Relevant bibliographies by topics / Nyhavn

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  2. Dissertations / Theses
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Academic literature on the topic 'Nyhavn'

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Published: 29 July 2024
Last updated: 30 July 2024

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Journal articles on the topic "Nyhavn"

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Cabiati, Manuela, Raffaele Caruso, Alessandro Verde, Laura Sabatino, Maria-Aurora Morales, and Silvia Del Ry. "Transcriptomic Profiling of the Four Adenosine Receptors in Human Leukocytes of Heart Failure Patients." BioMed Research International 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/569438.

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In this study the transcriptomic profiling of adenosine receptors (ARs) in human leukocytes of heart failure (HF) patients as a function of clinical severity, assessing the possible changes with respect to healthy subjects (C), was evaluated. Total RNA was extracted from leukocytes ofC(n=8) and of HF patients (NYHA I-IIn=9; NYHA III-IVn=14) with a PAXgene Blood RNA Kit. An increase as a function of clinical severity was observed in each AR (A1R:C=0.02±0.009, NYHAI-II=0.21±0.09, NYHAIII-IV=3.6±1.3,P=0.03 Cversus NYHA III-IV,P=0.02NYHA I-II versus NYHA III-IV; A2aR:C=0.2±0.05, NYHAI-II=0.19±0.04, NYHAIII-IV=1.32±0.33,P=0.005 Cversus NYHA III-IV,P=0.003NYHA I-II versus NYHA III-IV; A2bR:C=1.78±0.36, NYHAI-II=1.35±0.29, NYHAIII-IV=4.07±1.21,P=0.03: NYHA I-II versus NYHA III-IV; A3R:C=0.76±0.21, NYHAI-II=0.94±0.19, NYHAIII-IV=3.14±0.77,P=0.01 Cversus NYHA III-IV and NYHA I-II versus NYHA III-IV, resp.). The mRNA expression of the ectonucleoside triphosphate diphosphohydrolase (CD39) and the ecto-5′-nucleotidase (CD73) were also evaluated. They resulted up-regulated. These findings show that components of adenosine metabolism and signalling are altered to promote adenosine production and signalling in HF patients. Thus, HF may benefit from adenosine-based drug therapy after confirmation by clinical trials.
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Kim, Myoung-Gook, Kyu-Ho Yang, Nam-Ki Choi, and Seon-Mi Kim. "LESCH-NYHAN SYNDROME: A CASE REPORT." JOURNAL OF THE KOREAN ACADEMY OF PEDTATRIC DENTISTRY 38, no. 3 (August 31, 2011): 284–89. http://dx.doi.org/10.5933/jkapd.2011.38.3.284.

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Millichap, J. Gordon. "Lesch-Nyhan Syndrome." Pediatric Neurology Briefs 2, no. 5 (May 1, 1988): 37. http://dx.doi.org/10.15844/pedneurbriefs-2-5-9.

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Nyhan, W. L. "Lesch-Nyhan Disease." Nucleosides, Nucleotides and Nucleic Acids 27, no. 6-7 (July 23, 2008): 559–63. http://dx.doi.org/10.1080/15257770802135745.

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Nyhan, William L. "LESCH-Nyhan Disease." Journal of the History of the Neurosciences 14, no. 1 (March 9, 2005): 1–10. http://dx.doi.org/10.1080/096470490512490.

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Torres, R. J., and J. G. Puig. "Lesch-Nyhan syndrome." Drugs of the Future 35, no. 5 (2010): 421. http://dx.doi.org/10.1358/dof.2010.035.05.1490758.

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Smith, Brian M., Bruce J. Cutilli, and Michael Fedele. "Lesch-Nyhan syndrome." Oral Surgery, Oral Medicine, Oral Pathology 78, no. 3 (September 1994): 317–18. http://dx.doi.org/10.1016/0030-4220(94)90061-2.

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Torres, R. J., and J. G. Puig. "Lesch-Nyhan syndrome." Drugs of the Future 35, no. 5 (2010): 421. http://dx.doi.org/10.1358/dof.2010.35.5.1490758.

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Holt, Kenneth S. "THE LESCH-NYHAN SYNDROME." Developmental Medicine & Child Neurology 11, no. 3 (November 12, 2008): 382–84. http://dx.doi.org/10.1111/j.1469-8749.1969.tb01452.x.

