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PubMed2004

Combining FDI and AI approaches within causal-model-based diagnosis.

This paper presents a model-based diagnostic method designed in the context of process supervision. It has been inspired by both artificial intelligence and control theory. AI contributes tools for qualitative modeling, including causal modeling, whose aim is to split a complex process into elementary submodels. Control theory, within the framework of fault detection and isolation (FDI), provides numerical models for generating and testing residuals, and for taking into account inaccuracies in the model, unknown disturbances and noise. Consistency-based reasoning provides a logical foundation for diagnostic reasoning and clarifies fundamental assumptions, such as single fault and exoneration. The diagnostic method presented in the paper benefits from the advantages of all these approaches. Causal modeling enables the method to focus on sufficient relations for fault isolation, which avoids combinatorial explosion. Moreover, it allows the model to be modified easily without changing any aspect of the diagnostic algorithm. The numerical submodels that are used to detect inconsistency benefit from the precise quantitative analysis of the FDI approach. The FDI models are studied in order to link this method with DX component-oriented reasoning. The recursive on-line use of this algorithm is explained and the concept of local exoneration is introduced.

Algorithms↗

PubMed2000

The causal influences of attributions on emotions: a procedural priming approach.

According to attributional theories of emotion, feelings of guilt presuppose that the causes of a negative event are located within the individual (internal attribution), whereas feelings of anger presuppose that the causes of the eliciting event are located outside the individual (external attribution). This study tested whether these attributions in fact exert the claimed causal influence on emotional experiences. The study employed a procedural priming technique in which neutral events were repeatedly attributed either to oneself (internal attribution) or to another person (external attribution). Subsequently, participants were exposed to a negative event that was ambiguous as to its causes. The results reveal that the prior repeated use of internal attributions enhanced the tendency to experience guilt, whereas the repeated use of external attributions enhanced the tendency to experience anger. These findings support the assumption that attributions exert a causal influence on emotions.

Adult↗

PubMed2002

Causal capture: contextual effects on the perception of collision events.

In addition to perceiving the colors, shapes, and motions of objects, observers can perceive higher-level properties of visual events. One such property is causation, as when an observer sees one object cause another object to move by colliding with it. We report a striking new type of contextual effect on the perception of such collision events. Consider an object (A) that moves toward a stationary object (B) until they are adjacent, at which point A stops and B starts moving along the same path. Such "launches" are perceived in terms beyond these kinematics: As noted in Michotte's classic studies, observers perceive A as being the cause of B's motion. When A and B fully overlap before B's motion, however observers often see this test event as a completely noncausal "pass": One object remains stationary while another passes over it. When a distinct launch event occurs nearby, however, the test event is "captured": It too is now irresistibly seen as causal. For this causal capture to occur, the context event need be present for only 50 ms surrounding the "impact," but capture is destroyed by only 200 ms of temporal asynchrony between the two events. We report a study of such cases, and others, that help define the rules that the visual system uses to construct percepts of seemingly high-level properties like causation.

Adult↗

PubMed2026

Unveiling the BMI Risk Threshold for Osteoarthritis: Multi-Database Causal and Nonlinear Evidence.

OBJECTIVE: To characterize the nonlinear relationship between BMI and osteoarthritis (OA), and to identify BMI thresholds that inform precise prevention strategies. METHODS: This multi-database study integrated Global burden of disease 2021, National Health and Nutrition Examination Survey 2007-2018, and Genome-Wide Association Studies. A generalized additive model was performed to visualize the BMI-OA relationship, adjusting for multiple confounders. We applied segmented logistic regression models to identify potential threshold effects and used Mendelian randomization to estimate the causal effects of BMI on OA subtypes. RESULTS: From 1990 to 2021, the age-standardized prevalence and years lived with disability rates for OA were highest in regions with high SDI. OA prevalence rose nonlinearly with BMI, with breakpoints at 24.00 and 41.58 kg/m2. Each unit increase in BMI was associated with higher odds of OA between 24.00 and 41.58 kg/m2 (OR = 1.022, 95% CI: 1.003-1.041) and above 41.58 kg/m2 (OR = 1.055, 95% CI: 1.022-1.090). Women and individuals aged ≥ 45 years exhibited a higher susceptibility to knee osteoarthritis. BMI was causally associated with knee osteoarthritis (OR = 1.63, 95% CI 1.50-1.77) and hip osteoarthritis (OR = 1.54, 95% CI 1.40-1.70). CONCLUSIONS: These findings suggest that OA risk awareness and weight-management strategies should begin before BMI reaches the high range, particularly among individuals with BMI exceeding 24.00 kg/m2.

