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PubMed2002

Monitoring the structural consequences of Phe12-->D-Phe and Leu15-->Aib substitution in human/rat corticotropin releasing hormone. Implications for design of CRH antagonists.

A new human/rat CRH analogue has been synthesized using the Fmoc/tBu solid-phase synthetic protocol. The sequence of the new peptide differs from the original in two positions, 12 and 15, at which the native amino acids l-phenylalanine 12 and l-leucine 15 have been replaced by the nonprotein amino acids d-phenylalanine and alpha-aminoisobutyric acid (Aib), respectively. The high resolution three-dimensional solution structure of [d-Phe12, Aib15]CRH has been determined by 688 distance constraints (656 meaningful NOE and 32 H-bonds distance limits) and 21 angle constraints. A family of 40 energy-minimized conformers was obtained with average rmsd of 0.39 +/- 0.16 A and 0.99 +/- 0.13 A for backbone and heavy atoms, respectively, and distance penalty functions of 0.42 +/- 0.03 A2. The NMR data acquired in a solvent system of water/trifluoroethanol (34%/66%, v/v) revealed that this 41-polypeptide adopts an almost linear helical structure in solution with helical content which reaches an 84% of the residues. Structural analysis confirmed the existence of two helical peptide fragments. The first was comprised of residues Ile6-Arg16 and the second of residues Glu20-Ile40, forming an angle of 34.2 degrees. The structural differences with respect to the native peptide have been identified in the region d-Phe12-Glu20 where double substitution at positions 12 and 15 seems to perturb the elements of the native 35-residue helix. These structural rearrangements promote non-native intramolecular interactions in the region of the molecule between either the hydrophobic side-chains of d-Phe12, Aib15 and Leu18, or the charged groups of the residue pairs Arg16-Glu20 and His13-Glu17 being responsible for changes in hormonal functionality. This CRH analogue currently exhibits lack of any activity.

Amino Acid Sequence↗
PubMed1992

Quantitative study of blood-brain barrier permeability changes after experimental whole-brain radiation.

Basic mechanisms underlying the tolerance and reaction of the central nervous system to ionizing radiation are not known precisely. We investigated the possibility of a change in blood-brain barrier (BBB) function as a causative factor for early delayed whole-brain radiation-induced cerebral dysfunction. Rats were exposed to conventional fractionation (200 cGy/d, 5 d/wk; total dose, 4000 cGy). BBB changes were assessed by means of the quantitative 14C-alpha-aminoisobutyric acid technique and electron microscopy. Studies of the passage of horseradish peroxidase across the BBB permitted comparative quantitative isotopical and qualitative morphological data. Experiments were carried out 2 to 3 weeks after the completion of the radiation exposure. The transport of 14C-alpha-aminoisobutyric acid across the BBB increased significantly in cerebral cortex and cerebellar gray matter, averaging 1.3 to 1.5 times over the normal values. Electron microscopy disclosed an intense vesicular response of the cortical microvascular endothelium that occurred without the opening of the tight junctions and resulted in an intense transport of HRP across the intact endothelium. The present data indicate that moderate doses of whole-brain radiation induce well-defined changes in BBB function, which possibly are involved in the pathogenesis of radiation-induced cerebral dysfunction in humans.

Aminoisobutyric Acids↗
PubMed1977

Tritium suicide selection of mammalian cell mutants defective in the transport of neutral amino acids.

Mouse lymphocytic cells of the established line GF-14 were allowed to accumulate intracellular 3H-labeled aminoisobutyric acid (AIB), frozen, and stored over liquid N2. After internal radiation had reduced survival to 1 in 10(4), survivors were plated and tested for their ability to transport AIB. Out of 200 clones tested, two (designated GF-17 and GF-18) were found to have reductions to 13-35% of the parent in the rate of transport of AIB, L-alanine, L-proline, and L-serine; GF-18 also showed significant reductions in the rate of transport of L-glutamate and DL-cysteine. Little or no change was observed for 10 other amino acids or for thymidine. Kinetic analyses revealed that the mutants were not altered in Km for AIB uptake, but had Vmax values approximately 20% the value of the parent strain, GF-14, suggesting that either the number of AIB transport sites or the turnover rate of the sites has been reduced in the two mutants.

Amino Acids↗
PubMed1989

Inhibition of amino acid transport and protein synthesis by HgCl2 and methylmercury in astrocytes: selectivity and reversibility.

