Gotowe bibliografie tematyczne / NNos

Gotowa bibliografia na temat „NNos”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 25 maja 2024

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Artykuły w czasopismach na temat "NNos"

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Rao, Y. Manjula, Arun Chaudhury i Raj K. Goyal. "Active and inactive pools of nNOS in the nerve terminals in mouse gut: implications for nitrergic neurotransmission". American Journal of Physiology-Gastrointestinal and Liver Physiology 294, nr 3 (marzec 2008): G627—G634. http://dx.doi.org/10.1152/ajpgi.00519.2007.

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Nitric oxide (NO) is responsible for nitrergic neurotransmission in the gut, and its release is dependent on its de novo synthesis by neuronal nitric oxide synthase (nNOS). The magnitude of NO synthesis and release during neurotransmission may be related to the fraction of catalytically active nNOS out of a larger pool of inactive nNOS in the nerve terminals. The purpose of the present study was to identify catalytically active and inactive pools of nNOS in the varicosities from mouse gut. Enteric varicosities were confirmed as nitrergic by colocalization of nNOS with the nerve varicosity marker synaptophysin. Low-temperature SDS-PAGE of these varicosity extracts showed 320-, 250-, and 155-kDa bands when blotted with anti-nNOS1422–1433 and 320- and 155-kDa bands when blotted with anti-nNOS1–20 antibodies, respectively. The 320- and 155-kDa bands represent dimers and monomers of nNOSα; the 250- and 135-kDa bands represent dimers and monomers of nNOSβ. Immunoprecipitation with calmodulin (CaM) showed that a portion of nNOSα dimer was bound with CaM. On the other hand, a portion of nNOSα dimer, nNOSβ dimer, and all monomers lacked CaM binding. The CaM-lacking nNOS fractions reacted with anti-serine 847-phospho-nNOS. In vitro assays of NO production revealed that only the CaM-bound dimeric nNOSα was catalytically active; all other forms were inactive. We suggest that the amount of catalytically active nNOSα dimers may be regulated by serine 847 phosphorylation and equilibrium between dimers and monomers of nNOSα.
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Saur, Dieter, Winfried L. Neuhuber, Bernd Gengenbach, Andrea Huber, Volker Schusdziarra i Hans-Dieter Allescher. "Site-specific gene expression of nNOS variants in distinct functional regions of rat gastrointestinal tract". American Journal of Physiology-Gastrointestinal and Liver Physiology 282, nr 2 (1.02.2002): G349—G358. http://dx.doi.org/10.1152/ajpgi.00226.2001.

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5′ mRNA variants of neuronal nitric oxide synthase (nNOS) are generated either by alternative promoter usage resulting in different mRNAs that encode for the same protein (nNOSα) or alternative splicing encoding NH2-terminally truncated proteins (nNOSβ/γ) that lack the PDZ/GLGF domain for protein-protein interaction of nNOSα. We studied the expression of 5′ nNOS mRNA forms and nNOS-interacting proteins (postsynaptic density protein-95; PSD-95) in the rat gastrointestinal tract and analyzed the more distinct localization of nNOS protein variants in the duodenum by immunohistochemistry with COOH- and NH2-terminal nNOS antibodies. 5′ nNOS mRNA variants showed a site-specific expression along the gastrointestinal tract with presence of all forms (nNOSα-a, -b, -c; nNOSβ) in the muscle layer of esophagus, stomach, duodenum, longitudinal muscle layer of jejunum/ileum, proximal colon, and rectum. In contrast, a lack of nNOSα-a and nNOSβ mRNA was observed in pylorus, circular muscle layer of jejunum/ileum, and cecum. Expression of nNOSα and nNOSβ cDNAs revealed proteins of ∼155 kDa and 135/125 kDa, respectively. Immunohistochemistry showed a differential distribution of COOH- and NH2-terminal nNOS immunoreactivity in distinct layers of rat duodenum, suggesting a cell-specific expression and distinct compartmentalization of nNOS proteins. Observed distribution of 5′ nNOS mRNA variants and proteins argue for a complex control of nNOS expression by usage of separate promoters, cell- and site-specific splicing mechanisms, and translational initiation. These mechanisms could be involved in gastrointestinal motor diseases and may explain the phenotype of nNOSα knockout mice with gastric stasis and pyloric stenosis, due to a total loss of nNOS in the pyloric sphincter region.
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Huber, Andrea, Dieter Saur, Manfred Kurjak, Volker Schusdziarra i Hans-Dieter Allescher. "Characterization and splice variants of neuronal nitric oxide synthase in rat small intestine". American Journal of Physiology-Gastrointestinal and Liver Physiology 275, nr 5 (1.11.1998): G1146—G1156. http://dx.doi.org/10.1152/ajpgi.1998.275.5.g1146.

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The aim of this study was to characterize neuronal nitric oxide synthase (nNOS) activity and 5′-end splice variants in rat small intestine. nNOS was predominantly expressed in the longitudinal muscle layer, with attached myenteric plexus (LM-MP). The biochemical properties of NOS activity in enriched nerve terminals resemble those of nNOS isolated from the brain. Western blot analysis of purified NOS protein with an nNOS antibody showed a single band in the particulate fraction and three bands in the soluble fraction. Rapid amplification of 5′ cDNA ends-PCR revealed the presence of three different 5′-end splice variants of nNOS. Two variants encode for nNOSα, which has a specific domain for membrane association. The third variant encodes for nNOSβ, which lacks the domain for membrane association and should therefore be soluble. nNOS is predominantly expressed in LM-MP and can be enriched in enteric nerve terminals. We present the first evidence that three 5′-end splice variants of nNOS encoding two different proteins are expressed in rat small intestine. These two nNOS enzymes exhibit different subcellular locations and might be implicated in different biological functions.
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Chaudhury, Arun, Y. Manjula Rao i Raj K. Goyal. "PIN/LC8 is associated with cytosolic but not membrane-bound nNOS in the nitrergic varicosities of mice gut: implications for nitrergic neurotransmission". American Journal of Physiology-Gastrointestinal and Liver Physiology 295, nr 3 (wrzesień 2008): G442—G451. http://dx.doi.org/10.1152/ajpgi.90280.2008.

