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Daya Zhang,1,&ast; Lijun Zhang,2,&ast; Shiju Chen,1,&ast; Runxiang Chen,1 Xiaodong Zhang,1 Feihu Bai3,4 1Graduate School, Hainan Medical University, Haikou, People’s Republic of China; 2Medical Examination Center, The Second Affiliated Hospital of Hainan Medical University, Haikou, People’s Republic of China; 3Department of Gastroenterology, The Second Affiliated Hospital of Hainan Medical University, Haikou, People’s Republic of China; 4The Gastroenterology Clinical Medical Center of Hainan Province, Haikou, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Feihu Bai, Chief Physician and Professor of Department of Gastroenterology, The Second Affiliated Hospital of Hainan Medical University, Yehai Avenue, &num;368, Longhua District, Haikou, Hainan Province, People’s Republic of China, Tel +86-18995181963, Fax +86 898-66809168, Email 328473521@qq.comBackground: The prevalence of metabolism-related fatty liver disease (MAFLD) has been rarely reported in hospital staffs. The aim of this study was to assess the prevalence and risk factors for MAFLD in hospital staffs aged ≥ 18 years.Methods: Based on type B ultrasonic, hospital staffs who underwent medical examinations at the second Affiliated Hospital of Hainan Medical University from January 2022 to March 2022 were classified into health control group (661 subjects) and MAFLD group (223 subjects), demographic, biochemical and blood examination information were compared between 2 groups. Independent risk factors for MAFLD were determined by logistic regression. Predictive values of risk factors of MAFLD were evaluated by receiver operating characteristic (ROC) curves.Results: The prevalence of MAFLD was 33.7%. Older age (OR=1.08, p< 0.001), H. pylori infection (OR=0.234, p=0.02), triglyceride-glucose (TyG) (OR=7.001, p< 0.001), low-density lipoprotein cholesterol (LDL-C) (OR=2.076, p= 0.028), red blood cell (RBC) (OR=2.386, p=0.001), eating out (OR=0.048, p=0.001), regular exercise (OR=23.017, p< 0.001), and overweight (OR=3.891, p= 0.003) were independently associated factors for MAFLD. The AUC of model predicting MAFLD is 0.910 [95% CI (0.886, 0.934)], with 0.794 sensitivity, 0.908 specificity. The diagnostic value of model was higher in the female MAFLD group after stratified analysis according to gender. The model showed that TyG was the factor contributing more to MAFLD. The diagnostic value of TyG was higher in the female MAFLD group than male MAFLD group.Conclusion: The prevalence of MAFLD among hospital staffs was 33.7%. TyG can be used to predict MAFLD especially for female hospital staffs for early intervention.Keywords: metabolic-associated fatty liver disease, MAFLD, hospital staffs, risk factors, triglyceride-glucose index, TyG, red blood cell, RBC, H. pylori infection

Primary Sjogren's syndrome (pSS) is an autoimmune exocrinopathy characterized by dryness symptoms. This review briefly describes recent advances in the targeted therapies for pSS. Biologics evaluated for pSS treatment mainly include B cell-depleting agents, inhibitors of B cell activation, and agents that target co-signaling molecules or proinflammatory cytokines. Small molecule inhibitors that target signaling pathways have also been evaluated. However, current evidence for the efficacy of targeted therapies in pSS is still sparse. Although ianalumab (an anti-B cell-activating factor [BAFF]-receptor antibody) and iscalimab (an anti-CD40 antibody) are promising biologics for pSS, their efficacy still needs to be evaluated in larger clinical trials. For other biologics, clinical trials have found no differences versus placebo in the change from baseline in European League Against Rheumatism Sjogren's Syndrome Disease Activity Index (ESSDAI) score and fatigue score. Possible causes of the disappointing outcomes mainly include the inefficacy of those evaluated biologics in treating pSS, the high heterogeneous nature of pSS, irreversible exocrine glandular failure at advanced disease stages, inappropriate recruitment strategy in clinical trials, and outcome measures. Early diagnosis and glandular function-centered outcome measures may help to improve the current situation in the systemic therapy of pSS.

