Helicobacter pylori(HP) infection is associated with non-alcoholic fatty liver disease (NAFLD) and insulin resistance; however, the correlation between HP eradication and NAFLD remains controversial. This systematic review and meta-analysis examined the effect of HP treatment on clinical and laboratory parameters in NAFLD patients.

We conducted a literature search of the PubMed, Embase, Scopus, and Web of Science databases through Septem ber 2023 for randomized controlled trials (RCTs) examining the effect of HP treatment on NAFLD patients versus lifestyle changes alone. The primary outcome was the change in steatosis parameters. The secondary endpoints were changes in anthropometric parameters, inflammatory markers (TNF-α), and metabolic parameters (fasting blood glucose, homeostasis model assessment of insulin resistance, AST/ALT, and lipid profile). The random effects model was used to calculate the standardized mean difference (SMD) with associated 95% confidence intervals (CIs) for our desired outcome.

Four RCTs met our inclusion criteria. A total of 453 patients were included (mean age 42.8 years, 58.5% males), 228 (50.3%) of whom were in the HP eradication group and 225 (49.7%) of whom were in the lifestyle modification group. Compared with lifestyle modification alone, HP eradication had a significant effect on reducing liver steatosis and TNF-α levels (SMD: - 0.9; 95% CI - 14.67, - 3.82, I² = 0% and SMD: - 6.3; 95% CI - 9.04, - 3.56, I² = 0%, respectively). No significant effect on other metabolic parameters was found.

HP eradication significantly reduced liver steatosis and TNF-α levels in NAFLD patients. However, HP eradi cation did not significantly affect other metabolic indices compared to lifestyle changes alone.

Diet plays a crucial role in insulin resistance and diabetes, with high-fat and high-carbohydrate diets being major contributors. However, the type of fat consumed is critical, as different fatty acids impact insulin sensitivity differently.

This review examines the potential benefits of avocado oil, which is rich in monounsaturated fatty acids (MUFAs), in improving glycaemic control and lipid metabolism. It also explores variations in avocado oil composition across different avocado cultivars.

Experimental and clinical studies were analysed to assess the metabolic effects of avocado oil. The impact of MUFAs on insulin sensitivity, lipid profiles, and metabolic health was reviewed, alongside the influence of fruit quality, maturity, and cultivar differences.

Avocado oil may enhance glycaemic control and lipid metabolism, benefiting individuals with diabetes and hypercholesterolemia. However, its composition varies significantly across avocado variants such as Hass, Reed, Ettinger, and Fuerte, influencing its therapeutic properties.

Avocado oil’s high MUFA content offers promising metabolic benefits. Further research is needed to standardize its therapeutic application, considering cultivar-dependent variations in composition.

Hypoxia plays a critical role in the pathophysiology of cardiomyopathy, myocardial infarction, and heart failure. Promoting ketone metabolism has been shown to be beneficial for myocardial cells under hypoxic conditions. However, the expression and regulatory mechanisms of key enzymes in the ketone pathway under hypoxic conditions are still unclear. This study aimed to investigate the effects of hypoxia on the expression of key enzymes in the ketone metabolic pathway and the underlying regulatory mechanisms involved.

H9C2 myocardial cells were cultured for 6 h in an oxygen-glucose-deprived state, and the expression of various genes was detected by quantitative real-time PCR. ELISA and lactate dehydrogenase (LDH) cytotoxicity assay were used to measure CoAs, itaconic acid, and LDH levels, respectively, and the dependence of gene expression on hypoxia-inducible factor-1 alpha (HIF-1α) was evaluated using the inhibitor LW6.

H9C2 cardiomyocytes exhibited increased ketone body metabolism in response to hypoxia. Hypoxia induced the expression of the ketone body enzymes succinyl-CoA:3-oxoacid CoA transferase (SCOT/OXCT1), 3-hydroxybutyrate dehydrogenase 2 (BDH2), and acyl-CoA: cholesterol acyltransferase 1 (ACAT1) in cardiomyocytes, with a concomitant increase in the level of acyl-CoA and a decrease in the level of succinyl-CoA. The HIF-1α inhibitor LW6 could partially reverse the expression of BDH2 and ACAT1, as well as the levels of succinyl-CoA. Interestingly, however, hypoxia-induced SCOT/ OXCT1 expression was not regulated by the HIF-1α inhibitor. In addition, hypoxia promoted the expression of inflammatory factors.

