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Artykuły w czasopismach na temat „NOS2A”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 20 lutego 2023

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1

Lepiller, Sandrine, Nathalie Franche, Eric Solary, Johanna Chluba i Véronique Laurens. "Comparative analysis of zebrafish nos2a and nos2b genes". Gene 445, nr 1-2 (wrzesień 2009): 58–65. http://dx.doi.org/10.1016/j.gene.2009.05.016.

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Bloch, Kenneth D., Johanna R. Wolfram, Donna M. Brown, Jesse D. Roberts, David G. Zapol, John J. Lepore, Galina Filippov, Jeffrey E. Thomas, Howard J. Jacob i Donald B. Bloch. "Three Members of the Nitric Oxide Synthase II Gene Family (NOS2A, NOS2B, and NOS2C) Colocalize to Human Chromosome 17". Genomics 27, nr 3 (czerwiec 1995): 526–30. http://dx.doi.org/10.1006/geno.1995.1086.

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3

Chai, Jun, Qinglu Wang, Bo Qin, Shengkui Wang, Youtao Wang, Muhammad Shahid, Kai Liu, Yifang Zhang i Weijie Qu. "Association of NOS2A gene polymorphisms with susceptibility to bovine tuberculosis in Chinese Holstein cattle". PLOS ONE 16, nr 6 (17.06.2021): e0253339. http://dx.doi.org/10.1371/journal.pone.0253339.

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Bovine tuberculosis (bTB) is a global zoonotic disease that has detrimental economic impacts worldwide. The NOS2A gene plays a key role in immunological control of many infectious diseases. However, research on the association between NOS2A polymorphisms and bTB infection in Holstein cattle reared on the Yunnan-Guizhou plateau of China is scarce. This study investigated a possible linkage between NOS2A polymorphisms and risk of developing bTB in Chinese Holstein cattle. The NOS2A gene was genotyped in 144 bTB-infected Holstein cows and 139 healthy controls were genotyped through nucleotide sequencing. Ten single-nucleotide polymorphisms (SNPs) were detected, six of which were associated with susceptibility/resistance patterns of bTB. Furthermore, the C/T genotypes of 671 and 2793, and T/T genotype of E22 (+15) were significantly associated with susceptibility risk; the G/A genotype of 2857, T/T genotype of E9 (+65), and C/C genotype of E9 (+114) probably increased resistance to bTB. In addition, the haplotypes of NOS2A-2 and NOS2A-9 were risk factors for bTB susceptibility, while the NOS2A-5 and NOS2A-8 haplotypes were contributing protective variants against tuberculosis. There is a significant association between variation in SNPs of NOS2A and tuberculosis susceptibility/resistance pattern. These findings suggest that substitution of genetic selection would be helpful for eradicating bTB. However, further investigation is required to study the underlying mechanism through which NOS2A polymorphisms affect bTB infection.

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4

Tsutsumi, Seiji, Xi Zhang, Keiko Takata, Kazuhiro Takahashi, Richard H. Karas, Hirohisa Kurachi i Michael E. Mendelsohn. "Differential regulation of the inducible nitric oxide synthase gene by estrogen receptors 1 and 2". Journal of Endocrinology 199, nr 2 (27.08.2008): 267–73. http://dx.doi.org/10.1677/joe-07-0292.

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Estrogen has both rapid and longer term direct effects on cardiovascular tissues mediated by the two estrogen receptors, ESR1 and ESR2. Previous work identified that estrogen regulates the expression of inducible nitric oxide synthase (NOS2A) in vascular smooth muscle cells (VSMC). ESR2 knockout mice have vascular dysfunction due to dysregulation of NOS2A expression and these mice are hypertensive (Zhu et al. Science 2002 295 505–508). Here, we report studies to examine the differential regulation of NOS2A gene expression by ESR1 and 2. Immunoblotting and RT-PCR studies revealed that different VSMC lines expressed different levels of ESR1 and ESR2 protein and mRNA. VSMC from different vascular beds were studied, including aortic VSMC expressing ESR1 and radial (Rad) VSMC expressing ESR2. E2 inhibited NO production and NOS2A protein expression in aortic VSMC. Human NOS2A promoter–reporter studies revealed suppression of NOS2A reporter activity by E2 in aortic VSMC, and stimulation of NOS2A reporter activity by E2 in Rad arterial VSMC. In heterologous expression studies of COS-7 cells lacking endogenous ER, E2 treatment of COS-7 cells did not alter NOS2A reporter activity in the presence of ESR1, while reporter activity increased 2.3-fold in the presence of ESR2. Similar experiments in COS-7 cells using the selective estrogen receptor modulator raloxifene showed that raloxifene caused a reduction in NOS2A reporter activity with ESR1 coexpression and an increase with ESR2 coexpression. Rat VSMC expressing ESR2 but not ESR1 also showed increased NOS2A reporter activity with E2 treatment, an effect lost when ESR1 was introduced into the cells. Taken together, these data support that hNOS2A transcription is regulated positively by ESR2 and negatively by ESR1 in VSMC, supporting differential actions of these two estrogen receptors on a physiologically relevant gene in VSMC.

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5

Gogna, Rajan, Esha Madan i Periannan Kuppusamy. "RPA-Dependent Melting of Triplex DNA at NOS2a Gene Promoter is Indispensible for p53-Mediated NOS2a Synthesis and Cardioprotection". Free Radical Biology and Medicine 53 (listopad 2012): S168. http://dx.doi.org/10.1016/j.freeradbiomed.2012.10.460.

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6

Batozhargalova, B. Ts, Yu L. Mizernitsky, S. E. Dyakova, N. V. Petrova i R. A. Zinchenko. "Clinical and genetic associations of NO-synthase and arginase gene polymorphisms and gene-gene interactions in children with bronchial asthma". Voprosy praktičeskoj pediatrii 15, nr 5 (2020): 7–17. http://dx.doi.org/10.20953/1817-7646-2020-5-7-17.

