Polarization-Current-Based FDTD Near-to-Far-Field Transformation

A new near-to-far-field transformation algorithm for three-dimensional finite-different time-domain is presented in this article. This new approach is based directly on the polarization current of the scatterer, not the scattered near fields. It therefore eliminates the numerical errors originating from the spatial offset of the E and H fields, inherent in the standard near-to-far-field transformation. The proposed method is validated via direct comparisons with the analytical Lorentz-Mie solutions of plane waves scattered by large dielectric and metallic spheres with strong forward-scattering lobes.Comment: 8 pages, 2 figures. Submitted to publis

Role of the intestinal microbiota in colorectal cancer

RESUMEN : Cada vez más se reconoce la importancia de la relación entre la microbiota intestinal y la salud humana. Ahora está bien establecido que una microbiota intestinal saludable es en gran parte responsable de la salud general del huésped. Así mismo la microbiota intestinal cada vez más se asocia con una gran variedad de enfermedades humanas como el cáncer colorrectal (CCR). La microbiota intestinal produce una serie de metabolitos y factores que afectan el metabolismo y la inmunidad del huésped. Dichas alteraciones del huésped conllevan a la aparición del CCR que se caracteriza por inflamación, disfunción de la barrera intestinal y estando involucrados mecanismos moleculares en el contexto de una disbiosis intestinal. Debido al gran impacto de la microbiota intestinal tanto en la salud como en la enfermedad se plantea la presente revisión que trata de analizar la reciente evidencia del impacto de la microbiota intestinal en el CCR considerando los microorganismos relacionados así como el papel que juega el biofilm en la incidencia del CCR. El objetivo es proporcionar un análisis del conocimiento actual del papel de la microbiota en la eficiencia y toxicidad de las terapias contra el CCR y la necesidad de integración de los datos del microbioma en la medicina de precisión para la prevención diagnóstico y tratamiento del CCR. Finalmente se incide en la modulación de la microbiota con fines terapéuticos.ABSTRACT : The importance of the relationship between the gut microbiota and human health is increasingly recognized. It is now well established that a healthy intestinal microbiota is largely responsible for the general health of the host. Likewise, intestinal microbiota are increasingly associated with a wide variety of human diseases such as colorectal cancer (CRC). The gut microbiota generates a series of metabolites and factors that affect the metabolism and immunity of the host. Such alterations of the host lead to the appearance of CRC characterized by inflammation, dysfunction of the intestinal barrier and molecular mechanisms involved in the context of an intestinal dysbiosis. Given the great impact of the gut microbiota on health and disease, this review considers the recent evidence of the impact of the intestinal microbiota on colorectal cancer considering related microorganisms and the role of biofilm in the incidence of colorectal (CRC). The objective is to provide an analysis of the current knowledge of the role of microbiota in the efficiency and toxicity of CRC therapies and the need for integration of microbial data into precision medicine for the prevention, diagnosis and treatment of CRC. Finally this revision points out, the modulation of the microbiota used for therapeutic purposes.Grado en Medicin

Circulating smooth muscle cell plasticity in the development of transplant arteriosclerosis

To date, chronic transplant dysfunction (CTD) is recognized as the major cause of long-term transplant loss (&gt;1 year) after transplantation. CTD presents histologically with obliterated intragraft arteries as a result of intimal hyperplasia referred to as transplant arteriosclerosis (TA). Neointimal lesions predominantly consist of vascular smooth muscle cells (VSMCs) intermingled with some inflammatory cells. The pathogenesis of TA is believed to be multifactorial, and many risk factors have been identified. Because the precise pathogenetic mechanisms underlying TA are still largely unknown, adequate prevention and treatment protocols are not available. In this review, we discus the origin (donor vs recipient, bone marrow vs non-bone marrow) of neointimal endothelial cells (ECs) and VSMCs in TA lesions, which were formerly believed to be solely graft-derived. On the basis of the data obtained in both clinical and experimental transplantation, it appears that the process leading to TA is heterogeneous and that neointimal ECs and VSMCs can be recruited from different sources, possibly depending on the severity of vascular damage. These data suggest a significant role of host-derived circulating EC-VSMC progenitor cells, which may be partly bone marrow-derived. These circulating progenitor cells are potential targets for therapeutic intervention to ameliorate TA development or occlusive vascular disease in general.</p

Long-Term Type 1 Diabetes Enhances In-Stent Restenosis after Aortic Stenting in Diabetes-Prone BB Rats

