How To Double Your Facebook Reach With Rebekah Radice [Podcast]

How To Double Your Facebook Reach With Rebekah Radice [Podcast] Organic reach: How do you boost yours? It’s one of those things that you might find to be a mystery, but it doesn’t have to be that way. Today we’re talking to Rebekah Radice, a social media strategist and the Chief Marketing Officer of Post Planner. With her help and expertise, Post Planner managed to double their Facebook organic reach. Rebekah has one of the top 10 social media blogs for 2015 and 2016, according to Social Media Examiner. She’s the author of the e-book, Shine Online, and she has been featured on NBC, Social Media Today, Steam Feed, Maximize Social Business, and others. She’s also a keynote speaker and is passionate about educating entrepreneurs and future business leaders. Some of the topics that you’ll hear discussed today include: Some information about Post Planner, as well as details on what Rebekah’s position as CMO entails. The biggest challenge with Facebook that marketers struggle to resolve. How Post Planner has achieved such great success with Facebook, and why organic growth is their main focus. How having big, crazy goals and a narrow focus contributed to Post Planner’s success. The importance of visual marketing and letting your personality shine through in your content. Rebekah’s advice for marketers who want to improve their Facebook organic reach.

Risk and Hedging Essay Example | Topics and Well Written Essays - 250 words

Risk and Hedging - Essay Example The exposure is also related to a case whereby the company borrows money in a foreign currency. Coca Cola Company usually relies on lending’s from the subsidiaries that are found in other countries (Vigna, 2012). An economic exposure is one that measures the changes in the present value of Coca Cola Company and it results from changes in the future expected cash flows that may be caused by exchange rate changes that are not expected. The exposure in Coca Cola Company mainly affects the selling price and the sales volume of the company. An accounting exposure is used in measuring the changes that are derived from accounting as a result of coca cola Company translating its financial statements that are found in a foreign currency into a reporting currency that is single. That will affect issues such as the payment of the corporate tax incurred by the company. Coca cola company therefore hedges so as to avoid risks that are involved with foreign transactions (Murphy,

Monopoly...is a great enemy to good management. Adam Smith, (1776), Essay

Monopoly...is a great enemy to good management. Adam Smith, (1776), The Wealth of Nations, Book I, Chapter XI. Discuss - Essay Example In the light of this statement therefore this question involves the discussion of the various market structures and their contribution to the achievement of the highest possible level of allocative and productive efficiency (in both static and dynamic senses).The question already suggests that the Monopolised market structure is not conducive to â€Å"good management† or efficient resource allocation. Resource allocation in a modern economy demands allocative efficiency which means that resources should be allocated to match the wants of society. Essentially this would mean a point of allocation where no redistribution would enable one individual to be made better off without making someone else worse off. Allocative efficiency would therefore consider both the consumer (demand) and the producer (supply) and that it should satisfy the needs of both. This essay will mainly discuss the two main extremes of competing market structures i.e. monopoly and perfect competition and to a slightly lesser extent similar models along the vast range of economic models falling halfway between these extremes for example Oligopolies. Perfect Competition represents the efficiency achieved by an industry which has extensive competition and almost no interference in the market forces either by the sellers or buyers or the government. Monopoly on the other hand represents a rather inefficient means of market structure characterised by lack of competition and extensive market control. 3.The reason the statement by Adam Smith seems to resent Monopoly power is because of the complete market control by the monopolist who as the only seller in the market will control the supply of goods in the market and is able to influence the price of its product sometimes in an unfair way. Perfect competition, in contrast is preferred in this regard as a market structure where each firm has neither got any significant

Tucson 4th ave streetcar Essay Example | Topics and Well Written Essays - 1500 words

Tucson 4th ave streetcar - Essay Example So far, the development plan is underway and the streetcar is soon getting an operation, however, the project draws a number of criticisms right from its planning to the effects of the finished railroad in the city. Efficiency in transportation reduces time lost in traffic thereby making the economy more efficient. For a long time the city of Tucson has merely relied on the efficient road network to provide connections to all the places within the city. The city has a dedicated metropolitan bus service coupled with a number of private taxi services that have by far ensured efficient transportation in and out of the city. However, the city just as any other part of the country is expanding. The city continues to attract more investors, which implies that more people move into the city all of who require effective means of transportation. This implies that while the sizes and the conditions of the road network have remained unchanged for quite some time, the demand has significantly in creased resulting in both congestion in the public places such as bus stations and traffic jams on the roads and major highways. The city therefore needed some more radical means of transportation, one which could transport a large number of people and do so efficiently fast. This could drastically reduce congestion and save time. Expansion of the road networks seemed more expensive and had more severe economic ramifications, the rest of the world and even New York among other cities in the United States have all tried and tested the efficiency of streetcars a feature, which prompted the council government of Tucson to employ one. However, the cost constructing one would overburden the taxpayers, which is the key source of revenue for the council government. The project, which expected to complete in June 2013, had an initial budget of one hundred and fifty million dollars but that has since increased to two hundred million owing to readjustments on a number of construction features (Golem and Janet 33). The project draws its funding from the voter approved regional transportation authority and federal agents both of which rely on taxes. Once completed the project is expected to relieve the public transport system and revamp business in the city’s major business districts. The project has so far served as one of the highest employers in the city of Tucson, its construction process alone has caused more than a thousand temporary construction jobs but the streetcar project is expected to create more than two thousand permanent jobs once it gets operational. Additionally, more than twenty construction companies set up in the neighborhood to sustain the construction process. More than one thousand five hundred more people will be employed by the Sun Link Tucson Transport Company to sustain the entire transportation process. Furthermore, the electricity powered streetcar promises efficiency, The Sun Link Tucson, which is the company mandated with operating t he streetcar, has a success history with managing public transportation and won the Best Transit system in 2005. It is therefore expected that the streetcar project will attain similar efficiency thereby decongesting the city. The mapping of the streetcar route passes

