Myofascial release for the treatment of pain and dysfunction in patients with chronic mechanical neck pain: Systematic review and meta-analysis of randomised controlled trials.

OBJECTIVE: To explore the effects of myofascial release (MFR) on pain and dysfunction in individuals with chronic mechanical neck pain (MNP). DATA SOURCES: PubMed, Embase, Medline, Wiley Online Library, Web of Science, CNKI, VIP, WanFang Data, and the Cochrane Library were searched until 12 September 2022. REVIEW METHODS: This study was registered in PROSPERO (CRD42022302485). Methodological quality was assessed using Cochrane risk of bias assessment, and the quality of the evidence followed the GRADE recommendation. The outcomes pain, cervical mobility (Flexion, Extension, Rotation, lateral flexion), trapezius and suboccipital pressure pain thresholds (PPT), neck disability index (NDI), and adverse effects were extracted. RESULTS: After screening of 346 studies, 13 studies and 601 participants met the inclusion criteria. All studies were of moderate methodological quality. Compared with the control group, the participants in the MFR group showed significantly greater improvements trapezius PPT SMD 0.41 (95% CI 0.11-0.72), suboccipital PPT SMD 0.47 (95% CI 0.21-0.72), respectively. The differences were not significant to support the MFR treatment on pain, flexion, extension, rotation, lateral flexion angle, and NDI. None of the studies reported any adverse events. CONCLUSION: This systematic review suggests that MFR is an effective treatment for the improvement of PPT of trapezius and suboccipital muscle in patients with chronic MNP. However, there is low to moderate evidence and may change over time.

Expression of CFTR, a hallmark gene of ionocytes, is downregulated in salivary glands of Sjögren's syndrome patients.

INTRODUCTION: The autoimmune exocrinopathy, Sjögren's syndrome (SjS), is associated with secretory defects in salivary glands. The cystic fibrosis transmembrane conductance regulator (CFTR) of the chloride channel is a master regulator of fluid secretion, but its role in SjS has not been investigated. Our research found a link between CFTR and SjS at the genetic and protein levels, as well as through clinical data. METHODS: We used single-cell RNA sequencing to identify the presence of CFTR in glandular epithelial cells of the human salivary gland (scRNA-seq) and confirmed the difference using immunofluorescence tests in labial glands and clinical data statistics from 44 non-SjS and 36 SjS patients. RESULTS: The changes of CFTR expression in salivary glands of SjS patients was assessed at both mRNA and protein levels. According to the scRNA-seq analyses, CFTR was the hallmark gene of ionocytes. We firstly identified that SjS had a lower level of CFTR expression in the labial glands than non-SjS at mRNA level. Using immunofluorescence assays, we also found that CFTR expression was decreased in SjS patients compared to non-SjS. The results of the clinical statistics revealed that CFTR expression was adversely correlated with feelings of dry mouth, lymphocyte infiltration in the labial glands, and certain autoantibodies in serum (antinuclear antibody, anti-Ro/SSA, and anti-La/SSB antibodies). CONCLUSION: Those findings above proved an obviously downregulated expression of CFTR in salivary glands of SjS patients and its clinical significance. Dysfunction in CFTR or ionocytes may contribute to SjS pathogenesis and represents a promising therapeutic target.

Abnormal Histones Acetylation in Patients with Primary Sjögren's Syndrome.

INTRODUCTION: Aberrant histone acetylation is increasingly thought to play important roles in the pathogenesis of autoimmune diseases. However, there are very few data on histone acetylation in primary Sjögren's syndrome (pSS). We aimed to investigate whether there was abnormal histones acetylation in patients with pSS. METHODS: We investigated the expressions of histone acetyltransferase (HAT) genes (p300, CREBBP and PCAF) by real-time PCR in the peripheral blood mononuclear cells (PBMCs) of pSS patients. HAT activity and histone H3/H4 acetylation activity were measured by activity kit, and histone H3/H4 acetylation was verified by Western blot (WB). Spearman test was utilized to analyze the association between HAT activity levels and clinical parameters of pSS patients. RESULTS: The mRNA expressions of p300, CREBBP and PCAF in PBMCs from pSS patients were decreased in comparison with healthy controls (P < 0.05). HAT activity and histone H3/H4 acetylation were reduced in PBMCs from pSS patients (P < 0.05). We found that HAT activity was negatively correlated with CRP (P = 0.040) and TNF-α (P = 0.012), and was positively correlated with C4 (P = 0.041). CONCLUSIONS: Histone hypoacetylation is observed in patients with pSS and is involved in the pathogenesis of pSS. KEY POINTS: • The mRNA expressions of p300, CREBBP and PCAF in PBMCs from pSS patients were decreased in comparison with HCs. • HAT activity and histone H3/H4 acetylation were reduced in PBMCs from pSS patients. • HAT activity was correlated with disease characters. • We show for the first time that the histone hypoacetylation may be involved in the pathogenesis of pSS.

The effect of concomitant chronic kidney disease on the recurrence of atrial fibrillation after catheter ablation: A protocol for systematic review and meta-analysis.

BACKGROUND: Some new trials have reported the effectiveness of chronic kidney disease on recurrence of atrial fibrillation following catheter ablation. Limited by small number of studies and insufficient outcomes, previous meta-analyses also failed to draw a consistent conclusion on this topic. We thus conducted a new meta-analysis to systematically analyze the effect of chronic kidney disease on recurrence of atrial fibrillation following catheter ablation. METHODS: Two independent investigators followed The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) reporting guidelines to conduct the present meta-analysis. From the inception to June 2021, the EMBASE, PubMed, Web of Science, and Cochrane Library electronic databases were searched using the key phrases "atrial fibrillation," "chronic kidney disease," "catheter ablation," "renal failure," "renal function," "renal insufficiency," "end-stage renal disease," and "dialysis" for all relevant English-language trials. Observational or randomized controlled trial focusing on assessing the effectiveness of chronic kidney disease on recurrence of atrial fibrillation following catheter ablation was included. P < .05 was set as the significance level. RESULTS: Our hypothesis was that chronic kidney disease is associated with increased atrial fibrosis and a higher risk of arrhythmia recurrence and that restoration of normal rhythm through catheter ablation is associated with improved kidney function. REGISTRATION NUMBER: 10.17605/OSF.IO/3WJAE.

Reduced Activity of HDAC3 and Increased Acetylation of Histones H3 in Peripheral Blood Mononuclear Cells of Patients with Rheumatoid Arthritis.

Aberrant histone acetylation and deacetylation are increasingly thought to play important roles in the pathogenesis of rheumatoid arthritis (RA). However, limited data from studies about the activity of histone deacetylases (HDACs) and histone acetyltransferase (HAT) in RA are controversial. Those conflicting results may be caused by sample size, medication, and age- and sex-matched controls. The aim of this study is to investigate the expression and activity of class I HDACs (1-3.8) and their effects on histone acetylation in peripheral blood mononuclear cells (PBMCs) from RA patients. The expression of class I HDACs in PBMCs from RA patients was decreased in both mRNA and protein levels in comparison with HCs. The nuclear HAT activities were dramatically increased. Further, we found HDAC3 activity to be the most significantly reduced in overall reduction of HDACs in the RA group. The extent of total histone H3, but not H4, acetylation in PBMCs from RA patients was increased compared to that in healthy controls (HCs) (p < 0.01). In RA PBMCs, the activity and expression of class I HDACs are decreased, which is accompanied with enhanced HAT activity. An altered balance between HDAC and HAT activity was found in RA PBMCs.