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At least 973 records · Page 54Linked to original sources
PubMed2001

Effect of gold(I) compounds on the virulence of an amyocarditic strain of coxsackievirus B3.

Coxsackieviruses, especially B strains (CVB), are known etiological agents of myocarditis. Both amyocardititc and myocarditic strains exist and at least one amyocarditic strain, CVB3/0, can convert to virulence when passaged through selenium or vitamin E-deficient mice. Gold(I)-containing compounds, such as aurothiomalate (ATM) and aurothioglucose (ATG), can act as selenium antagonists. In this study, we examined the effect of intraperitoneal administration of equal doses of ATM or ATG on the virulence of CVB3/0. ATM but not ATG increased mortality in CVB3/0-infected mice. CVB3/0-infected mice treated with ATM had total necrosis of the pancreatic exocrine tissue. Heart damage also occurred in ATM-treated mice but did not correlate with mortality. Increased viral titers and persistence were observed in ATM-treated mice and, to a lesser extent, in ATG-treated mice. Thus, under our conditions, only ATM increased the virulence of CVB3/0, whereas ATG did not. On the other hand, both ATG and ATM inhibited thioredoxin reductase activity in heart and pancreas, but neither affected glutathione peroxidase activity. In contrast, dietary selenium deficiency reduces both enzyme activities. Thus, it is unlikely that these compounds affect virulence by acting as selenium antagonists.

Animals↗
PubMed1996

Training older adults to use automatic teller machines.

The present study assessed the success of several instructional programs in teaching the use of automatic teller machines (ATMs). Fifty-six older adults (aged 61 to 81) participated in the study, randomly assigned to each of four, 14-member groups. The description group received only a general overview of an ATM; the text guide group received written instructions for performing various transactions on an ATM; the pictorial guide group received written instructions accompanied by pictures of corresponding ATM screens; and the online tutorial group completed a step-by-step tutorial on a simulated ATM. Participants practiced on an ATM simulator. They were tested after a 24-h interval on their ability to perform familiar transactions on an unfamiliar ATM simulator and to perform completely novel transactions. Accuracy was best for the online tutorial group, intermediate for the text and pictorial guide groups, and worst for the description group. These data demonstrate both the importance of providing older adults with ATM training and the fact that the type of training influences the level of performance. The online tutorial, which provided specific practice on the task components, best facilitated acquisition and transfer performance.

Age Factors↗
PubMed1996

A survey of automatic teller machine usage across the adult life span.

The purpose of this study was to analyze automatic teller machine (ATM) usage across the adult life span. We conducted an extensive survey of 9000 people in the Memphis and Atlanta metropolitan areas. Approximately 17% of those people responded. The survey assessed detailed demographic information, experience with technology in general, experience specifically related to ATMs, problems and dislikes with ATMs, and reasons that people do not use ATMs. The survey provided a valuable set of data. First, we have detailed information about the demographics and individual characteristics of ATM users and nonusers; importantly, these data are stratified across the adult life span. In addition, we know the likes and dislikes of ATM users and the types of problems they typically have using ATMs. Moreover, we have detailed analysis of why adults of all ages may choose not to use ATMs. Training and design implications of these data are discussed.

Adult↗
PubMed1999

Decrease in multiple sclerosis with acute transverse myelitis in Japan.

Acute transverse myelitis (ATM) may be a manifestation of multiple sclerosis (MS) and was reported to be more common among Japanese MS patients than in Caucasian MS patients. Recently there are arguments whether clinical manifestations of MS may have changed. Therefore, we studied the frequency of ATM in MS and the clinical subtypes of MS in 86 clinically definite MS patients whose onsets were in 1970-1979, 1980-1989, and 1990-1998 in Sendai City, Japan. Fifty-six of the patients were women and 30 were men. Forty-four patients had the conventional form of MS (C-MS) commonly seen in Western countries, and 42 had optic-spinal or spinal forms of MS (OSS-MS). Twenty MS patients had ATM, and all of them were belong to optic-spinal form of MS. ATM was not seen in any cases of C-MS. The mean onset age (years) of the clinical subtypes was 25.5 in C-MS, 34.1 in OSS-MS without ATM, and 30.9 in OSS-MS with ATM. Among the patients whose onset of the disease was in 1970-1979, 60.0% of them were cases of OSS-MS with ATM, but such cases were markedly decreased to 5.3% in 1990-1998. In contrast, the frequency of C-MS increased to 63.2% in 1990-1998 compared with 20.0% in 1970-1979. Analysis of the data by the year of birth of the patients showed similar results. Our data suggest that the frequency of ATM in MS markedly decreased, and that of C-MS increased during the last 30 years in Sendai, Japan. Since the genetic background of Japanese has not changed, some exogenous factors, such as food, infectious microorganisms, and chemicals in our environment, may be responsible for the change.

