I’m working on a management report and need support to help me learn.I have a management assignment. I copied the instructions below.Choose a company to research and analyze its Corporate Social Responsibility efforts and ethics. Use class lectures, textbook readings, and Online Assignments to discuss the two concepts by providing examples from the company. Make sure to clearly distinguish between the two concepts of Ethics and Corporate Social Responsibility. Organizations can be chosen from media sources such as newspapers, magazines, videos, and blogs. You also can choose an organization where you work or have worked in the past. Make sure you choose an organization where you have enough information to draw conclusions.Cite all references used in your research. It does not matter which citation format you use as long as you remain consistent. Your paper should be a maximum of THREE (3 pages ), double-spaced in a Microsoft Word document. The page count suggested is the maximum, but answers can be shorter if they are well written, concise, and include a depth of content.NO PLAGIARISM. REALLY STRICT
PU Corporate Social Responsibility & Ethics Organizational Management Discussion
As with the Case Assignment, make sure you have thoroughly reviewed the background readings and understand the key concepts of job redesign and job crafting. Then think about your own job and workplace and how these concepts apply to your own work life. Once you have finished reviewing the background readings and have carefully thought about how these concepts relate to your own job, write a 2- to 3-page paper answering the following questions:
Of the three main types of job redesign (job enlargement, job rotation, job enrichment), which one do you think would be the most effective in your current workplace? Explain your reasoning, and cite Bauer and Erdogan (2012) or Griffin (2007) as part of your answer.
Suppose your supervisor decides to use job enrichment to redesign your job. Of the five core job characteristics discussed in Bauer and Erdogan (2012) or page 9 of Griffin (2007), which one do you think should be changed as part of your job redesign?
Which specific job crafting strategy or intervention do you think would be most effective at your organization or for your specific job? Refer to one of the specific strategies or interventions discussed in Wrzesniewski (2014) or Dik and Duffy (2012).
SLP Assignment Expectations
Answer the assignment questions directly in 2 to 3 written pages.
Stay focused on the precise assignment questions; don’t go off on tangents or devote a lot of space to summarizing general background materials.
Make sure to use reliable and credible sources as your references. Articles published in established newspapers or business journals/magazines are preferred. If you use articles from the Internet, make sure they are from credible sources.
Reference your sources of information with both a bibliography and in-text citations.
Bauer, T., & Erdogan, B. (2012) Chapter 6.1: Motivating employees through job design. Introduction to Organizational Behavior. Flatworld Knowledge. http://2012books.lardbucket.org/books/an-introduction-to-organizational-behavior-v1.0/s10-01-motivating-employees-through-j.html
Griffin, R. (2007). Chapter 6: Organization structure and design. Principles of Management. Houghton Mifflin, New York. http://college.cengage.com/business/griffin/sas_principles/1e/assets/students/know_bank/griffin_sas_KB_6.1.pdf
Now that you have read up on traditional approaches to job design, read up on job crafting. This reading is by Amy Wrzesniewski, who you saw in one of the videos above:
Wrzesniewski, A. (2014). Chapter 6: Engage in job crafting. In Dutton, J. E., & Spreitzer, G. M. (eds). How to Be a Positive Leader: Small Actions, Big Impact. San Francisco, CA, USA: Berrett-Koehler Publishers. [EBSCO eBook Collection]
Complete 2 page Essay for SLP (TRIDENT)
Managing employment relations
Write a report, of 3000 words, which draws on examples of organisationalpractice and academic literature to evaluate the extent to whichthe management of employment relations is becoming increasinglyfragmented and blurred owing to structural labour market changes andinter-firm network relationships. Explain the implications that your reviewhas for the management of employment relations at an organisational level.The word count is 3000 words +/-10%
Effects of an oil price shock on importing and exporting countries
