Gotowe bibliografie tematyczne / INOS

Gotowa bibliografia na temat „INOS”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 11 marca 2023

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Artykuły w czasopismach na temat "INOS"

1

Vodovotz, Y., C. Bogdan, J. Paik, Q. W. Xie i C. Nathan. "Mechanisms of suppression of macrophage nitric oxide release by transforming growth factor beta." Journal of Experimental Medicine 178, nr 2 (1.08.1993): 605–13. http://dx.doi.org/10.1084/jem.178.2.605.

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Activated mouse peritoneal macrophages produce nitric oxide (NO) via a nitric oxide synthase that is inducible by interferon gamma (IFN-gamma): iNOS. We have studied the mechanisms by which transforming growth factor beta 1 (TGF-beta) suppresses IFN-gamma-stimulated NO production. TGF-beta treatment reduced iNOS specific activity and iNOS protein in both cytosolic and particulate fractions as assessed by Western blot with monospecific anti-iNOS immunoglobulin G. TGF-beta reduced iNOS mRNA without affecting the transcription of iNOS by decreasing iNOS mRNA stability. Even after iNOS was already expressed, TGF-beta reduced the amount of iNOS protein. This was due to reduction of iNOS mRNA translation and increased degradation of iNOS protein. The potency of TGF-beta as a deactivator of NO production (50% inhibitory concentration, 5.6 +/- 2 pM) may reflect its ability to suppress iNOS expression by three distinct mechanisms: decreased stability and translation of iNOS mRNA, and increased degradation of iNOS protein. This is the first evidence that iNOS is subject to other than transcriptional regulation.
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Gunnett, Carol A., Donald D. Heistad, Angela Loihl i Frank M. Faraci. "Tumor necrosis factor-α impairs contraction but not relaxation in carotid arteries from iNOS-deficient mice". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, nr 5 (1.11.2000): R1558—R1564. http://dx.doi.org/10.1152/ajpregu.2000.279.5.r1558.

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We used mice deficient in expression of inducible NO synthase (iNOS −/−) to directly examine the role of iNOS in impaired vasoconstrictor responses following tumor necrosis factor-α (TNF-α). In iNOS +/+ mice, contraction of carotid arteries in response to prostaglandin F2α(PGF2α) was impaired following TNF-α (100 μg/kg ip)( n = 10, P < 0.01). In contrast to responses in wild-type mice, contraction to low concentrations of PGF2αwere normal, but maximum contraction to PGF2αwas impaired in arteries from iNOS −/− mice treated with TNF-α [0.35 ± .0.02 g ( n = 8) following vehicle and 0.25 ± 0.02 g ( n = 7) following TNF-α ( P < 0.05)]. Aminoguanidine, a relatively selective inhibitor of iNOS, partially restored contraction to PGF2αin vessels from iNOS +/+ mice but had no effect in iNOS −/− mice injected with TNF-α, suggesting that a mechanism(s) other than iNOS contributes to impaired responses. In contrast to contractile responses, relaxation of the carotid artery in response to acetylcholine and nitroprusside was not altered following TNF-α in iNOS +/+ or iNOS −/−mice. Responses of carotid arteries from iNOS −/− mice and effects of aminoguanidine suggest that both iNOS-dependent and iNOS-independent mechanisms contribute to impaired contractile responses following TNF-α.
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Cutler, David. "Unhelpful iNOS". Trends in Pharmacological Sciences 22, nr 12 (grudzień 2001): 609. http://dx.doi.org/10.1016/s0165-6147(00)01963-5.

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Farley, K. S., L. F. Wang, H. M. Razavi, C. Law, M. Rohan, D. G. McCormack i S. Mehta. "Effects of macrophage inducible nitric oxide synthase in murine septic lung injury". American Journal of Physiology-Lung Cellular and Molecular Physiology 290, nr 6 (czerwiec 2006): L1164—L1172. http://dx.doi.org/10.1152/ajplung.00248.2005.

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Inducible nitric oxide synthase (iNOS) contributes importantly to septic pulmonary protein leak in mice with septic acute lung injury (ALI). However, the role of alveolar macrophage (AM) iNOS in septic ALI is not known. Thus we assessed the specific effects of AM iNOS in murine septic ALI through selective AM depletion (via intratracheal instillation of clodronate liposomes) and subsequent AM reconstitution (via intratracheal instillation of donor iNOS+/+ or iNOS−/− AM). Sepsis was induced by cecal ligation and perforation, and ALI was assessed at 4 h: protein leak by the Evans blue (EB) dye method, neutrophil infiltration via myeloperoxidase (MPO) activity, and pulmonary iNOS mRNA expression via RT-PCR. In iNOS+/+ mice, AM depletion attenuated the sepsis-induced increases in pulmonary microvascular protein leak (0.3 ± 0.1 vs. 1.4 ± 0.1 μg EB·g lung−1·min−1; P < 0.05) and MPO activity (37 ± 4 vs. 67 ± 8 U/g lung; P < 0.05) compared with that shown in non-AM-depleted mice. In AM-depleted iNOS+/+ mice, septic pulmonary protein leak was restored by AM reconstitution with iNOS+/+ AM (0.9 ± 0.3 μg EB·g lung−1·min−1) but not with iNOS−/− donor AM. In iNOS−/− mice, sepsis did not induce pulmonary protein leak or iNOS mRNA expression, despite increased pulmonary MPO activity. However, AM depletion in iNOS−/− mice and subsequent reconstitution with iNOS+/+ donor AM resulted in significant sepsis-induced pulmonary protein leak and iNOS expression. Septic pulmonary MPO levels were similar in all AM-reconstituted groups. Thus septic pulmonary protein leak is absolutely dependent on the presence of functional AM and specifically on iNOS in AM. AM iNOS-dependent pulmonary protein leak was not mediated through changes in pulmonary neutrophil influx.
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Hardiman, Karin M., J. Russell Lindsey i Sadis Matalon. "Lack of amiloride-sensitive transport across alveolar and respiratory epithelium of iNOS(−/−) mice in vivo". American Journal of Physiology-Lung Cellular and Molecular Physiology 281, nr 3 (1.09.2001): L722—L731. http://dx.doi.org/10.1152/ajplung.2001.281.3.l722.

