Time series analysis of PM2.5 pollution risk based on the supply and demand of PM2.5 removal service: a case study of the urban areas of Beijing.

Demonstrating the temporal changes in PM2.5 pollution risk in regions facing serious PM2.5 pollution problems can provide scientific evidence for the air pollution control of the region. However, research on the variation of PM2.5 pollution risk on a fine temporal scale is very limited. Therefore, we developed a method for quantitative characterizing PM2.5 pollution risk based on the supply and demand of PM2.5 removal services, analyzed the time series characteristics of PM2.5 pollution risk, and explored the reasons for the temporal changes using the urban areas of Beijing as the case study area. The results show that the PM2.5 pollution risk in the urban areas of Beijing was close between 2008 and 2012, decreased by approximately 16.3% in 2016 compared to 2012, and further decreased by approximately 13.2% in 2021 compared to 2016. The temporal variation pattern of the PM2.5 pollution risk in 2016 and 2021 showed significant differences, including an increase in the number of risk-free days, a decrease in the number of heavily polluted days, and an increase in the stability of the risk day sequence. The significant reduction in risk level was mainly attributed to Beijing's air pollution control measures, supplemented by the impact of COVID-19 control measures in 2021. The results of PM2.5 pollution risk decomposition indicate that compared to the previous 2 years, the stability and predictability of the risk variation in 2016 increased, but the overall characteristics of high risk from November to February and low risk from April to September did not change. The high risk from November to February was mainly due to the demand for coal heating during this period, a decrease in PM2.5 removal service supply caused by plant leaf fall, and the common occurrence of temperature inversions in winter, which hinders the diffusion of air pollutants. This study provides a method for the analysis of PM2.5 pollution risk on fine temporal scales and may provide a reference for the PM2.5 pollution control in the urban areas of Beijing.

Rare oxoisoaporphine alkaloids from Menispermum dauricum with potential anti-inflammatory activity.

Eleven alkaloids including four previously undescribed oxoisoaporphine alkaloids, menisoxoisoaporphines A-D (1-4), four known analogues (5-8), and three aporphine alkaloids (9-11), were isolated and identified from the rhizomes of Menispermum dauricum. Their structures were elucidated by extensive spectroscopic data and single-crystal X-ray diffraction analyses. Among them, compounds 1 and 4 were the first samples of oxoisoaporphine with C-6 isopentylamino moiety, and 2 was a rare C-4 methylation product of oxoisoaporphine alkaloid. The in vitro anti-inflammatory activity of compounds 1-11 was performed by evaluating the inhibition of NO level in LPS-induced RAW264.7 macrophages. Among them, compound 4 exhibited the most potent NO inhibition activity with an IC50 value of 1.95 ± 0.33 µM. The key structure-activity relationships of those oxoisoaporphine alkaloids for anti-inflammatory effects have been summarized.

Decrypting the skeletal toxicity of vertebrates caused by environmental pollutants from an evolutionary perspective: From fish to mammals.

The rapid development of modern society has led to an increasing severity in the generation of new pollutants and the significant emission of old pollutants, exerting considerable pressure on the ecological environment and posing a serious threat to both biological survival and human health. The skeletal system, as a vital supportive structure and functional unit in organisms, is pivotal in maintaining body shape, safeguarding internal organs, storing minerals, and facilitating blood cell production. Although previous studies have uncovered the toxic effects of pollutants on vertebrate skeletal systems, there is a lack of comprehensive literature reviews in this field. Hence, this paper systematically summarizes the toxic effects and mechanisms of environmental pollutants on the skeletons of vertebrates based on the evolutionary context from fish to mammals. Our findings reveal that current research mainly focuses on fish and mammals, and the identified impact mechanisms mainly involve the regulation of bone signaling pathways, oxidative stress response, endocrine system disorders, and immune system dysfunction. This study aims to provide a comprehensive and systematic understanding of research on skeletal toxicity, while also promoting further research and development in related fields.

