencies of both Co and Mo from a spent Co-Mo catalyst at a high pulp density of 10% by supplementing extracellular polymeric substances (EPSs). The results showed that the addition of 0.6 g L-1 EPSs harvested a maximum release of 73.6% for Co and 72.5% for Mo after 9 days of contact, with an evident elevation of 22.6% for Co and 24.4% for Mo, in contrast to no addition, respectively. The added EPS not only promoted the growth of plankton cells to produce more active molecules but also boosted the adhesion of leaching cells to the spent catalyst to form stable aggregates. Moreover, the resulting aggregates allowed for the gathering and confinement of the active small molecules, including Fe3+ and Fe2+, inside the micro-areas between the spent catalysts and the cells for quick electronic transfer as an interface oxidation/reduction reaction to free both Co and Mo from the spent catalyst.

Precision detection of hepatocellular carcinoma-associated telomerase RNA with SA@Comb-HCR nanosystem.

Accurate intracellular visualization of human telomerase RNA (hTR) is imperative for early diagnosis and treatment monitoring of hepatocellular carcinoma (HCC). While isothermal amplification-based DNA cascade strategies are promising, challenges persist in achieving great intake efficiency of detection probes within tumor cells and enhancing intracellular reaction efficiency. This study introduces a SA@Comb-HCR nanosystem, a highly effective approach for in situ hTR detection in HCC cells. Sodium alginate-coated liposomes ensures efficient nanoprobe delivery, which are then combined with proximity effect-inspired signal amplification. The coating of sodium alginate facilitates receptor-mediated endocytosis, prevents serum protein adhesion, and mitigates cationic liposome cytotoxicity. The designed Comb-like consolidated hairpin probe enhances the concentration of the local reactant, resulting in cascade amplification upon hTR activation. This technique achieves precision detection of intracellularly overexpressed hTR in HCC cells with a remarkable detection limit of 0.7 pM. This approach holds great promise for advancing targeted and sensitive early clinical diagnosis of HCC.

Assembled collagen films modified using polyacrylic acid with improved mechanical properties via mineralization.

The imperative task of enforcing collagen materials holds paramount significance in the field of hard tissue repair. We hereby present mineralized collagen fiber films via mineralization with improved mechanical properties. Self-extracted collagen was assembled into an array with an aligned fibrous pattern and then modified with polyacrylic acid (PAA) followed by mineralization in cationic polyacrylamide (CPAM)-SBF. Biomineralization occurred at the inner and outer surface of the assembled collagen fiber films. A tensile strength of up to 40.38 ± 3.08 MPa of mineralized collagen was obtained, for the first time, which may be attributed to the synergistic effect of polyanion and polycation on the mineralization process of assembled intrafibrillar collagen fibers. It was argued that PAA may facilitate the intra-fiber interaction of collagen, which extends the elongation at break of collagen fibers. This study introduces a pioneering approach for the preparation of mineralized collagen materials with superior mechanical properties, which would be beneficial for hard tissue repair.

5 mC modification of steroid hormone biosynthesis-related genes orchestrates feminization of channel catfish induced by high-temperature.

To elucidate the mechanism behind channel catfish feminization induced by high temperature, gonad samples were collected from XY pseudo-females and wild-type females and subjected to high-throughput sequencing for Whole-Genome-Bisulfite-Seq (WGBS) and transcriptome sequencing (RNA-Seq). The analysis revealed 50 differentially methylated genes between wild-type females and XY pseudo-females, identified through the analysis of KEGG pathways and GO enrichment in the promoter of the genome and differentially methylated regions (DMRs). Among these genes, multiple differential methylation sites observed within the srd5a2 gene. Repeatability tests confirmed 7 differential methylation sites in the srd5a2 gene in XY pseudo-females compared to normal males, with 1 specific differential methylation site (16608174) distinguishing XY pseudo-females from normal females. Interestingly, the expression of these genes in the transcriptome showed no difference between wild-type females and XY pseudo-females. Our study concluded that methylation of the srd5a2 gene sequence leads to decreased expression, which inhibits testosterone synthesis while promoting the synthesis of 17ß-estradiol from testosterone. This underscores the significance of the srd5a2 gene in the sexual differentiation of channel catfish, as indicated by the ipu00140 KEGG pathway analysis.

