The escalating pressure from global population growth, climate change, and resource consumption is intensifying the burden on traditional agricultural production. Against this backdrop, soil degradation and pollution present increasingly severe challenges, creating a vicious cycle with rising food demands. Maintaining soil health and its ecosystem services has thus become a critical prerequisite for achieving sustainable agriculture in the future. This review explores the impacts of soil carbon (C) and nitrogen (N) dynamics on soil microbial communities and their interactions. Soil C and N are key determinants of microbial diversity and community structure, intrinsically linked to soil C/N cycling, crop productivity, and ecological balance. Environmental factors such as nitrogen fertilizer application, organic matter amendment application, litter decomposition, elevated CO₂ concentrations, and nitrogen deposition significantly influence soil C and N dynamics. Changes in soil C and N content regulate microbial community dynamics and the synergistic, competitive, and antagonistic interactions among microorganisms. Meanwhile, microbial communities actively respond to alterations in soil C and N availability. The resulting shifts in microbial communities and their interactions subsequently regulate soil C/N cycling and ecosystem stability, ultimately influencing ecosystem functions. By elucidating the mechanisms underlying soil carbon-nitrogen-microbial interactions, this review significantly advances our understanding of soil ecosystem responses and feedback mechanisms in the context of global change, while also providing crucial practical guidance for enhancing soil fertility and promoting sustainable agricultural development through microbial regulation.
Soil Microbiology ; Nitrogen/metabolism* ; Carbon/metabolism* ; Soil/chemistry* ; Bacteria/growth & development* ; Fungi/metabolism* ; Ecosystem ; Fertilizers ; Agriculture

Pneumothorax during pediatric laparoscopic surgery is a potentially fatal complication that may not be promptly recognized. It can occur due to congenital anatomical abnormalities, pre-existing pulmonary disease, or operative factors during laparoscopy. Clinical presentation may range from asymptomatic to acute respiratory distress, pleuritic chest pain, and even life-threatening circulatory collapse. Here, we report a case of sudden intraoperative pneumothorax accompanied by extensive subcutaneous emphysema of the neck and chest wall during laparoscopic high ligation of the hernial sac in a child. The child presented with a reducible left lower abdominal mass and mild pain 3 days prior but did not seek medical attention. Symptoms worsened 1 day prior to admission, with difficulty reducing the mass. On April 8, 2021, the patient was admitted to the Department of Anesthesiology, Zhuzhou Hospital Affiliated to Xiangya School of Medicine of Central South University, with a diagnosis of "left inguinal hernia." On the second day of hospitalization, laparoscopic high ligation of the left inguinal hernia sac was performed under general anesthesia. During the procedure, the patient developed a sudden increase in airway pressure, marked hemodynamic fluctuations, crepitus in the neck and right anterior chest regions, and significantly diminished breath sounds in the right lung. Emergent bedside chest X-ray confirmed a right-sided pneumothorax. Immediate intervention including thoracic needle decompression, closed thoracic drainage, the lung re-expansion was performed. The patient was discharged on the 7th postoperative day with full recovery. This case highlights the need for clinicians to remain vigilant for iatrogenic pneumothorax during pediatric laparoscopic surgery. Close intraoperative monitoring of vital signs is crucial for early detection, recognition, and timely management of pneumothorax to ensure patient safety during minimally invasive procedures.
Humans ; Laparoscopy/methods* ; Pneumothorax/etiology* ; Ligation/methods* ; Hernia, Inguinal/surgery* ; Male ; Intraoperative Complications/etiology* ; Child ; Herniorrhaphy/methods* ; Female ; Subcutaneous Emphysema/etiology*

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Objective To investigate the protective effect of verapamil on hyperuricemia nephropathy(HN)in mice through modulating TXNIP/NLRP3 inflammasome signaling pathway.Methods Thirty-two male C57BL/6J mice(8 weeks old,weighing 18～22 g)were randomly divided into a blank control group,a model group,an allopurinol group(10 mg/kg),and a verapamil group(40 mg/kg),with 8 animals in each group.Except for the control mice,the other mice were given 10%fructose water and adenine to establish a mouse model of HN.After successful establishment of model mice,the corresponding interventions were administered to the mice of the other 3 groups for 4 consecutive weeks.The levels of serum uric acid(UA),creatinine(Cr),urea(UREA),aspartate aminotransferase(AST)and alanine aminotransferase(ALT)were measured.HE staining was used to assess the alterations in renal morphology and the infiltration of inflammatory cells,while Masson's staining was employed to evaluate renal fibrosis.Moreover,ELISA was employed to measure the contents of IL-1β and IL-6 in kidney tissue,while serum levels of malondialdehyde(MDA),superoxide dismutase(SOD),and glutathione peroxidase(GSH-Px)were detected by colorimetric assay.Furthermore,immunohistochemical staining and Western blot analysis were conducted to examine the expression of TXNIP,NLRP3,IL-1β,MMP7,FN1,CD68,and MPO proteins in the kidney.Results Compared to the control group,HN mice exhibited increased serum UA,Cr,and UREA levels(P<0.05),renal pathological changes including renal tubular regeneration,interstitial or periglomerular fibrosis and prominent infiltration of inflammatory cells,and significantly increased renal contents of IL-1β and IL-6 and serum MDA level(P<0.05),while reduced serum SOD and GSH-Px contents(P<0.05),as well as up-regulation of kidney proteins TXNIP,NLRP3,IL-1β,CD68,MPO,FN1 and MMP7(P<0.01).Verapamil treatment notably reduced serum UA and Cr levels(P<0.01),improved kidney lesions to some extents,decreased collagen volume fraction(CVF)(P<0.01),and restored pro-inflammatory cytokines and oxidative stress markers(P<0.05)when compared with the levels in the model group.Further research found that the expression of kidney proteins TXNIP,NLRP3,IL-1β,CD68,MPO,FN1,and MMP7 was significantly down-regulated by verapamil treatment(P<0.05).Conclusion Verapamil exhibits a renal protective effect on HN mice through its anti-inflammatory,antioxidant,and antifibrotic properties,and its mechanism may be related to the inhibition of the TXNIP/NLRP3 inflammasome signaling pathway.

