Mediation of mitochondrial DNA copy number and oxidative stress in fluoride-related bone mineral density alteration in Chinese farmers.

Excessive fluoride can adversely affect bone mineral density (BMD). Oxidative stress and mitochondrial dysfunction are crucial mechanisms of health damage induced by fluoride. Here, a cross-sectional survey involving 907 Chinese farmers (aged 18-60) was carried out in Tongxu County in 2017, aiming to investigate the significance of mitochondrial DNA copy number (mtDNAcn) and oxidative stress in fluoride-related BMD change. Concentrations of urinary fluoride (UF), serum oxidative stress biomarkers, including total antioxidant capacity (T-AOC), total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA), as well as relative mtDNAcn in peripheral blood were determined. The multivariable linear model and mediation analysis were performed to assess associations between UF, oxidative stress, and relative mtDNAcn with BMD. Results showed that GSH-Px levels increased by 6.98 U/mL [95% confidence interval (CI) 3.41-10.56)] with each 1.0 mg/L increment of UF. After stratification, the T-AOC, relative mtDNAcn, and BMD decreased by 0.04 mmol/L (-0.08 ~ -0.01), 0.29-unit (-0.55 ~ -0.04), and 0.18-unit (-0.33 ~ -0.03) with every 1.0 mg/L elevation of UF in the excessive fluoride group (EFG, adults with UF > 1.6 mg/L), respectively. Furthermore, T-AOC and relative mtDNAcn were favorably related to the BMD in the EFG (ß = 0.82, 95%CI 0.16-1.48 for T-AOC; ß = 0.11, 95%CI 0.02-0.19 for relative mtDNAcn). Mediation analysis showed that relative mtDNAcn and T-AOC mediated 15.4% and 17.1% of the connection between excessive fluoride and reduced BMD, respectively. Findings suggested that excessive fluoride was related to lower BMD in adults, and the decrement of T-AOC and relative mtDNAcn partially mediate this relationship.

Risk of heavy metal(loid) compositions in fine particulate matter on acute cardiovascular mortality: a poisson analysis in Anyang, China.

Fine particulate matter (PM2.5) is a risk factor of cardiovascular disease. Associations between PM2.5 compositions and cardiovascular disease are a point of special interest but inconsistent. This study aimed to explore the cardiovascular effects of heavy metal(loid) compositions in PM2.5. Data for mortality, air pollutants and meteorological factors in Anyang, China from 2017 to 2021 were collected. Heavy metal(loid) in PM2.5 were monitored and examined monthly. A Case-crossover design was applied to the estimated data set. The interquartile range increase in cadmium (Cd), antimony (Sb) and arsenic (As) at lag 1 was associated with increment of 8.1% (95% CI: 3.3, 13.2), 4.8% (95% CI: 0.2, 9.5) and 3.5% (95% CI: 1.1, 6.0) cardiovascular mortality. Selenium in lag 2 was inversely associated with cerebrovascular mortality (RR = 0.920 95% CI: 0.862, 0.983). Current-day exposure of aluminum was positively associated with mortality from ischemic heart disease (RR = 1.083 95% CI: 1.001, 1.172). Stratified analysis indicated sex, age and season modified the cardiovascular effects of As (P < 0.05). Our study reveals that heavy metal(loid) play key roles in adverse effects of PM2.5. Cd, Sb and As were significant risk factors of cardiovascular mortality. These findings have potential implications for accurate air pollutants control and management to improve public health benefits.

Reactivity of unactivated peroxymonosulfate and peroxyacetic acid with thioether micropollutants: Mechanisms and rate prediction.

Thioether compounds, prevalent in pharmaceuticals, are of growing environmental concern due to their prevalence and potential toxicity. Peroxy chemicals, including peroxymonosulfate (PMS) and peroxyacetic acid (PAA), hold promise for selectively attacking specific thioether moieties. Still, it has been unclear how chemical structures affect the interactions between thioethers and peroxy chemicals. This study addresses this knowledge gap by quantitatively assessing the relationship between the structure of thioethers and intrinsic reaction rates. First, the results highlighted the adverse impact of electron-withdrawing groups on reactivity. Theoretical calculations were employed to locate reactive sites and investigate structural characteristics, indicating a close relationship between thioether charge and reaction rate. Additionally, we established a SMILES-based model for rapidly predicting PMS reactivity with thioether compounds. With this model, we identified 147 thioether chemicals within the high production volume (HPV) and Food and Drug Administration (FDA) approved drug lists that PMS could effectively eliminate with the toxicity (-lg LC50) decreasing. These findings underscore the environmental significance of thioether compounds and the potential for their selective removal by peroxides.

