ObjectiveTo investigate the T lymphocyte subset levels and viral loads in newly human immunodeficiency virus (HIV) antibody-confirmed positive cases in Suzhou (2021‒2024), and to analyze potential influencing factors by integrating their demographic characteristics, immune status, and viral replication patterns, thereby providing evidence for HIV/acquired immune deficiency syndrome (AIDS) prevention and control. MethodsPeripheral whole blood samples were collected from newly confirmed HIV-positive cases in Suzhou from 2021 to 2024. T lymphocyte subset analysis and viral load testing were performed, and influencing factors were identified in combination with demographic characteristics. Logistic regression models were employed to identify factors associated with CD4⁺T lymphocyte counts ≤350 cells·μL^-1, and Spearman’s rank correlation test was used to analyze the correlation between logarithmic value of viral load and CD4⁺/CD8⁺ ratio. ResultsAmong the 3 022 confirmed HIV-positive samples, the median CD4⁺T lymphocyte count was 298.00 cells·μL^-1, with 882 cases (29.19%) showing CD4⁺ T lymphocyte counts <200 cells·μL^-1. The median CD8⁺T lymphocyte count was 1 011.00 cells·μL^-1. The median CD4⁺/CD8⁺ ratio was 0.28, with 32.46% of cases exhibiting CD4⁺/CD8⁺ ratios <0.20, and there were statistically significant differences in CD4⁺/CD8⁺ ratio among different genders, age groups, marital status, and sample sources (all P<0.05). Multivariate logistic regression analyses indicated that individuals aged ≥20 years, those who were divorced or widowed, and cases identified through medical institutions had a significantly higher proportion of CD4⁺T lymphocyte counts ≤350 cells·µL⁻¹ compared to those aged <20 years, unmarried individuals, and cases sourced from voluntary counseling and testing (VCT) clinics, respectively. The mean logarithmic value of viral load was (4.29±1.15) copies·mL^-1. The logarithmic value of viral load demonstrated a significantly negative correlation with both CD4⁺/CD8⁺ ratio (r=-0.43, P<0.001) and CD4⁺T lymphocyte count (r=-0.37, P<0.001). ConclusionA substantial proportion of newly diagnosed HIV/AIDS cases in Suzhou are late presenters with high viral load levels. Targeted interventions should prioritize high-risk populations through enhanced active surveillance and the implementation of combined T lymphocyte subsets analysis and viral load testing, which can enable earlier case-finding and timely antiretroviral therapy initiation.

