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Biomedical subjects

I Baker

Publications and source records attributed to I Baker.

At least 19 recordsLinked to original sources
PubMed2005

Meta-analysis of vitamin D receptor polymorphisms and pulmonary tuberculosis risk.

Several case-control studies performed in populations where the incidence of tuberculosis (TB) is high have examined genetic susceptibility to TB. The Vitamin D receptor (VDR) gene is a good candidate, because it influences immune response, and associations between TaqI and FokI polymorphisms in the VDR gene and pulmonary TB risk have been found. Furthermore, if a relationship between these polymorphisms and TB risk is confirmed this will be important evidence pointing to vitamin D as a potential preventive agent for TB. We carried out a systematic review and meta-analysis, and found that results were inconclusive and studies were underpowered.

Genetic Predisposition to Disease↗
PubMed2004

An EBSP study of isothermally-annealed cold-rolled nickel.

Scanning electron microscopy and electron backscattered patterns, EBSP, have been employed to reveal both the grain structure and texture of 90% cold-rolled polycrystalline nickel after 1-hour anneals at a variety of temperatures. After annealing at either 400 degrees or 500 degrees C, small, cube-oriented, equi-axed grains were produced via primary recrystallization. At 600 degrees C, large [124]<211> oriented grains accounted for an increasing proportion of the microstructure, until at 1000 degrees C only large grains ( approximately 600 microm) and a sharp [124]<211> texture were present. Detailed EBSP analyses of the grain boundaries surrounding the large abnormally grown grains observed at 600 degrees C demonstrated that formation of the secondary recrystallization texture was due to migration of high-mobility, random high-angle boundaries around grains that had a size advantage, consistent with the Abbruzzese-Lücke model.

Crystallization↗
PubMed2003

Imaging dislocations in ice.

Three techniques have been used to study dislocations in ice: etch pitting-replication, transmission electron microscopy, and X-ray topography (XT). It is shown that, because ice is a weak absorber of X-rays and can be produced with a low dislocation density, allowing relatively thick specimens to be studied, the most useful technique is XT. The observations that have been made with conventional XT are briefly outlined. However, the introduction of high-intensity synchrotron radiation, with its concomitant short exposure times, showed that images obtained through conventional XT observations were of dislocations that had undergone recovery. The important dynamic observations and measurements that have been made using synchrotron X-ray topography are presented. Dynamic synchrotron X-ray topography observations of ice single crystals undergoing deformation in situ have shown that slip mainly occurs by the movement of screw and 60 degrees (1/3) [1120] dislocations on the basal plane, although non-basal slip by edge dislocations can also occur. The operation of Frank-Read and other dislocation multiplication sources have been clearly demonstrated and dislocation velocities have been measured. In contrast, in polycrystals, dislocation generation occurred at grain boundaries where there are stress concentrations before lattice dislocation generation mechanisms operate. Faulted dislocation loops have been determined to be mainly interstitial in both polycrystals and single crystals.

Crystallization↗
PubMed2001

Observation of impurities in ice.

This paper presents a new method for determining the microstructural location of impurities in polycrystalline ice, which involves allowing the ice to sublimate under vacuum and then identifying the concentrated impurities using energy dispersive X-ray microanalysis in a low-vacuum scanning electron microscope. The method allows the presence of impurities in both the grain boundaries and the lattice of natural polycrystalline ice to be observed. Using this technique on natural ice, filaments consisting chiefly of NaCl were observed in some grain boundaries, small amounts of sulfur and chlorine were found in the grain interiors of the ice, and large concentrations of sulfur were observed in inclusions.

Electron Probe Microanalysis↗
PubMed2001

Influenza A among patients with human immunodeficiency virus: an outbreak of infection at a residential facility in New York City.

Although annual influenza vaccination is recommended for persons who are infected with human immunodeficiency virus (HIV), data are limited regarding the epidemiology of influenza or the effectiveness of influenza vaccination in this population. We investigated a 1996 outbreak of infection with influenza A at a residential facility for persons with AIDS. We interviewed 118 residents and employees, reviewed 65 resident medical records, and collected serum samples for measurement of influenza antibody titers. After controlling for history of smoking, influenza vaccination, and resident or employee status, in a multivariate model, HIV infection was not statistically associated with influenza-like illness (ILI). Symptoms and duration of ILI were similar for most HIV-infected and HIV-uninfected persons. However, 8 (21.1%) of 38 HIV-infected persons with ILI (vs. none of 15 HIV-uninfected persons) were either hospitalized, evaluated in an emergency room, or had ILI lasting > or = 14 days (P=.06). Vaccination effectiveness (VE) was similar for HIV-infected and HIV-uninfected persons. Vaccination was most effective among HIV-infected persons with CD4 cell counts of >100 cells/microL (VE, 65%; 95% CI, 36%--81%) or HIV type 1 virus load of <30,000 copies/mL (VE, 52%; 95% CI, 11%--75%). Providers should continue to offer influenza vaccination to HIV-infected persons.

