Causal conjunction fallacies: The roles of causal strength and mental resources

In two experiments we tested the prediction derived from Tversky and Kahneman's (1983) work on the causal conjunction fallacy that the strength of the causal connection between constituent events directly affects the magnitude of the causal conjunction fallacy. We also explored whether any effects of perceived causal strength were due to graded output from heuristic Type 1 reasoning processes or the result of analytic Type 2 reasoning processes. As predicted, Experiment 1 demonstrated that fallacy rates were higher for strongly than for weakly related conjunctions. Weakly related conjunctions in turn attracted higher rates of fallacious responding than did unrelated conjunctions. Experiment 2 showed that a concurrent memory load increased rates of fallacious responding for strongly related but not for weakly related conjunctions. We interpret these results as showing that manipulations of the strength of the perceived causal relationship between the conjuncts result in graded output from heuristic reasoning process and that additional mental resources are required to suppress strong heuristic output.

Who is susceptible to conjunction fallacies in category-based induction?

Recent evidence suggests that the conjunction fallacy observed in people's probabilistic reasoning is also to be found in their evaluations of inductive argument strength. We presented 130 participants with materials likely to produce a conjunction fallacy either by virtue of a shared categorical or a causal relationship between the categories in the argument. We also took a measure of participants' cognitive ability. We observed conjunction fallacies overall with both sets of materials but found an association with ability for the categorical materials only. Our results have implications for accounts of individual differences in reasoning, for the relevance theory of induction, and for the recent claim that causal knowledge is important in inductive reasoning.

Molecular pathology of RUNX3 in human carcinogenesis

A major goal of molecular biology is to elucidate the mechanisms underlying cancer development and progression in order to achieve early detection, better diagnosis and staging and novel preventive and therapeutic strategies. We feel that an understanding of Runt-related transcription factor 3 (RUNX3)-regulated biological pathways will directly impact our knowledge of these areas of human carcinogenesis. The RUNX3 transcription factor is a downstream effector of the transforming growth factor-beta (TGF-beta) signaling pathway, and has a critical role in the regulation of cell proliferation and cell death by apoptosis, and in angiogenesis, cell adhesion and invasion. We previously identified RUNX3 as a major gastric tumor suppressor by establishing a causal relationship between loss of function and gastric carcinogenesis. More recently, we showed that RUNX3 functions as a bona fide initiator of colonic carcinogenesis by linking the Wnt oncogenic and TGF-beta tumor suppressive pathways. Apart from gastric and colorectal cancers. a multitude of epithelial cancers exhibit inactivation of RUNX3, thereby making it a putative tumor suppressor in human neoplasia. This review highlights our current understanding of the molecular mechanisms of RUNX3 inactivation in the context of cancer development and progression. (C) 2009 Elsevier B.V. All rights reserved.

Does infection by Nosema ceranae cause "Colony Collapse Disorder" in honey bees (Apis mellifera)?

Nosema ceranae is an emergent and potentially virulent pathogen of the honey bee (Apis mellifera) that has spread across the world in the last 10 or so years. Its precise origin and timing of spread are currently unclear because of a lack of appropriate genetic markers and inadequate sampling in putative Asian source populations. Though it has been dismissed as a cause of CCD in the USA based on correlational analyses of snapshot sampling of diseased hives, observations of naturally infected colonies suggest that it leads to colony collapse in Spain. Experiments are sorely needed to investigate its impact on individuals and colonies, and to pin down a causal relationship between N. ceranae and colony collapse. Whether N. ceranae is displacing N. apis is uncertain. For temperate zone apiculturalists, global climate change may mean that N. ceranae presents more of a challenge than has hitherto been considered the case.

The role of adiposity in cardiometabolic traits:a Mendelian randomization analysis

The association between adiposity and cardiometabolic traits is well known from epidemiological studies. Whilst the causal relationship is clear for some of these traits, for others it is not. We aimed to determine whether adiposity is causally related to various cardiometabolic traits using the Mendelian randomization approach.