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Objective. To analyze the association between NOS1, NOS2, NOS3, ARG1, and ARG2 gene polymorphisms and clinical, laboratory, and functional characteristics of bronchial asthma (BA) in children by evaluating gene-gene interactions. Patients and methods. We have evaluated the associations between the NOSs and ARG genes and gene-gene interactions in 107 children with BA. We performed comparative genetic analysis of associations between polymorphic variants of candidate genes in 107 BA patients and clinical manifestations of the disease, laboratory, and functional parameters. Results. We have found an association between the short (S) allele and SS genotype of the NOS1 (AAT)n gene and early disease onset (<5 years), severe BA, and antiinflammatory targeted therapy (with omalizumab and combination inhaled corticosteroids with long-acting β2-agonists). We have also revealed an association between the short (S) allele and SS genotype of the NOS1 (AAT)n gene, as well as long (L) alleles and LL genotypes of the NOS2A (CCTTT)n gene in BA patients and elevated FeNO levels in the exhaled air. The following association have also been identified: between alleles and genotypes containing long (L) tandem repeats in the NOS2A (CCTTT)n gene and reduced FEV1; between AG genotype of the ARG2 gene (rs3742879), alleles and genotypes containing long tandem repeats (L) of the NOS2А (CCTTT)n gene and reduced FEV1/ FVC; between alleles and genotypes containing long tandem repeats (L), combinations of genotypes SL+LL of the NOS2А (CCTTT)n and impaired patency at the level of the middle bronchi FEF50; between allele G, heterozygous genotype AG of the ARG2 (rs3742879) gene with impaired patency at the level of peripheral bronchi FEF75. Conclusion. Our analysis of gene-gene interactions has demonstrated phenotypic characteristics of BA: early BA onset, severe BA, decreased FEV1 and FEF50, increased NO concentration in exhaled air, and presence of fungal and epidermal sensitization. Key words: children, bronchial asthma, NOS and ARG gene polymorphisms, gene-gene interactions

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7

De Luca, Chiara, Agnese Gugliandolo, Carlo Calabrò, Monica Currò, Riccardo Ientile, Desanka Raskovic, Ludmila Korkina i Daniela Caccamo. "Role of Polymorphisms of Inducible Nitric Oxide Synthase and Endothelial Nitric Oxide Synthase in Idiopathic Environmental Intolerances". Mediators of Inflammation 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/245308.

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Oxidative stress and inflammation play a pathogenetic role in idiopathic environmental intolerances (IEI), namely, multiple chemical sensitivity (MCS), fibromyalgia (FM), and chronic fatigue syndrome (CFS). Given the reported association of nitric oxide synthase (NOS) gene polymorphisms with inflammatory disorders, we aimed to investigate the distribution of NOS2A −2.5 kb (CCTTT)nas well as Ser608Leu and NOS3 −786T>C variants and their correlation with nitrite/nitrate levels, in a study cohort including 170 MCS, 108 suspected MCS (SMCS), 89 FM/CFS, and 196 healthy subjects. Patients and controls had similar distributions of NOS2A Ser608Leu and NOS3 −786T>C polymorphisms. Interestingly, the NOS3 −786TT genotype was associated with increased nitrite/nitrate levels only in IEI patients. We also found that the NOS2A −2.5 kb (CCTTT)11allele represents a genetic determinant for FM/CFS, and the (CCTTT)16allele discriminates MCS from SMCS patients. Instead, the (CCTTT)8allele reduces by three-, six-, and tenfold, respectively, the risk for MCS, SMCS, and FM/CFS. Moreover, a short number of (CCTTT) repeats is associated with higher concentrations of nitrites/nitrates. Here, we first demonstrate that NOS3 −786T>C variant affects nitrite/nitrate levels in IEI patients and that screening for NOS2A −2.5 kb (CCTTT)npolymorphism may be useful for differential diagnosis of various IEI.

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8

Varadé, Jezabel, José Ramón Lamas, Miguel Fernández-Arquero, Juan Ángel Jover, Emilio G. de la Concha, Alfonso Martínez, Benjamín Fernández-Gutierrez i Elena Urcelay. "NO role of NOS2A susceptibility polymorphisms in rheumatoid arthritis". Nitric Oxide 21, nr 3-4 (grudzień 2009): 171–74. http://dx.doi.org/10.1016/j.niox.2009.07.005.

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9

Xu, Weiming, Steve Humphries, Masafumi Tomita, Toshiko Okuyama, Michihiro Matsuki, David Burgner, Dominic Kwiatkowski, Lizhi Liu i Ian G. Charles. "Survey of the Allelic Frequency of a NOS2A Promoter Microsatellite in Human Populations: Assessment of the NOS2A Gene and Predisposition to Infectious Disease". Nitric Oxide 4, nr 4 (sierpień 2000): 379–83. http://dx.doi.org/10.1006/niox.2000.0290.

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10

Schulte, C., M. Sharma, J. C. Mueller, P. Lichtner, J. Prestel, D. Berg i T. Gasser. "Comprehensive association analysis of the NOS2A gene with Parkinson disease". Neurology 67, nr 11 (11.12.2006): 2080–82. http://dx.doi.org/10.1212/01.wnl.0000247672.41736.bd.

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11

Catana, Andreea, Alma Maniu, Doinel Radeanu, Radu A. Popp, Roxana F. Ilies i Iuliu V. Catana. "Possible association between -954G/C iNOS polymorphism in nasal polyposis. A case-control study in a population group of Northern Romania". Romanian Journal of Rhinology 6, nr 24 (1.12.2016): 197–201. http://dx.doi.org/10.1515/rjr-2016-0023.

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Abstract BACKGROUND. Polymorphisms for genes encoding chemosensitive signalling proteins like NOS2 might contribute to the variability in individual susceptibility to nasal polyposis. NO produced by the inducible NO synthase enzyme NOS2A is generated at high levels in certain types of inflammation, so that the role of NOS2 might also be important in nasal polyposis etiopathogeny. MATERIAL AND METHODS. This is a cross-sectional, randomized, case-control study for the evaluation of the frequency of -954G/C NOS2A2 alleles among patients with nasal polyposis. The study included 91 cases of nasal polyposis diagnosed patients (nasal endoscopy and CT scan examination), and 117 healthy unrelated controls. NOS2 genotyping was carried out using PCR amplification of relevant gene fragment and it was followed by restriction enzyme digestion. Detection of the variant alleles was determined through analysis of resulting restriction fragment length polymorphism (RFLP) followed by gel electrophoresis. RESULTS. Molecular analysis revealed an increased frequency of NOS2 variant allele in the study group compared to the control group (p=0.019, OR=1.991, CI=1.08-3.67). A statistically significant finding was highlighted among allergic and nonallergic patients with nasal polyposis (p=0.046, OR=0.449. CI=0.208-0.969) and a relationship between nasal polyposis patients with asthma and non-asthmatic patients (p=0.119, OR=1.825, CI=0.875-3.80). CONCLUSION. The main finding of our study is that -954G/C polymorphism of NOS gene seems to be associated with an increased risk for nasal polyposis.

