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Artykuły w czasopismach na temat "GEWE"
Lorenz, Friederike. "Gewe(r)bliche Ware". kma - Klinik Management aktuell 11, nr 09 (wrzesień 2006): 16–19. http://dx.doi.org/10.1055/s-0036-1573889.
Pełny tekst źródłaRab, M. Abdur, i Jasmin Akhter. "Sine-Function Method In The Soliton Solution Of Nonlinear Partial Differential Equations". GANIT: Journal of Bangladesh Mathematical Society 32 (4.02.2013): 55–60. http://dx.doi.org/10.3329/ganit.v32i0.13647.
Pełny tekst źródłaAgarwala, Ajita, i Rishu Chaujar. "Noise analysis of gate electrode work function engineered recessed channel (GEWE-RC) MOSFET". Journal of Physics: Conference Series 367 (21.05.2012): 012013. http://dx.doi.org/10.1088/1742-6596/367/1/012013.
Pełny tekst źródłaObermayer-Pietsch, B., i M. Ulbing. "MicroRNAs in der Osteologie". Osteologie 24, nr 04 (2015): 219–24. http://dx.doi.org/10.1055/s-0037-1622069.
Pełny tekst źródłaGupta, Neha, i Rishu Chaujar. "Quantum analysis based extraction of frequency dependent intrinsic and extrinsic parameters for GEWE-SiNW MOSFET". Journal of Computational Electronics 16, nr 1 (24.01.2017): 61–73. http://dx.doi.org/10.1007/s10825-016-0949-4.
Pełny tekst źródłaGupta, Neha, Ajay Kumar i Rishu Chaujar. "Oxide bound impact on hot-carrier degradation for gate electrode workfunction engineered (GEWE) silicon nanowire MOSFET". Microsystem Technologies 22, nr 11 (7.05.2015): 2655–64. http://dx.doi.org/10.1007/s00542-015-2557-9.
Pełny tekst źródłaChaujar, Rishu, Ravneet Kaur, Manoj Saxena, Mridula Gupta i R. S. Gupta. "Design considerations and impact of technological parametric variations on RF/microwave performance of GEWE-RC MOSFET". Microwave and Optical Technology Letters 52, nr 3 (8.01.2010): 652–57. http://dx.doi.org/10.1002/mop.25008.
Pełny tekst źródłaGupta, Neha, Ajay Kumar i Rishu Chaujar. "Impact of device parameter variation on RF performance of gate electrode workfunction engineered (GEWE)-silicon nanowire (SiNW) MOSFET". Journal of Computational Electronics 14, nr 3 (18.06.2015): 798–810. http://dx.doi.org/10.1007/s10825-015-0715-z.
Pełny tekst źródłaGupta, N., i R. Chaujar. "Investigation of temperature variations on analog/RF and linearity performance of stacked gate GEWE-SiNW MOSFET for improved device reliability". Microelectronics Reliability 64 (wrzesień 2016): 235–41. http://dx.doi.org/10.1016/j.microrel.2016.07.095.
Pełny tekst źródłaGupta, Neha, i Rishu Chaujar. "Optimization of high-k and gate metal workfunction for improved analog and intermodulation performance of Gate Stack (GS)-GEWE-SiNW MOSFET". Superlattices and Microstructures 97 (wrzesień 2016): 630–41. http://dx.doi.org/10.1016/j.spmi.2016.07.021.
Pełny tekst źródłaRozprawy doktorskie na temat "GEWE"
Gewe, Susanne [Verfasser], i KLAUS-MICHAEL [Akademischer Betreuer] BRAUMANN. "Gesundheitsbildung im Sport an der Berufsschule : Untersuchung, Entwicklung und praxisbezogene Überprüfung eines Curriculumbausteins im Fach Sport am Beispiel von Medizinischen und Zahnmedizinischen Fachangestellten in der Ausbildung / Susanne Gewe. Betreuer: Klaus-Michael Braumann". Hamburg : Staats- und Universitätsbibliothek Hamburg, 2014. http://d-nb.info/1046460242/34.