essay writing service free From the middle of twentieth century, due to exceptional importance of the crude oil in the supply of the world’s energy demands, it has become one of the major indicators of economic activities of the world. Even after the appearance of alternate forms of energy like solar power, water and wind, the importance of crude oil as the main source of energy still cannot be denied. This sharp increase in the world oil prices and the volatile exchange rates are generally regarded as the factors of discouraging economic growth. Particularly, the very recent highs, recorded in the world oil market bring apprehension about possible slump in the economic growth in both developed and developing countries. A large number of researchers proposed that exchange rate volatility and oil price fluctuations have considerable consequences on real economic activities. The impact of oil price fluctuation is expected to be different between in oil exporting and in oil importing countries. An oil price increase should be considered as bad news for oil importing countries and good news for oil exporting countries, while the reverse should be expected when the oil price decreases. Through demand and supply transmission mechanism, oil prices impacts the real economic activity. The supply side effects are associated with the fact that crude oil is a basic input to production, and an increase in oil price leads to a rise in production costs ultimately that result in firms’ lower output. Oil prices changes also entail demand-side effects on investment and consumption. Consumption is also affected indirectly through its positive relation with disposable income. Moreover, oil prices have an adverse impact on investment by increasing firms’ costs. On the other hand it is generally recognized that the depreciation of exchange rate would reduce imports and expand exports, while the appreciation of exchange rate would encourage imports and discourage exports. Especially a depreciation of the exchange rate leads to income transfer to exporting countries from importing countries through a shift in the terms of trade. Since 2003, oil prices increased continuously, even touched the peak of $137 per barrel in July 2008, but after that a declining trend was observed. After 1970s, many negative oil shocks hit the world economies. The first one was during 1973-74 caused by OPEC oil prohibition, and secondly in 1978-79 when the OPEC put restraints on its oil production. This rising trend in oil prices continued until mid 1980s, subsequently, Iraq-Iran war in early 1980s further shoot up the prices. However in 1986, when Saudi Arabia increased its crude oil production, oil price tend to decreased. In 1990s, Iraq-Kuwait war was a major factor of oil price increase but it was ended in a year because of Asian financial crisis. In 1999-2000 the OPEC again narrow its production leading to another price shock. The latest and last oil price shock was started in the year 2003 which continued till July 2008. In other words, oil prices have always remained quite volatile. According to report of IEA (2004) , these price shocks have raised serious concerns among the policy makers all over the world. The adverse economic impact of higher oil prices on oil-importing developing countries is generally considered as more worse than for the developed countries because of their more reliance on imported oil and are more energy-intensive. Malik. A (2007) also mentioned in her research that, the recent surge in the oil prices especially after 2000 has worried many economists about its possible adverse impacts. This increasing trend in the oil prices has hurt many of the economies worldwide including that of Pakistan, in terms of creating inflationary pressures, increasing budget deficit and balance of payment problems. According to ADB (2005) report, supply, demand, and speculative factors, and their interrelationships, all leads towards the steady rise in oil prices. From the last many years, all over the world, the demand for oil grew due to economic strength and growth in the US, as well as strong economic performance in developing Asian countries specially China and India. From 1990’s to 2003 global demand for oil grew at the rate of 1.3 % whereas for the People Republic of China and India the combined rates is at 7 % and accounted for almost 40 percent of the demand growth. There are various empirical literatures, investigating the relationship between oil price variations and economic growth. The existence of a negative relationship between macro-economic activities and oil prices has become widely accepted especially after Hamilton’s 1983 work. He pointed out that increase in oil prices, reduced US output growth from 1948 to 1980. Hamilton’s findings have been confirmed and extended by many authors and researcher. Hooker (1996) confirmed and extended Hamilton’s work for the period 1948 to 1972 and demonstrated that the oil price level and its changes do reflect the influence on GDP growth. This is shown in the third and fourth quarters after the shock that rise of 10% in oil prices lead to a GDP growth decrease of approximately 0.6 %. Accordingly, Lee et al. (1995) Mork (1989), and Hamilton (1996) presented the non-linear transformations of oil prices to re-establish the negative association between oil prices increases and economic decline, as well as these researchers also analyzed Granger causality between both variables. The result of Granger causality test proved that oil prices Granger cause U.S. economy before 1973 but no longer Granger