[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.

Objective:To explore the benefits of transradial diagnostic cerebral angiography in elderly patients and its correlation with morphometric parameters of the aortic arch.Methods:Clinical data and aortic arch CTA imaging parameters of patients who underwent cerebral angiography at the Department of Neurosurgery, Beijing Hospital, between May 2022 and April 2023 were retrospectively analyzed.The study aimed to compare the time taken for angiography via radial artery access in elderly patients versus younger patients, as well as via femoral artery access, and to evaluate the associated aortic arch morphology parameters.Results:A total of 101 patients' data were analyzed, with 67 males(66.3%)and an average age of 63.4±12.0 years.Among them, 69 patients(68.3%)were aged 60 and above.The arterial approach for 44 patients(43.6%)was radial, while 57 cases(56.4%)used the femoral artery approach.In the elderly group, 14 cases(20.6%), 31 cases(45.6%), and 23 cases(33.8%)had type Ⅲ aortic arch, respectively.For younger patients, 17 cases(53.1%), 12 cases(37.5%), and 3 cases(9.4%)fell into these categories.The distribution difference was statistically significant( χ2=12.765, P=0.002).Elderly patients had a larger aortic arch width angle compared to younger patients(106°±12°and 100°±12°, t=2.334, P=0.022).The time for whole-brain angiography via radial artery was shorter for elderly patients than via femoral artery(39.8±29.5 minutes and 52.2±28.4 minutes, respectively, t=1.845, P=0.070).In young patients, there was no significant time difference between the two approaches(42.3±30.4 minutes for radial artery and 34.6±11.2 minutes for femoral artery, t=1.026, P=0.313).In the type Ⅱ aortic arch group, the average times for transradial and transfemoral approaches were 38.1±21.7 minutes and 46.7±32.2 minutes, respectively( t=1.020, P=0.314).The average times for the type Ⅲ aortic arch group were 41.9±37.3 minutes and 48.9±20.7 minutes, respectively.Correlation analysis revealed a significant negative correlation between the duration of radial artery access and the distance from the origin of the innominate artery to the left subclavian artery(Pearson correlation coefficien( r=-0.372, P=0.014). Conclusions:In elderly patients, particularly those with type Ⅱ or Ⅲ aortic arch or a wide aortic arch, diagnostic cerebral angiography using transradial access is preferable to femoral access.The distance between the innominate artery and the left subclavian artery origin could impact the duration of the procedure.

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*