Richard Lucas

PurposeThe purpose of this paper is to present a preliminary analysis of age and gender across a number of questions asked in a survey of ethical attitudes of professionals in the information and communication technology industry in Australia. While a large number of demographic questions regarding ethics and regulation, only those concerning age and gender are examined here.Design/methodology/approachAn online survey was conducted of the ICT workplace in Australia. The results were analyzed using SPSS.FindingsThere are some significant differences across the generations as well between the genders. Gen Y is different when compared to the others on how important ethical regulations ought to be. Gen Y thinks that ethical regulations ought to be less important. When gender was examined it was clear that males thought that ethical regulations ought to be significantly less important when compared with what females thought.Research limitations/implicationsWhile a larger sample size was desired, the consistency of the replies, when compared against a number of comparative populations, indicated that the replies we received were representative of the ICT workforce.Originality/valueThis paper raises many issues that demand greater care and attention be given when constructing new models of governing ethics within the Australian ICT workplace.

Rationale: Antibiotic treatment of patients infected with G- or G+ bacteria promotes release of the toxins lipopolysaccharide and pneumolysin in their lungs. Growth Hormone-releasing Hormone agonist JI-34 protects human lung microvascular endothelial cells, expressing splice variant 1 of the receptor, from PLY-induced barrier dysfunction. We investigated whether JI-34 also blunts LPS-induced hyperpermeability. Since GHRH receptor signaling can potentially stimulate both cAMP-dependent barrier-protective pathways as well as barrier-disruptive protein kinase C pathways, we studied their interaction in GHRH agonist-treated HL-MVEC, in the presence of PLY, by means of siRNA-mediated protein kinase A depletion. Methods: Barrier function measurements were done in HL-MVEC monolayers using Electrical Cell substrate Impedance Sensing and VE-cadherin expression by Western blotting. Capillary leak was assessed by Evans Blue dye incorporation. Cytokine generation in broncho-alveolar lavage fluid was measured by multiplex analysis. PKA and PKC-a activity were assessed by Western blotting. Results: GHRH agonist JI-34 significantly blunts LPS-induced barrier dysfunction, at least in part by preserving VE-cadherin expression, while not affecting inflammation. In addition to activating PKA, GHRH agonist also increases PKC-α activity in PLY-treated HL-MVEC. Treatment with PLY significantly decreases resistance in control siRNA-treated HL-MVEC, but does so even more in PKA-depleted monolayers. Pretreatment with GHRH agonist blunts PLY-induced permeability in control siRNA-treated HL-MVEC, but fails to improve barrier function in PKA-depleted PLY-treated monolayers. Conclusions: GHRH signaling in HL-MVEC protects from both LPS and PLY-mediated endothelial barrier dysfunction and concurrently induces a barrier-protective PKA-mediated and a barrier-disruptive PKC-a-induced pathway in the presence of PLY, the former of which dominates the latter. © 2014 Czikora, Sridhar, Gorshkov, Alieva, Kasa, Gonzales, Potapenko, Umapathy, Pillich, Rick, Block, Verin, Chakraborty, Matthay, Schally and Lucas.