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Artykuły w czasopismach na temat "Potential biomaker"
Pavoni-Ferreira, P. C., A. S. Petrilli, M. T. Alves, R. Jesus-Garcia Filho i S. R. Toledo. "Angiogenic biomaker study in osteosarcoma". Journal of Clinical Oncology 27, nr 15_suppl (20.05.2009): e21507-e21507. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e21507.
Pełny tekst źródłaHashimoto, T., T. Hata, Y. Mori, J. Suzuki, Y. Kamata, K. Yoshimura, M. Kunou i in. "P17-3 Evaluating event-related potential P50 suppression for diagnostic biomaker for psychiatric disorders". Clinical Neurophysiology 121 (październik 2010): S203—S204. http://dx.doi.org/10.1016/s1388-2457(10)60836-x.
Pełny tekst źródłaLi, Chen, Hui Geng, Linhua Ji, Xiaojing Ma, Qichao Yin i Hua Xiong. "ESM-1: A Novel Tumor Biomaker and its Research Advances". Anti-Cancer Agents in Medicinal Chemistry 19, nr 14 (16.12.2019): 1687–94. http://dx.doi.org/10.2174/1871520619666190705151542.
Pełny tekst źródłaNafi’u, S. A., K. Suleiman, M. K. Ahmad i M. Zakariyya. "Effect of Paraquat Herbicide on Oxidative Stress Biomaker Enzyme Activities in C. Gariepinus". Dutse Journal of Pure and Applied Sciences 7, nr 3b (6.01.2022): 48–59. http://dx.doi.org/10.4314/dujopas.v7i3b.6.
Pełny tekst źródłaLiu, Tianju, Andrew E. Rinke, Kevin Flaherty i Sem Hin Phan. "Soluble B7H3 induction in pulmonary fibrosis is associated with disease severity". Journal of Immunology 204, nr 1_Supplement (1.05.2020): 146.9. http://dx.doi.org/10.4049/jimmunol.204.supp.146.9.
Pełny tekst źródłaB. Veena, B. Veena. "Bioinformatics Analysis of Mirna Data for Potential Biomarker Discovery". International Journal of Scientific Research 2, nr 8 (1.06.2012): 45–47. http://dx.doi.org/10.15373/22778179/aug2013/16.
Pełny tekst źródłaMcNamara, Aoife E., i Lorraine Brennan. "Potential of food intake biomarkers in nutrition research". Proceedings of the Nutrition Society 79, nr 4 (2.07.2020): 487–97. http://dx.doi.org/10.1017/s0029665120007053.
Pełny tekst źródłaK. Mohammed, Lona, i Sarhang S. Gul. "Diagnostic Potential of Salivary Biomarker Profiles in Epidemiological Survey of Periodontitis". Sulaimani dental journal 7, nr 2 (12.01.2020): 36–44. http://dx.doi.org/10.17656/sdj.10114.
Pełny tekst źródłaPriya, Shalini, Alina Peluso, Mayanka Chandra Shekhar, Ioana Danciu, Jordan Miller i Heidi A. Hanson. "Abstract 4191: Assessing performance of biomarker extraction from electronic health records: Data augmentation methods for a hierarchical self-attention network (HiSAN)". Cancer Research 83, nr 7_Supplement (4.04.2023): 4191. http://dx.doi.org/10.1158/1538-7445.am2023-4191.
Pełny tekst źródłaEbadi, Maryam, i Vera C. Mazurak. "Potential Biomarkers of Fat Loss as a Feature of Cancer Cachexia". Mediators of Inflammation 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/820934.
Pełny tekst źródłaRozprawy doktorskie na temat "Potential biomaker"
Frederickx, Nancy. "The SLC22A18 transporter, a potential biomarker for chemotherapeutic treatment". Doctoral thesis, Universite Libre de Bruxelles, 2015. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/217862.
Pełny tekst źródłaDoctorat en Sciences
info:eu-repo/semantics/nonPublished
Santos, Joana Rita Faneca. "TAU Thr231 phosphorylation as a potential Alzheimer's disease biomarker". Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22056.
