Esther Piltcher Haber

Hebrew University of Jerusalem

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Rui Curi

Instituto Butantan

ÂR

Ângelo Rafael Carpinelli

Universidade de São Paulo

Carla Roberta de Oliveira Carvalho

Universidade de São Paulo

Sandro Massao Hirabara

Universidade Cruzeiro do Sul

Rafael Nesher

Hadassah Medical Center

Nikolaos Grigoriadis

AHEPA University Hospital

Erol Cerasi

Hadassah Medical Center

Hanna Rosenmann

Hadassah Medical Center

Maria Cristina Picinato Medeiros de Araújo

Universidade de São Paulo

W. S. Lee

Harvard University Press

Cooperative Institutions

Universidade de São Paulo

Harvard University Press

Hadassah Medical Center

Hebrew University of Jerusalem

Ben-Gurion University of the Negev

University Medical Center

Soroka Medical Center

Hadassah Academic College

Harvard University

Karolinska Institutet

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The stylistic role of the anticipatory genitive construction in sumerian literature

Revue d assyriologie et d archéologie orientale (2011)

Esther Piltcher Haber

Résumé La construction génitivale inversée est assurément une construction morpho-syntaxique sumérienne originale; elle dérive de la construction génitivale standard et est employée comme outil stylistique dans la littérature. La construction génitivale inversée constitue un outil particulier pour mettre l’accent sur le nom régi, en le déplaçant au début de la construction génitivale. Une des fonctions stylistiques les plus significatives du génitif inverse est la singularisation d’un ou de plusieurs mots clés à l’intérieur d’une composition littéraire, en le(s) plaçant au début de la phrase. Un examen des textes sumériens littéraires montre que ce phénomène, à la fois grammatical et stylistique, est largement répandu. Dans ces compositions, le mot-clé apparaît souvent au début de la phrase, qu’il soit sujet, objet ou mot régi, et cela en dépit de l’ordre des mots habituel en sumérien.

Genitive case

10.3917/assy.103.0037

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Diabetes associated cell stress and dysfunction: role of mitochondrial and non‐mitochondrial ROS production and activity

The Journal of Physiology (2007)

Philip Newsholme Esther Piltcher Haber Sandro Massao Hirabara Eduardo Rebelato J. Procópio

It is now widely accepted, given the current weight of experimental evidence, that reactive oxygen species (ROS) contribute to cell and tissue dysfunction and damage caused by glucolipotoxicity in diabetes. The source of ROS in the insulin secreting pancreatic beta-cells and in the cells which are targets for insulin action has been considered to be the mitochondrial electron transport chain. While this source is undoubtably important, we provide additional information and evidence for NADPH oxidase-dependent generation of ROS both in pancreatic beta-cells and in insulin sensitive cells. While mitochondrial ROS generation may be important for regulation of mitochondrial uncoupling protein (UCP) activity and thus disruption of cellular energy metabolism, the NADPH oxidase associated ROS may alter parameters of signal transduction, insulin secretion, insulin action and cell proliferation or cell death. Thus NADPH oxidase may be a useful target for intervention strategies based on reversing the negative impact of glucolipotoxicity in diabetes.

Mitochondrial ROS

10.1113/jphysiol.2007.135871

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CARACTERIZAÇÃO DA LIGAÇÃO DO HORMÔNIO DE CRESCIMENTO HUMANO À MEMBRANA MICROSSOMAL DE FÍGADO DE MULHER GRÁVIDA

Esther Piltcher Haber

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Melatonin inhibits insulin secretion and decreases PKA levels without interfering with glucose metabolism in rat pancreatic islets

Journal of Pineal Research (2002)

Maria Cecília Picinato Esther Piltcher Haber José Cipolla‐Neto Rui Curi Carla Roberta de Oliveira Carvalho

