This paper introduces the setting and configuration of our hospital's fPACS workstation, which is developed by the First Military Medical University. The fPAX video workstations are used as the terminals, including fPAX sampling workstation for video, picture and number, fPAX diagnosis workstation, fPAX clinician workstation and fPAX consultation center workstation. The workstation is equipped with an IBM4 2G host computer, an 80G fixed disc, an EMS memory more than 512M and a SONY 21″ pure flat display. Our experience of building PACS workstation proves that the reasonable setting and configuration is helpful to save the money and increase the efficiency.

Objective To investigate the role of long noncoding RNA-AK001903 in the pathogenesis of primary gout arthritis (GA).Methods The subjects were divided into four groups:30 acute gout patients (AGA),24 non-acute gout patients (NAGA),24 healthy controls and 24 hyperuricemia (HUA).Real-time quantitative polymerase chain reaction (RT-qPCR) was employed to examine the expression of AK001903 in peripheral blood mononuclear cells (PBMCs) from four groups.100 μg/ml monosodium (MSU) was used to stimulate the peripheral blood of NAGA and healthy control patients.Then the expression of AK001903 was detected by RT-qPCR.Kruskal-Wallis test,Mann-Whitney test,Spearman correlations were used for statistical analysis.Results The expression level of AK001903 in the AGA group (0.079±0.022) and the NAGA group (0.071±0.021) were higher than the healthy control group (0.014±0.004).There was no significant difference between the NAGA group and the NAGA group (Z=-0.655,P＞0.05).Those of the GA group (0.078±0.018) and the HUA group(0.047±0.016) was higher than the healthy control group (0.014±0.004) (Z=-2.887,Z=-4.157;P＜0.05).Compared with the control group,the expression of AK001903 in NAGA and the healthy control group which were stimulated by MSU was significantly increased.The Spearman correlation analysis found that the AK001903 expression levels in the GA groups were correlated with TG (r=0.938,P＜0.05),VLDL (r=0.873,P＜0.05),GLU9 (r=0.671,P＜0.05) and were negatively correlated with apoA1 (r=-0.661,P＜0.05).Conclusion Altered expression of AK001903 may be involved in the process of imbalance between lipid metabolism and hyperuricemia,and takes part in the pathogenesis of GA.

At present, the major public health challenges caused by novel coronavirus infection have gradually subside. However, a large number of people are still suffering from long-novel coronavirus syndrome or post-novel coronavirus syndrome. The clinical manifestations of long coronavirus syndrome are related to multiple systems, such as respiratory, circulatory, nervous, digestive and musculoskeletal systems, with various long-term persistent symptoms after novel coronavirus infection. At the same time, the infection of the novel coronavirus is an important cause of frailty and sarcopenia in the elderly population. However, at present, the scholars have not paid enough attention to the skeletal muscle weakness caused by the novel coronavirus. Therefore, this paper focuses on the long-novel coronavirus syndrome and sarcopenia to explore the pathological mechanism of skeletal muscle attenuation caused by the SARS-CoV-2 mediated "cytokine storm", mitochondrial damage, hypoxia state and other links, so as to raise the attention of clinical and academic researchers and improve the clinical strategy of frailty and sarcopenia after novel coronavirus infection.

Objective: To construct the BCMA-CAR using the B-cell maturation antigen (BCMA) specific ligand APRIL as antigen binding region and to validate the effect of BCMA-CAR modified T cells (BCMA-CAR-T) on myeloma cells. Methods: The BCMA-CAR was constructed using the BCMA specific ligand APRIL as antigen binding domain and 4-1BB as the costimulatory domain. The specific cytotoxicity against BCMA⁺ myeloma cell lines and primary multiple myeloma (MM) cells in vitro were evaluated. In addition, BCMA⁺ myeloma xenograft mouse model was established to assess the anti-tumor effect of BCMA-CAR-T cell therapy in vivo. Results: BCMA-CAR-T cells could specifically kill BCMA⁺ myeloma cell lines (For BCMA-CAR-T cells, BCMA⁺ cells are almost undetectable in the E∶T ratio of 1∶4) and MM patients’ bone marrow mononuclear cells (the proportion of residual cells in BCMA-CAR-T and vector-T groups was 16.0% vs 66.85%, P=0.003) with significant degranulation (CAR-T and vector-T cells cocultured with MM1.S, H929 and U266 had degranulation levels of 33.30% vs 5.62%, 16.97% vs 2.95% and 25.87% vs 2.97%, respectively, P<0.001) and cytokines release (P<0.01) in vitro. In a human BCMA⁺ myeloma xenograft mouse model, BCMA-CAR-T cells could significantly prolong the survival of mice (The median survival time of mice treated with BCMA-CAR-T and vector-T cells was 87.5 days and 67.5 days, respectively, P<0.001) . Conclusion The ligand-based BCMA-CAR-T cells could be a promising strategy for BCMA⁺ multiple myeloma treatment.