Готові списки джерел за темами / Molecular delineation

Добірка наукової літератури з теми "Molecular delineation"

Автор: Grafiati
Опубліковано: 12 травня 2022

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  1. Статті в журналах
  2. Дисертації
  3. Книги
  4. Частини книг
  5. Тези доповідей конференцій
  6. Звіти організацій

Статті в журналах з теми "Molecular delineation":

1

Arini, Pedro David, Sergio Liberczuk, Javier Gustavo Mendieta, Martín Santa María, and Guillermo Claudio Bertrán. "Electrocardiogram Delineation in a Wistar Rat Experimental Model." Computational and Mathematical Methods in Medicine 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/2185378.

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Background and Objectives. The extensive use of electrocardiogram (ECG) recordings during experimental protocols using small rodents requires an automatic delineation technique in the ECG with high performance. It has been shown that the wavelet transform (WT) based ECG delineator is a suitable tool to delineate electrocardiographic waveforms. The aim of this work is to implement and evaluate the ECG waves delineation in Wistar rats applying WT. We also describe the ECG signal of the Wistar rats giving the characteristics of its spectrum among other useful information. Methods. We evaluated a delineator based on WT in a Wistar rat electrocardiograms database which was annotated manually by experienced observers. Results. The delineation showed an “overall performance” such as sensitivity and a positive predictive value of 99.2% and 83.9% for P-wave, 100% and 99.9% for QRS complex, and 100% and 99.8% for T-wave, respectively. We also compared temporal analysis based ECG delineator with the WT based ECG delineator in RR interval, QRS duration, QT interval, and T-wave peak-to-end duration. The results showed that WT outperforms the temporal delineation technique in all parameters analyzed. Conclusions. Finally, we propose a WT based ECG delineator as a methodology to implement in a wide diversity of experimental ECG analyses using Wistar rats.
2

Lévy, Jonathan, Aurélie Coussement, Céline Dupont, Fabien Guimiot, Clarisse Baumann, Géraldine Viot, Sandrine Passemard, et al. "Molecular and clinical delineation of 2p15p16.1 microdeletion syndrome." American Journal of Medical Genetics Part A 173, no. 8 (June 1, 2017): 2081–87. http://dx.doi.org/10.1002/ajmg.a.38302.

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3

Letcher, Peter M., Martha J. Powell, James G. Chambers, Joyce E. Longcore, Perry F. Churchill, and Phillip M. Harris. "Ultrastructural and molecular delineation of the Chytridiaceae (Chytridiales)." Canadian Journal of Botany 83, no. 12 (December 2005): 1561–73. http://dx.doi.org/10.1139/b05-115.

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The Chytridiomycota is in need of taxonomic revision, especially the largest order, the Chytridiales. We analyzed 25 isolates in, or allied to, the Chytridium clade of this order. Isolates were selected based on one or more of the following criteria: (i) having a large subunit molecular sequence similar to that of the type of the genus Chytriomyces, (ii) having specific zoospore morphology, and (iii) currently classified as a species in the genus Chytriomyces . We examined ultrastructural characters and partial sequences of large subunit and small subunit rDNA and generated a phylogenetic hypothesis using maximum parsimony and Bayesian analyses. The sequence analyses strongly supported the Chytridiaceae, Phlyctochytrium, and Chytriomyces angularis clades, and each clade had a specific zoospore type. Developmental morphology of the thallus did not mirror the DNA-based phylogeny. Based on the results of phylogenetic analyses of sequences and ultrastructural characters, we emend the Chytridiaceae by including exogenous and polycentric development and define the family on the basis of a single zoospore type. Species identified as being in the genus Chytriomyces occur in several separate, well-supported clades along with species currently classified in seven other genera ( Asterophlyctis , Entophlyctis , Obelidium , Physocladia , Podochytrium , Rhizoclosmatium , and Siphonaria ), indicating that Chytriomyces as currently defined is polyphyletic.
4

Tassano, E., M. G. Alpigiani, A. Calcagno, P. Salvati, L. De Miglio, P. Fiorio, C. Cuoco, and G. Gimelli. "Clinical and molecular delineation of a 16p13.2p13.13 microduplication." European Journal of Medical Genetics 58, no. 3 (March 2015): 194–98. http://dx.doi.org/10.1016/j.ejmg.2014.12.016.

