Castilla A.M.,Ministry of Environment |
Huey R.B.,University of Washington |
Calvete J.J.,Institute of Biomedicine of Valencia |
Richer R.,Cornell College |
Al-Hemaidi A.H.M.,Ministry of Environment
Journal of Arid Environments
We review the literature on the geographic and taxonomic diversity of species of lizards and scorpions that are involved in predator-prey interactions. Somewhat surprisingly, lizards are often the predators in these interactions. Consequently, our goals were to evaluate whether lizard predators had evolved morphological or physiological resistance to scorpion venom or whether the rely on behavioral evasions, and also to document co-evolutionary patterns. Diverse lizards prey on scorpions, but most studies are surprisingly anecdotal. Whether lizard predators tolerate scorpion venom is largely unexplored. Our review highlights opportunities for studies of the evolution of tolerance to scorpion venom by lizards and of the ecology and evolution of lizard-scorpion interactions in arid zones. Progress will be facilitated by collaborations between experts in ecology and toxicology, and by incorporating molecular approaches such as proteomics and transcriptomics. Much is to be learned about scorpion venoms and their effects on predators, with potential benefits to humans. © 2014 Elsevier Ltd. All rights reserved. Source
Hallmann A.-L.,University of Munster |
Hallmann A.-L.,Max Planck Institute for Molecular Biomedicine |
Arauzo-Bravo M.J.,Biodonostia Health Research Institute |
Arauzo-Bravo M.J.,Ikerbasque |
And 14 more authors.
Stem Cell Research
Reprogramming technology enables the production of neural progenitor cells (NPCs) from somatic cells by direct transdifferentiation. However, little is known on how neural programs in these induced neural stem cells (iNSCs) differ from those of alternative stem cell populations in vitro and in vivo. Here, we performed transcriptome analyses on murine iNSCs in comparison to brain-derived neural stem cells (NSCs) and pluripotent stem cell-derived NPCs, which revealed distinct global, neural, metabolic and cell cycle-associated marks in these populations. iNSCs carried a hindbrain/posterior cell identity, which could be shifted towards caudal, partially to rostral but not towards ventral fates in vitro. iNSCs survived after transplantation into the rodent brain and exhibited in vivo-characteristics, neural and metabolic programs similar to transplanted NSCs. However, iNSCs vastly retained caudal identities demonstrating cell-autonomy of regional programs in vivo. These data could have significant implications for a variety of in vitro- and in vivo-applications using iNSCs. © 2016. Source
Redondo S.,Complutense University of Madrid |
Ruiz E.,Complutense University of Madrid |
Gordillo-Moscoso A.,Complutense University of Madrid |
Navarro-Dorado J.,Complutense University of Madrid |
And 6 more authors.
Aims/hypothesis: Inflammation is a common feature in cardiovascular diseases, including diabetes mellitus. In addition to the well-known inflammatory role of cyclooxygenase-2 (COX-2), this protein has also been implicated in apoptosis resistance in tumour cells. Vascular smooth muscle cells (VSMC) from diabetic patients are also resistant to apoptosis because of an increased abundance of B cell lymphoma 2 protein (BCL2). In this work, we investigated whether overproduction of COX-2 was involved in the resistance to apoptosis in VSMC fromdiabetic patients. Methods: VSMC were obtained from internal mammary arteries from patients who had undergone coronary artery bypass graft surgery. Apoptosis was measured by DNA fragmentation, BCL2 degradation and cytochrome c release. Results: Apoptosis induced by C-reactive protein in cells from non-diabetic patients was mediated by COX-2. VSMC from diabetic patients showed higher basal levels of COX-2 compared with those from non-diabetic patients. Transfection of VSMC from non-diabetic patients with a plasmid containing COX-2 (also known as PTGS2) increased basal production of COX-2 and BCL2 and mimicked the resistance to apoptosis that occurs in diabetic patients. We also found a significant correlation (R=0.846, p=0.016) between COX-2 and BCL2 production in arterial rings from diabetic patients measured by confocal microscopy. However, inhibition of COX-2 production by small interfering RNA proved unable to reverse BCL2 production in diabetic VSMC. Conclusions/interpretation: These results suggest a link between inflammation (COX-2) and apoptosis resistance (BCL2) in the arteries of diabetic patients. This relationship is not causative and the common production of these two proteins may be co-regulated by shared regulatory elements in diabetes. © Springer-Verlag 2010. Source
Haworth A.,Neurogenetics Unit |
Bertram L.,Max Planck Institute for Molecular Genetics |
Carrera P.,San Raffaele Scientific Institute |
Elson J.L.,Northumbria University |
And 21 more authors.
The rate of DNA variation discovery has accelerated the need to collate, store and interpret the data in a standardised coherent way and is becoming a critical step in maximising the impact of discovery on the understanding and treatment of human disease. This particularly applies to the field of neurology as neurological function is impaired in many human disorders. Furthermore, the field of neurogenetics has been proven to show remarkably complex genotype-to-phenotype relationships. To facilitate the collection of DNA sequence variation pertaining to neurogenetic disorders, we have initiated the "Neurogenetics Consortium" under the umbrella of the Human Variome Project. The Consortium's founding group consisted of basic researchers, clinicians, informaticians and database creators. This report outlines the strategic aims established at the preliminary meetings of the Neurogenetics Consortium and calls for the involvement of the wider neurogenetic community in enabling the development of this important resource. © Springer-Verlag 2011. Source
Diaz-Moralli S.,University of Barcelona |
Ramos-Montoya A.,University of Barcelona |
Marin S.,University of Barcelona |
Fernandez-Alvarez A.,Institute of Biomedicine of Valencia |
And 3 more authors.
American Journal of Physiology - Endocrinology and Metabolism
Carbohydrate response element-binding protein (ChREBP) is a transcription factor that mediates glucose signaling in mammalian liver, leading to the expression of different glycolytic and lipogenic genes, such as pyruvate kinase (L-PK) and fatty acid synthase (FAS). The current model for ChREBP activation in response to sugar phosphates holds that glucose metabolization to xylulose 5-phosphate (X-5-P) triggers the activation of protein phosphatase 2A, which dephosphorylates ChREBP and leads to its nuclear translocation and activation. However, evidence indicates that glucose 6-phosphate (G-6-P) is the most likely signal metabolite for the glucose-induced transcription of these genes. The glucose derivative that is responsible for carbohydrate-dependent gene expression remains to be identified. The difficulties in measuring G-6-P and X-5-P concentrations simultaneously and in changing them independently have hindered such identification. To discriminate between these possibilities, we adapted a liquid chromatography mass spectrometry method to identify and quantify sugar phosphates in human hepatocarcinoma cells (Hep G2) and rat hepatocytes in response to different carbon sources and in the presence/absence of a glucose-6-phosphate dehydrogenase inhibitor. We also used this method to demonstrate that these cells could not metabolize 2-deoxyglucose beyond 2-deoxyglucose-6-phosphate. The simultaneous quantification of sugar phosphates and FAS and L-PK expression levels demonstrated that both X-5-P and G-6-P play a role in the modulation of gene expression. In conclusion, this report presents for the first time a single mechanism that incorporates the effects of X-5-P and G-6-P on the enhancement of the expression of carbohydrate-responsive genes. © 2012 the American Physiological Society. Source