Saturday, October 26, 2019

Treatment Options in Recurrent GBM Research

Treatment Options in Recurrent GBM Research Strategies for clinical applications The multi-omics data may also reveal important leads for therapeutic applications. A very recent review on GBM, reported outcomes of clinical trials investigating current treatment options in recurrent GBM, including anti-angiogenic, signaling pathway blockade and immunotherapy based approaches (1). However the genetic and cellular heterogeneity reflects in the modest results obtained so far. This necessitates identification and validation of better therapeutic targets and active strategies to combat GBM. Some novel strategies are showing promise in Phase II trials and preliminary data is becoming available, such as, EGFRvIII peptide vaccine, Rindopepimut; CD95 targeted monoclonal antibody, APG100 and multi-targeted tyrosine kinase inhibitor cabozantinib (1). A multi-pronged approach targeting a panel of proteins may thus hold the key to eliciting a synergistic response and prove more beneficial than current treatment modalities targeting individual markers. When it comes to circulat ory or plasma-based biomarkers, in view of the technical limitations encountered in deep and direct plasma analysis as discussed earlier, alternate methods which would allow prediction of tumor related molecules and their targeted exploration would be highly useful. One of the outcomes of the study was the identification of effective strategies for data analysis and integration, facilitated by the bioinformatics tools available today. It shows experimental identification of proteins passed through the screen to ensure analytical rigor and functional relevance as above (Stage 1). Biologically important and potential tumor specific proteins identified in expression studies are then assessed for their secretory potential based on computational prediction algorithms for signal peptide and transmembrane domain containing proteins, such as, SignalP and TMHMM, respectively and via non-classical secretory mechanisms using SecretomeP. These proteins are further prioritized based on their de tectability and occurrence in proteomic data for secretome, CSF and plasma analysis (normal or patient) (Stage 2). The potential secretory candidates are then explored in plasma in a targeted manner (Stage 3). Interestingly, some of these proteins were identified in analysis of plasma or CSF from GBM patients (2, 3). Once bioinformatically scrutinized as above and compiled, the candidate biomarker panels, can be subjected to validation and experimentation in cohorts of tissue sections, blood plasma/serum specimens from patients (Stage 4). We believe construction of such high confidence protein panels would be a valuable paradigm for studies in larger cohorts in clinical experimental designs. High confident lead candidates for experimental application GBM Secreted proteins Secreted proteins have an integral role in GBM tumorigenesis through cell growth, migration, invasion, and angiogenesis besides being important in normal physiological processes and thus instrumental to the discovery of cancer biomarkers. Besides being useful as markers for typing the tumor, their presence in easily accessible body fluids makes them useful for monitoring the disease progression or treatment response and recurrence. A thorough survey of all available literature was done to identify the several candidate biomarkers have been reported in serum or plasma of GBM patients and these are shown in Table 1 in Chapter 1. However, such potential and promising new biomarkers are yet to be rigorously evaluated for application against this unmet need. Non-invasive methods based on circulatory biomarkers would be useful for monitoring not only GBM patients but also for lower grades Grade II and III tumors that exhibit longer survival periods. Further, some new reports on circulating tumor DNA (ctDNA) that have identified in the plasma of GBM patients such as mutated IDH1 DNA (4), methylated MGMT DNA (5) and EGFRvIII mutant DNA (6). The highly sensitive sequencing based methods for detection of circulatory tumor DNA (ctDNA) in patients plasma are under progress (7). These ctDNA markers shed by dead tumor cells may surface in future to be reasonable indicators for tumor diagnostics. Kinases in GBM Identification of GnRH signaling pathway using an alternate approach As mentioned in Chapter 2, I used alternate approaches to enhance pathway views by targeting specific protein families, i.e. kinases. Protein kinases (PKs) are well known therapeutic targets in different cancers and a family of proteins that are major components of signal transduction pathways acting as membrane receptors (RTKs) or as intracellular signaling mediators (non-receptor PKs) and several protein kinases have been implicated in gliomagenesis (8, 9). Several studies have also shown altered expression of protein kinases in GBM and targeted therapies directed towards RTKs using kinase inhibitors are in clinical trials (10, 11). There is renewed optimism in the use of kinase inhibitors to treat GBM (12). New therapeutic strategies have emerged that use multi-targeted kinase inhibitors to simultaneously disrupt multiple kinases (13). The GBM data was found to be enriched with several kinases. A total of 102 kinases were present in GBM datasets; 77 different kinases in transcript omics data and 30 kinases in proteomics data with 26 in common between them.   