Fe-AZT and Pd-AZT Synthesis and Effects

Fe-AZT and Pd-AZT Synthesis and Effects Synthesis and Effects of Fe-AZT and Pd-AZT on Viability of Human Hepatocytes and Hepatocellular Carcinoma Cells Submitted by: Anna Harutyunyan Introduction Cancer is one of the major causes of mortality in the world. In 2015, according to the National Cancer Institute, over 1.6 million new cases of cancer were reported in the United States. The estimated cancer deaths for the year of 2015 were over 500,000. According to the National Cancer Institute projections, in 2016 an estimated 1.7 million new cases of cancer were diagnosed in the United States and 595,690 people will die from the disease (National Cancer Institute). Although new cancer treatments and therapies are designed and implemented every year, cancer is still the number two cause of mortality in the United States, therefore developing and testing new effective anticancer agents is crucial. Hepatocellular carcinoma (HCC) is one of the deadliest forms of cancers (Venook et al., 2010). The overall 5-year survival rate of HCC is less than 17%, making HCC the fastest rising cause of cancer related death in the United States (American Cancer Society 2016; Mittal and El-Serag, 2013). The annual age-adjusted incidence rates of HCC increased from 1.4 per 100,000 individuals in 1975-77 to 4.8 per 100,000 in 2005-07. An estimated 39,230 new cases of liver cancer (including intrahepatic bile duct cancers) were expected to occur in the US during 2016, approximately three-fourths of which would be hepatocellular carcinoma. An estimated 27,170 liver cancer deaths were expected in 2016 (American Cancer Society 2016). In 80-90% cases HHC occurs with and after cirrhosis. HCCs major risk factors are Hepatitis B and C viruses, cirrhosis, non-alcoholic fatty liver disease (NAFLD), overconsumption of alcohol and exposure to other carcinogenic substances (Mittal and El-Serag, 2013). Liver ca ncer is the sixth most common neoplasm and the third leading cause of cancer-related deaths, accounting for approximately 600,000 deaths annually (Venook et al., 2010). Because of early metastasis and progression, HCCs treatment is difficult, and traditional chemotherapy has shown limited success (Sabokrough et al, 2014). A research study published in 2015 suggested that an organometallic complex of platinum (II) azidothymidine (Pt (II)-AZT) has an antitumor effect on rat hepatocellular carcinoma cells. It was shown that this complex was significantly more effective in tumor suppression than the AZT without platinum (Sabokrough et al., 2014). Several organometallic complexes of AZT (with Zinc, Cobalt, Copper and Iron) were synthesized and characterized previously. The Iron complex of AZT (Fe-AZT) was shown to be the most stable (Shirvastav et al.) and have antimicrobial activity against 4 groups of bacteria. Electron rich ligands like AZT effectively bind and interact with metal ions producing metallodrugs which offer promising therapeutic application in terms of combating the drug-resistant strains of pathogens. It is also logical that a metal ion can influence the biological activity and therapeutic efficacy of the bio-molecule they bind (Shirvastav et al.) Thus it is useful to investigate the effect of a metal ion on the efficacy and mode of action of AZT in suppressing malignant cells and inducing apoptosis. To date, no research has been published regarding synthesis of Pd-AZT the inhibitory effect of both Fe-AZT and Pd-AZT on malignant cells. The aim of this research project is to synthesize Fe-AZT and Pd-AZT, confirm their structure and molecular mass and test their effects on viability of human hepatocellular carcinoma cells and normal human hepatocytes. Background Normal cell cycle In order to understand the biology of cancer it is crucial to understand the cell cycle of normal cells and cancerous cells. All cells in a given organism are under strict control of multiple regulatory agents, such as RB or p53 that control cell growth and keep the proliferative index stable. If there is a need for the cell to divide, the proliferative genes will turn on, or the suppressor genes that keep proliferation from occurring will be shut down, which will result in cell division (Hardin et al., 2014). The normal cell cycle consists of the following phases: G1, S, G2, M. During the G1 phase duplication of organelles, membrane systems and other important components happens. There is an important checkpoint at the end of this phase referred to as the restriction checkpoint, which verifies that DNA synthesis was successful and no errors have been detected. Next is the S phase during which the cell duplicates each chromosome. During the G2 the rest of the components that were not synthesized in the G1 phase are synthesized. A checkpoint after this phase makes sure the cell is ready to divide, and no errors in chromosome duplication were made. Mitosis is the next phase, when the cell physically divides (cytokinesis) making two identical daughter cells. A checkpoint during this phase checks if both of the daughter cells received the correct number of chromosomes. After division, the cell may remain in its silent G0 phase, when it does not divide, but continues to function. If any errors are detected on any of the checkpoints, the cell cycle