Correlations between bone metabolism biomarkers and fluoride exposure in adults and children.

Increased exposure to fluoride, which notably affects bone metabolism, is a global concern. However, the correlations and sensitivity of bone metabolism to fluoride remain controversial. In this cross-sectional study, 549 children (aged 7-12 years) and 504 adults (≥ 18 years old) were recruited in the high-fluoride areas of the Henan Province. Urinary fluoride (UF) level was determined using a fluoride electrode. Fasting venous blood serum was collected to measure bone metabolism biomarkers. The selected bone metabolism biomarkers for children included bone alkaline phosphatase (BALP), serum alkaline phosphatase (ALP), osteocalcin (OCN), calcitonin (CT), parathyroid hormone (PTH), phosphorus (P5+), and calcium (Ca2+). For adults, the biomarkers included ALP, CT, PTH, ß-CrossLaps (ß-CTX), P5+, and Ca2+. The correlations between UF and bone metabolism biomarkers were analyzed using binary logistic regression, a trend test, a generalized additive model, and threshold effect analysis. Regression analysis indicated a significant correlation between serum OCN, PTH, and UF levels in children aged 7-9 years. Serum OCN, PTH, and BALP contents were significantly correlated with UF in boys (P < 0.05). Furthermore, the interaction between age and UF affected serum P5+ and PTH (P < 0.05). The generalized additive model revealed nonlinear dose-response relationships between P5+, BALP, and UF contents in children (P < 0.05). Serum OCN level was linearly correlated with the UF concentration (P < 0.05). Similarly, a significant correlation was observed between ß-CTX and UF levels in adults. In addition, significant correlations were observed between UF-age and serum Ca2+, ß-CTX, and PTH contents. There was a non-linear correlation between serum Ca2+, P5+, and ß- CTX and UF levels (P < 0.05). Overall, serum OCN, BALP, and P5+ levels can serve as sensitive bone metabolism biomarkers in children, while ß-CTX, P5+, and Ca2+ can be considered fluoride-sensitive bone metabolism biomarkers in adults.

Relationships between root exudation and root morphological and architectural traits vary with growing season.

Plants allocate a substantial amount of C belowground for root exudates and for the construction and adjustment of root morphological and architectural traits. What relationships exist between root exudates and other root traits and these relationships change with growing season, however, remain unclear. We quantified the root exudation rate and root morphological traits, including total root length (RL), total root surface area (RS), root diameter (RD), specific root length (SRL), specific root area (SRA) and root tissue density (RTD), and architectural traits, such as branching intensity (BI), and investigated their associations during the rapidly growing season (April and August) and the slowly growing season (December) of three common native tree species, Liquidambar formosana, Michelia maudiae and Schima superba, in subtropical China. We found that the linkages of RD, SRL, SRA, RTD and BI did not change with the growing season, reflecting their highly conservative relationships. The root exudation rate varied significantly with growing season (P < 0.05) and produced various associations with other root traits at different growing seasons. During the rapidly growing season (i.e., April), the exudation rate was the highest and was positively correlated with RL. The exudation rate was the lowest during the slowly growing season (i.e., December) and was negatively associated with RL, RS and RTD. Our findings demonstrate the seasonality of the linkages of root exudation rate with other root traits, which highlights the highly plastic and complex associations of belowground root traits. These findings help to deepen our understanding of plant nutrient acquisition strategies.

Proteomics Sequencing Reveals the Role of TGF-ß Signaling Pathway in the Peripheral Blood of Offspring Rats Exposed to Fluoride.