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12

Bugeja, Matthew J., David R. Booth, Bruce H. Bennetts, Robert N. S. Heard, David Burgner i Graeme J. Stewart. "An investigation of NOS2A promoter polymorphisms in Australian multiple sclerosis patients". European Journal of Human Genetics 13, nr 7 (27.04.2005): 815–22. http://dx.doi.org/10.1038/sj.ejhg.5201422.

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13

Manna, Ida, Maria Liguori, Paola Valentino, Francesca Condino, Antonella La Russa, Alessandra Clodomiro, Rita Nisticò, Gemma Di Palma i Aldo Quattrone. "Preliminary evidences of a NOS2A protective effect from Relapsing–Remitting Multiple Sclerosis". Journal of the Neurological Sciences 264, nr 1-2 (styczeń 2008): 112–17. http://dx.doi.org/10.1016/j.jns.2007.08.007.

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14

Blanco, Yolanda, Jordi Yag�e, Francesc Graus i Albert Saiz. "No association of inducible nitric oxide synthase gene ( NOS2A ) to multiple sclerosis". Journal of Neurology 250, nr 5 (1.05.2003): 598–600. http://dx.doi.org/10.1007/s00415-003-1047-7.

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15

Velez, Digna Rosa, William F. Hulme, Jamie L. Myers, J. Brice Weinberg, Marc C. Levesque, Martin E. Stryjewski, Eduardo Abbate i in. "NOS2A, TLR4, and IFNGR1 interactions influence pulmonary tuberculosis susceptibility in African-Americans". Human Genetics 126, nr 5 (3.07.2009): 643–53. http://dx.doi.org/10.1007/s00439-009-0713-y.

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16

Bohanec Grabar, Petra, Dušan Logar, Matija Tomšič, Blaž Rozman i Vita Dolžan. "Genetic Polymorphisms Modifying Oxidative Stress Are Associated with Disease Activity in Rheumatoid Arthritis Patients". Disease Markers 26, nr 1 (2009): 41–48. http://dx.doi.org/10.1155/2009/147356.

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Reactive oxygen and nitrogen species are involved in the pathology of rheumatoid arthritis (RA). Polymorphisms in genes coding for superoxide dismutases (SOD2 and SOD3), catalase (CAT), tumor necrosis factor-alpha (TNFA) and inducible NO synthase (NOS2A) may influence RA activity. We determined SOD2 Ala-9Val, SOD3 Arg213Gly, CAT C-262T, TNFA G-308A, TNFA C-857T and NOS2A (CCTTT)npolymorphisms in 327 RA patients. Carriers of CAT -262T and TNFA -308A allele had lower mean disease activity score of 28 joint count (DAS28) values than patients with CAT -262CC and TNFA -308GG genotypes (p= 0.014 andp= 0.046, respectively). Patients with the combination of CAT -262T and TNFA -308A allele had lower mean DAS28 values and a higher probability for low disease activity than non-carriers (p= 0.003, OR = 3.585, 95% CI = 1.538–8.357). Our results suggest that CAT and TNFA polymorphisms alone and in combination influence the activity of RA.

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17

Tyugaeva, E. A., V. I. Korchagin, K. O. Mironov i A. E. Platonov. "Genetic Factors in Individual Predisposition toward Hemorrhagic Fever with Renal Syndrome". Epidemiology and Vaccinal Prevention 18, nr 2 (1.05.2019): 113–22. http://dx.doi.org/10.31631/2073-3046-2019-18-2-113-122.

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Hemorrhagic fever with renal syndrome (HFRS) is a zoonotic infection disease caused by Orthohantavirus which belongs to Hantaviridae family. This article is a brief review of recent data about genetic factors which play a role in individual predisposition toward HFRS. There are reports discovered associations of polymorphic sites with HFRS severity and risk complications. Polymorphic sites in genes which code proteins of immune (МНС, TNF, IL1) and endothelial (VE-cadherin) systems, blood coagulation (SERPINE1, ITGA2B, NOS) and detoxification (CYP1A1, GSTP1) systems and their links with disease are described in this article. HLA haplotypes B*08-DRB1*03 and B*46-DRB1*09, B*51-DRB1*09 are associated with severe forms of HFRS-PUUV and HFRS-HTNV respectively. TNF A-allele and AA-genotype in -308G>A SNP (rs1800629), CDH5 ТТ-genotype in 1550T>C SNP, SERPINE1 G-allele in -844A>G SNP (rs2227631), alleles HPA3 b, NOS2A*11 and NOS2A*11/NOS2A*12-genotype, CYP1A1 1А2С-genotype in SNP (rs1048943) and GSTP AG-genotype in SNP (rs1695) demonstrated associations with severe HFRS. Differences in the expression levels of GATA3, T-BET, CD3, IFNβ, NFkB, STAT1 and MxA genes in cell cultures stimulated by hantavirus. Expression of GATA3 was significantly higher in cell cultures of patients with severe HFRS than with a mild form. In contrast, MxA gene expression was up-regulated in cell cultures of patients with mild HFRS-PUUV. Considering individual genetic factors of HFRS patients would allow defining the best tactic of therapy and prophylaxis in this way. And as a result of applying this treatment in the clinical practice decrease of unfavorable disease outcome would occur.

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18

Barcellos, L. F., P. P. Ramsay, S. J. Caillier, S. Sawcer, J. Haines, S. Schmidt, M. Pericak-Vance i in. "Genetic variation in nitric oxide synthase 2A (NOS2A) and risk for multiple sclerosis". Genes & Immunity 9, nr 6 (26.06.2008): 493–500. http://dx.doi.org/10.1038/gene.2008.41.

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19

Jena, Mamata, Amit Kumar Srivastava, Rajnish Kumar Singh, Prithvi Raj Sharma, P. K. Das i Rameshwar N. K. Bamezai. "NOS2A promoter (CCTTT)n association with TB lacks independent functional correlation amongst Indians". Tuberculosis 94, nr 1 (styczeń 2014): 81–86. http://dx.doi.org/10.1016/j.tube.2013.10.004.

