Objective: To validate the performance of the Procleix UltrioPlex E assay (Grifols, Spain) on the Procleix Panther automated nucleic acid detection platform, which employs the TMA method to simultaneously detect HIV-1/HIV-2/HCV/HBV/HEV viruses, and to evaluate its value for screening transfusion-associated infectious diseases. Methods: In accordance with the requirements of ISO15189"Application of the Guidelines for the Accreditation of Quality and Capabilities of Medical Laboratories in the Field of Molecular Diagnostics (CNAS-CL02-A009: 2018)", "Guidelines for Performance Validation of Molecular Diagnostic Testing Procedures (CNAS-GL039: 2019)", and the "Technical Operating Procedures for Blood Banks (2019 Edition)", this study validated the reagent's performance in terms of analytical sensitivity validation, performance consistency validation, interference resistance, and cross-contamination resistance. Results: Probit analysis revealed that the 95% detection limits (95% confidence interval) for HBV, HCV, HIV, and HEV were 2.0 IU/mL, 1.5 IU/mL, 18.0 IU/mL and 3.7 IU/mL, respectively, which were consistent with the minimum detection limits stated in the kit's package insert and were comparable to the Procleix Ultrio Elite kit. Both kits were used to test the performance validation serum plate simultaneously, yielding results consistent with the serum plate (Kappa=1), indicating stable performance. Detection of medium-and low-concentration lipemia and weakly positive hemolysis samples demonstrated good interference resistance. Cross-contamination performance validation showed that the kit exhibited excellent cross-contamination resistance. Conclusion: The Procleix UltrioPlex E nucleic acid detection kit enables combined detection of HIV-1, HIV-2, HCV, HBV, and HEV, allowing single-test screening for multiple viruses in donor blood. The kit's analytical performance is stable and meets basic laboratory requirements, making it suitable for screening transfusion-associated infectious diseases in blood banks.

Diabetic tendinopathy is a common and disabling musculoskeletal complication of diabetes, clinically characterized by tendon thickening, pain, impaired healing capacity and compromised biomechanical performance, collectively undermining joint function and quality of life. Its pathogenesis is multifactorial. On the one hand, chronic hyperglycaemia promotes the abnormal accumulation of advanced glycation end products (AGEs) within tendon collagen, leading to non-enzymatic crosslinking and engagement of the receptor for AGEs (RAGE), which in turn triggers inflammasome activation and sustains inflammatory responses. On the other hand, the diabetic milieu disrupts collagen metabolic homeostasis, impairs microvascular function and induces peripheral neuropathy; together, these alterations drive extracellular matrix degeneration and weaken the mechanical properties of tendon. Exercise, as a non-pharmacological intervention, can ameliorate these pathological changes through multiple integrated mechanisms. First, exercise attenuates tendon inflammation and restores microenvironmental homeostasis. Regular physical activity reduces AGE-RAGE signalling, thereby suppressing downstream expression of tumour necrosis factor (TNF) and interleukin-1β (IL-1β), while upregulating the anti-inflammatory cytokine interleukin-10 (IL-10). This shift from a pro-inflammatory to a pro-resolving milieu not only restrains chronic inflammation but may also limit excessive inflammasome activation in tenocytes and tissue-resident immune cells. Second, exercise enhances local expression of insulin-like growth factor 1 (IGF-1), thereby activating the phosphoinositide 3-kinase (PI3K)-protein kinase B (Akt) signalling pathway. This axis stimulates tenocyte proliferation, augments synthesis of type I collagen —— the principal load-bearing component of tendon —— and thereby promotes tissue repair, preserves tensile strength and supports matrix synthesis and structural integrity. In addition, exercise improves blood supply and nutrient delivery to tendon by increasing the expression of vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF) and the small leucine-rich proteoglycan decorin (DCN), thereby enhancing capillary growth, coordinating collagen fibrillogenesis and actively suppressing pathological vascular calcification. Exercise also increases the expression of angiopoietin-like 4 (ANGPTL4), fibroblast growth factor 2 (FGF-2) and CD34. Through the concerted actions of these factors, exercise promotes angiogenesis, restores the microvascular network and ensures adequate oxygen and nutrient supply to relatively ischaemic tendon tissue. Finally, exercise elevates levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), supporting neuronal survival, axonal growth and the function of sensory and