bluuebunny/crossref_metadata_2025 huggingface dataset:
Acoustic telemetry observation systems: challenges encountered and overcome in the Laurentian Great Lakes
Authors: Krueger Charles C. , Holbrook Christopher M. , Binder Thomas R. , Vandergoot Christopher S. , Hayden Todd A. , Hondorp Darryl W. , Nate Nancy , Paige Kelli , Riley Stephen C. , Fisk Aaron T. , Cooke Steven J.
Published: December 2017

The Great Lakes Acoustic Telemetry Observation System (GLATOS), organized in 2012, aims to advance and improve conservation and management of Great Lakes fishes by providing information on behavior, habitat use, and population dynamics. GLATOS faced challenges during establishment, including a funding agency-imposed urgency to initiate projects, a lack of telemetry expertise, and managing a flood of data. GLATOS now connects 190+ investigators, provides project consultation, maintains a web-based data portal, contributes data to Ocean Tracking Network’s global database, loans equipment, and promotes science transfer to managers. The GLATOS database currently has 50+ projects, 39 species tagged, 8000+ fish released, and 150+ million tag detections. Lessons learned include (1) seek advice from others experienced in telemetry; (2) organize networks prior to when shared data is urgently needed; (3) establish a data management system so that all receivers can contribute to every project; (4) hold annual meetings to foster relationships; (5) involve fish managers to ensure relevancy; and (6) staff require full-time commitment to lead and coordinate projects and to analyze data and publish results.
Testing the Validity of the ‘Local’ and ‘Global’ GKLS Master Equations on an Exactly Solvable Model
Authors: González J. Onam , Correa Luis A. , Nocerino Giorgio , Palao José P. , Alonso Daniel , Adesso Gerardo
Published: December 2017

When deriving a master equation for a multipartite weakly-interacting open quantum systems, dissipation is often addressed locally on each component, i.e. ignoring the coherent couplings, which are later added ‘by hand’. Although simple, the resulting local master equation (LME) is known to be thermodynamically inconsistent. Otherwise, one may always obtain a consistent global master equation (GME) by working on the energy basis of the full interacting Hamiltonian. Here, we consider a two-node ‘quantum wire’ connected to two heat baths. The stationary solution of the LME and GME are obtained and benchmarked against the exact result. Importantly, in our model, the validity of the GME is constrained by the underlying secular approximation. Whenever this breaks down (for resonant weakly-coupled nodes), we observe that the LME, in spite of being thermodynamically flawed: (a) predicts the correct steady state, (b) yields with the exact asymptotic heat currents, and (c) reliably reflects the correlations between the nodes. In contrast, the GME fails at all three tasks. Nonetheless, as the inter-node coupling grows, the LME breaks down whilst the GME becomes correct. Hence, the global and local approach may be viewed as complementary tools, best suited to different parameter regimes.
Open System Model for Quantum Dynamical Maps with Classical Noise and Corresponding Master Equations
Authors: Kropf Chahan M. , Shatokhin Vyacheslav N. , Buchleitner Andreas
Published: December 2017

We show how random unitary dynamics arise from the coupling of an open quantum system to a static environment. Subsequently, we derive a master equation for the reduced system random unitary dynamics and study three specific cases: commuting system and interaction Hamiltonians, the short-time limit, and the Markov approximation.
Total State Dynamics in the GKSL Regime
Authors: Megier Nina , Strunz Walter T.
Published: December 2017

We develop a framework that allows us to describe the dynamics of the total state of an open quantum system and its bosonic environment in the usual Born (weak coupling) and Markov approximation. By shifting the whole time-dependence into an unnormalized s-operator of the open system, the full dynamics is captured by an s-master equation of similar structure than the well-known Gorini-Kossakowski-Sudarshan-Lindblad (GKSL) master equation for the reduced dynamics. By varying the ordering parameter s (0 ≤ s ≤ 1) we obtain the partial Husimi representation (s = 0) and the partial Glauber-Sudarshan representation (s = 1) for the dynamics of the total state. For the reduced density operator the GKSL master equation can be derived easily. The case of s = 1/2, leading to a partial Wigner representation, is helpful to study the overlap of states in the total Hilbert space of system and environment.
Excitation conduction in Meissner's plexus of rabbit small intestine.
Authors: Yokoyama S , Ozaki T , Kajitsuka T
Published: December 2017

Excitation conduction in Meissner's plexus of the rabit small intestine was investigated by analyzing the records of potentials evoked by a single electrical stimulus applied to this plexus. Experiments were performed on the Meissner's plexus that remained attached to the circular muscle after the longitudinal muscle and mucous membrane were removed from intestinal segment. Conduction velocities of nerve impulses were 0.3-0.7 m/s, chronaxie of the nerve bundle was 0.06-0.12 ms. While the distance between the stimulating and recording electrodes was increased, the latency of evoked potentials was prolonged, the number increased, and the amplitude decreased; no potentials could be recorded when the distance was more than 4 mm. Evoked potentials recorded at relatively long conduction distance were reduced in amplitude or abolished after a repeated stimulation with high frequencies above 50/s, after hexamethonium application, and in a state of lack of oxygen. It was concluded that, in Meissner's plexus, nerve impulses spread through multiple pathways and make synaptic transmission at a relatively short conduction distance.
Ileal mucosal cyclic AMP and Cl secretion: serosal vs. mucosal addition of cholera toxin.
Authors: Sheerin H E , Field M
Published: December 2017

