Search PubMed⌕ Search

Biomedical subjects

K H Yang

Publications and source records attributed to K H Yang.

At least 145 records · Page 8Linked to original sources

Renal abnormalities in schoolchildren.

To establish prevalence of some renal abnormalities in schoolchildren, an epidemiologic study of 132,686 schoolchildren, including 69,903 boys and 62,783 girls, was conducted from March 1987 to May 1988 in the city of Taipei. At the health station of each school, the students were screened quickly by a physician with portable real-time ultrasound equipment. When a renal abnormality was detected or suspected, the examinee was referred to Taipei Municipal Women and Children's Hospital for further investigation. Radiologic and urologic procedures were then selectively performed to establish the correct diagnosis. Renal abnormalities were detected in 645 students (approximately 0.5% of total population screened). There were 256 cases of hydronephrosis, 103 cases of unilateral renal agenesis, 128 cases of unilateral small kidney, 90 cases of renal cystic disorders, 30 cases of ectopic kidney, and 38 cases of other abnormalities. Surgically correctable lesions were demonstrated in 50 of these students. Rapid renal ultrasonography was found to effectively detect some renal abnormalities initially, and prevalence could then be established after further investigations.

Adolescent↗

Role of the transfer of metabolites from hepatocytes to splenocytes in the suppression of in vitro antibody response by dimethylnitrosamine.

The metabolism and subsequent immunosuppressive effects of dimethylnitrosamine (DMN) were investigated in mixed cultures of mouse hepatocytes and mouse splenocytes. Hepatocytes were shown to activate DMN to an immunosuppressive form that caused the suppression of the in vitro antibody response to the T-dependent antigen, sheep erythrocytes (SRBC). A significant increase in the binding of DMN metabolites to trichloroacetic acid (TCA) precipitable material in splenocytes was induced when 94 microM [14C-methyl]DMN was added to the co-culture medium, indicating that reactive intermediates of DMN were transferred from hepatocytes to splenocytes and resulted in alkylation of macromolecules in splenocytes. The amount of [14C]DMN bound to TCA precipitable material in splenocytes increased in a time-dependent manner up to 4 hr of incubation. Aminoacetonitrile (AAN), a high-affinity DMN demethylase inhibitor, reversed the suppression by low concentrations of DMN (0.5 to 5 mM), but not by high concentrations of DMN (greater than 5 mM). AAN also inhibited the binding of [14C]DMN to both hepatocytes and splenocytes. These results suggest that reactive metabolites of DMN are released from hepatocytes and that the suppression of the antibody response by DMN is mediated via these reactive intermediates.

Alkylation↗

The subunit composition of Portunus trituberculatus hemocyanin polymers.

The subunit composition of isolated polymeric forms of Portunus trituberculatus hemocyanin were analysed by immunological techniques. The dodecamers contain four monomeric subunits corresponding to subunits I, II, III and IV, whereas the hexamers are devoid of subunit IV. These results suggest that subunit IV is required as a joining piece for the assembly of dodecamers.

Animals↗

Presence of hexobarbital in primary cultures of rat hepatocytes maintains cytochrome P-450 levels and drug metabolizing enzyme activities.

Addition of hexobarbital (1 mM) to the culture medium of rat hepatocytes protected against the rapid decline in the level of cytochrome P-450 and the activities of various drug metabolizing enzymes. While the hepatocytes cultured for 72 hr without hexobarbital had only 30% of their original level of cytochrome P-450, the cells maintained with hexobarbital had 75% of the initial level of the hemoprotein. After 72 hr in culture, the activities of aminopyrine N-demethylase and biphenyl 4-hydroxylase were 22-24% of the original rate for the nontreated cells and 73-78% for the hexobarbital treated cells. The activities of 7-ethoxycoumarin O-deethylase and aryl hydrocarbon hydroxylase in the cultures of treated cells were even higher than those of the freshly isolated hepatocytes. Additions of other substrates of hepatic mixed function oxidase to the culture medium did not protect against the loss of cytochrome P-450 and enzyme activities.

1-Butanol↗

Suppression of in vitro antibody production by dimethylnitrosamine in mixed cultures of mouse primary hepatocytes and mouse splenocytes.

The suppression of in vitro antibody responses by dimethylnitrosamine (DMN) was produced in a mouse hepatocyte and splenocyte co-culture system. Mouse hepatocytes were isolated from female B6C3F1 mice and cultured for 20-24 hr to allow the formation of a monolayer on collagen-coated plastic petri dishes. Spleen cells were isolated from the same hybrid and were co-cultured with the hepatocytes along with DMN. Cyclophosphamide (CP), an immunosuppressive agent requiring metabolic activation that was included as an initial positive control, produced a marked suppression of the in vitro antibody responses to LPS, DNP-Ficoll, and SRBCs in 4 hr in the co-culture system. Under comparable conditions DMN markedly suppressed the response to SRBCs, marginally suppressed the response to DNP-Ficoll, and did not suppress the polyclonal response to LPS. The suppression by DMN was related to the rocking speed during the 4-hr co-culture period and was optimally produced when the cultures were not rocked. Addition of serum into the medium (10% fetal calf serum) during the co-culture period did not change the effects of DMN on the antibody response. However, the addition of extracellular DNA (1 mg calf thymus DNA/ml) prevented the suppression of the antibody response by DMN. These results suggest that DNA represents the primary macromolecular target for the reactive intermediate of DMN, and indicate that a syngeneic co-culture system can be used to characterize the in vitro immunosuppression

Animals↗

Immunosuppression induced by chemicals requiring metabolic activation in mixed cultures of rat hepatocytes and murine splenocytes.

