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Biomedical subjects

C Power

Publications and source records attributed to C Power.

At least 91 records · Page 5Linked to original sources
PubMed1998

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↗
PubMed1998

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↗
PubMed1998

Gender, work roles and psychosocial work characteristics as determinants of health.

This paper aims to identify gender similarities and differences in psychosocial work characteristics for those in and out of paid employment, to inform research on possible health-related effects. Specifically five questions are addressed: do women report poorer work characteristics than men; are gender differences related to specific characteristics; do work characteristics differ between full- and part-time women workers and between those in paid and unpaid work; are socio-economic gradients in work characteristics similar for men and women; and, if there are gradients, do they differ between women in paid and unpaid work? Analyses are based on the 33 year follow-up of the 1958 British birth cohort. Four psychosocial work characteristics were examined: learning opportunities, monotony, pace of work, and flexibility of breaks. Women reported more negative work characteristics than men, primarily because of differences in learning opportunities (26% lacked opportunity compared with 13% of men) and monotonous work (47 and 31% respectively). Women in full-time employment reported fewer negative characteristics (27%) than part-time (39%) or home-workers (36%). Home-workers had fewer opportunities for learning (36%) and greater monotony (49%) than paid workers (21 and 22% respectively), however fewer home-workers reported inability to control the work pace (11% compared to 23%) and inflexibility of breaks (21% compared to 47%). Socio-economic gradients in work characteristics were similar among men and women, except for flexibility of break times. A socio-economic gradient in work characteristics was found for full- and part-time workers, but not among home-workers. Differences in self reported health were also examined: a social gradient was found for all employment status groups, being strongest for home-workers despite the absence of a gradient in negative work characteristics. In conclusion, these marked gender differences in psychosocial work characteristics need to be considered in future research on work and health.

Adult↗
PubMed1998

The relationship between parental separation in childhood and problem drinking in adulthood.

AIMS: To investigate the association between parental separation and alcohol consumption and problem drinking in early adulthood (at ages 23 and 33). DESIGN: The study used longitudinal data from the 1958 British birth cohort study, a large representative national sample followed to age 33. SETTING: Great Britain. PARTICIPANTS: 11,407 subjects were interviewed at age 33 in 1991 (69% of the target population). Analyses are based on 4606 men and 4892 women with data at ages 23 and 33. MEASUREMENTS: Units of alcohol consumed in the previous week at ages 23 and 33. Heavy drinking was defined as more than 20 units/week (women) and more than 35 units/week (men). Problem drinking was indicated by the four-item CAGE measure. Information on parental separation was reported by subjects at age 33; parental deaths were ascertained from data recorded in childhood sweeps of the survey. FINDINGS: At age 23, the relationship between parental separation and alcohol consumption was weak and inconsistent, but by age 33 a stronger and more consistent relationship had emerged. Higher levels of alcohol consumption, heavy drinking and problem drinking (odds ratios 1.29-1.90) were found for those who had experienced parental divorce in childhood, but not later parental divorce or parental death. These results were not substantially attenuated by possible mediating factors, such as marital status or socio-economic circumstances. CONCLUSIONS: The risk associated with early parental divorce appeared to strengthen between ages 23 and 33. Life-course factors influencing the manifestation of alcohol problems in those from divorced families need to be identified.

Adult↗
PubMed1998

Anaesthetic depth at induction. An evaluation using clinical eye signs and EEG polysomnography.

We describe the stages of non-REM sleep induced by anaesthesia with sevoflurane 8% in oxygen and relate these stages to clinical eye positions. We explored John Snow's observation (1847) that 'when voluntary movement ceases, with the eyes fixed in an upward gaze during the gas induction of anaesthesia, the patient is protected against the risk of mental suffering' (awareness). Unpremedicated ASA 1 patients undergoing elective tonsillectomy were studied using EEG polysomnographic principles and clinical eye movement tracking. The results expressed as median and range were: latency to stage 1 sleep 4.5 min [2.5-7.5], stage 2 sleep 5 min [3.5-8.5], stage 3 sleep 5.5 min [4-12] and stage 4 sleep 6 min [4.5-15.5]. Eye position 5, the point of no further eye movement, was reached after 9 min [5.5-18.5]. This was significantly longer than the time taken to reach the stage 4 sleep EEG, p < 0.01, supporting Snow's observation and encouraging investigation into eye movement tracking technology as a potential monitor of anaesthetic depth.