ObjectiveThe malaria parasites remodel the host erythrocyte structure by exporting parasite proteins that interact with the membrane skeleton proteins of red blood cells (RBCs), facilitating their intracellular survival and pathogenicity. Skeleton-binding protein 1 (SBP1) is a conserved exported protein across Plasmodium species. In Plasmodium falciparum, SBP1 has been reported to interact with erythrocyte membrane skeleton proteins 4.1R and spectrin, while its contribution to erythrocyte remodeling and parasite virulence in Plasmodium berghei (Pb) remains unclear. This study aims to determine whether PbSBP1 associates with the host cytoskeletal protein 4.1R and to investigate its role in the remodeling of host RBCs and the pathogenicity of Plasmodium berghei. MethodsIn Plasmodium berghei, the relationship between PbSBP1 and the erythrocyte cytoskeletal protein 4.1R was examined using co-immunoprecipitation. A Pbsbp1 gene knockout mutant of Plasmodium berghei (Pbsbp1∆) was generated based on the principle of double crossover homologous recombination. The deformability of erythrocytes infected with Pbsbp1∆ parasites was assessed using microfluidic methods. Microchannels with an array of cylindrical pillars were used to detect modifications in infected RBC deformability. The infected RBCs were squashed between the rows and recovered between the columns and the transit velocity (μm/s) of infected RBCs travelling through the microchannel was recorded. The component of the erythrocyte membrane skeleton junctional complex, tropomodulin (TMOD), was fluorescently labeled, and the cytoskeletal network of infected erythrocytes was imaged using super-resolution stochastic optical reconstruction microscopy (STORM) to analyze ultrastructural changes in the cytoskeleton of wild-type (WT) and Pbsbp1∆-infected erythrocytes. Actin-based junctional complexes were displayed as individual clusters by the labeled TMOD in the STORM images, and the cluster densities and distances between adjacent clusters of infected RBCs were calculated. Additionally, rodent malaria models (BALB/c mice) and experimental cerebral malaria models (C57BL/6 mice) were employed to monitor the growth of Pbsbp1∆ and WT parasites during the intraerythrocytic stage and their capacity to induce cerebral malaria in mice. ResultsPbSBP1 may participate in the remodeling of infected erythrocytes through direct or indirect interaction with the erythrocyte cytoskeletal protein 4.1R. Microfluidic assays revealed that the deformability of erythrocytes infected with Pbsbp1∆ parasites was significantly enhanced compared to those infected with WT parasites. STORM imaging further demonstrated that the ultrastructure of the erythrocyte cytoskeleton in Pbsbp1∆-infected cells was altered relative to that in WT-infected erythrocytes. The distances between nearest neighbors of clusters had a tendency to increase while the cluster densities were decreased in Pbsbp1∆-infected RBCs compared to WT-infected RBCs. Subsequent phenotypic analysis indicated that the growth rate of Pbsbp1∆ parasites during the intraerythrocytic stage was significantly slower than that of WT parasites, and their ability to induce cerebral malaria in mice was also attenuated. These findings suggest that PbSBP1 is involved in the remodeling of the erythrocyte membrane skeleton, likely through its direct or indirect interaction with protein 4.1R, thereby regulating the deformability of infected erythrocytes and influencing the pathogenicity of the blood-stage parasites. ConclusionThis study establishes a role for PbSBP1 in host erythrocyte remodeling and parasite virulence, providing new research strategies for the prevention and treatment of malaria.

Treatment resistance, recurrence, and metastasis of breast cancer remain critical issues affecting long-term patient survival. Chronic psychological stress may act as a host biological driver of breast cancer treatment resistance rather than a mere comorbidity. Through the sustained activation of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis, also referred to as the "brain-tumor axis", stress signaling reshapes inflammatory, immune, and metabolic networks within the tumor microenvironment and thereby influences chemotherapy, endocrine therapy, anti-HER2 therapy, immunotherapy, and radiotherapy. Current evidence indicates that the key pathways with translational potential are mainly the β-adrenergic axis and the glucocorticoid receptor (GR) pathway. The former is more involved in amplifying inflammatory responses, promoting immunosuppression and metastasis, whereas the latter is closely associated with anti-apoptosis, maintenance of tumor stemness, and reprogramming of estrogen receptor function. This review focuses on the discrepancies in evidence regarding these pathways between population-based studies and preclinical models, and discusses clinically operable non-pharmacologic interventions such as cognitive behavioral stress management, nurse navigation and treatment adherence support, and exercise interventions during the neoadjuvant phase. Although high-level evidence for direct survival benefit remains limited, these interventions have shown favorable effects on cortisol levels, depressive symptoms, quality of life, adherence, relative dose intensity, and some biology-related intermediate endpoints, making them valuable complementary approaches in comprehensive breast cancer management.

