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Organic Chemistry Borohydride Reduction of 2 Methylcyclohexane Lab Report

Organic Chemistry Borohydride Reduction of 2 Methylcyclohexane Lab Report.

Post Lab Report Format (typed, printed, page numbered, single spacing) (make sure to put Your Name and Your Partner’s Name together)Title (Borohydride Reduction of 2-Methylcyclohexanone)Purpose (why we did the exp.)Chemical Structure (make sure to put the reference) You can draw your own structure with free software (any chemical structure drawing software is ok. However, put the name of the software below the structures)Safety Information/Physical Data (physical properties of compounds)Procedure (Your own paragraph form (3rd person))Clean-Up (how to clean up the wastes)Observational Data Presentation% yield? Final mass of 2-Methylcyclohexanol? IR? Briefly explain IR of the product. (See the attached IR in this announcement)Discussion (in PARAGRAPH FORM)What is reduction? Why sodium borohydride?How does the reaction occur? Why sodium hydroxide?Why dichloromethane? Why saturated sodium chloride solution (NaCl)?Why sodium sulfate? How the distillation works on this exp.?Explain the IR of 2-Methylcyclohexanol. (Attached)Is It different from the reactant IR (2-Methylcyclohexanone) in the lab manual? How different?Low % yield? Any possible sources of error?References (ACS format for discussion)Side reaction: N/A% yield: show your calculation work.Mechanisms: N/AAnalysis of TLC/IR/NMR: show the IR again and explain the IR of 2-Methylcyclohexanol in detail.Post Lab Questions: N/A
Organic Chemistry Borohydride Reduction of 2 Methylcyclohexane Lab Report

MGT 321 Saudi Electronic University Lead in Toys and Drinking Water Case Study.

Instructions – PLEASE READ THEM CAREFULLYundefinedBlackboard (WORD format only) via allocated folder.Students are advised to make their work clear and well presented; marks may be reduced for poor presentation. This includes filling your information on the cover page.must mention question number clearly in their answer.Late submission will NOT be accepted.Avoid plagiarism, the work should be in your own words, copying from students or other resources without proper referencing will result in ZERO marks. No exceptions.All answered must be typed using Times New Roman (size 12, double-spaced) font. No pictures containing text will be accepted and will be considered plagiarism)((I attached a file on the thread and a file on the article to extract from it))
MGT 321 Saudi Electronic University Lead in Toys and Drinking Water Case Study

This essay will analyze a major political trend, attitude, conflict or event between 1812 and 1860.. I’m trying to study for my History course and I need some help to understand this question.

The Antebellum Period
you will analyze a major political trend, attitude, conflict, or event between 1812 and 1860 and explain its historical significance. Your analysis should answer in depth the question: Why is this particular idea or event important to the study of early U.S. history? This is a seemingly easy question to answer, but the goal is to uncover the details and nuances of whichever topic you choose in order to fully appreciate its value.
Examples you might choose from (but are not limited to) include:

the development of the Republican Party;
Free Soil Movement;
Free Labor Party;
transportation revolution (or related projects);
emergence of working class/middle class/wealthy business elites;
Indian Removal policies;
Nullification crisis;
formation of Whig Party;
Mexican American War;
Texan independence;
any antebellum reform movement;
Underground Railroad;
Fugitive Slave act;
the list goes on! Again, this is a short list to get you started. Basically anything you find of interest from chapters 9-14 is fair game! If you want to confirm your topic with me before you begin this paper, I would be happy to give you some preliminary feedback.

Based upon the textbook readings as well as two additional academic sources, you will write a 4-page essay (in addition to a cover page and Bibliography page) that examines the significance of your topic of choice.
To get started, you will create an annotated bibliography to be submitted prior to the actual essay. The annotated bibliography has a separate submission section here: Essay 2 Annotated Bibliography which also includes further instructions.
Below are the requirements:

4 pages minimum (not including the cover page and bibliography)
typed, Times New Roman, 12 point font, double spaced
1 inch margins
cover page, bibliography page, Chicago style citations
reference to at least three secondary sources (can include textbook)
Submit via Canvas, due Sunday, December 8, 11:59pm

This essay will analyze a major political trend, attitude, conflict or event between 1812 and 1860.