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5

Iida, Shinsuke, and Ryuzo Ueda. "Multistep Tumorigenesis of Multiple Myeloma: Its Molecular Delineation." International Journal of Hematology 77, no. 3 (April 2003): 207–12. http://dx.doi.org/10.1007/bf02983776.

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6

Al-Khalaf, Fawziya A., Adel Ismail, Ashraf T. Soliman, David E. C. Cole, and Tawfeg Ben-Omran. "Neonatal severe hyperparathyroidism: further clinical and molecular delineation." European Journal of Pediatrics 170, no. 5 (October 23, 2010): 625–31. http://dx.doi.org/10.1007/s00431-010-1335-z.

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7

Roquet, Cristina, Llorenç Sáez, Juan José Aldasoro, Alfonso Susanna, María Luisa Alarcón, and Núria Garcia-Jacas. "Natural Delineation, Molecular Phylogeny and Floral Evolution in Campanula." Systematic Botany 33, no. 1 (March 1, 2008): 203–17. http://dx.doi.org/10.1600/036364408783887465.

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8

Koolen, D. A., A. J. Sharp, J. A. Hurst, H. V. Firth, S. J. L. Knight, A. Goldenberg, P. Saugier-Veber, et al. "Clinical and molecular delineation of the 17q21.31 microdeletion syndrome." Journal of Medical Genetics 45, no. 11 (November 1, 2008): 710–20. http://dx.doi.org/10.1136/jmg.2008.058701.

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9

Aqua, Mfon S., Patrizia Rizzu, Elizabeth A. Lindsay, Lisa G. Shaffer, Elaine H. Zackai, Joan Overhauser, and Antonio Baldini. "Duplication 3q syndrome: Molecular delineation of the critical region." American Journal of Medical Genetics 55, no. 1 (January 2, 1995): 33–37. http://dx.doi.org/10.1002/ajmg.1320550111.

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10

Laurell, Tobias, Johanna Lundin, Britt-Marie Anderlid, Jerome L. Gorski, Giedre Grigelioniene, Samantha J. L. Knight, Ana C. V. Krepischi, et al. "Molecular and clinical delineation of the 17q22 microdeletion phenotype." European Journal of Human Genetics 21, no. 10 (January 30, 2013): 1085–92. http://dx.doi.org/10.1038/ejhg.2012.306.

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Статті в журналах Дисертації

Дисертації з теми "Molecular delineation":

1

McDonnell, Aoibhinn. "Molecular delineation of cyathostome species." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247701.

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2

Geli, Janos. "Further delineation of molecular alterations in adreno-medullary tumors /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-306-1/.

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3

Hood, Rebecca. "Molecular and Clinical Delineation of Rare Disorders of Stature." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36067.

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There are more than 7000 described rare genetic disorders; however, the molecular basis underlying approximately half of these disorders is unknown, and the majority are currently untreatable. Stature and growth abnormalities are a common clinical feature of many rare disorders including: Floating-Harbor syndrome (FHS), a short stature syndrome characterized by delayed osseous maturation, language deficits, and unique dysmorphic facial features; Weaver syndrome, an overgrowth syndrome characterized by advanced osseous maturation, developmental delay, and macrocephaly; and Sotos syndrome with cutis laxa, an overgrowth syndrome with marked tissue laxity in addition to the typical Sotos characteristics of developmental delay, macrocephaly, and a unique facial gestalt. The genetic basis underlying these three rare stature conditions were unknown at the outset of this study. We utilized high-throughput exome sequencing approaches to investigate the molecular etiology of these rare disorders and identified truncating mutations in the final exon of SRCAP as the genetic cause underlying FHS, missense mutations in EZH2 in Weaver syndrome, and novel mutations in the Sotos syndrome gene NSD1 in Sotos syndrome with cutis laxa. Next, we investigated the spectrum of SRCAP mutations in FHS and established the clustering of truncating SRCAP mutations in the final exon as being highly suggestive of a non-haploinsufficiency mutational mechanism in FHS. Finally, global methylation array analysis identified a unique methylation ‘epi-signature’ in FHS individuals, providing further insight into FHS disease mechanism and a diagnostic signature. These studies have delineated the molecular etiology of these three rare stature/growth disorders, furthered our understanding of the associated clinical spectrum, and provided biological insight into disease pathogenesis.
4

Nielsen, Janne T. "Molecular Genetic Approaches to Species Identification and Delineation in Elasmobranchs." NSUWorks, 2004. http://nsuworks.nova.edu/occ_stuetd/278.

