Towards Environmental Retrofitting of Egyptian Transitional Spaces: Courtyard-Building in Alexandria University, Egypt

Consuming huge amount of energy and emitting large amount of heat can be assumed as one of the main problems facing urban environment in the world today. These problems associated with current high urban density and less of vegetation within urban fabric. For instance, in Egypt, Universities are today facing rising problem of offering more educational spaces especially in large cities such as Cairo and Alexandria. The study thus focuses on Revival Egyptian buildings in Alexandria University based on hierarchical transitional spaces. As Egyptian transitional spaces, such as courtyards historically were essential outdoor spaces for multiple uses and purposes. As part of retrofitting research project of existed transitional spaces in Alexandria University, this paper focused on one parameter which is building height. This is by targeting to find the maximum height of courtyard building with minimum negative effect on air and thermal flow. This simulation is done with consideration to the surrounding urban context in Alexandria University. The simulation approach is based on two years of field measurement of thermal conditions and air velocity in the Universityrsquos transitional spaces. The study is usingfield-measurement data for nurturing the Computational Fluid Dynamics (CFD) model, and for validating the simulation results. The Computational Fluid Dynamics (CFD) study is done by introducing four cases of different building heights to investigating the changing air and thermal flow inside the existed courtyard. nbs

Can Europe recover without credit?

Data from 135 countries covering five decades suggests that creditless recoveries, in which the stock of real credit does not return to the pre-crisis level for three years after the GDP trough, are not rare and are characterised by remarkable real GDP growth rates: 4.7 percent per year in middle-income countries and 3.2 percent per year in high-income countries. However, the implications of these historical episodes for the current European situation are limited, for two main reasons. First, creditless recoveries are much less common in highincome countries, than in low-income countries which are financially undeveloped. European economies heavily depend on bank loans and research suggests that loan supply played a major role in the recent weak credit performance of Europe. There are reasons to believe that, despite various efforts, normal lending has not yet been restored. Limited loan supply could be disruptive for the European economic recovery and there has been only a minor substitution of bank loans with debt securities. Second, creditless recoveries were associated with significant real exchange rate depreciation, which has hardly occurred so far in most of Europe. This stylised fact suggests that it might be difficult to re-establish economic growth in the absence of sizeable real exchange rate depreciation, if credit growth does not return

Genetic variation in the TLL1 gene is not associated with fibrosis in patients with metabolic associated fatty liver disease

Metabolic associated fatty liver disease (MAFLD) is the most prevalent liver disease in Western nations, with high heritability. A recent study of Japanese patients with the disease suggested that TLL1 rs17047200 is associated with fibrosis; whether a similar association is observed in Caucasian patients with MAFLD is unknown. We investigated the association of the TLL1 rs17047200 polymorphism with liver fibrosis in a cohort of Caucasian patients with MAFLD (n = 728). We also investigated whether TLL1 expression is altered during liver injury in humans, in murine models of fibrosis, and in in-vitro. While TLL1 expression is upregulated in the liver of humans with MAFLD and in mice, the rs17047200 variant was not associated with fibrosis or any other histological features, or with hepatic TLL1 expression. In conclusion, the TLL1 rs17047200 variant is not a risk variant for fibrosis in Caucasian patients with MAFLD. However, TLL1 could be involved in the pathogenesis of liver fibrosis

Copy number variation and expression of exportin-4 associates with severity of fibrosis in metabolic associated fatty liver disease

