Objective: To investigate the impact of RhE antigen-matched transfusion during liver transplantation on early postoperative recovery and complications. Methods: In this retrospective cohort study, ninety-five patients undergoing liver transplantation at Kunming First People's Hospital between January 2022 and July 2025 were enrolled. Patients were divided into two groups: Group 1 (RhE-mismatched transfusion, n=57) and Group 2 (RhE-matched transfusion, n=38). The baseline data, complete blood counts, hepatic and renal function, coagulation parameters, and complication rates between the two groups were compared at postoperative days 1, 3, 5, 7, and 10. Survival analysis was performed using the Kaplan-Meier method. Results: The baseline characteristics were well-balanced and comparable between the two groups (all P>0.05). The early postoperative mortality rate in the mismatched group (31.58%, 18/57) was significantly higher than that in the matched group (10.53%, 4/38) (P=0.017). The incidence of postoperative hepatic encephalopathy was significantly higher in the mismatched group (50.88%, 29/57) than in the matched group (10.53%, 4/38) (P<0.001). The incidence of postoperative haemorrhage in the mismatched group (24.56%, 14/57) was higher than that in the matched group (5.26%, 2/38), with a statistically significant difference (P=0.014). The incidence of perioperative infection in the mismatched group (28.07%, 16/57) was higher than that in the matched group (10.53%, 4/38), with a statistically significant difference (P=0.04). Corresponding odds ratios (OR) and 95% confidence intervals indicated a lower risk of these adverse events in the matched group. On postoperative day 1, the change in activated partial thromboplastin time (-1.6, 20.5) in the mismatched group was greater than in the matched group (-0.2, 5.5). The change in international normalised ratio (-0.56, 1.22) in the mismatched group was greater than in the matched group (-0.18, 0.32), while the change in albumin (-4.0, 4.8) was smaller in the mismatched group than in the matched group (-2.5, 8.8). On postoperative day 5, the change in albumin (-0.41±7.83) in the mismatched group was smaller than in the matched group (2.68±4.53). At postoperative day 7, the change in albumin in the mismatched group (-0.61±7.38) was smaller than that in the matched group (2.51±5.85), while the change in D-dimer in the mismatched group (0.73, 7.4) was greater than that in the matched group (-1.6, 4.3). On postoperative day 10, the mismatched group exhibited significantly higher fibrinogen levels (-1.21, 1.78) than the matched group (-0.49, 0.97), and significantly longer prothrombin times (-11.3, -2.7) than the matched group (-6.2, -0.8) (all P<0.05). The matched group exhibited a mean overall survival (OS) of 32.803 months (95% CI:29.171-36.436 months), significantly exceeding the mismatched group's 28.996 months (95% CI:24.202-33.790 months). The log-rank test yielded statistically significant results (χ =4.307, P=0.038). Conclusion: Implementing RhE blood group-matched transfusion during liver transplantation may help reduce early postoperative mortality and the incidence of major complication rates, promote faster recovery of coagulation and liver function, and thereby improve short-term patient outcomes.

