Anomalous acoustic streaming is observed emanating from sharp edges of solid bodies that are vibrating in fluids. The streaming velocities can be orders of magnitude higher than expected from the Rayleigh streaming at similar amplitudes of vibration. Acoustic velocity of fluid relative to a solid body diverges at a sharp edge, giving rise to a localized time-independent body force acting on the fluid. This force results in a formation of a localized jet. Two-dimensional numerical simulations are performed to predict acoustic streaming for low amplitude vibration using two methods: (1) Steady-state solution utilizing perturbation theory and (2) direct transient solution of the Navier-Stokes equations. Both analyses agree with each other and correctly predict the streaming of a sharp-edged vibrating blade measured experimentally. The origin of the streaming can be attributed to the centrifugal force of the acoustic fluid flow around a sharp edge. The dependence of this acoustic streaming on frequency and velocity is examined using dimensional analysis. The dependence law is devised and confirmed by numerical simulations.
Background: Dementia is more prevalent among people with type 2 diabetes, but little is known regarding the influence of antidiabetic agents on this association. Objective: This study assessed the impact of various antidiabetic agents on the risk of dementia among patients with Type 2 diabetes mellitus. Methods: Relevant studies were retrieved from the PubMed, Embase, Cochrane Central Register of Controlled Trials (CENTRAL), and ClinicalTrials.gov databases. Nine antidiabetic agents were included in the search. Data were pooled via network meta-analysis and meta-analysis. Results: Nine studies were selected for the network meta-analysis with 530,355 individuals and 17 studies for the meta-analysis with 1,258,879 individuals. The analysis excluded glucagon-like peptide 1 (GLP-1) analogs and sodium-dependent glucose transporter 2 (SGLT-2) inhibitors due to the absence of relevant data. The use of dipeptidyl peptidase-4 (DPP-4) inhibitors, metformin, thiazolidinedione, and sulfonylurea was associated with a decreased risk of dementia in comparison to no treatment with antidiabetic agents (hazard ratio [HR] for DPP-4 inhibitors, 0.54; 95% confidence interval [CI], 0.38-0.74, HR for metformin, 0.75; 95% CI, 0.63-0.86; HR for sulfonylurea, 0.85; 95%CI, 0.73-0.98 and HR for thiazolidinedione, 0.70; 95% CI, 0.55-0.89, respectively). However, the node-splitting analysis showed the inconsistency of direct and indirect estimates in sulfonylurea (P = 0.042). DPP-4 inhibitors, metformin, thiazolidinedione, and sulfonylurea exhibited a significant impact on the risk of dementia in diabetics compared with insulin (HR, 0.35; 95%CI, 0.20-0.59, HR, 0.48; 95% CI, 0.30-0.77, HR, 0.45; 95% CI, 0.29-0.73 and HR, 0.55; 95% CI, 0.34-0.88, respectively). DPP-4 inhibitors also exhibited a protective effect on the risk of Alzheimer's dementia compared with the no treatment with antidiabetic agents (HR, 0.48; 95% CI, 0.25-0.92). The meta-analysis demonstrated a protective effect of using metformin and DPP-4 inhibitors on the risk of dementia (HR, 0.86; 95% CI, 0.74-1.00 and HR, 0.65; 95% CI, 0.55-0.76, respectively). Further analysis showed insulin was associated with an increased risk of Alzheimer's dementia (HR, 1.60; 95% CI, 1.13-2.26). Only two case-control studies mentioned GLP-1 analogs and SGLT-2 inhibitors, and the pooled ORs showed no evidence of an association with dementia (GLP-1 analogs: 0.71; 95% CI, 0.46-1.10 and SGLT-2 inhibitors: 0.74; 95% CI, 0.47-1.15). Conclusion: This analysis indicated that patients with type 2 diabetes under treatment with DPP-4 inhibitors presented with the lowest risk of dementia, followed by those treated with metformin and thiazolidinedione, while treatment with insulin was associated with the highest risk. For the increasing focus on the protective effect on dementia, further specific clinical studies are needed to evaluate the impact of GLP-1 analogs and SGLT-2 inhibitors on the risk of dementia.
The proliferation of glomerular mesangial cells (GMCs) and secretion of extracellular matrix (ECM) in rat Thy-1 nephritis (Thy-1N), resembling human mesangioproliferative glomerulonephritis (MsPGN), have been studied for many years, but the mechanisms, especially the role of signalling pathway activation and its regulation in GMCs triggered by sublytic C5b-9 complexes in Thy-1N rats remain largely unclear. In the study, the proliferation of GMCs and production of ECM as well as the role of PI3K/Akt and its regulation, both in GMCs induced by sublytic C5b-9 (in vitro) and in the renal tissues of rats with Thy-1N (in vivo), were determined and the results revealed that GMCs proliferation and ECM secretion, both in vitro and in vivo, were notably increased, and that PI3K/Akt1 activation and its regulation, such as TNF receptor-associated factor 6 (TRAF6)-mediated Akt1 ubiquitination and PI3K-dependent Akt1 phosphorylation, were involved in the process of Thy-1N induction. On the other hand, silence of the TRAF6, PI3K or Akt1 genes could obviously diminish the proliferative damages and urinary protein secretion of Thy-1N rats. Together, these data implicated that sublytic C5b-9 complexes in Thy-1N rats could promote GMCs proliferation and ECM production through TRAF6-mediated PI3K-dependent Akt1 activation, in which the ubiquitination and phosphorylation of the Akt1 signal molecule played an important role in the initiation and development of the proliferative changes in the rats with Thy-1N.