Pathway analysis using these kinases revealed GnRH signaling as the top pathway that has still not investigated in the context of GBM. We observe an overall enrichment of about 129 entities from omics datasets of which 26 kinases and 57 non-kinase members are coming from the concordant (n=711) transcriptome and proteome dataset. The 26 concordant kinases along with their fold changes are shown in the Figure 48 below. A large proportion of GnRH pathway entities include kinases (MAPKs, CAMKs, and RTKs) that enabled its identification as a top pathway using this approach. A targeted search of other non-kinase members of the pathway resulted in additional members of the pathway in omics datasets that further increased its significance value. In GBM, it has been shown that human GnRH receptors are expressed in tumor cells and receptor activation affects apoptosis, adhesion and angiogenesis to promote tumorigenesis. GnRH signalling as a possible therapeutic target in cancer has already been suggested and put together with my observations it strongly supports this possibility in the context of GBM. The expanded hand-curated map of GnRH signaling is a valuable resource for the scientific community. Expression of GnRH and GnRH receptor has been reported in GBM cell lines and tissue samples at both mRNA and protein levels concordant with clinical data obtained using GBM tumor tissues and treatment with GnRH agonists resulted in anti-proliferative activity (14-16).There is also evidence that the analogues can cross the blood-brain barrier, indicating suitability for treatment of malignant glioblastomas (17). Given the significance of this pathway in cancers and GBM, further understanding the molecular interplay involving GnRH signalling pathway in light of my findings will reveal is use as a potential molecular and therapeutic target.      Ã‚   Glioma Amplicon and Risk Regions The protein coding genes implicated in Glioma and other cancers were clustered based on their chromosomal locations using Gene Set Enrichment Analysis tools to compute overlaps with positional gene sets from Molecular Signatures database and further clustered based on proximity to other known oncogenes from Atlas of Genetics and Cytogenetics in Oncology and Haematology data resource, to identify colocalized gene clusters on Chr. 12 and other chromosomes as shown in Chapter 3. An important finding was that larger number of overexpressed differential regulated genes in glioma datasets mapped to two significant regions the glioma amplicon (n=37) in 12q13-15 region and the glioma susceptibility (n=16) in the 12p13 region implicated as a major risk region in patients with a family history of gliomas. The discovery of these two clusters of overexpressed genes provides a biological validation of mass-spectrometry derived data. Apart from these two essential regions, several genes from the glioma dataset were found to cluster around amplicons on other chromosomes and other known cancer associated genes that were not identified in GBM datasets but present in close proximity to them. These can be investigated in a more targeted manner in glioma.   Many studies have been done to understand the biological significance of these amplicon regions in gliomas that indicate that these amplifications are more frequent in gliomas than previously thought and have different distribution patterns in low grade versus high grade tumors (18, 19). Overall, a relative high degree of amplifications and deletions are seen in GBM that have implications on the expression of the genes involved and contribute to relevant pathogenic genes (20). Novel genes and isoforms Alternative splicing increases the repertoire of protein functionality and heterogeneity and aberrant splicing events have been frequently seen in several cancers, including GBM and increasing evidence now points to their important role in tumor initiation and progression. The concept of proteogenomics has emerged rapidly as a valuable approach to integrate mass spectrometry (MS)-derived proteomic data with transcriptomic data to identify novel splice variants. However, the role of alternative splicing in GBM is still nascent and needs to be explored as potential biomarkers or molecular targets. As detailed in Chapter 4, the identification of a novel variant of NCAM1, using a proteogenomics approach with 5 peptide evidences from MS data spanning a novel exonic region, is very significant finding in GBM. NCAMs are well characterized glycoproteins that mediate cell-cell or cell-matrix adhesion among neurons and between neurons and muscle. Several splice variants of NCAM1 have been identified (21, 22) and alterations in these have been found in serum and tissues of brain tumors (23, 24). NCAM1 has 5 known isoforms and also exhibits glycoforms as it can be post-translationally modified by the addition of polysialic acid (PSA), which is thought to abrogate its homophilic binding properties and affect the adhesive properties of NCAM (25). Further, PSA conjugated NCAM, was shown to potentiate migration via FGFR signaling distinct from its adhesion capability (26).   The following observations may be noted with respect to this novel variant: The observation is supported in transcriptomics data in 18 out of 25 RNAseq samples. Multiple gene modelling software such as Augustus, GenScan, AceView and Ensemble support the presence of this novel exon in their gene models and a high degree of conservation was seen as expected for an exonic region. This variant was also separately identified in MS-derived Human Proteome and IvyGAP RNAseq datasets NCAM1 is upregulated in several cancers; however, in GBM both transcript and protein data support its down regulation.   