Relevant bibliographies by topics / Phenotypes

Academic literature on the topic 'Phenotypes'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Phenotypes"

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Catalán, Pablo, Andreas Wagner, Susanna Manrubia, and José A. Cuesta. "Adding levels of complexity enhances robustness and evolvability in a multilevel genotype–phenotype map." Journal of The Royal Society Interface 15, no. 138 (January 2018): 20170516. http://dx.doi.org/10.1098/rsif.2017.0516.

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Robustness and evolvability are the main properties that account for the stability and accessibility of phenotypes. They have been studied in a number of computational genotype–phenotype maps. In this paper, we study a metabolic genotype–phenotype map defined in toyLIFE , a multilevel computational model that represents a simplified cellular biology. toyLIFE includes several levels of phenotypic expression, from proteins to regulatory networks to metabolism. Our results show that toyLIFE shares many similarities with other seemingly unrelated computational genotype–phenotype maps. Thus, toyLIFE shows a high degeneracy in the mapping from genotypes to phenotypes, as well as a highly skewed distribution of phenotypic abundances. The neutral networks associated with abundant phenotypes are highly navigable, and common phenotypes are close to each other in genotype space. All of these properties are remarkable, as toyLIFE is built on a version of the HP protein-folding model that is neither robust nor evolvable: phenotypes cannot be mutually accessed through point mutations. In addition, both robustness and evolvability increase with the number of genes in a genotype. Therefore, our results suggest that adding levels of complexity to the mapping of genotypes to phenotypes and increasing genome size enhances both these properties.
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von Both, Ulrich, Anna Buerckstuemmer, Kirsten Fluegge, and Reinhard Berner. "Heterogeneity of Genotype-Phenotype Correlation among Macrolide-Resistant Streptococcus agalactiae Isolates." Antimicrobial Agents and Chemotherapy 49, no. 7 (July 2005): 3080–82. http://dx.doi.org/10.1128/aac.49.7.3080-3082.2005.

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ABSTRACT Seventy-four erythromycin-resistant group B Streptococcus isolates were analyzed regarding their phenotype-genotype and phenotype-serotype correlation. Four different phenotypes were assessed, one of them for the first time. ermB and ermTR were the most frequent genotypes (80%). The most prevalent serotype III showed great phenotypic variability while serotype V was strongly associated only with two different phenotypes.
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Volkova, G. V., O. A. Kudinova, and O. F. Vaganova. "Diversity of virulence phenotypes of Puccinia triticinain different agroclimatic zones of the North Caucasus." Rossiiskaia selskokhoziaistvennaia nauka, no. 6 (December 15, 2019): 23–26. http://dx.doi.org/10.31857/s2500-26272019623-26.

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The phenotypic composition of the North Caucasian population of wheat leaf rust pathogen (Puccinia triticina Erikks.) in various agro-climatic zones of the region in 2016-2018 is analyzed. 233 single pustule isolates were studied, of which 212 virulence phenotypes were identified. In all the years of research, a high level of population diversity was established (the Shannon index (Sh) was 0.92-0.99). The dominant phenotype in 2016 was the PHRS phenotype, which was identified in the southern foothill, western Azov and eastern steppe agro-climatic zones. In the population of 2016, phenotypes with a high and medium number of virulence genes prevailed. In 2017, the most represented are the phenotypes of DCRL, LBLL (Western Azov zone) and PCQB (Northern zone). Avirulent phenotype BBBB was common for populations of 20162018. In 2016, a phenotype with virulence to Lr9 (TLGS) was first detected. In 2017 and 2018, phenotypes virulent to the Lr24 gene (PKTT, SFGQ, CFPQ, TKTS, MKTT, LKSR) were detected in the populations of the fungus. A high level of population differences in phenotypic composition between the years of research was established (Rogers index (R) was 0.96 -0.99).
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Zhang, Tracy D., Scott C. Kolbe, Leah C. Beauchamp, Ella K. Woodbridge, David I. Finkelstein, and Emma L. Burrows. "How Well Do Rodent Models of Parkinson’s Disease Recapitulate Early Non-Motor Phenotypes? A Systematic Review." Biomedicines 10, no. 12 (November 24, 2022): 3026. http://dx.doi.org/10.3390/biomedicines10123026.

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The prodromal phase of Parkinson’s disease (PD) is characterised by many non-motor symptoms, and these have recently been posited to be predictive of later diagnosis. Genetic rodent models can develop non-motor phenotypes, providing tools to identify mechanisms underlying the early development of PD. However, it is not yet clear how reproducible non-motor phenotypes are amongst genetic PD rodent models, whether phenotypes are age-dependent, and the translatability of these phenotypes has yet to be explored. A systematic literature search was conducted on studies using genetic PD rodent models to investigate non-motor phenotypes; cognition, anxiety/depressive-like behaviour, gastrointestinal (GI) function, olfaction, circadian rhythm, cardiovascular and urinary function. In total, 51 genetic models of PD across 150 studies were identified. We found outcomes of most phenotypes were inconclusive due to inadequate studies, assessment at different ages, or variation in experimental and environmental factors. GI dysfunction was the most reproducible phenotype across all genetic rodent models. The mouse model harbouring mutant A53T, and the wild-type hα-syn overexpression (OE) model recapitulated the majority of phenotypes, albeit did not reliably produce concurrent motor deficits and nigral cell loss. Furthermore, animal models displayed different phenotypic profiles, reflecting the distinct genetic risk factors and heterogeneity of disease mechanisms. Currently, the inconsistent phenotypes within rodent models pose a challenge in the translatability and usefulness for further biomechanistic investigations. This review highlights opportunities to improve phenotype reproducibility with an emphasis on phenotypic assay choice and robust experimental design.
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Angelone, Steven, Iván Piña-Torres, Israel Padilla-Guerrero, and Michael Bidochka. "“Sleepers” and “Creepers”: A Theoretical Study of Colony Polymorphisms in the Fungus Metarhizium Related to Insect Pathogenicity and Plant Rhizosphere Colonization." Insects 9, no. 3 (August 17, 2018): 104. http://dx.doi.org/10.3390/insects9030104.

