899 resultados para strict and absolute liability


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Epistemological foundationalism has for centuries attempted to unify all scientific inquiry into the context of one grand science, the first philosophy. One of the most important tasks of this tradition has been to ground all knowledge on absolutely certain foundations. In this master s thesis I ask the following question: To what extent and under what conditions is it possible to achieve absolute certainty in the sense of the attempts of Cartesian foundationalism? By examining how the 20th century philosophers, Edmund Husserl (1859-1938), Hannah Arendt (1906-1975) and Maurice Merleau-Ponty (1908-1961) interpret the epistemological methodology of René Descartes, I claim that the Cartesian achievement of absolute certainty rests on the implicit presupposition of an epistemologically prior form of faith in the world and trust (pistis) in other conscious beings. I show that knowledge is possible only within the context of a common world that is inhabited by several conscious beings that share a common linguistic system. This threefold element is shown to be the bedrock condition for any kind of philosophical inquiry. The main literature sources for this thesis are The Life of the Mind by Hannah Arendt, Le Visible et l invisible by Maurice Merleau-Ponty, Meditationes de Prima Philosophiae by René Descartes and Erfahrung und Urteil by Edmund Husserl.

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Drop formation at conical tips which is of relevance to metallurgists is investigated based on the principle of minimization of free energy using the variational approach. The dimensionless governing equations for drop profiles are computer solved using the fourth order Runge-Kutta method. For different cone angles, the theoretical plots of XT and ZT vs their ratio, are statistically analyzed, where XT and ZT are the dimensionless x and z coordinates of the drop profile at a plane at the conical tip, perpendicular to the axis of symmetry. Based on the mathematical description of these curves, an absolute method has been proposed for the determination of surface tension of liquids, which is shown to be preferable in comparison with the earlier pendent-drop profile methods.

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The appropriate frequency and precision for surveys of wildlife populations represent a trade-off between survey cost and the risk of making suboptimal management decisions because of poor survey data. The commercial harvest of kangaroos is primarily regulated through annual quotas set as proportions of absolute estimates of population size. Stochastic models were used to explore the effects of varying precision, survey frequency and harvest rate on the risk of quasiextinction for an arid-zone and a more mesic-zone kangaroo population. Quasiextinction probability increases in a sigmoidal fashion as survey frequency is reduced. The risk is greater in more arid regions and is highly sensitive to harvest rate. An appropriate management regime involves regular surveys in the major harvest areas where harvest rate can be set close to the maximum sustained yield. Outside these areas, survey frequency can be reduced in relatively mesic areas and reduced in arid regions when combined with lowered harvest rates. Relative to other factors, quasiextinction risk is only affected by survey precision (standard error/mean × 100) when it is >50%, partly reflecting the safety of the strategy of harvesting a proportion of a population estimate.

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In this chapter, we look at the step beyond reporting, to the external audit or assurance function. The role of any audit engagement is to provide a professional opinion on a set of financial or non-financial assertions reported by an organization's management, based on an agreed evaluative framework. Any such opinion is not a guarantee that the underlying report is free from fraud or misstatement. Where an audit opinion on financial statements is incorrect, this is referred to as an audit failure. Specifically, the textbook definition of audit failure has two components: that the financial statements contain a serious error and that the auditor has failed to detect the error due to the auditor's failure during the audit process.