cause was found from 1973 to 1994. Recently, Hamilton (2003) and Jimenez and Rodríguez (2004) also confirms the non-linear relationship between the economic growth of U.S. economy and increases of oil prices The quantitative exercise conducted by the IEA in alliance with the OECD (Organization for Economic Co-operation and development) department of Economics and with the assistance of IMF Research department in 2004, indicated that a continued $10 per barrel increase in oil price would result in the decrease of about 0.4 % OECD as a whole, in the first and second years of higher prices. Inflation would increase by half a percentage and unemployment would also increase in this case. The OECD imported the oil at a cost of over $260 billion in 2003 which is 20% more than its 2001 oil need. European countries, which are highly dependent on oil imports, would suffer most in the short term, their GDP dropping by 0.5% and inflation rising by 0.5% in 2004. The U.S would suffer the least, with GDP falling by 0.3%, because its indigenous production meets a bigger share of its oil needs. Japan’s GDP would fall 0.4%, This analysis assumes constant exchange rates and economic growth for the US economy. The present paper is the extension of the existing empirical literature in two directions. First, we have not focused on the oil importing US economy only , rather we analyzed the effects of an oil price shock in two different type of countries which include five oil exporting countries i.e. Saudi Arabia, Norway, Venezuela, Kuwait , Nigeria and five oil importing country i.e. Pakistan, India , China, Japan , Germany. Secondly, we will not only demonstrate the relationship between oil prices and real economic growth but we will also analyze the role of the real exchange rate for real economic growth. Oil Importing Countries China China’s real GDP has increased continuously at surprising rate of 10% per year in recent years. Simultaneously with strong economic growth, its demand for energy is also surging rapidly. The figure 1 clearly shows about the oil consumption and production behavior of the country which tends the country to import from different countries. China produces 3798 thousand barrels per day and consumes 8200 thousand barrels per day of oil in 2009. This means that China has to import roughly 4402 thousand barrels per day to meet its consumption needs per day. In the year 2007, China was declared as the world’s third largest net importer of oil behind the U.S and Japan. In July 2005, the reform of the exchange rate system was introduced by the central bank of China. After the reforms, the exchange rate of yuan was set according to a basket of other currencies. At the end of 2007, the yuan was appreciated by 7.5% approx. against the dollar, in consequence of these reforms. India According to the Oil
Through the Eyes of the Patient and the Health Care Professional
Please read the case studies that I attached and fill out the document named “HLT-324V-RS-CarePlanTemplate”. Please submit that same exact template with the answers. Here is the instructions for my assignment: Assessment Descriiption Allied health professionals are confronted with different death and dying practices. An effective allied health professional recognizes the importance of understanding different cultural practices, and learns how to evaluate the death, dying, and spiritual beliefs and practices across the cultures. Read the two specified case histories and choose one for this assignment. Chapter 4, “Stories of Abby: An Ojibwa Journey” and Chapter 14, “Stories of Shanti: Culture and Karma,” by Gelfland, Raspa, and Sherylyn, from End-of-Life Stories: Crossing Disciplinary Boundaries (2005), from the GCU Library. Identify your role as a health care professional in supporting Abby’s or Shanti’s dying rituals, and in creating strategies for displaying respect while still providing quality care. Identify communication strategies necessary in caring for your select person. Integrate your strategies as you develop a care plan describing how you would approach the situation and care for the patient. Review the “Care Plan” template prior to beginning. Include the following in your care plan: Communication: family and patient Treatment options that align with the specific culture Education: family and patient Family roles in the process Spiritual beliefs Barriers Cultural responses Any additional components that you feel would need to be addressed (from your perspective as a health care professional) Prepare this assignment according to the guidelines found in the APA Style Guide, located in the Student Success Center. An abstract is not required.
Role of PINK1 in α-synuclein Aggregation
