Abstract: To explore the molecular mechanism by which long non-coding RNA Surfactant Associated 1 Pseudogene(SFTA1P) promotes the proliferation and migration of clear cell renal cell carcinoma(ccRCC) cells by regulating the microRNA-182-5p(miR-182-5p)/fibronectin 1(FN1) pathway. Methods: GEPIA2 software was utilized to analyze the expression ofSFTA1Pin ccRCC tissues from the TCGA database. Quantitative real-time PCR(qPCR) was employed to detect the expression ofSFTA1Pin ccRCC tissues, normal kidney tissues and ccRCC cell lines. A subcellular localization experiment was performed to explore the localization ofSFTA1Pwithin the human renal cell adenocarcinoma cell line(ACHN) derived from ccRCC. ACHN cells were then divided into the following groups: si-Con group, si-SFTA1P #2 group, mimic NC group, miR-182-5p mimic group, anti-miR-Con group, anti-miR-182-5p group, anti-miR-182-5p+si-FN1 group, si-Con+anti-miR-Con group, si-SFTA1P #2+anti-miR-Con group, and si-SFTA1P #2+anti-miR-182-5p group. CCK-8 and Transwell chamber experiments were conducted to assess cell proliferation and migration abilities. qPCR, Western blot, and dual-luciferase reporter assays were employed to elucidate the regulatory interactions amongSFTA1P,miR-182-5p, andFN1. Results: Analysis of The Cancer Genome Atlas(TCGA) database indicated thatSFTA1Pwas overexpressed in ccRCC tissues(P<0.05). When compared to normal kidney tissues,SFTA1Pexpression was markedly elevated in ccRCC tissues(P<0.01). Furthermore, the expression levels ofSFTA1Pin ccRCC cell lines 786-O, SN12-PM6, ACHN, and A498 were significantly higher than those in human renal proximal tubule cells(HK-2)(allP<0.01). Subcellular localization experiments revealed thatSFTA1Ppredominantly localized in the cytoplasm of ACHN cells. Compared to the si-Con group, the si-SFTA1P #2 group exhibited a significant reduction in proliferation and migration abilities of ACHN cells, accompanied by a decrease inFN1mRNA and protein expression(P<0.05). Compared to the mimic NC group, the expression ofFN1mRNA and protein in ACHN cells in the miR-182-5p mimic group reduced(P<0.01). In comparison to the anti-miR-Con group, the expression levels ofFN1mRNA and protein in ACHN cells were significantly elevated in the anti-miR-182-5p group. Additionally, there was a significant enhancement in both cell proliferation and migration capabilities(P<0.05). Conversely, the proliferation and migration abilities of ACHN cells in the anti-miR-182-5p+si-FN1 group were significantly reduced compared to the anti-miR-182-5p group(P<0.05). Furthermore, relative to the si-SFTA1P #2+anti-miR-Con group, the ACHN cells in the si-SFTA1P #2+anti-miR-182-5p group demonstrated increased proliferation and migration abilities, along with elevatedFN1mRNA and protein expression levels(P<0.05). Conclusion SFTA1Pexhibits elevated expression levels in ccRCC and facilitates the proliferation and migration of ccRCC cells through the modulation of themiR-182-5p/FN1signaling pathway.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Health science popularization is one of the important carriers for public hospitals to carry out public welfare.However,there are some problems in the process of children's health science popularization,such as low enthusiasm of science communicators,single form of communication and vague audience of science popularization.In the past ten years,Children's Hospital of Soochow University has set up a volunteer service team of"Xiaoding Youth Volunteer Camp",by leading the innova-tion of the team management style of the youth,the innovation of the popular science style around the project,and the innovation of the brand building aimed at the audience.It has launched the project of popularizing the science of Children's health in schools,the project of micro-video on popularizing the science of Children's health,the project of live broadcast by the radio sta-tion"Joint construction of Forensic Medicine",and the project of caring for the health of children in difficult circumstances.This paper explores and practices a path of integration of youth volunteer service and child health science popularization in public hos-pitals,analyzes the working mode and effect of"Xiaoding youth volunteer camp"in Children's Hospital of Soochow University,in order to provide new ideas and methods for the mode of children's health science popularization in public hospitals.

Objective To investigate the characteristics of epitope distribution on HLA class Ⅰ antigen in the regular platelet donors from Nanjing area and establish the HLA epitope database for regular platelet donors.Methods High-resolution HLA typing was per-formed using Sanger method for the blood samples from 649 regular platelet donors in Nanjing area.The polymorphism of HLA antigen epitopes corresponding to the high-resolution HLA typing results was analyzed using the HLA Eplet Registry website.The frequencies of allele frequencies,HLA haplotype,and HLA antigen epitope were calculated by using the direct counting method.Results Among the 649 regular platelet donors,38 HLA-A alleles were detected,corresponding to 36 HLA-A epitopes,and the higher frequencies were 79GT,144K and 138MI.Seventy-three HLA-B alleles were detected corresponding to 35 HLA-B epitopes,and the higher frequencies were 131S,69TNT,and 80N.Sixty-four HLA class Ⅰ antigen epitopes were detected,in which the higher frequencies were 79GT,131S,and 144K.Conclusions The distribution of HLA antigen epitopes in the regular platelet donors of Nanjing area exhibited u-nique polymorphic characteristics.The epitope matching strategies should be established based on the distribution characteristics of HLA antigen epitopes,which may expand the range of available donors and reduce the incidence of platelet transfusion refractoriness.

