Faultlines of Federation: Australia\u27s Intergovernmental Cooperation and Human Rights during the Pandemic

The COVID-19 pandemic has challenged previously understood boundaries between jurisdictions and the balance of power between national, state and territory governments in Australia. The crisis served as a catalyst for long called for-yet unexpected-reform of the peak intergovernmental body, the Council of Australian Governments (\u27COAG\u27) which was replaced by the National Cabinet to ensure coordinated intergovernmental responses. This article examines whether the new National Cabinet has emerged as an effective institution of intergovernmental cooperation in Australia\u27s federalist structure. Is it capable of protecting human rights? Three main areas of rights protection were examined including health, work and rights of residents in aged care. The National Cabinet has been effective in providing decisive responses to contain and suppress COVID-19. However, second-wave outbreaks, particularly in Victoria, have revealed fault lines in the system. Within the three areas of rights protection examined we found that intergovernmental cooperation through the National Cabinet was most effective when there was a clear delineation of responsibility between the levels of government. However, the protection of aged care residents in particular has revealed serious systemic deficiencies leading to blame-shifting between the levels of government over the boundaries of responsibility. As an institution of intergovernmental cooperation, the National Cabinet offers some advantages over the COAG. Frequent internet meetings of the National Cabinet have alleviated some criticisms that haunted COAG as being ineffective and overburdened with unnecessary procedure. Further, the heightened attention of the mass media has somewhat countered complaints about opaque decision-making and lack of accountability. Conversely, some fault lines begin to emerge around states acting in self-interested ways —hard-line border closures damaging both economic interests and individuals\u27 freedom of movement. There are also indicators of centralisation with the emerging National Cabinet structure containing potential for power to shift from states and territories—which currently hold most of the constitutional powers relating to emergencies —to the Commonwealth. The National Cabinet served as a political and symbolic tribune for the Prime Minister rather than premiers and chief ministers. Whether the National Cabinet can overcome these fault lines remains to be seen. At least we note some positive signs that cooperative approaches are possible and effective when most needed

“Xi Jinping Thought”

Introduction: A context of epochal change Xi Jinping’s full report to the 19th Chinese Communist Party (CCP) Congress in October 2017 seeks to “ensure and improve living standards through sustainable development;” it condones market “reform and opening” (gaige kaifang 改 革 开 放) and encourages Chinese enterprises to “go out” (zou chuqu 走出去) especially along the Silk Road Economic Belt and 21st Century Maritime Silk Road (2017: 2). China’s relatively slow growth rate since 2009 has required a re..

Cytochrome P4501A is Induced in Endothelial Cell Lines From the Kidney and Lung of the Bottlenose Dolphin, \u3ci\u3eTursiops truncatus\u3c/i\u3e

Marine mammals respond to the presence of polycyclic and planar halogenated aromatic hydrocarbons (PAH or PHAH) with the induced expression in endothelium of cytochrome P4501A1, regulated through the aryl hydrocarbon receptor (AHR) transcription factor. Physiological responses in other animals, such as edema and inflammation indicate that the endothelium may be compromised by exposure to AHR agonists, which are ubiquitous in the marine environment. In other mammals and fish the cellular and molecular consequences of exposure to AHR agonists have been elucidated in cultured endothelial cells. We have cultured and characterized cetacean endothelial cells (EC) and used them in induction studies. Endothelial cells were cultured from the lung and kidney of the bottlenose dolphin, Tursiops truncates, and exposed to the AHR agonists β-naphthoflavone (βNF) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). βNF (1–3 μM) induced significant increases in CYP1A1 (O-deethylation of 7-ethoxyresorufin to resorufin; EROD) activity to 3.6 and 0.92 pmol/mg/min in lung and kidney EC, respectively. TCDD was more potent than βNF, and more efficacious, with maximum induction of CYP1A1 activity of 10.1 and 15.2 pmol/mg/min in lung and kidney EC at 3–10 nM TCDD. The differential response indicates that the lung and kidney endothelial cells in culture retain the ability to respond in a selective manner to specific stimuli. Both the molecular mechanisms of induction and the physiological consequences, especially in the vasculature, of toxicant exposure can be studied in this system