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This chapter provides an overview of a recent shift in regulatory strategies to address copyright infringement toward enlisting the assistance of general purpose Internet Service Providers. In Australia, the High Court held in 2012 that iiNet, a general purpose ISP, had no legal duty to police what its subscribers did with their internet connections. We provide an overview of three recent developments in Australian copyright law since that decision that demonstrate an emerging shift in the way that obligations are imposed on ISPs to govern the actions of their users without relying on secondary liability. The first is a new privately negotiated industry code that introduces a 'graduated response' system that requires ISPs to pass on warnings to subscribers who receive allegations of infringement. The second involves a recent series of Federal Court cases where rightsholders made a partially successful application to require ISPs to hand over the identifying details of subscribers whose households are alleged to have infringed copyright. The third is a new legislative scheme that will require ISPs to block access to foreign websites that 'facilitate' infringement. We argue that these shifts represent a greater sophistication in approaches to enrolling general purpose intermediaries in the regulatory project. We also suggest that these shifts represent a potentially disturbing trend towards enforcement of copyright law in a way that does not provide strong safeguards for the legitimate constitutional due process interests of users. We conclude with a call for greater attention and research to better understand how intermediaries make decisions when governing the conduct of users, how those decisions may be influenced by both state and non-state actors, and how the rights of individuals to due process can be adequately protected.

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There has been much debate over recent years about whether Australian copyright law should adopt a fair use doctrine. In this chapter we argue by pointing to the historical record that the incorporation of the term 'copyrights' in the Australian Constitution embeds a notion of balance and fair use in Australian law and that this should be taken into account when interpreting the Australian Copyright Act 1968. English case law in the 18th and 19th centuries developed a principle that copyright infringement did not occur where a person had made a fair use of a work. Fair use was generally established where the defendant had made a productive use that did more than alter the original work for the purpose of evading liability, and where the defendant had made an original contribution to the resulting work. Additionally, fairness was shown by a use that did not supersede or prejudice the market for the original work. At the time of including the copyright power in the Constitution, the UK Parliament’s understanding of “copyrights” included the notion of fair use as it had been developed in U.K. precedent. In this chapter we argue that the work “copyrights” in the Australia Constitution takes its definition from copyright in 1900 and as it has evolved since. Importantly, the word “copyrights” is infused with a particular meaning that incorporates the principle of copyright balance. The constitutional notion of copyright, therefore, is not that of an unlimited power to prevent all copying. Rather, copyright distinguishes between infringing copying and non-infringing copying and grants to the copyright owner only the power to control the former. Non-infringing copying includes well-accepted limitations on the copyright owner’s rights, including the copying of ideas, the copying of public domain works and the copying of insubstantial parts of copyrighted works. In this chapter we argue that non-infringing copying also includes copying to make a fair use of a work. The sections that distinguish infringing copying from non-infringing copying in the Copyright Act 1968 are sections 36(1) and 101(1), which define infringement as the doing, without licence, of an “act comprised in the copyright”. An infringing copy is an act comprised the copyright, whereas a non-infringing copy is not. We argue that space for fair uses of copyrighted works is built into the Copyright Act 1968 through these sections, because a fair use will not produce an infringing copy and so is not an act comprised in the copyright.

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In The Fissured Workplace, David Weil dissects the ways in which ostensibly ‘large’ American businesses have come to shed direct employees and instead source their labour needs through a ‘complicated network of smaller business units’. As he notes, this has increased the profitability of these ‘lead’ businesses, at the expense of those who (ultimately) work for them: Wage setting and supervision shift from core businesses to a myriad of organizations, each operating under the rigorous standards of lead businesses but facing fierce competitive pressures. Although lead businesses set demanding goals and standards, and often detailed work practice requirements for subsidiary companies, the actual liability, oversight, and supervision of the workforce become the problem of one or more other organizations. And by replacing a direct employment relationship with a fissured workplace, employment itself becomes more precarious, with risk shifted onto smaller employers and individual workers, who are often cast in the role of independent businesses in their own right.

