ObjectiveThe present study aimed to investigate alterations in white matter microstructure and spontaneous neural activity in male college smokers, and to further explore their associations with nicotine dependence. Given that adolescence and early adulthood represent critical periods for brain maturation, particularly for white matter development, understanding the neural correlates of smoking behavior during this stage is of substantial importance for both neuroscience and public health. MethodsA total of 115 male undergraduate students were initially recruited for this study. After quality control and exclusion procedures, 52 male college smokers and 42 demographically matched healthy non-smokers were included in the final analysis. All participants underwent multimodal magnetic resonance imaging (MRI), including diffusion tensor imaging (DTI) and resting-state functional MRI (rs-fMRI). White matter fiber tracts were reconstructed using the automated fiber quantification (AFQ) method, which enables precise identification and quantification of major fiber bundles. Eighteen major white matter tracts were segmented for each participant. Along the core trajectory of each tract, 100 equidistant nodes were sampled. Fractional anisotropy (FA) was calculated at each node to assess white matter microstructural integrity, while amplitude of low-frequency fluctuation (ALFF) was computed to evaluate spontaneous neural activity within white matter tracts. Between-group differences in FA and ALFF were assessed using two-sample t-tests, with appropriate corrections applied for multiple comparisons. Furthermore, Pearson correlation analyses were conducted to examine the relationships between imaging-derived metrics (FA and ALFF values in regions showing significant group differences) and nicotine dependence severity, as measured by the Fagerström test for nicotine dependence (FTND). ResultsCompared with healthy non-smokers, male college smokers exhibited significantly increased FA values in several white matter tracts, including the left thalamic radiation, right corticospinal tract, forceps major of the corpus callosum, left uncinate fasciculus, and right arcuate fasciculus. These findings suggest altered microstructural organization or increased directional coherence within these pathways. In addition, smokers demonstrated significantly elevated ALFF values in the forceps major, right uncinate fasciculus, and left arcuate fasciculus, indicating enhanced spontaneous neural activity in these white matter regions. Correlation analyses revealed that FA values in the left thalamic radiation and right corticospinal tract were negatively correlated with FTND scores, suggesting that higher levels of nicotine dependence were associated with reduced microstructural integrity or altered fiber organization in these regions. In contrast, ALFF values in the forceps major and right uncinate fasciculus were positively correlated with FTND scores, indicating that greater nicotine dependence was associated with increased spontaneous neural activity in specific white matter pathways. ConclusionThe present study provides evidence that male college smokers exhibit distinct alterations in both white matter microstructure and functional activity. These abnormalities are not uniformly distributed but rather localized to specific fiber tracts implicated in sensorimotor processing, interhemispheric communication, and higher-order cognitive and emotional regulation. Importantly, the observed associations between imaging metrics and nicotine dependence severity suggest that these structural and functional alterations may reflect neurobiological mechanisms underlying addiction. The combination of AFQ-based tract profiling and multimodal MRI offers a sensitive approach for detecting subtle changes along white matter pathways, highlighting its potential utility in identifying neuroimaging biomarkers of nicotine dependence. Overall, these findings indicate that smoking during early adulthood may disrupt ongoing white matter maturation, potentially leading to long-term consequences for brain function. This study provides novel insights into the neural basis of nicotine dependence and underscores the importance of early intervention and prevention strategies targeting young smokers.

BACKGROUND:The application of high-frequency ultrasound technology provides an effective tool for the precise assessment of skeletal muscle morphology in the elderly.However,the correlation between the morphological parameters of skeletal muscle obtained and physical activity capacity remains unclear. OBJECTIVE:To explore the correlation between morphological parameters of the gastrocnemius muscle and physical activity capacity in elderly females using high-frequency ultrasound imaging technology,thereby identifying effective predictive indicators for physical activity capacity in the elderly. METHODS:Fifty-nine elderly female subjects over the age of 60 with the ability to live independently were recruited in the communities surrounding Shanghai Sanda University.High-frequency ultrasound images of the subjects'gastrocnemius muscles were collected to obtain the relevant parameters,including muscle thickness,fiber length,pennation angle,and fiber length/muscle thickness(Lf/Tm)index.Physical activity capacity tests were also conducted and relevant indicators included the 10-meter walk test,timed up-and-go test,30-second chair stand test,and grip strength test.Correlation analyses were performed between various morphological parameters and physical activity capacity test indicators. RESULTS AND CONCLUSION:Significant correlations were found between various muscle morphological parameters(P<0.05).The pennation angle showed significant correlations with the 10-meter walking speed(r=-0.35,P<0.05)and timed up-and-go test results(r=0.32,P<0.05).The Lf/Tm index was positively correlated with 10-meter walking speed and grip strength test results(r=0.39,P<0.01;r=0.30,P<0.05),but was negatively correlated with timed up-and-go test results(r=-0.32,P<0.05).All these findings indicate that the pennation angle and Lf/Tm index of the gastrocnemius muscle show a good correlation with physical activity capacity in elderly females,which can serve as effective predictive indicators for physical activity capacity.

