Objective: To characterize perioperative dynamic changes in immune-cell phenotypes and inflammatory cytokines in patients undergoing CPB (cardiopulmonary bypass) cardiac surgery, and to explore their associations with postoperative outcomes. Methods: In this prospective cohort study, 120 adult patients who underwent elective cardiac surgery under CPB at West China Hospital from May 2022 to March 2023 were enrolled. Perioperative immune-cell phenotypes and concentrations of 40 inflammation-related cytokines were measured. The primary outcomes were the sequential organ failure assessment (SOFA) score at 24 h after surgery and ΔSOFA (the peak SOFA score within 48 h after surgery minus the preoperative SOFA score). Secondary outcomes included major adverse cardiovascular events (MACE), acute kidney injury (AKI), respiratory failure, severe liver injury, and infection. Results: The mean age of enrolled patients was 57±10 years. Of these, 52% (62/120) were male and 90% (108/120) underwent valve surgery. During the rewarming to the end of CPB, neutrophil counts rapidly increased (7.39×10 /L vs preoperative 3.07×10 /L, P<0.001), with significant upregulation of CD11b (7.30×10 /L vs preoperative 3.05×10 /L, P<0.001) and CD54 (7.15×10 /L vs preoperative 2.99×10 /L, P<0.001). Lymphocyte counts increased at the end of CPB (1.75×10 /L vs preoperative 1.12×10 /L, P<0.001) but decreased significantly at 24 h after surgery (0.59×10 /L vs preoperative 1.12×10 /L, P<0.001). Plasma analysis showed that multiple pro-inflammatory cytokines increased during CPB and remained elevated up to 24 h after surgery; five chemokines and the anti-inflammatory cytokine IL-10 peaked at the end of CPB. The SOFA score increased from 1 (1, 2) preoperatively to 7 (5, 10) at 24 h after surgery, with a ΔSOFA of 6 (4, 8). Within 30 days after surgery, 48 patients (40.0%) developed AKI, 17 (14.2%) developed infection, 4 (3.3%) developed severe liver injury, 3 (2.5%) developed respiratory failure, and 3 (2.5%) experienced MACE. During the 2-year follow-up, 8 patients (6.7%) experienced MACE and 5 (4.2%) died. Conclusion: Multi-organ dysfunction is common after cardiac surgery under CPB (median ΔSOFA, 6), accompanied by perioperative activation of multiple immune-cell subsets and upregulation of pro-inflammatory, anti-inflammatory, and chemotactic mediators. This study provides data-driven evidence and research clues for further investigation of the associations between CPB-related immune perturbations and postoperative organ dysfunction and clinical outcomes.

ObjectiveTo investigate the effects of salidroside （SAL） on the impaired bioactivity of endothelial progenitor cells （EPCs） in atherosclerotic （As） mice and the potential mechanisms regarding AMP-activated protein kinase （AMPK）. MethodsAtherosclerosis was induced in 8-week-old male ApoE^-/- mice with high-fat diet. Intragastric administration of SAL was given to one mice group to investigate the effects of SAL on aortic plaque burden， plasma NO level， the migration and angiogenic capabilities of bone marrow-derived EPCs （BM-EPCs）. The proliferation， migration and vasculogenic properties of EPCs isolated from As mice were investigated in vitro. AMPK-sh-RNA or the AMPK inhibitor Compound C was used to investigate the role of AMPK/Akt/eNOS pathway in the regulatory effects of SAL. ResultsCompared with As group， NO level was significantly elevated in SAL group. The sizes of atherosclerotic plaques at the aortic root were reduced with smaller lipid cores in SAL group compared with As group. Moreover， the migration and angiogenesis capacity of EPCs markedly decreased in As mice， while SAL treatment reversed these impairments. Incubation with SAL at concentrations of 20， 40， and 80 μmol/L for 48 hours significantly promoted the proliferation， migration， and angiogenesis of EPCs. AMPK-sh-RNA transfection abrogated the 20 μmol/L SAL improvement in EPC biological activities. Western blot analysis further demonstrated that treatment with Compound C blocked the activation of AMPK/Akt/eNOS signaling pathway induced by SAL. ConclusionSAL upregulates the biological functions of EPCs through activating the AMPK/Akt/eNOS signaling pathway， thereby ameliorating EPC dysfunction during the pathological progression of atherosclerosis.