AIDS-Related Opportunistic Infections↗
PubMed2001

The incidence and aetiology of stroke in the Caerphilly and Speedwell Collaborative Studies I: methods and incidence of events.

Stroke mortality and morbidity remain high despite downward trends in incidence and case fatality. Population-based longitudinal studies which include collection of risk factor data are required for a better understanding of stroke aetiology. From a representative cohort of men from South Wales and South-west England, followed up for a median of 17 y, details of possible cerebrovascular events were collected from questionnaires, hospital admission data, general practitioner records, death certificates, radiology records and post-mortem reports. Radiology records, and strokes and transient ischaemic attacks were independently validated. There were 433 strokes and 163 transient ischaemic attacks identified during follow-up. Of these, 333 were the first ever in a lifetime strokes of which 139 were definite ischaemic, 20 were haemorrhagic and 168 were probable ischaemic strokes. The crude incidence rate for stroke was 445 (95% confidence interval 398-493) per 100 000 person years. The age-standardised rates for 10 y age-bands were: 45-54 y 91 (10-172); 55-64 y 351 (269-432) and 65-74 y 855 (669-1040). The 30 d case-fatality rate was 21.0% (70/333) for all strokes and 19.2% (60/312) for ischaemic strokes. For transient ischaemic attacks the age-standardised incidence rates for the same 10 y age bands were 92 (4-179), 111 (64-157), and 273 (167-80), respectively. These rates for stroke transient ischaemic attack are likely to be accurate given the high ascertainment of events in this representative population of middle-aged men. Such studies, reporting reliable measures of cerebrovascular events, are important for measuring burden of disease, and for analysis of risk factor associations to help improve understanding of stroke aetiology and inform preventive efforts.

Cohort Studies↗
PubMed2001

The incidence and aetiology of stroke in the Caerphilly and Speedwell Collaborative Studies II: risk factors for ischaemic stroke.

Reduction of stroke burden requires preventive interventions targeted at important risk factors. This report presents the analysis of risk factors for ischaemic stroke from a representative cohort of middle aged men from South Wales and south-west England. Data on risk factors were collected through validated questionnaires and physical and clinical measurements. Details of possible cerebrovascular events were retrieved, classified into ischaemic, haemorrhagic and uncertain subtypes, and validated. The ratio of definite ischaemic to definite haemorrhagic strokes was calculated. This showed that the vast majority of strokes of unknown subtype were likely to ischaemic. After exclusion of known haemorrhagic strokes and subarrachnoid haemorrhages the remaining strokes were labelled ischaemic. Hazard ratios for possible risk factors were calculated for all ischaemic, and for fatal and non-fatal strokes. There were 293 ischaemic strokes. Statistically significant age-adjusted hazard ratios were: 1.50 (95% confidence interval 1.16-1.95) for being in a manual social class, 1.82 (1.24-2.67) if smoking >15 cigarettes/d at enrollment, 1.19 (1.13-1.24) and 1.23 (1.14-1.34) per 10 mmHg increase in systolic and diastolic blood pressure, respectively, 0.67 (0.46-0.96) for the top quintile high density lipoprotein-cholesterol:cholesterol ratio compared to the bottom quintile, 2.04 (1.40-2.99) for presence of angina, 3.90 (2.01-7.58) for presence of atrial fibrillation, and 3.35 (1.90-5.80) for presence of diabetes. Risk factors were more strongly associated with fatal than non-fatal strokes. Multivariate analyses revealed that, while there was some attenuation of the effect of social class, angina and elevated BP, the risks from atrial fibrillation and diabetes were increased.

Brain Ischemia↗
PubMed2000

Dopamine induces cell death, lipid peroxidation and DNA base damage in a catecholaminergic cell line derived from the central nervous system.

Dopamine can be autoxidized to superoxides and quinones. Superoxides can form hydroxyl radicals that are highly reactive with lipids, proteins and DNA leading to neuronal damage and cell death. We used a clonal catecholaminergic cell line (CATH.a) derived from the central nervous system to evaluate the effects of dopamine on cell death, lipid peroxidation and DNA base damage. Dopamine produces cell death in CATH.a cells and this is associated with an increase in annexin binding, which is an early indicator of apoptosis. Incubation of CATH.a cells with deferoximine, an iron chealator, partially antagonizes dopamine-induced cell death. In CATH.a cells, dopamine produces an increase in both lipid peroxidation, as measured by cis-parinaric acid fluorescence, and DNA oxidative base damage, as measured by 8-hydroxy-2'-deoxyguanosine formation. Cell death was inhibited 84-92% by the hydrophilic antioxidants, dithiothreitol, L-cysteine, and N-acetylcysteine. The lipophilic vitamins, retinol and vitamin E and the vitamin E analog, Trolox, inhibited dopamine-induced cell death by 18-33%. The lipophilic antioxidants probucol, propyl glycol and butylated hydroxyanisone had no inhibitory effect on dopamine-induced cell death. These data suggest that damage to DNA and lipids may be partially responsible for dopamine-induced cell death in CATH.a cells.