The previously reported observation that submicromolar concentrations of HgCl2 inhibit glutamate uptake reversibly in astrocytes, without effect on 2-deoxyglucose uptake, suggested that elemental mercury vapor, which is oxidized to mercuric mercury in the brain, might cause neurodegenerative change through the mediation of glutamate excitotoxicity. Here, selectivity is explored further by measuring the inhibition of other amino acid transporters and protein synthesis as a function of HgCl2 concentration. The properties of MeHgCl were compared under identical conditions, and some morphological correlates of function were examined. Inhibition of amino acid transport by HgCl2 was selective, whereas MeHgCl was nonselective. The 50% inhibitory concentrations of HgCl2 for uptake of alpha-aminoisobutyric acid by system A, uptake of alpha-aminoisobutyric acid or kynurenine by a system L variant, and uptake of gamma-aminobutyric acid were all two- to fourfold greater than that for uptake of glutamate. The submicromolar concentrations of HgCl2 that inhibited glutamate transport also inhibited protein synthesis, but in a rapidly reversible fashion, and elicited only discrete ultrastructural changes (heterochromatin, increased numbers of lysosomal bodies, and increased complexity of cell surface). In contrast, inhibition of protein synthesis by MeHgCl was acutely (1-h) irreversible and became marked only at concentrations higher than those that elicited gross morphologic change in the form of "bleb"-like swellings. The results lend support to the proposed excitotoxic mediation of mercury vapor neurotoxicity and reveal a sharp contrast between the effects of HgCl2 and MeHgCl on astrocytes.

Amino Acids↗
PubMed1985

Presence of a nonmetabolizable solute that is translocated with Na+ enhances Na+-dependent pH homeostasis in an alkalophilic Bacillus.

The presence of a nonmetabolizable solute whose uptake is coupled to the inward translocation of Na+ has been found to enhance Na+-dependent pH homeostasis and survival of an obligately alkalophilic bacterium. Upon shift of cells of Bacillus firmus RAB from growth medium to buffers at pH 10.5, viability and maintenance of a relatively acidified cytoplasm depended upon the presence of Na+ and was augmented by the inclusion of alpha-aminoisobutyric acid in the buffer. Similarly, when cells were first equilibrated at pH 8.5 and then shifted to buffer at pH 10.5, an extraordinary capacity to maintain a relatively low pHin was exhibited, but only in the presence of Na+. In this protocol, the inclusion of alpha-aminoisobutyric acid actually resulted in an early overshoot of proton influx and also rendered a suboptimal concentration of Na+ efficacious in pH homeostasis. When a protonophoric uncoupler was added to the equilibration and shift buffers, Na+-dependent acidification of the interior was inhibited at early time points. The results support the conclusion drawn from earlier work that a Na+/H+ antiporter plays a critical role in pH homeostasis in the obligately alkalophilic bacilli. Moreover, the current findings indicate that the Na+/solute symporters are a physiologically functional pathway for completing the sodium cycle that controls pHin.

Aminoisobutyric Acids↗
PubMed1989

Serum glucocorticoids have persistent and controlling effects on insulinlike growth factor I action under serum-free assay conditions in cultured human fibroblasts.

The biological actions of insulinlike growth factor I (IGF-I) measured under serum-free assay conditions were found to be significantly influenced by prior subculture conditions for adult human fibroblasts. Glucocorticoids seemed to be the major medium variable affecting IGF-I action. IGF-I added to serum-free cultures had little or no effect on [14C]aminoisobutyric acid uptake or [3H]thymidine incorporation in human fibroblasts previously maintained in media containing serum with low glucocorticoid levels or in serum stripped of endogenous steroids. However, a 48-h preincubation with dexamethasone resulted in a marked synergistic increase in IGF-I stimulation of [14C]aminoisobutyric acid uptake and [3H]thymidine incorporation in these cultures. In contrast, IGF-I in serum-free medium seemed to be a potent mitogenic and metabolic stimulus for human fibroblasts which had been subcultured in media with a high glucocorticoid content, either endogenous or supplemented. After these culture conditions, a 48-h preexposure to dexamethasone had no further enhancing effect on IGF-I action. Dexamethasone also potentiated IGF-I, insulin, and epidermal growth factor stimulation of fibroblast replication depending on the earlier subcultivation conditions. Thus, glucocorticoids are important modulators of IGF-I bioactivity in cultured human fibroblasts. Serum glucocorticoids can exert a profound influence on the biological phenomena measured in cell culture, even when the serum has been removed before the actual experiment, and must be carefully taken into account for accurate evaluation of the biological function of IGF-I and other growth factors.

