Congenital lower urinary tract obstruction (CLUTO) is a spectrum of fetal malformations caused by anatomical abnormalities of the urethra, characterized by high rates of perinatal complications and mortality. The 2024 joint guideline from the European Association of Urology (EAU) and the European Society for Paediatric Urology (ESPU) introduced systematic revisions to the comprehensive management of CLUTO. Key updates encompass advancements in prenatal and postnatal screening and precise diagnosis, refined fetal prognosis assessment, clearer indications and modality selection for prenatal intervention, optimization of postnatal treatment strategies, and the establishment of a lifelong follow-up framework within an integrated care pathway. This article elucidates these key updates by comparing the 2024 EAU/ESPU guideline with the 2022 European Rare Kidney Disease Reference Network (ERKNet) consensus. It also discusses ongoing controversies and future research directions. The aim is to provide clinicians with the latest evidence-based insights to inform practice, ultimately improving outcomes and quality of life for children with CLUTO.
Humans ; Urology ; Female ; Urethral Obstruction/therapy* ; Pregnancy ; Child ; Europe ; Prenatal Diagnosis ; Infant, Newborn ; Urethra/abnormalities*

BackgroundThe adolescent mood disorders become more prevalent， imposing progressively greater perceived and actual caregiving burdens on caregivers， while the current health education resources， delivery formats and training programs remain insufficient in addressing their needs. ObjectiveTo evaluate the effect of structured health education on the caregiver burden associated with adolescent mood disorders， thereby informing evidence-based strategies for alleviating the burden. MethodsA total of 195 caregivers of adolescent inpatients with mood disorders admitted to a tertiary general hospital in Mianyang from June 1， 2020 to July 31， 2022 were consecutively enrolled and randomly assigned to either the research group （n=99） or the control group （n=96） using random number table method. Both groups received routine health education. In addition， the research group participated in a structured health education program comprising three modules covering disease knowledge， medication management， coping with family stress， and guidance for daily living. Upon admission， baseline information regarding both caregivers and adolescent inpatients was collected though a self-administered questionnaire. Caregiver Strain Index （CSI） was administered to assess caregiver burden at admission， discharge， and 1， 3 and 6 months post-discharge. A self-designed health education feedback questionnaire was administered on the day of discharge to evaluate caregivers' feedback on the health education. At 6 months post-discharge， data on any hospital readmission were collected. ResultsUltimately， 85 caregivers （85.86%） in the research group and 84 caregivers （87.50%） in the control group completed the study. Generalized estimating equation analysis revealed significant time effects and group-by-time interaction effects on CSI scores between the two groups （Wald χ²=790.347， 10.047， P<0.05 or 0.01）. There was no statistically significant difference between the two groups in terms of access to disease information， trust preference and core information needs （P>0.05）. Additionally， caregivers in the research group reported significantly better understanding of the disease-related knowledge and higher ratings on the effectiveness of health education when compared to the control group， with statistically significant differences （P<0.01）. ConclusionIn contrast to routine health education， structured health education may help alleviate caregiving burden among caregivers of adolescents with mood disorders.［Funded by Sichuan Medical Association Project （number， Q190004）］

Objective:To investigate the preventive and therapeutic effects and mechanisms of Dachaihu decoction(DCD)on dextran sodium sulfate(DSS)-induced ulcerative colitis(UC)and liver injury in mice,as well as the association between DCD benefits and gut microbiota modulation.Methods:Mice were treated with DCD(20.10 and 10.05 g/kg)for 2 weeks,with free access to drinking water containing 3%DSS in the second week to induce UC.Histopathological examination,RT-qPCR and 16S rRNA sequencing were used to investigate the effect of DCD on UC mice.Results:DCD pretreatment significantly alleviated weight loss,bloody diarrhea with mucus,histopathological abnormalities of the colon,and colon shortening in mice with DSS-induced UC.In addition,DCD pretreat-ment significantly upregulated the levels of Occludin,ZO-1,and MUC-2 in the colon and protected the intestinal barrier of mice.DCD pretreatment also alleviated inflammatory cell infiltration in the colon and the liver and significantly reduced the expression levels of the proinflammatory factors such as IL-1β,IL-6,TNF-α,iNOS,COX-2,and NLRP3,thereby exerting a protective effect against UC and liver injury.It should be noted that DCD corrected gut micro-biota imbalance in UC mice by enriching probiotic bacteria such as Lactobacillus and Bifidobacterium and reducing harmful bacteria such as Norank_f_Desulfovibrionaceae and Escherichia-Shigella.Conclusion:DCD can alleviate DSS-induced UC and exert a liver-protecting effect by protecting intestinal barrier,inhibiting inflam-mation,and regulating gut microbiota.