The underlying mechanism of fluorosis has not been fully elucidated. The purpose of this study was to explore the mechanism of fluorosis induced by sodium fluoride (NaF) using proteomics. Six offspring rats exposed to fluoride without dental fluorosis were defined as group A, 8 offspring rats without fluoride exposure were defined as control group B, and 6 offspring rats exposed to fluoride with dental fluorosis were defined as group C. Total proteins from the peripheral blood were extracted and then separated using liquid chromatography-tandem mass spectrometry. The identified criteria for differentially expressed proteins were fold change > 1.2 or < 0.83 and P < 0.05. Gene Ontology function annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed using the oeCloud tool. The 177 upregulated and 22 downregulated proteins were identified in the A + C vs. B group. KEGG pathway enrichment analysis revealed that transforming growth factor-ß (TGF-ß) signaling pathway significantly enriched. PPI network constructed using Cytoscape confirmed RhoA may play a crucial role. The KEGG results of genes associated with fluoride and genes associated with both fluoride and inflammation in the GeneCards database also showed that TGF-ß signaling pathway was significantly enriched. The immunofluorescence in HPA database showed that the main expression sites of RhoA are plasma membrane and cytosol, while the main expression site of Fbn1 is the Golgi apparatus. In conclusion, long-term NaF intake may cause inflammatory response in the peripheral blood of rats by upregulating TGF-ß signaling pathway, in which RhoA may play a key role.

T-2 toxin induces mitochondrial dysfunction in chondrocytes via the p53-cyclophilin D pathway.

Kashin-Beck disease is an endemic joint disease characterized by deep chondrocyte necrosis, and T-2 toxin exposure has been confirmed its etiology. This study investigated mechanism of T-2 toxin inducing mitochondrial dysfunction of chondrocytes through p53-cyclophilin D (CypD) pathway. The p53 signaling pathway was significantly enriched in T-2 toxin response genes from GeneCards. We demonstrated the upregulation of the p53 protein and p53-CypD complex in rat articular cartilage and ATDC5 cells induced by T-2 toxin. Transmission electron microscopy showed the damaged mitochondrial structure of ATDC5 cells induced by T-2 toxin. Furthermore, it can lead to overopening of the mitochondrial permeability transition pore (mPTP), decreased mitochondrial membrane potential, and increased reactive oxygen species generation in ATDC5 cells. Pifithrin-α, the p53 inhibitor, alleviated the increased p53-CypD complex and mitochondrial dysfunction of chondrocytes induced by T-2 toxin, suggesting that p53 played an important role in T-2 toxin-induced mitochondrial dysfunction. Mechanistically, T-2 toxin can activate the p53 protein, which can be transferred to the mitochondrial membrane and form a complex with CypD. The increased binding of p53 and CypD mediated the excessive opening of mPTP, changed mitochondrial membrane permeability, and ultimately induced mitochondrial dysfunction and apoptosis of chondrocytes.

Source identification of sedimentary organic carbon in coastal wetlands of the western Bohai Sea.

Coastal wetlands play a vital role in mitigating climate change, yet the characteristics of buried organic carbon (OC) and carbon cycling are limited due to difficulties in assessing the composition of OC from different sources (allochthonous vs. autochthonous). In this study, we analyzed the total organic carbon (TOC) to total nitrogen (TN) ratio (C/N), stable carbon isotope (δ13C) composition, and n-alkane content to distinguish different sources of OC in the surface sediments of the coastal wetlands on the western coast of the Bohai Sea. The coupling of the C/N ratio with δ13C and n-alkane biomarkers has been proved to be an effective tool for revealing OC sources. The three end-member Bayesian mixing model based on coupling C/N ratios with δ13C showed that the sedimentary OC was dominated by the contribution of terrestrial particulate organic matter (POM), followed by freshwater algae and marine phytoplankton, with relative contributions of 47 ± 21 %, 41 ± 18 % and 12 ± 17 %, respectively. The relative contributions of terrestrial plants, aquatic macrophytes and marine phytoplankton assessed by n-alkanes were 56 ± 8 %, 35 ± 9 % and 9 ± 5 % in the study area, respectively. The relatively high salinity levels and strong hydrodynamic conditions of the Beidagang Reservoir led to higher terrestrial plants source and lower aquatic macrophytes source than these of Qilihai Reservoir based on the assessment of n-alkanes. Both methods showed that sedimentary OC was mainly derived from terrestrial sources (plant-dominated), suggesting that vegetation plays a crucial role in storing carbon in coastal wetlands, thus, the coastal vegetation management needs to be strengthened in the future. Our findings provide insights into the origins and dynamics of OC in coastal wetlands on the western coast of the Bohai Sea and a significant scientific basis for future monitoring of the blue carbon budget balance in coastal wetlands.

