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Biomedical subjects

M C Chou

Publications and source records attributed to M C Chou.

53 records · Page 3Linked to original sources
PubMed1990

Mutagenicity of airborne particles from four cities in Taiwan.

The mutagenicity of airborne particles from 8 urban and suburban locations in each of four cities, Taipei, Hsinchu, Taichung, and Kaohsiung, in Taiwan area were investigated with S. typhimurium strain TA98 by Ames Salmonella/microsomal test. The average mutagenic activity of airborne particulate samples from Taipei and Kaohsiung was higher than that from Hsinchu and Taichung with or without metabolic activation. The major direct-acting mutagenic compounds of airborne particulate samples from Taipei and Kaohsiung was similar to that of standard dinitropyrenes mixture (DNPs) in the retention time of HPLC. Moreover, the contents of DNPs of airborne particulate samples from Taipei and automobile exhaust partially purified through Sephadex LH-20 gel filtration and semipreparative HPLC were determined by HPLC. DNPs was major direct-acting mutagens of the urban air samples from Taipei and their major pollutants might be from automobile exhaust. However, the major mutagenic compounds of airborne particulate samples from Hsinchu and Taichung did not correspond to any of the standard compounds tested. The content of benzo[a]pyrene (B[a]P) of airborne particulate samples was also determined by HPLC. The concentration of B[a] P was 0.05-0.62 ng/m3 air sample. The B[a] P contents of airborne particulate samples from four cities in Taiwan did not show good correlation with their mutagenic activity. Thus, we concluded that B[a] P was not a major indirect-acting mutagenic compound in the tested air samples.

Air Pollutants↗
PubMed1983

Exposure of dog thyroid slices to acetylcholine induces refractoriness to its subsequent stimulation of glucose oxidation.

An initial incubation of dog thyroid slices with 0.1 or 1 microM acetylcholine (ACH) for at least 2 h decreases its subsequent stimulation of [1-14C]glucose oxidation. Refractoriness persists for as long as 6 h in the absence of ACH. While new protein synthesis is essential for recovery, it is not necessary for its induction. Refractoriness is prevented when 25 microM tropicamide, an atropine-like drug, is present from the beginning of the initial incubation, but not when it is added after 2 h of incubation of slices with ACH, indicating that at this time ACH is no longer necessary for refractoriness. During refractoriness induced by ACH, stimulation of glucose oxidation by thyroid-stimulating hormone, prostaglandin E1, dibutyryl cyclic AMP, and cholera toxin, but not menadiol, is also significantly diminished. Incubation of thyroid slices with ACH does not modify its stimulation of iodide organification or 32Pi incorporation into phospholipids. These results suggest that the desensitization is not due to changes in the ACH receptor but rather to intracellular metabolic effects. This phenomenon may be important in the regulation of cholinergic effects on the thyroid.

Acetylcholine↗
PubMed1983

Absence of hepatic extraction of pancreatic polypeptide in conscious dogs.

In 15 conscious dogs basal portal vein pancreatic polypeptide (PP) (306 +/- 8 pg/ml) exceeded both hepatic vein PP (255 +/- 8 pg/ml) and arterial PP (244 +/- 9 pg/ml) and increased rapidly 10 min after oral glucose administration. In contrast to oral glucose, intraportal glucose infusion decreased PP levels from 45 min until the end of the infusion. Meat ingestion rapidly and promptly increased PP. During the basal state, hepatic extraction of total immunoreactive PP was 10 +/- 4%, not significantly different from zero, of the 150 +/- 14 ng/min presented to the liver. Fractional hepatic extraction of PP did not change after oral glucose, meat ingestion, or intraportal glucose infusion. Chromatographic analysis showed at least four different components of immunoreactive PP. The first peak eluted with the void volume, the second peak between the void volume and authentic PP, and the third peak coincided with authentic PP. When present, the fourth peak eluted after authentic PP. More than half of the immunoreactive PP in the basal state eluted with authentic PP, whereas about one-third was found in the second peak. The marked alterations in PP after meat, oral glucose, or intraportal glucose and atropine reflected primarily changes in the third peak. The fractional hepatic extraction of all the components was very similar.