Pełny tekst źródłaVasanwala, Farha Huseini. "Gene manipulations for cancer gene therapy". Diss., The University of Arizona, 2002. http://hdl.handle.net/10150/289776.
Pełny tekst źródłaBashiardes, Evy. "Gene polymorphisms, gene expression and atherosclerotic plaques". Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420882.
Pełny tekst źródłaPayne, Katie Emma. "β₃ integrin gene polymorphisms and gene regulation". Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413197.
Pełny tekst źródłaLodhi, Saad Salman Khan. "Unraveling gene gene interactions in rheumatoid arthritis". Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-19908.
Pełny tekst źródłaSmith, Erin N. "Gene-environment interaction in yeast gene expression /". Thesis, Connect to this title online; UW restricted, 2008. http://hdl.handle.net/1773/5025.
Pełny tekst źródłaLi, Wei. "Analyzing Gene Expression Data in Terms of Gene Sets: Gene Set Enrichment Analysis". Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/math_theses/79.
Pełny tekst źródłaCarmo, Ana Paula Santos do. "Estudo da distribuiÃÃo da frequÃncia de genÃtipos de Helicobacter pylori em lesÃes gÃstricas". Universidade Federal do CearÃ, 2011. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=9557.
Pełny tekst źródłaA bactÃria Helicobacter pylori, à um agente etiolÃgico bem estabelecido para o desenvolvimento de lesÃes gÃstricas como gastrite, Ãlcera pÃptica, metaplasia e doenÃas malignas, com alta incidÃncia de infecÃÃo em todo mundo, porÃm cerca de 80% dos indivÃduos infectados permanecem assintomÃticos e apenas uma minoria desenvolve doenÃas a ela relacionadas. Estudos tÃm sido realizados na tentativa de identificar a relaÃÃo de genes determinantes da patogenicidade de H. pylori, entretanto, atà o momento apenas os genes cagA e o alelo de vacA s1m1 sÃo considerados marcadores de virulÃncia para o desenvolvimento de lesÃes gÃstricas mais graves. A bactÃria H. pylori possui uma alta variabilidade genÃtica, sendo que um dos mecanismos propostos para o desenvolvimento de lesÃo seria atravÃs da inflamaÃÃo. DiferenÃas na intensidade de respostas inflamatÃrias poderiam ser decorrentes do perfil genotÃpico da cepa infectante. Recentes trabalhos apontam a importÃncia dos genes cagE, virB11 de H. pylori, em cÃncer gÃstrico. Entretanto, estudos em lesÃes gÃstricas sÃo restritos. Assim, o objetivo deste trabalho foi determinar o perfil genotÃpico das cepas de H. pylori quanto a presenÃa dos genes de virulÃncia cagA, cagE, virB11, vacA e flaA, circulantes no estado do Cearà em 201 casos de lesÃes gÃstricas de diferentes gravidades, coletadas de pacientes dispÃpticos atendidos em trÃs hospitais de Fortaleza-CE. A detecÃÃo de H. pylori foi feita atravÃs da amplificaÃÃo do gene ureC, os genes estudados por amplificaÃÃo de fragmentos especÃficos, usando a tÃcnica de PCR, foram observados em gel de agarose 1% e poliacrilamida a 6% e 8%. Neste estudo houve um predomÃnio do sexo feminino 59% (119/201), principalmente