Search PubMed⌕ Search

Biomedical subjects

K Thompson

Publications and source records attributed to K Thompson.

At least 37 records · Page 2Linked to original sources
PubMed1998

Immunohistochemical identification of epithelial and mesenchymal cell types in the chorioallantoic and yolk sac placentae of the guinea-pig.

To define the epithelial and mesenchymal cell types of the guinea-pig placenta, immunostaining patterns were determined for the intermediate filament proteins cytokeratin and vimentin. Chorionic and yolk sac placentae were studied at 15, 20, 25, 29-30, 44-45, 55 and 65 days of gestation. Immunohistochemistry was performed on 5-microm thick sections of paraffin embedded tissue using specific antibodies against cytokeratin, a marker for epithelial cells, including trophoblast, and vimentin, a marker for mesenchymal cells and stromal decidua. Immunostaining was identified by the avidin-biotin-peroxidase technique with diaminobenzidine as the chromogen. Most of the surface of the placenta is covered by the columnar epithelium of the parietal yolk sac, beneath which is found a layer of chorionic giant cells. In the guinea-pig, a sheet of mesenchymal cells interposed between these cell layers immunostained for vimentin, a protein that is expressed only intracellularly, and had nuclei orientated parallel to the surface of the placenta. This cell layer is quite different from Reichert's membrane in the rat or mouse, which is acellular. Within the main placenta, cytokeratin immunostaining demonstrated that the trophoblasts lining the large maternal blood sinuses are different in character from the surrounding syncytiotrophoblast, confirming earlier ultrastructural observations. In the subplacenta, some trophoblast did not immunostain for cytokeratin and there was non-specific staining of cellular debris, so that immunostaining for vimentin provided the clearest indication of the maternal-fetal interface. In later stages of gestation (30-55 days), trophoblasts invading the walls of maternal arteries immunostained for cytokeratin and were vimentin negative. In early gestation, however, trophoblast invasion of the maternal vessels was indicated by cells that were immunoreactive for both cytokeratin and vimentin.

Allantois↗
PubMed1998

Hippocampal stimulation produces neuronal death in the immature brain.

We re-examined the proposed resistance of the immature brain to seizure-induced damage. In awake, freely moving rat pups, intermittent perforant path stimulation produced selective hippocampal cell loss and reduction in paired-pulse inhibition. During 16 h of stimulation, animals showed frequent wet dog shakes and hind-limb scratching movements but no convulsive motor activity. In situ end-labelling performed 2 h after the end of stimulation showed an intense band of positively-labelled eosinophilic cells with condensed profiles bilaterally in the dentate granule cell layer of stimulated animals. Control animals showed no in situ end-labelling positivity in the dentate gyrus. These cells were not observed 24 h later, suggestive of rapidly scavenged apoptotic cells. One day after the end of stimulation, many necrotic interneurons with eosinophilic cytoplasm and pyknotic nuclei were observed in the hilus of the stimulated dentate gyrus in all rats tested. Hippocampal pyramidal cells in CA1, CA3 and subiculum showed bilateral damage greater on the side of stimulation, and prepiriform cortex sustained bilateral symmetrical lesions. One month after perforant path stimulation, Cresyl Violet staining showed the number of large hilar interneurons (>15 microm) was reduced on the stimulated side (54.1 +/- 12.2) compared to the non-stimulated side (100.5 +/- 10.2 cells, P<0.01). Immunohistochemical analysis showed significant losses in somatostatin (8.5 +/- 1.6 stimulated side, 22.8 +/- 3.8 unstimulated side, P<0.05) and neuropeptide Y (12.8 +/- 3.2 stimulated side, 17.0 +/- 4.1 unstimulated side, P<0.05) immunoreactive cells in the stimulated hilus but no loss of parvalbumin-immunoreactive cells. Significant reductions in paired-pulse inhibition were found after stimulation but there was some return of inhibition by one month. These combined data demonstrate that the immature brain can incur damage as a result of prolonged seizure-like hippocampal activity mimicking status epilepticus in immature rats. The hippocampal damage produced by perforant path stimulation is associated with the immediate loss of physiological inhibition suggesting important modification of excitatory control in an extremely epileptogenic region of the brain.

Animals↗
PubMed1998

Determinants of four functional tasks among older adults: an exploratory regression analysis.

