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Biomedical subjects

M R Brown

Publications and source records attributed to M R Brown.

At least 235 records · Page 13Linked to original sources
PubMed1987

Toxic and antifeeding actions of melittin in the corn earworm, Heliothis zea (Boddie): comparisons to bee venom and the insecticides chlorpyriphos and cyromazine.

The acute and sublethal effects of melittin were compared to whole bee venom, chlorpyriphos and cyromazine injected into the corn earworm, Heliothis zea (Boddie). Melittin had twice the toxicity of crude venom, but only 3% that of chlorpyriphos. Melittin significantly reduced growth rate, diet consumption and food utilization efficiencies of fourth instar larvae. Bee venom and insecticides reduced these parameters to a lesser extent.

Bee Venoms↗
PubMed1987

Media for study of growth kinetics and envelope properties of iron-deprived bacteria.

Ion-exchange chromatography was used to remove iron from complex and chemically defined laboratory media. The kinetics of metal cation removal from the media was investigated by using atomic absorption spectrophotometry, and the results indicated that over 90% of the iron could be eliminated from certain complex media by this treatment. The treated medium was used for growth studies in a gram-positive and a number of gram-negative organisms that were isolated from infections in humans. High-molecular-weight outer membrane proteins that are known to be induced under iron-depleted growth conditions (iron-regulated membrane proteins) were observed when a number of gram-negative pathogens were cultivated in the treated media. Iron uptake by Staphylococcus aureus varied, depending on the iron content of the medium.

Bacterial Outer Membrane Proteins↗
PubMed1987

Multiple effects of phorbol ester on secretory activity in rabbit gastric glands and parietal cells.

Acid secretory activity and respiration in rabbit gastric glands are stimulated by cAMP-dependent and -independent agonists. Potentiation between agonists suggests interaction of the activation pathways. Regulation of secretory response by protein kinase C was investigated with 12-0-tetradecanoyl phorbol-13-acetate (TPA). TPA elevated basal respiration, pepsin release, and acid secretion but inhibited histamine and carbachol stimulation of acid secretion by gastric glands, as measured by [dimethylamino-14C]aminopyrine accumulation. The inhibition of histamine response was specific for protein kinase C activators, occurred after a 20-min lag, and was not reversed by removal of TPA after 3 min of preincubation. TPA pretreatment inhibited acid secretory responses to cholera toxin and forskolin but enhanced the response to cAMP analogues. Cholera toxin and pertussis toxin simulated ADP-ribosylation of 45 and 41 kDa proteins, respectively, in parietal cell membranes. Therefore, both stimulatory (Gs) and inhibitory (Gi) GTP binding proteins of adenylyl cyclase appear to be present in parietal cells. Pretreatment with pertussis toxin attenuated PGE2 but not TPA inhibition of histamine stimulation of aminopyrine accumulation. Thus, the inhibitory effect of TPA does not appear to be associated with an action on Gi. The results with histamine and carbachol suggest that protein kinase C may regulate both cAMP-dependent and -independent stimulation of parietal cell acid secretion.

Adenosine Diphosphate↗
PubMed1987

Histamine increases phosphorylation of 27- and 40-kDa parietal cell proteins.

Purified, hormonally responsive parietal cells from rabbit gastric mucosae were used as a model to study intracellular mechanisms controlling parietal cell HCl secretion. Using a high-resolution, two-dimensional electrophoretic technique, we demonstrate that histamine increases phosphorylation of two parietal cell proteins with approximate molecular weights of 27 and 40 kDa and respective pIs of 5.9 and 6.2. The increase in phosphorylation appears to be mediated via an adenosine 3',5'-cyclic monophosphate (cAMP)-dependent mechanism because cAMP analogues and forskolin stimulate phosphorylation of these proteins, whereas the cholinergic agonist, carbachol, which elevates parietal cell intracellular free calcium concentration but not cAMP content, and the calcium ionophore, ionomycin, do not. Both phosphoproteins are located in low-speed particulate fractions. The 40-kDa phosphoprotein was found in both enriched chief and parietal cells. This phosphoprotein may be cytoskeleton associated, since it is detected in a Triton-insoluble particulate fraction after prolonged exposure of parietal cells to Triton X-100. The 27-kDa phosphoprotein was detected in parietal but not in enriched chief cells and appeared to be localized in a low-speed fraction previously shown to contain increased H+-K+-ATPase activity after histamine stimulation. The location and rapid increase in phosphorylation of the 27-kDa phosphoprotein upon histamine stimulation make this protein an attractive candidate for future studies of intracellular regulation of parietal cell HCl secretion. The 40-kDa phosphoprotein may play a more general role in control of cytoskeletal activity, and perhaps, in morphological transformations associated with stimulus-secretion coupling.