sympathetic nerve endings within tendon, thereby exerting neurotrophic and neuromodulatory effects and improving tendon innervation and neuromuscular control. Moreover, exercise upregulates collapsin response mediator protein 2 (CRMP-2), a molecule involved in axonal guidance and regeneration, and moderately increases the activity of substance P (SP), thereby helping to regulate neurogenic inflammation, pain perception and trophic support for tenocytes. Drawing together current evidence, this review systematically summarizes the mechanisms underlying diabetic tendinopathy and examines the mechanistic basis of exercise intervention, with the aim of providing a theoretical framework for the development of precise exercise strategies for affected individuals. However, several key issues remain unresolved: the therapeutic efficacy and mechanistic specificity of different exercise modalities in diabetic tendinopathy have yet to be defined, and early diagnostic biomarkers remain insufficiently characterized. Future studies should apply multi-omics approaches to profile AGE subtypes, miRNA signatures and collagen metabolic products, and should also clarify the adverse effects and underlying mechanisms of excessive exercise or mechanical overloading in diabetic tendinopathy. Such efforts will further elucidate the therapeutic effects and mechanisms of exercise in diabetic tendinopathy and provide a stronger basis for precision exercise prescription and fitness guidance in patients with diabetes.

The CDH23 gene is a pathogenic mutant gene of the USH1D subtype in Usher syndrome.In this study,two wild-type Cdh23 full-length plasmids(～16 kb)with different promoters were construc-ted,and fluorinated polyethylene imine(FPEI)was used as a delivery vector to transfect the house ear institute-organ of corti 1(HEI-OC1)and the optimal expression plasmid was obtained by evaluating the transfection efficiency in vitro.Firstly,the results of the synthesis of FPEI were analyzed using Fourier transform infrared absorption spectroscopy to prove the successful synthesis of FPEI.After that,the plas-mid encapsulation ability of FPEI and the surface potential and hydration diameter of the formed comple-xes were characterized by agarose gel blocking assay,Zeta potential assay,and dynamic light scattering assay.It was found that FPEI had good plasmid encapsulation ability,and the FPEI plasmid complexes were all positively charged at high mass ratio,with the distribution of particle sizes in the range of 100-300 nm.The low cytotoxicity and high transfection efficiency of FPEI in HEI-OC1 cells were verified by Cell Counting Kit-8(CCK-8)and flow cytometry.Comparing FPEI with Lipofectamine 3000 and differ-ent quality PEI(25K,40K)transfection reagents,the transfection efficiency of FPEI was found to be significantly better than that of the traditional transfection reagents.Quantitative real-time polymerase chain reaction(qRT-PCR)and Western blot results showed that the CAG promoter was better than the CMV promoter,which could be used as the optimal expression plasmid for the subsequent in vivo experi-ments.In addition,it was verified by cellular immunofluorescence that CDH23 was mainly distributed in the cytoplasm after overexpression.The above results demonstrated that FPEI can be used as an efficient delivery vector for in vitro overexpression of large genes represented by Cdh23,which provides an impor-tant experimental basis for subsequent in vivo gene therapy of USH1D syndrome.

Objective:In the context of China's cardiovascular disease(CVD)high-risk population screening and intervention project,this study systematically evaluates the applicability of the EQ-5D-5L and SF-6Dv2 instruments among individuals at high risk of CVD.Methods:Convergent validity was assessed using Spearman's correlation coefficient.Measurement agreement was evaluated through intraclass correlation coefficients(ICC)and Bland-Altman plots.Factors influencing utility differences were explored using multiple linear regression analysis.Kruskal-Wallis test and t-test were used to examine discriminant validity.Sensitivity was compared by effect size(ES),relative efficiency(RE),and the area under the receiver operating characteristic curve(ROC-AUC).Floor and ceiling effects were also compared.Results:Among 5,415 individuals at high risk of CVD,the two instruments showed moderate overall correlation and acceptable convergent validity,but dimension-specific correlations were weak,and measurement consistency was low(ICC=0.367).Both instruments effectively distinguished different health states,yet the SF-6Dv2 demonstrated superior sensitivity and a milder ceiling effect.Conclusion:When measuring the health utility value of CVD patients,scale selection should be cautious,especially for high-risk groups,and SF-6Dv2 is more appropriate.