These data confirm the critical role of ketone metabolism in myocardial hypoxia and help to elucidate the pathophysiology of cardiomyopathy, myocardial infarction and heart failure.

Atrial natriuretic peptide (ANP) and Zn^2⁺ have been shown to confer cardioprotection against ischemia/reperfusion (I/R) injury. Zn^2⁺ alleviates myocardial hypertrophy and pulmonary hypertension by regulating ANP expression, but its precise role in ANP-mediated cardioprotection remains unclear. This study aimed to investigate whether ANP protects the heart during reperfusion by modulating Zn^2⁺ levels and to explore the underlying mechanisms involved.

In this study, we utilized an isolated reperfused heart model in rats, as well as wild-type (WT) and ANP knockout (ANP^−/−) mouse models, for in vivo I/R experiments. For clinical investigations, plasma samples were collected from 216 patients with ischemia-related diseases. Evans blue and TTC staining, radioimmunoassay, ICP‒OES, echocardiography, Hydro-Cy3-mediated ROS detection, and Western blotting were employed to evaluate the effect of ANP on Zn^2⁺ homeostasis.

Plasma ANP levels were significantly elevated in patients with ST-elevation myocardial infarction (STEMI), nonST-elevation myocardial infarction (NSTEMI), and heart failure (HF). ANP secretion increased during reperfusion, rather than infarction, both ex vivo and in vivo, promoting Zn^2⁺ accumulation in reperfused tissue. ANP and Zn^2⁺ protected mitochondria and reduced infarct size; these effects were reversed by the Zn^2⁺ chelator TPEN. In WT and ANP^−/− mice, EF% and FS% decreased after reperfusion, with ANP^−/− mice exhibiting significantly worse cardiac function. ANP pretreatment alone improved cardiac function, but combined pretreatment with ANP and TPEN decreased EF% and FS% while increasing LVID. Reperfusion increased ROS levels in both WT and ANP^−/− hearts, which were reduced by ANP pretreatment. I/R injury elevated Zn^2⁺ transporter 8 (ZnT8) expression, an effect that was counteracted by ANP, although this effect was reversed by TPEN. Hypoxia-inducible factor 1-alpha (HIF-1α) expression was elevated in I/R rats and ANP^−/− mice, and it was inhibited by both Zn^2⁺ and ANP pretreatment. However, the HIF-1α inhibitor 2-Me did not reverse the effect of ANP on ZnT8 expression. Additionally, ANP increased PI3K expression in both WT and ANP^−/−I/R mice, but this effect was blocked by the PI3K inhibitor LY294002.

ANP modulates Zn2⁺ homeostasis during reperfusion injury by downregulating ZnT8 through the PI3K signalling pathway, thereby reducing myocardial I/R injury.

This study aimed to investigate the association between insulin resistance and the risk of cardiovascular disease.

A cross-sectional study including 2128 participants aged 40-79 years was conducted using data from the National Health and Nutrition Examination Survey from 1999 to 2018. The quantitative insulin sensitivity check index (QUICKI) and homeostasis model assessment of β-cell function (HOMA-β) were used as independent variables. The 10-year risk of a first hard atherosclerotic cardiovascular event was used as the dependent variable, with other potential confounding factors considered. Multivariate linear regression models and smooth curve fitting were used to assess the associations between insulin resistance and 10-year risk.

A total of 2128 patients, comprising 1191 men and 937 women, were included in our analysis. The regression analyses revealed a negative correlation between the QUICKI score and the 10-year risk of a first hard atherosclerotic cardiovascular event [β = - 8.85, CI (- 15.77, - 1.93)] after adjusting for age, race, body mass index, systolic blood pressure, diastolic blood pressure, hypertension treatment, smoking, diabetes, and low-density lipoprotein cholesterol. Conversely, an increase in HOMA-β was associated with 10-year risk [β = 6.84, CI (0.45, 13.23)]. Gender-specific subgroup analysis indicated that the QUICKI had a β value of 0.077 (0.046, 0.108) for men and 0.080 (0.061, 0.094) for women.

This study demonstrated that increased insulin resistance is linked to an increased risk of cardiovascular disease.

