Analysis of Sorting Algorithms Using a WSN and Environmental Pollution Data based on FPGA

Wireless Snesor Network (WSN) based sys- tems with a focus on Internet of Things (IoT) applications generate a large amount of data. Many applications that need to process data in real time make use of microcontroller-based architectures with sequential pro- gramming. Systems based on sequential programming can emulate parallelism up to a certain number of in- structions, which is not the case with Field Programmable Gate Array (FPGA). The main objective of this work is to monitor a network of 40 CO2 sensors and to perform real-time sorting of all data. In addition, the run time analysis of two sorting algorithms is performed: bubble sort and insertion sort. For this purpose, an FPGA- based architecture is implemented, controlled by a finite state machine(FSM), which executes each of the sorting algorithms. The results show that the insertion sort algorithm is faster than the burbble sort, but consumes more hardware resources in the FPG

Response and resistance to BET bromodomain inhibitors in triple-negative breast cancer

Triple-negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. BET bromodomain inhibitors, which have shown efficacy in several models of cancer have not been evaluated in TNBC. These inhibitors displace BET bromodomain proteins such as BRD4 from chromatin by competing with their acetyl-lysine recognition modules, leading to inhibition of oncogenic transcriptional programs. Here we report the preferential sensitivity of TNBCs to BET bromodomain inhibition in vitro and in vivo, establishing a rationale for clinical investigation and further motivation to understand mechanisms of resistance. In paired cell lines selected for acquired resistance to BET inhibition from previously sensitive TNBCs, we failed to identify gatekeeper mutations, new driver events or drug pump activation. BET-resistant TNBC cells remain dependent on wild-type BRD4, which supports transcription and cell proliferation in a bromodomain-independent manner. Proteomic studies of resistant TNBC identify strong association with MED1 and hyper-phosphorylation of BRD4 attributable to decreased activity of PP2A, identified here as a principal BRD4 serine phosphatase. Together, these studies provide a rationale for BET inhibition in TNBC and present mechanism-based combination strategies to anticipate clinical drug resistance

Response and resistance to BET bromodomain inhibitors in triple-negative breast cancer.

Triple-negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. BET bromodomain inhibitors, which have shown efficacy in several models of cancer, have not been evaluated in TNBC. These inhibitors displace BET bromodomain proteins such as BRD4 from chromatin by competing with their acetyl-lysine recognition modules, leading to inhibition of oncogenic transcriptional programs. Here we report the preferential sensitivity of TNBCs to BET bromodomain inhibition in vitro and in vivo, establishing a rationale for clinical investigation and further motivation to understand mechanisms of resistance. In paired cell lines selected for acquired resistance to BET inhibition from previously sensitive TNBCs, we failed to identify gatekeeper mutations, new driver events or drug pump activation. BET-resistant TNBC cells remain dependent on wild-type BRD4, which supports transcription and cell proliferation in a bromodomain-independent manner. Proteomic studies of resistant TNBC identify strong association with MED1 and hyper-phosphorylation of BRD4 attributable to decreased activity of PP2A, identified here as a principal BRD4 serine phosphatase. Together, these studies provide a rationale for BET inhibition in TNBC and present mechanism-based combination strategies to anticipate clinical drug resistance

Role of cyclooxygenase-2 in the progression of tumors of the lung and the mammary gland

