Objective To investigate the mRNA and protein expressions of Nav 1.1 and Nav 1.2 in hippocampus following traumatic brain injury ( TBI) in rats.Methods After the lateral fluid percussion model was established in adult male Sprague Dawley rats,the rats were sacrificed at 2,12,24 and 72 hours after percussion and collected ipsilateral hippocampus for detecting mRNA and protein expressions of Nav 1.1 and Nav 1.2 by means of fluorescent quantitation RT-PCR,Western blot and immunofluo rescence staining.Results The mRNA expressions of Nav 1.1 and Nav 1.2 were significantly down-regulated (P<0.01) in hippocampus and reached the lowest level at 2 hours following TBI.The protein expression of Nav 1.1 was significantly down-regulated (P<0.01) but recovered near to level of control group at 72 hours after TBI.While there was no statistical difference on protein expression of Nav 1.2 in hippocampus after TBI compared with control group (P>0.05).Conclusion TBI induces significant down-regulated mRNA and protein expressions of Nav 1.1 in the hippocampus,which may be one of molecular mechanisms for functional alternation of sodium channels and excitotoxic action following TBI.

This article reports a rare case of proliferative glomerulonephritis with monoclonal immunoglobulin deposits. The patient, a middle-aged woman, exhibited clinical manifestations including nephrotic syndrome, microscopic hematuria, renal insufficiency, hyperglycemia, and bilateral diabetic retinopathy. Notably, monoclonal bands were absent in both blood and urine immunofixation electrophoresis. Renal biopsy revealed membranoproliferative glomerulonephritis, with immunofluorescence revealing exclusive petal-like deposition of IgG3 subtype along the capillary loop. Electron microscopy demonstrated segmental thickening of the glomerular basement membrane, along with electron dense deposits in the subendothelial and mesangial areas, lacking discernible substructure. The diagnosis comprised proliferative glomerulonephritis with monoclonal immunoglobulin deposition concurrent with diabetic nephropathy. Subsequent sequential treatment with daratumumab and cyclophosphamide over 6 months led to partial remission of nephrotic syndrome, normalization of renal function, and significant improvement of anemia. During the 24-month follow-up period, no serious adverse reactions occurred.