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Article ; Online: Cocaine self-administration disrupted by the N-methyl-D-aspartate receptor antagonist ketamine: a randomized, crossover trial.

Dakwar, E / Hart, C L / Levin, F R / Nunes, E V / Foltin, R W

2017 Volume 22, Issue 1, Page(s) 76–81

Abstract: ... evidence suggests a single sub-anesthetic dose of the N-methyl-D-aspartate receptor antagonist ketamine ...

Abstract	Repeated drug consumption may progress to problematic use by triggering neuroplastic adaptations that attenuate sensitivity to natural rewards while increasing reactivity to craving and drug cues. Converging evidence suggests a single sub-anesthetic dose of the N-methyl-D-aspartate receptor antagonist ketamine may work to correct these neuroadaptations and restore motivation for non-drug rewards. Using an established laboratory model aimed at evaluating behavioral shifts in the salience of cocaine now vs money later, we found that ketamine, as compared to the control, significantly decreased cocaine self-administration by 67% relative to baseline at greater than 24 h post-infusion, the most robust reduction observed to date in human cocaine users and the first to involve mechanisms other than stimulant or dopamine agonist effects. These findings signal new directions in medication development for substance use disorders.
MeSH term(s)	Adult ; Central Nervous System Stimulants/pharmacology ; Cocaine/pharmacology ; Cocaine-Related Disorders/drug therapy ; Craving/drug effects ; Cross-Over Studies ; Cues ; Female ; Humans ; Ketamine/metabolism ; Ketamine/pharmacology ; Ketamine/therapeutic use ; Male ; Middle Aged ; Motivation ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors ; Self Administration
Chemical Substances	Central Nervous System Stimulants ; Receptors, N-Methyl-D-Aspartate ; Ketamine (690G0D6V8H) ; Cocaine (I5Y540LHVR)
Language	English
Publishing date	2017-01
Publishing country	England
Document type	Journal Article ; Randomized Controlled Trial
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/mp.2016.39
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Zs.A 4812: Show issues

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Article ; Online: Plasma cell depletion with bortezomib in the treatment of refractory N-methyl-d-aspartate (NMDA) receptor antibody encephalitis. Rational developments in neuroimmunological treatment.

Keddie, S / Crisp, S J / Blackaby, J / Cox, A / Coles, A / Hart, M / Church, A J / Vincent, A / Zandi, M / Lunn, M P

European journal of neurology

2018 Volume 25, Issue 11, Page(s) 1384–1388

Abstract: ... in the treatment of refractory N-methyl-d-aspartate receptor (NMDAR) antibody encephalitis and its potential ...

Abstract	Background and purpose: The aim was to assess the therapeutic potential of bortezomib in the treatment of refractory N-methyl-d-aspartate receptor (NMDAR) antibody encephalitis and its potential in other immune-mediated, B-cell-driven neurological diseases. Methods: Two cases of severe NMDAR antibody encephalitis, resistant to first and second line therapy with steroids, intravenous immunoglobulins, plasma exchange, cyclophosphamide and rituximab, were treated with four and five cycles of 1.3 mg/m Results: Both patients showed significant clinical improvement with reductions of NMDAR antibody titres following bortezomib treatment. This is the first case in the literature where the NMDAR antibody level was undetectable following treatment with bortezomib. Conclusion: Bortezomib's unique ability to target long-lived autoreactive plasma cells appears to be a useful adjunct to standard second line immunosuppressive therapy in treatment-refractory NMDAR antibody encephalitis. The drug's pharmacodynamics, cell targeting and mechanism of action are reviewed, and it is postulated that bortezomib may be useful in a host of B-cell-driven neuroimmunological diseases.
MeSH term(s)	Adult ; Anti-N-Methyl-D-Aspartate Receptor Encephalitis/drug therapy ; Antineoplastic Agents/therapeutic use ; Bortezomib/therapeutic use ; Female ; Humans ; Plasma Cells ; Receptors, N-Methyl-D-Aspartate/immunology ; Treatment Outcome
Chemical Substances	Antineoplastic Agents ; Receptors, N-Methyl-D-Aspartate ; Bortezomib (69G8BD63PP)
Language	English
Publishing date	2018-08-31
Publishing country	England
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1280785-0
ISSN	1468-1331 ; 1351-5101 ; 1471-0552
ISSN (online)	1468-1331
ISSN	1351-5101 ; 1471-0552
DOI	10.1111/ene.13759
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Zs.A 4738: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: First observation of the decays B(0) --> D(-)p_p pi+ and B(0) --> D(-)p_n.

