I have a project proposal about Fantasy Football (attached). I need someone to help me put it into the software Microsoft Project (create a Microsoft project document), and write up the written response (Microsoft word). My proposal is attached. Here are the requirements:Project Schedule Due by 15 AUG 2016 (Monday) at NoonThis assignment consists of two (2) parts: a project schedule, and a written response. You must submit both parts as separate files for the completion of this assignment. Label each file name according to the part of the assignment it is written for.Part A: Project Schedule (Submit as one  Microsoft Project file)In Assignment 2, you developed a project plan. Now, using the information from your project proposal, create a multi-level work breakdown structure (WBS) and detailed project schedule. Your project must include the following criteria: The project must consist of at least twenty-five (25) tasks. Each task must contain a start date, a finish date, and have main staffing and non-staffing resources assigned. Assume that your work activities are completed during normal weekdays (no weekend work) under normal conditions (8 hours per day). In terms of holidays, you can assume no work will be done the following days: New Year’s Day, President’s Day, Good Friday, Good Monday, Friday before Memorial Day, Memorial Day, the business day before Independence Day, Independence Day, the Friday before Labor Day, Labor Day, the day before Thanksgiving Day, Thanksgiving Day, Black Friday (day after Thanksgiving), the business day before Christmas, Christmas Day, the business day after Christmas Day, and New Year’s Eve.Part B: Written Response (Submit as a Microsoft Word file)Write a one to two (1-2) page response in which you:Analyze your project in terms of project completion, critical path, and slack / float. Specifically, be sure to answer the following: When will the project be completed? What is the critical path for the project?How much slack / float is in your project? What activities have the greatest slack / float?Summarize the recommendations or improvements you would make to your project schedule. Specifically, be sure to answer the following: Identify the top three (3) activities that you believe could impact the project completion date.What additional activities would you add to this project to make it more complete, from a project management viewpoint?Format your assignment according to the following formatting requirements: Typed, double spaced, using Times New Roman font (size 12), with one-inch margins on all sides.Include a cover page containing the title of the assignment, the student’s name, the professor’s name, the course title, and the date. The cover page is not included in the required page length.
Microsoft Project Management, assignment help
I’m working on a computer science report and need a sample draft to help me study.
1. need to know those type of diagram, (Management )2. read case study and ans. (Computer science)3. Do excel calculations The essay will be 1400 – 1800 words long. Please see the questions shown in the screenshot. I will send you all info after hired, eg PPTs, student access etc. Please send a draft in 12hrs-1 day time, day 2, and day 3 as well. + Will need to to draft some questions to ask the teacher
BISM 1201 AU Transforming Business with Information Systems Business Process Essay
Assignment Question(s): (Marks 5) Q1. ABC company is issuing eight-year bonds with a coupon rate of 6.5 percent and semiannual coupon payments. If the current market rate for similar bonds is 8 percent, what will be the bond price? If the company wants to raise $1.25 million, how many bonds does the firm have to sell? (1 mark)Ans:Q2. You are interested in purchasing the common stock of Inch, Inc., which is currently priced at $ 40. The company is expected to pay a dividend of $3 next year and to grow at a constant rate of 8 percent. What should the market value of the stock be if the required rate of return is 15.75 percent? (1mark)Is this a good buy? Why or why not? (1mark)AnsQ3. Raneem owns shares in HP Inc. Currently, the market price of the stock is $36.34. Management expects dividends to grow at a constant rate of 6 percent for the foreseeable future. Its last dividend was $3.25. Raneem’s required rate of return for such stocks is 16 percent. She wants to find out whether she should sell his shares or add to her holdings. What is the value of this stock? (1 Mark) Based on your answer above, should Raneem buy additional shares in Honda Inc.? Why or why not? (1 Mark) My requests:i want clear and enoughAvoid plagiarism, the work should be in your own words, copying from students or other resources without proper referencing will result in ZERO marks. Must mention question numbers clearly in their answers.
