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Soil contamination with heavy metals from industrial and mining activities poses significant environmental and public health risks, necessitating effective remediation strategies. This review examines the utilization of sulfate-reducing bacteria (SRB) for bioremediation of heavy metal-contaminated soils. Specifically, it focuses on SRB metabolic pathways for heavy metal immobilization, interactions with other microorganisms, and integration with complementary remediation techniques such as soil amendments and phytoremediation. We explore the mechanisms of SRB action, their synergistic relationships within soil ecosystems, and the effectiveness of combined remediation approaches. Our findings indicate that SRB can effectively immobilize heavy metals by converting sulfate to sulfide, forming stable metal sulfides, thereby reducing the bioavailability and toxicity of heavy metals. Nevertheless, challenges persist, including the need to optimize environmental conditions for SRB activity, address their sensitivity to acidic conditions and high heavy metal concentrations, and mitigate the risk of secondary pollution from excessive carbon sources. This study underscores the necessity for innovative and sustainable SRB-based bioremediation strategies that integrate multiple techniques to address the complex issue of heavy metal soil contamination. Such advancements are crucial for promoting green mining practices and environmental restoration. [ABSTRACT FROM AUTHOR]

O-Glycan synthesis enzyme glucosaminyl (N-acetyl) transferase 3 (GCNT3) is closely related to the occurrence and development of various cancers. However, the regulatory mechanism and function of GCNT3 in nasopharyngeal carcinoma (NPC) are still poorly understood. This study aims to explore the regulatory mechanism of EBV-encoded latent membrane protein 2A (LMP2A) on GCNT3 and the biological role of GCNT3 in NPC. The results show that LMP2A can activate GCNT3 through the mTORC1 pathway, and there is a positive feedback between the mTORC1 and GCNT3. GCNT3 regulates EMT progression by forming a complex with ZEB1 to promote cell migration. GCNT3 can also promote cell proliferation. These findings indicate that targeting the LMP2A-mTORC1-GCNT3 axis may represent a novel therapeutic target in NPC. [ABSTRACT FROM AUTHOR]

Exploring the allometric characteristics and driving mechanisms of economic development (ED) and carbon emissions (CE) is significant for promoting regional sustainable development. This study applied the panel grey relational model and the Driscoll–Kraay estimation method to investigate the internal mechanism of economic development and carbon emissions, to analyse their spatiotemporal correlation and allometric characteristics, and finally to characterize the impact mechanism of their allometric growth of the Yangtze River Delta urban agglomeration (YRDUA). The results show that (1) the spatiotemporal distribution patterns of economic development and carbon emissions are coincident and positively correlated, with the strength of the time-series correlation between them being less than the average value of 0.757 from 2016 onward. (2) The economic development-carbon emissions vertical allometric growth coefficient showed a trend of increasing and then decreasing and was always in a negative allometric growth state. The relative growth rate of carbon emissions was lower than that of economic development, and the per unit GDP carbon emissions decreased slightly. The horizontal allometric growth coefficient showed that more than 90% of the cities are in the negative allometric growth state, and that the negative allometric II and III levels are the main ones. (3) Per capita GDP, industrial structure, and energy structure are the boosting factors of the allometric growth coefficient, while population density and environmental regulation play a restraining role. Trade openness showed a restraining effect in 2010–2015 and turned into a promoting effect in 2016–2020. In both stages, the energy structure is one of the most crucial driving factors. The findings reported in this study can provide support for urban agglomerations to achieve low-carbon city development goals. [ABSTRACT FROM AUTHOR]

Exhausted CD8+ T lymphocytes and tumor-associated macrophages play critical roles in determining cancer prognosis and the efficacy of immunotherapy. Our study revealed a negative correlation between exhausted CD8+ T lymphocytes and prognosis in thyroid carcinoma (THCA). Consensus clustering divided patients into two subgroups of exhaustion with different prognoses, as defined by marker genes of exhausted CD8+ T cells. Subsequently, we constructed an eight-gene prognostic signature, and developed a risk score named the exhaustion-related gene score (ERGS) to forecast both prognosis and immunotherapy response in THCA. Bulk RNA sequencing analysis revealed a higher prevalence of M2 macrophages, indicative of an immunosuppressive tumor microenvironment (TME), in the high-ERGS group. Single-cell RNA sequencing showed that SPP1+ macrophages and CD14+ monocytes infiltrations were positively associated with higher ERGS. Functionally, it was determined that SPP1+ macrophages exert an immunosuppressive role, while CD14+ monocytes were implicated in promoting tumor progression and angiogenesis. Analysis of cell–cell interactions between SPP1+ macrophages and T cells highlighted the activation of the SPP1-CD44 and MIF-CD74 axes, both of which could foster an immunosuppressive TME. Therapeutic strategies that target SPP1+ macrophages, CD14+ monocytes, and the SPP1-CD44 and MIF-CD74 axes may potentially improve the prognosis and amplify the immunotherapy response in THCA patients. [ABSTRACT FROM AUTHOR]