Journal Article↗
PubMed1999

Brain-derived and glial cell line-derived neurotrophic factors protect a catecholaminergic cell line from dopamine-induced cell death.

Brain-derived neurotrophic factor (BDNF) promotes the survival of dopaminergic neurons in primary cultures and protects these neurons from the neurotoxic effects of 6-hydroxydopamine. The protective mechanism of BDNF on neurotoxicity was evaluated using CATH.a cells, a clonal catecholaminergic cell line derived from the central nervous system. Dopamine produced a dose-dependent cell death in CATH.a cells. Treatment of CATH.a cells with BDNF or glia cell line-derived neurotrophic factor (GDNF) reduced dopamine-induced cell death by approximately 60-70%. Nerve growth factor, basic fibroblast growth factor, neurotrophin-4/5 and insulin had no protective effect on dopamine-induced cell death. Dopamine decreased the activity of superoxide dismutase and the levels of glutathione in the CATH.a cells and these decreases were reversed by BDNF. In addition, BDNF treatment alone increased superoxide dismutase activity by 108%. These results suggest that BDNF may safeguard CATH.a cells from dopamine-induced cell death by maintaining or enhancing components of the cell, which protect from oxidative stress.

Animals↗
PubMed1999

The Bristol Shared Care Glaucoma Study: reliability of community optometric and hospital eye service test measures.

BACKGROUND/AIMS: Primary open angle glaucoma patients and glaucoma suspects make up a considerable proportion of outpatient ophthalmological attendances and require lifelong review. Community optometrists can be suitably trained for assessment of glaucoma. This randomised controlled trial aims to assess the ability of community optometrists in the monitoring of this group of patients. METHODS: Measures of cup to disc ratio, visual field score, and intraocular pressure were taken by community optometrists, the hospital eye service and a research clinic reference "gold" standard in 405 stable glaucoma patients and ocular hypertensives. Agreement between and within the three centres was assessed using mean differences and intraclass correlation coefficients. Tolerance limits for a change in status at the level of individual pairs of measurements were also calculated. RESULTS: Compared with a research clinic reference standard, measurements made by community optometrists and those made in the routine hospital eye service were similar. Mean measurement differences and variability were similar across all three groups compared for each of the test variables (IOP, cup to disc ratio, and visual field). Overall, the visual field was found to be the most reliable measurement and the cup to disc ratio the least. CONCLUSIONS: Trained community optometrists are able to make reliable measurements of the factors important in the assessment of glaucoma patients and glaucoma suspects. This clinical ability should allow those optometrists with appropriate training to play a role in the monitoring of suitable patients.

Community Health Services↗
PubMed1997

Increased cyclic AMP response to forskolin in Epstein-Barr virus-transformed human B-lymphocytes derived from schizophrenics.

Phorbol 12-myristate-13-acetate (PMA), a protein kinase C (PKC) activator, elevated basal cyclic AMP levels and enhanced isoproterenol-, prostaglandin E1- (PGE1), forskolin- and cholera toxin-stimulated cyclic AMP accumulation in Epstein-Barr virus (EBV)-transformed human B-lymphocytes. Staurosporine, a PKC inhibitor, significantly antagonized the increase in cyclic AMP accumulation produced by PMA, whereas the inactive phorbol ester, 4 alpha-phorbol 12,13-didecanoate (4 alpha PDD), had no effect. Basal levels of cyclic AMP and the accumulation of cyclic AMP produced by PMA, isoproterenol, PGE1, cholera toxin and the combination of these compounds with PMA were not significantly different between schizophrenics and controls. The cyclic AMP response to forskolin in the presence and absence of PMA was significantly greater in EBV-transformed human B-lymphocytes from schizophrenics. These results suggest that activation of adenylyl cyclase by forskolin is elevated in EBV-transformed B-lymphocytes derived from schizophrenics and that this elevation is further enhanced through a PKC-dependent phosphorylation mechanism.

Adult↗
PubMed1996

Chronic cocaine administration increases tyrosine hydroxylase activity in the ventral tegmental area through glutaminergic- and dopaminergic D2-receptor mechanisms.