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Different strains of Metarhizium exhibit a range of polymorphisms in colony phenotypes. These phenotypes range from highly conidiating colonies to colonies that produce relatively more mycelia and few conidia. These different phenotypes are exhibited in infected insects in the soil. In this paper, we provide a theoretical consideration of colony polymorphisms and suggest that these phenotypes represent a range of strategies in the soil that Metarhizium exhibits. We call these different strategies “sleepers” and “creepers”. The “sleeper” phenotype produces relatively greater amounts of conidia. We use the term “sleeper” to identify this phenotype since this strategy is to remain in the soil as conidia in a relatively metabolically inactive state until a host insect or plant encounter these conidia. The “creeper” phenotype is predominantly a mycelial phenotype. In this strategy, hyphae move through the soil until a host insect or plant is encountered. We theoretically model the costs and benefits of these phenotypic polymorphisms and suggest how evolution could possibly select for these different strategies.
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Adams, Dean C., and Michael L. Collyer. "Phylogenetic Comparative Methods and the Evolution of Multivariate Phenotypes." Annual Review of Ecology, Evolution, and Systematics 50, no. 1 (November 2, 2019): 405–25. http://dx.doi.org/10.1146/annurev-ecolsys-110218-024555.

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Evolutionary biology is multivariate, and advances in phylogenetic comparative methods for multivariate phenotypes have surged to accommodate this fact. Evolutionary trends in multivariate phenotypes are derived from distances and directions between species in a multivariate phenotype space. For these patterns to be interpretable, phenotypes should be characterized by traits in commensurate units and scale. Visualizing such trends, as is achieved with phylomorphospaces, should continue to play a prominent role in macroevolutionary analyses. Evaluating phylogenetic generalized least squares (PGLS) models (e.g., phylogenetic analysis of variance and regression) is valuable, but using parametric procedures is limited to only a few phenotypic variables. In contrast, nonparametric, permutation-based PGLS methods provide a flexible alternative and are thus preferred for high-dimensional multivariate phenotypes. Permutation-based methods for evaluating covariation within multivariate phenotypes are also well established and can test evolutionary trends in phenotypic integration. However, comparing evolutionary rates and modes in multivariate phenotypes remains an important area of future development.
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Iwasaki, Takeshi, Hiroshi Doi, Hideaki Tsuji, Yuya Tabuchi, Motomu Hashimoto, Koji Kitagori, Shuji Akizuki, et al. "Phenotypic landscape of systemic lupus erythematosus: An analysis of the Kyoto Lupus Cohort." Modern Rheumatology 32, no. 3 (August 12, 2021): 571–76. http://dx.doi.org/10.1093/mr/roab020.

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ABSTRACT Objectives The present study aimed to clarify comprehensive relationships among the clinical variables of systemic lupus erythematosus (SLE). Methods We retrospectively surveyed 32 clinical variables in 581 patients and conducted comprehensive association studies among SLE clinical phenotypes. A univariate analysis of all possible combinations was performed, and the results of phenotypic correlations were reduced into two dimensions. We also created a regression formula using L1 regularisation (LASSO) to calculate the probability of exhibiting each phenotype. Results The univariate analysis identified 26 correlations, including multiple phenotypes with low complement. Some unpredicted correlations were identified, including fever and the anti-Sm antibody (odds ratio; OR = 2.3, p = 1.6 × 10–5) or thrombocytopenia and psychosis (OR = 3.7, p = 3.2 × 10–5). The multivariate analysis accurately estimated the probability of exhibiting each phenotype (area under the curve > 0.7) in 10 out of 20 phenotypes. Conclusions The present results show the phenotypic architecture of SLE and represent a model for estimating the probability of exhibiting each phenotype. They also offer insights into the pathology of SLE and estimating the probability of the onset of new phenotypes in clinical practice.
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Ju, Meizhi, Andrea D. Short, Paul Thompson, Nawar Diar Bakerly, Georgios V. Gkoutos, Loukia Tsaprouni, and Sophia Ananiadou. "Annotating and detecting phenotypic information for chronic obstructive pulmonary disease." JAMIA Open 2, no. 2 (April 26, 2019): 261–71. http://dx.doi.org/10.1093/jamiaopen/ooz009.