Prognostic implications of STK11 with different mutation status and its relationship with tumor-infiltrating immune cells in non-small cell lung cancer.

Background: Mutations in STK11 (STK11Mut) gene may present a negative impact on survival in Non-small Cell Lung Cancer (NSCLC) patients, however, its relationship with immune related genes remains unclear. This study is to unveil whether overexpressed- and mutated-STK11 impact survival in NSCLC and to explore whether immune related genes (IRGs) are involved in STK11 mutations. Methods: 188 NSCLC patients with intact formalin-fixed paraffin-embedded (FFPE) tissue available for detecting STK11 protein expression were included in the analysis. After immunohistochemical detection of STK11 protein, patients were divided into high STK11 expression group (STK11High) and low STK11 expression group (STK11Low), and then Kaplan-Meier survival analysis and COX proportional hazards model were used to compare the overall survival (OS) and progression-free survival (PFS) of the two groups of patients. In addition, the mutation data from the TCGA database was used to categorize the NSCLC population, namely STK11 Mutated (STK11Mut) and wild-type (STK11Wt) subgroups. The difference in OS between STK11Mut and STK11Wt was compared. Finally, bioinformatics analysis was used to compare the differences in IRGs expression between STK11Mut and STK11Wt populations. Results: The median follow-up time was 51.0 months (range 3.0 - 120.0 months) for real-life cohort. At the end of follow-up, 64.36% (121/188) of patients experienced recurrence or metastasis. 64.89% (122/188) of patients ended up in cancer-related death. High expression of STK11 was a significant protective factor for NSCLC patients, both in terms of PFS [HR=0.42, 95% CI= (0.29-0.61), P<0.001] and OS [HR=0.36, 95% CI= (0.25, 0.53), P<0.001], which was consistent with the finding in TCGA cohorts [HR=0.76, 95%CI= (0.65, 0.88), P<0.001 HR=0.76, 95%CI= (0.65, 0.88), P<0.001]. In TCGA cohort, STK11 mutation was a significant risk factor for NSCLC in both lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD) histology in terms of OS [HR=6.81, 95%CI= (2.16, 21.53), P<0.001; HR=1.50, 95%CI= (1.00, 2.26), P=0.051, respectively]. Furthermore, 7 IRGs, namely CALCA, BMP6, S100P, THPO, CGA, PCSK1 and MUC5AC, were found significantly overexpressed in STK11-mutated NSCLC in both LUSC and LUAD histology. Conclusions: Low STK11 expression at protein level and presence of STK11 mutation were associated with poor prognosis in NSCLC, and mutated STK11 might probably alter the expression IRGs profiling.

MiR-106a-5p targets PFKFB3 and improves sepsis through regulating macrophage pyroptosis and inflammatory response.

The enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase isoform 3 (PFKFB3) is a critical regulator of glycolysis and plays a key role in modulating the inflammatory response, thereby contributing to the development of inflammatory diseases such as sepsis. Despite its importance, the development of strategies to target PFKFB3 in the context of sepsis remains challenging. In this study, we employed a miRNA-based approach to decrease PFKFB3 expression. Through multiple meta-analyses, we observed a downregulation of miR-106a-5p expression and an upregulation of PFKFB3 expression in clinical sepsis samples. These changes were also confirmed in blood monocytes from patients with early sepsis and from a mouse model of lipopolysaccharide (LPS)-induced sepsis. Overexpression of miR-106a-5p significantly decreased the LPS-induced increase in glycolytic capacity, inflammatory response, and pyroptosis in macrophages. Mechanistically, we identified PFKFB3 as a direct target protein of miR-106a-5p and demonstrated its essential role in LPS-induced pyroptosis and inflammatory response in macrophages. Furthermore, treatment with agomir-miR-106a-5p conferred a protective effect in an LPS mouse model of sepsis, but this effect was attenuated in myeloid-specific Pfkfb3 KO mice. These findings indicate that miR-106a-5p inhibits macrophage pyroptosis and inflammatory response in sepsis by regulating PFKFB3-mediated glucose metabolism, representing a potential therapeutic option for the treatment of sepsis.

Intestinal Barrier Impairment Induced by Gut Microbiome and Its Metabolites in School-Age Children with Zinc Deficiency.

