Effectiveness of a Game-Based Mobile Application in Educating Nursing Students on Venous Blood Specimen Collection: A Randomized Controlled Trial.

Aim: Incorporating mobile applications into traditional clinical teaching methods to assess the impact of game-based mobile applications on the practical knowledge and skill levels of venous blood specimen collection among nursing students. Background: Although game-based mobile applications are recognized as teaching aids that replicate clinical practice in a safe environment, their impact and effectiveness are relatively unknown in the education of nursing students. Design: In September 2021, a single-blind randomized controlled trial was conducted in a university-affiliated hospital in China. Methods: One hundred five nursing students were randomly divided into the control group (n = 53) and the experimental group (n = 52). All participants received the same theoretical and operational training. For the next 7 days, the experimental group used a game-based mobile application, and the control group practiced venous blood specimen collection using traditional teaching methods. We observed the before-and-after comparison of the skill performance and learning curve of both groups of participants. Results: The final skill performance scores of the nursing students in the experimental group were higher than that of the nursing students in the control group (P < 0.001). Analysis of the learning curve showed that to master the skills, the experimental and control groups needed an average of 8 and 10 repetitions, respectively. Conclusion: This mobile application has a positive learning effect on nursing students' venous blood specimen collection skills in the short term. It should be applied to the training of clinical nursing skills.

IgG4-related disease with massive pericardial effusion diagnosed clinically using FDG-PETCT: a case report.

Background: IgG4-related disease (IgG4-RD) is a systemic inflammatory disease which involves various organs such as the pancreas, lacrimal gland, salivary gland, retroperitoneum, and so on. These organs can be affected concomitantly. 18-Fluorodeoxyglucose positron emission tomography computed tomography (FDG-PETCT) is a systemic examination which can identify active inflammation and detect multiple organ involvement simultaneously. Pericardial involvement is rare in IgG4-RD, early detection and treatment can greatly improve the prognosis of patients. Case summary: We reported a 82-year-old female patient referred to our department complaining of chest tightness and abdominal fullness for 8 months and massive pericardial effusion for 2 months. A large amount of pericardial effusion was found during the hospitalization of Gastroenterology. Then she was transferred to cardiology. Although infectious, tuberculous, and neoplastic pericardial effusions were excluded, there was still no diagnosis. The patients were examined by FDG-PETCT which considered IgG4-RD. After coming to our department, the results of the patient's laboratory tests showed that immunoglobulin subgroup IgG4 was 14.0 g/L. Then we performed a biopsy of the right submandibular gland. Pathological morphology and immunohistochemistry suggested IgG4-RD. Combined with level of IgG4, clinical, pathological and immunohistochemical results, we determined the final diagnosis of IgG4 related diseases. Then we gave glucocorticoid and immunosuppressant treatment. At the end, pericardial effusion was completely absorbed. As prednisone acetate was gradually reduced, no recurrence of the disease has been observed. Conclusion: Pericardial effusion can be the initial presentation in IgG4-RD. For patients with massive pericardial effusion of unknown cause, early detection of IgG4 is recommended, and PETCT may be helpful for obtaining the diagnosis.

Downregulation of miR-98-5p expression induces interleukin-6 expression in rheumatoid fibroblast-like synoviocytes.

AIM: The increased level of interleukin-6 (IL-6) plays a significant role in the pathogenesis of rheumatoid arthritis (RA). Specific blockade of IL-6 or its receptor has been used successfully in treating RA. MicroRNAs can regulate gene expression and act as regulators of target genes. Manipulation of specific microRNAs provides a novel therapeutic strategy for treating/preventing diseases. This study explored the role of miR-98-5p in the regulation of IL-6 expression in rheumatoid fibroblast-like synoviocytes (RA-FLSs). METHODS: Real-time PCR was used to detect miR-98-5p expression in RA-FLSs and normal human fibroblast-like synovial cells (HFLSs). Site-directed gene mutagenesis and reporter gene assay were performed to identify the interaction between miR-98-5p and IL-6. Manipulation of miR-98-5p expression in RA-FLS used transfection with miR-98-5p mimic or inhibitor. Stimulation of FLSs with IL-1ß induced IL-6 production. Enzyme-linked immunosorbent assay was used to detect the level of IL-6 secreted into the RA-FLS culture supernatant. RESULTS: Compared with HFLSs, the expression of miR-98-5p in RA-FLSs was significantly downregulated, and was negatively correlated with DAS28 scores and rheumatoid factor. In patients with anti-keratin antibody-positive RA, the expression level of miR-98-5p was lower. miR-98-5p negatively regulated the expression of IL-6 in RA-FLSs. After IL-1ß stimulation, the expression of miR-98-5p decreased and the level of IL-6 protein was upregulated during IL-6 secretion. CONCLUSION: These data suggest that manipulation of miR-98-5p, which negatively modulates IL-6 expression, may be a potential clinical approach in RA.