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Abstract Objectives Chronic obstructive pulmonary disease (COPD) phenotypes cover a range of lung abnormalities. To allow text mining methods to identify pertinent and potentially complex information about these phenotypes from textual data, we have developed a novel annotated corpus, which we use to train a neural network-based named entity recognizer to detect fine-grained COPD phenotypic information. Materials and methods Since COPD phenotype descriptions often mention other concepts within them (proteins, treatments, etc.), our corpus annotations include both outermost phenotype descriptions and concepts nested within them. Our neural layered bidirectional long short-term memory conditional random field (BiLSTM-CRF) network firstly recognizes nested mentions, which are fed into subsequent BiLSTM-CRF layers, to help to recognize enclosing phenotype mentions. Results Our corpus of 30 full papers (available at: http://www.nactem.ac.uk/COPD) is annotated by experts with 27 030 phenotype-related concept mentions, most of which are automatically linked to UMLS Metathesaurus concepts. When trained using the corpus, our BiLSTM-CRF network outperforms other popular approaches in recognizing detailed phenotypic information. Discussion Information extracted by our method can facilitate efficient location and exploration of detailed information about phenotypes, for example, those specifically concerning reactions to treatments. Conclusion The importance of our corpus for developing methods to extract fine-grained information about COPD phenotypes is demonstrated through its successful use to train a layered BiLSTM-CRF network to extract phenotypic information at various levels of granularity. The minimal human intervention needed for training should permit ready adaption to extracting phenotypic information about other diseases.
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Monés, Jordi, and Marc Biarnés. "Geographic atrophy phenotype identification by cluster analysis." British Journal of Ophthalmology 102, no. 3 (July 20, 2017): 388–92. http://dx.doi.org/10.1136/bjophthalmol-2017-310268.

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Background/aimsTo identify ocular phenotypes in patients with geographic atrophy secondary to age-related macular degeneration (GA) using a data-driven cluster analysis.MethodsThis was a retrospective analysis of data from a prospective, natural history study of patients with GA who were followed for ≥6 months. Cluster analysis was used to identify subgroups within the population based on the presence of several phenotypic features: soft drusen, reticular pseudodrusen (RPD), primary foveal atrophy, increased fundus autofluorescence (FAF), greyish FAF appearance and subfoveal choroidal thickness (SFCT). A comparison of features between the subgroups was conducted, and a qualitative description of the new phenotypes was proposed. The atrophy growth rate between phenotypes was then compared.ResultsData were analysed from 77 eyes of 77 patients with GA. Cluster analysis identified three groups: phenotype 1 was characterised by high soft drusen load, foveal atrophy and slow growth; phenotype 3 showed high RPD load, extrafoveal and greyish FAF appearance and thin SFCT; the characteristics of phenotype 2 were midway between phenotypes 1 and 3. Phenotypes differed in all measured features (p≤0.013), with decreases in the presence of soft drusen, foveal atrophy and SFCT seen from phenotypes 1 to 3 and corresponding increases in high RPD load, high FAF and greyish FAF appearance. Atrophy growth rate differed between phenotypes 1, 2 and 3 (0.63, 1.91 and 1.73 mm2/year, respectively, p=0.0005).ConclusionCluster analysis identified three distinct phenotypes in GA. One of them showed a particularly slow growth pattern.
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Greenbury, Sam F., Iain G. Johnston, Ard A. Louis, and Sebastian E. Ahnert. "A tractable genotype–phenotype map modelling the self-assembly of protein quaternary structure." Journal of The Royal Society Interface 11, no. 95 (June 6, 2014): 20140249. http://dx.doi.org/10.1098/rsif.2014.0249.

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The mapping between biological genotypes and phenotypes is central to the study of biological evolution. Here, we introduce a rich, intuitive and biologically realistic genotype–phenotype (GP) map that serves as a model of self-assembling biological structures, such as protein complexes, and remains computationally and analytically tractable. Our GP map arises naturally from the self-assembly of polyomino structures on a two-dimensional lattice and exhibits a number of properties: redundancy (genotypes vastly outnumber phenotypes), phenotype bias (genotypic redundancy varies greatly between phenotypes), genotype component disconnectivity (phenotypes consist of disconnected mutational networks) and shape space covering (most phenotypes can be reached in a small number of mutations). We also show that the mutational robustness of phenotypes scales very roughly logarithmically with phenotype redundancy and is positively correlated with phenotypic evolvability. Although our GP map describes the assembly of disconnected objects, it shares many properties with other popular GP maps for connected units, such as models for RNA secondary structure or the hydrophobic-polar (HP) lattice model for protein tertiary structure. The remarkable fact that these important properties similarly emerge from such different models suggests the possibility that universal features underlie a much wider class of biologically realistic GP maps.
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Dissertations / Theses on the topic "Phenotypes"

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Sailer, Zachary. "Predicting Phenotypes in Sparsely Sampled Genotype-Phenotype Maps." Thesis, University of Oregon, 2019. http://hdl.handle.net/1794/24231.

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Naturally evolving proteins must navigate a vast set of possible sequences to evolve new functions. This process depends on the genotype-phenotype map. Much effort has been directed at measuring protein genotype phenotype maps to uncover evolutionary trajectories that lead to new functions. Often, these maps are too large to comprehensively measure. Sparsely measured maps, however, are prone to missing key evolutionary trajectories. Many groups turn to computational models to infer missing phenotypes. These models treat mutations as independent perturbations to the genotype-phenotype map. A key question is how to handle non-independent effects known as epistasis. In this dissertation, we address two sources of epistasis: 1) global and 2) local epistasis. We find that incorporating global epistasis improves our predictive power, while local epistasis does not. We use our model to infer unknown phenotypes in the Plasmodium falciparum chloroquine transporter (PfCRT) genotype-phenotype map, a protein responsible for conferring drug resistance in malaria. From these predictions, we uncover key evolutionary trajectories that led high resistance. This dissertation includes previously published and unpublished co-authored material.
2020-01-11
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Arbon, Jed. "Phenotype-genotype correlation between the Hippo pathway and 3D craniofacial phenotypes." Thesis, University of Iowa, 2016. https://ir.uiowa.edu/etd/3042.