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AlFadhli, Suad, Eiman M. A. Mohammed i Asmahan Al Shubaili. "Association analysis of nitric oxide synthases: NOS1, NOS2A and NOS3 genes, with multiple sclerosis". Annals of Human Biology 40, nr 4 (lipiec 2013): 368–75. http://dx.doi.org/10.3109/03014460.2013.786756.

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21

Mineharu, Youhei, Kayoko Inoue, Sumiko Inoue, Shigeki Yamada, Kazuhiko Nozaki, Katsunobu Takenaka, Nobuo Hashimoto i Akio Koizumi. "Association Analysis of Common Variants of ELN, NOS2A, APOE and ACE2 to Intracranial Aneurysm". Stroke 37, nr 5 (maj 2006): 1189–94. http://dx.doi.org/10.1161/01.str.0000217408.91389.4d.

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Xu, Weiming, Lizhi Liu, Piers Emson, Charles R. Harrington, Ian G. McKeith, Robert H. Perry, Christopher M. Morris i Ian G. Charles. "The CCTTT polymorphism in the NOS2A gene is associated with dementia with Lewy bodies". NeuroReport 11, nr 2 (luty 2000): 297–99. http://dx.doi.org/10.1097/00001756-200002070-00015.

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23

Burgner, D., K. Rockett, H. Ackerman, J. Hull, S. Usen, M. Pinder i D. P. Kwiatkowski. "Haplotypic relationship between SNP and microsatellite markers at the NOS2A locus in two populations". Genes & Immunity 4, nr 7 (październik 2003): 506–14. http://dx.doi.org/10.1038/sj.gene.6364022.

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24

Martín, M. Carmen, Alfonso Martinez, J. Luis Mendoza, Carlos Taxonera, Manuel Díaz-Rubio, Miguel Fernández-Arquero, Emilio G. de la Concha i Elena Urcelay. "Influence of the inducible nitric oxide synthase gene (NOS2A) on inflammatory bowel disease susceptibility". Immunogenetics 59, nr 11 (23.10.2007): 833–37. http://dx.doi.org/10.1007/s00251-007-0255-1.

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25

Sjöstrand, C., H. Modin, T. Masterman, K. Ekbom, E. Waldenlind i J. Hillert. "Analysis of Nitric Oxide Synthase Genes in Cluster Headache". Cephalalgia 22, nr 9 (listopad 2002): 758–64. http://dx.doi.org/10.1046/j.1468-2982.2002.00452.x.

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The aetiology of cluster headache is still not yet completely understood, but the potential relevance of genetic factors has been recognized during recent years. Nitric oxide (NO) plays a critical role in the regulation of vasodilation, neurotransmission, inflammation and many other events throughout the body. NO also appears to be an important mediator of vascular headache pathophysiology. In this study we have performed an association analysis of five polymorphic micro-satellite markers in the three different NO synthase (NOS) genes; nNOS (NOS1), iNOS (NOS2A) and eNOS (NOS3). Ninety-one cluster headache patients diagnosed according to International Headache Society criteria and 111 matched controls were studied. Phenotype and allele frequencies were similarly distributed in patients and controls except for an iNOS (NOS2A) pentanucleotide repeat allele which was significantly more common in controls. We observed a higher phenotype frequency of this allele in our control group compared with rates in control groups of other studies, whereas the frequency in our patients was similar to that in controls from previous reports. Thus, we conclude that it is unlikely that genetic variations within the NOS genes contribute greatly to cluster headache susceptibility.

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26

Gerashchenko, G. V., O. V. Grygoruk, O. A. Kononenko, O. P. Gryzodub, E. O. Stakhovsky i V. I. Kashuba. "EXPRESSION PATTERN OF GENES ASSOCIATED WITH TUMOR MICROENVIRONMENT IN PROSTATE CANCER". Experimental Oncology 40, nr 4 (22.12.2018): 315–22. http://dx.doi.org/10.31768/2312-8852.2018.40(4):315-322.

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Aim: To assess relative expression (RE) levels of CAF-, TAM-specific, immune defense-associated genes in prostate tumors and to show correlation of RE with clinical, pathological and molecular characteristics, with the aim to define clinically significant specific alterations in a gene expression pattern. Methods: RE of 23 genes was analyzed by a quantitative polymerase chain reaction in 37 freshly frozen samples of prostate cancer tissues of a different Gleason score (GS) and at various tumor stages, compared with RE in 37 paired conventionally normal prostate tissue (CNT) samples and 20 samples of prostate adenomas. Results: Differences in RE were shown for 11 genes out of 23 studied, when tumor samples were compared with corresponding CNTs. 7 genes, namely ACTA2, CXCL14, CTGF, THY1, FAP, CD163, CCL17 were upregulated in tumors. 4 genes, namely CCR4, NOS2A, MSMB, IL1R1 were downregulated in tumors. 14 genes demonstrated different RE in TNA at different stages: CXCL12, CXCL14, CTGF, FAP, HIF1A, THY1, CCL17, CCL22, CCR4, CD68, CD163, NOS2A, CTLA4, IL1R1. RE changes of 9 genes — CXCL12, CXCL14, HIF1A, CCR4, CCL17, NOS2A, CTLA4, IL1R1, IL2RA — were found in tumors with different GS. Moreover, 9 genes showed differences in RE in TNA, dependently on the presence or absence of the TMPRSS2/ERG fusion and 7 genes showed differences in RE of groups with differential PTEN expression. Significant correlations were calculated between RE of 9 genes in adenocarcinomas and the stage, and GS; also, between RE of 2 genes and the fusion presence; and between RE of 4 genes and PTEN expression. Conclusions: Several gene expression patterns were identified that correlated with the GS, stage and molecular characteristics of tumors, i.e. presence of the TMPRSS2/ERG fusion and alterations in PTEN expression. These expression patterns can be used for molecular profiling of prostate tumors, with the aim to develop personalized medicine approaches. However, the proposed profiling requires a more detailed analysis and a larger cohort of patients with prostate tumor.

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Highet, A., S. Thompson, D. Furness, V. Zhang, G. Dekker i C. Roberts. "114. HYPERTENSIVE DISORDERS OF PREGNANCY ARE ASSOCIATED WITH IMMUNOREGULATORY GENE POLYMORPHISMS". Reproduction, Fertility and Development 22, nr 9 (2010): 32. http://dx.doi.org/10.1071/srb10abs114.

