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Results for “causality”

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PubMed1998

Causal mechanisms of subjective cognitive dysfunction in schizophrenic and depressed patients.

We examined causal mechanisms of subjective cognitive (dis)abilities in schizophrenic and depressed patients, and in patient and normal control groups. This exploratory study included objective cognitive performance (Continuous Performance Task) as well as mood and mental effort ratings. Self-report of cognitive dysfunction in patients was not correlated with objective cognitive deficits. Correlational patterns differed between groups. Our findings in schizophrenic and depressed patients point to different causal mechanisms of their subjective cognitive malaise, despite similar subjective ratings. Depressed patients associate high mental effort during task performance with a reduced cognitive efficacy, whereas schizophrenic patients associate high effort with cognitive symptoms like distractibility and overload.

Adult↗

PubMed1978

A causal model of health services for diabetic patients.

A causal model of health services which includes patient and provider variables, perceived access to care, utilization of services, continuity of care, technical quality of the care process, technical quality of the care outcome, and patient satisfaction is applied to a group of diabetic patients enrolled in the Seattle Prepaid Health Care Project. The enrollees received comprehensive health services at zero out-of-pocket cost from either a prepaid group practice plan or an independent practice plan. Surveys were periodically conducted to determine health status, satisfaction, and demographic characteristics of the enrollees; utilization of services was monitored throughout the experiment. The causal model is operationalized through the use of path analysis. Significant relationships (p less than or equal to .10) were established between satisfaction and perceived access to care, family size, sex, and professional qualifications of the provider; between outcome of care and health status, female education, and physician performance; between physician performance and professional qualifications; between continuity of care and health status and female education; between utilization and perceived access, specialty of provider, and provider system; and between access to care and provider system. The policy implications of the results are discussed.

Consumer Behavior↗

PubMed1989

Patient satisfaction and the use of health services. Explorations in causality.

Little research exists that examines the causal relationship between patient satisfaction and the use of health services. This study of a representative sample of low income families suggests that a relationship does exist. Furthermore, results reported indicate it is bidirectional and reciprocal in nature, and that it is highly related to the provider from which patients seek care. Analysis according to the five major area clinics that were main sources of medical care for an upstate New York community (two HMOs, two hospital-affiliated teaching clinics, and one continuity-of-care clinic) revealed that, in some providers, the association between use and satisfaction is positive, in others negative. Further evidence for a "patient provider" interaction hypothesis was found, suggesting that background characteristics, including health status and race, are related to use and satisfaction in different ways in different clinics. The findings provide evidence for the existence of a causal relationship between use and satisfaction, which is dependent on the context in which medical care is given, and also suggest structural characteristics that might be responsible for these effects. A final conceptual model of satisfaction is offered, permitting reciprocal causation with use and satisfaction with emphasis on patient provider interactions, and this model provides an identification of short- and long-term processes. Progress in this area might require a shift in perspective upward toward structural and systems variables or a shift downward toward "microanalytic" processes, which detail patient-provider interactions.

Consumer Behavior↗

PubMedDate not supplied

Circulating testosterone levels and aggression in adolescent males: a causal analysis.

Empirical analyses conducted within a causal-analytic framework (path analysis) on a sample of normal adolescent human males suggested that circulating levels of testosterone in the blood had a direct causal influence on provoked aggressive behavior (self-reports): A high level of testosterone led to an increased readiness to respond vigorously and assertively to provocations and threats. Testosterone also had an indirect and weaker affect on another aggression dimension: High levels of testosterone made the boys more impatient and irritable, which in turn increased their propensity to engage in aggressive-destructive behavior. Two somewhat parallel dimensions of behavior, intermale and irritable aggression, have been identified in animal research to be under testosterone control.

Adolescent↗

PubMed1992

Cognitive dysfunction in a patient with long-term occupational exposure to ethylene oxide. Role of ethylene oxide as a causal factor.

This case illustrates a comprehensive approach to assessing causality in a woman with apparent cognitive dysfunction, as measured by neuropsychological testing, and a 10-year history of occupational exposure to ethylene oxide. The analysis included a multidisciplinary examination of the patient, which took place several years after the termination of her exposure. In addition, all of the patient's prior medical and psychiatric records were reviewed, as were the records of her employer to ascertain her exposure history. Our evaluation revealed a pattern of neuropsychological findings not consistent with nervous system damage secondary to an organic effect of ethylene oxide. A more likely causal hypothesis is adopted: the patient's apparent cognitive dysfunction had a psychiatric etiology. This case also illustrates the potential impact of a patient's involvement in legal proceedings related to claims of neurocognitive dysfunction.