Background:The mechanism of sublytic C5b-9-mediated glomerular mesangial cell (GMC) apoptosis in rat Thy-1 nephritis remains unclear. Results: GMC apoptosis was induced by sublytic C5b-9 via the interferon regulatory factor-1 (IRF-1)/caspase 8-dependent pathway, in which IRF-1 up-regulated caspase 8 activity. Conclusion: Sublytic C5b-9 could promote GMC apoptosis in Thy-1 nephritis through IRF-1-activation of caspase 8. Significance: IRF-1 might provide a potential target for human mesangioproliferative glomerulonephritis treatment.
Background Artificial intelligence (AI) assistance has been considered as a promising way to improve colonoscopic polyp detection, but there are limited prospective studies on real‐time use of AI systems. Methods We conducted a prospective, multicenter, randomized controlled trial of patients undergoing colonoscopy at six centers. Eligible patients were randomly assigned to conventional colonoscopy (control group) or AI‐assisted colonoscopy (AI group). AI assistance was our newly developed AI system for real‐time colonoscopic polyp detection. Primary outcome is polyp detection rate (PDR). Secondary outcomes include polyps per positive patient (PPP), polyps per colonoscopy (PPC), and non‐first polyps per colonoscopy (PPC‐Plus). Results A total of 2352 patients were included in the final analysis. Compared with the control, AI group did not show significant increment in PDR (38.8% vs. 36.2%, p = 0.183), but its PPC‐Plus was significantly higher (0.5 vs. 0.4, p < 0.05). In addition, AI group detected more diminutive polyps (76.0% vs. 68.8%, p < 0.01) and flat polyps (5.9% vs. 3.3%, p < 0.05). The effects varied somewhat between centers. In further logistic regression analysis, AI assistance independently contributed to the increment of PDR, and the impact was more pronounced for male endoscopists, shorter insertion time but longer withdrawal time, and elderly patients with larger waist circumference. Conclusion The intervention of AI plays a limited role in overall polyp detection, but increases detection of easily missed polyps; ChiCTR.org.cn number, ChiCTR1800015607.
The apoptosis of glomerular mesangial cells (GMCs) in rat Thy-1 nephritis (Thy-1N), a model of human mesangioproliferative glomerulonephritis (MsPGN), is accompanied by sublytic C5b-9 deposition. However, the mechanism by which sublytic C5b-9 induces GMC apoptosis is unclear. In the present studies, the effect of X-linked inhibitor of apoptosis-associated factor 1 (XAF1) expression on GMC apoptosis and the role of p300 and interferon regulatory factor-1 (IRF-1) in mediating XAF1 gene activation were determined, both in the GMCs induced by sublytic C5b-9 (in vitro) and in the renal tissues of rats with Thy-1N (in vivo). The in vitro studies demonstrated that IRF-1-enhanced XAF1 gene activation and its regulation by p300-mediated IRF-1 acetylation were involved in GMC apoptosis induced by sublytic C5b-9. The element of IRF-1 binding to XAF1 promoter and two acetylated sites of IRF-1 protein were also revealed. In vivo, silence of p300, IRF-1 or XAF1 genes in the renal tissues diminished GMC apoptosis and secondary GMC proliferation as well as urinary protein secretion in Thy-1N rats. Together, these data implicate that sublytic C5b-9 induces the expression of both p300 and IRF-1, as well as p300-dependent IRF-1 acetylation that may contribute to XAF1 gene activation and subsequent GMC apoptosis in Thy-1N rats.
To examine and quantify the potential relation between diabetic retinopathy (DR) and risk of all-cause mortality, stroke and heart failure (HF).The resources of meta-analysis of epidemiological observational studies were from Pub-med, EMBASE, CINAHL, Cochrane Library, conference, and proceedings.Random/fixed effects models were used to calculate pooled subgroup analysis stratified by different grades of DR was performed to explore the potential source of heterogeneity. Statistical manipulations were undertaken using program STATA.Of the included 25 studies, comprising 142,625 participants, 19 studies were concluded to find the relation of DR to all-cause mortality, 5 for stroke, and 3 for HF. Risk ratio (RR) for all-cause mortality with the presence of DR was 2.33 (95% CI 1.92–2.81) compared with diabetic individuals without DR. Evidences showed a higher risk of all-cause mortality associated with DR in patients with T2D or T1D (RR 2.25, 95% CI 1.91–2.65. RR 2.68, 95% CI 1.34–5.36). According to different grades of DR in patients with T2D, RR for all-cause mortality varied, the risk of nonproliferative diabetic retinopathy (NPDR) was 1.38 (1.11–1.70), while the risk of proliferative diabetic retinopathy (PDR) was 2.32 (1.75–3.06). There was no evidence of significant heterogeneity (Cochran Q test P = 0.29 vs 0.26, I2 = 19.6% vs 22.6%, respectively). Data from 5 studies in relation to DR and the risk of stroke showed that DR was significantly associated with increased risk of stroke (RR = 1.74, 95%CI: 1.35–2.24), compared with patients without DR. Furthermore, DR (as compared with individuals without DR) was associated with a marginal increased risk of HF in patients with diabetes mellitus (DM) (n = 3 studies; RR 2.24, 95% CI 0.98–5.14, P = 0.056).Our results showed that DR increased the risk of all-cause mortality, regardless of the different stages, compared with the diabetic individuals without DR. DR predicted increased risk of stroke and HF. Although only 3 studies about HF were available, the association between DR and HF should be careful.
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