Adult↗
PubMed2001

Superoxide stress identifies neurons at risk in a model of ataxia-telangiectasia.

Ataxia-telangiectasia (A-T) is an autosomal recessive disorder caused by mutations in the ATM gene. A-T children demonstrate sensitivity to ionizing radiation, predisposition to hematological malignancies, and telangiectasias. However, the hallmark of A-T is fulminant degeneration of cerebellar Purkinje cells accompanied by a progressive ataxia with features of both cerebellar and basal ganglia dysfunction. Although the ATM gene product (ATM) is known to be involved in DNA repair, the mechanisms that link loss of ATM with neurodegeneration remain unknown. Recently, it has been suggested that abnormalities in redox status contribute to the A-T phenotype. To address this question in the nervous system, we measured reactive oxygen species (ROS) in brain regions and specific neuronal populations in ATM-/- mice. We found increased ROS levels in cerebellum and striatum but not cortex of ATM-/- mice compared to ATM+/+ mice. Confocal microscopic examination revealed elevated superoxide levels in cerebellar Purkinje cells and nigral dopaminergic neurons but not cortical neurons, thus mapping increased superoxide levels onto the neuronal populations selectively affected in A-T. These data are the first demonstration of elevated levels of ROS in neurons at risk in any genetic neurodegenerative disorder and, furthermore, suggest that ATM acts as a pro-survival signal in post-mitotic Purkinje cells and dopaminergic neurons by modifying superoxide radical handling in these selectively vulnerable neurons.

Animals↗
PubMed2001

Lipid peroxidation, circulating cytokine and endothelin 1 levels in healthy volunteers undergoing hyperbaric oxygenation.

BACKGROUND: The aim of the present study was to evaluate the effects of hyperbaric oxygenation on lipid peroxidation, on the release of circulating cytokines (TNFa, IL6, IL1b) and endothelin-1 (ET1). METHODS EXPERIMENTAL DESIGN: single arm, prospective study. SETTING: ICU hyperbaric division of a University Hospital. PATIENTS: fifteen healthy volunteers (10 male and 5 female, mean age 32+/-7 years) studied during hyperbaric oxygenation divided at random into two groups: group A (7 subjects) and group B (8 subjects). INTERVENTIONS: Both groups were consecutively pressurized at 2 atmospheres (2 atm abs) and 2.8 atm abs, with a constant descending rate of 1 m/min; in accordance with the experimental design, group A breathed pure oxygen continuously through facial masks and group B breathed chamber air during pressurization. MEASURES: Twenty millilitres of blood were drawn from all individuals at the following times: 1) basal, before HBO; 2) after 10 min at 2 atm abs; 3) after 10 min at 2.8 atm abs; 4) 30 min after the end of HBO. In all collected samples thiobarbituric reacting substances were evaluated, using the spectrophotometric technique, IL1 TNF and IL6 serum levels by ELISA and endothelin 1 plasma levels by radioimmunoassay. RESULTS: In both groups, TBARS levels showed a twofold increase (p<0.05) in relation to the baseline, during and after hyperbaric oxygenation. Serum IL6 and IL1b values did not significantly change over the study in any of the volunteers. TNFa amounts significantly increased (p<0.05) during HBO, at 2 atm abs and 2.8 atm abs in both groups, with almost twofold increments. ET1 plasma values increased (p<0.05) in all volunteers during and after HBO: at 2 atm abs (range 7 to 24 pg/ml), 2.8 atm abs (range 7 to 19 pg/ml) and 30 min after (range 8 to 17 pg/ml) in relation to baseline (range 4 to 12 pg/ml). All the studied compounds had a similar trend in the two groups. CONCLUSIONS: Hyperbaric oxygenation in healthy volunteers can induce not only lipid peroxidation, but also liberation of compounds such as TNFa and endothelins, no matter whether pure oxygen is breathed or not. These results suggest that the phenomenon behind this release might be leukocyte activation as induced by HBO. The possible role of ET1 in determining vasoconstriction occurring during HBO is also suggested.