Anderson, S / Frolov, V V / Kubota, Y / Lee, S J / Mahapatra, R / O'Neill, J J / Poling, R / Riehle, T / Smith, A / Stepaniak, C J / Urheim, J / Ahmed, S / Alam, M S / Athar, S B / Jian, L / Ling, L / Saleem, M / Timm, S / Wappler, F /

Anastassov, A / Duboscq, J E / Eckhart, E / Gan, K K / Gwon, C / Hart, T / Honscheid, K / Hufnagel, D / Kagan, H / Kass, R / Pedlar, T K / Schwarthoff, H / Thayer, J B / von Toerne, E / Zoeller, M M / Richichi, S J / Severini, H / Skubic, P / Undrus, A / Chen, S / Fast, J / Hinson, J W / Lee, J / Miller, D H / Shibata, E I / Shipsey, I P / Pavlunin, V / Cronin-Hennessy, D / Lyon, A L / Thorndike, E H / Jessop, C P / Marsiske, H / Perl, M L / Savinov, V / Zhou, X / Coan, T E / Fadeyev, V / Maravin, Y / Narsky, I / Stroynowski, R / Ye, J / Wlodek, T / Artuso, M / Ayad, R / Boulahouache, C / Bukin, K / Dambasuren, E / Karamov, S / Majumder, G / Moneti, G C / Mountain, R / Schuh, S / Skwarnicki, T / Stone, S / Viehhauser, G / Wang, J C / Wolf, A / Wu, J / Kopp, S / Mahmood, A H / Csorna, S E / Danko, I / McLean, K W / Márka, S / Xu, Z / Godang, R / Kinoshita, K / Lai, I C / Schrenk, S / Bonvicini, G / Cinabro, D / McGee, S / Perera, L P / Zhou, G J / Lipeles, E / Pappas, S P / Schmidtler, M / Shapiro, A / Sun, W M / Weinstein, A J / Würthwein, F / Jaffe, D E / Masek, G / Paar, H P / Potter, E M / Prell, S / Sharma, V / Asner, D M / Eppich, A / Hill, T S / Morrison, R J / Briere, R A / Chen, G P / Behrens, B H / Ford, W T / Gritsan, A / Roy, J / Smith, J G / Alexander, J P / Baker, R / Bebek, C / Berger, B E / Berkelman, K / Blanc, F / Boisvert, V / Cassel, D G / Dickson, M / Drell, P S / Ecklund, K M / Ehrlich, R / Foland, A D / Gaidarev, P / Gibbons, L / Gittelman, B / Gray, S W / Hartill, D L / Heltsley, B K / Hopman, P I / Jones, C D / Kandaswamy, J / Kreinick, D L / Lohner, M / Magerkurth, A / Meyer, T O / Mistry, N B / Nordberg, E / Patterson, J R / Peterson, D / Riley, D / Thayer, J G / Urner, D / Valant-Spaight, B / Warburton, A / Avery, P / Prescott, C / Rubiera, A I / Yelton, J / Zheng, J / Brandenburg, G / Ershov, A / Gao, Y S / Kim, D Y / Wilson, R / Browder, T E / Li, Y / Rodriguez, J L / Yamamoto, H / Bergfeld, T / Eisenstein, B I / Ernst, J / Gladding, G E / Gollin, G D / Hans, R M / Johnson, E / Karliner, I / Marsh, M A / Palmer, M / Plager, C / Sedlack, C / Selen, M / Thaler, J J / Williams, J / Edwards, K W / Janicek, R / Patel, P M / Sadoff, A J / Ammar, R / Bean, A / Besson, D / Davis, R / Kwak, N / Zhao, X

Physical review letters

2001 Volume 86, Issue 13, Page(s) 2732–2736

Abstract: We report the first observation of exclusive decays of the type B-->D(*)N_NX, where N is a nucleon ... and B(B0-->D(*-)p_n) = (14.5(+3.4)(-3.0)+/-2.7)x10(-4). Antineutrons are identified ... Storage Ring, we measure the branching fractions B(B0-->D(*-)p_p pi(+)) = (6.5(+1.3)(-1.2)+/-1.0)x10(-4 ...

