Background: Systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) are autoimmune diseases with some overlapping clinical manifestations. Recent studies have revealed that Toll-like receptors (TLRs) play essential roles in autoimmune diseases' pathogenesis. To investigate the expression of TLR genes in SLE and SSc that are specific to the character of these diseases' pathogenesis.Methods: We recruited patients with SLE (n = 15) and SSc (n = 9) from China Medical University Hospital hospital in Taiwan from 2016 to 2017. Included were healthy reference controls and SLE datasets from the NCBI database. RNA was extracted from peripheral blood cells of the patients for next-generation sequencing (NGS). Results in identified differentially expressed genes were compared to explore TLRs' association with SLE and SSc pathogenesis. Housekeeping genes, including ACTB, GAPDH, PGK1, PPIB, SDHA, and TBP, were used to normalize the expression levels of the TLR genes. Results: There were significant differences in raw gene expression for patients with SLE and SSc (p < 0.05). No significant difference between patients with SLE and control datasets with SLE (p >0.05). The expression levels of TLR1 (p = 0.018) and TLR3 (p = 0.031) were significantly upregulated in the patients with SSc compared with those with SLE, normalized by GAPDH. Compared with many housekeeping genes, ACTB, GAPDH, and TBP indicated a significant difference (p < 0.05) in the expression of TLR1and TLR3. Conclusions: TLR1 and TLR3 can serve as biomarkers to distinguish the gene expression between SLE and SSc, normalized with housekeeping genes such as ACTB, GADPH, and TBP.

Background: Systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) are autoimmune diseases with some overlapping clinical manifestations. SLE is characterized by systemic inflammation with vasculitis and multiple organ damage, whereas SSc manifests as low-grade inflammation with vasculopathy and tissue fibrosis. Recent studies have revealed that Toll-like receptors (TLRs) play essential roles in the pathogenesis of autoimmune diseases. This study investigated the expression of TLR genes in SLE and SSc to determine their roles in the pathogenesis of these diseases.Methods: Patients with SLE (n = 15) and SSc (n = 9) were recruited from a hospital in Taiwan from 2016 to 2017. RNA was extracted from peripheral blood cells of the patients for next-generation sequencing (NGS). Then, We identified differentially expressed genes and associated pathways to explore the association of TLRs with SLE and SSc pathogenesis. Several housekeeping genes, including ACTB, GAPDH, PGK1, PPIB, SDHA, and TBP, were used to normalize the expression levels of the TLR genes.Results: GAPDH, PGK1, PPIB and SDHA are significantly different (p < 0.05) in patients of SLE and SSc. The expression levels of TLR1 (p = 0.018) and TLR3 (p = 0.031) were significantly upregulated in the patients with SSc compared with those with SLE, normalized by GAPDH.Conclusions: TLR1 and TLR3 can serve as biomarkers to distinguish the gene expression between SLE and SSc, normalized with housekeeping genes such as ACTB, GADPH and TBP.

Introduction: This systematic review and meta-analysis aimed to assess the efficacy and safety of cupping therapy in patients with metabolic syndrome (MetS). Methods: This systematic review focused on patients with MetS and included randomized controlled trials (RCTs) that compared the effects of cupping therapy with control groups. A total of 12 electronic databases were searched from inception until February 03, 2023. The main outcome after the meta-analysis was waist circumference; the others included anthropometric variables, blood pressure, lipid profile, fasting blood glucose level, and high-sensitivity C-reactive protein level. The incidence of adverse events and the follow-up courses were also evaluated. Risk of bias (ROB) was evaluated using ROB 2.0 from the Cochrane Handbook. Results: This systematic review included five studies involving 489 patients. Some risks of bias were also identified. The meta-analysis revealed a statistically significance in waist circumference (MD = −6.07, 95% CI: −8.44 to −3.71, P < .001, I 2 = 61%, τ 2 = 3.4), body weight (MD = −2.46, 95% CI: −4.25 to −0.68, P = .007, I 2 = 0%, τ 2 = 0) and body mass index (MD = −1.26, 95% CI: −2.11 to −0.40, P = .004, I 2 = 0%, τ 2 = 0) between the cupping therapy and control groups. However, there were no significant results in total fat percentage and blood pressure values. Regarding biochemical markers, cupping significantly lowered the concentration of low-density lipoprotein cholesterol (MD = −3.98, 95% CI: −6.99 to −0.96, P = .010, I 2 = 0%, τ 2 = 0) but had no significant effect on total cholesterol, triglyceride, high-density lipoprotein cholesterol, fasting blood glucose, and high-sensitivity C-reactive protein. 3 RCTs reported no adverse events. Conclusions: Despite some ROB and low to substantial heterogeneity of the included studies, cupping therapy can be considered a safe and effective complementary intervention for reducing waist circumference, body weight, body mass index, and low-density lipoprotein cholesterol in patients with MetS. In the future, well-designed, high-quality, rigorous methodology, and long-term RCTs in this population are required to assess the efficacy and safety of cupping therapy.

Objectives:Malar rash is one of clinical phenotypes seen in systemic lupus erythematosus (SLE). However, the pathogenesis of malar rash is not clear for each case of SLE patients. In this paper we endeavored to investigate the linking of clinical phenotype from the gene expression profiles between both patients with malar rash and without malar rash. Therefore we might perform better evaluation of the possible prognosis for different SLE patients in the future.Methods: This study utilizes transcriptome sequencing (RNA-Seq) technologies to discover underlying gene expression profile for systemic lupus erythematosus patients. We performed transcriptome sequencing experiments and analyzed differentially expressed genes (DEGs) and associated pathways.Results: From the analysis of gene expression profiling, we identified the gene DAAM2 is the most differentially expressed gene for patients with malar rash. Using a gene set enrichment analysis, we discuss the linkage between DAAM2 and the possible pathways for systemic lupus erythematosus with malar rash.Conclusions: We identified DAAM2 as a candidate biomarker for the clinical phenotype of malar rash for systemic lupus erythematosus.JRC and PWH did the analysis on the patient data. JRC, PWH, BJW, SIC, CMC, HHC and HTC discussed the project and jointly wrote the manuscript. HTC and HHC leaded the project. All authors read and approved the final manuscript.