Objective To study the hemodynamic effects of enhanced external counter pulsation(EECP)on typical coronary artery disease and microcirculation angina.Methods A physiological model of the right dominant coronary artery,including the coronary conduit arteries and coronary microcirculation,was established using lumped parameter models.Pathological conditions,such as one-vessel lesions,three-vessel lesions,and microcirculation angina,were simulated.EECP intervention models were established,and the hemodynamic effects of EECP on pathological models was simulated.Results The simulation results of the coronary physiological model,pathological models,and EECP intervention model established in this study were consistent with experimental data in related literature.EECP improved coronary blood flow in all three pathological conditions.For one-vessel lesions,EECP could not recover the blood flow of left main coronary artery to a normal level after the stenosis rate reached 80%-85%.For three-vessel lesions,EECP treatment could not be used if the stenosis rate in one of the three vessels exceeded 90%.For microcirculation angina,EECP was effective when critical condition myocardial blood flow was>1.03 mL/min·g and coronary flow reserve was>1.64.Conclusions The model of coronary disease under EECP interference established in this study meets expectations,and the obtained simulation data have certain reference values for the clinical application of EECP.

ObjectiveTo investigate the therapeutic effect of ganoderic acid A （GA-A） on a mouse model of concanavalin A （ConA）-induced autoimmune hepatitis （AIH）. MethodsA total of 35 mice were randomly divided into control group （NC group）， model group （ConA group）， and low-， middle-， and high-dose GA-A treatment groups （GA-A-L， GA-A-M， and GA-A-H groups， respectively）， with 7 mice in each group. ConA was injected via the caudal vein of mice to establish a classic mouse model of AIH， and different doses of GA-A were administered via intraperitoneal injection 1 hour later for treatment. Proteomic techniques were used to investigate the protective mechanism of GA-A on hepatocytes， and HL-60 cells were differentiated into dHL-60 neutrophils by all-trans retinoic acid in vitro to validate the mechanism of action of GA-A. Related indicators were measured， including inflammatory markers （the activities of serum alanine aminotransferase ［ALT］ and aspartate aminotransferase ［AST］， HE staining， and inflammation-related genes）， apoptosis markers （TUNEL staining）， neutrophils， and neutrophil extracellular trap （NET） markers （myeloperoxidase ［MPO］， citrullinated histone H3 ［CitH3］， Ly6G， and free double-stranded DNA ［dsDNA］）， and p38 phosphorylation markers. The independent samples t-test was used for comparison of continuous data between two groups； a one-way analysis of variance was used for comparison between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsCompared with the NC group， the ConA group had significant increases in the serum levels of ALT and AST （both P<0.001）， and compared with the ConA group， GA-A treatment significantly reduced the levels of ALT and AST （both P<0.01）. HE staining showed that the mice in the ConA group had significant liver necrosis， while GA-A treatment significantly reduced the area of liver necrosis and the number of TUNEL-positive cells （both P<0.05）. Compared with the ConA group， the GA-A group had significant reductions in the expression levels of the inflammatory factors interleukin-6， tumor necrosis factor-α， and interferon gamma in serum and liver tissue （all P<0.05）. The proteomic analysis showed that GA-A alleviated ConA-induced acute immune liver injury by inhibiting the release of NET and the p38 MAPK pathway. Immunofluorescent staining of mouse liver tissue showed that compared with the ConA group， the GA-A group had significant reductions in the number of MPO-positive neutrophils and the number of cells with positive Ly6G and CitH3 （all P<0.01）. Western Blot and dsDNA testing showed that GA-A significantly inhibited the levels of the NET markers dsDNA and CitH3 and the level of p38 phosphorylation in liver tissue and dHL-60 cells （all P<0.05）. ConclusionGA-A alleviates liver inflammatory response and hepatocyte death by inhibiting the p38 MAPK pathway and the release of NET， thereby alleviating ConA-induced acute immune liver injury. This study provides a theoretical basis for the use of GA-A to treat immune liver injury by regulating neutrophil function.

The circadian rhythm of the body is mainly regulated by the biological clock gene,which is the result of biological evolution and plays an important role in maintaining the normal function of the organ-ism.When the circadian rhythm is disturbed or disordered,it will produce adverse health consequences.The current researches find that circadian rhythm disorder mediated by biological clock gene plays an important regulatory role in the occurrence and development of acute inflammatory diseases,such as sepsis,ischemia-reperfusion injury and COVID-19.This paper reviews the research progress of biological clock gene in acute inflammatory diseases in recent years,and discusses the role of targeted biological clock gene in the treatment of inflammatory related diseases and the existing problems.

Humans ; Whooping Cough/prevention & control* ; Vaccines, Acellular ; China