ENDNOTE: A EXPERIÊNCIA DA FMVZ/USP NA CAPACITAÇÃO E NORMALIZAÇÃO DE TRABALHOS

O presente trabalho relata a experiência da Biblioteca Virginie Buff D’Ápice da FMVZ/USP na capacitação do uso do software EndNote e sua aplicabilidade por seus usuários; objetiva ainda demonstrar o potencial de uso dessa ferramenta na normalização de trabalhos científicos e acadêmicos. Com dados preliminares obtidos entre os anos de 2009 e 2010, além da experiência vivenciada nesse período, foi possível constatar que o uso do EndNote pelos estudantes que participaram da capacitação oferecida pela biblioteca promoveu um índice de acerto na normalização de seus trabalhos muito acima daqueles que não foram capacitados e/ou não o utilizaram o programa. Dessa forma, pode-se considerar que uma capacitação efetiva e o uso adequado do EndNote facilitam o trabalho do pesquisador que, ao utilizá-lo, pode focar mais seus esforços na escrita do trabalho, bem como o da biblioteca responsável pela normalização de trabalhos científicos/acadêmicos

Normalização de nomes de autores em fontes de informação institucionais: proposta de um método automático de verificação de erros

A recuperação da produção científica por autoria é um desafio para diversos mantenedores de bases de dados, devido à ambiguidade causada por problemas derivados da falta de controle no momento da indexação. Este estudo apresenta um método automático para verificação de ocorrência de erros em dados de autorias da base de produção científica da Universidade de São Paulo (Dedalus) tomando como base o banco institucional de recursos humanos. Por meio de algoritmos de busca aproximada, compararam-se esses dados com os dados de autoria registrados no banco de produção científica de quatro unidades da USP (período de 2006-2010). Com base nesse estudo piloto foi possível estabelecer mecanismos de interoperabilidade entre o banco da produção e os bancos institucionais de recursos humanos, além de permitir mapear a porcentagem de erros, desenvolver mecanismos de interferência e estabelecer um cronograma para ampliar o estudo as demais unidades USP, bem como procedimentos de normalização.

Fontes de informação institucionais para normalização de nomes de autores: proposta de um método automático

A recuperação da produção científica por autoria é um desafio para diversos mantenedores de bases de dados, devido à ambiguidade causada por problemas de homonímia e possíveis variações e alterações de nome de uma mesma pessoa. A abordagem deste problema de pesquisa vem sendo proposta conjuntamente por pesquisadores das áreas de Ciência da Computação e Ciência da Informação, fazendo uso de metodologias diversas. Este estudo apresenta um método automático para verificação de ocorrência de erros em dados de autorias da base de produção científica da Universidade de São Paulo (Dedalus) tomando como base o banco corporativo de funcionários ,tanto informações administrativas e acadêmicas do sistema Tycho, ambos da USP. O Tycho forneceu informações de contexto (lista de autoridades) permitindo, por meio de algoritmos de busca aproximada, a identificação e contagem automática das variações dos nomes, bem como potenciais problemas nos registros bibliográficos.

El futuro de la profesión pasa por BIM

[ES]Presentación. BIM: Situación en el panorama nacional e internacional, Sergio Muñoz, Presidente de la BuildingSmart Spanish Chapter. ¿Qué BIM implantamos? Jesús Martínez, Arquitecto BIM Manager. BIM. Casos prácticos. Ciclo de vida de la edificación, Alejandro Núñez Noda, Director Técnico IMC Gestión Integral de la edificación. BG. BIM. Casos prácticos. Modelos BIM As-Built, Josep Coll, EiPM. BG. Smart Cities ¿Burbuja o Tendencia? Félix Herrera, responsable del Área de Ingeniería Telemática, Universidad de La Laguna. Láser Scaner 3D en la conservación del patrimonio y trabajo en grandes infraestructuras, Raúl Rubio, Captae. BG. Virtual BIM – Realidad Aumentada, Sergi Florensa, Virtual BIM.

