Objective To analyze the epidemiological characteristics and immunization history of pertussis cases in Yichang City, Hubei Province from 2018 to 2023. Methods Data on the incidence and immunization history of pertussis cases were collected in Yichang City from 2018 to 2023, and the epidemiological characteristics was analyzed and described. Results A total of 109 cases of pertussis were reported in Yichang from 2018 to 2023, and the annual average reported incidence rate was 0.45/100,000. The incidence rate reported in each year was between 0～1.58/100,000. The area with the highest annual reported incidence rate was Xiling District (1.19/100,000). There was a statistically significant difference in the incidence rate between different years (χ²=208.26, P < 0.001). The annual reported incidence rate showed a significant increasing trend (χ² trend =125.71, P < 0.001). The ratio of male to female cases was 1.22. There was no significant difference in the annual reported incidence rates between males and females (χ²=0.85, P=0.36). Children aged 3-9 years accounted for 60.55%. Students and scattered children accounted for 45.87% and 36.70%, respectively. Before the onset of the disease, 72.48% had a history of immunization with pertussis-containing vaccine, and 27.52% had no history of immunization. The shortest interval between the last dose of pertussis-containing vaccine and the onset of the disease was 8 days, the longest was 4057 days, and the median was 1882 days. Conclusion From 2018 to 2023, the reported incidence of pertussis in Yichang City has been on the rise, with the majority of cases occurring in children and students under the age of 9. It is recommended to strengthen pertussis disease monitoring.

Iron overload is strongly associated with heart disease. Ferroptosis is a new form of regulated cell death indicated in cardiac ischemia-reperfusion (I/R) injury. However, the specific molecular mechanism of myocardial injury caused by iron overload in the heart is still unclear, and the involvement of ferroptosis in iron overload-induced myocardial injury is not fully understood. In this study, we observed that ferroptosis participated in developing of iron overload and I/R-induced cardiomyopathy. Mechanistically, we discovered that Parkin inhibited iron overload-induced ferroptosis in cardiomyocytes by promoting the ubiquitination of long-chain acyl-CoA synthetase 4 (ACSL4), a crucial protein involved in ferroptosis-related lipid metabolism pathways. Additionally, we identified p53 as a transcription factor that transcriptionally suppressed Parkin expression in iron-overloaded cardiomyocytes, thereby regulating iron overload-induced ferroptosis. In animal studies, cardiac-specific Parkin knockout mice (Myh6-CreER ^T2 /Parkin ^fl/fl ) fed a high-iron diet presented more severe myocardial damage, and the high iron levels exacerbated myocardial I/R injury. However, the ferroptosis inhibitor Fer-1 significantly suppressed iron overload-induced ferroptosis and myocardial I/R injury. Moreover, Parkin effectively protected against impaired mitochondrial function and prevented iron overload-induced mitochondrial lipid peroxidation. These findings unveil a novel regulatory pathway involving p53-Parkin-ACSL4 in heart disease by inhibiting of ferroptosis.

Acetaminophen (APAP) is the primary cause of drug-induced acute liver failure. Ovarian tumor deubiquitinase 6A (OTUD6A), a recently discovered deubiquitinase of the OTU family, has been primarily studied in tumor contexts. However, its role in APAP-induced liver injury (AILI) remains unclear. Therefore, this study aimed to investigate the involvement of OTUD6A in the pathogenesis of AILI. Our findings demonstrated a substantial upregulation of OTUD6A in both the liver tissue and isolated hepatocytes of mice following APAP stimulation. OTUD6A knockout exacerbated APAP-induced inflammation, hepatocyte necrosis, and liver injury, whereas OTUD6A overexpression alleviated these pathologies. Mechanistically, OTUD6A directly interacted with the enhancer of zeste homolog 2 (EZH2) and selectively removed K48-linked polyubiquitin chains from EZH2, enhancing its stability. This resulted in increased protein levels of EZH2 and H3K27me3, as well as reduced endoplasmic reticulum (ER) stress and cell death in hepatocytes. Collectively, our research uncovers a novel role for OTUD6A in mitigating APAP-induced liver injury by promoting EZH2 stabilization.