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While the method using specialist herbivores in managing invasive plants (classical biological control) is regarded as relatively safe and cost-effective in comparison to other methods of management, the rarity of strict monophagy among insect herbivores illustrates that, like any management option, biological control is not risk-free. The challenge for classical biological control is therefore to predict risks and benefits a priori. In this study we develop a simulation model that may aid in this process. We use this model to predict the risks and benefits of introducing the chrysomelid beetle Charidotis auroguttata to manage the invasive liana Macfadyena unguis-cati in Australia. Preliminary host-specificity testing of this herbivore indicated that there was limited feeding on a non-target plant, although the non-target was only able to sustain some transitions of the life cycle of the herbivore. The model includes herbivore, target and non-target life history and incorporates spillover dynamics of populations of this herbivore from the target to the non-target under a variety of scenarios. Data from studies of this herbivore in the native range and under quarantine were used to parameterize the model and predict the relative risks and benefits of this herbivore when the target and non-target plants co-occur. Key model outputs include population dynamics on target (apparent benefit) and non-target (apparent risk) and fitness consequences to the target (actual benefit) and non-target plant (actual risk) of herbivore damage. The model predicted that risk to the non-target became unacceptable (i.e. significant negative effects on fitness) when the ratio of target to non-target in a given patch ranged from 1:1 to 3:2. By comparing the current known distribution of the non-target and the predicted distribution of the target we were able to identify regions in Australia where the agent may be pose an unacceptable risk. By considering risk and benefit simultaneously, we highlight how such a simulation modelling approach can assist scientists and regulators in making more objective decisions a priori, on the value of releasing specialist herbivores as biological control agents.

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Polycyclic Aromatic Hydrocarbons (PAHs) represent a major class of toxic pollutants because of their carcinogenic and mutagenic characteristics. People living in urban areas are regularly exposed to PAHs because of abundance of their emission sources. Within this context, this study aimed to: (i) identify and quantify the levels of ambient PAHs in an urban environment; (ii) evaluate their toxicity; and (iii) identify their sources as well as the contribution of specific sources to measured concentrations. Sixteen PAHs were identified and quantified in air samples collected from Brisbane. Principal Component Analysis – Absolute Principal Component Scores (PCA- APCS) was used in order to conduct source apportionment of the measured PAHs. Vehicular emissions, natural gas combustion, petrol emissions and evaporative/unburned fuel were the sources identified; contributing 56%, 21%, 15% and 8% of the total PAHs emissions, respectively, all of which need to be considered for any pollution control measures implemented in urban areas.

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The permanent mammalian kidney (metanephros) develops as a result of complex reciprocal tissue interactions between a ureteric epithelium and the renal mesenchyme. The overall goal of the research in this thesis was to gain data that will eventually help in elucidating the formation of congenital renal malformations. The experiments in my thesis aimed to reveal the mechanisms by which Notch, Wnt and GDNF/Ret signalling pathways regulate the development of functional kidney. The function of Notch pathway was studied by a transgenic mouse model, where it was shown that overactivation of Notch signalling disturbs kidney development and alters the expression of Gdnf and Ret/GFRa1. This indicates that Notch signalling interplays with GDNF/Ret in the regulation of the primary ureteric budding and its subsequent branching. The data also suggested that strict spatio-temporal regulation of these two pathways is required for determination of ureteric tip-identity, which appeared to be crucial for the branch formation. The function of Wnt signalling in the ureteric morphogenesis was studied by in vivo and in vitro methods to show that a canonical pathway is required for ureteric branching. Stabilisation and deletion of the canonical pathway mediator, b-catenin specifically in the ureteric epithelium result in renal aplasia/hypodysplasia. These defects originate from severe blockage of ureteric branching due to the disrupted Ret signalling. Consequently, ureteric tip specific markers are lost and ureteric stalk identity is expanded throughout the whole epithelium. Thus, the data demonstrates that the Wnt/b-catenin pathway plays an essential role in the patterning and branching of the ureteric epithelium. A novel in vitro method was generated and utilised in nephron induction studies to reveal the mechanisms through which nephrogenesis is induced. Transient GSK3 inhibition results in stabilisation of b-catenin in the isolated renal mesenchyme, which efficiently triggers nephron formation. Also genetic stabilisation of b-catenin specifically in the mesenchyme results in spontaneous nephrogenesis. The results show that activation of the canonical Wnt pathway is sufficient to initiate nephrogenesis, and suggest that this pathway mediates the nephron induction in murine kidney mesenchymes. Taken together, this thesis demonstrates Notch and Wnt signalling pathways as novel regulators of ureteric branching morphogenesis, and that activation of the canonical Wnt pathway is sufficient for nephron induction. The studies also indicate that the Notch and Wnt pathways cross-talk with GDNF/Ret signalling in the patterning of ureteric epithelium.

