Emerging corporate disclosure of environmental social and governance (ESG) risks: An Australian study

Today, companies across all industries around the globe face the challenges of unprecedented disruption due to climate change and other social disruptions. It is the responsibility of standard setters and regulators of the financial sector to constantly encourage industries to adopt and respond instead of ignoring the disruption. Environmental Social and Governance (ESG) risk disclosure is one of the main emerging corporate disclosures of rising importance. Specifically with new Australian Securities Exchange (ASX) listing rules companies listed in the ASX are expected to comply with new Environmental Social and Governance (ESG) risk discloser requirements from the year 2016 and if they do not comply, the \u27if not, why not\u27 rule applies. This study seeks to provide insight into the current ESG risk disclosure practices in the Australian context giving particular reference to the extractive sector companies for which ESG disclosure has become a crucial reporting requirement

Editorial Volume 16 Issue 2. March 2022.

This Special Issue is based on selected papers from the Environmental Social and Governance (ESG) and Sustainability Conference (2021). This is the second ESG conference held by Victoria University Business School (VUBS) and the Institute of Sustainable Industries and the Liveable Cities (ISILC) of Victoria University, Melbourne, Australia

Determinants of public sector accounting reforms: A case study of Sri Lanka in rapidly developing Asia

Special Issue: International Public Sector Accounting Standards (IPSAS): Current status, practices, and future agend

The Surge of Environmental Social and Governance Reporting and Sustainable Development Goals: Some Normative Thoughts

The rising demand for Environmental Social and Governance (ESG) disclosure by stakeholders has created a new tide of sustainability reporting, including Sustainable Development Goals (SDGs). With this new rising tide, the need for enhanced credibility in ESG information has stimulated the development of carbon accounting, ESG disclosure measures and regulations around the world. The aim of this article is to analyse the risks and opportunities of ESG practices and the impact of different stakeholders on the measures, tools and frameworks, including SDGs used among different sectors to report sustainability performance. This study finds that business leaders worldwide have an opportunity to use transparent information about ESG risks and opportunities to promote more effective engagement with investors and other stakeholders and global, national and organisational leaders have a legal and ethical responsibility to deliver sustainable outcomes to their global and local communities

The Surge of Environmental Social and Governance Reporting and Sustainable Development Goals: Some Normative Thoughts

The rising demand for Environmental Social and Governance (ESG) disclosure by stakeholders has created a new tide of sustainability reporting, including Sustainable Development Goals (SDGs). With this new rising tide, the need for enhanced credibility in ESG information has stimulated the development of carbon accounting, ESG disclosure measures and regulations around the world. The aim of this article is to analyse the risks and opportunities of ESG practices and the impact of different stakeholders on the measures, tools and frameworks, including SDGs used among different sectors to report sustainability performance. This study finds that business leaders worldwide have an opportunity to use transparent information about ESG risks and opportunities to promote more effective engagement with investors and other stakeholders and global, national and organisational leaders have a legal and ethical responsibility to deliver sustainable outcomes to their global and local communities

CLU blocks HDACI-mediated killing of neuroblastoma

Clusterin is a ubiquitously expressed glycoprotein with multiple binding partners including IL-6, Ku70, and Bax. Clusterin blocks apoptosis by binding to activated Bax and sequestering it in the cytoplasm, thereby preventing Bax from entering mitochondria, releasing cytochrome c, and triggering apoptosis. Because increased clusterin expression correlates with aggressive behavior in tumors, clusterin inhibition might be beneficial in cancer treatment. Our recent findings indicated that, in neuroblastoma cells, cytoplasmic Bax also binds to Ku70; when Ku70 is acetylated, Bax is released and can initiate cell death. Therefore, increasing Ku70 acetylation, such as by using histone deacetylase inhibitors, may be therapeutically useful in promoting cell death in neuroblastoma tumors. Since clusterin, Bax, and Ku70 form a complex, it seemed likely that clusterin would mediate its anti-apoptotic effects by inhibiting Ku70 acetylation and blocking Bax release. Our results, however, demonstrate that while clusterin level does indeed determine the sensitivity of neuroblastoma cells to histone deacetylase inhibitor-induced cell death, it does so without affecting histone deacetylase-inhibitor-induced Ku70 acetylation. Our results suggest that in neuroblastoma, clusterin exerts its anti-apoptotic effects downstream of Ku70 acetylation, likely by directly blocking Bax activation

Bifidobacterium Infantis 35624 Protects Against Salmonella-Induced Reductions in Digestive Enzyme Activity in Mice by Attenuation of the Host Inflammatory Response

OBJECTIVES: Salmonella-induced damage to the small intestine may decrease the villi-associated enzyme activity, causing malabsorption of nutrients and diarrhea, and thus contribute to the symptoms of infection. The objective of this study was to determine the mechanism by which different doses and durations of Salmonella infection and lipopolysaccharide (LPS) affect brush border enzyme activity in the mouse, and to determine if the probiotic Bifidobacterium longum subspecies infantis 35624 could attenuate the intestinal damage. METHODS: BALB/c mice were challenged with Salmonella enterica serovar Typhimurium UK1 at various doses (10(2)-10(8) colony-forming unit (CFU)) and durations (10(6) CFU for 1-6 days). Mice were also treated with B. longum subsp. infantis 35624 for 2 weeks before and during a 6-day S. Typhimurium challenge (10(6) CFU), or before injection of LPS. The small intestine was assessed for morphological changes, mRNA expression of cytokines, and activity of the brush border enzymes sucrase-isomaltase, maltase, and alkaline phosphatase. RESULTS: S. Typhimurium infection significantly reduced the activity of all brush border enzymes in a dose- and time-dependent manner (P<0.05). This also occurred following injection of LPS. Pre-treatment with B. longum subsp. infantis 35624 prevented weight loss, protected brush border enzyme activity, reduced the small intestinal damage, and inhibited the increase in interleukin (IL)-10 and IL-8 expression due to Salmonella challenge. CONCLUSIONS: Salmonella infection reduces the small intestinal brush border enzyme activity in mice, with the level of reduction and associated weight loss increasing with dose and duration of infection. B. longum subsp. infantis 35624 treatment attenuated the effect of Salmonella infection on brush border enzyme activity and weight loss, which may be due to modulation of the host immune response

Molecular association of glucose-6- phosphate isomerase and pyruvate kinase M2 with glyceraldehyde-3-phosphate dehydrogenase in cancer cells

Background: For a long time cancer cells are known for increased uptake of glucose and its metabolization through glycolysis. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a key regulatory enzyme of this pathway and can produce ATP through oxidative level of phosphorylation. Previously, we reported that GAPDH purified from a variety of malignant tissues, but not from normal tissues, was strongly inactivated by a normal metabolite, methylglyoxal (MG).Molecular mechanism behind MG mediated GAPDH inhibition in cancer cells is not well understood. Methods: GAPDH was purified from Ehrlich ascites carcinoma (EAC) cells based on its enzymatic activity. GAPDH associated proteins in EAC cells and 3-methylcholanthrene (3MC) induced mouse tumor tissue were detected by mass spectrometry analysis and immunoprecipitation (IP) experiment, respectively. Interacting domains of GAPDH and its associated proteins were assessed by in silico molecular docking analysis. Mechanism of MG mediated GAPDH inactivation in cancer cells was evaluated by measuring enzyme activity, Circular dichroism (CD) spectroscopy, IP and mass spectrometry analyses. Result: Here, we report that GAPDH is associated with glucose-6-phosphate isomerase (GPI) and pyruvate kinase M2 (PKM2) in Ehrlich ascites carcinoma (EAC) cells and also in 3-methylcholanthrene (3MC) induced mouse tumor tissue. Molecular docking analyses suggest C-terminal domain preference for the interaction between GAPDH and GPI. However, both C and N termini of PKM2 might be interacting with the C terminal domain of GAPDH. Expression of both PKM2 and GPI is increased in 3MC induced tumor compared with the normal tissue. In presence of 1 mM MG,association of GAPDH with PKM2 or GPI is not perturbed, but the enzymatic activity of GAPDH is reduced to 26.8 ± 5 % in 3MC induced tumor and 57.8 ± 2.3 % in EAC cells. Treatment of MG to purified GAPDH complex leads to glycation at R399 residue of PKM2 only, and changes the secondary structure of the protein complex. Conclusion: PKM2 may regulate the enzymatic activity of GAPDH. Increased enzymatic activity of GAPDH in tumor cells may be attributed to its association with PKM2 and GPI. Association of GAPDH with PKM2 and GPI could be a signature for cancer cells. Glycation at R399 of PKM2 and changes in the secondary structure of GAPDH complex could be one of the mechanisms by which GAPDH activity is inhibited in tumor cells by MG