Objective To explore the mechanism of Huoxin pill(HXP)in the prevention and treatment of heart failure(HF)based on transcriptomics and network pharmacology.Methods The mice were randomly divided into the normal control group,model control group,positive control group treated with sacubitril/valsartan(60 mg·kg-1),low-dose group treated with HXP(31.2 mg·kg-1),and high-dose group treated with HXP(62.4 mg·kg-1).The model control group and each drug treat-ment group were subcutaneously injected with an equal volume of ISO(5 mg·kg-1)for modeling,while the normal control group was given an equal volume of sterile saline.Six hours later,each drug administration group was gavaged with the corresponding drug for intervention,and the normal control and model control groups were gavaged with an equal volume of sterile water.The modeling and drug administration were continued for 21 days.The cardiac function parameters of the mice were measured using color Doppler ultrasound imaging;ELISA was used to detect the levels of mouse serum cAMP,NT-proBNP,and BNP;HE staining and Masson's trichrome staining were used to evaluate the pathological morphology of cardiac tissue,and the CVF was calculated.Network pharmacology combined with transcriptomics was used to predict potential targets and signaling pathways of HXP in the prevention and treatment of HF,and molecular biology methods were used for validation.Results Compared with the normal control group,the model control group showed an increase in LVESd and LVEDd(P＜0.01),and a decrease in LVEF and LVFS(P＜0.01);BNP,NT-proBNP,and cAMP levels were increased(P＜0.01);myocardial collagen fibers increased and CVF in-creased(P＜0.01).Compared with the model control group,the HXP low-dose group,HXP high-dose group,and positive control groups showed a decrease in LVESd and LVEDd(P＜0.01),and an increase in LVEF and LVFS(P＜0.01);serum levels of BNP,NT-proBNP,and cAMP decreased(P＜0.05);the degree of myocardial fibrosis decreased and CVF decreased(P＜0.01).Network pharmacology combined with transcriptomics predicted 10 key targets for HXP in the prevention and treatment of HF:CACNA1H,SCN10A,FGF12,PVALB,ACAN,LGALS3,SERPINE1,MMP3,GSTM1,VDR.Western blot results showed that the protein activation levels of PKA and CREB in myocardial tissue were increased in the model control group compared with the nor-mal control group(P＜0.01).Compared with the model control group,HXP low-dose group、HXP high-dose group,and positive control groups showed a decrease in the protein activation levels of PKA and CREB in myocardial tissue(P＜0.05).Conclusion HXP has an improvement effect on ISO-induced HF in mice,which may involve numerous targets and the cAMP/PKA signaling pathway.

Objective To evaluate the reliability of Vitek 2 AST-N335 card for determining the susceptibility of Acinetobacter bauman-nii(AB)to cefoperazone/sulbactam.Methods A total of 318 non-repeated clinical isolates of AB collected in 2023 were tested for antimicrobial susceptibility to cefoperazone/sulbactam using broth microdilution(BMD),the AST-N335 card,and the Kirby-Bauer(K-B)disk diffusion method.Using BMD as the reference method,the reliability of AST-N335 card was assessed,and the accuracy of K-B disk diffusion method as the confirmatory test was validated.Results Compared with BMD,the susceptibility testing of 318 AB strains to cefoperazone/sulbactam using the AST-N335 card showed categorical agreement(CA)of 87.8％(279/318),very major er-ror(VME)of 6.0％(19/318),major error(ME)of 0％(0/318),and minor error(mE)of 1.9％(6/318),which fall outside of the acceptable error range.In contrast,the K-B method achieved CA of 99.4％(316/318),VME of 0％,ME of 0.3％(1/318),and mE of 0.3％(1/318),all within acceptable limits.Of these,the errors with AST-N335 card occurred within the minimum inhibitory concentration(MIC)range of 8-32 μg/mL.Using BMD as the reference method,further analysis was performed on the 171 AB strains with AST-N335 card MIC values of 8-32 μg/mL for cefoperazone/sulbactam.It was revealed that at MIC of 32 μg/mL,the CA was 0％;at MIC of 16 μg/mL,CA was 5.3％(1/19)and VME rate was 84.2％(16/19),both of which substantially exceeded accepta-ble error ranges.At MIC of 8 μg/mL,the CA was 94.9％(131/138)and VME was 2.2％(3/138),both approaching the acceptable ranges.Conclusion The results obtained with Vitek 2 AST-N335 card in determining for cefoperazone/sulbactam are unreliable when the MIC values fall within the range of 8-32 μg/mL,which leads to an underestimation of the resistance rate to cefoperazone/sulbac-tam.This issue requires urgent attention in both laboratories and clinical practice.The K-B disk diffusion method could serve as a sup-plementary verification approach in routine laboratories.