Changes in ion transport and cyclic AMP (cAMP) concentration produced by addition of cholera toxin to the serosal side of isolated rabbit ileal mucosa (CTs) were compared to the changes produced by addition to the mucosal side (CTm). CTs increased short-circuit current (SCC) as did CTm but it did so more slowly. CTs, unlike CTm, did not significantly decrease electrical conductance. Inhibition of the SCC response to theophylline, a measure of preexisting secretion, was almost complete 180 min after CTm but was not yet significant 180 min after CTs. Longer (280 min) after CTs, the SCC response to theophylline was reduced by 59%, a significant reduction but less than that caused by CTm. A statistically significant change in net Cl flux could not be demonstrated after CTs, although at 280 min the measured flux was halfway between the fluxes for control and CTm tissues. Cyclic AMP concentrations were determined at 190 min, 10 min after addition of theophylline. CTs, despite little or no effect on ion transport, increased cAMP to the same level as did CTm, and the effect on cAMP of adding toxin to both sides was additive. We conclude that 1) active secretion is probably stimulated by cholera toxin added on the serosal side, although more slowly than after addition to the mucosal side and 2) much of the toxin-stimulated cAMP content of the mucosa is not coupled to secretion.
Effect of hypophysectomy on calcium transport by rat duodenum.
Authors: Krawitt E L , Kunin A S , Sampson H W , Bacon B F
Published: December 2017

To examine the effect of hypophysectomy on intestinal calcium absorption, studies were performed on immature rats 7, 14, and 21 days after hypophysectomy. Duodenal calcium transport was measured in vitro utilizing everted gut sacs and in vivo by a luminal perfusion technique. Hypophysectomy produced no differences in the ability of everted gut sacs to transport calcium. Similarly, when in vivo transport data were expressed on the basis of intestinal length, no significant differences were noted. However, when transport data were expressed on the basis of mucosal weight, increases in absorption and lumen-to-plasma fluxes were apparent in hypophysectomized animals. No differences were seen in plasma-to-lumen fluxes. The results indicate that when the transport data are corrected for mass of intestinal mucosa, the duodenum from hypophysectomized animals absorbs calcium more avidly due to an increase in lumen-to-plasma flux.
Aldosterone metabolism in isolated perfused rat kidney.
Authors: Nakane H , Nakane Y , Reach G , Corvol P , Menard J
Published: December 2017

The renal metabolism and handling of [1,2-3H]aldosterone ([3H]A) was studied using isolated perfused rat kidney under different perfusion conditions. The metabolite production rate (MPR) and the urinary excretion of [3H]A together with its radiometabolites (UV/P3H) were studied. Among the formed metabolites, no acid-labile conjugate of aldosterone (ALC) was detected. The MPR was not altered in studies using nonfiltering kidney, a result that suggests that the majority of metabolites were formed without requirement of the process of glomerular filtration and tubular uptake of the hormone. High perfusion pressure (high PP) resulted in a striking increase in whole metabolic clearance rate of aldosterone (MCR[3H]A) due mostly to an enhanced urinary excretion of intact aldosterone and, to a lesser degree, to a significant increase in MPR. Factors determining the excretion rate of [3H]A and its metabolites were than investigated under administration of diuretics. Mannitol (44 mM) induced a marked increase in urine volume (UV) accompanied by a significant UV/P3H increase. Meanwhile, 0.1 mM furosemide resulted in an increase only in UV, but not in UV/P3H. These results revealed the UV dependence of aldosterone excretion in certain diuretic conditions.
Enhanced fluid transport across gallbladder mucosa in experimental cholelithiasis.
Authors: Lee S P
Published: December 2017

Fluid transport of the gallbladder has been studied in two models of experimental cholelithiasis: dihydrocholesterol-induced gallstones in the rabbit and lincomycin-induced gallstones in the guinea pig. Using the noneverted explained gallbladder of the rabbit and the guinea pig, the transport of luminal to serosal fluid has been quantitated before, during, and after stone formation. The everted gallbladder preparation of the rabbit has also been used to measure fluid transport before and during gallstone formation. In both models, an increased fluid transport was observed in the phase of gallstone induction and a return to normal after stones were formed. This abnormality preceded the appearance of conventional histological features of cholecystitis. There was also a coincidental increase in glycoprotein production from and cell proliferation of the gallbladder epithelium. This enhancement of fluid transfer may play a contributing role in the genesis of gallstones.
Effect of growth hormone on acute glucagon and insulin release.
Authors: Sirek A , Vranic M , Sirek O V , Vigas M , Policova Z
Published: December 2017

The aim was to clarify whether or not sudden spike concentrations of plasma growth hormone (GH) can affect the endocrine pancreas in vivo. The peaking of GH was reproduced by an injection (10 mg/kg iv) of bovine GH to anesthetized normal, pancreatectomized, and alloxan-diabetic dogs. In portal but not in peripheral blood, immunoreactive plasma glucagon (IRG), glucagon-like activity (GLI), and immunoreactive insulin (IRI), were significantly elevated within 10 min in normal and alloxan-diabetic dogs. In pancreatectomized dogs, GH did not affect either IRG or GLI. When a physiological dose of GH (6 microgram/kg) calculated to produce ambient peak plasma concentrations of 40 ng/ml was given to four conscious, normal dogs with indwelling portal catheters, a rise of IRG from 108 +/- 19 to 170 +/- 17 pg/ml and of IRI from 20 +/- 12 to 67 +/- 19 muU/ml (mean +/- SE) occurred within 2 min. GLI was not affected. Thus a sudden rise in GH concentration can stimulate the release of a) GLI in the presence but not in the absence of the pancreas, and b) pancreatic IRG and IRI but not extrapancreatic IRG.
Molecular forms of immunoreactive pancreatic cationic trypsin in pancreatitis patient sera.
Authors: Brodrick J W , Geokas M C , Largman C , Fassett M , Johnson J H
Published: December 2017