Objective:To analyze the predictive role of WT1 expression levels pre-and early post-transplantation on relapse and overall survival(OS)in patients with acute myeloid leukemia(AML)undergoing allogeneic hematopoietic stem cell transplantation(allo-HSCT)during their first complete remission(CR1).Methods:A retrospective analysis was conducted on the clinical data of 107 adult AML patients who underwent allo-HSCT during their CR1 at our center between May 2012 and December 2021.The predictive role of bone marrow WT1 expression levels before transplantation and at 3 and 6 months post-transplantation on relapse and OS was explored in combination with relevant clinical factors.Results:The median follow-up time for the 107 patients was 70(range:11-117)months.Among the patients,15 cases died.Kaplan-Meier survial analysis showed that the 3-year overall survival(OS)rate was 85.0％.20 patients experienced relapse,with a median time to relapse of 8(range:0.5-44)months and a l-year cumulative relapse rate of 13.1％.The overall median value of WT1 before transplantation,3 months after transplantation,and 6 months after transplantation was 0.26％(range:0％-23.64％),with an upper quartile value of 0.74％.No statistically significant differences in WT1 expression levels were observed among the pre-transplantation,3-month post-transplantation,and 6-month post-transplantation time points(P=0.227).Univariate analysis showed that patients with WT1 levels＞0.74％at 3 months post-transplantation had a higher 1-year relapse rate(P=0.029)and lower 3-year OS rate(P＜0.001)compared to patients with WT1 levels ≤0.74％.Other significant factors affecting 1-year relapse included stem cell source(P=0.041)and chronic graft-versus-host disease(cGVHD)(P=0.013).For 3-year OS,additional influencing factors were genetic high risk(P=0.048)and stem cell source(P=0.016).Multivariate analysis revealed that WT1 level＞0.74％at 3 months post-transplantation had a trend to affect 1-year relapse rate(HR=3.309,95％CI:0.958-11.431,P=0.058),while the absence of cGVHD was an independent risk factor for 1-year relapse(HR=3.473,95％CI:0.749-16.100,P=0.037).Only WT1 level＞0.74％at 3 months post-transplantation was an independent risk factor for 3-year OS(HR=6.886,95％CI:2.402-19.738,P＜0.001).Conclusion:High WT1 expression level at 3 months post-transplantation in AML patients undergoing allo-HSCT during CR1 affects the 1-year relapse rate and 3-year OS,and is an independent risk factor affecting 3-year OS.These findings suggest that dynamic monitoring of WT1 expression levels has certain value in prognostic assessment of AML patients who received allo-HSCT during CR1.

Objective To investigate the mechanism by which Yangmai Tongluo formula improves microcirculation disorders induced by high homocysteine(Hcy)levels via regulation of the acid sphingomyelinase(ASM)and endoplasmic reticulum(ER)stress pathways.Methods Fifty male C57BL/6J mice were divided randomly into a control group,Hcy model group,Yangmai Tongluo formula low-/high dose groups(5.3,10.4 g/kg,respectively),and a folic acid group(0.08 g/kg).Except for the control group,microcirculation disorders were induced in all mice using drinking water containing 1.8 g/L Hcy for 6 weeks.After modeling for 2 weeks,mice were administered the corresponding treatments by gavage for 4 weeks.Serum Hey concentrations and the blood perfusion volume of the lower extremity microvessels were measured.Protein expression levels of zonula occludens ZO-1,ZO-2,intercellular adhesion molecule-1(ICAM-1),vascular cell adhesion molecule-1(VCAM-1),ASM,glucose-regulated protein 78(GRP78),and C/EBP homologous protein(CHOP)in the cardiac microvascular endothelium were analyzed using immunofluorescence.Results Serum Hcy levels were significantly increased in the Hcy model group compared with the control group(P＜0.05).Yangmai Tongluo formula did not significantly reduce Hey levels compared with the Hey model group,but blood perfusion in the lower extremities was significantly increased(P＜0.01)and expression levels of ZO-1 and ZO-2 in the cardiac microvascular endothelium were restored(P＜0.001)in the Yangmai Tongluo formula high dose group.It also inhibited the expression of ICAM-1,VCAM-1,ASM,GRP78,and CHOP(P＜0.05),with comparable effects to folic acid.Conclusions Yangmai Tongluo formula improves Hcy-induced microcirculation disorders and endothelial dysfunction by inhibiting ASM activity and alleviating ER stress,via a mechanism closely related to the regulation of endothelial inflammation and barrier stability.These result provide experimental evidence to support the use of traditional Chinese medicine to treat microvascular diseases.