Independence in Accounting Rhetorical Analysis & Existential Threat Discussion

Independence in Accounting Rhetorical Analysis & Existential Threat Discussion.

Selecting one of the essays we have discussed so far in class (see below), perform a rhetorical analysis of approximately 650-750 words (2.5-3 pages max/double spaced/12 point font) in length. Your thesis should propose a claim addressing if the text succeeds or fails in its purpose as well as the reasoning for how/why some aspect of the argument works to convince/persuade or not convince/persuade the audience of the author’s claim. (Remember: Thesis = Claim + Reason.) In performing your rhetorical analysis you do not have to focus on the entirety of the text but only perform a close reading examining a particular aspect of the text and its effectiveness or ineffectiveness in fulfilling the author’s purpose/convincing its intended audience. In the body of your essay you will go on to analyze how well a key component of the argument works to convince or move (or not convince or move) the essay’s audience, paying specific attention to the rhetorical devices and appeals discussed in class (ethos, logos, pathos; logical and appropriate use of credible/unbiased evidence and reasoning; as well as style, word choice, tone, etc.). In performing your analysis, ask yourself specific questions, such as: What is the purpose of the argument? Who is its intended audience and what are its expectations? What is the time and place in which it was written? (ie. The context of the argument). What claim is it making? Does it serve a particular interest or does the author seem to have a hidden bias or agenda in making his argument? What appeals or techniques does the author use – ethos, logos, pathos – to support that claim? What is the genre of the argument (informational, definitional, proposal, evaluation, political writing, advertisement, etc.)? Who is making the argument, and what ethos does he create? How does the author establish credibility? Does the author come across as fair-minded and trustworthy? If the author appeals to pathos, does he do so fairly? If the author appeals to logos, is his logic rational or is it based on faulty reasoning or overgeneralization? What authorities does the argument rely on and are they creditable? Is the argument rational and feasible? What facts, reasons, examples, and evidence does the argument employ as support and are they effectively presented? Or does the author misrepresent his examples or take them out of context in order to fit his stance? How is the argument organized and arranged? How does the language, tone and style (humor, sarcasm, diction, formality, seriousness) of the argument work to convince or turn off its audience? Perform a close reading of the text in question and use specific examples/quotations in your analysis to demonstrate how the language and rhetoric work to form a competent, coherent (or incompetent, invalid) argument, explaining your reasoning by deeply analyzing your support. Your analysis should stay in the 3rd person and be structured effectively in adherence to the guidelines and conventions of scholarly writing as covered in the textbooks and discussed in class (formal diction, effective argument structure, grammatically correct, demonstrates flow and coherency in language usage, etc.). Your essay must be properly cited in MLA format (See relevant pages in The Little Seagulls Handbook) and include a one page works-cited as the last page of your paper (See pages 144-146, #19, in the Little Seagulls Handbook on citing a work from an anthology for formatting guidelines). For a model of an effective rhetorical analysis see the sample essay handed out in class. Remember: Whether you agree or disagree with an author’s argument does not matter in writing a rhetorical analysis essay, but it is rather your job as a fair-minded and unbiased reader and critic to analyze and prove how a text works (or fails) to convince its audience and fulfill its purpose (i.e. is the author’s argument valid/effective and why or why not?).Essays:“An Argument against Veganism… from a Vegan?” Pages: 609-614“from World without Mind: The Existential Threat of Big Tech” Pages: 719-722
Independence in Accounting Rhetorical Analysis & Existential Threat Discussion

research methodology discussion

i need help writing an essay research methodology discussion.