Aim To investigate the role and regulatory mechanism of CREB regulated transcription coactivator 2(CRTC2)in cardiomyocyte hypertrophy.Methods A pathological cardiomyocyte hypertrophy model was established in C57BL/6 mice by intraperitoneal injection of isoproterenol(ISO),the expression of CRTC2 in cardiac tissue was detec-ted by Western blot.The CRTC2 knockout mice model was constructed,the cardiac function of mice was detected by small animal echocardiography,the collagen fiber content in mice cardiac tissue was detected by Masson staining,the car-diomyocyte hypertrophy related proteins:skeletal muscle α1-actin(ACTA1)and brain natriuretic peptide(BNP),as well as ferroptosis related proteins:acyl-CoA synthetase long chain family member 4(ACSL4),solute carrier family 7 member 11(SLC7A11)and glutathione peroxidase 4(GPX4)in mice cardiac tissue were detected by Western blot,the iron ion content in mice cardiac tissue was detected by iron ion kit,to evaluate the correlation between CRTC2 and cardiomyocyte hypertrophy and ferroptosis.H9c2 cells were induced by ISO to construct an in vitro model of cardiomyocyte hypertrophy,the protein expressions of CRTC2,ACTA1,BNP,ACSL4,SLC7A11 and GPX4 were detected after intervention with fer-roptosis inhibitor ferrostatin-1(Fer-1).H9c2 cells with CRTC2 overexpression induced by ISO were used to construct an in vitro model of cardiomyocyte hypertrophy,the related indicators of cardiomyocyte hypertrophy and ferroptosis were detec-ted to explore the mechanism of CRTC2 in cardiomyocyte hypertrophy.Results Compared with the control group,the expression of CRTC2 protein in the cardiac tissue of ISO induced cardiomyocyte hypertrophy mice was increased(P＜0.05).Compared with wild-type mice,CRTC2-/-mice showed worsened cardiac function,manifested as increased left ventricular end-diastolic diameter(LVEDD),left ventricular end-systolic diameter(LVESD),left ventricular posterior wall thickness(LVPWT),heart weight/tibia length(HW/TL)and heart weight/body weight(HW/BW),decreased short axis shortening(FS)and ejection fraction(EF),increased collagen fiber content in cardiac tissue,upregulated ex-pression of cardiomyocyte hypertrophy-related proteins ACTA1 and BNP,increased mRNA and protein expression of ferrop-tosis-related protein ACSL4,decreased mRNA and protein expression of SLC7A11 and GPX4,and elevated iron ion content in cardiac tissue(P＜0.05 or P＜0.01).In vitro experiments showed that compared with ISO group,the ISO+Fer-1 group had no significant change in CRTC2 protein expression(P＞0.05),the expression of ACTA1 and BNP protein decreased,the surface area of cardiomyocyte reduced,the expression of ACSL4 protein decreased,and the expression of SLC7A11 and GPX4 proteins increased(P＜0.05 or P＜0.01).Compared with the ISO group,the LV-CRTC2+ISO group showed a decrease in surface area of cardiomyocytes(P＜0.01),a decrease in ACTA1,BNP and ACSL4 protein ex-pression,an increase in SLC7A11 and GPX4 protein expression,and a decrease in ROS and iron ion content(P＜0.05 or P＜0.01).Conclusion CRTC2 alleviates cardiomyocyte hypertrophy and protect cardiac function by suppressing fer-roptosis in cardiomyocytes.