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This investigation demonstrates the presence and binding of the protein LC8 (described as “protein inhibitor of nNOS” or PIN in some reports) to different components of neuronal nitric oxide synthase (nNOS) in nitrergic varicosities of mice gut. Whole varicosity extracts showed three (320-, 250-, and 155-kDa) nNOS bands with anti-nNOS1422–1433 antibody and a 10-kDa band with anti-LC8 antibody. The LC8 immunoprecipitate (IP) showed three nNOS bands, suggesting that LC8 was bound with all three forms of nNOS but dissociated from them during SDS-PAGE. Studies using LC8 IP and supernatant and probed with anti-CaM showed that LC8 was not associated with CaM-bound 320-kDa nNOS but was present in the CaM-lacking fraction. Probing these fractions with anti-serine847-P-nNOS showed that 320-kDa serine847-phosphorylated-nNOS consisted of LC8-bound and LC8-lacking components. Subsequent studies with varicosity membrane and cytosolic fractions separately showed that membrane contained CaM-bound and CaM-lacking, serine847-phosphorylated 320-kDa nNOS; both these fractions lacked LC8. On the other hand, the cytosolic fraction contained CaM-lacking, serine847-phosphorylated 320-kDa, 250-kDa, and 155-kDa nNOS bands that were all associated with LC8. These studies, along with in vitro nitric oxide assays, show that in gut nitrergic nerve varicosities 1) all cytosolic serine847-phosphorylated nNOS was catalytically inactive and bound with LC8, and 2) membrane-associated nNOS consisted of catalytically active, CaM-bound and catalytically inactive, CaM-lacking, serine847-phosphorylated nNOSα dimers, both of which lacked LC8. These results suggest that LC8 may dissociate from the 320-kDa nNOSα dimer upon binding to membrane, thus supporting the view that LC8 may transport nNOSα dimer to the varicosity membrane for participation in nitrergic neurotransmission.
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Smith, Cheryl A., Beth Santymire, Aaron Erdely, Vasuki Venkat, György Losonczy i Chris Baylis. "Renal nitric oxide production in rat pregnancy: role of constitutive nitric oxide synthases". American Journal of Physiology-Renal Physiology 299, nr 4 (październik 2010): F830—F836. http://dx.doi.org/10.1152/ajprenal.00300.2010.

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Functional studies show that increased renal nitric oxide (NO) mediates the renal vasodilation and increased glomerular filtration rate that occur during normal pregnancy. We investigated whether changes in the constitutive NO synthases (NOS), endothelial (eNOS) and neuronal (nNOS), were associated with the increased renal NO production in normal midterm pregnancy in the rat. In kidneys from midterm pregnant (MP: 11–13 days gestation), late-term pregnant (LP: 18–20 days gestation), and similarly aged virgin (V) rats, transcript and protein abundance for eNOS and the nNOSα and nNOSβ splice variants, as well as the rate of l-arginine-to-l-citrulline conversion, were determined as a measure of NOS activity. At MP, renal cortical abundance of the total eNOS protein and phosphorylated (Ser1177) eNOS was reduced, and l-arginine-to-l-citrulline conversion in the cortical membrane fraction was decreased; these declines were also seen in LP. There were no changes in the eNOS transcript. In contrast, l-arginine-to-l-citrulline conversion in the soluble fraction of renal cortex increased at MP and then declined at LP. This MP increase was ablated by S-methylthiocitrulline, a nNOS inhibitor. Using Western blotting, we did not detect a change in the protein abundance or transcript of the 160-kDa nNOSα, but protein abundance and transcript of the nNOSβ were increased at MP in cortex. Collectively, these studies suggest that the soluble nNOSβ is responsible for the increased renal cortical NO production during pregnancy.
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Tu, Angyan, Jun Ye i Bing Wang. "Neutrosophic Number Optimization Models and Their Application in the Practical Production Process". Journal of Mathematics 2021 (19.04.2021): 1–8. http://dx.doi.org/10.1155/2021/6668711.

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In order to simplify the complex calculation and solve the difficult solution problems of neutrosophic number optimization models (NNOMs) in the practical production process, this paper presents two methods to solve NNOMs, where Matlab built-in function “fmincon()” and neutrosophic number operations (NNOs) are used in indeterminate environments. Next, the two methods are applied to linear and nonlinear programming problems with neutrosophic number information to obtain the optimal solution of the maximum/minimum objective function under the constrained conditions of practical productions by neutrosophic number optimization programming (NNOP) examples. Finally, under indeterminate environments, the fit optimal solutions of the examples can also be achieved by using some specified indeterminate scales to fulfill some specified actual requirements. The NNOP methods can obtain the feasible and flexible optimal solutions and indicate the advantage of simple calculations in practical applications.
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Sampath, Chethan, Abhinav V. Raju, Michael L. Freeman, Shanthi Srinivasan i Pandu R. Gangula. "Nrf2 attenuates hyperglycemia-induced nNOS impairment in adult mouse primary enteric neuronal crest cells and normalizes stomach function". American Journal of Physiology-Gastrointestinal and Liver Physiology 322, nr 3 (1.03.2022): G368—G382. http://dx.doi.org/10.1152/ajpgi.00323.2021.

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Primary neuronal cell crust (pENCs) in the intestine habitats nNOS and Nrf2, which was suppressed in diabetic gastroparesis. Activation of Nrf2 restored nNOS by suppressing inflammatory markers in pENCs cells. Inhibition of Nrf2 reveals a negative feedback mechanism for the activation of GSK-3. Activation of Nrf2 alleviates STZ-induced delayed gastric emptying and nitrergic relaxation in female mice. Activation of Nrf2 restored impaired gastric BH4 biosynthesis enzyme GCH-1, nNOSα expression thus regulating nitric oxide levels.
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Ihara, Hideshi, Atsushi Kitamura, Shingo Kasamatsu, Tomoaki Ida, Yuki Kakihana, Hiroyasu Tsutsuki, Tomohiro Sawa, Yasuo Watanabe i Takaaki Akaike. "Superoxide generation from nNOS splice variants and its potential involvement in redox signal regulation". Biochemical Journal 474, nr 7 (15.03.2017): 1149–62. http://dx.doi.org/10.1042/bcj20160999.

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We previously demonstrated different spacial expression profiles of the neuronal nitric oxide (NO) synthase (nNOS) splice variants nNOS-µ and nNOS-α in the brain; however, their exact functions are not fully understood. Here, we used electron paramagnetic resonance to compare the electron-uncoupling reactions of recombinant nNOS-µ and nNOS-α that generate reactive oxygen species (ROS), in this case superoxide. nNOS-µ generated 44% of the amount of superoxide that nNOS-α generated. We also evaluated the ROS production in HEK293 cells stably expressing nNOS-α and nNOS-µ by investigating these electron-uncoupling reactions as induced by calcium ionophore A23187. A23187 treatment induced greater ROS production in HEK293 cells expressing nNOS-α than those expressing nNOS-µ. Also, immunocytochemical analysis revealed that A23187-treated cells expressing nNOS-α produced more 8-nitroguanosine 3′,5′-cyclic monophosphate, a second messenger in NO/ROS redox signaling, than did the cells expressing nNOS-µ. Molecular evolutionary analysis revealed that the ratio of nonsynonymous sites to synonymous sites for the nNOS-µ-specific region was higher than that for the complete gene, indicating that this region has fewer functional constraints than does the complete gene. These observations shed light on the physiological relevance of the nNOS-µ variant and may improve understanding of nNOS-dependent NO/ROS redox signaling and its pathophysiological consequences in neuronal systems.
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Zhao, Tianxue, Qian Li, Qianyun Mao, Kaida Mu i Chen Wang. "Hepatic nNOS impaired hepatic insulin sensitivity through the activation of p38 MAPK". Journal of Endocrinology 248, nr 3 (marzec 2021): 265–75. http://dx.doi.org/10.1530/joe-20-0322.