Microbial Necromass, Lignin, and Glycoproteins for Determining and Optimizing Blue Carbon Formation.

Coastal wetlands contribute to the mitigation of climate change through the sequestration of "blue carbon". Microbial necromass, lignin, and glycoproteins (i.e., glomalin-related soil proteins (GRSP)), as important components of soil organic carbon (SOC), are sensitive to environmental change. However, their contributions to blue carbon formation and the underlying factors remain largely unresolved. To address this paucity of knowledge, we investigated their contributions to blue carbon formation along a salinity gradient in coastal marshes. Our results revealed decreasing contributions of microbial necromass and lignin to blue carbon as the salinity increased, while GRSP showed an opposite trend. Using random forest models, we showed that their contributions to SOC were dependent on microbial biomass and resource stoichiometry. In N-limited saline soils, contributions of microbial necromass to SOC decreased due to increased N-acquisition enzyme activity. Decreases in lignin contributions were linked to reduced mineral protection offered by short-range-ordered Fe (FeSRO). Partial least-squares path modeling (PLS-PM) further indicated that GRSP could increase microbial necromass and lignin formation by enhancing mineral protection. Our findings have implications for improving the accumulation of refractory and mineral-bound organic matter in coastal wetlands, considering the current scenario of heightened nutrient discharge and sea-level rise.

Cost-of-illness of gastroenteritis caused by rotavirus in Chinese children less than 5 years.

Acute gastroenteritis (AGE) caused by rotavirus (RV) remains a public health issue in China. To accelerate the mass rotavirus vaccination, it is important to inform the policy maker, and the public of the economic burden caused by rotavirus infection. A meta-analysis was conducted applying standardized algorithms. Articles published before January 1, 2023, in English and Chinese were searched through PubMed, CNKI, and WanFang Data. Studies with cost analysis of RV AGE were included. A random-effects model was applied to synthesize the total cost of RV AGE from the societal perspective. A prospective survey aimed to measure the cost of RV AGE was conducted in 2021 and 2022 in Shaoxing city, Zhejiang province, that can represent the developed region. The cost data was applied as deviation indicator, in comparison with the pooled estimate generated from meta-analysis. Totally 286 articles were identified, and eventually 12 studies were included. The pooled total social cost of RV AGE was US$282.1 (95%CI: US$213.4-350.7). The pooled private cost of RV AGE was US$206.4 (95%CI: US$155.2-257.5). RV AGE hospitalized and RV AGE incurred in developed regions caused remarkable higher burden (US$631.2 [95%CI: US$512.6-749.8], and US$333.6 [95%CI: US$234.1-433.2] respectively), compared to RV AGE treated at outpatient, and incurred in less developed regions. Our study demonstrates that RV AGE causes a significant economic burden in China. Given the promising effectiveness and highly cost-effective, introduction of rotavirus vaccines in national immunization programs could substantially reduce the economic burden in China.

Possible association between cerebral white matter atrophy and impaired performance of activities of daily living in patients with Parkinson's disease.

INTRODUCTION: The contribution of brain abnormalities in patients with Parkinson's disease (PD) to impaired functional status remains uncertain. Our study assessed whether global and regional brain structural abnormalities are associated with impaired performance of activities of daily living (ADL) in PD patients. MATERIAL AND METHODS: A retrospective analysis was conducted of 46 patients with PD, recruited prospectively from a movement disorder clinic. Motor impairment and disability were assessed using the Hoehn and Yahr (H-Y) scale and Unified Parkinson's Disease Rating Scale Part III (UPDRS-III). Cognitive status was evaluated with Montreal Cognitive Assessment (MoCA). The performance of ADL was indexed by the sum score of the Physical Self-Maintenance Scale (PSMS) and Lawton Instrumental ADL scale. Brain magnetic resonance imaging (MRI) was performed to assess white matter hyperintensities and medial temporal lobe atrophy (MTLA). Global brain atrophy, indexed by the relative grey matter volume (RGM), relative white matter volume (RWM) and average cortical thickness of the whole brain, was quantified by voxel-based morphometry (VBM). RESULTS: The ADL score (where higher scores indicate poorer performance) negatively correlated with RWM (where greater volume indicates less severe atrophy; r = -0.41, p = 0.004) and RGM (where greater volume indicates less severe atrophy; r = -0.43, p = 0.003) but not with the average cortical thickness ( r = -0.16, p = 0.29). With ADL score as the dependent variable in a linear regression model, H-Y stage and RWM significantly correlated with the ADL score after adjusting for age and MoCA score, and together accounted for 51% of the variance therein. RGM was not significantly correlated with the ADL score after adjusting for age and MoCA score. CONCLUSIONS: Cerebral white matter atrophy may be associated with the performance of ADL in patients with PD, indicating an important role of white matter impairment in their functional status.