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Introduction: The purpose of this study was to examine phenotypic expression of craniofacial form, shape, and size as it relates to the genotype of an individual. Shape analyses were completed on 3-D images of each subject's craniofacial structure by landmarking 45 points of interest on the cranial base, facial bones, and upper and lower jaws. A candidate gene analysis was undertaken focusing on specific genes in the Hippo Signaling Pathway to examine genotype-phenotype correlations that play a role in craniofacial development. This study is a continuation of a larger project aimed at the identification of candidate genes associated with human dento-skeletal bite problems led by Dr. Lina Moreno-Uribe. Methods: The sample size for our study included 166 individuals who had never been treated orthodontically at the time of records. Each individual was genotyped and a CBCT of the craniofacial complex was captured. Each CBCT image was landmarked by a single observer using 45 points to mark points on the cranial base and facial bones including the maxilla and mandible. General Procrustes superimposition was used to find correlations with phenotype and genotype. Size analysis was completed with average Euclidean Distances and ANOVA analysis. Results: 2 SNP's from the FOX03 gene had significant associations with size. The AA genotyped individuals appeared larger in overall size than AB genotyped individuals. 3 SNP's had statistically significant associations with facial form. The FOX06 SNPs had significant associations with increased anterior-posterior growth of the maxilla. The AJUBA SNP had significant associations with increased overall craniofacial breadth. Conclusion: Genes in the Hippo signaling pathway have specific roles in the development of facial form and size.
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Bloomfield, Kelly Louise, and n/a. "Investigation of the Role of Thioredoxin in the Invasive Phenotype and its Interaction with the Transcription Factor Sp1." Griffith University. School of Biomolecular and Biomedical Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20031021.120018.

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Thioredoxin is a small ubiquitous oxido-reductase found in all species. The highly conserved active site, which facilitates thioredoxins redox activity, contains two redox active cysteine residues. Thioredoxin has numerous protein substrates to which it donates H+ ions and it can also function as a free radical scavenger. Through these activities thioredoxin is able to influence the redox state of not only its protein targets, but also the entire cellular environment. Thioredoxin has been implicated in many biological functions, and one mechanism by which it influences these functions is through interactions with a number of transcription factors including NF-kappa-B and p53. Thioredoxin also has numerous extracellular biological roles. It has been shown that thioredoxin is actively secreted from a number of normal and transformed cell lines including fibroblasts and activated B and T cells. This study investigates the role of thioredoxin in embryonic implantation and cancer cell metastasis, two physiological functions which rely on the same basic processes. Thioredoxin expression has previously been shown to be increased in many cancers. However it has not yet been established whether this increase is a causative or a side effect of the cancerous phenotype. Similarly thioredoxin expression has previously been shown to be increased during different phases of the oestrus cycle and pregnancy. This thesis describes the role of thioredoxin in embryonic implantation using a marmoset model. A thioredoxin cDNA was isolated and subsequently sequenced. Preliminary antibody experiments indicated that the anti human thioredoxin monoclonal antibodies available in our laboratory would recognise marmoset thioredoxin. Subsequently immunocytochemistry using anti human thioredoxin antibodies was carried out on sectioned marmoset uterus and embryonic tissue. The results indicated that thioredoxin is expressed by cells at the embryonic-maternal interface of early implantation sites. Further studies demonstrated that thioredoxin is also expressed and secreted by cultured blastocysts in vitro. This thesis also describes the role of thioredoxin in cancer cell metastasis. Results of this study indicate that thioredoxin is actively involved in facilitating the invasive phenotype of breast cancer cells. The two cell lines utilised were MCF-7, a well differentiated, relatively non-invasive breast cancer cell line; and MDA-MB-231, a poorly differentiated, highly invasive breast cancer cell line. The cell lines were transfected with thioredoxin sense, antisense and 1SS (encodes thioredoxin with both active cysteine residues mutated to serine residues and is thus redox inactive) constructs. The results demonstrate that when endogenous thioredoxin levels are increased, i.e. transfected with a sense thioredoxin construct, the invasive breast cancer cell line MDA-MB-231 becomes more invasive, conversely when endogenous levels are decreased, i.e. transfected with antisense or 1SS constructs, the invasive capacity of these cells decreases. However, when the endogenous level of thioredoxin was manipulated in the relatively non-invasive cell line MCF-7 very little effect was observed. Results also indicate that thioredoxin has the ability to act as a chemoattractant for actively invading breast cancer cells. Both of these functions appear to be dependent on thioredoxin's redox activity. Additional studies described in this thesis have shown that thioredoxin is involved in the regulation of Sp1 in vitro. Sp1 is a transcription factor known to regulate the transcription of a number of genes whose products are intimately involved in the invasive phenotype. The results in this study suggest that Sp1 DNA binding is regulated by thioredoxin such that when reduced by the enzyme its binding to DNA is facilitated. Results also indicate that Sp1 may regulate the transcription of thioredoxin by binding to Sp1 sites within the thioredoxin promoter.
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Bloomfield, Kelly Louise. "Investigation of the Role of Thioredoxin in the Invasive Phenotype and its Interaction with the Transcription Factor Sp1." Thesis, Griffith University, 2003. http://hdl.handle.net/10072/366170.