Building Information Modelling (BIM) Effectiveness in Performing Life Cycle Assessment of Building

The scope of this project is to study the effectiveness of building information modelling (BIM) in performing life cycle assessment in a building. For the purposes of the study will be used “Revit” which is a BIM software and Tally which is an LCA tool integrated in Revit. The project is divided in six chapters. The first chapter consists of a theoretical introduction into building information modelling and its connection to life cycle assessment. The second chapter describes the characteristics of building information modelling (BIM). In addition, a comparison has been made with the traditional architectural, engineering and construction business model and the benefits to shift into BIM. In the third chapter it will be a review of the most well-known and available BIM software in the market. In chapter four life cycle assessment (LCA) will be described in general and later on specifically for the purpose of the case study that will be used in the following chapter. Moreover, the tools that are available to perform an LCA will be reviewed. Chapter five will present the case study that consists of a model in a BIM software (Revit) and the LCA performed by Tally, an LCA tool integrated into Revit. In the last chapter will be a discussion of the results that were obtained, the limitation and the possible future improvement in performing life cycle assessment (LCA) in a BIM model.

La strategia BIM a supporto del progetto della sicurezza nel cantiere edile: il caso dell'ospedale di primo soccorso a Lampedusa.

Throughout this research, the whole life cycle of a building will be analyzed, with a special focus on the most common issues that affect the construction sector nowadays, such as safety. In fact, the goal is to enhance the management of the entire construction process in order to reduce the risk of accidents. The contemporary trend is that of researching new tools capable of reducing, or even eliminating, the most common mistakes that usually lead to safety risks. That is one of the main reasons why new technologies and tools have been introduced in the field. The one we will focus on is the so-called BIM: Building Information Modeling. With the term BIM we refer to wider and more complex analysis tool than a simple 3D modeling software. Through BIM technologies we are able to generate a multi-dimension 3D model which contains all the information about the project. This innovative approach aims at a better understanding and control of the project by taking into consideration the entire life cycle and resulting in a faster and more sustainable way of management. Furthermore, BIM software allows for the sharing of all the information among the different aspects of the project and among the different participants involved thus improving the cooperation and communication. In addition, BIM software utilizes smart tools that simulate and visualize the process in advance, thus preventing issues that might not have been taking into consideration during the design process. This leads to higher chances of avoiding risks, delays and cost increases. Using a hospital case study, we will apply this approach for the completion of a safety plan, with a special focus onto the construction phase.

L'approccio interdisciplinare BIM e la sostenibilità integrata: progetto residenziale per una villetta monofamiliare in Sicilia.

Il BIM (Building Information Modeling ) è un processo coordinato per agevolare l’integrazione delle informazioni pertinenti alle varie fasi di progettazione dell’opera edilizia. La rappresentazione digitale di un edificio, completa di tutte le sue parti ed informazioni sempre aggiornate, affidabili ed accessibili, aiuta il confronto decisionale, la produzione di elaborati, la stima dei costi e tanti altri aspetti del processo edilizio che vengono così ad essere trattati in maniera più efficiente, immediata e con meno sprechi rispetto a molti approcci tradizionali ancora in uso. Con queste premesse la tesi ha voluto indagare potenzialità e criticità di strumenti progettuali avanzati per giungere ad una costruzione efficace e sostenibile. A questo scopo Revit di Autodesk si è dimostrato un software che permette di avere in un unico spazio di lavoro tutti i dati pertinenti alle figure professionali che intervengono durante il processo edilizio. Nel modello BIM realizzato per progettare realisticamente una villetta monofamiliare localizzata a Mezzojuso, in provincia di Palermo, sono stati esaminati molteplici aspetti: dal modello fisico, alla visualizzazione grafica 2D e 3D, alla modellazione parametrica di un modello concettuale energetico che coinvolge analisi di comfort termico ed igrometrico, ad un modello dei venti (per arrivare ad un design energetico ottimale). Il metodo di progetto è stato applicato facendo largo uso di elementi parametrici non standard nei modelli 3D e di altri prodotti realmente esistenti nel mercato italiano. Il risultato finale è stato quello di giungere ad una valutazione delle geometrie più idonee per il controllo degli spazi rispetto alla normativa locale, allo studio di più tipologie di pacchetti murari per risolvere i problemi di raffrescamento estivo e isolamento invernale, alla realizzazione di un computo metrico di massima: sono stati solo questi alcuni degli aspetti considerati per approcciare la tematica da un più ampio punto di vista multidisciplinare.