Objective: To investigate the iodine nutrition status of children aged 8-10 in Guangming, Longhua and Yantian District of Shenzhen in 2023, and to explore the influencing factors of thyroid volume. To evaluate prevention strategies and to provide a scientific basis for the elimination of iodine deficiency disorders. Methods: Urine and household salt samples were randomly collected from 580 non-boarding students aged 8-10 years foriodine content detection. Thyroid volume was measured using a fully digital ultrasound imaging system, and goiter prevalence was calculated. Results: A total of 580 samples was tested. The median salt iodine concentration was 23.86 mg/kg, with 93.62% qualified iodized salt and 94.48% coverage rate. The median of urinary iodine was 265.00 μg/L, mainly distributed between 200 - < 300 μg/L and ≥300 μg/L. The proportion of children with ap⁃ propriate iodine was 20. 86% , and the proportion of children with insufficient or excessive urinary iodine levels was 10. 86% and 68. 28% of the total surveyed population , respectively. The median thyroid volume was 3. 27 mL , and the goiter rate was 1. 72% . Multiple linear regression analysis showed that age was the risk factor for thyroid volume (8=0 328, P<0.05). while urinary iodine was the protective factor for thyroid volume(B=-4.134x10-4,P<0.05). Conclusion The qualified iodized salt rate, median of urinary iodine,and goiter prevalence of 580 children aged 8 - 10 meet the elimination criteria for iodine deficiency disorders. Age and urinary iodine are closely related to thyroid volume change. The urinary iodine level of children is generally high and requires serious attention.

Myelin is an essential structure that facilitates rapid saltatory conduction in the nervous system. Discrepancies in myelin microstructure are a hallmark of numerous neurological disorders, rendering the assessment of myelin integrity and content an indispensable tool in clinical diagnostics and neuroscience research. Extensive research has been dedicated to scrutinizing its biochemical makeup and morphology under normal, pathological, and experimental conditions over the years. In this review, we present an updated summary of the myelin sheath's structure, composition, and developmental trajectory. We systematically enumerate and contrast eight prevalent myelin staining techniques across dimensions of sensitivity, specificity, and resolution, delving into their underlying staining principles. With an initial application of myelin histology on the mouse demyelination model, our review accentuates the accurate delineation of myelination and the microstructural analysis of the myelin sheath. Such insights are anticipated to significantly contribute to the evaluation and understanding of white matter pathologies.
Myelin Sheath/metabolism* ; Animals ; Humans ; Demyelinating Diseases/pathology* ; Staining and Labeling/methods*

Stem cells play a crucial role in maintaining tissue regenerative capacity and homeostasis. However, mechanisms associated with stem cell senescence require further investigation. In this study, we conducted a proteomic analysis of human dental pulp stem cells (HDPSCs) obtained from individuals of various ages. Our findings showed that the expression of NUP62 was decreased in aged HDPSCs. We discovered that NUP62 alleviated senescence-associated phenotypes and enhanced differentiation potential both in vitro and in vivo. Conversely, the knocking down of NUP62 expression aggravated the senescence-associated phenotypes and impaired the proliferation and migration capacity of HDPSCs. Through RNA-sequence and decoding the epigenomic landscapes remodeled induced by NUP62 overexpression, we found that NUP62 helps alleviate senescence in HDPSCs by enhancing the nuclear transport of the transcription factor E2F1. This, in turn, stimulates the transcription of the epigenetic enzyme NSD2. Finally, the overexpression of NUP62 influences the H3K36me2 and H3K36me3 modifications of anti-aging genes (HMGA1, HMGA2, and SIRT6). Our results demonstrated that NUP62 regulates the fate of HDPSCs via NSD2-dependent epigenetic reprogramming.
Humans ; Dental Pulp/cytology* ; Nuclear Pore Complex Proteins/genetics* ; Cellular Senescence/genetics* ; Stem Cells/metabolism* ; Epigenesis, Genetic ; Cell Proliferation ; Cell Differentiation ; Histone-Lysine N-Methyltransferase/metabolism* ; Cells, Cultured ; Cellular Reprogramming ; Cell Movement ; Proteomics

Objective To investigate the risk factors for the occurrence of metabolic dysfunction-associated steatotic liver disease(MASLD)in lean individuals and construct a risk prediction model.Methods Based on the National Health and Nutrition Examination Survey(NHANES)database in the United States(from January 2017 to March 2020),1 123 adult individuals were included in this study.Then the participants were randomly divided into a training set(n=561)and a validation set(n=562)through simple random sampling.Data on their demographics,anthropometrics,lifestyle,underlying diseases,and laboratory test results were collected.LASSO regression analysis was used to screen potential variables in the training set,and multivariate logistic regression was employed to identify independent risk factors for lean MASLD.Based on these risk factors,a prediction model for lean MASLD was constructed(LMPM).To evaluate the clinical value of the LMPM,it was compared with two commonly used prediction models for non-alcoholic fatty liver disease,the fatty liver index(FLI)and the hepatic steatosis index(HSI).The performance of the model was evaluated and internally validated using the area under the receiver operating characteristic curve(AUC),net reclassification index(NRI),integrated discrimination improvement(IDI),calibration curve,decision curve,and clinical impact curve.Results Age,waist circumference,and triglycerides(TG)were identified as independent risk factors for the development of MASLD in lean individuals.The LMPM,constructed based on these indicators,demonstrated good discriminative ability in both the training and validation sets,with AUC values of 0.86(95%CI:0.82～0.89)and 0.81(95%CI:0.77～0.85),respectively,which were significantly better than those of FLI[training set:AUC=0.83(95%CI:0.79～0.87);validation set:AUC=0.74(95%CI:0.70～0.79)]and HSI[training set:AUC=0.71(95%CI:0.66～0.76);validation set:AUC=0.71(95%CI:0.65～0.76)].Compared with FLI and HSI,the LMPM showed improvements in NRI and IDI in both the training and validation sets.The calibration curve demonstrated its high accuracy,and both the decision curve analysis and the clinical impact curve analysis indicated that the LMPM provided greater clinical benefits.Conclusion Age,waist circumference,and TG are independent risk factors for lean MASLD.Based on these factors,a prediction model,named LMPM,is developed to assess the risk of MASLD in lean individuals,which exhibits good predictive performance and has certain guiding significance for the timely identification of high-risk populations.

Objective To elucidate the effects of miR-616 on the malignant biological processes of osteosarcoma and to preliminarily explore its potential mechanisms.Methods In situ hybridization(ISH)was employed to analyze miR-616 expression in 11 paraffin-embedded osteosarcoma specimens collected in our department during January 2018 to December 2019.Quantitative real-time PCR(qRT-PCR)was used to compare the mRNA expression level of miR-616 in the osteoblast cell line hFOB1.19 and osteosarcoma cell lines 143B and HOS.Stable cell lines with miR-616 knockdown or overexpression were established via lentiviral transfection in 143B and HOS cells.Cell proliferation and apoptosis were detected by flow cytometry,while cell invasion and migration were assessed using Transwell and colony formation assays,respectively.To evaluate the effect of miR-616 on tumor growth in vivo,10 female nude mice(4 weeks old,weighing 18～20 g)were randomized into a control group and a miR-616 overexpression group.After the xenograft tumor model was constructed,the growth of subcutaneous tumors was monitored.Finally,next-generation sequencing and a dual-luciferase reporter assay were performed to identify the target genes of miR-616.Results ISH results showed that miR-616 expression was up-regulated in osteosarcoma tissues than adjacent tissues,and primarily localized in the cytoplasm.qRT-PCR confirmed that miR-616 level was significantly higher in 143B and HOS cells than hFOB1.19 cells(P<0.05).In vitro experiments revealed that miR-616 overexpression enhanced the proliferation,migration and invasion,while suppressing apoptosis in 143B and HOS cells(P<0.01).Conversely,miR-616 knockdown weakened these malignant phenotypes(P<0.05),with miR-616-3p showing a stronger effect on apoptosis than miR-616-5p.Animal experiments demonstrated that the tumor weight in the miR-616 overexpression group was significantly greater than that of the control group(98.00±17.22 vs 33.60±8.08 mg,P<0.01).Furthermore,KLF2 was identified and confirmed as a direct target of miR-616.Conclusion MiR-616 promotes malignant biological behaviors in osteosarcoma,and its expression level indicates that it may serve as a potential therapeutic target.