Animals↗
PubMed1982

Recovery from thyroid-stimulating hormone-induced refractoriness in thyroid slices: effect of removal of hormone and new protein synthesis.

An initial incubation of bovine thyroid slices with TSH causes decreased responsiveness to the subsequent addition of the hormone when the adenylate cyclase -cAMP system and other metabolic parameters are measured. After the initial incubation with TSH, refractoriness persists despite incubation of thyroid slices for 24 h in the absence of added TSH. Removal of persistently bound TSH by trypsin or antibody to TSH did not reverse the refractoriness during a subsequent 2 h incubation without added TSH. However, normal TSH responsivity was restored by the removal of TSH bound during the first incubation by the addition of either trypsin or antibody to TSH at the beginning of a 24-h second incubation. Restitution of TSH responsiveness after treatment with trypsin or antibody to TSH requires new protein synthesis. While TSH-induced refractoriness does not modify stimulation of cAMP by cholera toxin, its effect on glucose oxidation is significantly diminished. Menadiol stimulation of glucose oxidation is not inhibited in thyroid slices refractory to TSH. Thus, the effect of menadiol is subsequent to the block induced by TSH, whereas that of cholera toxin is proximal to it.

Adenylyl Cyclases↗
PubMed1981

The effect of tolbutamide and hepatic extraction of insulin and glucagon and hepatic glucose output in anesthetized dogs.

The effects of tolbutamide and insulin infusion on hepatic extraction of insulin and glucagon and on hepatic glucose output were compared in anesthetized dogs. The basal hepatic extraction of insulin was not significantly different in the two experiments (62 +/- 7% vs. 49 +/- 8%). The fraction of insulin extracted by the liver was not changed by either tolbutamide or insulin administration. In contrast, hepatic extraction of glucagon significantly increased from a basal value of 12 +/- 8% to 41 +/- 12% 30 min after tolbutamide, coincident with hypoglycemia and increased secretion of glucagon. The percent hepatic extraction of glucagon did not change during insulin infusion despite similar hypoglycemia and an even greater increase in the amount of glucagon reaching the liver. Tolbutamide and insulin produced a transient fall in hepatic glucose output which was associated with a significant increase in the insulin to glucagon molar ratio of the portal vein. Despite the persistence of hypoglycemia, hepatic glucose production returned to control values, and the portal venous insulin to glucagon molar ratio returned toward normal. Thus, the initial hypoglycemia after tolbutamide and insulin treatment reflects decreased hepatic glucose production, while the later effects represent increased peripheral glucose utilization. Hepatic glucose output correlated better with the portal venous insulin to glucagon molar ratio than the ratio of the hormones removed by the liver. These findings indicate that insulin and glucagon extraction by the liver are quite different and are independently regulated. Tolbutamide directly increases the fraction of glucagon removed by the liver. Because of changes in hepatic extraction after tolbutamide, increased pancreatic secretion of glucagon might not be reflected in its peripheral concentration.

Animals↗
PubMed1980

The effect of somatostatin on the hepatic extraction of insulin and glucagon in the anesthetized dog.