Role of PINK1 in α-synuclein Aggregation. The role of PINK1 in α-synuclein aggregation and toxicity in Parkinson’s disease State-of-the-art Misfolding and aggregation of α-synuclein (ASYN) is the major component of Lewy bodies (LBs) , the pathological hallmark of Parkinson’s disease (PD) [2, 3]. Although clinical and experimental studies suggest the involvement of protein misfolding, oxidative stress and mitochondrial dysfunction [4, 5], the fundamental cause of the disease, its underlying mechanism remains elusive. The normal function of ASYN is still unclear, but it is thought to be involved in the vesicular trafficking, regulation of dopamine neurotransmission and in synaptic function and plasticity [6, 7]. PTEN-induced kinase 1 (PINK1) was identified as an interactor of ASYN. In worms, mitochondrial fragmentation induced by expression of ASYN is rescued by co-expression of PINK1 . Also, in flies, overexpression of PINK1 rescues motor and developmental defects induced by ASYN . More than 70 mutations in the PINK1 gene were identified in familial PD in an autosomal recessive manner [10, 11]. Previous studies suggests that PINK1 plays a critical role in PD pathogenesis and dysregulation of PINK1 may contribute to the development of PD [12, 13]. However, whether PINK1 also plays a role in the ASYN pathology has not been addressed so far, and will be one of the central goals of this proposal. In this context, we pretend investigate that whether ASYN pathology differs in the absence of PINK1 in cell culture and in vivo. Thus, we hypothesize that the possible interaction between PINK1 and ASYN may be favorable to the cells through the decrease of ASYN aggregation and cell death. Project aims The central aims of this project are to study the modulatory effect of PINK1 on ASYN aggregation and toxicity, in vitro and in vivo, which would be important for therapeutic intervention in synucleinopathies, particularly in PD. Experimental design To assess the interaction between PINK1 and ASYN Over the past decade, mutations in several genes, among which ASYN and PINK1, have been identified in inherited PD [14, 15] and whether there is a direct interaction of PINK1 and ASYN awaits further research. In order to study if there is a direct interaction between PINK1 and ASYN in vivo, we will perform a co-immunoprecipitation analysis of ASYN and PINK1 proteins from brain lysate of wild type Sprague-Dowley adult female rats. Following the immunoprecipitation of endogenous ASYN, endogenous PINK1 will be detected using a PINK1 specific antibody. To investigate the effect of PINK1 in ASYN aggregation Although the process of ASYN aggregation has been extensively studied in vitro, it is still unclear which cellular pathways are involved. To investigate the effect of PINK1 on ASYN aggregation, recombinant ASYN will be incubated in the presence of total protein lysates from cells overexpressing either EGFP-PINK1 or EGFP, as a control. ASYN fibrillization will be followed by monitoring ThT fluorescence at 482 nm. ThT is an amyloid-specific dye whose fluorescence dramatically increases upon binding to cross-β sheet structures such as those formed during ASYN self-assembly. To assess the interaction between PINK1 and ASYN and the effect in mitochondrial morphology and membrane potential Mitochondrial dysfunction has long been implicated in PD pathogenesis due to reduced activity in complex I [16, 17]. PINK1 contains a putative N-terminal mitochondrial targeting sequence, and evidence exists that PINK1 is targeted to mitochondria . However, the influence of ASYN in mitochondrial targeting of PINK1 is not entirely settled. To assess putative mitochondrial defects caused by a loss of PINK1 function, we will verify mitochondrial morphology by fluorescence microscopy in SH-SY5Y cells expressing wild-type (WT) ASYN under control of the Tet-off regulatory expression system before and after siRNA mediated downregulation of PINK1. To determine whether possible mitochondrial morphology alterations are associated with functional impairments, we will measure the mitochondrial membrane potential by TMRM fluorescence activated cell sorting (FACS). To determine the effects of PINK1 in ASYN aggregation and toxicity in vivo. The increase of ASYN aggregation was reported in synucleinophaties cell culture models in which PINK1 was silenced via RNA interference . However, a detailed research of the interaction between PINK1 and ASYN toxicity in vivo is still missing. Several different genetic mouse models have been generated based on the expression of ASYN driven by a diversity of promoters. To assess the influence of PINK1 in ASYN aggregation we will use the animal model which express full-length human WT ASYN under the Thy-1 promoter [20, 21]. Firstly, we will determine whether overexpression of PINK1 influences ASYN aggregation in the brain of transgenic mice. For this propose, we will inject adeno-associated viruses (AAV) encoding PINK1 in SN of transgenic or WT littermate control mice. Next, we will execute behavioral analysis and then we will sacrifice the animals to determine whether PINK1 increases ASYN aggregation and controls neuronal loss. Thus, we will perform immunohistochemistry and Thioflavin S staining, to assess whether inclusions display amyloid-like properties. Interestingly, although fly models