Adult↗
PubMed1985

The movement of radioactive molecules across dentine in vivo in the dog.

Using a technique for measuring the movement of circulating molecules across the odontoblast-dentinal complex, the movement of water and alpha-aminoisobutyric acid through dentine and into a flow cell prepared on the tooth is described. The movement of water depended on dentine thickness, and varied from 0.40 microliter/min per cm2 in a flow cell overlying an average thickness of 0.74 mm of dentine, to 1.23 microliter/min per cm2 in a flow cell with a dentinal floor of 0.40 mm average thickness. The data suggest that alpha-aminoisobutyric-acid concentrations were lower in dentinal fluid than in blood plasma.

Aminoisobutyric Acids↗
PubMed1977

Effect of tryptophan and nicotinamide loads on urinary excretion of RNA metabolites by bladder cancer patients.

In a comparative study of tryptophan metabolism and urinary excretion of nucleic acid derivatives (including beta-aminoisobutyric acid, 7-methylguanine, pseudouridine, and urate) in 12 male bladder cancer patients, the excretion of pseudouridine and 7-methylguanine decreased significantly after an oral dose of 2 g L-tryptophan. A similar decrease occurred after an oral nicotinamide load of 50 mg four times a day, which indicated a possible common mode of action of tryptophan and nicotinamide. No definite resolution could be made as to the causal mechanism for the observed descrase in RNA turnover.

Aminoisobutyric Acids↗
PubMed1981

Adrenalectomy decreases amino-acid transport in hepatocytes.

The effect of adrenalectomy on basal and hormone-stimulated amino-acid transport in liver was investigated by measuring the uptake of alpha-aminoisobutyric acid in freshly isolated rat hepatocytes. Adrenalectomy resulted in a 50% decrease in the transport capacity of hepatocytes; this change was accounted for by a diminution in the Vmax of a low affinity component of transport and specifically affected the A-transport system. Cortisone therapy fully restored the capacity of hepatocytes to transport amino acids. Sensitivity and responsiveness of hepatocytes from adrenalectomized animals to insulin, glucagon and dexamethasone, tested for the capacity of these hormones to stimulate AIB transport in vitro, were essentially identical with that of hepatocytes from control rats. The results support the concept of a positive (stimulatory) role of glucocorticoids in vivo, in the regulation of amino acid transport in the liver.

Adrenalectomy↗
PubMed1986

Mechanisms controlling renal hemodynamics and electrolyte excretion during amino acids.

Our purpose was to investigate the mechanisms by which increased plasma amino acids elevate renal blood flow (RBF) and glomerular filtration rate (GFR). Since transport of amino acids and Na+ is linked in the proximal tubule, we hypothesized that increased amino acids might stimulate proximal tubular Na+ reabsorption (PRNa) and thus increase RBF and GFR by a macula densa feedback mechanism. A solution of four amino acids (Ala, Ser, Gly, Pro) was infused intravenously (0.075 mmol X kg-1 X min-1 total) into anesthetized dogs with normal kidneys (NK) and with kidneys in which the tubuloglomerular feedback mechanism was blunted by lowering renal artery pressure (LPK) or blocked by making the kidneys nonfiltering (NFK). In NK, RBF and GFR increased by 35 +/- 4% and 30 +/- 7% after 90 min of amino acid infusion, while PRNa (estimated from lithium clearance) and O2 consumption increased by 31 +/- 5% and 29 +/- 5% and distal Na+ delivery remained relatively constant. Autoregulation of RBF and GFR in response to step decreases in renal artery pressure was impaired during amino acids in NK. The hemodynamic responses to amino acids were abolished in LPK and NFK. Infusion of the nonmetabolized alpha-aminoisobutyric acid (0.075 mmol X kg-1 X min-1) into NK produced changes in renal hemodynamics that were similar to the responses observed with the four metabolizable amino acids. These data are consistent with the hypothesis that elevation of plasma amino acids increases RBF and GFR by a mechanism that requires an intact macula densa feedback. Metabolism of the amino acids does not appear to be necessary for these changes to occur.