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Neuronal nitric oxide synthase (nNOS) interacts with its adaptor protein NOS1AP through its PZD domain in the neurons. Previously, we had reported that NOS1AP enhanced hepatic insulin sensitivity through its PZD-binding domain, which suggested that nNOS might mediate the effect of NOS1AP. This study aimed to examine the role and underlying mechanisms of nNOS in regulating hepatic insulin sensitivity. nNOS co-localized with NOS1AP in mouse liver. The overexpression of NOS1AP in mouse liver decreased the level of phosphorylated nNOS (p-nNOS (Ser1417)), the active form of nNOS. Conversely, the liver-specific deletion of NOS1AP increased the level of p-nNOS (Ser1417). The overexpression of nNOS in the liver of high-fat diet-induced obese mice exacerbated glucose intolerance, enhanced intrahepatic lipid accumulation, decreased glycogen storage, and blunted insulin-induced phosphorylation of IRbeta and Akt in the liver. Similarly, nNOS overexpression increased triglyceride production, decreased glucose utilization, and downregulated insulin-induced expression of p-IRbeta, p-Akt, and p-GSK3beta in the HepG2 cells. In contrast, treatment with Nω-propyl-L-arginine (L-NPA), a selective nNOS inhibitor, improved glucose tolerance and upregulated insulin-induced phosphorylation of IRbeta and Akt in the liver of ob/ob mice. Furthermore, overexpression of nNOS increased p38MAPK phosphorylation in the HepG2 cells. In contrast, inhibition of p38MAPK with SB203580 significantly reversed the nNOS-induced inhibition of insulin-signaling activity (all P < 0.05). This indicated that hepatic nNOS inhibited the insulin-signaling pathway through the activation of p38MAPK. These findings suggest that nNOS is involved in the development of hepatic insulin resistance and that nNOS might be a potential therapeutic target for diabetes.
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Choate, J. K., E. J. F. Danson, J. F. Morris i D. J. Paterson. "Peripheral vagal control of heart rate is impaired in neuronal NOS knockout mice". American Journal of Physiology-Heart and Circulatory Physiology 281, nr 6 (1.12.2001): H2310—H2317. http://dx.doi.org/10.1152/ajpheart.2001.281.6.h2310.

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The role of nitric oxide (NO) in the vagal control of heart rate (HR) is controversial. We investigated the cholinergic regulation of HR in isolated atrial preparations with an intact right vagus nerve from wild-type (nNOS+/+, n = 81) and neuronal NO synthase (nNOS) knockout (nNOS−/−, n = 43) mice. nNOS was immunofluorescently colocalized within choline-acetyltransferase-positive neurons in nNOS+/+ atria. The rate of decline in HR during vagal nerve stimulation (VNS, 3 and 5 Hz) was slower in nNOS−/− compared with nNOS+/+ atria in vitro ( P < 0.01). There was no difference between the HR responses to carbamylcholine in nNOS+/+ and nNOS−/− atria. Selective nNOS inhibitors, vinyl-l-niohydrochloride or 1–2-trifluoromethylphenyl imidazole, or the guanylyl cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one significantly ( P < 0.05) attenuated the decrease in HR with VNS at 3 Hz in nNOS+/+ atria. NOS inhibition had no effect in nNOS−/− atria during VNS. In all atria, the NO donor sodium nitroprusside significantly enhanced the magnitude of the vagal-induced bradycardia, showing the downstream intracellular pathways activated by NO were intact. These results suggest that neuronal NO facilitates vagally induced bradycardia via a presynaptic modulation of neurotransmission.
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Rozprawy doktorskie na temat "NNos"

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Simmers, Jessica L. "nNos localization, muscle function and atrophy in skeletal muscle disorders". Thesis, The Johns Hopkins University, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=3573097.

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In skeletal muscle, loss of neuronal nitric oxide synthase (nNOS) from the sarcolemma has been observed in a few muscular dystrophies and myopathies. However, the extent of this phenomenon, its mechanism, and its physiological impact are not well understood. Using immunofluorescent staining for nNOS, a survey of 161 patient biopsies found absent or reduced sarcolemmal nNOS in 43% of patients. Patient mobility and muscle functional status correlated with nNOS mislocalization from the sarcolemma. Mouse models of inherited and acquired myopathies showed similar loss of sarcolemmal nNOS and impaired mobility and muscle function. A proteomic approach, using mass spectrometry and differentially labeled control and steroid-induced myopathy (SIM) mouse samples, found novel nNOS binding proteins including alpha-actinin-3 (ACTN3), which exhibited decreased interaction with nNOS after steroid treatment. It revealed a potential explanation for impaired muscle function in SIM as nNOS interactions were lost at the sarcomere and gained at the sarcoplasmic reticulum impairing contractility. Treating nNOS-deficient mice with steroids demonstrated that loss of sarcolemmal nNOS reduces muscle contractility and strength in SIM through increased nitric oxide (NO) signaling. In SIM mice treated with a nitric oxide donor and steroids, nitric oxide partially protects the muscle from atrophy and improves muscle fatigability and recovery suggesting nNOS mislocalization also decreases NO availability. These findings show that loss of sarcolemmal nNOS is a common phenomenon that negatively impacts muscle function. Therapeutic strategies targeting nNOS or NO signaling need to allow for the complexity of local nitric oxide content and cellular context.

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BALDELLI, SARA. "Ruolo dell'ossido nitrico sintasi neuronale (nNOS) nella modulazione dell'omeostasi redox intracellulare". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/861.

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L' ossido nitrico (NO) è una molecola in grado di svolgere funzioni diverse e contrapposte in dipendenza della sua concentrazione e del sito di produzione: ad alte concentrazioni (? ­M-mM) può provocare effetti tossici, mentre a basse concentrazioni (nM) può funzionare da secondo messaggero e da antiossidante. Per chiarire i meccanismi attraverso i quali l' NO esplica la sua funzione di antiossidante e di mantenimento dell' omeostasi cellulare, abbiamo esaminato gli effetti del trattamento con derivati organosolfurici dellâ aglio (DADS e GE), in grado di incrementare i livelli intracellulari di ROS in cellule di neuroblastoma umano SH-SY5Y, che esprimono costitutivamente la nNOS. I seguenti studi ci hanno dimostrato che i derivati organosolfurici dell' aglio potrebbero modulare il contenuto di nNOS e suggeriscono come l' NO potrebbe svolgere un importante ruolo nel bloccare la citotossicità indotta dai ROS. Accanto all' azione antiossidante dell'NO, ogni cellula presenta un sistema di difesa antiossidante indispensabile nel bloccare lo stress ossidativo/nitrosativo. In particolare, il sistema nervoso rappresenta una regione dell' organismo altamente aerobia e i livelli della sua difesa antiossidante sono relativamente bassi, si ipotizza, quindi, che la nNOS con il suo prodotto NO e gli antiossidanti intracellulari, interagiscano allo scopo di mantenere l'equilibrio della cellula nervosa. La SOD1 e il GSH rappresentano due degli antiossidanti che potrebbero interagire in modo diretto o indiretto con la nNOS o con l' NO, a livello del sistema nervoso. I seguenti studi propongono come un flusso endogeno di NO, dovuto a sovraespressione dell' enzima nNOS, possa influenzare l' omeostasi cellulare e l' espressione di un antiossidante intracellulare, il GSH. Infine, abbiamo mostrato come la nNOS, attraverso un meccanismo NO-indipendente, sembra regolare negativamente la trascrizione del gene che codifica per la SOD1, interagendo direttamente con il fattore di trascrizione Sp1 impedendo il suo legame al promotore del gene sod1 e down-regolando, così, il suo contenuto in mRNA, l' attività e il contenuto proteico.
Nitric oxide (NO) plays an important role in both physiological and pathophysiological mechanisms involving properties at the chemical, cellular, and physiological levels. The relatively low concentration of NO required being an antioxidant suggests that in addition to its involvement with cyclic GMP, this radical molecule serves to counterbalance oxidative stress. This balance between NO and oxidative stress provides an important regulatory mechanism in numerous physiological effects. Imbalance in this redox symbiotic relationship can lead to different pathophysiological conditions. Here we demonstrate the neuroprotective role played by nNOS/NO in counteracting the ROS-mediate ciotoxicity, induced by treatment with garlic derivatives. In particular, we found that, besides their role in promoting growth arrest and apoptosis, either oil-soluble derivatives DADS or water GE significantly increased the content of nNOS in neuronal cell lines. Next to the antioxidant action of NO, each cell is equipped with an extensive antioxidant system to counteract their harmful properties directly by interception or indirectly through reversal of oxidative damage. In central nervous system, the antioxidant defence system and nNOS may interact to ensure the integrity and homeostasis of neuronal cells. Especially in the nervous system the nNOS/NO may directly or indirectly modulate the activity and expression of antioxidant defence systems. Indeed, we further analysed the influence of endogenous overproduction on NO on the intracellular antioxidants SOD1 and GSH in cell lines of neuronal and non-neuronal origin. We report that nNOS over-expression induced a NO-dependent increase in the concentration of GSH thus reinforcing the idea that it represents a protective agent against NO cytotoxicity. On the other hand, the nNOS over-expression causes a NO-indipendent down-regulation of SOD1 in terms of mRNA, protein and activity levels.
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SAGRATI, ANDREA. "Neuronal nitric oxide synthase positive cells in the human corpus callosum and indusium griseum". Doctoral thesis, Università Politecnica delle Marche, 2021. http://hdl.handle.net/11566/291083.