Objective:To explore the potential profile categories of self-disgust in young and middle-aged breast cancer patients, and analyze the influencing factors of different categories.Methods:A convenience sampling method was used, and 270 young and middle-aged breast cancer patients admitted to the thyroid and breast cancer ward and oncology ward of Fenyang Hospital in Shanxi Province from September 2023 to April 2024 were the study subjects. The survey was conducted transect surveys using the general information questionnaire, Questionnaire for the Assessment of Self-Disgust, Social Constraints Scale, the Chronic Illness Rejection and Discrimination Scale. Potential categories of self-disgust in young and middle-aged breast cancer patients were explored using latent profile analysis, and unordered multinomial Logistic regression was employed to investigate their influencing factors.Results:A total of 234 young and middle-aged female breast cancer patients were included, with the age of (45.61±10.90) years old. Latent profile analysis revealed three potential categories of self-hatred in these patients: low disgust group (45.30%, 106/234), medium disgust group (41.45%, 97/234), and generalized high disgust group (13.25%, 31/234). Compared to the low disgust group, patients with more comorbidities and poorer self-care ability were more likely to belong to the generalized high disgust group ( OR=0.244, 8.775, both P<0.05). Patients with a longer duration of illness and higher scores on the social constraints scale and chronic illness rejection and discrimination scale were more likely to fall into the medium disgust group and the generalized high disgust group ( OR values were 0.156 - 1.317, all P<0.05). Conclusions:The level of self-disgust in young and middle-aged breast cancer patients is significantly heterogeneous. Nursing staff should formulate personalized intervention strategies according to this classification characteristic, which can be cut from the perspective of reducing patients' social restriction and chronic illness rejection and discrimination to improve patients' acceptance of the disease and self-acceptance level, and then reduce their self-disgust.

Objective To investigate the effects of asperuloside(ASP)on airway inflammation and the interleukin-6/Janus kinase 2/signal transducer and activator of transcription 3(IL-6/JAK2/STAT3)signaling pathway in juvenile rats with bronchial asthma.Methods A juvenile rat model of bronchial asthma was constructed and randomly separated into a Model group,low,medium,and high dose asperuloside groups(ASP-L,ASP-M,ASP-H groups),and high-dose asperuloside+pathway activator group(ASP-H+CA1 group),with 12 rats in each group.An additional 12 healthy rats were included as Control group.All rats were evaluated for lung function.The number of inflammatory cells in bronchoalveolar lavage fluid(BALF),and the levels of inflammatory factors in BALF and serum were detected.HE staining was applied to observe the pathological morphology of lung tissue.Western blot was applied to detect the expression of proteins related to the IL-6/JAK2/STAT3 signaling pathway.Results Compared with Control group,the lung tissue of rats in the Model group showed severe damage and higher levels of inflammatory cell infiltration,the PEF,Cdyn,and FEV/FVC indexes were greatly decreased,the numbers of inflammatory cells(WBC,EOS,NEU,LYM),levels of inflammatory factors(IL-1β,TNF-α,and IL-6)in BALF and serum,and the expression levels of signaling pathway proteins(IL-6,p-JAK2/JAK2,p-STAT3/STAT3)were obviously increased(P＜0.05).Compared with the Model group,with the increase of ASP dosage,the degree of lung tissue damage and inflammatory cell infiltration of rats in the ASP-L,ASP-M,and ASP-H groups were significantly reduced,the PEF,Cdyn,and FEV/FVC indexes were gradually increased,the numbers of inflammatory cells(WBC,EOS,NEU,LYM),levels of inflammatory factors(IL-1β,TNF-α,and IL-6)in BALF and serum,and the expression levels of signaling pathway proteins(IL-6,p-JAK2/JAK2,p-STAT3/STAT3)were gradually decreased(P＜0.05).Compared with the ASP-H group,the lung tissue of rats in the ASP-H+CA1 group showed severe damage,the infiltration of inflammatory cells increased,the PEF,Cdyn,and FEV/FVC indexes were decreased,the numbers of inflammatory cells(WBC,EOS,NEU,LYM),levels of inflammatory factors(IL-1β,TNF-α,and IL-6)in BALF and serum,and the expression levels of signaling pathway proteins(IL-6,p-JAK2/JAK2,p-STAT3/STAT3)were greatly increased(P＜0.05).Conclusion Asperuloside can improve lung tissue damage,reduce inflammation levels,and improve lung ventilation function in rats with bronchial asthma.Its effect may be related to the regulation of the IL-6/JAK2/STAT3 signaling pathway.