The struggle for safe staffing levels in the USA: A political economy of evidence-based practice

This paper examines the debate over nursing staff to patient ratios through the lens of Marxist political economy, arguing that the owners and controllers of healthcare in the USA have a vested interest in opposing mandated minimum ratios, while those involved in carrying out nursing care have a vested interest in their implementation, which coincides with the interests of patients. We examine how evidence-based practice articulates with social power, and proceed to interrogate the research methods used to generate evidence for practice, noting that randomised controlled trials are not suitable for evaluating nurse/patient ratios, which means that observational studies are the primary source of evidence. Representatives of nursing managers have used the fact that observational studies, while demonstrating an association between high ratios and poor outcomes, have not established a causal relationship, to support their argument that there is not sufficient evidence for the imposition of mandatory ratios. We argue that the precautionary principle provides firm justification for mandatory ratios, unless and until a causal relationship has been disproved. We conclude that those involved in the generation of evidence have to choose between technical arguments about the inferiority of observational studies, or emphasising their sufficiency in triggering the precautionary principle.

Plasma Clusterin Levels and the rs11136000 Genotype in Individuals with Mild Cognitive Impairment and Alzheimer's Disease

Aim: Substantial evidence links atherosclerosis and Alzheimer's disease (AD). Apolipoproteins, such as apolipoprotein E, have a causal relationship with both diseases. The rs11136000 SNP within the CLU gene, which encodes clusterin (apolipoprotein J), is also associated with increased AD risk. The aim of this study was to investigate the relationship between plasma clusterin and the rs11136000 genotype in mild cognitive impairment (MCI) and AD.

Methods: Plasma and DNA samples were collected from control, MCI and AD subjects (n=142, 111, 154, respectively). Plasma clusterin was determined by ELISA and DNA samples were genotyped for rs11136000 by TaqMan assay.

Results: Plasma clusterin levels were higher in MCI and AD subjects vs. controls (222.3 +/- 61.3 and 193.6 +/- 58.2 vs. 178.6 +/- 52.3 mu g/ml, respectively; p

Conclusion: This study examined control, MCI and AD subjects, identifying for the first time that plasma clusterin levels were influenced, not only by the presence of AD, but also the transitional stage of MCI, while rs11136000 genotype only influenced plasma clusterin levels in the control group. The increase in plasma clusterin in MCI and AD subjects may occur in response to the disease process and would be predicted to increase binding capacity for amyloid-beta peptides in plasma, enhancing their removal from the brain.

Still Unequal at Birth: Birth Weight, Socioeconomic Status and Outcomes at Age 9

The prevalence of low birth weight is an important aspect of public health which has been linked to increased risk of infant death, increased cost of care, and a range of later life outcomes. Using data from a new Irish cohort study, I document the relationship between birth weight and socio-economic status. The association of maternal education with birth weight does not appear to be due to the timing of birth or complications during pregnancy, even controlling for a wide range of background characteristics. However, results do suggest intergenerational persistence in the transmission of poor early life conditions. Birth weight predicts a number of outcomes at age 9, including test scores, hospital stays and health. An advantage of the data is that I am able to control for a number of typically unmeasured variables. I determine whether parental investments (as measured by the quality of interaction with the child, parenting style, or school quality) mediate the association between birth weight and later indicators. For test scores, there is evidence of non-linearity, and boys are more adversely affected than girls. I also consider whether there are heterogeneous effects by ability using quantile regression. These results are consistent with a literature which finds that there is a causal relationship between early life conditions and later outcomes.

