Vibration Parameter Optimization of a Linear Vibrating Banana Screen Using DEM 3D Simulation

In this paper, the effects of vibration parameters of a banana screen, i.e. frequency, amplitude and vibration direction angle, on the screening efficiency per unit time were studied using the discrete element method (DEM). The simulations were validated according to data collected from an experimental prototype screen. Functional relationships between vibration parameters and screening efficiency per unit time are presented. The results showed that the screening efficiency per unit time first displays an increase and later a decrease when the frequency, amplitude or vibration direction angle increased respectively. Vibration parameter optimization was also investigated, using an orthogonal experiment. Based on the banana screen model, it can be concluded that when the frequency is 22 Hz, the amplitude is 2.2 mm and the vibration direction angle is 39°, the screening efficiency of a banana screen is optimal

Vibration Parameter Optimization of a Linear Vibrating Banana Screen Using DEM 3D Simulation

In this paper, the effects of vibration parameters of a banana screen, i.e. frequency, amplitude and vibration direction angle, on the screening efficiency per unit time were studied using the discrete element method (DEM). The simulations were validated according to data collected from an experimental prototype screen. Functional relationships between vibration parameters and screening efficiency per unit time are presented. The results showed that the screening efficiency per unit time first displays an increase and later a decrease when the frequency, amplitude or vibration direction angle increased respectively. Vibration parameter optimization was also investigated, using an orthogonal experiment. Based on the banana screen model, it can be concluded that when the frequency is 22 Hz, the amplitude is 2.2 mm and the vibration direction angle is 39°, the screening efficiency of a banana screen is optimal

A Novel Graphene Quantum Dot-Based mRNA Delivery Platform

During the last decades, there has been growing interest in using therapeutic messager RNA (mRNA) together with drug delivery systems. Naked, unformulated mRNA is, however, unable to cross the cell membrane and is susceptible to degradation. Here we use graphene quantum dots (GQDs) functionalized with polyethyleneimine (PEI) as a novel mRNA delivery system. Our results show that these modified GQDs can be used to deliver intact and functional mRNA to Huh-7 hepatocarcinoma cells at low doses and, that the GQDs are not toxic, although cellular toxicity is a problem for these first-generation modified particles. Functionalized GQDs represent a potentially interesting delivery system that is easy to manufacture, stable and effective

T Cells Development Is Different between Thymus from Normal and Intrauterine Growth Restricted Pig Fetus at Different Gestational Stage

This experiment was conducted to evaluate the development of T cells in intrauterine growth retarded (IUGR) piglets at different gestational stages, and tentatively explore the relationship between T cells development and the Notch signaling pathway. A total of 18 crossbred (Landrace×Large white) primiparous sows were mated at similar weights and estruses and euthanized at d 60, 90 and 110 of gestation with six replicates for each time point. One IUGR and one normal fetus were picked from each litter. The T-cell subsets, mRNA expression of Delta-like1, Delta-like4, Jagged1, and Notch2 genes in the thymus were investigated. Compared to normal piglets, CD3+CD4−CD8+ cells in IUGR fetuses at d 90 was 0.13% lower (p<0.05). At d 110 of gestation CD8+ T cells in IUGR fetuses was 0.19% lower (p<0.05). The percentage of CD8+ T cells was 3.14% lower (p<0.05) of the total T cells in IUGR pigs at d 60. The abundance of Notch2 and Delta-like4 mRNA at d 110 was 20.93% higher and 0.77% (p<0.05) lower, and Delta-like1 mRNA at d 90 was 0.19% (p<0.05) higher compared to normal pigs. These results suggested that normal fetuses had a greater proportion of T-cell subsets at earlier gestation periods, and the Notch signaling pathway was likely partially responsible for these differences to some degree

Causal association of gastroesophageal reflux disease with obstructive sleep apnea and sleep-related phenotypes: a bidirectional two-sample Mendelian randomization study

BackgroundThe interactions and associations between obstructive sleep apnea (OSA), sleep-related phenotypes (SRPs), and gastroesophageal reflux disease (GERD) are complex, thus it is hard to explore the effect and direction of causalities.Study objectivesA bidirectional Mendelian randomization (MR) study was performed to explore causal associations of GERD with OSA and SRPs (including insomnia, morningness, sleep duration, ease of getting up, daytime napping, daytime dozing, and snoring).MethodsFirst, we gathered summary statistics from publicly available databases. Subsequently, we identified single-nucleotide polymorphisms without strong linkage (r2 ≤ 0.001) by referencing relevant genome-wide association studies that met genome-wide significance criteria. Our primary analysis relied on inverse variance weighted to estimate the causal relationship. To ensure the validity of our findings, we also conducted several sensitivity analyses. These included MR Pleiotropy RESidual Sum and Outlier to detect and correct for potential pleiotropic effects, MR-Egger to assess directional pleiotropy, and weighted median analysis to further evaluate heterogeneity and pleiotropy. For the initial MR analysis, when causality was indicated by the results, instrumental variables that were significantly linked to the aforementioned confounding factors were removed. We will re-analyze the data after excluding outcome-related single nucleotide polymorphisms to confirm that the results are still consistent with the previous results.ResultsGERD was found to increase the risk of OSA (OR = 1.53, 95% CI = 1.37–1.70, p = 5.3 × 10−15), insomnia (OR = 1.14, 95% CI = 1.10–1.19, p = 1.3 × 10−10), snoring (OR = 1.09, 95% CI = 1.04–1.13, p = 6.3 × 10−5) and less sleep duration (OR = 0.94, 95% CI = 0.91–0.97, p = 3.7 × 10−4). According to the reverse-direction analysis, there is an elevated risk of GERD associated with OSA (OR = 1.07, 95% CI = 1.02–1.12, p = 0.005), insomnia (OR = 1.95, 95% CI = 1.60–2.37, p = 1.92 × 10−11) and snoring (OR = 1.74, 95% CI = 1.37–2.21, p = 4.4 × 10−6).ConclusionGenetic susceptibility to GERD can elevate the likelihood of experiencing insomnia, snoring, and OSA, in addition to diminishing sleep duration. Conversely, a reverse MR analysis indicates that ameliorating any one of insomnia, snoring, or OSA can mitigate the risk of developing GERD

