Energy-use modelling for residential buildings in the metropolitan area of Gran Mendoza (AR)

Most of the world's population is concentrated in cities and there is necessary to intervene in the management of energy consumptions to ensure a high quality of people life with good air quality and thermal comfort and an overall livability of the urban environment. Anthropic activities are the main cause of greenhouse gas emissions and this suggests the need of a different management of energy consumptions especially of buildings, one of the principal contributor of GHG emissions. The goal of this work is the evaluation of a simplified energy model that allows quantifying the spatial distribution of energy consumption at urban scale with a GIS tool. The case study is the metropolitan area of Gran Mendoza, an urban conglomerate comprising six departamentos in the central-western region of Argentina. The model estimates the energy consumption for space heating of residential buildings, after having classified the buildings according to their characteristics. This simplified model has been validated by the comparison with the real consumption data provided by the local company distributing natural gas. With this model, it is possible to elaborate energy strategies based on the real buildings heritage, identifying critical areas requiring a priority of intervention

The Transantral Endoscopic Approach: A Portal for Masses of the Inferior Orbit\u2014Improving Surgeons' Experience Through Virtual Endoscopy and Augmented Reality

In the past years, endoscopic techniques have raised an increasing interest to perform minimally invasive accesses to the orbit, resulting in excellent clinical outcomes with inferior morbidities and complication rates. Among endoscopic approaches, the transantral endoscopic approach allows us to create a portal to the orbital floor, representing the most straightforward access to lesions located in the inferior orbital space. However, if endoscopic surgery provides enhanced magnified vision of the anatomy in a bloodless field, then it has several impairments compared with classic open surgery, owing to restricted operative spaces. Virtual surgical planning and anatomical computer-generated models have proved to be of great importance to plan endoscopic surgical approaches, and their role can be widened with the integration of surgical navigation, virtual endoscopy simulation, and augmented reality (AR). This study focuses on the strict conjugation between the technologies that allow the virtualization of surgery in an entirely digital environment, which can be transferred to the patient using intraoperative navigation or to a printed model using AR for pre-surgical analysis. Therefore, the interaction between different software packages and platforms offers a highly predictive preview of the surgical scenario, contributing to increasing orientation, awareness, and effectiveness of maneuvers performed under endoscopic guidance, which can be checked at any time using surgical navigation. In this paper, the authors explore the transantral approach for the excision of masses of the inferior orbital compartment through modern technology. The authors apply this technique for masses located in the inferior orbit and share their clinical results, describing why technological innovation, and, in particular, computer planning, virtual endoscopy, navigation, and AR can contribute to empowering minimally invasive orbital surgery, at the same time offering a valuable and indispensable tool for pre-surgical analysis and training

The transcriptional regulator ZNF398 mediates pluripotency and epithelial character downstream of TGF-beta in human PSCs

Human pluripotent stem cells (hPSCs) have the capacity to give rise to all differentiated cells of the adult. TGF-beta is used routinely for expansion of conventional hPSCs as flat epithelial colonies expressing the transcription factors POU5F1/OCT4, NANOG, SOX2. Here we report a global analysis of the transcriptional programme controlled by TGF-beta followed by an unbiased gain-of-function screening in multiple hPSC lines to identify factors mediating TGF-beta activity. We identify a quartet of transcriptional regulators promoting hPSC self-renewal including ZNF398, a human-specific mediator of pluripotency and epithelial character in hPSCs. Mechanistically, ZNF398 binds active promoters and enhancers together with SMAD3 and the histone acetyltransferase EP300, enabling transcription of TGF-beta targets. In the context of somatic cell reprogramming, inhibition of ZNF398 abolishes activation of pluripotency and epithelial genes and colony formation. Our findings have clear implications for the generation of bona fide hPSCs for regenerative medicine

Metabolic control of DNA methylation in naive pluripotent cells.

Naive epiblast and embryonic stem cells (ESCs) give rise to all cells of adults. Such developmental plasticity is associated with genome hypomethylation. Here, we show that LIF-Stat3 signaling induces genomic hypomethylation via metabolic reconfiguration. Stat3-/- ESCs show decreased α-ketoglutarate production from glutamine, leading to increased Dnmt3a and Dnmt3b expression and DNA methylation. Notably, genome methylation is dynamically controlled through modulation of α-ketoglutarate availability or Stat3 activation in mitochondria. Alpha-ketoglutarate links metabolism to the epigenome by reducing the expression of Otx2 and its targets Dnmt3a and Dnmt3b. Genetic inactivation of Otx2 or Dnmt3a and Dnmt3b results in genomic hypomethylation even in the absence of active LIF-Stat3. Stat3-/- ESCs show increased methylation at imprinting control regions and altered expression of cognate transcripts. Single-cell analyses of Stat3-/- embryos confirmed the dysregulated expression of Otx2, Dnmt3a and Dnmt3b as well as imprinted genes. Several cancers display Stat3 overactivation and abnormal DNA methylation; therefore, the molecular module that we describe might be exploited under pathological conditions

Metabolic control of DNA methylation in naive pluripotent cells.

Naive epiblast and embryonic stem cells (ESCs) give rise to all cells of adults. Such developmental plasticity is associated with genome hypomethylation. Here, we show that LIF-Stat3 signaling induces genomic hypomethylation via metabolic reconfiguration. Stat3-/- ESCs show decreased α-ketoglutarate production from glutamine, leading to increased Dnmt3a and Dnmt3b expression and DNA methylation. Notably, genome methylation is dynamically controlled through modulation of α-ketoglutarate availability or Stat3 activation in mitochondria. Alpha-ketoglutarate links metabolism to the epigenome by reducing the expression of Otx2 and its targets Dnmt3a and Dnmt3b. Genetic inactivation of Otx2 or Dnmt3a and Dnmt3b results in genomic hypomethylation even in the absence of active LIF-Stat3. Stat3-/- ESCs show increased methylation at imprinting control regions and altered expression of cognate transcripts. Single-cell analyses of Stat3-/- embryos confirmed the dysregulated expression of Otx2, Dnmt3a and Dnmt3b as well as imprinted genes. Several cancers display Stat3 overactivation and abnormal DNA methylation; therefore, the molecular module that we describe might be exploited under pathological conditions