Effects of somatostatin (250 ng/kg . min) or saline infusion on hepatic extraction of endogenous and exogenous insulin and glucagon were investigated in anesthetized dogs. After a 20-min control period, somatostatin or saline was infused into the superior mesenteric vein for 100 min. During the final 50 min of the somatostatin or saline infusion, insulin (1.7 mU/kg . min) and glucagon (20 ng/kg . min) were also infused. These infusions were then replaced with a saline infusion for an additional 30 min. Somatostatin rapidly and significantly decreased portal vein insulin and glucagon concentrations. Hepatic extraction of endogenous insulin decreased from the control value of 61 +/- 5% to 29 +/- 10% during the final 20 min of somatostatin infusion before exogenous insulin and glucagon were added to the infusion. The decrease in hepatic extraction of endogenous insulin is based on the mean of the individual values of the eight dogs in the group and may be spurious because of the very low concentrations of insulin which were being measured and the fact that at such low concentrations, some dogs appeared to have negative hepatic extraction of inulin. Glucagon extraction was unchanged (9 +/- 6% compared to 7 +/- 12%) during the first 50 min of infusion of somatostatin. Column chromatography demonstrated that the 3500 mol wt fraction of glucagon comprised 75 +/- 4% of the total glucagon immunoreactivity in the portal vein during the control period and 67 +/- 13% during the infusion of somatostatin. During the final 20 min of somatostatin infusion before the addition of insulin and glucagon, the blood glucose significantly decreased and hepatic glucose output fell from 2.4 +/- 0.4 to 1.4 +/- 0.3 mg/kg . min. However, the insulin to glucagon (3500 mol wt fraction) molar ratio did not change significantly (4.2 +/- 1.1 to 2.6 +/- 0.5). During the final 20 min of the combined infusion of somatostatin, insulin, and glucagon, hepatic extraction of insulin returned to control values and glucagon extraction rose from 7 +/- 12% to 35 +/- 11%. Hepatic glucose output increased without any significant change in the portal vein insulin to glucagon molar ratio. After the termination of the combined infusion, hepatic extraction of insulin was unchanged, but glucagon removal returned to control values. At this time, the portal vein insulin to glucagon ratio rose, and hepatic production of glucose fell below control values. These results demonstrate that somatostatin may influence peripheral insulin and glucagon values by modifying their hepatic extraction and inhibiting their pancreatic secretion. Hepatic glucose output did not always reflect the portal vein insulin to glucagon molar ratio.

Anesthesia↗
PubMed1980

Time-action characteristics of regular and NPH insulin in insulin-treated diabetics.

The time course of action of regular and NPH insulins injected sc was studied in 15 insulin-treated diabetics over a 24-h period during which they received a constant infusion of glucose. The blood glucose began to decline in 1.2 +/- 0.1 h (range, 0.5--2) and reached its nadir in 5.7 +/- 0.3 h (range, 4--8) after the sc injection of regular insulin. The peak effect of regular insulin usually persisted for several hours, and the total duration of action was 16.2 +/- 1.1 h (range, 9--24). Both the time of peak effect and the total duration of action were considerably prolonged compared to data provided in standard textbooks. Free insulin increased to a peak in 2.7 +/- 0.3 h (range, 1--4) after regular insulin injection and then returned to baseline by 8.8 +/- 0.96 h. Subcutaneous injection of NPH insulin decreased the blood glucose by 2.4 +/- 0.5 h (range, 1--7), with a maximal effect at 11.0 +/- 1.4 h (range, 5--19). The total duration of effect on blood glucose was 25.1 +/- 0.7 h (range, 20--29). These values are similar to those in standard textbooks. Although the total insulin levels increased after the injection of NPH insulin, there was very little if any elevation in free insulin. Recognition of the prolonged effect of regular insulin is important in establishing an insulin treatment regime for diabetic patients.

Adolescent↗
PubMed1978

Hepatic insulin and glucagon extraction after their augmented secretion in dogs.

Effects of intravenous arginine and cholecystokinin-pancreozymin (CCK-PZ) infusion on hepatic extraction of insulin (EI) and glucagon (EGG) and also on hepatic glucose output (HGO) were studied in anesthetized dogs. Because insulin and glucagon exert antagonistic effects on HGO, insulin:glucagon (I/GG) molar ratios were determined in the portal vein and also in peripheral vessels. During the arginine-CCK-PZ infusion the amount of insulin and glucagon coming to the liver increased 12- and 15-fold, respectively. In contrast EI decreased significantly from a control value of 62 +/- 6% to a nadir of 22 +/- 13%. EGG (control value 19 +/- 9%), however, was unaffected by arginine-CCK-PZ. The absence of any alteration in EGG cannot be attributed to the molecular heterogeneity of the immunoreactive glucagon. HGO increased fourfold in response to the pancreatic stimulation, whereas portal I/GG decreased significantly from 8.2 +/- 0.9 to 5.0 +/- 0.7. The concurrent femoral arterial I/GG (control 3.7 +/- 1.0) and mesenteric venous I/GG (control 2.1 +/- 0.5) increased significantly. These observations indicate that portal, but not peripheral, I/GG measurements reflect hepatic events in anesthetized dogs, probably because of the different extraction patterns for insulin and glucagon.