This study aimed to explore a novel method that integrates the segmentation guidance classification and the diffusion model augmentation to realize the automatic classification for tibial plateau fractures (TPFs).

YOLOv8n-cls was used to construct a baseline model on the data of 3781 patients from the Orthopedic Trauma Center of Wuhan Union Hospital. Additionally, a segmentation-guided classification approach was proposed. To enhance the dataset, a diffusion model was further demonstrated for data augmentation.

The novel method that integrated the segmentation-guided classification and diffusion model augmentation significantly improved the accuracy and robustness of fracture classification. The average accuracy of classification for TPFs rose from 0.844 to 0.896. The comprehensive performance of the dual-stream model was also significantly enhanced after many rounds of training, with both the macro-area under the curve (AUC) and the micro-AUC increasing from 0.94 to 0.97. By utilizing diffusion model augmentation and segmentation map integration, the model demonstrated superior efficacy in identifying Schatzker I, achieving an accuracy of 0.880. It yielded an accuracy of 0.898 for Schatzker II and III and 0.913 for Schatzker IV; for Schatzker V and VI, the accuracy was 0.887; and for intercondylar ridge fracture, the accuracy was 0.923.

The dual-stream attention-based classification network, which has been verified by many experiments, exhibited great potential in predicting the classification of TPFs. This method facilitates automatic TPF assessment and may assist surgeons in the rapid formulation of surgical plans.

The study aimed to develop machine learning (ML) models to predict the mortality of patients with acute gastrointestinal bleeding (AGIB) in the intensive care unit (ICU) and compared their prognostic performance with that of Acute Physiology and Chronic Health Evaluation II (APACHE-II) score.

A total of 961 AGIB patients admitted to the ICU of Renmin Hospital of Wuhan University from January 2020 to December 2023 were enrolled. Patients were randomly divided into the training cohort (n = 768) and the validation cohort (n= 193). Clinical data were collected within the first 24 h of ICU admission. ML models were constructed using Python V.3.7 package, employing 3 different algorithms: XGBoost, Random Forest (RF) and Gradient Boosting Decision Tree (GBDT). The area under the receiver operating characteristic (ROC) curve (AUC) was used to evaluate the performance of different models.

A total of 94 patients died with an overall mortality of 9.78% (11.32% in the training cohort and 8.96% in the validation cohort). Among the 3 ML models, the GBDT algorithm demonstrated the highest predictive performance, achieving an AUC of 0.95 (95% CI 0.90-0.99), while the AUCs of XGBoost and RF models were 0.89 (95% CI 0.82-0.96) and 0.90 (95% CI 0.84-0.96), respectively. In comparison, the APACHE-II model achieved an AUC of 0.74 (95% CI 0.69-0.87), with a specificity of 70.97% (95% CI 64.07-77.01). When APACHE-II score was incorporated into the GBDT algorithm, the ensemble model achieved an AUC of 0.98 (95% CI 0.96-0.99) with a sensitivity of 85.71% and a specificity up to 95.15%.

The GBDT model serves as a reliable tool for accurately predicting the in-hospital mortality for AGIB patients. When integrated with the APACHE-II score, the ensemble GBDT algorithm further enhances predictive accuracy and provides valuable insights for prognostic evaluation.

Stroke is a main cause of disability and mortality worldwide. It has been reported that ischemic preconditioning (IP) has neuroprotective effects against stroke. This study aimed to verify the mechanism by which calcium-sensing receptor (Casr) inhibition-mediated M2 microglial transformation in the IP protects against stroke, which will provide a potential therapeutic target for stroke.

Middle cerebral artery occlusion (MCAO) rats and oxygen-glucose deprivation (OGD) neurons were used in this study. IP was induced via the transient MCAO and OGD methods. RNA sequencing (RNA-Seq) was used to explore the underlying key molecules. Western blotting and immunohistochemistry were performed to detect the expression of Casr and the M1 and M2 microglial markers. CCK8 was used to detect cell viability. The calcium concentration was detected via the use of Fluo-4 AM, a fluorescence probe. The Casr inhibitor NPS2143 and the Casr activator R568 were used to explore the role of Casr in M2 microglial transformation and neuroprotection.

We first revealed that IP induced M2 microglial transformation in ischemic injury. In addition, MCAO injury increased Casr expression and the calcium concentration, which was inhibited by IP. Furthermore, Casr activation inhibited the M2 microglial transformation induced by IP. Finally, we found that Casr inhibition improved the survival rate, alleviated neurological deficits, and reduced the infarct volume induced by MCAO.