Zinc deficiency affects the physical and intellectual development of school-age children, while studies on the effects on intestinal microbes and metabolites in school-age children have not been reported. School-age children were enrolled to conduct anthropometric measurements and serum zinc and serum inflammatory factors detection, and children were divided into a zinc deficiency group (ZD) and control group (CK) based on the results of serum zinc. Stool samples were collected to conduct metagenome, metabolome, and diversity analysis, and species composition analysis, functional annotation, and correlation analysis were conducted to further explore the function and composition of the gut flora and metabolites of children with zinc deficiency. Beta-diversity analysis revealed a significantly different gut microbial community composition between ZD and CK groups. For instance, the relative abundances of Phocaeicola vulgatus, Alistipes putredinis, Bacteroides uniformis, Phocaeicola sp000434735, and Coprococcus eutactus were more enriched in the ZD group, while probiotic bacteria Bifidobacterium kashiwanohense showed the reverse trend. The functional profile of intestinal flora was also under the influence of zinc deficiency, as reflected by higher levels of various glycoside hydrolases in the ZD group. In addition, saccharin, the pro-inflammatory metabolites, and taurocholic acid, the potential factor inducing intestinal leakage, were higher in the ZD group. In conclusion, zinc deficiency may disturb the gut microbiome community and metabolic function profile of school-age children, potentially affecting human health.

A field study of a novel permeable-reactive-biobarrier to remediate chlorinated hydrocarbons contaminated groundwater.

Chlorinated hydrocarbons (CHs) pose significant health risks due to their suspected carcinogenicity, necessitating urgent remediation efforts. While the combination of zero-valent iron (Fe0) and microbial action shows promise in mitigating CH contamination, field studies on this approach are scarce. We devised a novel three-layer permeable reactive barrier (PRB) material incorporating Fe0 and coconut shell biochar, effectively implemented at a typical CH-contaminated site. Field monitoring data revealed conducive conditions for reductive dechlorination of CHs, characterized by low oxygen levels and a relatively neutral pH in the groundwater. The engineered PRB material consistently released organic carbon and iron, fostering the proliferation of CH-dechlorinating bacteria. Over a 250-day operational period, the pilot-scale PRB demonstrated remarkable efficacy in CH removal, achieving removal efficiencies ranging from 21.9% to 99.6% for various CH compounds. Initially, CHs were predominantly eliminated through adsorption and iron-mediated reductive dechlorination. However, microbial reductive dechlorination emerged as the predominant mechanism for sustained and long-term CHs removal. These findings underscore the economic viability and effectiveness of our approach in treating CH-contaminated groundwater, offering promising prospects for broader application in environmental remediation efforts.

Relationship between human epididymal protein 4 and depth of tumor invasion, postoperative recurrence, and metastasis of epithelial epithelial ovarian cancer.

This study aimed to analyze the relationship between human epididymal protein 4 (HE4) and infiltration depth, postoperative recurrence, and metastasis of epithelial ovarian cancer (OVCA). Immunohistochemistry was used to detect the expression level of HE4 in cancer tissues and adjacent tissues of 90 patients with epithelial OVCA admitted to our hospital from May 2017 to January 2018. Cox regression was used to analyze the factors affecting the prognosis of epithelial OVCA. The relationship between HE4 and the prognosis of epithelial OVCA was analyzed by the receiver operating characteristic curve and Kaplan-Meier survival curve. The positive expression rate of HE4 in epithelial OVCA was 85.56%, which was higher than 34.44% in adjacent tissues (p < 0.01). The International Federation of Gynecology and Obstetrics stage, infiltration depth, lymph node metastasis, postoperative recurrence and metastasis, and HE4 positivity were independent risk factors for the prognosis, and platinum-based chemotherapy sensitivity was an independent protective factor for the prognosis of patients with epithelial OVCA (p < 0.05). The area under the curve of HE4 in diagnosing epithelial OVCA and predicting recurrence was 0.863 and 0.700, the sensitivity was 91.60% and 85.60%, and the specificity was 90.20% and 65.60%. The median progression-free survival and overall survival were 26.1 and 30.2 months in HE4-positive epithelial OVCA patients, while these were 31.4 and 35.6 months in HE4-negative epithelial OVCA patients (p < 0.05). In conclusion, HE4 was highly expressed in epithelial OVCA tissues. Its expression level was related to the depth of tumor invasion, postoperative recurrence and metastasis, and other clinicopathological characteristics of patients with epithelial OVCA.