Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
[Short-term efficacy of rituximab in children with calcineurin inhibitor resistant steroid resistant nephrotic syndrome].
Zhonghua Er Ke Za Zhi
January 2025
Department of Nephrology, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai Kidney Development and Pediatric Kidney Disease Research Center State, Key Laboratory of Kidney Diseases, Shanghai201102, China.
To investigate the short-term efficacy and safety of rituximab (RTX) in children with calcineurin inhibitor (CNI) resistant steroid resistant nephrotic syndrome (SRNS). A retrospective case analysis was conducted. Thirteen children with CNI resistant SRNS who were regularly treated with RTX (375 mg/m per dose (maximum dose 500 mg), 1 dose per week, a total of 4 doses) in Department of Nephrology, Children's Hospital of Fudan University from January 2016 to December 2023 were enrolled.
View Article and Find Full Text PDFThe mechanism of enterogenous toxin methylmalonic acid aggravating calcium-phosphorus metabolic disorder in uremic rats by regulating the Wnt/β-catenin pathway.
Mol Med
January 2025
Department of Nephrology, The Affiliated Hospital of Hebei University, No. 212 Yuhua East Road, Lianchi District, Baoding, 071000, Hebei Province, China.
Background: Uremia (UR) is caused by increased UR-related toxins in the bloodstream. We explored the mechanism of enterogenous toxin methylmalonic acid (MMA) in calcium-phosphorus metabolic disorder in UR rats via the Wnt/β-catenin pathway.
Methods: The UR rat model was established by 5/6 nephrectomy.
gene mutation through CRISPR RNA-guided base editing weakens bacterial virulence and immune evasion.
Virulence
December 2025
Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
The resistance of commonly used clinical antibiotics, such as daptomycin (DAP), has become increasingly serious in the fight against () infection. It is essential to explore key pathogenicity-driven genes/proteins in bacterial infection and antibiotics resistance, which contributes to develop novel therapeutic strategies against infections. The gene of , encoding 5'-nucleotidase (NT5), is nearly unknown for its function in drug resistance and bacterial infection.
View Article and Find Full Text PDFCOVID-19 infection and risk of adverse drug reactions: Cohort study.
Therapie
January 2025
Centre régional de pharmacovigilance, hôpital Nord, CHU de Saint-Étienne, 42055 Saint-Étienne cedex, France.
Aim: During coronavirus disease 2019 (COVID-19), the incidence rate of adverse drug reactions (ADRs) in hospitalized patients seemed higher than before the pandemic. Severe inflammation triggered by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was cited as an explanation. We aimed to determine whether COVID-19 infection was associated with a higher risk of ADRs compared to other infectious diseases.
View Article and Find Full Text PDFBacterial cellulose-based scaffold modified with anti-CD29 antibody to selectively capture urine-derived stem cells for bladder repair.
Carbohydr Polym
March 2025
Qingdao Key Laboratory of Materials for Tissue Repair and Rehabilitation, Shandong Engineering Research Center for Tissue Rehabilitation Materials and Devices, School of Rehabilitation Sciences and Engineering, University of Health and Rehabilitation Sciences, Qingdao 266113, China. Electronic address:
Acellular cellulose-based biomaterials hold promising potential for treating bladder injuries. However, the compromised cellular state surrounding the wound impedes the complete reconstruction of the bladder. This necessitates the development of a bio-instructive cellulose-based biomaterial that actively controls cell behavior to facilitate effective bladder regeneration.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!