Wicked problems in public policy

Some of the most difficult policy problems of the modern era have been described as complex, intractable, open-ended and 'wicked'. What are the key features of such problems? And are they really very different in nature from more routine problems? Are we developing better ways to address these wicked problems? This paper sketches some key aspects of wicked problems, and illustrates the discussion with two contemporary Australian examples - recent attempts to address the causes and possible solutions to Indigenous disadvantage; and policy responses to climate change

Wicked Problems in Public Policy

This is an open access book. This book offers the first overview of the ‘wicked problems’ literature, often seen as complex, open-ended, and intractable, with both the nature of the ‘problem’ and the preferred ‘solution’ being strongly contested. It contextualises the debate using a wide range of relevant policy examples, explaining why these issues attract so much attention. There is an increasing interest in the conceptual and practical aspects of how ‘wicked problems’ are identified, understood and managed by policy practitioners. The standard public management responses to complexity and uncertainty (including traditional regulation and market-based solutions) are insufficient. Leaders often advocate and implement ideological ‘quick fixes’, but integrative and inclusive responses are increasingly being utilised to recognise the multiple interests and complex causes of these problems. This book uses examples from a wide range of social, economic and environmental fields in order to develop new insights about better solutions, and thus gain broad stakeholder acceptance for shared strategies for tackling ‘wicked problems’

Wicked Problems in Public Policy

This is an open access book. This book offers the first overview of the ‘wicked problems’ literature, often seen as complex, open-ended, and intractable, with both the nature of the ‘problem’ and the preferred ‘solution’ being strongly contested. It contextualises the debate using a wide range of relevant policy examples, explaining why these issues attract so much attention. There is an increasing interest in the conceptual and practical aspects of how ‘wicked problems’ are identified, understood and managed by policy practitioners. The standard public management responses to complexity and uncertainty (including traditional regulation and market-based solutions) are insufficient. Leaders often advocate and implement ideological ‘quick fixes’, but integrative and inclusive responses are increasingly being utilised to recognise the multiple interests and complex causes of these problems. This book uses examples from a wide range of social, economic and environmental fields in order to develop new insights about better solutions, and thus gain broad stakeholder acceptance for shared strategies for tackling ‘wicked problems’

Urban water security - what does it mean?

This research is focussed on understanding what urban water security means–a surprisingly elusive concept given the global shift from rural to urban living. We first make the case for a distinct urban water security definition. We then identify 25 unique water security definitions, of which three relate to the urban context but all with scope for improvement. Applying novel indices, we assess the prevalence, complexity and evolution of themes and dimensions within all definitions and find a stable spectrum of themes; but note a shifting emphasis towards environmental and social dimensions, away from quality and quantity of supply. Overall the definitions are becoming more comprehensive by simply listing more outcomes to be achieved. Instead of this ‘shopping-list’ approach, we propose a simplified urban water security definition with a focus on agreement of needs with community stakeholders, while using the themes to guide what the objectives might be

The Progression of β-amyloid Deposition in the Frontal Cortex of the Aged Canine

Brains from 41 aged canines (≥10 years of age) were examined immunohistochemically to characterize the laminar distribution and age-related progression of β-amyloid (Aβ) in frontal cortex. We classified the Aβ patterns into four distinct types. Type I was characterized by small, faint deposits of Aβ in deep cortical layers. Type II consisted of diffuse deposits of Aβ mainly in layers V and VI. Type III had both dense plaques in superficial layers, and diffuse deposits in deep layers. Finally, Type IV had solely dense plaques throughout all layers of cortex. We compared the Aβ distribution pattern between the Old canines (10–15 years, n=22) and the Very Old canines (\u3e15 years, n=19). The Old group primarily had negative staining, or Type I and Type II patterns of amyloid deposition (73%). Conversely, the Very Old group had predominantly Types II, III and IV deposits (89.5%), a difference that was significant (Pβ deposition in canine frontal cortex is a progressive age-related process beginning with diffuse deposits in the deep cortical layers followed by the development of deposits in outer layers. In support of this hypothesis, the deeper layer diffuse plaques in the Very Old group of dogs also contain the largest proportion of β-amyloid with an isomerized aspartic acid residue at position 7, indicating that these deposits had been present for some time. We also observed fiber-like Aβ immunoreactivity within regions of diffuse Aβ deposits. These fibers appeared to be degenerating neurites, which were negative for hyperphosphorylated tau. Therefore, these fibers may represent a very early form of neuritic change that precede tau hyperphosphorylation or develop by an alternative pathway

Neuronal Deletion of Caspase 8 Protects against Brain Injury in Mouse Models of Controlled Cortical Impact and Kainic Acid-Induced Excitotoxicity

system. mice demonstrated superior survival, reduced seizure severity, less apoptosis, and reduced caspase 3 processing. Uninjured aged knockout mice showed improved learning and memory, implicating a possible role for caspase 8 in cognitive decline with aging.Neuron-specific deletion of caspase 8 reduces brain damage and improves post-traumatic functional outcomes, suggesting an important role for this caspase in pathophysiology of acute brain trauma

Natural flavonoids as potential multifunctional agents in prevention of diabetic cataract

Cataract is one of the earliest secondary complications of diabetes mellitus. The lens is a closed system with limited capability to repair or regenerate itself. Current evidence supports the view that cataractogenesis is a multifactorial process. Mechanisms related to glucose toxicity, namely oxidative stress, processes of non-enzymatic glycation and enhanced polyol pathway significantly contribute to the development of eye lens opacity under conditions of diabetes. There is an urgent need for inexpensive, non-surgical approaches to the treatment of cataract. Recently, considerable attention has been devoted to the search for phytochemical therapeutics. Several pharmacological actions of natural flavonoids may operate in the prevention of cataract since flavonoids are capable of affecting multiple mechanisms or etiological factors responsible for the development of diabetic cataract. In the present paper, natural flavonoids are reviewed as potential agents that could reduce the risk of cataract formation via affecting multiple pathways pertinent to eye lens opacification. In addition, the bioavailability of flavonoids for the lens is considered

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders