Air Pollution Exposure Induces Vascular Injury and Hampers Endothelial Repair by Altering Progenitor and Stem Cells Functionality

Extensive evidence indicates an association of air pollution exposure with an increased risk of cardiovascular disease (CVD) development. Fine particulate matter (PM) represents one of the main components of urban pollution, but the mechanisms by which it exerts adverse effects on cardiovascular system remain partially unknown and under investigation. The alteration of endothelial functions and inflammation are among the earliest pathophysiological impacts of environmental exposure on the cardiovascular system and represent critical mediators of PM-induced injury. In this context, endothelial stem/progenitor cells (EPCs) play an important role in vascular homeostasis, endothelial reparative capacity, and vasomotor functionality modulation. Several studies indicate the impairment of EPCs’ vascular reparative capacity due to PM exposure. Since a central source of EPCs is bone marrow (BM), their number and function could be related to the population and functional status of stem cells (SCs) of this district. In this review, we provide an overview of the potential mechanisms by which PM exposure hinders vascular repair by the alteration of progenitor and stem cells’ functionality

Microwave Schottky diagnostic systems for the Fermilab Tevatron, Recycler, and CERN LHC

A means for non-invasive measurement of transverse and longitudinal characteristics of bunched beams in synchrotrons has been developed based on high sensitivity slotted waveguide pickups. The pickups allow for bandwidths exceeding hundreds of MHz while maintaining good beam sensitivity characteristics. Wide bandwidth is essential to allow bunch-by-bunch measurements by means of a fast gate. The Schottky detector system is installed and successfully commissioned in the Fermilab Tevatron, Recycler and CERN LHC synchrotrons. Measurement capabilities include tune, chromaticity, and momentum spread of single or multiple beam bunches in any combination. With appropriate calibrations, emittance can also be measured by integrating the area under the incoherent tune sidebands

Progress with PXIE MEBT Chopper

A capability to provide a large variety of bunch patterns is crucial for the concept of the Project X serving MW-range beam to several experiments simultaneously. This capability will be realized by the Medium Energy Beam Transport's (MEBT) chopping system that will divert 80% of all bunches of the initially 5mA, 2.1 MeV CW 162.5 MHz beam to an absorber according to a pre-programmed bunch-by-bunch selection. Being considered one of the most challenging components, the chopping system will be tested at the Project X Injector Experiment (PXIE) facility that will be built at Fermilab as a prototype of the Project X front end. The bunch deflection will be made by two identical sets of travelling-wave kickers working in sync. Currently, two versions of the kickers are being investigated: a helical 200 Ohm structure with a switching-type 500 V driver and a planar 50 Ohm structure with a linear 250 V amplifier. This paper will describe the chopping system scheme and functional specifications for the kickers, present results of electromagnetic measurements of the models, discuss possible driver schemes, and show a conceptual mechanical design.Comment: 3 pp. 3rd International Particle Accelerator Conference (IPAC 2012) 20-25 May 2012. New Orleans, Louisian

Performance Enhancement in CZTS Solar Cells by SCAPS-1D Software

This is the abstract, usually it does not have references. Usually the reader will read this part first to know what this paper is about and decide upon it to continue reading or not. The font of main text is 10 Times New Roman with single line spacing of 6 pt after and 0 pt before. The titles of sections are font 12, bold and they have single line spacing of 6pt before, 12 pt after, subsections are font 12, Italic and they have single line spacing of 6pt before, 12 pt after. Both upper line and lower line enclosing this part is paper-specific and changes according to the paper, usually it is very similar to the journal header background color, abstract contents are Times New Roman size 10, no line spacing

Phenotypically Heterogeneous Podoplanin-expressing Cell Populations Are Associated with the Lymphatic Vessel Growth and Fibrogenic Responses in the Acutely and Chronically Infarcted Myocardium