Humans↗

PubMed2026

Cell Type-Resolved Causal Inference and Spatial Transcriptomic Integration Reveal Immune-Specific Genetic Drivers of Autoimmune and Malignant Thyroid Disease.

BACKGROUND: Thyroid diseases, including autoimmune thyroid disease (AITD) and thyroid cancer, are characterized by immune dysregulation, yet the cell type-specific genetic mechanisms underlying these conditions remain poorly understood. Most genome-wide association studies (GWAS) have relied on bulk tissue expression quantitative trait loci (eQTL), which cannot resolve the heterogeneity of immune cell populations. METHODS: We performed two-sample Mendelian randomization (MR) analyses using single-cell cis-eQTLs from 14 immune cell subtypes (OneK1K cohort) as instrumental variables against GWAS summary statistics for four thyroid outcomes: autoimmune hyperthyroidism, autoimmune hypothyroidism, thyroid cancer and autoimmune thyroiditis. Causal associations were validated through Bayesian colocalization, phenome-wide association analysis (PheWAS) and multi-layered transcriptomic validation encompassing spatial transcriptomics of AITD tissue (GSE248205), bulk RNA-seq of thyroid cancer (GSE3678) and single-cell RNA-seq of thyroid tumours (GSE250521). gsMap spatial LD score regression was applied to map disease heritability onto spatial tissue architecture. RESULTS: We identified six Bonferroni-significant causal gene-cell type pairs for autoimmune hyperthyroidism, including protective effects of ABHD16A in naïve/immature B cells (OR = 0.440), HIST1H3H in CD8 NC T cells (OR = 0.324), HMGN4 in NK recruiting cells (OR = 0.556) and ZKSCAN4 in CD8 S100B T cells (OR = 0.427), with five pairs showing strong colocalization (PP.H4 ≥ 86%). Three pairs reached significance for autoimmune hypothyroidism, including a risk association of HLA-F in CD4 NC T cells (OR = 1.139). For autoimmune thyroiditis, FAM134B/RETREG1 showed consistent suggestive protective associations across both CD4 and CD8 NC T cells (PP.H4 ≥ 90% for both), suggesting a possible involvement of ER phagy regulation in thyroiditis susceptibility. Thyroid cancer showed a suggestive association with HLA-G in classical monocytes (OR = 1.899, PP.H4 = 53%). Spatial transcriptomic validation demonstrated progressive immune infiltration from control tissue to Graves' disease to Hashimoto's thyroiditis (7.7%-15.7%, 46.1%-54.1%, respectively) and strong spatial correlation between target gene expression and corresponding cell type enrichment (e.g., plasma cell-HLA-DQB1: r = 0.491, p < 10-300). HLA-G was independently validated in thyroid cancer bulk (log2fc = 0.542, p = 9.51 × 10-3, AUC = 0.857) and single-cell datasets. PheWAS revealed no significant associations detected for the core candidates. gsMap identified significant enrichment of autoimmune hypothyroidism heritability in gastrointestinal tract, adrenal gland and adipose tissue (all Bonferroni p < 0.002). CONCLUSIONS: This study establishes a multi-scale analytical framework integrating cell type-resolved genetic inference with spatial tissue validation, revealing distinct immunogenetic architectures underlying autoimmune versus malignant thyroid disease. Protective genetic programs in autoimmune hyperthyroidism converge on chromatin remodelling (HIST1H3H, HMGN4, ZKSCAN4) and lipid metabolism (ABHD16A) across lymphocyte subsets, whereas thyroid cancer risk involves immune escape mediated by HLA-G in myeloid cells. The ER-phagy receptor RETREG1 represents a candidate pathway warranting further investigation in autoimmune thyroiditis. These findings provide genetically supported, cell type-specific therapeutic targets and demonstrate a generalizable strategy for dissecting the immune-mediated mechanisms of complex thyroid diseases.

