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Awide range of camera apps and online video conferencing services support the feature of changing the background in real-time for aesthetic, privacy, and security reasons. Numerous studies show that theDeep-Learning (DL) is a suitable option for human segmentation, and the ensemble of multiple DL-based segmentation models can improve the segmentation result. However, these approaches are not as effective when directly applied to the image segmentation in a video. This paper proposes an Adaptive N-Frames Ensemble (AFE) approach for high-movement human segmentation in a video using an ensemble of multiple DL models. In contrast to an ensemble, which executes multiple DL models simultaneously for every single video frame, the proposed AFE approach executes only a single DL model upon a current video frame. It combines the segmentation outputs of previous frames for the final segmentation output when the frame difference is less than a particular threshold. Our method employs the idea of the N-Frames Ensemble (NFE) method, which uses the ensemble of the image segmentation of a current video frame and previous video frames. However, NFE is not suitable for the segmentation of fast-moving objects in a video nor a video with low frame rates. The proposed AFE approach addresses the limitations of the NFE method. Our experiment uses three human segmentation models, namely Fully Convolutional Network (FCN), DeepLabv3, and Mediapipe. We evaluated our approach using 1711 videos of the TikTok50f dataset with a single-person view. The TikTok50f dataset is a reconstructed version of the publicly available TikTok dataset by cropping, resizing and dividing it into videos having 50 frames each. This paper compares the proposed AFE with single models and the Two-Models Ensemble, as well as the NFE models. The experiment results show that the proposed AFE is suitable for low-movement as well as high-movement human segmentation in a video. [ABSTRACT FROM AUTHOR]

Tissues actively involved in energy metabolism are more likely to face metabolic challenges from bioenergetic substrates and are susceptible to mitochondrial dysfunction, leading to metabolic diseases. The mitochondria receive signals regarding the metabolic states in cells and transmit them to the nucleus or endoplasmic reticulum (ER) using calcium (Ca2+) for appropriate responses. Overflux of Ca2+ in the mitochondria or dysregulation of the signaling to the nucleus and ER could increase the incidence of metabolic diseases including insulin resistance and type 2 diabetes mellitus. Mitochondrial transcription factor A (Tfam) may regulate Ca2+ flux via changing the mitochondrial membrane potential and signals to other organelles such as the nucleus and ER. Since Tfam is involved in metabolic function in the mitochondria, here, we discuss the contribution of Tfam in coordinating mitochondria-ER activities for Ca2+ flux and describe the mechanisms by which Tfam affects mitochondrial Ca2+ flux in response to metabolic challenges. [ABSTRACT FROM AUTHOR]

We theoretically analyze diffusion trajectories of an anisotropic object moving on a two dimensional space in the absence of an external field. In determining diffusion parameters associated with the shape anisotropy, we devise a measure based on the gyration tensor and obtain its analytic expression exactly. Its efficiency and statistical convergence are examined in comparison with the fourth cumulant of particle displacement. We find that the estimation of diffusion constants based on the gyration measure is more efficient than the analysis adopting the fourth cumulant. [ABSTRACT FROM AUTHOR]

Selenoprotein W (SelW) is a selenium-containing protein with a redox motif found abundantly in the skeletal muscle of rodents. Previous in vitro studies suggest that SelW plays an antioxidant role; however, relatively few in vivo studies have addressed the antioxidant role of SelW. Since oxidative stress is a causative factor for the development of insulin resistance in obese subjects, we hypothesized that if SelW plays a role as an antioxidant, SelW deficiency could aggravate the oxidative stress and insulin resistance caused by a high-fat diet. SelW deficiency did not affect insulin sensitivity and H2O2 levels in the skeletal muscle of control diet-fed mice. SelW levels in the skeletal muscle were decreased by high-fat diet feeding for 12 wk. High-fat diet induced obesity and insulin resistance and increased the levels of H2O2 and oxidative stress makers, which were not affected by SelW deficiency. High-fat diet feeding increased the expression of antioxidant enzymes; however, SelW deficiency did not affect the expression levels of antioxidants. These results suggest that SelW does not play a protective role against oxidative stress and insulin resistance in the skeletal muscle of high-fat diet-fed obese mice. [ABSTRACT FROM AUTHOR]