Specific coenzyme preference switching for an aldo-keto reductase that synthesizes the chiral intermediate of duloxetine.

The synthesis of chiral intermediates for the traditional antidepressant duloxetine has gained significant attention as the number of depressed patients continues to grow. S-N, N-Dimethyl-3-hydroxy-3-(2-thienyl)-1-propanamide (S-DHTP) is a critical intermediate in the synthesis of duloxetine, and the chemical synthesis process is complex and environmentally unfriendly. Reduced nicotinamide adenine dinucleotide phosphate (NADPH) is a major cost driver in the biocatalytic production of S-DHTP from N, N-Dimethyl-3-keto-3-(2-thienyl)-1-propanamide (DKTP). Here, we successfully modified the coenzyme preference of an aldo-keto reductase (AKR7-2-1) to use the cheaper reduced nicotinamide adenine dinucleotide (NADH) through a coenzyme preference modification approach. We utilized protein engineering to create a superior mutant, Y53F, which increased the coenzyme specificity of AKR7-2-1 by 875-fold and improved its thermal stability, enhancing its potential for industrial applications. Molecular dynamics simulations were performed to demonstrate the effect of mutations at key sites on the protein, revealing the altered coenzyme preference and increased thermal stability from structural and energetic changes. This study validates the viability of the coenzyme preference modification strategy for aldo-keto reductase, offering valuable insights for fellow researchers and guiding future investigations.

Prominent Vessel Signs After Endovascular Thrombectomy Corelates with Unexplained Neurological Deterioration and is a More Reliable Imaging Predictor of Prognosis in Anterior Large Vessel Occlusion Stroke.

OBJECTIVE: Fifty percent of patients who undergo endovascular thrombectomy (EVT) for large-vessel occlusion exhibit unfavorable outcomes. The primary factor is attributed to persistent brain impairment even after successful EVT. The prominent vessel sign (PVS) on magnetic resonance susceptibility-weighted imaging reflects the territory of dysmetabolism and may facilitate an expeditious assessment for prognostication. We aimed to examine the relationship between PVS after EVT and the occurrence of early neurological deterioration (END) and 3-month outcomes. METHODS: Patients who underwent EVT and multimodal magnetic resonance imaging were included. END was defined as an increase of ≥2 in the National Institutes of Health Stroke Scale within 72 hours after EVT. Symptomatic intracranial hemorrhage, malignant edema, and surgical complications were defined as definite END, whereas the other symptoms were categorized as unexplained END (ux-END). The PVS-Alberta Stroke Program Early CT Score (ASPECTS) score was used to evaluate the asymmetric cerebral venous signal on the susceptibility-weighted imaging sequences semiquantitatively. RESULTS: A total of 116 eligible patients were included, 18 (15.5%) of whom presented with ux-END. The 72 hour National Institutes of Health Stroke Scale was strongly correlated with diffusion-weighted imaging infarct volume and PVS-ASPECTS and was significantly higher in the ux-END group (16 ± 6 vs. 5 ± 4, P = 0.001). The PVS-ASPECTS score was significantly associated with poor outcomes (odds ratio 2.551, 95% confidence interval (CI) 1.722-3.780, P＜0.001), and PVS-ASPECTS (area under the curve 0.884, 95% CI 0.815-0.953, P < 0.001) was superior to diffusion-weighted imaging infarct volume (area under the cure 0.720, 95% CI 0.620-0.820, P = 0.001) in predicting 3-month poor outcome. At the optimal cut-off of 2, the PVS-ASPECT predicted poor outcomes with a sensitivity of 89.7% and a specificity of 78.2%. CONCLUSIONS: PVS 72 hours after EVT correlated with ux-END. The PVS-ASPECTS is a more reliable predictor of stroke prognosis and provides valuable information regarding post-EVT management.

