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Soils are heterogeneous and microbial spatial distribution can clearly indicate the spatial characteristics of the soil carbon and nitrogen cycle. However, it is not clear how long-term fertilization affects the spatial distribution of microbial biomass in fluvo-aquic soil. We collected fluvo-aquic soil samples (topsoil 0-7.5 cm and sub-topsoil 7.5-20 cm) using a spatially-explicit design within three 40.5 m2 plots in each of four fertilization treatments. Fertilization treatments were: cropping without fertilizer inputs (CK); chemical nitrogen, phosphorus, and potassium fertilizer (NPK); chemical fertilizer with straw return (NPKS); and chemical fertilizer with animal manure (NPKM). Variables included soil microbial biomass carbon (MBC) and nitrogen (MBN), and MBC/MBN. For both soil layers, we hypothesized that: microbial biomass was lowest in CK but with the largest spatial heterogeneity; and microbial biomass was highest in NPKM and NPKS but with the lowest spatial heterogeneity. Results showed that: (1) Fertilization significantly increased MBC and MBN more in topsoil than sub-topsoil but had no MBC/MBN changes. (2) The coefficient of variation (CV) and Cochran's C showed that variation was largest in CK in topsoil and NPK in sub-topsoil and that variation of topsoil was generally lower than in sub-topsoil. The sample size of the three variables was largest in CK in topsoil but had little variation among the other treatments. (3) The trend-surface model showed that within-plot heterogeneity varied substantially with fertilization (NPKM = NPK > NPKS > CK), but Moran's I and the interpolation map showed that spatial variability with fertilization followed the order NPK > NPKS > CK = NPKM at a fine scale in topsoil. In sub-topsoil, the trend-surface model showed that within-plot heterogeneity followed the order NPKM = CK > NPK > NPKS and that the fine-scale pattern was NPKM>NPK = NPKS>CK. MBC had the highest spatial heterogeneity among the three variables in both soil layers. Our results indicate that the application of organic fertilizer (straw or manure) reduced the variation of MBC and MBN but increased the spatial variability of MBC and MBN. The spatial variation of the three variables was MBC > MBN > MBC/MBN regardless of whether variation was considered at the plot-scale or the fine-scale in both layers.

Yes-associated protein (YAP) is a pivotal regulator in cellular proliferation, survival, differentiation, and migration, with significant roles in embryonic development, tissue repair, and tumorigenesis. At the maternal–fetal interface, emerging evidence underscores the importance of precisely regulated YAP activity in ensuring successful pregnancy initiation and progression. However, despite the established association between YAP dysregulation and adverse pregnancy outcomes, insights into the impact of aberrant YAP levels in fetal-derived, particularly trophoblast cells, and the ensuing dysfunction at the maternal–fetal interface remain limited. This review comprehensively examines YAP expression and its regulatory mechanisms in trophoblast cells throughout pregnancy. We emphasize its integral role in placental development and maternal–fetal interactions and delve into the correlations between YAP dysregulation and pregnancy complications. A nuanced understanding of YAP's functions during pregnancy could illuminate intricate molecular mechanisms and pave the way for innovative prevention and treatment strategies for pregnancy complications. 59X2rQyhJem7PrxahrMaVy Video Abstract