We confirmed that Casr-related neuroprotection induced by IP is associated with the transformation of M2 microglia. These findings can be used to understand the protective mechanisms of IP against ischemic stroke.

To elucidate the regulatory mechanism of circRNAs in diabetic retinopathy.

Next-generation sequencing (NGS) was employed to identify circRNAs that are abnormally expressed in endothelial progenitor cells (EPCs) under hyperglycemia (HG) conditions. The regulatory mechanism and predicted targets of this circRNA were also studied via bioinformatics analysis, luciferase reporter assays, angiogenic differentiation experiments, flow cytometry, and RT-qPCR.

Circ-astrotactin 1 (circ-Astn1) expression was decreased in EPCs under HG conditions, and circ-Astn1 overexpres-

These findings suggest that circ-Astn1 promotes SIRT1 expression by sponging miR-138-5p. Circ-Astn1 over-

Chemoresistance, such as paclitaxel (PTX) resistance, has become a great obstacle in non-small cell lung cancer (NSCLC) treatment. The natural agent salidroside (SAL) has been shown to exert an antitumor effect on NSCLC. Nonetheless, it is unclear whether SAL can decrease the resistance of NSCLC to PTX.

PTX-resistant NSCLC cells (H1299/PTX and A549/PTX) were generated. Cell Counting Kit-8 (CCK-8) assay was used to detect cell viability. Colony formation assay and flow cytometry were utilized to assess cell proliferation and apoptosis, respectively. Immunofluorescence staining and TOP/FOP flash luciferase assay were employed to estimate β-catenin activation. Western blotting was implemented to estimate the protein levels of apoptosis-, proliferation-, and Wnt/β-catenin signaling-associated markers. A xenograft mouse model was established to investigate the impact of SAL on PTX resistance in vivo.

SAL increased PTX-induced suppression of proliferation and promoted apoptosis in PTX-resistant NSCLC cells.

SAL enhances the sensitivity of NSCLC cells to PTX by blocking the Wnt/β-catenin signal transduction.

Tumour cells in a hypoxic state are more invasive, have stronger self-renewal capabilities, and are difficult to treat because of their ability to promote tumour recurrence and metastasis. The glycolysis inhibitor 3-bromopyruvic acid (3-BrPA) can completely inactivate glycolytic enzymes at extremely low drug concentrations, thereby exerting a strong inhibitory effect on the glucose energy metabolism of tumor cells. Therefore, we tested the inhibitory effect of 3-BrPA on hepatocellular carcinoma cells (HepG2) in vitro; then, we used the VX2 liver cancer model to study the antitumour effect of 3-BrPA combined with interventional embolization on liver cancer.

In vitro, a CCK-8 assay was used to detect the inhibitory effect of different concentrations of 3-BrPA on HepG2 cells, and light microscopy confirmed that the HepG2 cells were completely dead. Western blotting was used to detect the expression of key proteins involved in apoptosis. A total of 30 New Zealand white rabbits were used to establish a liver cancer model and were randomly divided into 3 groups 2 weeks after tumor establishment: the control group was perfused with saline in the hepatic artery; the transcatheter arterial embolization (TAE) group was given TAE; and the experimental group was perfused with 3-BrPA combined with TAE. The tumor-bearing rabbits were killed one week after surgery. The tumor volume and tumor necrosis ratio were calculated via the histopathological examination.

In vitro, the inhibitory effect of 3-BrPA on HepG2 cells increased with increasing concentration. 3-BrPA (100 μmol/L) could induce the necrosis of HepG2 cells. Stimulation with 50 μmol/L 3-BrPA could activate the tumor cell apoptosis pathway. 3-BrPA combined with TAE treatment could significantly inhibit tumor growth and cause more complete tumor necrosis.

Hepatocellular carcinoma (HCC), a lethal cancer with high global mortality, may be targeted through ferroptosis, an iron-dependent form of cell death. Despite its potential, the prognostic value of ferroptosis in HCC is underexplored.

