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Biomedical subjects

B He

Publications and source records attributed to B He.

275 records · Page 16Linked to original sources
PubMedDate not supplied

On the estimation of the Laplacian electrocardiogram during ventricular activation.

Body surface Laplacian electrocardiogram (ECG) mapping using a set of disk electrodes is explored by both computer simulation and human experiments in 12 healthy subjects. The Laplacian ECG was estimated from body surface potentials using finite difference estimation algorithms. The performance of the finite difference Laplacian estimators was evaluated by both computer simulation and human experiments. The present experimental results show that the two types of finite difference Laplacian estimates are highly correlated and have a consistent spatial distribution over the anterolateral chest during normal ventricular activation. The present computer simulation and human experiment results suggest the feasibility of estimating the body surface Laplacian maps (BSLMs) from potentials using the finite difference algorithm over the anterior chest in male subjects. The noise levels of the BSLMs over the anterolateral chest were quantitatively compared to the noise levels in corresponding body surface potential maps (BSPMs) in 12 healthy subjects. The simulation and experiment results indicate that the noise to signal ratios in the BSLMs over the anterolateral chest during ventricular activation is about 5 times that of the BSPMs, when no signal processing is performed.

Adolescent↗
PubMedDate not supplied

Silica increases tumor necrosis factor (TNF) production, in part, by upregulating the TNF promoter.

Silica causes release of tumor necrosis factor (TNF) from mononuclear phagocytes. One hypothesis is that silica increases TNF production, in part, by upregulating the TNF gene. To evaluate this hypothesis, THP-1 cells (a myelomonocytic cell line) were exposed to various amounts of silica and then the TNF gene transcription was evaluated. In this study silica caused a dose-dependent increase in TNF mRNA and the peak response occurred at 3 h following stimulation. A transient transfection assay also showed that silica upregulated expression of a TNF CAT construct in THP-1 cells. Furthermore, a nuclear run-on assay demonstrated that silica particles induce increased TNF gene transcription in exposed cells. THP-1 cells cultured for various periods of time in the presence of silica released TNF into the cell supernatants. These studies show that silica can upregulate the TNF gene, which results in the release of TNF protein from the cells.

Autoimmunity↗
PubMedDate not supplied

Synergistic activation of the human cytomegalovirus major immediate early promoter by prostaglandin E2 and cytokines.

Human cytomegalovirus (HCMV) is a common cause of morbidity and mortality in immunosuppressed patients, especially transplant recipients. In this population, infection is frequently due to reactivation of latent virus. The major immediate early promoter of HCMV controls production of immediate early gene products, which are both trans- and cis-active and are responsible for reactivation. Activation of this promoter is therefore a crucial step in regulation of reactivation infection. It is known that there are cAMP-response elements in the HCMV major immediate early promoter. We hypothesized that prostaglandins (PG), like PGE2, which are known to increase cAMP, as well as cytokines known to be released during acute inflammation, may be important in the regulation of this promoter and thus in reactivation of HCMV. To examine this, we transfected pCAT760, a plasmid containing the major immediate early promoter of HCMV upstream of a chloramphenicol acetyltransferase (CAT) gene, into THP-1 cells. These cells were subsequently stimulated with PGE2 and/or one of a variety of cytokines. We found that PGE2, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1 beta each upregulated the HCMV major immediate early promoter. TNF-alpha, IL-1 beta, IL-6, and IL-10 were each synergistic or additive with PGE2 in upregulating the promoter. Since PGE2 and the cytokines are all products of activated macrophages, we suggest that acute inflammation and macrophage activation may predispose to reactivation of latent HCMV.

Cytokines↗