Pełny tekst źródłaAlzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the presence of extracellular amyloid plaques (senile plaques) and intracellular neurofibrillary tangles formed by hyperphosphorylated TAU protein. TAU protein when hyperphosphorylated loses the ability to bind to microtubules and can be released into peripheral fluids. This process leads to neuronal degradation and neuronal death. Phosphorylation at threonine 231 has been shown to be specific for AD and to precede assembly of paired helical filaments in the human brain. In order to understand more about this residue we analysed SH-SY5Y cells undifferentiated and in differentiated cells induced by retinoic acid (RA). Treatment with RA increased expression of TAU phosphorylated at Thr231 (TAUpThr231) as determined by Western blot analysis. We further explored TAU phosphorylation by immunocytochemistry and noticed that in undifferentiated SH-SY5Y cells, TAUpThr231 was located mainly in the nucleus. In contrast, TAU and TAUpThr231 was redistributed to the neurites and in the soma of SH-SY5Y cells, which were induced to differentiate by retinoic acid (RA). In order to evaluate the potential of TAUpThr231 as a biomarker, we measured TAUpThr231 in CSF by a sandwich enzyme immunoassay and observed that the ratio of TAUpThr231/TAU levels discriminated significantly the AD group for the non-AD group. These findings indicate that TAUpThr231/t-TAU ratio levels may be a valuable marker for the clinical diagnosis of AD, irrespective of age and gender.
A doença de Alzheimer (AD) é uma doença neurodegenerativa progressiva caracterizada pela presença de placas de amilóide extracelulares (placas senis) e tranças neurofibrilhares intracelulares formadas pela proteína TAU hiperfosforilada. A proteína TAU quando hiperfosforilada perde a capacidade de se ligar a microtúbulos e pode ser libertada para fluidos periféricos. Este processo leva à degradação neuronal e à morte neuronal. A fosforilação na treonina 231 tem-se demonstrado ser específica para a AD e preceder a formação de filamentos helicoidais emparelhados no cérebro humano. Para melhor perceber a função deste resíduo e a contribuição para a localização da TAU, analisámos células SH-SY5Y indiferenciadas e células diferenciadas, pela adição de ácido retinoico (RA). O tratamento com RA aumentou a expressão de TAU fosforilada na Thr231 (TAUpThr231) conforme determinado por Western blot. Explorámos ainda a fosforilação da TAU por imunocitoquímica e percebemos que em células SH-SY5Y indiferenciadas, a phosphoTAU231 estava localizada principalmente no núcleo. Em contraste, TAU e phosphoTAU231 foram redistribuídas para as dendrites e citosol das células SH-SY5Y diferenciadas pelo ácido retinoico (RA). Para avaliar o potencial deste resíduo como biomarcador; medimos TAUpThr231 em CSF por meio de um imunoensaio enzimático em sanduíche e observámos que a proporção de níveis de TAUpThr231 / TAU discriminou de forma significativa o grupo AD do grupo não-AD. Essas descobertas podem indicar que os níveis da relação TAUpThr231 / t-TAU podem ser um marcador valioso para o diagnóstico clínico de AD, independentemente da idade e do género.
Almeida, João Carlos Moutinho de. "DNA methylation as a potential biomarker for Alzheimer disease". Master's thesis, Universidade de Aveiro, 2013. http://hdl.handle.net/10773/13261.
Pełny tekst źródłaDNA methylation is the major studied epigenetic mechanism and consists in the addiction of a methyl group to 5’ carbon position of the cytosine ring. Methylation of promoter gene regions are directly correlated with gene silencing, which can allow the development of certain diseases since relevant genes may be inhibited due to its promoter methylation; being that the opposite can also occur. This epigenetic mechanism has been linked to cancer and recently it is also being pointed to have an important role in neurological disorders, such as Alzheimer’s Disease (AD). Furthermore, aging is the major risk factor for AD, and also the process underlying many of the epigenetic alterations. As AD etiology and pathological development is not complete understood, alterations in epigenetic mechanisms like DNA methylation may underlie the basis of gene expression alterations. Hence, in this study, possible AD patients and age- and sex-matched controls were used. Genomic DNA was extracted from blood samples and the global methylation levels were determined using an ELISA-type assay, The possible AD patients exhibit lower methylation levels (0,75%±0,29) than age- and sex-matched controls (0,86%±0,29). Gene specific methylation profiles of AD related genes, namely APP and ApoE, was carried out using Combine Bisulfite Restriction Analysis (COBRA), Methylation Sensitive-High Resolution Melting (MS-HRM) and Bisulfite Direct Sequencing. The APP promoter region did not reveal any methylation by COBRA and MS-HRM. For the ApoE promoter region evaluated no differences in the methylation levels could be detected between patients and controls using these two techniques. However, by sequencing analysis of this ApoE promoter region, differences arise in specific CpG sites, indicating a tendency for increased methylation of CpG1, CpG3 and CpG 5 and a decreased methylation of CpG6 in AD patients when compared with age- and sex-matched controls. In this study AD patients exhibited a tendency for lower global methylation levels when compared to control individuals and the ApoE promoter region exhibited a tendency for a pattern of methylation that maybe related to AD pathology.
