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Biomedical subjects

C Power

Publications and source records attributed to C Power.

At least 73 records · Page 4Linked to original sources

Social support at age 33: the influence of gender, employment status and social class.

This paper investigates the conceptualisation and operationalisation of social support and it's relationship to gender, employment status and social class. Clarification of these relationships is sought in order to better understand associations between social support and health. We used data from the 33-year survey of the 1958 British birth cohort study. Individual items and subscales of practical and emotional support were examined. In general, men had lower support than women and social classes IV and V had lower support than classes I and II. Emotional support, either from personal (for example, from friends or family), or combined with organisational sources of support (such as from a church or a financial institution), showed consistent gender and social class patterns. This suggests that emotional support is a robust concept across socio-demographic groups. Less consistent trends were found for practical support, in that socio-demographic trends depended on how practical support was measured. In particular, it depended on whether both personal and organisational sources of support were examined. Gender differences in social support were large and might therefore be expected to contribute to gender differences in health, whereas social class differences in social support were modest, suggesting a minor explanatory role for this factor in accounting for inequalities in health.

Adult↗

Does financial hardship account for elevated psychological distress in lone mothers?

Lone mothers have been shown to have higher levels of psychological distress than married mothers, but it is not clear how this difference arises. Using data from the 1958 British birth cohort followed to age 33, we investigated alternative explanations for the excess distress of lone mothers. Logistic regression models were used to estimate odds ratios for distress (measured using the Malaise Inventory) in lone vs married mothers. Odds ratios were adjusted to assess the contribution of explanatory factors. At age 33, psychological distress was greater among lone than married mothers (OR 2.59, 95% CI 1.97, 3.41). The odds ratio decreased to 1.43 (95% CI 1.02, 2.01) after adjustment for all explanatory factors (prior psychological distress, age of youngest child and number of children in the household, and contemporary measures of financial hardship, employment, and social support). Attenuation of the odds ratio was most marked after taking account of financial hardship. Psychological distress was greater among divorced mothers than never married mothers, though not significantly (OR = 1.70, 95% CI 0.88, 3.28). This difference was not explained by the factors examined, and was not due to the immediate distress associated with a recent divorce. Elevated psychological distress of lone mothers appears to be related to financial hardship, while other explanations, including social support and selection, have a more modest impact. Not all of the elevated psychological distress among lone mothers was accounted for, particularly among divorced lone mothers.

Adolescent↗

Marital status transitions and psychological distress: longitudinal evidence from a national population sample.

BACKGROUND: Evidence is conflicting as to whether the association between marital status and psychological distress is due to selection (i.e. distress influences marital status) or causation (marital status influences distress). We investigate: (i) whether differences in psychological distress pre-date marital transitions; (ii) whether levels of distress change following transitions; and (iii) potential mediating and moderating factors. METHODS: Data on psychological distress (indicated by the Malaise Inventory) and marital status at ages 23 and 33 were analysed for 4514 men and 4842 women from the 1958 birth cohort. RESULTS: Higher levels of distress were found among the divorced and lower levels among the single and the married. Selection was seen in the lower initial mean symptoms of those who married (1.69 for men; 2.84 for women) compared to those remaining single (2.41 for men; 3.26 for women). Causation was indicated by the relative deterioration in distress of those who divorced compared to the continuously married (an increase of 0.31 and 0.03 respectively for men), especially in women (a decrease of 0.18 versus 0.71). This was most evident in women who were downwardly mobile and those with children. Recently separated men and women showed especially large increases in distress. CONCLUSIONS: The relationship between marital status and psychological distress involves selection and causation. Findings failed to support ideas of marriage being protective (through social support), or detrimental (through family roles). Divorce increased distress, with both acute and longer-term components moderated by secondary factors such as childcare and declining socioeconomic status.

Adult↗

Heavy alcohol consumption and marital status: disentangling the relationship in a national study of young adults.

AIMS: To investigate why alcohol consumption varies by marital status, assessing (i) differences in heavy consumption prior to changes in marital status (indicating selection) and increases or decreases in heavy consumption associated with changes in marital status (indicating causation), (ii) whether such increases or decreases are transient, and (iii) the possible mediating effect of parental status. DESIGN: Longitudinal cohort. SETTING: Great Britain. PARTICIPANTS: Data from the 23- and 33-year surveys of the 1958 British birth cohort (all born in England, Wales and Scotland, 3-9 March 1958). MEASUREMENTS: Heavy drinking, defined as more than 35 (men) and 20 (women) units/week; changes between ages 23 and 33 in consumption and marital status. FINDINGS: The divorced had the highest consumption levels at both ages, the married had the lowest. Selection effects were minimal in both sexes. Overall, heavy drinking declined between ages 23 and 33 (21.4-13.0% in men, 6.4-3.4% in women), but increased among individuals who divorced, compared to the continuously married (adjusted OR = 2.05, 95% CI = 1.49, 2.83 for men; OR = 2.61, 95% CI = 1.67, 4.09 for women), most strikingly for recent divorces (adjusted OR = 4.97, 95% CI = 2.86, 8.57 and OR = 5.25, 95% CI = 2.60, 10.65). High rates of heavy drinking persisted for never married men (19.1%) and women (5.2%). CONCLUSIONS: The heavy drinking level of divorced young adults was not due to selection. Marital separation was accompanied by increases in heavy drinking, with pronounced short-term effects. Adverse alcohol-related health consequences may occur in the immediate period around divorce. Individuals who never marry appear to have a chronic heavy consumption pattern that may contribute to their increased mortality.

