Widening access to refugees : Responses of Austrian public universities

Europe has been a scene of mass migration unparalleled in scale since the World War II in the last couple of years. With the recent migration flow, higher education institutions have confronted with the new challenge of managing a diverse student body from refugees and asylum seekers. Likewise, refugee and asylum seeking students have encountered various barriers in accessing higher education. Whilst significance of higher education for refugees is well-documented in the literature, higher education has not been prioritized for international support and education of refugees has received little attention until recently. Being one of the main transit countries for refugees, Austria has received approximately 90.000 asylum applications in 2015, an increase of 200% as compared to 2014, which is equivalent to about 1 percent of country's population. While policy discussions in Austria have revolved around handling the refugee crisis and offering humanitarian aid, the role of higher education in integrating refugees has not yet been considered by the policy side. In this context, the aim of this study is to analyze how the Austrian higher education system is responding to including refugees and asylum seekers and what policies and strategies they are adopting to this end. The study adopts qualitative methodology, and employs documentary research and interviews as data collection tools. Data were collected through semi-structured interviews from various stakeholders representing Austrian higher education system; universities, students, student unions and analysis of the official documents "Leistungsvereinbarung" (performance agreements) of public universities. Findings reveal that language, funding and lack of documentation constitute major obstacles for refugee students' access to higher education. While efforts are being exerted by individual universities and NGOs to meet immediate challenges, funding and support from the policy side of higher education remain scarce. Thus, a concerted national action plan for education of refugees is needed

BRAF Activation Initiates but Does Not Maintain Invasive Prostate Adenocarcinoma

Prostate cancer is the second leading cause of cancer-related deaths in men. Activation of MAP kinase signaling pathway has been implicated in advanced and androgen-independent prostate cancers, although formal genetic proof has been lacking. In the course of modeling malignant melanoma in a tyrosinase promoter transgenic system, we developed a genetically-engineered mouse (GEM) model of invasive prostate cancers, whereby an activating mutation of BRAFV600E–a mutation found in ∼10% of human prostate tumors–was targeted to the epithelial compartment of the prostate gland on the background of Ink4a/Arf deficiency. These GEM mice developed prostate gland hyperplasia with progression to rapidly growing invasive adenocarcinoma without evidence of AKT activation, providing genetic proof that activation of MAP kinase signaling is sufficient to drive prostate tumorigenesis. Importantly, genetic extinction of BRAFV600E in established prostate tumors did not lead to tumor regression, indicating that while sufficient to initiate development of invasive prostate adenocarcinoma, BRAFV600E is not required for its maintenance

Widening access to refugees : Responses of Austrian public universities

Europe has been a scene of mass migration unparalleled in scale since the World War II in the last couple of years. With the recent migration flow, higher education institutions have confronted with the new challenge of managing a diverse student body from refugees and asylum seekers. Likewise, refugee and asylum seeking students have encountered various barriers in accessing higher education. Whilst significance of higher education for refugees is well-documented in the literature, higher education has not been prioritized for international support and education of refugees has received little attention until recently. Being one of the main transit countries for refugees, Austria has received approximately 90.000 asylum applications in 2015, an increase of 200% as compared to 2014, which is equivalent to about 1 percent of country's population. While policy discussions in Austria have revolved around handling the refugee crisis and offering humanitarian aid, the role of higher education in integrating refugees has not yet been considered by the policy side. In this context, the aim of this study is to analyze how the Austrian higher education system is responding to including refugees and asylum seekers and what policies and strategies they are adopting to this end. The study adopts qualitative methodology, and employs documentary research and interviews as data collection tools. Data were collected through semi-structured interviews from various stakeholders representing Austrian higher education system; universities, students, student unions and analysis of the official documents "Leistungsvereinbarung" (performance agreements) of public universities. Findings reveal that language, funding and lack of documentation constitute major obstacles for refugee students' access to higher education. While efforts are being exerted by individual universities and NGOs to meet immediate challenges, funding and support from the policy side of higher education remain scarce. Thus, a concerted national action plan for education of refugees is needed

A prostatic intraepithelial neoplasia-dependent p27 Kip1 checkpoint induces senescence and inhibits cell proliferation and cancer progression.

Transgenic expression of activated AKT1 in the murine prostate induces prostatic intraepithelial neoplasia (PIN) that does not progress to invasive prostate cancer (CaP). In luminal epithelial cells of Akt-driven PIN, we show the concomitant induction of p27(Kip1) and senescence. Genetic ablation of p27(Kip1) led to downregulation of senescence markers and progression to cancer. In humans, p27(Kip1) and senescence markers were elevated in PIN not associated with CaP but were decreased or absent, respectively, in cancer-associated PIN and in CaP. Importantly, p27(Kip1) upregulation in mouse and human in situ lesions did not depend upon mTOR or Akt activation but was instead specifically associated with alterations in cell polarity, architecture, and adhesion molecules. These data suggest that a p27(Kip1)-driven checkpoint limits progression of PIN to CaP

Evaluation of the results of MOTAKK hepatitis C virus RNA genotyping and hepatitis delta virus external quality assessment programs during 2015-2016

Background/Aims: To evaluate the HCV RNA genotyping and HDV RNA tests that are performed in molecular microbiology laboratories in Turkey as part of a national external quality assessment programme, MOTAKK (Molekuler Tanida Kalite Kontrol) (English translation: Quality control in molecular diagnostics)

Stress response gene ATF3 is a target of c-myc in serum-induced cell proliferation

The c-myc proto-oncogene encodes a transcription factor that promotes cell cycle progression and cell proliferation, and its deficiency results in severely retarded proliferation rates. The ATF3 stress response gene encodes a transcription factor that plays a role in determining cell fate under stress conditions. Its biological significance in the control of cell proliferation and its crosstalk regulation, however, are not well understood. Here, we report that the serum response of the ATF3 gene expression depends on c-myc gene and that the c-Myc complex at ATF/CREB site of the gene promoter plays a role in mediating the serum response. Intriguingly, ectopic expression of ATF3 promotes proliferation of c-myc-deficient cells, mostly by alleviating the impeded G1-phase progression observed in these cells, whereas ATF3 knockdown significantly suppresses proliferation of wild-type cells. Our study demonstrates that ATF3 is downstream of the c-Myc signaling pathway and plays a role in mediating the cell proliferation function of c-Myc. Our results provide a novel insight into the functional link of the stress response gene ATF3 and the proto-oncogene c-myc