Dissertations / Theses on the topic 'Shona novels'
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Mitchell, Andrea Michelle. "Ngozi : a novel." Thesis, University of Canterbury. School of Humanities, 2009. http://hdl.handle.net/10092/4450.
Full textBrightwell, Sara. "Identifying novel regulators of reprogramming using RNA interference." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/16156.
Full textEvans, Matthew C. "Quantitative Analysis of Novel Chemical and shRNA Based Methods to Increase Survival of Motor Neuron Protein Levels." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/566.
Full textKim, Yun Cheol. "Novel strategies for studying gene and protein function random shRNA library synthesis and trasnposon directed base-exchange mutagenesis /." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1693038461&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.
Full textMiller, Tyler Eugene. "Identifying Novel In Vivo Epigenetic Dependencies in Glioblastoma." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1464856610.
Full textZigara, Herbert. "Gender bias in selected Shona novels." Diss., 2016. http://hdl.handle.net/10500/22168.
Full textAfrican Languages
M.A. (African Languages)
Nenduva, Aphios. "Investigating moral perversion in post-Independence Shona detective novels." Thesis, 2018. http://uir.unisa.ac.za/handle/10500/25689.
Full textThe study unravels moral perversion in selected post-independence detective Shona novels. Moral perversion is a multi-faceted concept and the study focuses on corruption, sexual harassment, abuse of office, stealing, poaching and illegal manufacturing of intoxicating products as the key definers of moral perversion. Afrocentricity merged with Kawaida philosophy are the lenses used to pass critical judgements on the extent the selected literary practitioners portrayed literature rooted in the African ontological existence on moral perversion. Fictional works used as primary sources are Sajeni Chimedza (1984), Mutikitivha Dumbuzenene (1991), Munzwa mundove (1999) and Dandemutande, (1998). All the novels are set in the post-independence era in Zimbabwe when moral perversion is rife. The study is qualitative in nature and data was gathered using questionnaires and interviews from literary critics, publishers and novelists. Particular attention is paid on the causes of moral perversion, images of people in leadership positions and the implications of character assassination of leaders in relation to the development of purposeful literature. The study contends that moral insanity is an acknowledged problem in the post-independence era and novelists are portraying leaders as the chief culprits manning factionalism and unorthodox ways of acquiring resources at the expense of the majority of citizenry. Guided and informed by Afrocentricity, the study argues that novelists are raising pertinent issues although their views are myopic, simplistic and self-defeating because they are failing to see that the leaders are also victims who are victimizing other victims. Blaming the leadership on moral perversion ignoring the impact of colonialism, and neo-colonialism in shaping African personality creates more harm than good as this exonerates the imperialistic system of exploitation which impinges on African culture and personality. Therefore, the study argues that novelists erroneously blame individuals for the sins of a system. There is need to interrogate both external and internal factors to establish sustainable home-grown problem solving solutions to improve human condition and the development of functional literature in Africa.
African Languages
D. Litt. et Phil. (African Languages)
Mapara, Jacob. "The Bible and literature: a case of biblical influence in some Shona novels." Diss., 2003. http://hdl.handle.net/10500/1235.
Full textAfrican Languages
M.A. (African Languages)
Wasosa, Wellington. "Deviance and moralisiation as portrayed in selected post-independence Shona novels and short stories." Thesis, 2014. http://hdl.handle.net/10500/19842.
Full textAfrican Languages
D. Litt. et Phil.
Viriri, Eunitah. "The promotion of unhu in Zimbabwean secondary schools through the teaching of Shona literature : Masvingo urban district, a case study." Thesis, 2017. http://hdl.handle.net/10500/23737.
Full textAfrican Languages
D. Litt. et Phil. (African Languages)
Nyaungwa, Oscar. "Folktale influence on the Shona novel." Thesis, 2008. http://hdl.handle.net/10500/2710.
Full textAfrican Languages and Literature
Thesis (M.A.)
Mazuruse, Mickson. "The theme of protest in the post-independence Shona novel." Diss., 2010. http://hdl.handle.net/10500/3949.
Full textAfrican languages
M.A. (African languages)
Mapara, Jacob. "An analysis of the reliability and validity of the Shona novel as a historical document." Thesis, 2007. http://hdl.handle.net/10500/1341.
Full textAfrican Languages
D.Litt. et Phil. (African Languages)
Yen, Meng-Chi, and 顏孟畿. "The novel approach for cancer therapy:by skin delivery of IDO shRNA." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/49566124315074026533.