is put on hold and the cell will undergo apoptosis. This process is governed my many enzymes and complexes, and theoretically, malfunction of any of these enzymes may result in uncontrolled cell division/proliferation. This can be the onset of carcinogenesis. Figure 1. The cell cycle phases with their checkpoints. Cancer cell cycle It is important to note that the normal cell cycle is under control of thousands of regulatory elements that are coded for by different genes. If mutations occur in the genes that code for the key elements keeping cell proliferation at bay, one level of control over the cell cycle is lost. There are cell signaling mechanisms through which immune cells detect faulty cells, send them death signals and the faulty cell undergoes apoptosis. It takes more than one mutation for a normal cell to start behaving like a cancer cell. Usually it is either the loss of the function of suppressor genes, or overexpression of proliferative genes that result in uncontrolled cell proliferation. When the cell becomes malignant, it loses the ability to respond to death signals, thus does not undergo apoptosis. The malignant cell cycle is slower than the normal cell cycle, however, since the cancer cells keep dividing and do not die, their number grows exponentially resulting in tumors (Weinberg, 2014). There is distinct cytological difference between normal and cancer cells (Figure 2). A normal cell has a smaller, regularly shaped nucleus, a low nucleus/cytoplasm ratio, is well differentiated and has well defined borders. Cancer cells have larger, irregularly shaped nucleus, high nucleus/cy toplasm ratio, are less differentiated and have irregular borders. In contract with normal cells that adhere to each other, cancer cells are less adhesive and break away from each other (Weinberg, 2014). Figure 2. The comparison of the cytology of normal cells and cancer cells. Azidothymidine (AZT), Fe(III)AZT, Pd(II)AZT Azidothymidine (AZT, Zidovudine) is a thymidine derivative in which the 3-hydroxy group is replaced by an azido group (Figure 3). It has been shown to have antitumor effects on different animal carcinoma cells both in vitro and in vivo through inhibition of telomerase activity and by causing cell cycle arrest (Gomez et al., 2012; Hadizadeh et al., 2014, Cooper and Lovett, 2011; Matteucci et al., 2015). Figure 3. Thymidine (left), Azidothymidine (right). Since cancer cells have higher proliferation rate than normal cells, their thymidine turnover rate is higher, which could contribute to their increased sensitivity to AZT. Several studies conducted by Fang et al., have shown that a hepatocellular carcinoma cell line (HepG2) is significantly more sensitive to AZT toxicity as compared to the normal hepatocyte (THLE2) sensitivity (Fang et al., 2014; Fang and Beland, 2009). The current hypothesis on how AZT affects the cell suggests that AZT is phosphorylated intracellularly yielding AZT-triphosphate and AZT-monophosphate. The AZT-monophosphate can be incorporated into the DNA structure instead of thymidine due to its similar molecular structure and shape. However, in contrast with thymidine, AZT lacks the 3 hydroxyl group which is the group that forms phosphodiester bonds between nucleotides in the DNA backbone structure. This means, wherever the AZT phosphate is incorporated in one of the DNA strands during DNA replication, the elongat ion of that strand halts (Figure 4). This is one of the mechanisms through which AZT causes damage to DNA (Fang et al, 2014). The commercial name of AZT is Zidovudine, and it is the basis of AIDS treatments. AZT blocks the replication of HIV-1 virus by competitively inhibiting the viral reverse transcriptase (RT). In other words, HIV RT prefers AZT to normal nucleotides. As described above, AZT is phosphorylated to AZT-triphosphate and is incorporated into viral DNA, halting nucleotide chain elongation. It is also known that AZT-triphosphate can be incorporated into eukaryotic DNA, although its affinity for DNA polymerases is lower than that for RT (Gomez et al, 2012). It was shown that Pt(II)-AZT is more effective in suppressing cancer cells than AZT, thus it has been suggested that having a transition metal bound to the central nitrogen atom of the azido group increases the complexs affinity for G-C and A-T base pairs and the P-backbone of DNA (Das and Pitre, 2007; Sabokrouh et al, 2015). Materials and Methods Fe-AZT and Pd-AZT synthesis To carry out the synthesis of Pd and Fe complexes, solid AZT and a standard ion solution of each metal (iron nitrate nonahydrate (Fe(NO3)3 ·9H2O and palladium chloride (PdCl2)) will be purchased from Sigma Aldrich (St. Louis, MO). Synthesis will be performed according to the protocol by Das and Pitre (2007). A 1:1 molar ratio of aqueous solution of AZT and metal ion will be refluxed for 3 hours. The volume of the reaction mixture will be reduced by 75% in order for the complex to precipitate. The solid product will be vacuum filtered, washed twice with ice-cold water, recrystallized and air-dried overnight. Infrared absorbance spectra will recorded for the AZT, Fe-AZT and Pd-AZT complexes. In the experiment conducted by Das and Pitre (2007) the comparison of IR spectra of pure AZT and its complex with Fe, the spectrum indicated a shift in bands from 2170 to 2150 