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Xiaobo Xu,1 Mengya Xia,2 Qinghua Chen,3 Weiguo Pang4 1School of Psychology, Shanghai Normal University, Shanghai, People’s Republic of China; 2T. Denny Sanford School of Social and Family Dynamics, Arizona State University, Tempe, AZ, USA; 3Department of Psychology, Hefei Normal University, Hefei, People’s Republic of China; 4School of Psychology and Cognitive Science, East China Normal University, Shanghai, People’s Republic of ChinaCorrespondence: Xiaobo Xu, School of Psychology, Shanghai Normal University, 100# Guilin Road, Shanghai, 200234, People’s Republic of China, Email xbxu@shnu.edu.cn Weiguo Pang, School of Psychology and Cognitive Science, East China Normal University, 3663# North Zhongshan Road, Shanghai, 200062, People’s Republic of China, Email wgpang@psy.ecnu.edu.cnPurpose: Prior studies revealed several beneficial aspects of being authentic, such as higher subjective well-being, more harmonious interpersonal relationships, and better workplace performance. However, how authenticity relates to unethical cheating behaviors in the academic context remains to be seen. Based on the literature review, the present study hypothesized that authenticity may be negatively linked to academic cheating through the mediating path of mastery approach goals.Methods: In Study 1, 250 college students self-reported their demographics and academic performance, and completed the scales of authenticity, academic cheating, mastery approach goals, and social desirability. In Study 2, 111 college students completed the same measures as in Study 1 at two different time points (5 months in between).Results: In Study 1, the results indicated that authenticity was positively associated with mastery approach goals, and both were negatively associated with academic cheating. After controlling for the confounding effect of gender, age, academic performance, and social desirability, mastery approach goals were identified as a mediator in the authenticity–a

Using Household Economic Survey (HES) data in New Zealand and Household, Income and Labour Dynamics in Australia (HILDA) data in 2018, retiree direct financial market participation proves to be an effective approach to improve retirees’ post-retirement financial wellbeing, shown in objective and subjective measurements. More specially, those retiree participants enjoy a higher annuitised net wealth and financial situation satisfaction in New Zealand, where universal superannuation is applied. Australian retiree participants have a higher replacement ratio and annuitised net wealth, along with a higher level of subjective financial situation satisfaction, and Australia uses the means-tested age pension system. Financial market participation strongly influences retiree income sufficiency in the objective and subjective measures in both universal and means-tested pension systems. Moreover, age, gender, partnership status, living area, eligibility for government pension, and employment status play certain roles in retiree post-retirement income sufficiency. Different methods, alternative calculations for income sufficiency, and alternative questions for subjective wellbeing results are all consistent with the main results. There is a clear policy implication for governments to encourage retiree financial market participation for better retirement life. The retiree’s income sufficiency gap is decomposed in Australia and New Zealand using the HILDA and HES datasets in 2018. The Oaxaca method decomposes different influences of demographic traits, individual financial positions, and unobserved factors on retirees’ income sufficiency in Australia and New Zealand with different pension systems. The results show that Australian retirees have a higher level of annuitised net wealth; New Zealand retirees have better life satisfaction. There is no significant difference in subjective financial situation satisfaction. Specifically, Australian retirees benefit more from individual

OBJECTIVE: Growing evidence suggests that a phenotypic switch converting pancreatic acinar cells to duct-like cells can lead to pancreatic intraepithelial neoplasia and eventually to invasive pancreatic ductal adenocarcinoma. Histologically, the onset of this switch is characterised by the co-expression of acinar and ductal markers in acini, a lesion called acinar-to-ductal metaplasia (ADM). The transcriptional regulators required to initiate ADM are unknown, but need to be identified to characterise the regulatory networks that drive ADM. In this study, the role of the ductal transcription factors hepatocyte nuclear factor 6 (HNF6, also known as Onecut1) and SRY-related HMG box factor 9 (Sox9) in ADM was investigated. DESIGN: Expression of HNF6 and Sox9 was measured by immunostaining in normal and diseased human pancreas. The function of the factors was tested in cultured cells and in mouse models of ADM by a combination of gain and loss of function experiments. RESULTS: Expression of HNF6 and Sox9 was ectopically induced in acinar cells in human ADM as well as in mouse models of ADM. HNF6 and, to a lesser extent, Sox9 were required for repression of acinar genes, for modulation of ADM-associated changes in cell polarity and for activation of ductal genes in metaplastic acinar cells. CONCLUSIONS: HNF6 and Sox9 are new biomarkers of ADM and constitute candidate targets for preventive treatment in cases when ADM may lead to cancer. This work also shows that ectopic activation of transcription factors may underlie metaplastic processes occurring in other organs.

