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Biomedical subjects

T Duong

Publications and source records attributed to T Duong.

At least 37 records · Page 2Linked to original sources
PubMed1999

The duration of human ocular Chlamydia trachomatis infection is age dependent.

We studied the relationship between age and prevalence, duration and incidence of clinical and laboratory evidence of ocular Chlamydia trachomatis infection in a cohort of Gambian subjects examined bi-weekly for 6 months. The duration of disease and infection, estimated by stratified survival analysis, proportional hazards regression and Weibull modelling, was markedly age-dependent. The estimated median duration of disease was 13.2 weeks in 0-4-year-old subjects and 1.7 weeks in those age 15 and over. Adjustment for multiple infections, and for missing observations did not alter this trend. The cumulative incidence rate of disease was reduced threefold with age. More rapid disease resolution is the main source of reduction in prevalence of active trachoma and ocular C. trachomatis infection with age; disease incidence was reduced to a lesser extent. This age-dependent resolution may be effected by adaptive cellular immune mechanisms. Mechanisms responsible for natural immunity should receive appropriate emphasis in vaccine design.

Adolescent↗
PubMed1999

Cold stress-induced modulation of inflammatory responses and intracerebral cytokine mRNA expression in acute murine toxoplasmosis.

The effects of a physical stressor, cold water stress (CWS), within the central nervous system were investigated in the acute phase of infection with Toxoplasma gondii. Female BALB/c mice were subjected to CWS for 5 min each day for 8 days prior to oral infection with 20 cysts of the low virulent ME 49 strain. Animals were killed at 10-day intervals to detect inflammation, gliosis, and expression of intracerebral cytokine mRNAs. Zones of inflammation were detected by Nissl staining and gliosis by immunoreactivity to glial fibrillary acidic protein. Larger zones of inflammation and reactive astrogliosis were consistently observed in mice subjected to CWS and infected (CWS +INF) compared to control infected (INF) mice. Expression of interleukin (IL)-1beta, IL-2, IL-12, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, and inducible nitric oxide synthase (iNOS) were decreased in CWS+INF mice at 10 days postinoculation (PI), followed by a gradual increase after day 20 PI. This was in contrast to increased expression of these cytokines at 10 days PI in INF mice with a gradual decline thereafter. Inflammation and astrogliosis in CWS+INF mice were associated with an increased expression of IL-1beta, IL-6, IL-12, and TNF-alpha between 20 and 30 days PI. These findings correlated with the continuous gene expression of tachyzoite surface antigen (SAG)-1 mRNA in CWS+INF mice compared to its sharp decline in INF mice after 20 days PI. These results suggest that CWS delays regulation and control of intracerebral Toxoplasma gondii during acute infection in BALB/c mice by decreasing the early expression of IFN-gamma, IL-2, TNF-alpha, iNOS, IL-1beta, and IL-12, while increasing the expression of IL-6, a counterregulatory cytokine.

Acute Disease↗
PubMed1998

Generation of destabilized green fluorescent protein as a transcription reporter.

The green fluorescent protein (GFP) is a widely used reporter in gene expression and protein localization studies. GFP is a stable protein; this property allows its accumulation and easy detection in cells. However, this stability also limits its application in studies that require rapid reporter turnover. We created a destabilized GFP for use in such studies by fusing amino acids 422-461 of the degradation domain of mouse ornithine decarboxylase (MODC) to the C-terminal end of an enhanced variant of GFP (EGFP). The fusion protein, unlike EGFP, was unstable in the presence of cycloheximide and had a fluorescence half-life of 2 h. Western blot analysis indicated that the fluorescence decay of EGFP-MODC-(422-461) was correlated with degradation of the fusion protein. We mutated key amino acids in the PEST sequence of EGFP-MODC-(422-461) and identified several mutants with variable half-lives. The suitability of destabilized EGFP as a transcription reporter was tested by linking it to NFkappaB binding sequences and monitoring tumor necrosis factor alpha-mediated NFkappaB activation. We obtained time course induction and dose response kinetics similar to secreted alkaline phosphatase obtained in transfected cells. This result did not occur when unmodified EGFP was used as the reporter. Because of its autofluorescence, destabilized EGFP can be used to directly correlate gene induction with biochemical change, such as NFkappaB translocation to the nucleus.

