Assessment of habitat quality and landscape connectivity for forest-dependent cracids in the Sierra Madre del Sur Mesoamerican biological corridor, Mexico

Assessing landscape connectivity allows us to identify critical areas that impede or facilitate the movement of organisms and their genes and to plan their conservation and management. In this article, we assessed landscape connectivity and ecological condition of the habitat patches of a highly biodiverse region in Chiapas, Mexico. We employed data of three cracid species with different characteristics in habitat use and mobility. The habitat map of each species was derived from a spatial intersection of the models of potential distribution and a high-resolution map of current land cover and land use. The ecological condition of vegetation types was evaluated using 75 field plots. Structure of landscape was estimated by fragmentation metrics, while functional connectivity was assessed using spatially explicit graph analysis. The extent of suitable habitat for Oreophasis derbianus, Penelopina nigra, and Penelope purpurascens correspond to 25%, 46%, and 55% of the study area (5,185.6 km2), respectively. Although the pine-oak forests were the most fragmented vegetation type, habitats of the three species were well connected, and only 4% to 9% of the fragments located on the periphery of the corridor had low connectivity. Landscape connectivity depends mainly on land uses with an intermediate and lower ecological condition (secondary forests and coffee agroforestry systems). Therefore, we suggest that in addition to promoting the improvement in connectivity in fragmented forests, conservation efforts should be aimed at preventing the conversion of mature forests into agricultural uses and maintaining agroforestry systems

Complete Genome Sequence of a bla OXA-58 -Producing Acinetobacter baumannii Strain Isolated from a Mexican Hospital

ABSTRACT In this study, we present the complete genome sequence of a blaOXA-58- producing Acinetobacter baumannii strain, sampled from a Mexican hospital and not related to the international clone

ELEMENTOS SOBRE LA HISTORIA DEL CONCEPTO DE DESARROLLO SEGÚN LOS ECONOMISTAS THEOTONIO DOS SANTOS Y GILBERT RIST

El artículo tiene como propósito presentar la percepción y las inquietudes que dos importantes pensadores económicos ofrecen a través de sus obras sobre dependencia económica y desarrollo, como punto de partida en la reflexión que se ha iniciado sobre algunos conceptos que se convierten en clave para una discusión o debate. El estudio de una de las obras de Theotonio Dos Santos y otra de Gilbert Rist sobre la temática mencionada, le deja al grupo de investigación importantes inquietudes para la construcción de un pensamiento propio y alternativo

Linking of psoriasis with osteopenia and osteoporosis: A cross‑sectional study

Psoriasis is a multisystem disease which has been related to vitamin‑D deficiency through chronic inflammation. This psoriasis‑related inflammatory state and vitamin‑D deficiency may induce bone mineral density loss. The purpose of this study is to assess the relationship of psoriasis with bone mineral density, by comparing psoriatic patients with healthy controls and patients with osteopenia/osteoporosis. Psoriatic patients showed worse hip and lumbar spine bone mineral density levels than healthy controls (P = 0.001) and better levels than osteoporotic patients (P < 0.001). Multivariate analysis demonstrated a negative association of age and a positive association of body mass index in hip bone mineral density in psoriatic patients. Bone mineral density levels in psoriatic patients are situated halfway between healthy controls and patients with osteopenia/osteoporosis. In addition, the higher body mass index in patients with psoriasis appears to confer a protective effect against further development of lower bone mineral density

Charged-particle multiplicities in pp interactions at root s=900 GeV measured with the ATLAS detector at the LHC

The first measurements from proton-proton collisions recorded with the ATLAS detector at the LHC are presented. Data were collected in December 2009 using a minimum-bias trigger during collisions at a centre-of-mass energy of 900 GeV. The charged-particle multiplicity, its dependence on transverse momentum and pseudorapidity, and the relationship between mean transverse momentum and charged-particle multiplicity are measured for events with at least one charged particle in the kinematic range |eta|500 MeV. The measurements are compared to Monte Carlo models of proton-proton collisions and to results from other experiments at the same centre-of-mass energy. The charged-particle multiplicity per event and unit of pseudorapidity at eta = 0 is measured to be 1.333 +/- 0.003 (stat.) +/- 0.040 (syst.), which is 5-15% higher than the Monte Carlo models predict