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Pinardi, Beatriz A., Liliana E. Romagnoli, Silvia S. Bonzani, Perla Robert, and Gonzalo J. Ferreyra. "Síndrome de Lesch-Nyhan." Piel 21, no. 9 (November 2006): 459–61. http://dx.doi.org/10.1016/s0213-9251(06)72539-4.

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Dissertations / Theses on the topic "Nyhavn"

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Råberg, Knut Sigurd. "Nyhavna arkivbibliotek." Thesis, Norges teknisk-naturvitenskapelige universitet, Fakultet for arkitektur og billedkunst, 2014. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-26690.

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Sætre, Marie, and Line Myrenget. "Å skifte status : trosnøytralt seremonibygg på Nyhavna." Thesis, Norges teknisk-naturvitenskapelige universitet, Fakultet for arkitektur og billedkunst, 2012. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-17648.

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Lorenz, Veronika. "Komplexe Veränderungen in der Genexpression der Ecto-Nukleosid-5-Triphosphat-Diphosphohydrolase bei Hypoxanthin-Phosphoribosyltransferase-Defizienz." kostenfrei, 2008. http://www.opus-bayern.de/uni-regensburg/volltexte/2009/1207/.

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Galloon, Terry. "Biochemical and genetic properties of HPRT Cape Town." Master's thesis, University of Cape Town, 1987. http://hdl.handle.net/11427/26591.

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An unusual partial HPRT deficient mutant, HPRT Cape Town was observed to have a low activity in erythrocyte lysates at high concentrations of the purine substrates, hypoxanthine and guanine. This substrate inhibition was not observed with the substrate PPRP. The low activity was not associated with changes in the Km or Vmax for any of the substrates (Steyn and Harley, 1984). The kinetics of the proband's enzyme was studied in lymphoblast extracts. The characteristic substrate inhibition was observed which showed that this phenomenon was not confined to erythrocytes but was a more generalized phenomenon. This result implies that the decreased HPRT activity observed in the proband is due to substrate inhibition by the purine bases. The HPRT enzyme is coded for by a gene which is located on the X chromosome (Pai et al., 1980). The proband's daughter was therefore studied in order to determine the cause of the mutation. It was not known whether the substrate inhibition was the result of a mutation in the gene coding for the enzyme, a mutation which results in altered post-translational modification or the absence or alteration of factors influencing normal HPRT kinetics. The daughter's transformed lymphoblasts exhibited growth patterns in selective media that resembled those of her father. The daughter's enzyme prepared from lymphoblast extracts exhibited the characteristic substrate inhibition. These results suggest that this cell line results from the selection of a clone or clones which have suppressed the function of the X chromosome carrying the maternal and presumably normal HPRT allele. The daughter's enzyme prepared from erythrocyte lysates exhibited intermediate enzyme activity between that of the proband and a normal control. This result suggests that the daughter is an obligate heterozygote and that the defect is due to a mutation in the HPRT gene itself. The defect was studied at the gene level. No difference was observed in the banding patterns of the proband's DNA and control DNA which were digested with various restriction enzymes and hybridized to ³²p-labelled HPRT cDNA. The size of the HPRT mRNA of the proband was the same as the control. These results imply that there is no major gene alteration; this is expected since the proband only has a partial deficiency of the enzyme. The HPRT cDNA was subcloned into a riboprobe vector, pGEM-3. The T7 promoter was used to transcribe antisense RNA strands which were then hybridized to the proband's RNA and control RNA. No difference was observed in the size of the protected fragment. This result does not exclude the possibility of a point mutation as the cause of the defect in HPRT Cape Town.
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Boyd, Marie. "Evaluation of screening strategies for the detection of molecular pathologies." Thesis, University of Glasgow, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295318.

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Heshka, Timothy William. "Effects of hypoxanthine upon dopamine neurons : an animal model for Lesch-Nyhan disease." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59392.

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In Lesch-Nyhan disease, concentrations of hypoxanthine are elevated especially in the brain and cerebrospinal fluid; dopamine and its metabolites are reduced in the caudate and putamen. Hence we investigated the possibility that hypoxanthine has direct effects on dopamine neurons.
Hypoxanthine, adenine or allopurinol was delivered unilaterally into the rat brain. Behavioural effects were monitored by apomorphine-induced rotation; ipsilateral turning was time and dose-dependent. Turning was competitively blocked by a non-specific DA antagonist, suggesting that dopamine neurons were altered. In hypoxanthine treated animals, a D1 antagonist specifically blocked rotation; catalepsy occurred after caffeine administration.
After two or three weeks treatment all groups had elevated purine levels in the caudate nuclei, while catecholamine levels were variably altered.
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Bavaresco, Caren Serra. "Efeito in vitro das substâncias acumuladas na doença de Lesch-Nyhan sobre a atividade da Na+,K+-ATPase em estriado de ratos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2004. http://hdl.handle.net/10183/5764.