lacking PINK1 expression display a drastic phenotype, ranging from mitochondrial dysfunction to significant dopaminergic neurodegeneration and motor deficits  the PINK1 knockout and knockdown mouse models developed so far display mild neurodegenerative changes . To investigate whether ASYN pathology differs in the absence of PINK1 in vivo, we will generate PINK1 knockdown mice by local delivery of a rAAV2/7-mediated, microRNA-based, short-hairpin RNA against PINK1 [24, 25]. We will analyze the vulnerability of the nigral dopaminergic neurons to a-synuclein toxicity when the PINK1 levels are reduced or absent. For this approach, we will deliver a rAAV2/7-a-synuclein WT vector to the SN of both PINK1 knockdown and PINK1 knockout mice. References 1. Spillantini MG, Schmidt ML, Lee VM, Trojanowski JQ, Jakes R, et al. (1997) Alpha-synuclein in Lewy bodies. Nature 388: 839-840. 2. de Lau LM, Breteler MM (2006) Epidemiology of Parkinson’s disease. Lancet Neurol 5: 525-535. 3. Goedert M (2001) Alpha-synuclein and neurodegenerative diseases. Nat Rev Neurosci 2: 492-501. 4. Fasano M, Lopiano L (2008) Alpha-synuclein and Parkinson’s disease: a proteomic view. Expert Rev Proteomics 5: 239-248. 5. Outeiro TF, Lindquist S (2003) Yeast cells provide insight into alpha-synuclein biology and pathobiology. Science 302: 1772-1775. 6. Schneider BL, Seehus CR, Capowski EE, Aebischer P, Zhang SC, et al. (2007) Over-expression of alpha-synuclein in human neural progenitors leads to specific changes in fate and differentiation. Hum Mol Genet 16: 651-666. 7. Crews L, Mizuno H, Desplats P, Rockenstein E, Adame A, et al. (2008) Alpha-synuclein alters Notch-1 expression and neurogenesis in mouse embryonic stem cells and in the hippocampus of transgenic mice. J Neurosci 28: 4250-4260. 8. Kamp F, Exner N, Lutz AK, Wender N, Hegermann J, et al. (2010) Inhibition of mitochondrial fusion by alpha-synuclein is rescued by PINK1, Parkin and DJ-1. Embo j 29: 3571-3589. 9. Todd AM, Staveley BE (2012) Expression of Pink1 with alpha-synuclein in the dopaminergic neurons of Drosophila leads to increases in both lifespan and healthspan. Genet Mol Res 11: 1497-1502. 10. Valente EM, Abou-Sleiman PM, Caputo V, Muqit MM, Harvey K, et al. (2004) Hereditary early-onset Parkinson’s disease caused by mutations in PINK1. Science 304: 1158-1160. 11. Valente EM, Bentivoglio AR, Dixon PH, Ferraris A, Ialongo T, et al. (2001) Localization of a novel locus for autosomal recessive early-onset parkinsonism, PARK6, on human chromosome 1p35-p36. Am J Hum Genet 68: 895-900. 12. Exner N, Treske B, Paquet D, Holmstrom K, Schiesling C, et al. (2007) Loss-of-function of human PINK1 results in mitochondrial pathology and can be rescued by parkin. J Neurosci 27: 12413-12418. 13. Oliveras-Salva M, Macchi F, Coessens V, Deleersnijder A, Gerard M, et al. (2014) Alpha-synuclein-induced neurodegeneration is exacerbated in PINK1 knockout mice. Neurobiol Aging 35: 2625-2636. 14. Farrer MJ (2006) Genetics of Parkinson disease: paradigm shifts and future prospects. Nat Rev Genet 7: 306-318. 15. Gasser T (2009) Mendelian forms of Parkinson’s disease. Biochim Biophys Acta 1792: 587-596. 16. Lin MT, Beal MF (2006) Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature 443: 787-795. 17. Olanow CW, Tatton WG (1999) Etiology and pathogenesis of Parkinson’s disease. Annu Rev Neurosci 22: 123-144. 18. Gandhi S, Muqit MM, Stanyer L, Healy DG, Abou-Sleiman PM, et al. (2006) PINK1 protein in normal human brain and Parkinson’s disease. Brain 129: 1720-1731. 19. Liu W, Vives-Bauza C, Acin-Perez R, Yamamoto A, Tan Y, et al. (2009) PINK1 defect causes mitochondrial dysfunction, proteasomal deficit and alpha-synuclein aggregation in cell culture models of Parkinson’s disease. PLoS One 4: e4597. 20. Rockenstein E, Mallory M, Hashimoto M, Song D, Shults CW, et al. (2002) Differential neuropathological alterations in transgenic mice expressing alpha-synuclein from the platelet-derived growth factor and Thy-1 promoters. J Neurosci Res 68: 568-578. 21. Chesselet MF, Richter F, Zhu C, Magen I, Watson MB, et al. (2012) A progressive mouse model of Parkinson’s disease: the Thy1-aSyn (“Line 61”) mice. Neurotherapeutics 9: 297-314. 22. Clark IE, Dodson MW, Jiang C, Cao JH, Huh JR, et al. (2006) Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin. Nature 441: 1162-1166. 23. Oliveras-Salva M, Van Rompuy AS, Heeman B, Van den Haute C, Baekelandt V (2011) Loss-of-function rodent models for parkin and PINK1. J Parkinsons Dis 1: 229-251. 24. Heeman B, Van den Haute C, Aelvoet SA, Valsecchi F, Rodenburg RJ, et al. (2011) Depletion of PINK1 affects mitochondrial metabolism, calcium homeostasis and energy maintenance. J Cell Sci 124: 1115-1125. 25. Osorio L, Gijsbers R, Oliveras-Salva M, Michiels A, Debyser Z, et al. (2014) Viral vectors expressing a single microRNA-based short-hairpin RNA result in potent gene silencing in vitro and in vivo. J Biotechnol 169: 71-81. Role of PINK1 in α-synuclein Aggregation
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