Full text國立成功大學
基礎醫學研究所
97
Indoleamine 2,3-dioxygenase (IDO) is a rate-limiting enzyme of tryptophan degradating pathway and a negative immunoregulatory molecule of dendritic cells. IDO-expressing dendritic cells suppress proliferation and activation of effector T cells and induce proliferation of regulatory T cells. We hypothesized that knockdown the IDO expression of dendritic cells could elicit the antitumor response. Besides the IDO specific inhibitor, short hairpin RNA (shRNA) is another approach to silence the IDO expression of dendritic cells. Thus, the IDO specific short hairpin RNA (shRNA) was constructed and evaluated the silencing efficiency on the mRNA and protein expression in vitro and in vivo. We observed the slower tumor growth rate and better survival rate on mouse bladder tumor cell MBT-2 and mouse colon cancer cell CT-26 bearing mice after IDO shRNA vaccinated. Adoptive transfer of CD11c+ cells which were isolated from IDO shRNA vaccinated mice was shown delayed tumor progression. The data indicated that IDO low-expressing CD11c+ cells played a critical role in antitumor response. Depletion the CD8+ and CD4+T cells abolished the IDO shRNA induced antitumor responses. Mice vaccinated with IDO shRNA targeting to different sequence induced similar therapeutic efficacy. IDO shRNA-resistant IDO expression vector delivered into dendritic cells abolished the therapeutic effect. It was suggesting that the therapeutic effect is not due to off-target and is dependent on IDO. In addition, the therapeutic effect was dependent on the vaccinated dose of IDO shRNA plasmid. IDO shRNA fused with Her2/neu DNA vaccine further enhanced the therapeutic effect on the bladder cancer model. On the other hand, IDO2 was an IDO-like protein. IDO2 shRNA induced similar antitumor immune responses with IDO siRNA, but the interaction between IDO and IDO2 was still unknown in this study. In conclusion, we provide a novel and simple approach to induce the antitumor immune response through skin delivery of IDO shRNA. Her2/neu DNA vaccine fused with IDO shRNA further enhanced the therapeutic efficacy. Moreover, the IDO2 might involve in immune regulation of dendritic cells.
Ntabeni, Sally-Susan. "Theme and character : some reflections on the historical context of the Ndebele novel." Diss., 1999. http://hdl.handle.net/10500/15668.
Full textAfrican Languages
M.A. (African Languages)
Muwati, Itai. "Interface of history and fiction : the Zimbabwean liberation war novel." Thesis, 2009. http://hdl.handle.net/10500/18686.
Full textAfrican Languages
D. Litt. et Phil. (African Languages)
Tsai, Yi-Hsuan, and 蔡依璇. "Using a novel lipoplex LPPC-Cetuximab with the shRNA-expressed transgenes for therapy of mutant EGFR-expressed lung carcinoma." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/01810063323022983123.
Full text國立交通大學
分子醫學與生物工程研究所
101
Recent studies have revealed that EGFR inhibitors were no longer effective in the treatment of EGFR-activating lung cancer due to the development of resistance. Although the irreversible second-generation EGFR TKIs were clinically developed to overcome the resistances, there was still the emergence of other resistant mechanisms. Therefore, our strategy was to search for the potent therapeutic genes which were commonly over-expressed in EGFR-activating lung cancer and directly silenced the genes for tumor inhibition. With powerful analysis tools of bioinformatics and rich online published microarray datasets from Gene Expression Omnibus (GEO), we developed a screening system and to search for the best therapeutic targets of lung tumors. The total gene profiles of 55 lung cancer cell lines and 279 clinical lung cancer samples were obtained from online GEO datasets. Following the process of screening filters, we got the 22 candidate genes which were commonly over-expressed and all associated with cell cycle regulation. After ranking the importance and experimental verification, we finally chose the potent therapeutic gene for further lung cancer gene therapy. By using the well-established LPPC/cetuximab delivery system, we delivered the shRNA-expressed transgene into EGFR-mutant NCI-H1650 and verified its anti-cancer effects.
Chen, Yu-tsung Shane. "Structural Dynamics and Novel Biological Function of Topoisomerase 2." Diss., 2015. http://hdl.handle.net/10161/9919.