The molecular forms of immunoreactive pancreatic cationic trypsin in sera of patients with acute pancreatic inflammation have been characterized using a radioimmunoassay technique that is capable of detecting trypsinogen as well as trypsin bound to alpha 1-antitrypsin. Trypsin bound to alpha 2-macroglobulin is not immunoreactive under normal assay conditions. However, alpha 2-macroglobulin-bound trypsin can be detected after gel filtration of serum on Bio-Gel A-0.5 m and acid treatment of column fractions. The average serum level of immunoreactive cationic trypsin from 20 patients with acute pancreatic inflammation was 1,590 ng/ml. An average normal value of 26 ng/ml has been obtained previously. Serum samples from 14 patients with pancreatic inflammation were chromatographed under conditions that resolve trypsinogen, alpha 1-antitrypsin-bound trypsin, and alpha 2-macroglobulin-bound trypsin. In each case, the major portion of the immunoreactive material eluted at a position corresponding to free trypsinogen, while a minor fraction of the immunoreactive material appeared to be trypsin bound to alpha 1-antitrypsin. The zymogen nature of the major peak was confirmed in one case by activation with human enteropeptidase. In 11 of 14 patients, acid treatment of the alpha 2-macroglobulin peak yielded immunoreactive trypsin.
Metabolic effects of L-phenyllactate in perfused kidney, liver, and muscle
Authors: Collier V. U. , Butler D. O. , Mitch W. E.
Published: December 2017

L-Phenyllactate (L-PL) can promote growth of normal and germ-free rats eating a phenylalanine (Phe)-free diet, but the sites and pathway of its conversion to Phe have not been extensively studied. We perfused rat kidneys, livers, and hindquarters with L-PL and measured Phe release and effects on organ function. Renal release of Phe the during perfusion with L-PL was 3.0 times control (P less than 0.001) and increased 2.5-fold with addition of glutamine (P less than 0.001); with phenylpyruvate (PP), it was 3.5 times control (P less than 0.001). Sixty-four percent of L-PL disappearance could be accounted for by appearance of PP and Phe. Although renal gluconeogenesis from lactate was inhibited 28% by L-PL, neither glomerular filtration rate (0.44 ml . min-1 . g wet weight-1) nor sodium reabsorption (94.3%) were impaired. There was no net release of Phe or PP by rat livers or hindquarters perfused with L-PL and hepatic gluconeogenesis, urea synthesis, and potassium balance were unaffecte by L-PL. Thus, the kidney, but not skeletal muscle or liver, converts L-PL to Phe, presumably by the pathway L-PL leads to PP leads to Phe. In acute experiments with isolated organs, L-PL does not cause significant renal or hepatic dysfunction.
Influence of sodium balance on ACTH/adrenal corticosteroid dose-response curves in the dog
Authors: Gordon R. D. , Nicholls M. G. , Tree M. , Fraser R. , Robertson J. I.
Published: December 2017

In order to define short-term ACTH/corticosteroid dose-respone characteristics, we infused ACTH for 1 h at each of five incremental rates into pedigreed male beagle dogs in four different states of sodium balance. Progressive sodium depletion was associated with progressive increased in basal (pre-ACTH) plasma levels of renin, angiotensin II, aldosterone, 18-hydroxycorticosterone (18-OH-B), and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC). Administration of dexamethasone significantly reduced the preinfusion levels of cortisol, aldosterone, 18-OH-B, and 18-OH-DOC. The threshold dose of ACTH required to elicit an aldosterone response during low-sodium intake was similar to that for cortisol, but was higher during normal or high-sodium intake. Steepest portions of the dose-response curves were at lower rates of ACTH infusion for cortisol than for aldosterone, and maximum increment was much greater for cortisol (60-fold) than for aldosterone (12-fold). Whereas the slopes of ACTH/aldosterone and ACTH/18-OH-B dose-response curves were steepened by lower sodium diets, the ACTH/cortisol response was significantly flattened by severe sodium depletion. We conclude that ACTH is a potent and direct-acting short-term regulator of aldosterone secretion, subject to modification by altered sodium balance.
Parathyroid hormone modulates protein kinase in giant cell tumors of human bone
Authors: Ausiello D. A. , Rosenblatt M. , Dayer J. M.
Published: December 2017

The physiological effects of parathyroid hormone (PTH) in bone are mediated at least in part by cyclic AMP. The biochemical events subsequent to this step have not been well characterized in this tissue. Giant cell tumors of bone (GT) increase cyclic AMP in response to PTH. This response can be inhibited by an analogue of bovine PTH, [Nle8, Nle18, Tyr34] bPTH-(3-34) amide (PTH-Inh). Cyclic AMP content and cyclic AMP-dependent protein kinase (cAMP-PK) were assayed in fresh tumors and cells in culture incubated with 1 microgram/ml of bPTH and/or PTH-Inh. PTH fully activated cAMP-PK in GT, and PTH-Inh completely inhibited PTH-stimulated increases in cyclic AMP content and cAMP-PK activity. When endogenous protein substrates were sought for cAMP-PK, three phosphoproteins of 55,000, 43,000, and 38,000 mol wt maximally increased their phosphorylation by 30% after 12-min incubation with bPTH. Dephosphorylation of proteins of 200,000 and 120,000 mol wt was also observed. These data are consistent with the hypothesis that PTH action in bone is mediated by the phosphorylation and dephosphorylation of specific substrates.
Maturation of hypothalamic-pituitary-thyroid response in the rat to acute cold
Authors: Frankel S. , Lange G.
Published: December 2017