Adolescent↗
PubMed1998

Neuropsychiatric systemic lupus erythematosus and the syndrome of inappropriate secretion of antidiuretic hormone: a case report with very late onset systemic lupus erythematosus.

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with neuropsychiatric lupus (NP-SLE) is rare. We report a case of SIADH associated with the new onset of SLE in an 88-yr-old female. The unique features of this case include the extreme age of onset of SLE presenting with neuropsychiatric manifestations and positive antiribosomal P antibody titres. Both the NP manifestations of SLE and SIADH were highly correlated with the SLE disease activity. This case illustrates a novel presentation of NP-SLE with SIADH which may develop due to antibody-mediated hypothalamic dysfunction.

Aged↗
PubMed1998

Neuronal death induced by brain-derived human immunodeficiency virus type 1 envelope genes differs between demented and nondemented AIDS patients.

Human immunodeficiency virus type 1 (HIV-1) infection of the brain results in viral replication primarily in macrophages and microglia. Despite frequent detection of viral genome and proteins in the brains of AIDS patients with and without HIV dementia, only 20% of AIDS patients become demented. To investigate the role of viral envelope gene variation in the occurrence of dementia, we examined regions of variability in the viral envelope gene isolated from brains of AIDS patients. Brain-derived HIV-1 V1-V2 envelope sequences from seven demented and six nondemented AIDS patients displayed significant sequence differences between clinical groups, and by phylogenetic analysis, sequences from the demented group showed clustering. Infectious recombinant viruses containing brain-derived V3 sequences from both clinical groups were macrophagetropic, and viruses containing brain-derived V1, V2, and V3 sequences from both clinical groups spread efficiently in macrophages. In an indirect in vitro neurotoxicity assay using supernatant fluid from HIV-1-infected macrophages, recombinant viruses from demented patients induced greater neuronal death than viruses from nondemented patients. Thus, the HIV-1 envelope diversity observed in these patient groups appeared to influence the release of neurotoxic molecules from macrophages and might account in part for the variability in occurrence of dementia in AIDS patients.

AIDS Dementia Complex↗
PubMed1998

Neurovirulence in feline immunodeficiency virus-infected neonatal cats is viral strain specific and dependent on systemic immune suppression.

Feline immunodeficiency virus (FIV) is a lentivirus that causes immune suppression and neurological disease in cats. Among animal viruses, individual viral strains have been shown to be neurovirulent, but the role of viral strain specificity among lentiviruses and its relationship to systemic immune suppression in the development of neurological disease remains uncertain. To determine the extent to which different FIV strains caused neurological disease, FIV V1CSF and Petaluma were compared in ex vivo assays and in vivo. Both viruses infected and replicated in macrophage and mixed glial cell cultures at similar levels, but V1CSF induced significantly greater neuronal death than Petaluma in a neurotoxicity assay. V1CSF-infected animals showed significant neurodevelopmental delay compared to the Petaluma-infected and uninfected animals. Magnetic resonance spectroscopy studies of frontal cortex revealed significantly reduced N-acetyl aspartate/creatine ratios in the V1CSF group compared to the other groups. Cyclosporin A treatment of Petaluma-infected animals caused neurodevelopmental delay and reduced N-acetyl aspartate/creatine ratios in the brain. Reduced CD4(+) and CD8(+) cell counts were observed in the V1CSF-infected group compared to the uninfected and Petaluma-infected groups. These findings suggest that neurodevelopmental delay and neuronal injury is FIV strain specific but that systemic immune suppression is also an important determinant of FIV-induced neurovirulence.

