Fungal infection characterization in a Peritoneal Dialysis Unit

Dubois Jean-Jacques. B. Lizet, F. de Ravignan ; Comprendre un paysage. Guide pratique de recherche. 1987. In: Hommes et Terres du Nord, 1987/4. Tourisme et développement local et régional. p. 256

A telomerase e a terapêutica do cancro: futuras perspectivas

Os telómeros localizam-se nas terminações dos cromossomas, sendo essenciais para a manutenção da sua integridade, prevenindo fusões terminais. Grande parte das proteínas com localização nos telómeros foram recentemente identificadas, contudo muitas das suas funções continuam por esclarecer. Mutações em genes codificantes destas proteínas causam diversas síndromes genéticas raras, caracterizadas por instabilidade genética, cromossómica e predisposição para cancro. A compreensão do funcionamento biológico do telómero, permitirá o desenvolvimento de novos métodos de diagnóstico, prevenção e terapêuticas mais eficazes para cada síndrome. Telomeres are located at chromosomes ends, having essential roles in preventing terminal fusions. Several telomeric proteins were recently identified, however most of their functions are not yet understood. Mutations at the genes encoding these proteins cause a number of rare genetic syndromes, characterized by genetic and/or chromosome instability and predisposition to cancer. The understanding of the whole mechanism of operation of telomere biology, will enable the development of new methods of diagnosis, prevention and more effective treatment for each syndrome

A telomerase e a terapêutica do cancro: futuras perspectivas

Os telómeros localizam-se nas terminações dos cromossomas, sendo essenciais para a manutenção da sua integridade, prevenindo fusões terminais. Grande parte das proteínas com localização nos telómeros foram recentemente identificadas, contudo muitas das suas funções continuam por esclarecer. Mutações em genes codificantes destas proteínas causam diversas síndromes genéticas raras, caracterizadas por instabilidade genética, cromossómica e predisposição para cancro. A compreensão do funcionamento biológico do telómero, permitirá o desenvolvimento de novos métodos de diagnóstico, prevenção e terapêuticas mais eficazes para cada síndrome. Telomeres are located at chromosomes ends, having essential roles in preventing terminal fusions. Several telomeric proteins were recently identified, however most of their functions are not yet understood. Mutations at the genes encoding these proteins cause a number of rare genetic syndromes, characterized by genetic and/or chromosome instability and predisposition to cancer. The understanding of the whole mechanism of operation of telomere biology, will enable the development of new methods of diagnosis, prevention and more effective treatment for each syndrome

Epigenetic Telomere Protection by Drosophila DNA Damage Response Pathways

Analysis of terminal deletion chromosomes indicates that a sequence-independent mechanism regulates protection of Drosophila telomeres. Mutations in Drosophila DNA damage response genes such as atm/tefu, mre11, or rad50 disrupt telomere protection and localization of the telomere-associated proteins HP1 and HOAP, suggesting that recognition of chromosome ends contributes to telomere protection. However, the partial telomere protection phenotype of these mutations limits the ability to test if they act in the epigenetic telomere protection mechanism. We examined the roles of the Drosophila atm and atr-atrip DNA damage response pathways and the nbs homolog in DNA damage responses and telomere protection. As in other organisms, the atm and atr-atrip pathways act in parallel to promote telomere protection. Cells lacking both pathways exhibit severe defects in telomere protection and fail to localize the protection protein HOAP to telomeres. Drosophila nbs is required for both atm- and atr-dependent DNA damage responses and acts in these pathways during DNA repair. The telomere fusion phenotype of nbs is consistent with defects in each of these activities. Cells defective in both the atm and atr pathways were used to examine if DNA damage response pathways regulate telomere protection without affecting telomere specific sequences. In these cells, chromosome fusion sites retain telomere-specific sequences, demonstrating that loss of these sequences is not responsible for loss of protection. Furthermore, terminally deleted chromosomes also fuse in these cells, directly implicating DNA damage response pathways in the epigenetic protection of telomeres. We propose that recognition of chromosome ends and recruitment of HP1 and HOAP by DNA damage response proteins is essential for the epigenetic protection of Drosophila telomeres. Given the conserved roles of DNA damage response proteins in telomere function, related mechanisms may act at the telomeres of other organisms

Bambu: Caminhos para o Desenvolvimento Sustentável

publicação de livroEste livro foi produzido a partir da iniciativa de construção de uma rede de pesquisa em bambu. Desta forma, colaboraram na construção coletiva do material, pesquisadores da Universidade Federal de Santa Catarina (UFSC), Universidade Tecnológica do Paraná (UTFPR), Universidade Estadual de Londrina (UEL), UNESP (Universidade Estadual Paulista Júlio de Mesquita Filho) e Universidade Estadual de Campinas (UNICAMP). Em uma linguagem acessível apresenta o conteúdo voltado ao entendimento das características biológicas do bambu, suas propriedades e etapas da cadeia produtiva como forma de estimular o desenvolvimento produtivo sustentável no Brasil.Sem financiamento

Dual Role of Topoisomerase II in Centromere Resolution and Aurora B Activity

Chromosome segregation requires sister chromatid resolution. Condensins are essential for this process since they organize an axial structure where topoisomerase II can work. How sister chromatid separation is coordinated with chromosome condensation and decatenation activity remains unknown. We combined four-dimensional (4D) microscopy, RNA interference (RNAi), and biochemical analyses to show that topoisomerase II plays an essential role in this process. Either depletion of topoisomerase II or exposure to specific anti-topoisomerase II inhibitors causes centromere nondisjunction, associated with syntelic chromosome attachments. However, cells degrade cohesins and timely exit mitosis after satisfying the spindle assembly checkpoint. Moreover, in topoisomerase II–depleted cells, Aurora B and INCENP fail to transfer to the central spindle in late mitosis and remain tightly associated with centromeres of nondisjoined sister chromatids. Also, in topoisomerase II–depleted cells, Aurora B shows significantly reduced kinase activity both in S2 and HeLa cells. Codepletion of BubR1 in S2 cells restores Aurora B kinase activity, and consequently, most syntelic attachments are released. Taken together, our results support that topoisomerase II ensures proper sister chromatid separation through a direct role in centromere resolution and prevents incorrect microtubule–kinetochore attachments by allowing proper activation of Aurora B kinase

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field