Diversos tipos de tumores poseen elevados niveles de expresión de la ciclooxigenasa-2 y de producción de prostaglandinas. El uso de los antiinflamatorios no esteroides resultó beneficioso en el tratamiento de distintos modelos tumorales, a veces independientemente de la expresión de las ciclooxigenasas, sus blancos primarios. Nuestro objetivo en este trabajo de tesis fue estudiar el papel de la COX-2 en la progresión de distintos modelos tumorales. Utilizamos el adenocarcinoma de pulmón murino LP07 y hallamos que la COX-2 es un componente importante del comportamiento maligno de estas células. En este modelo, la inhibición de la COX-2 redujo el crecimiento del tumor primario y el desarrollo metastásico así como también los síndromes paraneoplásicos provocados por el tumor. La COX-2 y la PGE2 tienen un papel clave en la modulación de la supervivencia de las células LP07, que ejerce modulando las actividades de las quinasas Akt y p38, así como también la actividad del factor de transcripción NF-κB. En los adenocarcinomas de mama murinos LM3 y LMM3 la importancia de la COX-2 es menos relevante, ya que si bien el uso de un inhibidor selectivo de esta enzima, el celecoxib, produjo esencialmente los mismos resultados que en las células LP07, un análogo carente de actividad inhibitoria se comportó de manera similar. La PGE2 exógena no revirtió ninguno de los efectos del celecoxib. En estas células, la modulación de la biología tumoral involucró también un aumento de la apoptosis y el arresto del ciclo celular posiblemente mediado por p21 y p27. Finalmente, utilizamos un modelo más complejo, con el cocultivo de células de un carcinoma ductal in situ de mama humano y fibroblastos inflamatorios de artritis reumática. Las células del CDIS MCF10DCIS.com no expresan COX-2, la cual es inducida cuando son cocultivadas con los fibroblastos de AR. Encontramos que los fibroblastos inducen la progresión hacia el carcinoma invasivo, en parte modulada por la COX-2, cuya inhibición disminuyó los niveles de la MMP-14 y la actividad de la MMP-9. La inhibición de la COX-2, el NF-κB y la MMP-9 redujo la capacidad invasiva de las células MCF10DCIS.com inducida por las interacciones con los fibroblastos inflamatorios. En conjunto, este trabajo sugiere la utilidad de los inhibidores de la COX-2 para el tratamiento de la progresión tumoral y la participación de esta enzima en la modulación del comportamiento de algunos tumores ya sea mediante su expresión constitutiva o inducida por un microambiente inflamatorio

Rol de la ciclooxigenasa-2 en la progresión de tumores de pulmón y mama

Diversos tipos de tumores poseen elevados niveles de expresión de la ciclooxigenasa-2 y de producción de prostaglandinas. El uso de los antiinflamatorios no esteroides resultó beneficioso en el tratamiento de distintos modelos tumorales, a veces independientemente de la expresión de las ciclooxigenasas, sus blancos primarios. Nuestro objetivo en este trabajo de tesis fue estudiar el papel de la COX-2 en la progresión de distintos modelos tumorales. Utilizamos el adenocarcinoma de pulmón murino LP07 y hallamos que la COX-2 es un componente importante del comportamiento maligno de estas células. En este modelo, la inhibición de la COX-2 redujo el crecimiento del tumor primario y el desarrollo metastásico así como también los síndromes paraneoplásicos provocados por el tumor. La COX-2 y la PGE2 tienen un papel clave en la modulación de la supervivencia de las células LP07, que ejerce modulando las actividades de las quinasas Akt y p38, así como también la actividad del factor de transcripción NF-κB. En los adenocarcinomas de mama murinos LM3 y LMM3 la importancia de la COX-2 es menos relevante, ya que si bien el uso de un inhibidor selectivo de esta enzima, el celecoxib, produjo esencialmente los mismos resultados que en las células LP07, un análogo carente de actividad inhibitoria se comportó de manera similar. La PGE2 exógena no revirtió ninguno de los efectos del celecoxib. En estas células, la modulación de la biología tumoral involucró también un aumento de la apoptosis y el arresto del ciclo celular posiblemente mediado por p21 y p27. Finalmente, utilizamos un modelo más complejo, con el cocultivo de células de un carcinoma ductal in situ de mama humano y fibroblastos inflamatorios de artritis reumática. Las células del CDIS MCF10DCIS.com no expresan COX-2, la cual es inducida cuando son cocultivadas con los fibroblastos de AR. Encontramos que los fibroblastos inducen la progresión hacia el carcinoma invasivo, en parte modulada por la COX-2, cuya inhibición disminuyó los niveles de la MMP-14 y la actividad de la MMP-9. La inhibición de la COX-2, el NF-κB y la MMP-9 redujo la capacidad invasiva de las células MCF10DCIS.com inducida por las interacciones con los fibroblastos inflamatorios. En conjunto, este trabajo sugiere la utilidad de los inhibidores de la COX-2 para el tratamiento de la progresión tumoral y la participación de esta enzima en la modulación del comportamiento de algunos tumores ya sea mediante su expresión constitutiva o inducida por un microambiente inflamatorio