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Pregnancy is a controlled state of inflammation. Deregulation of cytokine networks can lead to adverse pregnancy outcomes including preeclampsia (PE). We aimed to identify single nucleotide polymorphisms in immunoregulatory genes that signify an increased risk of the gestational hypertensive disorders PE and gestational hypertension (GH). 1169 nulliparous pregnant women and their partners were recruited prospectively for the Adelaide SCOPE study. PE and GH were classified using strict guidelines. Uncomplicated pregnancies served as controls. Peripheral blood from couples and cord blood from neonates were collected. DNA was extracted and genotyped for Interleukin (IL)-6 rs1800795, IL-4 rs2243250, IL-10 rs1800896 and rs1800871, mannose binding lectin (MBL) rs1800450, transforming growth factor beta 1 (TGFβ-1) rs1800469 and cyclooxygenase (COX)-2 rs20417 & rs5275 and inducible nitric oxide synthase (NOS2A) rs1137933 using the Sequenom MassARRAY system. Genotypes for Caucasian PE (n = 75) and GH (n = 102) were compared with controls (n = 422) and analysed using Chi-Square. In neonates IL-6 G allele carriage was associated with PE (P = 0.011, OR=2.0, 95% CI = 1.2–3.7) and the CC genotype associated with GH (P = 0.002). Neonatal IL-10 RS180071 AA genotype associated with PE (P = 0.041) and IL-10 RS1800896 AA associated with GH (P = 0.022). Paternal NOS2A C allele was more frequent in PE (P = 0.03, OR = 2.1, 95% CI = 1.1–4.5), and maternal NOS2A CC more frequent in GH (P = 0.018). Increased neonatal carriage of MBL rs1800450 AA+GA genotypes associated with GH (P = 0.03, OR = 2.2, 95% CI = 1.1–4.5). No associations were observed between TGFβ-1 or COX2 genotypes and PE or GH. Associations between neonatal IL-6 G, which confers high placental IL-6 expression, and PE suggest a possible mechanism by which PE is a pro-inflammatory exacerbation of placental origin. Since placental IL-10 is important for maternal tolerance of the fetus, genotypes predisposing to low IL-10 expression in the neonate which associate with both PE and GH, suggest a role for decreased placental IL-10 in these disorders.

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Zakaria, Nur Atikah, Md Asiful Islam, Wan Zaidah Abdullah, Rosnah Bahar, Abdul Aziz Mohamed Yusoff, Ridhwan Abdul Wahab, Shaharum Shamsuddin i Muhammad Farid Johan. "Epigenetic Insights and Potential Modifiers as Therapeutic Targets in β–Thalassemia". Biomolecules 11, nr 5 (18.05.2021): 755. http://dx.doi.org/10.3390/biom11050755.

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Thalassemia, an inherited quantitative globin disorder, consists of two types, α– and β–thalassemia. β–thalassemia is a heterogeneous disease that can be asymptomatic, mild, or even severe. Considerable research has focused on investigating its underlying etiology. These studies found that DNA hypomethylation in the β–globin gene cluster is significantly related to fetal hemoglobin (HbF) elevation. Histone modification reactivates γ-globin gene expression in adults and increases β–globin expression. Down-regulation of γ–globin suppressor genes, i.e., BCL11A, KLF1, HBG-XMN1, HBS1L-MYB, and SOX6, elevates the HbF level. β–thalassemia severity is predictable through FLT1, ARG2, NOS2A, and MAP3K5 gene expression. NOS2A and MAP3K5 may predict the β–thalassemia patient’s response to hydroxyurea, a HbF-inducing drug. The transcription factors NRF2 and BACH1 work with antioxidant enzymes, i.e., PRDX1, PRDX2, TRX1, and SOD1, to protect erythrocytes from oxidative damage, thus increasing their lifespan. A single β–thalassemia-causing mutation can result in different phenotypes, and these are predictable by IGSF4 and LARP2 methylation as well as long non-coding RNA expression levels. Finally, the coinheritance of β–thalassemia with α–thalassemia ameliorates the β–thalassemia clinical presentation. In conclusion, the management of β–thalassemia is currently limited to genetic and epigenetic approaches, and numerous factors should be further explored in the future.

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Batozhargalova, B. T., S. E. Diakova, N. V. Petrova, Yu L. Mizernitsky i R. A. Zinchenko. "Association of polymorphisms of NO synthases and arginase genes, clinical, laboratory and functional indicators with the level of nitrogen oxide in exhaled air in children with bronchial asthma". Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 64, nr 5 (16.11.2019): 55–68. http://dx.doi.org/10.21508/1027-4065-2019-64-5-55-68.

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The article presents the results of a study of the associations of NO synthase and arginase genes in children with bronchial asthma with clinical, laboratory and functional parameters depending on the level of nitrogen oxide in exhaled air (FeNO). We examined 107 children with bronchial asthma, they were divided into 2 groups depending on the level of FeNO. We found a number of associations in the group of patients with an elevated level of FeNO (≥20 ppb): carriage of alleles and genotypes containing short tandem repeats of S (9–11) NOS1(AAT)n gene, with an early debut and severe course of the disease, an increased level of total IgE in blood serum; carriage of alleles and genotypes containing long tandem repeats L (12–16) of the NOS2A(CCTTT) n gene, with a moderate course of the disease, with an increased level of IgE; carriage of the allele *A of the ARGII gene (rs3742879) with a moderate course of the disease; carriage of the *G allele and heterozygous *AG genotype of the ARGII gene (rs3742879) with a decreased level of FEV1/FVC; carriage of L alleles and a combination of the SL and LL genotypes of the NOS1(AAT)n gene with elevated blood eosinophils (eosinophilia); a combination of S/L + L/L genotypes of the NOS1(AAT)n gene with fungal sensitization. The authors established the correlations between disease severity and NOS1(AAT)n; the age of the manifestation of the disease and NOS1(AAT)n; FEV1/FVC and ARGII (rs3742879); feedback between blood eosinophilia and NOS1(AAT)n. The authors also determined a number of associations in the group of patients with low level of FeNO (<20 ppb): carriage of alleles and genotypes containing short tandem repeats of S (9–11) gene NOS1(AAT)n, with fungal sensitization; carriage of alleles and genotypes containing long tandem repeats of L (12–16) gene NOS2A(CCTTT)n, with reduced FEV1 and FEV1/FVC; carriage of the homozygous genotype of *GG gene ARGII(rs3742879) with epidermal sensitization. With a reduced level of FeNO, the study determined a relationship between the severity of bronchial asthma and NOS1(AAT)n; degree of effectiveness of anti-inflammatory basic therapy and NOS1(AAT)n; fungal sensitization and NOS1(AAT)n; feedback between FEV1 and NOS2(CCTTT)n; FEV1/FVC and NOS2(CCTTT)n.