Adult↗
PubMed2001

Replication protein A2 phosphorylation after DNA damage by the coordinated action of ataxia telangiectasia-mutated and DNA-dependent protein kinase.

Replication protein A (RPA, also known as human single-stranded DNA-binding protein) is a trimeric, multifunctional protein complex involved in DNA replication, DNA repair, and recombination. Phosphorylation of the RPA2 subunit is observed after exposure of cells to ionizing radiation (IR) and other DNA-damaging agents, which implicates the modified protein in the regulation of DNA replication after DNA damage or in DNA repair. Although ataxia telangiectasia-mutated (ATM) and DNA-dependent protein kinase (DNA-PK) phosphorylate RPA2 in vitro, their role in vivo remains uncertain, and contradictory results have been reported. Here we show that RPA2 phosphorylation is delayed in cells deficient in one of these kinases and completely abolished in wild-type, ATM, or DNA-PK-deficient cells after treatment with wortmannin at a concentration-inhibiting ATM and DNA-PK. Caffeine, an inhibitor of ATM and ATM-Rad3 related (ATR) but not DNA-PK, generates an ataxia-telangiectasia-like response in wild-type cells, prevents completely RPA2 phosphorylation in DNA-PKcs deficient cells, but has no effect on ataxia-telangiectasia cells. These observations rule out ATR and implicate both ATM and DNA-PK in RPA2 phosphorylation after exposure to IR. UCN-01, an inhibitor of protein kinase C, Chk1, and cyclin-dependent kinases, has no effect on IR-induced RPA2 phosphorylation. Because UCN-01 abrogates checkpoint responses, this observation dissociates RPA2 phosphorylation from checkpoint activation. Phosphorylated RPA has a higher affinity for nuclear structures than unphosphorylated RPA suggesting functional alterations in the protein. In an in vitro assay for DNA replication, DNA-PK is the sole kinase phosphorylating RPA2, indicating that processes not reproduced in the in vitro assay are required for RPA2 phosphorylation by ATM. Because RPA2 phosphorylation kinetics are distinct from those of the S phase checkpoint, we propose that DNA-PK and ATM cooperate to phosphorylate RPA after DNA damage to redirect the functions of the protein from DNA replication to DNA repair.

Androstadienes↗
PubMed2003

Oxidative stress is responsible for deficient survival and dendritogenesis in purkinje neurons from ataxia-telangiectasia mutated mutant mice.

Atm gene-disrupted mice recapitulate the majority of characteristics observed in patients with the genetic disorder ataxia-telangiectasia (A-T). However, although they exhibit defects in neuromotor function and a distinct neurological phenotype, they do not show the progressive neurodegeneration seen in human patients, but there is evidence that ataxia-telangiectasia mutated (Atm)-deficient animals have elevated levels of oxidized macromolecules and some neuropathology. We report here that in vitro survival of cerebellar Purkinje cells from both Atm "knock-out" and Atm "knock-in" mice was significantly reduced compared with their wild-type littermates. Although most of the Purkinje neurons from wild-type mice exhibited extensive dendritic elongation and branching under these conditions, most neurons from Atm-deficient mice had dramatically reduced dendritic branching. An antioxidant (isoindoline nitroxide) prevented Purkinje cell death in Atm-deficient mice and enhanced dendritogenesis to wild-type levels. Furthermore, administration of the antioxidant throughout pregnancy had a small enhancing effect on Purkinje neuron survival in Atm gene-disrupted animals and protected against oxidative stress in older animals. These data provide strong evidence for a defect in the cerebellum of Atm-deficient mice and suggest that oxidative stress contributes to this phenotype.

Animals↗
PubMed2004

Topoisomerase poisons differentially activate DNA damage checkpoints through ataxia-telangiectasia mutated-dependent and -independent mechanisms.