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A doença de Lesch-Nyhan é um erro inato do metabolismo das purinas caracterizado pela deficiência na enzima hipoxantina- guanina fosforibosiltransferase. O bloqueio dessa reação resulta no acúmulo tecidual de hipoxantina, xantina e ácido úrico. A doença caracteriza-se por hiperuricemia, variado grau de retardo mental e motor, espasticidade e auto-mutilação. No sistema nervoso central, a Na+, K+ - ATPase é responsável pela manutenção da homeostase dos íons Na+ e K+, regulando o volume celular, a excitabilidade neuronal, o transporte de neurotransmissores e outras moléculas. Evidências na literatura demonstram que a redução na atividade da Na+, K+ - ATPase está relacionada com diversas doenças neurodegenerativas, tais como isquemia cerebral e doenças de Parkinson e de Alzheimer. No presente estudo, investigamos o efeito in vitro da hipoxantina, xantina e ácido úrico sobre a atividade da Na+, K+- ATPase em membrana plasmática sináptica de estriado de ratos. Estudamos, também, a cinética de inibição causada pela hipoxantina e de interação entre hipoxantina, xantina e ácido úrico. Nossos resultados demonstram que hipoxantina, xantina e ácido úrico inibem significativamente a atividade da Na+, K+- ATPase. O estudo dos mecanismos de inibição da atividade enzimática causados pela hipoxantina demonstrou um efeito inibitório não competitivo com o substrato ATP. Além disso, o estudo de interação cinética entre hipoxantina, xantina e ácido úrico sugere que esses compostos atuem em um mesmo sítio de ligação na enzima. Verificamos, também, o efeito da preincubação de homogeneizado de estriado de ratos na presença de hipoxantina (10 µM) sobre a atividade da Na+, K+- ATPase de membrana plasmática sináptica com a adição ou não de antioxidantes (glutationa e trolox), bem como alguns parâmetros de estresse oxidativo denominados TBARS (medida de lipoperoxidação) e TRAP (capacidade antioxidante tecidual não-enzimática) no intuito de verificar a participação do estresse oxidativo nos mecanismos de inibição enzimática provocados pela hipoxantina. Os resultados monstraram que a hipoxantina inibe significativamente a atividade da Na+, K+- ATPase. Adicionalmente, nossos resultados demonstraram que glutationa, mas não o trolox, na concentração de 1 mM, foi capaz de prevenir a inibição enzimática causada pela hipoxantina. Nossos resultados também mostraram que a hipoxantina, na mesma concentração, aumentou TBARS e diminuiu TRAP que essa substância induz o estresse oxidativo. É possível que a inibição na atividade da Na+, K+- ATPase possa estar envolvida nos mecanismos pelos quais as oxipurinas são neurotóxicas. Acreditamos que nossos resultados possam contribuir, pelo menos em parte, na compreensão da disfunção neurológica encontrada em pacientes portadores da doença de Lesch-Nyhan.
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Ruillier, Valentin. "Utilisation des cellules souches pluripotentes pour le criblage à haut débit de molécules thérapeutiques dans la maladie de Lesch-Nyhan." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLE011/document.