Background: Liver fibrosis risk is a heritable trait, the outcome of which is the net deposition of extracellular matrix by hepatic stellate cell-derived myofibroblasts. Whereas nucleotide sequence variations have been extensively studied in liver fibrosis, the role of copy number variations (CNV) in which genes exist in abnormal numbers of copies (mostly due to duplication or deletion) has had limited exploration. Methods: The impact of the XPO4 CNV on histological liver damage was examined in a cohort comprised 646 Caucasian patients with biopsy-proven MAFLD and 170 healthy controls. XPO4 expression was modulated and function was examined in human and animal models. Findings: Here we demonstrate in a cohort of 816 subjects, 646 with biopsy-proven metabolic associated liver disease (MAFLD) and 170 controls, that duplication in the exportin 4 (XPO4) CNV is associated with the severity of liver fibrosis. Functionally, this occurs via reduced expression of hepatic XPO4 that maintains sustained activation of SMAD3/SMAD4 and promotes TGF-β1-mediated HSC activation and fibrosis. This effect was mediated through termination of nuclear SMAD3 signalling. XPO4 demonstrated preferential binding to SMAD3 compared to other SMADs and led to reduced SMAD3-mediated responses as shown by attenuation of TGFβ1 induced SMAD transcriptional activity, reductions in the recruitment of SMAD3 to target gene promoters following TGF-β1, as well as attenuation of SMAD3 phosphorylation and disturbed SMAD3/SMAD4 complex formation. Interpretation: We conclude that a CNV in XPO4 is a critical mediator of fibrosis severity and can be exploited as a therapeutic target for liver fibrosis. Funding: ME and JG are supported by the Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney; a National Health and Medical Research Council of Australia (NHMRC) Program Grant (APP1053206) and Project and ideas grants (APP2001692, APP1107178 and APP1108422). AB is supported by an Australian Government Research Training Program (RTP) scholarship. EB is supported by Horizon 2020 under grant 634413 for the project EPoS

Is there a Common European Business Cycle? New Insights from a Frequency Domain Analysis

To assess the synchronization of business cycles in Europe we extract the cyclical component of industrial production in five European countries using the filter of Baxter and King (1999). The hypothesis of a joint business cycle is tested by using the frequency domain common cycle test suggested by Breitung and Candelon (2000). The common cycle hypothesis is clearly rejected for U.K. data whereas some weak evidence for a joint cyclical pattern is found for France, The Netherlands, Austria and Germany. Zusammenfassung Gibt es einen gemeinsamen europäischen Konjunkturzyklus? Neue Erkenntnisse durch eine Spektralanalyse Um die Synchronität der Konjunkturzyklen in Europa zu bewerten, wird die Zykluskomponente der Industrieproduktion in fünf europäischen Ländern identifiziert, indem der Baxter-King-Filter (1999) angewendet wird. Die Hypothese eines gemeinsamen Konjunkturzyklus wird durch einen Test auf einen gemeinsamen Zyklus im Frequenzbereich nach Breitung und Candelon (2000) überprüft. Ein gemeinsamer Konjunkturzyklus muss demnach für Großbritannien klar zurückgewiesen werden, wohingegen einige schwache Anzeichen für ein gemeinsames Konjunkturmuster für Frankreich, die Niederlande, Österreich und Deutschland gefunden werden konnten

Mistranslation Drives Alterations in Protein Levels and the Effects of a Synonymous Variant at the Fibroblast Growth Factor 21 Locus

Fibroblast growth factor 21 (FGF21) is a liver-derived hormone with pleiotropic beneficial effects on metabolism. Paradoxically, FGF21 levels are elevated in metabolic diseases. Interventions that restore metabolic homeostasis reduce FGF21. Whether abnormalities in FGF21 secretion or resistance in peripheral tissues is the initiating factor in altering FGF21 levels and function in humans is unknown. A genetic approach is used to help resolve this paradox. The authors demonstrate that the primary event in dysmetabolic phenotypes is the elevation of FGF21 secretion. The latter is regulated by translational reprogramming in a genotype- and context-dependent manner. To relate the findings to tissues outcomes, the minor (A) allele of rs838133 is shown to be associated with increased hepatic inflammation in patients with metabolic associated fatty liver disease. The results here highlight a dominant role for translation of the FGF21 protein to explain variations in blood levels that is at least partially inherited. These results provide a framework for translational reprogramming of FGF21 to treat metabolic diseases