Cardiac lymphatic vasculature undergoes substantial expansion in response to myocardial infarction (MI). However, there is limited information on the cellular mechanisms mediating post-MI lymphangiogenesis and accompanying fibrosis in the infarcted adult heart. Using a mouse model of permanent coronary artery ligation, we examined spatiotemporal changes in the expression of lymphendothelial and mesenchymal markers in the acutely and chronically infarcted myocardium. We found that at the time of wound granulation, a three-fold increase in the frequency of podoplanin-labeled cells occurred in the infarcted hearts compared to non-operated and sham-operated counterparts. Podoplanin immunoreactivity detected LYVE-1-positive lymphatic vessels, as well as masses of LYVE-1-negative cells dispersed between myocytes, predominantly in the vicinity of the infarcted region. Podoplanin-carrying populations displayed a mesenchymal progenitor marker PDGFRalpha, and intermittently expressed Prox-1, a master regulator of the lymphatic endothelial fate. At the stages of scar formation and maturation, concomitantly with the enlargement of lymphatic network in the injured myocardium, the podoplanin-rich LYVE-1-negative multicellular assemblies were apparent in the fibrotic area, aligned with extracellular matrix deposits, or located in immediate proximity to activated blood vessels with high VEGFR-2 content. Of note, these podoplanin-containing cells acquired the expression of PDGFRbeta or a hematoendothelial epitope CD34. Although Prox-1 labeling was abundant in the area affected by MI, the podoplanin-presenting cells were not consistently Prox-1-positive. The concordance of podoplanin with VEGFR-3 similarly varied. Thus, our data reveal previously unknown phenotypic and structural heterogeneity within the podoplanin-positive cell compartment in the infarcted heart, and suggest an alternate ability of podoplanin-presenting cardiac cells to generate lymphatic endothelium and pro-fibrotic cells, contributing to scar development

Phenotypically Heterogeneous Podoplanin-expressing Cell Populations Are Associated with the Lymphatic Vessel Growth and Fibrogenic Responses in the Acutely and Chronically Infarcted Myocardium

Cardiac lymphatic vasculature undergoes substantial expansion in response to myocardial infarction (MI). However, there is limited information on the cellular mechanisms mediating post-MI lymphangiogenesis and accompanying fibrosis in the infarcted adult heart. Using a mouse model of permanent coronary artery ligation, we examined spatiotemporal changes in the expression of lymphendothelial and mesenchymal markers in the acutely and chronically infarcted myocardium. We found that at the time of wound granulation, a three-fold increase in the frequency of podoplanin-labeled cells occurred in the infarcted hearts compared to non-operated and sham-operated counterparts. Podoplanin immunoreactivity detected LYVE-1-positive lymphatic vessels, as well as masses of LYVE-1-negative cells dispersed between myocytes, predominantly in the vicinity of the infarcted region. Podoplanin-carrying populations displayed a mesenchymal progenitor marker PDGFRalpha, and intermittently expressed Prox-1, a master regulator of the lymphatic endothelial fate. At the stages of scar formation and maturation, concomitantly with the enlargement of lymphatic network in the injured myocardium, the podoplanin-rich LYVE-1-negative multicellular assemblies were apparent in the fibrotic area, aligned with extracellular matrix deposits, or located in immediate proximity to activated blood vessels with high VEGFR-2 content. Of note, these podoplanin-containing cells acquired the expression of PDGFRbeta or a hematoendothelial epitope CD34. Although Prox-1 labeling was abundant in the area affected by MI, the podoplanin-presenting cells were not consistently Prox-1-positive. The concordance of podoplanin with VEGFR-3 similarly varied. Thus, our data reveal previously unknown phenotypic and structural heterogeneity within the podoplanin-positive cell compartment in the infarcted heart, and suggest an alternate ability of podoplanin-presenting cardiac cells to generate lymphatic endothelium and pro-fibrotic cells, contributing to scar development

Hydrolytic Degradation of Polylactic Acid Fibers as a Function of pH and Exposure Time

