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At least 1,063 records · Page 59Linked to original sources
PubMed1989

Acute effects of low-dose cranial irradiation on regional capillary permeability in experimental brain tumors.

To determine the acute effects of low-dose cranial irradiation (CRT) on regional capillary permeability (RCP) of normal brain, brain tumor and damaged brain surrounding the tumor, we used quantitative autoradiography (QAR) to measure regional blood-to-tissue transport (K) of [14C]aminoisobutyric acid (AIB) in experimental C6 brain tumors 3-4 h after a single dose of 3 Gy CRT. K increased 63% in cortex, 30% in basal ganglia and 31% in brain surrounding the tumor (BST) vs. controls (P less than 0.005). K did not change in the tumor or in the brain adjacent to the tumor (BAT), suggesting that capillaries of normal parenchyma are more sensitive to the acute effects of CRT than capillaries of damaged parenchyma or tumor.

Aminoisobutyric Acids↗
PubMed1989

Comparison of uptake kinetics in freshly isolated suspensions and short-term primary cultures of rat hepatocytes.

The apparent kinetics of uptake of various model substrates were examined for hepatocytes in suspension and primary culture up to 72 h. The ability of hepatocytes to take up taurocholate and ouabain was decreased in culture. Vmax for uptake of both substrates diminished rapidly with increasing time in culture. An increase in Km was observed in cultures 6 h after plating, but there was no further change with prolongation of culture time. The decrease of uptake of taurocholate and ouabain during culture may be due to the reduction in the number of transport carriers plus a decrease of affinity of the carrier to substrates. The nonsaturable component of cadmium uptake was much reduced in cultured cells compared with the suspensions. The saturable process was lower in 6 h culture but increased to a level comparable with the fresh cells at longer culture time. No significant change was found in the Km between suspensions and cultures. Uptake of alpha-aminoisobutyric acid was greater in culture while that of 3-O-methyl-D-glucose was relatively stable but about one-half that found in cell suspension. Thus, uptake of two substrates, taurocholate and ouabain, is clearly compromised with increasing time in primary culture, while uptake of the other substrates does not reflect such a dramatic decrease. It is therefore apparent that the cell preparation of choice in uptake studies depends on the substrate and the nature of the experiments.

2,4-Dinitrophenol↗
PubMed1973

Metabolic effects of plasmin digests of human growth hormone in the rat and man.

As a first step in our study of structure-function relationships among primate and non-primate growth hormones, human growth hormone (hGH) was subjected to the limited digestive activity of human plasmin. The lyophilized whole digest, containing less than 2% of unchanged hormone, had an average of 2.3 new amino-terminal groups per mole. The digest had the same potency as the native hormone (a) in causing weight gain in hypophysectomized rats; (b) in stimulating somatomedin production in hypophysectomized rats; (c) in stimulating upake of [(3)H]leucine into isolated diaphragm of hypophysectomized rats; (d) in accelerating transport of [(14)C]alpha-aminoisobutyric acid into isolated diaphragm of hypophysectomized rats; (e) in stimulating uptake of [3-0-methyl-(14)C]glucose by isolated adipose tissue of hypophysectomized rats; (f) in accelerating conversion of [(14)C]glucose to (14)CO(2) by isolated epididymal adipose tissue of hypophysectomized rats. The digest also caused glucosuria in partially pancreatectomized rats treated with dexamethasone. These metabolic actions of plasmin-digested hGH in the array of animal tests were confirmed by comparable effects elicited in 11 human subjects (nine pituitary-deficient children and adolescents and two nondeficient adults). A single injection of the plasmin digest caused an increase in plasma free fatty acids and a fall in plasma amino acids. Seven daily injections caused positive balances of nitrogen, phosphorous, sodium, and potassium, gain in body weight, and in two of three subjects impairment of glucose tolerance. The potency of the plasmin digest in producing these metabolic effects in man was comparable to that of native hGH.Thus, 2-3 bonds in the hGH molecule can be cleaved by plasmin without impairing the hormone's growthpromoting, anabolic, diabetogenic, and adipokinetic actions for rat and man.

Adipose Tissue↗
PubMed1989

Insulin receptor monoclonal antibodies that mimic insulin action without activating tyrosine kinase.

HTC rat hepatoma cells were transfected with human insulin receptor cDNA to a level of 40,000 receptors/cell. In these cells, as well as in nontransfected cells, insulin stimulated the uptake of alpha-aminoisobutyric acid. Two monoclonal antibodies directed against the human insulin receptor alpha subunit, like insulin, stimulated amino acid uptake in transfected HTC cells, but not in nontransfected HTC cells. The antibodies, in contrast to insulin, failed to stimulate insulin receptor tyrosine kinase activity, both in intact transfected cells and in cell free extracts prepared from them. These data suggest, therefore, that activation of insulin receptor tyrosine kinase may not be an obligatory step in all of the transmembrane signaling mechanisms of the insulin receptor.

