The Araucaria dendrochronological network: growth patterns and climatic signals of paraná-pine on the Southern Brazilian plateau.

Ameridendro

Diabetes Causes Bone Marrow Autonomic Neuropathy and Impairs Stem Cell Mobilization via Dysregulated p66Shc and Sirt1

Diabetes compromises the bone marrow (BM) microenvironment and reduces circulating CD34 + cells. Diabetic autonomic neuropathy (DAN) may impact the BM, because the sympathetic nervous system (SNS) is prominently involved in BM stem cell trafficking. We hypothesize that neuropathy of the BM affects stem cell mobilization and vascular recovery after ischemia in diabetes. We report that, in patients, cardiovascular DAN was associated with fewer circulating CD34 + cells. Experimental diabetes (STZ and Ob/Ob ) or chemical sympathectomy in mice resulted in BM autonomic neuropathy, impaired Lin - cKit + Sca1 + (LKS) cell and endothelial progenitor cells (EPC, CD34 + Flk1 + ) mobilization and vascular recovery after ischemia. DAN increased expression of p66Shc and reduced expression of Sirt1 in mice and humans. p66Shc KO in diabetic mice prevented DAN in the BM, and rescued defective LKS cell and EPC mobilization. Hematopoietic Sirt1 KO mimicked the diabetic mobilization defect, while hematopoietic Sirt1 overexpression in diabetes rescued defective mobilization and vascular repair. Through p66Shc and Sirt1 , diabetes and sympathectomy elevated the expression of various adhesion molecules, including CD62L . CD62L KO partially rescued the defective stem/progenitor cell mobilization. In conclusion, autonomic neuropathy in the BM impairs stem cell mobilization in diabetes with dysregulation of the lifespan regulators p66Shc and Sirt1

Polineuropatía desmielinizante inflamatoria crónica como forma de presentación de lupus eritematoso sistémico

Se describe el caso de una mujer de 35 años que presenta polineuropatía desmielinizante inflamatoria crónica como compromiso neurológico en su diagnóstico inicial de lupus eritematoso sistémico (LES). Si bien el compromiso neurológico es de una prevalencia variable en lupus, la asociación que se describe no es frecuente y tiene importantes connotaciones en el tratamiento

Quantifying n -Photon Indistinguishability with a Cyclic Integrated Interferometer

We report on a universal method to measure the genuine indistinguishability of n photons - a crucial parameter that determines the accuracy of optical quantum computing. Our approach relies on a low-depth cyclic multiport interferometer with N=2n modes, leading to a quantum interference fringe whose visibility is a direct measurement of the genuine n-photon indistinguishability. We experimentally demonstrate this technique for an eight-mode integrated interferometer fabricated using femtosecond laser micromachining and four photons from a quantum dot single-photon source. We measure a four-photon indistinguishability up to 0.81±0.03. This value decreases as we intentionally alter the photon pairwise indistinguishability. The low-depth and low-loss multiport interferometer design provides an original path to evaluate the genuine indistinguishability of resource states of increasing photon number

The Peritoneum as a Natural Scaffold for Vascular Regeneration

Objective: The peritoneum has the same developmental origin as blood vessels, is highly reactive and poorly thrombogenic. We hypothesize that parietal peritoneum can sustain development and regeneration of new vessels. Methods and Results: The study comprised two experimental approaches. First, to test surgical feasibility and efficacy of the peritoneal vascular autograft, we set up an autologous transplantation procedure in pigs, where a tubularized parietal peritoneal graft was covered with a metal mesh and anastomosed end-to-end in the infrarenal aorta. Second, to dissect the contribution of graft vs host cells to the newly developed vessel wall, we performed human-to-rat peritoneal patch grafting in the abdominal aorta and examined the origin of endothelial and smooth muscle cells. In pig experiments, the graft remodeled to an apparently normal blood vessel, without thrombosis. Histology confirmed arterialization of the graft with complete endothelial coverage and neointimal hyperplasia in the absence of erosion, inflammation or thrombosis. In rats, immunostaining for human mitochondri revealed that endothelial cells and smooth muscle cells rarely were of human origin. Remodeling of the graft was mainly attributable to local cells with no clear evidence of c-kit+ endothelial progenitor cells or c-kit+ resident perivascular progenitor cells. Conclusions: The parietal peritoneum can be feasibly used as a scaffold to sustain the regeneration of blood vessels, whic

The Redox Enzyme p66Shc Contributes to Diabetes and Ischemia-Induced Delay in Cutaneous Wound Healing

OBJECTIVE: The redox enzyme p66Shc produces hydrogen peroxide and triggers proapoptotic signals. Genetic deletion of p66Shc prolongs life span and protects against oxidative stress. In the present study, we evaluated the role of p66Shc in an animal model of diabetic wound healing. RESEARCH DESIGN AND METHODS: Skin wounds were created in wild-type (WT) and p66Shc(-/-) control and streptozotocin-induced diabetic mice with or without hind limb ischemia. Wounds were assessed for collagen content, thickness and vascularity of granulation tissue, apoptosis, reepithelialization, and expression of c-myc and beta-catenin. Response to hind limb ischemia was also evaluated. RESULTS: Diabetes delayed wound healing in WT mice with reduced granulation tissue thickness and vascularity, increased apoptosis, epithelial expression of c-myc, and nuclear localization of beta-catenin. These nonhealing features were worsened by hind limb ischemia. Diabetes induced p66Shc expression and activation; wound healing was significantly faster in p66Shc(-/-) than in WT diabetic mice, with or without hind limb ischemia, at 1 and 3 months of diabetes duration and in both SV129 and C57BL/6 genetic backgrounds. Deletion of p66Shc reversed nonhealing features, with increased collagen content and granulation tissue thickness, and reduced apoptosis and expression of c-myc and beta-catenin. p66Shc deletion improved response to hind limb ischemia in diabetic mice in terms of tissue damage, capillary density, and perfusion. Migration of p66Shc(-/-) dermal fibroblasts in vitro was significantly faster than WT fibroblasts under both high glucose and hypoxia. CONCLUSIONS: p66Shc is involved in the delayed wound-healing process in the setting of diabetes and ischemia. Thus, p66Shc may represent a potential therapeutic target against this disabling diabetes complication