Aflatoxin Exposure and Associated Human Health Effects, a Review of Epidemiological Studies

flatoxins are fungal toxins that possess acute life threatening toxicity, carcinogenic properties and other potential chronic adverse effects. Dietary exposure to aflatoxins is considered a major public health concern, especially for subsistence farming communities in sub-Saharan Africa and South Asia, where dietary staple food crops such as groundnuts and maize are often highly contaminated with aflatoxin due to hot and humid climates and poor storage, together with low awareness of risk and lack of enforcement of regulatory limits. Biomarkers have been developed and applied in many epidemiological studies assessing aflatoxin exposure and the associated health effects in these high-risk population groups. This review discusses the recent epidemiological evidence for aflatoxin exposure, co-exposure with other mycotoxins and associated health effects in order to provide evidence on risk assessment, and highlight areas where further research is necessary. Aflatoxin exposure can occur at any stage of life and is a major risk factor for hepatocellular carcinoma, especially when hepatitis B infection is present. Recent evidence suggests that aflatoxin may be an underlying determinant of stunted child growth, and may lower cell-mediated immunity, thereby increasing disease susceptibility. However, a causal relationship between aflatoxin exposure and these latter adverse health outcomes has not been established, and the biological mechanisms for these have not been elucidated, prompting further research. Furthermore, there is a dearth of information regarding the health effects of co-exposure to aflatoxin with other mycotoxins. Recent developments of biomarkers provide opportunities for important future research in this area.

Aircraft Cost Modelling using the Genetic Causal Technique within a Systems Engineering Approach

The paper is primarily concerned with the modelling of aircraft manufacturing cost. The aim is to establish an integrated life cycle balanced design process through a systems engineering approach to interdisciplinary analysis and control. The cost modelling is achieved using the genetic causal approach that enforces product family categorisation and the subsequent generation of causal relationships between deterministic cost components and their design source. This utilises causal parametric cost drivers and the definition of the physical architecture from the Work Breakdown Structure (WBS) to identify product families. The paper presents applications to the overall aircraft design with a particular focus on the fuselage as a subsystem of the aircraft, including fuselage panels and localised detail, as well as engine nacelles. The higher level application to aircraft requirements and functional analysis is investigated and verified relative to life cycle design issues for the relationship between acquisition cost and Direct Operational Cost (DOC), for a range of both metal and composite subsystems. Maintenance is considered in some detail as an important contributor to DOC and life cycle cost. The lower level application to aircraft physical architecture is investigated and verified for the WBS of an engine nacelle, including a sequential build stage investigation of the materials, fabrication and assembly costs. The studies are then extended by investigating the acquisition cost of aircraft fuselages, including the recurring unit cost and the non-recurring design cost of the airframe sub-system. The systems costing methodology is facilitated by the genetic causal cost modeling technique as the latter is highly generic, interdisciplinary, flexible, multilevel and recursive in nature, and can be applied at the various analysis levels required of systems engineering. Therefore, the main contribution of paper is a methodology for applying systems engineering costing, supported by the genetic causal cost modeling approach, whether at a requirements, functional or physical level.

Temporal information and children's and adults' causal inferences

Three experiments examined whether children and adults would use temporal information as a cue to the causal structure of a three-variable system, and also whether their judgements about the effects of interventions on the system would be affected by the temporal properties of the event sequence. Participants were shown a system in which two events B and C occurred either simultaneously (synchronous condition) or in a temporal sequence (sequential condition) following an initial event A. The causal judgements of adults and 6-7-year-olds differed between the conditions, but this was not the case for 4-year-olds' judgements. However, unlike those of adults, 6-7-year-olds' intervention judgements were not affected by condition, and causal and intervention judgements were not reliably consistent in this age group. The findings support the claim that temporal information provides an important cue to causal structure, at least in older children. However, they raise important issues about the relationship between causal and intervention judgements.