Febuxostat mitigates IL-18-induced inflammatory response and reduction of extracellular matrix gene.

BACKGROUND: Osteoarthritis (OA) is a disease commonly diagnosed in the elderly population. It is reported that the reduction of extracellular matrix and infiltrated inflammation are two main factors responsible for the pathogenesis of OA. This investigation aims to explore the potential protective effects of Febuxostat against IL-18-induced insults in chondrocytes, as well as the possible mechanism. MATERIALS AND METHODS: The viability of chondrocytes was evaluated using the MTT assay. QRT-PCR and ELISA were used to measure the expressions and concentrations of IL-6, TNF-α, and CCL5, respectively. The accumulation of glycosaminoglycans (GAGs) was measured using Alcian blue assay. The chondrocytes were transfected with siRNA against Sox-9 in order to establish the Sox-9 knock-down chondrocytes. The expressions of iNOS, Col2a1, Acan, and Sox-9 were measured using qRT-PCR. The production of NO was measured using Diaminofluorescein-FM diacetate (DAF-FM DA) staining. RESULTS: The up-regulated expressions of IL-6, TNF-α, CCL5, iNOS, and NO stimulated by IL-18 were down-regulated by the introduction of Febuxostat. The expressions of Col2a1, Acan, and Sox-9 were significantly reduced by IL-18 but greatly promoted by Febuxostat. The increased gene expressions of Col2a1 and Acan induced by Febuxostat were abolished by knocking down Sox-9 in the chondrocytes. CONCLUSION: Febuxostat might mitigate IL-18-induced inflammatory response and reduction of the extracellular matrix gene mediated by Sox-9.

MicroRNA-101-3p inhibits fibroblast-like synoviocyte proliferation and inflammation in rheumatoid arthritis by targeting PTGS2.

OBJECTIVE: Rheumatoid arthritis (RA) is the most frequently occurring inflammatory arthritis. The present study was performed to characterize the role of microRNA-101-3p (miR-101-3p) and prostaglandin-endoperoxide synthase 2 (PTGS2) in inflammation and biological activities of fibroblast-like synoviocytes (FLSs) in RA. METHODS: Initially, miR-101-3p and PTGS2 expression in RA tissues of RA patients and RA rats was detected by qRT-PCR and Western blot analysis. Rat model of type II collagen-induced arthritis (CIA) was adopted to simulate RA, followed by injection of miR-101-3p mimics or siRNA against PTGS2. Next, the apoptosis in synovial tissue and the levels of tumor necrosis factor (TNF)-α, IL-1ß and IL-6 were identified. Subsequently, FLSs in RA (RA-FLSs) were isolated, after which in vitro experiments were conducted to analyze cell proliferation, apoptosis, migration and invasion upon treatment of up-regulated miR-101-3p and silenced PTGS2. Furthermore, the relationship of miR-101-3p and PTGS2 was determined by bioinformatics prediction and luciferase activity assay. RESULTS: We identified poorly expressed miR-101-3p and highly expressed PTGS2 in synovial tissues of RA patients and RA rats, which showed reduced synoviocyte apoptosis and enhanced inflammation. In response to miR-101-3p mimics and si-PTGS2, the RA-FLSs were observed with attenuated cell proliferation, migration and invasion, corresponding to promoted apoptosis. Down-regulation of PTGS2 could rescue the effect of inhibited miR-101-3p in synovial injury and phenotypic changes of FLS in RA rats. Notably, miR-101-3p was found to negatively regulate PTGS2. CONCLUSION: Taken together, miR-101-3p reduces the joint swelling and arthritis index in RA rats by down-regulating PTGS2, as evidenced by inhibited FLS proliferation and inflammation.

