The Experts below are selected from a list of 54 Experts worldwide ranked by ideXlab platform
Yanyi Peng - One of the best experts on this subject based on the ideXlab platform.
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activation of nicotinic receptor induced postsynaptic responses to luteinizing hormone releasing hormone in bullfrog sympathetic ganglia via a na dependent mechanism
Proceedings of the National Academy of Sciences of the United States of America, 1998Co-Authors: Yanyi PengAbstract:Nicotine at very low doses (5–30 nM) induced large amounts of luteinizing hormone-releasing hormone (LHRH) release, which was monitored as slow membrane depolarizations in the ganglionic neurons of bullfrog sympathetic ganglia. A nicotinic antagonist, d-Tubocurarine Chloride, completely and reversibly blocked the nicotine-induced LHRH release, but it did not block the nerve-firing-evoked LHRH release. Thus, nicotine activated nicotinic acetylcholine receptors and produced LHRH release via a mechanism that is different from the mechanism for evoked release. Moreover, this release was not caused by Ca2+ influx through either the nicotinic receptors or the voltage-gated Ca2+ channels because the release was increased moderately when the extracellular solution was changed into a Ca2+-free solution that also contained Mg2+ (4 mM) and Cd2+ (200 μM). The release did not depend on Ca2+ release from the intraterminal Ca2+ stores either because fura-2 fluorimetry showed extremely low Ca2+ elevation (≈30 nM) in response to nicotine (30 nM). Moreover, nicotine evoked LHRH release when [Ca2+] elevation in the terminals was prevented by loading the terminals with 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid and fura-2. Instead, the nicotine-induced release required extracellular Na+ because substitution of extracellular NaCl with N-methyl-d-glucamine Chloride completely blocked the release. The Na+-dependent mechanism was not via Na+ influx through the voltage-gated Na+ channels because the release was not affected by tetrodotoxin (1–50 μM) plus Cd2+ (200 μM). Thus, nicotine at very low concentrations induced LHRH release via a Na+-dependent, Ca2+-independent mechanism.
Blythe Max - One of the best experts on this subject based on the ideXlab platform.
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Dr Gordon Jackson Rees in interview with Dr Max Blythe: Interview 2
Oxford Brookes University, 2017Co-Authors: Rees, Gordon Jackson, Blythe MaxAbstract:This interview covers the major part of Gordon Jackson Rees' career - his work in paediatric anaesthesia. At the start of the interview Dr Rees talks about the paediatric surgeon Isabella Forshall, whom he worked with till she retired in 1965. He reflects on her pioneering role in her specialty; increasing knowledge in an under-researched area, making surgery more humane, and her view that anaesthesia was central to the development of paediatric surgery. Dr Rees outlines his early career in paediatric anaesthesia; he was among the pioneers of intravenous inductions in children, and the wide use of relaxants and artificial ventilation. He speaks of developments in paediatric surgery in Liverpool in the 1950s; the growth of the neonatal surgery with the arrival of Peter Rickham, and the publication of the first textbook on paediatric anaesthesia. The interview then focuses on Dr Rees' continued collaboration with Cecil Gray. He describes the publication of joint papers on the philosophy behind anaesthesia, the growing national and international reputation of anaesthesia in Liverpool, and Gray's pioneering taught postgraduate course in anaesthesia. Next, Dr Rees outlines developments in paediatric surgery in 1950s and 60s, particularly thoracic surgery, and early attempts at open-heart surgery combining cardiopulmonary bypass with surface cooling. The interview ends with a discussion of his role in the major research in paediatric anaesthesia. This includes: investigating levels of sensitivity to d-Tubocurarine Chloride in neonates; and developing ventilation techniques, some of which are now widely used in adult intensive care
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Professor Cecil Gray CBE KCSG FRCS FRCP FRCA in interview with Dr Max Blythe: Interview 2
Oxford Brookes University, 2017Co-Authors: Gray T Cecil, Blythe MaxAbstract:Following the first interview in which Professor T Cecil Gray discusses the start of a career as an anaesthetist, this interview takes up the account of his career from 1944 after being invalided home from North Africa, where he served in the Royal Army Medical Corps. Professor Gray begins by speaking of resuming work as an anaesthetist in Liverpool and the start of his pioneering work on curare in anaesthetic practice, in collaboration with the anaesthetist, John Halton.In the mid-forties, John Halton divided his time between service as a medical officer in the Royal Air Force and working with the distinguished thoracic surgeon, Hugh Morriston Davies, at Clatterbridge Hospital. John Halton learnt from American Air Force colleagues of the first use of curare as a muscle relaxant in anaesthesia (by Harold Griffith in Montreal in 1942), and managed to obtain curare in the form of a crude extract of the vine, Chondodendron tomentosum - a constituent of the South American arrow poison. Professor Gray and John Halton began to experiment with the extract in their respective anaesthetic practices and when supplies ran low started to use the pure alkaloid, Curarin (d-Tubocurarine Chloride), which they obtained from Rod Gregory. Rod