Adult↗

PubMed2000

Latanoprost and cystoid macular edema: is there a causal relation?

Published reports of the occurrence of cystoid macular edema (CME) in eyes being treated with latanoprost have led to concern regarding a possible causal relation between the two. Review of all published cases (28 eyes in 25 patients), plus another case reported here for the first time, indicates that all eyes had independent risk for development of CME, so that definitive conclusions about a causal relation cannot be established. In addition, controlled clinical trials and experimental studies with latanoprost have given no indication that latanoprost causes clinical CME. Pharmacokinetic considerations indicate that the concentration of latanoprost expected in the posterior segment of the eye is too low to have a pharmacologic effect, and latanoprost is not known to exhibit vasoactive or inflammatory properties. Nevertheless, reports of a possible association between CME and latanoprost use must be given serious consideration, and in eyes that are at risk for CME, an increased level of surveillance for its development is recommended.

Aged↗

PubMed2006

Melanoma, Parkinson's disease and levodopa: causal or spurious link? A review of the literature.

Since the early 1970s, a number of case reports have suggested that levodopa therapy for Parkinson's disease increases the risk of cutaneous malignant melanoma. As yet, no formal epidemiological study has been conducted to verify this hypothesis. To elucidate the relationship between levodopa and the risk of cutaneous malignant melanoma, a systematic literature search using computerized bibliographic databases was done. This review presents the case history evidence for and against the hypothesis of a causal association, and explores possible epidemiological, genetic, social, biochemical and toxicological factors that may increase the risk of melanoma in Parkinson's disease patients. All the case reports in the literature were considered. We concluded that (1) there is no epidemiological or experimental evidence of a causal role of levodopa in increasing the risk of melanoma incidence or progression; (2) there is good evidence of an excess risk of melanoma in patients with Parkinson's disease; (3) there is good evidence of a protective effect of tobacco smoking on the risk for Parkinson's disease; (4) there is good evidence of positive correlation between social class and melanoma risk; (5) the relationship between the risk of Parkinson's disease and the risk of melanoma may be due to a common genetic profile or it can be attributed to a confounding role of social class, associated with both melanoma and Parkinson's disease possibly through an inverse relationship with tobacco smoking.

Animals↗

PubMed2006

Lipoma on the corpus callosum in a patient with schizophrenia-like episode: is there a causal relationship?

Disturbed interhemispheric communication has been proposed as responsible for schizophrenia. We present a case of a schizophrenia-like episode with no neurologic or other psychiatric symptoms. However, magnetic resonance imaging revealed a lipoma on the splenium of the corpus callosum. Neuropsychologic examination revealed normal interhemispheric transfer, but a slight dysfunction associated with right-hemispheric anterior regions. Rather than supporting the hypothesis of a causal relationship between callosal abnormality and schizophrenia-like symptoms, our findings argue against a direct causal relationship between lesion site and psychotic episode. We conclude that cerebral abnormality per se may represent a risk factor for neuropsychiatric symptoms.

Adult↗

PubMed2026

Identification of putative causal associations between MicroRNAs and breast cancer via Mendelian randomization and bioinformatic analysis.

MicroRNAs (miRNAs) are implicated in breast cancer progression and prognosis. This study employed a Mendelian randomization (MR) framework to investigate causal relationships between plasma circulating miRNAs and breast cancer. miRNA expression quantitative trait loci were extracted from 2 independent cohorts. High-confidence miRNAs and their associated single-nucleotide polymorphisms were selected for 2-sample MR analyses using inverse-variance weighted and MR-Egger methods. Differential expression analysis and univariate Cox regression identified survival-associated genes in breast cancer, while enrichment analyses revealed pathways and biological processes linked to candidate targets. Pan-cancer analyses of miRNAs and targets were conducted via the ENCORI platform. Initial MR analyses in the discovery phase identified hsa-miR-100-5p, hsa-miR-125b-5p, and hsa-miR-339-5p as significantly associated with reduced breast cancer risk (P < .05), suggesting potential protective roles. A total of 1291 survival-associated differentially expressed genes were identified, with 39 overlapping targets implicated in miRNA-mediated breast cancer intervention. Enrichment analyses highlighted their involvement in cell cycle regulation and p53 signaling pathway. In the validation cohort, only hsa-miR-339-5p confirmed a protective effect on breast cancer risk, while hsa-miR-100-5p and hsa-miR-125b-5p did not reach significance. Pan-cancer profiling demonstrated aberrant miRNA expression across malignancies, prognostic relevance in multiple cancers, and significant negative correlations between miRNAs and target genes in breast tumors. Our findings provide novel insights into the causal roles of miRNAs in breast cancer pathogenesis and underscore their potential as noninvasive biomarkers and therapeutic targets. Future studies should prioritize functional validation and clinical translation of these miRNAs.