Electrokinetic methods are efficient in probing the electrostatic surface properties of charged systems. However, anomalies observed in experiments indicate that the classical electrokinetic theory should be reconsidered. Using Green’s function methods and hydrodynamic simulations, we investigate electro-osmosis driven by electric-field-induced ion motion near a charged planar substrate with smooth or rough boundary. First, a reformulation of electro-osmotic theory for planar charged surfaces employing Green’s functions shows that the Helmholtz-Smoluchowski (HS) relation between electrostatic potential and solvent velocity is exact for smooth surfaces, even in the presence of ion correlations. Deviations from HS theory are caused by combined hydrodynamic and electric surface friction, as our hydrodynamic simulations of ions at smooth and corrugated charged surfaces in lateral electric fields demonstrate. Within the simulations, hydrodynamic interactions are treated in the continuum limit and the presence of a no-slip boundary condition at the surface is taken into account. While electrofriction is relevant in highly charged system and/or for multivalent ions, hydrodynamic friction is dominant in systems with moderate surface charge density and/or low ionic valency. We also derive the effective electrokinetic surface charge from the electro-osmotic solvent profiles, which is substantially reduced when compared with the bare value and shows qualitative agreement with the experimental tendency. [ABSTRACT FROM AUTHOR]

Obesity is a major public health issue worldwide and is frequently associated with erectile dysfunction (ED). Both conditions may share an internal pathologic environment, also known as common soil. Their main pathophysiologic processes are oxidative stress, inflammation, and resultant insulin and leptin resistance. Moreover, the severity of ED is correlated with comorbid medical conditions, including obesity. Therefore, amelioration of these comorbidities may increase the efficacy of ED treatment with phosphodiesterase 5 inhibitors, the first-line medication for patients with ED. Although metformin was originally developed as an insulin sensitizer six decades ago, it has also been shown to improve leptin resistance. In addition, metformin has been reported to reduce oxidative stress, inflammatory response, and body weight, as well as improve ED, in animal and human studies. Moreover, administration of a combination of metformin and phosphodiesterase 5 inhibitors improves erectile function in patients with ED who have a poor response to sildenafil and are insulin resistant. Thus, concomitant treatment of metabolic derangements associated with obesity in patients with ED who are obese would improve the efficacy and reduce the refractory response to penile vasodilators. In this review, we discuss the connecting factors between obesity and ED and the possible combined treatment modalities. [ABSTRACT FROM AUTHOR]

Clusterin is a secretory glycoprotein that is involved in multiple physiopathological processes, including lipid metabolism. Previous studies have shown that clusterin prevents hepatic lipid accumulation via suppression of sterol regulatory elementbinding protein (SREBP) 1. In this study, we examined the role of clusterin in renal lipid accumulation in clusterin-knockout mice and NRK52e tubular epithelial cells. Clusterin deficiency increased the expression of SREBP1 and its target genes and decreased malonyl-CoA decarboxylase protein levels in the kidney. Expression of the endocytic receptor, megalin, and scavenger receptor class A was increased in clusterindeficient mice. Functional analysis of lipid metabolism also revealed that lipid uptake and triglyceride synthesis were increased and fatty acid oxidation was reduced, leading to increased lipid accumulation in clusterin-deficient mice. These phenomena were accompanied by mesangial expansion, fibrosis and increased urinary proteinto- creatinine ratio. High-fat feeding aggravated these clusterin deficiency-induced pathological changes. Clusterin knockdown in NRK52e cells increased lipogenic gene expression and lipid levels, whereas overexpression of clusterin by treatment with adenovirus or recombinant clusterin protein suppressed lipogenic gene expression and lipid levels. Transforming growth factor-beta 1 (TGFB1) expression increased in the kidney of clusterin-deficient mice and suppression of TGFB1 in NRK52e cells suppressed lipid accumulation. These results suggest that clusterin deficiency induces renal lipid accumulation by dysregulating the expression of lipid metabolism-related factors and TGFB1, thereby leading to chronic kidney disease. Hence, clusterin may serve as a therapeutic target for lipid-induced chronic kidney disease. [ABSTRACT FROM AUTHOR]