A metilação de DNA é, de todos os mecanismos epigenéticos, o mais estudado e consiste na adição de um grupo metil ao carbono da posição 5 do anel de uma citosina. A metilação da região promotora de genes está diretamente relacionada com silenciamento genético, podendo conduzir ao desenvolvimento de determinadas patologias, uma vez que genes importantes não são expressos devido a este mecanismo. Este mecanismo epigenético tem vindo a ser estudado a nível do cancro e, recentemente, tem adquirido alguma importância ao nível de doenças neurológicas, como a doença de Alzheimer (DA). O envelhecimento é o maior factor de risco para a DA e ao mesmo tempo está na base de muitas das alterações nos mecanismos epigenéticos. Como a patologia e etiologia da DA ainda não é completamente conhecida, alterações ao nível de mecanismos epigenéticos, como a metilação de DNA, podem ajudar a entender as alterações de expressão de genes nesta doença. Neste estudo, utilizaram-se amostras de pacientes com possível DA e controlos com idades semelhantes. O DNA genómico foi extraído de amostras de sangue e os níveis de metilação global foram avaliados por um ensaio de ELISA. Os pacientes apresentaram uma tendência para uma diminuição da metilação global (0,75%±0,29) relativamente aos controlos (0,86%±0,29). Os perfis de metilação dos genes envolvidos na DA, APP e ApoE, foram obtidos por Combine Bisulfite Restriction Analysis (COBRA), Methylation Sensitive - High Resolution Melting (MS-HRM) e Bisulfite Direct Sequencing (BDS). Para a região promotora do gene ApoE, não foram encontradas diferenças entre pacientes e controlos assim como a região promotora do gene APP não apresentou metilação através do método COBRA e MS-HRM. De igual modo, a região promotora do gene ApoE também não apresentou diferenças usando estas 2 técnicas. No entanto, a BDS evidenciou diferenças em locais CpGs específicos, mostrando que existe uma tendência para o aumento da metilação nos CpGs 1, 3 e 5; e para diminuição da metilação no CpG 6 dos pacientes relativamente aos indivíduos control. Este estudo permitiu verificar uma tendência para de diminuição da metilação global dos pacientes com possível DA relativamente aos controlos e também a existência de um possível padrão de metilação da região promotora do gene ApoE, que pode estar relacionado com a patologia da DA .
Sharpe, Benjamin Peter. "Prostate cancer stem cells : potential new biomarkers". Thesis, University of Bath, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.698969.
Pełny tekst źródłaRankin, Naomi. "Immunoglobulin G glycoslation as a potential biomarker for multiple sclerosis". Thesis, University of Strathclyde, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538908.
Pełny tekst źródłaThomas, Joanna. "Brown adipose tissue a potential early biomarker of metabolic syndrome /". Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p3356437.
Pełny tekst źródłaTitle from first page of PDF file (viewed July 9, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
Thermaenius, Elisabeth. "Prostasome ELISA - a potential marker for prostate cancer diagnosis". Thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-179493.
Pełny tekst źródłaHamid, Umi Marshida Abd. "Glycosylation-based approaches for potential breast cancer biomarkers". Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.540155.
Pełny tekst źródłaAshtaputre, Ravina M. "Potential Biomarkers for Preterm Delivery in Amniotic Fluid". Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1464186519.