Objective To investigate the clinical characteristics and outcomes of Coronavirus Dis-ease 2019 in immunocompromised hosts.Methods A retrospective analysis was conducted on the clinical data of 230 hospitalized patients diagnosed with Coronavirus Disease 2019 at Nanjing Yimin Hospital from December 2022 to November 2023.The patients were divided into three groups based on their immune status:immunocompromised group(n=59),relatively immunocompromised group(n=129),and immunocompetent group(n=42).The clinical characteristics(such as clinical manifesta-tions,imaging features,and laboratory examinations)and outcomes(such as length of hospital stay and in-hospital mortality)were compared among three groups.Results Compared with there latively immunocompromised and immunocompetent groups,the immunocompromised group showed no obvious specific clinical manifestations.However,the proportions of patients with symptoms such as cough and expectoration were lower,and the occurrences of symptoms such as myalgia and fatigue were less fre-quent in the immunocompromised group(P＜0.05).The chest CT findings in the immunocompro-mised group also lacked specific changes,mainly presenting as subpleural ground-glass opacities and consolidations with multilobar distribution,but fibrotic changes were more common(P＜0.05).The proportion of patients with decreased absolute lymphocyte counts in the immunocompromised group was higher than that in the immunocompetent group,and the proportion of patients with elevated procalcitonin levels was higher than that in the other two groups(P＜0.05).The proportion of severe case sand the length of hospital stay in the immunocompromised group were higher and longer than those in the relatively immunocompromised and immunocompetent groups(P＜0.05).The in-hospital mortality rates in the immunocompromised,relatively immunocompromised,and immunocompetent groups were 10.17％,6.98％,and 2.38％,respectively,with no statistically significant difference(P＞0.05).Conclusion After Coronavirus Disease 2019,immunocompromised hosts do not show obvi-ous clinical and imaging features.However,they have a prolonged length of hospital stay,a signifi-cantly higher proportion of severe cases,and a tendency towards increased in-hospital mortality,which should be given high clinical attention.

Objective To assess the therapeutic efficacy of low-intensity focused ultrasound(LIFU)on knee arthrofibrosis in rats and explore its underlying mechanisms.Methods Fifteen male SD rats(8 weeks old,weighing 250～300 g)were randomly divided into a blank control group,a model group,and an ultrasound treatment group,with 5 animals in each group.Rat model of knee joint stiffness was established in the model and ultrasound treatment group.The rats in the ultrasound group received LIFU intervention(frequency:1 MHz,power:1.5 W,20 min per session,5 times/week)for 4 weeks.The knee ranges of motion(ROM,flexion and extension)were measured in all 3 groups at 0,14 and 28 d after intervention.Histological analysis was conducted for the morphological changes in the posterior capsular area of the knee.After the synovial fibroblasts were primary isolated from rat knee joints,the cells were divided into blank control,LIFU,TGF-β(10 ng/mL),and TGF-β+LIFU groups.Changes in fibrosis-related indicators and the TGF-β/Smad signaling pathway were assessed in each group.Results In the animal experiments,LIFU intervention for 14 d resulted in significantly improved flexion-extension ROM in knee joints when compared with the rats in the model group(P<0.05),and the improvement was more obvious at 28 d after intervention(P<0.05).After 28 d of LIFU intervention,the fibrosis of the posterior capsule of the knee joint was notably improved in the ultrasound group than the model group,and the expression levels of fibrosis-related indicators(α-SMA,TGF-β)were decreased(P<0.05).In the cellular experiments,the TGF-β group exhibited remarkable up-regulation of fibrosis-related molecules(α-SMA,COL1A1,COL3A1)at both protein and mRNA levels(P<0.05),and activation of the TGF-β/Smad signaling pathway when compared to the blank control group.While LIFU intervention inhibited the expression of TGF-β-induced upregulation of fibrotic indicators(α-SMA,COL1A1,COL3A1)and the activation of TGF-β/Smad signaling pathway(P<0.05).Conclusion LIFU can effectively improve knee arthrofibrosis in rats,which potentially through the inhibition of fibroblast activation and modulation of the TGF-β/Smad signaling pathway.

This article introduces the novel conceptual framework of small vulnerable newborns (SVN) and delineates three classification approaches. It further analyzes regional disparities in SVN prevalence and examines complex contributing factors encompassing environmental influences, maternal health status, and socioeconomic determinants. Finally, the discussion focuses on SVN management and preventive strategies, emphasizing the critical importance of preconception/prenatal care, nutritional supplementation, and targeted disease interventions in reducing SVN incidence.

Objective:To compare the sustained virological response (SVR) and viral recurrence in patients with chronic hepatitis C (CHC) after antiviral treatment, and to further analyze the influencing factors of liver-related events (LRE).Methods:This was a retrospective cohort study. A total of 1 844 CHC patients who visited the Department of Infectious Diseases of Hainan General Hospital from January 1st, 2013 to December 31st, 2022 were included. After screening, 891 patients were selected and divided into direct-acting antiviral agent (DAA) treatment group, interferon treatment group and non-antiviral treatment group based on different intervention measures. Propensity score matching was performed, and SVR and viral recurrence were compared among the three groups. Statistical analysis was performed using the chi-square test, and multivariate Cox regression analysis was used to evaluate the risk factors for LRE.Results:The confirmed CHC patients showed an increasing trend year by year (average annual change percentage=19.97%, 95% confidence interval ( CI) 10.46% to 30.30%, t=4.32, P<0.001). After propensity score matching, the total sample size of 891 CHC patients was 451, including 100 in the interferon treatment group, 311 in the DAA treatment group, and 40 in the non-antiviral treatment group. In the interferon treatment group, 89 cases (89.00%) achieved SVR and nine cases (9.00%) had recurrence. In the DAA treatment group, 306 cases (98.39%) achieved SVR and 10 cases (3.22%) had recurrence. The differences were statistically significant ( χ2=17.84 and 6.22, respectively, both P<0.05). Cox multivariate regression analysis showed that age (hazard ratio ( HR)=1.065, 95% CI 1.028 to 1.104, P<0.001), alcohol consumption ( HR=3.034, 95% CI 1.302 to 7.071, P=0.010) were independent risk factors for LRE in CHC patients, while albumin ( HR=0.858, 95% CI 0.802 to 0.917, P<0.001), DAA treatment ( HR=0.267, 95% CI 0.103 to 0.692, P=0.007) were protective factors. In CHC patients receiving antiviral treatment, diabetes ( HR=6.719, 95% CI 2.242 to 20.137, P<0.001), total bilirubin ( HR=1.111, 95% CI 1.054 to 1.171, P<0.001) and viral recurrence ( HR=4.646, 95% CI 1.322 to 16.321, P=0.017) were independent risk factors for LRE. Conclusions:Compared with interferon treatment, DAA treatment has a significantly higher SVR rate and a lower recurrence rate. Age and alcohol consumption are independent risk factors for LRE, while higher albumin levels and DAA treatment are protective factors. In CHC patients receiving antiviral treatment, diabetes, viral recurrence, and total bilirubin are independent risk factors for LRE.