Camptothecin and Adriamycin are clinically important inhibitors for topoisomerase (Topo) I and Topo II, respectively. The ataxia-telangiectasia mutated (ATM) product is essential for ionizing radiation-induced DNA damage responses, but the role of ATM in Topo poisons-induced checkpoints remains unresolved. We found that distinct mechanisms are involved in the activation of different cell cycle checkpoints at different concentrations of Adriamycin and camptothecin. Adriamycin promotes the G(1) checkpoint through activation of the p53-p21(CIP1/WAF1) pathway and decrease of pRb phosphorylation. Phosphorylation of p53(Ser20) after Adriamycin treatment is ATM dependent, but is not required for the full activation of p53. The G(1) checkpoint is dependent on ATM at low doses but not at high doses of Adriamycin. In contrast, the Adriamycin-induced G(2) checkpoint is independent on ATM but sensitive to caffeine. Adriamycin inhibits histone H3(Ser10) phosphorylation through inhibitory phosphorylation of CDC2 at low doses and down-regulation of cyclin B1 at high doses. The camptothecin-induced intra-S checkpoint is partially dependent on ATM, and is associated with inhibitory phosphorylation of cyclin-dependent kinase 2 and reduction of BrdUrd incorporation after mid-S phase. Finally, apoptosis associated with high doses of Adriamycin or camptothecin is not influenced by the absence of ATM. These data indicate that the involvement of ATM following treatment with Topo poisons differs extensively with dosage and for different cell cycle checkpoints.

Antibiotics, Antineoplastic↗
PubMed1994

Myocardial protection during coronary angioplasty with autoperfusion and forced perfusion: an in vitro comparison.

During coronary angioplasty, perfusion distal to the inflated angioplasty balloon can be maintained with autoperfusion balloon catheters and coronary perfusion pumps. The blood flow rates through the autoperfusion balloon catheters and the flow rates achieved with a perfusion pump were compared in vitro with fresh human blood at 37 degrees C. In a specially designed system, blood flow rates through Stack autoperfusion balloon catheters were measured at 40, 60 and 80 mmHg continuous pressure. In another system, driving pressures were measured during perfusion with the pump, through a specially designed forced perfusion catheter at 20, 40 and 60 ml/min flow. The pressure applied in the autoperfusion experiments was converted into atmospheres (atm) to facilitate comparison with the driving pressures measured during pumping (1 mmHg = 1.316 x 10(-3) atm). Mean flow rates through the autoperfusion balloon catheters were: 46 ml/min at 0.05 atm, 66 ml/min at 0.09 atm and 75 ml/min at 0.1 atm. Mean pressures during pumping were: 1.8 atm at 20 ml/min, 3.5 atm at 40 ml/min, 5 atm at 60 ml/min. Due to the phasic nature of coronary blood flow, the flow through autoperfusion balloons is generally lower than the minimum required for adequate myocardial protection (= 60 ml/min). Thus, autoperfusion balloon catheters are simpler and cheaper devices than perfusion pumps, but generally they are not able to provide adequate myocardial protection.

Angioplasty, Balloon, Coronary↗
PubMed1993

[Ambulatory monitoring of patients with suspected sleep apnea syndrome using a thermistor sensor in comparison with nocturnal polysomnography].

Simple ambulatory monitoring methods can be used in step-by-step diagnosis of sleep apnoea syndrome to differentiate between high-risk and low-risk patients, or to exclude the syndrome for achieving more efficient utilisation of sleep laboratory facilities. The question was whether a new method using a thermistor sensor measuring respiration-conditioned thermal convection at the mouth and nose can reliably record the frequency of apnoea (ambulatory thermistor method = ATM). The study was subdivided into two sections. In phase I the respiratory impulses measured via ATM were polygraphically recorded in 20 patients simultaneously with conventional cardiopulmonary data of nocturnal polygraphy (heart rate, oxygen saturation, thorax and abdominal excursions and oronasal respiratory flow). 40 patients participated in phase II. During a first night the patients slept under ATM in their patient rooms. In the 2nd night nocturnal polygraphy was conducted with the parameters mentioned above; the results of both nights were then compared. Taking 35 phases of apnoea in one night as threshold or baseline value, a sensitivity of 100% and a specificity of 84.6% were attained in phase I, the simultaneous comparison of ATM and nocturnal polygraphy, in the recording of an enhanced nocturnal apnoea frequency by ATM. In phase 2 (1st night ATM, 2nd night polygraphy) ATM also yielded a sensitivity of 100% and a specificity of 76%. When measuring with a borderline value of 70 nocturnal phases of apnoea, ATM yielded a specificity and sensitivity of 100%, in phase 2 a sensitivity of 80.7% and a specificity of 88.5%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1977

New observations on pressure-induced motor disturbances in a small mammal.