Tumor necrosis factor sensitizes primary murine hepatocytes to Fas/CD95-induced apoptosis in a Bim- and Bid-dependent manner

Fas/CD95 is a critical mediator of cell death in many chronic and acute liver diseases and induces apoptosis in primary hepatocytes in vitro. In contrast, the proinflammatory cytokine tumor necrosis factor α (TNFα) fails to provoke cell death in isolated hepatocytes but has been implicated in hepatocyte apoptosis during liver diseases associated with chronic inflammation. Here we report that TNFα sensitizes primary murine hepatocytes cultured on collagen to Fas ligand (FasL)-induced apoptosis. This synergism is time-dependent and is specifically mediated by TNFα. Fas itself is essential for the sensitization, but neither Fas up-regulation nor endogenous FasL is responsible for this effect. Although FasL is shown to induce Bid-independent apoptosis in hepatocytes cultured on collagen, the sensitizing effect of TNFα is clearly dependent on Bid. Moreover, both c-Jun N-terminal kinase activation and Bim, another B cell lymphoma 2 homology domain 3 (BH3)-only protein, are crucial mediators of TNFα-induced apoptosis sensitization. Bim and Bid activate the mitochondrial amplification loop and induce cytochrome c release, a hallmark of type II apoptosis. The mechanism of TNFα-induced sensitization is supported by a mathematical model that correctly reproduces the biological findings. Finally, our results are physiologically relevant because TNFα also induces sensitivity to agonistic anti-Fas-induced liver damage. CONCLUSION: Our data suggest that TNFα can cooperate with FasL to induce hepatocyte apoptosis by activating the BH3-only proteins Bim and Bid.

Synergistic induction of cell death in liver tumor cells by TRAIL and chemotherapeutic drugs via the BH3-only proteins Bim and Bid

Although death receptors and chemotherapeutic drugs activate distinct apoptosis signaling cascades, crosstalk between the extrinsic and intrinsic apoptosis pathway has been recognized as an important amplification mechanism. Best known in this regard is the amplification of the Fas (CD95) signal in hepatocytes via caspase 8-mediated cleavage of Bid and activation of the mitochondrial apoptosis pathway. Recent evidence, however, indicates that activation of other BH3-only proteins may also be critical for the crosstalk between death receptors and mitochondrial triggers. In this study, we show that TNF-related apoptosis-inducing ligand (TRAIL) and chemotherapeutic drugs synergistically induce apoptosis in various transformed and untransformed liver-derived cell lines, as well as in primary human hepatocytes. Both, preincubation with TRAIL as well as chemotherapeutic drugs could sensitize cells for apoptosis induction by the other respective trigger. TRAIL induced a strong and long lasting activation of Jun kinase, and activation of the BH3-only protein Bim. Consequently, synergistic induction of apoptosis by TRAIL and chemotherapeutic drugs was dependent on Jun kinase activity, and expression of Bim and Bid. These findings confirm a previously defined role of TRAIL and Bim in the regulation of hepatocyte apoptosis, and demonstrate that the TRAIL-Jun kinase-Bim axis is a major and important apoptosis amplification pathway in primary hepatocytes and liver tumor cells.

Thiazolide-induced apoptosis in colorectal cancer cells is mediated via the Jun kinase-Bim axis and reveals glutathione-S-transferase P1 as Achilles' heel

Glutathione-S-transferase of the Pi class (GSTP1) is frequently overexpressed in a variety of solid tumors and has been identified as a potential therapeutic target for cancer therapy. GSTP1 is a phase II detoxification enzyme and conjugates the tripeptide glutathione to endogenous metabolites and xenobiotics, thereby limiting the efficacy of antitumor chemotherapeutic treatments. In addition, GSTP1 regulates cellular stress responses and apoptosis by sequestering and inactivating c-Jun N-terminal kinase (JNK). Thiazolides are a novel class of antibiotics for the treatment of intestinal pathogens with no apparent side effects on the host cells and tissue. Here we show that thiazolides induce a GSTP1-dependent and glutathione-enhanced cell death in colorectal tumor cell lines. Downregulation of GSTP1 reduced the apoptotic activity of thiazolides, whereas overexpression enhanced it. Thiazolide treatment caused strong Jun kinase activation and Jun kinase-dependent apoptosis. As a critical downstream target of Jun kinase we identified the pro-apoptotic Bcl-2 homolog Bim. Thiazolides induced Bim expression and activation in a JNK-dependent manner. Downregulation of Bim in turn significantly blocked thiazolide-induced apoptosis. Whereas low concentrations of thiazolides failed to induce apoptosis directly, they potently sensitized colon cancer cells to TNF-related apoptosis-inducing ligand- and chemotherapeutic drug-induced cell death. Although GSTP1 overexpression generally limits chemotherapy and thus antitumor treatment, our study identifies GSTP1 as Achilles' heel and thiazolides as novel interesting apoptosis sensitizer for the treatment of colorectal tumors.