Growing evidence suggests that a phenotypic switch converting pancreatic acinar cells to duct-like cells can lead to pancreatic intraepithelial neoplasia and eventually to invasive pancreatic ductal adenocarcinoma. Histologically, the onset of this switch is characterised by the co-expression of acinar and ductal markers in acini, a lesion called acinar-to-ductal metaplasia (ADM). The transcriptional regulators required to initiate ADM are unknown, but need to be identified to characterise the regulatory networks that drive ADM. In this study, the role of the ductal transcription factors hepatocyte nuclear factor 6 (HNF6, also known as Onecut1) and SRY-related HMG box factor 9 (Sox9) in ADM was investigated., Journal Article, Research Support, N.I.H. Extramural, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published

Growing evidence suggests that a phenotypic switch converting pancreatic acinar cells to duct-like cells can lead to pancreatic intraepithelial neoplasia and eventually to invasive pancreatic ductal adenocarcinoma. Histologically, the onset of this switch is characterised by the co-expression of acinar and ductal markers in acini, a lesion called acinar-to-ductal metaplasia (ADM). The transcriptional regulators required to initiate ADM are unknown, but need to be identified to characterise the regulatory networks that drive ADM. In this study, the role of the ductal transcription factors hepatocyte nuclear factor 6 (HNF6, also known as Onecut1) and SRY-related HMG box factor 9 (Sox9) in ADM was investigated., Journal Article, Research Support, N.I.H. Extramural, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published

Udgivelsesdato: 2009-Aug-7, We have previously reported that the loss of Arx and/or Pax4 gene activity leads to a shift in the fate of the different endocrine cell subtypes in the mouse pancreas, without affecting the total endocrine cell numbers. Here, we conditionally and ectopically express Pax4 using different cell-specific promoters and demonstrate that Pax4 forces endocrine precursor cells, as well as mature alpha cells, to adopt a beta cell destiny. This results in a glucagon deficiency that provokes a compensatory and continuous glucagon+ cell neogenesis requiring the re-expression of the proendocrine gene Ngn3. However, the newly formed alpha cells fail to correct the hypoglucagonemia since they subsequently acquire a beta cell phenotype upon Pax4 ectopic expression. Notably, this cycle of neogenesis and redifferentiation caused by ectopic expression of Pax4 in alpha cells is capable of restoring a functional beta cell mass and curing diabetes in animals that have been chemically depleted of beta cells.

Udgivelsesdato: 2009-Aug-7, We have previously reported that the loss of Arx and/or Pax4 gene activity leads to a shift in the fate of the different endocrine cell subtypes in the mouse pancreas, without affecting the total endocrine cell numbers. Here, we conditionally and ectopically express Pax4 using different cell-specific promoters and demonstrate that Pax4 forces endocrine precursor cells, as well as mature alpha cells, to adopt a beta cell destiny. This results in a glucagon deficiency that provokes a compensatory and continuous glucagon+ cell neogenesis requiring the re-expression of the proendocrine gene Ngn3. However, the newly formed alpha cells fail to correct the hypoglucagonemia since they subsequently acquire a beta cell phenotype upon Pax4 ectopic expression. Notably, this cycle of neogenesis and redifferentiation caused by ectopic expression of Pax4 in alpha cells is capable of restoring a functional beta cell mass and curing diabetes in animals that have been chemically depleted of beta cells.