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The extent to which endogenously generated nitric oxide alters Na+transport across the mammalian alveolar epithelium in vivo has not been documented. Herein we measured alveolar fluid clearance and nasal potential differences in mice lacking the inducible form of nitric oxide synthase [iNOS; iNOS(−/−)] and their corresponding wild-type controls [iNOS(+/+)]. Alveolar fluid clearance values in iNOS(+/+) and iNOS(−/−) anesthetized mice with normal oxygenation and acid-base balance were ∼30% of instilled fluid/30 min. In both groups of mice, fluid absorption was dependent on vectorial Na+movement. Amiloride (1.5 mM) decreased alveolar fluid clearance in iNOS(+/+) mice by 61%, whereas forskolin (50 μM) increased alveolar fluid clearance by 55% by stimulating amiloride-insensitive pathways. Neither agent altered alveolar fluid clearance in iNOS(−/−) mice. Hyperoxia upregulated iNOS expression in iNOS(+/+) mice and decreased their amiloride-sensitive component of alveolar fluid clearance but had no effect on the corresponding values in iNOS(−/−) mice. Nasal potential difference measurements were consistent with alveolar fluid clearance in that both groups of mice had similar baseline values, which were amiloride sensitive in the iNOS(+/+) but not in the iNOS(−/−) mice. These data suggest that nitric oxide produced by iNOS under basal conditions plays an important role in regulating amiloride-sensitive Na+channels in alveolar and airway epithelia.
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Si, Chuanping, Ruihua Zhang, Yuan Hu, Hui Zhang i Huabao Xiong. "Distinct roles of dendritic cell-derived iNOS in the control of effective and regulative dendritic cell differentiation." Journal of Immunology 196, nr 1_Supplement (1.05.2016): 59.2. http://dx.doi.org/10.4049/jimmunol.196.supp.59.2.

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Abstract The immune system exists in a delicate equilibrium between response and tolerance. Dendritic cells (DC) are a plastic lineage able to process and integrate signals from the microenvironment. But the regulation how DCs differentiate to effective or regulatory DC cells are incompletely understood. Inducible nitric oxide synthase (iNOS) derived NO plays critical roles in immune suppression of immune cells. But, it is still not clear what the function of DC cells-derived iNOS is in the regulation in inflammatory diseases. In this study, we demonstrated that DC-derived iNOS regulates balance of effective and regulatory DC cell differentiation. iNOS deficient mice displayed an increased effective DC phenotypes, whereas the percentage of regulatory DCs were comparable in wild-type and iNOS deficient mice in vivo and in vitro. The results were further supported by increased effective DCs from iNOS−/− BMDC cells. Activation of DCs by LPS/IFNg resulted in the expression of iNOS in WT mice. The iNOS inhibitor L-NIL enhanced effective DCs differentiation, mimicking the effect observed in iNOS deficient mice. NO donor SNAP suppressed effective DCs. iNOS−/− DCs result in more enhanced T cell activation. iNOS−/− mice infected with Citrobacter Rodentium led to more severe intestinal inflammation compared to WT mice and the results were correlated with more inflammatory cells infiltration in iNOS−/− in colon tissues. And iNOS−/− mice showed increased effective DCs in colon tissues than that in WT mice. Our results suggest that DC-derived iNOS negatively controls effective DC development and targeting DC-derived iNOS would lead to the new therapies for autoimmune/inflammatory diseases.
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Melillo, G., T. Musso, A. Sica, L. S. Taylor, G. W. Cox i L. Varesio. "A hypoxia-responsive element mediates a novel pathway of activation of the inducible nitric oxide synthase promoter." Journal of Experimental Medicine 182, nr 6 (1.12.1995): 1683–93. http://dx.doi.org/10.1084/jem.182.6.1683.

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Picolinic acid, a catabolite of L-tryptophan, activates the transcription of the inducible nitric oxide synthase gene (iNOS) in IFN-gamma-treated murine macrophages. We performed functional studies on the 5' flanking region of the iNOS gene linked to a CAT reporter gene to identify the cis-acting element(s) responsible for the activation of iNOS transcription by picolinic acid. Transient transfection assays showed that the full-length iNOS promoter in the murine macrophage cell line ANA-1 was activated by the synergistic interaction between IFN-gamma and picolinic acid. Deletion or mutation of the iNOS promoter region from -227 to -209, containing a sequence homology to a hypoxia-responsive enhancer (iNOS-HRE), decreased picolinic acid- but not LPS-induced CAT activity by more than 70%. Functional studies using a tk promoter-CAT reporter gene plasmid demonstrated that the iNOS-HRE was sufficient to confer inducibility by picolinic acid but not by IFN-gamma or LPS. Electrophoretic mobility shift assays confirmed that picolinic acid alone induced a specific binding activity to the iNOS-HRE. Furthermore, we found that the iNOS-HRE activity was inducible by hypoxia and that hypoxia in combination with IFN-gamma activated the iNOS promoter in transient transfection assays and induced iNOS transcription and mRNA expression. These data establish that the iNOS-HRE is a novel regulatory element of the iNOS promoter activity in murine macrophages and provide the first evidence that iNOS is a hypoxia-inducible gene.
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Chu, Wei, Lirong Cao, Gui Daokun i Jiali Zhao. "iNOS Promotes the Development of Osteosarcoma via Wnt/β-Catenin Pathway". Journal of Immunology Research 2021 (16.08.2021): 1–10. http://dx.doi.org/10.1155/2021/4549221.