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Les mutations affectant la fonction d'enzymes impliquées dans le cycle des purines sont responsables d'une multitude de syndromes pédiatriques, caractérisés par des atteintes neurologiques et comportementales. A ce jour, aucune stratégie thérapeutique n'a été réellement efficace pour contrôler ces symptômes. La maladie de Lesch-Nyhan (MLN), associée à la perte de fonction de l'enzyme de recyclage HGPRT, constitue un bon modèle d'étude. Mon travail a consisté à utiliser la technologie des cellules souches induites à la pluripotence, reprogrammées à partir de fibroblastes de patients atteints des formes sévères de la MLN, pour identifier des phénotypes neuronaux associés à la perte de fonction de l'HGPRT. Ces marqueurs phénotypiques ont ensuite été utilisés pour identifier, par une approche de criblage à haut débit, de nouvelles molécules chimiques capables de corriger ces défauts. Plus de 3000 molécules ont été testées et 6 composés, tous dérivés de l'adénosine, ont pu être identifiés comme compensant le métabolisme par un mécanisme d'action indépendant de l'HGPRT. De manière intéressante, un des composés, la S-adenosylmethionine (SAM) a par le passé déjà démontré des effets bénéfiques sur les symptômes comportementaux typiques de la MLN dans plusieurs études de cas. Cela démontre que la stratégie abordée ici a permis l'identification de cibles thérapeutiques permettant d'améliorer les symptômes neurospychiatriques de cette pathologie et constitue un modèle réplicable pour différentes pathologies touchant le métabolisme cérébral
Mutations in genes coding for enzymes involved in purine synthesis or recycling lead to dramatic neurological conditions with poor pharmacological options. Lesch–Nyhan disease (LND) is caused by deficiency of the salvage pathway enzyme HGPRT that compromises recycling of guanine and hypoxanthine into GMP and IMP. LND is characterized by severe neuropsychiatric symptoms that are out of reach of pharmacological treatments. Here we use human cortical neural stem cells and neurons derived from iPSC of children affected by severe forms of LND to identify neural phenotypes associated with HGPRT-deficiency and of interest to develop a target-agnostic based drug screening system. We screened more than 3000 molecules and identified 6 compounds, all possessing an adenosine moiety, that corrected LND related neuronal phenotypes by promoting metabolism compensations in a HGPRT-independent manner. One of these compound, S-adenosylmethionine (SAM), has already been reported as providing amelioration of behavioral symptoms in some LND cases, demonstrating that our screening allowed the identification of pathways that can be relevant therapeutic targets to ease the devastating neuropsychiatric symptoms associated with this pathology. Interestingly, these pathways can be activated in LND patients via simple food supplementation. This experimental paradigm can also be easily adapted to other purine associated neurological disorders affecting normal brain development
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Petitgas, Céline. "Etude des mécanismes pathogéniques de la maladie de Lesch-Nyhan en relation avec le système dopaminergique chez un organisme modèle, Drosophila melanogaster." Thesis, Paris Sciences et Lettres (ComUE), 2019. http://www.theses.fr/2019PSLET049.

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L’adénine phosphoribosyltransférase (APRT) et l’hypoxanthine-guanine phosphoribosyltransférase (HGPRT) sont deux enzymes majeures impliquées dans le recyclage des purines chez les Mammifères, une voie métabolique essentielle permettant la récupération des bases puriques dérivées de l’alimentation ou de la dégradation des nucléotides. La voie de sauvetage des purines est en effet moins coûteuse en énergie que la voie de synthèse de novo et son dysfonctionnement induit diverses pathologies. En particulier, des mutations héréditaires supprimant l’activité de l’HGPRT sont associées à la maladie de Lesch-Nyhan (MLN), une pathologie infantile rare liée à l’X caractérisée par une hyperuricémie et de graves troubles neurocomportementaux tels que dystonie, spasticité et automutilations. Des études ont montré que les patients présentent une diminution significative des taux de dopamine dans les ganglions de la base, sans que l’on comprenne clairement le lien entre la neurotransmission dopaminergique et l’absence d’activité de l’HGPRT. L’objectif de cette thèse a donc été d’étudier la relation entre le sauvetage des purines et le système dopaminergique chez un organisme modèle, la drosophile, afin de mieux comprendre les mécanismes impliqués dans la MLN. La drosophile n’a pas d’homologue de l’HGPRT, ce qui suggère que l’homologue de l’APRT, désignée Aprt, est l’unique enzyme de recyclage des purines chez cet organisme. Nos travaux montrent que des drosophiles mutantes déficientes en Aprt présentent des défauts physiologiques en partie comparables à ceux associés à l’absence d’HGPRT chez l’Homme, notamment un taux élevé d’acide urique ainsi que des altérations des marqueurs dopaminergiques et des troubles neurocomportementaux. A l’inverse, des perturbations génétiques du système dopaminergique induisent une diminution de l’expression et de l’activité de l’Aprt. Nos résultats confirment ainsi la conservation d’un lien physiologique entre le recyclage des purines et le système dopaminergique chez la drosophile, et indiquent de plus que cette régulation fait intervenir la signalisation adénosinergique. Ce nouveau modèle pourrait donc s’avérer utile à terme pour identifier de nouvelles cibles thérapeutiques permettant d’améliorer le traitement de cette maladie dramatique
Adenine phosphoribosyltransferase (APRT) and hypoxanthine-guanine phosphoribosyltransferase (HGPRT) are two major enzymes involved in purine recycling in mammals, an essential metabolic pathway that allows the recovery of free purine bases derived from diet or the degradation of nucleotides. The purine salvage pathway is indeed less energy costly than de novo purine synthesis and its dysfunction induces various pathologies. In particular, inherited mutations suppressing HGPRT enzyme activity are associated with Lesch-Nyhan disease (LND), a rare X-linked metabolic and neurophysiological disorder in children, characterized by hyperuricemia and severe neurobehavioural disturbances such as dystonia, spasticity and compulsive self-injury. Studies have shown that LND patients have markedly reduced dopamine levels specifically in the basal ganglia, but the mechanisms linking the lack of HPRT activity and dopaminergic neurotransmission have not been elucidated to date. In this thesis work, we have been studying the relation between purine metabolism and the dopaminergic system in a model organism, Drosophila, with the aim to find new clues about the mechanisms involved in LND. No HGPRT homologue is present in the Drosophila genome, which suggests that the APRT homologue, named Aprt, is the only purine-recycling enzyme in this organism. Our work shows that Aprt-deficient flies have defects partly comparable to those associated with HGPRT deficiency in humans, notably an increase in uric acid levels, as well as alterations in dopaminergic markers and neurobehavioural defects. Conversely, genetic disruptions of the dopaminergic system decrease the expression and activity level of Aprt. Our results therefore confirm the conservation of a physiological link between purine recycling and the dopaminergic system in Drosophila, and further indicate that this regulation requires adenosinergic signaling. This new model could therefore prove valuable to find new therapeutic targets and possibly improve the cure of this dramatic disease
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Bavaresco, Caren Serra. "Alterações bioquímicas e comportamentais em ratos submetidos à administração intra-estriatal de hipoxantina." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2008. http://hdl.handle.net/10183/13329.