Purpose: High-fat (HF) feeding induces hypothalamic leptin resistance via the activation of toll-like receptor 4 (TLR4). TLR4 deficiency confers resistance to diet-induced obesity. Udenafil, an anti-impotence drug, inhibits TLR4 in airway epithelial cells in vitro. In this study, we evaluated whether udenafil suppressed the hypothalamic expression of TLR4 and reduced body weight. Materials and Methods: The hypothalamic expression of TLR4, phosphodiesterase 5 (PDE5), nuclear factor-κB (NF-κB), and myeloid differentiation primary response gene 88 (Myd88) was analyzed by real-time polymerase chain reaction after treating mice for 2 days with udenafil (0, 12, 120, or 600 μg/d). Furthermore, the hypothalamic expression of TLR4, pro-opiomelanocortin (POMC), and neuropeptide Y (NPY) was analyzed after 9 days' treatment with udenafil and/or leptin. We also measured body weight and food intake following 9 days of udenafil and/or leptin treatment in control- and HF-fed mice. Results: Udenafil suppressed hypothalamic TLR4 mRNA expression dose-dependently. The changes were associated with decreased PDE5, NF-κB, and Myd88 expression. Udenafil treatment for 9 days reduced body weight and caloric intake in HF-fed mice. This may have been associated with the suppression of NPY expression that was elevated by HF feeding. POMC expression was not affected by udenafil. However, udenafil did not augment the effects of leptin on the reduction of body weight and caloric intake in HF-fed mice. Conclusions: These results suggested that udenafil reduced body weight by suppressing hypothalamic TLR4 mRNA expression in HF-fed mice and the combination effect of udenafil and leptin was additive rather than synergistic. [ABSTRACT FROM AUTHOR]

Regulation of lipogenesis by pathophysiological factors in the liver and skeletal muscle is well understood; however, regulation in the kidney is still unclear. To elucidate nutritional regulation of lipogenic factors in the kidney, we measured the renal expression of lipogenic transcriptional factors and enzymes during fasting and refeeding in chow-fed and high-fat-fed mice. We also examined the regulatory effect of the liver X receptor (LXR) on the expression of lipogenic factors. The renal gene expression of sterol regulatory element-binding protein (SREBP)-1c and fatty acid synthase (FAS) was reduced by fasting for 48 h and restored by refeeding, whereas the mRNA levels of forkhead box O (FOXO)1/3 were increased by fasting and restored by refeeding. Accordingly, protein levels of SREBP-1, FAS, and phosphorylated FOXO1/3 were reduced by fasting and restored by refeeding. The patterns of lipogenic factors expression in the kidney were similar to those in the liver and skeletal muscle. However, this phasic regulation of renal lipogenic gene expression was blunted in diet-induced obese mice. LXR agonist TO901317 increased the lipogenic gene expression and the protein levels of SREBP-1 precursor and FAS but not nuclear SREBP-1. Moreover, increases in insulin-induced gene mRNA and nuclear carbohydrate-responsive element binding protein (ChREBP) levels were observed in the TO901317-treated mice. These results suggest that the kidney shows flexible suppression and restoration of lipogenic factors following fasting and refeeding in lean mice, but this is blunted in obese mice. LXR is involved in the renal expression of lipogenic enzymes, and ChREBP may mediate the response. [ABSTRACT FROM AUTHOR]

Close to equilibrium, the exchange of particles and heat between macroscopic systems at different temperatures and different chemical potentials is known to be governed by a matrix of transport coefficients which are positive and symmetric. We investigate the amounts of heat and particles that are exchanged between two small quantum systems within a given time, and find them characterized by a transport matrix which neither needs to be symmetric nor positive. At larger times even spontaneous transport can be observed in the total absence of temperature and chemical potential differences provided that the two systems are different in size. All these deviations from standard transport behavior can be attributed to the fact that work is done on the system in the processes contacting and separating those parts of the system that initially possess different temperatures and chemical potentials. The standard transport properties are recovered for vanishing work and also in the limit of large systems and sufficiently large contact times. The general results are illustrated by an example. [ABSTRACT FROM AUTHOR]