Sensitive fluorescence assay of chloramphenicol coupled with two-level isothermal amplification using a self-powered catalyzed hairpin assembly and entropy-driven circuit.

Two levels of nucleic acids-based isothermal amplification normally require a long reaction time due to the low concentration of catalyst, which limits its practical application. A sensitive fluorescence assay of chloramphenicol (CAP) was developed coupled with two-level isothermal amplification using a self-powered catalyzed hairpin assembly (CHA) and entropy-driven circuit (EDC). CAP can bind with its aptamer to open its closed structure. The opened hairpin can initiate self-powered CHA and EDC. The product of CHA can circularly catalyze the CHA with increasing concentration. In principle, the product of CHA plays the role of catalyst and increases with the progression of the reaction. Compared with the normal two levels of amplification, the amplification efficiency of our strategy is much higher due to the self-powered reaction by the CHA product. Thus, the reaction time is shortened to 110 min in this strategy. Moreover, the detection limit for CAP can achieve 0.1 pM and shows promising prospects for practical application.

Harnessing Ash for Sustainable CO2 Absorption: Current Strategies and Future Prospects.

This review explores the potential of using different types of ash, namely fly ash, biomass ash, and coal ash etc., as mediums for CO2 capture and sequestration. The diverse origins of these ash types - municipal waste, organic biomass, and coal combustion - impart unique physicochemical properties that influence their suitability and efficiency in CO2 absorption. This review first discusses the environmental and economic implications of using ash wastes, emphasizing the reduction in landfill usage and the transformation of waste into value-added products. Then the chemical/physical treatments of ash wastes and their inherent capabilities in binding or reacting with CO2 are introduced, along with current methodologies utilize these ashes for CO2 sequestration, including mineral carbonation and direct air capture techniques. The application of using ash wastes for CO2 capture are highlighted, followed by the discussion regarding challenges associated with ash-based CO2 absorption approach. Finally, the article projects into the future, proposing innovative approaches and technological advancements needed to enhance the efficacy of ash in combating the increasing CO2 levels. By providing a comprehensive analysis of current strategies and envisioning future prospects, this review aims to contribute to the field of sustainable CO2 absorption and environmental management.

CPK10 protein kinase regulates Arabidopsis tolerance to boron deficiency through phosphorylation and activation of BOR1 transporter.

Boron (B) is crucial for plant growth and development. B deficiency can impair numerous physiological and metabolic processes, particularly in root development and pollen germination, seriously impeding crop growth and yield. However, the molecular mechanism underlying boron signal perception and signal transduction is rather limited. In this study, we discovered that CPK10, a calcium-dependent protein kinase in the CPK family, has the strongest interaction with the boron transporter BOR1. Mutations in CPK10 led to growth and root development defects under B-deficiency conditions, while constitutively active CPK10 enhanced plant tolerance to B deficiency. Furthermore, we found that CPK10 interacted with and phosphorylated BOR1 at the Ser689 residue. Through various biochemical analyses and complementation of B transport in yeast and plants, we revealed that Ser689 of BOR1 is important for its transport activity. In summary, these findings highlight the significance of the CPK10-BOR1 signaling pathway in maintaining B homeostasis in plants and provide targets for the genetic improvement of crop tolerance to B-deficiency stress.

Mismatch repair protein deficiency and its implications on distant metastasis in colorectal cancer: A comprehensive analysis.