Tumor necrosis factor-α (TNF-α) inhibitors are the main types of biological conventional synthetic disease-modifying antirheumatic drugs and have efficacy in treating ankylosing spondylitis (AS) which is not sensitive for nonsteroidal anti-inflammatory drug. However, the impact of TNF-α inhibitors on immune cells in patients with AS is still clearly undefined, and the impact of immune cells on treatment response is also largely elusive. This study is aimed at evaluating the longitudinal changes of circulating immune cells after anti-TNF-α therapy and their associations with treatment response in AS patients. Thirty-five AS patients receiving the treatment of anti-TNF-α therapy were included into this prospective observational study. The frequencies of immune cells including Th1, Th2, Th17, regulatory T cell (Treg), T follicular helper cell (Tfh), and regulatory B cell (Breg) in the peripheral blood were measured by flow cytometry at baseline and 4 time points after therapy. The difference in the circulating immune cells between responders and nonresponders was compared. This study suggested that anti-TNF-α therapy could significantly reduce circulating proinflammatory immune cells such as Th17 and Tfh, but significantly increased the percentages of circulating Treg and Breg. Moreover, circulating Breg may be a promising predictor of response to anti-TNF-α therapy in AS patients.

A miniaturized frequency selective rasorber (FSR) that has a wide absorption band in the S–C band and a wide transmission band based on X-band is presented in this paper. The FSR consists of a lossy layer loaded with lumped resistors and a bandpass layer with a three-screen cascade structure, which has the advantages of low insertion loss, wide passband bandwidth, and stable structural performance in the operating band. The rectangular spiral resonant (RSR) is loaded in the middle of the four arms of the cross to form a lossy layer. The aggregate resistance is loaded between the units to form a closed loop, which will absorb the detection signal and thus greatly reduce the radar cross section (RCS). The bandpass layer is divided into three layers, with two identical square patches coupled with a layer of complementary cross grids to form a multi-order bandpass filter. Furthermore, the operating mechanism of low absorption and high transmission is analyzed and verified based on equivalent circuit theory and impedance matching theory. The simulation results show that the 1 dB transmission band of the FSR is 8.0–12.5 GHz and the 10 dB absorption band is 2.8–6.6 GHz. The highest transmittance reaches over 97% at 10.0–11.5 GHz and the lowest insertion loss is 0.012 dB. It has important theoretical reference value and great application in the field of the new stealthy radome.

Primary Sjögren's syndrome (pSS) is an autoimmune exocrinopathy characterized by dryness symptoms. This review briefly describes recent advances in the targeted therapies for pSS. Biologics evaluated for pSS treatment mainly include B cell-depleting agents, inhibitors of B cell activation, and agents that target co-signaling molecules or proinflammatory cytokines. Small molecule inhibitors that target signaling pathways have also been evaluated. However, current evidence for the efficacy of targeted therapies in pSS is still sparse. Although ianalumab (an anti-B cell-activating factor [BAFF]-receptor antibody) and iscalimab (an anti-CD40 antibody) are promising biologics for pSS, their efficacy still needs to be evaluated in larger clinical trials. For other biologics, clinical trials have found no differences versus placebo in the change from baseline in European League Against Rheumatism Sjögren's Syndrome Disease Activity Index (ESSDAI) score and fatigue score. Possible causes of the disappointing outcomes mainly include the inefficacy of those evaluated biologics in treating pSS, the high heterogeneous nature of pSS, irreversible exocrine glandular failure at advanced disease stages, inappropriate recruitment strategy in clinical trials, and outcome measures. Early diagnosis and glandular function-centered outcome measures may help to improve the current situation in the systemic therapy of pSS.

