The walls of gated communities in Brazil and Turkey: security, separation or status?

Gated communities are common types of housing estates found in many countries. They are based on strictly controlled access of people. Houses, and at times high-rise apartment blocks, are built behind a common wall, along private internal streets. Both in Brazil and in Turkey these types of residential neighborhoods can be found mainly on the outskirts of large urban areas. This paper investigates the reasons for the increase of such residential areas, in relation to the two countries urban problems. In Brazil the dominant reason for the proliferation of gated communities, found in the literature and in advertisement of such estates, is security, in view of the countries high crime rates. In Turkey the main reason for a family to choose to live in such residential areas is status and privacy. Although Brazil and Turkey have very different cultural backgrounds, in both countries gated communities are increasingly popular. The attraction of these so-called communities must therefore be analyzed. Are people more vulnerable in large mega-cities? Also, the impact on urban prospects as a whole must be discussed. Socio-cultural and psychological concepts such as territoriality, security, privacy, which can be represented by a pattern of behavior of an individual or group, as based on control of space, are thus touched on in the paper. Conclusions confirm that the reasons for preferences for gated communities are the feeling of belonging to a special place, fear of crime and a sense security and determine decision making of families in their homeownership choices

Bax affects intracellular Ca2+ stores and induces Ca2+ wave propagation

In the present study, we evaluated proapoptotic protein Bax on mitochondria and Ca2+ homeostasis in primary cultured astrocytes. We found that recombinant Bax (rBax, 10 and 100 ng/ml) induces a loss in mitochondrial membrane potential (DeltaPsi(m)). This effect might be related to the inhibition of respiratory rates and a partial release of cytochrome c, which may change mitochondrial morphology. the loss of DeltaPsi(m) and a selective permeabilization of mitochondrial membranes contribute to the release of Ca2+ from the mitochondria. This was inhibited by cyclosporin A (5 muM) and Ruthenium Red (1 mug/ml), indicating the involvement of mitochondrial Ca2+ transport mechanisms. Bax-induced mitochondrial Ca2+ release evokes Ca2+ waves and wave propagation between cells. Our results show that Bax induces mitochondrial alteration that affects Ca2+ homeostasis and signaling. These changes show that Ca2+ signals might be correlated with the proapoptotic activities of Bax.Universidade Federal de São Paulo, UNIFESP, INFAR, Dept Pharmacol, BR-04044020 São Paulo, BrazilNINDS, Biochem Sect, NIH, Bethesda, MD 20892 USAUniv São Paulo, Inst Quim, Dept Biochem, São Paulo, BrazilUniversidade Federal de São Paulo, UNIFESP, INFAR, Dept Pharmacol, BR-04044020 São Paulo, BrazilWeb of Scienc

Análise crítica da aplicação do custeio-meta no desenvolvimento de empreendimentos de habitação de interesse social

O custeio-meta é uma abordagem amplamente aplicada na manufatura e representa uma inovação no processo de desenvolvimento de produtos, em que o custo, a qualidade e a funcionalidade não são conseqüências do processo de projeto, mas parâmetros de entrada. Este artigo investiga a aplicabilidade da abordagem custeio-meta no desenvolvimento de empreendimentos habitacionais de interesse social (EHIS). Tais empreendimentos possuem muitas peculiaridades em relação a produtos da manufatura, não havendo evidências de que esta abordagem seja adequada ao desenvolvimento de EHIS, nem mesmo de produtos da construção civil em geral. Este artigo se propõe a investigar como e por que algumas características dos EHIS - a maioria delas comuns também a outros tipos de empreendimentos de construção - influenciam a aplicabilidade do custeio-meta. Estas questões foram analisadas com base na adaptação de conceitos da manufatura para a construção civil e num estudo de caso exploratório conduzido em uma companhia estadual de provisão habitacional. O estudo propõe adaptar o custeio-meta às condições do contexto de análise, concentrar esforços nas atividades mais vantajosas ou ajustar o contexto de análise de modo a maximizar os seus benefícios e minimizar incertezas