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CHAPTER 2 The burgeoning shark-fishing industry has caused severe declines in many shark populations, prompting an urgent need for conservation and management of sharks on a species-specific basis. Many fisheries are managed on the basis of species groups due to difficulty in identifying the morphologically similar requiem sharks (Carcharhinidae) and their body parts. One diagnostic trait readily discernible in landed shark carcasses is the presence or absence of an interdorsal ridge, which allows shark carcasses to be categorized as either ridgeback or non-ridgeback sharks and narrows the identification process. Further identification to species, however, remains problematic and is a major impediment to management and conservation on a species-specific basis. To facilitate the goal of species-specific management, I have developed a rapid and cost-efficient DNA-based method for use in species identification. It employs a high-density, multiplex polymerase chain reaction (PCR) assay that combines seven species-specific primers and two universal primers to discriminate one ridgeback (Galeocerdo cuvier) and six non-ridgeback (Carcharhinus brevipinna, C. limbatus, C. acronotus, C. isodon, C. leucas, and Negaprion brevirostris) sharks common in U.S. Atlantic fisheries. The primers were designed based on species-specific nucleotide differences in the nuclear ITS2 locus. These seven primers were tested on 73 non-target species worldwide to assess their diagnostic utility on a global scale. Five of the seven primers are species-specific, with only the C. leucas and the C. limbatus primers each amplifying one other congener, C. perezi and C. tilstoni, respectively. This diagnostic assay was tested in a practical management context and successfully identified shark fins confiscated by NMFS law enforcement agents, indicating that it will be useful in management of the U.S. Atlantic shark fishery. Furthermore, the primers developed for G. cuvier, C. leucas and C. brevipinna successfully identified their respective target species from the Atlantic and Pacific Oceans, suggesting that they will also be useful for global applications such as monitoring international trade in shark products. CHAPTER 3 Accurate species delineation is essential to sound management and conservation of fishery resources. The species status of two butterfly rays, Gymnura marmorata and G. crebripunctata, occurring in the fisheries in the Gulf of California and on the Pacific Mexican coast, has long been debated. Direct sequence comparison and a phylogenetic analysis were carried out using a segment of the mitochondrial cytochrome b locus to elucidate the relationship between G. marmorata and G. crebripunctata and five other congeners. Sequence divergence between G. marmorata and G. crebripunctata was minimal compared to sequence divergence among the five other established congeners. A neighbor-joining analysis showed strong statistical (100%) support and a maximum likelihood analysis showed reasonable support (62%) for the monophyletic clade consisting. of G. marmorata and G. crebripunctata. Importantly, neither analysis supported the reciprocal monophyly of either species, as would be expected for true separate species. These data suggest that the current classification of G. marmorata and G. crebripunctata as two separate species needs to be revised to support their designation as a single species. Genetic analysis of the cyt b locus also revealed three single-nucleotide synapomorphies that partitioned animals from the two geographic sites sampled in Mexico (Sahuimaro, Sonora and Bahia Almejas, Baja California Sur), indicating the existence of possible population genetic structure between the two sites. By analyzing cyt b sequences from seven ofthe 10 described Gymnura species, I also provide the first phylogenetic hypothesis for interspecies relationships in the genus Gymnura.
5

Vukovic, Milica. "Delineation of molecular events that occur in a PKCα-KR-mediated murine model of CLL". Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3675/.