Adult↗

Antisense oligodeoxynucleotides targeting internal exon sequences efficiently regulate TNF-alpha expression.

ABSTRACT Exon sequences upstream of splice sites play a critical role in mRNA processing, which is dependent on spliceosome interactions with these sites. Using antisense oligodeoxynucleotides (ODN), we targeted these and other sequences of the proinflammatory tumor necrosis factor-alpha (TNF-alpha) gene because it is multiply spliced and has been difficult to regulate with ODN in the past. ODN targeting exon sequences upstream of the donor splice sites of internal exons 2 (ORF4) and 3 (ORF6) significantly reduced TNF-alpha levels in stimulated U937 cells by 62%+/-7% and 51%+/-9%, respectively, in a dose-dependent manner but did not affect interleukin-6 (IL-6) levels. In contrast, ODN targeting the exon sequences downstream of the acceptor splice sites of exons 1, 2, and 3 failed to reduce TNF-alpha levels significantly under the same conditions. End-phosphorothioated ORF4 (ORF4-PE) significantly reduced TNF-alpha mRNA levels by greater than 80% (p < 0.001) and protein levels by 60% (p < 0.001) in U937 cells. ORF4-PE reduced newly synthesized TNF-alpha protein levels by >80% in lipopolysaccharide (LPS)-stimulated human macrophages, by greater than 60% in phorbol myristate acetate/phyto-hemagglutinin (PMA/PHA)-stimulated human peripheral blood mononuclear cells (PBMC), and by approximately 50% in LPS-stimulated murine monocytes. These results suggest that exon sequences flanking donor splice sites are highly susceptible target domains for antisense inhibition of TNF-alpha gene expression.

Animals↗

V3 recombinants indicate a central role for CCR5 as a coreceptor in tissue infection by human immunodeficiency virus type 1.

Binding of the human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein gp120 to both CD4 and one of several chemokine receptors (coreceptors) permits entry of virus into target cells. Infection of tissues may establish latent viral reservoirs as well as cause direct pathologic effects that manifest as clinical disease such as HIV-associated dementia. We sought to identify the critical coreceptors recognized by HIV-1 tissue-derived strains as well as to correlate these coreceptor preferences with site of infection and dementia diagnosis. To reconstitute coreceptor use, we cloned HIV-1 envelope V3 sequences encoding the primary determinants of coreceptor specificity from 13 brain-derived and 6 colon-derived viruses into an isogenic (NL4-3) viral background. All V3 recombinants utilized the chemokine receptor CCR5 uniformly and efficiently as a coreceptor but not CXCR4, BOB/GPR15, or Bonzo/STRL33. Other receptors such as CCR3, CCR8, and US28 were inefficiently and variably used as coreceptors by various envelopes. CCR5 without CD4 present did not allow for detectable infection by any of the tested recombinants. In contrast to the pathogenic switch in coreceptor specificity frequently observed in comparisons of blood-derived viruses early after HIV-1 seroconversion and after onset of AIDS, the characteristics of these V3 recombinants suggest that CCR5 is a primary coreceptor for brain- and colon-derived viruses regardless of tissue source or diagnosis of dementia. Therefore, tissue infection may not depend significantly on viral envelope quasispeciation to broaden coreceptor range but rather selects for CCR5 use throughout disease progression.

AIDS Dementia Complex↗

Productive infection of human peripheral blood mononuclear cells by feline immunodeficiency virus: implications for vector development.

Feline immunodeficiency virus (FIV) is a lentivirus causing immune suppression and neurological disease in cats. Like primate lentiviruses, FIV utilizes the chemokine receptor CXCR4 for infection. In addition, FIV gene expression has been demonstrated in immortalized human cell lines. To investigate the extent and mechanism by which FIV infected primary and immortalized human cell lines, we compared the infectivity of two FIV strains, V1CSF and Petaluma, after cell-free infection. FIV genome was detected in infected human peripheral blood mononuclear cells (PBMC) and macrophages at 21 and 14 days postinfection, respectively. Flow cytometry analysis of FIV-infected human PBMC indicated that antibodies to FIV p24 recognized 12% of the cells. Antibodies binding the CCR3 chemokine receptor maximally inhibited infection of human PBMC by both FIV strains compared to antibodies to CXCR4 or CCR5. Reverse transcriptase levels increased in FIV-infected human PBMC, with detection of viral titers of 10(1.3) to 10(2.1) 50% tissue culture infective doses/10(6) cells depending on the FIV strain examined. Cell death in human PBMC infected with either FIV strain was significantly elevated relative to uninfected control cultures. These findings indicate that FIV can productively infect primary human cell lines and that viral strain specificity should be considered in the development of an FIV vector for gene therapy.

