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.

OBJECTIVE: To observe the effects of electroacupuncture at the pterygopalatine region on nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)-mediated pyroptosis and inflammatory factors in rats with allergic rhinitis (AR). METHODS: Twenty-four SD rats were randomly divided into a blank group, a model group, an acupuncture group and an electroacupuncture group, 6 rats in each group. Except for the blank group, OVA-induced AR model was established in the remaining groups. In the electroacupuncture group, the rats were treated with electroacupuncture at the bilateral pterygopalatine region, with disperse-dense wave, in frequency of 2 Hz/100 Hz and current of 0.5-1 mA, 15 min each time, once every other day, for 3 times. In the acupuncture group, the rats were treated with acupuncture at bilateral pterygopalatine region simply, without electrical stimulation. The rhinitis symptom score was observed, the pathomorphology of the nasal mucosa was observed by HE staining; the serum levels of OVA-specific immunoglobulin E (OVA-sIgE), interleukin (IL)-4, IL-6 and IL-1β were detected by ELISA; the mRNA expression of NLRP3, apoptosis-associated speck-like protein containing CARD (ASC), cysteinyl aspartate specific proteinase-1 (caspase-1) and IL-18 in the nasal mucosa was detected by real-time PCR; the protein expression of NLRP3, ASC, caspase-1 and IL-18 in the nasal mucosa was detected by Western blot. RESULTS: Compared with the blank group, in the model group, the rhinitis symptom score was increased (P<0.01), the serum levels of OVA-sIgE, IL-4, IL-6 and IL-1β were increased (P<0.05), the nasal mucosa showed pathomorphology of inflammatory infiltration; the mRNA and protein expression of NLRP3, ASC, caspase-1 and IL-18 in the nasal mucosa was increased (P<0.05). Compared with the model group, in the electroacupuncture group, the rhinitis symptom score was reduced (P<0.01), the pathology of the nasal mucosa was improved; the serum levels of OVA-sIgE, IL-4, IL-6 and IL-1β were decreased (P<0.05); the mRNA and protein expression of NLRP3, ASC, caspase-1 and IL-18 in the nasal mucosa was decreased (P<0.05). CONCLUSION Electroacupuncture at the pterygopalatine region can exerting the anti-inflammatory effect by inhibiting NLRP3-mediated pyroptosis and inflammatory factor imbalance, thus alleviate rhinitis symptoms in AR rats.
Animals ; Electroacupuncture ; NLR Family, Pyrin Domain-Containing 3 Protein/immunology* ; Rats ; Rats, Sprague-Dawley ; Rhinitis, Allergic/physiopathology* ; Pyroptosis ; Male ; Acupuncture Points ; Humans ; Female ; Interleukin-1beta/genetics* ; Interleukin-18/immunology* ; Interleukin-6/genetics* ; Caspase 1/immunology*

Immune thrombocytopenia (ITP) is a hemorrhagic autoimmune disease characterized by antibody-mediated platelet injury. ITP has complicated immunopathological mechanisms that need further elucidation. It is well known that the costimulatory molecules OX40 ligand (OX40L) and OX40 play essential roles in the immunological mechanisms of autoimmune diseases. Previously, we discovered that the expression of OX40L and OX40 is significantly increased in the peripheral blood mononuclear cells (PBMCs) of ITP patients. In our present study, OX40L-induced follicular helper T (Tfh) cells exhibited an activated phenotype with elevated expression of inducible T-cell costimulator (ICOS), programmed cell death protein-1 (PD-1), and cluster of differentiation 40 ligand (CD40L) in vitro. Moreover, aberrant OX40L‒OX40 expression might promote the Tfh1-to-Tfh2 shift in vivo, inducing the generation of autoantibodies by enhancing the helper function of Tfh cells for B lymphocytes in a mouse model, which might accelerate the progression of ITP. Additionally, signal transduction through the OX40L‒OX40 axis might be related to the activation of tumor necrosis factor receptor-associated factor (TRAF)‒nuclear factor-κB (NF-κB) and Janus kinase (JAK)‒signal transducer and activator of transcription (STAT) signaling pathways. Overall, OX40L‒OX40 signaling is proposed as a potential novel therapeutic target for ITP.
Animals ; OX40 Ligand/physiology* ; Purpura, Thrombocytopenic, Idiopathic/immunology* ; Cell Differentiation ; Mice ; T-Lymphocytes, Helper-Inducer/cytology* ; T Follicular Helper Cells/cytology* ; Signal Transduction ; Receptors, OX40 ; Mice, Inbred C57BL ; Humans ; Female

Cemental tear is a rare and indetectable condition unless obvious clinical signs present with the involvement of surrounding periodontal and periapical tissues. Due to its clinical manifestations similar to common dental issues, such as vertical root fracture, primary endodontic diseases, and periodontal diseases, as well as the low awareness of cemental tear for clinicians, misdiagnosis often occurs. The critical principle for cemental tear treatment is to remove torn fragments, and overlooking fragments leads to futile therapy, which could deteriorate the conditions of the affected teeth. Therefore, accurate diagnosis and subsequent appropriate interventions are vital for managing cemental tear. Novel diagnostic tools, including cone-beam computed tomography (CBCT), microscopes, and enamel matrix derivatives, have improved early detection and management, enhancing tooth retention. The implementation of standardized diagnostic criteria and treatment protocols, combined with improved clinical awareness among dental professionals, serves to mitigate risks of diagnostic errors and suboptimal therapeutic interventions. This expert consensus reviewed the epidemiology, pathogenesis, potential predisposing factors, clinical manifestations, diagnosis, differential diagnosis, treatment, and prognosis of cemental tear, aiming to provide a clinical guideline and facilitate clinicians to have a better understanding of cemental tear.
Humans ; Dental Cementum/injuries* ; Consensus ; Diagnosis, Differential ; Cone-Beam Computed Tomography ; Tooth Fractures/therapy*

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.