Animals↗
PubMed1987

CRF initiates biological actions within the brain that are observed in response to stress.

Corticotropin-releasing factor (CRF) is thought to be an endogenous mediator of adrenocorticotropic hormone release following stress. We examined if CRF initiates further biological actions that are observed in response to stressful events. Male beagle dogs (10-12 kg) were fitted with a chronic intracerebroventricular cannula, intra-arterial and intravenous catheters, as well as a gastric fistula. Synthetic human CRF was microinjected into the third cerebral ventricle in conscious animals. CRF (0.1-1.0 nmol/kg) significantly (P less than 0.01) increased plasma concentrations of epinephrine, norepinephrine, glucagon, and glucose and elevated mean arterial pressure and heart rate. Pretreatment of the animals with the ganglionic blocking agent chlorisondamine completely abolished the increases in plasma catecholamine and glucose concentrations as well as the elevations in blood pressure and heart rate. CRF significantly (P less than 0.01) inhibited gastric acid secretion, but not plasma gastrin concentrations stimulated by an 8% liquid peptone meal. The gastric inhibitory action of CRF was completely prevented by chlorisondamine and, in part, by naloxone and a vasopressin antagonist. In contrast, bilateral truncal vagotomy did not affect the gastric inhibitory action of CRF. The results of this study indicate that CRF acts within the central nervous system to increase plasma glucose and glucagon concentrations, mean arterial pressure, and heart rate by activation of the autonomic nervous system. CRF inhibits meal-stimulated gastric acid secretion by activation of the sympathetic nervous system and, in part, by opiate and vasopressin-dependent pathways and not by inhibition of gastrin release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Corticotropin-releasing factor receptor antagonist: effects on the autonomic nervous system and cardiovascular function.

The corticotropin-releasing factor (CRF) receptor antagonist, alpha-helical [Glu27]-corticotropin-releasing factor 9-41 (CRF 9-41) has been assessed for its ability to modify plasma concentrations of epinephrine and norepinephrine, mean arterial pressure (MAP) and heart rate (HR). Basal concentrations of epinephrine and norepinephrine were not altered by lateral ventricular (icv) administration of CRF 9-41. However, this CRF antagonist, given icv, attenuated the rise of plasma epinephrine following 30% hemorrhage and insulin-induced hypoglycemia. CRF 9-41 did not alter the increased plasma concentrations of epinephrine or norepinephrine following icv administration of bombesin. Icv administration of CRF 9-41 blunted CRF-induced elevation of MAP and HR in normal animals. However, this CRF antagonist did not modify the MAP or HR in spontaneously hypertensive rats. Similarly, this CRF antagonist administered to Sprague-Dawley rats neither prevented the rise of MAP or HR following electrical stimulation of the central nucleus of the amygdala, nor did it affect nitroprusside-induced hypotension and tachycardia.

Amygdala↗
PubMed1986

Glucocorticoid suppression of the sympathetic nervous system and adrenal medulla.