Objective To explore the role of secreted phosphoprotein 1(SPP1)and myeloid differentiation primary response 88(MYD88)in morphine-induced cardiomyocyte apoptosis.Methods A morphine addiction model was established in Sprague-Dawley(SD)rats.Twelve SD rats were randomly assigned to the normal saline(NS)group or the morphine-dependent(DAM)group.Histopathological analysis was employed to observe and compare myocardial tissue morphology between the two groups.Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL)staining was performed to assess the number of apoptotic cells in each group.The expression levels of SPP1 and MYD88 were evaluated using immunohistochemistry.Quantitative real-time poly merase chain reaction(RT-qPCR)and Western blot were used to detect the mRNA and protein expression of SPP1,MYD88,Bax,Bcl2,Caspase-3,and Caspase-9.Simultaneously,Western blot analysis was used to detected the expression of Cleaved Caspase-3 and Cleaved Caspase-9 proteins.In vitro,SPP1 expression was knocked down in primary neonatal rat cardiomyocytes(NRCMs),and cells were divided into three groups:control(CON),morphine treated(DA),and shSPP1#3+DA.Cell viability was assessed using the CCK-8 assay,and apoptosis rates were determined by flow cytometry.Results HE and TUNEL staining of myocardial tissues from morphine-addicted SD rats revealed that,compared with the NS group,myofibrils in the DAM group exhibited partial disruption and a significant increase in apoptotic cells(P<0.05).Western blot and RT-qPCR analyses demonstrated that,relative to the NS group,the mRNA and protein levels of SPP1,MYD88,Bax,Caspase-3,and Caspase-9 were significantly upregulated in the DAM group(P<0.05),whereas Bcl2 expression was significantly downregulated at both mRNA and protein levels(P<0.05),and the protein expression levels of Cleaved Caspase-3 and Cleaved Caspase-9 were also increased.with all differences being statistically significant.In NRCMs following morphine intervention,cell viability in the DA group was markedly reduced compared to the CON group(P<0.05),accompanied by a signifi-cant increase in apoptosis rate(P<0.05).Consistently,Western blot and RT-qPCR results showed elevated mRNA and protein expression of SPP1,MYD88,Bax,Caspase-3,and Caspase-9 in the DA group(P<0.05),along with decreased Bcl2 expression(P<0.05).The protein expression levels of Cleaved Caspase-3 and Cleaved Caspase-9 were elevated simultaneously.In contrast,the shSPP1#3+DA group exhibited opposing trends compared to the DA group,with statistically sig nificant differences(P<0.05).Conclusion SPP1 and MYD88 play critical roles in mediating morphine-induced cardiomyocyte apoptosis,and silencing SPP1 has been shown to significantly reduce the extent of cardiomyocyte apoptosis following morphine exposure.

Objective To investigate the efficacy of cannabidiol(CBD)in improving renal function and protecting the kidney in mice with unilateral ureteral obstruction(UUO).Methods A total of 24 healthy,8-week-old,WTC57BL/6 male mice were divided into the Sham group,UUO group and UUO+CBD group,with 8 rats in each group.The UUO models were established by ligating one side of the ureter and removing the contralateral kidney to ensure unilateral kidney hydronephrosis.In the UUO+CBD group,5 mg/kg CBD was intraperitoneally injected immediately after the operation,once a day for 10 days.The Sham and UUO groups were given the same amount of normal saline.Blood sample was collected through the inner canthus venous plexus of the orbit 24 hours after the last administration.The levels of serum creatinine(Scr),blood urea nitrogen(BUN),tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),superoxide dismutase(SOD),and malondialdehyde(MDA)were detected with an automatic biochemistry analyzer.The histopathological sections were prepared,the pathological changes of renal tissues were observed under a light microscope,and the pathological injuries were scored.Mitochondrial quantity and morphological structure changes were observed with a transmission electron microscopy.Results Compared with the Sham group,the UUO group exhibited significantly higher levels of Scr[(22.55±3.29)μmol/L vs.(12.11±3.32)μmol/L],BUN[(18.62±2.15)mmol/L vs.(10.05±1.19)mmol/L],TNF-α[(21.04±2.56)pg/mL vs.(9.26±0.47)pg/mL],IL-1β[(10.25±1.25)pg/mL vs.(5.44±0.99)pg/mL],and MDA[(31.26±1.17)nmol/mL vs.(17.12±1.39)nmol/mL],but significantly lower level of SOD[(90.26±2.11)U/mL vs.(136.54±3.05)U/mL],all P＜0.000 1.Compared with the UUO group,the UUO+CBD group showed a significant decrease in the levels of Scr[(16.82±0.89)μmol/L vs.(22.55±3.29)μmol/L],BUN[(14.35±0.99)mmol/L vs.(18.62±2.15)mmol/L],TNF-α[(16.29±0.88)pg/mL vs.(21.04±2.56)pg/mL],IL-1β[(6.23±0.95)pg/mL vs.(10.25±1.25)pg/mL],MDA[(20.36±1.23)nmol/mL vs.(31.26±1.17)nmol/mL],and renal pathological damage score[(1.88±0.64)vs.(2.50±0.76)],but a significant increase in SOD level[(117.84±1.57)U/mL vs.(90.26±2.11)U/mL],all P＜0.000 1.Under electron microscopy,mitochondrial swelling,loss of inner membrane structure,and membrane rupture were observed in the UUO group,while the UUO+CBD group showed milder morphological changes.Conclusion CBD improves renal function in UUO model mice through anti-inflammatory,antioxidant and mitochondrial protection,and is a potential therapeutic drug for renal protection in clinic.

