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We focus on political marketing and conduct a systematic literature review of journal articles exploring political marketing on social media. The systematic literature review delineates the current state of political social media marketing literature. It spans six databases and comprises sixty-six journal articles published between 2011 and 2020. We identify and categorize the variables studied in the literature and develop an integrative framework that links these variables. We describe the research themes that exist in the literature. The review demonstrates that the field is growing. However, the literature is fragmented, along with being predominantly based in the US context. Conceptual and theoretical shortcomings also exist. Moreover, the literature ignores pertinent contemporary topics such as co-creation, influencer marketing, and political advertising on social media. Nevertheless, a nascent domain with growing practical significance, political social media marketing provides various exciting avenues for further research, which we outline in this study.

PurposeThis study investigates the role of personal resource (i.e. psychological empowerment) in reducing the negative impact of emotional exhaustion of frontline employees on their engagement. It also examines the moderating effects of ethical climate and transformational leadership in mitigating the negative influence of emotional exhaustion on engagement among frontline service employees (FLEs).Design/methodology/approachData were collected from 671 frontline employees from financial services sector. Confirmatory factor analysis (CFA) and hierarchical regression analysis (HRA) were used to test the hypothesized relationships.FindingsResults show that the impact of emotional exhaustion on employee engagement is greatly affected by psychological empowerment. Transformational leadership moderates the negative effects of emotional exhaustion on psychological empowerment, while ethical climate weakens the negative impact of emotional exhaustion on employee engagement.Practical implicationsService firms need to provide enough autonomy to emotionally exhausted frontline employees so that they feel valued. The emotionally exhausted employees can be engaged if they are empowered to discharge their job most effectively and a climate is ensured which can keep them motivated toward accomplishing their targets. A fair and just treatment shall boost their morale to perform better and to strengthen their staying intentions.Originality/valueThe novelty of our study lies in examining and fostering engagement among emotionally exhausted FLEs. It shows that job resources at the individual level (i.e. psychological empowerment), team level (i.e. transformational leadership) and organizational level (i.e. ethical climate) can help in encouraging work engagement among emotionally exhausted FLEs.

Proximal tubule (PT) transports most of the renal Ca2+, which was usually described as paracellular (passive). We found a regulated Ca2+ entry pathway in PT cells via the apical transient receptor potential canonical 3 (TRPC3) channel, which initiates transcellular Ca2+ transport. Although TRPC3 knockout (−/−) mice were mildly hypercalciuric and displayed luminal calcium phosphate (CaP) crystals at Loop of Henle (LOH), no CaP + calcium oxalate (CaOx) mixed urine crystals were spotted, which are mostly found in calcium nephrolithiasis (CaNL). Thus, we used oral calcium gluconate (CaG; 2%) to raise the PT luminal [Ca2+]o further in TRPC3−/− mice for developing such mixed stones to understand the mechanistic role of PT-Ca2+ signaling in CaNL. Expectedly, CaG-treated mice urine samples presented with numerous mixed crystals with remains of PT cells, which were pronounced in TRPC3−/− mice, indicating PT cell damage. Notably, PT cells from CaG-treated groups switched their mode of Ca2+ entry from receptor-operated to store-operated pathway with a sustained rise in intracellular [Ca2+] ([Ca2+]i), indicating the stagnation in PT Ca2+ transport. Moreover, those PT cells from CaG-treated groups demonstrated an upregulation of calcification, inflammation, fibrotic, oxidative stress, and apoptotic genes; effects of which were more robust in TRPC3 ablated condition. Furthermore, kidneys from CaG-treated groups exhibited fibrosis, tubular injury and calcifications with significant reactive oxygen species generation in the urine, thus, indicating in vivo CaNL. Taken together, excess PT luminal Ca2+ due to escalation of hypercalciuria in TRPC3 ablated mice induced surplus CaP crystal formation and caused stagnation of PT [Ca2+]i, invoking PT cell injury, hence mixed stone formation.

Appendices: Appendix 1 see Table 7. Appendix 2: You are tasked with evaluating ‘Experience WA’, a smart tourism app, while participating in a tourism experience in Western Australia. Your holiday is coming. You intend to take a five-day long trip to Perth, Western Australia. You come across ‘Experience WA’, a smart tourism app that can augment your tourism experience in Perth. ‘Experience WA’ gives you location-based information on your surroundings and can be used to plan your vacation in Perth, look up events nearby, find nearby tourism attractions, and share your holiday plans with your friends. You can use ‘Experience WA’ to search for information and plan your trip in Perth. ‘Experience WA’ can be found at the following links: Google Play Store. Apple App Store. Copyright © The Author(s) 2022. The paper identifies and analyses customers’ motives to co-create when interacting with smart services by integrating the self-determination theory with coordination mechanisms. The study also examines the how and to what extent value co-creation impacts on word-of-mouth and customer-based brand equity. An online questionnaire was employed for empirically validating the research model. The relationships were examined using partial least square path modelling. The findings show that intrinsic and extrinsic motives are significant antecedents of value co-creation. The coordination mechanisms namely, relating and knowing also significantly influence customers’ involvement in the value co-creation process. Results also show that value co-creation mediates the relationship between customers motives (intrinsic and extrinsic) to co-create and consequences. Findings of this study adds to the human–computer interaction literature by strengthening the nomological network of value co-creation when interacting with smart services by proposing a novel model integrating both the antecedents and outcomes of value co-creation. By recognizing how this practice could be motivated, service providers can bolster customer-firm interactions and enable favourable firm level consequences. Open Access funding enabled and organized by CAUL and its Member Institutions.