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Inducible nitric oxide synthase (iNOS), accompanied with protumor and antitumor activity, has been studied in multiple cancers. However, the role of iNOS expression in osteosarcoma (OS) is far from being fully understood. In present work, iNOS levels were detected in OS tissues and cell lines. Colony formation assay, Transwell assay, and fow cytometer were used to assess proliferation, migration, invasion, and apoptosis abilities in vitro after iNOS inhibition. Western blotting determined the expressions of iNOS, MMP2, MMP9, C-MYC, Ki67, PCNA, and β-catenin. Mice transfected with OS cells were to evaluate tumor formation. IHC assay was to evaluate the expressions of iNOS and β-catenin in mice. The results showed that iNOS was upregulated in both OS tissues and cells compared with that in matched normal tissues or cells. And we found that proliferation, migration, and invasion numbers of OS cells were decreased, and apoptosis numbers of OS cells were increased after iNOS inhibition. MMP2, MMP9, C-MYC, Ki67, and PCNA levels were also reduced in OS cells treated with iNOS inhibition. Else, iNOS inhibition would suppress β-catenin expression in OS cells to regulate MMP2, MMP9, C-MYC, Ki67, and PCNA expressions. In addition, tumor formation, iNOS expression, and β-catenin expression were inhibited in mice transplanted with iNOS knockout OS cells. These results indicated that iNOS might be a potential therapeutic target for OS.
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Miller, Barbara H., Rutilio A. Fratti, Jens F. Poschet, Graham S. Timmins, Sharon S. Master, Marcos Burgos, Michael A. Marletta i Vojo Deretic. "Mycobacteria Inhibit Nitric Oxide Synthase Recruitment to Phagosomes during Macrophage Infection". Infection and Immunity 72, nr 5 (maj 2004): 2872–78. http://dx.doi.org/10.1128/iai.72.5.2872-2878.2004.

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ABSTRACT Inducible nitric oxide synthase (iNOS) is a cytoplasmic protein responsible for the generation of nitric oxide (NO · ) in macrophages. In this work, we hypothesized that the intracellular localization of iNOS is significant for effective delivery of NO · to phagosomes containing ingested microorganisms. Using immunofluorescence microscopy and Western blot analysis, iNOS was shown to localize in the vicinity of phagosomes containing latex beads in stimulated macrophages. iNOS also localized to phagosomes containing Escherichia coli. The colocalization of iNOS with ingested latex beads was an actin-dependent process, since treatment with the actin microfilament disrupter cytochalasin D prevented iNOS recruitment to latex bead phagosomes. In contrast to E. coli and inert particle phagosomes, mycobacterial phagosomes did not colocalize with iNOS. This study demonstrates that (i) iNOS can be recruited to phagosomes; (ii) this recruitment is dependent on a functional actin cytoskeleton; (iii) certain microorganisms have the ability to prevent or reduce colocalization with iNOS; and (iv) spatial exclusion of iNOS may play a role in Mycobacterium tuberculosis pathogenesis.
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Chicoine, Louis G., Edith Tzeng, Rebekah Bryan, Steven Saenz, Michael L. Paffett, Joelle Jones, C. Richard Lyons, Thomas C. Resta, Leif D. Nelin i Benjimen R. Walker. "Intratracheal adenoviral-mediated delivery of iNOS decreases pulmonary vasoconstrictor responses in rats". Journal of Applied Physiology 97, nr 5 (listopad 2004): 1814–22. http://dx.doi.org/10.1152/japplphysiol.00193.2004.

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We hypothesized that adenovirus-mediated inducible nitric oxide synthase (iNOS) gene transduction of the lung would result in time-dependent iNOS overexpression and attenuate the vascular constrictor responses to a thromboxane mimetic, U-46619. Rats were treated via the trachea with surfactant alone (sham), surfactant containing an adenoviral construct with a cytomegalovirus promoter-regulated human iNOS gene (Adeno-iNOS), or an adenoviral construct without a gene insert (Adeno-Control). Adeno-iNOS-transduced rats demonstrated human iNOS mRNA and increased iNOS protein levels only in the lungs. Immunohistochemistry of lungs from Adeno-iNOS-treated animals demonstrated transgene expression in alveolar wall cells. In the lungs from Adeno-iNOS-transduced rats, the expression of iNOS protein and exhaled nitric oxide concentrations were increased on days 1–4 and 7 but returned to baseline values by day 14. The administration of the selective iNOS inhibitor l- N6-(1-iminoethyl)lysine dihydrochloride (l-NIL) decreased exhaled nitric oxide concentrations to levels found in Adeno-Control-transduced lungs. In a second group of rats, the segmental vasoconstrictor responses to U-46619 were determined in isolated, perfused lungs 3 days after transduction. Lungs from rats transduced with Adeno-iNOS had reduced total, arterial, and venous vasoconstrictor responses to U-46619 compared with sham, Adeno-Control, and control groups. In a third set of experiments, the response to 400 nM U-46619 in the presence of 10 μM l-NIL was not different in the isolated lungs from Adeno-Control- and Adeno-iNOS-transduced rats. We conclude that adenovirus-mediated iNOS gene transduction of the lung results in time-dependent iNOS overexpression, which attenuates the vascular constrictor responses to the thromboxane mimetic U-46619.
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Rozprawy doktorskie na temat "INOS"

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Duarte, Andressa. "Participação da via PI3K/AKT na produção de óxido nítrico por macrófagos peritoneais". Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-21102013-112320/.