Aminoisobutyric Acids↗
PubMed1990

Model for drug uptake by brain tumors: effects of osmotic treatment and of diffusion in brain.

A mathematical model describing drug uptake into brain tumors, directly from blood and indirectly from neighboring tissue, is presented. The model quantitatively describes uptake into tumor, brain surrounding tumor (BST), and normal brain and uptake following reversible osmotic blood-brain barrier (BBB) and blood-tumor barrier disruption. It employs published data on the time course for reclosure of the BBB following osmotic treatment and on the brain and tumor uptake of [14C]alpha-aminoisobutyric acid by Walker 256 carcinomas and C6 gliomas implanted into the rat brain. Constant infusion and bolus injection infusion schedules are considered. In untreated brain, the BST acts as a sink, reducing the integrated exposure of the adjacent tumor to the drug, whereas following osmotic treatment, tumor exposure to drug is enhanced, not only by increased delivery from blood but also by diffusion (and bulk flow) from neighboring brain. The model provides a quantitative framework for examining the efficacy of osmotic treatment to enhance chemotherapy of brain tumors.

Aminoisobutyric Acids↗
PubMed1997

Long-term effect of norepinephrine on iodide uptake in FRTL-5 cells.

The sympathetic nervous system plays a role in the regulation of thyroid function. In FRTL-5 rat thyroid cells, norepinephrine (NE) acutely depresses intracellular I- by increasing I- efflux. The present study was undertaken to determine the effect of NE on iodide transport after a longer time period. NE inhibited the ability of thyrotropin (TSH) to induce iodide uptake by FRTL-5 cells after 48 or 72 hours, but not after 24 hours. The effect of NE was more evident with increasing concentrations of TSH. NE did not modify the rate of I- efflux. Inhibition was associated with a decrease in the Vmax and no change in the Km for iodide influx. To determine if this was a generalized effect of NE on thyroid cell membrane, the uptake of alpha-aminoisobutyric acid (a nonmetabolizable aminoacid) and of 2-deoxyglucose was measured. NE did not inhibit TSH stimulation of the uptake of the two compounds. NE inhibited the action of dibutyryl cAMP (dbcAMP) on iodide uptake in a similar manner to TSH, but did not alter the cyclic adenosine monophosphate (cAMP) levels increased by TSH. The effects of different adrenoreceptor agonists and antagonists demonstrated that norepinephrine acts through an alpha1-adrenergic receptor.

Adrenergic alpha-Agonists↗
PubMed1999

Maternal epidermal growth factor deficiency causes fetal hypoglycemia and intrauterine growth retardation in mice: possible involvement of placental glucose transporter GLUT3 expression.

We investigated the physiological role of epidermal growth factor (EGF) in fetal growth in mice in which midgestational sialoadenectomy induced maternal EGF deficiency. Sialoadenectomy decreased the fetal weight significantly, indicating that maternal EGF deficiency caused intrauterine growth retardation. The weight of the fetal liver in the sialoadenectomized mice was reduced in proportion to the decrease in body weight (82.7+/-10.2 vs. 70.9+/-10.9 mg), whereas the brain weight was not reduced. Sialoadenectomy significantly decreased the glucose concentration in fetal plasma (86.0+/-13.0 vs. 63.0+/-11.8 mg/dl) without affecting the maternal plasma level of glucose. Transplacental transfer of 3H-2-deoxyglucose was significantly decreased by sialoadenectomy (5.17+/-1.25 vs. 2.94+/-1.02%), but transfer of 14C-aminoisobutyric acid was not affected. Northern blot analysis and in situ hybridization of glucose transporter isoform GLUT1 and GLUT3 messenger RNAs (mRNAs) in placenta revealed that sialoadenectomy significantly reduced the expression of GLUT3 mRNA without affecting GLUT1 mRNA levels. Administration of anti-EGF antiserum enhanced the effects of EGF deficiency, which were almost completely corrected by EGF supplementation. These results indicate that EGF plays an important role in fetal growth by regulating the transplacental supply of glucose via GLUT3 expression in the placenta.

Aminoisobutyric Acids↗
PubMed1998

Influence of hypoglycemic coma on brain water and osmolality.