Animals↗

The duration and timing of exposure: effects of socioeconomic environment on adult health.

OBJECTIVES: This study investigated timing and duration effects of socioeconomic status (SES) on self-rated health at 33 years of age and established whether health risks are modified by changing SES and whether cumulative SES operates through education. METHODS: Data were from the 1958 British birth cohort. Occupational class at birth and at 16, 23, and 33 years of age was used to generate a lifetime SES score. RESULTS: At 33 years of age, 12% of men and women reported poor health. SES at birth and at 16, 23, and 33 years of age was significantly associated with poor health: all ages except 16 years in men made an additional contribution to the prediction of poor health. No large differences in effect sizes emerged, suggesting that timing was not a major factor. Odds of poor health increased by 15% (men) and 18% (women) with a 1-unit increase in the lifetime SES score. Strong effects of lifetime SES persisted after adjustment for education level. CONCLUSIONS: SES from birth to 33 years of age had a cumulative effect on poor health in early adulthood. This highlights the importance of duration of exposure to socioeconomic conditions for adult health.

Adult↗

Rhetoric to practice: the challenge of collaboration of academe and industry.

Community health nursing is a complex practice that encompasses nurses working in many diverse settings. This article discusses the development of a project which focused on better preparation of students for potential employment in community settings. The formation of the working team and the development of the curriculum is outlined. A focus is given to the linking of primary health care principles in the teaching and facilitation of students within hospital and community settings. Comprehensive conclusions cannot be made yet from the project's preliminary findings. However, the process of collaboration has demonstrated several issues. These will have an impact on everyone who has been part of this project, and the issues are discussed in this article. The article provides an overview of the first year of collaboration of a 4-year project.

Community Health Nursing↗

Childhood predictors of adult obesity: a systematic review.

OBJECTIVE: To identify factors in childhood which might influence the development of obesity in adulthood. BACKGROUND: The prevalence of obesity is increasing in the UK and other developed countries, in adults and children. The adverse health consequences of adult obesity are well documented, but are less certain for childhood obesity. An association between fatness in adolescence and undesirable socio-economic consequences, such as lower educational attainment and income, has been observed, particularly for women. Childhood factors implicated in the development of adult obesity therefore have far-reaching implications for costs to the health-services and economy. SEARCH STRATEGY: In order to identify relevant studies, electronic databases--Medline, Embase, CAB abstracts, Psyclit and Sport Discus-were searched from the start date of the database to Spring 1998. The general search structure for electronic databases was (childhood or synonyms) AND (fatness or synonyms) AND (longitudinal or synonyms). Further studies were identified by citations in retrieved papers and by consultation with experts. INCLUSION CRITERIA: Longitudinal observational studies of healthy children which included measurement of a risk factor in childhood (<18 y), and outcome measure at least 1 y later. Any measure of fatness, leanness or change in fatness or leanness was accepted. Measures of fat distribution were not included. Only studies with participants from an industrialized country were considered, and those concerning minority or special groups, e.g. Pima Indians or children born preterm, were excluded. FINDINGS: Risk factors for obesity included parental fatness, social factors, birth weight, timing or rate of maturation, physical activity, dietary factors and other behavioural or psychological factors. Offspring of obese parent(s) were consistently seen to be at increased risk of fatness, although few studies have looked at this relationship over longer periods of childhood and into adulthood. The relative contributions of genes and inherited lifestyle factors to the parent-child fatness association remain largely unknown. No clear relationship is reported between socio-economic status (SES) in early life and childhood fatness. However, a strong consistent relationship is observed between low SES in early life and increased fatness in adulthood. Studies investigating SES were generally large but very few considered confounding by parental fatness. Women who change social class (social mobility) show the prevalence of obesity of the class they join, an association which is not present in men. The influence of other social factors such as family size, number of parents at home and childcare have been little researched. There is good evidence from large and reasonably long-term studies for an apparently clear relationship for increased fatness with higher birth weight, but in studies which attempted to address potential confounding by gestational age, parental fatness, or social group, the relationship was less consistent. The relationship between earlier maturation and greater subsequent fatness was investigated in predominantly smaller, but also a few large studies. Again, this relationship appeared to be consistent, but in general, the studies had not investigated whether there was confounding by other factors, including parental fatness, SES, earlier fatness in childhood, or dietary or activity behaviours. Studies investigating the role of diet or activity were generally small, and included diverse methods of risk factor measurement. There was almost no evidence for an influence of activity in infancy on later fatness, and inconsistent but suggestive evidence for a protective effect of activity in childhood on later fatness. No clear evidence for an effect of infant feeding on later fatness emerged, but follow-up to adulthood was rare, with only one study measuring fatness after 7y. Studies investigating diet in childhood were limited and inconc

Adult↗

Inequalities in self-rated health: explanations from different stages of life.

