Short-term clinical observations of belimumab in the treatment of recently diagnosed systemic lupus erythematosus.

OBJECTIVE: To explore the therapeutic effectiveness and safety of belimumab in the treatment of recently diagnosed systemic lupus erythematosus (SLE). METHODS: Between January 2019 and February 2022, a total of 30 patients who had been recently diagnosed with SLE were selected for 6 months of belimumab treatment at the Department of Rheumatology and Immunology, Tianjin First Central Hospital. Laboratory test results and related adverse reactions were recorded at baseline and after treatment. RESULTS: Participants' white blood cell counts and complement 3, complement 4, and hemoglobin levels were higher after treatment than at baseline. Participants' immunoglobulin G and immunoglobulin M levels, SLE Disease Activity Index 2000 scores, glucocorticoid doses, erythrocyte sedimentation rates, and serum albumin/globulin ratios were lower after treatment. These differences were all statistically significant (p < .05). CONCLUSION: Belimumab was safe and effective in patients recently diagnosed with SLE and might help to reduce the use of glucocorticoids and to improve anemia with few adverse reactions. Belimumab might be applied in the treatment of patients recently diagnosed with SLE with high disease activity.

Identification of Tissue-Specific Expressed Hub Genes and Potential Drugs in Rheumatoid Arthritis Using Bioinformatics Analysis.

Background: Rheumatoid arthritis (RA) is a common autoimmune disease characterized by progressive, destructive polyarthritis. However, the cause and underlying molecular events of RA are not clear. Here, we applied integrated bioinformatics to identify tissue-specific expressed hub genes involved in RA and reveal potential targeted drugs. Methods: Three expression profiles of human microarray datasets involving fibroblast-like synoviocytes (FLS) were downloaded from the Gene Expression Omnibus (GEO) database, the differentially expressed mRNAs (DEGs), miRNAs (DEMs), and lncRNAs (DELs) between normal and RA synovial samples were screened using GEO2R tool. BioGPS was used to identified tissue-specific expressed genes. Functional and pathway enrichment analyses were performed for common DEGs using the DAVID database, and the protein-protein interaction (PPI) network of common DEGs was constructed to recognize hub genes by the STRING database. Based on receiver operating characteristic (ROC) curve, we further investigated the prognostic values of tissue-specific expressed hub genes in RA patients. Connectivity Map (CMap) was run to identify novel anti-RA potential drugs. The DEM-DEG pairs and ceRNA network containing key DEMs were established by Cytoscape. Results: We obtain a total of 418 DEGs, 23 DEMs and 49 DELs. 64 DEGs were verified as tissue-specific expressed genes, most derive from the hematologic/immune system (20/64, 31.25%). GO term and KEGG pathway enrichment analysis showed that DEGs focused primarily on immune-related biological process and NF-κB pathway. 10 hub genes were generated via using MCODE plugin. Among them, SPAG5, CUX2, and THEMIS2 were identified as tissue-specific expressed hub genes, these 3 tissue-specific expressed hub genes have superior diagnostic value in the RA samples compared with osteoarthritis (OA) samples. 5 compounds (troleandomycin, levodopa, trichostatin A, LY-294002, and levamisole) rank among the top five in connectivity score. In addition, 5 miRNAs were identified to be key DEMs, the lncRNA-miRNA-mRNA network with five key DEMs was formed. The networks containing tissue-specific expressed hub genes are as follows: ARAP1-AS2/miR-20b-3p/TRIM3, ARAP1-AS2/miR-30c-3p/FRZB. Conclusion: This study indicates that screening for identify tissue-specific expressed hub genes and ceRNA network in RA using integrated bioinformatics analyses could help us understand the mechanism of development of RA. Besides, SPAG5 and THEMIS2 might be candidate biomarkers for diagnosis of RA. LY-294002, trichostatin A, and troleandomycin may be potential drugs for RA.

Boosting visual perceptual learning by transcranial alternating current stimulation over the visual cortex at alpha frequency.

