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Abstract Abdominal pain represents greater than 20% of US Emergency Department (ED) visits due to a wide range of illnesses. There are currently no reliable blood biomarkers to predict serious outcomes in patients with abdominal pain. Our previous studies have identified three mRNA transcripts related to innate immune activation: alkaline phosphatase (ALPL), interleukin-8 receptor-β (IL8RB), and defensin-1 (DEFA1) as promising candidates to detect an intra-abdominal infection. The objective of this study was to evaluate the accuracy of these mRNA biomarkers to predict likely infection, hospitalization and surgery in Emergency Department patients with undifferentiated abdominal pain. We prospectively enrolled Emergency Department patients with undifferentiated abdominal pain who received an abdominal CT scan as part of their evaluation. Clinical outcomes were abstracted from the CT scan and medical records. mRNA biomarker levels were calculated independent of the clinical outcomes and their accuracy was assessed to predict infectious diagnoses, surgery and hospital admission. 89 patients were enrolled; 21 underwent surgery; 47 underwent hospital admission; and, no deaths were observed within 30 days. In identifying which cases were likely infectious, mRNA biomarkers’ AUC values were: ALPL, 0.83; DEFA1 0.51; IL8RB, 0.74; and ALPL + IL8RB, 0.79. In predicting which Emergency Department patients would receive surgery, the AUC values were: ALPL, 0.75; DEFA1, 0.58; IL8RB, 0.75; and ALPL + IL8RB, 0.76. In predicting hospital admission, the AUC values were: ALPL, 0.78; DEFA1, 0.52; IL8RB, 0.74; and, ALPL + IL8RB, 0.77. For predicting surgery, ALPL + IL8RB’s positive likelihood ratio (LR) was 3.97; negative LR (NLR) was 0.70. For predicting hospital admission, the same marker’s positive LR was 2.80 with an NLR of 0.45. Where the primary cause for admission was a potentially infectious disorder, 33 of 34 cases (97%) had positive RNA scores. In a pragmatic, prospective diagnostic accuracy trial in Emergency Department patients with undifferentiated abdominal pain, mRNA biomarkers showed good accuracy to identify patients with potential infection, as well as those needing surgery or hospital admission.

Microglia are the principal resident immune cells in the central nervous system (CNS) and play important roles in the development of CNS disorders. In recent years, there have been significant developments in our understanding of microglia, and we now have greater insight into the temporal and spatial patterns of microglia activation in a variety of CNS disorders, as well as the interactions between microglia and neurons. A variety of signaling pathways have been implicated. However, to date, all published clinical trials have failed to demonstrate efficacy over placebo. This review summarizes the results of recent important studies and attempts to provide a mechanistic view of microglia activation, inflammation, tissue repair, and CNS disorders.

The arachidonic acid pathway metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) contributes to ischemia/reperfusion brain injury. Inhibition of 20-HETE formation can protect the developing brain from global ischemia. In previous studies, we have found that treatment with the 20-HETE synthesis inhibitor N-hydroxy-N-4-butyl-2-methylphenylformamidine (HET0016) can protect the immature brain from traumatic brain injury (TBI), but its hydrophobic nature limits its full potential. We designed a reactive oxygen species-responsive HET0016 prodrug, which consists of a thioketal link between HET0016 and stearyl alcohol (HET-TK-SA), and used the nanoprodrug strategy to successfully synthesize liposomes HET0016 prodrug liposomes (HPLs) to facilitate the application of HET0016 in protection from TBI. HPLs demonstrated spherical shape, size of about 127.8 nm, a zeta potential of −28.8 mv, a narrow particle size distribution and good stability. Male rats at postnatal day 16–17 underwent controlled cortical impact (CCI) followed by intravenous injection with vehicle or HET0016 (1 mg/kg, 2 h post-injury, once/day for 3 days). The results of the in vivo demonstrated that HPLs has good biosafety and can pass through the blood-brain barrier. Not only that compared with HET0016, HPLs better-inhibited inflammation and improved neuronal degeneration, which further led to lesion volume reduction, upgraded behavioral task performance, and ameliorated the degree of TBI impairment. Our results demonstrated HPLs could be a new strategy for juvenile TBI therapy.