Irregularities in the cellular uptake of thyroid hormones significantly affect muscle development and regeneration. Herein, we report indispensable role of transthyretin (TTR) in maintaining cellular thyroxine level. TTR was found to enhance recruitment of muscle satellite cells to the site of injury, thereby regulating muscle regeneration. Fluorescence-activated cell sorting (FACS) and immunofluorescence analysis of TTRwt (TTR wild type) and TTRkd (TTR knock-down) cells revealed that TTR controlled cell cycle progression by affecting the expression of Cyclin A2. Deiodinase 2 (D2) mediated increases in triiodothyronine levels were found to regulate the expression of myogenic marker, myogenin (MYOG). Moreover, use of a coumarin derivative (CD) revealed a significant reduction in cellular thyroxine, thereby indicating that TTR play a role in the transport of thyroxine. Taken together, these findings suggest that TTR mediated transport of thyroxine represents a survival mechanism necessary for the myogenic program. The results of this study will be highly useful to the strategic development of novel therapeutics to combat muscular dystrophies. [ABSTRACT FROM AUTHOR]

Background: Hyperglycemia, a characteristic feature of diabetes, induces glucotoxicity in pancreatic (3-cells, resulting in further impairment of insulin secretion and worsening glycemic control. Thus, preservation of insulin secretory capacity is essential for the management of type 2 diabetes. In this study, we evaluated the ability of an Orthosiphon stamineus (OS) extract to prevent glucotoxicity in insulin-producing cells. Methods: We measured insulin mRNA expression and glucose-stimulated insulin secretion (GSIS) in OS-treated INS-1 cells after exposure to a high glucose (HG; 30 mM) concentration. Results: The hexane extract of OS elevated mRNA expression of insulin as well as pancreatic and duodenal homeobox-1 of INS- 1 cells in a dose-dependent manner. The hexane OS extract also increased the levels of phosphorylated phosphatidylinositol 3-kinase (PI3K) in a concentration-dependent manner. Additionally, Akt phosphorylation was elevated by treatment with 100 and 200 μmol of the hexane OS extract. Three days of HG exposure suppressed insulin mRNA expression and GSIS; these expressions were restored by treatment with the hexane OS extract. HG elevated peroxide levels in the INS-1 cells. These levels were unaffected by OS treatment under both normal and hyperglycemic conditions. Conclusion: Our results suggested that the hexane extract of OS elevates insulin mRNA expression and prevents glucotoxicity induced by a 3-day treatment with HG. This was associated with the activation of PI-3K and Akt. [ABSTRACT FROM AUTHOR]

The rapid increase in the number of patients with chronic diseases is an important public healthcare issue in many countries, which accelerates many studies on a healthcare system that can, whenever and wherever, extract and process patient data. A patient with a chronic disease conducts self-management in an out-of-hospital environment, particularly in an at-home environment, so it is important to provide integrated and personalized healthcare services for effective care. To help provide effective care for chronic disease patients, we propose a service flow and a new cloud-based personalized healthcare system architecture supporting both at-home and at-hospital environments. The system considers the different characteristics of at-hospital and at-home environments, and it provides various chronic disease care services. A prototype implementation and a predicted cost model are provided to show the effectiveness of the system. The proposed personalized healthcare system can support cost-effective disease care in an at-hospital environment and personalized self-management of chronic disease in an at-home environment. [ABSTRACT FROM AUTHOR]

Females are more often affected by constipation than males, especially during pregnancy, which is related to the menstrual cycle. Although still controversial, alterations of progesterone and estrogen may be responsible. Therefore, this study was conducted in order to determine whether the female sex steroid hormone itself is responsible for development of constipation in both female and male mice. Administration of estrogen resulted in a decrease in weight of accumulated feces on days 2, 3, 4, and 5 in male mice and on day 5 in female mice, compared with the control group, but progesterone administration did not. Administration of estrogen resulted in a decrease in gastrointestinal movement, compared to normal; however, no significant change was observed by administration of progesterone. In conclusion, estrogen, rather than progesterone, may be a detrimental factor of constipation via decreased bowel movement in mice. [ABSTRACT FROM AUTHOR]