Studies were performed to evaluate the effects of glucocorticoids on the activity of the sympathetic nervous system and adrenal medulla. Plasma concentrations of norepinephrine and epinephrine were measured in rats in which endogenous glucocorticoids were removed by bilateral adrenalectomy and in rats to which exogenous glucocorticoids were administered. In intact rats, dexamethasone (2.5, 25 or 250 micrograms) pretreatment suppressed ether vapor-induced elevations of norepinephrine and epinephrine concentrations in plasma. Corticosterone (3 mg/kg), similar to dexamethasone, attenuated the elevation of plasma concentrations of norepinephrine and epinephrine in rats exposed to ether vapor. Glucocorticoids did not alter the elevation of plasma catecholamines stimulated by intracerebroventricular injections of corticotropin-releasing factor or calcitonin gene-related peptide, thus demonstrating functional integrity of the sympathetic nervous system and adrenal medulla. Adrenalectomy resulted in elevation of basal plasma norepinephrine levels and accentuation of ether vapor-induced elevations of plasma norepinephrine concentrations in rats. Dexamethasone (25 ug) administration blunted the effects of adrenalectomy on both basal and ether vapor-stimulated levels of plasma norepinephrine. It is concluded that glucocorticoids acting at as yet undefined sites may be involved in the regulation of sympathetic nervous system and adrenal medullary function.

Adrenal Medulla↗
PubMed1986

Release of intracellular Ca2+ and elevation of inositol trisphosphate by secretagogues in parietal and chief cells isolated from rabbit gastric mucosa.

The fluorescent intracellular Ca2+ indicator, fura2/AM, was used to determine the effects of carbachol, cholecystokinin octapeptide (CCK-8), gastrin and histamine on intracellular Ca2+ ([Ca2+]i) in parietal cells from rabbit gastric mucosa enriched to more than 95% purity by a new Nycodenz gradient/centrifugal elutriation technique. Changes in [Ca2+]i in response to the same agonists were also measured in enriched chief cells. Carbachol, histamine, gastrin and CCK-8 increased parietal cell [Ca2+]i with the response to carbachol greater than CCK -8 = histamine = gastrin. Prestimulation with msximal doses of carbachol blocked histamine-induced increases in [Ca2+]i. In chief cells, carbachol increased [Ca2+]i but to a lesser degree than CCK-8, while histamine had no significant effect on [Ca2+]i. Neither removal of extracellular Ca2+ coupled with acute addition of 1 mM EGTA nor addition of the Ca2+-channel blocker nicardipine prevented agonist-induced changes in [Ca2+]i in either cell type. In the presence and absence of 10 mM LiCl2, carbachol and CCK-8 were found to increase inositol trisphosphate (IP3) content in both parietal and chief cells while histamine had no significant effect on this phosphoinositide hydrolysis product. From these results and previous observations with gastric glands (Chew, C.S. (1986) Am. J. Physiol. 13, G814-G823) we conclude that: carbachol, CCK-8, gastrin and histamine increase parietal cell [Ca2+]i initially by release of Ca2+ from the same intracellular store(s); the release of [Ca2+]i in response to carbachol and CCK-8 in both chief and parietal cells appear to be mediated by IP3; however, other mechanisms may be involved in histamine-induced release of parietal cell Ca2+.

Animals↗
PubMed1986

Mosquito trypsin: immunocytochemical localization in the midgut of blood-fed Aedes aegypti (L.).

A polyclonal antibody was raised against trypsin purified from the midgut of blood-fed Aedes aegypti. Using this antibody and our modification of the peroxidase-antiperoxidase immunocytochemical reaction, strong activity was found in the lumen of the midgut at the light-microscopical level. The activity was localized mainly in the posterior part of the distensible, abdominal midgut, along the periphery of the blood bolus and within the peritrophic membrane. Immunoreactivity appeared 8 h after the blood meal and was most prominent around 24 h, coinciding with our previous spectrophotometric determinations of trypsin. At the electron-microscopical level, secretory granules, immunocytochemically labelled with anti-trypsin antibody and protein A-colloidal gold, were first detected about 12 h after the blood meal. At 18 h, the secretory pathway could be followed immunocytochemically from the formation of granules in the Golgi complex until their release by exocytosis in the midgut lumen. By 24 h, there was a reduction in secretory granules, and large lysosomes appeared. The process of secretion described for this mosquito is comparable to similar events in vertebrate secretory systems and the presence of an intracellular trypsinogen is suggested.

Aedes↗
PubMed1986

Inhibition of gastric acid secretion by brain peptides in the dog. Role of the autonomic nervous system and gastrin.