Objective To evaluate the reliability of Vitek 2 AST-N335 card for determining the susceptibility of Acinetobacter bauman-nii(AB)to cefoperazone/sulbactam.Methods A total of 318 non-repeated clinical isolates of AB collected in 2023 were tested for antimicrobial susceptibility to cefoperazone/sulbactam using broth microdilution(BMD),the AST-N335 card,and the Kirby-Bauer(K-B)disk diffusion method.Using BMD as the reference method,the reliability of AST-N335 card was assessed,and the accuracy of K-B disk diffusion method as the confirmatory test was validated.Results Compared with BMD,the susceptibility testing of 318 AB strains to cefoperazone/sulbactam using the AST-N335 card showed categorical agreement(CA)of 87.8％(279/318),very major er-ror(VME)of 6.0％(19/318),major error(ME)of 0％(0/318),and minor error(mE)of 1.9％(6/318),which fall outside of the acceptable error range.In contrast,the K-B method achieved CA of 99.4％(316/318),VME of 0％,ME of 0.3％(1/318),and mE of 0.3％(1/318),all within acceptable limits.Of these,the errors with AST-N335 card occurred within the minimum inhibitory concentration(MIC)range of 8-32 μg/mL.Using BMD as the reference method,further analysis was performed on the 171 AB strains with AST-N335 card MIC values of 8-32 μg/mL for cefoperazone/sulbactam.It was revealed that at MIC of 32 μg/mL,the CA was 0％;at MIC of 16 μg/mL,CA was 5.3％(1/19)and VME rate was 84.2％(16/19),both of which substantially exceeded accepta-ble error ranges.At MIC of 8 μg/mL,the CA was 94.9％(131/138)and VME was 2.2％(3/138),both approaching the acceptable ranges.Conclusion The results obtained with Vitek 2 AST-N335 card in determining for cefoperazone/sulbactam are unreliable when the MIC values fall within the range of 8-32 μg/mL,which leads to an underestimation of the resistance rate to cefoperazone/sulbac-tam.This issue requires urgent attention in both laboratories and clinical practice.The K-B disk diffusion method could serve as a sup-plementary verification approach in routine laboratories.

Objective To explore the mechanism of Huoxin pill(HXP)in the prevention and treatment of heart failure(HF)based on transcriptomics and network pharmacology.Methods The mice were randomly divided into the normal control group,model control group,positive control group treated with sacubitril/valsartan(60 mg·kg-1),low-dose group treated with HXP(31.2 mg·kg-1),and high-dose group treated with HXP(62.4 mg·kg-1).The model control group and each drug treat-ment group were subcutaneously injected with an equal volume of ISO(5 mg·kg-1)for modeling,while the normal control group was given an equal volume of sterile saline.Six hours later,each drug administration group was gavaged with the corresponding drug for intervention,and the normal control and model control groups were gavaged with an equal volume of sterile water.The modeling and drug administration were continued for 21 days.The cardiac function parameters of the mice were measured using color Doppler ultrasound imaging;ELISA was used to detect the levels of mouse serum cAMP,NT-proBNP,and BNP;HE staining and Masson's trichrome staining were used to evaluate the pathological morphology of cardiac tissue,and the CVF was calculated.Network pharmacology combined with transcriptomics was used to predict potential targets and signaling pathways of HXP in the prevention and treatment of HF,and molecular biology methods were used for validation.Results Compared with the normal control group,the model control group showed an increase in LVESd and LVEDd(P＜0.01),and a decrease in LVEF and LVFS(P＜0.01);BNP,NT-proBNP,and cAMP levels were increased(P＜0.01);myocardial collagen fibers increased and CVF in-creased(P＜0.01).Compared with the model control group,the HXP low-dose group,HXP high-dose group,and positive control groups showed a decrease in LVESd and LVEDd(P＜0.01),and an increase in LVEF and LVFS(P＜0.01);serum levels of BNP,NT-proBNP,and cAMP decreased(P＜0.05);the degree of myocardial fibrosis decreased and CVF decreased(P＜0.01).Network pharmacology combined with transcriptomics predicted 10 key targets for HXP in the prevention and treatment of HF:CACNA1H,SCN10A,FGF12,PVALB,ACAN,LGALS3,SERPINE1,MMP3,GSTM1,VDR.Western blot results showed that the protein activation levels of PKA and CREB in myocardial tissue were increased in the model control group compared with the nor-mal control group(P＜0.01).Compared with the model control group,HXP low-dose group、HXP high-dose group,and positive control groups showed a decrease in the protein activation levels of PKA and CREB in myocardial tissue(P＜0.05).Conclusion HXP has an improvement effect on ISO-induced HF in mice,which may involve numerous targets and the cAMP/PKA signaling pathway.