Pełny tekst źródłaMacedo, Bárbara Beatriz Pinto. "Aldehyde dehydrogenases as potential biomarkers in myeloid neoplasias". Master's thesis, Universidade de Aveiro, 2018. http://hdl.handle.net/10773/22674.
Pełny tekst źródłaA superfamília das desidrogenases dos aldeídos (ALDH) é constituída por 19 enzimas cuja principal função é a proteção do organismo contra aldeídos tóxicos. As ALDHs têm sido associadas ao desenvolvimento de múltiplas doenças. As síndromes mielodisplásicas (SMD) são caracterizadas por hematopoiese ineficaz associada a citopenias no sangue periférico e elevada predisposição para transformação leucémica. A leucemia mieloide aguda (LMA) é caracterizada por crescimento anómalo de células mieloides imaturas no sangue e na medula óssea. A fisiopatologia das SMDs e LMAs é um processo complexo de múltiplas etapas que envolve alterações genéticas e epigenéticas numa ampla variedade de genes associados à diferenciação, proliferação, auto-renovação e apoptose celulares. Uma vez que as ALDHs estão envolvidas em alguns destes processos biológicos, a desregulação destas enzimas pode influenciar o desenvolvimento de SMD e LMA. O objetivo deste estudo é avaliar a expressão génica das ALDHs em doentes com SMD e LMA de modo a verificar seu potencial como biomarcadores de diagnóstico e/ou prognóstico destas doenças. Neste contexto, analisou-se a expressão da ALDH1A1, ALDH1A2, ALDH1A3, ALDH1B1, ALDH1L1, ALDH1L2, ALDH2, ALDH3A1, ALDH3A2, ALDH3B1, ALDH3B2, ALDH4A1, ALDH5A1, ALDH7A1, ALDH16A1 e ALDH18A1 por PCR de transcriptase reversa. Os genes diferencialmente expressos (ALDH3A2, ALDH3B1, ALDH4A1 e ALDH18A1) foram quantificados, por PCR em tempo real, em 54 doentes, 34 com SMD e 20 com LMA, e em 34 controlos saudáveis. A análise estatística foi realizada com recurso aos testes de Kolmogorov-Smirnov, Mann-Whitney, Kruskal-Wallis e análise ROC. As diferenças foram consideradas significativas quando p<0.05. Os resultados mostraram que para as ALDH1A3, ALDH1L1, ALDH1L2, ALDH3A1, ALDH3B2 e ALDH5A1 não existem diferenças de expressão entre doentes com SMD, doentes com LMA e controlos. Os doentes com SMD e LMA apresentam níveis de expressão de ALDH3A2 (SMD: mediana 1.9251; distância interquartil 1.28; p=0.000618; LMA: mediana 1.5096; distância interquartil 0.99; p=0.008) e ALDH4A1 (SMD: mediana 0.1841; distância interquartil 0.47; p=0.01134; LMA: mediana 0.1635; distância interquartil 0.78; p=0.124) superiores aos observados nos controlos (ALDH3A2: mediana 0.4624; distância interquartil 1.53; ALDH4A1: mediana 0.0388; distância interquartil 0.12). Por outro lado, os doentes com SMD apresentam níveis de expressão mais elevados de ALDH3B1 (mediana 1.6445; distância interquartil 1.39) do que os doentes com LMA (mediana 0.4541; distância interquartil 0.47; p=0.000314) e controlos (mediana 0.3521; distância interquartil 0.51; p=5.9942E-07). Os diferentes subtipos de SMD apresentam expressão diferencial de ALDH3A2 e ALDH3B1. Além disso, os doentes com SMD e com LMA com alterações mielodisplásicas não expressam ALDH18A1. Seguidamente avaliou-se a expressão das ALDHs nos doentes de SMD estratificados de acordo com o WPSS (WHO classification-based Prognostic Scoring System) e verificou-se que os doentes de muito baixo risco apresentaram maior expressão de ALDH3B1 (mediana 17.6934; distância interquartil 16.32) comparativamente aos de risco intermédio (mediana 1.2352; distância interquartil 2.55; p=0.010) . Por fim, a expressão das isoformas de ALDH não parece influenciar a sobrevivência global de doentes com SMD e LMA ou a evolução de SMD para LMA. Em conclusão, este trabalho sugere que as isoformas de ALDH apresentam expressão diferencial em doentes com SMD e LMA relativamente a indivíduos saudáveis e entre si. A expressão de ALDH3B1 poderá ser um potencial biomarcador de diagnóstico de SMD. Além disso, uma vez que nenhum doente com SMD e LMA com alterações mielodisplásicas apresenta expressão da ALDH18A1, a expressão desta isoforma poderá ser um bom biomarcador de diagnóstico de mielodisplasia. Por fim, a expressão de ALDH3A2 demostrou ser um possível biomarcador de diagnóstico de LMA. No entanto, estudos adicionais com um maior número de amostras são necessários para provar o potencial dessas enzimas como biomarcadores de diagnóstico.