Fosinopril improves liver fibrosis by upregulating ACE2/Angiotensin-(1-7) axis activation in rats with nonalcoholic steatohepatitis

The aim of this research was to evaluate the effect of the angiotensin converting enzyme (ACE) inhibitor fosinopril on liver fibrosis in rats with high fat diet (HFD) induced nonalcoholic steatohepatitis (NASH). We found that treatment with fosinopril improved liver fibrosis. Moreover, treatment with fosinopril decreased serum Angiotensin (Ang) II, leptin, transforming growth factor β1 and hyaluronic acid concentrations, increased serum ACE2, Ang-(1-7), and adiponectin concentrations in rats fed with HFD. In the liver, fosinopril led to decreased leptin, α-smooth muscle actin, and collagen I expression, increased ACE2 and adiponectin expression. In conclusion, Fosinopril improves liver fibrosis by upregulating ACE2/Ang-(1-7) axis activation in rats with HFD-induced NASH. Furthermore, fosinopril might regulate the progression of liver fibrosis through the downregulation of leptin and the upregulation of adiponectin.Colegio de Farmacéuticos de la Provincia de Buenos Aire

Surgery induces neurocognitive disorder via neuroinflammation and glymphatic dysfunction in middle-aged mice with brain lymphatic drainage impairment

BackgroundBrain lymphatic drainage impairment is a prevalent characteristic in both aging and neurodegeneration. Surgery is more likely to induce excessive neuroinflammation and postoperative neurocognitive disorder (PND) among patients with aging and neurodegeneration. We hypothesized that surgical trauma may aggravate PND through preexisting cerebral lymphatic drainage impairment. However, there remains limited understanding about the role of surgery in changes of neurocognitive function in the populations with preoperative brain lymphatic drainage impairment. This study aims to expand our insight into surgery-induced glymphatic dysfunction, neuroinflammation and PND in middle-aged mice with preoperative brain lymphatic drainage impairment.Materials and methodsDeep cervical lymph nodes ligation (LdcLNs) was performed on middle-aged mice to establish preoperative brain lymphatic drainage impairment. A month later, laparotomy was performed on these mice with or without LdcLNs followed by analysis of brain neuroinflammation, glymphatic function, neuronal damage, and behavioral test.ResultsLdcLNs disrupted meningeal lymphatic drainage. In middle-aged mice with LdcLNs, surgery exacerbated more serious glymphatic dysfunction accompanied by aggravation of A1 astrocytes activation and AQP4 depolarization. Furthermore, surgery caused neuronal damage via reducing expression of neuronal nuclei (NeuN), post-synaptic density protein 95 (PSD95) and synaptophysin (SYP), as well as impairment in exploratory behavior and spatial working memory in middle-aged mice with LdcLNs. Additionally, surgery induced neuroinflammation with elevated microglia activation and increased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, as well as activated more expression of HMGB1/TLR-4/NF-κB pathway in middle-aged mice with LdcLNs.ConclusionSurgery exacerbates neuroinflammation and glymphatic dysfunction, ultimately resulting in neuronal damage and neurocognitive disorder in middle-aged mice with preoperative brain lymphatic drainage impairment. These results suggest that brain lymphatic drainage impairment may be a deteriorating factor in the progression of PND, and restoring its function may serve as a potential strategy against PND

Empagliflozin rescues pro-arrhythmic and Ca 2+ homeostatic effects of transverse aortic constriction in intact murine hearts

We explored physiological effects of the sodium-glucose co-transporter-2 inhibitor empagliflozin on intact experimentally hypertrophic murine hearts following transverse aortic constriction (TAC). Postoperative drug (2–6 weeks) challenge resulted in reduced late Na+ currents, and increased phosphorylated (p-)CaMK-II and Nav1.5 but not total (t)-CaMK-II, and Na+/Ca2+ exchanger expression, confirming previous cardiomyocyte-level reports. It rescued TAC-induced reductions in echocardiographic ejection fraction and fractional shortening, and diastolic anterior and posterior wall thickening. Dual voltage- and Ca2+-optical mapping of Langendorff-perfused hearts demonstrated that empagliflozin rescued TAC-induced increases in action potential durations at 80% recovery (APD80), Ca2+ transient peak signals and durations at 80% recovery (CaTD80), times to peak Ca2+ (TTP100) and Ca2+ decay constants (Decay30–90) during regular 10-Hz stimulation, and Ca2+ transient alternans with shortening cycle length. Isoproterenol shortened APD80 in sham-operated and TAC-only hearts, shortening CaTD80 and Decay30–90 but sparing TTP100 and Ca2+ transient alternans in all groups. All groups showed similar APD80, and TAC-only hearts showed greater CaTD80, heterogeneities following isoproterenol challenge. Empagliflozin abolished or reduced ventricular tachycardia and premature ventricular contractions and associated re-entrant conduction patterns, in isoproterenol-challenged TAC-operated hearts following successive burst pacing episodes. Empagliflozin thus rescues TAC-induced ventricular hypertrophy and systolic functional, Ca2+ homeostatic, and pro-arrhythmogenic changes in intact hearts