Background Resistance to androgen deprivation therapy remains a major challenge for the clinical treatment of patients with castration-resistant prostate cancer (CRPC). CYP1B1, a critical enzyme that catalyzes the conversion of estradiol to 4-Hydroxy-17β-estradiol (4-OHE2), has been reported to promote the development and progression of hormone-related cancer, but its role in CRPC is unclear. Methods To explore the underlying mechanism which CYP1B1 promotes the prostate cancer stem cells (PCSCs) characteristics, bioinformatics analyses of human clinical prostate cancer (PCa) datasets were performed. CYP1B1, IL6, and estrogen receptor-α (ERα) expression levels were evaluated in PCa and CRPC tissues via immunohistochemistry. The high-performance liquid chromatography-mass spectrometry assay was carried out to examine intracellular 4-OHE2 levels. Serum-free suspension culture and flow cytometry assays were performed to evaluate PCSCs. Chromatin immunoprecipitation was used to validate that 4-OHE2 recruited ERα to the IL6 promoter. Results CYP1B1 expression was significantly increased in CRPC tissues and androgen-independent PCa cell lines. CYP1B1 + PCa cells were significantly enriched in bicalutamide-treated LNCaP cells, and CYP1B1 knockdown reduced the cell viability under bicalutamide treatment. In addition, CYP1B1 knockdown decreased the intracellular 4-OHE2 concentration, accompanied by reduced PCSC characteristics. In PCa cells, 4-OHE2 stimulated ERα transcriptional activity and upregulated the expression of IL6 and downstream genes of the IL6-STAT3 signaling. 4-OHE2 increased cell viability under bicalutamide treatment and promoted PCSC characteristics, while IL6 neutralizing antibody reversed these effects. Mechanistically, siERα and the ER antagonist ICI182780 significantly attenuated 4-OHE2-induced IL6 expression, and 4-OHE2 promoted the binding of ERα to the estrogen response element of the IL6 promoter. Conclusions Our findings indicate that CYP1B1-catalyzed 4-OHE2 enhanced PCSC characteristics and attenuated bicalutamide sensitivity by ERα-mediated the IL6-STAT3 pathway activation. Our study further emphasizes the role of CYP1B1 in castration resistance and illustrates a novel mechanism of CRPC development. Graphical Abstract 54dyAth8NatsYXqV4_5FMe Video Abstract .

Telomere length (TL) shortening is a pivotal indicator of biological aging and is associated with many human diseases. The genetic determinates of human TL have been widely investigated, however, most existing studies were conducted based on adult tissues which are heavily influenced by lifetime exposure. Based on the analyses of terminal restriction fragment (TRF) length of telomere, individual genotypes, and gene expressions on 166 healthy placental tissues, we systematically interrogate TL-modulated genes and their potential functions. We discover that the TL in the placenta is comparatively longer than in other adult tissues, but exhibiting an intra-tissue homogeneity. Trans-ancestral TL genome-wide association studies (GWASs) on 644,553 individuals identify 20 newly discovered genetic associations and provide increased polygenic determination of human TL. Next, we integrate the powerful TL GWAS with placental expression quantitative trait locus (eQTL) mapping to prioritize 23 likely causal genes, among which 4 are functionally validated, including MMUT , RRM1 , KIAA1429 , and YWHAZ . Finally, modeling transcriptomic signatures and TRF-based TL improve the prediction performance of human TL. This study deepens our understanding of causal genes and transcriptomic determinants of human TL, promoting the mechanistic research on fine-grained TL regulation. Variation in human telomere length has been well studied, but most previous studies have used adult telomere length. Here, the authors explore the genetic basis of telomere length in the placenta and find suggestive causal genes modulating human telomere length.

Purpose The objectives of the study were (1) to quantify the long-term effects of nitrogen-phosphorus fertilizer (NP) and a combination of nitrogen-phosphorus with organic manure (NPM) on total soil organic carbon (SOC) and total soil inorganic carbon (SIC), (2) to identify the changes of SOC and SIC in soil particle-size fractions, and (3) to investigate the relationship between SOC and SIC. Materials and methods Two long-term field experiments (sites A and B) were performed in 1984 (site A) and 1979 (site B) in the North China Plain. The soil samples were collected in 2006 and separated for clay, silt and sand size particle fractions and then determined for SOC and SIC. Results and discussion The long-term fertilization significantly increased SOC in 0–20 cm soil layer by 9–68% but significantly decreased or had no effect on SIC. In total, soil carbon storage was little affected by NP, but significantly increased by NPM application ( p  < 0.05). Fertilization affected both SOC and SIC in sand- and silt-sized particles but not in clay-size fraction. Both NP and NPM increased SOC in sand- and silt-sized particles by 8.7–123.9% in the 0–20 cm layer but decreased SIC up to 80.4% in the 40–60 cm layer. The SOC concentration in the particle-size fractions was negatively correlated with SIC concentration, which may imply an antagonistic interaction between organic and inorganic carbon levels. Conclusions These results illustrate the importance of soil inorganic carbon pool in evaluating soil total carbon pool in semi-arid farmlands. Previous assessments of the effects of fertilizers on the soil carbon pool, using only SOC determinations, require re-evaluation with the inclusion of SIC determinations.