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A síndrome de Lesch Nyhan é um erro inato do metabolismo das purinas, de característica recessiva, ligado ao sexo. Caracteriza-se, bioquimicamente, pela deficiência na atividade da enzima hipoxantina-guanina fosforribosiltransferase (HGPRT), resultando principalmente no acúmulo tecidual de hipoxantina. O quadro clínico manifestado é bastante característico incluindo alterações motoras e cognitivas, retardo mental, espasticidade e automutilação. Considerando que os mecanismos envolvidos nas alterações cerebrais encontradas nessa síndrome ainda são pouco conhecidos, os objetivos do presente estudo foram investigar o efeito da administração intraestriatal de hipoxantina sobre parâmetros bioquímicos cerebrais (atividades da Na+, K+- ATPase e acetilcolinesterase (AChE), parâmetros de estresse oxidativo, hidrólise dos nucleotídeos da adenina) e comportamentais (tarefas do labirinto aquático de Morris, campo aberto e esquiva inibitória) em ratos. Os resultados mostraram que a administração intra-estriatal de hipoxantina reduziu as atividades das enzimas Na+, K+- ATPase e AChE em estriado, hipocampo e no córtex cerebral de ratos. A infusão de hipoxantina aumentou a quimioluminescência,, substâncias reativas ao ácido tiobarbitúrico (TBARS) e atividade da enzima glutationa peroxidase (GPx), e reduziu a capacidade antioxidante tecidual (TRAP) e as atividades das enzimas superóxido dismutase (SOD) e catalase (CAT) em estriado de ratos. As hidrólises dos nucleotídeos da adenina também foram inibidas pela administração de hipoxantina. Os efeitos relatados possivelmente ocorreram através da geração de radicais livres, uma vez que a administração de vitaminas E e C previniu tais efeitos, com exceção do TRAP. Considerando as alterações neuroquímicas induzidas pela administração de hipoxantina observadas em nosso modelo experimental, a próxima etapa desse trabalho foi investigar o papel da administração de hipoxantina sobre a memória/ aprendizagem em ratos na tarefa do labirinto aquático de Morris e esquiva inibitória. A atividade motora dos animais também foi avaliada na tarefa de campo aberto. Os resultados mostraram que a hipoxantina provocou um déficit de V memória/ aprendizado em ambas as tarefas realizadas, contudo não alterou o comportamento motor dos animais. Nossos resultados, em conjunto, mostram que a administração intra-estriatal de hipoxantina provoca uma série de alterações bioquímicas e comportamentais as quais podem, pelo menos em parte, contribuir para as disfunções neurológicas características observadas nesta síndrome. Além disso, se nossas evidências se confirmarem em humanos, a utilização de antioxidantes, tais como as vitaminas E e C, poderão ser utilizados como estratégias terapêuticas a fim de evitar as alterações neurológicas nos pacientes portadores da síndrome de Lesch Nyhan.
Lesch Nyhan is an inborn X-linked recessive disease of purine metabolism characterized by deficiency of hypoxanthine-guanine phosphoribosyltranspherase (HGPRT) activity, resulting mainly in tissue accumulation of hypoxanthine. Affected patients present motor and cognitive deficits, spasticity, and self-mutilation behavior. Considering that the mechanisms involved in brain dysfunction found in this syndrome are poorly understood, the general objective of this study was to investigated the effect on intrastriatal hypoxanthine administration on some cerebral biochemical parameters (activities of Na+, K+- ATPase and acetylcholinesterase (AChE), oxidative stress parameters, adenine nucleotide hydrolysis) and behavioral (water-maze, step-down inhibitory avoidance and open field tasks) in rats. Results showed that intrastriatal hypoxanthine administration inhibited Na+, K+- ATPase and AChE in striatum, hippocampus and cerebral cortex of rats. We also verified that hypoxanthine administration increased chemiluminescence, thiobarbituric acid reactive substance (TBARS) and glutathione peroxidase (GPx) activity and reduced total radical-trapping antioxidant parameter (TRAP) and also superoxide dismutase (SOD) and catalase (CAT) activities in striatum of rats. Moreover, adenine nucleotide hydrolysis was also inhibited by hypoxanthine administration. These effects could be probably related to free radical generation since pretreatment with vitamins E and C prevented those effects, excepting for TRAP. Considering the neurochemical alterations provoked by hypoxanthine administration in this experimental model, the next step in this study was to investigate the effect of intrastriatal hypoxanthine administration on memory/ learning of rats in water-maze and step-down inhibitory avoidance tasks. The motor activity of the rats was evaluated by open field task. Results showed that hypoxanthine administration impaired memory/ learning in both tasks, however the motor activity of rats was not altered. Taken together, our results showed that intrastriatal hypoxanthine administration induced various biochemical and behavioral modification that could contribute, at least in part, to the characteristically neurological dysfunction observed in this syndrome. Moreover, if our evidences also occur in human, supplementation with antioxidants, like vitamins E and C, could be used as therapeutically strategies in order to avoid the neurological disturbances present in Lesch Nyhan patients.
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Books on the topic "Nyhavn"