Renal tubule Cpt1a overexpression protects from kidney fibrosis by restoring mitochondrial homeostasis

Chronic kidney disease (CKD) remains a major epidemiological, clinical, and biomedical challenge. During CKD, renal tubular epithelial cells (TECs) present a persistent inflammatory and profibrotic response. Fatty acid oxidation (FAO), the main source of energy for TECs, is reduced in kidney fibrosis and contributes to its pathogenesis. To determine whether gain of function in FAO (FAO-GOF) could protect from fibrosis, we generated a conditional transgenic mouse model with overexpression of the fatty acid shuttling enzyme carnitine palmitoyl-transferase 1A (CPT1A) in TECs. Cpt1a-knockin (CPT1A-KI) mice subjected to 3 models of renal fibrosis (unilateral ureteral obstruction, folic acid nephropathy [FAN], and adenine-induced nephrotoxicity) exhibited decreased expression of fibrotic markers, a blunted proinflammatory response, and reduced epithelial cell damage and macrophage influx. Protection from fibrosis was also observed when Cpt1a overexpression was induced after FAN. FAO-GOF restored oxidative metabolism and mitochondrial number and enhanced bioenergetics, increasing palmitate oxidation and ATP levels, changes that were also recapitulated in TECs exposed to profibrotic stimuli. Studies in patients showed decreased CPT1 levels and increased accumulation of short- and middle-chain acylcarnitines, reflecting impaired FAO in human CKD. We propose that strategies based on FAO-GOF may constitute powerful alternatives to combat fibrosis inherent to CKD

Efecto del cloruro de cadmio sobre la expresión del represor transcripcional REST/NRSF y su gen blanco CDH1 en tejido pulmonar de ratones ICR-CD1

REST (RE1-Silencing Transcription factor) is a transcription factor with zinc fingers that represses its transcriptional targets through its interaction with the RE1 (Restrictive Element 1) sequence. Although some metals such as cadmium can alter protein function by competing with zinc, studies at the molecular level have not been performed to determine this effect on REST. The CDH1 gene is a transcriptional target of REST that codes for the cell adhesion glycoprotein E-cadherin and the deregulation of its expression has been associated with the cancerous process. The objective of this work was to evaluate the effect of exposure to 1.3 µM/3 days with CdCl2 in ICR-CD1 mice on the levels of REST and its target gene CDH1 in lung tissue. CDH1 mRNA levels were determined by RT-PCR, while E-cadherin and REST protein levels were assessed by Western blot. After CdCl2 treatment, the levels of CDH1 and its product E-cadherin increased in relation to the loss of REST expression. In conclusion, cadmium promotes a decrease in REST at the protein level, as well as an increase in the levels of CDH1 messenger RNA and its E-cadherin product. The increase in E-cadherin is probably due to CDH1 transcriptional relaxation mediated by loss of REST expression.REST (RE1-Silencing Transcription factor) es un factor de transcripción con dedos de zinc que reprime a sus blancos transcripcionales a través de su interacción con la secuencia RE1 (Restrictive Element 1). Aunque algunos metales como el cadmio pueden alterar la función de proteínas al competir con el zinc, no se han realizado estudios a nivel molecular para para determinar dicho efecto sobre REST. El gen CDH1 es un blanco transcripcional de REST que codifica para la glicoproteína de adhesión celular E-cadherina y la desregulación de su expresión ha sido asociada al proceso canceroso. El objetivo de este trabajo fue evaluar el efecto de la exposición a 1.3 µM/3 días con CdCl2 en ratones ICR-CD1 sobre los niveles de REST y de su gen blanco CDH1 en tejido pulmonar. Los niveles del mRNA de CDH1 se determinaron por RT-PCR, mientras que los niveles de las proteínas E-cadherina y REST se evaluaron mediante Western blot. Después del tratamiento con CdCl2 los niveles de CDH1 y de su producto E-cadherina se incrementaron en relación con la pérdida de la expresión de REST. En conclusión, el cadmio promueve la disminución de REST a nivel de proteína, así como el incremento de los niveles de ARN mensajero de CDH1 y de su producto E-cadherina. El incremento de E-cadherina probablemente se debe a la relajación transcripcional de CDH1 mediado por la pérdida de la expresión de REST

Cancer genomics paves the way to targeted therapy.