Objective To explore the factors predicting the reliability of platelet-impedance(PLT-I)re-sults through a retrospective analysis of non-aggregated samples with abnormal platelet histograms.Methods A total of 322 samples with abnormal platelet histograms were collected from the Sysmex XN9000 automatic hematology analyzer,all of which showed no platelet aggregation as determined by the DI-60 auto-matic digital image analysis system.Using the platelet count fluorescent(PLT-F)results as a standard,the absolute and relative deviations of PLT-I results were calculated,and the parameters of samples with devia-tions within and outside the allowable range were analyzed.Logistic regression analysis was used to identify potential factors associated with deviations of PLT-I from PLT-F beyond the allowable range.The receiver op-erating characteristic(ROC)curve was used to evaluate the predictive value of these potential factors for devi-ations beyond the allowable range.Results The deviations of PLT-I from PLT-F were within the allowable range in 279 cases(86.65％)and outside the allowable range in 43 cases(13.35％).Comparisons between the two groups revealed statistically significant differences in mean red blood cell valume(MCV),red blood cell distribution width-cuefficient of variation(RDW-SD),DI-60 red cell fragments,platelet distribution width(PDW),and DI-60 large platelet ratio(P＜0.05).Logistic regression indicated that DI-60 red cell fragments and DI-60 large platelet ratio were independent potential factors for deviations of PLT-I from PLT-F beyond the allowable range(P＜0.05).The cut off values for predicting deviations beyond the allowable range were 1.75 for DI-60 red cell fragments and 66％for DI-60 large platelet ratio.The area under the curve(AUC)for the combined diagnosis of the two factors was 0.813,with a sensitivity of 88.4％and a specificity of 66.3％,indicating a higher predictive value than individual factors(P＜0.05).Conclusion When platelet histograms are abnormal,DI-60 large platelet ratio and DI-60 red cell fragments are independent potential factors predic-ting the reliability of PLT-I results,and their combination has a high predictive value.

Objective:To explore the clinical efficacy of a free superficial palmar branch of the radial artery (SPBRA)-pedicled wrist crease flap for bridging and repairing finger C-shape soft tissue defect.Methods:From March 2021 to January 2023, the clinical data of patients with finger C-shape soft tissue defects in Department of Orthopedics, the Affiliated Changzhou No. 2 People’s Hospital of Nanjing Medical University were retrospectively analyzed. Preoperatively, color Doppler was used to locate the perforator point, and the position and size of the flap were designed. A free SPBRA-pedicled wrist crease flap was used in a Flow-through method to bridge and repair the defects. Postoperatively, the survival, color, texture, sense, and shape of the skin flap were observe, and the healing of the donor site was assessed. The clinical efficacy was evaluated using Evaluation Trail Standards for Replantation Function of Chinese Society of Hand Surgery.Results:All 10 patients completed the entry result analysis, including 8 males and 2 females. The age ranged from 22 to 54 years old. Among them, 3 cases involved the index finger, 5 cases involved the middle finger, and 2 cases involved the ring finger. All of them showed segmental defects of the unilateral volar medial artery with combined digital nerve defects, including 7 cases of radial injury and 3 cases of ulnar injury. 3 cases of the vascular defect ranged in the proximal phalanx areas, 6 cases in the middle phalanx region, and 1 case in the middle to distal phalanx region. The length of the proper artery defect ranged from 1.0 cm to 1.8 cm, the area of skin defect ranged from 1.0 cm×2.5 cm to 2.2 cm×4.0 cm, and the harvested flap area range ranged from 1.2 cm×2.8 cm to 2.5 cm×5.0 cm. The patients were followed up for 10 to 19 months. All flaps survived and healed well, with no bulky appearance, and a texture similar to normal finger skin. The static two-point discrimination ranged from 7.0~ 10.0 mm (average 8.5 mm). Superficial infection around the flap occurred in 1 case after surgery. It improved after dressing change. No vascular crisis occurred. The wounds at the donor site healed primarily, leaving linear scars. The flexion and extension activities of the wrist joint were not affected. According to the Evaluation Trail Standards for Replantation Function of Chinese Society of Hand Surgery: 8 cases received excellent results, 2 cases were good, and the patient satisfaction was high.Conclusion:The free SPBRA-pedicled wrist crease flap has good and accurate efficacy in bridging and repairing finger C-shape soft tissue defects. It has the advantages of convenient harvesting, minimal trauma, and low complication rate, and has clinical promotion and application value.

Multi-family therapy (MFT), as an extension of traditional family therapy, refers to a treatment method in which family members from multiple families participate at the same time. Although its application in severe mental disorders such as schizophrenia is mature, its potential in a wider field and its localization pathway need to be systematically discussed. This paper aims to summarize the development, treatment settings and requirements of the early classic model of MFT, analyze its core mechanism, focus on summarizing the emerging application model variants and effectiveness of MFT in medical care (schizophrenia, eating disorders), school education (refusing to intervene in school) and social work (treating ADHD children, traumatized families, etc.), and comprehensively explore the research methods of effect evaluation.However, there are still some limitations in the current researches, such as lax evaluation, unclear specific action pathway, family vulnerability and lack of cross-cultural adaptability research. Finally, the future development direction is prospected to provide reference for promoting the application practice of MFT.