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L’obbiettivo del nostro studio è stato quello di comprendere il meccanismo che controlla la regolazione del flusso sanguigno cerebrale nel corpo calloso (CC) umano con il fine di spiegare l’effetto BOLD, precedentemente scoperto da Fabri e collaboratori nel 2011. Le analisi per determinare la presenza, il numero, la distribuzione e la morfologia delle cellule immunopositive all’enzima ossido nitrico sintetasi neuronale (nNOS) sono eseguite sul corpo calloso e sul’indusium griseum (IG). L’Ossido nitrico (NO) è un neurotrasmettitore gassoso largamente diffuso nel cervello umano ed ha, tra le altre funzioni, un potente effetto vasodilatante e perciò contribuisce a regolare il flusso sanguigno cerebrale. Sezioni seriali sagittali ottenute da blocchetti in paraffina e da taglio del tessuto in congelato sono state utilizzate per l’analisi immunoistochimica sul CC e sul IG. L’intensa marcatura che si è ottenuta ha dimostrato la presenza di cellule immunopositive al nNOS, e grazie alla microscopia a fluorescenza ne è stata confermata la loro natura neuronale e astrocitaria. Cellule neuronali immunopositive all’nNOS sono state osservate sia nel CC che nell’IG mentre gli astrociti che lo esprimono erano solo presenti nel CC. I neuroni nNOS positivi hanno mostrato diverse morfologie e risultavano essere piu abbondanti a 1mm a partire dalla linea mediana, per l’IG e a 4mm per il CC con un picco di massima abbondanza nel corpo del CC. In alcuni casi questi nueroni erano localizzati principalmente nell’interfaccia tra IG e CC e piu specificatamente in prossimita delle arterie piali, arteriole che originano dall’arteria sopracallosale che poi si affosano nel corpo calloso. La presenza di neuroni nNOS positivi in prossimità di vasi sanguigni, in questi due tessuti suggeriscono un loro plausibile ruolo nella regolazione neurovascolare del CC che potrebbero quindi ipoteticamente spiegare l’effetto BOLD osservato in risonanza. l’IG inoltre potrebbe giocare un ruolo attivo nel controllo della vascolarizzazione del CC, ed è quindi probabile e che non sia solo un tessuto di rimanenza embrionale come precedentemente si riteneva ma un tessuto con un sua funzione specifica. Infine è stata osservata per la prima volta la presenza di astrociti nNOS positivi nel corpo calloso umano. Queste cellule variavano nella presenza, nel numero e nelle loro distribuzione in base a diverse condizioni di ossigenazione sistemica che avvenivano nel momento del decesso. Infatti nei soggetti deceduti dopo una breve ipossia gli astrociti nNOS positivi erano assenti, mentre risultavano essere molto abbondanti nei soggetti deceduti con un ipossia prolungata. L’immunopositività degli astrociti sembrerebbe quindi essere correlata alla durata dell’ipossia cerebrale al momento della morte.
The aim of the present study is to investigate the possible mechanism for the control of cerebral blood flow in the corpus callosum (CC), that could explain the BOLD effect previously found (Fabri et al., 2011). The presence, number, distribution and morphology of neuronal Nitric Oxyde Sinthase (nNOS) positive cells was investigated in the corpus callosum (CC) and indusium griseum (IG). Nitric Oxyde (NO) is a gaseous neurotransmitter largely diffused in the brain, whichexerts a powerful vasodilatory effect, and therefore it can contribute to regulate the cerebral blood flow. Sagittal serial sections from paraffin or frozen autoptic specimens of human adult CC and overlying IG were processed for immunohistochemistry and immunofluorescence analysis, using an antibody against the neuronal form of the enzyme Nitric Oxyde Synthase (nNOS). The stainings revealed the presence of many nNOS immunopositive cells. By double labeling technique with immunofluorescence at confocal microscopy, it has been shown that in the CC both neurons and astrocytes positive to nNOS antibody were present, and their number varied in different conditions, as detailed below. In the IG, only neurons nNOS positive were found. Neurons showed different morphologies, were more numerous 1 mm apart from the medial line in IG and 4 mm in CC, with a peak over the body of the CC. In some cases, they were located at the boundary between IG and CC, more densely packed in proximity to the pial arteries penetrating into the CC. The significant presence of nNOS immunopositive neurons in these two structures suggests that they might have a role in the neurovascular regulation of CC, moreover the IG could plays a functional role in the adult brain. The presence of nNOS positive astrocytes in the human CC has been here demostrated for the first time. As previously mentioned, their number and distribution varied in different conditions: nNOS positive astrocytes were absent in samples from subjects deceased after a short hypoxia; their number and labeling intensity increased with the hypoxia prolongation. Neuronal NOS immunopositivity of CC astrocytes seems thus related to the hypoxia duration and the consequent brain damage.
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Cheung, Nathan Yiutung. "Serotonin receptor and neuronal nitric oxide synthase expression in the rat brain : implications for MDMA toxicity". Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368095.

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Jähne, Sebastian [Verfasser]. "Kompensationsmechanismen im Skelettmuskel von neuronaler Stickstoffmonoxid-Synthase (nNOS) defizienten Mäusen / Sebastian Jähne". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2010. http://d-nb.info/1027814905/34.

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Lim, Gregory B. S. "nNOS-derived nitric oxide modulation of the ryanodine receptor calcium release channel". Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.533867.