Polylactic acid (PLA) is a widely used bioresorbable polymer in medical devices owing to its biocompatibility, bioresorbability, and biodegradability. It is also considered a sustainable solution for a wide variety of other applications, including packaging. Because of its widespread use, there have been many studies evaluating this polymer. However, gaps still exist in our understanding of the hydrolytic degradation in extreme pH environments and its impact on physical and mechanical properties, especially in fibrous materials. The goal of this work is to explore the hydrolytic degradation of PLA fibers as a function of a wide range of pH values and exposure times. To complement the experimental measurements, molecular-level details were obtained using both molecular dynamics (MD) simulations with ReaxFF and density functional theory (DFT) calculations. The hydrolytic degradation of PLA fibers from both experiments and simulations was observed to have a faster rate of degradation in alkaline conditions, with 40% of strength loss of the fibers in just 25 days together with an increase in the percent crystallinity of the degraded samples. Additionally, surface erosion was observed in these PLA fibers, especially in extreme alkaline environments, in contrast to bulk erosion observed in molded PLA grafts and other materials, which is attributed to the increased crystallinity induced during the fiber spinning process. These results indicate that spun PLA fibers function in a predictable manner as a bioresorbable medical device when totally degraded at end-of-life in more alkaline conditions

Preclinical Models of Visceral Sarcomas

Visceral sarcomas are a rare malignant subgroup of soft tissue sarcomas (STSs). STSs, accounting for 1% of all adult tumors, are derived from mesenchymal tissues and exhibit a wide heterogeneity. Their rarity and the high number of histotypes hinder the understanding of tumor development mechanisms and negatively influence clinical outcomes and treatment approaches. Although some STSs (~20%) have identifiable genetic markers, as specific mutations or translocations, most are characterized by complex genomic profiles. Thus, identification of new therapeutic targets and development of personalized therapies are urgent clinical needs. Although cell lines are useful for preclinical investigations, more reliable preclinical models are required to develop and test new potential therapies. Here, we provide an overview of the available in vitro and in vivo models of visceral sarcomas, whose gene signatures are still not well characterized, to highlight current challenges and provide insights for future studies

Regulación epigenética del IFN-y en tuberculosis

M. tuberculosis (Mtb) es el principal asesino microbiológico en el mundo. Las modificaciones epigenéticas son claves en la plasticidad del sistema inmune y como mediadores entre el ambiente y los fenotipos celulares. El IFN-v, media la respuesta protectiva frente a Mtb, pero se desconocen los mecanismos epigenéticos que regularían su activación y mediarían la susceptibilidad a la tuberculosis.Área: Ciencias Biológicas, Ambiente y Salud

Healing of Prosthetic Arterial Grafts

Numerous synthetic biomaterials have been developed as vascular substitutes. In vitro, ex vivo and in vivo studies have demonstrated that in animals, selected materials, i.e., Dacron and ePTFE (expanded polytetrafluoroethylene) grafts, are successfully incorporated in both the large and the small caliber host arteries through a process which is generally referred to as graft healing. Morphologically, this process consists of a series of complex events including fibrin deposition and degradation, monocyte-macrophage recruitment and flow-oriented cell-layer generation, this last event being the complete endothelialization of the arterial substitute. In contrast to experimental animals, the flow surface of synthetic vascular grafts remains unhealed in humans, particularly in the small caliber conduits. Healing in man consists of graft incorporation by the perigraft fibrous tissue response with a surface covered by more or less compacted, cross-linked fibrin. It is therefore obvious that: i) marked differences in graft healing exist between animals and man; and ii) the usual mechanisms of graft endothelialization are partially ineffective in man. In order to guarantee the patency of synthetic vascular grafts for human small artery bypass, new strategies and approaches have recently been attempted. In particular, the endothelial cell seeding approach has been successfully accomplished in animals and is being experimented in human clinical studies. The problems and results of this biological approach are outlined in this paper