To study the effects of pronounced hypoglycemia on brain osmolality and brain edema formation, fasted rats were rendered hypoglycemic by injection of insulin, and subjected to 30 min of hypoglycemic coma. Recovery was accomplished by glucose administration. The change in water content in different brain regions was measured as a change in specific gravity after 30 min of hypoglycemic coma, or 30, 60, and 180 min after glucose administration. Plasma and brain tissue osmolality were measured in separate animals. The results show a significant decrease in specific gravity (increase in water content) in all structures measured (caudoputamen, neocortex, hippocampus, and cerebellum) at the end of the period of coma, as well as after 30 min and 60 min of recovery. At 180 min of recovery, brain water was normalized. The edema affected all structures to the same degree regardless of their vulnerability to hypoglycemic damage. Brain tissue osmolality showed a tendency to decrease with decreasing tissue glucose content. The decrease was significant (P<0.01) at 30 min of isoelectric coma. In the recovery phase, normal brain osmolality was restored within 30 min. Measurements of blood-brain barrier (BBB) permeability after 30 min of hypoglycemic coma showed no extravasation of Evan's blue, though a small but significant increase in the permeability for aminoisobutyric acid (AIB) in caudoputamen and in cerebellum was found. To analyze the importance of tissue acidosis for formation of edema, hypoglycemic animals were made acidotic by increasing the CO2 concentration in inspired air to produce an arterial plasma pH of 6.8-6.9. In these animals the edema was of a similar degree to the normocapnic animals, and the permeability for AIB was normal. We conclude that osmolytic mechanisms are not the primary cause of the selective neuronal vulnerability in hypoglycemic coma. Furthermore, the BBB is largely intact during a hypoglycemic insult.

Acidosis↗
PubMed2004

Chiroptical transcription of helical information through supramolecular harmonization with dynamic helices.

With biologically important "peptide bundling" as the motif, new chromophoric cyclic host 1 was designed, which consists of two zinc porphyrin units that are connected by dynamic peptide helices of nonameric aminoisobutyric acid (Aib) units. Upon inclusion of pyridine-anchored helical peptides between the zinc porphyrin units, 1 displayed an intense exciton-coupled circular dichroism (CD) band at 410-450 nm, whose sign reflected the helical sense of the guest peptides. Studies with conformationally defined dehydrophenylalanine-containing analogues indicated that the dynamic helical chains in the host are stereochemically harmonized with right- or left-handed helices of the guest peptides in a confined nano space, leading to either clockwise- or anticlockwise-twisted geometry (chiroptical output) of the connecting zinc porphyrin chromophores.

Aminoisobutyric Acids↗
PubMedDate not supplied

Nucleoside excretion in breast cancer: comparison with other biochemical tumour-index-substances.

[We have measured four urinary nucleosides (dimethylguanosine, 1-methylinosine, pseudouridine and beta-aminoisobutyric acid)in patients with benign breast disease and patients with early and advanced breast cancer in order to assess their value as tumour-index-substances. We compared the results with other biochemical indices of breast cancer and sought and correlations between these indices. The results indicate that few abnormalities occurred in patients without overt metastases and these did not predict early relapse. In those with metastatic disease, dimethylguanosine excretion was most frequently elevated. Correlations were observed between some of the nucleosides and lysozyme and alpha1-antirypsin.

Aminoisobutyric Acids↗
PubMed1981

Syncytiotrophoblast membrane vesicles: a model for examining the human placental cholinergic system.

A membrane vesicle preparation was used to examine characteristics of the human placental cholinergic system. Plasma membrane vesicles were prepared from the microvillous surface of the human placental syncytiotrophoblast. Membranes were purified 18 -to 20-fold as indicated by 5'-nucleotidase activity. Vesicle cholinesterase activity was enriched and had a substrate preference consistent with that of acetylcholinesterase (acetylcholine greater than acetyl-beta-methylcholine greater than butyryl-choline). Choline acetyltransferase specific activity was reduced 80%. The synthetic muscarinic ligand, [3H]-quinuclidinyl benzilate (QNB), was used to identify two classes of muscarinic cholinergic binding sites. The dissociation constant of QNB binding was 80 pM and 30 nM for the two sites. The sites were saturable and bound 9 fmoles and 910 fmoles per mg protein for the high and low affinity sites, respectively. Specific binding was inhibited by scopolamine, atropine, carbamylcholine (CCH), and diphenhydramine, but not by non-muscarinic ligands-i.e. GABA, glycine, d-amphetamine, kappa-bungarotoxin and nicotine. The cholinergic agonist CCh had no effect on active AIB transport, although pharmacologic doses (lmM) of atropine, scopolamine and lidocaine reduced Na-gradient active transport of kappa-aminoisobutyric acid (AIB). No effect on Na-independent AIB transport was observed. Thus, these drugs apparently reduced AIB uptake through their shared local anesthetic activity and not through a central cholinergic mechanism. In contrast, CCh was able to stimulate Ca2+ uptake by the vesicles in a dose-dependent manner paralleling its ability to inhibit QNB binding. The CCh-stimulated Ca2+ uptake was inhibited by scopolamine, implying its mediation via cholinergic-type binding sites. The membrane vesicle preparation therefore provides a useful model for examination of the role of the human placental cholinergic system.