Gregory, who was a senior lecturer and then professor in the physiology department of the University of Liverpool, was to remain an important research collaborator.Professor Gray then goes on to describe the dramatic muscle relaxation effect produced when he first administered Curarin intravenously to a patient undergoing abdominal surgery, using Pentothal and cyclopropane as the anaesthetic. There is discussion of how initially Curarin was given in a low dose so that respiration was not abolished completely, but with experience the dose was gradually increased and respiration was controlled. This technique permitted the use of light anaesthesia for surgery and greatly assisted post-operative recovery. The discussion then progresses to the development of the technique with the use of physostigmine and then prostigmine in conjunction with atropine to reverse the effect of the Curarin.In March 1946 the Liverpool group's early results were presented at a meeting of the Royal Society of Medicine and were published subsequently in the Proceedings of the Society, in what is now recognised as a landmark paper in anaesthesia literature. (General acceptance by anaesthetists of the use of controlled ventilation with muscle relaxants did not come until later, and at first Tubocurarine was used almost exclusively as an adjuvant to anaesthesia in the spontaneously respiring patient.) Professor Gray talks of the award of an MD degree in 1947 and his appointment as reader to head a new academic department of anaesthesia at the University of Liverpool, and he acknowledges the support of the professor of surgery, Charles Wells. He then speaks of the appointment to a demonstratorship of Dr Gordon Jackson Rees, who became a highly valued colleague and friend over many years, contributing to both the teaching and research of the department. In the following part of the interview, Professor Gray discusses setting up an administrative structure for anaesthetists in Liverpool and the origins of the renowned Liverpool course in anaesthetics. A discussion follows of a joint publication with Dr Gordon Jackson Rees on the role of apnoea in major surgery, and the essence of the 'Liverpool Technique' being the application of the anaesthetic triad, unconsciousness, analgesia and muscle relaxation.The interview moves on to Professor Gray's involvement with teaching initiatives in Europe, including the WHO course at the Anaesthesiology Centre in Copenhagen. The final part of the interview covers Dr Gordon Jackson Rees' entry into the field of paediatric anaesthesia, the impact of the introduction of the National Health Service, and Professor Gray's invitation in 1948 to join the board of the newly created Faculty of Anaesthetists of the Royal College of Surgeons
Mark J Zoran - One of the best experts on this subject based on the ideXlab platform.
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activity dependent induction of functional secretory properties at cultured neuromuscular synapses of helisoma
Journal of Neurophysiology, 1996Co-Authors: James C Poyer, Mark J ZoranAbstract:1. The role of activity-dependent mechanisms in target-mediated induction of secretory properties was investigated at regenerating neuromuscular synapses of the American pond snail, Helisoma trivolvis, in cell culture. 2. Identified motoneurons were isolated into cell culture conditions that promoted neurite outgrowth. Buccal neurons 19 (B19) were cultured alone for 2 days, at which time dissociated muscle fibers were manipulated into contact with newly formed neurites. 3. Immediately before the plating of muscle fibers, the sodium channel blocker, tetrodotoxin (TTX), or the acetylcholine receptor antagonist, d-Tubocurarine Chloride (curare), was added to the culture dish. After 48 h of exposure, the inhibitors were removed by repeated dilution of the culture medium and electrophysiological analyses were performed. 4. Cholinoceptive assay cells were manipulated into contact with the presynaptic neurons to assess secretory properties along neuronal processes. Assay cells were used to control for variations in postsynaptic sensitivity that could result from long-term exposure to activity inhibitors. 5. These analyses demonstrated that inhibition of TTX-sensitive presynaptic activity and inhibition of curare-sensitive postsynaptic activation both blocked the induction of excitation-secretion coupling typically induced in these motoneurons by appropriate target contact. Neuron B5, which rapidly acquires functional synaptic properties in vitro, was unaffected in its secretory function by 48 h of activity inhibition. 6. Acquisition of secretory competence was not suppressed due to a reduction in the viability or long-term changes in excitability of the activity-inhibited neurons, as indicated by analyses of electrophysiological properties. 7. Although target-contact and activity both participated in the induction of secretory modifications in neuron B19, target-mediated changes did not involve retrograde effects on presynaptic neuronal excitability. 8. We hypothesize that contact-mediated mechanisms govern the initiation of presynaptic modifications in B19, however, our data indicate that the acquisition of functional excitation-secretion coupling also involves activity-dependent mechanisms. Although the mechanistic role of activity remains undefined, our results suggest that the activation of the target muscle plays a critical role in a retrograde signaling pathway underlying maturation of a functional secretory apparatus in target-contacted neuronal processes.