Animals↗
PubMed1998

M. tuberculosis molecular variation in CNS infection: evidence for strain-dependent neurovirulence.

OBJECTIVE: To determine the molecular diversity among Mycobacterium tuberculosis isolates associated with central nervous system tuberculosis (CNS TB) in a defined cohort of HIV uninfected patients. DESIGN/METHODS: A retrospective analysis was performed of clinical and laboratory data for all patients with CNS TB diagnosed in Manitoba, Canada, between 1979 and 1996. Restriction fragment-length polymorphisms (RFLP) of archival isolates of M. tuberculosis from CNS TB patients were determined and interpreted against the frequency of different isolates from all TB patients in the years 1992 to 1996. RESULTS: Among 2,334 patients with active TB, CNS TB was diagnosed in 42 (1.8%); meningitis with or without tuberculoma in 76%; and tuberculoma alone in 24%. CNS TB patients were significantly more likely to be young (<40 years old), female, and of Aboriginal origin. Morbidity (fixed/recurrent CNS deficit) rate was 29% and mortality rate was 26%. An adverse outcome, either morbidity or mortality, was significantly more common in those with meningitis. RFLP analysis of isolates (n=19) from CNS TB patients revealed 13 distinct restriction patterns with a predominance of the type 1 pattern (n=6). The frequency of type 1 restriction pattern was significantly greater in patients with CNS TB compared to all TB patients in Manitoba. CONCLUSIONS: CNS TB continues to have a high morbidity and mortality despite modern methods of detection and treatment. Although several strains of M. tuberculosis cause CNS TB, the current study suggests that the occurrence of CNS TB may be strain-dependent.

Adult↗
PubMed1998

Brain-derived HIV-1 tat sequences from AIDS patients with dementia show increased molecular heterogeneity.

HIV-1 infection results in a dementing illness affecting 20% of patients with AIDS. Several HIV-1 genes have been implicated in the pathogenesis of HIV-induced neurological disease. To search for distinct HIV-1 sequences associated with the development of dementia, brain-derived tat, env, and pol sequences were examined from AIDS patients defined pre-mortem as demented (HIV-D)[n=5] or non-demented (HIV-ND)[n=5]. Estimations of evolutionary distances and frequency of non-synonymous mutation rates revealed significant differences between brain-derived tat, env, and pol-encoded reverse transcriptase sequences. However, established zidovudine-associated resistance mutations in reverse transcriptase sequences were identified in only one HIV-D and one HIV-ND patient despite prolonged treatment of some patients. Non-synonymous/synonymous substitution rates among the tat sequences derived from patients with HIV-D were significantly higher compared to the HIV-ND group (P < 0.001). The ratios of transversions to transitions were also significantly higher among the HIV-D tat sequences (P< 0.01). Phylogenetic analyses showed clustering of sequences from each clinical group among the brain-derived tat and env sequences. These studies indicated that differing selective forces act on individual HIV-1 genes in the brain which may influence the development of dementia.

AIDS Dementia Complex↗
PubMed1997

Origins of health inequalities in a national population sample.

BACKGROUND: Explanations for social inequalities in health are often explored but remain largely unresolved. To elucidate the origins of health inequalties, we investigated the extent to which adult-disease risk factors vary systematically according to social position over three decades of early life. METHODS: We used the 1958 birth cohort (all children born in England, Scotland, and Wales on March 3-9, 1958) with data up to age 33 years from parents, teachers, doctors, and cohort members (n = 11,407 for age 33 interview). FINDINGS: Social class of origin was associated with physical risk factors (birthweight, height, and adult body-mass index); economic circumstances, including household overcrowding, basic amenities, and low income; health behaviour of parents (breastfeeding and smoking) and of participants (smoking and diet); social and family functioning and structure, such as divorce or separation of participants or their parents, emotional adjustment in adolescence, social support in early adulthood; and educational achievement and working career, in particular no qualifications, unemployment, job strain, and insecurity. With few exceptions, there were strong significant trends of increasing risk from classes I and II to classes IV and V. Self-perceived health status and symptoms were worse in participants with lower class origins. INTERPRETATION: An individual's chance of encountering multiple adverse health risks throughout life is influenced powerfully by social position. Social trends in adult-disease risk factors do not emerge exclusively in mid-life, but accumulate over decades. Investment in educational and emotional development is needed in all social groups to strengthen prevention strategies relating to health behaviour, work-place environment, and income inequality.

Adult↗
PubMed1997

The Tat protein of HIV-1 induces tumor necrosis factor-alpha production. Implications for HIV-1-associated neurological diseases.

Human immunodeficiency virus (HIV) infection may cause a dementing illness. HIV-mediated dementia is clinically and pathologically correlated with the infiltration of activated macrophages and elevated levels of tumor necrosis factor (TNF)-alpha, both of which occur in an environment of small numbers of infected cells. We examined the possibility that HIV protein Tat, which is released extracellularly from infected cells, may induce the production of TNF-alpha. Tat induced TNF-alpha mRNA and protein production dose-dependently, primarily in macrophages but also in astrocytic cells. The TNF-alpha induction was NF-kappaB-dependent and could be eliminated by inhibiting protein kinase A or protein tyrosine kinase activity. In addition, Tat-induced TNF-alpha release was also linked to phospholipase C activation. However, Tat effects were independent of protein kinase C. These observations suggest that Tat may provide an important link between HIV and macrophage/glial cell activation and suggest new therapeutic approaches for HIV dementia.