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Thioredoxin is a small ubiquitous oxido-reductase found in all species. The highly conserved active site, which facilitates thioredoxins redox activity, contains two redox active cysteine residues. Thioredoxin has numerous protein substrates to which it donates H+ ions and it can also function as a free radical scavenger. Through these activities thioredoxin is able to influence the redox state of not only its protein targets, but also the entire cellular environment. Thioredoxin has been implicated in many biological functions, and one mechanism by which it influences these functions is through interactions with a number of transcription factors including NF-_B and p53. Thioredoxin also has numerous extracellular biological roles. It has been shown that thioredoxin is actively secreted from a number of normal and transformed cell lines including fibroblasts and activated B and T cells. This study investigates the role of thioredoxin in embryonic implantation and cancer cell metastasis, two physiological functions which rely on the same basic processes. Thioredoxin expression has previously been shown to be increased in many cancers. However it has not yet been established whether this increase is a causative or a side effect of the cancerous phenotype. Similarly thioredoxin expression has previously been shown to be increased during different phases of the oestrus cycle and pregnancy. This thesis describes the role of thioredoxin in embryonic implantation using a marmoset model. A thioredoxin cDNA was isolated and subsequently sequenced. Preliminary antibody experiments indicated that the anti human thioredoxin monoclonal antibodies available in our laboratory would recognise marmoset thioredoxin. Subsequently immunocytochemistry using anti human thioredoxin antibodies was carried out on sectioned marmoset uterus and embryonic tissue. The results indicated that thioredoxin is expressed by cells at the embryonic-maternal interface of early implantation sites. Further studies demonstrated that thioredoxin is also expressed and secreted by cultured blastocysts in vitro. This thesis also describes the role of thioredoxin in cancer cell metastasis. Results of this study indicate that thioredoxin is actively involved in facilitating the invasive phenotype of breast cancer cells. The two cell lines utilised were MCF-7, a well differentiated, relatively non-invasive breast cancer cell line; and MDA-MB-231, a poorly differentiated, highly invasive breast cancer cell line. The cell lines were transfected with thioredoxin sense, antisense and 1SS (encodes thioredoxin with both active cysteine residues mutated to serine residues and is thus redox inactive) constructs. The results demonstrate that when endogenous thioredoxin levels are increased, i.e. transfected with a sense thioredoxin construct, the invasive breast cancer cell line MDA-MB-231 becomes more invasive, conversely when endogenous levels are decreased, i.e. transfected with antisense or 1SS constructs, the invasive capacity of these cells decreases. However, when the endogenous level of thioredoxin was manipulated in the relatively non-invasive cell line MCF-7 very little effect was observed. Results also indicate that thioredoxin has the ability to act as a chemoattractant for actively invading breast cancer cells. Both of these functions appear to be dependent on thioredoxin's redox activity. Additional studies described in this thesis have shown that thioredoxin is involved in the regulation of Sp1 in vitro. Sp1 is a transcription factor known to regulate the transcription of a number of genes whose products are intimately involved in the invasive phenotype. The results in this study suggest that Sp1 DNA binding is regulated by thioredoxin such that when reduced by the enzyme its binding to DNA is facilitated. Results also indicate that Sp1 may regulate the transcription of thioredoxin by binding to Sp1 sites within the thioredoxin promoter.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Berry, Mike A. "An exploration of asthma phenotypes." Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/29513.

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In this thesis the long term stability of eosinophilic bronchitis has been investigated in a longitudinal study. Induced sputum has been used to investigate a possible difference in expression of IL-13 in asthma and eosinophilic bronchitis. Bronchoscopy has been used to compare the airway immunopathology of eosinophilic and non eosinophilic asthma and the long term stability and response to inhaled corticosteroids in non eosinophilic asthma was studied in a prospective randomised controlled trial. Alveolar nitric oxide concentration has been validated as a measure of distal lung inflammation. Finally the role of TNF-alpha and response to etanercept has been investigated in patients with refractory asthma. Evolution from eosinophilic bronchitis into asthma was rare, decline in lung function was not increased, although female gender, smoking and prolonged eosinophilic airway inflammation were independent risk factors for an accelerated decline. IL-13 concentrations were elevated in asthma compared to eosinophilic bronchitis, suggesting a role for this cytokine in the development of airway hyperresponsiveness. Non eosinophilic asthma remained stable over the period of investigation and was associated with reduced response to inhaled corticosteroids. Mast cells were present in airway smooth muscle in eosinophilic and non eosinophilic asthma but not normal controls. Subepithelial layer thickening was a feature of eosinophilic but not non eosinophilic asthma. Alveolar nitric oxide was increased in refractory asthma and reduced by oral but not inhaled corticosteroids.
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Yuan, Qiu-Ping. "Trinucleotide repeats and neuropsychiatric phenotypes /." Stockholm : [Karolinska institutets bibl.], 2001. http://diss.kib.ki.se/2001/91-7349-058-X/.

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Jadon, Deepak. "Biomarkers of psoriatic arthritis phenotypes." Thesis, University of Bath, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.683546.