The effect of melatonin (0.1 microM) on freshly isolated islets from adult rats was investigated. Melatonin caused a marked decrease of insulin secretion by islets in response to glucose. The mechanism involved was then examined. Melatonin did not interfere with glucose metabolism as indicated by the measurement of glucose oxidation. However, the content of the protein kinase A (PKA) catalytic alpha-subunit was significantly decreased in islets exposed to melatonin for 1 hr in the presence of 8.3 mM glucose, whereas that of the protein kinase C (PKC) alpha-subunit remained unchanged. Melatonin also inhibited forskolin-induced insulin secretion, a well known activator of adenylate cyclase (AC) activity. This may explain the low content of insulin found in islets incubated in the presence of melatonin for 3 hr. In fact, 3',5' -cyclic adenosine monophosphate (cAMP), a product of AC activity, stimulates insulin synthesis. These findings led us to postulate that a down-regulation of the PKA signaling pathway may be the mechanism involved in the melatonin inhibition of the process of glucose-induced insulin secretion.

Pancreatic Islets

Carbohydrate Metabolism

10.1034/j.1600-079x.2002.02903.x

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Citations (127)

E2A-BP, A protein binding to E12/E47, inhibits differentiation of myoblasts

Wilson O. Endege Mukesh K. Jain Chih-Lin Hsieh C J Kho Nicholas E. S. Sibinga

C2C12

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Corrigendum to “Efficacy and safety of immunization with phosphorylated tau against neurofibrillary tangles in mice” [Exp. Neurol. 224/2 (2010) 472–485]

Experimental Neurology (2013)

Moran Boimel Nikolaos Grigoriadis Athanasios Lourbopoulos Esther Piltcher Haber Oded Abramsky

10.1016/j.expneurol.2013.03.013

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Palmitate acutely raises glycogen synthesis in rat soleus muscle by a mechanism that requires its metabolization (Randle cycle)

FEBS Letters (2003)

Sandro Massao Hirabara Carla Roberta de Oliveira Carvalho José Roberto Mendonça Esther Piltcher Haber Luiz Cláudio Fernandes

The acute effect of palmitate on glucose metabolism in rat skeletal muscle was examined. Soleus muscles from Wistar male rats were incubated in Krebs–Ringer bicarbonate buffer, for 1 h, in the absence or presence of 10 mU/ml insulin and 0, 50 or 100 μM palmitate. Palmitate increased the insulin‐stimulated [ 14 C]glycogen synthesis, decreased lactate production, and did not alter D ‐[U‐ 14 C]glucose decarboxylation and 2‐deoxy‐ D ‐[2,6‐ 3 H]glucose uptake. This fatty acid decreased the conversion of pyruvate to lactate and [1‐ 14 C]pyruvate decarboxylation and increased 14 CO 2 produced from [2‐ 14 C]pyruvate. Palmitate reduced insulin‐stimulated phosphorylation of insulin receptor substrate‐1/2, Akt, and p44/42 mitogen‐activated protein kinases. Bromopalmitate, a non‐metabolizable analogue of palmitate, reduced [ 14 C]glycogen synthesis. A strong correlation was found between [U‐ 14 C]palmitate decarboxylation and [ 14 C]glycogen synthesis ( r =0.99). Also, palmitate increased intracellular content of glucose 6‐phosphate in the presence of insulin. These results led us to postulate that palmitate acutely potentiates insulin‐stimulated glycogen synthesis by a mechanism that requires its metabolization (Randle cycle). The inhibitory effect of palmitate on insulin‐stimulated protein phosphorylation might play an important role for the development of insulin resistance in conditions of chronic exposure to high levels of fatty acids.

Decarboxylation

10.1016/s0014-5793(03)00316-8

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Citations (54)

Potential roles of tyrosine phosphatase mkp-1 in the proliferation of rat vascular smooth muscle cells

Kwok‐On Lai H. Wang W. S. Lee M. E. Lee Esther Piltcher Haber

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Glial cell line-derived neurotrophic factor (GDNF) induced migration of spermatogonial cells in vitro via MEK and NF-kB pathways

Differentiation (2013)

Mahmoud Huleihel Emma Fadlon A. AbuElhija Esther Piltcher Haber Eitan Lunenfeld

10.1016/j.diff.2013.06.005