Groups of rats 3, 4, 5, 7, and 10 wk of age were tested for their ability to respond to acute cold (4 degrees C for 30 min). Thyroid reactions were estimated from intrathyroidal colloid droplet (CD) counts, serum thyrotropin (TSH) and thyroxine (T4) levels. Normally CD counts increased to a maximum in the 5-wk-old rats were lower in the 7-wk-old, and still lower in the 10-wk-old animals. The significant finding was that exposure to cold caused a decrease in CD counts in 3-, 4-, 5-wk-old rats but an increase in mature animals. This CD decrease was apparent within 10 min in the 4- and 5-wk-old rats, Injections of TSH and thyrotropin-releasing hormone (TRH) raised CD counts in all age groups but had little effect on response to cold. TSH serum levels were higher in the 5-wk-old than in the 3- and 4-wk-old animals; cold caused a greater TSH reduction in the 5-wk-old rats than in younger groups. Serum T4 levels were approximately the same in 3-, 4-, and 5-wk-old rats; when they were exposed to cold, the level rose despite the fact that CD counts dropped. These data indicate that in rats hypothalamic-pituitary-thyroid reactions to acute cold attain the adult pattern between 5 and 7 wk after birth.
Epitrochlearis muscle. II. Metabolic effects of contraction and catecholamines
Authors: Nesher R. , Karl I. E. , Kipnis D. M.
Published: December 2017

Effects of isometric contraction and catecholamines on glucose and glycogen metabolism in skeletal muscle were investigated with the in vitro rat epitrochlearis preparation. Mechanical performance and glycogenolysis exhibited two phases. During the initial 30 min, muscle work was 30% greater and glycogenolysis 8- to 10-fold faster than the steady-state values in the subsequent 3–4 h of contraction. Glucose uptake was increased by contraction and remained relatively constant during stimulation. Epinephrine (10(-9) to 10(-6) M) and norepinephrine (10(-7) to 10(-5) M) produced inotropic and glycogenolytic effects blocked by propranolol but not phentolamine. Chemical sympathectomy and propranolol blocked the initial glycogenolytic and inotropic effects produced by isometric contraction, suggesting that they were caused by the release of endogenous catecholamines. Net lactate production in resting muscles accounted for > 50% of total glucosyl units utilized. During contraction net lactate production accounted < 10–15% of total glycosyl flux indicating that rat fast-twitch pale muscle is capable of significant rates of aerobic glucose oxidation. Oleate and caprylate did not affect mechanical performance, glycogen, or glucose metabolism in resting or contracting muscles.
25(OH)D3 metabolism in kidney cell cultures: lack of a direct effect of estradiol
Authors: Henry H. L.
Published: December 2017

There are several reports of increased production of 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3] by the kidney of birds in response to estrogen treatment. To determine whether estradiol influences the renal cell directly, primary cultures of chick kidney cells were exposed to the steroid under a variety of conditions. In the absence of 1,25(OH)2D3, treatment of cultures for 20-24 h with 10(-5) and 10(-6) M estradiol led to inhibition of 25-hydroxyvitamin D3 [25(OH)D3]-1-hydroxylase activity. When the 1-hydroxylase was suppressed and 25(OH)2D3-24-hydroxylase was induced by treatment with 1,25(OH)2D3, estradiol in concentrations of 10(-9) and 10(-5) M either had no effect or slightly inhibited 1,25(OH)2D3 production. Similarly, 24R,25-dihydroxyvitamin D3[24,25(OH)2D3] production was not affected consistently by estradiol. These results were unaltered when either testosterone (10(-6) M) or insulin (5 micrograms/ml) was present in the medium. Shorter treatments (0.5, 2, 4, and 8 h) with estradiol resulted in a transient decrease in both 1,25(OH)2D3 and 24,25(OH)2D3 production, but at no time was stimulation observed. These results suggest that the effects of estrogens on 25(OH)D3 metabolism observed in vivo are exerted elsewhere than directly at the renal cell.
Insulin binding and sensitivity in rat skeletal muscle: effect of starvation
Authors: Brady L. J. , Goodman M. N. , Kalish F. N. , Ruderman N. B.
Published: December 2017

In contrast to adipose tissue and heart, the in vitro sensitivity of skeletal muscle to insulin is enhanced by starvation. To determine the basis for this, insulin binding and its ability to stimulate glucose metabolism were examined in the incubated rat soleus. In solei from 50-g rats, starvation for 48 h enhanced insulin binding by 50-100% at concentrations of 100 ng/ml or less. Starvation also resulted in higher basal and insulin-stimulated rates of glycogen synthesis, glycolysis, and glucose uptake. The enhanced effect of insulin only occurred at concentrations less than 50-75 ng/ml, in keeping with the increased binding of insulin in this concentration range. On the other hand, under conditions in which binding at equilibrium was the same, glucose uptake was still higher in the starved group, suggesting that some postreceptor event may have been more sensitive to insulin. These studies confirm that the in vitro sensitivity of rat skeletal muscle to insulin is enhanced by 48 h of starvation. They suggest that this is due at least partially to an increase in insulin binding at physiological concentrations.
Effect of maternal canine starvation on fetal and neonatal liver metabolism
Authors: Miettinen E. L.
Published: December 2017

Heptic glycolytic and gluconeogenic intermediates from fasted newborns of five control and five 3-day starved canine mothers (MCS) were studied at 0, 3, 6, 9, and 24 h of age. MCS did not affect fetal hepatic glycogen concentration; however, a significant increase in uridine diphosphate glucose (UDPG) (0.186 vs. 0.106 mumol/g), fructose 6-phosphate (0.084 vs. 0.034), pyruvate (0.321 vs. 0.126), and citrate (0.190 vs. 0.140) concentrations occurred. At 3 h, the intrahepatic glucose concentration among the MCS newborns declined (3.09 vs. 6.34) and remained lower than the controls for up to 9 h. UDPG concentration, however, remained elevated throughout the 24 h. In addition intrahepatic pyruvate was significantly elevated in the MCS group. Elevated phosphoenolpyruvate concentrations were observed between 3 and 6 h. Malate levels were lower than controls between 6 and 9 h and alpha-ketoglutarate was significantly higher between 6 and 24 h. Calculated cytoplasmic NAD/NADH ratio was elevated throughout the 24 h. Hepatic triglycerides were higher than controls up to 9 h. A decline in hepatic triglycerides was observed between 9 and 24 h. The results suggest increased glycolysis and suppressed gluconeogenesis in the MCS puppies, probably because of increased triglyceride synthesis and decreased free fatty acid oxidation resulting in a lack of cytoplasmic NADH.
Regulation of calcium homeostasis in the fetal and neonatal rat
Authors: Thomas M. L. , Anast C. S. , Forte L. R.
Published: December 2017

