Guohai Su

In this study, we identified novel pro-angiogenic peptides from Spirulina and elucidated their molecular mechanisms. Among the three fractions (A, B, and C) purified from the Spirulina protein extract by RP-HPLC, fraction B displayed the most potent pro-angiogenic activity. Through LC-MS/MS analysis, bioinformatics screening, and molecular docking, 20 candidate peptides were selected. In zebrafish models, five of these peptides, MFDCLR, MDMWGK, MNPGCR, MYDNFCK, and MPGLGR, significantly stimulated subintestinal vessel plexus (SIVP) growth and rescued intersegmental vessel (ISV) injury induced by Vatalanib (PTK787). Cellular experiments further showed that the five peptides reversed VEGFR tyrosine kinase inhibitor II (VRI)-induced impairments in proliferation, migration, and tube formation, with MDMWGK exhibiting the most pronounced pro-angiogenic effect. Moreover, the Matrigel plug assay confirmed that MDMWGK promoted extensive neovascularization in vivo . Subsequent mechanistic investigations revealed that the pro-angiogenic effect of MDMWGK was associated with activation of the VEGFA/PI3K-Akt signaling pathway, as evidenced by increased phosphorylation of PI3K and Akt. Collectively, this study provides an integrated screening strategy for discovering bioactive peptides from Spirulina and establishes a theoretical basis for developing pro-angiogenic agents.

Background: To compare the accuracy of coronary artery calcium scores (CACSs) automatically measured by two artificial intelligence (AI) systems on nonelectrocardiogram (ECG)-gated chest computed tomography (CT) and to investigate the relationship between CACS and the degree of coronary artery stenosis. Materials and Methods: A retrospective study was conducted on 182 patients who underwent both ECG-gated Coronary computed tomography angiography (CTA) and non-ECG-gated chest CT. Images from all patients were processed using postprocessing software and two AI systems (Software A/B). The manually measured CACS by experienced physicians using ECG-gated Coronary CTA was used as the gold standard. The agreement between two AI systems and the gold standard was assessed using the intraclass correlation coefficient (ICC) and Bland–Altman analysis. In addition, Spearman’s correlation analysis was performed to evaluate the relationship between CACS and the degree of coronary artery stenosis. Results: Both AI systems demonstrated high ICCs for CACS measurement (0.90, 95% confidence interval [CI]: 0.871–0.926 for Software A; 0.96, 95% CI: 0.943–0.968 for Software B). The mean differences (95% limits of agreement) were 23.59 ± 442.35 for Software A and −80.35 ± 292.99 for Software B. Both systems showed good agreement in CACS measurement, with Software B exhibiting higher accuracy than Software A. Spearman’s correlation analysis revealed weak-to-moderate positive correlations between CACS measured by different methods and the degree of coronary artery stenosis ( r = 0.151–0.560, P < 0.05) across all coronary branches. Conclusion: The two AI-based CACS systems, when applied to nongated chest CT, demonstrated consistency with manually measured CACS from ECG-gated coronary CTA. Software B showed superior accuracy compared to Software A. The correlation between CACS and the degree of vascular stenosis is influenced by vascular remodeling patterns, with positive remodeling reducing its consistency. Therefore, a comprehensive assessment of vascular stenosis should integrate vascular remodeling patterns and other diagnostic indicators.

Cardiac fibrosis is a pivotal pathological process driving adverse cardiac remodeling and a defining feature of end-stage heart disease. Nicotine, a princi

The early and accurate diagnosis of acute myocardial infarction (AMI) remains a significant clinical challenge. To this end, we profiled the surface proteo

The emergence of antibiotic resistance in Helicobacter pylori led to a sharp decline in eradication rates, but there are limited data regarding the prevalence and genetic mechanisms of antibiotic resistance in Shandong. This study aims to assess the prevalence and molecular mechanisms of H. pylori antibiotic resistance to commonly used antibiotics in Shandong populations. Antimicrobial susceptibility testing was performed for clarithromycin, levofloxacin, metronidazole, tetracycline, rifampicin, amoxicillin, azithromycin, and moxifloxacin using E-test method. PCR amplified resistance-associated genes for all the strains, and 32 were whole-genome sequenced. 62 H. pylori strains were obtained and the infection rate was 30.1% (62/206). No resistance to amoxicillin was observed. Two and four strains were resistant to tetracycline and rifampicin, respectively, and no resistance-associated mutations were found in the 16S rRNA and rpoB genes. The resistance rates of azithromycin, clarithromycin, levofloxacin, and moxifloxacin were 56.45% (35/62), 33.87% (21/62), 48.39% (30/62), and 56.45% (35/62), respectively. The percentages of dual, triple, and quadruple resistance were 32.26% (20/62), 24.19% (15/62), and 1.61% (1/62), respectively, and only one isolate was resistant to quadruple antibiotics. Phenotypic resistance associated with the A2143G mutations in 23S rRNA for azithromycin and clarithromycin (kappa coefficient, 0.808 and 0.671, respectively), and gyrA mutations (N87K/N87I/D91G/D91Y/D91N) for levofloxacin and moxifloxacin (kappa coefficient, 0.526 and 0.442, respectively). Metronidazole resistance was observed in 43.55% (27/62) isolates and most of the metronidazole-resistant strains had truncated rdxA and frxA. The detection of a truncated rdxA gene correlated with phenotypic resistance results (kappa coefficient, 0.728). There was no association between whole-genome phylogeny and antibiotic resistance profiles. Our results revealed the high resistance rates and multiple resistance of H. pylori to commonly used antibiotics. Continued surveillance of H. pylori antibiotic resistance is crucial in Shandong to establish effective eradication therapy for this population.