cm-1 due to complexation through N atom of azido group. A similar band shift in the IR spectrum of Fe-AZT and Pd-AZT is expected. A Matrix Assisted Laser Ioniation/Distortion Time-of-Flight (MALDI TOF) mass spectrometry analysis will be performed for the Fe-AZT and Pd-AZT to determine the molar mass and the stoichiometry of the complexes. The matrix for analysis will be composed of 1:1 saturated Anthranilic Acid and Nicotinic Acid (Sigma Aldrich, St. Louis, MO). The samples and matrix will be dissolved in 45% acetonitrile: 55% water (van Kampen et al., 2004). Cell cultures HepG2, THLE2. Liver carcinoma cell line HepG2 and normal human liver cell line THLE2 will be obtained from American Type Culture Collection (Manassas, VA). The standard protocol recommended by ATCC will be used for establishing and maintaining hepatic cell lines. The cell lines will be plated at a density of 5 x 103 cells/cm2. HepG2 cells will be cultured in DMEM with 10% fetal bovine serum and antibiotics (penn/strep). THLE2 cells will be cultured in LHC-8 medium with 70ng/ml phosphoethanolamine, 5ng/ml epidermal growth factor, 10% fetal bovine serum and antibiotics (Fang et al., 2009). After ensuring sufficient cell growth and several passages of each cell line, the two cell lines will be divided into 4 groups each: control (no treatment) and treated with each drug: AZT, Fe-AZT and Pd-AZT (Table 1). Table 1. The experimental setup of the control and experimental groups of cells. Control 1 (C1) THLE2 cell line (no treatment) Control 2 (C2) HepG2 cell line (no treatment) Experimental 1 (E1) THLE2 cell line+AZT Experimental 2 (E2) HepG2 cell line+AZT Experimental 3 (E3) THLE2 cell line+Fe-AZT Experimental 4 (E4) HepG2 cell line+Fe-AZT Experimental 5 (E5) THLE2 cell line+Pd-AZT Experimental 6 (E6) HepG2 cell line+Pd-AZT The cells in the treated groups will be further categorized by the concentrations of the drug. HepG2 cells will be incubated with 2, 20 or 100  µM aqueous solution of AZT, Fe-AZT or Pd-AZT for 14 days. THLE2 cells will be incubated with 50, 500 or 2500  µM aqueous solution of AZT, Fe-AZT or Pd-AZT for 14 days. Each group of cells will be seeded at 5 x 103 cells/cm2 density in 6-well plates. The cells will be passaged weekly during the two-week treatment period. The dosage and incubation time were chosen based on a similar study (Fang et al., 2013; Matteucci et al., 2015; Sabokrouh et al., 2015). Cell viability assay After 14-day treatment period, 103 106 cells from each group will be seeded in a 96-well plate, incubated for 4 hours, and treated with MTT reagent, followed by a 8-12 hours incubation at 37 °C. After the incubation with MTT, when the cells have metabolized the yellow tetrazolium dye (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) to purple formazan, the cells will be treated by a detergent to release the formazan into the solution, and the absorbance will be measured at 570nm using an ELIZA reader. The number of metabolically active cells will be determined using a previously made calibration curve. The statistical differences will be calculated using a Two-Way ANOVA and Tukeys Post-Hoc Test. Anticipated outcomes. The expected mass-to-charge ratio from mass spectrometry analysis of Fe-AZT complex is 323.1, that of Pd-AZT is 373.6. Based on the published literature and the adopted hypothesis, all three drugs are expected to decrease cell viability. The concentration of either drug should have positive correlation with decrease in cell viability. Based on previous observations, it is expected that the HepG2 cells will be significantly more sensitive to both complexes, thus will be significantly less viable after the treatment compared to the THLE-2 cells. Study Participants and Timeline Anna Harutyunyan is the primary author of this study. She is currently a senior biology and chemistry major at Wilson College. This project will serve as Annas senior research project. She will conduct the research and present the results with the supervision of her advisors Dr. Deborah S. Austin (Sponsoring PAS member) and Dr. M. Dana Harriger (PAS Member). The research study began in September 2016 and will be completed by April 2017. Annas research findings will be analyzed and written as her senior thesis. Anna will also present her findings at the 2017 Pennsylvania Academy of Science meeting and at the Wilson College research colloquium. Budget Item Price MTT Assay Kit (ThermoFisher) $235.00 Zidovudine (Sigma) $124.00 LHC-8 medium (Gibco) $140.00 Total $499.00 Facilities and Equipment The MALDI TOF mass spectrophotometer will be provided by Pennsylvania State College of Medicine Mass Spectrometry Facility under supervision of Bruce Stanley, PhD. All materials, other instruments, and equipment not listed, including cell culture media and supplies, will be provided by the Department of Physical and Life Science of Wilson College. References       American Cancer Society. Cancer Facts Figures 2016. Atlanta: American Cancer Society; 2016. Bilsland AE, Stevenson K, Liu Y, Hoare S, Cairney CJ, Roffey J, et al. (2014) Mathematical Model of a Telomerase Transcriptional Regulatory Network Developed by Cell-Based Screening: Analysis of Inhibitor Effects and Telomerase Expression Mechanisms. PLoS Comput Biol 10(2): e1003448. doi:10.1371/journal.pcbi.1003448 