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Common diseases such as endometriosis (ED), Alzheimer's disease (AD) and multiple sclerosis (MS) account for a significant proportion of the health care burden in many countries. Genome-wide association studies (GWASs) for these diseases have identified a number of individual genetic variants contributing to the risk of those diseases. However, the effect size for most variants is small and collectively the known variants explain only a small proportion of the estimated heritability. We used a linear mixed model to fit all single nucleotide polymorphisms (SNPs) simultaneously, and estimated genetic variances on the liability scale using SNPs from GWASs in unrelated individuals for these three diseases. For each of the three diseases, case and control samples were not all genotyped in the same laboratory. We demonstrate that a careful analysis can obtain robust estimates, but also that insufficient quality control (QC) of SNPs can lead to spurious results and that too stringent QC is likely to remove real genetic signals. Our estimates show that common SNPs on commercially available genotyping chips capture significant variation contributing to liability for all three diseases. The estimated proportion of total variation tagged by all SNPs was 0.26 (SE 0.04) for ED, 0.24 (SE 0.03) for AD and 0.30 (SE 0.03) for MS. Further, we partitioned the genetic variance explained into five categories by a minor allele frequency (MAF), by chromosomes and gene annotation. We provide strong evidence that a substantial proportion of variation in liability is explained by common SNPs, and thereby give insights into the genetic architecture of the diseases.

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Major depressive disorder (MDD) is a common complex disorder with a partly genetic etiology. We conducted a genome-wide association study of the MDD2000+ sample (2431 cases, 3673 screened controls and >1 M imputed single-nucleotide polymorphisms (SNPs)). No SNPs achieved genome-wide significance either in the MDD2000+ study, or in meta-analysis with two other studies totaling 5763 cases and 6901 controls. These results imply that common variants of intermediate or large effect do not have main effects in the genetic architecture of MDD. Suggestive but notable results were: (a) gene-based tests suggesting roles for adenylate cyclase 3 (ADCY3, 2p23.3) and galanin (GAL, 11q13.3); published functional evidence relates both of these to MDD and serotonergic signaling; (b) support for the bipolar disorder risk variant SNP rs1006737 in CACNA1C (P=0.020, odds ratio=1.10), and; (c) lack of support for rs2251219, a SNP identified in a meta-analysis of affective disorder studies (P=0.51). We estimate that sample sizes 1.8- to 2.4-fold greater are needed for association studies of MDD compared with those for schizophrenia to detect variants that explain the same proportion of total variance in liability. Larger study cohorts characterized for genetic and environmental risk factors accumulated prospectively are likely to be needed to dissect more fully the etiology of MDD.