Full textEukaryotic Topoisomerase 2 is an essential enzyme that solves DNA topological problems such as DNA knotting, catenation, and supercoiling. It alters the DNA topology by introducing transient double strand break in one DNA duplex as a gate for the passage of another DNA duplex. Two different aspects of studies about eukaryotic Topoisomerase 2 will be covered in this thesis. In the first half of the thesis, we investigated conformational changes of human Topoisomerase 2 (hsTop2) in the presence of cofactors and inhibitors. In the second half, we focused on an unknown regulatory function in the C-terminal domain (CTD) of Drosophila Topoisomerase 2 (Top2).
In the project of studying enzyme conformational changes, we adapted a previously developed methodology, Pulse-Alkylation Mass Spectrometry, with monobromobimane to study the protein dynamics of hsTop2. Using this method, we captured the evidence of conformational changes in the presence of ATP and Mg2+ or the Top2 inhibitor, ICRF-193 which were not previously observed. Last, by using CTD truncated hsTop2, the increasing reactivity of Cys427 suggested the CTD domain might be tethered adjacent to the core enzyme.
Following the study of enzyme conformational changes, we switched gear to examine an interaction between Drosophila Top2 and Mus101, homolog of human TopBP1. We first found that Mus101 interacts with CTD of Top2 in a phosphorylation-dependent manner. Next, in the co-immunoprecipitation and pull-down experiments using truncated or mutant Top2 with various Ser to Ala substitutions, we mapped the binding motif to the last amino acids of Top2 and identified that phosphorylation of Ser1428 and Ser1443 is important for Top2 to interact with the N-terminus of Mus101, which contains BRCT1/2 domains (BRCT, BRCA1 C-terminus). The binding affinity of the N-terminal Mus101 with a synthetic phosphorylated peptide covering the last 25 amino acids of Top2 (with pS1428 and pS1443) was determined by surface plasmon resonance with a Kd of 0.57 μM. In an in vitro decatenation assay, Mus101 can specifically reduce the decatenation activity of Top2, and dephosphorylation of Top2 attenuates this response to Mus101. Next, we endeavored to establish a cellular system for testing the biological function of Top2-Mus101 interaction. Top2-silenced S2 cells rescued by Top220, truncation of 20 amino acids from the C-terminus of Top2, developed abnormally high chromosome numbers, which implies an infidelity in chromosome segregation during mitosis. Lastly, Top2-null flies rescued by Top2 with S1428A and S1443A were found to be viable but sterile. After investigating spermatogenesis, telophase of meiosis I was delayed, indicating Top2-Mus101 interaction is also important in segregating DNA in meiosis.
Dissertation
Mund, Julie Ann. "A Synthetic Lethal shRNA Screen and Genetic Proof of Concept Identifies RAC1 as a Novel Target to Disrupt Plexiform Neurofibroma Formation." Diss., 2019. http://hdl.handle.net/1805/21933.
Full textNeurofibromatosis Type 1 (NF1) is a highly penetrant autosomal dominant genetic disorder where mutations in the tumor suppressor gene NF1 leads to decreased neurofibromin. The most debilitating manifestation is the presence of complex multilineage Schwann cell-derived plexiform neurofibromas (PN). Historically, little clinical success has been achieved targeting PN through surgery or chemotherapies. I performed an shRNA library screen of patient-derived Schwann cell lines to identify novel therapeutic targets to disrupt PN formation and progression. An shRNA library screen of human kinases and Rho-GTPases was performed in NF1-/- and paired NF1 competent immortalized Schwann cell lines. Following sequencing, candidates were identified. We previously developed a novel mouse model of NF1 wherein a neural crest specific Postncre targeted loxp-flanked Nf1 that replicated the PN found in patients. Additional cohorts of mice were generated with biallelic deletion of Rac1 (Nf1f/fRac1f/f Postn-Cre+; DKO ). Mice were aged for 9 months and peripheral nerves were harvested and fixed in formalin. Peripheral nerve size was measured and tumors were identified through blinded analysis of hematoxylin and eosin and Masson’s Trichrome (collagen) stained slides. Rho family members, including RAC1, were identified as candidates through an shRNA library screen. Genetic disruption of Rac1 in the Schwann cell lineage resulted in the prevention of tumor formation in DKO mice, as observed by peripheral nerve size and histological analysis. I observed an average of 14.8 +/- 2.65 tumors per mouse in the Nf1f/f Postnviii Cre+ cohort compared to 0 tumors in the DKO (p<0.0001). Following an shRNA library screen, RAC1 was identified as a candidate to modulate PN formation. Biallelic deletion of Rac1 in vivo prevented PN formation. I demonstrate that a candidate identified in an shRNA library screen can translate to an biological effect in a mouse model of PN.