BIOL2060 Cell Cycle [Photograph found in Department of Biology Memorial University of Newfoundland]. (2015). In Hardin Bertoni (Authors). Retrieved March 30, 2016, from http://www.mun.ca/biology/desmid/brian/BIOL2060/BIOL2060-19/CB19.html Chen, Yi-Bin. Liver Cancer Hepatocellular Carcinoma: MedlinePlus Medical Encyclopedia. U.S National Library of Medicine. U.S. National Library of Medicine, 1 Aug. 2015. Web. 10 Apr. 2016. Cooper, D. L., Lovett, S. T. (2011). Toxicity and tolerance mechanisms for azidothymidine, a replication gap-promoting agent, in Escherichia coli. DNA Repair, 10(3), 260-270. http://doi.org/10.1016/j.dnarep.2010.11.007 Das, R., Pitre, K. S. (september 2007). Bioinorganic studies on Fe (II)- zidovudine (azt) complex. Indian Journal of Chemical Technology, 14, 526-528. Retrieved February 20, 2016. Fang, J.-L., Beland, F. A. (2009). Long-Term Exposure to Zidovudine Delays Cell Cycle Progression, Induces Apoptosis, and Decreases Telomerase Activity in Human Hepatocytes. Toxicological Sciences, 111(1), 120-130. http://doi.org/10.1093/toxsci/kfp136 Fang, J., Han, T., Wu, Q., Beland, F., Chang, C., Guo, L., Fuscoe, J. (2014). Differential gene expression in human hepatocyte cell lines exposed to the antiretroviral agent zidovudine. Archives Of Toxicology, 88(3), 609-623. doi:10.1007/s00204-013-1169-3 Gomez, D. E., Armando, R. G., Alonso, D. F. (2012). AZT as a telomerase inhibitor. Frontiers in Oncology, 2, 113th ser. Retrieved March 11, 2016, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3434370/ Hadizadeh, S., Najafzadeh, N., Mazani, M., Amani, M., Mansouri-Torshizi, H., Niapour, A. (2014). Cytotoxic Effects of Newly Synthesized Palladium(II) Complexes of Diethyldithiocarbamate on Gastrointestinal Cancer Cell Lines. Biochemistry Research International, 1-9.doi:10.1155/2014/813457 Hardin, J., Bertoni, G., Kleinsmith, L. J., Becker, W. M. (2014). Beckers world of the cell (8th ed.). Boston: Benjamin Cummings. Harrington, J. A., Reardon, J. E., Spector, T. (1993). 3-azido-3-deoxythymidine (AZT) monophosphate: an inhibitor of exonucleolytic repair of AZT-terminated DNA. Antimicrobial Agents and Chemotherapy, 37(4), 918-920. van Kampen Jeroen J.A., Fraaij Pieter L.A., Vishal Hira, van Rossum Annemarie M.C., Hartwig, Nico G., de Groot Ronald, Luider Theo M.. A new method for analysis of AZT- triphosphate and nucleotide-triphosphates. Biochemical and Biophysical Research Communications, Volume 316, Issue 3, 9 April 2004, 151-159] Matteucci, C., Minutolo, A., Marino-Merlo, F., Grelli, S., Frezza, C., Mastino, A., Macchi, B. (2015). Characterization of the enhanced apoptotic response to azidothymidine by pharmacological inhibition of NF-kB. Life Sciences, 127, 90-97. doi:10.1016/j.lfs.2015.01.038 Mittal, S., El-Serag, H. B. (2013). Epidemiology of HCC: Consider the Population. Journal ofClinical Gastroenterology, 47(0), S2-S6.http://doi.org/10.1097/MCG.0b013e3182872f29 National Cancer Institute. (n.d.). Surveillance, Epidemiology, and End Results Program. Retrieved February 16, 2016, from http://seer.cancer.gov/statfacts/html/all.html Neto, V. (2013, January). AZT action [Photograph found in Organic Chemistry]. Retrieved April 1, 2016, from http://wwwblogvine.blogspot.com/2013/01/azt-was-originally-intendedto- treat.html (Originally photographed 2013, January 20) Normal And Cancer Cells Structure [Photograph found in Cells or Tissue Abnormal Cells or Tissue Cells or Tissue Normal Cells or Tissue Historical Graphics, National Cancer Institute]. (2001, January 1). In P. Kenny (Illustrator). Retrieved April 1, 2016, from https://visualsonline.cancer.gov/details.cfm?imageid=2512 (Originally illustrated 1990, April) Pichard, L., Raulet, E., Fabre, G., Ferrini, J. B., Ourlin, J. C., Maurel, P. (2006, February). Human hepatocyte culture. Retrieved March 11, 2016, from https://www.researchgate.net/publication/7063976_Human_hepatocyte_culture Sabokrouh, A., Vaisi-Raygani, A., Goodarzi, M. T., Khatami, S., Taghizadeh-jahed, M., Shahabadi, N., à ¢Ã¢â€š ¬Ã‚ ¦ Shakiba, Y. (2015). Comparison between Platinum-Azidothymidine and Azidothymidine Effects on Bcl-2 and Telomerase Gene Expression in Rats with Hepatocellular Carcinoma. Avicenna Journal of Medical Biotechnology, 7(2), 50-56. Sabokrouh, A., Goodarzi, M. T., Vaisi-Raygani, A., Khatami, S., Taghizadeh-Jahed, M. (2014). Effects of Treatment with Platinum Azidothymidine and Azidothymidine on Telomerase Activity and Bcl-2 Concentration in Hepatocellular Carcinoma-Induced Rats. Avicenna Journal Of Medical Biotechnology, 6(4), 200-209. Telomere Shortening Determines the Proliferative Lifespan of Human Diploid Fibroblasts. 2001. Nature Reviews. By Nicole F. Mathon and Alison C. Lloyd. Web. 21 Mar. 2016. ThermoFisher Scientific. (n.d.). MRNA Extraction. Retrieved March 11, 2016, from https://www.thermofisher.com/us/en/home/life-science/dna-rna-purification-analysis/rna- extraction/rna-types/mrna-extraction.html Venook, A. P., Papandreou, C., Furuse, J., De Guevara, L. L. (2010). The Incidence and Epidemiology of Hepatocellular Carcinoma: A Global and Regional Persprective. The Oncologist, 4(15), 5-13. Retrieved March 11, 2016, from http://theoncologist.alphamedpress.org/content/15/suppl_4/5.long Weinberg, Robert A. The Biology of Cancer. 2nd ed. New York, NY: Garland Science, 2014. Print.