Objective:To investigate the prevalence and risk factors of overweight and obesity among Chinese children aged 3-18 years from 11 provinces, antonomous regions, or municipalities.Methods:This national cross-sectional community health survey utilized a multistage stratified cluster-random sampling method to recruit 193 997 nationally representative participants from 11 provinces, autonomous regions, or municipalities between January 2017 and December 2019. All participants underwent physical examinations, and their caregivers completed questionnaires assessing participants′ dietary, lifestyle, familial, and perinatal information. Multilevel multinomial logistic regression models were employed to identify the potential risk factors.Results:The cohort comprised 193 997 children (102 178 boys, 91 819 girls),aged (10±4) years. Overall prevalence rates were 30 574(15.8%)overweight children and 17 217(8.9%) obesity children. Boys exhibited higher overweight and obesity rates than girls (17.0% (17 368/102 178) vs. 14.4% (13 206/102 178), 11.3% (11 553/91 819) vs. 6.2% (5 664/91 819), χ2=249.12,1 578.69,both P<0.001). The detection rates of obesity in Tanner stage 2 and 3 were the highest in boys and girls, with 13.4%(2 231/16 665) and 8.6%(880/10 221) respectively. Risk factors for obesity included parental overweight (paternal OR=2.34 and maternal OR=2.29), annual household income of 100 000-200 000 yuan (compared with<100 000 yuan, OR=1.04), higher paternal education (compared with below high school,high school and a college education OR=1.09,1.14), birth weight >4.0 kg (≤5 and>5 years old OR=1.74, 1.44,respectively), and western food consumption≥1 time/month (compared with<1, 1-2, 3-4,>4 times/month OR=1.36, 1.30, 1.67(≤5 years), 1.19, 1.16, 1.15 (>5 years), respectively) (all P<0.05). Conversely, coarse grain intake≥1 times/week (compared with<1 times/week, every day, 3-4, 1-2 times/week OR=0.74, 0.80, 0.71 (≤5 years), 0.75, 0.87, 0.90(>5 years), respectively, all P<0.05) was associated with reduced obesity risk. Conclusions:Obesity epidemiology in children demonstrates significant heterogeneity across age, gender, geographic regions, and pubertal stages. It is necessary to establish a personalized prevention and control strategy.

Objective:To analyze the value of marginal donor livers in liver transplantation for patients with acute-on-chronic liver failure (ACLF).Methods:Clinical data of 58 patients with ACLF undergoing liver transplantation at the First Affiliated Hospital of Guangxi Medical University from January 2020 to June 2023 were retrospectively analyzed, including 33 males and 25 females, aged (40.4±14.4) years. According to the source of donor (marginal or standard), recipients were divided into the marginal group ( n=28), and standard group ( n=30). The preoperative model for end-stage liver disease (MELD) score, cold/warm ischemia time, intraoperative blood loss, postoperative tracheal intubation time, intensive care unit (ICU) stay, liver function, renal function, coagulation function, postoperative complications, and survival situation were compared between the groups. Results:The MELD score, cold/warm ischemia time, intraoperative blood loss, postoperative tracheal intubation time, length of ICU stay, alanine transaminase, aspartate transaminase, total bilirubin, serum creatinine, blood urea nitrogen, estimated glomerular filtration rate, fibrinogen, postoperative infection, primary graft nonfunction, biliary complications, and vascular complications were compared between the groups (all P>0.05). The incidence of delayed graft function (DGF) recovery was 28.6%(8/28) in marginal group, higher than that in standard group 6.7%(2/30) ( χ2=5.13, P=0.038). The one-year cumulative survival rates were 89.3% and 93.3% in marginal group and standard group, respectively ( P=0.580). Conclusion:The therapeutic effect of marginal donor liver in ACLF recipients is comparable to that of standard donor liver. The incidence of DGF is higher in recipients with marginal donor liver.