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Chronic lymphocytic leukaemia (CLL) is the most prevalent leukaemia of the Western world, and despite the recent evolution in clinical treatment of the disease, it remains incurable. Although current therapies such as allogeneic hematopoietic stem cell (HSC) transplantation have been successfully used to treat CLL, this is an option for only a minority, as most CLL patients are diagnosed over the age of sixty and cannot withstand the harsh transplantation procedures. Combination chemotherapy, such as fludarabine and cyclophosphamide, has been shown to significantly improve response rate and prolonged remission in CLL patients, however, no improvement in overall survival has been observed. Patients eventually relapse due to re-emergence of minimal residual disease (MRD). Therefore it is critical that further clinical therapies are investigated in order to eliminate MRD, and offer hope to patients that are unresponsive to current treatments. CLL is marked by the presence of the accumulation of long-lived mature monoclonal B cells in peripheral lymphoid organs, bone marrow and peripheral blood with the specific phenotype of CD19hi, CD5+, CD23+ and IgMlo that resist apoptosis. The in vivo accumulation of leukaemic lymphocytes is highly facilitated by interactions of CLL cells with other cells present in their microenvironment, including stromal cells and soluble factors such as IL4. Studies have established a variety of mechanisms potentially responsible for disease progression in CLL, including chromosomal abnormalities and intrinsic defects in the apoptotic machinery due to higher levels of the anti-apoptotic protein Bcl-2 family member proteins Bcl-2 and Mcl-1, thus making this disease extremely heterogeneous. Although the apoptotic machinery is certainly dysregulated in CLL, it is not simply a disease of a clonal accumulation of B cells, rather, proliferation is occurring as well as apoptosis, accounting for up to 2% of the clone size per day. CLL B cell proliferation centres exist within lymph nodes (LN) and bone marrow (BM) where B cells receive signals from their B cell antigen receptor (BCR) to proliferate, generating a very aggressive form of the disease. In addition, evidence suggests that stimulation through the BCR plays a pivotal role in pathogenesis of CLL since CLL B cells have a phenotypic profile of B cells activated by antigen interaction and a genetic expression profile of antigen experienced B cells. During the course of our studies assessing the impact of modulating protein kinase C (PKC) signaling in B cell development in vitro or in vivo, we developed a unique model system to investigate the mechanisms underlying the induction of CLL. Introduction of full length, catalytically inactive PKCα (PKCα-KR) into HSCs derived from wild type mouse fetal liver (FL), and subsequent culture of the cells either in vitro or in vivo resulted in the generation of a population of B lymphocytes that are phenotypically similar to human CLL cells (CD19hi, CD5+, CD23+, IgMlo). PKCα-KR-expressing FL cells also expressed enhanced proliferative capacity over untransduced cells and were refractory to apoptosis. These results indicate that the subversion of PKCα signaling acts as an oncogenic trigger for developing B lymphocytes. The aim of this project was to identify similarities between our murine CLL (mCLL) model and human CLL and investigate putative translational therapeutic targets. The main findings of this study implicate PKCβII as an important survival and proliferation signal within mCLL. Cyclin D1 is also upregulated within mCLL, linked to an increase in the proliferative capacity of mCLL cells, and is regulated through transcriptional repressor 4EBP1, which appears inactive in both mCLL and human CLL. In addition, PKCα-KR transduced cells harbour the potential for lineage plasticity in a microenvironment-dependent manner, whereby PKCα-KR B cells lineage switch to T cells upon Notch ligation. The reprogramming occurs via a reduction in B cell specific genes and an upregulation of T cell specific genes, implicating the deregulation of PKCα activity/expression as a potential mechanism for lineage trans-differentiation during malignancies. Importantly, in human CLL, PKCα is downregulated at the transcript and protein levels implicating it a tumour suppressor, highlighting the translational capacity of our CLL mouse model.
6

Burkitt, Wright Emma Mary Milborough. "De novo germline disorders of the Ras-MAPK pathway : clinical delineation, molecular diagnosis and pathogenesis." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/de-novo-germline-disorders-of-the-rasmapk-pathwayclinical-delineation-molecular-diagnosis-and-pathogenesis(9688dc20-7b1b-46f1-a638-b4d1809f430b).html.