Structures of the holoenzyme TglHI required for 3-thiaglutamate biosynthesis.

Structural diverse natural products like ribosomally synthesized and posttranslationally modified peptides (RiPPs) display a wide range of biological activities. Currently, the mechanism of an uncommon reaction step during the biosynthesis of 3-thiaglutamate (3-thiaGlu) is poorly understood. The removal of the ß-carbon from the Cys in the TglA-Cys peptide catalyzed by the TglHI holoenzyme remains elusive. Here, we present three crystal structures of TglHI complexes with and without bound iron, which reveal that the catalytic pocket is formed by the interaction of TglH-TglI and that its activation is conformation dependent. Biochemical assays suggest a minimum of two iron ions in the active cluster, and we identify the position of a third iron site. Collectively, our study offers insights into the activation and catalysis mechanisms of the non-heme dioxygen-dependent holoenzyme TglHI. Additionally, it highlights the evolutionary and structural conservation in the DUF692 family of biosynthetic enzymes that produce diverse RiPPs.

Effects of STN-DBS surgery on cerebral glucose metabolism and distribution of DAT in Parkinson's disease.

INTRODUCTION: Parkinson's disease (PD) is a neurodegenerative disorder that affects millions of people worldwide. Subthalamic nucleus (STN) deep brain stimulation (DBS) has been shown to be an effective treatment for PD; however, the effects of this surgery on cerebral metabolism and presynaptic dopamine transporter (DAT) distribution are still being studied. METHODS: In this study, we included 12 PD patients (6 male and 6 female) who underwent STN-DBS surgery and had both 18 F-FDG and 11 C-CFT PET/CT imaging before and 1 year after the surgery. We used paired t-tests to identify changes in cerebral metabolism and calculated PD-related metabolic covariance pattern (PDRP) scores. We also assessed the uptake of 11 C-CFT in the striatum using striatal-to-occipital ratios (SORs). RESULTS: One year after surgery, we observed significant reductions in tremor, rigidity, akinesia, postural instability/gait disturbance, and Unified Parkinson's Disease Rating Scale Part III scores (p < .01, p < .001, p < .001, p < .001, and p < .001, respectively). Hamilton Depression Rating Scale and quality of life (PDQ-39 SI) were also significantly reduced (p < .05 and p < .01, respectively). The mean PDRP score decreased by 37% from 13.0 ± 6.6 to 8.2 ± 7.9 after STN-DBS surgery (p < .05). We observed decreased 18 F-FDG uptake in several areas, including the temporal lobe (BA22), thalamus, putamen, and cingulate gyrus (BA24), whereas it was increased in the supplementary motor area, postcentral gyrus, lingual gyrus, and precuneus (p < .05). SORs of 11 C-CFT in the bilateral caudate nucleus and ipsilateral posterior putamen were significantly decreased compared to preoperative levels (p < .05). CONCLUSION: Our findings suggest that STN-DBS surgery modifies the metabolic network of PD patients and improves motor symptoms, depression, and quality of life. However, it does not prevent the decrease of DAT in striatal areas.

Pan-cancer analysis of G6PD carcinogenesis in human tumors.

