Transient behavior in Single-File Systems

We have used Monte-Carlo methods and analytical techniques to investigate the influence of the characteristics, such as pipe length, diffusion, adsorption, desorption and reaction rates on the transient properties of Single-File Systems. The transient or the relaxation regime is the period in which the system is evolving to equilibrium. We have studied the system when all the sites are reactive and when only some of them are reactive. Comparisons between Mean-Field predictions, Cluster Approximation predictions, and Monte Carlo simulations for the relaxation time of the system are shown. We outline the cases where Mean-Field analysis gives good results compared to Dynamic Monte-Carlo results. For some specific cases we can analytically derive the relaxation time. Occupancy profiles for different distribution of the sites both for Mean-Field and simulations are compared. Different results for slow and fast reaction systems and different distribution of reactive sites are discussed.Comment: 18 pages, 19 figure

The polarized image of a synchrotron-emitting ring of gas orbiting a black hole

High Energy Astrophysic

Constraints on black-hole charges with the 2017 EHT observations of M87*

InstrumentationHigh Energy Astrophysic

The variability of the black hole image in M87 at the dynamical timescale

The black hole images obtained with the Event Horizon Telescope (EHT) are expected to be variable at the dynamical timescale near their horizons. For the black hole at the center of the M87 galaxy, this timescale (5–61 days) is comparable to the 6 day extent of the 2017 EHT observations. Closure phases along baseline triangles are robust interferometric observables that are sensitive to the expected structural changes of the images but are free of station-based atmospheric and instrumental errors. We explored the day-to-day variability in closure-phase measurements on all six linearly independent nontrivial baseline triangles that can be formed from the 2017 observations. We showed that three triangles exhibit very low day-to-day variability, with a dispersion of ∼3°–5°. The only triangles that exhibit substantially higher variability (∼90°–180°) are the ones with baselines that cross the visibility amplitude minima on the u–v plane, as expected from theoretical modeling. We used two sets of general relativistic magnetohydrodynamic simulations to explore the dependence of the predicted variability on various black hole and accretion-flow parameters. We found that changing the magnetic field configuration, electron temperature model, or black hole spin has a marginal effect on the model consistency with the observed level of variability. On the other hand, the most discriminating image characteristic of models is the fractional width of the bright ring of emission. Models that best reproduce the observed small level of variability are characterized by thin ring-like images with structures dominated by gravitational lensing effects and thus least affected by turbulence in the accreting plasmas.https://iopscience.iop.org/article/10.3847/1538-4357/ac332e/pdfPublished versio

Event Horizon Telescope observations of the jet launching and collimation in Centaurus A

InstrumentationLarge scale structure and cosmolog

Broadband multi-wavelength properties of M87 during the 2017 Event Horizon Telescope campaign

High Energy AstrophysicsInstrumentatio

Hypothalamic endoplasmic reticulum stress and insulin resistance in off spring of mice dams fed high-fat diet during pregnancy and lactation

FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ – CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO CIENTÍFICO E TECNOLOGICOThe goal of this study was to determine the presence early of markers of endoplasmic reticulum stress (ERS) and insulin resistance in the offspring from dams fed HFD (HFD-O) or standard chow diet (SC-O) during pregnancy and lactation. To address this question, we evaluated the hypothalamic and hepatic tissues in recently weaned mice (d28) and the hypothalamus of newborn mice (d0) from dams fed HFD or SC during pregnancy and lactation. Body weight, adipose tissue mass, and food intake were more accentuated in HFD-O mice than in SC-O mice. In addition, intolerance to glucose and insulin was higher in HFD-O mice than in SC-O mice. Compared with SC-O mice, levels of hypothalamic IL1-β mRNA, NFκB protein, and p-JNK were increased in HFD-O mice. Furthermore, compared with SC-O mice, hypothalamic AKT phosphorylation after insulin challenge was reduced, while markers of ERS (p-PERK, p-eIF2α, XBP1s, GRP78, and GRP94) and p-AMPK were increased in the hypothalamic tissue of HFD-O at d28 but not at d0. These damages to hypothalamic signaling were accompanied by increased triglyceride deposits, activation of NFκB, p-JNK, p-PERK and p-eIF2α. These point out lactation period as maternal trigger for metabolic changes in the offspring. These changes may occur early and quietly contribute to obesity and associated pathologies in adulthood. Although in rodents the establishment of ARC neuronal projections occurs during the lactation period, in humans it occurs during the third trimester. Gestational diabetes and obesity in this period may contribute to impairment of energy homeostasis.The goal of this study was to determine the presence early of markers of endoplasmic reticulum stress (ERS) and insulin resistance in the offspring from dams fed HFD (HFD-O) or standard chow diet (SC-O) during pregnancy and lactation. Materials/Methods To address this question, we evaluated the hypothalamic and hepatic tissues in recently weaned mice (d28) and the hypothalamus of newborn mice (d0) from dams fed HFD or SC during pregnancy and lactation. Results Body weight, adipose tissue mass, and food intake were more accentuated in HFD-O mice than in SC-O mice. In addition, intolerance to glucose and insulin was higher in HFD-O mice than in SC-O mice. Compared with SC-O mice, levels of hypothalamic IL1-β mRNA, NFκB protein, and p-JNK were increased in HFD-O mice. Furthermore, compared with SC-O mice, hypothalamic AKT phosphorylation after insulin challenge was reduced, while markers of ERS (p-PERK, p-eIF2α, XBP1s, GRP78, and GRP94) and p-AMPK were increased in the hypothalamic tissue of HFD-O at d28 but not at d0. These damages to hypothalamic signaling were accompanied by increased triglyceride deposits, activation of NFκB, p-JNK, p-PERK and p-eIF2α. Conclusion These point out lactation period as maternal trigger for metabolic changes in the offspring. These changes may occur early and quietly contribute to obesity and associated pathologies in adulthood. Although in rodents the establishment of ARC neuronal projections occurs during the lactation period, in humans it occurs during the third trimester. Gestational diabetes and obesity in this period may contribute to impairment of energy homeostasis635682692FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ – CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO CIENTÍFICO E TECNOLOGICOFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ – CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO CIENTÍFICO E TECNOLOGICOsem informaçãosem informaçã

Hypothalamic Endoplasmic Reticulum Stress And Insulin Resistance In Offspring Of Mice Dams Fed High-fat Diet During Pregnancy And Lactation

