La auditoría tributaria preventiva y los riesgos tributarios en las empresas industriales de Puente Piedra-Lima 2020

Explica acerca de la auditoría tributaria preventiva y cómo se relaciona con los riesgos tributarios en las empresas industriales en el distrito de Puente Piedra en Lima-Perú. En el marco del desarrollo empresarial y la inseguridad jurídica tributaria, las empresas tienen mayores riesgos de que la SUNAT les desconozca la deducción de sus costos y gastos, y la emisión de resolución de multas a las compañías por incumplimiento formales y sustanciales por ello la necesidad de realizar auditoria tributaria preventiva para subsanar estas omisiones y de este modo alertar a la gerencia las medidas de mejoras a sus procesos de documentación empresarial y sustento de los hechos económicos de la empresa. Por último, también sirve para la implementación de un sistema de control interno de este modo prevenir cualquier error en la determinación de los impuestos a declarar. Finalmente, en el presente estudio se comprueba que la auditoria tributaria preventiva disminuye los riesgos tributarios en las compañías que lo aplican y se logra una empresa con menos multas, menos reparos en las fiscalizaciones esto debido a una determinación correcta de sus impuestos, y el control documentario y validación de la información que llega al departamento de contabilidad para el cierre mensual y anual de los impuestos y con la evidencia suficiente para sustentar las operaciones de las empresas

Estudio de los factores bHLH E2-2 en la represión de cadherina-E y la transición epitelio-mesénquima: comparación con E47

Tesis doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Medicina. Departamento de Bioquímica. Fecha de lectura: 18 de Junio 200

SeDiCI - Desafíos y experiencias en la vida de un repositorio digital

Desde su creación en el año 2003, el Servicio de Difusión de la Creación Intelectual ha afrontado diversas dificultades que han influido directa o indirectamente en su desarrollo y crecimiento. En este documento se presentan algunas de estas experiencias, describiendo en cada caso el problema, su contexto y las vías de acción tomadas para superarlo. Adicionalmente se describen algunas de las diferentes líneas de investigación y desarrollo actuales, orientadas a expandir y mejorar los servicios proporcionados a la comunidad de usuarios. De ahí que el objetivo principal de este trabajo sea exponer la experiencia adquirida, con la intención de que resulte de utilidad para aquellas instituciones que se encuentren en el proceso de creación de sus propios repositorios.Since its creation in the year 2003, the Intellectual Creation Dissemination Service has faced up many difficulties. Thus the initiative has been directly and indirectly affected during its development and growth. This work presents some of these experiencies, describing problems, context and solution approaches. This document also describes some of the new and most recent challenges and the current research and development trends, which are oriented to improve and extend the services provided by SeDiCI. The main purpose of this document is to share the lived experiences with this project, which may be useful to other institutions working on their own digital repositories.Servicio de Difusión de la Creación Intelectual (SEDICI

The genetic history of Scandinavia from the Roman Iron Age to the present

The authors acknowledge support from the National Genomics Infrastructure in Stockholm funded by Science for Life Laboratory, the Knut and Alice Wallenberg Foundation and the Swedish Research Council, and SNIC/Uppsala Multidisciplinary Center for Advanced Computational Science for assistance with massively parallel sequencing and access to the UPPMAX computational infrastructure. We used resources from projects SNIC 2022/23-132, SNIC 2022/22-117, SNIC 2022/23-163, SNIC 2022/22-299, and SNIC 2021-2-17. This research was supported by the Swedish Research Council project ID 2019-00849_VR and ATLAS (Riksbankens Jubileumsfond). Part of the modern dataset was supported by a research grant from Science Foundation Ireland (SFI), grant number 16/RC/3948, and co-funded under the European Regional Development Fund and by FutureNeuro industry partners.Peer reviewedPublisher PD