Objective To investigate the protective effect of hederagenin(HDG)on cisplatin(Cis)-induced acute kidney injury(AKI)in mice and its potential mechanism.Methods 24 male C57BL/6J mice were randomly divided into a control group,AKI model group,HDG low-dose group,and HDG high-dose group,with six mice in each group.AKI model was established by intraperitoneal injection of 20 mg/kg cisplatin(Cis).The HDG low-dose and HDG high-dose groups were given 20,40 mg/kg HDG by intragastric administration,respectively,and samples were collected 3 days later.The kidneys of the mice were collected for hematoxylin-eosin(HE)and periodic-acid-schiff(PAS)staining to evaluate the kidney pathology,and serum was collected to detect changes in serum creatinine(Scr)and blood urea nitrogen(BUN).The expression of p-P65,P65,IL-6,TNF-α,IL-1β,and other inflammatory-related proteins was detected by Western Blot.A TCMK1(renal tubular epithelial cell)inflammatory cell model was established by Cis(200 ng/mL)stimulation in vitro.Blank group,Cis model group,HDG low-dose group,HDG high-dose group,Axin2 overexpression group,HDG+Axin2 overexpression group were set up.In the Axin2-overexpression group,the expression of p-P65,P65,IL-6,TNF-α,IL-1β,Axin2,and AREG was detected among total cell proteins.Results Compared with the control group,AKI model mice exhibited significantly elevated serum creatinine and blood urea nitrogen levels(P<0.05),accompanied by pathological alterations including vacuolar degeneration of renal tubules,inflammatory cell infiltration,and glycogen deposition,and the expression of inflammation-related proteins(p-P65,TNF-α,IL-6,IL-1β)and Axin2 was markedly upregulated in AKI mice(P<0.05).HDG treatment induced a dose-dependent reduction in serum creatinine and blood urea nitrogen levels(high-dose>low-dose,P<0.05),alleviated renal histopathological damage,and concurrently suppressed the expression of these inflammatory mediators and Axin2(P<0.05).HDG was confirmed that dose-dependently inhibited Cis-induced upregulation of Axin2,and inflammatory cytokines in vitro experiments.Transcriptome sequencing revealed that Axin2 overexpression significantly increased amphiregulin(AREG)expression(P<0.05).Mechanistically,HDG reduced p-P65 phosphorylation by suppressing the Axin2/AREG axis(P<0.05),while Axin2 overexpression abolished the protective effects of HDG against Cis-induced renal tubular cell injury.Conclusions HDG protects against renal injury in AKI mice by reducing inflammation through the inhibition of Axin2/AREG axis activation.

AIM:To explore the potential of Huangqi sanqi mixture(AP)in improving renal fi-brosis by performing transcriptome sequencing of the kidneys of the unilateral ureteral ligation mouse group and the Huangqi sanqi mixture inter-vention group,and using bioinformatics to verify the signitficantly different lncRNAs mechanism.METHODS:Twenty-four C57 mice were divided in-to sham operation group,renal fibrosis group,Huangqi sanqi mixture intervention group(3.944 g/kg)and irbesartan positive control intervention group,with 6 mice in each group.A mouse model of renal fibrosis was established by unilateral ure-teral ligation(UUO).The animals were given intra-gastric administration after operation,and the ani-mals were sacrificed and the specimens were col-lected after seven consecutive days of administra-tion.The changes of Huangqi sanqi mixture on re-nal fibrosis pathological damage were analyzed by HE and Masson staining,and the protein levels of Fn and α-SMA in renal tissue of each group were detected by Western blot and immunohistochemis-try to evaluate the alleviating effect of Huangqi san-qi mixture on renal fibrosis.Subsequently,lncRNA expression information was obtained by transcrip-tome sequencing,and Quantitative Real-time PCR(qPCR)was performed after data quality,GO en-richment and differential lncRNA were analyzed.According to the differential lncRNA and target analysis results obtained by