BACKGROUND: While previous studies have indicated variability in distant metastatic potential among different mismatch repair (MMR) states in colorectal cancer (CRC), their findings remain inconclusive, especially considering potential differences across various ethnic backgrounds. Furthermore, the gene regulatory networks and the underlying mechanisms responsible for these variances in metastatic potential across MMR states have yet to be elucidated. METHODS: We collected 2058 consecutive primary CRC samples from the South West of China and assessed the expression of MMR proteins (MLH1, MSH2, MSH6, and PMS2) using immunohistochemistry. To explore the inconsistencies between different MMR statuses and recurrence, we performed a meta-analysis. To delve deeper, we employed Weighted Gene Co-expression Network Analysis (WGCNA), ClueGo, and iRegulon, pinpointing gene expression networks and key regulatory molecules linked to metastasis and recurrence in CRC. Lastly, both univariate and multivariate Cox regression analyses were applied to determine the impact of core regulatory molecules on metastasis. RESULTS: Of the samples, 8.2% displayed deficient MMR (dMMR), with losses of MLH1 and PSM2 observed in 40.8% and 63.9%, respectively. A unique 24.3% isolated loss of PMS2 without concurrent metastasis was identified, a result that diverges from established literature. Additionally, our meta-analysis further solidifies the reduced recurrence likelihood in dMMR CRC samples compared to proficient MMR (pMMR). Two gene expression networks tied to distant metastasis and recurrence were identified, with a majority of metastasis-related genes located on chromosomes 8 and 18. An IRF1 positive feedback loop was discerned in the metastasis-related network, and IRF1 was identified as a predictive marker for both recurrence-free and distant metastasis-free survival across multiple datasets. CONCLUSION: Geographical and ethnic factors might influence peculiarities in MMR protein loss. Our findings also highlight new gene expression networks and crucial regulatory molecules in CRC metastasis, enhancing our comprehension of the mechanisms driving distant metastasis.

Precision treatment in advanced hepatocellular carcinoma.

The past decade has witnessed significant advances in the systemic treatment of advanced hepatocellular carcinoma (HCC). Nevertheless, the newly developed treatment strategies have not achieved universal success and HCC patients frequently exhibit therapeutic resistance to these therapies. Precision treatment represents a paradigm shift in cancer treatment in recent years. This approach utilizes the unique molecular characteristics of individual patient to personalize treatment modalities, aiming to maximize therapeutic efficacy while minimizing side effects. Although precision treatment has shown significant success in multiple cancer types, its application in HCC remains in its infancy. In this review, we discuss key aspects of precision treatment in HCC, including therapeutic biomarkers, molecular classifications, and the heterogeneity of the tumor microenvironment. We also propose future directions, ranging from revolutionizing current treatment methodologies to personalizing therapy through functional assays, which will accelerate the next phase of advancements in this area.

Comparative transcriptomics reveals common and strain-specific responses of human macrophages to infection with Mycobacterium tuberculosis and Mycobacterium bovis BCG.

Mycobacterium tuberculosis (MTB) and Mycobacterium bovis (M. bovis) are closely related pathogenic mycobacteria known to cause chronic pulmonary infections in both humans and animals. Despite sharing nearly identical genomes and virulence factors, these two bacteria display variations in host tropism, epidemiology, and clinical presentations. M. bovis Bacillus Calmette-Guérin (BCG) is an attenuated strain of M. bovis commonly utilized as a vaccine for tuberculosis (TB). Nevertheless, the molecular underpinnings of these distinctions and the intricacies of host-pathogen interactions remain areas of ongoing research. In this study, a comparative transcriptomic analysis was conducted on human leukemia macrophages (THP-1) infected with either MTB H37Rv or M. bovis BCG (Tokyo strain) to elucidate common and strain-specific responses at the transcriptional level. RNA sequencing was utilized to characterize the transcriptomes of human primary macrophages infected with MTB or BCG at 6 and 24 h post-infection. The findings indicate that both MTB and BCG induce substantial and dynamic alterations in the transcriptomes of THP-1, with a notable overlap in the quantity and extent of differentially expressed genes (DEGs). Moreover, gene ontology (GO) enrichment analysis unveiled shared pathways related to immune response, cytokine signaling, and apoptosis. The immune response of macrophages to bacterial infections at 6 h exhibited significantly greater intensity compared to that at 24 h. Furthermore, distinct gene sets displaying notable variances between MTB and BCG infections were identified. The profound impact of MTB infection on macrophage gene expression, particularly within the initial 6 h, was evident. Additionally, downregulation of pathways such as Focal adhesion, Rap1 signaling pathway, and Regulation of actin cytoskeleton was observed. The pathways associated with inflammation reactions and cell apoptosis exhibited significant differences, with BCG triggering macrophage apoptosis and MTB enhancing the survival of intracellular bacteria. Our findings reveal that MTB and BCG provoke similar yet distinct transcriptional responses in human macrophages, indicating variations in their pathogenesis and ability to adapt to host environments. These results offer novel insights into the molecular mechanisms governing host-pathogen interactions and may contribute to a deeper understanding of TB pathogenesis.