In this paper, a radar absorber with composite structure of metasurface/honeycomb is proposed. Carbon coating is used as a loss material, and honeycomb sandwich structure is used as a support layer to enhance mechanical strength. Introducing impedance matching layer in the top layer of honeycomb absorber can significantly improve the low-frequency absorption performance. The simulation results show that the absorption efficiency of the combined structure absorber can reach more than 90% in the frequency range of 3.65–17.3 GHz. We verified the simulation results through experiments. This method provides an idea for the design of ultra-wideband absorber and has a potential application prospect in stealth material design.

Background/objective The neurological involvement associated with primary Sjogren's syndrome (pSS) can be life threatening. However, the specific characteristics of pSS-related neurological involvement remain obscure. This study aimed at determining the clinical characteristics of this neurological involvement in patients with pSS. Methods The clinical data of 205 patients with pSS who were admitted to our department between January 2015 and June 2017 were studied. Characteristics and laboratory findings of pSS patients with neurological abnormalities were compared with pSS patients without. Results Forty of the 205 patients with pSS exhibited neurological abnormalities (19.51%); of these, 13 patients exhibited central nervous system (CNS) involvement only, 20 patients exhibited peripheral nervous system (PNS) involvement only, and 7 patients exhibited both, yielding a total of 20 (9.76%) patients with CNS involvement and 27 (13.17%) patients with PNS involvement. The titers of anti-Sjogren's syndrome type A (SSA) antibodies were significant higher while the presence of anti-Sjogren's syndrome type B (SSB) antibodies was significant lower in patients with vs. without neurological involvement. Similar results were found in patients with CNS involvement. No significant differences between patients with and without neurological involvement were found for the other clinical parameters examined. Conclusions Neurological involvement in patients with pSS is common and needs to be carefully evaluated. Patients with pSS with a high titer of anti-SSA and low presence of anti-SSB antibodies might have a relatively high risk of developing neurological involvement. Future studies should focus on identifying biomarkers that may aid in the early diagnosis of neurological involvement in patients with pSS.

We read with interest the article by Felten et al which assessed the efficacy of interleukin 6 receptor inhibition (tocilizumab) in Sjogren’s syndrome (SjS).1 SjS is a chronic rheumatic disease characterised by immune infiltrates into exocrine glands such as salivary and lacrimal glands, which can impair glandular function and result in profound dryness.2 Despite the substantially expanded knowledge on its pathogenesis, the management of SjS has not been improved substantially in recent decades, and there are still some unmet needs in both the diagnosis and management of SjS.3 4 Currently available therapies for SjS are limited, and most clinical trials of targeted therapies in SjS including another recent trial of cytotoxic T lymphocyte-associated antigen-4-Ig (abatacept) have reported disappointing findings.1 5 6 There are some possible explanations for those negative findings, and the inefficacy of those evaluated biological drugs is undoubtedly a major possible reason.3 6 Apart from the inefficacy of those drugs, the adopted clinical trial design such as the outcome measures has been regarded as a possible contributor …

Introduction In recent axSpAx patients with remission lasting at least 3 months and later followed-up monthly for a median of 8 months, we compared the predictive value of baseline MRI of sacroiliac joints and constructed a nomogram model for predicting flare. Methods This study included 251 patients with axial spondyloarthritis, according to the ASAS axSpA classification criteria, who achieved Low Disease Activity (ASDAS) and underwent MRI examination. A total of 144 patients from the First Affiliated Hospital of Xiamen University were used as the nomogram training set; 107 from the First Affiliated Hospital of Fujian Medical University were for external validation. Results The median time of relapse was 8.705 months (95% CI 8.215–9.195) and 7.781 months (95% CI 7.075–8.486) for MRI-positive patients and 9.8 months (95% CI 9.273–10.474) for MRI negative patients, respectively. Both active sacroiliitis on MRI (HR 1.792, 95% CI 1.230–2.611) and anti-TNF-α treatments (HR 0.507, 95% CI 0.349–0.736) were significantly associated with disease flares. Gender, disease duration, HLA-B27, MRI, and anti-TNF-α treatment were selected as predictors of the nomogram. The areas under the ROC curve (AUROCs) of the 1-year remission probability in the training and validation groups were 0.71 and 0.729, respectively. Nomogram prediction models present better AUROCs, C-indices, and decision curve analysis cure than the clinical experience model. Conclusions Active sacroiliitis in MRI requires weighting in order to estimate remission and disease flares, when axSpA patients achieve low disease activity. The simple nomogram might be able to discriminate and calibrate in clinical practice. Trial registration ClinicalTrials, NCT03425812, Registered 8 February 2018, https://clinicaltrials.gov Supplementary Information The online version contains supplementary material available at 10.1007/s40744-021-00279-y.