Objective To systematic evaluate the impact of applying the clinical nursing pathway(CNP)on epidural anesthetic analgesia natural delivery.Methods The randomized controlled trial(RCT)and quasi-experimental researches on the application of CNP in epidural anesthetic analgesia natural delivery were retrieved from PubMed,Cochrane Library,Embase,Web of Science,China Knowledge Network database,Wanfang database,VIP and the Chinese Biomedical Literature Database.The retrieval time limit was from January 1,2014,to July 31,2024 with no language limitation.The meta analysis on the included studies was performed by applying RevMan5.4.1.Results A total of 5 RCTs and 2 quasi-experimental studies were in-cluded,involving 979 parturients with deliveries.The meta analysis showed that compared with the conven-tional nursing,CNP could shorten the duration of the first stage of labor(MD=—1.06,95％CI:—1.95——0.17,P=0.02)and the duration of the second stage of labor(MD=—0.12,95％CI:—0.21——0.03,P=0.006);decreased the rate of perineal lateral incision(RR=0.73,95％CI:0.65-0.83,P＜0.001)and inci-dence rate of postpartum urinary retention(RR=0.35,95％CI:0.20-0.63,P＜0.001);and shortened the time to lactation initiation(SMD=—1.52,95％CI:—2.38——0.66,P＜0.001).There was no influence on reducing postpartum 24 h hemorrhage amount(SMD=—0.51,95％CI:—1.23-0.21,P=0.16).The study subjects were divided into the primipara women subgroup and unclassified parturients subgroup.Compared with the conventional nursing group,compared with the conventional nursing,CNP had no impact on the dura-tion of the first stage of labor(MD=—0.32,95％CI:—0.61-0.98,P=0.63)and the duration of the second stage of labor(MD=—0.11,95％CI:—0.25-0.04,P=0.15)in the primipara women subgroup.CNP could reduce the postpartum 24 h hemorrhage volume in the unclassified parturients subgroup(SMD=—1.47,95％CI:—1.72——1.21,P＜0.001).Conclusion Application of CNP in parturients labor analgesia could reduce the perineal lateral incision rate and incidence rate of postpartum urinary retention and shorten the time to lac-tation initiation.Due to the heterogeneity among studies,the impact of CNP on the labor duration and the bleeding amount within postpartum 24 h still requires more high-quality studies to be conducted in the future for verification.