Glucose-6-phosphate dehydrogenase (G6PD) is involved in the catalytic pentose phosphate pathway (PPP), which is closely related to energy metabolism. G6PD plays a crucial role in many types of cancer, but the specific molecular mechanisms of G6PD in cancer remain unclear. Therefore, we investigated the potential oncogenic role of G6PD in various tumors based on The Cancer Genome Atlas (TCGA), the cBioPortal datasets, the University of California Santa Cruz (UCSC) Xena browser, and the UALCAN-based online tool. G6PD was highly expressed in several cancer tissues (hepatocellular carcinoma, glioma, and breast cancer) compared with normal tissues and was significantly associated with poor prognosis of hepatocellular carcinoma, clear cell renal cell carcinoma, and breast cancer. Promoter methylation levels of G6PD were lower in Bladder Urothelial Carcinoma (BLCA) (P = 2.77e-02), breast invasive carcinoma (BRCA) (P = 1.62e-12), kidney renal clear cell carcinoma (KIRC) (P = 4.23e-02), kidney renal papillary cell carcinoma (KIRP) (P = 2.64e-03), liver hepatocellular carcinoma (LIHC) (P = 1.76e-02), stomach adenocarcinoma (STAD) (P = 3.50e-02), testicular germ cell tumors (TGCT) (P = 1.62e-12), higher in prostate adenocarcinoma (PRAD) (P = 1.81e-09), and uterine corpus endometrial carcinoma (UCEC) (P = 2.96e-04) compared with corresponding normal tissue samples. G6PD expression was positively correlated with the infiltration level of immune cells in most tumors, suggesting that G6PD may be involved in tumor immune infiltration. In addition, the functional mechanism of G6PD also involves 'Carbon metabolism', 'Glycolysis/Gluconeogenesis', 'Pentose phosphate pathway', and 'Central carbon pathway metabolism in cancer signaling pathway'. This pan-cancer study provides a relatively broad understanding of the oncogenic role of G6PD in various tumors and presents a theoretical basis for the development of G6PD inhibitors as therapeutic drugs for multiple cancers.

Programmable and printable formaldehyde dehydrogenase as an excellent catalyst for biodegradation of formaldehyde.

As an environmental pollutant, formaldehyde can cause serious harm to the human body. Among many degradation methods, formaldehyde dehydrogenase from Pseudomonas putida (PFDH) exhibits broad potential because of its strong catalytic specificity and high degradation efficiency. However, the real application of PFDH in industry is limited by its instability and difficulties in recycling. In this work, the suitable printing conditions for immobilizing PFDH by three-dimensional (3D) printing technology were studied: the concentration of sodium alginate (SA) was 1.635 wt%, the concentration of CaCl2 was 7.4 wt%, the crosslinking time with CaCl2 was 8 min, and the temperature of the reaction was 31.5°C. 3D-printed PFDH/calcium alginate (CA) microspheres have 210% relative enzyme activity after seven repeated uses. Dried PFDH/CA particles were characterized by scanning electron microscope (SEM), Fourier transform infrared spectrometer (FT-IR), EDS elemental mapping, and thermogravimetric analysis (TGA) which proved that the enzyme was immobilized by the material. In addition, the recycling ability of 3D printing to immobilize different objects was explored and different shapes were designed by computer-aided design (CAD). In conclusion, 3D printing technology was applied to immobilize PFDH in this work, which provides a new idea to biodegrade formaldehyde in a green way.

Plant-soil feedback regulates the trade-off between phosphorus acquisition pathways in Pinus elliottii.

Plant-soil feedback (PSF) is conventionally characterized by plant biomass growth, yet it remains unclear how PSF affects plant nutrient acquisition strategies (e.g., nutrient absorption and nutrient resorption) associated with plant growth, particularly under changing soil environments. A greenhouse experiment was performed with seedlings of Pinus elliottii Englem and conditioned soils of monoculture plantations (P. elliottii and Cunninghamia lanceolata Hook). Soil sterilization was designed to test plant phosphorus (P) acquisition strategy with and without native soil fungal communities. Soils from P. elliottii and C. lanceolata plantations were used to explore the specific soil legacy effects on two different P acquisition pathways (absorption and resorption). Phosphorus addition was also applied to examine the separate and combined effects of soil abiotic factors and soil fungal factors on P acquisition pathways. Due to diminished mycorrhizal symbiosis, PSF prompted plants to increasingly rely on P resorption under soil sterilization. In contrast, P absorption was employed preferentially in the heterospecific soil, where species-specific pathogenic fungi could not affect P absorption. Higher soil P availability diluted the effects of soil fungal factors on the trade-off between the two P acquisition pathways in terms of the absolute PSF. Moreover, P addition plays a limited role in terms of the relative PSF and does not affect the direction and strength of relative PSF. Our results reveal the role of PSF in regulating plant P acquisition pathways and highlight the interaction between mycorrhizal and pathogenic fungi as the underlying mechanism of PSF.