RESUMEN: La lucha contra el cáncer es aún un desafío mayor, con cerca de 14 millones de nuevos casos de cáncer al año y más de 8 millones de muertes anuales atribuidas al cáncer. Con la ayuda de múltiples servicios clínicos del HUMV y otras Instituciones, trabajamos para demostrar la hipótesis de que análisis integrados de genómica y secuenciación dirigida de alta profundidad en especímenes quirúrgicos de rutina puede generar datos firmes y relevantes sobre la complejidad molecular, composición subclonal, índice mutacional, firmas mutacionales y mutaciones precisas en genes con implicaciones terapéuticas; así generando una herramienta diagnóstica robusta que permita predecir sensibilidad a terapias específicas. In este proyecto, hemos podido demostrar que los estudios genómicos del cáncer demuestran dianas útiles para la intervención terapéutica y que la combinación de múltiples terapias inactivando rutas oncogénicas convergentes representa una opción plausible para pacientes con cáncer avanzado.ABSTRACT: Cancer is still a mayor challenge with something more than 14M new cases per year in the world and more of 8M patients dying yearly because of cancer. With the collaboration of multiple clinical services at the HUMV and other clinical institutions, we are working to demonstrate the hypothesis that genomics integrative analysis and high-depth targeted mutational analysis in routine cancer specimens may generate consistent, relevant data informing about molecular complexity, subclonal composition, mutational rate, mutational signatures and precise mutations in genes with therapeutic implications; thus generating a robust, solid, diagnostic tool that may allow to predict the sensitivity to specific therapies. In this project we have been able to demonstrate that cancer genome studies do demonstrate actionable targets, and that the combination of multiple therapies targeting convergent pathways represent a plausible option for advanced cancer patients

Applied diagnostics in liver cancer. Efficient combinations of sorafenib with targeted inhibitors blocking AKT/mTOR

Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related deaths worldwide. There is increasing interest in developing specific markers to serve as predictors of response to sorafenib and to guide targeted therapy. Using a sequencing platform designed to study somatic mutations in a selection of 112 genes (HepatoExome), we aimed to characterize lesions from HCC patients and cell lines, and to use the data to study the biological and mechanistic effects of case-specific targeted therapies used alone or in combination with sorafenib. We characterized 331 HCC cases in silico and 32 paired samples obtained prospectively from primary tumors of HCC patients. Each case was analyzed in a time compatible with the requirements of the clinic (within 15 days). In 53% of the discovery cohort cases, we detected unique mutational signatures, with up to 34% of them carrying mutated genes with the potential to guide therapy. In a panel of HCC cell lines, each characterized by a specific mutational signature, sorafenib elicited heterogeneous mechanistic and biological responses, whereas targeted therapy provoked the robust inhibition of cell proliferation and DNA synthesis along with the blockage of AKT/mTOR signaling. The combination of sorafenib with targeted therapies exhibited synergistic anti-HCC biological activity concomitantly with highly effective inhibition of MAPK and AKT/mTOR signaling. Thus, somatic mutations may lead to identify case-specific mechanisms of disease in HCC lesions arising from multiple etiologies. Moreover, targeted therapies guided by molecular characterization, used alone or in combination with sorafenib, can effectively block important HCC disease mechanisms.FUNDING: Grants from ISCIII, co-financed by the European Union (FEDER) (PI16/00156), Ramón and Cajal research program from MINECO (RYC-2013-14097) and FUNDACIÓN LUCHAMOS POR LA VIDA to JPV. Grants from ISCIII (RD06/0020/0107-RD012/0036/0060) to MAP. Grant from ISCIII (Ref. PIE15/00079) to JC & JPV. NGD is a recipient of a UC-IDIVAL pre-doctoral fellow. I.V. was also supported by the Ramón and Cajal research program