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Type 1 diabetes (T1D) is a common, multifactorial disease with strong familial clustering. In Finland, the incidence of T1D among children aged 14 years or under is the highest in the world. The increase in incidence has been approximately 2.4% per year. Although most new T1D cases are sporadic the first-degree relatives are at an increased risk of developing the same disease. This study was designed to examine the familial aggregation of T1D and one of its serious complications, diabetic nephropathy (DN). More specifically the study aimed (1) to determine the concordance rates of T1D in monozygotic (MZ) and dizygotic (DZ) twins and to estimate the relative contributions of genetic and environmental factors to the variability in liability to T1D as well as to study the age at onset of diabetes in twins; (2) to obtain long-term empirical estimates of the risk of T1D among siblings of T1D patients and the factors related to this risk, especially the effect of age at onset of diabetes in the proband and the birth cohort effect; (3) to establish if DN is aggregating in a Finnish population-based cohort of families with multiple cases of T1D, and to assess its magnitude and particularly to find out whether the risk of DN in siblings is varying according to the severity of DN in the proband and/or the age at onset of T1D: (4) to assess the recurrence risk of T1D in the offspring of a Finnish population-based cohort of patients with childhood onset T1D, and to investigate potential sex-related effects in the transmission of T1D from the diabetic parents to their offspring as well as to study whether there is a temporal trend in the incidence. The study population comprised of the Finnish Young Twin Cohort (22,650 twin pairs), a population-based cohort of patients with T1D diagnosed at the age of 17 years or earlier between 1965 and 1979 (n=5,144) and all their siblings (n=10,168) and offspring (n=5,291). A polygenic, multifactorial liability model was fitted to the twin data. Kaplan-Meier analyses were used to provide the cumulative incidence for the development of T1D and DN. Cox s proportional hazards models were fitted to the data. Poisson regression analysis was used to evaluate temporal trends in incidence. Standardized incidence ratios (SIRs) between the first-degree relatives of T1D patients and background population were determined. The twin study showed that the vast majority of affected MZ twin pairs remained discordant. Pairwise concordance for T1D was 27.3% in MZ and 3.8% in DZ twins. The probandwise concordance estimates were 42.9% and 7.4%, respectively. The model with additive genetic and individual environmental effects was the best-fitting liability model to T1D, with 88% of the phenotypic variance due to genetic factors. The second paper showed that the 50-year cumulative incidence of T1D in the siblings of diabetic probands was 6.9%. A young age at diagnosis in the probands considerably increased the risk. If the proband was diagnosed at the age of 0-4, 5-9, 10-14, 15 or more, the corresponding 40-year cumulative risks were 13.2%, 7.8%, 4.7% and 3.4%. The cumulative incidence increased with increasing birth year. However, SIR among children aged 14 years or under was approximately 12 throughout the follow-up. The third paper showed that diabetic siblings of the probands with nephropathy had a 2.3 times higher risk of DN compared with siblings of probands free of nephropathy. The presence of end stage renal disease (ESRD) in the proband increases the risk three-fold for diabetic siblings. Being diagnosed with diabetes during puberty (10-14) or a few years before (5-9) increased the susceptibility for DN in the siblings. The fourth paper revealed that of the offspring of male probands, 7.8% were affected by the age of 20 compared with 5.3% of the offspring of female probands. Offspring of fathers with T1D have 1.7 times greater risk to be affected with T1D than the offspring of mothers with T1D. The excess risk in the offspring of male fathers manifested itself through the higher risk the younger the father was when diagnosed with T1D. Young age at onset of diabetes in fathers increased the risk of T1D greatly in the offspring, but no such pattern was seen in the offspring of diabetic mothers. The SIR among offspring aged 14 years or under remained fairly constant throughout the follow-up, approximately 10. The present study has provided new knowledge on T1D recurrence risk in the first-degree relatives and the risk factors modifying the risk. Twin data demonstrated high genetic liability for T1D and increased heritability. The vast majority of affected MZ twin pairs, however, remain discordant for T1D. This study confirmed the drastic impact of the young age at onset of diabetes in the probands on the increased risk of T1D in the first-degree relatives. The only exception was the absence of this pattern in the offspring of T1D mothers. Both the sibling and the offspring recurrence risk studies revealed dynamic changes in the cumulative incidence of T1D in the first-degree relatives. SIRs among the first-degree relatives of T1D patients seems to remain fairly constant. The study demonstrates that the penetrance of the susceptibility genes for T1D may be low, although strongly influenced by the environmental factors. Presence of familial aggregation of DN was confirmed for the first time in a population-based study. Although the majority of the sibling pairs with T1D were discordant for DN, its presence in one sibling doubles and presence of ESRD triples the risk of DN in the other diabetic sibling. An encouraging observation was that although the proportion of children to be diagnosed with T1D at the age of 4 or under is increasing, they seem to have a decreased risk of DN or at least delayed onset.

