Does school SES matter less for high-performing students than for their lower-performing peers? A quantile regression analysis of PISA 2018 Australia

Background While the relationship between school socioeconomic composition and student academic outcomes is well established, knowledge about differential effects is not extensive. In particular, little is known whether the relationship differs for students with varying levels of academic performance. We examined whether the school socioeconomic composition effect on academic achievement is stronger or weaker for high-performing students than for average- and low-performing students. Australia is a theoretically interesting case study as it has high levels of school socioeconomic segregation compared to other economically developed countries. Methods We conducted quantile regression analysis using data from the Australia PISA 2018 sample (N = 14,273 15-year-old students). We examined the effect of school socioeconomic status (school SES) on student performance in reading, mathematical and scientific literacy. Results We found that the school socioeconomic composition effect is substantial and is similar for all students, regardless of their level of academic performance. The findings also show that school SES is a stronger predictor than student SES for all student performance quintiles, and the size of the school SES effect relative to the size of student SES effect is larger in lower performance quintiles. Conclusions These results indicate no differential effect of school SES on reading, mathematical or scientific literacy for students of varying levels of academic performance. The relationship is similarly strong and positive for high-performing students as it is for their lower performing peers. As school SES is a strong predictor for all students regardless of their level of academic performance, we argue that equity of educational outcomes can be best achieved by policies and structures that promote socioeconomically mixed rather than segregated schools. We also call for more research that seeks to identify and understand possible differential effects of school socioeconomic composition on a range of academic and non-cognitive student outcomes

Gaining strategic insights into Logistics 4.0: expectations and impacts

YesThe developments brought by Industry 4.0 have spread to various components in a supply chain, where logistics is of utmost importance due to the intermediate role of logistics service providers (LSPs) operating among different actors. Despite such a vital role, the extant literature lacks from the extensive analysis of Industry 4.0 implementations in the logistics industry, particularly for LSPs. Accordingly, this study sets out to investigate, comprehensively, Industry 4.0 projections in logistics and their reflections on LSPs by adopting a multidimensional approach. In this respect, the key themes influenced by Industry 4.0 developments are initially determined through a structured survey conducted in the Turkish logistics industry. Then, in the same industry, both the probabilities and the impacts of Industry 4.0-focused thematic statements are examined through an integrative interview survey, which also incorporates ‘why-type’ of questions. Consequently, this study offers academic implications in terms of demonstrating possible changes in the logistics industry from the operational, financial, and human resources aspects. Additionally, the findings serve as a reference for logistics professionals while fostering their competitive Industry 4.0 initiatives and facilitating their strategic decisions

IRE1α-XBP1s pathway promotes prostate cancer by activating c-MYC signaling

Activation of endoplasmic reticulum (ER) stress/the unfolded protein response (UPR) has been linked to cancer, but the molecular mechanisms are poorly understood and there is a paucity of reagents to translate this for cancer therapy. Here, we report that an IRE1α RNase-specific inhibitor, MKC8866, strongly inhibits prostate cancer (PCa) tumor growth as monotherapy in multiple preclinical models in mice and shows synergistic antitumor effects with current PCa drugs. Interestingly, global transcriptomic analysis reveal that IRE1α-XBP1s pathway activity is required for c-MYC signaling, one of the most highly activated oncogenic pathways in PCa. XBP1s is necessary for optimal c-MYC mRNA and protein expression, establishing, for the first time, a direct link between UPR and oncogene activation. In addition, an XBP1-specific gene expression signature is strongly associated with PCa prognosis. Our data establish IRE1α-XBP1s signaling as a central pathway in PCa and indicate that its targeting may offer novel treatment strategies.</p

3, 3′5 Triiodo L Thyronine Induces Apoptosis in Human Breast Cancer MCF-7cells, Repressing SMP30 Expression through Negative Thyroid Response Elements