Niveles de interferón tipo I en pacientes con lupus eritematoso sistémico

Introducción: el interferón (IFN) tipo I es una citoquina que juega un rol fundamental en la patogenia del Lupus Eritematoso Sistémico (LES). Diferentes niveles de esta citoquina podrían explicar la heterogeneidad de esta patología y ser útil para evaluar la actividad de la misma. Objetivos: determinar los niveles de IFN tipo I sérico en pacientes con LES y evaluar su utilidad como biomarcador de actividad. Material y Métodos: 16 pacientes con LES (ACR 1997) y 16 controles. Métodos: Actividad de la enfermedad (SLEDAI-2K), daño orgánico (SLICC), IFN tipo I (HEK-Blue-IFNα/β), anticuerpos anti-DNAdc (Inmunofluorescencia Indirecta), anticuerpos anti-ENA (ELISA), C3-C4 (Inmunoturbidimetría). Estadística: InfoStat/Instat/MedCalc. Valores de p<0,05 fueron considerados estadísticamente significativos. Resultados: se observó un aumento de la concentración de IFN en el grupo LES con respecto al control (p<0,05). Los pacientes con valores de IFN superiores al punto de corte, se asociaron con la presencia de anticuerpos anti-DNAdc (OR:13,33;p<0,05). Pacientes con hipocomplementemia y aquellos con puntaje de SLEDAI-2K mayor a 8 presentaron mayores niveles de IFN comparados con pacientes con complemento normal y menor puntaje de índice, respectivamente (p<0,05). Conclusiones: estos resultados sugieren la importancia que podría tener la determinación de IFN tipo I para el monitoreo de la actividad del LES

Serum oxidative stress-induced repression of Nrf2 and GSH depletion: a mechanism potentially involved in endothelial dysfunction of young smokers

AbstractBackground: Although oxidative stress plays a major role in endothelial dysfunction (ED), the role of glutathione (GSH), ofnuclear erythroid-related factor 2 (Nrf2) and of related antioxidant genes (ARE) are yet unknown. In this study we combined an in vivo with an in vitro model to assess whether cigarette smoking affects flow-mediated vasodilation (FMD), GSHconcentrations and the Nrf2/ARE pathway in human umbilical vein endothelial cells (HUVECs).Methods and Results: 52 healthy subjects (26 non-smokers and 26 heavy smokers) were enrolled in this study. In smokerswe demonstrated increased oxidative stress, i.e., reduced concentrations of GSH and increased concentrations of oxidationproducts of the phospholipid 1-palmitoyl-2-arachidonyl-sn-glycero-3-phosphorylcholine (oxPAPC) in serum and inperipheral blood mononuclear cells (PBMC), used as in vivo surrogates of endothelial cells. Moreover we showedimpairment of FMD in smokers and a positive correlation with the concentration of GSH in PBMC of all subjects. In HUVECsexposed to smokers\u2019 serum but not to non-smokers\u2019 serum we found that oxidative stress increased, whereas nitric oxideand GSH concentrations decreased; interestingly the expression of Nrf2, of heme oxygenase-1 (HO-1) and of glutamatecysteineligase catalytic (GCLC) subunit, the rate-limiting step of synthesis of GSH, was decreased. To test the hypothesisthat the increased oxidative stress in smokers may have a causal role in the repression of Nrf2/ARE pathway, we exposedHUVECs to increasing concentrations of oxPAPC and found that at the highest concentration (similar to that found insmokers\u2019 serum) the expression of Nrf2/ARE pathway was reduced. The knockdown of Nrf2 was associated to a significantreduction of HO-1 and GCLC expression induced by oxPAPC in ECs.Conclusions: In young smokers with ED a novel further consequence of increased oxidative stress is a repression of Nrf2/ARE pathway leading to GSH depletion

Agricultural machinery adequacy for handling the mombaça grass biomass in agroforestry systems.

Abstract: The current scenario of Agroforestry Systems (AFS) worldwide lacks specific machinery, resulting in practically all operations being carried out manually. This leads to a significant physical effort for small-scale farmers and limits the implementation of AFS to small areas. The objective of the study was to evaluate the suitability of existing machines for performing agroforestry tasks. This research utilizes Descriptive Statistics and Exponentially Weighted Moving Average methods to evaluate the data and compare the treatments, where different machines are used to cut Mombaça grass (Megathyrsus maximus Jacq): (i) costal brushcutter (CBC); (ii) tractor-mounted rotary brushcutter (RBC); and (iii) mini grain reaper machine (GRM). The experiments were conducted in Jaguariúna, São Paulo, Brazil. GRM is recommended for achieving greater biomass production, reducing raking time, and minimizing operational costs. CBC is suitable for smaller areas due to its affordability and slow operation, which requires significant physical effort. RBC is recommended for reducing working time, physical effort, and personnel costs, making it suitable for larger-scale contexts