Circulating levels of calcium (Ca) and immunoreactive parathyroid hormone (IPTH), and the renal cyclic AMP responses to PTH, calcitonin (CT), and vasopressin (VP) were measured in fetal and neonatal rats. Serum Ca increased from a mean value of 9.1 mg/dl on the 19th day of gestation to 10.9 on day 20. Circulating IPTH decreased from 875 pg/ml to 213. Serum Ca declined rapidly after birth to a nadir of 7.6 by 3 h and IPTH increased to 2,006 pg/ml, indicating that fetal and newborn parathyroids are capable of responding appropriately to changes in circulating Ca. Renal responsiveness to hormones was assessed in vitro in the presence of methylisobutylxanthine, a phosphodiesterase inhibitor. The tissue cyclic AMP response to PTH and CT (15- to 18-fold over basal) was greatest at gestational days 18 and 19, progressively declined throughout the remainder of gestation, and remained low during the first 24 h after birth (6- to 7-fold). Renal cyclic AMP response to VP remained consistently low throughout this period. The depressed renal cyclic AMP response to PTH at the time of birth may contribute to the hypocalcemia found in newborn rats.
Alloxan action on glucose metabolism in cultured fibroblasts. II. Effects on pentose-monophosphate shunt and tricarboxylic acid pathways
Authors: Ishibashi F. , Bennett P. H. , Howard B. V.
Published: December 2017

The site of action of alloxan on glucose metabolism has been investigated using cultured human fibroblasts. Analysis of cell extracts after cell monolayers were exposed to D-[U-14C]glucose indicated that the initial stimulation of glucose incorporation by alloxan was observed primarily in the nucleotide fraction (ribose) with inhibition of lactate production. The subsequent inhibition of glucose incorporation was observed in the nucleotide fraction. Assay of 14CO2 production indicated that alloxan enhanced 14CO2 formation from D-[U-14C]glucose for approximately 10 min, followed by inhibition. To probe the site of alloxan action, rates of 14CO2 formation from 1- and 6-position labeled [14C]glucose, and [U-14C]pyruvate were compared. The initial stimulation was observed mainly in D-[1–14C]glucose oxidation, whereas inhibition was measurable with the 6-position tracer and [14C]pyruvate. The results suggest that alloxan initially stimulates the pentose-monophosphate shunt and then subsequently inhibits both the pentose-monophosphate shunt and tricarboxylic acid pathways.
Effects of GnRH and drugs that affect cAMP levels on LH synthesis and release
Authors: Liu T. C. , Wang P. S. , Jackson G. L.
Published: December 2017

We examined basal and gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone (LH) release and synthesis in response to drugs that raise intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels. Anterior pituitaries from ovariectomized rats were incubated with or without drugs in the presence of GnRH and [3H]glucosamine. Neither 8-bromo-cAMP (8-Br-cAMP) (10 mM), cholera toxin (10 micrograms/ml), nor phosphodiesterase inhibitors [theophylline, 2 and 8 mM; 3-isobutyl-1-methylxanthine (MIX), 0.2 mM] had any detectable effect on release of immunoreactive LH (IR-LH) when used alone. However, 8-Br-cAMP and the inhibitors potentiated (P less than 0.01) GnRH-induced release of IR-LH. Total radiolabeled LH in the system was elevated (P less than 0.01) by either GnRH, 8-Br-cAMP for cholera toxin, but reduced (P less than 0.01) by 8 mM theophylline and unaffected by MIX or 2 mM theophylline. 8-Br-cAMP did not alter the effect of GnRH on radiolabeled LH in the total system, whereas MIX and 2 mM theophylline reduced (P less than 0.05) it. These results suggest that 1) cAMP does not effect LH release directly, but may interact with GnRH to potentiate it, 2) GnRH and cAMP have a similar mode of action on LH glycosylation, and 3) phosphodiesterase inhibitors have additional actions that interfere with LH glycosylation.
Fetal fuels. IV. Regulation of branched-chain amino and keto acid metabolism in fetal brain
Authors: Shambaugh G. E. , Koehler R. A.
Published: December 2017

The regulation of branched-chain amino and keto acid metabolism was examined in fetal rat brains at 20 days gestation. When fetal brain slices were incubated with [1-14C]leucine, graded concentrations of beta-hydroxybutyrate or acetoacetate resulted in a progressive rise in labeled alpha-ketoisocaproic acid accompanied by a fall in 14CO2, whereas the sum of these products remained unchanged. These reciprocal relationships were maintained when leucine concentrations were varied from 0.4 to 4 mM. Increasing concentrations of glucose or pyruvate enhanced the formation of both 14CO2 and alpha-ketoisocaproic acid from [1–14C]leucine, but resulted in a progressive decrease in the conversion of alpha-ketoisocaproic acid to 14CO2. That glucose and ketone bodies probably acted via separate mechanisms was suggested by a further inhibition of alpha-ketoisocaproic acid decarboxylation whenever beta-hydroxybutyrate was added. When mothers were starved from days 18–20, a threefold rise in circulating branched-chain keto acids was reflected concordantly in the fetus and was attended by a significant enhancement of leucine transaminase activity in fetal brain. Because levels of circulating ketone bodies reported during maternal starvation were maximally effective in diminishing the conversion of alpha-ketoisocaproic acid to 14CO4, it is suggested that the inhibitory effects of beta-hydroxybutyrate on the critical dehydrogenase step in branched-chain keto acid metabolism in fetal brain could restrain oxidation of maternally derived alpha-ketoisocaproic acid, thereby permitting salvage for reversible transamination to leucine.
Protein synthesis in liver and small intestine in protein deprivation and diabetes
Authors: McNurlan M. A. , Garlick P. J.
Published: December 2017