Abstract	We report the first observation of exclusive decays of the type B-->D()N_NX, where N is a nucleon. Using a sample of 9.7x10(6)B_B pairs collected with the CLEO detector operating at the Cornell Electron Storage Ring, we measure the branching fractions B(B0-->D(-)p_p pi(+)) = (6.5(+1.3)(-1.2)+/-1.0)x10(-4) and B(B0-->D(*-)p_n) = (14.5(+3.4)(-3.0)+/-2.7)x10(-4). Antineutrons are identified by their annihilation in the CsI electromagnetic calorimeter.
Language	English
Publishing date	2001-03-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	208853-8
ISSN	1079-7114 ; 0031-9007
ISSN (online)	1079-7114
ISSN	0031-9007
DOI	10.1103/PhysRevLett.86.2732
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Article ; Online: Attractor reconstruction with reservoir computers: The effect of the reservoir's conditional Lyapunov exponents on faithful attractor reconstruction.

Hart, Joseph D

Chaos (Woodbury, N.Y.)

2024 Volume 34, Issue 4

Abstract: Reservoir computing is a machine learning framework that has been shown to be able to replicate the chaotic attractor, including the fractal dimension and the entire Lyapunov spectrum, of the dynamical system on which it is trained. We quantitatively ... ...

Abstract	Reservoir computing is a machine learning framework that has been shown to be able to replicate the chaotic attractor, including the fractal dimension and the entire Lyapunov spectrum, of the dynamical system on which it is trained. We quantitatively relate the generalized synchronization dynamics of a driven reservoir during the training stage to the performance of the trained reservoir computer at the attractor reconstruction task. We show that, in order to obtain successful attractor reconstruction and Lyapunov spectrum estimation, the maximal conditional Lyapunov exponent of the driven reservoir must be significantly more negative than the most negative Lyapunov exponent of the target system. We also find that the maximal conditional Lyapunov exponent of the reservoir depends strongly on the spectral radius of the reservoir adjacency matrix; therefore, for attractor reconstruction and Lyapunov spectrum estimation, small spectral radius reservoir computers perform better in general. Our arguments are supported by numerical examples on well-known chaotic systems.
Language	English
Publishing date	2024-04-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	1472677-4
ISSN	1089-7682 ; 1054-1500
ISSN (online)	1089-7682
ISSN	1054-1500
DOI	10.1063/5.0196257
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Article: Acute N-methyl-D,L-aspartate administration stimulates the luteinizing hormone releasing hormone pulse generator in the ovine fetus.

Bettendorf, M / de Zegher, F / Albers, N / Hart, C S / Kaplan, S L / Grumbach, M M

Hormone research

1999 Volume 51, Issue 1, Page(s) 25–30

Abstract: ... the capacity to respond to an exogenous stimulus, a synthetic excitatory amino acid analogue, N-methyl-D-L ... the oFSH response to NMDA (n = 5). Moreover, D, L-2-amino-5-phosphonovalerate, a specific competitive ... and a greater oFSH response (p < 0.03) than NMDA (n = 6). Desensitization of the fetal gonadotrope ...