We observed two known forms of NCAM1 as well as the novel form to be down regulated. It is interesting to note that the miRNA (hsa-mir-30a-5p) that regulates NCAM1 is upregulated in GBM indicating the deregulation of a putative oncogenic cascade. In summary, our findings demonstrate the usefulness of combining omics approaches to identify novel putative candidates in GBM. Although, it is not clear if the novel splice variant represents a major or minor form of NCAM1. At the transcript level, it seems to be a minor component; however, preliminary assessment at the protein level is suggestive of it being a predominant form. Regardless, it would be interesting to explore the biological significance of the novel splice variant of NCAM1 and examine its role in GBM tumorigenesis. Hence, in the light of this observation my identification of novel NCAM1 splice variant through proteogenomics analysis using GBM RNAseq data is a very important finding in GBM. The effect of this novel variant on cell-cell adhesion and migration in GBM needs to be further investigated in a targeted manner. Disease implications and targeted analysis Studies suggest that gliomas constitute a rapidly progressing neurodegenerative disease caused by the malignant growth of glial cells that nourish neurons, resulting in a loss of brain function. Glutamate excitotoxicity is observed in several neurological diseases, which is also utilized by gliomas to gain growth advantage (27). My observations that neurological conditions like Alzhiemers and Parkinsons disease share many common genes with gliomas possible indicate shared molecular mechanisms inducing neurodegeneration. Further, the chromosomal mapping of glioma differentials revealed two clusters; one around 12p13 implicated as a glioma risk region and another around 12q13-15 region harboring a glioma amplicon with several overexpressed and amplified genes. Hence, extracting gene/disease associations and generation of a glioma-centric functional and diseasome network is important for understanding GBM tumorigenesis. Further, this region was found to be enriched in several cancers in cluding other brain neoplasms and neurological diseases that may share disease genes and processes with gliomas. Only 22 of the observed 108 disease genes in the diseasome network were identified in our proteomic analysis. The other 86 disease genes implicated in gliomas but not identified in our dataset can be investigated in a more targeted manner in gliomas, providing a global view of linkages between disease phenotypes. Additionally, the finding that chromosomal proximity of genes may have an impact on their functions can be used to explore the functions of missing proteins mapping within functional cassettes of related protein/genes. Such investigations offer newer paradigms that may be valuable to investigate and present clinically important targets. Future Scope Metabolomic data integration and potential Compared to the genome and proteome, metabolome represents the phenotypic changes more closely and has already been investigated for malignancies such as breast, ovarian, colon, prostrate and esophageal cancers. This line of investigation has been extended to gliomas albeit on a smaller scale, revealing novel insights into the role of metabolites in GBM tumorigenesis (reviewed in ref. (28)). Previous studies have revealed how mutations can lead to generation of oncometabolites such as 2-hydroxyglutarate (2-HG) specifically in IDH1 mutated gliomas (29). The discovery by Otto Warburg that cancer cells prefer to metabolize glucose through a seemingly inefficient process of aerobic glycolysis   led to the application of 18-FDG-PET imaging to predict the histological grade of gliomas.   Using this technique we could now distinguish low grade gliomas that have low specific uptake (SUV) values from grade III and IV that have higher SUVs.   One study performed global metabolic profilin g using mass-spectrometry coupled to liquid/gas chromatography on patient derived tumor samples and found increased levels of glutathione, tryptophan and metabolites associated with phentose phosphate and nucleotide synthesis and glycolytic intermediates such as phosphoenolpyruvate (PEP) and 3-phosphoglycerate (30). These studies have collectively provided a window of opportunity for further investigation and integrating these changes with the changes at proteomic, transcriptomic and genomic levels will be the next big step in to study the underlying biology of these tumors. Improving pathway analysis with phosphoproteomics data Protein phosphorylation plays a central role in transmitting the signal from outside the cell through a cascade effect into an intracellular signal to control the biochemical pathways in all living cells. This mechanism of activation or deactivation can be orchestrated by protein kinases via phosphorylation and phosphatases via dephosphorylation. Modifications to these signaling networks via mutations or abnormal protein expression or post-translational modifications may underlie both development and progression of tumorigenesis. Glioma Repository In order to facilitate annotation of key terms and manage the collection of high-throughput data coming from different omics technologies and platforms and make it easier to store and retrieve large amounts of information, I proposed to a schema for data annotation, collection and deposition. The data will be stored in the backend, in separate tables in a relational database (RDBMS), to enable effortless retrieval of key information for particular candidates of interest and also allow for complex querying. The outline for the schema is given below. Figure 49: Schema for development of a glioma repository