Functional ability declines in later life. The purpose of this project was to determine if strength, postural control, and joint pain predict performance of four functional tasks among older adults. A sample of 28 older adults completed assessments of strength, postural control, joint pain, and four functional tasks. The duration to complete the functional tasks of: 1) getting out of bed, going to a chair, and then returning to bed; 2) crossing a street and getting onto a bus; 3) exiting the passenger side of a car; and 4) climbing a flight of 27 stairs was recorded. Step-wise regression equations indicated that seated row strength and dynamic postural control were significant predictors of all of the tasks and accounted for the largest proportion of the variance in each equation. These results indicate that measures of physical fitness may be more important predictors of functional tasks among older adults than chronological age.

Activities of Daily Living↗
PubMed1998

Histopathological features of lepromatous iridocyclitis; a case report.

A peripheral iridectomy specimen which included a portion of the ciliary body from an advanced lepromatous leprosy patient was studied histopathologically. The lepromatous granuloma in the iris was similar in content and appearance to that of skin lesions. It appeared that even in this advanced lepromatous patient the dilator muscles of the iris were preserved. This study agrees with the earlier observation that the dysfunction of the iris in lepromatous disease is most probably the result of autonomic nerve destruction. Further, it is possible that the lepromatous involvement of the iris may reflect the histopathological changes in the ciliary body.

Aged↗
PubMed1997

Lithium-pilocarpine status epilepticus in the immature rabbit.

Although status epilepticus in children is associated with neuronal pathologies, there are few developmental models of status epilepticus which produce damage in the immature brain. We have developed a new model of status epilepticus using systemically injected pilocarpine in immature rabbits pretreated with lithium. Injected animals demonstrated behavioral and electrographic seizures. Behavioral seizures were characterized by sustained or recurrent bouts of clonus in all limbs. The pilocarpine-induced seizures had a 40% mortality. All animals surviving the status epilepticus had hippocampal lesions when evaluated 48 h after the SE. Within the hippocampus, CA1 pyramidal cells were the most vulnerable cell population. Extrahippocampal damage was seen in the majority of animals. Our results show that severe seizures cause hippocampal lesions in the absence of hypoxemia and suggest that the presumed resistance of the immature brain to seizure-induced damage is not a general rule which can be applied to all models or species.

Animals↗
PubMed1997

In vivo production of A-protein, lipopolysaccharide, iron-regulated outer membrane proteins and 70-kDa serine protease by Aeromonas salmonicida subsp. salmonicida.

Using specific immunostaining of Western blots, the in vivo expression of several putative virulence factors of Aeromonas salmonicida subsp. salmonicida was demonstrated in infected muscle tissue of Atlantic salmon and rainbow trout. Three virulent isolates of A. salmonicida were used. One isolate was chosen because in vitro it was apparently a non-producer of the 70-kDa serine protease. Infected furuncle tissue was centrifuged and samples of the pellet and supernatant probed for evidence that the components of interest were bacterial cell-associated or secreted. The A-protein was detected in pelleted furuncle material but not in the supernatant. Lipopolysaccharide, both high and low molecular mass, was present in the pellet but only high molecular mass lipopolysaccharide was detected in the furuncle supernatant. Iron-regulated outer membrane proteins were detected in the furuncle pellet. The 70-kDa serine protease was detected in the furuncle supernatant of both protease-producing strains. However, whilst the protease-deficient isolate was demonstrated to produce low levels of the 70-kDa protease when grown in vitro under iron restricted conditions, none could be detected in vivo.

Aeromonas↗
PubMed1997

Partial protection of hippocampal neurons by MK-801 during perforant path stimulation in the immature brain.

We investigated whether the non-competitive NMDA receptor antagonist, MK-801, could protect neurons in the immature brain from the excitotoxic affects of perforant path stimulation. A high dose of MK-801 reduced the number of injured hilar interneurons in the stimulated hippocampus from 30.0 +/- 5.2 in unmedicated rats to 12.2 +/- 9.6 in MK-801 treated animals (P < 0.05). MK-801 injection also protected the animals from the scattered dentate granule cell injury observed in non-medicated animals 1 day after stimulation. Other effects of drug injection included exacerbated damage in limbic cortices, retrosplenial cortical damage, and reduced inhibition in a highly epileptogenic region of the dentate gyrus. Our results show that a subpopulation of hilar interneurons is vulnerable to NMDA-induced damage in the immature hippocampus but that non-competitive blockade of the NMDA receptor may be a dangerous therapeutic strategy.

Age Factors↗
PubMed1997

Minimal effects of dextroamphetamine on scopolamine-induced cognitive impairments in humans.