na faixa etÃria (15-44) 30% (61/201), alta taxa de infecÃÃo por H. pylori 97,5% (196/201). A gastrite crÃnica ativa (GCA) foi a lesÃo gÃstrica mais frequente (55,7%;112/201), associada a pacientes na faixa etÃria de 15-44 (36,6% : 41/112) opondo-se à metaplasia intestinal em que, a frequÃncia dos casos aumentou com a idade sendo maior em pacientes mais velhos 46% (16/35), o que concorda com a literatura. O Ãnico caso de displasia ocorreu numa paciente > 65 anos. As lesÃes gÃstricas foram predominantemente localizadas no antro. O gene cagA foi mais frequente na gastrite crÃnica ativa (GCA), estando tambÃm em alta frequÃncia na gastrite atrÃfica (GA) e metaplasia intestinal (MI). Na GCA foi observado tambÃm alta frequÃncia dos genes cagE, virB11, vacAm1 e flaA, com diferenÃa estatÃstica, quando comparada com a gastrite crÃnica inativa (GCI) (cagA - p=0,007 cagE- p=0,000, virB11 - p=0,005, vacAm1- p=0,047 e flaA - p=0,001), sendo que os genes virB11 e flaA foram mais frequentes na GCA do que na Ãlcera. Os alelos s1 e m1 de vacA , bem como a combinaÃÃo s1m1 foram os mais frequentes nas lesÃes gÃstricas. Os casos H. pylori positivos foram agrupados de acordo com a presenÃa dos genes estudados, levando em consideraÃÃo a presenÃa do alelo s1 e os genes da ilha. Nessas anÃlises foi observada maior frequÃncia de cepas contendo os genes vacA s1 e [Ia (cagA+, cagE+ e virB11+ ) + Ib (cagA+ e virB11+; cagE+ e virB11+) ; 47,7% ] na gastrite crÃnica ativa em relaÃÃo a gastrite crÃnica inativa (GCI), esta com maior frequÃncia de cepas dos grupos [Ic (cagA+ ou cagE+ ou virB11+ ou cagA+ e cagE+) +Id (ureC+); 62%]. Adicionalmente, maior frequÃncia de cepas pertencentes aos grupos Ia e Ib foi observada na metaplasia intestinal incompleta, (59%), enquanto que na metaplasia intestinal completa uma maior frequencia de cepas pertencentes aos grupos Ic + Id, (78%) (p=0,027). Todos os casos de gastrite atrÃfica e Ãlcera eram do grupo I, e um Ãnico caso de displasia pertencia ao grupo Ia. Esses dados evidenciam uma associaÃÃo de cepas com genÃtipos mais virulentos em lesÃes com potencialidade de malignizaÃÃo.
A bactÃria Helicobacter pylori à um agente etiolÃgico bem estabelecido para o desenvolvimento de lesÃes gÃstricas como gastrite, Ãlcera pÃptica, metaplasia e doenÃas malignas, com alta incidÃncia de infecÃÃo todo mundo, porÃm cerca de 80% dos indivÃduos infectados permanecem assintomÃticos e apenas uma minoria desenvolve doenÃas a ela relacionadas. Estudos tem sido realizados na tentativa de identificar a relaÃÃo de genes determinantes da patogenicidade de H. pylori, entretanto, atà o momento apenas os genes cagA e o alelo de vacA s1m1 sÃo considerados marcadores de virulÃncia para o desenvolvimento de lesÃes gÃstricas mais graves. A bactÃria H. pylori possui uma alta variabilidade genÃtica sendo que um dos mecanismos propostos para o desenvolvimento de lesÃo seria atravÃs da inflamaÃÃo. DiferenÃas na intensidade de respostas inflamatÃrias poderiam