Thursday, October 24, 2019

Interview With The Vampire :: essays research papers

This novel, “Interview with the Vampire';, by Anne Rice, is by far one of the best book I’ve ever read. It started with a young boy interviewing a vampire, and the vampire related him the whole story of his life, how he became a vampire, his thrilling adventures through the centuries and his complex relationships with both the mortals and the immortals. In my opinion, Anne Rice had done the best of jobs. The writing and the detailed descriptions, the composing of this novel, had brought out every emotion of the characters like the flick of a whip. The rage, the love, the hatred, the sufferings, the darkness, the pain and the terror, were all presented so vividly as if in front of my eyes, as if I were really part of the character. I think Anne Rice had created the most successful characters. Throughout the whole book, you can really look at the conflicts between them. They are, somehow, attached or attracted by each other, both the mortals and the immortals. Their love and hate and struggles go to such degrees, and yet limited by their nature, it was almost impossible to understand it at all. I believe Anne Rice had used those characters to express humanity, the whole plot was some kind of an irony. Something like a metaphor, though she exaggerated everything to make it poignant enough. Not only were the characters a success, the time and place details were incredible. The costumes, ways of manner, history and every background changes as the years passed, and she made the backgrounds so realistic that I could almost feel everything surrounding me. Actually I think Anne Rice had done such a great job that this book should be counted as literature.

Wednesday, October 23, 2019

Financial Management Questions

Q5. Putting yourself in the position of an existing shareholder(investor) of your company, using both the annual corporate report and the information about your company’s share price in the Financial Times, provide a recommendation (with reasons) whether you rate your company’s shares as Buy, Hold or Sell. There are a wide range of factors that affect share price. These include interest rates, inflation, the performance of the industry/sector the company is in, the performance of the company itself, and the market supply and demand for the companies’ shares.The following graph shows Marks and Spencer’s share price over the last 12 months. http://corporate. marksandspencer. com/investors/shareprice/chart Accessed: 05/12/11 By viewing the graph, we can see that there have been numerous fluctuations in share price over the last 12 months. At the start of the year share price was at around 370 pence per share and dropped down to around 330 pence per share afte r 3 months. There was then a surge in share price which reached over 400 pence per share at its peak in May.It then fell to its lowest point, just above 300 pence per share in September and there have since been small fluctuations in share price. Its current share price is at 329. 00 but we expect it to continue to fluctuate slightly before finally increasing again into the New Year, as share prices do generally remain low over the Christmas period. The following table is share information that was published in The Financial Times weekly update on Monday 5th December 2011. | |Price |Wks% Chg | Div |Div Cov |Mcap ? | Last xd | |Marks&Sp |330. 10 |+7. 3 |17 |2. 3 |5,233. 3 |16. 11 | Using the data available from this table and information published in the annual company report, we can work out dividend yield and dividend cover. â€Å"Dividend yield tells you the percentage cash return on the investment, and can be directly compared with interest rates and other investment opportuniti es. It expresses the dividend per share as a percentage of the current share price† (McKenzie, 2010:385).It is therefore worked out by dividing the dividend per share which is 17 pence, by the current price by share, which is 330. 10, and then multiplying the answer by 100. The dividend yield can then be worked out as 5. 17%. This would therefore be a worthwhile investment considering many interest rates for banks are less than 1%. The dividend cover â€Å"measures how many times the dividend could be paid from the available profits† (McKenzie, 2010:384). The financial times reveal that the dividend cover is 2. 3, and therefore the dividend could be paid 2. 3 times out of Marks and Spencer’s available profits.This shows that Marks and Spencer are using quite a substantial amount of profit to pay out dividends, nearly half. This may be rewarding for a shareholder looking for a quick return, however, shareholders who are looking to invest in Marks and Spencer in th e long run may find it more beneficial if Marks and Spencer’s reinvested their profits into the business. Taking everything into account, we would recommend a shareholder to hold their shares, as we believe that there will be a rise in share price in the coming months, so they will therefore make a better return if they do wish to sale in the future.The dividend yield shows that Marks and Spencer offer a good return on investment, compared with other alternatives such as bank interest rates. And also they use a considerable amount of their profits to pay shareholders dividends, so we believe it would be worthwhile holding onto the shares for the time being at least. Financial Times, Monday December 5 2011, p. 26 McKenzie, W. (2010) Using and Interpreting Company Accounts. FT Prentice Hall. p. 384-385