Protein synthesis (as a percent of the protein pool synthesized per day) has been measured in liver and small intestine of young male rats from the incorporation of 100 mumol [1–14C]leucine/100 g body wt into protein over 10 min. Dietary protein deprivation for 8 days depressed protein synthesis in liver (30%), jejunal mucosa (20%), and jejunal serosa (25%). In serosa, reduced levels of RNA relative to protein could account for altered synthesis; in liver and mucosa, the amount of protein synthesized per unit RNA was reduced. In liver of streptozotocin-diabetic rats protein synthesis was depressed 45%, whereas it was maintained in jejunal mucosa and serosa. Depressed synthesis in liver was accompanied by both a loss of RNA relative to protein and a reduction in the protein synthesized per RNA.
Up-regulation of hepatic prostaglandin E receptors in vivo induced by prostaglandin synthesis inhibitors
Authors: Rice M. G. , McRae J. R. , Storm D. R. , Robertson R. P.
Published: December 2017

Up-regulation in vivo of liver plasma membrane receptors for prostaglandin E (PGE) was studied in Sprague-Dawley rats using the prostaglandin synthesis inhibitors, acetylsalicylic acid (ASA) and indomethacin (Indo). Following 4 days of treatment with ASA, the concentration of receptors and the affinity for binding were both significantly increased (Ro - +37%, KA = +62%). Following 4 days of treatment with Indo, the number of receptors was increased but the binding-site affinity was decreased (Ro = +40%, KA = -71%). Animals were then examined after treatment with either ASA or Indo for 1 day, a time when there was no significant decrease in PGE. After 1 day of treatment, the opposite changes in binding-site affinity were again observed, but there were no changes in the number of receptors with either drug, suggesting that the changes in affinity resulted from non-prostaglandin-related effects of the drugs. To ascertain the physiologic consequences of up-regulation, adenylate cyclase activity was measured in control and up-regulated membranes. There were no significant changes in basal or in PGE-stimulated adenylate cyclase activity. These data demonstrate that decreased endogenous PGE causes up-regulation of PGE receptors, but that this is not accompanied by increased adenylate cyclase activity. These data may indicate that PGE-stimulated adenylate cyclase operates maximally under normal receptor concentrations and that therefore its activity cannot be increased by regulatory changes in receptor density.
Action of thyrotropin-releasing hormone on mammotrophs and thyrotrophs
Authors: Snyder G. , Naor Z. , Fawcett C. P. , McCann S. M.
Published: December 2017

Anterior pituitary cells from 15-day female rats were separated by unit gravity sedimentation into four populations (designated regions I-IV) based on the profile of cell distribution and the resulting content of radioimmunoassayable (RIA) hormones. The cells in regions II and IV released thyrotropin (TSH) in response to thyrotropin-releasing hormone (TRH, 5 ng/ml); however, those in region IV released only approximately 5% of their RIA content, whereas those in region II released approximately 26% in response to the same stimulus. Concomitant elevation of cAMP and of cGMP occurred in region II cells but only cGMP was elevated in region IV cells. Mammotrophs were localized in region III. They responded to TRH by releasing prolactin (PRL) and exhibiting increased cAMP content. These data provide support for the existence of two functionally distinct populations of thyrotrophs in 15-day-old female rats. The data also imply that cAMP is involved in TRH induced PRL release, whereas cGMP is involved in TRH-induced TSH release.
Hypothalamic control of endocrine thermogenesis
Authors: Marques P. R. , Illner P. , Williams D. D. , Gren W. L. , Kendall J. W. , Davis S. L. , Johnson D. G. , Gale C. C.
Published: December 2017

Hypothalamic and ruminal cooling raised serum thyrotropin (TSH), adrenocorticotropin (ACTH), norepinephrine (NE), and glucose in conscious goats in 20 degree C ambient temperature. Cooling of the preoptic anterior hypothalamus (POAH) for 2 h initially evoked shivering and vasoconstriction, leading to 1.5 degree C rise in rectal temperature (Tr). Pituitary-thyroid activation by POAH cooling was shown by peak rises in TSH of 60% at 40 min, in triiodothyronine (T3) of 54% at 80 min, and in thyroxine (T4) of 40% at 140 min. At 60 min, ACTH and NE peaked at 57 and 65%, respectively. TSH, ACTH, and NE declined during the 2nd h of POAH cooling as Tr plateaued; when POAH cooling was stopped, these hormones fell below basal level as vasodilation and panting restored Tr to normal. In contrast to the core hyperthermia evoked by POAH cooling, ruminal intubation with O degree C water (1 liter/10 kg) led to general hypothermia, Tpoah and Tr falling 1.6 degree C at 40 min. Pituitary-thyroid responses were less but ACTH and NE more, compared with POAH cooling. TSH peaked at 37% at 20 min, T3 at 55% at 60 min, and T4 at 18% at 200 min. ACTH peaked at 250% at 30 min and NE at 120% at 20 min. Thermosensitive neurons in the POAH seem to mediate more sensitive and complete control over TSH than over ACTH, or NE release, whereas extrahypothalamic core thermosensitivity (e.g., brain stem, spinal cord, abdomen) may influence ACTH and NE more than TSH release.
Thyroid hormone-sensitive brown adipose tissue respiration in the newborn rabbit
Authors: Klein A. H. , Jenkins J. J. , Reviczky A. , Fisher D. A.
Published: December 2017