Objective To report a case of tibial synovial sarcoma and review relevant literature to enhance understanding of this disease.Methods The clinical data of a patient with tibial synovial sarcoma treated at Kaifeng Central Hospital were retrospectively analyzed.A literature search was conducted in domestic and international databases,including China National Knowledge Infrastructure(CNKI),Wanfang Data,PubMed,Web of Science,and Embase,up to July 2024.Relevant literature was comprehensively reviewed to summarize the imaging and pathological characteristics,treatment,and prognosis of synovial sarcoma.Results A 29-year-old female patient was admitted with left lower extremity pain.X-ray examination revealed a proximal tibia space-occupying lesion suggestive of malignancy,and a mid-tibial space-occupying lesion considered benign.Contrast-enhanced computed tomography(CT)and plain magnetic resonance imaging(MRI)of the proximal tibial lesion also suggested malignancy.Ultrasound-guided biopsy of the proximal tibial tumor revealed a poorly differentiated malignant tumor.Immunohistochemistry results indicated monophasic synovial sarcoma,requiring genetic testing for definitive diagnosis.The patient underwent wide resection of the proximal left tibial malignancy with tumor-type artificial joint replacement,combined with curettage and bone cement filling for the left mid-tibial lesion under anesthesia.Postoperative pathology of space-occupying lesions in the proximal tibia confirmed monophasic synovial sarcoma,and fluorescence in situ hybridization(FISH)demonstrated a rupture of the synovial sarcoma translocation gene(SYT)(i.e.,SS18 positive).There was no recurrence or metastasis found in the patient during the reexamination 6 months after postoperative chemotherapy.As of July 2024,15 cases of genetically confirmed primary intraosseous synovial sarcoma have been reported internationally.Symptoms included pain and swelling,with a medical history of 1-2 years.The X-ray and CT findings showed osteolytic destruction with bone cortical discontinuity.In 13 cases,the intraosseous masses extended to the extraosseous area;in 2 cases,punctate calcifications were detected within the masses.Plain MRI scan showed iso-signal or hypo-signal on T1WI and hyper-signal,iso-signal,and hypo-signal on fat-suppressed T2WI,and enhanced MRI scan demonstrated heterogeneous enhancement.Pathological examination showed spindle-shaped cells under microscopy.Immunohistochemistry results showed positive epithelial membrane antigen(EMA),broad-spectrum cytokeratin(AE1/AE3),Ewing's sarcoma marker(CD99),and transducin-like enhancer of Split 1(TLE1).Twelve patients underwent surgical treatment;6 patients received adjuvant chemotherapy after surgery,of whom 4 developed local recurrence or distant metastasis at initial diagnosis,and 3 died during follow-up.Among the 6 patients who did not receive adjuvant chemotherapy,3 suffered from recurrence or distant metastasis.Conclusions Primary intraosseous synovial sarcoma is a rare malignant tumor with non-specific clinical manifestations.Imaging features typically include osteolytic destruction and intraosseous masses extending extraosseously,suggesting an intraosseous origin.Pathology and immunohistochemistry aid diagnosis,but definitive confirmation relies on further genetic testing.At present,the main treatment regimens for synovial sarcoma involve comprehensive therapies such as surgery and adjuvant chemotherapy,and the prognosis of patients is poor.

Numerous studies on the formation and consolidation of memory have shown that memory processes are characterized by phase-dependent and dynamic regulation. Memory retrieval, as the only representation of memory content and an active form of memory processing that induces memory reconsolidation, has attracted increasing attention in recent years. Although the molecular mechanisms specific to memory retrieval-induced reconsolidation have been gradually revealed, an understanding of the time-dependent regulatory mechanisms of this process is still lacking. In this study, we applied a transcriptome analysis of memory retrieval at different time points in the recent memory stage. Differential expression analysis and Short Time-series Expression Miner (STEM) depicting temporal gene expression patterns indicated that most differential gene expression occurred at 48 h, and the STEM cluster showing the greatest transcriptional upregulation at 48 h demonstrated the most significant difference. We then screened the differentially-expressed genes associated with that met the expression patterns of those cluster-identified genes that have been reported to be involved in learning and memory processes in addition to dipeptidyl peptidase 9 (DPP9). Further quantitative polymerase chain reaction verification and pharmacological intervention suggested that DPP9 is involved in 48-h fear memory retrieval and viral vector-mediated overexpression of DPP9 countered the 48-h retrieval-induced attenuation of fear memory. Taken together, our findings suggest that temporal gene expression patterns are induced by recent memory retrieval and provide hitherto undocumented evidence of the role of DPP9 in the retrieval-induced reconsolidation of fear memory.
Animals ; Fear/physiology* ; Male ; Dipeptidyl-Peptidases and Tripeptidyl-Peptidases/genetics* ; Memory Consolidation/physiology* ; Time Factors ; Mental Recall/drug effects* ; Mice ; Gene Expression Profiling