Amino Acids↗
PubMed1993

Effect of tumor necrosis factor or interleukin-1 on muscle amino acid uptake and the role of glucocorticoids.

Muscle amino acid uptake is inhibited during sepsis and endotoxemia. Cytokines, in particular tumor necrosis factor (TNF) and interleukin-1 (IL-1), have been implicated as mediators of metabolic alterations in sepsis and other critical illness. In this study, we examined the effect of TNF and IL-1 on muscle amino acid uptake and tested the hypothesis that cytokine-induced changes in muscle amino acid uptake are mediated by glucocorticoids. Intraperitoneal injection in rats of 100 micrograms per kilogram body weight of human recombinant TNF alpha (rTNF alpha) or rIL-1 alpha resulted, two hours later, in 36 and 24 percent reduction, respectively, of amino acid transport in incubated soleus muscles, determined as intracellular uptake of alpha-aminoisobutyric acid. When rats were treated with the glucocorticoid receptor antagonist RU 38486 (5 milligrams per kilogram of body weight) two hours before cytokine injection, the inhibitory effect on muscle amino acid transport of TNF was blocked, whereas that of IL-1 was unaffected. The present results suggest that TNF and IL-1 may regulate amino acid transport in skeletal muscle and that the effect of TNF, but not that of IL-1, is at least partly mediated by glucocorticoids.

Amino Acids↗
PubMedDate not supplied

Potential biologic markers in Burkitt's lymphoma.

Specific biochemical molecules used as potential biologic markers, including modified nucleosides, polyamines, and pyrimidine catabolic end-products, were quantitatively measured in the urine of seven patients with Burkitt's lymphoma before, during, and after one or more courses of therapy. The results of this preliminary study demonstrated that patients with this disease frequently excrete significantly increased amounts oof modified nuceleosides (considered to be derived primarily from transfer ribonucleic acid), polyamines, and beta-aminoisobutyric acid during the course of their disease. With successful treatment and rapid destruction of tumor cells, a concomitant rise in these molecules occurs. Elevations were observed prior to chemotherapy and changes in levels associated with treatment or tumor progression appeared to correlate with disease status and to aid in assessing antitumor response. Periodic follow-up analysis of these molecules may be helfful in appraising relapse or recurrence of the malignancy prior to overt evidence of tumor by existing clincial means.

Adolescent↗
PubMed1993

Competitive irreversible inhibition of dopamine uptake by 6-hydroxydopamine.

We examined the effects of 6-hydroxydopamine (6-OHDA) treatment on the human neuroblastoma cell line SK-N-SH-SY5Y (SY5Y) and the rat pheochromocytoma cell line, PC12. Structural and metabolic integrity was tested by measuring the ability of cells to transport the non-metabolizable amino acid analogue [3H]-alpha-aminoisobutyric acid (AIB). We determined that treatment with 6-OHDA at concentrations of 49 microM and 62 microM inhibited 50% of the AIB uptake in SY5Y and PC12 cells, respectively. Inhibition of AIB uptake was prevented by the addition of catalase, but was not influenced by the addition of 1 mM dopamine. This indicated that cell damage resulted from the generation of H2O2 and was independent of the catecholamine uptake system. Effects directly on the catecholamine uptake system were observed by measuring the uptake of 3H-dopamine. In contrast to the effects on amino acid uptake, dopamine uptake was significantly inhibited by 6-OHDA treatment, and this inhibition was not prevented by the addition of catalase. The results indicate a Ki of 430 microM for inhibition of dopamine uptake by 6-OHDA treatment of PC12 cells. The results are consistent with a competitive irreversible inhibition of the dopamine uptake sites by 6-OHDA or one of its metabolites. Thus, the lack of a catecholamine uptake-dependent cellular toxicity appears to result from the direct inactivation of catecholamine uptake sites. Similarly, the inhibition of dopamine uptake in vivo by 6-OHDA may be explained, at least in part, by direct inactivation of dopamine uptake sites rather than exclusively by intracellular transport and action of 6-OHDA.

Adrenal Gland Neoplasms↗
PubMed1985

The influence of temperature on the functions of cultured Sertoli cells.

