PubMed Health⌕ Search

Biomedical subjects

B Chang

Publications and source records attributed to B Chang.

At least 181 records · Page 10Linked to original sources
PubMed1987

Effect of delta-9-tetrahydrocannabinol on the in vitro uptake of alpha-amino isobutyric acid by term human placental slices.

Tetrahydrocannabinol (THC), the active component in marijuana smoke, crosses the placenta and is a potential fetotoxic agent. In both human and animal studies, the most consistent fetal effect of THC is intrauterine growth retardation. Since fetal somatic growth is dependent on placental transfer of nutrients, including essential amino acids, we studied the effect of THC upon the in vitro uptake of amino acid by term human placental slices. Uptake of alpha-amino isobutyric acid was inhibited in a dose-dependent fashion, correlating with the log of the dose (1-100 microM THC; r = 0.945; p less than 0.01). Compared to control tissue, significant impairment of alpha-amino isobutyric acid uptake began at 20 microM THC. Similar results were found for valine. The time course (30-120 min) for alpha-amino isobutyric acid uptake showed linearity for both control and THC-(50 microM) treated tissue, but there was a marked reduction in the THC slope. Uptake of alpha-amino isobutyric acid was significantly reduced at all times. The sustained effect of THC was slightly, but significantly, reversed by removal of THC from the medium after 90 min of 50 microM THC exposure. Only partial reversal may have been due to the 15- to 20-fold accumulation of THC in the placental tissue. Uptake kinetics showed noncompetitive inhibition with decreased Vmax: control Vmax = 51.66 +/- 6.26 versus 50 microM THC = 26.96 +/- 6.22 (mmol/liter intracellular water per h) (p less than 0.01); and no change in diffusion constant (Km): control Km = 0.78 +/- 0.08 versus 50 microM THC = 0.80 +/- 0.09 (mM).(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoisobutyric Acids↗
PubMed1986

Tumor uptake of 5-fluorouracil, methotrexate, and adriamycin vs gallium.

Since the imaging pattern of 67Ga-citrate is well known, it can be the benchmark for evaluation of potential tumor imaging agents. Tritium labeled 5-fluorouracil, Adriamycin, (doxorubicin/Adria) and Methotrexate/Lederle were compared at 2 h to 67Ga-citrate at 2 and 48 h by percent uptake per gram of various tissues and tumor in rats implanted with Walker 256 carcinosarcoma. 67Ga at 48 h showed approximately three times more uptake in the tumor than 5 fluorouracil and eight times more than the others. 5 Fluorouracil showed approximately three times greater uptake than Methotrexate or doxorubicin and 1.4 times the 2 h uptake of 67Ga. 5 Fluorouracil shows potential as an imaging agent especially where the waiting time between injection and imaging must be short.

Animals↗
PubMed1985

Ethanol and fetal nutrition: effect of chronic ethanol exposure on rat placental growth and membrane-associated folic acid receptor binding activity.

Rat placental composition and specific folate receptor activity were measured at 20 days gestation in dams exposed to chronic high doses of ethanol (6%, vol/vol) throughout gestation and in isocalorically pair-fed controls. Ethanol-exposed fetuses were smaller (ethanol = 3.28 +/- 0.08 vs. control = 4.01 +/- 0.10 g, p less than 0.001), but their placentae were larger (experimental = 0.534 +/- 0.02 vs. control = 0.399 +/- 0.01 g, p less than 0.001). The increased weight appears to be secondary to hyperplasia as total DNA was increased while the wet/dry, RNA/DNA, and protein/DNA ratios were not different. Despite larger placentae, specific folate receptor activity was significantly reduced in the ethanol-exposed tissue, whether expressed relative to membrane protein, placental weight, or total placental binding. These results confirm that ethanol exposure is placentotoxic and suggest an additional mechanism by which ethanol may lead to intrauterine growth retardation; namely, decreased folate receptor activity.

Animals↗
PubMed1982

Inhibition of Escherichia coli heat-stable enterotoxin effects on intestinal guanylate cyclase and fluid secretion by quinacrine.

Enterotoxigenic Escherichia coli may produce a heat-stable enterotoxin (ST) that causes diarrheal disease in humans and in animals ST activates particulate guanylate cyclase in intestinal mucosal cells and causes intestinal fluid secretion. In this study, we examined the effects of quinacrine on ST activation of guanylate cyclase and ST-mediated intestinal fluid secretion. Quinacrine significantly reduced ST activation of particulate guanylate cyclase in rat intestinal tissue. Additionally, quinacrine reduced ST-mediated fluid secretion in a rat intestinal loop assay (P less than 0.05). In the suckling mouse model, subcutaneous quinacrine (0.1 mumole/mouse) reduced ST-induced fluid secretion at a submaximally effective dose of the toxin, but it did not reduce ST-mediated fluid secretion at a near maximally effective dose. Quinacrine (0.1 mumole/mouse) did not significantly reduce intestinal fluid secretion induced by the analog of cyclic GMP, 8-bromo cyclic GMP. However, at a higher concentration of quinacrine (1 mumole/mouse), significant inhibition of 8-bromo cyclic GMP-induced secretion was observed. Inhibition by the antimalarial agent quinacrine of ST-induced fluid secretion, by a block prior to guanylate cyclase activation, suggests a possible role for a phospholipase early in the sequence of events of ST activation of guanylate cyclase. The results suggest that ST may activate membrane phospholipases prior to ST activation of guanylate cyclase.

