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Explaining lifetime criminal arrests among clients of a psychiatric probation and parole service.

This study examines the extent to which sociodemographic characteristics, clinical characteristics, substance abuse problems, and the array of lifetime criminal behavior may explain lifetime arrests among offenders supervised by the psychiatric probation and parole service. Three hundred twenty-five clients with new cases at a psychiatric probation and parole service in a large urban center were screened for major psychiatric disorders. They were also interviewed for socio-demographic characteristics, mental health treatment history, criminal behavior, and arrest history. Hierarchical block multiple regression analysis tested a model explaining lifetime arrests. After controlling for age and other demographic variables, the number of lifetime psychiatric hospitalizations and lifetime occurrences of mania diagnosis significantly explained lifetime arrests. The total model explained about 10 percent of the variance in lifetime arrests after controlling for opportunity variables, which explained 45 percent. The explanatory power of lifetime hospitalizations and mania support the contention that symptoms, rather than diagnosis, may be the most important clinical factor in explaining criminal arrest among persons with mental illness. Implications for psychiatric services include the development of effective jail diversion programs.

Adult↗

Explained randomness in proportional hazards models.

A coefficient of explained randomness, analogous to explained variation but for non-linear models, was presented by Kent. The construct hinges upon the notion of Kullback-Leibler information gain. Kent and O'Quigley developed these ideas, obtaining simple, multiple and partial coefficients for the situation of proportional hazards regression. Their approach was based upon the idea of transforming a general proportional hazards model to a specific one of Weibull form. Xu and O'Quigley developed a more direct approach, more in harmony with the semi-parametric nature of the proportional hazards model thereby simplifying inference and allowing, for instance, the use of time dependent covariates. A potential drawback to the coefficient of Xu and O'Quigley is its interpretation as explained randomness in the covariate given time. An investigator might feel that the interpretation of the Kent and O'Quigley coefficient, as a proportion of explained randomness of time given the covariate, is preferable. One purpose of this note is to indicate that, under an independent censoring assumption, the two population coefficients coincide. Thus the simpler inferential setting for Xu and O'Quigley can also be applied to the coefficient of Kent and O'Quigley. Our second purpose is to point out that a sample-based coefficient in common use in the SAS statistical package can be interpreted as an estimate of explained randomness when there is no censoring. When there is censoring the SAS coefficient would not seem satisfactory in that its population counterpart depends on an independent censoring mechanism. However there is a quick fix and we argue in favour of its use.

Antimetabolites, Antineoplastic↗

Less than 50% of variation in HDL cholesterol between and within individuals, is explained by established predictors.

Variation in serum high density lipoprotein cholesterol (HDL-C) concentrations is believed to be largely explained by triglycerides, but this has been mainly explored in cross-sectional analyses. Eight hundred and eighty one white male participants in a health screening program attended on a total of 2158 occasions for measurements that included fasting HDL-C, low density lipoprotein cholesterol (LDL-C) and homeostasis model assessment insulin resistance (HOMA-R). Baseline, change between-visit and repeated-measures regression models were used to analyse predictors of between- and within-individual variation in HDL-C. Independent predictors of between-individual variation included serum triglycerides (20.3 or 19.6% of the variance explained, depending on the model used), body mass index (BMI: 4.7 and 4.3%), cigarette smoking (3.3 and 1.5%) and alcohol consumption (0.4 and 1.1%). Within-individual variation in HDL-C was explained by changes in serum triglycerides (4.7 and 7.5%) and BMI (5.3 and 2.9%). In multivariate models, 24.3 and 24.9% of between-individual variation in HDL-C, and 7.9 and 8.8% of within-individual variation could be explained, depending on the model used. Sixty percent of the variation in HDL-C was due to unobserved factors. The majority of variation in HDL-C remains to be explained by influences other than the conventional variables: triglyceride and LDL cholesterol concentrations, insulin resistance, smoking and alcohol.

