Development of an Approach for Producing Architectural form in Architectural Design Education

AbstractAt the early stages of architectural education, it is observed that students have difficulty to produce forms. Students, during the design process, comfortably use basic geometrical elements one by one, however are not able to diversify them by transformation because of the fact that students are not capable enough to transform basic geometrical forms in accordance with arithmetical operations and geometrical transformation. In this study examining the architectural form creation; a three-month case study is conducted with first year students in Department of Architecture through which the software is used. Initially architectural projects of students designed in accordance with traditional methods and it is observed that students are not able to throughly transform the forms. At the second stage, students are expected to develop their projects through sofware transformations. Additionally, a questionaire is also conducted with students in order to define the possitive and negative aspects of forms created with this method

MITF-MIR211 axis is a novel autophagy amplifier system during cellular stress

Macroautophagy (autophagy) is an evolutionarily conserved recycling and stress response mechanism. Active at basal levels in eukaryotes, autophagy is upregulated under stress providing cells with building blocks such as amino acids. A lysosome-integrated sensor system composed of RRAG GTPases and MTOR complex 1 (MTORC1) regulates lysosome biogenesis and autophagy in response to amino acid availability. Stress-mediated inhibition of MTORC1 results in the dephosphorylation and nuclear translocation of the TFE/MITF family of transcriptional factors, and triggers an autophagy- and lysosomal-related gene transcription program. The role of family members TFEB and TFE3 have been studied in detail, but the importance of MITF proteins in autophagy regulation is not clear so far. Here we introduce for the first time a specific role for MITF in autophagy control that involves upregulation of MIR211. We show that, under stress conditions including starvation and MTOR inhibition, a MITF-MIR211 axis constitutes a novel feed-forward loop that controls autophagic activity in cells. Direct targeting of the MTORC2 component RICTOR by MIR211 led to the inhibition of the MTORC1 pathway, further stimulating MITF translocation to the nucleus and completing an autophagy amplification loop. In line with a ubiquitous function, MITF and MIR211 were co-expressed in all tested cell lines and human tissues, and the effects on autophagy were observed in a cell-type independent manner. Thus, our study provides direct evidence that MITF has rate-limiting and specific functions in autophagy regulation. Collectively, the MITF-MIR211 axis constitutes a novel and universal autophagy amplification system that sustains autophagic activity under stress conditions.No sponso

Autophagy and cancer dormancy

Metastasis and relapse account for the great majority of cancer-related deaths. Most metastatic lesions are micro metastases that have the capacity to remain in a non-dividing state called “dormancy” for months or even years. Commonly used anticancer drugs generally target actively dividing cancer cells. Therefore, cancer cells that remain in a dormant state evade conventional therapies and contribute to cancer recurrence. Cellular and molecular mechanisms of cancer dormancy are not fully understood. Recent studies indicate that a major cellular stress response mechanism, autophagy, plays an important role in the adaptation, survival and reactivation of dormant cells. In this review article, we will summarize accumulating knowledge about cellular and molecular mechanisms of cancer dormancy, and discuss the role and importance of autophagy in this context

Non-alcoholic fatty liver disease in obese children and the relationship between metabolic syndrome criteria

Aim: To investigate metabolic syndrome (MetS) and MetS criteria, and to establish whether metabolic syndrome criteria were associated with non-alcoholic fatty liver disease (NAFLD) in obese children