Animals↗
PubMed1982

Radiation therapy before cystectomy in the management of patients with bladder cancer.

During the preceding two decades, 309 patients with bladder cancer were treated by irradiation before cystectomy at the Memorial Sloan-Kettering Cancer Center. A radical tumour dose averaging 6000 cGy (rad) in six weeks was given to 104 patients who underwent radical cystectomy +/- one year later for persistent or recurrent cancer. Pre-operative pelvic irradiation was planned in 205 patients who received either 4000 cGy in four weeks (119) or 2000 cGy in one week (86) and underwent radical cystectomy after +/- six weeks and two days, respectively. The determinate five-year survival rates (41-43%) were similar with the three irradiation regimes; mortality under five years was mainly due to cancer recurrence locally and/or distally. Incidence of recurrence with radiation-induced stage reduction (21%) was lower, especially within the pelvis, than with no stage reduction (51%). Treatment results with planned pre-operative irradiation, especially in high stage tumours, were more favourable with the shorter 2000 cGy regimen of high fractional doses than with the conventionally fractionated 4000 cGy regimen.

Adult↗
PubMed1982

The mineralocorticoid hormone pathways in hypertension with hyperaldosteronism.

Simultaneous measurement of the 0800-hr plasma concentrations of deoxycorticosterone (DOC), corticosterone (B), 18-hydroxycorticosterone (18-OHB), aldosterone, 18-hydroxydeoxycorticosterone (18-OHDOC) and cortisol (F) in four types of primary aldosteronism provides evidence for primary adrenal disease. Elevated DOC with normal F concentrations in the presence of elevated 18-OHB and aldosterone, and suppressed renin concentration suggests a primary adrenal abnormality of the zona glomerulosa (ZG). Steroid production by the zona fasciculata (ZF), F, 18-OHDOC, and most often B, is normal. These patterns exist only for primary adrenal hyperplasia, aldosterone-producing adenoma (APA), and aldosterone-producing adrenocortical carcinoma (AP-Ca). Elevated DOC levels are rarely found in patients with idiopathic hyperaldosteronism (IHA or adrenal hyperplasia) and suggest that IHA is not a primary adrenal disorder and should be excluded from the syndrome of primary aldosteronism as they have been heretofore.

18-Hydroxydesoxycorticosterone↗
PubMed1982

Regulation of the mineralocorticoid hormones in adrenocortical disorders with adrenocorticotropin excess.

Chronic stimulation by adrenocorticotropin (ACTH) of the adrenal cortex produces different plasma mineralocorticoid hormone (MCH) patterns, depending on the amount of glucocorticoid hormones (cortisol) concurrently generated and the degree of activation of the renin angiotensin system (RAS). Patients with Cushing's disease or the ectopic ACTH-excess syndrome have normal or low production of the MCHs, aldosterone and 18-hydroxycorticosterone (18-OHB), by the zona glomerulosa (ZG), elevated cortisol and deoxycorticosterone (DOC) levels, and high-normal to elevated production of the MCHs corticosterone (B) and 18-hydroxydeoxycorticosterone (18-OHDOC) by the zona fasciculata (ZF). Prolonged administration of superphysiologic doses of ACTH to normal subjects yields similar patterns. Patients with simple virilizing 21-hydroxylase deficiency (21-OHD) have impaired ZF production of B and 18-OHDOC and elevated DOC, 18-OHB, and aldosterone secretion secondary to the superimposed RAS stimulation of the ZG. Patients with 17 alpha-hydroxylase deficiency (17 alpha-OHD) have elevated levels of the ZF MCHs DOC, B, 18-OHDOC, and 18-OHB and a functionally suppressed ZG. Patients with 11 beta-hydroxylase deficiency (11 beta-OHD) have only elevated production of DOC by the ZF and suppressed RAS and aldosterone. A significant negative correlation between cortisol and aldosterone concentrations suggests that cortisol is involved in the ACTH-mediated inhibition of aldosterone formation.

18-Hydroxydesoxycorticosterone↗
PubMed1980

Activation of intestinal guanylate cyclase by heat-stable enterotoxin of Escherichia coli: studies of tissue specificity, potential receptors, and intermediates.