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This work sought to investigate the clinical phenotypes and molecular basis of cardio-facio-cutaneous syndrome (CFC), a germline disorder of the Ras-MAPK pathway, like Noonan syndrome (NS) and neurofibromatosis type I, caused by mutations in genes encoding proteins that act within this signal transduction pathway. CFC is most commonly due to mutation in BRAF, and less commonly MAP2K1, MAP2K2 or KRAS. A proportion of patients currently have no mutation identified. Mutations and clinical features of patients with a molecular diagnosis of CFC were investigated, which demonstrated a wide range of causative mutations, and some unclassified variants. Both known and novel clinical features of CFC were identified. A strong association between severe contractures and the p.(Tyr130Cys) mutation in MAP2K1 was found, which has not previously been reported. In contrast to the large number of patients with a confirmed molecular diagnosis, several with a highly suggestive clinical phenotype have been found to have no mutationin any of the known CFC genes. The molecular basis of these presentations was investigated by conventional Sanger sequencing of candidate genes. Fourteen patients with the p.(Ser2Gly) mutation in SHOC2 were identified, with clinical presentations consistent with CFC, NS or CS. Target enrichment and massively parallel sequencing of selected genes was undertaken in ten patients. Mutations in known genes were identified in four patients (including the positive control). Candidate causative variants in novel genes were suggested in two further patients, one of which was confirmed on Sanger sequencing. Whole exome sequencing of patient-parent trios was also undertaken to identify de novo variants. Three trios were analysed, and in one patient with a clinical diagnosis of CFC, a frameshift mutation in NF1 was identified, which was confirmed by Sanger sequencing to be present and de novo. The molecular effects of CFC-associated mutations in BRAF on Ras-MAPK pathway signalling were studied in cell culture systems, using Western blotting for ERK1/2 phosphorylation, in vitro kinase assays and luciferase assays, to assess activity of downstream targets of the Ras-MAPK pathway. Altered pathway activity was demonstrated for novel variants that had not previously been characterised at the molecular level, which was in keeping with the findings of the effects of previously studied mutations. The cardiac phenotype in animal models of CFC, CS and NS/CFC was explored using expression microarrays to identify potentially important genes and pathways in the pathogenesis of hypertrophic cardiomyopathy (a progressive but potentially treatable disease feature) in these conditions. A signature of increased expression of Myh7, the embryonic form of myosin, was identified in the heart of the mouse model of CFC due to a B-Raf mutation at four weeks postnatal age, but comparative analysis suggested significant differences in either the mechanisms causing cardiac phenotypes, or the timescales over which these may exert their effects, in the three models. In summary, the most significant findings of this work were that SHOC2 mutation is a frequent cause of a severe NCFC presentation, and massively parallel sequencing can be an effective means of molecular investigation of this group of disorders. Novel features of CFC syndrome that were identified include severe contractures in association with p.(Tyr130Cys) mutations in MAP2K1. The analysis of mouse models of the NCFCs was hampered by heterogeneity within the expression microarray results, and low levels of expression of the H-Ras mutant allele in the mouse model of Costellosyndrome.
7

Park, Dongik [Verfasser], and Mathias [Akademischer Betreuer] Schmidt. "Molecular delineation of cellular pathways associated with the antidepressant treatment response / Dongik Park ; Betreuer: Mathias Schmidt." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1148941363/34.

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8

Hua, Brian L. "Delineation of the molecular mechanisms underlying DNA replication initiation and changes in gene copy number during Drosophila development." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/108891.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2017.
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Includes bibliographical references.
The study of differential DNA replication programs in Drosophila has provided important insight into the molecular control of replication initiation and fork progression during development. We investigated the mechanisms by which binding of the origin recognition complex (ORC) and replication fork inhibition give rise to locally underreplicated regions in Drosophila polyploid tissues. We identified copy number changes genome-wide in two additional polyploid tissues and compared our results to three previously profiled larval tissues. These results revealed a high level of tissue-specificity in the number of underreplicated sites within a given tissue but also highlighted the conservation of the locations of many of these underreplicated regions across tissues. By mapping ORC binding sites in the larval fat body, we found that the repression of replication initiation is a common mechanism of underreplication in polytene tissues. Our ORC localization studies also suggest that underreplication zones are hard-wired across tissues and that differential underreplication of these zones is dependent upon variation in fork progression across these regions. We then utilized the Drosophila amplicons in follicle cells (DAFCs) as a model replication system to dissect the molecular mechanisms underlying the activation of individual replication origins. Repression of the DAFC-22B origin is not achieved through changes in subnuclear localization but rather through effects of the surrounding chromatin. We identified two novel genomic sites at which origin activity is modulated directly by the surrounding chromatin environment. At one site, the surrounding chromatin promotes one additional round of origin firing at a specific developmental time point. At the other site, origin activity is repressed by the surrounding chromatin through inhibition of the localization of the MCM2-7 helicase complex. Origin repression at this site is not correlated with the establishment of heterochromatin, raising the possibility that the activity of individual replication origins are regulated by the chromatin environment on a greater, conformational level. Finally, we dissected the requirement of transcription in the activation of the DAFC-62D origin. Surprisingly, transcription is not required in cis for origin activation. These results indicate the requirement of a trans-acting factor specifically at this site and highlight the diversity of mechanisms that control metazoan origin activation.
by Brian L. Hua.
Ph. D.
9

Theodorou, Andria Soteri. "Screening and delineation of molecular mechanisms of action of HbF inducing agents for the treatment of β-thalassaemia". Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/screening-and-delineation-of-molecular-mechanisms-of-action-of-hbf-inducing-agents-for-the-treatment-of-thalassaemia(fbad43de-f2b2-49a1-980b-b6dfcc1a25c5).html.