Amino Acid Sequence↗
PubMed1998

The in vitro neuronal toxicity of pentraxins associated with Alzheimer's disease brain lesions.

Serum amyloid P component (AP) and C-reactive protein (CRP) are normal serum components which belong to the pentraxin family of proteins. These proteins have been previously localized by immunohistochemical method to the brain lesions of Alzheimer's disease (AD). AP is a constant constituent of amyloid deposits including those found in AD. Both AP and CRP have been localized to AD neurofibrillary tangles. An indirect role for these proteins has been previously suggested in the etiology of AD. We studied the effects of serum AP and CRP on a human-derived neuronal cell line (hNT). In treated cell cultures, AP and CRP were detected immunohistochemically within hNT neurons, indicating cellular uptake of these proteins. Serum AP at the lowest serum physiological concentration (8 microgram/ml) showed a marked toxicity to hNT neurons. CRP also displayed toxicity to the hNT neurons but at a level compatible with inflammatory states (50 microgram/ml). These results suggest a more direct role for serum AP and CRP in the pathogenesis of AD.

Acute-Phase Proteins↗
PubMed1998

Modelling the costs of paediatric HIV infection and AIDS: comparison of infected children born to screened and unscreened mothers.

OBJECTIVE: To estimate the cost of managing children with HIV/AIDS in the UK from a health service perspective. DESIGN AND METHODS: Epidemiological, resource use and unit cost data were combined within a decision analytic model. A Markov model was developed to predict the prognoses of HIV-infected children under different assumptions about natural history, treatment efficacy and the timing of antiretroviral therapy. Resource use estimates for various stages of HIV/AIDS were based on published data relating to the UK health service and clinical judgement; unit cost data were taken from a London centre. RESULTS: The base-case results suggest that the cost of caring for an HIV-infected child is higher if the mother's infection was known about at or before the child's birth (antenatal screened cohort): lifetime costs ranged from 46 427 pound sterling to 119 502 pound sterling per child in the screened cohort and from 38 691 pound sterling to 86 014 pound sterling in the unscreened cohort. However, the screened cohort benefited from longer life expectancy (base-case, 11.66 versus 10.09 years) and AIDS-free life expectancy (base-case, 7.13 years versus 6.22 years). Results are sensitive to assumptions about natural history and treatment efficacy: for example, if antiretroviral therapy was initiated at birth, and assuming optimistic natural history parameters, discounted costs could increase to 215 077 pound sterling and the additional lifetime cost of a child born to a screened mother could be 72 491 pound sterling. CONCLUSIONS: Results reflect the marked uncertainty regarding the cost of, and prognosis for, children with HIV/AIDS in the new era of more potent antiretroviral combination therapies. These results are part of an assessment of the relative cost-effectiveness of alternative antenatal HIV testing strategies.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Epidemiology and detection of HIV-1 among pregnant women in the United Kingdom: results from national surveillance 1988-96.

OBJECTIVE: To describe the epidemiology of HIV-1 infection in pregnant women in the United Kingdom. DESIGN: Serial unlinked serosurveillance for HIV-1 in neonatal specimens and surveillance through registers of diagnosed maternal and paediatric infections from reporting by obstetricians, paediatricians, and microbiologists. SETTING: United Kingdom, 1988-96. SUBJECTS: Pregnant women proceeding to live births and their children. MAIN OUTCOME MEASURES: Time trends in prevalence of HIV-1 seropositivity in newborn infants (as a proxy for infection in mothers); the proportions of mothers with diagnosed HIV-1 infections, and their characteristics. RESULTS: HIV-1 prevalence among mothers in London rose sixfold between 1988 and 1996 (0.19% of women tested; 1 in 520 in 1996). Apart from in Edinburgh and Dundee, levels remained low in Scotland (0.025%; 1 in 3970) and elsewhere in the United Kingdom (0.016%; 1 in 1930). Over a third of births to infected mothers in 1996 occurred outside London. In London the reported infections were predominantly among black African women, whereas in Scotland most were associated with drug injecting. The contribution of reported infection among African women increased over time as that of drug injecting declined. In Scotland 51% of mothers' infections were diagnosed before the birth. In England, despite a national policy initiative in 1992 to increase the antenatal detection rate of HIV, no improvement in detection was observed, and in 1996 only 15% of previously unrecognised HIV infections were diagnosed during pregnancy. CONCLUSIONS: HIV-1 infection affects mothers throughout the United Kingdom but is most common in London. Levels of diagnosis in pregnant women have not improved. Surveillance data can monitor effectively the impact of initiatives to reduce preventable HIV-1 infections in children.

