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PubMedDate not supplied

Using trend theory to explain heroin use trends.

Trend theory is an effort to integrate histories of populations and distribution systems to explain the key epidemiological question: why do these people in this place at this time experience a rapid increase in heroin use? The theory grew out of work on heroin trends in the Baltimore metropolitan area, specifically on epidemics among urban African-Americans in the 1960s and among suburban white youth in the 1990s. This overview represents trend theory as an instance of agent-based adaptive models characteristic of complexity theory.

Heroin Dependence↗

PubMed1999

Tiredness as a ticket of entry. The role of patients' beliefs and psychological symptoms in explaining frequent attendance. General Practice Fatigue Group.

OBJECTIVES: To test when patients presented with fatigue whether their beliefs about its cause was related to their frequency of attending; and to measure the association between their fatigue and psychological symptoms and their frequency of attendance during the study year. DESIGN: A cohort study. SETTING: Primary health care. PATIENTS: Patients presenting with fatigue as their main symptom. MAIN OUTCOME MEASURES: A fatigue questionnaire, the general health questionnaire (GHQ), an attribution scale, and measurement of consulting frequency during the 6 months before and after the patient presented. RESULTS: Patients who believed their fatigue was due to a physical or costly physical cause consult for any reason significantly more frequently than patients who reported that psychological as well as physical problems might have caused their fatigue. Patients' psychological distress measured with the GHQ was more closely associated with frequent attendance than their level of fatigue was. CONCLUSIONS: When patients present with fatigue it is important to inquire about their beliefs and psychological symptoms; these factors may be more important than the fatigue itself in explaining their help-seeking behaviour.

Adolescent↗

PubMed2003

Effects of bosentan on cellular processes involved in pulmonary arterial hypertension: do they explain the long-term benefit?

Pulmonary arterial hypertension is a rapidly progressing disease characterized by an over- expression of endothelin. In addition to its potent pulmonary vasoconstrictor effects, endothelin has been shown to produce many of the aberrant changes, such as hypertrophy, fibrosis, inflammation, and neurohormonal activation that underlie the shortened life span in pulmonary arterial hypertensive patients. The fact that endothelin expression correlates significantly with disease severity and outcome in these patients suggests that endothelin, through binding to both ETA and ETB receptor subtypes, is a key causative agent in the pathophysiology of pulmonary arterial hypertension. The orally active dual endothelin receptor antagonist bosentan competitively antagonizes the binding of endothelin to both endothelin receptor subtypes with high affinity and specificity. In animal models relevant for the pathophysiology of pulmonary hypertension, bosentan not only causes selective pulmonary vasodilation, but also prevents vascular hypertrophy and cardiac remodeling, attenuates pulmonary fibrosis, decreases vascular inflammation, and blunts neurohormonal activation. These experimental data may explain the effects on disease progression and the long-term benefit observed with bosentan in pulmonary arterial hypertension.

Animals↗

PubMed2006

Do reductions in the tar and nicotine yields of cigarettes help to explain recent reductions in lung cancer rates in young men and women in the United States?

Between 1985 and 2000, lung cancer rates in U.S. men and women aged 35-54 yr have declined. To investigate whether these declines can adequately be explained by changes in smoking prevalence, consumption, and duration, or if changes in tar and nicotine yields also contributed, two model-fitting approaches were used. Both approaches used individual person National Health Interview Survey data on smoking prevalence, age of starting and time of quitting, and national estimates of consumption per smoker and yields. Both approaches compared observed rates (by sex and age) relative to 1985, with those predicted after successively including various smoking variables into the model, making varying allowance for compensation for reduced yield. Approach A was simpler, based on mean smoking statistics estimated separately for current and former smokers. Approach B used the multistage model and individual smoking histories to estimate risk. Both approaches showed observed declines in risk were (except for men aged 35-39 yr) clearly greater than predicted based only on prevalence, consumption, and duration. Including yield generally improved the fit. At younger ages, models assuming substantial compensation (consistent with evidence from studies relating nicotine yield and intake) fitted well, but at age 50-54 yr in both sexes and age 45-49 yr in women, the decline was better fitted by models assuming little compensation. The conclusions were not sensitive to the precise parameter values assumed in the modeling. Interpretation is not straightforward, but the findings suggest declines in yields have contributed to the recent declines in rates in young U.S. men and women.

Adult↗

PubMed2001

The additional value of anticipated regret and psychopathology in explaining intended condom use among drug users.

