Objective: To explore the relationship between non suicidal self injury (NSSI) behavior and serum lipid levels as well as thyroid function among college students with depression. Methods: A total of 169 college students with depression in the psychiatry departments of tertiary hospitals (grade 3A and 3B) in Ningbo from December 2023 to April 2025 were selected. The Adolescent Self injury Scale (ASIS) was used to assess the presence of NSSI, and participants were accordingly divided into a NSSI group ( n =51) and a non NSSI group ( n =118). General demographic data (including gender, age, and family situation) were collected from both groups. Blood tests were performed to measure lipid profiles [triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C)] and thyroid hormones [triiodothyronine (T3), thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH)]. Multivariate Logistic regression was employed to analyze risk factors for NSSI, and receiver operating characteristic (ROC) curve analysis was used to evaluate the predictive value of serum lipid and thyroid hormone levels for NSSI occurrence in college students with depression. Results: The levels of TC, LDL-C, and TSH in the NSSI group were (4.02±0.73) mmol/L, (2.32±0.36) mmol/L, and (6.57±1.95) mU/L , which were significantly higher than those in the non NSSI group [(3.41±0.56) mmol/L, (2.00±0.27) mmol/L, and ( 4.48± 1.09) mU/L, respectively] ( t =5.32, 5.60, 7.20, all P <0.05). Logistic regression analysis revealed that college students from single parent/reconstituted families, those who had experienced school bullying, and those with higher levels of TC, LDL-C, and TSH had a significantly increased risk of engaging in NSSI ( OR =5.22, 6.12, 5.90, 83.64, 3.64, all P <0.05). ROC curve analysis demonstrated that the combined detection of TC, LDL-C, and TSH had high diagnostic efficacy for predicting NSSI in college students with depression, with a sensitivity of 86.3% and a specificity of 94.9%. Conclusions NSSI behavior in college students with depression is associated with serum lipid levels and thyroid function. These biomarkers may serve as useful reference indicators for assessing the conditions of these patients.

ObjectiveThis study aimed to investigate whether Bushen Tongluo prescription inhibits macrophage polarization by regulating the Wnt3a/β-catenin signaling pathway， thereby reducing epithelial-mesenchymal transition and excessive extracellular matrix deposition， in order to elucidate the anti-pulmonary fibrosis mechanisms of Bushen Tongluo prescription and provide a new theoretical basis for the clinical treatment of pulmonary fibrosis. MethodsFifty male Sprague-Dawley （SD） rats were randomly divided into a blank group， model group， pirfenidone group， and high- and low-dose Bushen Tongluo prescription groups. Except for the blank group， the pulmonary fibrosis model was established by intratracheal instillation of bleomycin. Intervention was initiated on day 28 after modeling. The high- and low-dose Bushen Tongluo prescription groups were administered Bushen Tongluo prescription at doses of 30.88， 15.44 g·kg^-1， respectively， by intragastric gavage. The pirfenidone group was administered pirfenidone capsules at 110 mg·kg^-1 by intragastric gavage. The blank and model groups were given an equal volume of normal saline by gavage， once daily for 90 days. After treatment， the level of transforming growth factor-β₁ （TGF-β₁） in bronchoalveolar lavage fluid （BALF） was detected by enzyme-linked immunosorbent assay （ELISA）. Morphological changes in lung tissue and the collagen volume fraction were compared. The protein distribution and expression of E-cadherin， cytokeratin 19， α-smooth muscle actin （α-SMA）， vimentin， collagen type Ⅰ （Col Ⅰ）， and collagen type Ⅲ （Col Ⅲ） in lung tissue were detected by immunohistochemistry. The protein distribution and expression of CD68， arginase-1 （Arg-1）， inducible nitric oxide synthase （iNOS）， Wnt3a， and β-catenin in lung tissue were detected by immunofluorescence. The protein expression of Wnt3a and β-catenin in lung tissue was detected by Western blot， and the mRNA expression of Wnt3a and β-catenin was detected by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultsCompared with the blank group， a large number of inflammatory cells infiltrated the airway walls， alveolar spaces， and interstitial tissue in the model group， with obvious fibrous tissue hyperplasia. The level of TGF-β₁ in BALF was significantly increased. The protein expression of E-cadherin and cytokeratin 19 in lung tissue was decreased， whereas the protein expression of α-SMA， Vimentin， Wnt3a， β-catenin， Col Ⅰ， and Col Ⅲ was increased. The fluorescence-positive area ratios of CD68， Arg-1， iNOS， Wnt3a， and β-catenin in lung tissue were increased. The protein and mRNA expression levels of Wnt3a and β-catenin in lung tissue were significantly increased （P<0.01）. Compared with the model group， all treatment groups showed varying degrees of improvement in inflammatory cell infiltration and fibrous tissue hyperplasia in the airway walls， alveolar spaces， and interstitial tissue， decreased TGF-β₁ levels in BALF， increased protein expression of E-cadherin and cytokeratin 19 in lung tissue， decreased protein expression of α-SMA， Vimentin， Col Ⅰ， and Col Ⅲ， decreased fluorescence-positive area ratios of CD68， Arg-1， iNOS， Wnt3a， and β-catenin in lung tissue， and decreased protein and mRNA expression levels of Wnt3a and β-catenin in lung tissue （P<0.05， P<0.01）. ConclusionBushen Tongluo prescription can improve bleomycin-induced pulmonary fibrosis in rats by inhibiting epithelial-mesenchymal transition and reducing excessive extracellular matrix deposition. The mechanism may be related to inhibition of the Wnt3a/β-catenin signaling pathway and the macrophage polarization mediated by this pathway.