Dual Inhibition of CDK4/6 and XPO1 Induces Senescence With Acquired Vulnerability to CRBN-Based PROTAC Drugs.

BACKGROUND & AIMS: Despite the increasing number of treatment options available for liver cancer, only a small proportion of patients achieve long-term clinical benefits. Here, we aim to develop new therapeutic approaches for liver cancer. METHODS: A compound screen was conducted to identify inhibitors that could synergistically induce senescence when combined with cyclin-dependent kinase (CDK) 4/6 inhibitor. The combination effects of CDK4/6 inhibitor and exportin 1 (XPO1) inhibitor on cellular senescence were investigated in a panel of human liver cancer cell lines and multiple liver cancer models. A senolytic drug screen was performed to identify drugs that selectively killed senescent liver cancer cells. RESULTS: The combination of CDK4/6 inhibitor and XPO1 inhibitor synergistically induces senescence of liver cancer cells in vitro and in vivo. The XPO1 inhibitor acts by causing accumulation of RB1 in the nucleus, leading to decreased E2F signaling and promoting senescence induction by the CDK4/6 inhibitor. Through a senolytic drug screen, cereblon (CRBN)-based proteolysis targeting chimera (PROTAC) ARV-825 was identified as an agent that can selectively kill senescent liver cancer cells. Up-regulation of CRBN was a vulnerability of senescent liver cancer cells, making them sensitive to CRBN-based PROTAC drugs. Mechanistically, we find that ubiquitin specific peptidase 2 (USP2) directly interacts with CRBN, leading to the deubiquitination and stabilization of CRBN in senescent liver cancer cells. CONCLUSIONS: Our study demonstrates a striking synergy in senescence induction of liver cancer cells through the combination of CDK4/6 inhibitor and XPO1 inhibitor. These findings also shed light on the molecular processes underlying the vulnerability of senescent liver cancer cells to CRBN-based PROTAC therapy.

Association of Muscle Fat Content and Muscle Mass With Impaired Lung Function in Young Adults With Obesity: Evaluation With MRI.

RATIONALE AND OBJECTIVES: Although low muscle mass is associated with decreased lung function, studies exploring the relationship between muscle fat content and lung function impairment are scarce. This study aimed to evaluate the association of muscle mass and fatty infiltration with lung function in young adults with obesity. MATERIALS AND METHODS: We performed a retrospective cross-sectional study of patients aged 18-45 years with obesity who had impaired pulmonary function (case group, n = 66) and those with normal pulmonary function (control group, n = 198) by matching age, sex, body mass index (BMI), and height to assess whether muscle characteristics differed. Muscle mass and muscle fat content were assessed by MRI using a chemical shift-encoded sequence (IDEAL-IQ). RESULTS: A total of 264 patients were enrolled (124 females; mean age 32.0 years). The case group had lower muscle mass than the control group (p = 0.012), and there was an association between low muscle mass and lung function impairment (odds ratio (OR), 3.74; 95% confidence interval (CI), 1.57-8.93). Furthermore, muscle fat content was significantly higher in cases compared to controls (7.4 (2.7) % vs. 6.2 (2.5) %, p = 0.001). Multiple logistic regression analysis showed that muscle fat content was associated with a higher risk of impaired lung function (OR, 2.10; 95% CI, 1.65-2.66), regardless of adiposity and muscle mass. CONCLUSION: Both muscle fat content and muscle mass are associated with impaired lung function in young adults with obesity.