The central anticholinergic drug scopolamine has been used to model aspects of the memory impairment that occurs in Alzheimer's disease and in aging. To determine whether nonspecific stimulant effects can attenuate the cognitive impairment induced by scopolamine, we studied the effects of scopolamine and the stimulant dextroamphetamine in 17 young normal volunteers. After a baseline day of cognitive testing, subjects participated in two study days, in which they received dextroamphetamine (d-AMP) (0.25 mg/kg p.o.) + scopolamine (0.5 mg i.v.) and placebo + scopolamine, in randomized order under double-blind conditions. There were no statistically significant differences in cognitive test performance between the two drug conditions with the exception of one of the category retrieval tasks. Stimulant effects were documented to occur by other measures. We conclude that d-AMP at the dose used does not attenuate the memory impairment induced by scopolamine.

Adult↗
PubMed1997

Inhibition of interleukin-10 during pregnancy results in neonatal growth retardation.

PROBLEM: Interleukin 10 is considered to be important in the survival of the fetus in murine pregnancies that are known to be at risk for fetal wastage. The function of IL-10 in a normal pregnancy is not known. METHODS: In this report, we attempted to neutralize Interleukin 10 by administering anti IL-10 monoclonal antibodies (mAb) to pregnant mice that have a low background risk for fetal resorptions. The first group of mice was sacrificed on gestation day 18 to study the fetal effects of anti IL-10 administration. The second group of mice was allowed to deliver to study the effects on the neonatal outcome. RESULTS: Administration of anti IL-10 mAb did not affect the duration of gestation or the fetal outcome. Neonates exposed to anti IL-10 mAb in utero showed signs of transient growth deficiency starting at 4 weeks of age that spontaneously corrected by 6 weeks of age. CONCLUSIONS: Administration of anti IL-10 mAb does not alter the duration of gestation or the fetal outcome in normal murine pregnancies; however, it appears to be associated with transient neonatal growth problems.

Animals↗
PubMed1996

High-performance liquid chromatographic separation of an HIV-1 reverse transcriptase inhibitor and its enantiomer.

This article describes the direct separation of an HIV-1 reverse transcriptase inhibitor and its enantiomer by HPLC on a silica-bonded polyacrylamide (ChiraSpher) column. The column selection was based on specific interactions between the individual enantiomers and the chiral stationary phase. The influence of some chromatographic conditions, such as concentration of the polar modifier in the mobile phase, column flow-rate and column temperature, on column performance was investigated. The separation was applied to the determination of the minor enantiomer in the bulk drug and as low as 0.3% of minor enantiomer was detectable.

Binding, Competitive↗
PubMed1996

Exogenous leukocyte and endogenous elastases can mediate mitogenic activity in pulmonary artery smooth muscle cells by release of extracellular-matrix bound basic fibroblast growth factor.

There is increasing evidence that extracellular matrix (ECM)-degrading proteinases contribute to the process of medial hypertrophy and neointimal proliferation in pulmonary vascular diseases. However, little is known about how proteinases, specifically elastases, induce vascular smooth muscle cell (SMC) hyperplasia. Our objective was to determine whether exogenous human leukocyte elastase (HLE), as well as endogenous vascular elastase, could release basic fibroblast growth factor (bFGF), a potent mitogen stored in the ECM surrounding SMCs. Cultured ovine and porcine pulmonary artery SMC were pre-incubated with [125I]-bFGF. After removal of unbound [125I]-bFGF, administration of HLE (0-1.0 microgram /ml, 1 h) resulted in a concentration-dependent accumulation of [125I]-bFGF in the conditioned medium, mirrored by depletion from the ECM. The serine elastase inhibitor elafin blocked this HLE-mediated action. Assessment by Western immunoblotting further demonstrated that HLE evoked the release of ECM-bound endogenous bFGF. When incubated with serum-starved SMC, conditioned medium from HLE-treated cells stimulated [3H]-thymidine incorporation, a feature neutralized by bFGF antibodies. In addition, SMC exposed to serum treated elastin (STE), previously shown to stimulate endogenous vascular elastase, liberated bioavailable bFGF from ECM stores, as determined by autoradiography, Western immunoblotting, and stimulation of DNA synthesis and SMC proliferation. Chondroitin sulfate, an inhibitor of STE-induced elastase activity, attenuated the release of bFGF. Our studies demonstrate that HLE, secreted by inflammatory cells, and endogenous vascular elastase release matrix-bound bFGF, suggesting a mechanism whereby elastases, through degradation of ECM, induce SMC proliferation associated with progressive vascular disease.

Animals↗
PubMed1996

Coping strategies and psychiatric morbidity in women attending breast assessment clinics.