BACKGROUND:Apoptosis plays an important role in secondary brain injury.Therefore,to explore the pathophysiological mechanism of promoting nerve cell survival after traumatic brain injury provides a new direction and theoretical basis for the prevention and treatment of traumatic brain injury. OBJECTIVE:To explore the expression changes of Lnx1 molecule in mammalian cortical neurons after brain injury and the possible mechanism involved in secondary brain injury. METHODS:Eighty adult SD rats were divided into 20 male and 20 female mice in sham operation group and 20 male and 20 female mice in traumatic brain injury group.The traumatic brain injury rat model was established by heavy falling method.At 6,12,24,48,and 72 hours after brain injury,the expression of related molecules in damaged cortical neurons was analyzed by RT-qPCR,western blot assay,and immunofluorescence staining. RESULTS AND CONCLUSION:(1)The brain tissue of traumatic brain injury group was bleeding and obvious tissue injury could be observed.Water content of brain tissue increased after traumatic brain injury.(2)Compared with the sham operation group,the expression of Lnx1 in cortical neurons after traumatic brain injury increased significantly at 24 hours after injury.(3)After traumatic brain injury,the expression of PBK and BCR protein decreased,and the pro-survival factor ctgf increased.(4)These findings suggest that after traumatic brain injury,the expression of Lnx1 is up-regulated in neurons,which may be due to the decrease of the expression of its target molecules PBK and BCR,and further promote the expression of living factor ctgf,which has a protective effect on the damaged neurons.

Objective:To retrieve, summarize and evaluate the best evidence for the non-pharmacological management of patients with cancer pain, so as to provide an evidence-based basis for the scientific management of cancer pain by healthcare professionals.Methods:A systematic search of the national and international literature on the non-pharmacological management of cancer pain was conducted, with a timeframe of January 2017 to January 2024. The quality of the included literature was evaluated, and evidence was extracted and summarized for those that met the quality criteria.Results:A total of 18 papers were included, including one clinical decision, seven guidelines, three expert consensus, and seven systematic reviews. Twenty-eight pieces of evidence were summarized around six themes of pain assessment, cognitive-behavioral interventions, physical therapy, interventional therapy and surgery, and self-management education and follow-up.Conclusions:Healthcare professionals should develop a patient-centered, appropriate and feasible non-pharmacological management plan for cancer pain with multiple agreements with patients and families, taking into account the clinical context and individual differences of patients in China, in order to improve the quality of life.

Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors worldwide. The traditional early screening modality of ultrasound,when combined with the biomarker alpha-fetoprotein (AFP),is deficient in sensitivity and specificity. In recent years,HCC risk assessment models based on statistical methods have been widely developed and validated due to advantages such as good efficacy,non-invasiveness,and ease of generalization. Currently,HCC risk assessment models adapted to the characteristics of patients with chronic liver disease,patients with hepatitis B and C,patients with cirrhosis,and the general population have been developed. The purpose of this review is to assist clinical diagnosis treatment,and scientific research by analyzing the current research status and development of liver cancer risk assessment models.

Objective:To retrieve, summarize and evaluate the best evidence for the non-pharmacological management of patients with cancer pain, so as to provide an evidence-based basis for the scientific management of cancer pain by healthcare professionals.Methods:A systematic search of the national and international literature on the non-pharmacological management of cancer pain was conducted, with a timeframe of January 2017 to January 2024. The quality of the included literature was evaluated, and evidence was extracted and summarized for those that met the quality criteria.Results:A total of 18 papers were included, including one clinical decision, seven guidelines, three expert consensus, and seven systematic reviews. Twenty-eight pieces of evidence were summarized around six themes of pain assessment, cognitive-behavioral interventions, physical therapy, interventional therapy and surgery, and self-management education and follow-up.Conclusions:Healthcare professionals should develop a patient-centered, appropriate and feasible non-pharmacological management plan for cancer pain with multiple agreements with patients and families, taking into account the clinical context and individual differences of patients in China, in order to improve the quality of life.

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.