Leveraging synthetic lethality to uncover potential therapeutic target in gastric cancer.

Since trastuzumab was approved in 2012 for the first-line treatment of gastric cancer (GC), no significant advancement in GC targeted therapies has occurred. Synthetic lethality refers to the concept that simultaneous dysfunction of a pair of genes results in a lethal effect on cells, while the loss of an individual gene does not cause this effect. Through exploiting synthetic lethality, novel targeted therapies can be developed for the individualized treatment of GC. In this study, we proposed a computational strategy named Gastric cancer Specific Synthetic Lethality inference (GSSL) to identify synthetic lethal interactions in GC. GSSL analysis was used to infer probable synthetic lethality in GC using four accessible clinical datasets. In addition, prediction results were confirmed by experiments. GSSL analysis identified a total of 34 candidate synthetic lethal pairs, which included 33 unique targets. Among the synthetic lethal gene pairs, TP53-CHEK1 was selected for further experimental validation. Both computational and experimental results indicated that inhibiting CHEK1 could be a potential therapeutic strategy for GC patients with TP53 mutation. Meanwhile, in vitro experimental validation of two novel synthetic lethal pairs TP53-AURKB and ARID1A-EP300 further proved the universality and reliability of GSSL. Collectively, GSSL has been shown to be a reliable and feasible method for comprehensive analysis of inferring synthetic lethal interactions of GC, which may offer novel insight into the precision medicine and individualized treatment of GC.

Long-term tralopyril exposure results in endocrinological and transgenerational toxicity: A two-generation study of marine medaka (Oryzias melastigma).

This study aims to investigate the impact of tralopyril, a newly developed marine antifouling agent, on the reproductive endocrine system and developmental toxicity of offspring in marine medaka. The results revealed that exposure to tralopyril (0, 1, 20 µg/L) for 42 days resulted in decreased reproductive capacity in marine medaka. Moreover, it disrupted the levels of sex hormones E2 and T, as well as the transcription levels of genes related to the HPG axis, such as cyp19b and star. Sex-dependent differences were observed, with females experiencing more pronounced effects. Furthermore, intergenerational toxicity was observed in F1 offspring, including increased heart rate, changes in retinal morphology and cartilage structure, decreased swimming activity, and downregulation of transcription levels of relevant genes (HPT axis, GH/IGF axis, cox, bmp4, bmp2, runx2, etc.). Notably, the disruption of the F1 endocrine system by tralopyril persisted into adulthood, indicating a transgenerational effect. Molecular docking analysis suggested that tralopyril's RA receptor activity might be one of the key factors contributing to the developmental toxicity observed in offspring. Overall, our study highlights the potential threat posed by tralopyril to the sustainability of fish populations, as it can disrupt the endocrine system and negatively impact aquatic organisms for multiple generations.

Biological biomarkers of oral cancer.

The oral squamous cell carcinoma (OSCC) 5 year survival rate of 41% has marginally improved in the last few years, with less than a 1% improvement per year from 2005 to 2017, with higher survival rates when detected at early stages. Based on histopathological grading of oral dysplasia, it is estimated that severe dysplasia has a malignant transformation rate of 7%-50%. Despite these numbers, oral dysplasia grading does not reliably predict its clinical behavior. Thus, more accurate markers predicting oral dysplasia progression to cancer would enable better targeting of these lesions for closer follow-up, especially in the early stages of the disease. In this context, molecular biomarkers derived from genetics, proteins, and metabolites play key roles in clinical oncology. These molecular signatures can help predict the likelihood of OSCC development and/or progression and have the potential to detect the disease at an early stage and, support treatment decision-making and predict treatment responsiveness. Also, identifying reliable biomarkers for OSCC detection that can be obtained non-invasively would enhance management of OSCC. This review will discuss biomarkers for OSCC that have emerged from different biological areas, including genomics, transcriptomics, proteomics, metabolomics, immunomics, and microbiomics.