Abstract	To assess whether fetal luteinizing hormone releasing hormone (LH-RH) neurosecretory neurons have the capacity to respond to an exogenous stimulus, a synthetic excitatory amino acid analogue, N-methyl-D-L-aspartate (NMDA; 15 mg/kg), was given rapidly intravenously to 8 chronically catheterized fetuses (130-142 days of gestation; term 147 +/- 3 days). All 8 fetuses exhibited a rise in plasma ovine luteinizing hormone (oLH) and ovine follicle-stimulating hormone (oFSH) within 5 min. The mean maximal increments of oLH (2.25 +/- 0.36 ng/ml) and oFSH (1.21 +/- 0.32 ng/ml) were significantly greater than in 6 normal saline-injected controls (oLH p < 0.0002; oFSH p < 0.03). The secretion of ovine prolactin (oPRL) and ovine growth hormone (oGH) was unaffected. LH-RH (5 microg) evoked a greater oLH response (p < 0.0009) and a greater oFSH response (p < 0.03) than NMDA (n = 6). Desensitization of the fetal gonadotrope by a potent LH-RH agonist, D-Trp6Pro9NEt-LH-RH (10 microg/day i.v. x 4 days), abolished the fetal oLH and the oFSH response to NMDA (n = 5). Moreover, D, L-2-amino-5-phosphonovalerate, a specific competitive antagonist for the NMDA receptor, completely inhibited the fetal oLH and oFSH response to NMDA, whereas D-L-2-amino-5-phosphonovalerate alone did not affect the plasma oLH or oFSH levels, the gonadotropin response to LH-RH, or the release of oGH or oPRL (n = 3). In primary ovine fetal pituitary cell cultures, NMDA (10(-10) to 10(-6) M) had no effect on oLH, oFSH, oGH, or oPRL secretion, whereas LH-RH stimulated oLH (10(-8) M; p < 0.0004) and oFSH (10(-8) M; p < 0. 0001) release, evidence that NMDA did not have a direct pituitary effect. The results suggest that NMDA induces oLH and oFSH secretion by stimulation of the fetal LH-RH pulse generator and is mediated by central NMDA receptors. Fetal LH and FSH secretion and the response to LH-RH decrease in late gestation in the ovine and human fetus. The relative importance of sex steroid dependent and sex steroid independent central nervous system inhibition in this developmental change is unclear. It appears that central neural inhibition in addition to sex steroid negative feedback contributes to the decrease in fetal gonadotropin concentrations in late gestation. NMDA did not affect fetal oGH or oPRL secretion.
MeSH term(s)	2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Cells, Cultured ; Feedback ; Female ; Fetal Blood ; Fetus/physiology ; Follicle Stimulating Hormone/blood ; Follicle Stimulating Hormone/secretion ; Gonadotropin-Releasing Hormone/agonists ; Gonadotropin-Releasing Hormone/pharmacology ; Growth Hormone/blood ; Growth Hormone/secretion ; Growth Hormone-Releasing Hormone/blood ; Growth Hormone-Releasing Hormone/secretion ; Humans ; Infusions, Intravenous ; Luteinizing Hormone/blood ; Luteinizing Hormone/secretion ; N-Methylaspartate/administration & dosage ; N-Methylaspartate/pharmacology ; Pituitary Gland/drug effects ; Pituitary Gland/secretion ; Pregnancy ; Prolactin/blood ; Prolactin/secretion ; Sheep ; Triptorelin Pamoate/analogs & derivatives ; Triptorelin Pamoate/pharmacology
Chemical Substances	Gonadotropin-Releasing Hormone (33515-09-2) ; Triptorelin Pamoate (57773-63-4) ; Tryptal (57773-65-6) ; N-Methylaspartate (6384-92-5) ; 2-Amino-5-phosphonovalerate (76726-92-6) ; Prolactin (9002-62-4) ; Luteinizing Hormone (9002-67-9) ; Follicle Stimulating Hormone (9002-68-0) ; Growth Hormone (9002-72-6) ; Growth Hormone-Releasing Hormone (9034-39-3)
Language	English
Publishing date	1999
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	124442-5
ISSN	1423-0046 ; 0301-0163
ISSN (online)	1423-0046
ISSN	0301-0163
DOI	10.1159/000023309
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Article: An assay for the enzyme N-acetyl-beta-D-glucosaminidase (NAGase) based on electrochemical detection using screen-printed carbon electrodes (SPCEs).