SEU Bonds Price Coupon Payment Interest Rate & Coupon Payments Worksheet
Writer’s Choice. Paper details Assignment: Agenda Comparison Grid and Fact Sheet or Talking Points Brief It may seem to you that healthcare has been a national topic of debate among political leaders for as long as you can remember. Healthcare has been a policy item and a topic of debate not only in recent times but as far back as the administration of the second U.S. president, John Adams. In 1798, Adams signed legislation requiring that 20 cents per month of a sailor’s paycheck be set aside for covering their medical bills. This represented the first major piece of U.S. healthcare legislation, and the topic of healthcare has been woven into presidential agendas and political debate ever since. As a healthcare professional, you may be called upon to provide expertise, guidance and/or opinions on healthcare matters as they are debated for inclusion into new policy. You may also be involved in planning new organizational policy and responses to changes in legislation. For all of these reasons you should be prepared to speak to national healthcare issues making the news. In this Assignment, you will analyze recent presidential healthcare agendas. You also will prepare a fact sheet to communicate the importance of a healthcare issue and the impact on this issue of recent or proposed policy. To Prepare: • Review the agenda priorities of the current/sitting U.S. president and the two previous presidential administrations. • Select an issue related to healthcare that was addressed by each of the last three U.S. presidential administrations. • Reflect on the focus of their respective agendas, including the allocation of financial resources for addressing the healthcare issue you selected. • Consider how you would communicate the importance of a healthcare issue to a legislator/policymaker or a member of their staff for inclusion on an agenda. The Assignment: (1- to 2-page Comparison Grid, 1-Page Analysis, and 1-page narrative) with a title page, an introduction, purpose statement, and a conclusion. This is an APA paper. Part 1: Agenda Comparison Grid Use the Agenda Comparison Grid Template found in the Learning Resources and complete the Part 1: Agenda Comparison Grid based on the current/sitting U.S. president and the two previous presidential administrations and their agendas related to the public health concern you selected. Be sure to address the following: • Identify and provide a brief description of the population health concern you selected and the factors that contribute to it. • Describe the administrative agenda focus related to the issue you selected. • Identify the allocations of financial and other resources that the current and two previous presidents dedicated to this issue. • Explain how each of the presidential administrations approached the issue. • At least 3 resources must be used Part 2: Agenda Comparison Grid Analysis Using the information you recorded in Part 1: Agenda Comparison Grid on the template, complete the Part 2: Agenda Comparison Grid Analysis portion of the template, by addressing the following: • Which administrative agency would most likely be responsible for helping you address the healthcare issue you selected? • How do you think your selected healthcare issue might get on the agenda for the current and two previous presidents? How does it stay there? • Who would you choose to be the entrepreneur/ champion/sponsor of the healthcare issue you selected for the current and two previous presidents? Part 3: Narrative Using the information recorded on the template in Parts 1 and 2, develop a 1-page narrative that you could use to communicate with a policymaker/legislator or a member of their staff for this healthcare issue. Be sure to address the following: • Summarize why this healthcare issue is important and should be included in the agenda for legislation. • Justify the role of the nurse in agenda setting for healthcare issues. • The response fully integrates at least 2 outside resources and 2-3 course specific resources that fully supports the summary provided. Writer’s Choice
Effect of Alterations in the FBN1 Gene
custom writing service Effect of Alterations in the FBN1 Gene. Specific alterations in FBN1 gene leads to different clinical outcomes as observed in Marfan lipodystrophy and geleophysic dysplasia 2 Fibrillin is an essential structural component found in connective tissue1. Humans have three types of fibrillin that are highly conserved and have similar structures—fibrillin 1, 2, and 31. These three types of fibrillin polymerize into microfibrils and therefore able to function in regulatory and structural roles in the extracellular matrix1. Microfibrils are found widely throughout the body in elastic and nonelastic connective tissues2. Specifically, fibrillin can be found in the connective tissue of the skin, vasculature, cartilage, tendon, muscle, lung, kidney, cornea, and cilary zonule2. Several different proteins associate with microfibrils by directly interacting with fibrillin, such as bone morphogenetic proteins1. Mutations in fibrillin or the associated proteins can lead to genetic disorders. There have been several genetic disorders associated with mutations in fibrillin 1 with a range of diverse phenotypes. Fibrillin 1 is encoded by the FBN1 gene found on chromosome 15 and contains 65 