Aldehyde Dehydrogenase (ALDH) superfamily is a group of 19 enzymes critical to the protection against toxic aldehydes, and have been associated with multiple diseases. Myelodysplastic syndromes (MDS) are characterized by ineffective hematopoiesis associated with peripheral blood cytopenias, and a predisposition toward leukemic transformation. Acute myeloid leukemia (AML) are characterized by disordered growth of immature myeloid blood cells in the blood and bone marrow. The pathophysiology of both, MDS and AML, is a complex multistep process that involves genetic and epigenetic abnormalities in a wide variety of genes associated with differentiation, cellular proliferation, self-renewal, and apoptosis. Since ALDHs are involved in some of these biological processes, the deregulation of these enzymes may influence MDS and AML development. The aim of the study is to evaluate the gene expression of ALDHs in patients with MDS and AML in order to verify their potential as a biomarker for the diagnosis and/or prognosis of these diseases. To this end, we did a preliminary analysis of the expression levels of ALDH1A1, ALDH1A2, ALDH1A3, ALDH1B1, ALDH1L1, ALDH1L2, ALDH2, ALDH3A1, ALDH3A2, ALDH3B1, ALDH3B2, ALDH4A1, ALDH5A1, ALDH7A1, ALDH16A1, and ALDH18A1. Then, we analyzed gene expression of ALDH3A2, ALDH3B1, ALDH4A1, and ALDH18A1 in 54 patients, 34 MDS and 20 AML, and 34 healthy controls. ALDH expression levels were analyzed using Reverse Transcriptase-PCR and differentially expressed genes were quantified by qPCR. The statistical analysis was carried out by the Kolmogorov-Smirnov Test, Mann-Whitney test, Kruskal-Wallis test, and ROC analysis. A value of p < 0.05 was considered significant. The results indicate that ALDH1A3, ALDH1L1, ALDH1L2, ALDH3A1, ALDH3B2, and ALDH5A1 did not show differences in their expression between MDS, AML, and controls. ALDH3A2, ALDH3B1, ALDH4A1, and ALDH18A1 had differential expression among study groups and were quantified by real time PCR. MDS and AML patients showed higher expression of ALDH3A2 (MDS: median 1.9251; interquartile range 1.28; p=0.000618; AML: median 1.5096; interquartile range 0.99; p=0.008) and ALDH4A1 (MDS: median 0.1841; interquartile range 0.47; p=0.01134; AML: median 0.1635; interquartile range 0.78; p=0.124) in comparison with controls (ALDH3A2: median 0.4624; interquartile range 1.53; ALDH4A1: median 0.0388; interquartile range 0.12). On the other hand, the expression of ALDH3B1 was higher in MDS patients (median 1.6445; interquartile range 1.39) than in AML patients (median 0.4541; interquartile range 0.47; p=0.000314) and controls (median 0.3521; interquartile range 0.51; p=5.9942E-07). ALDH3A2 and ALDH3B1 also showed statistically significant differences between the different subtypes of MDS. Additionally, patients with MDS and AML with myelodysplasia related changes (AML-MRC) did not expressed ALDH18A1. When we compared MDS patients according to WHO classification-based prognostic scoring system (WPSS) risk groups it was found that patients with very low risk had higher expression of ALDH3B1 (median 17.6934; interquartile range 16.32) in comparison with patients with intermediate risk (median 1.2352; interquartile range 2.55; p=0.010). Furthermore, the expression of ALDH isoforms does not appear to influence MDS and AML patient’s overall survival or MDS evolution to AML. In summary, ALDH isoforms have differential expression patterns in MDS and AML patients when compared with controls and each other. The ALDH3B1 is a potential diagnostic biomarker of MDS. Since none MDS and AML-MRC patients expressed ALDH18A1, the expression of this isoform may be a good diagnostic biomarker. Finally, ALDH3A2 could be a diagnostic biomarker of AML. However, further studies with a higher number of participants are needed to prove the potential of these enzymes as diagnostic biomarkers.