Tuesday, October 22, 2019

Web Design Essay

Web Design Essay Web Design Essay | Assesment One | Web Systems BN102 | | | Rachael Mayhew MIT 110101 | Tanya Linden | | 1.0 | Introduction The â€Å"bad† website I have chosen to critique is a website designed to advertise a book named â€Å"The Bombshell Manual of Style – by Laren Stover†. The website begins with a few flash images moving around, which then leads to you needing to remove images of underwear before you can move forward. You are given the option of completing a quiz designed to see if you are a ‘bombshell’, or the option to skip and move straight to the crux of the site. The website content mainly consists of little facts about the book or what a typical bombshell is as you move on, till you eventually get to the end at which point you are offered a way to purchase the book. 2.0 | Visual Effect 2.1 Colour Scheme The colour scheme is a white background with pink or black typography. Pink colours, depending on the shade, are sometimes associated with love, romance or youth from the viewer’s point of view. However white is seen as cold and sterile which is a contrast to the use of pink. There are many images used on this website so this may be the reason for a simple colour scheme (Empathizing Color Psychology in Web Design, 2013). 2.2 Imaging I am using a laptop with a screen resolution of 1366 x 768, and as can be seen in Appendix One from the original website, www.bombshellmanual.com, the images used are pixelated heavily. This is seen with every image used which is numerous, including the flash images. Most of the text throughout the website is a simple and readable font; however the hyperlinks to different parts of the website are cursive flash images. 2.3 Page Layout The main content of this page is centred with much space on either side. This however, may be a deliberate move due to the fact on more than one occasion you must ‘uncover’ the text by moving images from on top of the text to the outer text. 3.0 | Navigation The navigation, or lack thereof on this website, is a purely a forward momentum with no chance to go backward. If you step off the main path, there is no option to go back or even start again unless you refresh. After the initial quiz, if you chose to do so, you cannot skip if you change your mind halfway through. To continue forward there is an image of a dog that you must click and drag that urges the website to load the first content page. This dog image actually caused me to start again from the beginning due to not moving it all the way across when initially asked to move it. I then tried to move it a second time as I could not see the text (see Appendix Two) which prompted everything to begin again. As you progress by hitting the â€Å"more† hyperlink, it moves into a different spot after each page changes, making it difficult to move quickly through if you have already read these pages. At no point are you offered all of the options like â€Å"purchasing the book† or â€Å"Bombshell Bulletins and Resources† at once, nor can you skip to the end or the beginning at will. When you get to the very end, your only option is to go back to the previous page (the only time this option is offered) or to go to Amazon.com to purchase the book. Clicking the picture will direct you straight to their website by opening a new tab. The main fury in the navigation is that if you accidentally move forward, you have no way to get back. You cannot even go back a page on your browser (I am using Explorer 9). Many of the hyperlinks that suggest to some different content do not actually work. I am unsure whether this was because they actually did not go anywhere or the page could not move on. I opened this also on my iPhone where it promptly told me that I could not see all their moving images due to not having Adobe flash player. However, I was able to see the content much clearer than on Internet Explorer, the navigation through pages was just as difficult. 4.0 | Content Amazon’s write up of the book

