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Braverman Y.,Kimron Veterinary Institute | Frish K.,Kimron Veterinary Institute | Reis M.,Bar - Ilan University | Mumcuoglu K.Y.,The Institute for Medical Research Israel Canada
Entomologia Generalis | Year: 2012

Host preference determines which host will be bitten and therefore potentially be infected with vectored pathogenic microorganisms by hematophagous arthropods such as Culicoides. In Israel, the feeding behavior of 8 out of 60 Culicoides species was confirmed by using the precipitin tests. In the present study several morphometric parameters, which characterize bird and mammal feeders were used. By means of the number of antennomer bearing sensilla coeloconica, the following fourteen probable mammal feeders could be detected: Culicoides derisor, Culicoides fagineus, Culicoides fascipennis, Culicoides imicola, Culicoides montanus, Culicoides newsteadi, Culicoides obsoletus, Culicoides pulicaris, Culicoides punctatus, Culicoides puncticollis, Culicoides schultzei group, Culicoides shaklawensis, Culicoides pallidicornis, and Culicoides vitreipennis. In addition, the following eighteen probable bird feeders were identified: Culicoides begueti, Culicoides brunnicans, Culicoides cataneii, Culicoides circumscriptus, Culicoides kibunensis, Culicoides distinctipennis, Culicoides gejgelensis, Culicoides haranti, Culicoides indistinctus, Culicoides odiatus, Culicoides maritimus, Culicoides festivipennis, Culicoides pseudopallidus, Culicoides griseidorsum, Culicoides sejfadinei, Culicoides simulator and Culicoides univittatus. The probable bird feeders possessed a significantly larger third palpal segment. The values of the antennal ratio in probable feeders on birds were signifi-cantly higher than those in probable mammal feeders. The number of bulb-shaped sensilla in the pit of the third palpal segment was found unreliable for determining host groups. © 2012 E. Schweizerbart'sche Verlagsbuchhandlung, D-70176 Stuttgart. Source


Wikstrom J.D.,Hebrew University of Jerusalem | Israeli T.,Hebrew University of Jerusalem | Bachar-Wikstrom E.,Hebrew University of Jerusalem | Swisa A.,The Institute for Medical Research Israel Canada | And 6 more authors.
Molecular Endocrinology | Year: 2013

Experimental lipotoxicity constitutes a model for β-cell demise induced by metabolic stress in obesity and type 2 diabetes. Fatty acid excess induces endoplasmic reticulum (ER) stress, which is accompanied by ER morphological changes whose mechanisms and relevance are unknown. We found that the GTPase dynamin-related protein 1 (DRP1), a key regulator of mitochondrial fission, is an ER resident regulating ER morphology in stressed β-cells. Inhibition of DRP1 activity using a GTP hydrolysis-defective mutant (Ad-K38A) attenuated fatty acid-induced ER expansion and mitochondrial fission. Strikingly, stimulating the key energy-sensor AMP-activated protein kinase (AMPK) increased the phosphorylation at the anti-fission site Serine 637 and largely prevented the alterations in ER and mitochondrial morphology. Expression of a DRP1 mutant resistant to phosphorylation at this position partially prevented the recovery of ER and mitochondrial morphology by AMPK. Fatty acid-induced ER enlargement was associated with proinsulin retention in the ER, together with increased proinsulin/insulin ratio. Stimulation of AMPK prevented these alterations, as well as mitochondrial fragmentation and apoptosis. In summary, DRP1 regulation by AMPK delineates a novel pathway controlling ER and mitochondrial morphology, thereby modulating the response of β-cells to metabolic stress. DRP1 may thus function as a node integrating signals from stress regulators, such as AMPK, to coordinate organelle shape and function. © 2013 by The Endocrine Society. Source


Gur C.,The Institute for Medical Research Israel Canada | Gur C.,Hebrew University of Jerusalem | Enk J.,The Institute for Medical Research Israel Canada | Enk J.,Hebrew University of Jerusalem | And 15 more authors.
PLoS ONE | Year: 2013

NK cells rapidly kill tumor cells, virus infected cells and even self cells. This is mediated via killer receptors, among which NKp46 (NCR1 in mice) is prominent. We have recently demonstrated that in type 1 diabetes (T1D) NK cells accumulate in the diseased pancreas and that they manifest a hyporesponsive phenotype. In addition, we found that NKp46 recognizes an unknown ligand expressed by beta cells derived from humans and mice and that blocking of NKp46 activity prevented diabetes development. Here we investigated the properties of the unknown NKp46 ligand. We show that the NKp46 ligand is mainly located in insulin granules and that it is constitutively secreted. Following glucose stimulation the NKp46 ligand translocates to the cell membrane and its secretion decreases. We further demonstrate by using several modalities that the unknown NKp46 ligand is not insulin. Finally, we studied the expression of the NKp46 ligand in type 2 diabetes (T2D) using 3 different in vivo models and 2 species; mice and gerbils. We demonstrate that the expression of the NKp46 ligand is decreased in all models of T2D studied, suggesting that NKp46 is not involved in T2D. © 2013 Gur et al. Source

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