Is the Body Ownable :: Philosophy Papers

Is the Body Ownable The way Jennifer Church approaches the issue of body ownership in â€Å"Ownership and the Body†, it sounds as though that we own our bodies is a given fact, and the controversy is over what follows from this and why it is important to have a discussion of this fact. I, however, intend to argue that it is a bad move to allow for the idea of self-ownership (or any sort of ownership of subjects), that it is more likely to perpetuate problems than to solve them to think in this way, and that the belief in the possibility of body/self-ownership is rooted primarily in linguistic ambiguities (â€Å"property† vs. â€Å"properties†, different senses of â€Å"mine†, etc.). Mine We will begin with the seemingly innocuous assertion, â€Å"my body is mine†. 1[1]This is a truism only if â€Å"mine† is not construed as â€Å"being that which I own†. I do not own my mother, my boss, or my sneeze. In some cases, â€Å"mine† only means that something pertains to me, not that it necessarily belongs to me in the sense in which a product of my labour might. Surely a slave who says, â€Å"my master,† is not trying to reverse the relationship (a relationship which is, by my account, illegitimate to begin with). Now, Church does want to allow, in a sense, for me to be able to own my mother. She certainly would allow my mother, initially, to own me.2[2] One can make a claim, by her account, to some degree of ownership of another person based on the extent to which that person has become part of one’s self.3[3] Her example for this is the right that one’s close friends and relatives have to make decisions for one who is incapacitated. I do not see how the concern of close ones can be taken as a form of ownership. While we hope that it is our closest friends and family who will look out for us when we are unable to look out for ourselves, in no way are they granted the rights that one would have over property.4[4] I take ownership to include unrestricted private use of an object. Of course my definition excludes the possibility of owning a Is the Body Ownable :: Philosophy Papers Is the Body Ownable The way Jennifer Church approaches the issue of body ownership in â€Å"Ownership and the Body†, it sounds as though that we own our bodies is a given fact, and the controversy is over what follows from this and why it is important to have a discussion of this fact. I, however, intend to argue that it is a bad move to allow for the idea of self-ownership (or any sort of ownership of subjects), that it is more likely to perpetuate problems than to solve them to think in this way, and that the belief in the possibility of body/self-ownership is rooted primarily in linguistic ambiguities (â€Å"property† vs. â€Å"properties†, different senses of â€Å"mine†, etc.). Mine We will begin with the seemingly innocuous assertion, â€Å"my body is mine†. 1[1]This is a truism only if â€Å"mine† is not construed as â€Å"being that which I own†. I do not own my mother, my boss, or my sneeze. In some cases, â€Å"mine† only means that something pertains to me, not that it necessarily belongs to me in the sense in which a product of my labour might. Surely a slave who says, â€Å"my master,† is not trying to reverse the relationship (a relationship which is, by my account, illegitimate to begin with). Now, Church does want to allow, in a sense, for me to be able to own my mother. She certainly would allow my mother, initially, to own me.2[2] One can make a claim, by her account, to some degree of ownership of another person based on the extent to which that person has become part of one’s self.3[3] Her example for this is the right that one’s close friends and relatives have to make decisions for one who is incapacitated. I do not see how the concern of close ones can be taken as a form of ownership. While we hope that it is our closest friends and family who will look out for us when we are unable to look out for ourselves, in no way are they granted the rights that one would have over property.4[4] I take ownership to include unrestricted private use of an object. Of course my definition excludes the possibility of owning a

