The following were investigated, including the number of staff in Luzhou public hospital libraries, the administrative departments of Luzhou public hospitals, the education level and specialized subjects of administrative staff, the soft and hard ware and resource development in Luzhou public hospital libraries, followed by an analysis of the status quo in Luzhou public hospital libraries with suggestions put forward for their development .

Objective:To evaluate the effects of dexamethasone on systemic lupus erythematosus complicated with cognitive dysfunction.Methods:Ten wild type mice and 20 MRL/lpr mice were applied for the research.MRL/lpr mice were randomly assigned to a MRL/lpr group and a MRL/lpr + dexamethasone (1.5 mg/kg) group.Interleukin-6 (IL-6),IL-1β,and tumor necrosis factor alpha (TNF-α) in serum and hippocampus were detected.The protein phosphorylation levels of phosphoinositide 3-kinase (P-PI3K),protein kinase B (P-Akt),NF-kappa-B inhibitor alpha (P-IκBa) and nuclear transcription factor kappa-B p65 (P-NF-κB p65) were detected by Western blot,the level of P-NF-κB p65 also was detected by immunohistochemistry.Results:Treatment with dexamethasone (1.5 mg/kg) alleviated the cognitive dysfunction and decreased the levels of IL-6,IL-1 β and TNF-α in serum and hippocampus,and reduced the levels of P-PI3K,P-Akt,P-IκBa and P-NF-κB p65 in hippocampus in MRL/lpr mice.Conclusion:Dexamethasone may play a protective role in the cognitive function by decreasing the levels of TNF-α and IL-1 β in the hippocampus of MRL/lpr lupus mice.

Objective:To investigate the safety and efficacy of transcatheter genicular artery embolization (GAE) for moderate to severe knee osteoarthritis (KOA).Methods:This prospective study included 13 patients (17 knees) with KOA who were treated with GAE from October 2020 to March 2021. The Kellgren-Lawrence (K-L) grade was 2-3 for 11 knees, and 4 for 6 knees. The Western Ontario and McMaster Universities osteoarthritis index (WOMAC) and the Whole-Organ Magnetic Resonance Imaging Score (WORMS) assessments were performed for all the subjects before operation. The success rate, clinical efficacy and complications were recorded after operation. Clinical outcomes were evaluated at 1 day, 1week and 1, 3, 6 months after the operation.Results:The success rate of GAE in 17 cases was 100%, and the success rate of target artery superselection was 98.4%(63/64). The baseline WOMAC pain score was 11(10, 13) and total score was 44(38, 58) for 17 knees. Post-operation follow-up WOMAC pain score were 4(3, 7), 2(1, 5), 2(1, 6) and 4(2, 6) at 1 day, 1 week, 1 month, and 3 months. Post-operation follow-up WOMAC total score were 22 (15, 34),20 (12, 24),17 (12, 26) and 20 (12, 31) at 1 day, 1 week, 1 month, and 3 months. There were 16 knees with 6 month follow-up assessment, with the WOMAC pain score of 2.5(2, 5), and the total score of 15(12, 26). Significant difference was found in the WOMAC pain score between baseline and the 1 day, 1 week, 1, 3 and 6 months follow up ( Z=-3.631, -3.623, -3.622, -3.622, -3.532, all P<0.001); also, the total score was statistically significant different between the baseline and the 1 day, 1 week, 1, 3 and 6 months follow up ( Z=-3.639, -3.634, -3.646, -3.527, -3.532, all P<0.001). At 3 months follow-up, there was 1 knee recognized clinical failure. Post-operative adverse reaction in this group included skin ecchymosis in femoral artery puncture area ( n=3), knee joint stiffness and pain within 1 week ( n=4),and clanging joints during postoperative activities ( n=6). Conclusion:GAE is a feasible and safe procedure with obvious short-term curative effect, which can alleviate pain symptoms and improve restricted movement in patients with KOA.

Post-stroke anxiety disorder （PSA） is a common psychiatric complication of stroke， which jeopardizes patients' recovery and their quality of life. Recent studies suggest that inflammation plays an important role in the pathogenesis of PSA. Therefore， this paper reviewed the related licture about the association between PSA and serum inflammatory biomarkers in order to provide references for the intervention of PSA. In this study， a comprehensive search was performed in China National knowledge Infrastructure （CNKI）， Wanfang Data， Web of Science and PubMed database to identify the well qualified literature focusing on the relationship between PSA occurrence and serum inflammatory biomarkers， and a total of 13 studies were retrieved. Analysis indicates a certain association between PSA occurrence and serum inflammatory biomarkers， and denotes that the elevation of inflammatory biomarkers may be a trigger for the disease occurrence and its progression， but the specific mechanism underlying this relationship requires further study.

Background: Chronic exposure to elevated levels of saturated fatty acids results in pancreatic β-cell senescence. However, targets and effective agents for preventing stearic acid-induced β-cell senescence are still lacking. Although melatonin administration can protect β-cells against lipotoxicity through anti-senescence processes, the precise underlying mechanisms still need to be explored. Therefore, we investigated the anti-senescence effect of melatonin on stearic acid-treated mouse β-cells and elucidated the possible role of microRNAs in this process. Methods: β-Cell senescence was identified by measuring the expression of senescence-related genes and senescence-associated β-galactosidase staining. Gain- and loss-of-function approaches were used to investigate the involvement of microRNAs in stearic acid-evoked β-cell senescence and dysfunction. Bioinformatics analyses and luciferase reporter activity assays were applied to predict the direct targets of microRNAs. Results: Long-term exposure to a high concentration of stearic acid-induced senescence and upregulated miR-146a-5p and miR- 8114 expression in both mouse islets and β-TC6 cell lines. Melatonin effectively suppressed this process and reduced the levels of these two miRNAs. A remarkable reversibility of stearic acid-induced β-cell senescence and dysfunction was observed after silencing miR-146a-5p and miR-8114. Moreover, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (Mafa) was verified as a direct target of miR-146a-5p and miR-8114. Melatonin also significantly ameliorated senescence and dysfunction in miR-146a-5pand miR-8114-transfected β-cells. Conclusion These data demonstrate that melatonin protects against stearic acid-induced β-cell senescence by inhibiting miR-146a- 5p and miR-8114 and upregulating Mafa expression. This not only provides novel targets for preventing stearic acid-induced β-cell dysfunction, but also points to melatonin as a promising drug to combat type 2 diabetes progression.