The effects of thyroid hormone treatment on brown adipose tissue (BAT) and liver metabolism were assessed by measuring oxygen consumption, sodium-potassium adenosine triphosphatase (Na-K-ATPase), and mitochondrial alpha-glycerophosphate dehydrogenase (alpha-GPD) activities in tissues from triiodothyronine- (T3) and vehicle-injected (for 3 days) newborn and adult rabbits. In the newborns, basal BAT cellular respiration was increased [mean (%/- SE) = 119 +/- 18 vs. 65 +/- 4 microliter O2/10(6) cells-1 . h in controls (P less than 0.005)], whereas hepatic respiration was unchanged. Ouabain had no effect on basal BAT cellular respiration, but suppressed hepatic respiration by 30% in both newborn groups. T3 treatment had no effect on NE- (10(-6) M) stimulated BAT respiration, whereas adult hepatic respiration was increased almost twofold. alpha-GPD activities were increased in both newborn BAT and adult liver but not in newborn liver. Na-K-ATPase activity was significantly increased only in newborn liver. In conclusion, 1) both BAT and liver are thyroid-hormone sensitive in the newborn rabbit, but the responses to T3 treatment are different in the two tissues; 2) the failure to stimulate both hepatic alpha-GPD and respiration in the newborn appears to be a developmental phenomenon characteristic of the rabbit; 3) thyroid hormones have little effect on sodium transport-dependent respiration in either BAT of liver in the newborn rabbit.
Comparison of canine corticosteroid responses to mean and phasic increases in ACTH
Authors: Wood C. E. , Shinsako J. , Dallman M. F.
Published: December 2017

To determine the dynamics and magnitudes of adrenal corticosteroid responses to ACTH, we measured arterial plasma ACTH and corticosteroid concentrations in conscious dogs during infusions of ACTH or saline. Synthetic alpha 1-24-ACTH was infused at rates of 300,900, or 4,500 ng/30 min either as constant infusions or as three equal short infusions at 10-min intervals. In dogs infused with saline, plasma ACTH fluctuated, whereas corticosteroids did not, suggesting that ACTH is secreted episodically in dogs as in man. The magnitudes of the plasma corticosteroid responses to ACTH infusions were linearly related to the logarithm of the total amount of ACTH infused in 30 min and not to the pattern of administration. In all ACTH infusion experiments, the lag between an increase in arterial ACTH and corticosteroids was not less than 3 min. Mean ACTH half-disappearance time, metabolic clearance rate, and volume of distribution estimated from the different experiments ranged between 1.8 and 2.1 min, 24 and 38 ml . kg-1 . min-1, and 95 and 114 ml/kg, respectively. Collectively, these results explain the apparent paradox that corticosteroid responses to ACTH-releasing stimuli can be initiated before a detectable increase in ACTH above the highest control value (Wood et al. Apparent dissociation of ACTH and corticosteroid responses to ml/kg hemorrhage in conscious dogs. Endocrinology In press).
Transient hepatic response to glucagon in man: role of insulin and hyperglycemia
Authors: Ferrannini E. , DeFronzo R. A. , Sherwin R. S.
Published: December 2017

We infused glucagon into normal humans while preventing changes in plasma glucose and insulin. Insulin (0.45 mU . min-1 . kg-1) were infused for 90 min, while euglycemia was maintained by a variable glucose infusion. Subsequently, glucagon (6 ng . min-1 . kg-1) was added, and changes in plasma glucose were avoided by appropriately reducing the glucose infusion. With insulin alone, glucose production (GP) fell to zero. When hyperglucagonemia (530 +/- 32 pg/ml) was superimposed, GP rose promptly and then slowly declined. However, between 180 and 240 min, GP remained elevated (1.72 +/- 0.30 mg . min-1 . kg-1) as compared to an insulin control study (0.03 +/- 0.20, P less than 0.025). When hyperglycemia (+25 mg/100 ml) was induced between 180 and 240 min, glucagon-stimulated GP was completely suppressed. To determine whether this effect was mediated by hyperglycemia per se or glucose-induced hyperinsulinemia, between 180 and 240 min we increased either a) the insulin infusion (by 0.25 mU . min-1 . kg-1) while maintaining euglycemia or b) plasma glucose (+25 mg/100 ml) while blocking insulin release with somatostatin. When the insulin was increased, GP declined by 68 +/- 13% (P less than 0.02). When plasma glucose alone was raised, GP fell from 1.44 +/- 0.09 to 0.07 +/- 0.16 mg . min-1 . kg-1 (less than 0.002). In conclusion, the hepatic response to sustained hyperglucagonemia is more persistent if changes in plasma glucose are prevented, and its transient nature is in part explained by a feedback adjustment to glucagon-induced hyperglycemia and hyperinsulinemia.
Effects of glucose, pyruvate, lactate, and amino acids on muscle protein synthesis
Authors: Hedden M. P. , Buse M. G.
Published: December 2017

