Biomedical subjects

H G Choi

Publications and source records attributed to H G Choi.

24 records · Page 2Linked to original sources

PubMed1994

Multiresolution segmentation of respiratory electromyographic signals.

Analysis of respiratory electromyographic (EMG) signals in the study of respiratory control requires the detection of burst activity from background (signal segmentation), and focuses upon the determination of onset and cessation points of the burst activity (boundary estimation). This paper describes a new automated multiresolution technique for signal segmentation and boundary estimation. During signal segmentation, a new transitional segment is defined which contains the boundary between background and burst activity. Boundary estimation is then performed within this transitional segment. Boundary candidates are selected and a probability is attributed to each candidate, using an artificial neural network. The final boundary for a given transitional segment is the boundary estimate with the maximum a posteriori probability. This new method has proved accurate when compared to boundaries chosen by two investigators.

Action Potentials↗

PubMed1994

Respiratory muscle activities after birth in asphyxiated preterm lambs.

Laryngeal and pump muscle activities are important in the establishment and maintenance of functional residual capacity (FRC) after birth. The aim of this study was to determine the expiratory mechanisms by which laryngeal and diaphragmatic activities achieve the increments in FRC postnatally. Wire electrodes were placed in: the laryngeal abductor, a major laryngeal adductor, the inferior pharyngeal constrictor and the diaphragm of six fetal sheep. The lambs were delivered prematurely by cesarean section and a face mask with a pneumotachograph applied. A grunting respiratory pattern was characterized by severe expiratory airflow retardation, associated with laryngeal adductor activity. In grunting breaths, minimal volume loss at end-expiration and incremental increases in FRC occurred when the onset of diaphragmatic activity preceded the onset of laryngeal muscle activities associated with laryngeal opening. Thus the timing order of laryngeal and diaphragmatic muscle activities near end-expiration is a determinant of increments in FRC.

Animals↗

PubMed1993

Role of receptor complexes in resistance or sensitivity to growth inhibition by TGF beta in intestinal epithelial cell clones.

Untransformed rat intestinal epithelial cells (IEC-18) were chemically mutagenized, selected in the presence of TGF beta 1, and cloned by limiting dilution. Two clones (4-5, 4-6) were resistant to growth inhibition by both TGF beta 1 and TGF beta 2. Another clone (4-1) was more sensitive to both TGF beta isoforms (relative to parental IEC-18 cells). IC50 values for TGF beta 1 and 2 in the 4-1 cells were at least 1/9 those of the parental cells; growth rates were reduced by 49% for TGF beta 1 and by 26% for TGF beta 2 in this clone. This increased sensitivity to TGF beta was explained by the 5- to 10-fold increase, relative to parental cells, in binding of TGF beta 1 and TGF beta 2 to both the type I and II receptors. In contrast, the resistance to growth inhibition by TGF beta in the 4-5 and 4-6 cells could not be explained by a decrease in either TGF beta binding affinities or in total number of receptors expressed, by the presence of serum binding components, or by occupation of receptor binding sites with autocrine TGF-beta 1. However, in comparison to TGF beta-sensitive cells (IEC-18, 4-1), the resistant cells displayed a higher ratio of type II relative to type I receptor binding by TGF-beta 1. Thus, a critical ratio of binding to receptor subtypes correlated with growth inhibition by TGF-beta 1. Resistance to TGF-beta 2 in the same clones did not appear to be receptor related. Thus, different mechanisms for resistance to TGF-beta 1 and TGF-beta 2 were observed within a given clone.

Animals↗

PubMed1993

Laryngeal and diaphragmatic muscle activities and airflow patterns after birth in premature lambs.