There are some challenges and unmet needs in the early diagnosis and management of Sjogren's syndrome (SjS) such as prominent glandular dysfunction at diagnosis and long diagnostic delay. Those challenges are partly attributed to the lack of a good knowledge of the early stages of SjS, which is a major obstacle to delivering appropriate care to SjS patients. Findings from both clinical and experimental studies suggest the plausibility of a redefined SjS course consisting of 4 stages, which includes initiation stage, preclinical stage, asymptomatic SjS stage and overt SjS stage. More studies focusing on the pathological processes and changes during the early stages of SjS are needed. To enable early diagnosis and treatment for SjS, more useful biomarkers of the early stages of SjS need to be identified, and individuals at high risk of SjS development need to be identified. Appropriate screening can be performed to facilitate the early diagnosis of SjS among those high-risk individuals.

Though macrophages and neutrophils are considered to be the principal immune cells involved in gout inflammation, recent studies highlight an emerging role of T cell subsets in the pathogenesis of gout. Some studies found that abnormal functions of several T cell subsets and aberrant expressions of their signature cytokines existed in gouty arthritis. Additionally, recent studies also suggested that therapeutic strategies by targeting pro-inflammatory T cell subsets or their related cytokines could ameliorate monosodium urate (MSU) crystals-induced arthritis in mice. The important role of T cells in gouty arthritis may provide some explanation for the absence of acute gout attacks among individuals with severe hyperuricemia or clinical evidence of MSU crystals deposition. Nevertheless, the molecular mechanisms underlying the role of those T cell subsets in gouty arthritis and their role in the initiation, progression and resolution of gouty arthritis are largely elusive, which need to be elaborated in future research. Uncovering the role of those T cell subsets in gout may transform our understanding of gout and facilitate new promising preventive or therapeutic strategies for gouty arthritis.

Background: Gout is the most common inflammatory arthritis induced by monosodium urate crystal (MSU) precipitation.The incidence of gout attack was significantly higher in men than women, indicating the important role of oestrogen system in pathogenesis of gout, but the specific mechanisms underlying remained to be explored. GPR30, the newly defined estrogen receptor, had been proved participated in regulating inflammation in some diseases. As different estrogen receptors paly different role in inflammation regulation, how GPR30 was involved in the inflammation induced by MSU in gout was still unknown. Methods: In this work, we investigated the function of GPR30 in inflammation induced by MSU in cultured macrophages and in mouse model by using G-1(the agonist of GPR30). We further tested the expression of the TLR and NOD like receptor protein3 (NLRP3), which are the key receptor involved in pathogenesis of gout. ROS and cleaved-caspase-1 expression were also detected to confirm the regulation role in NLRP3 pathway. Seahorse analysis was used to detect the metabolism profile in macrophages by G-1 to investigate the mechanism of GPR30 in inflammation. The relative expression of GPR30 were detected according to the inflammation state to confirm the role of GPR30 in gout. Results: Negative regulation role of G-1 in IL-1β expression and NLRP3 expression were found both in vitro and in vivo. Moreover, the negative regulation of ROS production and NLRP3 as well as cleaved-caspase-1 expression were also found in G-1 stimulated macrophages. Our data also showed that G-1 inhibited aerobic glycolysis in LPS activated macrophages, which might be responsible for IL-1β and NLRP3 expression. Higher expression levels of GPR30 were found in patients with remitted gout inflammation. Conclusion: Together, our data suggested that GPR30 was involved in the negative inflammation regulation induced by MSU and high expression of GPR30 might contribute to part of the mechanism of inflammation remission of gout.