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The aim of this study was to deepen the understanding of eating disorders, body image dissatisfaction and related traits in males by examining the epidemiology and genetic epidemiology of these conditions in representative population-based twin samples. The sample of Study I included adolescent twins from FinnTwin12 cohorts born 1983 87 and assessed by a questionnaire at ages 14 y (N=2070 boys, N=2062 girls) and 17 y (N=1857 boys, N=1984 girls). Samples of Studies II-V consisted of young adult twins born 1974-79 from FinnTwin16 cohorts (Study II N=1245 men, Study III N=724 men, Study IV N=2122 men, Study V N=2426 women and N=1962 men), who were assessed by a questionnaire at the age 22-28 y. In addition, 49 men and 526 women were assessed by a diagnostic interview. The overall response rates for both twin cohorts in all studies were 80-90%. In boys, mainly genetic factors (82%, 95% confidence interval [CI] 72-92) explained the covariation of self-esteem between the ages 14 y and 17 y, whereas in girls, environmental factors (69%, 95% CI 43-93) were the largest contributors. Of young men, 30% experienced high muscle dissatisfaction, while 12% used or had used muscle building supplements and/or anabolic steroids on a regular basis. Muscle dissatisfaction exhibited a robust association with the indicators of mental distress and a genetic component (42%, 95% CI 23-59) for its liability in this population was found. The variation of muscle-building substance use was primarily explained by the environmental factors. The incidence rate of anorexia nervosa in males for the age of 10-24 y was 15.7 (95% CI 6.6-37.8) per 100 000 person-years, and its lifetime prevalence by the young adulthood was 0.24% (95% CI 0.03-0.44). All detected probands with anorexia nervosa had recovered from eating disorders, but suffered from substantial psychiatric comorbidity, which manifested also in their co-twins. Additionally, male co-twins of the probands displayed significant dissatisfaction with body musculature, a male-specific feature of body dysmorphic disorder. All probands were from twin pairs discordant for eating disorders. Of the five male probands with anorexia nervosa, only one was from an opposite-sex twin pair. Among women from the opposite-sex pairs, the prevalence of DSM-IV or broad anorexia nervosa was no significantly different compared to that of the women from monozygotic pairs or from dizygotic same-sex pairs. The prevalence of DSM-IV or broad bulimia nervosa did not differ in opposite- versus same-sex female twin individuals either. In both sexes, the overall profile of indicators on eating disorders was rather similar between individuals from opposite-sex and same-sex pairs. In adolescence, development of self-esteem was differently regulated in boys compared to girls: this finding may have far-reaching implications on the etiology of sex discrepancy of internalizing and externalizing disorders. In young men, muscle dissatisfaction and muscle building supplement/steroid use were relatively common. Muscle dissatisfaction was associated with marked psychological distress such as symptoms of depression and disordered eating. Both genetic and environmental factors explained muscle dissatisfaction in the population, but environmental factors appeared to best explain the use of muscle-building substances. In this study, anorexia nervosa in boys and young men from the general population was more common, transient and accompanied by more substantial co-morbidity than previously thought. Co-twins of the probands with anorexia nervosa displayed significant psychopathology such as male specific symptoms of body dysmorphic disorder, but none of them had had an eating disorder: taken together, these traits are suggestive for an endophenotype of anorexia nervosa in males. Little evidence was found on that the risk for anorexia nervosa, bulimia nervosa, disordered eating or body dissatisfaction were associated with twin zygosity. Thus, it is unlikely that in utero femininization, masculinization or postnatal socialization according to the sex of the co-twin have a major influence on the later development of eating disorders or related traits.