This study examined the role of coping strategies and personality characteristics in mediating psychiatric morbidity in subjects facing possibly serious breast disease. Participating were 121 women aged 20 to 65 undergoing breast fine needle biopsy for a suspicious lesion on mammography. All subjects received psychosocial assessments including the 12-item General Health Questionnaire (GHQ-12), the Eysenck Personality Inventory (EPI) and the Coping Strategies Inventory. The results show that neuroticism was the only EPI subscore significantly correlated with GHQ-12 score. A habitual method of coping with adversity known as 'engagement' has a negative correlation with GHQ-12 score; that is, patients who actively confront their illness and the uncertainty that surrounds it show better psychological health. Stepwise multiple regression reveals that neuroticism and an engagement coping strategy are the most significant predictors towards GHQ-12 score prior to the diagnosis of breast cancer.

Adaptation, Psychological↗
PubMed1996

DNA-based immunization by in vivo transfection of dendritic cells.

Delivery of antigen in a manner that induces effective, antigen-specific immunity is a critical challenge in vaccine design. Optimal antigen presentation is mediated by professional antigen-presenting cells (APCs) capable of taking up, processing and presenting antigen to T cells in the context of costimulatory signals required for T-cell activation. Developing immunization strategies to optimize antigen presentation by dendritic cells, the most potent APCs, is a rational approach to vaccine design. Here we show that cutaneous genetic immunization with naked DNA results in potent, antigen-specific, cytotoxic T lymphocyte-mediated protective tumor immunity. This method of immunization results in the transfection of skin-derived dendritic cells, which localize in the draining lymph nodes. These observations provide a basis for further development of DNA-based vaccines and demonstrate the feasibility of genetically engineering dendritic cells in vivo.

Amino Acid Sequence↗
PubMed1996

The pharmacokinetics, antigenicity, and fusion-inhibition activity of RSHZ19, a humanized monoclonal antibody to respiratory syncytial virus, in healthy volunteers.

Single ascending doses of RSHZ19 (also known as SB 209763), a humanized monoclonal antibody (MAb) directed to the fusion protein of respiratory syncytial virus, were administered to healthy men to evaluate the safety, pharmacokinetics, antigenicity, and fusion inhibition (FI) activity of RSHZ19. Doses of RSHZ19 (0.025-10.0 mg/kg) or placebo were infused over 30 min, and subjects were followed for 10 weeks. Plasma concentrations of RSHZ19 and RSHZ19-specific antibodies were determined by ELISAs. FI titers were used to evaluate the ability of plasma to inhibit virus-induced fusion of VERO cells previously infected with RS Long strain virus. Twenty-six subjects, mean age 24, completed the study. RSHZ19 was safe and well tolerated, and no subject developed antibodies to RSHZ19 during follow-up. RSHZ19 had low plasma clearance and a half-life of approximately 23 days, similar to native IgG. Increases in FI titers relative to pretreatment levels were seen 24 h after MAb administration in all 4 subjects given 10 mg/kg and in 2 of 4 given 5 mg/kg.

Adolescent↗
PubMed1996

Estrogen blocks early T cell development in the thymus.

PROBLEM: Pregnancy and estrogen are known to suppress B lymphopoiesis as well as lead to thymic involution in the mouse. Additionally, estrogen deficiency by oophorectomy reportedly causes a selective increase in the B220+ B cells in the murine bone marrow. The purpose of this study was to determine if estrogens played a regulatory role in T cell development. METHODS: The first experimental group consisted of 5-6-week-old Balb/c mice that received subcutaneous pellets of placebo, estriol, estradiol, or progesterone. The thymus glands were examined 2-4 weeks after treatment. The second group consisted of 6-week-old Balb/c mice who underwent either bilateral oophorectomy or a sham procedure. Two weeks after the surgery, extensive phenotypic characterization of the thymus and spleen cells was performed by flow cytometry using monoclonal antibodies to surface markers of T cell subsets. RESULTS: Estrogen treatment causes a dramatic reduction of thymic size and cellularity. All defined T cell subsets of CD4 and CD8 were reduced, with a disproportionate loss of CD4+CD8+ double positive cells. Examination of the triple negative (CD3-CD4-CD8-) subset revealed a striking loss of TN developmental progression of the early precursor cells. Based on the expression of CD44 (pgp-1) and CD25 (IL-2R alpha) markers, the TN thymic compartment was composed almost entirely of the earliest population (CD44+, CD25-), with the remaining maturational stages (CD44+, CD25+; CD44-, CD25+; CD44-, CD25-) depleted. In contrast, all T cell developmental stages in the thymus were found to be in normal proportions in the oophorectomized mice, with no differences in the splenic T and B cell subsets. CONCLUSIONS: The study demonstrates that estrogen but not progesterone blocks T cell development in the thymus. However, contrary to our expectation, estrogen deprivation by oophorectomy does not enhance T cell development.

Animals↗