Analysis of Sorting Algorithms Using a WSN and Environmental Pollution Data based on FPGA

Wireless Snesor Network (WSN) based sys- tems with a focus on Internet of Things (IoT) applications generate a large amount of data. Many applications that need to process data in real time make use of microcontroller-based architectures with sequential pro- gramming. Systems based on sequential programming can emulate parallelism up to a certain number of in- structions, which is not the case with Field Programmable Gate Array (FPGA). The main objective of this work is to monitor a network of 40 CO2 sensors and to perform real-time sorting of all data. In addition, the run time analysis of two sorting algorithms is performed: bubble sort and insertion sort. For this purpose, an FPGA- based architecture is implemented, controlled by a finite state machine(FSM), which executes each of the sorting algorithms. The results show that the insertion sort algorithm is faster than the burbble sort, but consumes more hardware resources in the FPG

Small Diameter Cell-Free Tissue-Engineered Vascular Grafts: Biomaterials and Manufacture Techniques to Reach Suitable Mechanical Properties

Vascular grafts (VGs) are medical devices intended to replace the function of a blood vessel. Available VGs in the market present low patency rates for small diameter applications setting the VG failure. This event arises from the inadequate response of the cells interacting with the biomaterial in the context of operative conditions generating chronic inflammation and a lack of regenerative signals where stenosis or aneurysms can occur. Tissue Engineered Vascular grafts (TEVGs) aim to induce the regeneration of the native vessel to overcome these limitations. Besides the biochemical stimuli, the biomaterial and the particular micro and macrostructure of the graft will determine the specific behavior under pulsatile pressure. The TEVG must support blood flow withstanding the exerted pressure, allowing the proper compliance required for the biomechanical stimulation needed for regeneration. Although the international standards outline the specific requirements to evaluate vascular grafts, the challenge remains in choosing the proper biomaterial and manufacturing TEVGs with good quality features to perform satisfactorily. In this review, we aim to recognize the best strategies to reach suitable mechanical properties in cell-free TEVGs according to the reported success of different approaches in clinical trials and pre-clinical trials

Beyond the Fantastic : Contemporary Art Criticism From Latin America

Mosquera offers his selection of 22 essays as an introduction to the ongoing critical debates within and without Latin America about Latin American art. The selections, Mosquera notes, are characteristic of newer theories since the 1980s, representing a shift away from the key concepts of the criticism of the 1960s, such as “resistance” and “revolution,” towards those like “hybridisation” and “appropriation” which share features with North American-style multiculturalism and mass culture. Brief biographical notes on the authors. Glossary, 2 p. Circa 290 bibl. ref

EN1 Is a Transcriptional Dependency in Triple-Negative Breast Cancer Associated with Brain Metastasis.

To define transcriptional dependencies of triple-negative breast cancer (TNBC), we identified transcription factors highly and specifically expressed in primary TNBCs and tested their requirement for cell growth in a panel of breast cancer cell lines. We found that EN1 (engrailed 1) is overexpressed in TNBCs and its downregulation preferentially and significantly reduced viability and tumorigenicity in TNBC cell lines. By integrating gene expression changes after EN1 downregulation with EN1 chromatin binding patterns, we identified genes involved in WNT and Hedgehog signaling, neurogenesis, and axonal guidance as direct EN1 transcriptional targets. Quantitative proteomic analyses of EN1-bound chromatin complexes revealed association with transcriptional repressors and coactivators including TLE3, TRIM24, TRIM28, and TRIM33. High expression of EN1 correlated with short overall survival and increased risk of developing brain metastases in patients with TNBC. Thus, EN1 is a prognostic marker and a potential therapeutic target in TNBC. SIGNIFICANCE: These findings show that the EN1 transcription factor regulates neurogenesis-related genes and is associated with brain metastasis in triple-negative breast cancer