sequencing,lncRNA Gm51500/Adam12 was overexpressed in vitro,and its mechanism in the protection of renal fibrosis by Huangqi sanqi mixture was studied by immunohis-tochemistry,immunofluorescence staining and qP-CR verification.RESULTS:Compared with the mod-el group,the renal fibrosis of the mice in the Huangqi sanqi mixture intervention group was sig-nificantly reduced,and the protein levels of α-SMA and Fn and the expression of lncRNA in the renal tis-sue were significantly down-regulated(P＜0.000 1).Three lncRNAs were screened and verified to in-crease in the model group and significantly de-crease after AP intervention,namely lncRNA Gm29994,Gm51500 and Gm35391.Target analysis showed that lncRNA Gm51500 had the most signifi-cant relationship with Adam12.The results of ani-mal experiments showed that Adam12 was highly expressed in the kidney of UUO mice and was sig-nificantly inhibited after AP intervention.Subse-quent cell experiments confirmed that overexpres-sion of lncRNA Gm51500 could up-regulate TGF-β-induced renal tubular cell fibrosis and Adam12 ex-pression.Cell recovery experiments confirmed that Adam12 overexpression reversed the inhibitory ef-fect of AP on renal tubular cell injury and fibrosis.CONCLUSION:Huangqi sanqi mixture can improve renal fibrosis.Based on transcriptomic sequencing,lncRNA Gm51500/Adam12 axis may be a potential target for Huangqi sanqi mixture to improve renal fibrosis.

Objective To investigate the efficacy of cannabidiol(CBD)in improving renal function and protecting the kidney in mice with unilateral ureteral obstruction(UUO).Methods A total of 24 healthy,8-week-old,WTC57BL/6 male mice were divided into the Sham group,UUO group and UUO+CBD group,with 8 rats in each group.The UUO models were established by ligating one side of the ureter and removing the contralateral kidney to ensure unilateral kidney hydronephrosis.In the UUO+CBD group,5 mg/kg CBD was intraperitoneally injected immediately after the operation,once a day for 10 days.The Sham and UUO groups were given the same amount of normal saline.Blood sample was collected through the inner canthus venous plexus of the orbit 24 hours after the last administration.The levels of serum creatinine(Scr),blood urea nitrogen(BUN),tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),superoxide dismutase(SOD),and malondialdehyde(MDA)were detected with an automatic biochemistry analyzer.The histopathological sections were prepared,the pathological changes of renal tissues were observed under a light microscope,and the pathological injuries were scored.Mitochondrial quantity and morphological structure changes were observed with a transmission electron microscopy.Results Compared with the Sham group,the UUO group exhibited significantly higher levels of Scr[(22.55±3.29)μmol/L vs.(12.11±3.32)μmol/L],BUN[(18.62±2.15)mmol/L vs.(10.05±1.19)mmol/L],TNF-α[(21.04±2.56)pg/mL vs.(9.26±0.47)pg/mL],IL-1β[(10.25±1.25)pg/mL vs.(5.44±0.99)pg/mL],and MDA[(31.26±1.17)nmol/mL vs.(17.12±1.39)nmol/mL],but significantly lower level of SOD[(90.26±2.11)U/mL vs.(136.54±3.05)U/mL],all P＜0.000 1.Compared with the UUO group,the UUO+CBD group showed a significant decrease in the levels of Scr[(16.82±0.89)μmol/L vs.(22.55±3.29)μmol/L],BUN[(14.35±0.99)mmol/L vs.(18.62±2.15)mmol/L],TNF-α[(16.29±0.88)pg/mL vs.(21.04±2.56)pg/mL],IL-1β[(6.23±0.95)pg/mL vs.(10.25±1.25)pg/mL],MDA[(20.36±1.23)nmol/mL vs.(31.26±1.17)nmol/mL],and renal pathological damage score[(1.88±0.64)vs.(2.50±0.76)],but a significant increase in SOD level[(117.84±1.57)U/mL vs.(90.26±2.11)U/mL],all P＜0.000 1.Under electron microscopy,mitochondrial swelling,loss of inner membrane structure,and membrane rupture were observed in the UUO group,while the UUO+CBD group showed milder morphological changes.Conclusion CBD improves renal function in UUO model mice through anti-inflammatory,antioxidant and mitochondrial protection,and is a potential therapeutic drug for renal protection in clinic.