Alcohol Drinking↗

Why does it run in families? Explaining family similarity in help-seeking behaviour by shared circumstances, socialisation and selection.

Why do contact frequencies with general practice of family members resemble each other? Many aspects related to the clustering of health-care utilisation within families have been studied, but the underlying mechanisms have not been addressed. This article considers whether family similarity in contact frequency with general practice can be explained as (a) a result of shared circumstances, (b) through socialisation, and (c) through homogeneity of background characteristics. Data from the second Dutch national survey of general practice were used to test these mechanisms empirically. This survey recorded all consultations in 2001 for 104 general practices in the Netherlands, serving 385,461 patients. Information about socio-demographic characteristics was collected by means of a patient survey. In a random sample, an extended health interview took place (n=12,699). Overall, we were able to show that having determinants in common through socialisation and shared circumstances can explain similarity in contact frequencies within families, but not all hypotheses could be confirmed. In specific terms, this study shows that resemblances in contact frequencies within families can be best explained by spending more time together (socialisation) and parents and children consulting a general practitioner simultaneously (circumstances of the moment). For general practitioners, the mechanisms identified can serve as a framework for a family case history. The importance of the mechanism of socialisation in explaining similarities in help-seeking behaviour between family members points to the significance of knowledge and health beliefs underlying consultation behaviour. An integrated framework including these aspects can help to better explain health behaviour.

Adolescent↗

Explaining variation in birth outcomes of Medicaid-eligible women with variation in the adequacy of prenatal support services.

OBJECTIVES: This study examines the contribution of the adequacy of nutrition, psychosocial, and health education support service delivery in explaining variation in birth outcomes among Medicaid-eligible women, their provider sites, and practice settings. METHODS: Logistic regression models for low birthweight and preterm birth outcomes are first fitted with medical record data on maternal risks and use of prenatal visits for more than 3,485 women receiving care at 27 ambulatory sites, correcting for clustering of women within sites. RESULTS: The change in variation explained by these models with the addition of the adequacy of support services indicates that providing at least one nutrition, psychosocial, and health education service session each trimester of care contributes significantly to explaining better birth outcomes when compared with providing fewer sessions. When the expected outcome rates calculated with the estimated effects in the models are compared with their observed rates across provider sites and setting types, however, adequacy of service delivery does not help to explain differences in outcomes at individual sites or types of settings. CONCLUSIONS: Although repeated support service sessions during prenatal care improve the chances of avoiding poor birth outcomes in low income women, further adjustments for other differences between women or service delivery are needed to explain variation in outcomes at different sites and practice settings.

Adult↗

Explaining the social gradient in coronary heart disease: comparing relative and absolute risk approaches.

STUDY OBJECTIVES: There are contradictory perspectives on the importance of conventional coronary heart disease (CHD) risk factors in explaining population levels and social gradients in CHD. This study examined the contribution of conventional CHD risk factors (smoking, hypertension, dyslipidaemia, and diabetes) to explaining population levels and to absolute and relative social inequalities in CHD. This was investigated in an entire population and by creating a low risk sub-population with no smoking, dyslipidaemia, diabetes, and hypertension to simulate what would happen to relative and social inequalities in CHD if conventional risk factors were removed. DESIGN, SETTING, AND PARTICIPANTS: Population based study of 2682 eastern Finnish men aged 42, 48, 54, 60 at baseline with 10.5 years average follow up of fatal (ICD9 codes 410-414) and non-fatal (MONICA criteria) CHD events. MAIN RESULTS: In the whole population, 94.6% of events occurred among men exposed to at least one conventional risk factor, with a PAR of 68%. Adjustment for conventional risk factors reduced relative social inequality by 24%. However, in a low risk population free from conventional risk factors, absolute social inequality reduced by 72%. CONCLUSIONS: Conventional risk factors explain the majority of absolute social inequality in CHD because conventional risk factors explain the vast majority of CHD cases in the population. However, the role of conventional risk factors in explaining relative social inequality was modest. This apparent paradox may arise in populations where inequalities in conventional risk factors between social groups are low, relative to the high levels of conventional risk factors within every social group. If the concern is to reduce the overall population health burden of CHD and the disproportionate population health burden associated with the social inequalities in CHD, then reducing conventional risk factors will do the job.

