Deuterium isotope effects on the enzymatic oxidative deamination of trace amines.
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Biomedical subjects
Publications and source records attributed to B Davis.
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A cluster of five cases of non-O group 1 (non-O1) V. cholerae gastroenteritis occurred in one Florida locality during November 1979. Clinical findings included nausea, vomiting, and abdominal cramping in all affected persons; two had bloody diarrhea. All five persons gave a history of eating raw oysters within four days of onset of illness. A case-control study statistically associated the eating of raw oysters with development of illness (p = 0.0008); this finding was confirmed by a retrospective cohort study of patients hospitalized for diarrhea (p = 0.0001). Non-O1 V. cholerae organisms were isolated from oysters and water samples taken from areas where ill persons had obtained their oysters. In at least one instance the same serotype was isolated from a patient's stool specimen and from the water where the patient had obtained oysters. Non-O1 V. cholerae infection must be considered in the differential diagnosis of shellfish-associated gastroenteritis.
In carrying out a new study of nucleotide concentrations in dystrophic muscle, we utilized myosin as a reference base. In nine control vastus lateralis muscle samples, nucleotide concentrations were 105 +/- 11 (SEM) moles of adenosine triphosphate (ATP) and 446 +/- 57 (SEM) nmoles of creatine phosphate (CP) per milligram of myosin. In seven Duchenne dystrophic vastus lateralis muscle samples, nucleotide concentrations were 127 +/- 25 (SEM) nmoles of ATP and 462 +/- 119 (SEM) moles of CP per milligram of myosin. The CP:ATP ratio of 3.6 +/- 0.367 from Duchenne muscle was not significantly different from normal, 4.32 +/- 0.243 ((p less than 0.20). In addition, myokinase activity, which is automatically assayed in these assays, was significantly increased in the Duchenne samples (p less than 0.10). The percent of myosin per total protein in the Duchenne biopsies was also diminished by 29% (p less than 0.01). These studies suggest that ATP and CP concentrations are not decreased in Duchenne dystrophic muscle when expressed in relation to the amount of contractile protein.
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Program planning and the initial experience of a new teaching ward for geriatric psychiatry are described. Elderly psychiatric patients, with diagnoses predominantly of depression and dementia, demonstrate more self-centeredness and less group awareness than do younger patients. Ward staff members often experience frustration, sadness and anger in response to working with them. Major problems unique to a geriatric psychiatry service include the paucity of adequate resources for post-discharge care and the necessity to obtain excellent medical-surgical consultation and support.
A service for 300 adult asthmatics is described. Since the service was started in 1970 only one death has occurred and this patient failed to comply with treatment or advice. Two patients required intermittent positive pressure ventilation. The success of the service is founded on two facts. Firstly, the natural history of life-threatening asthma usually allowed time to change treatment at home or in a clinic and this prevented the development of the severe grades. Secondly, the great majority of asthmatics could be taught how to recognise worsening of their asthma and to communicate with a doctor who then changed the treatment. An essential feature of the service is that the patients had at all times easy access to a doctor with appropriate knowledge and attitudes.
Our aim was to determine whether adrenergic as well as cholinergic nerves mediate secretion of fluids from tracheal submucosal glands and, if so, via which receptors. To do this, we studied the secretory responses of tracheal segments to electrical and pharmacologic stimulation in vitro in the presence and absence of a specific nerve blocker and autonomic antagonists. Stimulation caused small elevations, or "hillocks," the size of which we estimated by measuring their diameters. We found that electrical stimulation, acetylcholine, and phenylephrine each caused secretion but that terbutaline did not. Tetrodotoxin prevented the secretory response to electrical stimulation but did not prevent the responses to acetylcholine or phenylephrine. Neither atropine nor phentolamine alone prevented the response to electrical stimulation, but both drugs together did, and propranolol did not inhibit the adrenergic component of the response to electrical stimulation. Atropine blocked the response to acetylcholine, and phentolamine blocked the response to phenylephrine. We conclude that adrenergic and cholinergic nerves mediate secretion from the tracheal glands of ferrets via alpha-adrenergic and muscarinic receptors, respectively.