Monday, October 21, 2019

Freud1 essays

Freud1 essays In several of his books, including Introductory Lectures on Psychoanalysis and On Dreams, Freud combines the topics of forgetting a proper name and dream analysis, formulating a thesis that helps to clarify his theories on both. He describes in psychoanalytic terms the mechanisms behind forgetting of a proper name and how they relate to the methods used in dream analysis. By looking at the two topics from a joint perspective, we can gain a greater understanding of them and how they relate to other areas of psychoanalysis. The tendency toward forgetting of a proper name is an important theme in Freuds work. He explained the way in which forgetting something like a name was actually a substitute for forgetting something that, unconsciously, an individual does not wish to remember. He described the unconscious force that prompted this forgetfulness as a counter-will, or an unconscious desire parallel to an individuals conscious desire. According to Freud, there is a connection between what one consciously forgets and what one unconsciously wants to forget. When a person has some unpleasant thought or issue that they wish to banish from their mind, the will to forget may miss its target, and the wish to forget may manifest itself in some other way. In this case the individual may forget something seemingly unconnected to the thought they wish to banish, such as a proper name. Freud gives some relevant examples of this phenomenon in Introductory Lectures: For instance, if we have temporarily forgotten a name, we are annoyed about it, do all we can to remember it and cannot leave the business alone. Why in such cases do we so extremely seldom succeed in directing our attention, as we are after all anxious to do, to the word which (as we say) is on the tip of our tongue and which we recognize at once when we are told it? Or again: there are cases in which the parapraxes mul...

Sunday, October 20, 2019

Decolonization of the Filipino American Mind Essay Example

Decolonization of the Filipino American Mind Essay Example Decolonization of the Filipino American Mind Paper Decolonization of the Filipino American Mind Paper Berdahl, R. O. , Gumport, P. J. (Eds. ). (1999). American Higher Education in the Twenty-first Century: Social, Political, and Economic Challenges. Baltimore, MD: The John Hopkins University Press. Baldazo, P. G. (March 1991). The good, the bad, the beautiful, and the ugly in Filipino cultural values. Heritage, 5(1), p. 6. Barringer, H. R. , Takeuchi, D. T. , Xenos, P. (January 1990). Education, occupational prestige, and income of Asian Americans. Sociology of Education, 63(1), pp. 27-43. Blair, S. L. Qian, Z. (July 1998). Family and Asian students’ educational performance. Journal of Family Issues. 19(4), p. 355. California Postsecondary Education Commission (2000). College-Going Rates of California Public High School Graduates by Racial/ Ethnic Group, Fall 1997 to Fall 1999. Higher Education Performance Indicators. Sacramento, California. Callan, P. M. , Finney, J. E. , Bracco, K. R. , Doyle, W. R. (Eds. ). (1997) Public and Private Financing of Higher Education. Phoenix, AZ: Oryx Press. Constantino, R. (2000). The mis-education of the Filipino. Journal of Contemporary Asia. 30(3), pp. 428-44. Espiritu, Y. L.. (1992). Asian American Panethnicity: bridging institutions and identities. Philadelphia, PA: Temple University Press. Espiritu, Y. L. , Fujita Rony, D. , Kibria, N. , and Lipsitz, G. (June 2000). The Role of Race And Its Articulations for Asian Pacific Americans. Journal of Asian American Studies, pp. 127-137. Fong, T. (1998). The Contemporary Asian American Experience. Upper Saddle River, NJ: Prentice Hall. Fulgado, C. Q. (September 1991). Speaking on education. Heritage, 5(1), pp. 17-18. Gendrano, V. P. (Fall 1996). Understanding Filipino parents and grandparents. Heritage, 10(3), p. 20-21. Guillermo, E. (2002, February 5). Side-by-side: U. S. lies and broken promises. SF Gate. Retrieved December 4, 2002 from the World Wide Web: http://sfgate. com/cgi-bin/article. cgi? file=/gate/archive/2002/02/05/eguillermo. DTL. Harrison, F. V. (1995). The Persistent Power of â€Å"Race† in the Cultural and Political Economy of Racism. Annual Review of Anthropology, 24, 59. Heller, D. E. (Ed. ). (2001). The States and Public Higher Education Policy: Affordability, Access and Accountability. Baltimore, MD: The Johns Hopkins University Press. Kang, K. C. (1996, January 26). Filipinos happy with life in U. S. , but lack united voice. Los Angeles Times, p. A1. King, R. C. (June 2000). Racialization, Recognition, and Rights: Lumping and splitting Multiracial Asian Americans in the 2000 Census. Journal of Asian American Studies, pp. 191-217. Luzzo, D. A. (October 1993). Ethnic Differences in College Students’ Perceptions of Barriers to Career Development. Journal of Multicultural Counseling and Development, 21(4), pp. 227-236. Okamura, J. Y. Agbayani, A. R. (1997). Pamantasan: Filipino American Higher Education. In M. P. P. Root (Ed. ). Filipino Americans: Transformation and identity (pp. 183-197). Thousand Oaks, CA: Sage Publications Inc. Pimentel, B. (1999, January 31). White Man’s Forgotten War. San Francisco Chronicle. Retrieved December 4, 2002 from the World Wide Web: http://sfgate. com/cgi-bin/article. cgi? file=/chronicle/archive/1999/01/31/SC16131. DTL. Rodis, R. 2002, April 3). Losing track of one’s census. New California Media. Retrieved September 27, 2002 from the World Wide Web: http://news. ncmonline. com/news/view_article. html? article_id=119. Roley, B. A. (2001, August 20). Filipinos- the hidden majority. San Francisco Chronicle. Retrieved September 27, 2002 from the World Wide Web: http://sfgate. com/cgi-bin/a rticle. cgi? file=/chronicle/archive/2001/08/20/ED194136. DTL. Root, M. P. P. (Ed. ). (1997). Filipino Americans: Transformation and identity. Thousand Oaks, CA: Sage Publications Inc.. Rumbaut, R. G. (2002, May 22). Competing Futures: The children of America’s newest Immigrants. Migration Information Source. Retrieved September 27, 2002 from the World Wide Web: migrationinformation. org/Feature/print. cfm? ID=1. Sargon, E. (2001, January 19). California’s misplaced priorities deny equal rights. Daily Nexus Online. Retrieved September 27,2002 from the World Wide Web: dailynexus. com/opinion/2001/205. html. Schirmer, D. , Shalom, R. (Eds. ). (1987). The Philippines Reader: A history of colonialism, neocolonialism, dictatorship and resistance. South End Press. Takaki, R. (1989). Strangers From A Different Shore: A history of Asian Americans. New York: Penguin Books. The Filipino Crisis in Higher Education. Retrieved September 27, 2002 from the World Wide Web: ocv/berkeley. edu/~pass/crisis. html. U. S. Department of Education, National Center for Education Statistics. (July 2002). NCES Profile of Undergraduates in United States Postsecondary Institutions (1999-2000) Statistical Analysis Report (NCES 2002-168). Washington D. C. : Office of Educational Research and Improvement. Wolf, D. L. (Fall 1997). Family secrets: transnational struggles among children of Filipino immigrants. Sociological Perspectives, 40(3), p. 457(26)