We have studied the effects of 30 peptides administered intracerebroventricularly on basal and pentagastrin-stimulated (8 micrograms/kg s.c.) gastric acid secretion in conscious dogs. None of the peptides significantly increased basal gastric acid secretion. Twelve peptides (2 nmol/kg) significantly (p less than 0.01) decreased the pentagastrin-stimulated 2-h acid output (percentage inhibition in parentheses): human calcitonin (CT) (36%), neurotensin (NT) (52%), rat corticotropin-releasing factor (CRF) (59%), human calcitonin gene-related peptide (CGRP) (59%), ovine CRF (66%), beta-endorphin (beta-End) (80%), urotensin-I (81%), rat CT (81%), porcine gastrin-releasing peptide (GRP) (83%), sauvagine (Svg) (85%), rat CGRP (87%), and bombesin (Bom) (95%). Blockade of the autonomic nervous system with chlorisondamine abolished the gastric inhibitory action induced by CRF, beta-End, CT, and NT, but not by CGRP and Bom (1 nmol/kg each). Corticotropin-releasing factor, beta-End, CT, NT, CGRP, and Bom significantly inhibited gastric acid secretion stimulated by an intragastric 8% peptone meal for 2 h. None of these six peptides significantly altered plasma gastrin concentrations in response to the peptone meal as compared with control experiments. A rise of plasma concentrations of gastrin, CT, CRF, and CGRP could not be detected by radioimmunoassay in animals after intracerebroventricular administration of these four peptides. The results of this study indicate that CT, CGRP, NT, beta-End, and peptides of the CRF and Bom families act within the brain to inhibit pentagastrin- and meal-stimulated gastric acid secretion in conscious dogs. None of the 30 peptides administered intracerebroventricularly increased basal gastric acid secretion in the dog. Inhibition of gastric acid secretion induced by CRF, beta-End, CT, and NT, but not by CGRP and Bom is mediated by the autonomic nervous system. Gastrin does not appear to play a role in gastric acid inhibition induced by the six brain peptides studied.

Animals↗
PubMed1986

FMRFamide- and pancreatic polypeptide-like immunoreactivity of endocrine cells in the midgut of a mosquito.

Immunocytochemical surveys of midguts from female mosquitoes, Aedes aegypti, reveal that half of the estimated 500 endocrine cells in a midgut contain a substance recognized by antisera to bovine pancreatic polypeptide and a molluscan peptide, FMRFamide (phenylalanine-methionine-arginine-phenylalanine-amide). With light microscopy the cells resemble an endocrine type because of their basal position in the epithelium, conical shape, and, in some instances, apical extensions to the lumen. At the ultrastructural level, the immunoreactive substance is contained specifically within the secretory granules of such cells. Immunoreactive cells are distributed exclusively in the midgut region where blood is stored, and ingestion of vertebrate blood reduces the number of such cells and the intensity of reaction in others. These two facts suggest that a blood meal stimulates release of the immunoreactive substance from the cells. Since the immunocytochemical localization is supplemented by a demonstrated secretory response, the cells are considered to be peptidergic endocrine cells.

Aedes↗
PubMed1986

Effects on mastitis of overmilking in conjunction with pulsation failure.

Half-udder comparisons were made using 56 cows for 2 months, in an experiment involving high bacterial challenge, to assess the combined effects of 5 min overmilking and pulsation failure (resulting from the use of shortened teacup liners) on teat condition and mastitis. Only three new infections were confirmed in over 12500 quarter milkings in quarters milked with control liners (of 148 mm effective length) indicating little or no effect of prolonged overmilking in these quarters. A 3.5-fold increase in the new infection rate (NIR) based on bacteriological diagnosis alone (P less than 0.01), or a 9-fold increase in NIR based on bacteriological diagnosis plus raised cell count and/or N-acetyl-beta-D-glucosaminidase (P less than 0.01), occurred in quarters milked with the same liners shortened to an effective length of 120-130 mm. The mean interval to infection or teat canal colonization (41 v. 60 milkings), and for a quarter infection to be confirmed by other diagnostic tests (45 v. 79 milkings) was significantly less in quarters overmilked with short liners. The results confirm that NIR increases whenever pulsation fails. Overmilking may increase NIR when it is associated with pulsation failure.

Animals↗
PubMed1986

Deliberate overfeeding in women and men: energy cost and composition of the weight gain.