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A imunidade inata é responsável pela resposta inicial aos microrganismos, uma vez que impede, controla ou elimina a infecção. Esse sistema consiste em barreiras epiteliais, proteínas plasmáticas e células circulantes e teciduais. Dentre esses componentes, os macrófagos possuem grande importância, sendo capazes de controlar e eliminar agentes patogênicos através da fagocitose e produção de espécies reativas de oxigênio e nitrogênio. A ativação de PRRs por constituintes oriundos dos patógenos em macrófagos desencadeia eventos da resposta imune inata, ativados por diversas vias de sinalização intracelular. A via das PI3Ks é conhecida por regular várias funções nas células, como a regulação do ciclo celular, migração e produção de espécies reativas de oxigênio e nitrogênio. O NO é um mediador central na imunidade inata que, após estímulos inflamatórios, é produzido em altas quantidades através da iNOS. Macrófagos deficientes em PI3K produzem menos NO e apresentam prejudicado controle da infecção quando infectados por T. cruzi. O objetivo do presente trabalho foi investigar o papel da via PI3K na produção de NO por macrófagos peritoneais estimulados com LPS. Os macrófagos empregados no estudo, WT e PI3K-/-, possuem o mesmo fenótipo. Observamos que macrófagos PI3K-/- possuem uma menor produção de NO e expressam menos iNOS. A reduzida expressão de iNOS, após estímulo com LPS, é também observada quando macrófagos WT são tratados com inibidores seletivos da PI3K e AKT. Além disso, demonstramos que, concomitantemente à menor expressão da iNOS, ocorre deficiência na fosforilação da AKT e diminuição da ativação do fator de transcrição NF-kB, sugerindo que a PI3K participa da ativação do NF-kB. Foi observado ainda que o tratamento com PTX também diminui a expressão da iNOS. No entanto, macrófagos PAFR-/- expostos ao LPS presentam maior expressão da iNOS, enquanto os macrófagos CCR2-/- apresentam menor expressão dessa enzima nessas condições. Para investigar a implicação da via PI3K in vivo foi administrado LPS i.v., como modelo de choque endotoxemico, no qual observamos maior sobrevida em animais PI3K-/- comparado aos animais WT e menores níveis de nitrito no soro. Nossos dados sugerem que a enzima PI3K é crítica para expressão de iNOS e produção de NO pelos macrófagos, possivelmente através da ativação do receptor CCR2, estando envolvida na fisiopatologia do choque induzido por LPS.
Innate immunity is the initial response to microorganisms, since it prevents, controls and eliminates infection. This system consists in epithelial barriers, plasma proteins and circulating and tissue cells. Among these components, macrophages have great importance, being capable of control and eliminate pathogen agents through phagocytosis and production of reactive oxygen and nitrogen species. Activation of PRRs by pathogens constituents in macrophages triggers events of the innate immune response, activated by various intracellular signaling pathways. PI3Ks pathway is known to regulate several functions in the cell, such as regulation of the cell cycle, migration and production of reactive oxygen and nitrogen species. NO is a central mediator in innate immunity, which after inflammatory stimuli, is produced in high levels by iNOS. PI3K-deficient macrophages produce less NO and exhibit impaired control of infection when infected by T. cruzi. The aim of the present study is to investigate the role of PI3K pathway in NO production by LPS-estimulated peritoneal macrophages. The macrophages used in this study, WT and PI3K- / -, have the same phenotype. We observed that PI3K- / - macrophages have a lower NO production and express less iNOS. The low expression of iNOS after stimulation with LPS was also observed in WT macrophages treated with selective inhibitors of PI3K and AKT. Furthermore, we demonstrate that, along to lower iNOS expression, there is deficiency in AKT phosphorylation and decreased activation of the transcription factor NF-kB, suggesting that PI3K participates of the NF-kB activation. It was also observed that PTX treatment has decreased iNOS expression. However, LPS-exposed PFAR-/- macrophages present greater expression of iNOS, while CCR2-/- macrophage exhibit lower expression of this enzyme under these conditions. To investigate involvement of the PI3K pathway has \"in vivo\",LPS was administered i.v., as an endotoxic model, in which we observed a higher survival in PI3K- / - animals compared to WT animals and lower nitrite levels in serum. Our data suggest that PI3K enzyme is critical to iNOS expression and NO production by macrophages, possibly through activation of the CCR2 receptor, being involved in the LPS-induced shock pathophysiology
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Gather, Fabian Matthias [Verfasser]. "Analyse der Expression der humanen induzierbaren NO-Synthase (iNOS)Einfluss der 5’-UTR auf die Expression der humanen iNOS und Expression der humanen iNOS in Modellen der neuronalen Differenzierung / Fabian Matthias Gather". Mainz : Universitätsbibliothek Mainz, 2020. http://d-nb.info/1205813624/34.

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Zholobenko, Aleksey. "Biomimetic vectors for breast cancer iNOS gene therapy". Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.580137.

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While the field of gene delivery has matured dramatically in the last decade, there is still no gene delivery agent that can combine safety, efficacy and specificity into a single vehicle. In this work two protein based vectors, the Designer Biomimetic Vector (DBV) and RALA were investigated for the delivery of the gene coding for iNOS to breast cancer cells. Protein based vectors have the advantage of biocompatibility, bioderadabiliy and the high degree of control over the composition of the vector. They are not, however, widely studied at the present day. The DBV is a multi-domain recombinant chimeric protein, while RALA is a synthetic peptide with a single bi-functional domain. The DBV was found to form nanoparticles in the range of around 100mn and achieve a transfection efficacy of up to 10% in ZR-75-1 cells when complexed with pEG FP-NI. When complexed with a plasmid which allowed expression of iNOS under a constitutive CMV promoter (pENi), high concentrations of NO were produced (10μM) and near total cell kill was observed. Consequently, when the DBV/pEGP-N1 was tested in vivo, transfection was found in all organs and tissues tested, including tumour. Treatment with DBV/pENi nanoparticles resulted in a tumour growth delay of 17 days for both single dose and bi-weekly dose groups. Bi-weekly dosing was found to be toxic in an iNOS dependant manner. RALA was tested as an alternative vector and found ton form nanoparticles between 30-1 OOmn in diameter and give a transfection efficacy of up to 35% in ZR-75-1 cells when complexed with pEGFP-Nl. In in vivo models, RALAlpEGFP-N1 was found to transfect all organs and tissues tested, including tumour. In addition, in immunocompetant C57B mouse models, RALA was found to be no more immunogenic than mock injections while reducing the immunogenicity of plasmid DNA. RALA/pEGFP-N1 nanoparticles were found to protect the cargo DNA from both serum and freeze-drying. The relative efficacy and tolerability of both the DBV and RALA set aside a role for the two vehicles as prototypes for future targeted gene delivery systems
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Zheng, Xilong. "Tyrosine kinase pathways, smooth muscle function and iNOS induction". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq24569.pdf.

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Campbell, Holly R. 1976. "Chlorine-induced lung injury and the role of iNOS". Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111574.