Adult↗

A simple model based on mutation and selection explains trends in codon and amino-acid usage and GC composition within and across genomes.

BACKGROUND: Correlations between genome composition (in terms of GC content) and usage of particular codons and amino acids have been widely reported, but poorly explained. We show here that a simple model of processes acting at the nucleotide level explains codon usage across a large sample of species (311 bacteria, 28 archaea and 257 eukaryotes). The model quantitatively predicts responses (slope and intercept of the regression line on genome GC content) of individual codons and amino acids to genome composition. RESULTS: Codons respond to genome composition on the basis of their GC content relative to their synonyms (explaining 71-87% of the variance in response among the different codons, depending on measure). Amino-acid responses are determined by the mean GC content of their codons (explaining 71-79% of the variance). Similar trends hold for genes within a genome. Position-dependent selection for error minimization explains why individual bases respond differently to directional mutation pressure. CONCLUSIONS: Our model suggests that GC content drives codon usage (rather than the converse). It unifies a large body of empirical evidence concerning relationships between GC content and amino-acid or codon usage in disparate systems. The relationship between GC content and codon and amino-acid usage is ahistorical; it is replicated independently in the three domains of living organisms, reinforcing the idea that genes and genomes at mutation/selection equilibrium reproduce a unique relationship between nucleic acid and protein composition. Thus, the model may be useful in predicting amino-acid or nucleotide sequences in poorly characterized taxa.

Amino Acids↗

Chronic stress conditions do explain posttraumatic brain injury depression.

Psychosocial and biologic mechanisms are implicated in depression after traumatic brain injury (TBI). Using McEwen's stress theory of allostasis as a guidepost, this study examined whether pre- and postinjury chronic stress conditions could explain post-TBI depressive symptoms. Seventy-five community-dwelling persons who sustained a mild-to-moderate TBI and were within 2 years of the injury participated in this cross-sectional study. The participants completed measures of chronic stress and depression, measured with the Neurobehavioral Functioning Inventory. Data were collected also on brain injury severity. Using multiple regression analysis, the frequency of childhood adversities and postinjury stress explained post-TBI depression. When time-since-injury was in the regression model, the frequency of preinjury stressors and postinjury stress significantly explained post-TBI depressive symptoms while the combined effect of childhood adversity with postinjury stress was not significant in explaining depressive symptoms. Pre- and postinjury chronic stress explained post-TBI depressive symptoms. These findings support stress-diathesis theory within the psychiatric literature and a linkage between chronic stress, an indicator of allostatic load, and post-TBI depression. These findings are important for nurse specialists working with persons who sustained brain injury, for chronic stress can be buffered by efficient and effective support systems.

Adult↗

Evaluation of bioassays versus contaminant concentrations in explaining the macroinvertebrate community structure in the Rhine-Meuse delta, The Netherlands.