Background: Observational studies have found an association between increased whole body water mass (BWM) and atrial fibrillation (AF). However, the causality has yet to be confirmed. To provide feasible protective measures on disease development, we performed Mendelian randomization (MR) design to estimate the potential causal relationship between increased BWM and AF. Methods: We implemented a two-sample MR study to assess whether increased BWM causally influences AF incidence. For exposure, 61 well-powered genetic instruments extracted from UK Biobank (N = 331,315) were used as the proxies of BWM. Summary genetic data of AF were obtained from FinnGen (Ncase = 22,068; Ncontrol = 116,926). Inverse-variance weighted (IVW), MR-Egger and weighted median methods were selected to infer causality, complemented with a series of sensitivity analyses. MR-Pleiotropy Residual Sum and Outlier (MR-PRESSO) and Radial MR were employed to identify outliers. Furthermore, risk factor analyses were performed to investigate the potential mechanisms between increased BWM and AF. Results: Genetic predisposition to increased BWM was demonstrated to be significantly associated with AF in the IVW model (OR = 2.23; 95% CI = 1.47–3.09; p = 1.60 × 10−7), and the result was consistent in other MR approaches. There was no heterogeneity or pleiotropy detected in sensitivity analysis. MR-PRESSO identified no outliers with potential pleiotropy after excluding outliers by Radial MR. Furthermore, our risk factor analyses supported a positive causal effect of genetic predicted increased BWM on edematous diseases. Conclusions: MR estimates showed that a higher BWM could increase the risk of AF. Pathological edema is an important intermediate link mediating this causal relationship.

The continuous development of mini-LEDs has led to higher requirements for chip transfer technology, which makes it difficult for the intermittent transfer method with a mechanical ejector pin to meet these requirements. To solve this problem, a novel compliant 2-DOF ejector pin mechanism for the mass transfer of robotic mini-LED chips is proposed in this paper. The compliance matrix method and the Newton method are employed for system kinematic modeling and dynamics modeling, respectively. The static and dynamic analyses of the mechanism are carried out via ANSYS Workbench, and the results of FEA are demonstrated the effectiveness of theoretical calculation. Then, an ILC is utilized to control the device via a parameters regulation approach in the frequency domain. Finally, an open-loop test and a trajectory tracking test for the prototype are carried out verify the effectiveness of proposed device. The test results indicate that the working stroke of the mechanism reaches 120 μm, the natural frequency of the device is 250.85 Hz, the coupling rate is less than ±0.5% and the tracking errors of 10 Hz, 20 Hz and 30 Hz sinusoidal signals are all within ±1.5%. According to the results of theoretical analyses, FEA and test, it has been proved that the designed mechanism for the mass transfer of mini-LED chips is superiority and effective.

With the speedy progress in electrical engineering field globally, power electronics course has aroused attention from academic community. English immersion teaching methods applied to power electronics course aim to introduce advanced counterpart academic knowledge from abroad to China and equip students and teaching staffs with international views as well as English-oriented logical and critical thinking in power electronics, and thus to promote power electronics development in China in the long term. By utilizing English immersion teaching methods for power electronics course, which involves problem-based learning, English-project-based assessment method and English-based laboratory operation, the challenges that the innovative teaching methods confront could be solved during each process of power electronics course. For further illustration, English immersion teaching methods for energy storage will be analysed as a study case. Consequently, the new English immersion teaching methods for power electronics course in China can be spread and applied in other non-native English-speaking countries to upgrade and reform power electronics course and related discipline.

Abstract Background Lung injury induced by lipopolysaccharide (LPS) remains one of the leading causes of morbidity and mortality in children. The damage to membrane phospholipids leads to the collapse of the bronchial alveolar epithelial barrier during acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Phospholipase A2 (PLA2), a key enzyme in the hydrolysis of membrane phospholipids, plays an important traumatic role in pulmonary inflammation, and Clara cell secretory protein (CCSP) is an endogenous inhibitor of PLA2. Our previous study showed that polydatin (PD), a monocrystalline extracted from a traditional Chinese medicinal herb (Polygonum cuspidatum Sieb, et Zucc), reduced PLA2 activity and sPLA2-IIA mRNA expression and mitigated LPS-induced lung injury. However, the potential mechanism for these effects has not been well defined. We have continued to investigate the effect of PD on LPS-induced expression of CCSP mRNA and protein in vivo and in vitro. Results Our results suggested that the CCSP mRNA level was consistent with its protein expression. CCSP expression was decreased in lung after LPS challenge. In contrast, PD markedly increased CCSP expression in a concentration-dependent manner. In particular, CCSP expression in PD-pretreated rat lung was higher than in rats receiving only PD treatment. Conclusion These results indicated that up-regulation of CCSP expression causing inhibition of PLA2 activation may be one of the crucial protective mechanisms of PD in LPS-induced lung injury.