Background: In recent decades, the escalating prevalence of obesity has contributed to a significant increase in the global burden of disease, with cardiovascular diseases (CVDs) emerging as the leading cause among all diseases attributable to high body-mass index (BMI). Utilizing global burden of disease (GBD) dataset from 1990 to 2021, we conducted a comprehensive analysis of the global, regional, and national trends in deaths and disability-adjusted life years (DALYs) attributable to CVDs caused by high BMI. Age-standardized mortality rate (ASMR) and age-standardized DALY rate (ASDR) were also investigated. Furthermore, we examined the associations of gender, age, and socio-demographic index (SDI) with the burden of CVDs attributable to high BMI. Finally, we assessed the evolution of health inequalities across countries and projected the global deaths and DALYs due to high BMI-related CVDs over the next two decades.Methods: The absolute numbers and the rates of age-standardized death, Disability-Adjusted Life Years (DALYs) per 100,000 people due to high BMI-related CVDs between 1990 and 2021 were extracted from GBD 2021. The estimated annual percentage changes (EAPCs) of high BMI-related CVDs disease burdens were calculated under the GBD's comparative risk assessment framework. Additionally, the disease burden prediction of the high BMI-related CVDs from 2022 to 2041 was performed using the bayesian age-period-cohort (BAPC) statistical model.Results: In 2021, high BMI-related CVDs accounted for 1.90 million deaths globally, representing an increase of 120.63% compared to 1990, with DALYs rising by 115.47% over the same period. Notably, while ASMR and ASDR among male showed no decline, female experienced 11.30% reduction in ASMRs and 6.12% reduction in ASDR. The burden was disproportionately borne by middle-aged and older populations across all age groups. Global health inequalities related to high BMI-related CVDs demonstrated a narrowing trend from 1990 to 2010, followed by a reversal into a negative correlation and continued to widen until 2021. Looking ahead, the burden of high BMI-related CVDs is projected to rise significantly due to population growth, the increasing prevalence of obesity, and aging populations.Conclusion: The results indicate that from 1990 to 2021, the burden of CVDs caused by high BMI has significantly increased. Particular attention should be directed toward middle and low-middle SDI regions. To mitigate this burden, it is imperative to implement public health strategies that emphasize education and awareness regarding the correlation between high BMI and CVDs. Policies promoting healthy dietary habits and regular physical activity are essential for reducing the future impact of high BMI-related cardiovascular morbidity and mortality. Such measures are not only urgently needed but also offer substantial long-term benefits for global health.

Background: The neutrophil to high-density lipoprotein cholesterol ratio (NHR) has been proposed as a potential marker for predicting cardiovascular events. However, its prognostic role following percutaneous coronary intervention (PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI) remains unclear. This study aimed to evaluate the predictive value of NHR for left ventricular remodeling (LVR) and long-term outcomes in STEMI patients post-PCI.Methods: This retrospective study included 299 STEMI patients who underwent PCI and were followed for 24 months post-procedure. Echocardiography was performed upon admission and at 6 months post-myocardial infarction (MI). LVR was defined as an increase in left ventricular diastolic volume (LVEDV) of at least 20% from baseline. Based on their VR status, patients were divided into LVR (n = 81) and non-LVR (n = 218) groups and clinical data were compared. A weighted logistic regression model was used to study the correlation between NHR and LVR. Weighted Cox proportional risk models were used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs) for major adverse cardiovascular events (MACE). And the NHR was analyzed using receiver operating characteristic (ROC) curves to predict the occurrence of postoperative LVR and MACE in STEMI patients. Restricted cubic spline (RCS) analysis was used to explore the linear or non-linear relationship between NHR and LVR or MACE. Cox survival analysis was used to assess the relationship between NHR, LVR and survival time.Results: Among the 299 STEMI patients enrolled in the study, LVR was observed in 81 patients after 24 months of follow-up. The LVR group had significantly higher NHR levels compared to the non-LVR group (8.19 ± 1.95 vs. 6.23 ± 1.91, P < 0.001). After adjusting for potential confounders, a significant positive correlation was found between NHR and LVR. Each standard deviation increase in NHR was associated with a 43% higher risk of MACE (HR: 1.43, 95% CI: 1.25–1.64, P < 0.001). ROC curve analysis demonstrated that NHR could predict both LVR (AUC: 0.762) and MACE (AUC: 0.722). An NHR cut-off value of >8.13 was significantly linked to an increased risk of MACE (HR: 4.30, 95% CI: 2.41–7.69).Conclusions: NHR is an independent predictor of LVR and MACE after PCI in STEMI patients. Monitoring NHR may aid in identifying high-risk patients early, facilitating individualized treatment.

Nicotine-induced impairment of autophagic flux promotes the onset of myocardial remodelling, thereby exacerbating heart failure. In this study, we investigated the role and molecular mechanisms of the transcription factor CDX1 in cardiac fibroblasts (CFs) activation and cardiomyocyte hypertrophy induced by nicotine. We found that CDX1 expression was increased in response to nicotine. However, a decrease in CDX1 further exacerbated the nicotine-induced blockade of autophagic flux, thereby aggravating CFs activation and cardiomyocyte hypertrophy. This effect was attributed to the suppression of the autophagic regulator LAPTM4B transcription by CDX1 and the subsequent activation of the mTOR pathway. In contrast, CDX1 overexpression promoted LAPTM4B expression, resulting in the opposite effect. In conclusion, our study demonstrated that CDX1/LAPTM4B axis could alleviate nicotine-induced autophagy flux impairment by inhibiting mTORC1 pathway activation, thereby alleviating CFs activation and cardiomyocyte hypertrophy, and exerting cardioprotective functions.