An animal model of severe acute respiratory distress syndrome for translational research.

Background: Despite the fact that an increasing number of studies have focused on developing therapies for acute lung injury, managing acute respiratory distress syndrome (ARDS) remains a challenge in intensive care medicine. Whether the pathology of animal models with acute lung injury in prior studies differed from clinical symptoms of ARDS, resulting in questionable management for human ARDS. To evaluate precisely the therapeutic effect of transplanted stem cells or medications on acute lung injury, we developed an animal model of severe ARDS with lower lung function, capable of keeping the experimental animals survive with consistent reproducibility.

Insufficient pretransplant induction therapy is associated with diffuse intrahepatic cholangiopathy in ABO-incompatible living donor liver transplantation for acute liver failure.

Background: ABO-incompatible liver transplantation (ABOi LT) can now be successfully performed with standard pretransplant induction therapy. For patients with chronic end-stage liver disease (ESLD), ABOi LT can achieve long-term outcomes comparable to those of blood type-compatible (ABOc) LT. Outcomes of patients with acute liver failure (ALF) who undergo urgent transplantation surgery with a limited induction period should be further investigated.

Metabolic consequences and tubular function after augmentation cystoplasty in children with neurogenic bladder.

Background: Many studies have reported the renal outcomes and metabolic consequences after augmentation cystoplasty (AC), however few studies have discussed changes in renal tubular function. The aim of this study was to determine the prevalence of metabolic disturbances, evaluate renal tubular function and 24-hour urine chemistry to evaluate the association between metabolic alterations and urolithiasis after AC.

Methods: We investigated serum biochemistry, blood gas, and 24-hour urinary metabolic profile of children who underwent AC between January 2000 and December 2020.

Loss of Kmt2c or Kmt2d primes urothelium for tumorigenesis and redistributes KMT2A-menin to bivalent promoters.

Members of the KMT2C/D-KDM6A complex are recurrently mutated in urothelial carcinoma and in histologically normal urothelium. Here, using genetically engineered mouse models, we demonstrate that Kmt2c/d knockout in the urothelium led to impaired differentiation, augmented responses to growth and inflammatory stimuli and sensitization to oncogenic transformation by carcinogen and oncogenes. Mechanistically, KMT2D localized to active enhancers and CpG-poor promoters that preferentially regulate the urothelial lineage program and Kmt2c/d knockout led to diminished H3K4me1, H3K27ac and nascent RNA transcription at these sites, which leads to impaired differentiation.

A portable optical detection system for rapid quantification of two rheumatoid arthritis biomarkers.

Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes joint damage and progressive destruction of adjacent cartilage and bones. Quick and accurate detection of rheumatoid factors (RF) and anti-cyclic citrullinated peptide antibodies (anti-CCP) in serum is effective in diagnosing RA and preventing its progression. However, current methods for detecting these two biomarkers are costly, time-consuming, labor-intensive, and require specialized equipment.