Saturday, October 19, 2019

Marketing Research Plan Essay Example | Topics and Well Written Essays - 1500 words

Marketing Research Plan - Essay Example To ensure we get cooperation on the study, we intend to visit at least two universities that offer both fulltime and online degrees modules to their students. We will also visit two companies to study on those who are not studying but intend to study so as to know what would motivate them to study an online degree course. We intend to spit this study into three distinct steps as follow: The first step will involve use of a questionnaire that will be utilized to get at the base of motivations on what would happen if those working fulltime have other options of studying. This study would only involve only those who are studying the online degree programme. The second step would involve direct interviewing of all students on the university on what would motivate them to take an online degree. This interview would involve both those in fulltime and part-time base programme. We intend to approach the administration of the two universities that offer online degree programm... The Study 1 We intend to approach the administration of the two universities that offer online degree programmes. We will use over observational approach in this study whereby we will identify ourselves as researchers and clarify to them on the main rationale of the study. For this case, we will request them to give us the contacts of those studying online degree programmes in their university. We will get their contacts especially email address and we would send them our questionnaire to them. The following questionnaire will be use in this study. The students will be expected to fill the questionnaires and email them back to us on their views regarding online degree courses. Study 2 The second study will involve direct interviewing students at the university. We will pick students at random at the university and interview them concerning online degree courses. We will introduce ourselves to students as researchers and our intention our carrying out the research. We would spend around 15 to 20 minutes with the students and discuss their view in regard to online degree course. After this, we would compile discussion and come up with the correct ideas on the best view concerning online degree courses. Questionnaire Choice Question Note: Question 1 - 5 has no specific quantifiable value; they are intended to measure affiliation with those already studying online degree programme. I. Which degree programme did you use in your previous study Fulltime programme _______________ Online Programme _______________ II. Which degree programme would you prefer today Fulltime programme _______________ Online Programme _______________ III. Why do you prefer the degree programme chosen above Convenience ________________ Cost