Type 1 diabetic patients have increased risk of developing in-stent restenosis following endovascular stenting. Underlying pathogenetic mechanisms are not fully understood partly due to the lack of a relevant animal model to study the effect(s) of long-term autoimmune diabetes on development of in-stent restenosis. We here describe the development of in-stent restenosis in long-term (~7 months) spontaneously diabetic and age-matched, thymectomized, nondiabetic Diabetes Prone BioBreeding (BBDP) rats (n = 6-7 in each group). Diabetes was suboptimally treated with insulin and was characterized by significant hyperglycaemia, polyuria, proteinuria, and increased HbA1c levels. Stented abdominal aortas were harvested 28 days after stenting. Computerized morphometric analysis revealed significantly increased neointima formation in long-term diabetic rats compared with nondiabetic controls. In conclusion, long-term autoimmune diabetes in BBDP rats enhances in-stent restenosis. This model can be used to study the underlying pathogenetic mechanisms of diabetes-enhanced in-stent restenosis as well as to test new therapeutic modalities

Transplant Arteriosclerosis and In-Stent Restenosis: Experimental studies on pathomechanisms and therapeutic intervention

Doel van het onderzoek was het bestuderen van verschillende cellulaire/moleculaire aspecten onderliggend aan het vernauwen van bloedvaten in getransplanteerde organen (transplantaat arteriosclerosis [TA]) en na stenting (in-stent restenosis [ISR]). TA en ISR vertegenwoordigen twee belangrijke bloedvat-vernauwende afwijkingen aan slagaders die beiden gekenmerkt worden door endotheelschade, ontsteking en neointima (NI) vorming. Er zijn geen adequate therapieën voorhanden waarmee TA en ISR kan worden voorkomen of behandeld. Focus was het verkrijgen van nieuwe inzichten in het herstel van beschadigd endotheel, de herkomst van NI gladde spiercellen (SMCs) en factoren verantwoordelijk voor SMC rekrutering/celdeling in TA en ISR. Het onderzoek werd uitgevoerd in zowel pre-klinische in vivo als in vitro modellen. De belangrijkste uitkomsten van dit onderzoek luiden als volgt. Er bestaat een genetische aanleg voor de ontwikkeling van TA die geassocieerd is met de mogelijkheid van SMCs om zich te vermeerderen én een verhoogde frequentie van circulerende SMC voorlopercellen. De ontwikkeling van TA kon sterk worden geremd met rosiglitazone, een zogenaamde PPARγ-agonist. Dit medicijn wordt veel gebruikt om diabetes-patiënten te behandelen; het remmende effect op TA ontwikkeling was tot dusver onbekend. Daarnaast werd aangetoond dat SMCs in ISR niet uit het beenmerg afkomstig zijn, maar mogelijk uit de vaatwand zelf. Tenslotte bleek in een nieuw ontwikkeld experimenteel model dat diabetes de ontwikkeling van ISR bevordert; dit was geassocieerd met een verminderd angiogeen vermogen in de vaatwand. Deze bevindingen hebben het inzicht in TA/ISR ontwikkeling vergroot en kunnen bijdragen aan de ontwikkeling van nieuwe methoden om TA/ISR te voorkomen of behandelen.

Role of progenitor cells in transplant arteriosclerosis

To date, chronic transplant dysfunction (CTD) is recognized as the major cause of transplant loss long term after transplantation. CTD has the remarkable histologic feature that the luminal areas of the intragraft arteries become obliterated as a result of occlusive neointima formation. Neointimal lesions contain predominantly vascular smooth muscle cells (VSMCs) and extracellular matrix admixed with inflammatory cells. At the luminal side, neointimal lesions are covered with a monolayer of endothelial cells (ECs). The etiology of transplant arteriosclerosis (TA) is largely unknown, and adequate prevention and treatment protocols are not available. In contrast to the largely accepted "response-to-injury" hypothesis for the development of TA that attributes an important role to graft-derived ECs and VSMCs, recent data indicate that host-derived vascular progenitor cells play a major role in the development of TA. The process leading to TA appears to be heterogeneous, and neointimal ECs and VSMCs can be recruited from different sources, possibly depending on the severity and duration of vascular damage. These data suggest a significant role of host-derived circulating EC/VSMC progenitor cells, which may be partly bone marrow derived. Circulating vascular progenitor cells are potential targets for therapeutic intervention to ameliorate TA development. Therefore, identification of mediators and cellular mechanisms that promote recruitment of vascular progenitors to sites of injury is warranted to dissect their detrimental and Possible beneficial effects in the development of TA. (c) 2005, Elsevier Inc