পৃষ্ঠা 1 থেকে 17 ফলাফল
A number of short noncoding microRNAs (miRs) have been demonstrated to be highly expressed in many kidney diseases such as renal cancer and lupus nephritis (LN); however, these results have not been extensively investigated. The aim of the present study was to investigate the expression and function
Urinary lactic dehydrogenase, alkaline phosphatase and lysozyme determinations were performed on 70 patients with various kidney diseases such as acute and chronic pyelonephritis, acute and chronic glomerulonephritis, idiopathic nephrotic syndrome, diabetic nephropathy, nephrosclerosis, lupus
OBJECTIVE
To investigate the significance of the calcineurin (CaN) activation in active lupus nephritis patient.
METHODS
Peripheral blood mononuclear cells (PBMCs) were separated from twenty-one active LN patients and 12 healthy controls. Phosphatase activity of CaN was determined using the CaN
The objective of this study was to investigate the role of miR-148a-3p in lupus nephritis (LN) based on data from previous studies and a microRNA assay. We evaluated the miR-148a-3p expression level in LN renal tissues and blood serum to determine its clinicopathological significance and effect on
Signaling of the C3a anaphylatoxin through its G protein-coupled receptor, C3aR, is relevant in a variety of inflammatory diseases, but its role in lupus nephritis is undefined. In this study, we show that expression of C3aR was significantly increased in prediseased and diseased kidneys of MRL/lpr
There are several reports in the literature regarding microRNA (miR)‑130b. It has been reported that miR‑130b is involved in several diseases. The present study aimed to understand the association between the levels of miR‑130b and lupus nephritis in patients. A total of 61 blood samples were
This study was performed to investigate the role of cell-mediated immunity in lupus nephritis (LN). Frozen sections from 38 patients with LN were examined by indirect immunoalkaline-phosphatase labeling using monoclonal antibodies to identify the immune cells infiltrating into the interstitium and
Systemic lupus erythematosus (SLE) is a complex autoimmune disease that is characterized by systemic inflammation and multiple organ failures. Dysregulation of T cells plays a critical role in SLE pathogenesis. Our previous study indicates that JKAP (also named DUSP22) inhibits T-cell activation and
Inhibitory signaling is an emerging function of ITAM-bearing immunoreceptors in the maintenance of homeostasis. Monovalent targeting of the IgA Fc receptor (FcalphaRI or CD89) by anti-FcalphaRI Fab triggers potent inhibitory ITAM (ITAM(i)) signaling through the associated FcRgamma chain
Immunoreceptors can transduce either inhibitory or activatory signals depending on ligand avidity and phosphorylation status, which is modulated by the protein kinases Lyn and Fyn. Here we show that Lyn and Fyn control immune receptor signaling status. SHP-1 tyrosine 536 phosphorylation by Lyn
We characterized urinary excretion of C3 fragments among patients with systemic lupus erythematosus (SLE) as a possible indicator of renal involvement. 28 patients, representing a broad range of disease activity were admitted to our study. Urinary proteins were separated on 4-20% gradient SDS-PAGE
Systemic lupus erythematosus is a multi-system disease characterized by wide-spread DNA methylation changes. To identify epigenetic susceptibility loci for lupus nephritis, genome-wide DNA methylation changes in naïve CD4+ T cells were compared between two sets of lupus patients with and without a
BACKGROUND
Paroxysmal nocturnal hemoglobinuria is an acquired disorder of hemopoiesis and is characterized by recurrent episodes of intravascular hemolysis due to an increased sensitivity to complement-mediated hemolysis. Systemic lupus erythematosus with paroxysmal nocturnal hemoglobinuria is very
Our previous experiment confirmed that high-mobility group box chromosomal protein 1 (HMGB1) was involved in the pathogenesis of Lupus nephritis (LN) by upregulating the proliferation of the mouse mesangial cell line (MMC) through the cyclin D1/CDK4/p16 system, but the precise mechanism is still