exons2. Fibrillin 1 is observed in organs, provides structural support, and is predominately found in adult microfibrils2. Structurally, fibrillin has five distinct regions—46 EGF-like repeats that are interrupted by 8 cysteine rich motifs, a region of basic residues by the amino-terminal, another cysteine-rich region, the carboxy terminus, and a proline-rich domain2. Fibrillin 1 can form homodimers in the presence of calcium that are supported through disulfide bonds2. Important proteins in fibrillin 1 microfibril assembly are the ADAMTS proteins2,3. A widely studied disorder associated with mutations in FBN1 is Marfans syndrome. Some common symptoms of Marfans syndrome include problems with eyes, heart, and lungs, long bones that are overgrown, and decreased muscle and subcutaneous fat11. Researchers have found more than 3000 mutations in FBN1 that are known to cause Marfan syndrome1. These mutations are vast as they occur in 56 of the 65 exons in FBN12. Molecularly some patients had approximately half the amount of fibrillin synthesized while others maintain normal synthesis but had abnormal secretion of fibrillin11. Additionally, patients that had normal synthesis and secretion may not be able to incorporate fibrillin properly into the ECM11. Mutations associated with other exons are rarer and are phenotypically distinct2. Two disorders associated with FBN1 mutations and vary phenotypically are Marfan lipodystrophy and geleophysic dysplasia 2. In Marfan lipodystrophy, patients share some similar symptoms with Marfan syndrome, but not all6. In general, patients are tall but do not gain weight properly such that their growth rate in height is disproportionate to their weight gain4. Patients also have characteristic facial features including downslanting palpebral fissues and retrognathia, hyperextensibility of abnormally long fingers and toes, myopia, widening of dural sac around spinal cord and a progeroid appearance although these individuals are not prematurely aging4. Only some patients suffer from heart-related conditions-such as dilation of the aortic root2. Although geleophysic dysplasia 2 has mutations in the FBN1 gene, it has vastly different clinical outcomes than Marfan lipodystrophy. Instead of tall stature, patients are short with a full ‘happy’ face and wide spaced eyes2. Compared to Marfan lipodystrophy, patients suffer from more serious heart conditions including problems with their mitral, tricuspid, and aortic valves2. These heart conditions are often fatal in these patients2. The skeletal system of these patients also has decreased joint mobility and short tubular bones2. Considering the vast phenotypic differences between Marfan lipodystrophy and geleophysic dysplasia 2, it is quite intriguing that both diseases stem from mutations within the same gene—FBN1. Marfan lipodystrophy syndrome is quite rare and only a small population of patients have been diagnosed and studied. In general, patients with Marfan lipodystrophy syndrome display heterozygous mutations in exon 64 of the FBN1 gene5. Some patients have deletions that lead to frameshift mutations creating premature stop codons5. These deletions vary in size as one patient was reported to have a 2 base pair deletion while another patient had a 20 base pair deletion5. Other patients have splice site transversions5. Interesting in some patients, this introduced mutation was de novo and was not previously seen in the parents of the respective patients5. It is curious how certain mutations in this specific exon can lead to a distinct disorder from classic Marfan syndrome. Because not all mutations in exon 64 or premature stop codons produce Marfan lipodystrophy, it is especially intriguing to further study how the structure and function of fibrillin 1 is altered in patients with the genetic disorder6. Patients with Marfan lipodystrophy all have an introduced premature stop codon that have been predicted to evade nonsense-mediated decay (NMD)6. With the ability to bypass NMD, it is predicted that this leads to truncated fibrillin 1 proteins6. I am curious if patients have additional fibrillin 1 production or if all transcripts arising from the mutated gene are able to escape NMD considering the premature stop codon arises in the second to last codon6. Some research has shown that the amount of FBN1 mRNA levels correlates with the amount of adipose tissue in mice and rabbits12,13. It has also been shown in a rabbit model that without the C-terminus, there is reduced secretion and elastin found in the extracellular matrix13. This predicted truncated protein also affects a protein recently named asprosin—profibrillin’s C-terminal cleavage product7. Researchers originally found that asprosin is secreted by adipose cells and is transported to the liver where the end result is a rapid increase in blood glucose7. Recently a group of researchers were not able to reproduce Romere’s results thus calling the function of asprosin into further questioning8. Regardless of asprosin’s function, with the premature stop codon introduced with Marfan lipodystophy syndrome, asprosin synthesis may be limited. Subsequent studies have found decreased amounts of asprosin leads to lipodystrophy and a substantial decrease in blood glucose levels in rabbits13. Although the mechanism is not completely clear for Marfan lipodystrophy patients, it is probable that reduced amount