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Platz, Naja Alberdi. Bebop Bar: Roman. Kbh.]: Lindhardt og Ringhof, 2006.

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Åstveit, Leif Inge. Ormen lange nyhamna: NTNU vitenskapsmuseets arkeologiske undersøekelser. Trondheim: Tapir, 2008.

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Parker, James N., and Philip M. Parker. Lesch-Nyhan syndrome: A bibliography and dictionary for physicians, patients, and genome researchers [to Internet references]. San Diego, CA: ICON Health Publications, 2007.

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Sarrionandia, Joseba. Hnuy illa nyha majah yahoo: (poemak, 1985-1995). Donosita: Elkar, 2013.

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Lechner, Hannelore. Reanimationspraxis bei inoperablen Patienten mit einer Herzinsuffizienz im Stadium NYHA IV. [s.l.]: [s.n.], 1996.

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1966-, Heilemann John, Rogers David (Journalist), and Shorenstein Center on Media, Politics, and Public Policy, eds. Theodore H. White lecture on press and politics with Mark Halperin and John Heilemann and the awarding of the David Nyhan Prize for Political Reporting to David Rogers. Cambridge, Massachusetts: Harvard Kennedy School Shorenstein Center on Media, Politics and Public Policy, 2014.

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Joan Shorenstein Center on the Press, Politics, and Public Policy and John F. Kennedy School of Government, eds. Theodore H. White Lecture on press and politics with the honorable Alan K. Simpson: And the awarding of the David Nyhan Prize for political reporting to Leonard Pitts Jr. Cambridge, Massachusetts: Harvard Kennedy School, Shorenstein Center on Media, Politics and Public Policy, 2013.