Pemberton, R M / Hart, J P / Mottram, T T

The Analyst

2001 Volume 126, Issue 11, Page(s) 1866–1871

Abstract: An electrochemical assay for the enzyme N-acetyl-beta-D-glucosaminidase (NAGase) is described ... using bare screen-printed carbon electrodes (SPCEs). The enzyme substrate, 1-naphthyl-N-acetyl-beta-D ...

Abstract	An electrochemical assay for the enzyme N-acetyl-beta-D-glucosaminidase (NAGase) is described, using bare screen-printed carbon electrodes (SPCEs). The enzyme substrate, 1-naphthyl-N-acetyl-beta-D-glucosaminide, was added to the NAGase-containing sample under hydrodynamic conditions and was hydrolysed to 1-naphthol, which was monitored amperometrically at an Eapp of +650 mV versus SCE. A pH study revealed the apparent Vmax for the assay to occur at pH 4.5. corresponding to an apparent substrate Km of 0.28 mM. In order to be compatible with the analysis of biological fluids, a final operating pH of 5.4 was selected, and, using a data recording time of 100 s post-substrate addition, the assay gave a linear response (r2 = 0.988) over the range 3.1 to 108 mU ml(-1) NAGase (RSD = 15.4%). This assay has the potential to monitor NAGase levels in a number of application areas.
MeSH term(s)	Acetylglucosaminidase/analysis ; Animals ; Carbon ; Electrochemistry ; Electrodes ; Humans ; Naphthols/analysis
Chemical Substances	Naphthols ; 1-naphthol (2A71EAQ389) ; Carbon (7440-44-0) ; Acetylglucosaminidase (EC 3.2.1.52)
Language	English
Publishing date	2001-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	210747-8
ISSN	0003-2654
ISSN	0003-2654
DOI	10.1039/b104874k
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Zs.A 2423: Show issues

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Article: Purification and characterization of an O-GlcNAc selective N-acetyl-beta-D-glucosaminidase from rat spleen cytosol.

Dong, D L / Hart, G W

The Journal of biological chemistry

1994 Volume 269, Issue 30, Page(s) 19321–19330

Abstract: ... involved in removal of these sugars, a neutral and cytoplasmic N-acetyl-beta-D-glucosaminidase (O-GlcNAcase ... Glycosylation of nuclear and cytoplasmic proteins by O-linked N-acetylglucosamine (O-GlcNAc ...

Abstract	Glycosylation of nuclear and cytoplasmic proteins by O-linked N-acetylglucosamine (O-GlcNAc) monosaccharides is an abundant, ubiquitous, and transient post-translational modification. To characterize enzymes involved in removal of these sugars, a neutral and cytoplasmic N-acetyl-beta-D-glucosaminidase (O-GlcNAcase) with strong selectivity for O-GlcNAc-synthetic glycopeptides has been purified over 22,000-fold from rat spleen homogenate. The purified O-GlcNAcase has two major polypeptides of apparent M(r) = 54,000 (alpha subunit) and M(r) = 51,000 (beta subunit). Enzyme activity sediments at M(r) = 106,000 on sucrose gradients, indicating that the native O-GlcNAcase is an alpha beta heterodimer. The O-GlcNAcase also shows substantially stronger relative activity against O-GlcNAc-synthetic glycopeptides than other hexosaminidases. Unlike acidic lysosomal hexosaminidases, O-GlcNAcase is not inhibited by GalNAc or its analogs, has no other detectable glycosidase activities, and does not cross-react with antibodies against acidic hexosaminidases. Subcellular fractionation and latency studies demonstrate the cytoplasmic and nucleoplasmic localization of the enzyme and its ubiquitous presence in tissues. These studies suggest that O-GlcNAcase is involved in the regulated removal of O-GlcNAc from O-GlcNAc-bearing glycoproteins in the nucleoplasmic and cytoplasmic compartments of cells.
MeSH term(s)	Acetylglucosaminidase/isolation & purification ; Acetylglucosaminidase/metabolism ; Amino Acid Sequence ; Animals ; Cell Compartmentation ; Chromatography ; Cytosol/enzymology ; Hydrogen-Ion Concentration ; Molecular Sequence Data ; Molecular Weight ; Rats ; Spleen/enzymology ; Subcellular Fractions/enzymology ; Substrate Specificity ; beta-N-Acetylhexosaminidases/metabolism
Chemical Substances	Acetylglucosaminidase (EC 3.2.1.52) ; beta-N-Acetylhexosaminidases (EC 3.2.1.52)
Language	English
Publishing date	1994-07-29
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
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Article: The neurotoxicity induced by ethanol withdrawal in mature organotypic hippocampal slices might involve cross-talk between metabotropic glutamate type 5 receptors and N-methyl-D-aspartate receptors.