in FBN1 mRNA levels, reduced secretion, and a decreased amount of asprosin is essential for this phenotype7,12,13. Mutations within the FBN1 gene can lead to drastically distinct phenotypic differences as seen in geleophysic dysplasia 2. Autosomal dominant geleophysic dysplasia 2 patients have mutations in the TB5 region in exons 41 and 42 of the FBN1 gene which encode the 5th 8-cysteine domain9,10,15. Mutations were found in essential structural residues or large aromatic regions9. Some mutations introduced a reactive cysteine which could react to outside stimulus or form disulfide bonds within the fibrillin 1 protein2. The addition or loss of a cysteine residue could interrupt disulfide bonds and thus disturb the assembly of fibrillin 1. Mutations involving aromatics could also be deleterious considering disruption of protein folding. Due to misfolding of fibrillin 1, the protein may be aggregating and thus making it difficult to form microfibrils. Subsequently, researchers found that fibrillin 1, with some of these mutations, were able to be secreted into the ECM and incorporate into the microfibril network2. It would be beneficial to know the levels of microfibrils as compared to normal levels for these specific mutations. The mutations that were found in the TB5 region and associated with geleophysic dysplasia 2 have not been previously characterized with Marfan syndrome mutations2. Additionally, mutations in the ADAMTSLIKE-2 protein were found to cause recessive geleophysic dysplasia9. In a mouse model, ADAMTSLIKE-2 deficient mice did not form microfibrils with fibrillin 114. ADAMTSLIKE-2 affects endochondral ossification thus impairing longitudinal bone growth14. In mice, the absence of ADAMTSLIKE-2 drove aberrant FBN1 levels and led to aggregates near the cell membrane14. Genetic disorders stemming from mutations in the FBN1 gene can be profoundly phenotypically distinct. Patients with Marfan lipodystrophy are tall with little fat and appear to have prematurely aged whereas patients with geleophysic dysplasia 2 have short tubular bones and have heart problems. Each of the mentioned disorders have genetic mutations in a specific exon(s) in the FBN1 gene. The location of the mutations essentially determines the fate of the patient. In Marfan lipodystrophy, mutations in exon 64 leads to decreased FBN1 mRNA, secretion, and asprosin7,12,13. On the other hand, geleophysic dystrophy 2 has mutations in a cysteine-rich region that may affect the structure and assembly of fibrillin 1 and thus affect longitudinal bone growth14,15. Additionally, aberrant production ADAMTSLIKE-2 protein led to aggregation14. Overall, specific mutations in different regions of the FBN1 gene can lead to different clinical pictures. Works Cited Sakai, Lynn Y; Keene, Douglas R. (2018) Fibrillin protein pleiotrophy: Acromelic dysplasias. Matrix Biol, 80:6-13. Online Mendelian Inheritance in Man, OMIM®. Johns Hopkins University, Baltimore, MD. MIM Number: 134797: 02-28-19: World Wide Web URL: https://omim.org/ Hubmacher, Dirk; Apte, Suneel S. (2015) ADAMTS proteins as modulators of microfibril formation and function. Matrix Biol, 47:34-43. Takenouchi, Toshiki, et. al. (2013) Severe congenitial lipodystrophy and a progeroid appearance: Mutation in the penultimate exon of FBN1 causing a recognizable phenotype. American Journal of Medical Genetics Part A, 161(12). Online Mendelian Inheritance in Man, OMIM®. Johns Hopkins University, Baltimore, MD. MIM Number: 616914: 02-28-19: World Wide Web URL: https://omim.org/ Passarge, Eberhard; Robinson, Peter N; Graul-Neumann, Luitgard M. (2016) Marfanoid-progeroid-lipodystrophy syndrome: a newly recognized fibrillinopathy. European Journal of Human Genetics, 24:1244-1247. Romere, Chase; et. al. (2016) Asprosin, a fasting-induced glucogenic protein hormone. Cell 165(3): 566-579. Herrath, Matthias von; et al. (2019) Case reports of pre-clinical replication studies in metabolism and diabetes. Cell Metabolism 29: 795-802. Le Goff, Carine; et al. Mutations in TGFβ Binding-Protein-Like Domain 5 of FBN1 are Responsible for Acromicric and Geleophysic Dysplasias. American Journal of Human Genetics 89: 7-14. Online Mendelian Inheritance in Man, OMIM®. Johns Hopkins University, Baltimore, MD. MIM Number: 614185: 02-27-19: World Wide Web URL: https://omim.org/ Online Mendelian Inheritance in Man, OMIM®. Johns Hopkins University, Baltimore, MD. MIM Number: 154700: 06-05-19: World Wide Web URL: https://omim.org/ Davis, Margaret R; et. al. (2016) Expression of FBN1 during adipogenesis: Relevance to the lipodystrophy phenotype in Marfan syndrome and related conditions. Molecular Genetics and Metabolism 119: 174-185. Chen, Mao; et. al. (2018) Truncated C-terminus of fibrillin-1 induces Marfanoid-progeroid-lipodystrophy (MPL) syndrome in rabbit. Dis Model Mech 11: 4. Delhon, Laure; et. al. (2019) Impairment of chondrogenesis and microfibrillar network in Adamtsl2 deficiency. FASEB J. 33: 2707-2718. Cheng, SW; et. al. (2018) A report of three families with FBN1-related acromelic dysplasias and review of literature for genotype-phenotype correlation in geleophysic dysplasia. European Journal of Medical Genetics 61: 219-224. Effect of Alterations in the FBN1 Gene
MCW Unit 5 Impacts & Affection of Social Media on Youth Population Questions
MCW Unit 5 Impacts & Affection of Social Media on Youth Population Questions.