Three functions of Sertoli cells were examined with cells from rats aged 13 and 25 days at 34 C, 38 C, and 40 C, namely protein synthesis (incorporation of amino acids into material precipitated by trichloroacetic acid), transport of alpha-aminoisobutyric acid, and production of lactate. A fourth function, namely production of cAMP was examined at two temperatures (34 C and 38 C) in cells from rats aged 25 days. In all cases, activity was greater at 38 C than at 34 C and greater at 40 C than at 38 C. Lysate of Sertoli cells showed similar differences in protein synthesis at the three temperatures, again at both ages. Protein synthesis was higher at 38 C than at 34 C in Sertoli cell-enriched tubules from rats aged 25 days and in Sertoli cells from normal rats of the same age cultured on rat tail collagen. The difference in protein synthesis at the two temperatures was seen whether the cells were cultured, before the experiment, for 7 days at 38 C or at 34 C. Production of cAMP by Sertoli cells was greater at 38 C than at 34 C. It is concluded that Sertoli cells do not show in vitro any inhibitory effect of body temperature on any of the functions tested, but on the contrary, are more active at body than at scrotal temperature. The possible significance of the differences seen is discussed.

Aminoisobutyric Acids↗
PubMed1991

Parallel modulation of brown adipose tissue GDP-binding, substrate uptake and (Na(+)-K+)-ATPase activity in the rat.

Brown adipose tissue (Na(+)-K+)-ATPase activity, in vitro glucose uptake and 2-aminoisobutyric acid uptake, as well as mitochondrial GDP-binding and succinate dehydrogenase activity were determined in order to study the relationship between these parameters in control, cold acclimated and cafeteria-fed rats. GDP-binding, (Na(+)-K+)-ATPase and glucose uptake were increased in interscapular brown adipose tissue from cold-acclimated and cafeteria-fed rats, whereas 2-aminoisobutyric acid uptake was only increased in cafeteria-fed rats. GDP-binding and (Na(+)-K+)-ATPase activity showed a high correlation coefficient suggesting a parallel modulation of both systems, which would probably share a common regulation mechanism.

Adipose Tissue, Brown↗
PubMed1981

Amino Acid Transport and stimulation by substrates in the absence of a Na2+ electrochemical potential gradient.

Uptake of alpha-aminoisobutyric acid (AIB) was examined in Ehrlich ascites tumor cells treated with the cation-exchange ionophore nigericin (20 microgram/ml). Membrane voltages were measured using the voltage-sensitive dye diethyloxadicarbocyanine (DOCC). In normal phosphate-buffered media, nigericin changed the distribution ratios of Na+ and K+ (the ratio of intra- to extracellular concentrations) nearly to unity, but AIB was still accumulated to a distribution ratio of approximately 9.0. When all but 40 mM Na+ in the medium was replaced by choline, nigericin resulted in K+ loss and Na+ gain and both cation distribution ratios approached 2.8-3.4, as would be expected if both ions were distributing near electrochemical equilibrium with a membrane voltage in the range of -28 to -33 mV. This conclusion was supported by the observation that the addition of 5 X 10(-7) M valinomycin to the nigericin-treated cell suspension produced no change in DOCC absorbance. In spite of the apparent zero electrochemical potential gradients for Na+ and K+, AIB was accumulated to a distribution ratio of 5.4 in the low-Na+ medium. Addition of 0.1 mM oubain or 50 microM vanadate did not alter the extent of AIB accumulation as would have been expected if a large component of the membrane voltage were due to electrogenic operation of the (Na+ + K+)-ATPase. Addition of lactate, pyruvate or glucose increased the AIB distribution ratios to 11.9, 9.4 and 15.3, respectively. The effect of glucose could be explained, at least in part, by an enhanced Na+ electrochemical potential gradient. However, neither lactate nor pyruvate produced any change either in membrane voltage or the intracellular Na+ concentration. Therefore, these results confirm the existence of a metabolic energy source which is coupled to AIB accumulation and operates in addition to the Na+ co-transport mechanism, and which is augmented by metabolic substrates such as lactate and pyruvate.

Amino Acids↗
PubMed1982

Glucocorticoid-induced insulin resistance: the importance of postbinding events in the regulation of insulin binding, action, and degradation in freshly isolated and primary cultures of rat hepatocytes.