Hemorrhagic shock is a common clinical emergency that can aggravate cell injury after resuscitation. Astrocytes are crucial for the survival of neurons because they regulate the surrounding ionic microenvironment of neurons. Although hemorrhagic shock and resuscitation (HSR) injury can impair cognition, it remains unclear how this insult directly affects astrocytes. In this study, we established an HSR model by bleeding and re-transfusion in mice. The social interaction test and new object recognition test were applied to evaluate post-operative cognitive changes, and the results suggest that mice experience cognitive impairment following exposure to HSR. In the HSR group, the power spectral density of β and γ oscillations decreased, and the coupling of the θ oscillation phase and γ oscillation amplitude was abnormal, which indicated abnormal neuronal oscillation and cognitive impairment after HSR exposure. In brief, cognitive impairment in mice is strongly correlated with Ca²⁺ signal strength in lateral septum astrocytes following HSR.
Animals ; Astrocytes/metabolism* ; Shock, Hemorrhagic/metabolism* ; Resuscitation/adverse effects* ; Male ; Mice ; Calcium Signaling/physiology* ; Mice, Inbred C57BL ; Septal Nuclei/metabolism* ; Cognitive Dysfunction/etiology* ; Disease Models, Animal ; Cognition Disorders/etiology*

Objective To systematically evaluate the effectiveness and acceptability of antidepressant drugs in the treatment of postpartum depression(PPD).Methods The PubMed,Cochrane Library,Embase,Web of Science,China National Knowledge Infrastructure(CNKI),Wanfang Database,VIP Journals of Chinese Scienc were searched,and Chinese Biomedical Literature Service System(SinoMed)database until November 2023.Screen randomized controlled trials(RCTs)of antidepressant drugs for the treatment of PPD.The treatment group was given antidepressant drugs,and the control group was given placebo or another antidepressant drug.Meta-analysis of effectiveness and acceptability is performed using Stata 17.0 software.Results A total of 27 RCTs with a total of 2 202 patients were included.The results of meta-analysis showed:The top three efficacy relative to placebo were mirtazapine[odds ratio(OR)=2.25,95％confidence interval(CI)=(1.20-3.30),P＜0.05],nortriptyline[OR=1.50,95％CI=(0.55-2.44),P＞0.05],venlafaxine[OR=1.35,95％CI=(0.13-2.56),P＞0.05].Acceptability is compared with placebo in the top three Chinese herbal medicine[OR=0.47,95％CI=(-0.72-1.66),P＞0.05],nortriptyline[OR=-0.08,95％CI=(-1.16-1.33),P＞0.05],venlafaxine[OR=-0.12,95％CI=(-1.47-1.24),P＞0.05].Conclusion Nortriptyline,venlafaxine,trazodone,and duloxetine are effective in treating PPD without obvious adverse drug reactions.

Objective To investigate the failure distribution characteristics of semiconductor coolers for medical devices and to analyze the failure mechanisms at different time periods.Methods Firstly,a sample of a pilot semiconductor cooler used in some medical device was used as the object,and all the failure data within the last 4 years were collected,screened and organized.Secondly,the failure data were fitted based on the Weibull distribution,and the failure distribution characteristics were analyzed by shape parameters.Finally,based on the failure distribution characteristics,mechanism analysis was carried out with the typical failure samples selected from three time periods of early failure,random failure and wear-out failure,and the causes of failure were found out.Results The failures of semiconductor coolers occurring in the three time periods presented different types of mechanisms,and the failure distribution conformed to the Weibull distribution.The causes included the mechanical stress damage for early failures,the process defect for random failures and water vapour penetration due to sealant aging after long-term operation of the semiconductor cooler.Conclusion The failure patterns of semiconductor coolers for medical devices are revealed effectively,providing a scientific basis for the design,improvement and reliability assessment of semiconductor coolers used in medical equipment.[Chinese Medical Equipment Journal,2025,46(5):34-38]