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McNamara, Tanner. "ENOS and nNOS contribution to reflex cutaneous vasodilation during dynamic exercise in humans". Thesis, Kansas State University, 2012. http://hdl.handle.net/2097/13788.

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Master of Science
Department of Kinesiology
B.J. Wong
Recent data suggests nNOS mediates the NO-component of reflex cutaneous vasodilation with passive heat stress. Our hypothesis was nNOS, but not eNOS, inhibition would attenuate reflex cutaneous vasodilation during dynamic exercise. Protocol 1: subjects performed a VO[subscript]2 peak test on a supine cycle ergometer. Protocol 2: with experimental arm at heart level subjects cycled in supine posture at 60% VO[subscript]2 peak to raise core temperature (Tc) 0.8-1.0°C (35-45 min). In protocol 2 subjects were equipped with 4 microdialysis fibers on the forearm and each randomly assigned as: 1) lactated Ringer’s (control); 2) 5mM NPLA (nNOS inhibition); 3) 10mM L-NIO (eNOS inhibition); and 4) 20mM L-NAME (non- selective NOS inhibition). At the end of protocol 2 all sites were locally heated to 43°C and infused with SNP to elicit maximal dilation. Mean arterial pressure (MAP), skin blood flow via laser- Doppler flowmetry (LDF), and Tc via ingestible telemetric pill were measured; cutaneous vascular conductance (CVC) was calculated as LDF/MAP and normalized to maximum. In protocol 2 there was no significant difference between control (62±5 %CVCmax) and NPLA (61±6 %CVCmax). L-NIO (38±4 %CVCmax) and L-NAME (41±7 %CVCmax) significantly attenuated CVC compared to control and NPLA (p<0.001 all conditions). There was no difference between L-NIO and L- NAME. We conclude eNOS, not nNOS, contributes to reflex cutaneous vasodilation during dynamic exercise.
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Sangüesa, Ferrer Juan F. "Modulation fonctionnelle et distribution du canal calcique Cav3. 2 : rôle de la nNOS". Montpellier 1, 2008. http://www.theses.fr/2008MON1T015.

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Le canal calcique Cav3. 2 joue un rôle capital dans de nombreux processus physiologiques, notamment dans la transmission de la douleur aigüe et chronique. Cependant, les mécanismes régulant la distribution et les propriétés de ces canaux restent encore mal connus. Au cours de ma thèse, j'ai participé au développement d'un nouveau modèle pour étudier ces mécanismes : la souris knock-in Cav3. 2-GFPécliptique. Cette souris permettra d'étudier la localisation et la dynamique de Cav3. 2 in vivo grâce à une étiquette fluorescente insérée dans la partie extracellulaire du canal. Des sites de recombinaison loxP ont été également introduits dans le génome de cette souris afin d'effectuer des invalidations tissu-spécifiques et/ou inductibles du canal. En parallèle, une approche protéomique m'a permis d'identifier un nouveau partenaire de Cav3. 2 : la nNOS, une enzyme responsable de la production d'oxyde nitrique (NO). En effet, nous avons montré que Cav3. 2 possède un motif très conservé dans sa région C-terminale qui lui permet d'interagir avec le domaine de PDZ de la nNOS. Cette interaction a des conséquences fonctionnelles pour les deux protéines. D'une part, la présence de la nNOS induit une diminution de la densité des courants générés par le canal Cav3. 2, grâce à un mécanisme qui nécessite l'activité de l'enzyme et la présence d'un centre coordinateur d'ions métalliques dans la partie extracellulaire du canal. D'autre part, nous avons montré que Cav3. 2 est capable de modifier la distribution subcellulaire de la nNOS. L'enzyme est emmenée par le canal à proximité de la membrane plasmique où elle est plus facilement activée par l'entrée de calcium. Cette association fonctionnelle Cav3. 2-nNOS pourrait être impliquée dans des processus comme la nociception, la mémoire et la régulation du tonus vasculaire.
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Sato, Vinicius Antonio Hiroaki. "Participação da serotonina no efeito tipo-antidepressivo induzido pela inibição da nNOS no hipocampo de ratos". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-22062011-090727/.

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Introdução: O óxido nítrico (NO) tem sido relacionado como um importante neuromodulador envolvido com a neurobiologia da adaptação ao estresse e da depressão. De fato, a administração sistêmica ou intra-hipocampal de inibidores da NO sintase neuronial (nNOS) induz efeitos do tipo antidepressivo em modelos animais. Evidências recentes indicam que os efeitos sistêmicos dos inibidores da nNOS são dependentes dos níveis de serotonina no encéfalo. O sistema serotoninérgico do hipocampo dorsal, por ativação dos receptores serotoninérgicos do tipo 1A (5HT1A), facilita a adaptação ao estresse e contribui para os efeitos comportamentais de drogas antidepressivas. Portanto, o objetivo do presente estudo foi testar a hipótese de que o efeito do tipo antidepressivo induzido pela administração hipocampal de inibidores da nNOS seria mediado pela facilitação da neurotransmissão serotoninérgica local e subseqüente ativação de 5HT1A. Métodos: Após cirurgia estereotáxica, ratos Wistar com cânulas-guia direcionadas ao hipocampo dorsal foram submetidos a sessão de pré-teste (PT 15 minutos de nado) e receberam administrações locais das drogas: N-propil-L-arginina (NPA, inibidor seletivo da nNOS: 0,00001 - 1 nmol/0,5 µL), fluoxetina (SSRI: 1, 3 e 10 nmol/0,5 µL), WAY100635 (antagonista seletivo para 5HT1A: 1, 3 e 10 nmol/0,5 µL) ou veículo (0,5 µL). 24h depois, o tempo de imobilidade foi registrado em uma sessão de 5 minutos de nado. Todos os protocolos foram aprovados por um comitê de ética local (Proc. No 08.1.1133.53.4) Resultados: A administração intra hipocampal de NPA ou fluoxetina reduziu significativamente o tempo de imobilidade em animais submetidos ao teste do nado forçado, um efeito tipo antidepressivo. A administração de WAY100635 não induziu efeito por si, mas foi capaz de bloquear os efeitos induzidos por fluoxetina ou NPA. Conclusões: A inibição da nNOS, pelo NPA, ou a inibição da recaptação de serotonina, pela fluoxetina, no DH induziu efeito do tipo antidepressivo de similar magnitude. O fato de que o pré-tratamento com WAY100635 foi capaz de bloquear os efeitos induzidos por NPA e fluoxetina indica que ambos os efeitos são mediados por facilitação da neurotransmissão serotoninérgica local e subseqüente ativação de 5HT1A. Assim, esses resultados sugerem que níveis aumentados de NO no DH poderiam levar a um déficit na neurotransmissão serotoninérgica local e, portanto, predispor ao desenvolvimento das conseqüências comportamentais do estresse.
Introduction: Nitric oxide (NO) has been suggested to play an important role in the neurobiology of stress adaptation and depression. In fact, systemic or hippocampal administration of neuronal NO synthase (nNOS) inhibitors induces antidepressant-like effects in animal models. Recent evidence indicates that the systemic effects of nNOS inhibitors are dependent on serotonin levels in the brain. The serotonergic system of the dorsal hippocampus (DH), through the activation of serotonin 1A (5-HT1A) receptors, is proposed to mediate stress adaptation and the behavioral effects of antidepressant drugs. Therefore, the aim of the present study was to test the hypothesis that the antidepressant-like effects induced by nNOS inhibition into the hippocampus would be mediated by a facilitation of the local serotonergic neurotransmission and subsequent 5-HT1A receptor activation. Methods: Male Wistar rats with guide-cannulae aimed at the DH were submitted to the pretest session (PT - 15 minutes of swimming) and received local administrations of the drugs: n-propyl-L-arginine (NPA, selective nNOS inhibitor: 0.00001 - 1 nmol/0.5 µL), fluoxetine (SSRI: 1, 3 and 10 nmol/0.5 µL), WAY100635 (selective 5-HT1A antagonist: 1, 3 and 10 nmol/0.5 µL) or vehicle (0.5 µL). One day later, the immobility time was registered at a 5 minutes swimming test session. All protocols were approved by a local ethical committee (Proc. N. 08.1.1133.53.4.) Results: The intrahippocampal administration of NPA or fluoxetine reduced the immobility time in animals submitted to the forced swimming test, an antidepressant-like effect in this model. WAY100635 did not induce any effect per se, but it was able to block the effects induced by fluoxetine or NPA. Conclusions: Inhibition of nNOS, by NPA, or inhibition of serotonin reuptake, by fluoxetine, in the DH induced antidepressant-like effects of similar magnitude. The fact that pretreatment with WAY100635 was able to block NPA- and fluoxetine-induced effects indicates that both effects are mediated by a facilitation of the local serotonergic neurotransmission and subsequent activation of 5-HT1A receptors. Therefore, these results suggest that increased NO levels in the DH could impair local serotonergic neurotransmission and, thus, predisposes to the development of stress-induced behavioral consequences, such as depressive-like behaviors.
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Sato, Vinicius Antonio Hiroaki. "Substratos neurais envolvidos com o desenvolvimento do comportamento de desamparo em ratos: possível envolvimento do NO". Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-20072016-091556/.