Soil salinization is a significant obstacle to agricultural development in arid and semiarid regions. While short-term experiments have demonstrated the effective improvement of saline soils through biochar amendment, the long-term efficacy in sustainably ameliorating such soils remains uncertain. Addressing this knowledge gap, this study investigated the long-term effects of biochar amendment in a field setting by applying different rates of biochar to a salt-affected soil and cultivating silage maize for three consecutive years. The comprehensive assessment includes not only maize growth but also changes in soil physical and chemical properties over the study period. The results reveal a notable elevation in maize above-ground dry matter, directly correlated to the enhanced uptake of nitrogen, phosphorous, and potassium. Additionally, biochar application improves saline soil physical properties, including reduced bulk density (1–23%), increased soil large pores (0.7–12%), and macroaggregates (24–141%), and chemical properties, including a decrease in exchangeable sodium percentage (35–48%), and an increase in soil total organic carbon (112–857%), total nitrogen (9–198%), available nitrogen (12–49%), phosphorus (141–538%) and potassium (57–895%). These improvements ultimately resulted in better maize growth. However, the amelioration effect of biochar on these soil properties gradually diminished over the three-year study. Consequently, this study suggests that biochar is a promising soil amendment that can enhance maize growth in saline soil for at least three years in a field experiment, providing valuable insights for sustainable agricultural practices in salt-affected regions.

Biochar was for the first time produced from Suaeda glauca. The immobilization of Pb and Cd by this biochar and pig manure biochar was examined in two types of soils by diethylene triamine pentaacetic acid (DTPA) extraction. Addition of biochars decreased DTPA extractable Pb and Cd in Fluvo-aquic soil with reduction rates being 11.3%–48.4% and 0.74%–64.9% compared with the control treatment. The pig manure biochar favored the immobilization of Pb and S. glauca biochar favored the immobilization of Cd. Biochars can effectively immobilize heavy metals in Fluvo-aquic soil. However, the addition of biochars increased extractable Pb and Cd in red soil, with pig manure biochars showing greater rates. This is ascribed to that the competition effects of ions released from biochar enhanced the moving of heavy metals from iron and manganese oxides bound form to organic matter bound form, and hence enhanced the mobility and bioavailability of heavy metals.

Background Preterm prelabor rupture of membranes (pPROM) is a leading cause of neonatal morbidity and mortality. While intra-amniotic infection is a well-established driver of pPROM, the role of sterile intra-amniotic inflammation remains unclear. Recent evidence suggests that interleukin-1 beta (IL-1β) promotes extracellular matrix (ECM) remodeling via downstream effectors, a disintegrin-like and metalloproteinase domain with thrombospondin type 1 motif 9 (ADAMTS9), while protein O-fucosyltransferase 2 (POFUT2) facilitates its O-fucosylation and secretion, amplifying ECM degradation. This study investigates how IL-1β-triggered nuclear factor kappa-B (NF-κB) activation promotes ADAMTS9 and POFUT2 expression, ultimately driving fetal membrane ECM remodeling and weakening in pPROM without signs of intra-amniotic infection. Methods A nested case-control study included maternal serum and fetal membrane samples from 60 pregnant women (34 pPROM, 26 full-term births [FTB]). ELISA measured serum levels of IL-1β and ADAMTS9, and their correlations were analyzed. Mechanistic studies utilized primary human amniotic epithelial cells (hAECs) and fetal membrane-decidua explants with IL-1β treatment. The role of NF-κB was explored using chromatin immunoprecipitation (ChIP) and luciferase assays to assess NF-κB binding to the promoters of ADAMTS9 and POFUT2. A murine model of sterile intra-amniotic inflammation under ultrasound-guided IL-1β injection was used to validate in vitro findings and assess pregnancy outcomes. Results Serum IL-1β and ADAMTS9 levels at 16 weeks of gestation were significantly higher in pPROM cases compared to FTB controls ( P  < 0.001). A combined model of these biomarkers demonstrated high predictive accuracy for pPROM (AUC = 0.83). Mechanistically, IL-1β activated NF-κB, leading to its binding to the promoters of ADAMTS9 and POFUT2. NF-κB activation promoted ADAMTS9 expression, while POFUT2 enhanced its secretion. Together, these processes drove versican degradation and ECM weakening. Intra-amniotic administration of IL-1β in mice induced fetal membrane weakening, preterm birth, and adverse neonatal outcomes, which were mitigated by the NF-κB inhibitor BAY 11-7082 treatment. Conclusion Maternal serum ADAMTS9 levels at mid-gestation are promising non-invasive biomarkers for pPROM risk stratification. Mechanistically, IL-1β-induced NF-κB activation promotes ADAMTS9 expression and POFUT2-dependent secretion, contributing to fetal membrane weakening. These findings provide new insights into the role and potential therapeutic target for sterile intra-amniotic inflammation in pPROM.