Cytochrome P4501A is induced in endothelial cell lines from the kidney and lung of the bottlenose dolphin, Tursiops truncatus

Author Posting. © The Authors, 2005. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Aquatic Toxicology 76 (2006): 295-305, doi:10.1016/j.aquatox.2005.10.005.Marine mammals respond to the presence of polycyclic and planar halogenated aromatic hydrocarbons (PAH or PHAH) with the induced expression in endothelium of cytochrome P4501A1, regulated through the aryl hydrocarbon receptor (AHR) transcription factor. Physiological responses in other animals, such as edema and inflammation indicate that the endothelium may be compromised by exposure to AHR agonists, which are ubiquitous in the marine environment. In other mammals and fish the cellular and molecular consequences of exposure to AHR agonists have been elucidated in cultured endothelial cells. We have cultured and characterized cetacean endothelial cells (EC) and used them in induction studies. Endothelial cells were cultured from the lung and kidney of the bottlenose dolphin Tursiops truncatus and exposed to the AHR agonists β-naphthoflavone (βNF) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). βNF (1-3 μM) induced significant increases in CYP1A1(O-deethylation of 7-ethoxyresorufin to resorufin;EROD) activity to 3.6 and 0.92 pmol/mg/min in lung and kidney EC, respectively. TCDD was more potent than βNF, and more efficacious, with maximum induction of CYP1A1activity of 10.1 and 15.2 pmol/mg/min in lung and kidney EC at 3-10 nM TCDD. The differential response indicates that the lung and kidney endothelial cells in culture retain the ability to respond in a selective manner to specific stimuli. Both the molecular mechanisms of induction and the physiological consequences, especially in the vasculature, of toxicant exposure can be studied in this system.Part of this work was completed during a faculty fellowship from Fordham University for RAG. The Faculty Research Council of Fordham University provided partial support for RAG. This research was supported by NIH grant 5- P42-ES07381 and by U.S.EPA grant R827102-01-0. This research is an outgrowth and continuing impact of Sea Grant Number Grant No. NA90- AA-D-SG480, project NA86RG0075-R/P61

Impact of Baseline Heart Failure Burden on Post-Implantable Cardioverter-Defibrillator Mortality Among Medicare Beneficiaries

ObjectivesThis study sought to assess the impact of baseline heart failure (HF) burden on survival with primary implantable cardioverter-defibrillator (ICD) among Medicare recipients.BackgroundSurvival after primary ICD implantation may differ between trial and Medicare populations.MethodsLinking data from the CMS (Centers for Medicare and Medicaid Services) ICD registry and the Medicare files (2005 to 2009), we identified primary ICD recipients age ≥66 years with ejection fraction ≤35%. Number of previous HF hospitalizations (prev-HF-hosp) and length of hospitalization prior to implantation were used to define HF burden. Crude all-cause mortality was estimated. Adjusted hazard ratios (HR) were derived from Cox models.ResultsOf 66,974 ICD recipients (73% men, 88% white, mean age 75 years), 11,876 died (average follow-up = 1.4 years), with 3-year mortality of 31%. Among patients with no prev-HF-hosp, 3-year mortality was 27% compared with 63% in those with ≥3 prev-HF-hosp (adjusted HR: 1.8). Among patients with same-day implantation, 3-year mortality was 25% compared with 53% in those with >1-week hospitalization days prior to implantation (adjusted HR: 1.9). Mortality at 3-year follow-up among the 31,685 ICD recipients with no prev-HF-hosp and same-day implantation (low HF burden) was similar to that in trials (22%).ConclusionsNearly one-third of Medicare ICD recipients died within 3 years, reflecting a population with more advanced age and disease than seen in trial populations for primary prevention ICD. Nearly one-half of Medicare recipients had a low HF burden and had a survival similar to trial ICD recipients. Future research is warranted to understand the effectiveness of primary ICD implantation among Medicare beneficiaries with heavy HF burdens

Cytochrome P450 induced differentially in endothelial cells cultured from different organs of Anguilla rostrata