Humans↗

PubMed2000

Causality in medicine: the case of tumours and viruses.

Clarification of the aetiology of chronic human diseases such as atherosclerosis or cancer is one of the dominant topics in contemporary medical research. It is believed that identification of the causal factors will enable more efficient prevention and diagnosis of these diseases and, in some instances, also permit more effective therapy. The task is difficult because of the multistep and multifactorial origin of these diseases. A special case in contemporary aetiological studies is definition of the role of viruses in the pathogenesis of human cancer. Virus-associated cancer develops only in a small minority of infected subjects, which implies that, if the virus does play a role in the pathogenesis of the malignancy, other factors must also be involved. In this paper the author attempts to review the present methodological approaches to aetiological studies of chronic diseases, discusses the role of criteria for identifying causal relationships and proposes guidelines that might help to determine the role of viruses in human cancer.

Humans↗

PubMed2025

An Updated Polygenic Index Repository: Expanded Phenotypes, New Cohorts, and Improved Causal Inference.

Polygenic indexes (PGIs) - DNA-based predictors of individual phenotypes - have become essential tools across biomedical and social sciences. We introduce Version 2 of the Polygenic Index Repository, which expands phenotype coverage from 47 to 61, increases the number of participating datasets from 11 to 20, and adopts a more consistent and improved methodology for PGI construction. For 16 phenotypes, we leverage summary statistics from an updated GWAS meta-analysis with greater statistical power compared to the original release, thereby improving the PGI's predictive power. To improve power for family-based analyses, we provide imputed parental PGIs in all datasets with first-degree relatives and offer a framework for interpreting results from analyses that control for parental PGIs. We illustrate the utility of parental PGIs using two applications: (1) comparing PGI associations with and without parental PGI controls for all phenotypes in two Repository datasets with family data, and (2) for BMI and diastolic blood pressure, exploring the contribution of causal versus non-causal components of PGI associations to the imperfect portability of PGIs across subgroups within a genetic ancestry. Collectively, the updates enhance predictive performance, broaden the Repository's scope, and introduce novel resources that reduce confounding bias and improve interpretability.

Journal Article↗

PubMed2025

Post-traumatic stress disorder and REM-sleep behavior disorder: exploring genetic associations and causal links.

OBJECTIVE: To explore potential genetic and/or causal associations between Post-Traumatic Stress Disorder and neurodegeneration-related isolated/idiopathic rapid-eye-movement sleep behavior disorder. METHODS: We conducted polygenic risk score, genetic correlation, and Mendelian randomization analyses using the latest genome-wide association studies summary statistics and individual genotyping data. Next, a blinded observer examined dopamine transporter imaging binding status-a marker of neurodegeneration-in patients with isolated/idiopathic rapid-eye movement sleep behavior disorder, with (N = 6) and without Post-Traumatic Stress Disorder (N = 32). RESULTS: Polygenic risk scores for Post-Traumatic Stress Disorder were associated with isolated/idiopathic rapid-eye-movement sleep behavior disorder, with each standard deviation increase linked to 14.7% higher odds (odds ratio = 1.15, 95% confidence interval: 1.04 to 1.26, p = 0.005). However, genetic correlation was weak, and Mendelian randomization did not support a potential causal relationship. The proportion of individuals with abnormal dopamine transporter imaging binding status was significantly higher in the Post-Traumatic Stress Disorder group compared to those without the disorder (p=0.01, X2 = 6.62). INTERPRETATION: Polygenic risk scores analysis identified an association between Post-Traumatic Stress Disorder and neurodegeneration-related isolated/idiopathic rapid-eye-movement sleep behavior disorder, consistent with the result from the small exploratory substudy. The lack of strong genetic correlation or causation may reflect limited sample size. Further research with larger and more diverse cohorts is crucial to clarify the genetic, biological and physiological mechanisms underlying this association.