Protein synthesis was measured in rat diaphragms incubated with serum amino acids + 0.35 mM L-[2,6-3H]tyrosine and different energy-yielding substrates. Muscles incubated with 5.5 mM glucose (with or without actinomycin D) synthesized more protein than those incubated with 11 mM pyruvate or 11 mM lactate. Tissue ATP decreased during incubation with lactate, but pyruvate maintained ATP, ADP, and creatine phosphate as well as glucose. Glucose 6-phosphate decreased in muscles incubated in glucose-free media. 14CO2 production from substrates was [1-14C]pyruvate greater than [1-14C]lactate greater than [3,4-14C]glucose. Intracellular lactate/pyruvate was measured to assess cytoplasmic free NADH/NAD+; the effect of different media on these ratios was lactate greater than glucose = lactate + pyruvate greater than pyruvate + glucose greater than pyruvate. Lactate + pyruvate (8.8 + 2.2 mM) supported protein synthesis better than pyruvate and as well as glucose. Adding glucose to pyruvate accelerated protein synthesis and increased NADH/NAD+. Iodoacetate (0.1 mM) inhibited glycolytic NAD reduction and abolished the stimulatory effect of glucose on protein synthesis in the presence of pyruvate. Supplementation of pyruvate media with 1 mM leucine or isoleucine stimulated protein synthesis, but beta-hydroxybutyrate, malate, alpha-ketoisocaproate, and all other amino acids were ineffective. The cytoplasmic redox potential may act as a translational modulator of protein synthesis in skeletal muscle.
Responses of ram lambs to active immunization against testosterone and luteinizing hormone-releasing hormone
Authors: Schanbacher B. D.
Published: December 2017

Active immunization of young ram lambs against testosterone and luteinizing hormone-releasing hormone (LHRH) was shown to block the growth attributes characteristic of intact ram lambs. Testosterone and LHRH-immunized lambs grew at a slower rate and converted feed to live weight gain less efficiently than albumin-immunized controls. Lambs immunized against testosterone and LHRH had high antibody titers for their respective antigens. Moreover, testosterone-immunized lambs had high serum concentrations of luteinizing hormone (LH) and testosterone, whereas LHRH-immunized lambs had low to nondetectable serum concentrations of these hormones. Release of LH and testosterone following the intravenous administration of LHRH (250 ng) was absent in LHRH-immunized lambs, but quantitatively similar for intact and albumin-immunized control lambs. Testosterone-immunized lambs responded as did conventional castrates with a large LH release, but testosterone concentrations were unchanged. These findings are discussed relative to the integrity of the hypothalamic-pituitary-testicular endocrine axis and the importance of gonadotropin support for normal testicular development. These data show that LHRH immunoneutralization effectively retards testicular development and produces a castration effect in young ram lambs.
Adipose lipoprotein lipase in insulin-treated diabetic lean and obese Zucker rats
Authors: Chan C. P. , Stern J. S.
Published: December 2017

Obese and lean alloxan-diabetic rats were given daily injections of insulin for 9 days. Plasma glucose and insulin concentrations were not different between the two genotypes given comparable amounts of insulin. Carcass fat and epididymal and retroperitoneal fat pad weights increased as the dose of insulin was increased. At each of four doses, fatties had larger fat cells, bigger pads, and more body fat than lean rats. Adipose lipoprotein lipase (LPL) activity per pad or per fat cell was increased by insulin. Except for the lowest dose of insulin, LPL activity was higher in obese rats than in lean rats. LPL activity per cell and cell size were highly correlated. However, when differences in cell size were corrected for, no significant effect of genotype existed. Cardiac LPL activities were different between the two genotypes only in nondiabetic rats. These results suggested that both insulin and some other genetic factors were important in elevating adipose LPL activities and thus fat deposition in obese Zucker rats.
Calcium channel and prolactin release in rat clonal pituitary cells: effects of verapamil
Authors: Ozawa S. , Kimura N.
Published: December 2017

Effects of verapamil on membrane electrical properties and prolactin release were studied in a rat anterior pituitary cell line GH3. Thyrotropin-releasing hormone (TRH), Ba2+, and high concentration of K+ enhance the release of prolactin from GH3 cells. These stimulatory actions on prolactin release were inhibited by adding 10(-4) M verapamil to the bathing mediums. The maximum rate of rise of the Ca action potential was reduced to 17% of the control by addition of 10(-4) M verapamil. Ba2+ caused a sustained membrane depolarization because Ba2+ goes through the Ca channels and blocks the development of the delayed rectification. This effect of Ba2+ was also inhibited by verapamil. Verapamil suppressed both the Na+ and outward K+ currents in addition to the Ca2+ current. The suppressive effect of verapamil on the voltage-sensitive Ca current is probably responsible for the inhibition of TRH- and high K+-stimulated prolactin release because the suppression of the Na+ and outward K+ currents does not inhibit the stimulatory actions of these secretagogues
Androgen resistance syndromes
Authors: Griffin J. E. , Leshin M. , Wilson J. D.
Published: December 2017

Hereditary defects that impede androgen action cause resistance to the hormone both during embryogenesis and in later life and hence usually cause developmental defects of the male urogenital tract. In genetic males such defects produce a phenotypic spectrum ranging from infertile but otherwise normal men to individuals with varying degrees of ambiguous genitalia to phenotypic women. These disorders can be classified on the basis of the step in androgen action that is impeded by the individual mutations. 5 alpha-Reductase deficiency is an autosomal recessive enzyme defect that impairs the conversion of testosterone to dihydrotestosterone. The internal male genital tract virilizes normally, but the external genitalia are predominantly female in character. The syndrome is the result of one of several mutations that impair the function of the 5 alpha-reductase enzyme. A variety of disorders influence the androgen receptor that mediates the action of both testosterone and dihydrotestosterone. At least four phenotypic variants can be distinguished: complete testicular feminization, incomplete testicular feminization, the Reifenstein syndrome, and the infertile male syndrome, each of which is inherited as an X-linked trait. Absence of receptor binding is found commonly in complete testicular feminization, but qualitative and/or less severe quantitative defects in receptor function can be associated with all four variants. A third type of disorder, receptor positive resistance, also causes variable defects in male development and is associated with normal 5 alpha-reductase activity and normal androgen receptor. The underlying defect is presumed to lie at the intranuclear site or sites of action of the hormone-receptor complex.