Computer simulation of fundamental processes in high voltage circuit breakers based on an automated modelling platform

Auto-expansion circuit breakers utilize the arc’s energy to generate the flow conditions required for current interruption. The operation of this type of circuit breaker is extremely complex and its interruption capability depends on the whole arcing history as well as a number of geometric factors. On the other hand, circuit breaker development based on test is extremely expensive and time consuming. The accumulated understanding of the underlying physical processes so far enables arc models be used as a tool for optimum design of switchgear product such as high voltage circuit breakers. For academic research, there is often a need to study the performance of a newly developed arc model by inspecting the distribution of relevant physical quantities during a simulation and their sensitivity to model parameters in an efficient and convenient approach. However the effective use of computer simulation by design engineers has been hindered by the complexity encountered in model implementation. This thesis presents the development and structure of an automated simulation tool, the Integrated Simulation and Evaluation Environment (ISEE), for the arcing process in gas-blast circuit breakers. The functionalities of ISEE are identified and developed based on the experience in real product design, which include visual creation and definition of components, automatic setup of arc models based on a commercial CFD software package as equation solver, simulation task management, and visualization of computational results in “real-time” mode. This is the first automated simulation platform in the community of switching arc simulation. Using ISEE as the simulation tool, different designs of auto-expansion circuit breakers have been investigated to reveal the fundamental characteristics of the arcing process under different test duties. Before attempting to investigate the capability of an auto-expansion circuit breaker, the fundamental issue of determining the turbulence parameter of the Prandtl mixing length model is addressed. Previous studies on turbulence arcs were mostly concerned with simple converging-diverging nozzles. There has been little work on real circuit breaker nozzles. In order to calibrate the turbulence parameter, real arcing conditions including interrupting currents, contact travels, and transient recovery voltages of two commercial circuit breakers, with rated voltage of 145 kV and 245 kV, have been used together with the geometry of the circuit breakers to calibrate the range of the turbulence parameter. The effect of nozzle ablation has been considered. All together 6 cases have been used for three circuit breakers with each pair of cases corresponding to a success and failure in its thermal recovery process. It has been found that a single parameter of 0.35 is applicable to all three circuit breakers with an auxiliary nozzle and a main nozzle of converge-flat throat-diverge shape. It must be noted that this value is obtained with the definition of thermal radius introduced in Chapter 3 and the assumption that the parameter linearly changes with the interrupting current from 0.05 at 15 kA to 0.35 at current zero. Using the calibrated turbulence model, a computational study of the thermal interruption performance of a 145 kV, 60 Hz auto-expansion circuit breaker with different arc durations has been carried out in Chapter 4. The relation between pressure peak and current peak in the auto-expansion circuit breaker is discussed. It has been found that a larger average mass flux in the main nozzle indicates a better interruption environment, enabling the circuit breaker to withstand a larger rate of rise of recovery voltage after current zero. Another important finding is that the auxiliary nozzle plays an important role in an auto-expansion circuit breaker both at the high current phase and during the current zero period. Therefore, the proper design and use of an auxiliary nozzle is a key factor to enhance the thermal interruption capability of high voltage auto-expansion circuit breakers. In Chapter 5 of the thesis, the transient pressure variation in auto-expansion circuit breakers was studied. The pressure variation has an extremely complex pattern and the pressure changes in different ways depending on the location in the arcing chamber. It is shown, for the first time, that the time lag between the current peak and pressure peak in the expansion volume can be explained by using an energy flow rate balance method, that is flow reversal occurs when the enthalpy exhaustion rate from the contact space equals the electrical power input. Following the flow reversal, a high enthalpy flow rate from the expansion volume into the contact gap first occurs for a short while (1 ms), which is followed by a high mass flow rate of relatively cool gas at less than 2000 K. This high mass flow rate causes a surplus in mass flow rate into the contact gap and results in the last temporary pressure peak in the contact space before the pressure and flow field finally settle down for arc quenching at current zero. The pressure change under different conditions, i.e. different arc durations, different current levels and different length of the heating channel, has also been studied in details. In summary the present research leads to original findings in three aspects of the operation of auto-expansion circuit breakers, i.e. the calibration of the turbulence parameter for the Prandtl mixing length model, interruption performance with different arc durations, and the transient pressure variation in the arcing process. The results are expected to provide useful information for the optimum design of auto-expansion circuit breakers

Case report: Targeted sequencing facilitates the diagnosis and management of rare multifocal pure ground-glass opacities with intrapulmonary metastasis

IntroductionTreatments for multiple ground-glass opacities (GGOs) for which the detection rate is increasing are still controversial. Next-generation sequencing (NGS) may provide additional key evidence for differential diagnosis or optimal therapeutic schedules.Case presentationWe first reported a rare case in which more than 100 bilateral pulmonary GGOs (91.7% of the GGOs were pure GGOs) were diagnosed as both multiple primary lung cancer and intrapulmonary metastasis. We performed NGS with an 808-gene panel to assess both somatic and germline alterations in tissues and plasma. The patient (male) underwent three successive surgeries and received osimertinib adjuvant therapy due to signs of metastasis and multiple EGFR-mutated tumors. The patient had multiple pure GGOs, and eight tumors of four pathological subtypes were evaluated for the clonal relationship. Metastasis, including pure GGOs and atypical adenomatous hyperplasia, was found between two pairs of tumors. Circulating tumor DNA (ctDNA) monitoring of disease status may impact clinical decision-making.ConclusionsSurgery combined with targeted therapies remains a reasonable alternative strategy for treating patients with multifocal GGOs, and NGS is valuable for facilitating diagnostic workup and adjuvant therapy with targeted drugs through tissue and disease monitoring via ctDNA