Journal Article↗

PubMed2005

Causal determination of acoustic group velocity and frequency derivative of attenuation with finite-bandwidth Kramers-Kronig relations.

Kramers-Kronig (KK) analyses of experimental data are complicated by the extrapolation problem, that is, how the unexamined spectral bands impact KK calculations. This work demonstrates the causal linkages in resonant-type data provided by acoustic KK relations for the group velocity (c(g)) and the derivative of the attenuation coefficient (alpha') (components of the derivative of the acoustic complex wave number) without extrapolation or unmeasured parameters. These relations provide stricter tests of causal consistency relative to previously established KK relations for the phase velocity (c(p)) and attenuation coefficient (alpha) (components of the undifferentiated acoustic wave number) due to their shape invariance with respect to subtraction constants. For both the group velocity and attenuation derivative, three forms of the relations are derived. These relations are equivalent for bandwidths covering the entire infinite spectrum, but differ when restricted to bandlimited spectra. Using experimental data from suspensions of elastic spheres in saline, the accuracy of finite-bandwidth KK predictions for c(g) and alpha' is demonstrated. Of the multiple methods, the most accurate were found to be those whose integrals were expressed only in terms of the phase velocity and attenuation coefficient themselves, requiring no differentiated quantities.

Acoustics↗

PubMed2005

Microscopic derivation of causal diffusion equation using the projection operator method.

We derive a coarse-grained equation of motion of a number density by applying the projection operator method to a non-relativistic model. The derived equation is an integrodifferential equation and contains the memory effect. The equation is consistent with causality and the sum rule associated with the number conservation in the low momentum limit, in contrast to usual acausal diffusion equations given by using the Fick's law. After employing the Markov approximation, we find that the equation has the similar form to the causal diffusion equation. Our result suggests that current-current correlations are not necessarily adequate as the definition of diffusion constants.

Journal Article↗

PubMed2000

Causal entropy bound for a spacelike region.

The identification of a causal-connection scale motivates us to propose a new covariant bound on entropy within a generic spacelike region. This "causal entropy bound," scaling as sqrt[EV], and thus lying around the geometric mean of Bekenstein's S/ER and holographic S/A bounds, is checked in various "critical" situations. In the case of limited gravity, Bekenstein's bound is the strongest while naive holography is the weakest. In the case of strong gravity, our bound and Bousso's holographic bound are stronger than Bekenstein's, while naive holography is too tight, and hence typically wrong.

Journal Article↗

PubMed2001

Causality of the brane universe.

Causal structure of the brane universe with respect to null geodesics in the bulk spacetime is studied. It is pointed out that apparent causality violation is possible for the brane universe which contains matter energy. It is also shown that there is no "horizon problem" in the Friedmann-Robertson-Walker brane universe.

Journal Article↗

PubMed2002

Positive mass from holographic causality.

For (n+1)-dimensional asymptotically anti-de Sitter (AdS) spacetimes which have holographic duals on their n-dimensional conformal boundaries, we show that the imposition of causality on the boundary theory is sufficient to prove positivity of mass for the spacetime when n> or =3, without the assumption of any local energy condition. We make crucial use of a time-delay formula relating the Ashtekar-Magnon mass of the spacetime to the time delay of a bulk null curve relative to that of a boundary null geodesic. We also discuss holographic causality for the negative mass AdS soliton and its implications for the positive energy conjecture of Horowitz and Myers.

Journal Article↗

PubMed2004

On the "Causality argument" in bouncing cosmologies.

We exhibit a situation in which cosmological perturbations of astrophysical relevance propagating through a bounce are affected in a scale-dependent way. Involving only the evolution of a scalar field in a closed universe described by general relativity, the model is consistent with causality. Such a specific counterexample leads to the conclusion that imposing causality is not sufficient to determine the spectrum of perturbations after a bounce provided it is known before. We discuss consequences of this result for string motivated scenarios.

Journal Article↗