Heat-stable enterotoxin (ST) of Escherichia coli increased guanylate cyclase activity in homogenates of rat and rabbit intestinal mucosa and stimulated intestinal fluid secretion in suckling mice. The ST effect on guanylate cyclase was dose-dependent, occurred without a time lag, and was confined to the particulate fraction. ST activation of guanylate cyclase was tissue-specific; ST did not alter activity of soluble or particulate rat liver, lung, heart, kidney, or cerebral cortex enzyme. The ST activity on guanylate cyclase and secretion was methanol-soluble and alkali-labile, and its effects were not altered by phentolamine, propranolol, or atropine. Monosialoganglioside did not reduce ST-induced secretion. However, indomethacin and butylated hydroxyanisole decreased the ST effect on both guanylate cyclase and secretion. Fluid secretion with ST sppears to result from specific activation of particulate intestinal guanylate cyclase. While adrenergic and cholinergic events are probably not involved in this process, the effects of ST may be mediated through prostaglandin synthesis or oxidative mechnanisms.

Alkalies↗
PubMed1980

Inhibition of Escherichia coli heat-stable enterotoxin by indomethacin and chlorpromazine.

Purified heat-stable enterotoxin (ST) from a procine strain of enterotoxigenic Escherichia coli activates quanylate cyclase in particulate fractions of rat intestinal tissue and induces fluid accumulation in suckling mice. These effects of ST were examined in the presence of either indomethacin or chlorpromazine. We also examined the effects of these two drugs on fluid accumulation in suckling mice induced by the 8-bromo analog of cyclic guanosine monophosphate. Either indomethacin or chlorpromazine reduced ST activation of guanylate cyclase. Both drugs also reduced intestinal fluid accumulation in suckling mice that resulted from submaximal doses of ST (both P < 0.001). However, there was no reduction in fluid secretion by either drug when a maximally effective dose of ST was used, suggesting that inhibition of fluid secretion by both drugs can be overcome by increasing the ST dose and that a threshold level of guanylate cyclase activity results in maximal secretory response. Both drugs also reduced basal guanylate cylase activity in rat intestinal tissue and fluid secreton in suckling mice. Chlorpromazine also reduced intestinal secretion mediated by 8-bromo cyclic guanosine monophosphate (P < 0.001). These findings indicate that chlorpromazine interferes with the effects of ST both before and after its activation of guanylate cyclase, whereas indomethacin interfers with ST only before its activation of guanylate cyclase.

Animals↗
PubMed1980

Clinical manifestation of adrenocorticotropin-determined plasma concentrations of mineralocorticoid hormones.

Chronic oversecretion of adrenocorticotropin (ACTH) in Cushing's disease and partial adrenal insufficiency results in a plasma pattern of mineralocorticoid hormones (MCHs) in which deoxycorticosterone, 18-hydroxycorticosterone and aldosterone remain within normal limits. In patients with deficiencies of 17 alpha- and 21-hydroxylation, the entire MCH pathway may be initially stimulated by ACTH alone in the presence of reduced cortisol production. An ACTH-induced intra-adrenal factor reflected by levels of cortisol production, or cortisol itself, may determine MCH levels by its inhibition (high) or lack of inhibition (low) of 11 beta- and 18-hydroxylation.

Adenoma↗
PubMed1979

Adrenocorticotropin inhibition of mineralocorticoid hormone production.

1. Adrenocorticotropin (ACTH)-induced steroidogenesis, obtained by continuous administration of ACTH for 3 days, produces in man (a) sustained elevations of plasma deoxycorticosterone and cortisol concentrations, (b) transient elevations of plasma aldosterone and 18-hydroxycorticosterone concentrations that return to near-control values, and (c) brisk initial increases in plasma 18-hydroxydeoxycorticosterone and corticosterone concentrations that fall to 20-68% of peak values 30 h thereafter. 2. Dexamethasone (8 mg/day, orally) treatment for 2 days in man permits a greater postural increase in plasma aldosterone and 18-hydroxycortisone concentrations. A dampening effect of ACTH is suggested. 3. An ACTH-initiated inhibition of 11 beta- and 18-hydroxylation is proposed to be operative in regulation of mineralocorticoid hormones.

18-Hydroxycorticosterone↗
PubMed1979

Transient traumatic "locked-in" syndrome.

The first clinical case of transient traumatic locked-in syndrome is presented. The locked-in state lasted for 3 months. The patient's neurologic deficit and the abnormal auditory evoked responses pointed to a lesion involving the left pons and ventral midbrain. The locked-in syndrome caused by a traumatic damage of the brain stem structures can be transient and thus it may have a better prognosis than the locked-in syndrome secondary to the occlusion of the basilar artery.

Accidents, Traffic↗