BackgroundFibrosis in most organs has proven to be an critical factor related to high risk of morbidity and mortality, but an adequate assessment of fibrosis severity is still challenging. This study tried to evaluate fibrosis severity through a fibrosis transcriptional signature.MethodsA fibrosis transcriptional signature was developed through an integrated analysis of multiple expression profiling datasets of human organs with fibrosis-related diseases. A fibrosis severity score for each sample was the calculated through gene set variation analysis (GSVA), and its role in evaluating fibrosis severity was then analyzed.ResultsTen expression profiling datasets of human tissues with organ failure were integrated with robust rank aggregation method, and a fibrosis severity score consisting of 149 genes. Most of those included genes were involved in fibrogenic pathways. GSEA analysis revealed that fibrosis transcriptional signature was significantly enriched in the fibrogenic tissues. Additionally, we found that fibrosis transcriptional signature could effectively differentiate fibrosis tissues and non-fibrosis tissues.ConclusionThis study developed an useful fibrosis transcriptional signature involved in fibrosis-related diseases. This fibrosis transcriptional signature is helpful in precisely evaluating the fibrosis severity in common organs at the transcriptional level.

Rheumatic diseases are extremely heterogeneous diseases with substantial risks of morbidity and mortality, and there is a pressing need in developing more safe and cost-effective treatment strategies. Peptide-based vaccination is a highly desirable strategy in treating noninfection diseases, such as cancer and autoimmune diseases, and has gained increasing attentions. This review is aimed at providing a brief overview of the recent advances in peptide-based vaccination therapy for rheumatic diseases. Tremendous efforts have been made to develop effective peptide-based vaccinations against rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), while studies in other rheumatic diseases are still limited. Peptide-based active vaccination against pathogenic cytokines such as TNF-α and interferon-α (IFN-α) is shown to be promising in treating RA or SLE. Moreover, peptide-based tolerogenic vaccinations also have encouraging results in treating RA or SLE. However, most studies available now have been mainly based on animal models, while evidence from clinical studies is still lacking. The translation of these advances from experimental studies into clinical therapy remains impeded by some obstacles such as species difference in immunity, disease heterogeneity, and lack of safe delivery carriers or adjuvants. Nevertheless, advances in high-throughput technology, bioinformatics, and nanotechnology may help overcome these impediments and facilitate the successful development of peptide-based vaccination therapy for rheumatic diseases.

Primary Sjögren’s syndrome (pSS) is a rheumatic disease characterized by the destruction of salivary and lacrimal glands, and its pathogenesis mechanism remains unclear. Gαq is the α-subunit of the heterotrimeric Gq protein. Researches demonstrated that Gαq was involved in the pathogenesis regulation of several rheumatic diseases. This study explored the role of Gαq in pSS. Gαq mRNA levels in peripheral blood mononuclear cells (PBMCs) from 39 patients and 26 healthy controls (HCs) were investigated using real-time PCR. IL-17A serum concentrations in 22 pSS patients and 23 HCs were tested by ELISA, and the clinical significance of Gαq was analyzed. The association of Gαq with interleukin-17A (IL-17A) expression was also analyzed in patients with pSS. We showed that Gαq expression in PBMCs from patients with pSS was significantly lower than that in PBMCs from HCs. Gαq expression level was closely associated with pSS disease activity. Furthermore, a negative association was also found in IL-17A and Gαq expression level. These data suggest that Gαq is involved in pSS pathogenesis regulation, possibly due to its regulation of Th17. These results provide new insights into the pSS pathogenesis mechanism involving abnormal Th17 regulation.