BACKGROUND: Transcranial alternating current stimulation (tACS) has been widely used to alter ongoing brain rhythms in a frequency-specific manner to modulate relevant cognitive functions, including visual functions. Therefore, it is a useful tool for exploring the causal role of neural oscillations in cognition. Visual functions can be improved substantially by training, which is called visual perceptual learning (VPL). However, whether and how tACS can modulate VPL is still unclear. OBJECTIVE: This work aims to explore how tACS modulates VPL and the role of neural oscillations in VPL. METHODS: A between-subjects design was adopted. Subjects were assigned to six groups and undertook five daily training sessions to execute an orientation discrimination task. During training, five groups received occipital tACS stimulation at 6, 10, 20, 40, and sham 10 Hz respectively, and one group was stimulated at the sensorimotor regions by 10 Hz tACS. RESULTS: Compared with the sham stimulation, occipital tACS at 10 Hz, but not at other frequencies, accelerated perceptual learning and increased the performance improvement. However, these modulatory effects were absent when 10 Hz tACS was delivered to the sensorimotor areas. Moreover, the tACS-induced performance improvement lasted at least two months after the end of training. CONCLUSION: TACS can facilitate orientation discrimination learning in a frequency- and location-specific manner. Our findings provide strong evidence for a pivotal role of alpha oscillations in boosting VPL and shed new light on the design of effective neuromodulation protocols that can facilitate rehabilitation for patients with neuro-ophthalmological disorders.

Prevalence and risk factors of active tuberculosis in patients with rheumatic diseases: a multi-center, cross-sectional study in China.

Evidence of active tuberculosis (ATB) in patients with rheumatic diseases are research priorities but limited data from China have been reported. Research targeting patients not taking anti-TNF biologics are especially insufficient. We aimed to investigate the prevalence and risk factors of ATB in this at-risk population. We conducted a tertiary hospital-based, multi-center, cross-sectional study by using stratified multi-stage cluster sampling strategy to screen ATB in patients with rheumatic diseases. We estimated the prevalence of ATB in patients with rheumatic diseases and identified risk factors among those who were not taking anti-TNF biologic. A total of 13,550 eligible patients were enrolled, and the result showed the standardized prevalence of ATB according to the composition ratio of various types of rheumatic disease was 882/100000 (95% confidence interval (CI): 706-1057). Multivariable logistic regression analysis in patients not taking anti-TNF biologics showed that the independent risk factors of ATB were having systemic lupus erythematosus (SLE) (OR=2.722, 95% CI: 1.437-5.159, p=0.002), having Behcet's disease (BD) (OR= 5.261, 95% CI: 2.071-13.365, p<0.001), taking azathioprine(AZA) within the past two years (OR=2.095, 95% CI: 0.986-4.450, p=0.054), exposing to glucocorticoids ≥30mg/d for more than four weeks within the past two years (OR=2.031, 95% CI: 1.247-3.309, p=0.004) and having evidences of previous TB (OR= 6.185, 95% CI: 3.487-10.969, p<0.001). The prevalence of ATB was higher in patients with rheumatic diseases compared to the general population. Patients with SLE or BD, prolonged exposure to moderate to high dose of glucocorticoids and previous TB were independent risk factors for ATB.

miR-496/MMP10 Is Involved in the Proliferation of IL-1ß-Induced Fibroblast-Like Synoviocytes Via Mediating the NF-κB Signaling Pathway.

Rheumatoid arthritis (RA) is a common chronic autoimmune disease featured by synovial inflammation. miR-496 is closely involved in various pathologic conditions. However, its role in RA has not yet been elucidated. Expression of miR-496 and MMP10 was determined based on the clinical samples with RA retrieved from the Gene Expression Omnibus (GEO) datasets. In vitro model of RA was constructed in MH7A cells stimulated by IL-1ß (10 ng/mL). Cell counting kit 8 (CCK-8) and flow cytometry experiments were implemented to investigate the cell viability and apoptosis rate of MH7A cells. TargetScan was applied to identify the targets of miR-496, and the regulation of miR-496 on MMP10 expression was validated by a dual-luciferase reporter gene assay. qRT-PCR and western blot analyses were conducted to examine the expression. miR-496 expression was decreased in RA tissues and MH7A cells after IL-1ß treatment. Overexpression of miR-496 significantly inhibited IL-1ß-treated MH7A cell viability. MMP10 was identified as a target of miR-496 and its expression was negatively regulated by miR-496. The effects of miR-496 on MH7A cell proliferation and apoptosis were reversed by MMP10. The activity of NF-κB pathway was associated with the miR-496/MMP10 axis in IL-1ß-stimulated MH7A cells. To summarize, this study demonstrated that miR-496 can impair the proliferative ability and facilitate the apoptosis of IL-1ß-treated MH7A through regulating MMP10 expression and NF-κB signaling pathway.