ser decorrentes do perfil genotÃpico da cepa infectante. Recentes estudos apontam a importÃncia dos genes cagE, virB11 de H. pylori, em cÃncer gÃstrico. Entretanto, estudos em lesÃes gÃstricas sÃo restritos. Assim, o objetivo deste trabalho foi determinar o perfil genotÃpico das cepas de H. pylori quanto a presenÃa dos genes de virulÃncia cagA, cagE, virB11, vacA e flaA, circulantes no estado do Cearà em 201 casos de lesÃes gÃstricas de diferentes gravidades, coletadas de pacientes dispÃpticos atendidos em trÃs hospitais de Fortaleza-CE. A detecÃÃo de H. pylori foi feita atravÃs da amplificaÃÃo do gene ureC, e os genes estudados por amplificaÃÃo de fragmentos especÃficos, usando a tÃcnica de PCR, e foram observados em gel de agarose 1% e poliacrilamida a 6% e 8%. Nesse estudo houve um predomÃnio do sexo feminino 59% (119/201), principalmente na faixa etÃria (15-44) 30% (61/201), e alta taxa de infecÃÃo por H. pylori 97,5% (196/201). A gastrite crÃnica ativa (GCA), foi a lesÃo gÃstrica mais frequente (55,7%;112/201), associada a pacientes na faixa etÃria de 15-44 (36,6% : 41/112) opondo-se à metaplasia intestinal onde a frequÃncia dos casos aumentou com a idade sendo maior em pacientes mais velhos 46% (16/35), o que concorda com a literatura. O Ãnico caso de displasia ocorreu numa paciente > 65 anos. As lesÃes gÃstricas foram predominantemente localizadas no antro. O gene cagA foi mais frequente na gastrite crÃnica ativa (GCA), estando tambÃm em alta frequÃncia na gastrite atrÃfica (GA) e metaplasia intestinal (MI). Na GCA foi observado tambÃm alta freqÃÃncias dos genes cagE, virB11, vacAm1 e flaA com diferenÃa estatÃstica quando comparada com a gastrite crÃnica inativa (GCI) (cagA - p=0,007 cagE- p=0,000, virB11 - p=0,005, vacAm1- p=0,047 e flaA - p=0,001), sendo que os genes virB11 e flaA foram mais frequentes na GCA que na Ãlcera. Os alelos s1 e m1 de vacA , bem como a combinaÃÃo s1m1 foram os mais frequentes nas lesÃes gÃstricas. Os casos H. pylori positivos foram agrupados de acordo com a presenÃa dos genes estudados, levando em consideraÃÃo a presenÃa do alelo s1 e os genes da ilha. Nestas anÃlises foi observada maior frequÃncia de cepas contendo os genes vacA s1 e [Ia (cagA+, cagE+ e virB11+ ) + Ib (cagA+ e virB11+; cagE+ e virB11+) ; 47,7% ] na gastrite crÃnica ativa em relaÃÃo a gastrite crÃnica inativa (GCI), esta Ãltima com maior frequÃncia de cepas dos grupos [Ic (cagA+ ou cagE+ ou virB11+ ou cagA+ e cagE+) +Id (ureC+); 62%]. Adicionalmente, maior frequÃncia de cepas pertencentes aos grupos Ia e Ib foi observada na metaplasia intestinal incompleta, (59%), enquanto que na metaplasia intestinal completa uma maior frequencia de cepas pertencentes aos grupos Ic + Id, (78%) (p=0,027). Todos os casos de gastrite atrÃfica e Ãlcera eram do grupo I, e o Ãnico caso de displasia pertencia ao grupo Ia. Esses dados evidenciam uma associaÃÃo de cepas com genÃtipos mais virulentos em lesÃes com potencialidade de malignizaÃÃo.