Role of TRAIL and the pro-apoptotic Bcl-2 homolog Bim in acetaminophen-induced liver damage

Acetaminophen (N-acetyl-para-aminophenol (APAP), paracetamol) is a commonly used analgesic and antipyretic agent. Although considered safe at therapeutic doses, accidental or intentional overdose causes acute liver failure characterized by centrilobular hepatic necrosis with high morbidity and mortality. Although many molecular aspects of APAP-induced cell death have been described, no conclusive mechanism has been proposed. We recently identified TNF-related apoptosis-inducing ligand (TRAIL) and c-Jun kinase (JNK)-dependent activation of the pro-apoptotic Bcl-2 homolog Bim as an important apoptosis amplification pathway in hepatocytes. In this study, we, thus, investigated the role of TRAIL, c-JNK and Bim in APAP-induced liver damage. Our results demonstrate that TRAIL strongly synergizes with APAP in inducing cell death in hepatocyte-like cells lines and primary hepatocyte. Furthermore, we found that APAP strongly induces the expression of Bim in a c-JNK-dependent manner. Consequently, TRAIL- or Bim-deficient mice were substantially protected from APAP-induced liver damage. This study identifies the TRAIL-JNK-Bim axis as a novel target in the treatment of APAP-induced liver damage and substantiates its general role in hepatocyte death.

The proapoptotic Bcl-2 family member Bim plays a central role during the development of virus-induced hepatitis

The proapoptotic Bcl-2 homolog Bim was shown to control the apoptosis of both T cells and hepatocytes. This dual role of Bim might be particularly relevant for the development of viral hepatitis, in which both the sensitivity of hepatocytes to apoptosis stimuli and the persistence of cytotoxic T cells are essential factors for the outcome of the disease. The relevance of Bim in regulating survival of cytotoxic T cells or induction of hepatocyte death has only been investigated in separate systems, and their relative contributions to the pathogenesis of T cell-mediated hepatitis remain unclear. Using the highly dynamic model system of lymphocytic choriomeningitis virus-mediated hepatitis and bone marrow chimeras, we found that Bim has a dual role in the development of lymphocytic choriomeningitis virus-induced, T cell-mediated hepatitis. Although the absence of Bim in parenchymal cells led to markedly attenuated liver damage, loss of Bim in the lymphoid compartment moderately enhanced hepatitis. However, when both effects were combined in Bim(-/-) mice, the effect of Bim deficiency in the lymphoid compartment was overcompensated for by the reduced sensitivity of Bim(-/-) hepatocytes to T cell-induced apoptosis, resulting in the protection of Bim(-/-) mice from hepatitis.

TRAIL enhances paracetamol-induced liver sinusoidal endothelial cell death in a Bim- and Bid-dependent manner

Paracetamol (acetaminophen, APAP) is a universally used analgesic and antipyretic agent. Considered safe at therapeutic doses, overdoses cause acute liver damage characterized by centrilobular hepatic necrosis. One of the major clinical problems of paracetamol-induced liver disease is the development of hemorrhagic alterations. Although hepatocytes represent the main target of the cytotoxic effect of paracetamol overdose, perturbations within the endothelium involving morphological changes of liver sinusoidal endothelial cells (LSECs) have also been described in paracetamol-induced liver disease. Recently, we have shown that paracetamol-induced liver damage is synergistically enhanced by the TRAIL signaling pathway. As LSECs are constantly exposed to activated immune cells expressing death ligands, including TRAIL, we investigated the effect of TRAIL on paracetamol-induced LSEC death. We here demonstrate for the first time that TRAIL strongly enhances paracetamol-mediated LSEC death with typical features of apoptosis. Inhibition of caspases using specific inhibitors resulted in a strong reduction of cell death. TRAIL appears to enhance paracetamol-induced LSEC death via the activation of the pro-apoptotic BH3-only proteins Bid and Bim, which initiate the mitochondrial apoptotic pathway. Taken together this study shows that the liver endothelial layer, mainly LSECs, represent a direct target of the cytotoxic effect of paracetamol and that activation of TRAIL receptor synergistically enhances paracetamol-induced LSEC death via the mitochondrial apoptotic pathway. TRAIL-mediated acceleration of paracetamol-induced cell death may thus contribute to the pathogenesis of paracetamol-induced liver damage.