Mendelian randomization↗

PubMed2005

Tests of causal linkages between cannabis use and psychotic symptoms.

AIM: To examine possible causal linkages between cannabis use and psychosis using data gathered over the course of a 25-year longitudinal study. DESIGN: A 25-year longitudinal study of the health, development and adjustment of a birth cohort of 1265 New Zealand children (635 males, 630 females). SETTING: The Christchurch Health and Development Study, a general community sample. PARTICIPANTS: A total of 1055 participants from the Christchurch Health and Development Study (CHDS) cohort for whom data on cannabis use and psychotic symptoms were available on at least one occasion from 18, 21 and 25 years. MEASUREMENTS: As part of this study, data were gathered on frequency of cannabis use and psychotic symptoms at ages 18, 21 and 25 years. FINDINGS: Regression models adjusting for observed and non-observed confounding suggested that daily users of cannabis had rates of psychotic symptoms that were between 1.6 and 1.8 times higher (P < 0.001) than non-users of cannabis. Structural equation modelling suggested that these associations reflected the effects of cannabis use on symptom levels rather than the effects of symptom levels on cannabis use. CONCLUSIONS: The results of the present study add to a growing body of evidence suggesting that regular cannabis use may increase risks of psychosis. The present study suggests that: (a) the association between cannabis use and psychotic symptoms is unlikely to be due to confounding factors; and (b) the direction of causality is from cannabis use to psychotic symptoms.

Adolescent↗

PubMed2005

Whither causal models in the neuroscience of ADHD?

In this paper we examine the current status of the science of ADHD from a theoretical point of view. While the field has reached the point at which a number of causal models have been proposed, it remains some distance away from demonstrating the viability of such models empirically. We identify a number of existing barriers and make proposals as to the best way for these to be overcome in future studies. These include the need to work across multiple levels of analysis in multidisciplinary teams; the need to recognize the existence of, and then model, causal heterogeneity; the need to integrate environmental and social processes into models of genetic and neurobiological influence; and the need to model developmental processes in a dynamic fashion. Such a model of science, although difficult to achieve, has the potential to provide the sort of framework for programmatic model-based research required if the power and sophistication of new neuroscience technologies are to be effectively exploited.

Attention Deficit Disorder with Hyperactivity↗

PubMed2005

Young children infer causal strength from probabilities and interventions.

We examine the interaction of two cues that children use to make judgments about cause-effect relations: probabilities and interventions. Children were shown a "detector" that lit up and played music when a block was placed on its surface. We varied the probabilistic effectiveness of the block, as well as whether the experimenter or the child was performing the interventions. In Experiment 1, we found that children can use probabilistic evidence to make inferences about causal strength. However, when the results of their own interventions are in conflict with the overall frequencies, preschoolers favor the results of their own interventions. In Experiment 2, children used probabilistic evidence to infer a hidden causal mechanism. Though they again gave preference to their own interventions, they did not do so when their interventions were explicitly confounded by an alternative cause.

Child↗

PubMed1992

Who caused it? Interpersonal causal inferences in young children.

Three experiments were designed to test 4- and 6-year-old children's causal inferences in interpersonal settings where emotions (glad, angry, and sad) were effect responses. The results showed that emotion and orientation (towards or away from) were central cues, and that sex and age also were used to some extent. Cues related to regularity philosophic notions (e.g. David Hume), such as contiguity in time and space, and time order of cause and effect were little used by comparison. The results raise questions about the basic role attributed to regularity cues both by philosophers and psychologists, and suggest a multiple cue contribution rather than a basic cue generalization approach to causal cognition development.

Child↗

PubMed1988

Population growth among U.S. regions and metropolitan areas: a test for causality.

"This paper explores theories of population growth, and implied economic growth, among the major U.S. metro areas and regions. One set of theoretical arguments [favors] the growth of large cities, while an alternative set of arguments [favors] the growth of the smaller urban areas. Still another set of arguments [combines] economic space and urban size in the concept of regional growth centers as the engines of regional growth. Granger causality tests are applied to determine the role of urban size or growth centers as engines of regional growth. The test results indicate no causal relationship exists."