Abstract In this study we examine determinants of intended condom use with casual and steady sex partners among drug users. Our aim was to find out whether anticipated regret and psychopathology represent additional factors in explaining condom use behaviour, on top of the constructs defined in traditional psychosocial models of behaviour. A questionnaire measuring intentions, attitude, beliefs, personal norm, subjective norm, descriptive norm, self-efficacy and anticipated regret toward condom use with steady and casual sex partners, and the Symptom Checklist '90 (to measure dimensions of psychopathology) were handed out to 150 Dutch drug users. The results showed that intended condom use with steady sex partners was mainly predicted by self-efficacy, personal norm and anticipated regret (total R2 = 0.41). Lower feelings of hostility and a more positive personal norm, subjective norm and attitude significantly predicted intended condom use with casual sex partners (total R2 = 0.24). The results also showed that intended condom use with steady sex partners seems to result from anticipating possible barriers, whereas condom use with casual sex partners is largely a matter of having safe sex norms. Practical implications of this study for Aids-preventive campaigns are also discussed.

Condoms↗

PubMed1988

Does incomplete repair explain the apparent failure of the basic LQ model to predict spinal cord and kidney responses to low doses per fraction?

Recent evidence indicates that isoeffect doses for spinal cord and kidney may be overestimated for fraction sizes as small as 1 or 2 Gy when calculated from a linear-quadratic (LQ) model fitted to data obtained for fraction sizes larger than 2 Gy. Reasons for this are unknown, but possible interpretations include exhaustion of repair capacity and incomplete repair in experiments designed to study the response to these small doses. The latter interpretation is motivated by the relatively short intervals between multiple daily doses given to the spinal cord (4 h) and kidney (5 h) when fraction sizes were small. The possibility that overestimation of isoeffect dose could be explained by incomplete repair during short intervals between doses was assessed by fitting experimental data to the incomplete-repair model. For the spinal cord the data could be interpreted by assuming that a repair process with a half-time of 1.7 h was incomplete; this half-time is negligibly different from the estimate obtained from repair-kinetics experiments with larger doses per fraction. The deviation from the (complete-repair) LQ model could be interpreted for the kidney in terms of a half-time of repair of 2.8 h (a negligibly different fit was obtained with the value 1.5 h). The clinical implication could be that multiple-fractions-per-day treatment would benefit from use of the longest feasible interfraction interval when late reactions are dose limiting.

Animals↗

PubMed1990

Does variation in the in vitro cellular radiosensitivity explain the shallow clinical dose-control curve for malignant melanoma?

In radiotherapy, clinical dose-control curves are generally more shallow than what should be expected from in vitro dose-survival curves for human cells of the same histology. One possible explanation is that a considerable inter-tumor heterogeneity in radiosensitivity flattens out the presumably steep individual dose-control curves. This paper compares dose-control curves for malignant melanomas derived from clinical data with curves derived from in vitro cell-survival experiments. Although inter-tumour variability in the in vitro dose and fractionation sensitivity may explain parts of the discrepancy between the steepness of clinical and in vitro dose-control curves, the present calculation indicates that a considerable additional variability, undetected by current in vitro assays, must be assumed to exist in order to resolve the discrepancy.

Cell Survival↗

PubMed1995

Inherent cellular differences may explain the dissimilar survival of RIF-1 and KHT tumour cells under aerobic and hypoxic conditions.

Although previous work has shown striking differences in radiobiological hypoxic fraction between KHT and RIF-1 murine sarcomas, intravascular oxyhaemoglobin (HbO2 saturations have revealed less substantial variations. Using quantitative histological techniques, we have also found minor differences in the distributions of distances between tumour cells and the nearest bloods vessel for KHT versus RIF-1 sarcomas. We report here, the results of an investigation of the inherent ability of these tumour cells to withstand conditions of hypoxia by in vitro culturing under aerobic and anoxic conditions. Tumours were dissociated, seeded into culture dishes, and placed in air-tight aluminium chambers. These chambers were repeatedly evacuated and refilled with a mixture of 95% N2 and 5% CO2 over a 2.5-h period. Following anoxic exposure, cells were removed and replated, and the in vitro plating efficiency (PE) was determined using a colony survival assay. After normalizing to aerobic controls, KHT tumour cells had a significantly lower PE, following a 16-hour exposure to anoxic conditions (0.4), than RIF-1 (0.6). Increasing the hypoxic exposure to 40 h resulted in normalized PEs of 0.07 for KHT versus 0.4 for RIF-1. Although these results support the hypothesis that the two tumour lines have different inherent abilities to withstand hypoxia, they do not explain the failure of direct measures of tumour oxygenation to correlate with the radiobiological hypoxic fraction. Additional factors such as differences in oxygen diffusivity or oxygen consumption rates between tumour lines may also be involved.

Aerobiosis↗

PubMed2002

Can differences in benefit levels explain duration and outcome of sickness absence?