Objective To analyze the status of 2 649 suspected pertussis patients in Xi'an and the changes in laboratory diagnostic indi-cators.Methods 2 649 patients with suspected pertussis who visited the Second Affiliated Hospital of Xi'an Jiaotong University from June 2023 to May 2025 were collected as the research subjects.Nasopharyngeal swabs were collected from the patients,and pertussis nucleic acid was detected by polymerase chain reaction(PCR)-fluorescence probe method.Laboratory diagnostic indicators were an-alyzed.Results Among the 2 649 samples tested,250 were positive for pertussis nucleic acid,with a positive detection rate of 9.44%.The detection rate in male patients was 9.37%(127/1 356),and in female patients was 9.51%(123/1 293),with difference no was statis-tically significant between the two groups(χ2=0.019,P=0.894).There was a statistically significant difference in the positive detection rate among different age groups(χ2=46.473,P<0.05),with the highest positive detection rate in the 7～19 age group(14.98%).The prevalence of pertussis showed a seasonal characteristic with a peak from April to September.21.2%(53/250)of the positive patients were mixed infections.In the 1～14 age group,the white blood cell count(WBC),lymphocyte percentage(LYMP%),and lymphocyte count(LYMP#)in the pertussis infection group were higher than those in the Mycoplasma pneumoniae(MP)infection group(t=10.179,5.819,8.614)and the Respiratory syncytial virus(RSV)infection group(t=16.570,2.618,7.185),and the differences were statistically significant(all P<0.01),respectively.In the＞14 age group,the LYMP%and LYMP#in the pertussis infection group were higher than those in the MP infection group(t=3.275,2.319)and the RSV infection group(t=2.401,4.617),and the differences were statistically significant(all P<0.05),respectively.Conclusion The pertussis infection status in Xi'an area from 2023 to 2025 shows significant char-acteristics in terms of age,season and laboratory test results.It is necessary to further improve the pertussis surveillance system in this area,optimize the clinical diagnosis and treatment process and strengthen the vaccination work of pertussis vaccine.

Aim To investigate the protective effects of methyl rosmarinate(MR)on myocardial injury in-duced by high-altitude hypoxia and explore its underly-ing mechanisms.Methods BALB/c mice were ran-domly divided into a control group,a model group,and low-,medium-,and high-dose MR groups(25,50,and 75 mg·kg-1,respectively).Except for the control group,all other groups were exposed to a hypobaric hypoxia chamber and administered MR via intraperitoneal injection daily for three days.After the experiment,myocardial tissues were collected for he-matoxylin and eosin(HE)staining to observe morpho-logical changes.Levels of malondialdehyde(MDA),glutathione(GSH),and superoxide dismutase(SOD)were measured to evaluate the anti-myocardial injury activity of MR.Network pharmacology was employed to predict drug-disease interaction targets,construct a protein-protein interaction(PPI)network,and identify core targets.Functional enrichment analysis was car-ried out using Gene Ontology(GO)and Kyoto Ency-clopedia of Genes and Genomes(KEGG)pathways.Molecular docking was used to verify the binding affini-ty of MR to core targets,and Western blot was conduc-ted to detect the expression of related proteins.Results MR significantly alleviated myocardial injury caused by high-altitude hypoxia.Network pharmacology analy-sis identified EGFR,Bcl-2,STAT3,MMP9,ESR1,and MTOR as key targets.Molecular docking con-firmed strong binding between MR and these core tar-gets.Western blot results demonstrated that MR im-proved myocardial injury by regulating the expression of STAT3,Bax,and Bcl-2 proteins.Conclusion MR may exert its protective effects on high-altitude hypoxi-a-induced myocardial injury through a multi-target mechanism.