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Background: Psoriatic arthritis (PsA) is a chronic heterogenous inflammatory arthritis with five phenotypes. The two least studied phenotypes are investigated in this thesis, including: psoriatic spondyloarthropathy (PsSpA) and psoriatic arthritis mutilans (PAM). The aims of this thesis were to determine the prevalence, clinical characteristics and radiographic characteristics of PsSpA and PAM in a cohort of PsA patients, and serum-soluble bone- turnover biomarkers of these phenotypes. Aims: Comparisons were made with PsA patients without axial disease (pPsA), and ankylosing spondylitis (AS) patients. Methods: A prospective single-centre cross-sectional study was conducted of PsA and AS patients. Serum on psoriasis-only patients (PsC) and healthy controls (HC) were also obtained. Multivariate clinical, radiographic, genetic and serum biomarker comparisons were made between these five groups of subjects. Results: The study enrolled 201 PsA and 201 AS patients, who were then reclassified as 118 PsSpA, 127 pPsA and 157 AS cases, alongside 200 PsC and 50 HC subjects. Several clinical biomarkers, imaging biomarkers, serum-soluble biomarkers and genetic biomarkers were identified that differentiate PsSpA from pPsA and AS. PsSpA affected a significant proportion of PsA patients, and was not a milder version of AS. PsSpA involvement was as disabling and clinically impactful as AS. PAM was found to be associated with PsSpA, and clinical biomarkers of PAM occurrence and radiographic progression were identified. Conclusions: In conclusion, this thesis indicates that PsSpA is on a spectrum of musculoskeletal disease, in between pPsA and AS; with PsSpA comprising a continuum itself, and with a phenotype expression related to disease duration. These findings may prompt the inception of an international-consensus classification system for PsSpA, for which there is a great clinical need. Given that PsSpA has its own discrete clinical and biomarker signature, its clinical management and research should be tailored from that of pPsA and AS. Ultimately this may further the effort for stratified and personalised medicine.
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Ding, Zhihao. "The genetics of cellular phenotypes." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708712.

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Heinzmann, Silke. "Nutritional modulation of metabolic phenotypes." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/6320.

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Diet and other lifestyle factors play a critical role in the risk of developing many diseases. Metabolic profiles contain a wealth of biochemical and physiological information and are influenced by various factors such as gender, age, BMI or genetic background. Diet is an important factor, and long-term dietary habits as well as short-term food challenges influence the metabolic phenotype. Metabolic profiling technology can be used to discover novel single or combination biomarkers of food intake. To aid personalised healthy lifestyle recommendations, it is necessary to characterise the metabolic phenotype of individuals and to establish the extent to which we can beneficially influence this phenotype by nutritional intervention. This thesis aims to evaluate metabonomics as a tool for systematically detecting metabolites related to inter-individual and food-related differences. In order to address these aims a nutrition study was undertaken, where individuals followed a strict diet regime consuming a standard diet including specific food challenges, spot urine collections were made throughout the study period. 1H NMR spectroscopy was performed to generate urinary metabolic profiles, which were subsequently analysed and interpreted using multivariate mathematical modelling methods. Clear metabolic signatures pertaining to the consumption of specific dietary components and ‘biomarker’ metabolites associated with particular foods were extracted. Further validation of a potential biomarker was undertaken interrogating a large-scale epidemiologic dataset, the INTERMAP Study. Inter-individual variation in the metabolic profile was observed, both in relation to differences in response to food ingestion and metabolic differences independent from immediate food ingestion. Among these alterations were metabolites originating from gut microbial-mammalian co-metabolism. The influence of the gut microbiota on the metabolic phenotype and obesity was further investigated using microbially modulated murine models. This thesis characterises the effects of the interaction of diet and microbial metabolism on the metabolic phenotype and provides a template for assessing complex dietary interventions with respect to beneficially modulating metabolism.
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Holberg, Catharine Jean 1944. "Genetic epidemiology of asthma phenotypes." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/565581.

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Books on the topic "Phenotypes"

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Frommlet, Florian, Małgorzata Bogdan, and David Ramsey. Phenotypes and Genotypes. London: Springer London, 2016. http://dx.doi.org/10.1007/978-1-4471-5310-8.

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Rollo, C. David. Phenotypes: Their epigenetics, ecology and evolution. London: Chapman & Hall, 1994.

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Patnaik, Ranjan. Engineering complex phenotypes in industrial strains. Hoboken, N.J: Wiley, 2012.

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Patnaik, Ranjan, ed. Engineering Complex Phenotypes in Industrial Strains. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118433034.

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Phenotypes: Their epigenetics, ecology and evolution. London: Chapman & Hall, 1994.

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Zysman, Michele Anne. Characterization of epigenetic phenotypes of endometrial cancer. Ottawa: National Library of Canada, 2002.

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Rice, Mabel, and Steven F. Warren. Developmental language disorders: From phenotypes to etiologies. Mahwah, N.J: Lawrence Erlbaum, 2004.

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Autism spectrum disorders: Phenotypes, mechanisms, and treatments. Basel: Karger, 2015.

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Gould, Todd D., ed. Mood and Anxiety Related Phenotypes in Mice. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-313-4.

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Gould, Todd D., ed. Mood and Anxiety Related Phenotypes in Mice. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-303-9.

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Book chapters on the topic "Phenotypes"

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Gobbetti, Marco, and Raffaella Di Cagno. "The Phenotypes." In Bacterial Communication in Foods, 21–37. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-5656-8_2.

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Sathya, Sethuraman, and Kasi Pandima Devi. "Ageing Phenotypes." In Nutrients and Nutraceuticals for Active & Healthy Ageing, 15–25. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-3552-9_2.

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Davis, Alan M. "System Phenotypes." In Great Software Debates, 119–24. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781119134657.ch21.

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Horn, Charles C. "Overlapping Phenotypes." In Pain Genetics, 115–30. Hoboken, NJ: John Wiley & Sons, Inc, 2013. http://dx.doi.org/10.1002/9781118398890.ch8.