Acetylcholine↗
PubMed1992

Effects of isoflurane on transport across the blood-brain barrier.

The blood-brain barrier (BBB) plays an important role in regulating and restricting transfer of molecules into the interstitial space of the brain. Anesthetic agents may affect the permeability of the BBB. In this investigation, the effect of isoflurane on the transport of small hydrophilic molecules across the BBB was studied in rats by measuring the blood-brain transfer coefficient (Ki) and the regional cerebral blood flow (rCBF) and by calculating the capillary permeability-surface area (PS) product. In the control group, after a femoral artery and vein were catheterized under isoflurane anesthesia, rats were allowed to remain awake for 2 h before measuring Ki (n = 6) or rCBF (n = 11). In the two experimental groups, rats were anesthetized with 1% and 2% isoflurane respectively, and their lungs were mechanically ventilated through a tracheal tube. Ki was measured (1% n = 6, 2% n = 7) using 14C-alpha-aminoisobutyric acid, and rCBF was measured (2% n = 7) using 14C-iodoantipyrine. Two percent isoflurane did not affect rCBF in 9 of 13 brain regions. Blood flow was less in the lateral and posterior cortex and greater in the medulla and pons when compared with the control group. Ki was less in 11 of 13 brain regions in both the 1% and 2% isoflurane groups than in the control group. There was no significant difference between 1 and 2% isoflurane in any brain region.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoisobutyric Acids↗
PubMed1999

Antenatal steroids decrease blood-brain barrier permeability in the ovine fetus.

Antenatal corticosteroid therapy reduces the incidence of intraventricular hemorrhage in premature infants. Enhanced microvascular integrity might provide protection against intraventricular hemorrhage. In the adult, there is evidence to suggest that the blood-brain barrier may be under hormonal control. We hypothesized that antenatal corticosteroids decrease blood-brain barrier permeability in the preterm ovine fetus. Chronically instrumented 120-day-gestation fetuses were studied 12 h after the last of four 6-mg dexamethasone (n = 5) or placebo (n = 6) injections had been given over 48 h to the ewes. Blood-brain barrier function was quantified with the blood-to-brain transfer constant (Ki) for alpha-aminoisobutyric acid (AIB). Ki was significantly lower across brain regions in the fetuses of ewes that received antenatal dexamethasone compared with placebo (ANOVA; interaction, F = 2.54, P < 0.004). In fetuses of dexamethasone- and placebo-treated ewes, Ki (microliter . g brain wt-1. min-1, mean +/- SD) was, respectively, 2.43 +/- 0.27 vs. 3.41 +/- 0.74 in the cortex, 4.46 +/- 0.49 vs. 5.29 +/- 0.85 in the cerebellum, and 3.70 +/- 0.49 vs. 5.11 +/- 0.70 in the medulla. We conclude that antenatal treatment with corticosteroids reduces blood-brain permeability in the ovine fetus.

Adrenal Cortex Hormones↗
PubMed1989

Modifications of the permeability of the blood-brain barrier and local cerebral metabolism in pentobarbital- and ketamine-anaesthetized rats.

The state of deep surgical anaesthesia, induced by intraperitoneal injection of pentobarbital sodium (54 mg/kg) or ketamine hydrochloride (150 mg/kg) in the rat, was accompanied by a significant reduction in the permeability of the blood-brain barrier evaluated by calculating a unidirectional blood-to-brain constant (Ki) for the circulating tracer [14C]alpha-aminoisobutyric acid. Pentobarbital-induced anaesthesia was also characterized by a widespread and marked depression of local cerebral glucose utilization; on the contrary, when rats were anaesthetized with ketamine, cerebral glucose utilization increased in the striatum and hippocampus and decreased in the cerebellum and brain-stem. It is suggested, as a hypothesis, that two different mechanisms, depending on the kind of the anaesthetic drug used, may be involved in the changes in the permeability of the blood-brain barrier, observed in anaesthetized animals: (a) a neurogenic component; (b) a direct interaction of the anaesthetic with elements of the microvasculature.

Aminoisobutyric Acids↗
PubMed1992

Ageing influences haloperidol-induced changes in the permeability of the blood-brain barrier in the rat.

The effect of the dopaminergic antagonist haloperidol on the permeability of the blood-brain barrier (BBB) to [14C]alpha-aminoisobutyric acid was studied in 10-12- and 28-30-week old rats. Following the intraperitoneal injection of haloperidol (1 mg kg-1), an increase in the permeability of the BBB, with respect to younger animals, was observed within the occipital cortex, striatum, hippocampus and hypothalamus in the older rats. No correlation was found between haloperidol-induced changes and age-related differences in the permeability of the BBB. Such age-associated increase in the vulnerability of the BBB when challenged with haloperidol might be related to a deterioration of the dopaminergic control of cerebrovascular permeability.

Aging↗