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Gorr T.A.,Institute of Veterinary Physiology | Wichmann D.,Institute of Veterinary Physiology | Hu J.,Institute of Veterinary Physiology | Hermes-Lima M.,University of Brasilia | And 9 more authors.
Physiological and Biochemical Zoology | Year: 2010

Many invertebrates and ectothermic vertebrates successfully cope with a fluctuating supply of ambient oxygen - and consequently, a highly variable tissue oxygenation - through increasing their antioxidant barriers. During chronic deprivation of oxygen, however, the hypometabolic defense mode of the fruit fly Drosophila, the hypoxia-induced behavioral hypothermia of the crayfish Pacifastacus leniusculus, and the production of ethanol during anoxia by the crucian carp Carassius carassius all indicate that these animals are also capable of utilizing a suite of genetic and physiological defenses to survive otherwise lethal reductions in tissue oxygenation. Normally, much of an organism's gene response to hypoxia is orchestrated via the hypoxia-inducible transcription factor HIF. Recent developments expand our view of HIF function even further by highlighting regulatory roles for HIF in the hypometabolism of insects, in the molting and the normoxic immune response of crustaceans, and in the control - via the downstream effector gene erythropoietin - of the hypoxic ventilatory response and pulmonary hypertension in mammals. These and related topics were collectively presented by the authors in a symposium of the 2008 ICA-CBP conference at Mara National Reserve, Kenya, Africa. This synthesis article communicates the essence of the symposium presentations to the wider community. © 2010 by The University of Chicago. All rights reserved. Source

Padrutt I.,Clinic for Small Animal Internal Medicine | Lutz T.A.,Institute of Veterinary Physiology | Reusch C.E.,Clinic for Small Animal Internal Medicine | Zini E.,Clinic for Small Animal Internal Medicine
Research in Veterinary Science | Year: 2015

Incretin analogues and inhibitors of the breakdown of endogenous incretins are antidiabetic drugs that increase β-cell proliferation and glucose-stimulated insulin secretion in rodents and humans. Objectives were to test whether exenatide, exenatide extended-release, and sitagliptin can be safely used in cats, to identify the most effective drug, and to test the effects of prolonged exenatide extended-release administration. Three cats each were given exenatide (0.2-2 μg/kg, q12h, subcutaneously, 5 days), exenatide extended-release (40-400 μg/kg, subcutaneously, once), and sitagliptin (1-10 mg/kg, q24h, orally, 5 days). Before and after treatment, glucose, insulin and glucagon areas under the curve (AUC) were assessed by meal response tests (MRT). Exenatide increased insulin AUC by 224%, 258%, 331% and 93%, exenatide extended-release by 127%, 169%, 178% and 95%, and sitagliptin by 32%, 69%, 62%, and 43%, respectively. The tested drugs are safe to use in cats and enhance insulin secretion. Incretin-based therapy may be beneficial in cats with diabetes mellitus. © 2014 Elsevier Ltd. Source

Pappo O.,Rabin Medical Center | Ben-Ari Z.,Rabin Medical Center | Ben-Ari Z.,Liver Institute | Shevtsov E.,Rabin Medical Center | And 6 more authors.
Canadian Journal of Physiology and Pharmacology | Year: 2010

Ischemia-reperfusion injury (I/R) is the main cause of primary graft nonfunction. Our aim was to evaluate the effect of excessive versus acute administration of erythropoietin (EPO) in attenuating the hepatic injury induced by I/R in mice. The effect of segmental (70%) hepatic ischemia was evaluated in a transgenic mouse line with constitutive overexpression of human EPO cDNA and in wild-type (WT) mice. Mice were randomly allocated to 5 main experimental groups: (i) WT-sham, (ii) WT ischemia, (iii) WT ischemia + recombinant human erythropoietin (rhEPO), (iv) transgenic-sham, and (v) transgenic ischemia. The EPO-pretreated mice showed a significant reduction in liver enzyme levels and intrahepatic caspase-3 activity and fewer apoptotic hepatocytes (p < 0.05 for all) compared with the WT untreated I/R group. EPO decreased c-Jun N-terminal kinase (JNK) phosphorylation and nuclear factor-kB (NF-kB) expression during I/R. In transgenic I/R livers, baseline histology showed diffused hepatic injury, and no significant beneficial effect was noted between the WT untreated and the transgenic I/R mice. In conclusion, acute pretreatment with EPO in WT mice attenuated in vivo I/R liver injury. However, in excessive EPO overexpression, the initial liver injury abolished the beneficial effect of EPO. These findings have important implications for the potential use of acute EPO in I/R injury during liver transplantation. Source

Eichelmann M.A.,University of Zurich | Fischer D.,University of Zurich | Heilmann M.,University of Zurich | Bernstorf Hydeskov H.,University of Zurich | And 19 more authors.
International Zoo Yearbook | Year: 2012

Previous reports in the literature indicate that primate species differ in their iron metabolism. Analyses were carried out of 229 serum samples of 18 different species, including marmosets, lemurs, woolly monkeys, colobines, macaques, baboons and great apes, for transferrin saturation (%TS), an indicator of iron absorption. In correspondence with our expectations based on the literature, lemurs and marmosets had significantly higher %TS values than great apes and macaques/baboons. The findings corroborate patterns previously described in individual studies, and underline that further efforts should be made to understand the reasons and consequences of these differences in iron metabolism. © 2012 The Author. International Zoo Yearbook © 2012 The Zoological Society of London. Source

Rozenberg I.,Institute Of Physiology Ir | Rozenberg I.,University of Zurich | Sluka S.H.M.,Institute Of Physiology Ir | Sluka S.H.M.,University of Zurich | And 21 more authors.
Arteriosclerosis, Thrombosis, and Vascular Biology | Year: 2010

Objective-: Enhanced endothelial permeability leading to intimal accumulation of low-density lipoproteins (LDL) stimulates the formation of atherosclerotic lesions. Histamine is known to increase vascular permeability. Whether this affects the formation of atherosclerotic lesions, however, remains elusive.Methods and results-: Apolipoprotein E-null (ApoE) mice treated with a histamine H1 receptor but not an H2 receptor antagonist developed 40% fewer atherosclerotic lesions in the aorta than placebo-treated controls. Similarly, genetic deletion of the H1 but not the H2 receptor resulted in a 60% reduction of lesions compared with ApoE controls. The H1 receptor enhanced LDL permeability and lipid accumulation in the aorta, whereas plasma lipoprotein levels remained unaltered. In contrast, the H1 receptor did not affect proliferation and migration of vascular smooth muscle cells. Bone marrow transplantation confirmed that the formation of atherosclerotic lesions depended on the H1 receptor in vascular cells, whereas its presence in bone marrow-derived cells was irrelevant for plaque development. Mice expressing the H1 receptor exhibited higher levels of the chemokine (C-C motif) ligand 5 and higher numbers of macrophages and T-helper lymphocytes in plaques, higher numbers of circulating lymphocytes, and larger spleens. Conclusion-: These data indicate that H1 but not H2 receptor activation drives the formation of atherosclerotic lesions through an increased vascular permeability for LDL, which is associated with an enhanced secondary aortic and systemic inflammation. These data open novel perspectives for the prevention and treatment of atherosclerotic vascular disease. © 2010 American Heart Association, Inc. Source

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