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Rice, Mabel, and Helen Tager-Flusberg. "Language Phenotypes." In Innovations in Cognitive Neuroscience, 227–43. Boston, MA: Springer US, 2016. http://dx.doi.org/10.1007/978-1-4614-3846-5_12.

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Broman, Karl W., and Śaunak Sen. "Non-normal phenotypes." In Statistics for Biology and Health, 135–51. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-92125-9_5.

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Sheth, Jamie, and MeiLan Han. "Phenotypes of COPD." In COPD, 147–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-47178-4_10.

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Francke, U. "Microdeletions and Mendelian Phenotypes." In Human Genetics, 201–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71635-5_24.

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Echevarria, David J., and Kanza M. Khan. "Sleep Phenotypes in Zebrafish." In The rights and wrongs of zebrafish: Behavioral phenotyping of zebrafish, 221–39. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-33774-6_10.

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Ullmann, Jeremy F. P., and Andrew L. Janke. "Neuroimaging Phenotypes in Zebrafish." In The rights and wrongs of zebrafish: Behavioral phenotyping of zebrafish, 273–89. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-33774-6_13.

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Conference papers on the topic "Phenotypes"

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Yin, Kejing, William K. Cheung, Yang Liu, Benjamin C. M. Fung, and Jonathan Poon. "Joint Learning of Phenotypes and Diagnosis-Medication Correspondence via Hidden Interaction Tensor Factorization." In Twenty-Seventh International Joint Conference on Artificial Intelligence {IJCAI-18}. California: International Joint Conferences on Artificial Intelligence Organization, 2018. http://dx.doi.org/10.24963/ijcai.2018/504.

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Non-negative tensor factorization has been shown effective for discovering phenotypes from the EHR data with minimal human supervision. In most cases, an interaction tensor of the elements in the EHR (e.g., diagnoses and medications) has to be first established before the factorization can be applied. Such correspondence information however is often missing. While different heuristics can be used to estimate the missing correspondence, any errors introduced will in turn cause inaccuracy for the subsequent phenotype discovery task. This is especially true for patients with multiple diseases diagnosed (e.g., under critical care). To alleviate this limitation, we propose the hidden interaction tensor factorization (HITF) where the diagnosis-medication correspondence and the underlying phenotypes are inferred simultaneously. We formulate it under a Poisson non-negative tensor factorization framework and learn the HITF model via maximum likelihood estimation. For performance evaluation, we applied HITF to the MIMIC III dataset. Our empirical results show that both the phenotypes and the correspondence inferred are clinically meaningful. In addition, the inferred HITF model outperforms a number of state-of-the-art methods for mortality prediction.
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Ryan, David T., Jingzhe Hu, Byron L. Long, and Amina A. Qutub. "Predicting Endothelial Cell Phenotypes in Angiogenesis." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93124.

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Controlling endogenous angiogenesis, or the formation of new capillaries, is a potential therapeutic strategy for numerous diseases including cancer, stroke and cardiovascular disease (1–4). These efforts have been met with mixed success in the clinic, partly due to an inadequate understanding, and thus control, of the mechanisms that influence the endothelial cells that form capillaries (1, 3). In order to control angiogenesis in an effort to improve treatment responses, quantitative information about endothelial cell behavior must be used to build accurate models of vascular network formation. In this paper, we introduce a method to identify and classify endothelial cell responses to angiogenic stimuli through sophisticated image analysis. The presented automated image processing tools and classification framework allow for rapid quantitative investigations of cellular images. Results of our analysis demonstrate that endothelial cells can be grouped into distinct morphological phenotypes as a function of their responses to combinations of angiogenic growth factor stimuli. Information on phenotypic behavior and responses will be applied towards predicting and guiding cell behavior for therapeutic design.
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Mascaró, Oscar, Joan Serra, Gianni Lucchetti, Xavier Gimeno, and Fernando Ruiz. "COPD Phenotypes and Comorbidities." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3610.

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Mallet, M. C., E. S. L. Pedersen, R. Makhoul, S. Blanchon, K. Hoyler, A. Jochmann, P. Latzin, et al. "Cough phenotypes in children." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.4530.

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Farias, Igor Braga, Bruno de Mattos Lombardi Badia, Gustavo Carvalho Costa, Roberta Ismael Lacerda Machado, Carolina Maria Marin, Wladimir Bocca Vieira de Rezende Pinto, Paulo Victor Sgobbi de Souza, and Acary Souza Bulle Oliveira. "Clinical and genetic profile of Brazilian patients with dysferlinopathies – A retrospective study." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.054.