Objective To detect the levels of anti-soluble liver antigen(anti-SLA)antibodies in the serum of patients with autoim-mune hepatitis(AIH)and analyze their value in liver injury.Methods A retrospective analysis was conducted on 33 AIH patients with anti-SLA antibody-positive and 33 age-and sex-matched anti-SLA antibody-negative AIH cases diagnosed at Nanjing Second Hos-pital from January 2017 to April 2024.The general and clinical data of the patients were collected along with the detection of anti-SLA antibody(by protein immunoblotting),anti-nuclear antibodies(by indirect immunofluorescence)and other autoimmune liver disease-related autoantibodies,the biochemical parameters,e.g.,total bilirubin(T-Bil),alanine aminotransferase(ALT),aspartate amin-otransferase(AST),gamma-glutamyl transferase(GGT),alkaline phosphatase(ALP),and the level of immunoglobulin IgG.The clinical characteristics,laboratory parameters,and liver histopathological features of the patients were analyzed and compared.Results There were no statistically significant differences were observed in gender,age,autoimmune liver disease-related antibodies(such as antinuclear antibody,anti-smooth muscle antibody,etc.)and liver function parameters(AST,ALT,GGT and ALP),between the two groups of patients(P＞0.05).However,in the patients with positive anti-SLA antibodies,the levels of T-Bil and IgG in serum were significantly higher than those of the negative group with both P value less than 0.05(P values of 0.017 and 0.048,respectively).The pathological examination for liver tissue revealed that the proportion of the patients with lymphocyte-plasma cell infiltration in anti-SLA-positive group was significantly higher than that in anti-SLA-negative group(χ2=4.243,P＜0.05),suggesting more active immune re-sponse.Conclusion The detection of anti-SLA antibodies levels in the serum of AIH patients may reflect the extent of liver injury,and should have the potential for assisting diagnosis and monitoring the disease condition.

Body mass index (BMI) has been increasing globally in recent decades. Previous studies reported that BMI was associated with sex hormone levels, but the results were generated via linear regression or logistic regression, which would lose part of information. Quantile regression analysis can maximize the use of variable information. Our study compared the associations among different regression models. The participants were recruited from the Center of Reproductive Medicine, The First Hospital of Jilin University (Changchun, China) between June 2018 and June 2019. We used linear, logistic, and quantile regression models to calculate the associations between sex hormone levels and BMI. In total, 448 men were included in this study. The average BMI was 25.7 (standard deviation [s.d.]: 3.7) kg m^-2; 29.7% (n = 133) of the participants were normal weight, 45.3% (n = 203) of the participants were overweight, and 23.4% (n = 105) of the participants were obese. The levels of testosterone and estradiol significantly differed among BMI groups (all P < 0.05). In linear regression and logistic regression, BMI was associated with testosterone and estradiol levels (both P < 0.05). In quantile regression, BMI was negatively associated with testosterone levels in all quantiles after adjustment for age (all P < 0.05). BMI was positively associated with estradiol levels in most quantiles (≤80^th) after adjustment for age (all P < 0.05). Our study suggested that BMI was one of the influencing factors of testosterone and estradiol. Of note, the quantile regression showed that BMI was associated with estradiol only up to the 80^th percentile of estradiol.
Male ; Humans ; Body Mass Index ; Cross-Sectional Studies ; Gonadal Steroid Hormones ; Regression Analysis ; Estradiol ; Testosterone

Chromodomain-helicase-DNA-binding protein 1 (CHD1) deletion is among the most common mutations in prostate cancer (PCa), but its role remains unclear. In this study, RNA sequencing was conducted in PCa cells after clustered regularly interspaced palindromic repeat (CRISPR)/CRISPR-associated protein 9 (Cas9)-based CHD1 knockout. Gene set enrichment analysis (GSEA) indicated upregulation of hypoxia-related pathways. A subsequent study confirmed that CHD1 deletion significantly upregulated hypoxia-inducible factor 1α (HIF1α) expression. Mechanistic investigation revealed that CHD1 deletion upregulated HIF1α by transcriptionally downregulating prolyl hydroxylase domain protein 2 (PHD2), a prolyl hydroxylase catalyzing the hydroxylation of HIF1α and thus promoting its degradation by the E3 ligase von Hippel-Lindau tumor suppressor (VHL). Functional analysis showed that CHD1 deletion promoted angiogenesis and glycolysis, possibly through HIF1α target genes. Taken together, these findings indicate that CHD1 deletion enhances HIF1α expression through PHD2 downregulation and therefore promotes angiogenesis and metabolic reprogramming in PCa.
Male ; Humans ; Von Hippel-Lindau Tumor Suppressor Protein/metabolism* ; DNA-Binding Proteins/metabolism* ; Prolyl Hydroxylases/metabolism* ; Hypoxia ; Prostatic Neoplasms/pathology* ; Glycolysis ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism* ; Cell Line, Tumor ; DNA Helicases/metabolism*

We reported the discovery of six novel coumarins, toddasirins A-F (1-6), each endowed with modified isoprenyl or geranyl side chains, derived from the roots of Toddalia asiatica. Comprehensive structural elucidation was achieved through multispectroscopic analyses, single-crystal X-ray diffraction experiments, and advanced quantum mechanical electronic circular dichroism (ECD) calculations. Furthermore, the anti-inflammatory activity of these compounds was assessed. Notably, compounds 1-3 and 6 demonstrated notable inhibitory effects on nitric oxide (NO) production in lipopolysaccharide (LPS)-induced RAW 264.7 cells, with 50% inhibitory concentration (IC₅₀) values of 3.22, 4.78, 8.90, and 4.31 μmol·L^-1, respectively.
Mice ; Animals ; Coumarins/chemistry* ; Rutaceae/chemistry* ; Anti-Inflammatory Agents/pharmacology* ; Plant Extracts/chemistry* ; RAW 264.7 Cells ; Nitric Oxide ; Molecular Structure