Background: The increasing prevalence of type 2 diabetes mellitus (T2DM) is associated with the rapid spread of obesity Obesity induces insulin resistance, resulting in 3-cell dysfunction and thus T2DM. Green tea extract (GTE) has been known to prevent obesity and T2DM, but this effect is stifi being debated. Our previous results suggested that circulating green tea gallated catechins (GCs) hinders postprandial blood glucose lowering, regardless of reducing glucose and cholesterol absorption when GCs are present in the intestinal lumen. This study aimed to compare the effect of GTE with that of GTE coadministered with poly-γ-glutamic acid (γ-PGA), which is likely to inhibit the intestinal absorption of GCs. Methods: The db/db mice and age-matched nondiabetic mice were provided with normal chow diet containing GTE (1%), γ-PGA(0.1%), or GTE+γ-PGA (1%:0. 1%) for 4 weeks. Results: In nondiabetic mice, none of the drugs showed any effects after 4 weeks. In db/db mice, however, weight gain and body fat gain were significantly reduced in the GTE+γ-PGA group compared to nondrug-treated db/db control mice without the corresponding changes in food intake and appetite. Glucose intolerance was also ameliorated in the GTE+γ-PGA group. Histopathological analyses showed that GTE+γ-PGA-treated db/db mice had a significantly reduced incidence of fatty liver and decreased pancreatic islet size. Neither GTE nor γ-PGA treatment showed any significant results. Conclusion: These results suggest that GTE+γ-PGA treatment than GTE or γ-PGA alone may be a useful tool for preventing both obesity and obesity-induced T2DM. [ABSTRACT FROM AUTHOR]

Background: Metformin, an oral biguanide insulin-sensitizing agent, is well known to decrease appetite. Although there is evidence that metformin could affect the brain directly, the exact mechanism is not yet known. Methods: To evaluate whether metformin induces anorexia via the hypothalamus, various concentrations of metformin were injected into the lateral ventricle of rats through a chronically implanted catheter and food intake was measured for 24 hours. The hypothalamic neuropeptides associated with regulation of food intake were also analyzed following 1 hour of intracerebroventricular (ICV) injections of metformin. Results: An ICV injection of metformin decreased food intake in a dose-dependent manner in unrestrained conscious rats. Hypothalamic phosphorylated AMP-activated protein kinase (pAMPK) increased by 3 μg with metformin treatment, but there was no further increase in pAMPK with increases in metformin dosage. The hypothalamic phosphorylated signal transducer and activator of transcription 3 (pSTAT3) increased by 3 μg with metformin treatment, but, there was no further increase in pSTAT3 level following increases of metformin dosage. Hypothalamic proopiomelanocortin was elevated with metformin treatment, while neuropeptide Y was not significantly changed. Conclusion: Our results suggest that metformin induces anorexia via direct action in the hypothalamus and the increase in pSTAT3, at least in part, is involved in the process. However, hypothalamic pAMPK appears not to contribute to metformin-induced appetite reduction in normal rats. Further studies exploring new pathways connecting metformin and feeding regulation are needed. [ABSTRACT FROM AUTHOR]

Objectives/Hypothesis: Leptin is a pleiotropic hormone that regulates food intake and metabolic and endocrine functions. Serum leptin levels have been reported to be increased in patients with allergic rhinitis and nasal polyposis; however, the explanation for this is unclear. We aimed to demonstrate the differential expression of leptin receptors in normal human nasal mucosa and nasal polyps, and to elucidate the effects of leptin on mucin gene expression in human nasal polyp epithelial cells. Study Design: Case-control and in vitro study. Methods: Normal ethmoid sinus mucosa was obtained from 10 subjects and used as a control; nasal polyps were obtained from 10 patients. Leptin receptor expression was analyzed using reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analysis. Leptin-induced expression of major respiratory mucins (MUC5AC and MUC5B) in the human nasal polyp epithelial cells was determined using RT-PCR and enzyme-linked immunosorbent assay. Results: The leptin receptor expression was stronger in the nasal polyps than in the normal nasal mucosa. In human nasal polyp epithelial cells, leptin increased the expression of MUC5AC and MUC5B, in a dose- and time-dependent manner, at the gene and protein levels. Leptin-induced mucin expression was inhibited by the leptin receptor antagonist. Conclusions: The increased expression of leptin receptors in nasal polyps implies leptin has a certain role in nasal polyposis. In addition, leptin appears to induce the expression of MUC5AC and MUC5B through leptin receptors in the human nasal polyp epithelial cells. Laryngoscope, 2010 [ABSTRACT FROM AUTHOR]