This assignment serves as a practice for student who is graduating next year. Based on the given research objective, student needs to define how the research will be conducted to collect reliable and useful data on the given research topic. The choice of the research techniques have to be justified.In addition, it needs to answer the following questions:-Which research will be conducted? Qualitative or Quantitative research ( or the combination of both)-Sampling technique ? ( in case Quantitative research is applied )-In case of Qualitative ( how many respondents are enough? , where could the respondents be approached, found?)_-Research population -Validity and Credibility of the research ( how to ensure the validity and credibility of this research – ( explain how to obtain data , how the choice of respondents, ( right respondents) , data collection could assure this) Research objective :To gain insight into travel motives and social media behaviors of Vietnamese travelers aged 24-35, in order to devise a social marketing communication plan that helps increase the brand awareness of Travelsmile ( travel company )towards this target group.Bear it mind that : Regarding the access to data : This company would provide the researcher the contacts of its previous client.
research methodology discussion

Applications of Genomics in Cancer

IN WHICH AREA OF HEALTH CARE CAN GENOMICS MAKE THE BIGGEST IMPACT, AND WHAT SCIENTIFIC ADVANCES ARE NEEDED TO MAKE THIS HAPPEN? Hozaifa S. Hassan Cancer management is one of the hottest areas in modern healthcare, especially with its increasing burden in both developing and developed countries. Genomics has changed the landscape of cancer management. This review highlights the current knowledge and concepts concerning how genomics with the advent of new technologies has revolutionised cancer management. Although we still have a long way to go till achieving full cure of cancer, the rapid development of cancer research carries fruitful promises for the near future. Keywords: Cancer, genomics, microRNA, immunotherapy The International Agency for Research on Cancer (IARC) has recently declared that global cancer burden rises to 14.1 million new cancer cases and 8.2 million cancer-related deaths occurred in 2012, compared with 12.7 million and 7.6 million, respectively, in 2008, with prediction of a substantive increase to 19.3 million new cancer cases per year by 2025. Prevalence estimates for 2012, show that there were 32.6 million people alive over the age of 15 years had a cancer diagnosed in the past five years. 1 This sets off the alarm bells, we have to develop more effective tools to face this current situation. Genome sequencing and the oncogenic landscape: Cancer is driven by various genomic alterations. The emergence of the draft human genome sequence in 2000 empowered the study of cancer genomes in many ways. With the arrival of the next generation sequencing (NGS) the tumour biology research has further revolutionized.2 With comprehensive sequencing of many cancer samples, huge number of mutated genes were discovered, so it is crucial to classify these genes into those whose mutations confer with selective gross advantage for the cancer ( driver genes mutations) and those which occur though the course of tumourigenesis and do not have great impact on the selective gross advantage (passenger mutations). There are about 140 driver genes identified till now. A typical tumour contains two to eight of these driver gene mutations. Driver genes can be classified into 12 signalling pathways that regulate three core cellular processes: cell fate, cell survival, and genome maintenance (Fig. 1). Therefore, targeting the driver genes or their products could have a great impact on tumour growth. Besides, the administration of unnecessary, costly, and potentially toxic treatment will be avoided.2 Fig ure 1. Cancer cell signaling pathways and the cellular processes they regulate. (Vogelstein et al ., 2013) Genomics and targeted therapy Targeted therapy towards the products of mutated driver genes has revolutionized the modern cancer therapy. This is best exemplified by imatinib which targets the Abelson (ABL) kinas in chronic myeloid leukaemia (CML). ABL kinase is a chimeric oncogenic fusion protein resulted from a reciprocal translocation of break point cluster (BCR) on chromosome 22 and ABL on chromosome 9. Food and drug administration (FDA) approved imatinib as first-line treatment for CML in 2001 for its magnificent response with 89% overall rate of 5-uear survival for patients treated. 