Harris, Barton R / Gibson, D Alex / Prendergast, Mark A / Blanchard, John A / Holley, Robert C / Hart, Stewart R / Scotland, Rebecca L / Foster, Thomas C / Pedigo, Norman W / Littleton, John M

Alcoholism, clinical and experimental research

2003 Volume 27, Issue 11, Page(s) 1724–1735

Abstract: ... the characteristics of an antagonist at metabotropic glutamate type 5 receptors (mGluR5s) rather than at N-methyl-d ...

Abstract	Background: We recently reported that the sodium salt of acamprosate (Na-acamprosate) demonstrates the characteristics of an antagonist at metabotropic glutamate type 5 receptors (mGluR5s) rather than at N-methyl-d-aspartate receptors (NMDARs). Because mGluR5s are able to enhance the function of NMDARs, this interplay may be involved in the dysregulation of glutamatergic transmission during ethanol withdrawal. The following studies use organotypic hippocampal slice cultures at a mature age to investigate the potential for this interplay in the neurotoxicity associated with withdrawal from long-term ethanol exposure. Methods: At 25 days in vitro, organotypic hippocampal slice cultures prepared from male and female 8-day-old rats were exposed to an initial concentration of 100 mM ethanol for 10 days before undergoing a 24-hr period of withdrawal. The effects of Na-acamprosate; 2-methyl-6-(2-phenylethenyl)pyridine (SIB-1893), a noncompetitive antagonist at mGluR5s; 7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester, a noncompetitive antagonist at mGluR1s; dizocilpine (MK-801), a noncompetitive NMDAR antagonist; and staurosporine on the neurotoxicity induced by ethanol withdrawal were assessed by determining differences in propidium iodide uptake. Polypeptide levels of mGluR5s and the NR1 and NR2B subunits of NMDARs were also determined via Western blot analyses after 10 days of ethanol exposure. Results: Significant neurotoxicity was always evident in the CA1 hippocampal region after a 24-hr withdrawal period. This spontaneous neurotoxicity resulted from intrinsic changes induced by the long-term presence of ethanol. Na-acamprosate (200-1000 microM), SIB-1893 (200-500 microM), MK-801 (20 microM), and staurosporine (200 nM) were all neuroprotective. The polypeptide levels of mGluR5s and NR1 and NR2B subunits of NMDARs were all increased after ethanol exposure; however, the increase in mGluR5s did not achieve statistical significance. Conclusions: From this model of long-term ethanol exposure and withdrawal, the functional interplay between mGluR5s and NMDARs might represent a novel target for the prevention of neurotoxicity associated with ethanol withdrawal.
MeSH term(s)	Animals ; Dizocilpine Maleate/pharmacology ; Ethanol/toxicity ; Female ; Hippocampus/drug effects ; Hippocampus/metabolism ; Male ; N-Methylaspartate/pharmacology ; Organ Culture Techniques ; Rats ; Rats, Sprague-Dawley ; Receptor, Metabotropic Glutamate 5 ; Receptors, Metabotropic Glutamate/agonists ; Receptors, Metabotropic Glutamate/antagonists & inhibitors ; Receptors, Metabotropic Glutamate/metabolism ; Receptors, N-Methyl-D-Aspartate/agonists ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors ; Receptors, N-Methyl-D-Aspartate/metabolism ; Substance Withdrawal Syndrome/metabolism
Chemical Substances	Receptor, Metabotropic Glutamate 5 ; Receptors, Metabotropic Glutamate ; Receptors, N-Methyl-D-Aspartate ; Ethanol (3K9958V90M) ; N-Methylaspartate (6384-92-5) ; Dizocilpine Maleate (6LR8C1B66Q)
Language	English
Publishing date	2003-11
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1097/01.ALC.0000093601.33119.E3
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Article ; Online: A history of home mechanical ventilation: The past, present and future.