Książki na temat "Potential biomaker"
Lee, Amanda Jayne. Potential biomarkers of cancer risk associated with exposure to hexavalent chromium. Birmingham: University of Birmingham, 2003.
Znajdź pełny tekst źródłaBallachey, Brenda Elizabeth. Biomarkers of damage to sea otters in Prince William Sound, Alaska, following potential exposure to oil spilled from the Exxon Valdez. Anchorage, AK: U.S. Fish and Wildlife Service, Alaska Fish and Wildlife Research Center, 1995.
Znajdź pełny tekst źródłaBallachey, Brenda Elizabeth. Biomarkers of damage to sea otters in Prince William Sound, Alaska, following potential exposure to oil spilled from the Exxon Valdez. Anchorage, AK: U.S. Fish and Wildlife Service, Alaska Fish and Wildlife Research Center, 1995.
Znajdź pełny tekst źródłaBallachey, Brenda Elizabeth. Biomarkers of damage to sea otters in Prince William Sound, Alaska, following potential exposure to oil spilled from the Exxon Valdez. Anchorage, AK: U.S. Fish and Wildlife Service, Alaska Fish and Wildlife Research Center, 1995.
Znajdź pełny tekst źródłaBlumenberg, Miroslav, red. Human Skin Cancer, Potential Biomarkers and Therapeutic Targets. InTech, 2016. http://dx.doi.org/10.5772/61922.
Pełny tekst źródłaTenovuo, Olli, Jean-charles Sanchez, Damir Janigro i Johan Undén, red. Biomarkers of Brain Damage – A Complex Challenge with Great Potential. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-754-3.
Pełny tekst źródłaCassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Roy A. J. Spence OBE, Miranda Payne i Gareth Morris-Stiff. Biomarkers and cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0040.
Pełny tekst źródłaNizari, Shereen, Cheryl Hawkes, Anusha Mishra i Yorito Hattori, red. The Neurovascular Unit as a Potential Biomarker and Therapeutic Target in Cerebrovascular Disease. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-238-5.
Pełny tekst źródłaProwle, John R. Renal injury biomarkers in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0302.
Pełny tekst źródłaFarooqui, Akhlaq A. Neurochemical Aspects of Alzheimer's Disease: Risk Factors, Pathogenesis, Biomarkers, and Potential Treatment Strategies. Elsevier Science & Technology Books, 2017.
Znajdź pełny tekst źródłaCzęści książek na temat "Potential biomaker"
Sloan, Philip. "The Bi-Directional Communication Between Tumour Cells and Other Components of the Tumour Microenvironment". W Critical Issues in Head and Neck Oncology, 1–9. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23175-9_1.
Pełny tekst źródłaNotter, Tina. "Immunological Processes in Schizophrenia Pathology: Potential Biomarkers?" W Biomarkers in Psychiatry, 389–410. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/7854_2018_43.
Pełny tekst źródłaMiyake, Hideaki, Atsushi Takenaka i Masato Fujisawa. "Biomarkers of Potential Therapeutic Value". W Prostate Cancer: A Comprehensive Perspective, 181–87. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2864-9_15.
Pełny tekst źródłaLotsberg, Maria Lie, i Stacey Ann D’mello Peters. "Publication Bias in Precision Oncology and Cancer Biomarker Research; Challenges and Possible Implications". W Human Perspectives in Health Sciences and Technology, 155–74. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92612-0_10.