Female↗
PubMed1998

Performance of antenatal HIV screening strategies in the United Kingdom.

BACKGROUND: In 1996 only 13.5% of previously undiagnosed HIV infected women were detected in pregnancy. In this study, all 265 maternity units in the United Kingdom were surveyed to determine the relation between screening strategy, uptake of testing, and detection rate. METHODS: Data on HIV screening strategy and uptake of testing were collected in 1997 by postal questionnaire. The proportion of women with previously undiagnosed HIV infection identified during pregnancy (detection rate) was calculated using data from national obstetric HIV surveillance and unlinked anonymous seroprevalence studies. RESULTS: 239 (90%) units responded; 25 of these (10%) had a universal offer strategy, 89 (37%) a selective offer, and 125 (52%) tested only women who requested it. All selective units offered testing to injecting drug users, but only 26% to women who had lived abroad in high prevalence areas. Uptake was over 10% in only eight units, all with a universal strategy, and in 76% of selective units it was below 0.1%. The detection rate was 14.7% in universal units, 7.8% in selective units, and 7.7% in on request units. In universal units, detection increased by 6.3% (95% confidence interval 3.7% to 8.8%) for every 10% increase in uptake of testing. There was evidence of both selective presentation for testing and avoidance of testing among infected women. CONCLUSIONS: All current antenatal HIV testing strategies fail to identify most infected women. Universal offer strategies achieve a very low uptake and a poor detection rate. Units with selective strategies tend to test only a minority of women at high risk and do not target all the main high risk groups.

Female↗
PubMed1997

p75 neurotrophin receptor immunoreactivity in the aged human hypothalamus.

Low-affinity p75 neurotrophin receptor (p75NTR) immunoreactivity in the aged human hypothalamus was examined in autopsied material. Numerous p75NTR-immunoreactive cells were found in the paraventricular and supraoptic hypothalamic nuclei. The suprachiasmatic nucleus was devoid of p75NTR-immunostaining. Many p75NTR-immunoreactive fibers extended laterally and ventrally from the paraventricular and supraoptic nuclei into the pituitary stalk and median eminence. Our results suggest that neurotrophins may be present within the human hypothalamo-hypophyseal system.

Aged↗
PubMed1997

C-reactive protein-like immunoreactivity in the neurofibrillary tangles of Alzheimer's disease.

C-reactive protein (CRP) is a plasma acute-phase protein, normally not found in the brain. Previous studies have demonstrated the presence of CRP in the senile plaques of Alzheimer's disease (AD). In this study, the presence of CRP-like immunoreactivity in AD neurofibrillary tangles (NFT) was demonstrated following pre-treatment of tissue sections with formic acid. CRP-like immunoreactivity was observed in both extracellular and intracellular NFT and was co-localized with the NFT marker PHF-1 and the amyloid P component (AP). The CRP-like immunoreactive NFT were less numerous and more limited in their distribution than PHF-1 or AP-immunoreactive NFT. The present results further support an involvement of inflammatory processes in the etiology of AD.

Aged↗
PubMed1997

Uptake of interventions to reduce mother-to-child transmission of HIV in the United Kingdom and Ireland.

OBJECTIVES: To describe the uptake of interventions to reduce mother-to-child transmission of HIV infection. DESIGN: Voluntary confidential reporting of HIV infection in pregnancy and childhood; telephone interview with key professionals in all London maternity units. SUBJECTS AND SETTING: HIV-infected pregnant women and children in the United Kingdom and Ireland. MAIN OUTCOME MEASURES: Trends in breastfeeding, use of zidovudine, mode of delivery and terminations of pregnancy. RESULTS: Between 1990 and 1995, 14 (4%) out of 314 women diagnosed with HIV infection before delivery breastfed compared with 109 (77%) out of 142 diagnosed after delivery. Since 1994, zidovudine use has increased in each 6-month period (14, 39, 67, and 75%; chi 2 = 17.5, P < 0.001), although in 1995 it was the policy of only 48% of London maternity units to offer zidovudine to HIV-infected women. During 1995, 44% of HIV-infected women were delivered by elective Cesarean section. Since 1990, 20% of women first diagnosed in pregnancy were reported to have their pregnancy terminated. CONCLUSIONS: Although detection of previously undiagnosed HIV infection in pregnancy remains low in the United Kingdom, and particularly in London, HIV-infected pregnant women who are aware of their status are increasingly active in taking up interventions to reduce transmission to their infants. If all HIV-infected women attending for antenatal care in London consented to testing and took up interventions and termination of pregnancy at the rates observed in this study, the number of vertically infected babies born in London each year could be reduced from an estimated 41 to 13.

Abortion, Induced↗
PubMed1994

Neuronal cytoskeletal abnormalities in human cerebral cortical dysplasia.

The cytoskeletal abnormalities of cortical neurons in human cerebral cortical dysplasia were compared by immunohistochemical methods to the neurofibrillary tangles of Alzheimer's disease (AD). Surgical specimens from cortical resections performed for the treatment of intractable childhood seizures as well as autopsied samples from AD patients were analyzed with different antibodies directed against high- or medium-molecular mass neurofilament epitopes, phosphorylated or non-phosphorylated forms of neurofilaments, ubiquitin, the microtubule-associated protein tau, and paired helical filaments (PHF), a defining feature of AD tangles. A strong abnormal increase in immunoreactivity to the high and medium molecular mass neurofilament epitopes was seen in hypertrophic neurons of cortical dysplasia. These neurofilamentous accumulations of cortical dysplasia as well as AD tangles also displayed immunoreactivity with antibodies against phosphorylated and non-phosphorylated neuro-filament epitopes, tau and ubiquitin. Only the AD tangles, however, were immunoreactive to the antiserum to PHF. These results replicate and extend our previous findings that the neurofibrillary accumulations in cerebral cortical dysplasia share some common antigens with the neurofibrillary tangles of AD but do not demonstrate immunoreactivity to PHF antiserum. The results also suggest that the cytoskeletal abnormalities observed in neurons of cortical dysplasia may result in part from alterations in the level of expression, in phosphorylation state or in transport of cytoskeletal components.

Aged↗
PubMed1994

Immunoreactivity patterns in neurofibrillary tangles of the inferior temporal cortex in Alzheimer disease.

The distributions of various immunohistochemical markers of neurofibrillary tangles (NFT) were compared to that of a normal nerve cell cytoskeletal marker, SMI32, in the inferior temporal cortex of Alzheimer brains and normal aged controls. NFT markers included antibodies to the microtubule-associated proteins tau, ubiquitin, or amyloid P component (AP). The results showed that, in our group of patients, the decrease of SMI32 immunoreactivity in the Alzheimer temporal cortex is paralleled by an increase in AP immunoreactivity in neurons and neurofibrillary tangles. This suggests that AP may play an important role in NFT formation or evolution in Alzheimer disease.

Aged↗
PubMed1993

Microtubule-associated proteins tau and amyloid P component in Alzheimer's disease.

The localization of the intracerebral microtubule-associated proteins tau (MAP-tau) has been compared to that of amyloid P component (AP), an extracerebral protein, by single- and double-antigen immunohistochemistry in neurofibrillary tangles of Alzheimer's brains. The results show that, individually, MAP-tau and AP may be observed in all stages of neurofibrillary tangle (NFT) formation. However, NFT labeled by MAP-tau and those labeled by AP largely do not overlap in their distribution. Furthermore, within the few NFT double-labeled by MAP-tau and AP, there was an inverse relationship between the immunoreactivity to MAP-tau and to AP. It is suggested that MAP-tau and AP are incorporated at different times into NFT and that this difference in the timing of NFT expression of these 2 proteins may be useful in the study of progressive NFT formation.

Aged↗
PubMed1993

Fatty acids may regulate aldosterone secretion and mediate some of insulin's effects on blood pressure.