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Recentemente, o óxido nítrico (NO) tem sido relacionado com a depressão. A administração de inibidores da NO sintase (NOS) induz efeitos do tipo antidepressivo em modelos animais e há um aumento da expressão da NOS em estruturas do sistema límbico em indivíduos depressivos e em animais expostos a estresse. Além disso, sabe-se que o estresse causa um aumento da ativação de neurônios localizados em estruturas do sistema límbico e que o tratamento com antidepressivos bem como com inibidor da NOS, diminui essa marcação. Contudo, ainda não se sabe como o sistema nitrérgico dessas estruturas está relacionado com os comportamentos relacionados à depressão. Assim nosso objetivo é testar a hipótese de que o desenvolvimento do desamparo (comportamento relacionado à depressão) em ratos seria causado por um aumento de atividade de neurônios que contém nNOS em estruturas envolvidas com a resposta emocional ao estresse, e que os diferentes tratamentos induzem efeitos do tipo antidepressivo no modelo apresentando através de um efeito final comum de diminuir essa ativação e, portanto, diminuir os níveis de NO. Para isso, ratos foram submetidos ao modelo do desamparo aprendido e tratados com drogas antidepressivas. Após o teste, foi feita a imunohistoquímica com marcação para Fos (Fos-IR; marcador de atividade neuronal) e nNOS (nNOS-IR). O tratamento repetido com desipramina (DES, na dose de 25, mas não na de 12,5 mg/Kg), fluoxetina (FXT, na dose de 15, mas não na de 30 mg/Kg) e imipramina (IMI, 15mg/Kg) induziu efeito do tipo-antidepressivo no teste do desamparo aprendido (LH). O tratamento agudo apenas com imipramina, mas não com FXT ou IMI, induziu o mesmo tipo de efeito. O tratamento com DES, FXT ou IMI também aumentou o número de cruzamentos entre choques no LH, porém não induziu aumento de atividade locomotora no teste do campo aberto. O tratamento repetido com DES diminuiu a Fos-IR na amígdala basolateral (BlAm), amígdala lateral (LAm), córtex pré-frontal medial (mPFC), região CA1 e CA3 do hipocampo dorsal (dHPC) e região CA3 do hipocampo ventral (vHPC). O tratamento agudo com DES induziu um aumento de Fos-IR na amígdala central (CeAm), amígdala medial (MeAm) e CA1 e CA3 do dHPC. O tratamento repetido com FXT diminuiu Fos-IR na BlAm e LAm, enquanto o tratamento agudo aumentou Fos-IR na CeAm. O tratamento repetido com IMI aumentou nNOS-IR na MeAm e a dupla marcação no núcleo leito da estria terminal (BST); e diminuiu o Fos-IR na região CA1 do dHPC e na região parvocelular do núcleo paraventricular do hipotálamo (pPVN). Por fim, foram encontradas relações positivas entre o número de células Fos-IR e o número de falhas em fugir ou escapar dos choques no LH na BlAm, LAm, CA1 e CA3 do dHPC e CA3 do vHPC; i.e., quanto mais células ativadas nessas estruturas, maior o número de choques que os animais receberam sem consegui fugir. Os resultados aqui apresentados são, em parte, corroborados pela literatura, mostrando a participação das estruturas analisadas no comportamento do desamparo aprendido e no efeito das drogas antidepressivas. Nesse contexto, acredita-se que o BST funcionaria como um núcleo de processamento da informação vinda do mPFC, HPC e amígdala, enviando projeções para o PVN e regulando o funcionamento do eixo HPA. O trabalho abre caminho para a identificação de subpopulações específicas de neurônios que expressam a nNOS, buscando compreender o papel destas na modulação das respostas comportamentais numa situação de estresse, na busca pela formulação de um cenário cada vez mais completo da participação do sistema nitrérgico dentro do complexo neurocircuito que regula as emoções
Recently, nitric oxide (NO) has been related with the neurobiology of depression. The NO synthase (NOS) inhibition induces antidepressant-like effects in animal models and there is an increase in the NOS expression in limbic structures of depressed patients or in stress exposed animals. Besides, it is well known that stressful events causes an increase in limbic structures neuronal activation and that antidepressant treatment as well as NOS inhibition attenuates this effect. However, it is still unknown how the limbic nitrergic system is related with depression-related behaviors. Then, the aim of this work is to test the hypothesis that the helplessness behavior development (a depression-related behavior) in rats would be induced by an increased activity of nNOS-containing neurons in structures related with the neurobiology of stress responses. Furthermore, the antidepressant-like effect induced by antidepressants treatment in this model would share a final effect, decreasing the activation of such neurons, and decreasing the levels of NO in these structures. For this aim, male rats were submitted to the learned helplessness model and treated with antidepressants. After the test, immunohistochemistry assay were performed, with double labeling for c-Fos (Fos-IR; neuronal activity marker) and nNOS (nNOS-IR). The repeated treatment with desipramine (DES, 25 mg/kg but not 12,5mg/kg), fluoxetine (FXT, 15 mg/Kg, but not 30 mg/Kg) and imipramina (IMI, 15 mg/KG) induced antidepressant-like effects in the learned helplessness test (LH). The acute treatment with IMI, but not with DES or FXT, induced the same effect. The repeated treatment with DES, FXT or IMI also increased the number of intertrial crossings in the LH, but not the locomotor activity score on the open field score. The repeated treatment with DES decreased the number of Fos-IR into the basolateral amygdala (BlAm), lateral amygdala (Lam), medial prefrontal cortex (mPFC), CA1 and CA3 regions of the dorsal hippocampus (dHPC), and CA3 region of the ventral hippocampus (vHPC). The acute treatment with DES increased the Fos-IR into the central amygdale (CeAm), medial amygdala (MeAm), and CA1 and CA3 regions of the dHPC. The repeated treatment with FXT decreases the number of Fos-IR into the BlAm and Lam, while the acute treatment increases the Fos-IR into the CeAm. The repeated treatment with IMI increased the nNOS-IR into the MeAm and the double- labeled cells into the bed nucleus of stria terminalis (BST); and decreased the Fos-IR into the CA1 region of the dHPC and into the parvocellular region of the paraventricular nucleus of the hypothalamus. Finally, positive correlations between the number of Fos-IR and the number of failures in escaping or avoiding the foot shocks on the LH were found into the BlAm, Lam, CA1 and CA3 of the dHPC, and CA3 of the vHPC, i.e., with more activated cells into these structures mentioned, more foot shocks the rats received. These results are (partially) corroborated with previous scientific papers, showing the analyzed structures participation in the learned helplessness behavior as well as in the antidepressant effect of antidepressant administration. Within this context, the BST would work as a relay center, processing the information coming from the mPFC, HPC and amygdaloid nuclei, and sending the output to the PVN, modulating the HPA axis. This work open some questions about the identification of specific nNOS-containing neuronal subpopulations, aiming to clarify their role in the stress response, and searching for the formulation of a more complete scenario of the nitrergic system participation in this complex emotion-regulating neurocircuit
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Książki na temat "NNos"