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Reactive airways dysfunction syndrome (RADS), a form of irritant-induced asthma (IIA) has been observed in humans following acute chlorine (Cl 2) gas exposure in occupational and domestic settings. Following Cl 2 injury, subepithelial fibrosis, mucous hyperplasia, and non-specific airway hyperresponsiveness have been reported. Based on the disease profile, we hypothesized that pulmonary damage may be oxidative in nature.
The aim of this work was to develop a murine model of irritant-induced asthma in order to investigate the pathogenic processes and potential oxidative mechanisms involved in response to Cl2 exposure, with a secondary aim of examining the role of iNOS in response to Cl2 inhalation.
A/J, C57BI/6J (wild type) and iNOS-1- mice exposed to various concentrations of Cl2 were mechanically ventilated for measurement of lung mechanics and responses to i.v. methacholine (MCh). Bronchoalveolar lavage was performed to examine total protein, cell populations and nitrate/nitrates. Tissues were harvested for histology and immunocytochemistry for iNOS, 3NT and carbonyl residues. To examine the role of iNOS, a subset of animals were treated with a selective iNOS inhibitor (1400W) and non-selective NOS inhibitor LNAME.
Chlorine exposure caused airway hyperresponsiveness, which appeared to be mitigated by iNOS blockade with 1400W, however this was not the case in iNOS-1- mice. Cl2 exposure also caused increases in total BAL protein, total cells, NOx, neutrophils, iNOS, 3NT and carbonyl residues.
In conclusion, chlorine exposure causes lung injury, similar to reactive airways dysfunction syndrome, characterized by airway hyperresponsiveness, epithelial sloughing, inflammatory cell influx, oxidative injury and increases in both the activity and expression of iNOS. Chlorine-induced airway hyperresponsiveness is mitigated, in part, by selective blockade of iNOS with the use of pharmacological intervention.
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Godoi, Fernanda Nascimento de. "?leo de soja em dietas para eq?inos atletas". Universidade Federal Rural do Rio de Janeiro, 2008. https://tede.ufrrj.br/jspui/handle/tede/580.

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This work aimed to evaluate intake in athletic horses fed diets with soybean oil inclusion and the effects of apparent digestibility of nutrients, digestive kinetics, faeces characters and physiologic, hematological and biochemical parameters and. In first essay, fifteen horses were used in a completely randomized design with three diets and five repetitions. Diets used were: diet without soybean oil inclusion (control); diet with inclusion of 8.5% soybean oil; diet with inclusion of 19.5% soybean oil. Trial had 34 days of duration, 30 days to adaptation of diets and four days to samples collection. Kinetics of liquid phase of digesta was estimated by LIPE? (Isolated Lignin Purified Enriched) in liquid form. The LIPE? was given only one time by oral infusion in 30th day of essay and faeces samples were collected at 2, 4, 8, 12, 16, 20, 24, 30, 36, 42, 48, 54, 60, 66, 72 and 78 hours after. Faeces characteristics were evaluate on 33th and 34th day of essay. Blood samples were taken before and at 34th day. Data were submitted to variance analysis and means compared by Student Newman-Keuls test, at 5% of significance. In secund essay, twelve horses were used in a completely randomized design with two diets and six repetitions. Diets used were: diet without soybean oil inclusion (control); diet with inclusion of 10% soybean oil. The trial had 82 days of duration, with three physical effort tests before, at 60th and at 82th day of trial. Heart frequency and body temperature were evaluation and blood samples for analyze of hematological and biochemical parameters were taken in five moments in function of physical effort tests. The first data collection, before the test, with horses at rest, and immediately after the test, and 10, 20 and 120 minutes after the physical effort tests. Data were submitted to non parametric analysis, at 5% of significance. There was a significant reduction of dry matter intake in horses fed high fat diet. Apparent digestibility of fat increased in high fat diets (P<0.05) and apparent digestibility of cellulose decrease (P>0.05) in diet with 19.5% soybean oil inclusion. Apparent digestibility of others nutrients, except crude protein, digestive kinetics and faeces characteristics were not affecting (P>0.05) in horses fed diets with soybean oil inclusion. Horses fed high fat diet increased (P<0.05) in blood level of erythrocytes, hemoglobin and triglycerides and reduction of mean corpuscular volume. Soybean oil in diets did not affect physiological, hematological and biochemical parameters along the time intake time and in function physical effort tests. High fat diets were palatable and safety without any colic or diarrheas cases. The soybean oil can used in diet for horses, reducing dry matter intake and increasing energy density of diets that is interesting to athletic horses
Objetivou-se avaliar o consumo de dietas com diferentes n?veis de inclus?o de ?leo de soja por eq?inos atletas e os efeitos na digestibilidade aparente dos nutrientes, cin?tica digestiva, caracter?sticas fecais, nos par?metros fisiol?gicos, hematol?gicos e bioqu?micos. No primeiro ensaio foram utilizados quinze eq?inos em delineamento experimental inteiramente casualizado com tr?s dietas e cinco repeti??es. As dietas utilizadas foram: dieta sem inclus?o de ?leo de soja (controle); dieta com inclus?o de 8,5% de ?leo de soja; dieta com inclus?o de 19,5% de ?leo de soja. O ensaio teve dura??o de 34 dias, sendo 30 dias de adapta??o dos eq?inos ?s dietas e quatro dias de coleta de amostras. A cin?tica da fase l?quida da digesta foi estimada pelo LIPE? (Lignina Isolada, Purificada e Enriquecida) na forma l?quida, fornecido no 30? dia de ensaio, em dose ?nica, e as amostras fecais foram coletadas nos tempos 0, 2, 4, 8, 12, 16, 20, 24, 30, 36, 42, 48, 54, 60, 66, 72 e 78 horas ap?s o fornecimento. As caracter?sticas fecais foram avaliadas no 33? e 34? dia e, as coletas das amostras sang??neas no in?cio e 34? dia do ensaio. Os resultados foram submetidos ? an?lise de vari?ncia e as m?dias comparadas pelo teste Student Newman-Keuls, com n?vel de signific?ncia de 5%. No segundo ensaio foram utilizados doze eq?inos em delineamento experimental inteiramente casualizado com duas dietas e seis repeti??es. As dietas utilizadas foram: dieta sem inclus?o de ?leo de soja (controle); dieta com inclus?o de 10% de ?leo de soja. O ensaio teve a dura??o de 82 dias, com a realiza??o de tr?s testes de esfor?o f?sico ao in?cio, 60? e 82? dia. Nesses testes foram avaliadas freq??ncia card?aca e temperatura corporal e coletadas amostras de sangue para an?lises hematol?gicas e bioqu?micas. A primeira coleta de dados ocorreu antes do teste, com os eq?inos em repouso e, imediatamente, 10, 20 e 120 minutos ap?s o t?rmino dos testes de esfor?o f?sico. Os valores m?dios dos par?metros fisiol?gicos, hematol?gicos e bioqu?micos foram submetidos ? an?lise n?o param?trica, a 5% de signific?ncia. Houve redu??o significativa no consumo de mat?ria seca das dietas com a inclus?o de ?leo de soja. O coeficiente de digestibilidade aparente do extrato et?reo aumentou (P<0,05) nas dietas hiperlipid?micas e o coeficiente de digestibilidade da celulose reduziu com a inclus?o de 19,5% de ?leo de soja. A digestibilidade dos demais nutrientes, exceto da prote?na bruta, a cin?tica da digesta no trato gastrointestinal e as caracter?sticas fecais n?o foram alteradas (P>0,05) pela inclus?o de ?leo nas dietas. Os eq?inos consumindo as dietas hiperlipid?micas apresentaram aumento (P<0,05) nos n?veis sang??neos de eritr?citos, hemoglobina e triglicer?dios e redu??o no volume corpuscular m?dio. N?o houve altera??o nos par?metros fisiol?gicos, hematol?gicos e bioqu?micos dos eq?inos alimentados com a dieta hiperlipid?mica ao longo do tempo de consumo das dietas e em fun??o dos testes de esfor?o f?sico. As dietas mostraram-se palat?veis e seguras, sem ocorr?ncia de casos de c?licas ou diarr?ias. O ?leo de soja pode ser utilizado nas dietas de eq?inos atletas visando suprir a demanda energ?tica e reduzir o consumo de mat?ria seca, desej?vel em eq?inos da modalidade esportiva Concurso Completo de Equita??o.
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Yang, Bo. "Mechanism of age-related cardiac dysfunction: Role of iNOS". Diss., The University of Arizona, 2003. http://hdl.handle.net/10150/289915.