Experiments in vitro and observation made in humans suggest that some unesterified fatty acids (FA) participate, as inhibitors, in the regulation of aldosterone secretion. Removal of FA from adrenal glomerulosa cells with albumin increases the responses to angiotensin II (AII) and dibutyryl cyclic AMP. Micromolar concentrations of some FA including arachidonic, oleic, linoleic, eicosapentaenoic, and docosahexaenoic inhibit aldosterone secretion by adrenal glomerulosa cells. Inhibition is specific--some acids like stearic are inactive, and the adrenal fasciculata is relatively resistant to inhibition. Oleic acid rapidly and reversibly inhibits aldosterone secretion by perfused dog adrenals. Observations in vivo suggest a reciprocal relationship between plasma levels of FA and aldosterone: insulin infusion into dogs lowers plasma FA and increases adrenal responsiveness to All; salt infusions into humans increase plasma FA as aldosterone falls; plasma FA are low in low-renin essential hypertension where adrenal responsiveness to All is high; plasma FA are inversely correlated with ratios of aldosterone to renin in black hypertensives; and plasma FA are high in some seriously ill patients whose aldosterone levels are inexplicably low. All receptors and the final step of aldosterone biosynthesis, oxidation at the 18 position, are the adrenal sites most sensitive to FA. Insulin's antinatriuresis may be mediated in part by its ability to lower plasma FA and thereby enhance adrenal response to secretagogues.

Aldosterone↗
PubMed1992

Immunohistochemical analysis of the basal forebrain in Alzheimer's disease.

An immunohistochemical analysis utilizing antibodies to glial fibrillary acid protein (GFAP), microglia, beta-amyloid, amyloid P-component, neurofibrillary tangles (NFT), and microtubule associated protein-tau (MAP-tau) was performed on the cholinergic basal forebrain in Alzheimer's disease (AD). This severely compromised system, which includes the nucleus basalis of Meynert, is largely responsible for the massive loss of cortical and subcortical cholinergic innervation in the diseased state. Our study juxtaposes the basal forebrain immunohistopathology to the hippocampus, amygdala, and entorhinal cortex in AD. Key findings include a progressive degeneration of these cholinergic neurons characterized by the formation of immunoreactively atypical NFT, the loss of intraneuronal lipofuscin, a lack of senile plaque and beta-amyloid deposition within the basal forebrain, and end-stage gliosis without residual extracellular NFT. These structural and compositional differences suggest a unique pathogenesis of the basal forebrain separate from other cortical regions in AD.

Acetylcholinesterase↗
PubMed1991

Altered excitatory amino acid function and morphology of the cerebellum of the spastic Han-Wistar rat.

A mutant strain of Han-Wistar rat carries an autosomal recessive gene producing spastic paresis which is characterized by ataxia, tremor and hind limb rigidity. Brains of affected rats and unaffected littermate controls were transected at the mesencephalon into rostral and caudal portions (the caudal portion contained the cerebellum and brainstem). Poly(A)+ mRNA was isolated from pooled rostral or caudal portions and injected into Xenopus oocytes. The oocytes were voltage-clamped and exposed to 1 mM L-glutamate, 500 microM kainate, 500 microM quisqualate, 200 microM N-methyl-D-aspartate (NMDA) or 1 mM gamma-aminobutyric acid (GABA). Oocytes injected with mRNA isolated from the caudal portions of the affected rat brains exhibited statistically significant increases in glutamate and kainate peak current responses compared to oocytes injected with mRNA from other brain samples. No differences were noted in the responses of the groups when exposed to quisqualate, NMDA or GABA. Cerebellar and brain stem mRNA were also isolated separately in different groups of mutants and unaffected littermates. Only oocytes injected with cerebellar mRNA from mutants displayed statistically significant increases in responses to glutamate and kainate. In parallel morphological studies changes in the cerebellum of mutants were also observed. These consisted of a loss of Purkinje cells and an asymmetrical disarrangement of the granule cell layer of cerebellar cortex. Taken together, the physiological and morphological results suggest that alterations in glutamate/kainate receptors in the cerebellum are phenotypic manifestations of the Han-Wistar mutation. The results are consistent with the hypothesis that this mutant rat might serve as a model of glutamate/kainate excitotoxicity in the brain.

Animals↗