Objective To investigate the mechanism of Bixie Fenqing Pills in improving renal injury caused by hyperuricemia (HUA). Methods The HUA model rats were induced by gavaging with oxonic acid potassium salt, adenine combined with 10% yeast powder feed for 2 weeks. The model was evaluated based on serum uric acid (SUA) level. The successfully modeled rats were randomly divided into model group, low-dose Bixie Fenqing Pills group, medium-dose Bixie Fenqing Pills group, high-dose Bixie Fenqing Pills group, and febuxostat group, with 8 rats in each group. The drug administration groups were gavaged with the corresponding drugs, while the control group and the model group were gavaged with an equal volume of 0.5% carboxymethyl cellulose sodium (CMC-Na). After 4 weeks of continuous drug administration, the rats were sacrificed for sampling. Biochemical method was used to detect the serum levels of SUA, adenosine deaminase (ADA), xanthine oxidase (XOD), blood urea nitrogen (BUN), and serum creatinine (SCr) in the rats in each group; hematoxylin-eosin (HE) staining was used to observe the pathological changes of renal tissues; the Western blot was used to detect the expression levels of ATP-binding cassette subfamily G member 2 (ABCG2), glucose transporter 9 (GLUT9), and multi-drug resistance-associated protein 4 (MRP4) in renal tissues; immunohistochemistry was used to detect the protein expression levels of phosphatidylinositol-3-kinase (PI3K), protein kinase B (AKT), and nuclear factor-κB (NF-κB) in renal tissues. Results HE staining showed that the renal unitstructure in the model group was incomplete, with multiple edema in the renal interstitium, a small number of glomeruli showing atrophy, and incomplete epithelial cells on the glomerular capsule wall; the serum levels of SUA, ADA, XOD, SCr and BUN in the model group were significantly increased (P < 0.01); the expression of GLUT9 protein in renal tissue was upregulated, while the expression levels of ABCG2 and MRP4 proteins were significantly decreased (P < 0.05); immunohistochemical results showed that the expression levels of PI3K, AKT and NF-κB proteins in renal tissues in the model group were increased significantly (P < 0.05). Compared with the model group, Bixie Fenqing Pills could significantly effectively improve renal injuryin HUA rats, reduce serum levels of SUA, ADA, XOD, SCr and BUN, downregulate the expression of GLUT9 protein in renal tissues, and increase the expression levels of ABCG2, MRP4, PI3K, AKT and NF-κB proteins (P < 0.05). Conclusion Bixie Fenqing Pills may affect the production and metabolism of uric acid by regulating the PI3K/AKT/NF-κB pathway and the expression of uric acid transporter proteins, thereby improving renal injury in HUA rats.

IgG 4-related disease (IgG 4-RD) is an immune-mediated fibroinflammatory condition characterized by tumefactive lesions in multi-organs. It is a novel entity presented by variable manifestations. In recent years, there has been progress toward recognizing IgG 4-RD. However, the diagnosis and treatment of IgG 4-RD still present challenges due to insufficient experience. To address this, the Chinese Rheumatology Association has developed standardized guidelines for the diagnosis and treatment of IgG 4-RD based on domestic and international experience. These guidelines aim to enhance the understanding and management of IgG 4-RD, ultimately improving the prognosis for patients with IgG 4-RD.

The MAPK signaling pathway can mediate a variety of cytokines to participate in the processes of inflammation, cancer, immune disorder, and neurodegenerative diseases, and it also plays an important role in the development and progression of hepatic echinococcosis. This article reviews the structure and regulation of the MAPK signaling pathway and elaborates on the role of the MAPK signaling pathway in hepatic echinococcosis. It is pointed out that the MAPK signaling pathway can activate both the cyst and the host in hepatic echinococcosis, participate in the development and progression of the disease, and exert an impact on its treatment. Drug therapy targeting the MAPK signaling pathway is expected to become a new strategy for the treatment of hepatic echinococcosis.