Comparative epidemiology of gestational diabetes in ethnic Chinese from Shanghai birth cohort and growing up in Singapore towards healthy outcomes cohort

Background Gestational diabetes mellitus (GDM) has been associated with adverse health outcomes for mothers and offspring. Prevalence of GDM differs by country/region due to ethnicity, lifestyle and diagnostic criteria. We compared GDM rates and risk factors in two Asian cohorts using the 1999 WHO and the International Association of Diabetes and Pregnancy Study Groups (IADPSG) criteria. Methods The Shanghai Birth Cohort (SBC) and the Growing Up in Singapore Towards healthy Outcomes (GUSTO) cohort are prospective birth cohorts. Information on sociodemographic characteristics and medical history were collected from interviewer-administered questionnaires. Participants underwent a 2-h 75-g oral glucose tolerance test at 24-28 weeks gestation. Logistic regressions were performed. Results Using the 1999 WHO criteria, the prevalence of GDM was higher in GUSTO (20.8%) compared to SBC (16.6%) (p = 0.046). Family history of hypertension and alcohol consumption were associated with higher odds of GDM in SBC than in GUSTO cohort while obesity was associated with higher odds of GDM in GUSTO. Using the IADPSG criteria, the prevalence of GDM was 14.3% in SBC versus 12.0% in GUSTO. A history of GDM was associated with higher odds of GDM in GUSTO than in SBC, while being overweight, alcohol consumption and family history of diabetes were associated with higher odds of GDM in SBC. Conclusions We observed several differential risk factors of GDM among ethnic Chinese women living in Shanghai and Singapore. These findings might be due to heterogeneity of GDM reflected in diagnostic criteria as well as in unmeasured genetic, lifestyle and environmental factors.Peer reviewe

Nutritional Interventions Improved Rumen Functions and Promoted Compensatory Growth of Growth-Retarded Yaks as Revealed by Integrated Transcripts and Microbiome Analyses

Growth retardation reduces the incomes of livestock farming. However, effective nutritional interventions to promote compensatory growth and the mechanisms involving digestive tract microbiomes and transcripts have yet to be elucidated. In this study, Qinghai plateau yaks, which frequently suffer from growth retardation due to malnutrition, were used as an experimental model. Young growth-retarded yaks were pastured (GRP), fed basal ration (GRB), fed basal ration addition cysteamine hydrochloride (CSH; GRBC) or active dry yeast (ADY; GRBY). Another group of growth normal yak was pastured as a positive control (GNP). After 60-day nutritional interventions, the results showed that the average daily gain (ADG) of GRB was similar to the level of GNP, and the growth rates of GRBC and GRBY were significantly higher than the level of GNP (P < 0.05). Basal rations addition of CSH or ADY either improved the serum biochemical indexes, decreased serum LPS concentration, facilitated ruminal epithelium development and volatile fatty acids (VFA) fermentation of growth-retarded yaks. Comparative transcriptome in rumen epithelium between growth-retarded and normal yaks identified the differentially expressed genes mainly enriched in immune system, digestive system, extracellular matrix and cell adhesion pathways. CSH addition and ADY addition in basal rations upregulated ruminal VFA absorption (SLC26A3, PAT1, MCT1) and cell junction (CLDN1, CDH1, OCLN) gene expression, and downregulated complement system (C2, C7) gene expression in the growth-retarded yaks. 16S rDNA results showed that CSH addition and ADY addition in basal rations increased the rumen beneficial bacterial populations (Prevotella_1, Butyrivibrio_2, Fibrobacter) of growth-retarded yaks. The correlation analysis identified that ruminal VFAs and beneficial bacteria abundance were significantly positively correlated with cell junction and VFA absorption gene expressions and negatively correlated with complement system gene expressions on the ruminal epithelium. Therefore, CSH addition and ADY addition in basal rations promoted rumen health and body growth of growth-retarded yaks, of which basal ration addition of ADY had the optimal growth-promoting effects. These results suggested that improving nutrition and probiotics addition is a more effective method to improve growth retardation caused by gastrointestinal function deficiencies

Glucose and Palmitate Differentially Regulate PFKFB3/iPFK2 and Inflammatory Responses in Mouse Intestinal Epithelial Cells