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It is well documented that in the human free of pathological change, there is cardiac diastolic dysfunction with decreased reserved systolic function. Inducible nitric oxide synthase (iNOS) expressed in cardiac myocytes is related to heart failure of various etiologies. We hypothesized that the high levels of nitric oxide (NO) produced by iNOS over-expressed in the myocardium caused age-related cardiac dysfunction by affecting calcium cycling proteins. To test our hypothesis, first, we validated the volumetric measurement of the conductance catheter system (CCS) in mice. The heart function characterized by CCS decreased in aged mice (16-month-old, n = 9) compared to Young mice (6-month-old, n = 9). The left ventricular (LV) dysfunction in aged WT mice was reversed by iNOS specific inhibitors, aminoguanidine (AMG, 10 mg/Kg, i.v. or infusion, n = 15) and S-methyl-isothiourea (MITU, 3 mg/Kg, i.v. n = 7) separately and worsened by substrate L-arginine (10 mg/Kg, i.v. n = 7). All three drugs had no effects on young WT mice or old (16-month-old) iNOS knockout (KO) mice. Cardiac iNOS mRNA and protein expression were identified with northern blot, western blot and immunohistochemistry singularly in old WT mice and not in young WT mice. The NOx and cGMP levels were significantly higher only in the old WT mice (n = 6) compared to young WT mice and cGMP levels decreased to normal with AMG administration in the old WT mice. Northern blot showed the expression of ryanodine receptor, sarco/endoplasmic reticulum (SERCA 2a) did not change in the aging process. However western blots showed that total phospholamban (PLB), phosphorylated PLB (p < 0.05) and more importantly the ratio of phosphorylated PLB to total PLB significantly decreased in aged mice (p < 0.01). AMG (10 mg/kg bolus iv) significantly improved diastolic function only in the old WT mice with decreased tau and increased dP/dtmin, but had no effects on both young or old PLB knockout mice. Taken together, we concluded that iNOS overexpression was one of the mechanisms leading to age-related cardiac dysfunction by affecting phosphorylation of PLB via iNOS/NO/cGMP pathways and inhibition of iNOS could reverse the age-related cardiac dysfunction.
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Vakkala, née Mustonen M. (Merja). "Apoptosis in breast lesions". Doctoral thesis, University of Oulu, 2000. http://urn.fi/urn:isbn:9514256506.

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Abstract In this work the extent of apoptosis was studied in a set of 504 benign and malignant breast lesions to elucidate its role in breast tumor development and progression. Also the correlation of apoptosis with estrogen and progesterone receptor positivity, cell proliferation and patients' prognosis was studied. The breast lesions were also analyzed immunohistochemically with antibodies to apoptosis regulating proteins bcl-2 and bax, and caspases 3, 6 and 8. In addition, the immunohistochemical expression of NO• synthesizing enzyme iNOS in relation to apoptosis and angiogenesis was studied. Furthermore, the expression of the antioxidative enzyme MnSOD was studied in relation to apoptosis and cell proliferation. According to the results, the apoptotic index was lowest in benign breast lesions. It was higher in in situ carcinomas, where a gradual increase in the extent of apoptosis from grade I to III in situ carcinoma was seen. The apoptotic index in invasive carcinomas was higher than in in situ carcinomas, and also in invasive carcinomas there was a gradual increase in apoptosis from grade I to III carcinomas. The apoptotic index was highest in recurrent carcinomas. Strong bcl-2 expression was usually found in benign breast lesions but the immunoreactivity decreased in in situ and invasive carcinomas. There was a significant inverse association between bcl-2 immunoreactivity and the extent of apoptosis. Low bcl-2 immunoreactivity also associated with estrogen- or progesterone receptor negativity. In contrast, bax expression did not show any significant association with apoptosis, hormone receptors or the histologic types of tumors. Strong cytoplasmic caspase 3, 6 and 8 immunoreactivity was found in most carcinomas. It was weaker in in situ carcinomas and only weak immunoreactivity could be seen in benign breast lesions. There was a significant association between the extent of apoptosis and caspase immunoreactivity. iNOS expression was found in both tumor and stromal cells. iNOS expression in tumor cells was more frequently found in invasive than in in situ carcinomas. Its expression correlated significantly with a high apoptotic index and high vascularization of the lesion. There was significantly less MnSOD immunoreactivity in invasive breast carcinomas compared to in situ carcinomas or benign hyperplasias. MnSOD immunoreactivity did not associate with the extent of apoptosis, but there was a marginal inverse association between cell proliferation and MnSOD expression. Increased apoptosis was significantly associated with a high cell proliferation, and inversely associated with a positive estrogen status. A high apoptotic index (< 0.50%) was associated with a decreased survival of the patients. The results of this study show that apoptosis plays a decisive role in the development and progression of breast carcinoma. It is influenced not only by apoptosis regulating proteins, such as bcl-2 and caspases, but also by the estrogen receptor status. Apoptosis was also associated with iNOS positivity, the effect of which is mediated through increased NO• production. In line with the suggested role of MnSOD as a tumor suppressor gene, its expression was downregulated in invasive breast carcinoma. In conclusion, the association of apoptosis with patient survival in breast carcinoma may be secondary to its association with tumor cell proliferation and high tumor grade, not necessarily suggesting any causal association between apoptosis and survival.
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Arevalo, Iracema. "Cutaneous leishmaniasis : iNOS gene expression and a novel immunomodulatory therapy". Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31183.