Preconditioning Involves Selective Mitophagy Mediated by Parkin and p62/SQSTM1

Autophagy-dependent mitochondrial turnover in response to cellular stress is necessary for maintaining cellular homeostasis. However, the mechanisms that govern the selective targeting of damaged mitochondria are poorly understood. Parkin, an E3 ubiquitin ligase, has been shown to be essential for the selective clearance of damaged mitochondria. Parkin is expressed in the heart, yet its function has not been investigated in the context of cardioprotection. We previously reported that autophagy is required for cardioprotection by ischemic preconditioning (IPC). In the present study, we used simulated ischemia (sI) in vitro and IPC of hearts to investigate the role of Parkin in mediating cardioprotection ex vivo and in vivo. In HL-1 cells, sI induced Parkin translocation to mitochondria and mitochondrial elimination. IPC induced Parkin translocation to mitochondria in Langendorff-perfused rat hearts and in vivo in mice subjected to regional IPC. Mitochondrial depolarization with an uncoupling agent similarly induced Parkin translocation to mitochondria in cells and Langendorff-perfused rat hearts. Mitochondrial loss was blunted in Atg5-deficient cells, revealing the requirement for autophagy in mitochondrial elimination. Consistent with previous reports indicating a role for p62/SQSTM1 in mitophagy, we found that depletion of p62 attenuated mitophagy and exacerbated cell death in HL-1 cardiomyocytes subjected to sI. While wild type mice showed p62 translocation to mitochondria and an increase in ubiquitination, Parkin knockout mice exhibited attenuated IPC-induced p62 translocation to the mitochondria. Importantly, ablation of Parkin in mice abolished the cardioprotective effects of IPC. These results reveal for the first time the crucial role of Parkin and mitophagy in cardioprotection

Análise do conforto ambiental em salas de aula: comparação entre dados técnicos e a percepção do usuário

Este trabalho trata da avaliação in loco do conforto ambiental de salas de aula de duas edificações com arquitetura e técnicas construtivas diferentes, que compõe a estrutura da Universidade Federal de Goiás. A pesquisa objetiva explorar essas edificações, buscando identificar a influência das tecnologias construtivas adotadas e da conformação física das mesmas no seu desempenho. Os dados técnicos levantados foram avaliados por modalidade de conforto. No conforto lumínico, realizaram-se medições próximas aos solstícios e equinócios. Os dados de conforto térmico coletados foram a temperatura e a umidade relativa do ar, por um período de onze meses. Já as medições acústicas buscaram a caracterização expedita do clima de ruídos (soundscape) em ambas as edificações, por meio da coleta dos níveis de pressão sonora ocorrentes ao longo de um dia de atividades cotidianas. Notou-se que apesar de as edificações possuírem orientação solar similar, os resultados de desempenho térmico e lumínico dos edifícios foram bastante diferenciados. Paralelamente às avaliações técnicas, foram aplicados questionários aos usuários das salas estudadas, que buscaram caracterizar a percepção destes, em relação a cada uma das modalidades de conforto. Da comparação dos dados técnicos e perceptivos, observou-se que as opiniões dos usuários não foram condizentes com os resultados da análise técnica. Detectou-se divergências entre a proposta de zona de conforto adotada e a satisfação dos usuários das edificações

Role of Mitofusin 2 in the Renal Stress Response

The role of mitofusin 2 (MFN2), a key regulator of mitochondrial morphology and function in the renal stress response is unknown. To assess its role, the MFN2 floxed gene was conditionally deleted in the kidney of mice (MFN2 cKO) by Pax2 promoter driven Cre expression (Pax2Cre). MFN2 cKO caused severe mitochondrial fragmentation in renal epithelial cells that are critical for normal kidney tubular function. However, despite a small (20%) decrease in nephron number, newborn cKO pups had organ or tubular function that did not differ from littermate Cre-negative pups. MFN2 deficiency in proximal tubule epithelial cells in primary culture induced mitochondrial fragmentation but did not significantly alter ATP turnover, maximal mitochondrial oxidative reserve capacity, or the low level of oxygen consumption during cyanide exposure. MFN2 deficiency also did not increase apoptosis of tubule epithelial cells under non-stress conditions. In contrast, metabolic stress caused by ATP depletion exacerbated mitochondrial outer membrane injury and increased apoptosis by 80% in MFN2 deficient vs. control cells. Despite similar stress-induced Bax 6A7 epitope exposure in MFN2 deficient and control cells, MFN2 deficiency significantly increased mitochondrial Bax accumulation and was associated with greater release of both apoptosis inducing factor and cytochrome c. In conclusion, MFN2 deficiency in the kidney causes mitochondrial fragmentation but does not affect kidney or tubular function during development or under non-stress conditions. However, MFN2 deficiency exacerbates renal epithelial cell injury by promoting Bax-mediated mitochondrial outer membrane injury and apoptosis

Wood Utilization Is Dependent on Catalase Activities in the Filamentous Fungus Podospora anserina

Catalases are enzymes that play critical roles in protecting cells against the toxic effects of hydrogen peroxide. They are implicated in various physiological and pathological conditions but some of their functions remain unclear. In order to decipher the role(s) of catalases during the life cycle of Podospora anserina, we analyzed the role of the four monofunctional catalases and one bifunctional catalase-peroxidase genes present in its genome. The five genes were deleted and the phenotypes of each single and all multiple mutants were investigated. Intriguingly, although the genes are differently expressed during the life cycle, catalase activity is dispensable during both vegetative growth and sexual reproduction in laboratory conditions. Catalases are also not essential for cellulose or fatty acid assimilation. In contrast, they are strictly required for efficient utilization of more complex biomass like wood shavings by allowing growth in the presence of lignin. The secreted CATB and cytosolic CAT2 are the major catalases implicated in peroxide resistance, while CAT2 is the major player during complex biomass assimilation. Our results suggest that P. anserina produces external H2O2 to assimilate complex biomass and that catalases are necessary to protect the cells during this process. In addition, the phenotypes of strains lacking only one catalase gene suggest that a decrease of catalase activity improves the capacity of the fungus to degrade complex biomass