Thyroid hormones regulate cell proliferation, differentiation as well as apoptosis. However molecular mechanism underlying apoptosis as a result of thyroid hormone signaling is poorly understood. The antiapoptotic role of Senescence Marker Protein-30 (SMP30) has been characterized in response to varieties of stimuli as well as in knock out model. Our earlier data suggest that thyroid hormone 3, 3'5 Triiodo L Thyronine (T(3)), represses SMP30 in rat liver.In highly metastatic MCF-7, human breast cancer cell line T3 treatment repressed SMP30 expression leading to enhanced apoptosis. Analysis by flow cytometry and other techniques revealed that overexpression and silencing of SMP30 in MCF-7 resulted in decelerated and accelerated apoptosis respectively. In order to identify the cis-acting elements involved in this regulation, we have analyzed hormone responsiveness of transiently transfected hSMP30 promoter deletion reporter vectors in MCF-7 cells. As opposed to the expected epigenetic outcome, thyroid hormone down regulated hSMP30 promoter activity despite enhanced recruitment of acetylated H3 on thyroid response elements (TREs). From the stand point of established epigenetic concept we have categorised these two TREs as negative response elements. Our attempt of siRNA mediated silencing of TRβ, reduced the fold of repression of SMP30 gene expression. In presence of thyroid hormone, Trichostatin- A (TSA), which is a Histone deacetylase (HDAC) inhibitor further inhibited SMP30 promoter activity. The above findings are in support of categorisation of both the thyroid response element as negative response elements as usually TSA should have reversed the repressions.This is the first report of novel mechanistic insights into the remarkable downregulation of SMP30 gene expression by thyroid hormone which in turn induces apoptosis in MCF-7 human breast cancer cells. We believe that our study represents a good ground for future effort to develop new therapeutic approaches to challenge the progression of breast cancer

Poverty in Consumer Culture:Towards a Transformative Social Representation

International audienceIn this article, we consider the representations of poverty within consumer culture. We focus on four main themes – social exclusion, vulnerability, pleasure and contentment – that capture some of the associations that contemporary understandings have made with poverty. For each theme, we consider the portrayals of poverty from the perspective of key agents (such as marketers, media, politicians) and then relate this to more emic representations of poverty by drawing on a range of contemporary poverty alleviating projects from around the world. We conclude with a set of guidelines for relevant stakeholders to bear in mind when elaborating their representations of poverty. These guidelines may act as a platform to transform marginalising representations of poverty into more empowering representations

Ubiquitously expressed hematological and neurological expressed 1 downregulates Akt-mediated GSK3ß signaling, and its knockdown results in deregulated G2/M transition in prostate cells

PubMed ID: 21323578As the molecular mechanism of ß-catenin deregulation is not well understood, and stabilized ß-catenin is known to translocate into the nucleus and activate genes for proliferation, a novel regulatory factor, hematological and neurological expressed 1 (HN1), for Akt-GSK3ß-ß- catenin axis is reported here. In our studies, HN1 gene structure was characterized. HN1 expression was found to be epidermal growth factor-responsive in PC-3 cells, and protein expression was also upregulated in PC-3 and LNCaP but not in DU145 cells. Additionally, HN1 was found to be downregulated by the specific AKT inhibitor wortmannin but not with PI3K or MAPK inhibitors, LY294002 and PD98059, respectively, in PC-3 and MCF-7 cells. Further, siRNA-mediated knockdown of HN1 resulted in considerable increase in Akt (S473) and GSK3ß (S9),(Y216) phosphorylations; moreover, subsequent accumulation of ß-catenin, increase in c-myc expression, and nuclear accumulation of cyclin D1 were observed in PC-3 cells. Knockdown of HN1 also resulted in prolongation of G 1 phase in cell cycle, increasing tetraploidy, presumably because of cells escaping from abnormal mitosis in PC-3 cells. Consistently, overexpression of HN1 reversed the cell-cycle-specific observations, resulted in accumulation of cells in G 2/M, and reduced the proliferation rate, which were investigated using flow cytometry and methylthiazol tetrazolium assays. As activating mutations of ß-catenin have been demonstrated in late-stage tumors, and ß-catenin stabilization was correlated with poor prognosis in previous reports, epidermal growth factor-upregulated HN1 expression might have a role in deregulating the AKT-GSK3ß (S9)-mediated signaling as a novel compensating mechanism. © 2011 Mary Ann Liebert, Inc

Understanding poverty and promoting poverty alleviation through transformative consumer research

Consumer research holds potential for expanding society's understanding of how people experience poverty and mechanisms for poverty alleviation. Capitalizing on this potential, however, will require more exploration of how consumption experiences shape individual and collective well-being among the poor. This article proposes a framework for transformative consumer research focused on felt deprivation and power within the lived experience of poverty. The framework points to consumer choice, product/service experiences, consumer culture, marketplace forces, and consumption capabilities as research streams with potential to help alleviate poverty. Future research in these areas will expand pathways for transforming the lives of the poor by alleviating stress, engaging marketplace institutions, fulfilling life aspirations, leveraging trust and social capital, and facilitating creativity and adaptation. © 2012 Elsevier Inc