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N. T. Z. Record Press. 2021-2025 Monthly Planner: Large Five Years Calendar Schedule Organizer 60 Months Novelty Gifts for Time Management - Nyhavn Denmark Cover. Independently Published, 2021.

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NYHAN. Nyhan Birth Defects. John Wiley & Sons Inc, 1989.

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Design, N. T. Z. Denmark Travel Journal: Blank Lined Notebook for Travels and Adventure of Your Trip Nyhavn Copenhagen Matte Cover 6 X 9 Inches 15. 24 X 22. 86 Centimetre 111 Pages. Independently Published, 2019.

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Book chapters on the topic "Nyhavn"

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Davis, Philip J. "Spectral Dialogue in Nyhavn." In Thomas Gray in Copenhagen, 67–72. New York, NY: Springer New York, 1995. http://dx.doi.org/10.1007/978-1-4757-4366-1_10.

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Conravey, Allison, and Ann Tilton. "Lesch-Nyhan Disease." In International Neurology, 638–39. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444317008.ch162.

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Chen, Harold. "Lesch-Nyhan Syndrome." In Atlas of Genetic Diagnosis and Counseling, 1–7. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6430-3_147-2.

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Pascual-Castroviejo, Ignacio, and Martino Ruggieri. "Lesch-Nyhan Syndrome." In Neurocutaneous Disorders Phakomatoses and Hamartoneoplastic Syndromes, 1017–22. Vienna: Springer Vienna, 2008. http://dx.doi.org/10.1007/978-3-211-69500-5_70.

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Little, Steven G., and Jennifer E. Rodemaker. "Lesch-Nyhan disease." In Health-related disorders in children and adolescents: A guidebook for understanding and educating., 386–91. Washington: American Psychological Association, 1998. http://dx.doi.org/10.1037/10300-054.

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Leung, Alexander K. C., William Lane M. Robson, Carsten Büning, Johann Ockenga, Janine Büttner, Hartmut Schmidt, Antonio V. Delgado-Escueta, et al. "Lesch-Nyhan Disease." In Encyclopedia of Molecular Mechanisms of Disease, 1156. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8924.

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Leung, Alexander K. C., William Lane M. Robson, Carsten Büning, Johann Ockenga, Janine Büttner, Hartmut Schmidt, Antonio V. Delgado-Escueta, et al. "Lesch-Nyhan Variant." In Encyclopedia of Molecular Mechanisms of Disease, 1156. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8925.

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Chen, Harold. "Lesch-Nyhan Syndrome." In Atlas of Genetic Diagnosis and Counseling, 1715–21. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-2401-1_147.

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Mateos, F. A., and J. G. Puig. "Prenatal Diagnosis of Lesch-Nyhan Syndrome." In Molecular Genetics, Biochemistry and Clinical Aspects of Inherited Disorders of Purine and Pyrimidine Metabolism, 27–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84962-6_4.

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Vagts, Dierk A., Heike Kaltofen, Uta Emmig, and Peter Biro. "Lesch-Nyhan-Syndrom/Kelly-Seegmiller-Syndrom." In Anästhesie bei seltenen Erkrankungen, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-44368-2_122-1.

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Conference papers on the topic "Nyhavn"

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Theranirajan, E., P. Sridevi, and K. Venkatesan Kannan. "G470 A rare case of lesch-nyhan syndrome." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference–Online, 25 September 2020–13 November 2020. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2020. http://dx.doi.org/10.1136/archdischild-2020-rcpch.403.

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Muñoz-Diosdado, A., L. Ramírez-Hernández, A. M. Aguilar-Molina, J. A. Zamora-Justo, R. A. Gutiérrez-Calleja, and C. D. Virgilio-González. "Multifractal analysis and the NYHA index." In XIII MEXICAN SYMPOSIUM ON MEDICAL PHYSICS. AIP Publishing LLC, 2014. http://dx.doi.org/10.1063/1.4901382.

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Seifar, Fatemeh, Diane Sutcliffe, and H. Jinnah. "Midbrain Dopamine Neurons Derived from Induced Pluripotent Stem Cells from Patients with Lesch Nyhan Disease and Gene-Edited Knock-In HPRT1 Mutations (P10-9.007)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000203414.