New insight into the effects of lead modulation on antioxidant defense mechanism and trace element concentration in rat bone

Risks of heavy metals-induced severe bone disorders generate interest to their toxicity. The present study was undertaken to monitor the biochemical and antioxidant status of bone of 30 and 80 days old male Wistar rats exposed to 5 week lead treatment. At the end of study, the rats were sacrificed, their long bone i.e. femur were excised, cleaned of soft tissue, minced and homogenized. Nucleic acid content, alkaline phosphatase, lipid peroxidation, catalase, glutathione S-transferase and superoxide dismutase were determined in bone. In both groups of treated animals lead treatment increased the production of malondialdehyde, while reducing activities of catalase, glutathione S-transferase and superoxide dismutase, indicating that it causes oxidative stress. Parallely with these effects lead significantly reduced the nucleic acid content and the activity of alkaline phosphatase, considered as biomarkers of osteoblast's function, conditions and development of bones. Moreover the concentrations of copper, zinc, iron and sodium were reduced in the excised bones. The present study indicates that the lead induced bone toxicity and its deteriorated development is the consequence of a primary oxidative stress. Our results may be helpful in understanding the modulation of biochemical parameters under lead toxicity

Dedifferentiation and Proliferation of Mammalian Cardiomyocytes

It has long been thought that mammalian cardiomyocytes are terminally-differentiated and unable to proliferate. However, myocytes in more primitive animals such as zebrafish are able to dedifferentiate and proliferate to regenerate amputated cardiac muscle.Here we test the hypothesis that mature mammalian cardiomyocytes retain substantial cellular plasticity, including the ability to dedifferentiate, proliferate, and acquire progenitor cell phenotypes. Two complementary methods were used: 1) cardiomyocyte purification from rat hearts, and 2) genetic fate mapping in cardiac explants from bi-transgenic mice. Cardiomyocytes isolated from rodent hearts were purified by multiple centrifugation and Percoll gradient separation steps, and the purity verified by immunostaining and RT-PCR. Within days in culture, purified cardiomyocytes lost their characteristic electrophysiological properties and striations, flattened and began to divide, as confirmed by proliferation markers and BrdU incorporation. Many dedifferentiated cardiomyocytes went on to express the stem cell antigen c-kit, and the early cardiac transcription factors GATA4 and Nkx2.5. Underlying these changes, inhibitory cell cycle molecules were suppressed in myocyte-derived cells (MDCs), while microRNAs known to orchestrate proliferation and pluripotency increased dramatically. Some, but not all, MDCs self-organized into spheres and re-differentiated into myocytes and endothelial cells in vitro. Cell fate tracking of cardiomyocytes from 4-OH-Tamoxifen-treated double-transgenic MerCreMer/ZEG mouse hearts revealed that green fluorescent protein (GFP) continues to be expressed in dedifferentiated cardiomyocytes, two-thirds of which were also c-kit(+).Contradicting the prevailing view that they are terminally-differentiated, postnatal mammalian cardiomyocytes are instead capable of substantial plasticity. Dedifferentiation of myocytes facilitates proliferation and confers a degree of stemness, including the expression of c-kit and the capacity for multipotency

Mitochondrial Fragmentation Is Involved in Methamphetamine-Induced Cell Death in Rat Hippocampal Neural Progenitor Cells

Methamphetamine (METH) induces neurodegeneration through damage and apoptosis of dopaminergic nerve terminals and striatal cells, presumably via cross-talk between the endoplasmic reticulum and mitochondria-dependent death cascades. However, the effects of METH on neural progenitor cells (NPC), an important reservoir for replacing neurons and glia during development and injury, remain elusive. Using a rat hippocampal NPC (rhNPC) culture, we characterized the METH-induced mitochondrial fragmentation, apoptosis, and its related signaling mechanism through immunocytochemistry, flow cytometry, and Western blotting. We observed that METH induced rhNPC mitochondrial fragmentation, apoptosis, and inhibited cell proliferation. The mitochondrial fission protein dynamin-related protein 1 (Drp1) and reactive oxygen species (ROS), but not calcium (Ca2+) influx, were involved in the regulation of METH-induced mitochondrial fragmentation. Furthermore, our results indicated that dysregulation of ROS contributed to the oligomerization and translocation of Drp1, resulting in mitochondrial fragmentation in rhNPC. Taken together, our data demonstrate that METH-mediated ROS generation results in the dysregulation of Drp1, which leads to mitochondrial fragmentation and subsequent apoptosis in rhNPC. This provides a potential mechanism for METH-related neurodegenerative disorders, and also provides insight into therapeutic strategies for the neurodegenerative effects of METH