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30

Warpeha, K. M., W. Xu, L. Liu, I. G. Charles, C. C. Patterson, F. Ah‐Fat, S. Harding, P. M. Hart, U. Chakravarthy i A. E. Hughes. "Genotyping and functional analysis of a polymorphic (CCTTT) n repeat of NOS2A in diabetic retinopathy". FASEB Journal 13, nr 13 (październik 1999): 1825–32. http://dx.doi.org/10.1096/fasebj.13.13.1825.

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Yee, LJ, S. Knapp, D. Burgner, BJW Hennig, AJ Frodsham, M. Wright, HC Thomas, AVS Hill i MR Thursz. "Inducible nitric oxide synthase gene (NOS2A) haplotypes and the outcome of hepatitis C virus infection". Genes & Immunity 5, nr 3 (26.02.2004): 183–87. http://dx.doi.org/10.1038/sj.gene.6364054.

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Yee, L. J., S. Knapp, D. Burgner, B. J. W. Hennig, A. J. Frodsham, M. Wright, H. C. Thomas, A. V. S. Hill i M. R. Thursz. "525 Inducible nitric oxide (NOS2A) haplotypes and the clinical outcomes of hepatitis C virus infection". Journal of Hepatology 40 (styczeń 2004): 154–55. http://dx.doi.org/10.1016/s0168-8278(04)90525-9.

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Tajouri, Lotti, Virginie Martin, Micky Ovcaric, Rob P. Curtain, Rod A. Lea, Peter Csurhes, Michael P. Pender i Lyn R. Griffiths. "Investigation of an inducible nitric oxide synthase gene (NOS2A) polymorphism in a multiple sclerosis population". Brain Research Bulletin 64, nr 1 (lipiec 2004): 9–13. http://dx.doi.org/10.1016/j.brainresbull.2004.04.019.

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Burgner, David, Stanley Usen, Kirk Rockett, Muminatou Jallow, Hans Ackerman, Alessandra Cervino, Margaret Pinder i Dominic P. Kwiatkowski. "Nucleotide and haplotypic diversity of the NOS2A promoter region and its relationship to cerebral malaria". Human Genetics 112, nr 4 (28.01.2003): 379–86. http://dx.doi.org/10.1007/s00439-002-0882-4.

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35

Burgner, David, Stanley Usen, Kirk Rockett, Muminatou Jallow, Hans Ackerman, Alessandra Cervino, Margaret Pinder i Dominic P. Kwiatkowski. "Nucleotide and haplotypic diversity of the NOS2A promoter region and its relationship to cerebral malaria". Human Genetics 114, nr 4 (1.03.2004): 401. http://dx.doi.org/10.1007/s00439-003-1068-4.

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Vigo, Ana González, Alfonso Martínez, Emilio G. de la Concha, Elena Urcelay i Antonio Ruiz de León. "Suggested Association of NOS2A Polymorphism in Idiopathic Achalasia: No Evidence in a Large Case–Control Study". American Journal of Gastroenterology 104, nr 5 (31.03.2009): 1326–27. http://dx.doi.org/10.1038/ajg.2009.72.

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Korneev, S. A., E. I. Korneeva, M. A. Lagarkova, S. L. Kiselev, G. Critchley i M. O'Shea. "Novel noncoding antisense RNA transcribed from human anti-NOS2A locus is differentially regulated during neuronal differentiation of embryonic stem cells". RNA 14, nr 10 (28.08.2008): 2030–37. http://dx.doi.org/10.1261/rna.1084308.

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Manna, Ida, Maria Liguori, Paola Valentino, Luana Vena, Francesca Condino, Rita Nisticò, Gemma Di Palma, Aldo Quattrone i Antonio Gambardella. "NOS2A as a candidate gene in Relapsing–Remitting Multiple Sclerosis: A haplotype study using selected subsets of single nucleotide polymorphisms". Journal of the Neurological Sciences 304, nr 1-2 (maj 2011): 75–77. http://dx.doi.org/10.1016/j.jns.2011.02.008.

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Gazquez, Irene, Jose A. Lopez-Escamez, Antonia Moreno, Colleen A. Campbell, Nicole C. Meyer, John P. Carey, Lloyd B. Minor i in. "Functional Variants in NOS1 and NOS2A Are Not Associated with Progressive Hearing Loss in Ménière's Disease in a European Caucasian Population". DNA and Cell Biology 30, nr 9 (wrzesień 2011): 699–708. http://dx.doi.org/10.1089/dna.2011.1259.

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MORRIS, Brian J., Cheryl L. GLENN, David E. L. WILCKEN i Xing Li WANG. "Influence of an inducible nitric oxide synthase promoter variant on clinical variables in patients with coronary artery disease". Clinical Science 100, nr 5 (10.04.2001): 551–56. http://dx.doi.org/10.1042/cs1000551.

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Pathophysiological processes in coronary artery disease (CAD) are influenced by genetic factors. Since (i) inducible nitric oxide synthase (iNOS) has important cardiovascular effects, and (ii) the promoter of the iNOS gene (NOS2A) is genetically modulated by a 4 bp insertion/deletion (+/-) polymorphism located 0.7 kb upstream, we decided to examine the influence of this variant on clinical variables in 856 CAD patients of Anglo-Celtic/Northern European extraction. We found that 2% of CAD patients were homozygous for the + allele, and 19% were heterozygous. Males made up 74% of the patient group, and in these the + allele was associated with 38% higher plasma glucose levels (P = 0.005), a 4.8% elevation in the waist/hip ratio (P = 0.009) and a 48% greater frequency of unstable angina (P = 0.014). The + allele, by influencing iNOS expression, could thus contribute to indices of insulin resistance and angina severity in male CAD patients.

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41

Falchi, Alessandra, Ignazio Stefano Piras, Laurianne Giovannoni, Pedro Moral, Giuseppe Vona i Laurent Varesi. "Population genetic data on four STR loci, PAI (CA)n, GpIIIa (CT)n, PLAT (TG)14 (CA)12, and NOS2A (CCTTT)n, in Mediterranean populations". Legal Medicine 9, nr 4 (lipiec 2007): 218–20. http://dx.doi.org/10.1016/j.legalmed.2007.01.001.