In cat trachea mounted in Ussing chambers, we studied the effects of an alpha-adrenergic agonist on mucus secretion measured with 35S bound to sulfated glycoproteins, and on fluxes of Na+ and Cl- ions measured with 22Na and 36Cl, under open-circuit conditions. Phenylephrine (10(-5) M), increased bound 35S-secretion by 147 +/- 24% (mean +/- SE, n = 13), increased JCl-S yields L from 2.54 +/- 0.23 to 7.40 +/- 1.19 microEq/cm2/h (n = 6), and increased JNaS yields L from 1.75 +/- 0.36 to 7.25 +/- 1.10 microEq/cm2/h (n = 6), it decreased 4Cl--L yields S from 2.69 +/- 0.41 to 2.46 +/- 0.41 microEq/cm2/h, but did not change JNa+L yields S. The stimulatory effects of (10(-5) M) phenylephrine were prevented by (10(-5) M) phentolamine, but were unaffected by (10(-5) M) propranolol. In contrast, (10(-5) M) terbutaline, a beta 2-adrenergic agonist, only increased bound 35S secretion by 43 +/- 7% (n = 22) and only increased JCl-S yields L from 3.76 +/- 0.46 to 4.55 +/- 0.41 microEq/cm2/h (n = 6); it did not change the other fluxes. These findings indicate that alpha-adrenergic stimulation causes secretion of sulfated glycoproteins and ion-mediated movement of water into the cat trachea.
The respiratory inductive plethysmograph, a monitor of ventilation that does not require a connection from the airway, was validated against spirometry during moderate exercise using a bicycle ergometer and a treadmill. One hundred seventy-three of 200 breaths during bicycle exercise from 6 young adults and 211 of 242 breaths during treadmill walking were within +/- 20% of the tidal volumes measured by simultaneous spirometry. The respiratory inductive plethysmograph appears to be a useful non-invasive monitor of ventilation during exercise.
We used a new non-invasive monitor of ventilation, the respiratory inductive plethysmograph, to determine the effects of breathing through a mouthpiece (with nose clip) and breathing through external dead spaces on ventilation at rest and during exercise. Six normal young subjects were studied during 5-min sequential periods at rest, submaximal exercise on a bicycle at a work load of 800 kgm/min, and recovery. Not surprisingly, the imposition on the respiratory system of breathing through a mouthpiece (with nose clip) and with external dead spaces of 150, 250, and 350 ml produced progressively greater ventilation than natural breathing during rest and submaximal bicycle exercise. However, when the actual tidal volumes were corrected for the increase in ventilation caused by the external dead space, ventilation both at rest and during exercise with mouthpiece breathing still remained higher than natural breathing. These data suggest that breathing through a mouthpiece (with nose clip) and breathing through external dead spaces stimulates ventilation both at rest and during exercise.
Our group developed two in vivo methods to study secretions from submucosal glands in exposed tracheal epithelium. (1) The exposed mucosal surface was coated with powdered tantalum; accumulated secretions produced elevations (hillocks) in the tantalum layer under which the duct openings were located. The rate of formation of the hillocks was observed through a dissecting microscope, and recorded by television on a video tape recorder. (2) Micropipets were used to collect timed samples from individual gland duct openings. With these techniques, the innervation of the submucosal glands and the autonomic regulation of their secretions were studied. We studied the control of ion movement across tracheal epithelium because active ion transport forms local osmotic gradients across epithelia which could regulate transepithelial water movement. We mounted pieces of the posterior wall of dog trachea in Ussing-type chambers and measured unidirectional fluxes of Cl- and Na+ under short-circuit conditions with 36Cl and 24Na. We found active transport of Cl- toward the lumen and Na+ toward the submucosa. With this technique we investigated the effect of parasympathomimetic drugs on ion movement. With a new in vitro method we studied output of 35S bound to sulfated mucins and movement of ions in cat trachea. We mounted pieces of anterior tracheal wall in Ussing-type chambers, added sodium 35S-sulfate to the submucosal side and monitored secretion of bound 35S in samples from the luminal side after dialysis. The unidirectional fluxes of Cl- and Na+ were measured with 36Cl and 22Na. With this method we examined the effect of alpha-adrenergic and beta-adrenergic agonists on mucin secretion and ion movement. Also with this preparation we studied the relationship between the permeability of the paracellular pathway to 14C-sucrose and the pattern of tight junction strands.
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The effect of various osmotica and lytic enzyme treatments, on the release of stable protoplasts from Aspergillus niger and two strains of Aspergillus fumigatus, has been investigated. Most osmotica supported protoplast release at a concentration of 0.6 M except for CaCl2 and Ca(NO3)2. Supplementation of 0.6 M KCl with 0.2 M CaCl2 enhanced release from both species, but depended upon strain of organism, concentration of osmoticum and enzyme system employed. More protoplasts were released at low concentrations of KCl and/or when chitinase was present in the digestion medium. This enhancement effect was concerned with the Ca2+ ion since addition of Ca(NO3)2 also gave a higher yield and EDTA severely depressed protoplast release. Further investigations suggested that the effect of Ca2+ was not primarily acting as a supplementary osmoticum or concerned with protoplast membrane stabilization. Experiments using 45CaCl2 showed that the enhancement effect was probably due to Ca2+ affecting chitinase activity.