Physcion 8­O­ß­glucopyranoside extracted from Polygonum cuspidatum exhibits anti­proliferative and anti­inflammatory effects on MH7A rheumatoid arthritis­derived fibroblast­like synoviocytes through the TGF­ß/MAPK pathway.

The present study aimed to investigate the anti­arthritic effect of physcion 8­O­ß­glucopyranoside (POGD) and its possible mechanisms. The anti­proliferative effects of POGD on MH7A cells were detected using a CCK­8 assay, and the release of pro­inflammatory cytokines, interleukin (IL)­1ß, IL­6, IL­8, IL­12 and IL­17A, were determined by ELISA. A type II collagen­induced arthritis (CIA) rat model was established to evaluate the anti­arthritic effect of POGD in vivo. The paw volumes, arthritis indices and serum levels of tumor necrosis factor (TNF)­α, IL­1ß, IL­6, IL­8, IL­17A were determined by ELISA. The mRNA expression levels of matrix metalloproteinase (MMP)­2, MMP­3, MMP­9, vascular endothelial growth factor and cyclooxygenase­2 were determined by reverse transcription­quantitative polymerase chain reaction analysis, and the expression levels of transforming growth factor (TGF)­ß1, small mothers against decapentaplegic (Smad)4, Smad7, c­Jun N­terminal kinase (JNK), phosphorylated (p­)JNK, p­P38, P38, p­extracellular signal­regulated kinase (ERK)1/2, ERK1/2, nuclear factor (NF)­κB p65 in the nucleus (N), cytosolic NF­κB p65 (C), and inhibitor of NF­κB (IκB) were determined by western blot analysis. The results indicated that POGD significantly inhibited MH7A cell growth. POGD markedly inhibited paw swelling and the arthritis indices of the CIA rats, and POGD may also inhibit the release of pro­inflammatory cytokines. Furthermore, POGD downregulated the expression levels of TGF­ß1, Smad4, NF­κB p65 (N), p38, p­p38, p­ERK1/2, JNK, p­JNK, TGF­ß1, Smad4, p­JNK, JNK, p­P38, P38, p­ERK1/2, ERK1/2 and NF­κB p65 (N), and upregulated the Smad7, NF­κB p65 (C) and IκB in TNF­α induced MH7A cells. In conclusion, the results suggested that POGD is a promising potential anti­inflammatory drug, and that POGD may decrease the expression of pro­inflammatory cytokines and mediators via inhibiting the TGF­ß/NF­κB/mitogen­activated protein kinase pathways.

LncRNA HOTAIR alleviates rheumatoid arthritis by targeting miR-138 and inactivating NF-κB pathway.

Rheumatoid arthritis (RA) is a chronic and autoimmune-mediated inflammatory disease. We aimed to investigate the regulation of lncRNA HOTAIR in LPS-treated chondrocytes and RA mouse. Our results showed that HOTAIR expression was significantly reduced in LPS-treated chondrocytes. The HOTAIR was then over-expressed in chondrocytes by transfecting recombinant lentivirus carrying sequences encoding HOTAIR. The LPS-induced reduction of cell proliferation rate and production of two inflammatory factors interleukin (IL)-17, IL-23 were markedly inhibited. Enforced expression of HOTAIR also led to the upregulation of proliferation-related protein Ki67 and proliferating cell nuclear antigen (PCNA). Moreover, a negative correlation was detected between the expression of HOTAIR and microRNA (miR)-138, and the expression of miR-138 was significantly increased in LPS-induced chondrocytes. The effects of HOTAIR over-expression on the proliferation and inflammation were partly reversed by miR-138 overexpression. Furthermore, the overexpression of HOTAIR significantly inhibited the activation of nuclear transcription factor-κB (NF-κB) in LPS-treated chondrocytes by suppressing p65 to cell nucleus, resulting in the down-regulation of IL-1ß and tumor necrosis factor (TNF)-α. In addition, the in vivo experiments exhibited that overexpression of HOTAIR increased cell proliferation and inhibited inflammation in RA rats, which were demonstrated by upregulation of Ki67 and PCNA, reduced CD4+IL-17+,CD4+IL-23+ cells, and down-regulation of p-p65, IL-1ß and TNF-α. In summary, our study suggests HOTAIR plays a protective role in RA by increasing proliferation rate and inhibiting inflammation, which may be related with the regulation of miR-138 expression and NF-κB signaling pathway. These results suggest that the regulation of HOTAIR may be a promising therapeutic strategy for RA.