ObjectivePrimary immune thrombocytopaenia (ITP) is highly heterogeneous. ANA-positive primary ITP may resemble the preclinical stage of connective tissue diseases (CTDs), but is still considered primary ITP due to a controversial CTD risk assessment in this group. The objective of this study was to clarify the risk of CTD in ANA-positive patients with primary ITP.MethodsWe performed a retrospective cohort study and a meta-analysis. 586 patients with newly diagnosed primary ITP were followed up and Cox regression analyses were used to analyse the associations of ANA positivity and other immune parameters with CTD development.ResultsThe mean follow-up time was 37 (19–56) months. ANA was positive in 21.33% (125 of 586) of patients with primary ITP in our retrospective cohort, and the overall rate of ANA positivity in the meta-analysis was 17.06% (369 of 2163). The adjusted HR for CTD in ANA-positive primary ITP was 6.15 (95% CI 2.66 to 14.23, pConclusionsThe findings suggest that ANA-positive primary ITP is a clinical entity distinct from other primary ITPs and is associated with increased risk of developing CTDs, especially SLE.

// Yuan Liu 1,* , Xining Liao 2,* , Ying Wang 3,* , Shiju Chen 1 , Yuechi Sun 1 , Qingyan Lin 1 and Guixiu Shi 1 1 Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, China 2 Medical College, Xiamen University, Xiamen, Fujian, China 3 Department of Endocrinology, The ChengGong Hospital Affiliated to Xiamen University, Xiamen, Fujian, China * Yuan Liu, Xining Liao and Ying Wang contribute equally to this study Correspondence to: Guixiu Shi, email: // Keywords : primary Sjogren’s syndrome; anti-MDM2 autoantibody; biomarker;Immunology and Microbiology Section; Immune response; Immunity Received : September 27, 2016 Accepted : January 17, 2017 Published : January 28, 2017 Abstract Introduction: Primary Sjogren’s Syndrome (pSS) is one of the autoimmune diseases characterized by polyclonal autoantibody production. The human homologue of the mouse double minute 2 (MDM2) is an important negative regulator of p53. Our previous study indicated that autoantibody to MDM2 can be detected in systemic lupus erythematosus patients. The purpose of this study is to study anti-MDM2 autoantibody in pSS patients. Methods: Anti-MDM2 autoantibody in sera from 100 pSS patients and 74 normal controls was investigated by ELISA. Positive samples were further confirmed by western blotting. Expression of MDM2 in labial gland tissue from pSS patients and normal controls was checked by immunohistochemistry. The difference in clinical characteristics and laboratory findings between anti-MDM2 positive and anti-MDM2 negative pSS patients was analyzed. Results: The presence of anti-MDM2 autoantibody in pSS patients was 21.0%, significantly higher than normal controls (5.40%). MDM2 was overexpressed in labial gland from pSS patients. pSS patients with positive anti-MDM2 were characterized by longer disease duration and more lymphocytes focal gathering in labial gland. Prevalence of anemia, thrombocytopenia and anti-SSB was significantly higher in pSS patients with anti-MDM2 autoantibody. Titer of anit-MDM2 was negatively associated with hemoglobin level, platelet count, complement 3 level and complement 4 level, positively associated with European Sjogren’s syndrome disease activity index (ESSDAI) and level of IgG. Conclusions: Anti-MDM2 autoantibody may be used as a potential serological biomarker in pSS disease activity evaluation. Study on the role of anti-MDM2 or MDM2 in pSS may help us know the pathogenesis mechanism of pSS better.