New observations on pressure-induced motor disturbances in a small mammal. Undersea Biomed. Res. 4(1):1-8.-Adult and baby mice were subjected to helium pressures up to 120 atm. Pressure-induced changes in motor acitivity (tremors and convulsions) were monitored both visually and with a noninvasive mechanical transducer. A study of five rates of compression showed that adult convulsion pressure thresholds (Pc) fell from a maximum of 90 atm at 20 atm/hr to a minimum of 63 atm at 610 atm/hr, Pc for baby mice rose from 53 atm at 8 days to reach the adult value (85-90 atm) at 21 days of age. Measurements of accommodation, or the decline in motor disturbances at constant pressure, are described. Animals allowed to accommodate for five hours at a pressure 9% higher than the first Pc (85 atm) and then compressed further showed a significantly higher second Pc (114 atm) than animals allowed one hour to accommodate (100 atm). The effects on including nitrogen in the heliox compression mixture on accommodation are also described.

Aging↗
PubMed2001

Trimethylamine oxide counteracts effects of hydrostatic pressure on proteins of deep-sea teleosts.

In shallow marine teleost fishes, the osmolyte trimethylamine oxide (TMAO) is typically found at <70 mmol/kg wet weight. Recently we found deep-sea teleosts have up to 288 mmol/kg, increasing in the order shallow < bathyal < abyssal. We hypothesized that this protein stabilizer counteracts inhibition of proteins by hydrostatic pressure, and showed that, for lactate dehydrogenases (LDH), 250 mM TMAO fully offset an increase in NADH K(m) at physiological pressure, and partly reversed pressure-enhanced losses of activity at supranormal pressures. In this study, we examined other effects of pressure and TMAO on proteins of teleosts that live from 2000-5000 m (200-500 atmospheres [atm]). First, for LDH from a grenadier (Coryphaenoides leptolepis) at 500 atm for 8 hr, there was a significant 15% loss in activity (P < 0.05 relative to 1 atm control) that was reduced with 250 mM TMAO to an insignificant loss. Second, for pyruvate kinase from a morid cod (Antimora microlepis) at 200 atm, there was 73% increase in ADP K(m) without TMAO (P < 0.01 relative to K(m) at 1 atm) but only a 29% increase with 300 mM TMAO. Third, for G-actin from a grenadier (C. armatus) at 500 atm for 16 hr, there was a significant reduction of F-actin polymerization (P < 0.01 compared to polymerization at 1 atm) that was fully counteracted by 250 mM TMAO, but was unchanged in 250 mM glycine. These findings support the hypothesis. J. Exp. Zool. 289:172-176, 2001.

Actins↗
PubMed1990

Continuously applied compressive pressure induces bone resorption by a mechanism involving prostaglandin E2 synthesis.

In previous research, we devised a specific culture chamber to examine the effect of continuously applied compressive pressure (CCP) on bone formation and resorption. The chamber was infused with compressed mixed gases with different O2 and CO2 composition to maintain the pO2, pCO2, and pH in the culture medium under pressures of +0.5 atm (1.5 atm total) to +2.0 atm (3.0 atm total) at the same levels as those at the ordinary pressure (1 atm). Using the specific culture chamber, we demonstrated that CCP greatly suppressed the differentiation of mouse osteoblast-like MC3T3-E1 cells. The inhibition by CCP appeared to be mediated by prostaglandin E2 (PGE2). In the present study, we examined the effect of CCP on osteoclastic bone resorption. CCP treatment of mouse bone marrow culture markedly increased both the PGE2 production and the number of tartrate-resistant acid phosphatase (TRACP)-positive mononuclear cells (possibly precursors of multinucleated osteoclasts). An autoradiographic study using [125I]-salmon calcitonin showed clearly that those TRACP-positive cells had calcitonin receptors. The CCP effect was the greatest at +1.0 atm (2.0 atm total). Isobutylmethylxanthine potentiated the production of TRACP-positive cells induced by CCP. Adding indomethacin completely inhibited both the TRACP-positive cell formation and the PGE2 production induced by CCP. CCP also increased the release of 45Ca from prelabeled mouse calvaria during later stages (2-6 days) of the 6-day culture period. CCP markedly increased PGE2 but not interleukin 1 in the culture media of mouse calvaria. These results indicate that, besides inhibiting osteoblast differentiation, CCP stimulates bone resorption by generating new osteoclasts through a mechanism involving PGE2 production.

Acid Phosphatase↗
PubMed1987

Pressure-adaptive differences in proteolytic inactivation of M4-lactate dehydrogenase homologues from marine fishes.