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ZHANG, J., B. S. LI, C. C. ZHOU, H. Y. YU, X. P. DING, M. P. SUN, H. LIU, G. Q. YU, H. S. LI i W. HUANG. "Single nucleotide polymorphisms in NOS2A and NOS3 genes are not associated with treatment response of non-small cell lung cancer patients following the definitive radiochemotherapy". Neoplasma 59, nr 06 (2012): 631–40. http://dx.doi.org/10.4149/neo_2012_080.

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Benbetka, Y., F. Messabih, M. C. Abadi i R. Amrane. "Étude de l’association des polymorphimes fonctionnels touchant les gènes TLR2, TIRAP, TNF, IL1B, IL1RN, IL12B et NOS2A avec la susceptibilité à la tuberculose pulmonaire en Algérie". Revue des Maladies Respiratoires 31 (styczeń 2014): A95. http://dx.doi.org/10.1016/j.rmr.2013.10.333.

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Cai, Li, Zhan Li, Xuhua Guan, Kun Cai, Lei Wang, Jiafa Liu i Yeqing Tong. "The Research Progress of Host Genes and Tuberculosis Susceptibility". Oxidative Medicine and Cellular Longevity 2019 (14.08.2019): 1–8. http://dx.doi.org/10.1155/2019/9273056.

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Background/Aims. Nucleotide diversity may affect the immune regulation of tuberculosis (TB) patients, leading to the individual susceptibility to TB. In recent years, there are a lot of researches on the association of host genetic factors and TB susceptibility which has attracted increasing attention, and the in-depth study of its mechanism is gradually clear. Materials. We made a minireview on the association of many candidate genes with TB based on recent research studies systematically, such as the human leukocyte antigen (HLA) gene, the solute carrier family 11 member 1 (SLC11A1) gene system, the vitamin D receptor (VDR) gene, the mannan-binding lectin (MBL) gene, the nitric oxide synthase 2A (NOS2A) gene, the speckled 110 (SP110) gene, and the P2X7 receptor (P2X7) gene. The discovery of these candidate genes could reveal the pathogenesis of TB comprehensively and is crucial to provide scientific evidence for formulating the related measures of prevention and cure. Discussion. The host genes play important roles in the development of TB, and the host genes may become new targets for the prevention and treatment of TB. Effective regulation of host genes may help prevent or even treat TB. Conclusion. This minireview focuses on the association of host genes with the development of TB, which may supply some clues for future therapies and novel drug targets for TB.

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45

Su, Jiechuang, Christopher P. Guise i William R. Wilson. "FSL-61 is a 6-nitroquinolone fluorogenic probe for one-electron reductases in hypoxic cells". Biochemical Journal 452, nr 1 (25.04.2013): 79–86. http://dx.doi.org/10.1042/bj20121695.

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One-electron reductases that reduce nitro compounds in hypoxic human tumour cells are poorly characterized, but are important for targeting hypoxia with nitroaromatic prodrugs. Fluorogenic probes with defined reductase profiles are needed to interrogate the activity of these enzymes in intact cells. In the present paper, we report a 6-nitroquinolone ester (FSL-61) as a fluorogenic probe for POR (NADPH:cytochrome P450 oxidoreductase) activity under hypoxia, and demonstrate its suitability of monitoring POR by flow cytometry. Reduction of FSL-61 by purified recombinant human POR generated the corresponding hydroxylamine, which was non-fluorescent, but was reduced further to the fluorescent amine in cells. Hydrolysis of the ester side chain facilitated cellular entrapment, enabling detection of heterogeneous POR expression in mixed populations of cells. In addition to POR, forced expression of three other diflavin reductases [MTRR (methionine synthase reductase), NDOR1 (NADPH-dependent diflavin oxidoreductase 1) and NOS2A (nitric oxide synthase 2A)] or NADPH:adrenoredoxin oxidoreductase in HCT116 cells significantly increased hypoxic activation of FSL-61. This reductase profile is similar to that for the dinitrobenzamide prodrug PR-104A under hypoxia, and fluorogenic metabolism of FSL-61 correlated significantly with PR-104A activation in a panel of 22 human tumour cell lines. The present study thus demonstrates the utility of FSL-61 for rapid and non-destructive interrogation of the activity of one-electron reductases in hypoxic cells at the single-cell level.

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46

Abhimanyu, Abhimanyu, Mridula Bose, Astha Giri i Mandira Varma-Basil. "Comparative Genetic Association Analysis of Human Genetic Susceptibility to Pulmonary and Lymph Node Tuberculosis". Genes 14, nr 1 (13.01.2023): 207. http://dx.doi.org/10.3390/genes14010207.

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Background: Tuberculosis (TB) manifests itself primarily in the lungs as pulmonary disease (PTB) and sometimes disseminates to other organs to cause extra-pulmonary TB, such as lymph node TB (LNTB). This study aimed to investigate the role of host genetic polymorphism in immunity related genes to find a genetic basis for such differences. Methods: Sixty-three, Single nucleotide polymorphisms (SNPs) in twenty-three, TB-immunity related genes including eleven innate immunity (SLCA11, VDR, TLR2, TLR4, TLR8, IRGM, P2RX7, LTA4H, SP110, DCSIGN and NOS2A) and twelve cytokine (TNFA, IFNG, IL2, Il12, IL18, IL1B, IL10, IL6, IL4, rs1794068, IL8 and TNFB) genes were investigated to find genetic associations in both PTB and LNTB as compared to healthy community controls. The serum cytokine levels were correlated for association with the genotypes. Results: PTB and LNTB showed differential genetic associations. The genetic variants in the cytokine genes (IFNG, IL12, IL4, TNFB and IL1RA and TLR2, 4 associated with PTB susceptibility and cytokine levels but not LNTB (p < 0.05). Similarly, genetic variants in LTA4H, P2RX7, DCSIGN and SP110 showed susceptibility to LNTB and not PTB. Pathway analysis showed abundance of cytokine related variants for PTB and apoptosis related variants for LNTB. Conclusions: PTB and LNTB outcomes of TB infection have a genetic component and should be considered for any future functional studies or studies on susceptibility to pulmonary and extra-pulmonary TB.

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Mercadante, Marcos T., Isabel Altenfelder Santos Bordin, Jair de Jesus Mari i Eurípedes C. Miguel. "Nossa revista, nossa missão". Revista Brasileira de Psiquiatria 24, nr 3 (wrzesień 2002): 107–8. http://dx.doi.org/10.1590/s1516-44462002000300001.

