The Pharmacovigilance Guidelines for Clinical Application of Oral Chinese Patent Medicines （hereinafter referred to as the Guidelines） is first specialized in the field of drug safety for oral Chinese patent medicines （OCPMs） in China. Rooted in China's healthcare context， the Guidelines address the unique usage patterns and risk characteristics of OCPMs， filling a regulatory gap in the pharmacovigilance framework specific to this category. To facilitate accurate understanding and effective implementation of the Guidelines， and to promote the standardized development of pharmacovigilance practices for OCPMs， this study offered a systematic interpretation based on its three core components. In the domain of risk monitoring and reporting， the paper analyzed the rationale for multi-source information integration and clarified the criteria for identifying key products and target populations for intensive monitoring. Regarding risk assessment， the Guidelines were examined from three dimensions of formulation components， medication behaviors， and population to address complex safety issues arising from medicinal constituents， irrational use， and individual susceptibility. In the area of risk control， the analysis focused on context-based interventions and dynamic closed-loop management strategies， exploring practical pathways to shift from passive response to proactive risk mitigation. Furthermore， this paper evaluated the applied value of the Guidelines and identified implementation challenges， such as insufficient capacity at the primary-care level and limited digital infrastructure. In response， the study proposed optimization strategies including establishing a dynamic updating mechanism， strengthening training at the grassroots level， and incorporating artificial intelligence to enhance pharmacovigilance capacity. This interpretation aims to provide actionable insights for marketing authorization holders （including manufacturers）， pharmaceutical distributors， healthcare institutions， and research organizations， ultimately supporting the establishment and refinement of a full lifecycle pharmacovigilance system for OCPMs.

Objective To develop a symptom and function assessment scale for patients after Nuss procedure for pectus excavatum and to test its reliability and validity. Methods Following the principles and procedures of patient-reported outcome (PRO) scale development stipulated by the U.S. Food and Drug Administration, an initial draft was formed through literature analysis, qualitative interviews, and Delphi expert consultation. The preliminary draft was used to conduct a pre-survey on patients who underwent Nuss procedure for pectus excavatum at Guangdong Provincial People's Hospital, and the reliability and validity of the scale were tested. Results A preliminary PRO-based symptom and function scale was constructed, covering two domains: symptoms and impact on daily functions. The symptom dimension included six items: chest tightness, palpitations, pain, shortness of breath, foreign body sensation of the steel plate, and distress; while the impact on daily functions included four items: difficulty in getting out of bed or lying down, raising arms, bending over, and standing or sitting for a long time. A total of 73 patients who underwent Nuss procedure for pectus excavatum were included in the questionnaire survey, with 70 valid questionnaires collected, including 64 males and 6 females, with 56 patients aged 12-17 years and 14 patients ≥18 years. Through exploratory factor analysis, two common factors were extracted, with a cumulative variance contribution rate of 70%. The Cronbach’s α coefficient of the scale was 0.917. Conclusion The scale developed in this study has good reliability and validity, high reliability and stability, and can be used as an evaluation tool for the recovery status of patients after Nuss procedure for pectus excavatum.