We have recently proposed that "down regulation" of the insulin receptor may be one of the many biological responses of a cell to insulin. In an attempt to further explore this hypothesis we have studied insulin action, binding, and degradation in freshly isolated hepatocytes from rats rendered insulin resistant by the administration of dexamethasone, 1.0 mg/kg every other day, for 1 and 4 wk, and in dexamethasone-treated (0.1 muM for 24 h) primary cultures of hepatocytes from normal rats. Dexamethasone treatment for 1 and 4 wk resulted in significant hyperinsulinemia and euglycemia when compared with age- and weight-matched control animals. Freshly isolated hepatocytes from rats treated with dexamethasone for 1 wk bound less insulin than cells from control animals. This decrease in insulin binding was reflected in a decrease in the total number of cellular insulin receptors upon solubilization of the cells. Insulin action was evaluated by the ability of insulin to stimulate the uptake of alpha-aminoisobutyric acid. The basal rate of aminoisobutyrate uptake in freshly isolated hepatocytes was enhanced by 1 wk of dexamethasone treatment, and although there was an apparent shift to the right in the dose-response curve for insulin-stimulated aminoisobutyrate uptake, at no insulin concentration was there a significant difference in the uptake by hepatocytes from control and dexamethasone-treated animals. This was true whether expressed as a percentage or absolute increment above basal. Insulin degradation was enhanced in hepatocytes from animals treated with dexamethasone for 1 wk but could not account for the observed changes in insulin binding. Hepatocytes from animals treated with dexamethasone for 4 wk were resistant to insulin with regard to aminoisobutyrate uptake, yet both insulin binding and insulin degradation returned to the levels observed in hepatocytes from control animals. Primary cultures of hepatocytes from normal rats exposed to dexamethasone, 0.1 muM, in vitro for 24 h were similar to hepatocytes from rats treated with dexamethasone for 4 wk in that they were insulin resistant with regard to aminoisobutyrate uptake and had normal to increased insulin binding. Insulin degradation was also similar. These cells were resistant to the ability of insulin, 0.1 muM, to down regulate its receptor whereas parallel cultures treated with insulin in the absence of dexamethasone had a 52% decrease in insulin binding. These data indicate that hepatocytes that are insulin responsive respond to in vivo hyperinsulinemia by a decrease in the number of insulin receptors and by increased insulin degradation. Hepatocytes rendered resistant to insulin both in vivo and in vitro are resistant to these effects of insulin. These studies emphasize the importance of postbinding events in the modulation of insulin binding, action, and degradation, and support the hypothesis that down regulation of the hepatocyte insulin receptor is one of the many biological actions of insulin. They also help explain how a cell can be insulin resistant and have a normal number of insulin binding sites in the presence of hyperinsulinemia.

Aminoisobutyric Acids↗
PubMed1990

Effect of steroids on edema and sodium uptake of the brain during focal ischemia in rats.

Steroids reduce permeability of the blood-brain barrier and inhibit active sodium transport by brain capillaries in vitro. Since the rate of edema formation during the early stages of ischemia is related to the rate of sodium transport from blood to brain, this study was designed to determine whether steroids reduce ischemic edema formation by inhibiting blood-brain barrier sodium transport. Dexamethasone was compared with progesterone since the latter is a more potent inhibitor of sodium transport in isolated capillaries. Sprague-Dawley rats were treated with vehicle (n = 22) or 2 mg/kg of either dexamethasone (n = 22) or progesterone (n = 17) 1 hour before occlusion of the middle cerebral artery. After 4 hours of ischemia, brain water content and blood-brain barrier permeability to [3H] alpha-aminoisobutyric acid and sodium-22 were determined. In controls, mean +/- SEM water content of tissue in the center of the ischemic zone was 82.4 +/- 0.2%. Brain edema was significantly reduced following pretreatment with either dexamethasone (80.6 +/- 0.1%, p less than 0.001) or progesterone (81.5 +/- 0.3%, p less than 0.05). There was also a significant reduction in blood-brain barrier permeability to alpha-aminoisobutyric acid in normal brain following either treatment (e.g., 2.21 +/- 0.19 and 1.37 +/- 0.10 microliters/g/min, p less than 0.001, for control and dexamethasone treatments, respectively), but no effect on the permeability to sodium (e.g., 1.19 +/- 0.05 and 1.12 +/- 0.11 microliters/g/min for control and dexamethasone treatments, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoisobutyric Acids↗