PURPOSE: The aim of this study is to examine the long- and short-term economic incentives inherent in the sickness and unemployment insurances. In particular, how the differences, in, for instance, benefit levels between the two systems, affect the duration and outcome of long-term sickness for the unemployed. METHOD: A sample of 280 sick-registered unemployed in the county of Värmland, Sweden was used in two regression models. Sickness duration was modelled in a linear regression and the outcome (healthy and non-healthy) in a logistic regression. RESULTS AND CONCLUSION: The study shows that economic incentives, i.e. differences in benefit levels, help in explaining sickness duration. The proven fact, that benefits from the sickness insurance are in general higher than from the unemployment insurance, results in the sickness spells being prolonged. Indications are also found of a preference for long-term income security through the sickness and disability insurances, using the length of unemployment before sickness registration, as a determinant of the outcome of the sickness spell.

Absenteeism↗

PubMed2005

Sex differences in plaque morphology may explain the higher male prevalence of myocardial infarction compared to angina pectoris. The Tromsø Study.

OBJECTIVES: To study whether the degree of carotid atherosclerosis and the male predominance of echolucent plaques could explain the sex difference in myocardial infarction (MI) compared to angina pectoris (AP). DESIGN: Ultrasound examination of the carotid artery was performed in 6727 persons. The presence of plaque, plaque thickness and number of segments with plaque were recorded. Plaque morphology in terms of echogenicity was scored as echolucent (soft plaque) or echogenic (hard plaque). A questionnaire was used to obtain information about coronary heart disease. RESULTS: In men with the most advanced atherosclerosis, the risk (OR, 95% CI) of having MI compared to those with no carotid atherosclerosis was less than half as the corresponding risk in women (2.2, 1.4-3.3 vs 5.3, 2.6-10.6). For MI, the male-to-female ratio was highest in the group with no carotid plaque and declined by increasing burden of atherosclerosis. For AP, the sex ratio was independent of the degree of atherosclerosis. CONCLUSIONS: The findings support the hypothesis that the sex difference in MI compared to AP is due to the higher male prevalence of echolucent plaque.

Age Distribution↗

PubMed2002

Self-rated health and mortality among young men: what is the relation and how may it be explained?

AIMS: This study examined the relation between self-rated health (SRH) and mortality among young men, and factors in youth and adolescence that could explain the relation. METHODS: Using logistic regression relative risks of mortality between various levels of self-rated health were compared in a longitudinal study of 49,321 men born in 1949-51, participating in a nationwide military conscription survey in 1969-70. RESULTS: Poor self-rated health at conscription was associated with increased mortality during 27 years of follow up for those stating Rather poor or Very poor compared with those stating Very good SRH. SRH was most strongly related to alcohol- and drug-related mortality. Three psychological factors (low emotional control, psychiatric diagnosis at conscription, and self-reported medication for nervous problems) were found to account for 84% of the increased mortality in the group stating Rather poor or Very poor SRH (remaining RR = 1.1). However, the explanatory power of the psychological factors was widely different for different diagnoses of death. CONCLUSIONS: Poor self-rated health among young men is a predictor of future mortality. Psychological factors seem to be important explanatory variables.

Adolescent↗

PubMed2006

Smoking and education: Do psychosocial variables explain the relationship between education and smoking behavior?

The effect of education, depressive symptoms, trait anxiety, and coping traits (approach-belief, monitoring-creating-executing, and self-regulating) were tested on smoking behavior among 574 young adult males. We hypothesized that depression, anxiety, and coping traits were mediators in the relationship between education and smoking. Univariate analyses showed a significant association between smoking behavior and depressive symptoms, higher trait anxiety score, and lower scores on approach-belief and self-regulating traits. Education was significantly associated with depressive symptoms and coping traits. Although we found significant associations between smoking and education, smoking and depression, and education and depression, the hypothesis was not supported. A similar pattern was found in the case of coping traits. A multivariate logistic regression showed that low education (OR = 4.29), severe depression (OR = 1.84), and low self-regulating coping traits (OR = 2.19) were independent risk factors for smoking. The relationship between education and smoking cannot be explained by these individual variables.

Adaptation, Psychological↗

PubMed2003

Explaining labor force status following spinal cord injury: the contribution of psychological variables.

OBJECTIVE: To investigate the relative influence of demographic, injury and psychological characteristics on the labor force status of people living with spinal cord injury. DESIGN: Cross-sectional survey. SUBJECTS: 459 persons who had experienced a traumatic spinal cord injury. All participants were patients of 1 of 2 specialist spinal cord injury services located in south-eastern Australia. METHODS: A survey, administered on average of 11.2 years after their injury, was used to collect the data. The study's main outcome measure was labor force status at the time of survey. Of those invited to participate in the study, 73% agreed to do so. RESULTS: Demographic, injury and psychological variables were found to explain 30% of the variance in the employment criterion: "in the labor force" vs "not in the labor force". Psychological variables contributed significantly to the separation of the 2 labor force groups. CONCLUSION: The inclusion of the selected psychological variables has advanced the understanding of the factors related to return to work following spinal cord injury, however this understanding is still not complete. Future efforts in this field would likely benefit from the inclusion of additional psychological characteristics, as well as environmental factors.