Objective:To study the subacute oral toxic effect of p-chloro-m-xylphenol on rats and provide a basis for its safety evaluation.Methods:SPF-grade Wistar rats were randomly divided into 4 groups according to body weight stratification randomization, with 20 rats in each group, half male and half female. The set concentrations of the p-chloro-m-xylphenol dose groups were 11.25, 22.50, and 45.00 mg/kg·BW respectively, with an intragastric volume of 10 ml/kg·BW. The blank control group was given the same amount of distilled water. The rats were treated with intragastric administration for 30 days. After intraperitoneal injection of 50 mg/kg·BW pentobarbital sodium for anesthesia, bloodletting and death, the organs were separated and weighed. Blood was collected from the abdominal aorta to determine the hematological and serum biochemical indicators of the whole blood of rats. Multiple groups comparison was performed by one-way analysis of variance, and pairwise comparison between groups was performed by the least significant difference test or Dunnett-t3 test.Results:The kidney weight in the 45.00 mg/kg·BW dose group of female rats [ (1.59±0.11) g] was lower than that in the blank control group [ (1.71±0.12) g], and the difference was statistically significant ( P<0.05) . The percentage of monocytes in the 11.25 mg/kg·BW dose group of male rats [ (4.81±0.74) %] was lower than that in the blank control group [ (5.86±0.58) %], the red blood cell count [ (6.93±0.26) ×10 12/L] and hemoglobin [ (134.30±4.95) g/L] in the 22.50 mg/kg·BW dose group of female rats were both lower than those in the blank control group[ (7.48±0.26) ×10 12/L, (146.20±4.42) g/L], the percentage of eosinophils in the 11.25 mg/kg·BW dose group of female rats [ (2.46±0.86) %] was higher than that in the blank control group [ (1.66±0.41) %], and the differences were statistically significant ( P<0.05) . Conclusion:P-chloro-m-xylphenol may have toxic effects on the blood system of rats, and the kidneys may be the potential target organs for its toxicity.

Objective:To investigate the short-term efficacy and safety of rituximab (RTX) in children with calcineurin inhibitor (CNI) resistant steroid resistant nephrotic syndrome (SRNS).Methods:A retrospective case analysis was conducted. Thirteen children with CNI resistant SRNS who were regularly treated with RTX (375 mg/m 2 per dose (maximum dose 500 mg), 1 dose per week, a total of 4 doses) in Department of Nephrology, Children′s Hospital of Fudan University from January 2016 to December 2023 were enrolled. The general data, disease related information, urinary protein/creatinine, serum albumin, blood creatinine before RTX treatment, immunosuppressants, adverse events, and monthly urinary protein/creatinine, serum albumin, and blood creatinine indexes within 6 months after RTX treatment were collected. The changes of urinary protein/creatinine, serum albumin and estimated glomerular filtration rate (eGFR) before and after RTX at 3 and 6 months were analyzed by using paired sample t test and Wilcoxon signed-rank test. Results:Among the 13 patients, 8 were male and 5 were female. The age of disease onset was 4.0 (2.9, 6.8) years and the age of RTX treatment was 9.8 (5.9, 13.6) years. There were 8 cases of focal segmental glomerulosclerosis, 3 cases of minimal change disease and 2 cases of mesangial proliferative glomerulonephritis. No clinically significant gene variation was detected in 12 cases and the other one did not receive gene test. Before RTX treatment, 11 cases were in chronic kidney disease stage G1, and 1 case each was in stage G2 and stage G3. Ten children completed 4 doses of RTX treatment, 1 patient completed 3 doses, and 2 patients completed 2 doses. Urinary protein/creatinine in 13 children at 3 and 6 months after RTX treatment was significantly lower than baseline (0.60 (0.13, 2.04), 0.49 (0.28, 1.10) vs. 1.44 (0.76, 4.11) mg/mg, Z=-2.34, -2.34, both P<0.05), and serum albumin was significantly higher than baseline ((35±8), (34±7) vs. (30±6) g/L, t=2.30, 2.60, both P<0.05). The eGFR at 6 months after RTX treatment was not significantly different from the baseline ((110±32) vs. (113±35) ml/(min·1.73 m 2), t=-0.76, P>0.05)). No serious adverse reactions occurred in this study. Conclusion:RTX could reduce urinary protein and increase serum albumin in short-term treatment in children with CNI resistant SRNS without significant side effects.