Highly Active and Water-Resistant Cu-Doped OMS-2 Catalysts for CO Oxidation: The Importance of the OMS-2 Synthesis Method and Cu Doping.

Porous cryptomelane-type Mn oxide (OMS-2) has an outstanding redox property, making it a highly desirable substitute for noble metal catalysts for CO oxidation, but its catalytic activity still needs to be improved, especially in the presence of water. Given the strong structure-performance correlation of OMS-2 for oxidation reactions, herein, OMS-2 is synthesized by solid state (OMS-2S), reflux (OMS-2R), and hydrothermal (OMS-2H) methods, aiming to improve its CO oxidation performance through manipulating synthesis parameters to tailor its particle size, morphology, and crystallinity. Characterization shows that OMS-2S has the highest CO oxidation activity in the absence of water due to its low crystallinity, high specific surface area, large oxygen vacancy content, and good redox property, but the presence of water can greatly reduce its CO oxidation activity. Doping Cu into an OMS-2 can not only improve its CO oxidation activity but also greatly improve its water tolerance. The Cu-doped OMS-2S catalyst with ∼4 wt % Cu can achieve a T90 of 49 °C (1% CO/10% O2/N2 and WHSV = 60,000 mL·g-1·h-1), ranking among the lowest reported T90 values for Mn oxide-based CO oxidation catalysts, and it can maintain nearly 100% CO conversion in the presence of 5 vol % water for over 50 h. In situ DRIFTs characterization indicates that the good water resistance of Cu-doped OMS-2S can be attributed to the significantly suppressed surface hydroxyl group generation because of Cu doping. This work demonstrates the importance of the synthesis method and Cu doping in determining the CO oxidation activity and water resistance of OMS-2 and will provide guidance for synthesizing highly active and water-resistant CO oxidation catalysts.

Dioxaphosphabicyclooctanes: small caged phosphines from tris(hydroxymethyl)phosphine.

Dioxaphosphabicyclo[2.2.2]octanes (L1-L4) have been prepared in a one-pot reaction from tris(hydroxymethyl)phosphine and various α,ß-unsaturated ketones. The non-volatile phosphines oxidise very slowly in air. They possess highly upfield 31P chemical shifts (-59 to -70 ppm), small cone angles (121-140°) and a similar electronic parameter to PPh3. Reaction of L1 with [Rh(acac)(CO)2] gave the complex [Rh(acac)(CO)(L1)] with a ν(CO) of 1981.5 cm-1, whereas reaction L1 with [Rh(CO)2Cl]2 gave [Rh(CO)(L1)2Cl] with a ν(CO) of 1979.9 cm-1, remarkably similar to the CO stretching frequencies reported for analogous PPh3 complexes. The cage phosphines were explored as ligands in rhodium catalysed hydroformylation of 1-octene. All of the ligands gave a linear selectivity to n-nonanal of 68%, regardless of the substituents. However the ligand substituents had a significant effect on the catalyst activity, with increased steric bulk around the coordination environment giving a three-fold increase in aldehyde yield. The phosphines undergo ligand subsitution with [Pd(MeCN)2Cl2] forming square planar trans-[Pd(L)2Cl2] complexes. Subsequent reduction with hydrazine furnishes homoleptic tetravalent [Pd(L1)4] which was applied as a catalyst in Suzuki-Miyaura couplings, furnishing the C-C coupled products in moderate yields.

Protective effect of Peucedanum praeruptorum Dunn extract on oxidative damage of LLC­PK1 cells induced by H2O2.