Elevated AGE-modified ApoB in sera of euglycemic, normolipidemic patients with atherosclerosis: relationship to tissue AGEs.:relationship to tissue AGEs

BACKGROUND: Advanced glycation endproducts (AGEs) are implicated in the pathogenesis of atherosclerotic vascular disease of diabetic and nondiabetic etiology. Recent research suggests that advanced glycation of ApoB contributes to the development of hyperlipidemia. AGE-specific receptors, expressed on vascular endothelium and mononuclear cells, may be involved in both the clearance of, and the inflammatory responses to AGEs. The aim of this study was to examine whether there is a relationship between serum AGE-ApoB and AGEs in arterial tissue of older normolipidemic nondiabetic patients with occlusive atherosclerotic disease, compared with age-matched and younger asymptomatic persons.

MATERIALS AND METHODS: Serum AGE-ApoB was measured by ELISA in 21 cardiac bypass patients. Furthermore, an AGE-specific monoclonal antibody, and polyclonal antibodies against anti-AGE-receptor (anti-AGE-R) 1 and 2 were used to explore the localization and distribution of AGEs and AGE-R immunoreactivity (IR) in arterial segments excised from these patients.

RESULTS: Serum AGE-ApoB levels were significantly elevated in the asymptomatic, older population, compared with those in young healthy persons (259 +/- 24 versus 180 +/- 21 AGE U/mg of ApoB, p < 0.01). Higher AGE-ApoB levels were observed in those patients with atherosclerosis (329 +/- 23 versus 259 +/- 24 AGE U/mg ApoB, p < 0.05). Comparisons of tissue AGE-collagen with serum AGE-ApoB levels showed a significant correlation (r = 0.707, p < 0.01). In early lesions, AGE-IR occurred mostly extracellularly. In fatty streaks and dense, cellular atheromatous lesions, AGE-IR was visible within lipid-containing smooth muscle cells and macrophages, while in late-stage, acellular plaques, AGE-IR occurred mostly extracellularly. AGE-R1 and -R2 were observed on vascular endothelial and smooth-muscle cells and on infiltrating mononuclear cells in the early-stage lesions, whereas in dense, late-stage plaques, they colocalized mostly with lipid-laden macrophages. On tissue sections, scoring of AGE-immunofluorescence correlated with tissue AGE and plasma AGE-ApoB.

CONCLUSIONS: (1) The correlation between arterial tissue AGEs and circulating AGE-ApoB suggests a causal link between AGE modification of lipoproteins and atherosclerosis. AGE-specific receptors may contribute to this process. (2) Serum AGE-ApoB may serve to predict atherosclerosis in asymptomatic patients.

Genetic Evidence for a Causal Role of Obesity in Diabetic Kidney Disease

Obesity has been posited as an independent risk factor for diabetic kidney disease (DKD), but establishing causality from observational data is problematic. We aimed to test whether obesity is causally related to DKD using Mendelian randomization, which exploits the random assortment of genes during meiosis. In 6,049 subjects with type 1 diabetes, we used a weighted genetic risk score (GRS) comprised of 32 validated BMI loci as an instrument to test the relationship of BMI with macroalbuminuria, end-stage renal disease (ESRD), or DKD defined as presence of macroalbuminuria or ESRD. We compared these results with cross-sectional and longitudinal observational associations. Longitudinal analysis demonstrated a U-shaped relationship of BMI with development of macroalbuminuria, ESRD, or DKD over time. Cross-sectional observational analysis showed no association with overall DKD, higher odds of macroalbuminuria (for every 1 kg/m(2) higher BMI, odds ratio [OR] 1.05, 95% CI 1.03-1.07, P < 0.001), and lower odds of ESRD (OR 0.95, 95% CI 0.93-0.97, P < 0.001). Mendelian randomization analysis showed a 1 kg/m(2) higher BMI conferring an increased risk in macroalbuminuria (OR 1.28, 95% CI 1.11-1.45, P = 0.001), ESRD (OR 1.43, 95% CI 1.20-1.72, P < 0.001), and DKD (OR 1.33, 95% CI 1.17-1.51, P < 0.001). Our results provide genetic evidence for a causal link between obesity and DKD in type 1 diabetes. As obesity prevalence rises, this finding predicts an increase in DKD prevalence unless intervention should occur.