1. Thirteen adult females and two males were overfed a total of 79-159 MJ (19,000-38,000 kcal) during a 3-week period at the Clinical Research Center, Rochester. The average energy cost of the weight gain was 28 kJ (6.7 kcal)/g, and about half the gain consisted of lean body mass (LBM) as estimated by 40K counting. 2. A survey of the literature disclosed twenty-eight normal males and five females who had been overfed a total of 104-362 MJ (25,000-87,000 kcal) under controlled conditions: twenty-five of these had assays of body composition, and three had complete nitrogen balances. 3. When these values were combined with those from our subjects (total forty-eight), there was a significant correlation between weight gain and total excess energy consumed (r 0.77, P less than 0.01) and between LBM gain and excess energy (r 0.49, P less than 0.01). Based on means the energy cost was 33.7 kJ (8.05 kcal)/g gain and 43.6% of the gain was LBM; from regression analysis these values were 33.7 kJ (8.05 kcal)/g gain and 38.4% of gain as LBM. 4. Individual variations in the response could not be explained on the basis of sex, initial body-weight or fat content, duration of overfeeding, type of food eaten, amount of daily food consumption or, in a subset of subjects, on smoking behaviour. 5. The average energy cost of the weight gain was close to the theoretical value of 33.8 kJ (8.08 kcal)/g derived from the composition of the tissue gained.

Adolescent↗
PubMed1986

Proximal muscle weakness and selenium deficiency associated with long term parenteral nutrition.

A 33-yr-old white female with short bowel syndrome secondary to trauma was maintained on home parenteral nutrition for 4 yr when her plasma, red cell, white cell, and platelet glutathione peroxidase (GSHPx) activities were found to be extremely low, as were her plasma and red cell selenium levels. During her first year on parenteral nutrition she noted the onset of an inability to rise from a squatting position, rapid tiring when stair climbing, and weakness when attempting to lift large or moderately heavy objects. Treatment with 400 micrograms/d of selenious acid intravenously was associated with a disappearance of her symptoms and an increase in proximal muscle strength within 6 wk. The plasma and red cell selenium levels, and the plasma and white cell GSHPx activities rose to normal levels within 6 wk. Red cell GSHPx activity returned to normal by 3 mo.

Adult↗
PubMed1986

The influence of the O and K antigens of Klebsiella aerogenes on surface hydrophobicity and susceptibility to phagocytosis and antimicrobial agents.

The surface hydrophobicity of Klebsiella aerogenes is influenced by the presence of capsular (K) and lipopolysaccharide (O) antigens. Loss of both K and O antigens (K-O-), but not the K antigen alone (K-O+), increased surface hydrophobicity and susceptibility to phagocytosis. Unheated serum (i.e., containing complement) increased the surface hydrophobicity and phagocytosis of the K-O+ and K-O- strains, but not of the K+O+ encapsulated parent strain. Despite the altered susceptibility to phagocytosis caused by the presence or absence of the K and O antigens, their loss did not influence sensitivity to a range of hydrophilic, hydrophobic or cationic antimicrobial agents.

Alkanes↗
PubMed1986

Influence of growth rate and iron limitation on the expression of outer membrane proteins and enterobactin by Klebsiella pneumoniae grown in continuous culture.

The influence of the growth rate on outer membrane protein composition and enterobactin production was studied with Klebsiella pneumoniae grown under conditions of iron limitation in chemostats. More enterobactin was produced at fast (D = 0.4 h-1) and slow (D = 0.1 h-1) growth rates in continuous cultures than in either logarithmic- or stationary-phase batch cultures. When the growth rate was controlled under conditions of carbon limitation and the iron level was reduced to 0.5 microM, the iron-regulated outer membrane proteins and enterobactin were induced at the fast growth rate. At the slow growth rate, although the iron-regulated outer membrane proteins were barely visible, a significant level of enterobactin was still produced. These results suggest that under conditions of either carbon or iron limitation, the growth rate can influence the induction of the high-affinity iron uptake system of K. pneumoniae. Other outer membrane proteins, including a 39-kilodalton peptidoglycan-associated protein, were found to vary with the growth rate and nutrient limitation.

Bacterial Outer Membrane Proteins↗