Self-reported sleep disturbance is significantly associated with depression, anxiety, self-efficacy, and stigma in Chinese patients with rheumatoid arthritis.

The objective of this article is to assess self-reported sleep disturbance and identify psychological, clinical, and sociodemographic factors that might influence sleep disturbance in patients with rheumatoid arthritis (RA). The study included 141 patients with confirmed RA (84.4% women, mean age 56.87 years). The Pittsburgh Sleep Quality Index, the Chinese version of rheumatoid arthritis self-efficacy scale, the Chinese version of Anxiety Depression Distress Inventory-27, the Chinese version of Stigma Scale for Chronic Illness, Visual Analogue Scale-Pain, disease activity index were used. Sleep disturbance was positively correlated with age, pain, disease activity, depression and anxiety, and stigma, while self-efficacy was correlated negatively with sleep disturbance. Multiple linear regression analysis revealed that depression, anxiety, self-efficacy, and stigma explained 77.4% of sleep quality variance. The data has demonstrated a suggestive relationship between low sleep quality and anxiety, depression, self-efficacy, and stigma. Patients reporting poor sleep, fatigue, and pain might have particular psychological intervention needs focusing on distress or anxiety symptoms, low self-efficacy, and high stigma.

Harnessing Pseudo-Jahn-Teller Disordering of Monoclinic Birnessite for Excited Interfacial Polarization and Local Magnetic Domains.

The symmetry in a polymorph is one of the most important elements for determining the inherent lattice nature. The MnO2 host tends to high-symmetry MnO6 octahedra as a result of the electronic structure t2g 3 eg 0 of Mn4+ ions, displaying an ordered structure accompanying with poor polarization loss and limiting its application toward high-performance microwave absorbers. Here, a pseudo-Jahn-Teller (PJT) distortion and PJT disordering design with abundant self-forming interfaces and local magnetic domains in the monoclinic birnessite-MnO2 host is first reported. The PJT distortion can give rise to asymmetric MnO6 octahedra, inducing the formation of interfaces and increased electron spin magnetic moment in the lattice. The resultant birnessite with PJT distortions and PJT disordering delivers an outstanding reflection loss value of -42.5 dB at an ultralow thickness of 1.7 mm, mainly derived from the excited interfacial polarization and magnetic loss. This work demonstrates an effective approach in regulating the lattice structure of birnessite for boosting microwave absorption performance.

Latent characteristics and influencing factors of stigma in rheumatoid arthritis: A latent class analysis.

To explore the latent classes of stigma in patients with rheumatoid arthritis, we analyzed the characteristics of the different categories. Adopting a convenient sampling method, socio-demographic and disease-related information from the outpatient clinics and wards of 3 tertiary care hospitals in China was collected. The Chinese version of the Internalized Stigma of Mental Illness scale-Rheumatoid Arthritis was used in this survey. Rheumatoid arthritis stigma was divided into 3 potential categories: Low Stigma-Strong Resistance (83, 41.5%), Medium Stigma-Strong Alienation (78, 39.0%), and High Stigma-Weak Resistance (39, 19.5%). Unordered multinomial logistic regression analysis showed that pain (OR = 1.540, P = .005; OR = 1.797, P < .001), elementary school education and below (OR = 4.051, P = .037), and duration of morning stiffness (OR = 0.267, P = .032) were risk factors for stigma, whereas family history was a protective factor against stigma (OR = 0.321, P = .046). Patients with longer morning stiffness, more severe pain, and less education have a greater risk of heavier stigma. Strong alienation is an early warning of heavy stigma. Resistance to stigma and family support can help patients overcome their psychological obstacles. More attention should be paid to constructing family centered support systems to help resist stigma.

microRNA-23 inhibits inflammation to alleviate rheumatoid arthritis via regulating CXCL12.