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Nguynen, Khoac Mnan. Nnoi lòng. [S.l: s.n., 1987.

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Centers for Disease Control (U.S.), red. NNIS manual: NNIS, National Nosocomial Infections Surveillance System. Atlanta, Ga: U.S. Dept. of Health and Human Services, Public Health Service, Centers for Disease Control, 1988.

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Buck, Pearl S. Nnoi đau thre kky. [Hà Nuoi]: NXB Văn học, 1996.

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Đno, Văn Trọn. Nnoi nisem mang theo. San Jose, CA (675 N. 1st St., Suite 611, San Jose 95112): Tusan báo Yêu, 1988.

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Du nnes Eis: Novelle. Berlin: Contumax-Verl., 2009.

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Anh, Hoàng Xuyên. Nnoi lòng cô phụ. San Jose, CA: NXB Chki Thkao, 1995.

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Đno, Thị Khôi Nguyên. Tuan cùng nnoi nhwo. [United States: s.n., 1989.

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Phương, Viuet. Trôi trong nnoi nhwo. Toronto, Ont: Làng Văn, 2000.

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Nguynen, Tran Hưng. Muot nnoi buson riêng: Tuap truyuen. Glendale, CA: Đại Nam, 1992.

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Ninh, Bkao. Nnoi buson chiren tranh: Truyuen dài. [Westminster, CA]: Hông Lĩnh, 1992.

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Części książek na temat "NNos"

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Tiro, Jasmin, Simon J. Craddock Lee, Steven E. Lipshultz, Tracie L. Miller, James D. Wilkinson, Miriam A. Mestre, Barbara Resnick i in. "Neuronal Nitric Oxide Synthase (nNOS)". W Encyclopedia of Behavioral Medicine, 1326. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_101144.

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Huang, P. L. "eNOS and nNOS in Stroke". W Handbook of Neurochemistry and Molecular Neurobiology, 47–63. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-30383-3_4.

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Saini, Rashmi, Zaffar Azam, Leena Sapra i Rupesh K. Srivastava. "Neuronal Nitric Oxide Synthase (nNOS) in Neutrophils: An Insight". W Reviews of Physiology, Biochemistry and Pharmacology, 49–83. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/112_2021_61.

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Xue, J. H., H. Yanamoto, I. Nagata, Z. W. Zhang i H. Kikuchi. "Increased Expression of nNos Following Cortical Spreading Depression in Rat Brain". W Maturation Phenomenon in Cerebral Ischemia V, 333–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18713-1_41.

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Hord, Jeffrey M., i John M. Lawler. "ROS and nNOS in the Regulation of Disuse-Induced Skeletal Muscle Atrophy". W The Plasticity of Skeletal Muscle, 231–50. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3292-9_11.

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Tellios, Vasiliki, Matthew Joseph Elias Maksoud i Wei-Yang Lu. "The Role of nNOS/NO on Cerebellar Development in Health and Disease". W Contemporary Clinical Neuroscience, 173–92. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23104-9_9.

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Kolev, Nikolay Ivanov. "Nichthomogene Nichtgleichgewichts-Zweiphasenströmung (NNZS)". W Transiente Zweiphasen-Strömung, 89–133. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-50107-4_8.

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Ikonomou, Pantelis F. "Nicht-NVV Nuklearwaffenstaaten (NNWS)". W Globale nukleare Entwicklungen, 159–84. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-15276-4_8.

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Brunetti, Jacopo, Walter D’Ambrogio, Annalisa Fregolent i Francesco Latini. "Substructuring Using NNMs of Nonlinear Connecting Elements". W Lecture Notes in Mechanical Engineering, 1426–40. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41057-5_116.

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Mamalakis, Antonios, Imme Ebert-Uphoff i Elizabeth A. Barnes. "Explainable Artificial Intelligence in Meteorology and Climate Science: Model Fine-Tuning, Calibrating Trust and Learning New Science". W xxAI - Beyond Explainable AI, 315–39. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04083-2_16.

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AbstractIn recent years, artificial intelligence and specifically artificial neural networks (NNs) have shown great success in solving complex, nonlinear problems in earth sciences. Despite their success, the strategies upon which NNs make decisions are hard to decipher, which prevents scientists from interpreting and building trust in the NN predictions; a highly desired and necessary condition for the further use and exploitation of NNs’ potential. Thus, a variety of methods have been recently introduced with the aim of attributing the NN predictions to specific features in the input space and explaining their strategy. The so-called eXplainable Artificial Intelligence (XAI) is already seeing great application in a plethora of fields, offering promising results and insights about the decision strategies of NNs. Here, we provide an overview of the most recent work from our group, applying XAI to meteorology and climate science. Specifically, we present results from satellite applications that include weather phenomena identification and image to image translation, applications to climate prediction at subseasonal to decadal timescales, and detection of forced climatic changes and anthropogenic footprint. We also summarize a recently introduced synthetic benchmark dataset that can be used to improve our understanding of different XAI methods and introduce objectivity into the assessment of their fidelity. With this overview, we aim to illustrate how gaining accurate insights about the NN decision strategy can help climate scientists and meteorologists improve practices in fine-tuning model architectures, calibrating trust in climate and weather prediction and attribution, and learning new science.
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Streszczenia konferencji na temat "NNos"

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Klinnikova, A. A., G. A. Danilova i N. P. Aleksandrova. "The role of neuronal NO synthase in the respiratory effects of TNF-α". W VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-115-118.