Background: Immunologic mechanisms have been one of the suggested causes of recurrent pregnancy loss (RPL). Antinuclear antibody positivity has been regarded as a typical feature of autoimmunity. Over past years many studies tried to clarify the association of ANA with RPL and the conclusions are controversial. The aim of this meta-analysis was to assess whether the presence of ANA directly increase the risk of RPL in women who did not have definite autoimmune diseases. Methods: We searched PubMed and Embase databases for relevant literatures, which included the data of ANA rate in RPL and control groups. Both fixed-effects and randomized-effects model were used to analyze the risk odds ratio with 95% confidence intervals (CIs) according to the heterogeneity across the selected studies. Findings: Twenty-one studies with 5038 participants including 2683 patients with RPL met the inclusion and exclusion criteria. The total positive rate of ANA was 22·4% (601/2683) in total RPL patients and 20·2% (397/1959) in unexplained RPL patients, respectively. Patients with total RPL or unexplained RPL had a significantly higher ANA positive rate than control groups [(OR =3·12, 95% CI:1·96, 4·97, I² = 77%), (OR = 3·47, 95% CI: 2·07, 5·81), I² = 74%], respectively]. Subgroup analysis demonstrated low titers of antibody (≤1: 80) were not associated with RPL patients [OR = 1·22, 95% CI (0·79, 1·90), I2 =86·1%], while higher ANA titer (≥1:160) showed a significant association between ANA and RPL patients [OR = 23·23, 95% CI (4·18,129·25, I 2 =0%)]. Higher rate of homogenous pattern in RPL group was observed [OR = 4·54, 95% CI (2·01, 10·24), I2=0%], and no significant difference in speckled pattern [OR = 1·08, 95% CI (0·69, 1·70), I 2 =0%] nor nucleolar pattern [OR = 3·52, 95% CI (0·93, 13·30), I 2 =0%] was found. Three studies detected the anti-dsDNA in two groups and the results demonstrated no significant difference between RPL group and controls [OR = 1·35, 95% CI (0·52, 3·54), I2=0%]. Interpretation: This is the first meta-analysis about the association between ANA positivity and RPL. The pooled data demonstrated increased prevalence of ANA in patients with RPL. ANA is suggested as a risk factor for RPL and should be recommended for this population. Funding Statement: The work was supported by Natural Science Foundation of China (NSFC) Grant U1605223 to Dr. Guixiu Shi, NSFC grant 81501407 to Dr. Yuan Liu; NSFC grant 81501369 to Dr. Shiju Chen; and the Leadership Program of the Technology Department of Fujian Province (Grant NO. 2015D011) to Dr. Guixiu Shi. Declaration of Interests: The authors declare no conflicts of interests. Ethics Approval Statement: The meta-analysis was performed in accordance with the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines.

Primary Sjogren's Syndrome (pSS) is a systemic inflammatory autoimmune of unknown aetiology affecting exocrine glands, particularly the lacrimal and salivary glands. Growing evidence that B-cell depletion therapies are remarkably efficacious in the disorder indicate a major role for B-cell in the immunopathogenesis of pSS. B cell-targeted therapies have raised new therapy promise for they interact with B-cell homeostasis. Anti-CD20 therapy is the unique effective non-symptomatic therapy used in pSS. Growing data suggest Rituximab a promising candidate for pSS therapy. We performed a search for publications on Rituximab in the treatment of pSS to explicate pathogenetic function of B cells and assesse the efficacy in glandular symptoms, systemic manifestations and laboratory parameters in pSS patients. However, the efficiency on glandular manifestations is rather disappointing and controversial. Whether pSS patients with a reasonable residual salivary flow and/or with shorter disease duration will benefit most from Rituximab treatment still remains unclear. Fatigue is the symptom that responds best to Rituximab therapy compared with other systematical involvements. The efficiency in laboratory parameters is unsatisfactory.