Americas↗

PubMed2005

Doubly robust estimation in missing data and causal inference models.

The goal of this article is to construct doubly robust (DR) estimators in ignorable missing data and causal inference models. In a missing data model, an estimator is DR if it remains consistent when either (but not necessarily both) a model for the missingness mechanism or a model for the distribution of the complete data is correctly specified. Because with observational data one can never be sure that either a missingness model or a complete data model is correct, perhaps the best that can be hoped for is to find a DR estimator. DR estimators, in contrast to standard likelihood-based or (nonaugmented) inverse probability-weighted estimators, give the analyst two chances, instead of only one, to make a valid inference. In a causal inference model, an estimator is DR if it remains consistent when either a model for the treatment assignment mechanism or a model for the distribution of the counterfactual data is correctly specified. Because with observational data one can never be sure that a model for the treatment assignment mechanism or a model for the counterfactual data is correct, inference based on DR estimators should improve upon previous approaches. Indeed, we present the results of simulation studies which demonstrate that the finite sample performance of DR estimators is as impressive as theory would predict. The proposed method is applied to a cardiovascular clinical trial.

Antidepressive Agents↗

PubMed2001

Chlamydia pneumoniae and atherosclerosis: does the evidence support a causal or contributory role?

The intracellular bacterial pathogen Chlamydia pneumoniae causes respiratory tract infection and has been associated with atherosclerosis and coronary artery disease. Since atherosclerosis is a progressive disease and is considered to be a chronic inflammation of the artery vessel wall, the interaction of C. pneumoniae with cells of the vasculature that can result in a local inflammatory response is of paramount importance. In this essay we review the pathophysiology of atherosclerosis in the context of C. pneumoniae infection and present an integrated model that includes the involvement of C. pneumoniae in all stages of atherogenesis including initiation, inflammation, fibrous plaque formation, plaque rupture and thrombosis. We hypothesize that acute and persistent infection of professional immune cells (T-cells, monocytes and macrophages) and non-immune cells (endothelial cells and smooth muscle cells) contributes to a sustained inflammatory response mediated by extensive cellular 'crosstalk' and numerous cytokines/chemokines. This cascade of inflammatory mediators may contribute to cellular dysfunction and tissue remodelling of the arterial intima. An improved understanding of the precise mechanism(s) of C. pneumoniae involvement in atherogenesis may help resolve the question of causality however, at the present time, we interpret the data as favoring a contributory rather than a causal role. Future research directed at the discovery of chlamydial virulence factors necessary for intracellular survival and subsequent alterations in host cell gene expression including signalling pathways may be important for the design of future clinical trials.

Animals↗

PubMed1984

Nutrition and health in childhood: causal and quantitative interpretations of dental caries.

The aim of the present study was to suggest a causal model of dental caries and to discuss some quantitative interpretations of this model. Three age groups of children (4, 8 and 13 yr) from three different areas in Sweden were included. The caries status of the children was examined. A 7-day record (4-and 8-yr-olds) and a dietary history (13-yr-olds) were used to estimate food intake. Sociodemographic data and data of caries preventive measures were obtained from parents/children. A causal model of dental caries is suggested and some quantitative interpretations are made by means of path analyses. Hypothetical examples of results of changes in caries determinants are given.

Adolescent↗

PubMed1988

Causal attributions of doctor and patients in a diabetes clinic.

This study investigated the level of congruence in causal attributions and diabetes-specific perceived control between doctor and patients during routine diabetes clinic consultations. The effectiveness of a strategy for improving the congruence of doctor and patients' attributions was examined. Fifty-four patients with poorly controlled insulin requiring diabetes mellitus were assigned to one of three forms of consultation: (1) routine consultation, (2) a consultation where doctor and patient explicitly negotiated and agreed the nature of the problem(s) to be discussed, (3) consultation as in (2) but doctor and patient negotiated and agreed not only the problems but also their causal attributions for the problems discussed. Analysis of covariance demonstrated that the experimental manipulations were successful in improving problem and attribution congruence across the groups. Predicted mismatches in perceived control between doctor and patient in Group I were demonstrated, and, as expected, were reduced in Groups II and III. The clinical implications of differing levels of congruence in attributions and perceived control were considered in analyses of glycaemic control and patients' satisfaction with their consultation.