It is often assumed that bioassays are better descriptors of sediment toxicity than toxicant concentrations and that ecological factors are more important than toxicants in structuring macroinvertebrate communities. In the period 1992 to 1995, data were collected in the enclosed Rhine-Meuse delta, The Netherlands, on macroinvertebrates, sediment toxicity, sediment contaminant concentrations, and ecological factors. The effect of various groups of pollutants (polycyclic aromatic hydrocarbons, trace metals, oil, polychlorinated biphenyls) and of ecological variables on the structure of the macroinvertebrate community were quantified. Ecological factors explained 17.3% of the macroinvertebrate variation, while contaminants explained 13.8%. Another 14.7% was explained by the covariation between ecological variables and contaminants. Polycyclic aromatic hydrocarbons explained a larger part of the variation than trace metals. The contributions of oil and polychlorinated biphenyls were small but significant. Elevated contaminant concentrations were significantly associated with differences in the macroinvertebrate food web structure. The response in bioassays (Vibrio fischeri, Daphnia magna, Chironomus riparius) was susceptible to certain contaminants but also to certain ecological factors. There was a weak correlation between in situ species composition and bioassays; 1.9% of in situ macroinvertebrate variation was explained by the bioassay responses. This seems to contradict the validity of using bioassays for a system-oriented risk assessment. Possible reasons for this discrepancy might be the manipulations of the sediment before the test and a higher pollutant tolerance of the in situ macroinvertebrates. Thus, macroinvertebrate field surveys and laboratory bioassays yield different types of information on ecotoxicological effects, and both are recommended in sediment risk assessment procedures.

Animals↗

Explained variation for logistic regression.

Different measures of the proportion of variation in a dependent variable explained by covariates are reported by different standard programs for logistic regression. We review twelve measures that have been suggested or might be useful to measure explained variation in logistic regression models. The definitions and properties of these measures are discussed and their performance is compared in an empirical study. Two of the measures (squared Pearson correlation between the binary outcome and the predictor, and the proportional reduction of squared Pearson residuals by the use of covariates) give almost identical results, agree very well with the multiple R2 of the general linear model, have an intuitively clear interpretation and perform satisfactorily in our study. For all measures the explained variation for the given sample and also the one expected in future samples can be obtained easily. For small samples an adjustment analogous to Radj2 in the general linear model is suggested. We discuss some aspects of application and recommend the routine use of a suitable measure of explained variation for logistic models.

Likelihood Functions↗

Explaining women's intentions and use of hormones with menopause.

The purposes of this theoretically-based study were (a) to examine the contributions of psychosocial variables (i.e., affect, beliefs, and norms), habit, and facilitating conditions to explaining women's intentions and use of hormones with menopause and (b) to assess whether clinical or demographic factors explained intentions and use, when controlling for psychosocial, habit, and facilitating conditions variables. In a cross-sectional design, 184 pre-, peri-, and postmenopausal women completed questionnaire measures. To explain intentions, data from 124 participants who were not using hormones were analyzed. To explain use, data from 125 peri- and postmenopausal participants were analyzed. In multivariate analyses, anxiety was associated inversely with use; norms were associated positively with intentions and use. Age was associated inversely with intentions; hot flashes were associated inversely with use. Future researchers can examine the combined influences of affect, beliefs, and norms on decisions about hormones. Clinicians can address anxieties and assess social influences about hormone use, as well as offer ways to deal with hot flashes.

Anxiety↗

Factors that explain the power line configuration wiring code-childhood leukemia association: what would they look like?

We explore the question of how to characterize a factor that would explain the patterns of wire code-childhood leukemia association observed in three major United States case-control studies. In positive studies, such a factor needs to be more prevalent in "high" wire codes than "low" whereas in negative studies, the factor should not be correlated to wire code. These concepts are quantified and we use these results to characterize potential factors that might explain the wire code-childhood leukemia association. We then re-evaluate findings from a survey of correlates of wire code in Connecticut with respect to potential for explaining the wire code-leukemia association. Under the presumption that the Connecticut correlations apply to the populations in which a wire code-leukemia association has been observed, only age and type of home are correlated enough to be potential explanatory factors. In particular, it appears very unlikely that traffic density can explain a significant portion of the wire code association. We suggest that correlation studies can be useful for identifying potential explanatory factors, but they must be done in regions where a wire code-childhood leukemia association has been observed.

Biometry↗

Re-assessing the virological approach to HIV pathogenesis: can it explain AIDS as an immunological disease?