The inactivation by hydrostatic pressure of muscle-type lactate dehydrogenase (M4-LDH, EC 1.1.1.27; L-lactate: NAD+ oxidoreductase) homologues from five shallow-living and six deep-living marine teleost fishes was compared. The pressures which inactivate these enzymes are much higher than the pressures experienced by any of the species. To determine whether hydrostatic pressure effects on protein aggregation state and conformation might influence proteolysis, the inactivation of LDH by the proteases, trypsin (EC 3.4.21.4) and subtilisin (EC 3.4.4.16) was determined at atmospheric pressure and 1,000 atm pressure. At 10 degrees C and atmospheric pressure, the enzymes of the shallow-living fishes are inactivated four times faster by trypsin and three times faster by subtilisin than are the homologues of the deep-living species. At 1,000 atm pressure, the homologues of shallow-occurring fishes were inactivated 28 to 64% more than predicted from the summed effects of denaturation by 1,000 atm pressure and tryptic inactivation at atmospheric pressure. In contrast, the homologues of the deep-sea species were inactivated by trypsin 0 to 21% more than expected. At 1,000 atm, inactivation by subtilisin increased to a similar degree for enzymes from both deep- and shallow-living species. However, at 1,000 atm, the M4-LDH homologues of the deep-sea species lost less activity (55.3%) than did the homologues of the shallow species (86.4%). In comparisons made at 200 atm, a pressure typical of the habitat of the deep-occurring species, tryptic inactivation of the LDH of the shallow-living Sebastes melanops was increased 14%. No pressure inactivation of the enzyme is evident at 200 atm.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed2001

Etoposide and adriamycin but not genistein can activate the checkpoint kinase Chk2 independently of ATM/ATR.

We have investigated the effects of three unrelated topoisomerase 2 inhibitors, genistein, adriamycin, and etoposide, on phosphorylation/activation of the checkpoint kinase Chk2 in normal or ATM-deficient (ATM-) human fibroblasts and in cells overexpressing a catalytically inactive ATR kinase. We demonstrate that genistein activates Chk2 in a strictly ATM-dependent manner, whereas etoposide and adriamycin can trigger Chk2 activation in long-term cultures of ATM- cells. Moreover, these two latter genotoxic compounds were found to activate Chk2 in fibroblasts expressing the dominant negative form of ATR. We also report a significant decrease in the accumulation in G2-phase of ATM- cells when genistein did not activate Chk2. In conclusion, our results strongly support that activation of Chk2 could be dependent on the type and/or extent of DNA damage and under the control of either an ATM-dependent or an ATM and, maybe, an ATR-independent pathway.

Ataxia Telangiectasia↗
PubMed1997

Phenotypic correction of ataxia-telangiectasia cellular defect by exogenously introduced human or mouse subchromosomal fragments.

A human-mouse hybrid containing a human 11q22-23 fragment including the ATM locus was used to examine its capability to correct the cellular defect of ataxia-telangiectasia (A-T). Examination of 21 A-T-derived hybrids indicated that the acquired radioresistance was observed in the clones where the 11q22-23 fragment was transferred intact, but not in those where donor-derived 11q segment was lost. In one exceptional clone, the ATM locus was deleted from the transferred fragment, while it was still partially radioresistant. This partially radioresistant clone was found to include the mouse-derived fragment containing the Atm gene, the mouse homologue of human ATM gene. Similar association of partial radioresistance with the presence of mouse Atm gene was observed in three additional hybrids. The results indicate that the cellular A-T defect can be corrected by the mouse subchromosomal fragment containing the Atm gene as well as by the human 11q22-23 fragment containing the ATM gene, but apparently to a lesser extent in the former.

Animals↗
PubMed1995

The effects of nitrous oxide on a glutamate-gated ion channel and their reversal by high pressure; a single channel analysis.

Nitrous oxide reversibly affects the kinetics, but not the conductance, of the qGluR channel of locust muscle. 0.5 atm N2O at 20.5 degrees C was without effect but both 1.5 and 2.7 atm significantly reduced the probability of the channel opening, the frequency of opening and the mean open time, and prolonged the mean closed time. 100 atm helium was without effect on these parameters, but when 98.5 atm He was combined with 1.5 atm N2O they, and the associated dwell time distributions, were restored to normal. 100 atm similarly combined with 2.7 atm N2O exerted a comparable trend which fell short of significance. The results are consistent with nitrous oxide binding to the channel with a significant molar volume increase, which pressure opposes. This suggests that nitrous oxide may cause conformational changes in the channel, and that the pressure reversal of nitrous oxide anaesthesia in animals could be caused by molecular antagonism.

Animals↗