The class I bHLH factors E2-2A and E2-2B regulate EMT

11 pages, 6 figures.Functional loss of the cell-cell adhesion molecule E-cadherin is an essential event for epithelial-mesenchymal transition (EMT), a process that allows cell migration during embryonic development and tumour invasion. In most carcinomas, transcriptional repression has emerged as the main mechanism responsible for E-cadherin downregulation. Here, we report the identification of class I bHLH factor E2-2 (TCF4/ITF2) as a new EMT regulator. Both isoforms of E2-2 (E2-2A and E2-2B) induce a full EMT when overexpressed in MDCK cells but without affecting the tumorigenic properties of parental cells, in contrast to other EMT inducers, such as Snail1 or class I bHLH E47. E-cadherin repression mediated by E2-2 is indirect and independent of proximal E-boxes of the promoter. Knockdown studies indicate that E2-2 expression is dispensable for maintenance of the EMT driven by Snail1 and E47. Comparative gene-profiling analysis reveals that E2-2 factors induce similar, yet distinct, genetic programs to that induced by E47 in MDCK cells. These results, together with the embryonic expression pattern of Tcf4 and E2A (which encodes E12/E47), support a distinct role for E2-2 and suggest an interesting interplay between E-cadherin repressors in the regulation of physiological and pathological EMT processes.This work was supported by the Spanish Ministry of Education and Science (SAF2004-00361; SAF2007-63051) and the EV (MRTN 2004-005428) to A.C., Consolider-Ingenio 2010 CDC2007-00017 to A.C. and M.A.N., and the EU (MRTN 2004-005428) to A.C. and by the Fundación Mutua Madrileña (to G.M.B.). V.R.S. was supported by an FPU fellowship from the Spanish Ministry of Education and Science. G.M.B. is a junior investigator of the Ramón y Cajal Program 2004.Peer reviewe

Viking warrior women? Reassessing Birka chamber grave Bj.581

Abstract: Please refer to full text to view abstract

Digital Expression

Welcome to the Third Edition of “Digital Expression”, interactive version. It has a totally new image and renovated contents that will improve your learning process! This eBook offers the bases to take advantage of the available digital media to create multimedia contents that include resources such as voice, text, sound, image, animation, and video in order to increase your chances to express creatively

Inhibition of calpain-regulated p35/cdk5 plays a central role in sildenafil-induced protection against chemical hypoxia produced by malonate

AbstractPhosphodiesterase 5 (PDE5) inhibitors have recently been reported to exert beneficial effects against ischemia–reperfusion injury in several organs but their neuroprotective effects in brain stroke models are scarce. The present study was undertaken to assess the effects of sildenafil against cell death caused by intrastriatal injection of malonate, an inhibitor of succinate dehydrogenase; which produces both energy depletion and lesions similar to those seen in cerebral ischemia. Our data demonstrate that sildenafil (1.5mg/kg by mouth (p.o.)), given 30min before malonate (1.5μmol/2μL), significantly decreased the lesion volume caused by this toxin. This protective effect can be probably related to the inhibition of excitotoxic pathways. Thus, malonate induced the activation of the calcium-dependent protease, calpain and the cyclin-dependent kinase 5, cdk5; which resulted in the hyperphosphorylation of tau and the cleavage of the protective transcription factor, myocyte enhancer factor 2, MEF2. All these effects were also significantly reduced by sildenafil pre-treatment, suggesting that sildenafil protects against malonate-induced cell death through the regulation of the calpain/p25/cdk5 signaling pathway. Similar findings were obtained using inhibitors of calpain or cdk5, further supporting our contention. Sildenafil also increased MEF2 phosphorylation and Bcl-2/Bax and Bcl-xL/Bax ratios, effects that might as well contribute to prevent cell death. Finally, sildenafil neuroprotection was extended not only to rat hippocampal slices subjected to oxygen and glucose deprivation when added at the time of reoxygenation, but also, in vivo when administered after malonate injection. Thus, the therapeutic window for sildenafil against malonate-induced hypoxia was set at 3h