Impact of pelvic floor ultrasound in diagnosis of postpartum pelvic floor dysfunction: A protocol of systematic review.

BACKGROUND: This study will appraise the impact of pelvic floor ultrasound (PFU) in diagnosis of postpartum pelvic floor dysfunction (PPPFD). METHODS: Studies that report the impact of PFU in diagnosis of PPPFD will be examined in Cochrane Library, MEDLINE, EMBASE, PSYCINFO, Scopus, Web of Science, Allied and Complementary Medicine Database, CNKI, and WANGFANG up to June 1, 2020. Grey literature sources will also be searched. All potential case-controlled studies (CCSs) exploring the impact of PFU in diagnosis of PPPFD will be considered for inclusion in this study. Data will be extracted from eligible CCSs for data pooling and meta-analysis. Whenever necessary, we will also perform summary effect size, heterogeneity across studies, study quality assessment, and reporting bias. RESULTS: The present study will estimate pooled outcome effects regarding the impact of PFU in diagnosis of PPPFD. CONCLUSION: This study may provide robust evidence to judge the impact of PFU on PPPFD SYSTEMATIC REVIEW REGISTRATION:: PROSPERO CRD42020187623.

Impact of ultrasound diagnosis for chronic pelvic pain.

BACKGROUND: This study aims to assess the impact of ultrasound diagnosis in patients with chronic pelvic pain (CPP). METHODS: We will carry out a comprehensive electronic search from the databases below: PUBMED, EMBASE, Cochrane Library, PSYCINFO, Web of Science, Cumulative Index to Nursing and Allied Health Literature, Allied and Complementary Medicine Database, Chinese Biomedical Literature Database, China National Knowledge Infrastructure, and WANGFANG databases from inception to July 1, 2019. The case-controlled studies focusing on impact of ultrasound diagnosis for patients CPP will be included in this study. Two authors will independently conduct all study selection, data collection, and risk of bias assessment. The risk of bias assessment will be assessed using Quality Assessment of Diagnostic Accuracy Studies tool. We will apply RevMan V.5.3 software and Stata V.12.0 software for data pooling and statistical analysis. RESULTS: This study will present pooled effect estimates regarding the impact of ultrasound diagnosis for CPP by assessing sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio of ultrasound to determine the diagnostic accuracy of ultrasound diagnosis for CPP. CONCLUSION: This study will provide modest evidence for the diagnostic accuracy of ultrasound in patients with CPP. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42019142799.

Rhein inhibits ATP-triggered inflammatory responses in rheumatoid rat fibroblast-like synoviocytes.

Rheumatoid arthritis (RA) is a chronic and systemic inflammatory disorder, which may lead to joint disabilities. So far the pathogenesis of RA remains largely undetermined, and there are still no potent drugs for clinical treatment. Rhein, a natural bioactive anthraquinone derivative, exhibited significant anti-inflammatory activities demonstrated by previous studies. Here we aimed to investigate the effects of rhein on ATP-induced inflammation responses in fibroblast-like synoviocytes isolated from a rat model of collagen induced arthritis (CIA). Our results showed that ATP triggered rapid cytosolic calcium concentration ([Ca2+]c) increase depending on extracellular Ca2+ entry. Given the major P2 subtypes expressed in rat synoviocytes were P2X4 and P2Y2 receptors, ATP-elicited calcium entry should be mainly resulted from activating P2X4. Interestingly, rhein could effectively block the ATP-induced [Ca2+]c increases in a dose-dependent manner. Besides, rhein also suppressed the production of intracellular reactive oxygen species (ROS) induced by ATP in synoviocytes that was resulted from P2X4-mediated Ca2+ entry. Brilliant blue G (BBG), which can block P2X4 receptor at high concentration, showed similar suppressive effects on above responses. Furthermore, in lipopolysaccharide-primed cells, application of ATP synergistically promoted the gene expression of cyclooxygenase-2, interleukin-6 and matrix metalloproteinase-9. Both rhein and BBG attenuated these inflammatory gene expressions enhanced by ATP. Above data together suggested a potential anti-arthritic role of rhein by inhibiting ATP-induced [Ca2+]c increase, ROS production and inflammatory gene expression targeting P2X4 in CIA rat synoviocytes, which will provide a novel insight in the therapy of RA.

Hypotonic stress promotes ATP release, reactive oxygen species production and cell proliferation via TRPV4 activation in rheumatoid arthritis rat synovial fibroblasts.

Rheumatoid arthritis (RA) is a chronic and systemic autoimmune-disease with complex and unclear etiology. Hypotonicity of synovial fluid is a typical characteristic of RA, which may play pivotal roles in RA pathogenesis. In this work, we studied the responses of RA synovial fibroblasts to hypotonic stress in vitro and further explored the underlying mechanisms. Data showed that hyposmotic solutions significantly triggered increases in cytosolic calcium concentration ([Ca2+]c) of synoviocytes. Subsequently, it caused rapid release of ATP, as well as remarkable production of intracellular reactive oxygen species (ROS). Meanwhile, hypotonic stimulus promoted the proliferation of synovial fibroblasts. These effects were almost abolished by calcium-free buffer and significantly inhibited by gadolinium (III) chloride (a mechanosensitive Ca2+ channel blocker) and ruthenium red (a transient receptor potential vanilloid 4 (TRPV4) blocker). 4α-phorbol 12,13-didecanoate, a specific agonist of TRPV4, also mimicked hypotonic shock-induced responses shown above. In contrast, voltage-gated channel inhibitors verapamil and nifedipine had little influences on these responses. Furthermore, RT-PCR and western blotting evidently detected TRPV4 expression at mRNA and protein level in isolated synoviocytes. Taken together, our results indicated that hypotonic stimulus resulted in ATP release, ROS production, and cell proliferation depending on Ca2+ entry through activation of TRPV4 channel in synoviocytes.