Objective The goal of this study was to determine the presence early of markers of endoplasmic reticulum stress (ERS) and insulin resistance in the offspring from dams fed HFD (HFD-O) or standard chow diet (SC-O) during pregnancy and lactation. Materials/Methods To address this question, we evaluated the hypothalamic and hepatic tissues in recently weaned mice (d28) and the hypothalamus of newborn mice (d0) from dams fed HFD or SC during pregnancy and lactation. Results Body weight, adipose tissue mass, and food intake were more accentuated in HFD-O mice than in SC-O mice. In addition, intolerance to glucose and insulin was higher in HFD-O mice than in SC-O mice. Compared with SC-O mice, levels of hypothalamic IL1-β mRNA, NFκB protein, and p-JNK were increased in HFD-O mice. Furthermore, compared with SC-O mice, hypothalamic AKT phosphorylation after insulin challenge was reduced, while markers of ERS (p-PERK, p-eIF2α, XBP1s, GRP78, and GRP94) and p-AMPK were increased in the hypothalamic tissue of HFD-O at d28 but not at d0. These damages to hypothalamic signaling were accompanied by increased triglyceride deposits, activation of NFκB, p-JNK, p-PERK and p-eIF2α. Conclusion These point out lactation period as maternal trigger for metabolic changes in the offspring. These changes may occur early and quietly contribute to obesity and associated pathologies in adulthood. Although in rodents the establishment of ARC neuronal projections occurs during the lactation period, in humans it occurs during the third trimester. Gestational diabetes and obesity in this period may contribute to impairment of energy homeostasis. © 2014 Elsevier Inc. All rights reserved.635682692Baud, V., Liu, Z.G., Bennett, B., Signaling by proinflammatory cytokines: Oligomerization of traf2 and traf6 is sufficient for jnk and ikk activation and target gene induction via an amino-terminal effector domain (1999) Genes Dev, 13 (10), pp. 1297-1308Chu, W.M., Ostertag, D., Li, Z.W., Jnk2 and ikkbeta are required for activating the innate response to viral infection (1999) Immunity, 11 (6), pp. 721-731Saltiel, A.R., Insulin resistance in the defense against obesity (2012) Cell Metab, 15 (6), pp. 798-804De Souza, C.T., Araujo, E.P., Bordin, S., Consumption of a fat-rich diet activates a proinflammatory response and induces insulin resistance in the hypothalamus (2005) Endocrinology, 146 (10), pp. 4192-4199Cai, D., Yuan, M., Frantz, D.F., Local and systemic insulin resistance resulting from hepatic activation of ikk-beta and nf-kappab (2005) Nat Med, 11 (2), pp. 183-190Barbuio, R., Milanski, M., Bertolo, M.B., Infliximab reverses steatosis and improves insulin signal transduction in liver of rats fed a high-fat diet (2007) J Endocrinol, 194 (3), pp. 539-550Melo, A.M., Bittencourt, P., Nakutis, F.S., Solidago chilensis meyen hydroalcoholic extract reduces jnk/ikappab pathway activation and ameliorates insulin resistance in diet-induced obesity mice (2011) Exp Biol Med (Maywood), 236 (10), pp. 1147-1155Lalli, C.A., Pauli, J.R., Prada, P.O., Statin modulates insulin signaling and insulin resistance in liver and muscle of rats fed a high-fat diet (2008) Metabolism, 57 (1), pp. 57-65Moraes, J.C., Coope, A., Morari, J., High-fat diet induces apoptosis of hypothalamic neurons (2009) PLoS One, 4 (4), p. 5045McNay, D.E., Briancon, N., Kokoeva, M.V., Remodeling of the arcuate nucleus energy-balance circuit is inhibited in obese mice (2012) J Clin Invest, 122 (1), pp. 142-152Gupta, A., Srinivasan, M., Thamadilok, S., Hypothalamic alterations in fetuses of high fat diet-fed obese female rats (2009) J Endocrinol, 200 (3), pp. 293-300Ashino, N.G., Saito, K.N., Souza, F.D., Maternal high-fat feeding through pregnancy and lactation predisposes mouse offspring to molecular insulin resistance and fatty liver (2012) J Nutr Biochem, 23 (4), pp. 341-348Shankar, K., Zhong, Y., Kang, P., Maternal obesity promotes a proinflammatory signature in rat uterus and blastocyst (2011) Endocrinology, 152 (11), pp. 