With the change of infectious disease incidence pattern and the development of related technologies, progresses have been made in the research of infectious disease epidemiology. In recent years, due to the change in the requirements of infectious disease prevention and control, the research focus has expanded from common infectious diseases to diseases which have been eliminated or might be eliminated, as well as emerging and re-emerging infectious diseases. Infectious disease data has been characterized by multiple sources and modalities. Along with the rapid development of pathogen detection methods, infectious disease surveillance has shifted from a single disease-targted one to a comprehensive one. Moreover, novel technologies such as multi-omics and artificial intelligence have been applied in infectious disease epidemiology research. The international cooperation in this field has become increasingly crucial, and the revision of the International Health Regulations and the negotiation of pandemic agreement will have a profound impact. In the future, infectious disease epidemiology research will develop with more powerful tools to improve its capabilities.

Objective:To analyze the key β-amyloid protein (Aβ) deposition in brain regions affecting the progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD).Methods:Based on the positron emission tomography data of Aβ in the Alzheimer's disease neuroimaging initiative database, the penalized generalized estimating equation (PGEE) and the mixed effects regression forest algorithm (MERF) were used to conduct dimensionality reduction analysis on 164 brain regions with Aβ deposition. Additionally, a multivariate longitudinal data joint model was used to screen the key Aβ deposition brain regions that influence the progression from MCI to AD.Results:Five key brain regions were commonly screened out by the PGEE and MERF models, they were the right prefrontal orbital cortex, the left superior temporal sulcus shore cortex, the right medial orbitofrontal cortex, the left putamen, and the right transverse temporal cortex, respectively. The results of the multivariate longitudinal data joint model based on these 5 Aβ deposition brain regions showed that, except the left superior temporal sulcus shore cortex, the longitudinal change trajectories of the other 4 Aβ deposition brain regions all affected the progression from MCI to AD ( P<0.05). Conclusion:The Aβ deposition in the right prefrontal orbital cortex, right medial orbitofrontal cortex, left putamen and right transverse temporal cortex affect the progression from MCI to AD.

Objective To investigate the effects and molecular mechanisms of regenerating islet-derived 3-Alpha(REG3A)on the proliferation,apoptosis and cisplatin(DDP)resistance of ovarian cancer(OC)cells.Methods Cancer tissue and adjacent tissue samples of 97 ovarian cancer patients admitted to Qinghai Fifth People's Hospital from January 2021 to December 2022 were collected.Quantitative reverse transcriptase-mediated PCR(qRT-PCR)and immunohis to chemistry(IHC)were used to detect the expression of REG3A in cancer tissues and adjacent tissues,and the relationship between its expression and the clinical pathological characteristics and prognosis of patients was analyzed.QRT-PCR was used to detect the expression of REG3A in human normal ovarian epithelial cell line OSE and human OC cell lines(ES2,HEY,A2780,and SKOV3).SKOV3 and DDP resistant OC cell lines(SKOV3/DDP)were selected and randomly divided into siNC group and siREG3A group.Cell counting kit-8(CCK-8)was used to detect cell proliferation activity.Determination of cell drug resistance by methylthiazolyl tetrazolium(MTT).Flow cytometry was used to detect proliferation cycle and apoptosis.Immunoblotting was used to detect the expression of resistance,proliferation,apoptosis and phsphatidylinostol 3-kinase(PI3K)/protein kinase B(Akt)pathway related proteins in OC cells.Results The expression of REG3A mRNA in ovarian cancer tissues was higher than that in adjacent tissues(1.46±0.43 vs 0.52±0.11),and the difference was statistically significant(t=20.858,P<0.001).The 5-year survival rate of patients with high expression of REG3A was 24.49%(12/49),which was lower than the 91.67%(44/48)of patients with low expression of REG3A,and the difference was statistically significant(χ2=44.841,P<0.001).The proportion of patients with FIGO stages III-IV,moderate to high differentiation and tumor size>3cm in the high expression group of REG3A was higher than that in the low expression group of REG3A,and the differences were statistically significant(χ2=4.537～9.972,all P<0.05).Compared with OSE,the mRNA and protein expression of REG3A in ES2,HKY,A2780 and SKOV3 increased significantly(t=6.725～30.234,all P<0.01).Compared with the siNC group,the expression of REG3A was downregulated in SKOV3 cells in the siREG3A group(0.23±0.02 vs 0.99±0.06),cell activity decreased at 24,48 and 72 hours of transfection,the proportion of G1 phase cells increased,while the proportion of S and G2 phase cells and apoptosis rate,MDR-1,Cyclin D1 and Cleaved caspase 3 protein expression,p-PI3K/PI3K and p-Akt/Akt ratios were decreased,and the differences were statistically significant(t=6.584～22.730,all P<0.01).After treatment with DDP at concentrations of 1.25,2.5,5,7.5 and 15 μg/ml,compared with the siNC group,the survival rates of SKOV3 and SKOV3/DDP cells in the siREG3A group gradually decreased,and the differences were statistically significant(t=2.888～11.135,all P<0.05).Conclusion REG3A is highly expressed in OC tissues and is associated with malignant progression and poor prognosis of OC.Its up-regulation promotes cancer cell proliferation and DDP resistance by activating the PI3K/Akt pathway,and inhibits apoptosis.