Neurodegenerative diseases (NDs), particularly Alzheimer’s disease (AD) and Parkinson’s disease (PD), and cardiovascular diseases (CVDs), including heart failure (HF) and coronary artery disease (CAD), are major chronic disorders associated with population aging. Their frequent coexistence in clinical practice suggests that they may not progress independently, but may instead be linked through bidirectional pathological communication within the brain-heart axis. Epidemiological evidence underscores this clinical burden: systematic reviews and meta-analyses have reported pooled relative risks for dementia of approximately 1.27 among individuals with a history of CAD and 1.60 among those with HF, while the pooled prevalence of cognitive impairment and dementia in patients with HF has been estimated at approximately 41.42% and 19.79%, respectively. This review synthesizes current evidence on the mechanistic links, disease-state manifestations, biomarkers, and potential therapeutic strategies involved in the comorbidity between NDs and CVDs from the perspective of the brain-heart axis. The brain and heart communicate through autonomic, neuroendocrine, neuroimmune, vascular, and humoral pathways. Sympathetic activation, parasympathetic withdrawal, vagal dysfunction, cerebral hypoperfusion, endothelial injury, blood-brain barrier (BBB) alterations, peripheral immune activation, and circulating inflammatory mediators may jointly contribute to cross-organ pathological signaling. Oxidative stress and inflammatory response are not specific to the brain-heart axis; rather, they may act as candidate amplifying processes within this network. Mitochondrial dysfunction and NADPH oxidase activation can increase the generation of reactive oxygen species and reactive nitrogen species, which may activate nuclear factor-κB, the NLRP3 inflammasome, and mitogen-activated protein kinase/c-Jun N-terminal kinase signaling. These pathways can promote the release of interleukin-1β, interleukin-6, tumor necrosis factor‑α, and other inflammatory mediators, which may in turn aggravate mitochondrial injury, endothelial dysfunction, immune cell activation, and further oxidant generation. Cytokines, chemokines, oxidized lipids, mitochondrial DNA, damage-associated molecular patterns, and extracellular vesicles may transmit these signals between the cardiovascular and central nervous systems, whereas autonomic reflexes provide an additional route for bidirectional amplification. Distinct disease states illustrate different manifestations of this network. The association between AD and CVDs may involve vascular risk factors, impaired amyloid-β clearance, abnormal cholesterol homeostasis, cerebral microvascular injury, neuroinflammation, and endothelial dysfunction. HF-related cognitive impairment may be linked to reduced cardiac output, recurrent cerebral hypoperfusion, hypoxia-related signaling, BBB dysfunction, circulating inflammation, and impaired autonomic feedback. In PD, cardiovascular autonomic dysfunction and abnormalities in heart rate and blood pressure regulation may interact with vascular injury, reduced cerebral perfusion, inflammation, and oxidative stress. However, the relationship between PD and CAD remains heterogeneous and may be modified by age, ethnicity, medication use, metabolic factors, and coexisting diseases. Biomarker evaluation should therefore move beyond isolated indicators. Traditional markers, including malondialdehyde, superoxide dismutase, glutathione, C-reactive protein, and interleukin-6, reflect systemic oxidative or inflammatory burden but lack sufficient specificity to distinguish primary neurodegeneration, cardiovascular injury, or a comorbid state involving both. Greater clinical value may be obtained from cross-system panels that combine oxidative stress and inflammatory markers with cardiac stress or injury biomarkers, such as N-terminal pro-B-type natriuretic peptide; glial or neuronal biomarkers, such as glial fibrillary acidic protein and neurofilament light chain; BBB- or endothelial injury-related biomarkers; and omics-derived candidates, including microRNAs, long non-coding RNAs, DNA methylation signatures, metabolites, and proteins. Multi-omics integration and artificial intelligence-assisted analysis may support risk stratification, disease monitoring, and prediction of treatment response. However, these approaches require standardized analytical platforms, validation in independent cohorts, and careful distinction between associative findings and causal mechanisms. Potential interventions include antioxidant, anti-inflammatory, mitochondria-targeted, and multi-target combination strategies, together with emerging approaches such as nanodelivery, CRISPR/Cas9- or CRISPR/dCas9-based regulation, mesenchymal stem cell-mediated mitochondrial transfer, and ergothioneine supplementation. Nevertheless, most available evidence is indirect, preclinical, or derived from other disease indications, and no single drug or technology can currently be regarded as specific to brain-heart axis comorbidity. The clinical relevance of these strategies will depend on whether they can be matched to dominant pathological phenotypes and improve both neurological and cardiovascular outcomes. Overall, comorbidity between NDs and CVDs is more appropriately understood as a heterogeneous cross-organ regulatory network than as a disorder driven by a single pathway. Future research should prioritize multicenter longitudinal cohorts, standardized clinical phenotyping, validation of cross-system biomarker panels, and mechanism-guided interventions in clearly defined patient subgroups, with integrated assessment of cognitive function, cardiovascular events, quality of life, long-term safety, and treatment response.