3 It is crucial to accurately match patients with the most appropriate drugs. Otherwise, some anti- cancer drugs would be clinically useless because the personal and financial costs would far outweigh the benefits. For example, targeted epidermal growth factor receptor (EGFR) inhibitors achieve a response rate of 71% in patients with non-small cell lung cancer whose tumour harbour an activating EGFR mutation compared with 1% for those without a mutation.3 There are many targeted drugs that are already used or will enter the clinic soon (Table 1).3 Genetic networks and pathways: one hit is not enough Genomics has shed the light on genetic networking and pathways, where tumourigenesis results from multiple mutations in different genetic networks driving one or more pathways that eventually lead to the acquisition of the growth advantage. This could explain why some targeted drugs are thwarted by resistance. Moreover, this could provide novel combinations for therapeutic intervention.4 For example, most of melanomas are driven by mitogen-activated protein kinase (MAPK) pathway which is composed of Ras-Raf-MEK-ERK switches. Melanoma patients who have B-RAF V600E variant greatly respond to the B-RAF inhibitors (vemurafenib and dabrafenib). Vemurafenib was approved by FDA in 2011 for increasing the survival in melanoma patients. 4 Unfortunately, this response is short-lived and regulation of two other agonists of MAPK- signalling, C-RAF and MAP3K8/COT, could bypass the requirement for B-RAF by re-activating the pathway downstream of the drug target. In a similar vein, Nazarian et al. (2010) have shown that another member in the same pathway called MEK – a downstream kinase to B-RAF- is also mutated in resistant cases. Therefore, adding MEK inhibitors to vemurafenib, could effectively eliminate most of resistant cells.4 Recently, Villanueva et al. (2013) have shown that the response rate to MEK inhibitor (trametinib) is decreasing. Resistance to MEK and BRAF inhibitors was conferred to MEK2-Q60P mutation and BRAF-V600E amplification, respectively, resulting in sustained MAPK activation in the resistant cells. Interestingly, concurrent use of both dabrafenib and trametinib from the start, not after developing resistance, could significantly improve the efficacy and decrease resistance to therapy. Moreover, a triple combination of dabrafenib, trametinib, and the PI3K/mTOR inhibitor GSK2126458 led to sustained tumour growth inhibition.5 This paves the way for novel combinations of drugs targeting multiple nodal points in cancer- driving pathways. As a result, cancer therapy will be more efficacious with less resistance. Oncogenic signatures: completing the atlas Many cancer genome projects unleashed in the past decade have identified essentially complete sets of protein-coding genes, coupled with the discovery of novel microRNAs. Moreover, deeper coverage of many cancer genomes has identified a wealth of somatic mutations, including copy- number changes (deletions and amplifications of DNA), rearrangements, point mutations and small insertions in many tumour types. However, the real challenge is to classify these enormous data sets and translate them into functional and actionable alterations.6 Recently, computational algorithms and functional genomics together with the sequencing of complete genomes of human cancers provide comprehensive catalogues of somatic mutations that fuel different types of cancers. Moreover, these catalogues predict possible targets for therapy in a resistance emerged towardsB-RAF inhibitors. Johannessen et al. (2010) have shown that up-selected cancer. *PARP denotes poly (adenosine diphosphate–ribose) polymerase. (McDermott et al., 2011) For example, The Cancer Genome Atlas (TCGA) provides molecular tumour maps in unprecedented detail. 3,299 TCGA tumours from 12 cancer types are classified according to their genetic and epigenetic alterations, and then they are gathered into pathways that affect oncogenesis with correlation between these functional alteration and available targeted therapy (Fig. 2). The globally coordinated International Cancer Genome Consortium (ICGC), of which TCGA is a member, will add thousands more samples and additional tumour types which together with computational algorisms will lead to better understanding of cancer.6 In the future, we would have a genomic atlas for different types of cancers guiding us through our quest for finding a cure for cancer. MicroRNA and cancer: tiny but powerful MicroRNAs (miRNAs) are small noncoding RNAs which enhance the cleavage or translational repression of specific mRNA with recognition site(s) in the 3’-untranslated region (3’UTR). They are involved in multiple biological activities as well as disease progression including cancer. Depending on the functions of their targets, they could act as either tumour suppressors or oncogenes. Dysregulation of miRNAs has been widely observed in different stages of cancer either by structural genetic alterations, epigenetic changes or abnormal biogenesis.7 Recently, miRNA-based anticancer therapies have been exploited, either alone or in combination with current targeted therapies. MicroRNA approaches could concurrently target multiple effectors of pathways involved in cell differentiation proliferation and survival (Fig. 3). 