Pełny tekst źródłaAnjum, Naser A., Sarvajeet Singh Gill, Armando C. Duarte i Eduarda Pereira. "Oxidative Stress Biomarkers and Antioxidant Defense in Plants Exposed to Metallic Nanoparticles". W Nanomaterials and Plant Potential, 427–39. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-05569-1_17.
Pełny tekst źródłaPhilips, Thomas, i Rita Sattler. "Glial Glutamate and Metabolic Transporters as a Target for Neurodegenerative Therapy and Biomarkers". W Pathological Potential of Neuroglia, 61–88. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0974-2_4.
Pełny tekst źródłaSimões e Silva, Ana Cristina, André Barreto Pereira, Mauro Martins Teixeira i Antônio Lúcio Teixeira. "Chemokines as Potential Markers in Pediatric Renal Diseases". W Biomarkers in Kidney Disease, 229–48. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-7699-9_39.
Pełny tekst źródłaSimões e Silva, Ana Cristina, André Barreto Pereira, Mauro Martins Teixeira i Antônio Lúcio Teixeira. "Chemokines as Potential Markers in Pediatric Renal Diseases". W Biomarkers in Kidney Disease, 1–20. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7743-9_39-1.
Pełny tekst źródłaPerkovic, Matea Nikolac, Gordana Nedic Erjavec, Dubravka Svob Strac i Nela Pivac. "Biomarkers of Depression: Potential Diagnostic Tools". W Understanding Depression, 35–51. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-6577-4_3.
Pełny tekst źródłaIuliano, Luigi, i Ulf Diczfalusy. "Oxysterols: Potential Biomarkers of Oxidative Stress". W Biomarkers for Antioxidant Defense and Oxidative Damage: Principles and Practical Applications, 99–115. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9780813814438.ch7.
Pełny tekst źródłaStreszczenia konferencji na temat "Potential biomaker"
Juratli, M., S. Sliwinski, E. Oppermann, A. Lorentzen, A. Pascher, WO Bechstein i M. Heikenwälder. "Ezrin-polarized circulating tumor cells as a potential biomaker in hepatocellular carcinoma". W 37. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0040-1721999.
Pełny tekst źródłaBrum, Wagner, Andrei Bieger, Joao Pedro Ferrari Souza, Marco de Bastiani, Andrea Benedet, Nicholas Ashton, Tharick Pascoal i in. "A THREE-RANGE APPROACH ENHANCES PROGNOSTIC UTILITY OF CSF BIOMARKERS IN ALZHEIMER’S DISEASE". W XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda022.
Pełny tekst źródłaKallingal, Nithusha, Kishor Kumar Sadasivuni, Issam Bahadur, Huseyin Cagatay Yalcin, Asiya Al-Busaidi, Hassen M. Ouakad i Somaya Al-Maadeed. "Colorimetry-based Detection of Exhaled Breath Biomarkers for Predicting Heart Failure". W Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0077.
Pełny tekst źródłaShah, Samar, Yaling Liu i Walter Hu. "Characterization of Biosensor Detection Process at Ultra-Low Concentration Through a Stochastic Particle Model". W ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13069.
Pełny tekst źródłaAzevedo, Fernanda Reis de, Michael Polydefkis, Simina Ticau, David Erbe, Anastasia McManus, Emre Aldinc, David Adams, Mary Reilly, Akshay Vaishnaw i Paul Nio. "Neurofilament Light Chain (NfL) as a Potential Biomarker of Treatment Response in Hereditary TransthyretinMediated (hATTR) Amyloidosis: Patisiran Global OLE Study". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.200.
Pełny tekst źródłaSeitkhaziyev, Yessimkhan Sherekhanovich, Nariman Danebekovich Sarsenbekov i Rakhim Nagangaliyevich Uteyev. "Geochemical Atlas of Oils and Source Rocks and Oil-Source Rock Correlations: A Case Study of Oil and Ggas Fields in the Mangyshlak Basin (Kazakhstan)". W SPE Annual Caspian Technical Conference. SPE, 2022. http://dx.doi.org/10.2118/212078-ms.
Pełny tekst źródłaOLIVEIRA, SANDRA MAXIMIANO DE, IGHOR LUIZ AZEVEDO TEIXEIRA, CAROLINA NUNES FRANÇA, CRISTIANE KAYSER, LUCAS GARCIA BIAGI i MARIA CRISTINA DE OLIVEIRA IZAR. "MICROPARTICLES IN SYSTEMIC SCLEROSIS: POTENTIAL NEW BIOMARKER?" W 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-514.