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Burton, Matthew J., Saul N. Rajak, Julien Bauer, Helen A. Weiss, Sonda B. Tolbert, Alice Shoo, Esmail Habtamu i in. "Conjunctival Transcriptome in Scarring Trachoma". Infection and Immunity 79, nr 1 (11.10.2010): 499–511. http://dx.doi.org/10.1128/iai.00888-10.

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ABSTRACTTrachoma is a poorly understood immunofibrogenic disease process, initiated byChlamydia trachomatis. Differences in conjunctival gene expression profiles between Ethiopians with trachomatous trichiasis (with [TTI] or without [TT] inflammation) and controls (C) were investigated to identify relevant host responses. Tarsal conjunctival swab samples were collected for RNA isolation andC. trachomatisPCR. Transcriptome-wide microarray experiments were conducted on 42 samples (TTI,n= 13; TT,n= 15; C,n=14). Specific results were confirmed by using multiplex quantitative reverse transcription-PCR for 16 mRNA targets in an independent collection of case-control samples: 386 case-control pairs (TTI,n= 244; TT,n= 142; C,n= 386). The gene expression profiles of cases were consistent with squamous metaplasia (keratins, SPRR), proinflammatory cytokine production (IL1β,CXCL5, andS100A7), and tissue remodeling (MMP7,MMP9,MMP12, andHAS3). There was no difference in the level ofIFNγ between cases and controls. However, cases had increasedINDO,NOS2A, andIL13RA2and reducedIL13.C. trachomatiswas detected in 1/772. Cases show evidence of ongoing inflammation and tissue remodeling, which were more marked where clinical inflammation was also present. Significantly, these processes appear to be active in the absence of currentC. trachomatisinfection. There was limited evidence of a TH1 response (INDOandNOS2A) and no association between a TH2 response and cases. The epithelium appears to be actively involved in late cicatricial stages of trachoma through the production of proinflammatory factors (IL1β,CXCL5, andS100A7). Longitudinal studies are needed to investigate which etiological factors and pathways are associated with progressive scarring and whether simply controlling chlamydial infection will halt progression in people with established cicatricial disease.

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Darrah, Rebecca, Edward McKone, Clare O'Connor, Christine Rodgers, Alan Genatossio, Sharon McNamara, Ronald Gibson i in. "EDNRA variants associate with smooth muscle mRNA levels, cell proliferation rates, and cystic fibrosis pulmonary disease severity". Physiological Genomics 41, nr 1 (marzec 2010): 71–77. http://dx.doi.org/10.1152/physiolgenomics.00185.2009.

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Airway inflammation and pulmonary disease are heterogeneous phenotypes in cystic fibrosis (CF) patients, even among patients with the same cystic fibrosis transmembrane conductance regulator (CFTR) genotype. Endothelin, a proinflammatory peptide and smooth muscle agonist, is increased in CF airways, potentially contributing to the pulmonary phenotype. Four cohorts of CF patients were screened for variants in endothelin pathway genes to determine whether any of these variants associated with pulmonary function. An initial cohort of 808 CF patients homozygous for the common CF mutation, ΔF508, showed significant association for polymorphisms in the endothelin receptor A gene, EDNRA ( P = 0.04), but not in the related endothelin genes ( EDN1, EDN2, EDN3, or EDNRB) or NOS1, NOS2A, or NOS3. Variants within EDNRA were examined in three additional cohorts of CF patients, 238 patients from Seattle, WA, 303 from Ireland and the U.K., and 228 from Cleveland, OH, for a total of 1,577 CF patients. The three additional groups each demonstrated a significant association between EDNRA 3′-untranslated region (UTR) variant rs5335 and pulmonary function ( P = 0.002). At the molecular level, single nucleotide primer extension assays suggest that the effect of the variants is quantitative. EDNRA mRNA levels from cultured primary tracheal smooth muscle cells are greater for the allele that appears to be deleterious to lung function than for the protective allele, suggesting a mechanism by which increased receptor function is harmful to the CF airway. Finally, cell proliferation studies using human airway smooth muscle cells demonstrated that cells homozygous for the deleterious allele proliferate at a faster rate than those homozygous for the protective allele.

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Schankin, CJ, M. Krumbholz, P. Sostak, VM Reinisch, R. Goldbrunner i A. Straube. "Headache in patients with a meningioma correlates with a bone-invasive growth pattern but not with cytokine expression". Cephalalgia 30, nr 4 (1.08.2009): 413–24. http://dx.doi.org/10.1111/j.1468-2982.2009.01945.x.

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We included 58 patients with meningioma in a prospective study to analyse the prevalence of and risk factors for different types of meningioma-associated headache. Twenty-three patients (40%) had meningioma-associated headache. Of these, the pain was migraine-like in five (22%) and tension-type headache (TTH)-like in 13 (57%). Sixteen of 21 (76%) experienced relief of pain intensity of at least 50% after 18–24 months. Univariate analysis revealed bone-invasive growth pattern ( P = 0.007) as a risk factor for headache and intake of antiepileptic drugs ( P = 0.04) or large surrounding oedema ( P = 0.04) as possible protective parameters. For migraine-like headache, risk factors were a positive history of migraine ( P = 0.009) and bone-invasive growth pattern ( P = 0.046) and, for TTH-like headache, only bone-invasive growth pattern ( P = 0.009). Binary logistic regression analysis added to assess predictability and interaction effects could not identify a single factor predicting the occurrence of headache in the presence of a meningioma (correct prediction in 74% by a model consisting of bone-invasive growth pattern, history of head surgery, intake of antiepileptic drugs, temporal tumour location and moderate and large surrounding oedema). Analysis of 38 tumour specimens could not confirm the hypothesis that the occurrence of headache correlates with the expression magnitude of signal substances known to be present in meningiomas [stroma cell-derived factor 1, interleukin (IL)-1β, IL-6, vascular endothelial growth factor A] or thought to be relevant to headache/pain pathophysiology [prostaglandin-endoperoxide synthase 2, calcitonin-related polypeptide alpha, nitric oxide synthase (NOS) 1, NOS2A, NOS3, transforming growth factor-alpha, tumour necrosis factor, tachykinin, vasoactive intestinal peptide]. The affection of bone integrity and the expression of molecules thought to be relevant to headache pathophysiology might be important for meningioma-associated headache in predisposed individuals.

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