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Current agents used for pharmacological reactivation of foetal haemoglobin (HbF) have limited application due to moderate therapeutic properties, variable patient response and potential cytotoxic effects. Therefore, identification of novel HbF inducing agents is still a major research goal to this day. Identification of new potential HbF inducers has been mainly based on screening of drug libraries. However, this approach has not been very successful in generating new promising agents. In the current project, I employed two approaches for identifying potential HbF inducers: 1) screening of agents that are structurally similar to compounds with known HbF inducing activity; 2) investigating molecular pathways of a known HbF inducer with the aim of identifying suitable targets for therapeutic manipulation and target-based drug design. The first approach involved screening of eleven xanthines including caffeine and nine hydroxystilbenic derivatives of resveratrol as potential HbF inducers. However, none of the agents had a potent enough HbF inducing activity in order to be considered as promising therapeutic agents. In the second approach, decitabine was chosen based on its high HbF inducing activity and moderate cytotoxicity in K562 cells and primary human erythroid cultures. Chromatin immunoprecipitation was used to characterise epigenetic changes in the β-globin gene locus, and quantitative real-time PCR for investigation of changes in gene expression levels of ten erythroid-related genes, in the presence of the agent. A quantitative iTRAQ proteomic approach coupled with mass spectrometry was used for identification of changes in the proteome of decitabine-treated and un-treated primary human erythroid cultures. The findings suggest that decitabine induces HbF production through activation of signal transduction pathways rather than through hypomethylation of gene promoters. One such possible pathway is the NF-κB pathway. Among the differentially expressed proteins, twenty-seven proteins were associated with the action of decitabine. Two of those proteins, ARHGAP4 and EGLN2, were previously implicated in hydroxyurea-mediated induction of γ-globin gene expression and hypoxia-mediated erythropoiesis, respectively. In addition, the de-ubiquitinating enzyme USP11 was substantially modulated in the presence of decitabine. The exact role of these proteins in γ-globin expression remains to be established.
10

Slotta, Tracey Ann Bodo. "Phylogenetics of the Malacothamnus alliance (Malvaceae): Assessing the role of hybridization and molecular and morphological variation in species delineation." Diss., Virginia Tech, 2004. http://hdl.handle.net/10919/11204.

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The Malacothamnus alliance consists of three genera, Iliamna, Malacothamnus, and Phymosia. The genera are considered taxonomically complex since hybridization freely occurs, polyploidy levels vary, and there is a lack of distinct morphological characters to delineate taxa. Several taxonomic treatments have been prepared for each genus, but relationships within the genera and the relationship of the Malacothamnus alliance to others in the Malvaceae remains unknown. This multifaceted study aimed to (a) examine the monophyly of the Malacothamnus alliance and its position in the Malvaceae, (b) determine the relationships between genera in the alliance, (c) compare variation of nuclear and chloroplast genes in the alliance, (d) prepare revised taxonomic treatments for Iliamna and Malacothamnus, and (e) examine the probability of successful hybridization in Iliamna. The monophyly of the Malacothamnus alliance was not confirmed using DNA sequences of both nuclear and chloroplast regions. In Iliamna, little sequence variation was detected among taxa in the Rocky Mountains; however, the nuclear and chloroplast regions conflicted with regard to the relationships of the western and eastern taxa. An ancestral copy of the chloroplast genome is shared between the two eastern U.S. Iliamna species and Phymosia (Bahamas and Mexico). The nuclear ITS sequences indicated the western U.S. Iliamna species were more closely related to Phymosia and Malacothamnus than to other species in Iliamna. Neither data set provided sufficient variation to resolve relationships of species in Malacothamnus. Genetic variation and the feasibility of hybridization in Iliamna supported the results of the broader phylogenetic studies. Iliamna corei and I. remota are recently derived from I. rivularis. Hybrid offspring of I. corei and I. remota had higher viability and fecundity than did hybrids between crosses of either species and I. rivularis. The Virginia populations of I. corei and I. remota are more genetically similar than either is to Illinois populations of I. remota. However, the species are morphologically distinct and can easily be distinguished from others in the genus. Revised taxonomic treatments for Iliamna and Malacothamnus based on surveys of herbarium material are presented. Taxonomic revisions include the new combinations of Iliamna grandiflora subsp. grandiflora and I. grandiflora supsp. crandallii and the resurrection of Malacothamnus hallii and M. orbiculatus.
Ph. D.
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Книги з теми "Molecular delineation":

1

Thomson, Sten. Delineation of the lectin site of the molecular chaperone calreticulin. 2005.