Objective To investigate the relationship between chromosomal karyotypes and reproductive factor levels in peripheral blood and adverse pregnancies in women.Methods A total of 105 pregnant women who received prenatal care and delivered at Yulin Hospital,the First Affiliated Hospital of Xi'an Jiaotong Uni-versity and Yulin Traditional Chinese Medicine Hospital from January 2020 to June 2024 were selected as the research subjects.Through the follow-up observation of pregnant women,there were 29 cases of pregnant women with adverse pregnancies(adverse pregnancy group)and 76 cases of pregnant and parturient women with normal pregnancies(good pregnancy group).The karyotypes of peripheral blood chromosomes and the levels of reproductive factors,as well as their correlations with adverse pregnancy outcomes,were analyzed re-spectively in the adverse pregnancy group and the good pregnancy group.Results There was a statistically significant difference in the proportion of autosomes and sex chromosomes in the number and structure of pe-ripheral blood between the adverse pregnancy group and the good pregnancy group(P＜0.05).The anti-Müllerian hormone(AMH)level in the adverse pregnancy group was higher than that in the good pregnancy group,while estradiol(E2)and progesterone(P)levels were lower than those in the good pregnancy group,and the differences were statistically significant(P＜0.05).Abnormalities in autosomal number,autosomal structure,sex chromosome number,sex chromosome structure,and AMH were all positively correlated with adverse pregnancy outcomes(r=0.369,0.445,0.528,0.665,0.785,P＜0.05).E2 and P were negatively cor-related with adverse pregnancy outcomes(r=-0.865,—0.562,P＜0.05).Conclusion Peripheral blood chromosomal karyotypes and reproductive factor levels are related to adverse pregnancies in women.By under-standing the relationship between these biomarkers and chromosomal abnormalities,adverse pregnancy out-comes can be better predicted and managed,and the accuracy of fertility treatment can be improved.

OBJECTIVE To evaluate the efficacy of sulbactam-durlobactam combined with meropenem in treating carbapenem-resistant Acinetobacter baumannii(CRAB)pulmonary infection.METHODS A total of 16 patients treated at China-Japan Friendship Hospital from Jan.1,2025 to Jun.1,2025 were included.Retrospective analy-sis was conducted on patients'basic situation,preliminary treatment regimens,infection-related diagnoses,etiolo-gy and clinical outcomes.Therapeutic drug monitoring(TDM)for sulbactam was also performed.RESULTS By the end of the treatment course,13 patients achieved etiological eradication of CRAB and clinical improvement,while 1 patient experienced CRAB recurrence within one month.Three patients showed treatment failure.TDM for sulbactam was performed in 13 patients.Except for one slightly lower,all achieved trough plasma concentra-tions above the minimum inhibitory concentration(MIC)(100％T＞MIC,MIC=4 mg/L based on clinical breakpoints).Dosage adjustments based on plasma concentrations were made for 4 patients,with 3 receiving re-duced doses and 1 receiving an increased dose.CONCLUSIONS Sulbactam-durlobactam combined with meropenem demonstrates superior efficacy in treating CRAB compared to other regimens.Under the recommended dosage,all patients can achieve the PK/PD target for sulbactam.