Over 10 years after the discovery of HIV, its molecular virology still fails to explain the clinical immunology of AIDS. The prevailing paradigm of AIDS pathogenesis, called here the "virological hypothesis", argues that viral attributes such as cytopathicity, replicability, syncytiality, cell tropism, emergent virulence, and viral load explain why infection develops to a life-threatening immunodeficiency. However, these attributes-singly and in combination-are shown here to be inadequate to explain the latency, immunological damage, and clinical dynamics of the disease of AIDS. The virological paradigm cannot explain the disease-free period (clinical latency); the mechanism and dynamics of CD4 T cell loss; the reason for the onset of disease at a given time-point; the relationship of CD4 T cell loss to AIDS-type disease; nor the idiosyncratic constellation of immunological and clinical phenomena that comprise AIDS as a unique syndrome. HIV as it is currently understood does not have the virological characteristics necessary to create a disease such as AIDS through direct classical (i.e. cytopathic) mechanisms. It is clear that the pathogenesis of AIDS remains unknown. Therefore, treatment based solely on inhibiting viral mechanisms-as with antivirals-is very likely to be insufficient. In addition, the molecular epidemiology of pathogenesis has been very poor; there is an enormous amount that is not known about the clinical immunology of AIDS, and the central question remains of how CD4 cell loss relates to clinical immunodeficiency. The conclusion drawn is that the virology of HIV has been pursed at the cost of understanding AIDS itself; that an emphasis on AIDS as an immunological disease is long overdue; and that appropriate treatment of AIDS will not be possible until the clinical immunology of AIDS is understood.

Acquired Immunodeficiency Syndrome↗

Acetylcholinesterase inhibition: does it explain the toxicity of organophosphorus compounds?

The hypothesis that acetylcholinesterase (AChE) inhibition is the mechanism of toxicity of organophosphorus (OP) compounds was examined by mathematically modeling the in vivo lethal effects of OP compounds and determining the amount of variation in OP toxicity that is explained by AChE inhibition. Mortality dose-response curves for several OP compounds (i.e., VX, soman, cyclosarin, sarin, tabun, diisopropylfluorophosphate and paraoxon) exhibited steep probit slopes (> 9.6) in guinea pigs. Steep probit slopes were also observed when the mortality dose-response curves for soman were examined in mice, rats, rabbits and non-human primates. The consistently steep probit slopes of the dose-response curves for highly toxic OP compounds suggested that these compounds have a single specific mechanism of toxicity regardless of the OP compound or the species in which it was tested. Regression analysis indicated that 93% of the 3,280-fold variation in the median lethal doses (i.e., LD(50)) of OP compounds in rats was explained by the variation in their in vitro rate constants for inhibition of AChE. Conversely, 91% of the 23-fold variation in the ability of the oximes pralidoxime and obidoxime to protect against the toxicity of OP compounds in guinea pigs was explained by the variation in the in vitro ability of oximes to reactivate OP-inhibited AChE. The best explanation for this variety of observations was that the primary mechanism of in vivo toxicity for highly toxic OP compounds is the inhibition of AChE, and the residual unexplained variation in OP toxicity that might be explained by other mechanisms represents < 10% of the total variation in OP toxicity.

Animals↗

Explaining bank vole cycles in southern Norway 1980-2004 from bilberry reports 1932-1977 and climate.

Correlations between mast fruiting of bilberry Vaccinium myrtillus and peak levels of Clethrionomys-voles have been reported from both Norway and Finland, but there has been a discussion whether this is a bottom-up or a top-down relationship. In a multiple regression model, 65% of the variation in a bilberry production index calculated from game reports from southern Norway 1932-1977 could be explained by the berry index of the two preceding years and climate factors acting during key stages of the flowering cycle. High vole populations in previous years did not contribute to explain the fluctuation in berry production. I used the selected model and climate data to predict bilberry production for the period 1978-2004. Predicted berry indices of the current and previous year explained 38% and the total amount of precipitation in May-June explained 16% of the variation in a log-transformed snap-trapping index of bank vole Clethrionomys glareolus 1980-2004. The vole index was not related to any of the climate variables used to predict berry production. This pattern supports the hypothesis that vole cycles are generated by changes in plant chemistry due to climate-synchronized mast fruiting.