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Nitric oxide (NO) has been shown to be lethal for a variety of intracellular pathogens including Leishmania. In murine models, the inducible nitric oxide synthase gene (iNOS) is expressed in activated macrophages and is involved in the synthesis of NO. Because the role of NO and iNOS in human leishmaniasis was less clear, we examined the expression of the iNOS gene in human macrophages infected with Leishmania in vitro and in biopsy tissue from subjects with cutaneous leishmaniasis.
Pentavalent antimony (Sb5+) in the form of Pentostam(TM) or Glucantime(TM) is still the treatment of choice despite its toxicity. Aldara(TM) (5% imiquimod) is an immune-response modifying agent that has been approved by the Food and Drug Administration in the USA for treating genital warts caused by papillomaviruses. We conducted an open-label, prospective study of combined Glucantime(TM) + Aldara(TM) therapy in subjects with CL who had previously failed a complete course of Glucantime(TM) treatment at regular doses. (Abstract shortened by UMI.)
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Vittur, Sebastian Bernhard Frederik [Verfasser]. "Kontraktion und Kompensation iNOS-überexprimierender Mauskardiomyozyten / Sebastian Bernhard Frederik Vittur". Gießen : Universitätsbibliothek, 2013. http://d-nb.info/1065394861/34.

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Książki na temat "INOS"

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Seyffarth, Gunter. The expression of iNOS and its control in human intrauterine tissues at term. Wolverhampton: University of Wolverhampton, 2001.

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Montejo, Ana María. Normativa contable para las obras sociales: Dec. PEN 1400/01, resoluciones de INOS, ANSSAL, SSSalud, y FACPCE. Buenos Aires: Ad-Hoc, 2004.

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Kasapinovic, Sonja. Evaluation of phenytoin and benzo[a]pyrene embryotoxicity using inducible nitric oxide synthase (iNOS) knockout mice in embryo culture. Ottawa: National Library of Canada, 2001.

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Pfister, Marcus. El pingüino Pedro. New York: Ediciones Norte-Sur, 1997.

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Pfister, Marcus. Pit il piccolo pinguino. Zurich, Switzerland: Nord-Sud, 1997.

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Meeting, International Neuro-ophthalmology Society. Highlights in neuro-ophthalmology: Proceedings of the Sixth Meeting of the International Neuro-ophthalmology Society (INOS), Hakone, Japan, 8-14 June, 1986. Redaktor Ishikawa Satoshi. Amsterdam, the Netherlands: Aeolus Press, 1987.

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P, Rome o. Emilio esta enfermo. Zaragoza: Edelvives, 2005.

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Penguin Pete. New York: North-South Books, 1997.

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Anne-Marie, Chapouton, red. Pit le petit pingouin. [Gossau Zürich, Suisse?]: Editions Nord-Sud, 1987.

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José, Moreno, red. El Pingüino Pedro. New York: Ediciones Norte-Sur, 1996.

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Części książek na temat "INOS"

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Fayet, Pierre. "“Inos” and “Sparticles”". W The Superworld I, 129–75. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-1318-2_5.

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Manning, Pamela T., Janice M. Thompson i Mark G. Currie. "Selective iNOS Inhibitors". W New Drugs for Asthma, Allergy and COPD, 156–59. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000062144.

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Qidwai, Tabish. "iNOS Genetic Polymorphisms". W Exploration of Host Genetic Factors associated with Malaria, 101–12. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4761-8_9.

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Boltz, Marie, Holly Rau, Paula Williams, Holly Rau, Paula Williams, Jane Upton, Jos A. Bosch i in. "Inducible Nitric Oxide Synthase (iNOS)". W Encyclopedia of Behavioral Medicine, 1058. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_100884.

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Buttery, Lee D. K., i Julia M. Polak. "iNOS and COX-2 in atherosclerosis". W Inducible Enzymes in the Inflammatory Response, 109–24. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8747-2_5.

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Ekmekcioglu, Suhendan, i Elizabeth A. Grimm. "Prognostic Significance of iNOS in Human Melanoma". W Nitric Oxide (NO) and Cancer, 293–307. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1432-3_16.

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Pascale, Rosa M., M. Frau i Francesco Feo. "Prognostic Significance of iNOS in Hepatocellular Carcinoma". W Nitric Oxide (NO) and Cancer, 309–28. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1432-3_17.

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Matsumoto, Manabu, Yuji Ohtsuki i Mutsuo Furihata. "Prognostic Significance of iNOS in Esophageal Cancer". W Nitric Oxide (NO) and Cancer, 329–40. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1432-3_18.

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Song, D. J., i R. Ruffini. "Determination of “Inos” Masses Composing Galactic Halos". W Observational Cosmology, 723–26. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3853-3_85.

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Zhou, P., i C. Iadecola. "iNOS and COX‐2 in Ischemic Stroke". W Handbook of Neurochemistry and Molecular Neurobiology, 33–45. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-30383-3_3.