Analysis of Genre, Stardom, Authorship and Gender Theory Essay

â€Å"Apparently no strictly logical distinctions can capture the variety of factors which create the genres we have† (Nicholas and Price, 1998) This quote demonstrates the complexity of allocating a particular genre to a film, as various aspects need to be considered. Although concrete groupings such as horror, science-fiction, crime and drama exist, the majority of movies contain more than one aspect which renders them difficult to categorise. For example, the difference between an ‘action’ and a ‘thriller’ film can be very fine. Should the length of footage of fight scenes determine them? Should the scale and intensity of adrenaline felt by the audience throughout the story line be considered? Apart from the concrete distinctions between fiction and non-fiction, many subcategories are used. Some genres are based on literature, such as ‘melodrama’ and ‘comedy’; others on the plot, for example the ‘war film’; and still others on media such as ‘the musical’. Furthermore, some genres are categorised by their budgets, censorship rating, racial identities, location, status amongst many others (Stam, 2000). Genres are a way of characterising a film in the simplest way, interpreting and judging without evaluating them. This allows viewers an easier choice when choosing which film to watch since the field has been narrowed down for them. Patterns such as in the plot, theme, and cinematographic technique and which branded star is used in the film are some of the ways the genres are often grouped. These are very commonly broadened because of the other forms of genre groups sometimes jumping in and out of a film are known as sub-genres. In the second edition (Nathan Abrams, 2010) of ‘Studying Film’ it is pointed out that not only are repetitions a requirement in identifying particular film genres, but so are their differences. Viewers take into account not only similarities but also variances between previous films they have seen. Thus when comparing a few films of the same genre, it is important to note that in spite of the recurring themes, each film will have its own individual plot. The use of genres and ‘putting films in boxes’, as it were, can lead to problems for the movie industry as story lines become repetitive, predictive and formulaic, perhaps causing some viewers to no longer hold the genre in such high regard. For this reason it is imperative that difference be a vital ingredient within categories as well as between them to provide more variation, innovation and flexibility within their general parameters. Films are automatically divided up using the genre categorisation, for example when you walk into a DVD store and looking for a film, they’ll be physically divided up through their classifications; Horror, Sci-fi, Crime, Drama, Action, Thriller, Social Realism and more. They might also classify the films by their rating, which in a sense is also a measurement of genre. Whether the film is a U classification for children, a rated 15 film or even a rated 18 film, these sub genres always crop up in promotional campaigns are also known for being genre specific; trailers in the cinema are also grouped together, like when watching a comedy, the trailers being shown in the previews will also be comedy. There are just a few examples as to how genre is divided without making overly noticeable to the audience. Martin Loop (cited in Barry, 2007) argues that genre in Hollywood does not really exist since so many films that are apparently made by an ‘auteur’ were simply influenced by society, and that Directors use different elements from different genres and the trends at the time to make their films. Taxi Driver narrates the story of Travis Bickle, an ex-marine unable to sleep at nights, so he decides to get a job as a night-time taxi driver. Played by Robert de Niro, Travis begins to date a woman working in the presidential campaign office of Charles Pallantine, but after taking her to watch a porn film they split up. Travis becomes increasingly paranoid and results in him buying an arsenal of weapons. After meeting a young prostitute ‘Iris’ played by Jodie Foster, he soon decides to make it his mission to save her from the life she leads. Thwarted in his attempt to assassinate Charles Pallantine, Taxi Driver’s climax occurs when Travis shoots and kills Iris’s pimp Matthew, played by Harvey Keitel and his henchmen. After the massacre Travis finds himself wounded and attempts to shot himself but comes short of bullets. The film ends with Travis being portrayed as a hero in the media for saving Iris’s life and taking her back to her parents. Travis’s search for to find meaning in his life is what motivates and drives the narrative forward. Taxi Driver is almost based exclusively on restricted narrative through the subjective consciousness of the narration of Travis filtering the narrative information through a single character. The camera emphasizes this by keeping a closed door to what is happening around him to a certain