The nature and control of early neonatal respiratory patterns were determined in 10 premature, asphyxiated lambs. Severe retardation of early expiratory airflow (braking) characterized an initial pattern (A), but was absent in a final one (B). During a transition pattern (pattern T), pattern A and B airflow types occurred. Close temporal relationships between the airflow patterns and posterior cricoarytenoid (PCA), thyroarytenoid (TA), and diaphragm (D) integrated muscle activities were demonstrated quantitatively. Specifically, in pattern A, the duration of braked expiratory airflow was related to the durations of TA burst activity and the absence of PCA burst activity (r2 = 0.99). In pattern A, pH, but not arterial PCO2 or arterial PO2, differed from that in patterns T and B [7.01 +/- 0.14 (A), 7.11 +/- 0.12 (T), 7.19 +/- 0.08 (B) (P < 0.03)]. Within-breath airflow and respiratory muscle activity relationships and differences in neural and mechanical respiratory timing intervals between patterns suggested that neural feedback was important in the control of central pattern generation. Thus activities of PCA, TA, and D shape the early neonatal airflow patterns and are influenced mainly by neuromechanical, and not chemical, feedback.

Animals↗

PubMed1990

Inhibitory effects of transforming growth factor beta 1 on mitogenic response, transforming growth factor alpha, and c-myc in quiescent, well-differentiated colon carcinoma cells.

Previously, we reported that exponentially proliferating cultures of well-differentiated human colon carcinoma cells responded to transforming growth factor beta 1 (TGF-beta) with growth inhibition, alterations in morphology, and increased secretion of the differentiation marker, carcinoembryonic antigen. Poorly differentiated cultures were unresponsive. Here we show that TGF-beta was ineffective in repressing nutrient-stimulated mitogenesis in quiescent, poorly differentiated cells. However, in quiescent, well-differentiated cells, TGF-beta repressed the mitogenic responses to both nutrients alone (by 90%) and to nutrients plus the exogenous stimulatory factors epidermal growth factor (E), insulin (I), and transferrin (T) (by 55-65%). Thymidine incorporation experiments indicated that TGF-beta reduced both the onset and peak mitogenic response to growth factors and/or nutrients in the well-differentiated cells. Additionally, TGF-beta repressed the growth factor (E + I + T)-stimulated upregulation of expression of both c-myc and of transforming growth factor alpha (TGF-alpha) mRNAs in quiescent, well-differentiated cells. TGF-beta also elicited a rapid (t1/2 approximately 1h) down-regulation of c-myc expression in the absence of prior growth factor (E + I + T) stimulation. In contrast, TGF-beta had no effect on c-myc or TGF-alpha mRNA expression in the poorly differentiated cells. The results suggest that TGF-beta exerts rapid inhibitory effects on proliferation-associated genes in quiescent and restimulated, well-differentiated cells. Expression of these genes (c-myc and TGF-alpha) may otherwise (in the absence of TGF-beta) play roles in the cellular signaling of mitogenic responses by growth stimulatory factors in well-differentiated colon carcinoma cells.

Blotting, Northern↗

PubMed1990

Evidence for c-myc in the signaling pathway for TGF-beta in well-differentiated human colon carcinoma cells.

Previously, we described a model culture system for comparing responsiveness of poorly differentiated and well-differentiated human colon carcinoma cells to exogenous growth factors. While polypeptide growth stimulators elicited an up-regulation of c-myc, as well as a mitogenic response in the well-differentiated cells, the poorly differentiated cells were insensitive to exogenous growth stimulators. We now show, by thymidine incorporation experiments and autoradiographic analysis, that transforming growth factor beta 1 (TGF-beta) abrogated the mitogenic responses to the growth factors epidermal growth factor + insulin + transferrin (IC50 = 0.8 ng/ml), as well as to nutrients (basal medium; IC50 = 0.2 ng/ml) in the well-differentiated cells. The poorly differentiated cells did not respond to TGF-beta. Moreover, TGF-beta (10 ng/ml) completely abrogated the growth factor-stimulated up-regulation of c-myc in the TGF-beta responsive, well-differentiated colon carcinoma cells. Addition of TGF-beta to the TGF-beta-responsive, well-differentiated cells, at a time after c-myc had been transiently up-regulated in response to growth stimulatory factors, resulted in a loss of responsiveness to TGF-beta. Addition of TGF-beta to these cells at increasing time periods after EIT stimulation also resulted in a loss of the TGF-beta-induced repression of c-myc. The results suggest an important role for c-myc in the mechanism of action of TGF-beta in well-differentiated human colon carcinoma cells.

Cell Differentiation↗