Background: Glutaredoxins (GRX)-1 is glutathione-dependent oxidoreductase. However, the role of these enzymes remains unknown in airway inflammatory diseases. Therefore, we aimed to establish the expression pattern of GRX-1 in the nasal polyps (NPs) and to assess the regulatory mechanisms associated with GRX-1 expression in interleukin (IL)-1beta-treated airway epithelial cells. Methods: The expression of GRX-1 in NPs and normal nasal mucosa were analyzed by reverse-transcription polymerase chain reaction and immunohistochemical staining. IL-1beta-induced reactive oxygen species (ROS) formation and GRX-1 expression in the airway epithelial cells was determined by flow cytometry and immunoassay. Results: The expression level of GRX-1 in NPs was significantly higher than in the normal nasal mucosa (p < 0.05). GRX-1 was highly expressed in the surface epithelial cells and the submucosal glandular cells in the NPs. IL-1beta increased the intracellular ROS formation and GRX-1 expression in airway epithelial cells. The inhibition of IL-1beta-induced ROS production by N-acetyl-cystein, an ROS scavenger, reduced GRX-1 expression. Diphenyleneiodonium and apocynin, NADPH oxidase inhibitors, did not abolish IL-1beta-induced ROS formation and GRX-1 expression, whereas budesonide attenuated it. Conclusion: High GRX-1 expression in NPs might be a primary defense against chronic inflammatory oxidative stress in nasal mucosa. IL-1beta-induced up-regulation of GRX-1 in airway epithelial cells is probably mediated by ROS. Glucocorticoids can regulate IL-1beta-induced ROS formation and GRX-1 expression. [ABSTRACT FROM AUTHOR]

Heat generation of uranium dioxide (UO2) powder and its pressureless rapid sintering behaviors have been studied using a high-frequency induction heating apparatus. The porous graphite housing has been used to prevent heat loss and to preheat the uranium oxides, simultaneously. At an elevated temperature, UO2 powder generated extra heat by itself. The synergism of individual heat generation between the graphite and UO2 powder could effectively heat the UO2 to the sintering temperature of 1700°C. Using this process, densification behavior of cylindrical and disk-type UO2 green pellets according to the heating rate and grain structure of sintered UO2 pellets were investigated. Rapid sintering caused a large crack around the circumference of the sintered pellet. The formation of cracks could be avoided when the heating rate or sample dimension are properly reduced. A dense and crack-free UO2 pellet with a relative density of up to 96% was produced within 5 min of the process time. The induction heat sintering process can be a potential candidate for the rapid fabrication of ceramics and composites. [ABSTRACT FROM AUTHOR]

A series of poly(amic acid)s have been synthesized from cyclobutane‐1,2,3,4‐tetracarboxylic dianhydride (CBDA), a functional diamine, 1‐(3,5‐diaminophenyl)‐3‐(1‐octadecyl)‐succinicimide and 4,4‐diaminodiphenylmethane (DDM) to give liquid crystal alignment layers with high pretilt angle after a rubbing process for vertically aligned liquid crystal display devices. Inherent viscosities of the poly(amic acid)s measured were in the range 0.2–1.56 dl/g, which decreased with an increase of content of 1‐(3,5‐diaminophenyl)‐3‐(1‐octadecyl)‐succinicimide. The cured polyimide films had good transparency, which was above 95% at 400 nm. Surface energies of all the polyimide films prepared from 1‐(3,5‐diaminophenyl)‐3‐(1‐octadecyl)‐succinicimide were below 40.7 dyn/cm before the rubbing process, which resulted in very high pretilt angles above 89°. By a rubbing process, the surface energy of the polyimide prepared from diamine mixture with 10 mol% of 1‐(3,5‐diaminophenyl)‐3‐(1‐octadecyl)‐succinicimide and 90% of DDM increased from 40.7 to 42.7 dyn/cm. Copyright © 2007 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