extent and seems to follow him almost obsessively as the film progresses. Has its genre made it more of a success? Maybe Taxi Driver being in the ‘Drama/thriller’ genre has enabled it to cross over two genres thus attracting a greater audience. Films are different from books or poems in that they are not simply constructed by a single person but require input from various people including a director, a producer, a screenwriter, actors and studio representatives to name a few. The notion of auteur theory, (translated from the French meaning ‘author’) in the filmmaking industry has therefore been heavily contended (Simpson, 2012). Andrew Sarris, the leading American proponent of the theory claimed in the 1950s and 60s that great filmmaking inspires the type of artistic expression and creativeness one would expect from a major literary author. For this reason we should be able to herald directors as ‘auteurs’, crediting them with ownership of the whole works. Critics maintain, however, that this notion completely ignores the rest of the film crew. A single ‘author’ does not appear to ascribe to movies due to the multiple actors involved. If each role plays an integral part in the process from beginning to end, how can one role claim the title of sole ‘author’? Furthermore, on what basis could ‘authorship’ be claimed? The tendency has been towards extending the title to the director; however perhaps not every director can be considered an ‘author’ if their work is not worthy. Sarris’ arguments have since been used to defend film as equivalent to the other arts; an important development considering earlier perceptions of the industry to be ‘less worthy’ of an artistic status. In this way perhaps in order to qualify as an ‘art’, a film needs an author. This label is particularly important for intellectual property rights and for status and identification. Nevertheless, the notion of ‘authorship’ also causes problems in other art forms; a composer is considered the true owner of the music he writes, but what about the music when it is used in performance at a concert or in a theatre piece? Having briefly outlined genre and authorship and their surrounding issues, this paper will seek to compare the theories to the film of Taxi Driver (1976)by Martin Scorcese to see how well they hold up and whether Martin Scorcese can shed further light on how genre and authorship should be  defined in the movie-making business. http://www. cs. grinnell. edu/~simpsone/Connections/Film/Author/index. html http://www. filmreference. com/encyclopedia/Academy-Awards-Crime-Films/Auteur-Theory-and-Authorship. html Studying film 2nd Edition, Nathan Abrams, Ian Bell, Jan Udris, Bloomsbury, 2010 Film History and Introduction, Kirsten Thomson, David Bordwell, McGraw-Hill, 1994

“King Charles is totally to blame for the civil war.” Do I Agree? Essay

The English Civil War took place in 1642 when Charles I raised his royal standard in Nottingham. The split between Charles and Parliament was such that neither side was willing to back down over the principles that they held and war was inevitable as a way in which all problems could be solved. The country split into those who supported the king and those who supported Parliament. Some historians say that Charles is totally to blame for this war, while some say that parliament is totally to blame for it. I am going to tell you about it. There were many reasons for why the king was to blame one of the reasons for why the king was to blame was because of his money problems. Charles was not good with money and always had very little. He had closed down parliament and had to think of ways of getting money without asking the parliament’s help. He had used old laws like ‘Ship Money’, which was a special tax to help the navy he used this idea to get money off the people of England. This made him very unpopular. Another reason for why the king was to blame was the way he had handled with religion. As he was the king, he had thought that he had the power to make the Scots use English prayer books. The scots were so furious that they decided to fight Charles I instead. This also made him unpopular to the scots as well as the people of England. When the scots had defeated him Charles had to pay lots of tax money which he couldn’t afford. So, Charles had to recall parliament, as only tax voted by parliament got rid of the scots. Charles believed in divine rights that God had chosen him to be king so he and Archbishop Laud started to decorate the church which he said that if the church is decorated, you will be closer to God. He also married a catholic princess from France which was very unpopular. Oliver Cromwell and Parliament still wanted more power and no return to the Catholic religion. To make things worse for Charles the Catholics in Ireland killed 100,000 Protestants. Also another reason why parliament is to blame is because the king and parliament always used to argue about who controls the army and parliament made the king angry by taking over them without his permission.