Numerical estimation and experimental verification of optimal parameter identification based on modern optimization of a three phase induction motor

The parameters of electric machines play a substantial role in the control system which, in turn, has a great impact on machine performance. In this paper, a proposed optimal estimation method for the electrical parameters of induction motors is presented. The proposed method uses the particle swarm optimization (PSO) technique. Further, it also considers the influence of temperature on the stator resistance. A complete experimental setup was constructed to validate the proposed method. The estimated electrical parameters of a 3.8-hp induction motor are compared with the measured values. A heat run test was performed to compare the effect of temperature on the stator resistance based on the proposed estimation method and the experimental measurements at the same conditions. It is shown that acceptable accuracy between the simulated results and the experimental measurements has been achieved

Acute and chronic metabolic effects of carvedilol in high-fructose, high fat diet-fed mice: Implication of β-arrestin2 pathway

We aimed to investigate the acute and chronic effects of carvedilol on insulin resistance in high-fructose, high-fat diet (HFrHFD)-fed mice and the implication of β-arrestin2 pathway. The acute effect of carvedilol (10 mg/kg, i.p.) on glucose tolerance and hepatic lipid signaling in normal and insulin resistant mice was investigated. Then, the chronic effect of carvedilol on insulin resistance and dyslipidemia in HFrHFD-fed mice was examined. Changes in β-arrestin2 and its down-stream signals in liver, skeletal muscle, and adipose tissue were measured. This involved measuring phosphatidylinositol 4,5-bisphosphate (PIP2) and diacylglycerol (DAG) levels and protein kinase B (Akt)-activity. Carvedilol acutely reduced fasting blood glucose levels in both normal and insulin resistant mice without significantly affecting the glucose tolerance. These acute effects were associated with increased hepatic PIP2 but decreased hepatic DAG levels. Chronic administration of carvedilol significantly ameliorated insulin resistance and dyslipidemia in HFrHFD-fed mice. These chronic effects were associated with increased β-arrestin2, PIP2 and Akt activity levels but decreased DAG levels in the classical insulin target tissues. In conclusion, carvedilol acutely maintains glucose homeostasis and chronically ameliorates insulin resistance and dyslipidemia in HFrHFD-fed mice. The insulin sensitizing effects of carvedilol are highly correlated with the upregulation of β-arrestin2 pathway.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Non‐classical monocytes frequency and serum vitamin D3 levels are linked to diabetic foot ulcer associated with peripheral artery disease

Abstract Aims/Introduction Peripheral artery disease (PAD) serves as a risk factor for diabetic foot ulcers (DFUs). PAD pathology involves atherosclerosis and impaired immunity. Non‐classical monocytes are believed to have an anti‐inflammatory role. 1,25‐Dihydroxy vitamin D (vitamin D3) is claimed to have immune‐modulating and lipid‐regulating roles. Vitamin D receptor is expressed on monocytes. We aimed to investigate if circulating non‐classical monocytes and vitamin D3 were implicated in DFUs associated with PAD. Materials and Methods There were two groups of DFU patients: group 1 (n = 40) included patients with first‐degree DFUs not associated with PAD, and group 2 (n = 50) included patients with DFU with PAD. The monocyte phenotypes were detected using flow cytometry. Vitamin D3 was assessed by enzyme‐linked immunosorbent assay. Results DFU patients with PAD showed a significant reduction in the frequency of non‐classical monocytes and vitamin D3 levels, when compared with DFU patients without PAD. The percentage of non‐classical monocytes positively correlated with vitamin D3 level (r = 0.4, P < 0.01) and high‐density lipoprotein (r = 0.5, P < 0.001), whereas it was negatively correlated with cholesterol (r = −0.5, P < 0.001). Vitamin D3 was negatively correlated with triglyceride/high‐density lipoprotein (r = −0.4, P < 0.01). Regression analysis showed that a high vitamin D3 serum level was a protective factor against PAD occurrence. Conclusions Non‐classical monocytes frequency and vitamin D3 levels were significantly reduced in DFU patients with PAD. Non‐classical monocytes frequency was associated with vitamin D3 in DFUs patients, and both parameters were linked to lipid profile. Vitamin D3 upregulation was a risk‐reducing factor for PAD occurrence

Ginseng^® Alleviates Malathion-Induced Hepatorenal Injury through Modulation of the Biochemical, Antioxidant, Anti-Apoptotic, and Anti-Inflammatory Markers in Male Rats

This study aims to see if Ginseng® can reduce the hepatorenal damage caused by malathion. Four groups of forty male Wistar albino rats were alienated. Group 1 was a control group that got orally supplied corn oil (vehicle). Group 2 was intoxicated by malathion dissolved in corn oil orally at 135 mg/kg/day. Group 3 orally received both malathion + Panax Ginseng® (300 mg/kg/day). Group 4 was orally given Panax Ginseng® at a 300 mg/kg/day dose. Treatments were administered daily and continued for up to 30 consecutive days. Malathion’s toxic effect on both hepatic and renal tissues was revealed by a considerable loss in body weight and biochemically by a marked increase in liver enzymes, LDH, ACP, cholesterol, and functional renal markers with a marked decrease in serum TP, albumin, and TG levels with decreased AchE and Paraoxonase activity. Additionally, malondialdehydes, nitric oxide (nitrite), 8-hydroxy-2-deoxyguanosine, and TNFα with a significant drop in the antioxidant activities were reported in the malathion group. Malathion upregulated the inflammatory cytokines and apoptotic genes, while Nrf2, Bcl2, and HO-1 were downregulated. Ginseng® and malathion co-treatment reduced malathion’s harmful effects by restoring metabolic indicators, enhancing antioxidant pursuit, lowering the inflammatory reaction, and alleviating pathological alterations. So, Ginseng® may have protective effects against hepatic and renal malathion-induced toxicity on biochemical, antioxidant, molecular, and cell levels