We developed methods to study secretions from airway submucosal glands in vivo: micropipettes with tips specially designed to seal around individual gland duct openings allowed us to collect all of the fluid secreted from individual glands. We visualized the secretions from large numbers of glands simultaneously by coating the airway surface with powdered tantalum; secreted mucus formed "hillocks" over each gland duct opening. Measurement of hillock size provided an estimate of secretion rate. We modified the "hillocks" method to study tracheal glands in vitro. To study regulation of mucin secretion in vitro, we measured the radioactivity from 35S bound to mucins secreted from the luminal surface of pieces of trachea mounted in Using-type chambers. Using these techniques, we demonstrated both cholinergic and alpha-adrenergic regulation of the glands.
The correspondence between complete serotype and biotype (P.A.D. Grimont and F. Grimont, J. Clin. Microbiol. 8:73-83, 1978) of 474 Serratia marcescens strains was studied. Of 127 serotypes, 70 were represented by two or more strains of the same serotype belonged to one biotype. However, for 91% of serotypes, strains of the same serotype belonged to one biogroup--i.e., a group of closely related biotypes. Biogroups are A1 (A1a, A1b); A2/6 (A2a, A2b, A6a, A6b); A3 (A3a, A3b, A3c, A3d); A4 (A4a, A4b); A5/8 (A5, A8a, A8b, A8c); and TCT (TCT, TT). Only two serotypes were composed of a mixture of pigmented and nonpigmented biogroups. Pigmented biogroups (A1 and A2/6) were otherwise differentiated from nonpigmented biogroups (A3, A4, A5/8, and TCT) by serotyping. Some biogroups preferentially occurred in some O serogroups: A4 in 01; A2/6 in O6, O8, and O14; and A3 in O9, O12, and O15. Three H serogroups were found to be biochemically homogeneous: H1, H7, and H20 were respectively and uniquely composed of biogroups A4, TCT, and A3. A square matrix of O versus H serogroups, with the corresponding biogroup for each O X H combination, was used for comparisons between O groups and between H groups. Identical patterns of biogroups were shown by serogroups O6, O8, and O14. Taxonomical, ecological, and practical consequences of these findings are discussed.
The output of secretions from the airway submucosal glands is regulated by vagal efferent nerves. Stimulation of cough receptors increases mucus output reflexly via the vagus nerves. Adrenergic agonists increase submucosal gland secretions in some species, which indicates that adrenergic receptors are present in these cells. However, evidence for adrenergic nervous pathways to the glands is limited. Irritants and drugs stimulate secretion from epithelial cells by direct effects. There is also evidence that the secretion of epithelial cells can be stimulated by parasympathetic nervous pathways in birds but not in mammals. Active ion transport of Cl- toward the lumen and of Na+ toward the submucosa results in net ion movement toward the airway lumen in unstimulated tracheal epithelia. Drugs and mediators increase the net movement of ions toward the lumen. No agents have yet been found that increase net ion movement toward the submucosa. The link between ion transport and water secretion in airway epithelia, although speculative, seems likely in view of the evidence from other epithelia. Since airway epithelium is a "tight junction" epithelium, modification of the tight junction may alter the transepithelial movement of water and ions. We suggest that the depth and consistency of the periciliary layer of airway secretions determine the ability of the cilia to propel the mucoprotein gel and thereby modify mucociliary transport. To achieve this, secretion of mucus must be controlled separately from the secretion of water. Studies are needed to determine which of the specialized functions of the epithelial cells interact to regulate the clearance of secretions from the airway. Is the sol maintained by secretion and reabsorption of fluid across the epithelium? Does the sol move with the gel by ciliary action or does it remain stationary? Do changes in the epithelial tight junctions influence net water movement and thus indirectly alter the depth of the sol layer? To answer these questions, techniques are needed to study subunits of the airway, including isolated surface cells and submucosal glands; and sensitive methods are required to analyze the very small samples of secretions for glycoprotein and electrolyte content. Intracellular measurements of electrolyte concentrations and electrical potentials may help to elucidate the mechanisms of transepithelial ion and water movement. The control system for the production and removal of respiratory tract secretions may be altered in disease. For instance, chronic stimulation of cough receptors causes reflex secretion and may be the cause of the hyperplasia of submucosal glands and of the abnormal secretions that occur in chronic bronchitis and asthma (50, 58). The abnormally viscid mucus in cystic fibrosis may be due to a defect in Cl- transport, which provides too little water for both the gel and sol layers. These speculations are intended to identify areas for further research, which hopefully will reduce the morbidity and mortality in these common lung diseases.
The authors report the incidence (2.7%) of shunt infection in a series of 778 consecutive shunt procedures. The management of these infections and an additional group of infected patients operated elsewhere is discussed. A protocol is given for the treatment of external infections, gram-positive internal infections and gram-negative internal infections.