Peucedanum praeruptorum Dunn extract (PPDE) is a well-known treatment used in traditional Chinese medicines, where it is most commonly used to treat coughs and symptoms such as headaches and fever. In the present study, the antioxidant capacity of PPDE in vitro was determined by scavenging experiments using DPPH, ABTS+·, ·OH, and ·O2-. The cell survival rate was determined by MTT assay. The MDA, SOD, CAT, GSH, and GSH-Px content were determined by colorimetry assays. The expression levels of antioxidant genes SOD, CAT, GSH, and GSH-Px were assessed by reverse transcription-quantitative PCR. HPLC was used to identify the PPDE components. The results suggested that PPDE had scavenging effects on DPPH, ABTS, hydroxyl, and superoxide anion radicals in a concentration-dependent manner; H2O2 treatment resulted in oxidative stress in LLC-PK1 cells, and the degree of injury of LLC-PK1 cells following PPDE treatment was improved, which was positively correlated with its concentration. Peucedanum praeruptorum Dunn extract treatment reduced the content of MDA and increased the content of CAT, SOD1, GSH, and GSH-Px. The mRNA expression levels of antioxidant genes detected by quantitative PCR were consistent with changes in CAT, SOD, GSS, and GSH-Px. Additionally, the trend in CAT, SOD1, GSH, and GSS protein expression levels was also consistent at the mRNA level. PPDE was found to consist of isochlorogenic acid C, myricetin, baicalin, luteolin, and kaempferol. Therefore, PPDE, which was formed of products derived from natural substances, functioned in the inhibition of oxidative damage. The present study aimed to obtain a better understanding of the traditional Chinese medicine Peucedanum praeruptorum Dunn and preliminarily elucidate its antioxidant mechanism at the cellular level. Further animal or human experiments are required to verify the antioxidant effects of PPDE for further development and utilization.

Colonization of multidrug-resistant Gram-negative bacteria increases risk of surgical site infection after hemorrhoidectomy: a cross-sectional study of two centers in southern China.

PURPOSE: The present study aims to determine the rectoanal colonization rate and risk factors for the colonization of present multidrug-resistant bacteria (MDRBs). In addition, the relationship between MDRB colonization and surgical site infection (SSI) following hemorrhoidectomy was explored. METHODS: A cross-sectional study was conducted in the Department of Colorectal Surgery of two hospitals. Patients with hemorrhoid disease, who underwent hemorrhoidectomy, were included. The pre-surgical screening of multidrug-resistant Gram-negative bacteria (MDR-GNB) colonization was performed using rectal swabs on the day of admission. Then, the MDRB colonization rate was determined through the rectal swab. Logistic regression models were established to determine the risk factors for MDRB colonization and SSI after hemorrhoidectomy. A p-value of < 0.05 was considered statistically significant. RESULTS: A total of 432 patients met the inclusion criteria, and the MDRB colonization prevalence was 21.06% (91/432). The independent risk factors for MDRB colonization were as follows: patients who received ≥ 2 categories of antibiotic treatment within 3 months (odds ratio (OR): 3.714, 95% confidence interval (CI): 1.436-9.605, p = 0.007), patients with inflammatory bowel disease (IBD; OR: 6.746, 95% CI: 2.361-19.608, p < 0.001), and patients with high serum uric acid (OR: 1.006, 95% CI: 1.001-1.010, p = 0.017). Furthermore, 41.57% (37/89) of MDRB carriers and 1.81% (6/332) of non-carriers developed SSIs, with a total incidence of 10.21% (43/421). Based on the multivariable model, the rectoanal colonization of MDRBs (OR: 32.087, 95% CI: 12.052-85.424, p < 0.001) and hemoglobin < 100 g/L (OR: 4.130, 95% CI: 1.556-10.960, p = 0.004) were independently associated with SSI after hemorrhoidectomy. CONCLUSION: The rectoanal colonization rate of MDRBs in hemorrhoid patients is high, and this was identified as an independent risk factor for SSI after hemorrhoidectomy.

Gγ subunit AT1/GS3-the "code" of alkaline tolerance in main graminaceous crops.

This brief article highlights the results of Zhang et al. (Science 379, eade8416, 2023), who recently found that the Gγ subunit AT1/GS3 contributes to alkaline tolerance in several main monocots crops, and revealed the molecular mechanism of AT1/GS3-mediated response to alkaline stress in plants, which involves regulating H2O2 levels by inhibiting the phosphorylation of aquaporin PIP2s.