In recent years, continuous efforts have been made to understand the impact of biochar on arable soil fertility. Little is known about whether the biochar derived from municipal sewage sludge has positive impacts on urban soil. In this study, we pyrolyzed spray-dried municipal sewage sludge at 200 °C, 300 °C, 500 °C, and 700 °C for 2 h in a muffle furnace and then amended it into an urban soil to grow turf grass in pots. The outcomes demonstrated that biochar incorporation caused remarkable increases in soil organic C, black C, total N, available P, and K by 3–8, 7–25, 2–9, 10–19, and 1.4–2 times, respectively. The dry matter of turf grass increased by 43–147%, probably due to the nutritional improvement after biochar addition. The turf grass grown in biochar-added soil had 4–70% lower heavy metals than that in the control, although the soils had much higher total heavy metals, which might imply that biochar amendment reduced the bioavailability of heavy metals. Considering the cost of biochar production and its impacts on both urban soil and grass, it would be alternative to convert the spray-dried municipal sewage sludge into biochar at 200 °C for 2 h and then used as an urban soil amendment.

Background Prostate cancer (PCa) is the second leading cause of mortality and a leading cause of malignant tumors in males. Prostate cancer stem cells (PCSCs) are likely the responsible cell types for cancer initiation, clinical treatment failure, tumor relapse, and metastasis. Estrogen receptor alpha (ERα) is mainly expressed in the basal layer cells of the normal prostate gland and has key roles in coordinating stem cells to control prostate organ development. Here, we investigated the roles of the estrogen-ERα signaling pathway in regulating PCSCs. Methods Correlation of CD49f and ERα/NOTCH1 was analyzed in human clinical datasets and tissue samples. Flow cytometry was used to sort CD49f Hi and CD49f Low cells. EZH2 recruitment by ERα and facilitation of ERα binding to the NOTCH1 promoter was validated by Co-IP and ChIP. Primary tumor growth, tumor metastasis and sensitivity to 17β-estradiol (E2) inhibitor (tamoxifen) were evaluated in castrated mice. Results ERα expression was significantly higher in CD49f Hi prostate cancer basal stem-like cells (PCBSLCs), which showed basal and EMT features with susceptibility to E2 treatment. ERα-induced estrogen effects were suggested to drive the NOTCH1 signaling pathway activity via binding to the NOTCH1 promoter. Moreover, EZH2 was recruited by ERα and acted as a cofactor to assist ERα-induced estrogen effects in regulating NOTCH1 in PCa. In vivo, E2 promoted tumor formation and metastasis, which were inhibited by tamoxifen. Conclusions Our results implicated CD49f+/ERα + prostate cancer cells associated with basal stem-like and EMT features, named EMT-PCBSLCs, in heightened potential for promoting metastasis. NOTCH1 was regulated by E2 in CD49f Hi EMT-PCBSLCs. These results contribute to insights into the metastatic mechanisms of EMT-PCBSLCs in PCa.