Objective To investigate the impacts of knocking-down Keratin 17(KRT17)on proliferation,apoptosis and epithelial mesenchymal transition(EMT)of bladder cancer cells by regulating Wnt/β-catenin signaling pathway.Methods The expression of KRT17 mRNA and protein in bladder cancer tissue,adjacent tissue,bladder cancer cell lines(5637,T24 and UM-UC-3)and human immortalized urothelial cell line SV-HUC-1 were detected by qRT-PCR and Western blot assay.Immunohistochemical staining was used to detect the expression of KRT17 in the tissues.Cells transfected with NC siRNA and KRT17 siRNA were labeled as the NC siRNA group and the KRT17 siRNA group,respectively.T24 cells treated with 20 mmol/L LiCl were labeled as the LiCl group.T24 cells transfected with KRT17 siRNA and treated with 20 mmol/L LiCl were labeled as the KRT17 siRNA+LiCl group.The non transfected cells were used as the blank group.CCK-8,cloning formation experiment and flow cytometry were applied to detect cell proliferation and apoptosis.QRT-PCR was applied to detect KRT17 mRNA expression.Western blot assay was applied to detect the expression levels of KRT17,β-catenin,Cyclin D1,EMT related proteins Vimentin,E-cadherin and Snail1 proteins.Results The expression of KRT17 mRNA and protein was greatly increased in bladder cancer tissue and cells(P＜0.05).The cell proliferation,colony count,KRT17 mRNA and protein expression,β-catenin,Cyclin D1,Vimentin,and Snail expression were lower in the KRT17 siRNA group than those in the NC siRNA group and the blank group,while apoptosis and E-cadherin expression were higher(P＜0.05).LiCl reversed the inhibition of KRT17 knockdown on the malignant behavior of bladder cancer.Conclusion Knocking-down KRT17 inhibits the proliferation and EMT of bladder cancer cells and promotes their apoptosis by inhibiting Wnt/β-catenin signaling pathway.

Objective To investigate the impacts of knocking-down Keratin 17(KRT17)on proliferation,apoptosis and epithelial mesenchymal transition(EMT)of bladder cancer cells by regulating Wnt/β-catenin signaling pathway.Methods The expression of KRT17 mRNA and protein in bladder cancer tissue,adjacent tissue,bladder cancer cell lines(5637,T24 and UM-UC-3)and human immortalized urothelial cell line SV-HUC-1 were detected by qRT-PCR and Western blot assay.Immunohistochemical staining was used to detect the expression of KRT17 in the tissues.Cells transfected with NC siRNA and KRT17 siRNA were labeled as the NC siRNA group and the KRT17 siRNA group,respectively.T24 cells treated with 20 mmol/L LiCl were labeled as the LiCl group.T24 cells transfected with KRT17 siRNA and treated with 20 mmol/L LiCl were labeled as the KRT17 siRNA+LiCl group.The non transfected cells were used as the blank group.CCK-8,cloning formation experiment and flow cytometry were applied to detect cell proliferation and apoptosis.QRT-PCR was applied to detect KRT17 mRNA expression.Western blot assay was applied to detect the expression levels of KRT17,β-catenin,Cyclin D1,EMT related proteins Vimentin,E-cadherin and Snail1 proteins.Results The expression of KRT17 mRNA and protein was greatly increased in bladder cancer tissue and cells(P＜0.05).The cell proliferation,colony count,KRT17 mRNA and protein expression,β-catenin,Cyclin D1,Vimentin,and Snail expression were lower in the KRT17 siRNA group than those in the NC siRNA group and the blank group,while apoptosis and E-cadherin expression were higher(P＜0.05).LiCl reversed the inhibition of KRT17 knockdown on the malignant behavior of bladder cancer.Conclusion Knocking-down KRT17 inhibits the proliferation and EMT of bladder cancer cells and promotes their apoptosis by inhibiting Wnt/β-catenin signaling pathway.