In feedback controls, measurement is an essential step in designing protocols according to outcomes. For quantum mechanical systems, measurement has another effect; to supply energy to the measured system. We verify that in feedback-controlled quantum engines, measurement plays a dual role; not only as an auxiliary to perform feedback control but also as an energy supply to drive the engines. We consider a specific engine cycle exploiting feedback control followed by projective measurement and show that the maximum bound of the extractable work is set by both the efficacy of the feedback control and the energy change caused by projective measurement. We take a concrete example of an engine using an immobile spin-1/2 particle as a working substance and suggest two possible scenarios for work extraction. [ABSTRACT FROM AUTHOR]

We investigate the initial ensemble dependence of the Jarzynski relation for nonequilibrium work performed on a classical system in the thermodynamic limit. It is shown that the Jarzynski equality holds also for a microcanonical ensemble only if the work process is quasi statically slow. If work is performed by a rapid perturbation, the average of exponentiated work expanded on a microcanonical system markedly deviates from the Jarzynski equality. Such deviation in fact quantifies the ratio of the energy distributions of nonequilibrium states in relative to equilibrium distribution. We exemplify these points in a simple model system both for the cases of deterministic and stochastic dynamics. [ABSTRACT FROM AUTHOR]

Oxidative stress plays an important role in tissue damage by hyperglycemia and hypoglycemia. It is well known that chronic exposure to hyperglycemia can lead to cellular dysfunction via oxidative stress and them are decreases in antioxidant enzymes in pancreatic β cells exposured to high glucose condition. As hyperglycemia worsens, the β cell steadily undergoes deterioration, secretes less and less insulin, and becomes a participant in a downward spiral of loss of function. However, little is known about correlation of oxidative stress with hypoglycemia in pancreatic β cells yet. To investigate the effect of hypoglycemia (obtained by low glucose media) on islets, we analyzed intracellular peroxide levels, insulin mRNA levels, PDX-1, MafA, mitochondrial function (intracellular ATP level) and GSIS in INS-1 cells and rat islets after culture at low glucose (2 mM) condition. The intracellular peroxide levels of the pancreatic islets (INS-1 cells, rat islets) measured by flow cytometry were increased in not only the high glucose (30 mM glucose in INS-1 cell or 50 mM ribose in rat islets) media but also low glucose media (2 mM) compared to 5.6 mM glucose media (p<0.05). The insulin mRNA levels, PDX-1, MafA, and GSIS were also decreased in both high and low glucose media compared to 5.6 mM glucose media (p<0.05). Also, the intracellular ATP level decreased in low glucose media compared to 5.6 mM glucose media (p<0.05). These results suggest that the β cell dysfunction of low glucose conditions is mainly due to ROS accumulation in INS-1 cells and rat islets, which is similar with glucose toxicity. [ABSTRACT FROM AUTHOR]

Long chain unsaturated fatty acid palmitate induces apoptosis in endothelial cells. AMP activated protein kinase(AMPK) activator, AICAR, is known to inhibit palmitate-induced apoptosis but the mechanism is not very clear. In the present study, we elucidated the inhibitory mechanism of AICAR on palmitate-induced apoptosis in bovine aortic endothelial cell (BAEC). Palmitate reduced cell survival and induced apoptosis in dose dependent manner measured by MTT and annexin V staining and procapase-3 protein level, respectively. Apoptosis caused by 250 µM palmitate resulted in increased production of reactive oxygen species (ROS) and increased phosphorylated NF-kB (pNF-kB). Adding 250 µM antioxidant n-acetyl cystein to 250 µM palmitate inhibited apoptosis, which was accompanied with reduced ROS production and pNF-kB level induced by palmitate. Treatment of 1 mM AICAR also inhibited palmitate induced apoptosis, ROS production, and pNF-kB level. In order to clear the mechanism of decrease in ROS production by AICAR, we measured UCP-2 protein level and found out that treatment of 1 mM AICAR for 24 hours increased UCP-2 protein level. In summary, palmitate induced apoptosis via increase in ROS production and AMPK activator, AICAR, reduced palmitate-induced apoptosis by increase in UCP-2 production. We suggest that increase in UCP-2 may reduce palmitate-induced increase in ROS production. [ABSTRACT FROM AUTHOR]