Adult↗

PubMed1996

Causal attributions for criminal offending and sexual arousal: comparison of child sex offenders with other offenders.

Causal attributions for their offending, and for sexual arousal and sexual behaviour, were investigated for 50 males convicted of child sex offences. These attributions were compared with those obtained from 150 males convicted of one of three other criminal offences: rape, property offences and violent offences against persons. In semi-structured interviews, the Offence and Sexual Arousal and Behaviour Attribution Questionnaires were administered. Offenders offered causal attributions for their offending and for their sexual arousal, and they rated these causes on attribution dimensions. Results showed that child sex offenders attributed both their offending and their sexual arousal to internal, stable and uncontrollable causes. Rapists and property offenders attributed their offending behaviour to external, stable and uncontrollable causes; and violent offenders to internal, stable and uncontrollable causes. In contrast to child sex offenders, the other three groups all attributed their sexual arousal and sexual behaviour to external, unstable and controllable causes. The findings are discussed in terms of their implications for intervention programmes.

Adolescent↗

PubMed1987

Attributional style and learned helplessness: relationship to the use of causal schemata and depressive symptoms in children.

The attributional style associated with learned helplessness in children is examined in terms of its stability over a six-month period; impact on causal schemata used by children; and association with depressive symptoms. Seventy-three fifth grade children provided attributions for success and failure and were divided into learned helpless and mastery-oriented groups on the basis of the attributions typically associated with these response patterns. The attributional styles were relatively stable, influenced responses to stimuli used to investigate the use of causal schemata and were related to depressive symptoms. These results are discussed in terms of research on learned helplessness in children and several research questions are identified.

Aptitude↗

PubMed2006

Physiological basis for a causal relationship of obstructive sleep apnoea to hypertension.

Obstructive sleep apnoea (OSA) is causally related to systemic hypertension through sustained sympathoexcitation. The causes of this sympathoexcitation remain uncertain; however, substantial animal and human data suggest that cyclic intermittent hypoxia (CIH), as is experienced at night by patients with OSA, provides the causal link between upper airway obstruction during sleep and sympathetic activation during waking. Direct and indirect evidence indicates that CIH leads to sympathoexcitation by two mechanisms: (1) augmentation of peripheral chemoreflex sensitivity (hypoxic acclimatization); and (2) direct effects on sites of central sympathetic regulation, such as the subfornical organ and the paraventricular nucleus of the hypothalamus. Initial reports suggest that the molecular mechanisms influencing peripheral chemoreflex sensitivity and central sympathetic activity may be the same, involving such neuromodulators as angiotensin II, endothelin and nitric oxide.

Animals↗

PubMed2002

Hepatocyte nuclear factor-1alpha is a causal factor responsible for interindividual differences in the expression of UDP-glucuronosyltransferase 2B7 mRNA in human livers.

UDP-glucuronosyltransferase (UGT) 2B7 is one of the most important UGT isozymes expressed in human livers. This enzyme is reported to show more than 10-fold interindividual differences in its enzyme activities. Thus, the amounts of UGT2B7 mRNA in 12 human livers were quantified by quantitative reverse transcription-polymerase chain reaction. The amounts of UGT2B7 mRNA in the subjects ranged from 0.22 to 2.63 copies/10(3) copies of beta-actin. A novel point mutation (-253G to A) found in this study did not affect the level of UGT2B7 mRNA in the subjects. To clarify a causal factor(s) determining the expression level of UGT2B7 mRNA, we examined the correlation between the amounts of mRNAs for UGT2B7 and hepatocyte nuclear factor (HNF)-1alpha, which regulates the expression of UGT2B7 gene. HNF-1alpha mRNA was expressed at a level ranging from 2.99 to 24.76 copies/10(6) copies of beta-actin in the subjects. The amounts of mRNAs for UGT2B7 expressed in these individual liver samples were highly associated with the amount of mRNA for HNF-1alpha (r = 0.786, p = 0.002), suggesting that HNF-1alpha is a factor limiting the expression of UGT2B7 mRNA and a causal factor responsible for an interindividual difference in human livers.

DNA-Binding Proteins↗