Copyright © 2022 The Authors. Brexit has caused a seismic shift in the British socio-economic and political landscapes, creating widespread uncertainties, while simultaneously giving hope and national pride to millions. The decision by a number of organizations to reshore their production has opened a new era for business management that challenges the axiomatic assumption of the benefits of offshored production. Although reshoring predates Brexit, the link between the two in the British context is not just serendipitous and they are argued to have reasonable interlinkages. However, there is inadequate empirical evidence to suggest that British consumers’ attitude towards Brexit has any effect on their intention to purchase reshored brands. Through a mixed-methods study comprising a survey of 415 respondents and 20 in-depth interviews, this paper addresses this research gap. Findings suggest that corporate social responsibility (CSR) and consumer reshoring sentiment (CRS) have positive effects on consumers’ attitude towards reshored brands. Despite CRS's positive influence on attitude towards Brexit, the latter does not have any significant effects on the intention to purchase a reshored brand, which is positively influenced by the attitude towards the same brand. As such, companies should enhance the image of their brands and CSR in order to harness the benefits of reshoring. University of Western Australia, as part of the Wiley – The University of Western Australia agreement via the Council of Australian University Librarians.

Purpose/Objective(s): Pancreatic ductal adenocarcinoma (PDAC) is characterized by an unusually high degree of hypoxia in the tumor microenvironment, which activates hypoxic signaling pathways orchestrated by hypoxia-inducible factor 1α (HIF1α). It has been shown previously that HIF1α significantly increases PDAC radioresistance and growth, though its mechanism of action is unknown. Here, we test the hypothesis that HIF1α confers these traits in PDAC through involvement in DNA damage repair and KRAS signaling in vitro. Materials/Methods: We performed studies with the KPC cell line (KrasLSL-G12D/+;TP53LSL-R172H/+). We used CRISPR-Cas9, a genome editing tool, to generate a HIF1α knockout (KO) cell line. Hypoxic microenvironments were induced using 100uM of the oxygen scavenger CoCl2. Radioresistance and double-strand DNA damage was evaluated and compared between wild-type (WT) and KO cells after treatment with increasing doses of ionizing radiation using neutral comet assays. Tumor signaling pathways were mapped and analyzed using western blot and co-immunoprecipitation. The KRASG12D inhibitor, BI-2852, was obtained from Boehringer-Ingelheim. Cancer cells were evaluated for growth and migration using cell proliferation assays and scratch wound assays following treatment with 50 uM BI-2852. Bioinformatic analysis was conducted using TCGA (The Cancer Genome Atlas) data; high and low expression were defined as samples with mRNA expression z-scores ≥ 1 and ≤ -1, respectively, Results: HIF1α KO cells demonstrated significantly increased radioresistance compared to WT cells following 8 and 10 Gy of radiation in hypoxic conditions (t-test, P Conclusion: Overall, this study demonstrates that HIF1α promotes DNA damage repair in PDAC and reveals a HIF1α/KRAS/p53 signaling axis. Future studies will test anti-HIF1α and anti-KRAS combination therapies in PDAC mouse models. Citation Format: Kevin J. Tu, Sanjit K. Roy, Amit Sawant, Hem D. Shukla. HIF1α is involved in radiation-induced DNA damage repair and anti-apoptotic pathways in pancreatic ductal adenocarcinoma. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 4810.

3-Bromopyruvate (3 BP) is a promising anticancer drug against pancreatic cancer. It exerts potent anticancer effects by inhibiting hexokinase II enzyme of glycolysis pathway and ATP generation in cancer cells. In present investigation we have examined the effect of 3-BromoPyruvate employing panc-2 cancer cells, and syngeneic pancreatic cancer mouse model. The clonogenic survival assay demonstrated dose dependent inhibition of cell growth, and we observed 95% cell death at 15 uM conc. Further, ATP production was severely inhibited in cancer cells treated with same concentration of 3-BP. We also observed that 3-BP in combination with low doses of irradiation was more effective in killing cancer cells than 3-BP alone. Electron microscopy revealed that 3-BromoPyruvate severely damaged mitochondrial integrity which might have severely affected ATP generation in cancer cells. We further tested 3-BromoPyruvate (2.5-10.0 mg/kg) in syngeneic panc-2 tumor mouse model and observed that 3-BP at10.0 mg/kg dose significantly reduced tumor growth (volume) about 35-40%. Immunohistochemistry (IHC) data showed that 3-BP inhibits hexokinase II (HK2) and TGFbeta1 and enhanced active caspase-3 expression in tumor tissues as compared to untreated control. The disruption of the interaction between VDAC1 and HK2 due to 3BP treatment was confirmed by CO-IP. Interestingly, 3 BP at higher dose induces caspase-3 activation in tumor derived organoid without showing any effect on normal pancreatic organoid. Altogether, the results in this study demonstrated that 3 BP could be a promising anti-tumor drug against pancreatic cancer and its efficacy could be improved in combination with radiation therapy. Citation Format: Sanjit K. Roy, Tijana Dukic, Binny Bhandary, Aneesh Acharya, Kevin J. Tu, Young H. Ko, Hem D. Shukla. 3-Bromopyruvate in combination with radiation inhibits pancreatic cancer growth by dismantling mitochondria and ATP generation in a preclinical mouse model [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5243.