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2

Thomson, Sten. Delineation of the lectin site of the molecular chaperone calreticulin. 2005.

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3

Mammoser, Aaron. Primary and Secondary Glioblastoma. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0127.

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Glioblastoma, formerly glioblastoma multiforme, is synonymous with WHO grade IV astrocytoma and is the most commonly diagnosed astrocytoma; it carries with it significant clinical, histologic, and molecular heterogeneity, with subtypes of the tumor and important new mutations associated with it characterized over the previous decade. Gene expression profiling has identified four tumor subgroups associated with specific mutational patterns, age of onset, and prognosis. The discovery of isocitrate dehydrogenase (IDH) mutations has led to further delineation between primary and secondary glioblastoma. Despite promising new investigational treatments, glioblastoma remains an incurable and fatal tumor.

Частини книг з теми "Molecular delineation":

1

Lauri, Sari E., Vernon R. J. Clarke, and Graham L. Collingridge. "Delineation of the Physiological Role of Kainate Receptors by Use of Subtype Selective Ligands." In Molecular Neuropharmacology, 27–46. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-672-0_2.

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2

Rajamanickam, Chellam, and Radhakrishnan Jeejabai. "Delineation of Sequences Essential for Specific Promoter Activation During Pressure Overloaded Hypertrophy or Factor-Induced Hypertrophy." In Molecular Cardiology, 251–60. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-879-x:251.

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3

Haase, Robert, Michael Andreeff, and Nasreddin Abolmaali. "On the Reliability of Automatic Volume Delineation in Low-Contrast [18F]FMISO-PET Imaging." In Molecular Radio-Oncology, 175–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-49651-0_9.

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4

Gaggelli, E., A. Lepri, N. Marchettini, and S. Ulgiati. "Selective 1H NMR Relaxation Delineation of Receptor Binding Equilibria." In Advanced Magnetic Resonance Techniques in Systems of High Molecular Complexity, 109–17. Boston, MA: Birkhäuser Boston, 1986. http://dx.doi.org/10.1007/978-1-4615-8521-3_9.

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5

Mayer-Jaekel, Regina E., and Brian A. Hemmings. "Molecular Complexity of Protein Phosphatase 2A Holoenzymes and Delineation of their Function." In Tyrosine Phosphorylation/Dephosphorylation and Downstream Signalling, 265–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78247-3_34.

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6

Beyens, Aude, Lore Pottie, Patrick Sips, and Bert Callewaert. "Clinical and Molecular Delineation of Cutis Laxa Syndromes: Paradigms for Elastic Fiber Homeostasis." In Advances in Experimental Medicine and Biology, 273–309. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-80614-9_13.

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7

Beyens, Aude, Lore Pottie, Patrick Sips, and Bert Callewaert. "Correction to: Clinical and Molecular Delineation of Cutis Laxa Syndromes: Paradigms for Elastic Fiber Homeostasis." In Advances in Experimental Medicine and Biology, C1. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-80614-9_16.

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8

Kishimoto, Tadamitsu, Toshio Hirano, Hitoshi Kikutani, and Atsushi Muraguchi. "Delineation of Human B Cell Differentiation: Immunological and Molecular Characterization of Human B Cell Differentiation Factor (BSF-2)." In Mechanisms of Lymphocyte Activation and Immune Regulation, 177–88. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5323-2_17.

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9

Katoh, Norio, Koichi Yasuda, Tohru Shiga, Masakaxu Hasegawa, Rikiya Onimaru, Shinichi Shimizu, Gerard Bengua, Masayori Ishikawa, Nagara Tamaki, and Hiroki Shirato. "A New Positron Emission Tomography (PET) Scanner with Semiconductor Detectors for Target Volume Delineation and Radiotherapy Treatment Planning in Patients with Nasopharyngeal Carcinoma." In Molecular Imaging for Integrated Medical Therapy and Drug Development, 52–59. Tokyo: Springer Japan, 2010. http://dx.doi.org/10.1007/978-4-431-98074-2_6.

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10

Fallarino, Francesca, Marco Gargaro, Giada Mondanell, Eric J. Downer, Md Jakir Hossain, and Bruno Gran. "Delineating the Role of Toll-Like Receptors in the Neuro-inflammation Model EAE." In Methods in Molecular Biology, 383–411. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3335-8_23.