The bacterium Helicobacter pylori is a well-established etiological factor in the development of gastric lesions such as gastritis, peptic ulcers, metaplasia and malignancy. The incidence of infection by this pathogen is high worldwide, but about 80% of infected individuals remain asymptomatic, and only a minority develops related diseases. Many studies have been conducted in an attempt to identify the involvement of genes in determining the pathogenicity of H. pylori, but so far, only the genes cagA and vacA allele s1m1 are considered virulence markers for the development of the more severe gastric lesions. H. pylori bacteria have a high genetic variability and one of the proposed mechanisms for lesion development is through inflammation. Differences in the intensity of inflammatory responses could be due to the genotypic profile of the infecting strain. Recent studies indicate the importance of the genes cagE and virB11, but mostly involving gastric cancer, while their role in gastric lesions is limited. The objective of this study was to determine the genetic subtypes of H. pylori strains and the presence of the virulence genes cagA, cagE, virB11 and flaA genes and vacA alleles, circulating in Ceara state, Brazil. Samples were collected from 201 cases of gastric lesions of varying severity, in dyspeptic patients treated at three hospitals in Fortaleza, Ceara State. The detection of H. pylori was performed using ureC gene amplification by PCR, and the detection of the genes studied was carried out by amplification of gene-specific fragments separated in 1% agarose gels. The sample was predominantly female (59%, 119/201) and mainly in the age group 15-44 years old (30%, 61/201), and had a high rate of H. pylori infection (97.5%, 196/201). Active chronic gastritis (ACG) was the most common gastric lesion (55.7%, 112/201), associated with patients aged 15-44 (36.6%, 41/112), unlike intestinal metaplasia, in which the frequency of cases increased with age, being higher in older patients (46%, 16/35), which agrees with the literature. A single case of dysplasia occurred in a patient > 65 years. The lesions were predominantly located in the gastric antrum and 30% of the cases had lesions located in the body and antrum simultaneously. The cagA gene was more frequent in ACG, showing a statistically significant correlation (r = 0.220, p = 0.007); it also showed a high frequency in atrophic gastritis and in intestinal metaplasia. In ACG, a high frequency of the genes cagE, virB11, flaA and vacAm1 was also statistically associated when compared to chronic inactive gastritis (ICG) (cagA - p = 0.007, cagE - p = 0.000, virB11 - p = 0.005, vacAm1 p = 0.047 and flaA - p = 0.001), and the genes virB11 and flaA were more frequent in ACG than in ulcer. The vacA alleles s1 and m1, and the combination s1m1, were the most frequent ones in gastric lesions. Considering the genotypes of H. pylori grouped by the presence of the genes studied, we observed a higher frequency of the most virulent strains in the ACG group (Ia + Ib, 47.7%) when compared to ICG, the latter showing a higher frequency of less virulent strains (Ic + Id, 62%). Additionally, a higher frequency of more virulent strains, belonging to groups Ia and Ib, was observed in incomplete intestinal metaplasia (59%), while in complete intestinal metaplasia an increased frequency of less virulent strains, belonging to the groups Ic + Id (78%) (p = 0.027), was found. All cases of atrophic gastritis and ulcer were in group I, and the single case of dysplasia belonged to group Ia (high virulence). These data indicate the important role of more virulent strains in potential malignant lesions.
Nastase, Mannila Maria. "Fibrinogen and susceptibility to myocardial infarction : role of gene-gene and gene-environment interactions /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-672-7/.
Pełny tekst źródłaRück, Andreas. "Myocardial gene therapy and gene expression in angina pectoris /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-648-4/.
Pełny tekst źródłaKsiążki na temat "GEWE"
Gede. Beijing Shi: Zhongguo he ping chu ban she, 1996.
Znajdź pełny tekst źródłaGene. Spain: Pocket Books, 2005.
Znajdź pełny tekst źródłaKarasu, Bilge. Gece. Istanbul: Metis Yayinlari, 1992.
Znajdź pełny tekst źródłaMasashi, Sada. Gege. Tōkyō: Gentōsha, 2002.
Znajdź pełny tekst źródłaCarolyn, Cook. Gene. Grantsville, MD: Hobby House Press, 1998.
Znajdź pełny tekst źródłaGene. Gene. Milano: Editoriale Giorgio Mondadori, 2020.
Znajdź pełny tekst źródłaCarolyn, Cook. Gene. Wyd. 3. Grantsville, Md: Hobby House Press, 2001.
Znajdź pełny tekst źródłaKarasu, Bilge. Gece. İstanbul: İletişim Yayınları, 1985.