Pełny tekst źródłaCelik, Emrah, Nicolas Rongione, Amelia Bahamonde, Zheng Ao i Ram Datar. "Isolation of Circulating Tumor Cells Using Stiffness-Based Filtration Platform". W ASME 2015 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/imece2015-53241.
Pełny tekst źródłaTanino, Y., X. Wang, Y. Inokoshi, K. Saito, N. Nakagawa, S. Sato, T. Ishii i in. "Syndecan-4 as a Potential Biomarker for Sarcoidosis." 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.a2267.
Pełny tekst źródłaNguyen, Thanh-Qua, Jeongyun Kim, Daewoong Lee, Ji-Seob Choi, Jaeho Park, Hojeong Jeon, Woo-Tae Park i Sangyoup Lee. "Immobilization of Magnetic Beads for Microfluidic Immunoassays". W ASME-JSME-KSME 2019 8th Joint Fluids Engineering Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/ajkfluids2019-5401.
Pełny tekst źródłaRaporty organizacyjne na temat "Potential biomaker"
Petkova, Boryana, Emilia Alova, Iliya Karagyozov, Polya Stoyanova, Vladimir Jekov, Milena Mourdjeva i Tsvetelina Oreshkova. IL-10: a Potential Prognostic Biomarker for Missed Abortion. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, lipiec 2019. http://dx.doi.org/10.7546/crabs.2019.07.16.
Pełny tekst źródłaMARTÍNEZ LEAL, LAURA DE LA CRUZ, i Carlos Romá Mateo. Preliminary proteomics analysis of the potential use of HMGB1 as sepsis biomarker. Fundación Avanza, maj 2023. http://dx.doi.org/10.60096/fundacionavanza/2312022.
Pełny tekst źródłaMa, Yunxing, Julia Brettschneider i Joanna Collingwood. A systematic review and meta-analysis of cerebrospinal fluid amyloid and tau levels in patients progressing from Mild Cognitive Impairment to Alzheimer’s Disease. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, lipiec 2022. http://dx.doi.org/10.37766/inplasy2022.7.0020.
Pełny tekst źródłaSwaby, Ramona. Cancer-Associated PCNA as a Potential Biomarker for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2010. http://dx.doi.org/10.21236/ada549224.
Pełny tekst źródłaPodlevsky, Joshua. Cas9 Protein Post-translational Modifications (PTMs): A Potential Biomarker of Gene-editing. Office of Scientific and Technical Information (OSTI), październik 2019. http://dx.doi.org/10.2172/1571552.
Pełny tekst źródłaCarlson, Kelsey, Kenneth J. Prusa, Chris A. Fedler, Ed M. Steadham, Elisabeth J. Huff-Lonergan i Steven M. Lonergan. Desmin and Peroxiredoxin-2 are Potential Biomarkers for Pork Tenderness. Ames (Iowa): Iowa State University, styczeń 2017. http://dx.doi.org/10.31274/ans_air-180814-313.
Pełny tekst źródłaCupples, Alison M. Development of Biomarkers for Assessing In Situ RDX Biodegradation Potential. Fort Belvoir, VA: Defense Technical Information Center, luty 2010. http://dx.doi.org/10.21236/ada573427.
Pełny tekst źródłaKarow, David S. MRI-Derived Cellularity Index as a Potential Noninvasive Imaging Biomarker of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, październik 2014. http://dx.doi.org/10.21236/ada616253.
Pełny tekst źródłaSun, Peiquing. Identification of Potential Biomarkers for the Early Diagnosis of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2003. http://dx.doi.org/10.21236/ada421783.
Pełny tekst źródłabao, qiangji, Xin ting Wu, Shu-Jun Chen, Jin-Tao Zhang, Kai Zhao Zhang, Yu Guo, Xiao-Feng Du i Ming-Fei Yang. Potential Biomarkers for Post-Stroke Depression: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, kwiecień 2022. http://dx.doi.org/10.37766/inplasy2022.4.0142.
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