Long chain unsaturated fatty acid palmitate induces apoptosis in endothelial cells. Adiponectin from adipocyte has anti-inflammatory and anti-apoptotic effects in endothelial cell. In the present study, we elucidated the effects of adiponectin in palmitate-induced apoptosis in human umbilical vein endothelial cell (HUVEC). Palmitate induced apoptosis measured by annexin V staining and caspase-3 activity in dose dependent manner. Treatment of 1, 5, and 10 µg/ml globular adiponectin inhibited apoptosis by 500 µM palmitate (incuation for 48 hours) in dose dependent manner and 5 and 10 µg/ml adiponectin completely inhibited apoptosis. Thus 5 µ/ml adiponectin was used for the present study. Treatment of adiponectin increased phosphorylated AMP activated protein kinase (AMPK), AKT, and intracellular cAMP level in HUVEC. Treatment of AMPK inhibitor, compound C (40 µM), to HUVEC containing 500 µM palmitate prevented inhibitory effects of adiponecin on palmitate-induced apoptosis, whereas AMPK activator, AICAR (1 mM), inhibited palmitate-induced apoptosis. PI-3 kinase inhibitor, LY294002 (50 µM), also prevented inhibitory effects of adiponecin on apoptosis, cAMP activator, cholera toxin (100 ng/ml) and foskolin (20 µM), inhibited palmitate-induced apoptosis, whereas PKA inhibitor, H-89 (10 µM) reversed inhibitory effects of adiponecin. These results suggest that adiponectin inhibits palmitate-induced apoptosis via AMPK-AKT and cAMP-PKA pathway. [ABSTRACT FROM AUTHOR]

We evaluated the effects of inducible NOS (iNOS) on lipid-infusion-induced insulin resistance in iNOS knockout (KO) mice. Twelve weeks of iNOS KO male mice and wild type litter mate were randomly divided into saline infused (Saline) and lipid-infused (Lipid) mice both in wild-type and iNOS KO groups and insulin sensitivity was accessed with hyperinsulinemic-euglycemic clamp technique. Four days before clamp, chronic catheter was inserted into jugular vein and connected to three-way to infuse insulin (15 pmol⋅kg[sup -1]⋅min[sup -1]) and 20% glucose on the day of clamp. After overnight fasting, 20% of intralipid and 33 U/ml of heparin were infused for 2 hours before and during clamp in lipid group, and saline was infused in saline group. Body weight was not different between wild-type and iNOS KO mice but epididymal fat mass was significantly elevated in iNOS KO mice. Glucose infusion rate (GIR) to maintain euglycemia was significantly reduced in Lipid compared with Saline in wild-type mice but GIR Was not reduced in Lipid compared with Saline in iNOS KO mice. Lipid-infusion produced whole body insulin resistance in wild-type mice but deficiency of iNOS prevented development of lipid-infusion-induced insulin resistance. Whole body insulin resistance was contributed by 30% decrease in skeletal muscle glucose uptake in wild-type mice, whereas, lipid-infusion had no effect on glucose uptake of skeletal muscle in iNOS KO mice. Skeletal muscle insulin resistance was accompanied with decrease in glycolysis in Lipid of wild-type mice. Glycogen synthesis rate was paradoxically increased in Lipid of iNOS KO mice. Lipid- infusion reduced hepatic insulin action both in wild type and iNOS KO mice. Skeletal muscle tumor necrosis factor-α(TNF-α) expression was elevated in Lipid of wild-type mice but deficiency of iNOS prevented elevation of TNF-α. These results suggest that deficiency of iNOS prevents whole body and skeletal muscle insulin resistance by lipid-infusion, which is mediated by inhibitory effect of lipid-infusion induced increased TNF-α expression. [ABSTRACT FROM AUTHOR]