Znajdź pełny tekst źródłaLong, Wu, red. Geye. Taibei Shi: Yi shu tu shu gong si, 1999.
Znajdź pełny tekst źródłaSchaffer, David V., i Weichang Zhou, red. Gene Therapy and Gene Delivery Systems. Berlin/Heidelberg: Springer-Verlag, 2005. http://dx.doi.org/10.1007/11542766.
Pełny tekst źródłaCzęści książek na temat "GEWE"
Moore, Sarah R. "Gene-Gene Interactions". W Encyclopedia of Personality and Individual Differences, 1757–59. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-24612-3_1472.
Pełny tekst źródłaGalik, Elizabeth, Shin Fukudo, Yukari Tanaka, Yori Gidron, Tavis S. Campbell, Jillian A. Johnson, Kristin A. Zernicke i in. "Gene-Gene Interaction". W Encyclopedia of Behavioral Medicine, 841–42. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_690.
Pełny tekst źródłaJiang, Rong. "Gene-Gene Interaction". W Encyclopedia of Behavioral Medicine, 925–26. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_690.
Pełny tekst źródłaZheng, Gang, Yaning Yang, Xiaofeng Zhu i Robert C. Elston. "Gene-Gene Interactions". W Analysis of Genetic Association Studies, 235–56. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2245-7_8.
Pełny tekst źródłaMoore, Sarah R. "Gene-Gene Interactions". W Encyclopedia of Personality and Individual Differences, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28099-8_1472-1.
Pełny tekst źródłaDeWan, Andrew T. "Gene-Gene and Gene-Environment Interactions". W Methods in Molecular Biology, 89–110. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7868-7_7.
Pełny tekst źródłaIvanov, V. I. "“Good Gene” /“Bad Gene”". W Genes and Resistance to Disease, 159–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-56947-0_14.
Pełny tekst źródłaDardick, Christopher D., i James N. Culver. "Gene-for-Gene Interactions". W Molecular Biology of Plant Viruses, 211–24. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5063-1_10.
Pełny tekst źródłaPalmer, Rohan, i Martin Hahn. "Gene". W Encyclopedia of Clinical Neuropsychology, 1549–50. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_1858.
Pełny tekst źródłaPalmer, Rohan, i Martin Hahn. "Gene". W Encyclopedia of Clinical Neuropsychology, 1135–36. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_1858.
Pełny tekst źródłaStreszczenia konferencji na temat "GEWE"
Chaujar, R., R. Kaur, M. Saxena, M. Gupta i R. S. Gupta. "GEWE-RC MOSFET: High performance RF solution to CMOS technology". W 2008 Asia Pacific Microwave Conference. IEEE, 2008. http://dx.doi.org/10.1109/apmc.2008.4958185.
Pełny tekst źródłaGupta, Neha, i Rishu Chaujar. "Implications of transport models on the analog performance of Gate Electrode Workfunction Engineered (GEWE) Silicon Nanowire MOSFET". W 2014 2nd International Conference on Devices, Circuits and Systems (ICDCS). IEEE, 2014. http://dx.doi.org/10.1109/icdcsyst.2014.6926154.
Pełny tekst źródłaGupta, Neha, Ajay Kumar i Rishu Chaujar. "Effect of dielectric engineering on analog and linearity performance of gate electrode workfunction engineered (GEWE) silicon nanowire MOSFET". W 2015 IEEE 15th International Conference on Nanotechnology (IEEE-NANO). IEEE, 2015. http://dx.doi.org/10.1109/nano.2015.7388768.
Pełny tekst źródłaChaujar, R., R. Kaur, M. Saxena, M. Gupta i R. S. Gupta. "GEWE-RC MOSFET: A solution to CMOS technology for RFIC design based on the concept of intercept point". W 2008 International Conference on Recent Advances in Microwave Theory and Applications (MICROWAVE). IEEE, 2008. http://dx.doi.org/10.1109/amta.2008.4762978.