Tyrosine hydroxylase activity was measured in the brain of rats treated chronically with saline or cocaine (10 mg/kg, 2 x day, for 7 days). Tyrosine hydroxylase activity was significantly increased in the ventral tegmental area 1, 6 and 12 weeks after the last treatment with cocaine. The increase in tyrosine hydroxylase activity at 6 weeks after the last cocaine injection was prevented by the prior administration of MK-801, haloperidol or clozapine but not by the D1 receptor antagonist, SCH-23390. SCH-23390 produced a significant increase in tyrosine hydroxylase activity when administered with saline. These data indicate that glutaminergic and dopaminergic D2-receptor mediated mechanisms are important in regulating the effect of cocaine on the ventral tegmental area.

Animals↗
PubMed1996

Evaluation of cyclic AMP accumulation in EBV-transformed human B-lymphocytes: effects of dopamine agonists, isoproterenol, prostaglandin E1, cholera toxin, forskolin, and phorbol 12-myristate-13 acetate.

1. Phorbol 12-myristate-13-acetate (PMA), a protein kinase C activator, elevated cyclic AMP accumulation in EBV-transformed human B-lymphocytes, and potentiated isoproterenol-, prostaglandin- (PGE1), cholera toxin-, and forskolin-stimulated cyclic AMP accumulation. 2. The dopamine D1 receptor agonist, SKF38393 (10(-7) to 10(-5) MH, had no effect on cyclic AMP accumulation in transformed human B-lymphocytes. 3. The dopamine D2 receptor agonist, quinpirole (10(-7) to 10(-5) MH did not inhibit cyclic AMP accumulation even when cyclic AMP accumulation was maximized by the addition of PMA and forskolin. 4. These data suggest that dopamine D1- and D2-receptor coupling to a cyclic AMP generating system is not present at detectable levels in transformed human B-lymphocytes.

Alprostadil↗
PubMed1996

Serum cytokine concentrations in patients with schizophrenia.

Interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha and the soluble interleukin-2 receptor were measured in the serum of 34 healthy controls and 48 patients with chronic schizophrenia using ELISA sandwich assays. No differences were found between the controls and patients.

Adolescent↗
PubMed1996

Dopamine induces apoptotic cell death of a catecholaminergic cell line derived from the central nervous system.

Dopamine produces a time- and dose-dependent increase in cell death in a clonal catecholaminergic cell line (CATH.a) derived from the central nervous system. Cell death also occurred after treatment with the catecholamines L-dihydroxyphenylalanine, norepinephrine, epinephrine, and isoproterenol, as well as the neurotoxic compound 6-hydroxydopamine. Cell death is not receptor mediated because selective noradrenergic and dopaminergic receptor agonists had no effect on CATH.a cell viability. Dopamine induces apoptotic cell death as indicated by DNA fragmentation measured by gel electrophoresis and by flow cytometric analysis. Apoptosis seems to be produced by dopamine autoxidation, because intracellular peroxides increase after dopamine treatment and cell death can be inhibited by catalase and N-acetylcysteine. N-acetylcysteine produced a dose-dependent decrease in dopamine-induced cell death; this correlated with a decrease in peroxide formation. In addition, antisense to the antioxidant protein bcl-2 increases the sensitivity of CATH.a cells to dopamine-induced cell death. These findings indicate that the oxidative products of dopamine cause neurotoxicity through apoptosis.

Animals↗
PubMed1994

Peripheral vascular disease: consequence for survival and association with risk factors in the Speedwell prospective heart disease study.

OBJECTIVE: To measure the prevalence and incidence of intermittent claudication, to describe the mortality associated wtih the condition, and to assess the relevance of risk factors for vascular disease. DESIGN: A standard questionnaire on calf pain when walking was given in the prospective Speedwell study, and a range of risk factors were measured. The men were re-examined at intervals of three years, and deaths over 11 years were identified. SETTING: The general population. PARTICIPANTS: All men aged 45 to 59 registered with 16 general practitioners. RESULTS: The prevalence of intermittent claudication increased from almost nil at ages 45-49 to 2.9% at ages 60-64. The annual incidence increased from 0.3% in the youngest men to 0.5% in those in their early 60s. Intermittent claudication was related to the existence of ischaemic heart disease, particularly angina, at the first examination. The relative odds of men with angina developing intermittent claudication was 6.7 (95% confidence interval (95% CI) 3.6 to 12.4). The risk of death in men with intermittent claudication was substantially raised. After standardisation for age and smoking the relative odds of death was 3.8 (95% CI 2.2 to 6.5). The excess was entirely from circulatory causes. Systolic blood pressure, fasting plasma glucose, triglycerides, and white cell count were all independently associated with the development of intermittent claudication, but the most striking association was with smoking. CONCLUSIONS: Intermittent claudication is an indicator for a very high risk of death. This is only partly explained by its strong association with ischaemic heart disease.

Age Factors↗
PubMed1992

Bones of contention.

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Attitude of Health Personnel↗