Author Posting. © The Authors, 2004. This is the author's version of the work. It is posted here by permission of Society for In Vitro Biology for personal use, not for redistribution. The definitive version was published in In Vitro Cellular & Developmental Biology - Animal 41 (2005): 57-63, doi:10.1290/0409063.1.Endothelial cells are a structural barrier and an active regulator of many bodily processes. CYP1A activity is induced in the endothelium of teleosts and mammals exposed to lipophilic xenobiotics, such as polycyclic aromatic hydrocarbons, and can have significant consequences for endothelial functions. We exposed cultures of characterized endothelial cells from the heart, kidney and rete mirabile of the eel, Anguilla rostrata, to AhR agonists. In heart endothelial cells the maximum response (based on EROD activity) to TCDD, 113 pmol/mg-min, was at 1 nM TCDD and the peak response to βNF, 135 pmol/mg-min, was at 3 μM βNF. The maximum response to TCDD in the kidney endothelial cells is 12 pmol/mg-min at 0.3 nM TCDD. The rete mirabile capillary endothelial cells responded minimally or not at all to exposure to TCDD and βNF. Both the heart and kidney endothelial cells (but not the rete mirabile capillary cells) have a low level of EROD activity (12.7 and 5.2 pmol/mg-min respectively) in untreated or DMSO-treated cells. The robust response of the heart endothelial cells to induction and the lack of response in the rete mirabile capillary endothelial cells indicate that these cells are a good resource to use to investigate the physiological consequences of AhR agonist exposure and CYP1A induction in different areas of the vasculature.The Faculty Research Council of Fordham University provided partial support for RAG. This research was supported by NIH grant 5-P42-ES07381 and by U.S.EPA grant R827102-01-0

Multidisciplinary Ophthalmic Imaging Progressive Loss of Retinal Ganglion Cells and Axons in Nonoptic Neuritis Eyes in Multiple Sclerosis: A Longitudinal Optical Coherence Tomography Study

Citation: Graham EC, You Y, Yiannikas C, et al. Progressive loss of retinal ganglion cells and axons in non-optic neuritis eyes in multiple sclerosis: a longitudinal optical coherence tomography study. Invest Ophthalmol Vis Sci. 2016;57:231157: -231757: . DOI:10.1167 PURPOSE. To examine the rate of retinal ganglion cell (RGC) layer and retinal nerve fiber layer (RNFL) changes in nonoptic neuritis (NON) eyes of relapsing remitting multiple sclerosis (RRMS) patients, and to find a specific imaging parameter useful for identifying disease progression. METHODS. Forty-five consecutive RRMS patients and 20 age-and sex-matched healthy subjects were enrolled. All patients were followed up for 3 years with annual optical coherence tomography (OCT) scans, which included a peripapillary ring scan protocol for RNFL analysis and a macular radial star-like scan to obtain RGC/inner plexiform layer (IPL) thickness measures. Healthy controls were scanned twice, 3 years apart. RESULTS. Retinal ganglion cell/inner plexiform layer and temporal RNFL (tRNFL) demonstrated highly significant thinning (P < 0.01), but all nasal segments and global RNFL (gRNFL) were not significantly different from normal controls. While receiver operating characteristics (ROC) analysis showed no advantage of RGC/IPL over tRNFL in cross-sectional detection of thinning, cut-off point based of fifth percentile in healthy controls demonstrated higher rate of abnormality for RGC/IPL. There was a significant progressive loss of RGC/IPL and tRNFL during the follow-up period. The largest thickness reduction was observed in tRNFL. ROC analysis demonstrated that tRNFL provided better sensitivity/specificity for detecting change over time than RGC/IPL (area under the curve [AUC] 0.78 vs. 0.52), which was confirmed by higher detection rate when 95 th percentile of progression in healthy controls was used as a cut-off. CONCLUSIONS. This study confirmed significant thinning of RGC/IPL and tRNFL in NON eyes of RRMS patients. Progressive losses were more apparent on tRNFL, while RGC/IPL showed less change over the follow-up period