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Background: The occurrence of immunity and inflammation outside the central nervous system frequently results in acute cognitive impairment among elderly patients. However, there is currently a lack of standardized methods for diagnosing acute cognitive impairment. The objective of our study was to identify potential mRNA biomarkers and investigate the pathogenesis of acute cognitive impairment in mice brains. Methods: To analyze changes in hub genes associated with acute cognitive impairment, bioinformatics analysis was performed on the mouse brain injury data of sterile saline control group and lipopolysaccharide (LPS) induced experimental group in Gene Expression Omnibus (GEO). Functional analysis was conducted using Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), which facilitated to identify some potential mRNA biomarkers for hub gene expression in mice brains. Additionally, the "CIBERSORT X″ R kit was employed to examine immune cell infiltrations of mice brains in LPS group and saline group. Results: In the LPS and saline group, 102 significantly upregulated differentially expressed genes (DEGs) and 32 downregulated DEGs were identified. The pathway enrichment analysis using GO and KEGG revealed that these DEGs were mainly related to the regulation of cytokine, cytokine-cytokine receptor interaction, as well as protein interaction with cytokine and cytokine receptor. Immune cell infiltration analysis indicated potential involvement of M1 macrophages, NK cells resting, T cells CD4 memory, and T cells CD8 naive in the process of cognitive impairment. By constructing a protein-protein interaction (PPI) network, five hub genes (Cxcl10, Cxcl12, Cxcr3, Gbp2, and Ifih1) showed significant associations with immune cell types by using a threshold Spearman's rank correlation coefficient of R > 0.50 and p < 0.05. Conclusion: The mRNA expression profile of the mice brain tissues in the LPS group differed from that in the normal saline group. These significantly expressed mRNAs may act an importance in the pathogenesis of acute cognitive impairment through mechanisms involving immunity and neuroinflammation.

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BACKGROUND: This study meta-analyzed the literature on possible association of 3 polymorphisms (-592, -1082, -819) in the interleukin-10 (IL-10) gene with susceptibility to human immunodeficiency virus (HIV)-1 infection. METHODS: PubMed, EMBASE, MEDLINE and Google Scholar were systematically searched to identify relevant studies in English. Meta-analyses were performed to examine the association of IL-10 polymorphisms -592, -1082, and -819 with susceptibility to HIV-1 infection. RESULTS: A significant association between the -592 polymorphism and susceptibility to HIV-1 infection was found in the total population (recessive model, odds ratios (OR) = 1.44, 95% CI = 1.06-1.96, P = .02; homozygous model, OR = 1.44, 95% CI = 1.02-2.02, P = .04). However, these results were not observed in subgroups based on ethnicity. The -1082 polymorphism was significantly associated with susceptibility to HIV-1 infection in Caucasians (OR = 1.30, 95% CI = 1.05-1.62, P = .02; recessive model, OR = 1.49, 95% CI = 1.09-2.03, P = .01; homozygous model, OR = 1.58, 95% CI = 1.01-2.46, P = .04), but not in Asians or the total population. None of the 5 genetic models suggested a significant association between the -819 polymorphism and HIV-1 infection. CONCLUSION: The available evidence indicates that the AA genotype of IL-10 -592 may confer increased susceptibility to HIV-1 infection, and that the AA genotype of -1082 may confer increased susceptibility in Caucasians. In contrast, the -819 polymorphism may not be associated with HIV-1 infection risk. These conclusions should be verified in large, well-designed studies.

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AIDS Research and Human Retroviruses officially retracts the paper entitled, "Association Between Polymorphisms in the Interleukin-10 Gene and Susceptibility to HIV-1 Infection," by Dan-Hui Fu, Wen-Juan Deng, Zhi Yang, Sen Hong, Qian-Ling Ding, Yang Zhao, Jia Chen, and Dan-Ke Su (AIDS Res Hum Retroviruses, epub: 16 Jun 2020; DOI: 10.1089/AID.2020.0011) due to a final, post-acceptance plagiarism review of the paper revealed a level of duplication of published sources that exceeded normal thresholds. The authors were provided an opportunity to adjust the problem, but the revision was returned with an even higher degree of duplication. The Editor and Publisher of AIDS Research and Human Retroviruses are committed to preserving the scientific literature and the community it serves.