Our study leveraged single-cell and bulk sequencing datasets to identify ferroptosis-related genes and developed a prognostic model via Cox and LASSO regression analyses. Survival and mutation analyses led to the creation of a nomogram for predicting patient prognosis. Furthermore, we investigated the role of GRINA, a ferroptosis-related gene, through functional assays, including cell proliferation, colony formation, and metastatic potential analyses. We also assessed mitochondrial abnormalities, intracellular iron, and ROS levels in GRINA-knockdown cells.

The developed ferroptosis-related model classified HCC patients into risk groups, revealing notable survival disparities. High-risk patients presented increased immune checkpoint gene expression. The nomogram revealed robust prognostic accuracy. Additionally, we found that GRINA suppression reduced HCC cell proliferation, colony formation, and metastatic potential. Cells with GRINA knockdown presented mitochondrial abnormalities and increased intracellular iron and ROS levels.

By analysing multiomics sequencing data, we established a connection between ferroptosis-related risk groups and the tumor immune microenvironment. These findings provide novel insights into the role of ferroptosis in HCC and suggest that GRINAinhibition is a potential therapeutic strategy, leading to mitochondrial damage and the induction of ferroptosis in HCC cell lines.

Close reduction and internal fixation have gained popularity for the treatment of pelvic fractures. However, the closed reduction of bilateral displaced posterior pelvic ring disruption is a great challenge even for the most experienced surgeon. In this study, we describe in detail a novel unlocking closed reduction technique (UCRT) frame that allows strong traction for bilateral posterior pelvic ring displacement and presents preliminary clinical outcomes.

We retrospectively reviewed 32 patients with bilateral displaced posterior pelvic ring disruptions (AO/OTA 61-C2 and C3) who were initially treated with this technique between July 2017 and July 2022. According to the AO/OTA classification, there were 9 cases (28.12%) of 61-C2, and 23 cases (71.88%) of 61-C3. There were 11 males, 21 females, with an average age of 38.1 years. The interval from injury to operation was 4-27 days, with a cut-off of 12.5 days (receiver operating characteristic curve). Operative time, blood loss, and postoperative radiographic findings were recorded. The functional outcomes and complications were followed.

A total of 30 (93.8%) patients achieved successful closed reduction, whereas 2 required open reduction. The successful closed reduction rate was 95.5% (21/22) in patients whose injury-to-operation time was less than 12.5 days. The vertical displacement percent correction of the obviously displaced hemipelvis was 70.20% ± 16.79% on average. The average degree of pelvic deformity correction was 64.86% ± 17.71%. Thirty patients were followed up for at least 12 months (12-36 months), and no complications of nonunion or redisplacement were observed. The Matta-Tornetta scoring standard revealed that the excellent (25/30) and good (4/30) rate was 96.7%. The Majeed clinical efficacy score revealed that the overall excellent and good rate was 100%. One patient had INFIX-related infection, and 2 reported numbness in the lateral thigh. The numbness was improved after INFIX removal.

This study presents an updated technique for closed reduction using a UCRT frame for bilateral posterior pelvic ring disruption, which has been shown to be effective, as indicated by excellent surgical and functional outcomes.

This study aimed to analyse the trend of the mental disorder spectrum in children and adolescents from 2014 to 2022 in one city in Central China and to provide actionable recommendations for the prevention and management of mental disorders.

In this hospital-based retrospective study, we utilized child and adolescent medical records data from the Wuhan Mental Health Center from January 2014 to December 2022 and examined the top 5 mental disorders (schizophrenia, depressive episode, bipolar disorder, pervasive developmental disorder, and unspecified mood disorder) that accounted for the overall proportion of patients admitted. The rank and proportion of these mental disorders, demographic characteristics and disease indicators were analysed.

There was a significant upwards trend in the number of children and adolescents diagnosed with mental disorders over the past 9 years, with a sharp decline in 2020 due to the COVID-19 pandemic, followed by a rebound in 2021 and a sustained level above prepandemic figures by 2022. The average age of hospitalization decreased significantly from 20.7 to 16.2 years, with a marked increase in the 12-17-year-old age group. The proportion of female hospitalizations increased from 39.2% to 55.2%, with a corresponding decrease in male hospitalizations. There was a notable decrease in the proportion of schizophrenia cases and an ascent of depressive episode to the most prevalent position.

This study emphasizes the critical need for targeted interventions and resources for severe mental disorders in children and adolescents and the importance of early detection and management of mental disorders to mitigate long-term effects on well-being and development.