[Objective]To investigate the pathogenesis,pathology,diagnosis and therapy of hyponatremia after acute spinal cord injury.[Method]Fifteen in-patients with hyponatremia after acute spinal cord injury from 2004 to 2006 were retrospectively analyzed.[Result]Serum sodium was lower than 130 mmol/L in all cases.Urine sodiumcanned was from 40 to 68 mmol/L and urine osmotic pressure was from 420 to 980 mmol/L.After limitation of water intake and appropriate salt intake,12 patients recovered at 2 to 3 weeks.Because of fever and avoiding limitation of water intake,the other 3 patients recovered slowly.[Conclusion]The more serious the acute spinal cord injury,the higher the frequency of hyponatremia;syndrome of inappropriate antidiuretic hormone secretion(SIADH) is its primary cause: appropriate measures should be taken to correct the hyponatremia according to the findings of serum sodium and urine osmotic pressure.

Objective To investigate the expressions of erythropoietin(EPO)and its receptor(EPO-R)in the spinal cord after acute traumatic injury in adult rats.Methods Sixty-nine Wistar rats were randomly divided into three groups:normal control group(n=5),spinal cord injury group(n=32),and sham operation group(n= 32).The injury group and sham operation group were further randomly divided into eight subgroups respectively (n=4)(1h,6h,12h,24h,3d,7d,14d,28 dafter operation).The expressions of EPO and EPO-R at different time points were detected by RT-PCR,Western blot and immunohistochemical staining.Results EPO was nut detected at any time point in the normal control grnup,spinal cord injury group or sham operation group.The EPO-R expression was not found in the normal control group or sham operation group.RT-PCR and Western blot analyses revealed EPO-R mRNA and protein expressions in the injury group as early as 6 h after injury.The EPO-R mRNA and protein expressions sharply increased at 12 h,peaked at 24 h to 7 d,and gradually declined after 7 d. They were still higher than those in the control rats 28 d after injury.The EPO-R immunoreactivity was chiefly found in neurons,oligodendrocytes,vascular endothelial and ependymal cells.Conclusion The EPO-R expression can be up-regulated obviously in the injured spinal cord,which provides a molecular basis for the nerooprotection of exogenous EPO.

Background: Evidence has revealed the involvement of microRNAs (miRNAs) in modulating osteogenic differentiation, implying the promise of miRNA-based therapies for treating osteoporosis. This study investigated whether miR-181a-5p influences osteogenic differentiation and bone formation and aimed to establish the mechanisms in depth. Methods: Clinical serum samples were obtained from osteoporosis patients, and MC3T3-E1 cells were treated with osteogenic induction medium (OIM) to induce osteogenic differentiation. miR-181a-5p-, Runt-related transcription factor 1 (Runx1)-, and/or allograft inflammatory factor-1 (AIF-1)-associated oligonucleotides or vectors were transfected into MC3T3-E1 cells to explore their function in relation to the number of calcified nodules, alkaline phosphatase (ALP) staining and activity, expression levels of osteogenesis-related proteins, and apoptosis. Luciferase activity, RNA immunoprecipitation, and chromatin immunoprecipitation assays were employed to validate the binding relationship between miR-181a-5p and Runx1, and the transcriptional regulatory relationship between Runx1 and AIF-1. Ovariectomy (OVX)-induced mice were injected with a miR-181a-5p antagonist for in vivo verification. Results: miR-181a-5p was highly expressed in the serum of osteoporosis patients. OIM treatment decreased miR-181a-5p and AIF-1 expression, but promoted Runx1 expression in MC3T-E1 cells. Meanwhile, upregulated miR-181a-5p suppressed OIM-induced increases in calcified nodules, ALP content, and osteogenesis-related protein expression. Mechanically, miR-181a-5p targeted Runx1, which acted as a transcription factor to negatively modulate AIF-1 expression. Downregulated Runx1 suppressed the miR-181a-5p inhibitor-mediated promotion of osteogenic differentiation, and downregulated AIF-1 reversed the miR-181a-5p mimic-induced inhibition of osteogenic differentiation. Tail vein injection of a miR-181a-5p antagonist induced bone formation in OVX-induced osteoporotic mice. Conclusion In conclusion, miR-181a-5p affects osteogenic differentiation and bone formation partially via the modulation of the Runx1/AIF-1 axis.

The twenty-first century has already recorded more than ten major epidemics or pandemics of viral disease, including the devastating COVID-19. Novel effective antivirals with broad-spectrum coverage are urgently needed. Herein, we reported a novel broad-spectrum antiviral compound PAC5. Oral administration of PAC5 eliminated HBV cccDNA and reduced the large antigen load in distinct mouse models of HBV infection. Strikingly, oral administration of PAC5 in a hamster model of SARS-CoV-2 omicron (BA.1) infection significantly decreases viral loads and attenuates lung inflammation. Mechanistically, PAC5 binds to a pocket near Asp49 in the RNA recognition motif of hnRNPA2B1. PAC5-bound hnRNPA2B1 is extensively activated and translocated to the cytoplasm where it initiates the TBK1-IRF3 pathway, leading to the production of type I IFNs with antiviral activity. Our results indicate that PAC5 is a novel small-molecule agonist of hnRNPA2B1, which may have a role in dealing with emerging infectious diseases now and in the future.
Animals ; Mice ; Antiviral Agents/pharmacology* ; COVID-19 ; Hepatitis B virus ; Interferon Type I/metabolism* ; SARS-CoV-2/drug effects* ; Heterogeneous-Nuclear Ribonucleoprotein Group A-B/antagonists & inhibitors*