Animals↗
PubMed1978

Effects of thyroid-stimulating hormone on human thyroid carcinoma and adjacent normal tissue.

Effects of TSH on the adenylate cyclase-cAMP system and some parameters of intermediary metabolism were investigated in human thyroid carcinoma and adjacent normal thyroid tissue. Basal adenylate cyclase activity and cAMP concentrations were significantly higher in carcinomatous tissue. Basal [1-14C]glucose oxidation, 32Pi incorporation into phospholipids, and organification of iodide were similar in both tissues. Stimulation of cAMP by TSH was significantly greater in normal compared to carcinomatous tissue. In neither tissue was there a good correlation between TSH stimulation of adenylate cyclase activity and cAMP concentrations. The TSH stimulation of 32Pi incorporation into phospholipids by TSH was significantly greater in normal tissue. The mean effect of TSH on iodide organification and glucose oxidation was similar in normal and carcinomatous tissue. Although specific binding of TSH was demonstrated in both normal and carcinomatous tissue, it did not correlate very well with stimulation of adenylate cyclase activity. Hormones other than TSH also augmented adenylate cyclase activity in two of the carcinomas. In individual patients, the relative responsivity of carcinomatous tissue compared to normal was not always consistent when all of the metabolic parameters were considered.

Adenylyl Cyclases↗
PubMedDate not supplied

O2-Hb reaction kinetics and the Fåhraeus effect during stagnant, hypoxic, and anemic supply deficit.

We modified our previous computer model of O2 and CO2 transport in the cerebral microcirculation to include nonequilibrium O2-Hb kinetics and the Fåhraeus effect (reduced tube hematocrit in small microvessels). The model is a steady-state multicompartmental simulation which includes three arteriolar compartments, three venular compartments, and one capillary compartment. Three different types of oxygen deficits (stagnant, hypoxic, and anemic conditions) were simulated by respectively reducing blood flow, arterial O2 saturation, and systemic hematocrit to one half of normal. Microcirculatory distributions for PO2, PCO2, O2 saturation and deviations from equilibrium, and the O2 and CO2 fluxes for each compartment were predicted for the three O2 supply deficits. Differences were found for O2 extraction ratios and relative contributions of arteriolar, venular, and capillary gas fluxes for each type of deficit. The Fåhraeus effect and O2-Hb kinetics reduced O2 extraction in all cases and altered microcirculatory gas distributions depending on the specific type of O2 supply deficits. The modified model continues to predict that capillaries are the major site where gas exchange takes place, and demonstrates that the Fåhraeus effect and nonequilibrium O2-Hb kinetics are important mechanisms that should not be neglected in O2 and CO2 transport modeling. While this model provides useful insight regarding the influence of the Fahraeus effect and O2-Hb kinetics under steady state, the addition of a distributed and dynamic simulation should further elucidate the effects of the brain's heterogeneous properties and transient behavior.

Algorithms↗
PubMedDate not supplied

Whole body 18F-2-deoxyglucose positron emission tomography to restage non-small cell lung cancer.

The helpfulness of 18F-2-deoxyglucose positron emission tomography (FDG-PET) in restaging non-small cell lung cancer (NSCLC) has not been extensively evaluated. A total of 156 patients referred for restaging of NSCLC were retrospectively evaluated. According to the classification of American Joint Committee on Cancer, stages I and II were defined as conventionally resectable, stage IIIA as locally advanced but resectable, stage IIIB as locally advanced but unresectable, and stage IV as absolutely unresectable. Compared to initial staging by chest computed tomographic findings, FDG-PET down-staged 45/156 (29%) and up-staged 52/156 (33%) NSCLCs. In addition, 37/156 (23%) patients were reclassified from resectable to unresectable and 22/156 (14%) patients were reclassified from unresectable to resectable. Our results prove the helpfulness of whole body FDG-PET for restaging NSCLC.

Biopsy↗