BACKGROUND: Inequalities in health are a major public-health concern. A greater understanding is needed on the relative importance of different causes. We investigated the contribution of risk factors identified at different life stages to inequalities in self-rated health. METHODS: We used data from 5606 men and 5799 women in the 1958 British birth cohort followed-up to age 33 years, on health behaviour, education, adolescent health, family structure and social support, work characteristics, and material circumstances. We assessed the contribution of different factors to social-class differences in self-rated health by adjustment of odds ratios (classes IV and V vs I and II). FINDINGS: Odds ratios of poor-rated health at age 33 were 3.15 for men and 2.30 for women, which decreased to 2.06 and 1.34, respectively, after adjustment for previously identified factors from birth to early adulthood. Adjustment for adult work characteristics, material circumstances, and health behaviour between ages 23 years and 33 years further decreased the odds ratios to 1.64 (men) and 1.11 (women). Most factors contributed to the reduction in odds ratios, although adolescent socioemotional adjustment, class at birth, educational qualifications, and psychosocial job strain were especially important. Additional key factors for men were adult smoking and job insecurity, and for women, housing during childhood, adult income, and age at first child. INTERPRETATION: There was no single cause of health inequality at age 33 years. Explanations spanned from early life to young adulthood. Policy implications include reduction of social differences in material circumstances and of differences in individual skills and resources acquired in early life.

Adult↗

Induction of monocyte chemoattractant protein-1 in HIV-1 Tat-stimulated astrocytes and elevation in AIDS dementia.

Activated monocytes release a number of substances, including inflammatory cytokines and eicosanoids, that are highly toxic to cells of the central nervous system. Because monocytic infiltration of the central nervous system closely correlates with HIV-1-associated dementia, it has been suggested that monocyte-derived toxins mediate nervous system damage. In the present study, we show that the HIV-1 transactivator protein Tat significantly increases astrocytic expression and release of monocyte chemoattractant protein-1 (MCP-1). Astrocytic release of beta-chemokines, which are relatively less selective for monocytes, including RANTES, macrophage inflammatory protein-1alpha, and macrophage inflammatory protein-1beta, was not observed. We also show that MCP-1 is expressed in the brains of patients with HIV-1-associated dementia and that, of the beta-chemokines tested, only MCP-1 could be detected in the cerebrospinal fluid of patients with this condition. Together, these data provide a potential link between the presence of HIV-1 in the brain and the monocytic infiltration that may substantially contribute to dementia.

AIDS Dementia Complex↗

Infrequent detection of human herpesvirus 6 DNA in peripheral blood mononuclear cells from multiple sclerosis patients.

Several studies have suggested an association between human herpesvirus 6 (HHV-6) infection and multiple sclerosis. As HHV-6 is predominantly a T-cell tropic virus, we examined the frequency of detection of HHV-6 genome in peripheral blood mononuclear cells from relapsing-remitting (n = 32) and chronic progressive (n = 14) patients and from healthy (n = 17) and neurological (n = 7) controls. Two sensitive polymerase chain reaction assays were used to target different regions within the HHV-6 genome. Depending on the polymerase chain reaction assay used, the detection of HHV-6 genome ranged from 11.7 to 23.5% (controls), 3.1 to 23.0% (relapsing-remitting), and 14.2 to 28.5% (chronic progressive). Although these observations do not exclude a pathogenic role for HHV-6 in multiple sclerosis, they indicate a lack of correlation between HHV-6 infection of peripheral blood mononuclear cells and the development of multiple sclerosis.

Adult↗

Parkinsonism with HIV infection.

We describe six patients with parkinsonism and another 10 patients with parkinsonian features with human immunodeficiency virus (HIV) infection. In 50% of these patients, the symptoms were precipitated by neuroleptics. In the remaining patients, no obvious cause other than HIV infection was identified. Discontinuation of the neuroleptics produced complete recovery in one patient and partial or no response in others. Rapid progression of parkinsonism was noted in two patients, one of whom was treated with high-dose zidovudine (AZT) and benztropine. We conclude that patients with AIDS are at risk of developing an akinetic parkinsonism which may be precipitated by the use of neuroleptics, response to treatment is variable, and parkinsonism may be another primary HIV-induced syndrome.

AIDS Dementia Complex↗