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Streszczenia konferencji na temat "INOS"

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Amoroso, Rosa. "Selective inhibition of the iNOS by acetamidine derivatives". W 7th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecmc2021-11491.

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Salim, Taha, i Elebeoba E. May. "In silico Kinetic Model of iNOS expression in macrophages". W 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6943801.

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Cortez e Castro, M., J. Ferreira, A. Matos i M. Bicho. "Endothelial dysfunction in asthma: enos, inos and ace polymorphisms". W ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.45.

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Callahan, LA, XH Song, LL Wang i GS Supinski. "Hyperglycemia-Induced Diaphragm Weakness Is Prevented by iNOS Inhibition." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6130.

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Marques, RH, CM Starling, FG Reis, R. Almeida-Reis, C. Cabido, RF Mizutani, EA Leick-Maldonado i in. "Repeated Physical Stress Increases Distal Lung Collagen Remodeling, Eosinophilic Inflammation and iNOS Activation Induced by Chronic Pulmonary Inflammation: Effects of iNOS Inhibition." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5622.

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Ibrahim, Mohammed M., Amy V. Paschall, Priscilla S. Redd i Kebin Liu. "Abstract LB-265: IRF8 is an essential transcriptional activator of iNOS although MDSCs up-regulate iNOS expression via an IRF8-independent mechanism". 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-lb-265.

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Tyryshkin, A., FM Gorgun, T. Mazumdar, S. Zeng i NT Eissa. "Src-Mediated Regulation of iNOS in Primary Airway Epithelial Cells." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4181.

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Song, W., G. Liu, C. Bosworth, WM Sullender, E. Abraham i S. Matalon. "Respiratory Syncytial Virus Inhibits Epithelial Na+Currents by Upregulating iNOS." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4946.

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Tufvesson, Ellen, Cecilia Andersson, Julie Weidner, Jonas Erjefält i Leif Bjermer. "iNOS expression is increased in peripheral airways of asthmatic patients". W Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa605.

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Kuo, Paul C. "OSTEOPONTIN IS AN NO-DEPENDENT TRANSREPRESSOR OF INOS GENE TRANSCRIPTION". W 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.243.

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Raporty organizacyjne na temat "INOS"

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Nosho, B. Z., B. R. Bennett, L. J. Whitman i M. Goldenberg. Spontaneous Growth of an InAs Nanowire Lattice in an InAs/GaSb Superlattice. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2002. http://dx.doi.org/10.21236/ada447719.

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Darby, Michael, John Haltiwanger i Mark Plant. The Ins and Outs of Unemployment: The Ins Win. Cambridge, MA: National Bureau of Economic Research, sierpień 1986. http://dx.doi.org/10.3386/w1997.

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Schultz, Peter Andrew. Simple intrinsic defects in InAs :. Office of Scientific and Technical Information (OSTI), marzec 2013. http://dx.doi.org/10.2172/1095951.

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Ives, L. K., M. Peterson, A. W. Ruff, J. S. Harris i P. A. Boyer. Wear due to printing inks. Gaithersburg, MD: National Bureau of Standards, 1987. http://dx.doi.org/10.6028/nbs.ir.87-3574.

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Ikossi, Kiki. InAs Device Process Development and Characterization. Fort Belvoir, VA: Defense Technical Information Center, maj 2003. http://dx.doi.org/10.21236/ada413747.

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Biaggne, Austin Robert, Michael D. McMurtrey, Joseph Louis Bass i Larry K. Aagesen Jr. Modeling Sintering Processes of Nanoparticle Inks. Office of Scientific and Technical Information (OSTI), sierpień 2019. http://dx.doi.org/10.2172/1546728.

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Santori, Charles, David Fattal, Jelena Vuckovic, Glenn S. Solomon i Yoshihisa Yamamoto. Single-Photon Generation With InAs Quantum Dots. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2004. http://dx.doi.org/10.21236/ada426389.

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Blair, William R. Chromatographic examination of Intaglio inks, resins and varnishes. Gaithersburg, MD: National Institute of Standards and Technology, 1991. http://dx.doi.org/10.6028/nist.ir.4949.

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Chandrasekaran, S., M. Worsley i A. Meike. 3D-Printable Inks for Energy and Environmental Applications. Office of Scientific and Technical Information (OSTI), grudzień 2021. http://dx.doi.org/10.2172/1836936.

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Megersa, Kelbesa. Strengths and Weaknesses of INGOs in Delivering Development Outcomes. Institute of Development Studies, czerwiec 2022. http://dx.doi.org/10.19088/k4d.2022.090.

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Compared to smaller or local NGOs, international non-governmental organisations (INGOs) have more influence or “voice” with decision-makers, funding agencies, and policymakers. As a result, INGOs are often better positioned to impact both domestic and international policy (Kreienkamp, 2017; Cooper, 2018; Morton, n.d.).This rapid review therefore seeks to find out the strengths and weaknesses of INGOs in delivering development and other outcomes?INGOs offer local CSOs valuable capacity-building opportunities as well as exposure to a broader range of expertise and development approaches. Many local CSOs see INGOs as a well-established and important part of the development industry. They collaborate with INGOs on funding or partnership arrangements, as well as non-funding collaborative approaches like knowledge and practice networks, or policy dialogue with governments, donors, or the private sector (Morton, n.d.; Jayawickrama and McCullagh, 2009; Green, 2015). Nonetheless, despite the unique contributions made by INGOs (and their peculiar characteristics that enable them to do so), these organisations have limitations that prevent them from reaching their full potential (Green, 2017; Jayawickrama and McCullagh, 2009; Cooper, 2018; Altahir, 2013).These include accountability,difficult working environment and coordination challenges among others explained in this report.Although this rapid evidence review has identified some key strengths and weaknesses of INGOs (i.e., in relation to their development or humanitarian work), many of the important findings are linked to a few relevant reports. Overall, there is a limited evidence base on the topic – since the literature rarely provides systematic and explicit documentation of the strengths/weaknesses of INGOs. Nonetheless, there is a voluminous literature (mostly project reports) on the works of individual INGOs.
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