Cell Line↗
PubMed1997

AIDS dementia complex with generalized myoclonus.

Focal and segmental, but not generalized, myoclonus have been described with human immunodeficiency virus (HIV) infection. We describe three patients with generalized myoclonus and acquired immunodeficiency syndrome (AIDS) dementia complex. In each, myoclonus persisted until death, invariably after a course of a few months. In two patients, myoclonus was elicited by sudden auditory stimuli and resembled a startle response. This form of myoclonus may be subcortical in origin. We suggest that the AIDS dementia complex be included among the causes of myoclonic dementia.

AIDS Dementia Complex↗
PubMed1997

Rabies viruses infect primary cultures of murine, feline, and human microglia and astrocytes.

Recent studies have reported the detection of rabies viral antigens and virions in astrocytes and microglia of rabies-infected animals. As a first step toward understanding whether these glial cells may be involved in rabies virus replication, persistence, and/or pathogenesis, we explored their potential to be infected in vitro. Primary cultures of murine, feline, and human microglia and astrocytes were infected with several different rabies viruses: two unpassaged street virus isolates, a cell culture-adapted strain, and a mouse brain-passaged strain. Infection, as determined by immunofluorescence, was detected in 15 of the 16 (94%) virus-glial cell combinations. Replication of infectious virus, determined by infectivity assay, was detected in 7 of the 8 (88%) virus-cell combinations. These results show that astrocytes and microglia can be infected by rabies viruses, suggesting that they may have a potential role in disease, perhaps contributing to viral spread, persistence and/or neuronal dysfunction.

Animals↗
PubMed1997

Comparing measures of health inequality.

Several methods are available to measure social inequalities in health. This paper discusses the advantages and disadvantages of different approaches, in particular the odds ratio, the slope and alpha. These methods are illustrated using data from subjects in the 1958 British birth cohort. The inequality measures are compared using health status at ages 23 and 33. Six health indicators are examined, including self-rated health, limiting long-standing illness, psychological health, respiratory symptoms, asthma and obesity. Two social indicators are compared, namely class at birth and educational qualifications. Conclusions do not differ substantially using the three methods for measuring inequality. However, consistent differences were evident between the measures of social position, with greater inequalities apparent for educational qualifications. Choice of social indicator therefore appears to be of primary importance in measuring health inequality.

Adult↗
PubMed1997

Feline immunodeficiency virus causes increased glutamate levels and neuronal loss in brain.

Feline immunodeficiency virus, like human immunodeficiency virus type 1, is a retrolentivirus causing neurological disease and immune suppression. Primary neurological complications, including human immunodeficiency virus encephalopathy and peripheral neuropathy, and neuropathological changes, including gliosis, neuronal injury and multinucleated giant cells, have been described for human immunodeficiency virus type 1 infection. Excitatory amino acids have been implicated as a basis for human immunodeficiency virus encephalopathy and the accompanying neuronal injury. Here, we test our hypothesis that feline immunodeficiency virus infection results in glial activation accompanied by enhanced glutamatergic activity, causing neuronal loss. Neurological signs observed in naturally and experimentally infected animals included ataxia, aggressivity and reduced motor activity. Neuropathological changes included gliosis, perivascular cuffing and neuronal dropout in the brains of both experimentally and naturally infected animals, but not in uninfected animals. Feline immunodeficiency virus antigen and genome were detected in the brains of all experimentally and naturally infected animals. Proton nuclear magnetic resonance spectroscopy revealed significantly increased glutamate levels in the feline immunodeficiency virus-infected animals. In contrast, glutamate decarboxylase levels in GABAergic neurons were reduced in feline immunodeficiency virus-infected animals. These findings provide direct in vivo evidence for enhanced glutamate levels in conjunction with neuronal loss, supporting the hypothesis of glutamate-mediated neurotoxicity as a major mechanism in the neuropathogenesis of retrolentiviral infections.

Animals↗