ObjectiveTo investigate the influence of histone deacetylase 3 (HDAC3) on the occurrence, development of psoriasis-like inflammation in mice, and the relative immune mechanisms. MethodsHealthy C57BL/6 mice aged 6-8 weeks were selected and randomly divided into 3 groups: control group (Control), psoriasis model group (IMQ), and HDAC3 inhibitor RGFP966-treated psoriasis model group (IMQ+RGFP966). One day prior to the experiment, the back hair of the mice was shaved. After a one-day stabilization period, the mice in Control group was treated with an equal amount of vaseline, while the mice in IMQ group was treated with imiquimod (62.5 mg/d) applied topically on the back to establish a psoriasis-like inflammation model. The mice in IMQ+RGFP966 group received intervention with a high dose of the HDAC3-selective inhibitor RGFP966 (30 mg/kg) based on the psoriasis-like model. All groups were treated continuously for 5 d, during which psoriasis-like inflammation symptoms (scaling, erythema, skin thickness), body weight, and mental status were observed and recorded, with photographs taken for documentation. After euthanasia, hematoxylin-eosin (HE) staining was used to assess the effect of RGFP966 on the skin tissue structure of the mice, and skin thickness was measured. The mRNA and protein expression levels of HDAC3 in skin tissues were detected using reverse transcription real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot (WB), respectively. Flow cytometry was employed to analyze neutrophils in peripheral blood and lymph nodes, CD4⁺ T lymphocytes, CD8⁺ T lymphocytes in peripheral blood, and IL-17A secretion by peripheral blood CD4⁺ T lymphocytes. Additionally, spleen CD4⁺ T lymphocyte expression of HDAC3, CCR6, CCR8, and IL-17A secretion levels were analyzed. Immunohistochemistry was used to detect the localization and expression levels of HDAC3, IL-17A, and IL-10 in skin tissues. ResultsCompared with the Control group, the IMQ group exhibited significant psoriasis-like inflammation, characterized by erythema, scaling, and skin wrinkling. Compared with the IMQ group, RGFP966 exacerbated psoriasis-like inflammatory symptoms, leading to increased hyperkeratosis. The psoriasis area and severity index (PASI) skin symptom scores were higher in the IMQ group than those in the Control group, and the scores were further elevated in the IMQ+RGFP966 group compared to the IMQ group. Skin thickness measurements showed a trend of IMQ+RGFP966>IMQ>Control. The numbers of neutrophils in the blood and lymph nodes increased sequentially in the Control, IMQ, and IMQ+RGFP966 groups, with a similar trend observed for CD4⁺ and CD8⁺ T lymphocytes in the blood. In skin tissues, compared with the Control group, the mRNA and protein levels of HDAC3 decreased in the IMQ group, but RGFP966 did not further reduce these expressions. HDAC3 was primarily located in the nucleus. Compared with the Control group, the nuclear HDAC3 content decreased in the skin tissues of the IMQ group, and RGFP966 further reduced nuclear HDAC3. Compared with the Control and IMQ groups, RGFP966 treatment decreased HDAC3 expression in splenic CD4⁺ and CD8⁺ T cells. RGFP966 treatment increased the expression of CCR6 and CCR8 in splenic CD4⁺ T cells and enhanced IL-17A secretion by peripheral blood and splenic CD4⁺ T lymphocytes. Additionally, compared with the IMQ group, RGFP966 reduced IL-10 protein levels and upregulated IL-17A expression in skin tissues. ConclusionRGFP966 exacerbates psoriatic-like inflammatory responses by inhibiting HDAC3, increasing the secretion of the cytokine IL-17A, and upregulating the expression of chemokines CCR8 and CCR6.

Hepatocellular carcinoma (HCC) expresses abundant glycolytic enzymes and displays comprehensive glucose metabolism reprogramming. Aldolase A (ALDOA) plays a prominent role in glycolysis; however, little is known about its role in HCC development. In the present study, we aim to explore how ALDOA is involved in HCC proliferation. HCC proliferation was markedly suppressed both in vitro and in vivo following ALDOA knockout, which is consistent with ALDOA overexpression encouraging HCC proliferation. Mechanistically, ALDOA knockout partially limits the glycolytic flux in HCC cells. Meanwhile, ALDOA translocated to nuclei and directly interacted with c-Jun to facilitate its Thr93 phosphorylation by P21-activated protein kinase; ALDOA knockout markedly diminished c-Jun Thr93 phosphorylation and then dampened c-Jun transcription function. A crucial site Y364 mutation in ALDOA disrupted its interaction with c-Jun, and Y364S ALDOA expression failed to rescue cell proliferation in ALDOA deletion cells. In HCC patients, the expression level of ALDOA was correlated with the phosphorylation level of c-Jun (Thr93) and poor prognosis. Remarkably, hepatic ALDOA was significantly upregulated in the promotion and progression stages of diethylnitrosamine-induced HCC models, and the knockdown of A ldoa strikingly decreased HCC development in vivo. Our study demonstrated that ALDOA is a vital driver for HCC development by activating c-Jun-mediated oncogene transcription, opening additional avenues for anti-cancer therapies.