Rheumatoid arthritis (RA) is a common systemic, inflammatory and autoimmune disorder. MicroRNAs (miRs) are strongly associated with the initiation and progression of RA. However, the functions and mechanisms underlying miR-23 in RA are not completely understood. Therefore, the present study aimed to investigate the molecular mechanisms underlying miR-23 in RA. A bioinformatics tool (StarBase) and a wide range of experimental assays, including reverse transcription-quantitative PCR, western blotting, luciferase reporter assays and ELISAs, were performed to investigate the biological role of miR-23 in RA. The results indicated that miR-23 was downregulated and chemokine C-X-C motif ligand 12 (CXCL12) was upregulated in RA samples compared with healthy samples. Furthermore, miR-23 overexpression suppressed inflammation via reducing TNF-α, IL-1ß and IL-8 expression levels compared with the NC mimic group. Regarding the underlying mechanism, compared with NC mimic, miR-23 mimic decreased CXCL12 mRNA expression by binding to its 3'-untranslated region. Additionally, CXCL12 overexpression reversed miR-23 mimic-mediated effects on inflammation. NF-κB signaling is associated with inflammation. Therefore, the present study indicated that CXCL12 promoted inflammation by activating NF-κB signaling. In conclusion, miR-23 inhibited inflammation to alleviate RA by regulating CXCL12 via the NF-κB signaling pathway, which may serve as a potential target for the diagnosis and treatment of RA.

PLD1 knockdown reduces metastasis and inflammation of fibroblast-like synoviocytes in rheumatoid arthritis by modulating NF-κB and Wnt/ß-catenin pathways.

Considered as an autoimmune disease, rheumatoid arthritis (RA) is an chronic inflammatory disorder that causes inflammation of the joints. This study is performed with the aim to clarify the expression of phospholipase D1 (PLD1) in RA and its specific regulation role of RA as well as the underlying mechanisms. In this study, synovial tissue samples were collected from RA patients, and RA-fibroblast-like synoviocytes (FLSs) were subsequently isolated. The expression levels of PLD1 and pathway-related proteins were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blotting or immunohistochemistry (IHC). Upon shPLD1 treatment, cell viability, proliferation, migration, invasion, and the level of inflammation-related factors were measured by Cell Counting Kit-8 (CCK-8), Edu, wound healing, Transwell and enzyme-linked immunosorbent assay (ELISA). Furthermore, C-reactive protein (CRP), rheumatoid factor (RF), arthritis score and synovial tissue lesions were assessed by collecting the blood or tissues from collagen induced arthritis (CIA) model rats. Our results showed that PLD1 level was increased in RA synovial tissues. Cell viability, proliferation, migration, invasion, and the level of inflammatory factors were reduced upon PLD1 knockdown in RA-FLSs. Moreover, p-IκBα/IκBα, ß-catenin, p-IKKß/IKKß and TCF-4 were inhibited under PLD1 knockdown treatment. PLD1 knockdown alleviated the collagen-induced addition of arthritis score, CRP and RF, as well as the filling of inflammatory cells and proliferation of synovium in CIA model rat. To sum up, knockdown of PLD1 could reduce RA-FLSs metastasis as well as inflammatory response by modulating the activity of NF-κB and Wnt/ß-catenin pathways.

12/15-Lipoxygenase inhibitor baicalein suppresses PPAR gamma expression and nuclear translocation induced by cerebral ischemia/reperfusion.

Accumulating evidences have demonstrated the beneficial actions of peroxisome proliferator-activated receptor gamma (PPAR gamma) in a variety of animal stroke models. Following middle cerebral artery occlusion (60 min) and 2-24 hr reperfusion in rats, we observed cerebral ischemia/reperfusion (I/R) induced up-regulation of PPAR gamma protein expression and translocation from the cytoplasm into the nucleus in a time-dependent manner. We also found that PPAR gamma agonist rosiglitazone enhanced whereas PPAR gamma antagonist GW9662 inhibited the alteration of PPAR gamma stimulated by I/R, suggesting that the changes of PPAR gamma may result from the activation by endogenous ligands. Moreover, the link between the 12/15-lipoxygenase and the production of activating ligands for PPAR gamma has been proved in various tissues. However, the relation of them in brain tissue has not been identified. We demonstrated that the I/R-induced PPAR gamma alteration was reversed by baicalein, the specific inhibitor of 12/15-lipoxygenase. Baicalein treatment significantly inhibited the up-regulation of PPAR gamma expression and, furthermore, suppressed PPAR gamma nuclear accumulation as well as maintained PPAR gamma cytoplasmic retention. Together, these results suggest that I/R induces both PPAR gamma expression and translocation, probably through the activation by endogenous ligands in a 12/15-lipoxygenase inhibitor-sensitive way.