Glucocorticoid-mediated acetylated regulation of glucocorticoid receptor and Histone3/Histone4 influence glucocorticoid heterogeneity in children patients with primary nephrotic syndrome.

Background: Glucocorticoid (GC) response heterogeneity has been recognized as an unfavorable prognostic factor, yet the underlying mechanism remains elusive. In this study, we endeavored to investigate the potential causes from an epigenetic perspective.

Methods: The protein expression levels of the glucocorticoid receptor (GR), acetylated GC receptor (Ac-GR), acetylated histone3 (Ac-H3), histone4 (Ac-H4), and the activity of nuclear factor-κB (NF-κB) were quantified in the peripheral blood lymphocytes of patients exhibiting diverse GC responses.

[Clinical phenotype characteristics and genetic analysis in children with nephronophthisis and related syndromes caused by different gene mutations].

Objectives: To improve the understanding of the clinical phenotypes and genetic characteristics of nephronophthisis (NPHP) and related syndromes in children.

Methods: A retrospective analysis was performed on the medical data of eight children with NPHP and related syndromes who were diagnosed and treated in the Department of Pediatrics of the Second Hospital of Hebei Medical University, from January 2018 to November 2022. The clinical characteristics and genetic testing results were analyzed.

Effect of modified C-reactive protein on complement activation: a possible complement regulatory role of modified or monomeric C-reactive protein in atherosclerotic lesions.

Objective: The capacity of human C-reactive protein (CRP) to activate/regulate complement may be an important characteristic that links CRP and inflammation with atherosclerosis. Recent advances suggest that in addition to classical pentameric CRP, a conformationally distinct isoform of CRP, termed modified or monomeric CRP (mCRP), may also play an active role in atherosclerosis. Although the complement activation behavior of CRP has been well established, the capacity of mCRP to interact with and activate the complement cascade is unknown.