BACKGROUND:Exosomes have been confirmed to be closely related to cartilage degeneration in osteoarthritis.However,the role and mechanism of exosome-derived genes in cartilage degeneration of osteoarthritis have not been fully elucidated.OBJECTIVE:Bioinformatics analyses were used to screen the genes related to cartilage degeneration in the synovial exosomes of patients with osteoarthritis,and to determine their biological functions and signaling pathways in order to provide new therapeutic targets for delaying cartilage degeneration in osteoarthritis.METHODS:Firstly,osteoarthritis-related exosome dataset GSE185059 and cartilage degeneration dataset GSE114007 were downloaded from Gene Expression Omnibus(GEO)database to screen exosome-derived cartilage degeneration related genes.GO functional and KEGG pathway enrichment analyses were performed based on the screened exosome-derived cartilage degeneration related genes.Protein-protein interaction network was drawn and Ingenuity Pathway Analysis(IPA)was conducted to screen and obtain key exosome-derived cartilage degeneration-related genes.Finally,qRT-PCR was used to verify the expression of key genes in osteoarthritis cartilage tissue and interleukin-1β stimulated chondrocyte models.RESULTS AND CONCLUSION:(1)There were 831 differentially expressed genes in the GSE185059 dataset and 5 323 differentially expressed genes in the GSE114007 dataset.A total of 94 exosome-derived cartilage degeneration related genes were screened after the intersection of these differentially expressed genes,of which 51 genes were down-regulated and 43 genes were up-regulated.(2)GO functional enrichment analysis showed that the up-regulated genes were mainly involved in the positive regulation of cell-cell adhesion,the positive regulation of T cell activation,and chronic inflammatory response,while the down-regulated genes were mainly involved in biological processes such as cell aggregation,cartilage differentiation and development,and skeletal system morphogenesis.(3)KEGG pathway enrichment analysis showed that exosome-derived cartilage degeneration-related genes were mainly involved in tryptophan enrichment metabolism,vitamin B6 metabolism,and leukocyte transendothelial migration.(4)The constructed protein-protein interaction network confirmed the existence of multiple interaction relationships among exosome-derived cartilage degeneration-related genes.Combined with five algorithms in CytoHubba software,four key exosome-derived cartilage degeneration-related genes were further screened,namely THY1,CYP1A1,NFKB2,and COL6A3.(5)The results of qRT-PCR showed that compared with normal cartilage,the expressions of THY1 and COL6A3 in osteoarthritic cartilage were increased,while the expression of CYP1A1 and NFKB2 was decreased.Similarly,compared with the unstimulated group,the expression of THY1 and COL6A3 in the interleukin-1β induced chondrocytes was upregulated,while the expression of CYP1A1 and NFKB2 was downregulated.(6)These results indicate that THY1,CYP1A1,NFKB2,and COL6A3 are genes related to cartilage degeneration in the exosomes of synovial fluid of patients with osteoarthritis,and may participate in the pathogenesis of osteoarthritis by regulating biological processes such as protein tyrosine kinase activity and lipid metabolism,as well as nuclear factor-κB signaling pathway and focal adhesion signaling pathway.However,the specific regulatory roles and molecular mechanisms of these key genes in cartilage degeneration need to be further verified by experiments.

[This corrects the article DOI: 10.1016/j.apsb.2022.05.019.].

Objective:To propose suggestions for the revision of quality standard of steviol glycosides through research on its major manufacturer's products.Methods:The inspection items in the current quality standards were inspected,with domestic and international quality standard of steviol glycosides.Results:Specific rotation was from-33.39° to-39.50°,pH was from 5.3 to 6.7,impurity absorbency was lower than 0.096 0,while the contents of weight loss on drying were lower than 5.0％,residue on ignition were lower than 0.043％,methanol residual were lower than 0.01％,ethanol residual were lower than 0.06％,residue on arsenic were lower than 0.000 054％,lead wasn't detected.The content of rebaudioside A and 13 kinds of steviol glycosides were 8.23％-68.48％and 85.78％-96.13％.Conclusion:The main components of the commercial steviol glycosides products were rebaudioside A and stevioside,with low safety risk of elemental impurities and solvent residues.It provided suggestions for the revision of quality standard of steviol glycosides in the Chinese Pharmacopoeia.