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Gallagher, Angela, Rebecca Lucas, and Martin Cowie. "39 Does NYHA class predict health-related quality of life?" In British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.39.

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Beyer, J., U. Schneider, K. Dawczynski, R. Biedermann, G. Färber, C. Schelenz, and E. Schleußner. "Maternale Herzinsuffizienz NYHA IV bei kritischer Aortenklappenstenose in der 24. SSW – ein Fallbericht." In 12. Jahrestagung der Mitteldeutschen Gesellschaft für Frauenheilkunde und Geburtshilfe e.V. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1645941.

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de Vries, Guus, Joop van der Meer, Harald Brennodden, and Stein Wendel. "Ormen Lange Gas Field, Immediate Settlement of Offshore Rock Supports." In ASME 2007 26th International Conference on Offshore Mechanics and Arctic Engineering. ASMEDC, 2007. http://dx.doi.org/10.1115/omae2007-29038.

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Located approximately 120 km offshore, Ormen Lange, with an estimated 400 billion m3 of natural gas, is the second-largest gas discovery on the Norwegian shelf. The water depth is up to 850 meters, making Ormen Lange the first deepwater project on the Norwegian Continental Shelf. The development of Ormen Lange is under shared operatorship between Norsk Hydro and Shell. Ormen Lange’s untreated well stream will be transported to shore in two 120 km long, 30-inch diameter pipelines to a processing plant at Nyhamna, Norway. From there, gas will be exported via a 42” 1200 km sub sea pipeline (Langeled) to Easington at the east coast of the UK. The pipelines have to pass over the Storegga slide edge which rises 200–300 meters toward the continental shelf in very steep slopes, which are also encountered in the nearshore Bjo¨rnsundet area. The uneven and steep seabed conditions require the use of approximately 2.8 million tons of rock to support and stabilize the pipelines. The sea bottom conditions on the Norwegian continental shelf are characterized by many outcrops as well as very soft clay deposits. The immediate settlement of the rock supports during installation form a significant amount of the total required rock volume. In this paper a procedure is presented on how to assess these immediate settlements recognizing four contributing components all being discussed separately. The calculation results are compared to a back-analysis, performed during the execution of the Ormen Lange rockworks, proving the suitability of the calculation method.
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Patel, Anjali, Reshma Rasheed, Imad Nazir, Ahmad Zarif, and Azad Mahmod. "131 Heart failure burden of mental health and frailty; correlation of efi, nyha with phq-9 and gad scores." In British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.131.

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Patel, Anjali, Reshma Rasheed, Imad Nazir, Ahmad Zarif, and Azad Mahmod. "131 Heart failure burden of mental health and frailty; correlation of efi, nyha with phq-9 and gad scores." In British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.131.

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S, Aggarwal, Lakshman Sai V, Pereira P, and Avarabeel S. "Uncovering the Unexpected: Rare Case of a Typical Presentation of Parathyroid Adenoma." In 4th International Conference on Gerontology and Geriatric Medicine. iConferences (Pvt) Ltd, 2024. http://dx.doi.org/10.32789/silverage.2023.1003.

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Abstract: The incidence of primary hyperparathyroidism in India is 2.5/1000 individuals. Primary hyperparathyroidism can be caused by a non-cancerous parathyroid adenoma, hyperplasia, or, rarely, parathyroid carcinoma. Most of these patients have few or no symptoms. A correct diagnosis can be reached through clinical settings, biochemical and radiological tests, and final confirmation by histopathology of the specimen. In our case, a 75-year-old male patient with an atypical presentation of hypercalcemia presented to the hospital with complaints of nausea since 1.5 months, loss of appetite and fatigue, loss of weight, decreased sleep, and breathlessness (Grade NYHA-2) since one month, for which further evaluation was done and led to the diagnosis of primary hyperthyroidism secondary to a parathyroid adenoma. This atypical presentation of hypercalcemia and the approach in which the diagnosis was made make this case truly unique in the elderly population. Keywords: Parathyroid adenoma, atypical presentation, elderly population
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Beyer, J., U. Schneider, K. Dawczynski, R. Biedermann, G. Färber, C. Schelenz, and E. Schleußner. "Fallbericht einer 35-jährigen III. Gravida, Patientin mit kardialer Dekompensation NYHA IV bei hochgradiger Aortenklappenstenose und iatrogener Frühgeburt 24/3 SSW." In 28. Deutscher Kongress für Perinatale Medizin. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1607827.

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