Adult↗

PubMedDate not supplied

How can be best explain retrograde amnesia in human memory disorder?

I firstly consider general issues relating to our attempts to understand retrograde amnesia. Three main hypotheses are reviewed that have been proposed to account for retrograde amnesia. A theory is outlined to explain the dense autobiographical amnesia that is a focal phenomenon in some cases of severe head injury. This theory postulates that autobiographical retrieval requires the activation of a distributed network of cognitive operations, and that autobiographical amnesia results from the occurrence of multiple areas of pathology, distributed over both space and time.

Age Factors↗

PubMedDate not supplied

Implicit memory: what must theories of amnesia explain?

In their target article on explaining functional deficits in amnesia, Mayes and Downes (this issue) discuss the relevance of implicit memory. Our commentary considers a number of implicit memory phenomena that may be especially pertinent to understanding the functional deficits of amnesia. Recent evidence suggests that amnesic patients do not benefit normally from an exact perceptual match of stimuli between study and text. We propose that this impairment may reflect one manifestation of a more general deficit in associative binding of information across different brain subsystems. This idea helps to clarify the distinction between implicit and explicit memory, and suggests that studies of implicit memory can help to elucidate the functional deficits in amnesia.

Amnesia↗

PubMed2003

Explaining the geographical variation of HIV among injection drug users in the United States.

Distinct physical and chemical types of street heroin exist worldwide, but their impact on behavior and disease acquisition is not well understood or documented. This article presents a hypothesis to explain the unequal diffusion of HIV among injection drug users in the United States by examining the distribution and use of one type of heroin--"Mexican black tar." Drawing on ethnographic, clinical, epidemiological, and laboratory data, we suggest that the chemical properties of black tar heroin promote the following safer injection practices: (1) the rinsing of syringes with water to prevent clogging; (2) the heating of cookers to promote dissolution; and (3) a rapid transition from venous injection to subcutaneous or intramuscular injections.

Blood-Borne Pathogens↗

PubMed1997

Costimulation by B7 modulates specificity of cytotoxic T lymphocytes: a missing link that explains some bystander T cell activation.

It has been proposed that some bystander T cell activation may in fact be due to T cell antigen receptor (TCR) cross-reactivity that is too low to be detected by the effector cytotoxic T lymphocyte (CTL). However, this hypothesis is not supported by direct evidence since no TCR ligand is known to induce T cell proliferation and differentiation without being recognized by the effector CTL. Here we report that transgenic T cells expressing a T cell receptor to influenza virus A/NT/68 nucleoprotein (NP) 366-374:Db complexes clonally expand and become effector CTLs in response to homologous peptides from either A/PR8/34 (H1N1), A/AA/60 (H2N2), or A/NT/68 (H3N2). However, the effector T cells induced by each of the three peptides kill target cells pulsed with NP peptides from the H3N2 and H2N2 viruses, but not from the H1N1 virus. Thus, NP366-374 from influenza virus H1N1 is the first TCR ligand that can induce T cell proliferation and differentiation without being recognized by CTLs. Since induction of T cell proliferation was mediated by antigen-presenting cells that express costimulatory molecules such as B7, we investigated if cytolysis of H1N1 NP peptide-pulsed targets can be restored by expressing B7-1 on the target cells. Our results revealed that this is the case. These data demonstrated that costimulatory molecule B7 modulates antigen specificity of CTLs, and provides a missing link that explains some of the bystander T cell activation.

Animals↗

PubMed2001

Deamidation of asparagine in a major histocompatibility complex-bound peptide affects T cell recognition but does not explain type B reactivity.

We have analyzed a panel of T cell hybridomas specific for the chemically dominant epitope of hen egg-white lysozyme 48-61 which has asparagine 59 as an important T cell receptor contact residue. A number of T cells recognize 48-61 with asparagine at position 59, but not the aspartic acid or isoaspartic acid derivatives. Conversely, we find T cells that specifically recognize 48-61 bearing an isoaspartic acid at residue 59, but not asparagine. For other T cells, asparagine, aspartic acid, or isoaspartic acid at residue 59 is irrelevant. We present evidence that our previous distinction between type A and type B T cells is not explained by asparagine deamidation at residue 59.

Animals↗