Animals↗

An attempt to explain why Tanzanian children drinking water containing 0.2 or 3.6 mg fluoride per liter exhibit a similar level of dental fluorosis.

The aim of this study was to identify factors that might explain the similar level of prevalence and severity of dental fluorosis in two neighboring areas in Tanzania: Kibosho; 0.2 mg fluoride/l, n = 96 and Arusha; 3.6 mg fluoride/l in drinking water, n = 80. Subjects aged 8-16 years were examined for dental fluorosis using the Thylstrup and Fejerskov Index (TFI). Based on the score on the upper left central incisor, the prevalence was not significantly different between the communities (TFI > or = 1). The severity, however, was significantly higher in Arusha. The areas had different food habits, e.g., type of weaning food used, and the use of magadi, a fluoride containing salt. In Arusha, 99% of the children had been given lishe, which is a magadi-free weaning food. Conversely in Kibosho, 61% used lishe while 39% used the magadi-containing weaning food kiborou. Magadi was used as food tenderizer in 'adult food' by 98% in Kibosho and 45% in Arusha. Residential area and use of magadi explained 5% of the variance in TFI scores in inter-area analyses. In intra-area analyses, weaning food in Kibosho and use of magadi in Arusha had a significant effect, but the total explained variance was only 5 and 4%, respectively. Apart from fluoride in the drinking water, other sources of fluoride such as use of magadi in weaning food (kiborou) and in the adult food may partly explain the high prevalence and severity of dental fluorosis in the community with 0.2 mg fluoride per liter in the drinking water.

Adolescent↗

Exercise participation and self-rated health: do common genes explain the association?

The purpose of this study is to investigate whether there is an association between exercise participation and self-rated health and whether this association can be explained by common genes and/or common environmental influences. In a sample of 5,140 Dutch adult twins and their non-twin siblings from 2,831 families, exercise participation (sedentaries, light or moderate, vigorous exercisers) and self-rated health were assessed by survey. To investigate the etiology of the association, bivariate genetic models using structural equation modeling were applied to the data. The correlation between exercise participation and self-rated health is significant but modest (r = 0.20). Exercise participation and self-rated health are both heritable (around 50% of the variance of both phenotypes is explained by genetic factors). The genetic factors influencing exercise participation and self-rated health partially overlap (r = 0.36) and this overlap fully explains their phenotypic correlation. We conclude that the association between exercise and self-rated health can be explained by genes predisposing to both exercise participation and self-rated health. These genes may directly influence both phenotypes (pleiotropy). Alternatively, genes that affect exercise or self-rated health may indirectly influence the other phenotype through a causal relationship. We propose that identification of the genes that cause differences in exercise behavior will help resolve the issue of causality.

Adolescent↗

Factors explaining the referral of the elderly to home nursing or home help.

Factors explaining the referral of the elderly to home nursing or home help or both were studied in a population (n = 1358) aged 60 years or over and living in the commune of Ahtäri, a semi-industrialized community in middle-western Finland, using social and health care registers and questionnaires in collecting data. The clients of home nursing and of combined home nursing and home help were predominantly women, whereas men were in the majority among those referred to home help. A stepwise regression analysis showed old age, living alone, low self-perceived health, low education and few visiting contacts to explain home nursing or home help among men. Among women, the most important variables explaining home nursing or home help in the regression model were old age, low self-perceived health, low standard of housing, high amount of symptoms and lowered functional capacity. The poor availability of social support is more important a factor explaining the referral to home care among elderly men than among women. On the other hand, low health status and poor functional capacity, as well as poor availability of physical support are more important factors among women than men.

Age Factors↗