Pełny tekst źródła"6th Belgian Brain Congress: The gene-environment tango in the healthy and diseased brain". W 6th Belgian Brain Congress: The gene-environment tango in the healthy and diseased brain. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-978-5.
Pełny tekst źródłaLi, Ling. "Mitochondrial fostering: the mitochondrial geme may play a role in plant orphan gene evolution". W ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1332405.
Pełny tekst źródłaKojima, T., M. Tanimoto, T. Kamiya, Y. Obata, K. Kurachi i H. Saito. "ANALYSIS OF FACTOR IX GENE IN NORMAL SUBJECTS AND HEMOPHILIA B PATIENTS IN JAPAN". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644077.
Pełny tekst źródłaTsakirpaloglou, Nikolaos. "Optimizing a high-throughput gene editing pipeline at the Texas A&M Crop Geme Editing Lab". W ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1053060.
Pełny tekst źródłaYasin, Jeshima. "Geme wide stress responsive gene network and miR target identification from an orphan legume Horsegram (Macrotyloma uniflorum)". W ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1332446.
Pełny tekst źródłaPolstein, Lauren R., i Charles A. Gersbach. "Photoregulated Gene Expression in Human Cells With Light-Inducible Engineered Transcription Factors". W ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80573.
Pełny tekst źródłaRaporty organizacyjne na temat "GEWE"
Marshall, Dana R., Olufemi J. Adegoke i Wei Zheng. Gene-Gene and Gene-Environment Interactions in the Etiology of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2007. http://dx.doi.org/10.21236/ada472397.
Pełny tekst źródłaWolstenhome, D. R. The plant mitochondrial mat-r gene/nad1 gene complex. Office of Scientific and Technical Information (OSTI), grudzień 1996. http://dx.doi.org/10.2172/763987.
Pełny tekst źródłaDing, Yi. Adenovirus-Mediated p202 Gene Transfer in Breast Cancer Gene Therapy. Fort Belvoir, VA: Defense Technical Information Center, maj 2005. http://dx.doi.org/10.21236/ada442740.
Pełny tekst źródłaWolstenholme, D. R. The plant mitochondrial mat-r gene/nad1 gene complex. Progress report. Office of Scientific and Technical Information (OSTI), czerwiec 1994. http://dx.doi.org/10.2172/10159855.
Pełny tekst źródłaSun, Jielin, Jianfeng Xu i Siqun L. Zheng. Systematic Search for Gene-Gene Interaction Effect on Prostate Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2012. http://dx.doi.org/10.21236/ada564269.
Pełny tekst źródłaSun, Jielin, Jianfeng Xu i Siqun L. Zheng. Systematic Search for Gene-Gene Interaction Effect on Prostate Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2013. http://dx.doi.org/10.21236/ada593732.
Pełny tekst źródłaEinstein, J. R., R. J. Mural, X. Guan i E. C. Uberbacher. Computer-based construction of gene models using the GRAIL Gene Assembly Program. Office of Scientific and Technical Information (OSTI), wrzesień 1992. http://dx.doi.org/10.2172/7160076.
Pełny tekst źródłaYang, Ning-Sun. A Novel Gene Gun-Mediated IL-12 Gene Therapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, październik 2000. http://dx.doi.org/10.21236/ada394902.
Pełny tekst źródłaKuchka, M. R. Post transcriptional regulation of chloroplast gene expression by nuclear encoded gene products. Office of Scientific and Technical Information (OSTI), styczeń 1992. http://dx.doi.org/10.2172/7309627.
Pełny tekst źródłaKuchka, M. R. Post transcriptional regulation of chloroplast gene expression by nuclear encoded gene products. Office of Scientific and Technical Information (OSTI), styczeń 1992. http://dx.doi.org/10.2172/5268747.
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