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Тези доповідей конференцій з теми "Molecular delineation":

1

Waterhouse, Dale J. "Multispectral endoscopy for delineation of adenoma in pituitary surgery (MAPS): a pilot study (Conference Presentation)." In Molecular-Guided Surgery: Molecules, Devices, and Applications V, edited by Brian W. Pogue and Sylvain Gioux. SPIE, 2019. http://dx.doi.org/10.1117/12.2507029.

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2

Seekell, Kevin C., Spencer Lewis, Christy Wilson, Gerald Grant, and Adam P. Wax. "Feasibility of Brain Tumor Delineation using Immunolabeled Gold Nanorods." In Optical Molecular Probes, Imaging and Drug Delivery. Washington, D.C.: OSA, 2013. http://dx.doi.org/10.1364/omp.2013.mw1c.3.

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3

Saito Nogueira, Marcelo, Michael Raju, Jacqueline E. Gunther, Siddra Maryam, Michael Amissah, Shane Killeen, Huihui Lu, Micheal O’Riordain, and Stefan Andersson-Engels. "Accurate colorectal cancer detection and delineation by probing superficial and deeper tissue biochemistry and microstructure using diffuse reflectance spectroscopy." In Molecular-Guided Surgery: Molecules, Devices, and Applications VIII, edited by Summer L. Gibbs, Brian W. Pogue, and Sylvain Gioux. SPIE, 2022. http://dx.doi.org/10.1117/12.2609547.

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4

Mishra, Deependra, John Wang, Steven T. Wang, Qian Cao, Helena Hurbon, Walter Akers, and Mikhail Y. Berezin. "Selection of Hyperspectral Endmember Extraction Algorithm for Tumor Delineation in Animal Models." In Optical Molecular Probes, Imaging and Drug Delivery. Washington, D.C.: OSA, 2021. http://dx.doi.org/10.1364/omp.2021.of2e.2.

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5

Christie, Jaryd R., Omar Daher, Hannah van Dongen, Rory Gilliland, Mohamed Abdelrazek, and Sarah A. Mattonen. "A semi-automatic threshold-based segmentation algorithm for lung cancer delineation." In Biomedical Applications in Molecular, Structural, and Functional Imaging, edited by Barjor S. Gimi and Andrzej Krol. SPIE, 2022. http://dx.doi.org/10.1117/12.2611501.

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6

Leigh, Steven Y., Danni Wang, Ye Chen, Michael J. Mandella, Henry Haeberle, Olav Solgaard, Christopher H. Contag, and Jonathan T. C. Liu. "Ratiometric Molecular Microscopy: Towards Real-Time Quantitative Delineation of Brain Tumor Margins." In Biomedical Optics. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/biomed.2012.bsu4b.5.

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7

Mallya, Yogish, Vijayananda J., Vidya M. S., Vasantha Kumar Venugopal, and Vidur Mahajan. "Automatic delineation of anterior and posterior cruciate ligaments by combining deep learning and deformable atlas based segmentation." In Biomedical Applications in Molecular, Structural, and Functional Imaging, edited by Barjor Gimi and Andrzej Krol. SPIE, 2019. http://dx.doi.org/10.1117/12.2512431.

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8

Tam, Clara, Sibo Tian, Johnathan J. Beitler, X. Jiang, Shuo Li, and Xiaofeng Yang. "Automated delineation of organs-at-risk in head and neck CT images using multi-output support vector regression." In Biomedical Applications in Molecular, Structural, and Functional Imaging, edited by Barjor Gimi and Andrzej Krol. SPIE, 2018. http://dx.doi.org/10.1117/12.2292556.

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9

Ward, Tarsha L. "Abstract 2056: Molecular delineation of TIP150 function underlying kinetochore microtubule dynamics during mitotic chromosome segregation." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2056.

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10

Song, Yurong, Qian Zhang, Ryan Bash, Chaoying Yin, Chunyu Yang, Debra Gilbert, Sophie Wang, et al. "Abstract 2854: Delineation of grade-specific molecular drivers in inducible preclinical mouse models of astrocytoma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2854.

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Звіти організацій з теми "Molecular delineation":

1

Worsham, Maria J., Usha Raju, and Gary Chase. Molecular Differentiation of Risk for Disease Progression: Delineating Stage-Specific Therapeutic Targets for Disease Management in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada418914.

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2

Worsham, Maria J., Usha Raju, Gary Chase, and Mei Lu. Molecular Differentiation of Risk for Disease Progression: Delineating Stage-Specific Therapeutic Targets for Disease Management in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada432140.

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