V. Theofanopoulos - One of the best experts on this subject based on the ideXlab platform.
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The Intranasal Absorption of the Quaternary Ammonium Compounds Neostigmine Bromide and Tubocurarine Chloride in the Rat
Drug Development and Industrial Pharmacy, 2008Co-Authors: K. P. Thadikonda, V. L. Thadikonda, V. TheofanopoulosAbstract:AbstractThe systemic absorptions of the quaternary ammonium compounds, neostigmine bromide and (+)-Tubocurarine Chloride, from the nasal cavity were compared in the adult male rat with those obtained by the oral and intravenous routes. By the oral route, neostigmine bromide was absorbed to a limited extent and Tubocurarine Chloride demonstrated undetectable plasma levels. In contrast, use of the intranasal route resulted in plasma drug levels that were either significantly higher or readily detectable. Greater systemic absorptions and, thereby, improved bioavailabilities were achieved by coadministering the title drugs with sodium glycocholate, a surfactant, or with amastatin, an aminopeptidase inhibitor. For both drugs, bioavailabilities in the presence of amastatin were greater than in the presence of sodium glycocholate (≥90% vs. ≥70%). Differences in the rate and extent of absorption of the quaternary ammonium compounds across the nasal mucosa appeared to reflect differences in molecular weight.
Peng Yan-yi - One of the best experts on this subject based on the ideXlab platform.
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Activation of nicotinic receptor-induced postsynaptic responses to luteinizing hormone-releasing hormone in bullfrog sympathetic ganglia via a Na(+)-dependent mechanism
The National Academy of Sciences, 1998Co-Authors: Cao Ying-jun, Peng Yan-yiAbstract:Nicotine at very low doses (5–30 nM) induced large amounts of luteinizing hormone-releasing hormone (LHRH) release, which was monitored as slow membrane depolarizations in the ganglionic neurons of bullfrog sympathetic ganglia. A nicotinic antagonist, d-Tubocurarine Chloride, completely and reversibly blocked the nicotine-induced LHRH release, but it did not block the nerve-firing-evoked LHRH release. Thus, nicotine activated nicotinic acetylcholine receptors and produced LHRH release via a mechanism that is different from the mechanism for evoked release. Moreover, this release was not caused by Ca(2+) influx through either the nicotinic receptors or the voltage-gated Ca(2+) channels because the release was increased moderately when the extracellular solution was changed into a Ca(2+)-free solution that also contained Mg(2+) (4 mM) and Cd(2+) (200 μM). The release did not depend on Ca(2+) release from the intraterminal Ca(2+) stores either because fura-2 fluorimetry showed extremely low Ca(2+) elevation (≈30 nM) in response to nicotine (30 nM). Moreover, nicotine evoked LHRH release when [Ca(2+)] elevation in the terminals was prevented by loading the terminals with 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid and fura-2. Instead, the nicotine-induced release required extracellular Na(+) because substitution of extracellular NaCl with N-methyl-d-glucamine Chloride completely blocked the release. The Na(+)-dependent mechanism was not via Na(+) influx through the voltage-gated Na(+) channels because the release was not affected by tetrodotoxin (1–50 μM) plus Cd(2+) (200 μM). Thus, nicotine at very low concentrations induced LHRH release via a Na(+)-dependent, Ca(2+)-independent mechanism