Objective:To investigate the life expectancy of antiretroviral treatment (ART) HIV-infected patients and its trends in Taizhou City, Zhejiang Province from 2014 to 2023.Methods:The data were obtained from the China Information System for Disease Control and Prevention , and the study subjects were HIV-infected patients received ART in Taizhou City. An abbreviated life expectancy table was prepared based on Chiang's method to analyze the differences in life expectancy of HIV-infected patients receiving ART in Taizhou City with different characteristics in 2023 and to compare the trends in life expectancy of patients with different CD4 +T lymphocytes (CD4) counts at the time of initiation of ART from 2014 to 2023. Results:A total of 4 825 patients were enrolled in this study, with a cumulative follow-up of 276 648.56 person-years, and a case-fatality rate of 18.07 (95% CI: 16.48-19.65) /1 000 person-years. In 2023, male patients had lower life expectancy than females in all age groups, and those who were married had higher life expectancy than those who were unmarried and those who were divorced or widowed; patients who had been transmitted heterosexually had lower life expectancy than those who had been transmitted through homosexual transmission. Patients with different CD4 counts at the time of initiating ART had different life expectancies in all age groups. The life expectancy of patients with CD4 counts ≥350 cells/μl when initiating the treatment was higher than that of patients with CD4 counts <200 cells/μl in all age groups. The life expectancy of HIV-infected patients on ART at age 20 and 50 increased from 39.0 years and 19.1 years in 2014 to 46.0 years and 24.1 years in 2023, respectively, with an average annual percentage change of 2.43% (95% CI: 0.81%-4.07%) and 3.34% (95% CI: 1.17%-5.56%). The change in life expectancy was similar for patients with CD4 counts ≥350 cells/μl and 200-349 cells/μl at the time of initiating treatment in 2016-2023, and was higher than that for patients with CD4 counts <200 cells/μl. The rate of increase in life expectancy for patients at age 50 was higher than that at age 20 for all CD4 counts. Conclusions:The rising trend of life expectancy among HIV-infected patients on ART in Taizhou City is obvious. But the disparity between patients with different characteristics is obvious, especially among patients with baseline CD4 counts <200 cells/μl, suggesting the importance of expanded testing, early diagnosis and timely initiation of ART to improve the life expectancy of HIV-infected patients.

Objective:To develop and validate clinical predictive models for identifying poor short-term response to recombinant human growth hormone(rhGH) treatment in children with short stature.Methods:A retrospective analysis was conducted on 118 children diagnosed with growth hormone deficiency or idiopathic short stature who were treated at the First Affiliated Hospital of Zhengzhou University and two other hospitals between January 1, 2020, and January 1, 2024. A poor response to rhGH was defined as a height increase of less than 0.2 standard deviation score(SDS) after 6 months of rhGH treatment. LASSO regression was used to identify predictive variables from baseline and follow-up data. Two logistic regression models were conducted: Model A(incorporating baseline variables only) and model B(incorporating both baseline and follow-up variables), and nomograms were created for visualization. External data and internal resampling were used for dual validation of the models, and their performance was compared.Results:A total of 118 children with short stature were included. Six baseline predictive variables(diagnosis, initial height SDS, bone age, bone age-chronological age difference, rhGH dose, and gender) and one follow-up variable(height SDS after 3 months of rhGH treatment) were identified. Area under the curve values for Model A and Model B were 0.753(95% CI 0.696-0.811) and 0.930(95% CI 0.891-0.975), respectively. Calibration curves, decision curve analysis, and other evaluation metrics demonstrated good discrimination and clinical utility for both models. Model B, incorporating the 3-month follow-up variable, showed superior predictive performance compared to Model A. Conclusions:The clinical prediction models developed in this study(Model A and Model B) are practical and reliable tools for quantitatively, conveniently, and intuitively identifying children with short stature at risk of poor response to rhGH treatment.