Objective To establish a high-throughput HPLC method for the simultaneous determination of 11 common antibacterial agents in acyclovir eye drops and to evaluate the quality and safety of the antibacterial agents in 42 batches of national drug inspection samples.Methods Gradient elution was performed on a Kromasil 100-5-C18(4.6 mm×250 mm,5 μm)column with acetonitrile-5 mmol·L-1 ammonium acetate aqueous solution(containing 1%triethylamine,pH adjusted to 4.5 by acetic acid)as the mobile phase.The detection wavelength was 262 nm.Results Good linear relationships were obtained for 11 antibacterial agents(r≥0.999 9).The average recovery range was 98.2%-101.8%,and the RSD was 0.7%-2.7%(n=9).As revealed by the systematic analysis of 42 batches of national drug inspection samples,some batches of samples were detected with out-of-prescription antibacterial agents 4-hydroxybenzoic acid and ethylparaben,and the results were 0.02-49 μg·mL-1.This indicated that ethylparaben degradation and colinear production pollution were the two major risk sources.Conclusions The method is accurate,sensitive,and specific and can be used for the qualitative and quantitative detection of antibacterial agents in acyclovir eye drops.Besides,some products have degradation of antibacterial agents and incomplete cleaning during co-linear production.It is still essential to further reinforce product quality control.

Retinopathy of prematurity (ROP) is a type of proliferative retinal disease occurring in premature, low birth weight infants, and is one of the most common blinding diseases in infants and young children.In recent years, anti-vascular endothelial growth factor (VEGF) therapy has shown good effect in treating ROP, and has become the preferred treatment for some ROP.However, the anti-VEGF treatment of ROP still faces the bottleneck of uncertain treatment timing and lack of objective criteria for efficacy evaluation.In recent years, artificial intelligence (AI) has not only been widely used in the screening and diagnosis of ROP, but also has made progress in evaluating treatment timing, therapeutic effect and follow-up plan in anti-VEGF treatment of ROP.At the same time, AI also shows potential in the prediction of efficacy and disease progression after anti-VEGF treatment of ROP.Therefore, based on recent relevant studies at home and abroad, this article reviews and looks forward to the application of AI in the evaluation of anti-VEGF treatment of ROP.

AIM:To investigate the effects of macrophage galactose-type lectin 1(Mgl1)gene deletion on he-matopoietic stem/progenitor cells(HSPCs)under steady-state conditions and inflammation.METHODS:Mice were di-vided into a control group(wild-type)and an experimental group(Mgl1 gene-deleted).Flow cytometry was used to ana-lyze the proportions of various hematopoietic cell lineages in the peripheral blood and bone marrow of both groups,assess-ing the impact of Mgl1 gene deletion on steady-state hematopoiesis(n=3～4).Transplantation and colony-forming assays were utilized to evaluate the effects of Mgl1 gene deletion onthe repopulation capacity and colony-forming ability of HSPCs(n=5).The LPS-induced inflammation model was employed to examine the effects of Mgl1 gene deletion on the inflamma-tory response of HSPCs both in vitro and in vivo(n=5～8).Western blot and RT-qPCR were conducted to analyze the alter-ations in signaling pathways regulated by Mgl1 in the inflammatory response of HSPCs(n=3).RESULTS:(1)Mgl1 gene deletion had no significant effecton steady-state hematopoiesis(P>0.05).(2)Mgl1 gene deletion promoted inflam-mation-induced cell differentiation of HSPCs(P<0.01).(3)Mgl1 gene deletion accelerated the exhaustion of HSPCs un-der prolonged inflammatory conditions(P<0.01).(4)Mgl1 was found to regulate the inflammatory response of HSPCs via the NF-κB signaling pathway.CONCLUSION:Mgl1 gene deletion enhances the inflammatory response of HSPCs via the NF-κB signaling pathway.