In order to investigate the lesions and proteins with differential expression in cells infected with the 2009 A (H1N1) virus and to determine the specific proteins involved in cell damage, the present study has been performed. BEAS-2B cells were infected with the 2009 A (H1N1) influenza virus or the seasonal H1N1 influenza virus for 12, 24, 48, and 72 h, and cell cycle and apoptosis were analyzed with flow cytometry. Total cellular proteins were extracted and underwent two-dimensional gel electrophoresis. The differentially expressed proteins underwent mass spectrometry for identification. The results showed that after 12 h, cells infected with the virus strain sourced from severe cases had the highest apoptosis rate (P < 0.05). After 48 h, cells infected with the virus strain sourced from fatal cases and severe cases had the highest apoptosis rate (P < 0.05), and after 72 h, cells infected with virus strains from fatal cases and ordinary cases had the highest apoptosis rate (P < 0.05). All the four influenza virus strains induced cell cycle arrest mainly at the G0/G1 phase. Eighteen differentially expressed proteins were identified, including galectin-1, cofilin-1, protein DJ-1, proteasome subunit α type-5, macrophage migration inhibitory factor, translationally controlled tumor protein, profilin 1, and interferon α-2. Galectin-1 was specifically observed in BEAS-2B infected with 2009 A (H1N1) influenza viruses, and cofilin-1 was specifically observed in BEAS-2B cells in the late stage of 2009 A (H1N1) influenza virus infection. In conclusion, differential effects of the 2009 A (H1N1) influenza virus and seasonal H1N1 influenza virus were identified on the cell cycle and apoptosis, and galectin-1 may play a role in cell apoptosis induced by 2009 A (H1N1) influenza virus.

MicroRNAs (miRNAs) have been identified to play important functions during osteoblast proliferation, differentiation, and apoptosis. The miR-17~92 cluster is highly conserved in all vertebrates. Loss-of-function of the miR-17-92 cluster results in smaller embryos and immediate postnatal death of all animals. Germline hemizygous deletions of MIR17HG are accounted for microcephaly, short stature, and digital abnormalities in a few cases of Feingold syndrome. These reports indicate that miR-17~92 may play important function in skeletal development and mature. To determine the functional roles of miR-17~92 in bone metabolism as well as osteoblast proliferation and differentiation. Murine embryonic stem cells D3 and osteoprogenitor cell line MC3T3-E1 were induced to differentiate into osteoblasts; the expression of miR-17-92 was assayed by quantitative real-time RT-PCR. The skeletal phenotypes were assayed in mice heterozygous for miR-17~92 (miR-17~92 +/Δ ). To determine the possibly direct function of miR-17~92 in bone cells, osteoblasts from miR-17~92 +/Δ mice were investigated by ex vivo cell culture. miR-17, miR-92a, and miR-20a within miR-17-92 cluster were expressed at high level in bone tissue and osteoblasts. The expression of miR-17-92 was down-regulated along with osteoblast differentiation, the lowest level was found in mature osteoblasts. Compared to wildtype controls, miR-17-92 +/Δ mice showed significantly lower trabecular and cortical bone mineral density, bone volume and trabecular number at 10 weeks old. mRNA expression of Runx2 and type I collagen was significantly lower in bone from miR-17-92 +/Δ mice. Osteoblasts from miR-17-92 +/Δ mice showed lower proliferation rate, ALP activity and less calcification. Our research suggests that the miR-17-92 cluster critically regulates bone metabolism, and this regulation is mostly through its function in osteoblasts.

Dermatomyositis (DM) is a subset of idiopathic inflammatory myopathies (IIM) which is characterized by chronic inflammation of skin and muscle weakness, and often involving other organs, such as skin, heart, gastrointestinal tract, pulmonary, and joints. Interstitial lung disease (ILD) is the most common internal organ manifestation that affects the prognosis of DM patients. The mortality is very high in DM-ILD patients especially in those with rapid ILD due to the lack of effective treatment. An early diagnosis of ILD in DM patients is critical important. In recent years, many studies focused on detecting serological biomarkers that can be used in prediction and evaluation of DM-ILD. Here we reviewed recent studies about serological biomarkers of DM-ILD. An overview of those biomarkers may help us have a better management of DM-ILD and may give us a better understanding about the pathogenesis of DM-ILD.