D'Cruz, Rebecca F / Hart, Nicholas

Chronic respiratory disease

2024 Volume 21, Page(s) 14799731241240776

Abstract: This state-of-the-art review provides an overview of the history of home mechanical ventilation (HMV), including early descriptions of mechanical ventilation from ancient and Renaissance perspectives and the mass development of ventilators designed for ... ...

Abstract	This state-of-the-art review provides an overview of the history of home mechanical ventilation (HMV), including early descriptions of mechanical ventilation from ancient and Renaissance perspectives and the mass development of ventilators designed for long-term use during the poliomyelitis epidemic. Seminal data from key clinical trials supports the application of HMV in certain patients with chronic obstructive pulmonary disease, neuromuscular disease and obesity-related respiratory failure. Innovative engineering coupled with refined physiological understanding now permits widespread delivery of home mechanical ventilation to a global population, using portable devices with advanced ventilatory modes and telemonitoring capabilities. Exponential growth in digital technology continues, and ongoing research is needed to understand how to harness clinical and physiological data to benefit patients and healthcare services in a clinically- and cost-effective manner.
MeSH term(s)	Humans ; Respiration, Artificial ; Obesity ; Pulmonary Disease, Chronic Obstructive/therapy
Language	English
Publishing date	2024-03-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2211488-9
ISSN	1479-9731 ; 1479-9723
ISSN (online)	1479-9731
ISSN	1479-9723
DOI	10.1177/14799731241240776
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: 2,3-didehydro-2,4-dideoxy-4-guanidino-N-acetyl-D-neuraminic acid (4-guanidino-Neu5Ac2en) is a slow-binding inhibitor of sialidase from both influenza A virus and influenza B virus.

Hart, G J / Bethell, R C

Biochemistry and molecular biology international

1995 Volume 36, Issue 4, Page(s) 695–703

Abstract: The effect of 2,3-didehydro-2,4-dideoxy-4-guanidino-N-acetyl-D-neuraminic acid (4-guanidino ...

Abstract	The effect of 2,3-didehydro-2,4-dideoxy-4-guanidino-N-acetyl-D-neuraminic acid (4-guanidino-Neu5Ac2en) on the sialidases from influenza virus reassortant X31 (which contains the sialidase from A/Aichi/2/68) and influenza virus B/Beijing/1/87 has been investigated. We find that 4-guanidino-Neu5Ac2en is a slow-binding inhibitor of both influenza A and influenza B virus sialidase, and that association and dissociation rate constants are almost identical for both enzymes. Furthermore, values for these rate constants are independent of whether purified enzyme or detergent-treated virus is used in the assays.
MeSH term(s)	Dose-Response Relationship, Drug ; Enzyme Inhibitors/metabolism ; Enzyme Inhibitors/pharmacology ; Guanidines ; Humans ; Influenza A virus/enzymology ; Influenza B virus/enzymology ; Kinetics ; Neuraminidase/antagonists & inhibitors ; Neuraminidase/isolation & purification ; Neuraminidase/metabolism ; Pyrans ; Sialic Acids/metabolism ; Sialic Acids/pharmacology ; Species Specificity ; Zanamivir
Chemical Substances	Enzyme Inhibitors ; Guanidines ; Pyrans ; Sialic Acids ; Neuraminidase (EC 3.2.1.18) ; Zanamivir (L6O3XI777I)
Language	English
Publishing date	1995-07
Publishing country	England
Document type	Comparative Study ; Journal Article
ZDB-ID	1144589-0
ISSN	1039-9712 ; 0158-5231
ISSN	1039-9712 ; 0158-5231
Database	MEDical Literature Analysis and Retrieval System OnLINE

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