Background: Familial hypercholesterolemia (FH) is an autosomal dominant disease of lipid metabolism mainly caused by mutations in the low-density lipoprotein receptor (LDLR) gene. Genetic detection of patients with FH help with precise diagnosis and treatment, thus reducing the risk of coronary heart disease (CHD) and other related diseases. The study aimed to identify the causative gene mutations in a Chinese FH family and reveal the pathogenicity and the mechanism of these mutations. Methods and results: Whole exome sequencing was performed in a patient with severe lipid metabolism dysfunction seeking fertility guidance from a Chinese FH family. Two LDLR variants c.1875 C > G (p.N625K; novel variant) and c.1448G > A (p.W483*) were identified in the family. Wildtype and mutant LDLR constructs were established by the site-direct mutagenesis technique. Functional studies were carried out by cell transfection to evaluate the impact of detected variants on LDLR activity. The two variants were proven to affect LDL uptake and binding, resulting in cholesterol clearance reduction to different degrees. According to The American College of Medical Genetics and Genomics (ACMG) Standards and Guidelines, the W483* variant was classified as "Pathogenic", while the N625K variant as "VUS". Conclusions: Our results provide novel experimental evidence of functional alteration by LDLR variants identified in our study and expand the mutational spectrum of LDLR mutation induced FH. [ABSTRACT FROM AUTHOR]

Existing studies on urbanization and carbon emissions are mostly based on a single pathway and lack the support of a theoretical framework. This study innovatively integrates Grossman's perspective of environmental effects analysis to develop a new framework to interpret the mechanism of multidimensional urbanization (MU) and carbon emissions (CEs). We first explored the spatial effects of MUs and CEs in the Yangtze River Delta urban agglomeration (YRDUA) and then introduced the "population-land-economic" urbanization variables into the S-STIRPAT model to determine the impact mechanisms of each factor on CEs under different urbanization dimensions. The results show that the spatiotemporal development patterns of MUs and CEs overlap to some extent. The Shanghai–Nanjing line is a high-value area of urbanization with different dimensions, as some edge cities are in low-value areas. However, there are local differences in the different dimensions of urbanization, e.g., population urbanization in the southern area is in a high-value area. CEs show a core-edge structure of "high in the center and low in the north and south". All factors, except for population urbanization, affect CEs locally, and their spillover effects are all positive, except for energy intensity, which has a negative influence on CEs in neighboring regions. Land urbanization has the largest positive impact on CEs, with a total effect coefficient of 0.409; economic urbanization has a coefficient of 0.195, and population urbanization has a coefficient of only 0.070. The findings can help to maximize urbanization growth while minimizing harmful environmental externalities. [ABSTRACT FROM AUTHOR]

Particulate matter (PM) induces and enhances oxidative stress and inflammation, leading to a variety of respiratory diseases, including acute lung injury. Exploring new treatments for PM-induced lung injury has long been of interest to researchers. Palmatine (PAL) is a natural extract derived from plants that has been reported in many studies to alleviate inflammatory diseases. Our study was designed to explore whether PAL can alleviate acute lung injury caused by PM. The acute lung injury model was established by instilling PM (4 mg/kg) into the airway of mice, and PAL (50 mg/kg and 100 m/kg) was administrated orally as the treatment groups. The effect and mechanism of PAL treatment were examined by immunofluorescence, immunohistochemistry, Western Blotting, ELISA, and other experiments. The results showed that oral administration of PAL (50 mg/kg and 100 m/kg) could significantly alleviate lung inflammation and acute lung injury caused by PM. In terms of mechanism, we found that PAL (50 mg/kg) exerts anti-inflammatory and anti-damage effects mainly by enhancing the activation of the Nrf2-related antioxidant pathway and inhibiting the activation of the NLRP3-related pyroptosis pathway in mice. These mechanisms have also been verified in our cell experiments. Further cell experiments showed that PAL may reduce intracellular reactive oxygen species (ROS) by activating Nrf2-related pathways, thereby inhibiting the activation of NLRP3-related pyroptosis pathway induced by PM in Beas-2B cell. Our study suggests that PAL can be a new option for PM-induced acute lung injury. [ABSTRACT FROM AUTHOR]