4158-4170Hotamisligil, G.S., Endoplasmic reticulum stress and the inflammatory basis of metabolic disease (2010) Cell, 140 (6), pp. 900-917Ryan, K.K., Woods, S.C., Seeley, R.J., Central nervous system mechanisms linking the consumption of palatable high-fat diets to the defense of greater adiposity (2012) Cell Metab, 15 (2), pp. 137-149Calegari, V.C., Torsoni, A.S., Vanzela, E.C., Inflammation of the hypothalamus leads to defective pancreatic islet function (2011) J Biol Chem, 286 (15), pp. 12870-12880Purkayastha, S., Zhang, H., Zhang, G., Neural dysregulation of peripheral insulin action and blood pressure by brain endoplasmic reticulum stress (2011) Proc Natl Acad Sci U S A, 108 (7), pp. 2939-2944Won, J.C., Jang, P.G., Namkoong, C., Central administration of an endoplasmic reticulum stress inducer inhibits the anorexigenic effects of leptin and insulin (2009) Obesity (Silver Spring), 17 (10), pp. 1861-1865Zhou, H., Zhang, K., Janciauskiene, S., Endoplasmic reticulum stress and lipid metabolism (2012) Biochem Res Int, 2012, p. 257528Milanski, M., Arruda, A.P., Coope, A., Inhibition of hypothalamic inflammation reverses diet-induced insulin resistance in the liver (2012) Diabetes, 61 (6), pp. 1455-1462Newberry, E.P., Xie, Y., Kennedy, S., Decreased hepatic triglyceride accumulation and altered fatty acid uptake in mice with deletion of the liver fatty acid-binding protein gene (2003) J Biol Chem, 278 (51), pp. 51664-51672Carr, T.P., Andresen, C.J., Rudel, L.L., Enzymatic determination of triglyceride, free cholesterol, and total cholesterol in tissue lipid extracts (1993) Clin Biochem, 26 (1), pp. 39-42Santos, G.A., Pereira, V.D., Roman, E.A., Hypothalamic inhibition of acetyl-coa carboxylase stimulates hepatic counter-regulatory response independent of ampk activation in rats (2013) PLoS One, 8 (4), p. 62669Yuan, M., Konstantopoulos, N., Lee, J., Reversal of obesity- and diet-induced insulin resistance with salicylates or targeted disruption of ikkbeta (2001) Science, 293 (5535), pp. 1673-1677Karin, M., Lin, A., Nf-kappab at the crossroads of life and death (2002) Nat Immunol, 3 (3), pp. 221-227Dutta, J., Fan, Y., Gupta, N., Current insights into the regulation of programmed cell death by nf-kappab (2006) Oncogene, 25 (51), pp. 6800-6816Li, J., Tang, Y., Cai, D., Ikkbeta/nf-kappab disrupts adult hypothalamic neural stem cells to mediate a neurodegenerative mechanism of dietary obesity and pre-diabetes (2012) Nat Cell Biol, 14 (10), pp. 999-1012Jiao, P., Ma, J., Feng, B., Ffa-induced adipocyte inflammation and insulin resistance: Involvement of ER stress and ikkbeta pathways (2011) Obesity (Silver Spring), 19 (3), pp. 483-491Nurnberger, S., Miller, I., Duvigneau, J.C., Impairment of endoplasmic reticulum in liver as an early consequence of the systemic inflammatory response in rats (2012) Am J Physiol Gastrointest Liver Physiol, 303 (12), pp. 1373-G1383Ozcan, L., Ergin, A.S., Lu, A., Endoplasmic reticulum stress plays a central role in development of leptin resistance (2009) Cell Metab, 9 (1), pp. 35-51Grayson, B.E., Levasseur, P.R., Williams, S.M., Changes in melanocortin expression and inflammatory pathways in fetal offspring of nonhuman primates fed a high-fat diet (2010) Endocrinology, 151 (4), pp. 1622-1632Hirosumi, J., Tuncman, G., Chang, L., A central role for jnk in obesity and insulin resistance (2002) Nature, 420 (6913), pp. 333-336Ozcan, U., Cao, Q., Yilmaz, E., Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes (2004) Science, 306 (5695), pp. 457-461Neville, M.C., Allen, J.C., Archer, P.C., Studies in human lactation: Milk volume and nutrient composition during weaning and lactogenesis (1991) Am J Clin Nutr, 54 (1), pp. 81-92Sohi, G., Revesz, A., Hardy, D.B., Nutritional mismatch in postnatal life of low birth weight rat offspring leads to increased phosphorylation of hepatic eukaryotic initiation factor 2 alpha in adulthood (2013) Metabolism, 62 (10), pp. 1367-1374Hummasti, S., Hotamisligil, G.S., Endoplasmic reticulum stress and inflammation in obesity and diabetes (2010) Circ Res, 107 (5), pp. 579-591Hotamisligil, G.S., Inflammation and endoplasmic reticulum stress in obesity and diabetes (2008) Int J Obes (Lond), 32 (SUPPL. 