The gene PFKFB3 encodes for inducible 6-phosphofructo-2-kinase, a glycolysis-regulatory enzyme that protects against diet-induced intestine inflammation. However, it is unclear how nutrient overload regulates PFKFB3 expression and inflammatory responses in intestinal epithelial cells (IECs). In the present study, primary IECs were isolated from small intestine of C57BL/6J mice fed a low-fat diet (LFD) or high-fat diet (HFD) for 12 weeks. Additionally, CMT-93 cells, a cell line for IECs, were cultured in low glucose (LG, 5.5 mmol/L) or high glucose (HG, 27.5 mmol/L) medium and treated with palmitate (50 mu mol/L) or bovine serum albumin (BSA) for 24 hr. These cells were analyzed for PFKFB3 and inflammatory markers. Compared with LFD, HFD feeding decreased IEC PFKFB3 expression and increased IEC proinflammatory responses. In CMT-93 cells, HG significantly increased PFKFB3 expression and proinflammatory responses compared with LG. Interestingly, palmitate decreased PFKFB3 expression and increased proinflammatory responses compared with BSA, regardless of glucose concentrations. Furthermore, HG significantly increased PFKFB3 promoter transcription activity compared with LG. Upon PFKFB3 overexpression, proinflammatory responses in CMT-93 cells were decreased. Taken together, these results indicate that in IECs glucose stimulates PFKFB3 expression and palmitate contributes to increased proinflammatory responses. Therefore, PFKFB3 regulates IEC inflammatory status in response to macronutrients.National Institutes of Health [HL108922, HL095556, R01DK095828, R01DK095862]; National Natural Science Foundation of China [81100562/H0711]; Hatch Program of National Institutes of Food and Agriculture (NIFA)SCI(E)[email protected]; [email protected]

Berberine Ameliorates Hepatic Steatosis and Suppresses Liver and Adipose Tissue Inflammation in Mice with Diet-induced Obesity

Increasing evidence demonstrates that berberine (BBR) is beneficial for obesity-associated nonalcoholic fatty liver disease (NAFLD). However, it remains to be elucidated how BBR improves aspects of NAFLD. Here we revealed an AMP-activated protein kinase (AMPK)-independent mechanism for BBR to suppress obesity-associated inflammation and improve hepatic steatosis. In C57BL/6J mice fed a high-fat diet (HFD), treatment with BBR decreased inflammation in both the liver and adipose tissue as indicated by reduction of the phosphorylation state of JNK1 and the mRNA levels of proinflammatory cytokines. BBR treatment also decreased hepatic steatosis, as well as the expression of acetyl-CoA carboxylase and fatty acid synthase. Interestingly, treatment with BBR did not significantly alter the phosphorylation state of AMPK in both the liver and adipose tissue of HFD-fed mice. Consistently, BBR treatment significantly decreased the phosphorylation state of JNK1 in both hepatoma H4IIE cells and mouse primary hepatocytes in both dose-dependent and time-dependent manners, which was independent of AMPK phosphorylation. BBR treatment also caused a decrease in palmitate-induced fat deposition in primary mouse hepatocytes. Taken together, these results suggest that BBR actions on improving aspects of NAFLD are largely attributable to BBR suppression of inflammation, which is independent of AMPK.National Institutes of Health [HL108922, HL095556, R01DK095828, R01DK095862]; National Natural Science Foundation of China [81100562/H0711]; Hatch Program of the National Institutes of Food and Agriculture (NIFA)SCI(E)[email protected]; [email protected]

Metformin Ameliorates Hepatic Steatosis and Inflammation without Altering Adipose Phenotype in Diet-Induced Obesity

Non-alcoholic fatty liver disease (NAFLD) is closely associated with obesity and insulin resistance. To better understand the pathophysiology of obesity-associated NAFLD, the present study examined the involvement of liver and adipose tissues in metformin actions on reducing hepatic steatosis and inflammation during obesity. C57BL/6J mice were fed a high-fat diet (HFD) for 12 weeks to induce obesity-associated NAFLD and treated with metformin (150 mg/kg/d) orally for the last four weeks of HFD feeding. Compared with HFD-fed control mice, metformin-treated mice showed improvement in both glucose tolerance and insulin sensitivity. Also, metformin treatment caused a significant decrease in liver weight, but not adiposity. As indicated by histological changes, metformin treatment decreased hepatic steatosis, but not the size of adipocytes. In addition, metformin treatment caused an increase in the phosphorylation of liver AMP-activated protein kinase (AMPK), which was accompanied by an increase in the phosphorylation of liver acetyl-CoA carboxylase and decreases in the phosphorylation of liver c-Jun N-terminal kinase 1 (JNK1) and in the mRNA levels of lipogenic enzymes and proinflammatory cytokines. However, metformin treatment did not significantly alter adipose tissue AMPK phosphorylation and inflammatory responses. In cultured hepatocytes, metformin treatment increased AMPK phosphorylation and decreased fat deposition and inflammatory responses. Additionally, in bone marrow-derived macrophages, metformin treatment partially blunted the effects of lipopolysaccharide on inducing the phosphorylation of JNK1 and nuclear factor kappa B (NF-κB) p65 and on increasing the mRNA levels of proinflammatory cytokines. Taken together, these results suggest that metformin protects against obesity-associated NAFLD largely through direct effects on decreasing hepatocyte fat deposition and on inhibiting inflammatory responses in both hepatocytes and macrophages