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It was shown that an increase level of proinflammatory cytokines has a modulating effect on the reflex control of respiration. The aim of this study was to investigate the involvement of neuronal nitric oxide synthase (nNOS) in the mechanisms of the influence of an increased level of Tumor necrosis factor – α (TNF-α) on the hypoxic ventilatory response. To achieve this goal, experiments were carried out on urethane anesthetized rats with intravenous administration of TNF-α before and after pretreatment with 7-nitroindazole specific nNOS inhibitor. The hypoxic ventilation response was assessed by rebreathing with a hypoxic gas mixture before and after administration of TNF-α. We found that TNF-α decreased the ventilatory response to hypoxia. Pretreatment with nNOS inhibitor reduced respiratory effects of TNF-α. Key words: cytokines, TNF-α, hypoxia, chemoreflex, respiration, ventilation, neuronal nitric oxide synthase.
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Yang, Sun, Zhen Yang i Frank L. Meyskens. "Abstract 5466: nNOS, a novel target for melanoma prevention and therapy". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5466.

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Lihong, Hou. "Impact of different exercise load on expression of hippocampal neurons nNOS in rats". W 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6028925.

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YANG, SUN, Zhen Yang, Richard B. Silverman, Thomas Poulos i Frank L. Meyskens. "Abstract 4744: Targeting nitric oxide signaling with nNOS inhibitors as a novel strategy for the therapy and prevention of human melanoma". W Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4744.

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Jackson, Claire L., Jacqueline King, Edith N. Quinn, Peter M. Lackie i Jane S. Lucas. "The Importance Of Being NNOS? Unique Localization Of Neuronal Nitric Oxide Synthase To Cilia And Investigating A Nitric Oxide Synthase-1 Polymorphism In Primary Ciliary Dyskinesia". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5504.

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Benussi, Elias, Andrea Patane', Matthew Wicker, Luca Laurenti i Marta Kwiatkowska. "Individual Fairness Guarantees for Neural Networks". W Thirty-First International Joint Conference on Artificial Intelligence {IJCAI-22}. California: International Joint Conferences on Artificial Intelligence Organization, 2022. http://dx.doi.org/10.24963/ijcai.2022/92.

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We consider the problem of certifying the individual fairness (IF) of feed-forward neural networks (NNs). In particular, we work with the epsilon-delta-IF formulation, which, given a NN and a similarity metric learnt from data, requires that the output difference between any pair of epsilon-similar individuals is bounded by a maximum decision tolerance delta >= 0. Working with a range of metrics, including the Mahalanobis distance, we propose a method to overapproximate the resulting optimisation problem using piecewise-linear functions to lower and upper bound the NN's non-linearities globally over the input space. We encode this computation as the solution of a Mixed-Integer Linear Programming problem and demonstrate that it can be used to compute IF guarantees on four datasets widely used for fairness benchmarking. We show how this formulation can be used to encourage models' fairness at training time by modifying the NN loss, and empirically confirm our approach yields NNs that are orders of magnitude fairer than state-of-the-art methods.
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Beyer, Michael, Christoph Schorn, Tagir Fabarisov, Andrey Morozov i Klaus Janschek. "Automated Hardening of Deep Neural Network Architectures". W ASME 2021 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/imece2021-72891.

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Abstract Designing optimal neural network (NN) architectures is a difficult and time-consuming task, especially when error resiliency and hardware efficiency are considered simultaneously. In our paper, we extend neural architecture search (NAS) to also optimize a NN’s error resilience and hardware related metrics in addition to classification accuarcy. To this end, we consider the error sensitivity of a NN on the architecture-level during NAS and additionally incorporate checksums into the network as an external error detection mechanism. With an additional computational overhead as low as 17% for the discovered architectures, checksums are an efficient method to effectively enhance the error resilience of NNs. Furthermore, the results show that cell-based NN architectures are able to maintain their error resilience characteristics when transferred to other tasks.
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"Session 5: Applications of NNs 4: NNs in modeling". W 2008 9th Symposium on Neural Network Applications in Electrical Engineering (NEUREL 2008). IEEE, 2008. http://dx.doi.org/10.1109/neurel.2008.4685603.

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Teodorescu, Horia-Nicolai L., i Mircea Hulea. "NNs Recognize Chaotic Attractors". W 2013 19th International Conference on Control Systems and Computer Science (CSCS). IEEE, 2013. http://dx.doi.org/10.1109/cscs.2013.7.

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Jeong, Sangoh, Doreen Cheng, Henry Song i Swaroop Kalasapur. "Nnon-collaborative interest mining for personal devices". W 2009 IEEE Symposium on Computational Intelligence and Data Mining (CIDM). IEEE, 2009. http://dx.doi.org/10.1109/cidm.2009.4938647.

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Raporty organizacyjne na temat "NNos"

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Burch, J. NNSS AUDIT. Office of Scientific and Technical Information (OSTI), luty 2023. http://dx.doi.org/10.2172/1959484.

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Kersley, L., i N. S. Wheadon. Scintillation Using NNSS Satellites. Fort Belvoir, VA: Defense Technical Information Center, styczeń 1985. http://dx.doi.org/10.21236/ada152804.

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Miller, Julianne J., Steve A. Mizell, George Nikolich i Scott Campbell. NNSS Soils Monitoring: Plutonium Valley (CAU366). Office of Scientific and Technical Information (OSTI), luty 2012. http://dx.doi.org/10.2172/1046465.

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Burris-Mog, Trevor. THE SCORPIUS ACCELERATOR AND THE NNSS. Office of Scientific and Technical Information (OSTI), czerwiec 2022. http://dx.doi.org/10.2172/1874883.

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Miller, Julianne J., Steve A. Mizell, George Nikolich, Greg McCurdy i Scott Campbell. NNSS Soils Monitoring: Plutonium Valley (CAU366) FY2012. Office of Scientific and Technical Information (OSTI), styczeń 2013. http://dx.doi.org/10.2172/1067381.

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Stromquist, W. R. DHWA Modeling Efforts for NNWS, FY 1985. Fort Belvoir, VA: Defense Technical Information Center, grudzień 1985. http://dx.doi.org/10.21236/ada165147.

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Nikolich, George, Steve Mizell, Greg McCurdy, Scott Campbell i Julianne J. Miller. NNSS Soils Monitoring: Plutonium Valley (CAU 366) FY2016. Office of Scientific and Technical Information (OSTI), październik 2017. http://dx.doi.org/10.2172/1404699.

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Nikolich, George, Steve A. Mizell, Greg McCurdy, Scott A. Campbell i Julianne J. Miller. NNSS Soils Monitoring: Plutonium Valley (CAU 366) FY2017. Office of Scientific and Technical Information (OSTI), maj 2018. http://dx.doi.org/10.2172/1438195.

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Nikolich, George, Kevin M. Heintz, Steve A. Mizell, Greg McCurdy, Austin Chapman, Julianne J. Miller i Susan Stillman. NNSS Soils Monitoring: Plutonium Valley (CAU 366) FY2019. Office of Scientific and Technical Information (OSTI), czerwiec 2020. http://dx.doi.org/10.2172/1634120.

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Nikolich, George, Steve Mizell, Greg McCurdy, Scott Campbell i Julianne J. Miller. NNSS Soils Monitoring: Plutonium Valley (CAU 366) FY2015. Office of Scientific and Technical Information (OSTI), luty 2017. http://dx.doi.org/10.2172/1344531.

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