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·AIM: To investigate the changes of serum levels of vascular endothelial growth factor ( VEGF ) , Endostatin (ES), thrombospondin (TSP), tissue kallikrein (TKLK) and soluble intercellular adhesion molecule-1 ( sICAM-1) in patients with diabetic retinopathy ( DR ) and its clinical significance.·METHODS:Selected 60 patients with non-proliferative diabetic retinopathy ( NPDR group ) , 60 patients with proliferative diabetic retinopathy ( PDR group ) were enrolled in this study. Sixty diabetic patients without diabetic retinopathy ( DM group ) and 60 healthy people ( control group) were also enrolled. Collection time was from January 2014 to December 2016. Serum levels of VEGF, ES, TSP, TKLK and sICAM-1 were measured and compared.·RESULTS: The levels of serum VEGF, TKLK and sICAM-1 in PDR group were significantly higher than those in NPDR group, DM group and control group ( P<0. 05). The ES of PDR group was significantly lower than that of NPDR group, DM group and control group ( P<0. 05). The levels of VEGF, TKLK and ES in the NPDR group were significantly higher than those in the DM group and the control group (P<0. 05). The serum VEGF in the NPDR group was positively correlated with the levels of ES, TKLK and sICAM-1 (P<0. 05). The serum VEGF of PDR group was positively related to the levels of TKLK and sICAM-1 (P<0. 05). There was no significant relationship between serum VEGF with ES and TSP in PDR group (P>0. 05).·CONCLUSION: The levels of serum ES, TSP, TKLK and sICAM - 1 in patients with DR have changed significantly, and the process of retinopathy has been affected by regulating the level of VEGF.

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OBJECTIVE: To synthesis 4-methyl-7-allyloxy coumarin by Williamson etherification from 4-methyl-7-hydroxy coumarin and apply as a substrate in hairy roots of Polygonum multiflorum. METHODS: The synthesis reaction of 4-methyl-7-allyloxy coumarin used the allyl bromide and potassium carbonate as catalysts, and acetone as solvent reacted for 17 hours, then the product was isolated. 4-methyl-7-allyloxy coumarin was added into the media of supension transgenic hairy roots of Polygonum multiflorum which had been precultured for 8 d, and then co-cultured for another 7 d. The biotransformation products were detected by TLC and HPLC and isolated by various chromatographic methods. RESULTS: Two biotransformation products, 4-methyl-7-hydroxy coumarin and 4-methyl-coumarin-7-O-beta-D-glucoside were isolated and identified. CONCLUSION: Hairy roots of Polygonum multiflorum contains not only glycosyltransferase but also hydrolysis enzymes.

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OBJECTIVE: To study the effect of FAM172A protein related to diabetic macroangiopathy on apoptosis and proliferation in HEK293 cells. METHODS: The pDrive-FAM172A plasmid constructed in our previous study was used as a template to amplify human FAM172A open reading frame by a polymerase chain reaction. The resulting PCR products were subcloned into the eukaryotic expression vector PDC315 to construct recombinant PDC315-FAM172A plasmid. PDC315-FAM172A plasmid was identified by enzyme cleavage and sequencing analysis. HEK293 cells were transiently transfected respectively with appropriate PDC315 or PDC315-FAM172A plasmid by Lipofectamine 2000 according to the manufacturer's instruction. XTT assay and growth curve were used to observe the effect of over-expression of FAM172A gene on HEK293 cell proliferation. PI and Annexin V/PI staining method were used to assess the effect of FAM172A gene on apoptosis and cell cycle of HEK293 cell. RESULTS: Eukaryotic expression vector PDC315-FAM172A was successfully constructed and identified by enzyme cleavage and sequencing analysis. Compared with PDC315 plasmid transfection, the XTT assay showed that optical density (A) value increased by 52% when transfected with PDC315-FAM172A plasmid (0.21±0.07 vs 0.32±0.06, P<0.01). Growth curve revealed that HEK293 cells transfected with PDC315-FAM172A plasmid proliferated faster than those transfected with PDC315 plasmid. PI staining showed that, as compared with PDC315 plasmid transfection, the apoptotic rate of HEK293 cells transfected with PDC315-FAM172A plasmid decreased by 38.5% (23.79±1.36 vs 14.64±0.95, P<0.01), cell percentage of G0-G1 phases significantly decreased (66.79±1.73 vs 58.16±0.75, P<0.01) and cell percentage of S phases significantly increased (22.62±1.16 vs 33.56±0.94, P<0.01). Annexin V/PI staining revealed that, as compared with PDC315 plasmid transfection, the percentage of early and advanced apoptotic cells decreased by 28% (13.63±0.56 vs 9.79±0.39, P<0.01) and 29% (7.70±0.29 vs 5.43±0.29, P<0.01) respectively. CONCLUSION: FAM172A protein promotes cell proliferation, inhibits cell apoptosis and facilitates S-phases entry. It indicates that FAM172A protein is involved in cell growth regulation. Our findings provide a clue for further study on its physiological functions and roles in diabetic macroangiopathy.

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