7), pp. 52-S54Cnop, M., Foufelle, F., Velloso, L.A., Endoplasmic reticulum stress, obesity and diabetes (2012) Trends Mol Med, 18 (1), pp. 59-68Gorski, J.N., Dunn-Meynell, A.A., Hartman, T.G., Postnatal environment overrides genetic and prenatal factors influencing offspring obesity and insulin resistance (2006) Am J Physiol Regul Integr Comp Physiol, 291 (3), pp. 768-R778Mayer, C.M., Belsham, D.D., Palmitate attenuates insulin signaling and induces endoplasmic reticulum stress and apoptosis in hypothalamic neurons: Rescue of resistance and apoptosis through adenosine 5' monophosphate-activated protein kinase activation (2010) Endocrinology, 151 (2), pp. 576-585Shoelson, S.E., Lee, J., Yuan, M., Inflammation and the ikk beta/i kappa b/nf-kappa b axis in obesity- and diet-induced insulin resistance (2003) Int J Obes Relat Metab Disord, 27 (SUPPL. 3), pp. 49-S52Kim, D.H., Woods, S.C., Seeley, R.J., Hypothalamic akt/pkb signaling in regulation of food intake (2012) Front Biosci (Schol Ed), 4, pp. 953-966Lee, J.Y., Kim, Y.R., Park, J., Inositol polyphosphate multikinase signaling in the regulation of metabolism (2012) Ann N y Acad Sci, 1271, pp. 68-74Minokoshi, Y., Alquier, T., Furukawa, N., Amp-kinase regulates food intake by responding to hormonal and nutrient signals in the hypothalamus (2004) Nature, 428 (6982), pp. 569-574Namkoong, C., Kim, M.S., Jang, P.G., Enhanced hypothalamic amp-activated protein kinase activity contributes to hyperphagia in diabetic rats (2005) Diabetes, 54 (1), pp. 63-68Stoppa, G.R., Cesquini, M., Roman, E.A., Intracerebroventricular injection of citrate inhibits hypothalamic ampk and modulates feeding behavior and peripheral insulin signaling (2008) J Endocrinol, 198 (1), pp. 157-168Andersson, U., Filipsson, K., Abbott, C.R., Amp-activated protein kinase plays a role in the control of food intake (2004) J Biol Chem, 279 (13), pp. 12005-12008Nazarians-Armavil, A., Menchella, J.A., Belsham, D.D., Cellular insulin resistance disrupts leptin-mediated control of neuronal signaling and transcription (2013) Mol Endocrinol, 27 (6), pp. 990-1003Stark, R., Ashley, S.E., Andrews, Z.B., Ampk and the neuroendocrine regulation of appetite and energy expenditure (2013) Mol Cell Endocrinol, 366 (2), pp. 215-223Kim, M.S., Lee, K.U., Role of hypothalamic 5'-amp-activated protein kinase in the regulation of food intake and energy homeostasis (2005) J Mol Med (Berl), 83 (7), pp. 514-520Breton, C., The hypothalamus-adipose axis is a key target of developmental programming by maternal nutritional manipulation (2013) J Endocrinol, 216 (2), pp. 19-R31Basseri, S., Austin, R.C., Endoplasmic reticulum stress and lipid metabolism: Mechanisms and therapeutic potential (2012) Biochem Res Int, 2012, p. 841362Fu, S., Yang, L., Li, P., Aberrant lipid metabolism disrupts calcium homeostasis causing liver endoplasmic reticulum stress in obesity (2011) Nature, 473 (7348), pp. 528-531Boden, G., She, P., Mozzoli, M., Free fatty acids produce insulin resistance and activate the proinflammatory nuclear factor-kappab pathway in rat liver (2005) Diabetes, 54 (12), pp. 3458-3465Muse, E.D., Lam, T.K., Scherer, P.E., Hypothalamic resistin induces hepatic insulin resistance (2007) J Clin Invest, 117 (6), pp. 1670-1678Prada, P.O., Zecchin, H.G., Gasparetti, A.L., Western diet modulates insulin signaling, c-jun n-terminal kinase activity, and insulin receptor substrate-1ser307 phosphorylation in a tissue-specific fashion (2005) Endocrinology, 146 (3), pp. 1576-1587Koutcherov, Y., Mai, J.K., Paxinos, G., Hypothalamus of the human fetus (2003) J Chem Neuroanat, 26 (4), pp. 253-270Vogt, M.C., Paeger, L., Hess, S., Neonatal insulin action impairs hypothalamic neurocircuit formation in response to maternal high-fat feeding (2014) Cell, 156 (3), pp. 495-50