As you learned in Unit 4, one indicator of bad science reporting in the popular press is the lack of reliance on peer-reviewed studies. Therefore, when reading a popular press article, it’s important to find out if the popular press article is based on results reported in a scholarly article.Good popular press articles indicate they’re based on results from a scholarly article by providing a link to those scholarly articles.For example, look at the first page of Kaplan’s (2013) popular press article “Most Depressing Brain Finding Ever” and the first page of Mooney’s (2013) popular press article, “Science Confirms: Politics Wrecks Your Ability to do Math.”Both of these two popular press articles link to the study on which they’re based with words such as “According to a new psychology paper, …” “The study, …” and “… research paper …”.Other popular press articles link to the study’s scholarly article at the end of their popular press article.For example, take another look at Fradera’s (2017) article, “How Much Are Readers Misled by Headlines that Imply Correlational Findings Are Causal?,” which you read during Unit 4.Go to the last page of Fradera’s (2017) popular press article to see where the author links to the research study on which the popular press article is based.The link is given as “How Readers Understand Causal and Correlational Expressions Used in News Headlines.”However, note that the link given to the scholarly article on which Fradera’s popular press article is based leads to only the journal article’s abstract. That’s because the scholarly article is not open access; it’s paywalled.If readers of the popular press article don’t have access to a university library, they won’t be able to read more than the abstract of the scholarly article, unless they’re willing to pay $11.95.Readers who won’t be able to read the entire scholarly article (unless they pay $11.95) include journalists who want to write popular press articles about that scholarly article.Find ten popular press articles on topics that interest you. For each of the ten popular press articles:Identify whether the popular press article is based on the results reported in a scholarly article.If the popular press article is based on the results reported in a scholarly article, identify whether the popular press article links to that scholarly article.If the popular press article is based on a scholarly article and if the popular press article links to that scholarly article, identify whether that scholarly article is open access or paywalled.Go to the Unit 5: Assignment #2 Discussion Board and make a new post in which you list (in a numbered list) the ten popular press articles. For each of the ten popular press articles:Provide a link to the popular press article (use the name of the popular press article for the text that you use for your embedded link, e.g., “Most Depressing Brain Finding Ever”);If the popular press article provided a link to the scholarly article, provide that link to the scholarly article (using the exact wording that was used in the popular press article, e.g., “According to a new psychology paper”) ANDtell us whether the scholarly article is available through open access or only through a (university library) paywall.To get your numbering — for your numbered list — you will need to do one of the following:type the numbers into the textbox yourself ORask the Discussion Board to number your list for you (by clicking on the numbering icon) ORtype the numbers into your Word or Google doc yourself, rather than relying on Word or Google doc to automatically number your list for you. (The numbers that Word or Google doc automatically add do not always copy over to the Discussion Board.)
MCW Unit 5 Impacts & Affection of Social Media on Youth Population Questions
ASCC Hedge Funds Statements on Public Corporations Exaggerated Earnings Questions
ASCC Hedge Funds Statements on Public Corporations Exaggerated Earnings Questions.
1. A critic recently claimed that hedge funds cause market volatility to increase when they publicize (and document) that a public corporation exaggerated its earnings. The critic argued that hedge funds should not be allowed to make such public statements, and should not be allowed to take short positions that bet against the firm that is being criticized. Write a short essay that supports or refutes this opinion.2. Should large securities firms be allowed to be independent and insulated from bank regulation, or should they be required to register as bank holding companies, and therefore be subject to bank regulations? Write a short essay that supports your opinion.
ASCC Hedge Funds Statements on Public Corporations Exaggerated Earnings Questions
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