Objective:To analyze the psychometric properties of the short-form Extended Barthel Index (EBI) in assessing ability in the activities of daily living (ADL).Methods:Data describing 295 discharged patients with stroke or traumatic brain injury were collected retrospectively, including their demographics, diagnoses, and functional assessments (EBI, FIM, MBI and MoCA). Then, data on 120 of them were used to construct short-form EBI models based on item-total advantage indices, while the remaining 175 patients served as a validation set to evaluate the acceptability, responsiveness, reliability, validity, and outcome consistency of the models. The optimal model was selected as the recommended short-form EBI.Results:The short-form EBI comprises seven items: personal hygiene, dressing/undressing, wheelchair-bed transfer, walking, social interaction during walking, problem-solving, and memory/learning/orientation, with each item scored 0-4 (total range: 0-28). The short-form EBI demonstrated good acceptability, with median and mean scores near the scale′s midpoint and no significant ceiling or floor effects. Its responsiveness (d=0.19) surpassed that of the original EBI (d=0.14). Moreover, the short-form EBI showed excellent reliability (Cronbach′s α=0.885; SEM=9.11) and validity, explaining 95.4% of the variance in EBI scores (adj. R 2=0.954). Concurrent validity with the EBI was strong (ρ=0.975, P≤0.001), and criterion validity with ρ=0.956 for FIM, 0.889 for MBI, and 0.806 for MoCA. The short-form and the original EBI exhibited good agreement [ICC=0.967 (95% CI: 0.769-0.989); score difference: 6.48±6.56]. Conclusions:The short-form EBI demonstrates excellent acceptability, responsiveness, reliability, validity, and outcome consistency, making it a practical tool for ADL assessment in cases of stroke or traumatic brain injury.

Objective:To investigate the association between prenatal environmental factors and attention defi-cit hyperactivity disorder(ADHD)and its symptom severity in children.Methods:Based on the Diagnostic and Statistical Manual of Mental Disorders,Fourth Edition(DSM-Ⅳ)diagnosis criteria,1 156 children with ADHD and 289 normal control children were included in this study.ADHD diagnoses were established using the Clinical Diag-nostic Interview Scale,core symptoms were assessed with the ADHD Rating Scale,and information on prenatal ex-posures were collected via self-developed questionnaires.Results:Maternal stress during pregnancy was associated with increased risk factor of ADHD in children(OR=1.22,P＜0.01).Among children with ADHD,preconception paternal alcohol consumption was positively associated with hyperactivity/impulsivity symptoms(β=0.08,P＜0.05),and maternal smoking during pregnancy was positively associated with total symptoms(β=0.07-0.09,P＜0.05).Conclusion:Maternal stress during pregnancy may increase the risk factor of ADHD in children.Both pre-conception paternal alcohol consumption and maternal smoking during pregnancy may be associated with increased ADHD symptom severity in children.

Aim To investigate the effect of cordycepin(COR)on gentamicin(GEN)-induced nephrotoxicity and the molecular mechanism of inhibiting oxidative stress and ferroptosis induced by GEN.Methods The oral SD rats were divided into a control group,GEN group,and GEN+COR group.Following the success-ful setting up of the animal model,the serum creatinine(CR)and urea nitrogen(BUN)levels of rats were measured,and renal tissue injury was assessed using HE staining.In addition,the contents of malondialde-hyde and glutathione in kidney tissues of SD rats in each group were detected,and the expressions of fer-roptosis markers GPX4 and SLC7A11 were analyzed by Western blot.Results Compared with the control group,CR and BUN in GEN-stimulated group signifi-cantly increased(P＜0.01),and the level of CR and BUN was effectively reduced after 50 mg·kg-1 COR oral administration.HE results also showed that COR could alleviate the kidney tissue damage caused by GEN.COR could reverse the increase of malondialde-hyde level and the decrease of glutathione level caused by GEN in rat kidney tissue,and COR could restore the decrease of GPX4 and SLC7A11 protein levels induced by GEN.Conclusion COR can reduce GEN-induced kidney injury by inhibiting oxidative stress and ferrop-tosis.