Primary cultures of adult rat hepatocytes (Fischer 344) were used as an in vitro metabolic activation system in immunotoxicological assays. Rat hepatocytes were isolated by a collagenase perfusion technique and cultured for 20 to 24 hr to allow the formation of a monolayer on collagen-coated plastic petri dishes. Spleen cells isolated from (C57BL/6 X C3H)F1 mice were cocultured with the hepatocytes along with the chemicals. Cyclophosphamide (CP) and Aflatoxin B1 (AFB1) were effectively activated in this coculture system and produced a dose-related suppression of the in vitro antibody responses to LPS, DNP-Ficoll, and SRBC in 3 hr. Neither CP (1 mM) nor AFB1 (10(-4) M) cultured with spleen cells alone produced any effects. Both CP and AFB1 also produced a dose-related suppression of the proliferative responses to LPS, Con A, and PHA. In contrast, up to 100 mM of N-nitrosodimethylamine (DMN) did not suppress any of these assays after a 3-hr incubation in the coculture system. These results indicate that a coculture system can be used to characterize the activity of immunosuppressive chemicals requiring metabolic activation.

Aflatoxin B1↗

Detection of DNA single-strand breaks induced by procarcinogens in Chinese hamster ovary cells cocultured with rat hepatocytes.

DNA single-strand breaks induced by procarcinogens were detected in Chinese hamster ovary (CHO) cells cocultured with adult rat hepatocytes. Freshly isolated adult rat hepatocytes were added to the CHO cell culture prelabeled with [3H]thymidine. After allowing the hepatocytes to attach on or near the CHO cells, aflatoxin B1 or benzo[a]pyrene was added to the culture and incubated for the desired time. DNA single-strand breaks in CHO cells were measured by the alkaline elution technique. Aflatoxin B1 induced some DNA single-strand breaks in CHO cells cultured alone, but in coculture system with hepatocytes the number of DNA single-strand breaks increased greatly. The magnitude of the increase was related to the dose and the time of exposure to aflatoxin B1. Addition of proteinase-K to the cell lysates increased the elution of DNA compared to that of samples without proteinase-K. Benzo[a]pyrene did not induce any DNA single-strand breaks in CHO cells in the absence of liver cells, but a significant number of single-strand breaks were detected in the coculture system.

Aflatoxin B1↗

Mechanism of facet load transmission as a hypothesis for low-back pain.

Low-back pain has a complex and multi-faceted etiology. The articular facets have been shown to be load-bearing structures and may be a site for low-back pain. The aim of this paper is to establish the mechanism for the transmission of axial load across a facet joint and to propose a facet-related hypothesis for low-back pain. The mechanism of load transmission was studied by two methods. Lumbar segments were instrumented with an intervertebral load cell (IVLC) to measure disc load so that facet load could be deduced. The applied load was moved 10 mm anteriorly and 12.5 mm posteriorly from the center of the vertebral body. The facets then were separated from the body and loaded axially to determine their stiffness in tension and compression and to observe the failure mode of the joint. It was shown optically that compressive loading of the isolated facet joints was equivalent to spinal extension and tensile loading to spinal flexion. Lastly, a finite element model of a lumbar motion segment was developed to simulate the transmission of facet load and to study the effects of disc degeneration on facet loads. Results of the study on six lumbar segments revealed that the normal facets carried 3-25%. If the facet joint was arthritic, the load could be as high as 47%. Experiments on isolated facet joints revealed that they behaved as a stiffening spring in compression and were weak in tension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effects of butylated hydroxytoluene (BHT) on biliary excretion of xenobiotics and bile flow in rats.

A significant enhancement in the biliary excretion of iv injected sulfobromophthalein (BSP), phenol- 3,6 -dibromphthalein disulfonate (DBSP), procaine amide ethobromide (PAEB) and ouabain was observed in rats maintained on diets containing 0.25% BHT for periods of 10 days. The enhanced biliary excretion of these drugs in BHT treated rats appears to be correlated with the increase in bile flow produced by BHT. The increased bile flow was due to an increase in canalicular bile production rather than a change in net ductular secretion or reabsorption of fluid since bile to plasma concentration ratios of erythritol were unchanged and no permeability change in the biliary tree was observed when mannitol was administered by retrograde intrabiliary injection. The increase in bile flow was not due to an enhanced excretion of bile salts into bile, because both the biliary bile acid concentration and total biliary excretion of bile acids were lower in BHT-treated rats than in control rats. It appears that the increase in bile flow produced by BHT is due to the osmotic choleresis related to the secretion of BHT and its metabolites into bile.

Animals↗

Effects of halogenated dibenzo-p-dioxins on plasma disappearance and biliary excretion of ouabain in rats.

A single dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,7-tribromodibenzo-p-dioxin (2,3,7-TBDD), 1,2,3,7,8,9-hexachlorodibenzo-p-dioxin (1,2,3,7,8,9-HCDD), 1,2,4,6,7,9-hexachlorodibenzo-p-dioxin (1,2,4,6,7,9-HCDD), or 1,3,6,8-tetrachlorodibenzo-p-dioxin (1,3,6,8-TCDD) was given to male rats (25 micrograms/kg, p.o.) and plasma concentration and biliary excretion of ouabain assessed 10 days later. Treatment of TCDD, 2,3,7-TBDD and to a lesser extent 1,2,3,7,8,9-HCDD increased the plasma concentration of ouabain and decreased its excretion into ouabain. TCDD, 2,3,7-TBDD and to a lesser extent, 1,2,3,7,8,9-HCDD decreased the bile flow. Liver wet weight was increased in TCDD and 2,3,7-TBDD treated rats. The magnitude of depression in ouabain excretion by those compounds was closely related to the reported relative binding affinity of the compound to liver cytosol and their induction potency of aryl hydrocarbon hydroxylase activity.

Animals↗