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Introduction: Dysferlinopathies are a group of conditions that are caused by mutations in the dysferlin gene. Objectives: To characterize the clinical phenotypes and genotypic spectrum of dysferlinopathies patients and to estimate the progression of functional and motor decline. Design and setting: Retrospective analysis of the medical records of patients followed up at our institution between 1995 and 2020. Methods: Patients were selected based on the following inclusion criteria:(i) Identification of a mutation defined as pathogenic in homozygosis or compound heterozygosis in the Dysf gene;or (ii)compatible clinical manifestations and decreased expression of dysferlin in immunohistochemistry on muscle biopsy. Classification of the phenotype was based on the first symptoms. Functionality was defined by the Gardner–Medwin & Walton(GMW) scale modified for dysferlinopathy. Results: 23 patients were included in the study. 16 were classified as limb-girdle muscular dystrophy autosomal recessive 2 (LGMDR2), 4 as Miyoshi muscular dystrophy, 2 as proximo-distal onset and 1 as asymptomatic hyperCKemia. Thighs adduction was the most affected movement in the first evaluation (mean strength=3). Plantar flexion was the movement with the greatest decline in strength(mean=-0.10 points on MRC/year;pT, Arg2042Cys and c.2643+1G>A, p.?(splicing), found 3 times each. There was no statistical difference in muscle strength in the first evaluation, motor and functional decline between the phenotypes. Conclusion: While LGMDR2 was the most common phenotype at onset, with the exception of asymptomatic hyperCKemia, there were not a clear difference in the pattern of progression between them.
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Zhelenina, Liudmila, Maryia Vakharlovskaya, Anna Galustyan, Olga Lavrova, Tatiyana Ivashchenko, and Maryia Kuropatenko. "Phenotypes of asthma in mothers have an influence on asthma phenotypes in children." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa323.

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Al-Nasser, A. "DIETARY LIPIDS AND IMMUNO-PHENOTYPES." In 18th International Multidisciplinary Scientific GeoConference SGEM2018. Stef92 Technology, 2018. http://dx.doi.org/10.5593/sgem2018/6.2/s25.019.

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Pires De Dias Marques, Alda Sofia, Ana Machado, Sara Souto-Miranda, Crsitina Jácome, Joana Cruz, Ana Oliveira, Vera Enes, et al. "Clinical characteristics of COPD Phenotypes." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2876.

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Bartusiak, Emily R., Miriam Barrabes, Aigerim Rymbekova, Julia Gimbernat-Mayol, Cayetana Lopez, Lorenzo Barberis, Daniel Mas Montserrat, Xavier Giro-I-Nieto, and Alexander G. Ioannidis. "Predicting Dog Phenotypes from Genotypes." In 2022 44th Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2022. http://dx.doi.org/10.1109/embc48229.2022.9870905.

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Theissen, Helen, Tapabrata Chakraborti, Stefano Malacrino, Korsuk Sirinukunwattana, Daniel Royston, and Jens Rittscher. "Learning Cellular Phenotypes through Supervision." In 2021 43rd Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2021. http://dx.doi.org/10.1109/embc46164.2021.9629898.

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Reports on the topic "Phenotypes"

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Ouyang, Zhiqiang, Qian Li, Guangrong Zheng, Tengfei Ke, Jun Yang, and Chengde Liao. Radiomics for predicting tumor microenvironment phenotypes in non-small cell lung cance: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0060.

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Review question / Objective: Tumor microenvironment (TIME) phenotype is an important factor to affect the response and prognosis of immunotherapy in non-small cell lung cancer (NSCLC). Recently, accumulating studies have noninvasivly perdited the TIME phenotypes of NSCLC by using CT or PET/CT based radiomics. We will conduct this study by means of meta-analysis to eveluate the power and value of CT or PET/CT based radiomics for predicting TIME phenotypes in NSCLC patients. Condition being studied: At present, several recent prospective or retrospective cohort studies and randomized controlled studies have confirmed that CT or PET/CT-based radiomics were the potential tools to predict TIME phenotypes in NSCLC. However, this conclusion is controversial because of the difference of prediction profermance of different studies. The published and unpublished investigations will be included in this study. We will comprehensively evaluate the heterogeneity of these investigations, and the power and value of radiomics for predicting TIME phenotypes.
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Shipley, James M. Modeling Phenotypes of Tuberous Sclerosis in the Mouse. Fort Belvoir, VA: Defense Technical Information Center, February 2006. http://dx.doi.org/10.21236/ada484673.

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Shipley, James M. Modeling Phenotypes of Tuberous Scerosis in the Mouse. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada535655.

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Shipley, James M. Modeling Phenotypes of Tuberous Scerosis in the Mouse. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ada466831.

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Stock, Joseph D., Biren R. Amin, Doyle E. Wilson, Caitlyn E. Abell, and Kenneth J. Stalder. Digital Evaluation of Structural Phenotypes Common among Higher Parity Crossbred Sows. Ames (Iowa): Iowa State University, January 2013. http://dx.doi.org/10.31274/ans_air-180814-1003.

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Hubbard, Rebecca A., Yong Chen, Jinbo Chen, Joanna Harton, Grace Choi, Arman Oganisian, Jing Huang, et al. Developing Statistical Methods for Estimating Phenotypes Using Electronic Health Record Data. Patient-Centered Outcomes Research Institute (PCORI), March 2021. http://dx.doi.org/10.25302/03.2021.me.151132666.

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Batchelder, Jake. AIRE Deficiency Exposes Inefficiencies of Peripheral Tolerance Leading to Variable APECED Phenotypes. Journal of Young Investigators, September 2016. http://dx.doi.org/10.22186/jyi.31.3.15-20.

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LaJeunesse, Dennis. Genetic and Molecular Characterization of Drosophia Brakeless: A Novel Modifier of Merlin Phenotypes. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada443662.

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LaJeunesse, Dennis. Genetic and Molecular Characterization of Drosophila Brakeless: A Novel Modifier of Merlin Phenotypes. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada428432.

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Malik, Abir, D. Lam, H. A. Enright, S. K. G. Peters, B. Petkus, and N. O. Fischer. Characterizing the Phenotypes of Brain Cells in a 3D Hydrogel Cell Culture Model. Office of Scientific and Technical Information (OSTI), August 2018. http://dx.doi.org/10.2172/1466140.

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