7 For example, O’Day et al. (2010) have shown that miR-24 inhibits proliferation through direct targeting of c-Myc, E2F1 and a number of related molecules. Interestingly, Ma et al. (2010) have shown the crucial role of miR-10b in breast cancer metastasis. This group has also exploited a possible therapeutic application, reporting that systemic treatment of tumour-bearing mice with miR-10b antagomirs suppresses breast cancer metastasis. This opens the door for the use of oligonucleotides or virus-based constructs to either block the expression of an oncogenic Figure 2. Map of functional and actionable alterations across 12 tumor types. Tumor types abbreviated as: BLCA, Bladder urothelial carcinoma; BRCA, Breast invasive carcinoma; COADREAD, Colon and rectum adenocarcinoma; GBM, Glioblastoma multiform; HNSC, Head and neck squamous cell carcinoma; KIRC, Kidney renal clear-cell carcinoma; LAML, Acute myeloid leukemia; LUAD, Lung adenocarcinoma; LUSC, Lung squamous cell carcinoma; OV, Ovarian serous cystadenocarcinoma; UCEC, Uterine corpus endometrioid carcinoma; MSS, Microsatellite stable; MSI, microsatellite instability; Ultra, ultramutators; Low CNA, endometrioid; RTK, receptor tyrosine kinase; DSB, double-strand break. (Ciriello et al., 2013) miRNA or to reintroduce a tumour suppressor miRNA lost in cancer.7 Cancer inunwtotherapy: awaken the giant For a cancer to develop and metastasise, it must first escape the immune surveillance. Cancer uses a Houdini mechanism to hide its antigens and deceive the immune system. Hanks et al. (2013) have shown that loss of tumour-expressed type III transforming growth factor receptor (TGF R3), enhance TGF-signalling within loco-regional dendritic cells (DCs) and up-regulated both the immune-regulatory enzyme indoleamine 2, 3- dioxygenase (IDO) in plasmacytoid DCs and the CCL22 chemokine in myeloid DCs. These alterations mediate T regulatory cells infiltration and the suppression of antitumor immunity.8 Interestingly, the therapeutic benefit derived from the combination of an antigen-specific vaccine with a TGF- signalling inhibitor in murine HER2/NEU-expressing 4T1 tumours was primarily mediated by an enhanced antitumor T cell response. This opens the door for using novel TGF- signalling inhibitor in enhancing the immune therapy.8 Another recent approach in this field is releasing the brakes of the immune system by using checkpoint blocking antibodies. For example, antibodies directed against cytotoxic T­ lymphocyte antigen 4 (CTLA-4) (e.g. Ipilimumab) and programmed death 1 receptor (PD-1) (e.g. Nivoluma) have demonstrated significant recent promise in the treatment of an expanding list of malignancies. Ipilimumab was approved by FDA in 2011 for significantly improving the survival of patients with metastatic melanoma. Further research will demonstrate much more checkpoints that can enhance immunotherapy either alone or with combinations with other drugs.9 Interestingly, cancerous cells also have some tricks to escape the radar of the natural killer cells (NKs). For example, cancerous cells down­ express their natural killer group 2, member D­ ligands (NKG2D-Ls) required for activation of NKG2D receptors on NKs. 10 Bedel et al. (2011) have shown a pivotal and novel role for signal transducer and activator of transcription 3 (STAT3) in modulating the expression ofMHC-I chain-related A (MICA) -one member ofNKG2D-L family- in cancer cells. Interestingly, neutralizing STAT3 with pharmacologic inhibitors or siRNA has led to an increase in NK degranulation and IFN–y Figure 3. MicroRNAs targeting the hallmarks of cancer. (Iorio et al., 2012) This sets the stage for developing novel effective immunotherapies in the future as well as increasing today’s ones efficacy. Conclusion Genomics has revolutionary changed the landscape of cancer management. Whole genome sequencing of many cancer types combined with computational algorithms will add a wealth of information to our current knowledge. In the future, complete comprehensive genomic atlas will be available for most cancer types. Therefore, the mutations driving an individual’s cancer could be exactly identified then precisely targeted by chemotherapeutics, immunotherapy, synthetic oligonucleotides or combinations of those. This will increase the efficacy of the therapy. Besides, the administration of unnecessary, costly, and potentially toxic treatment will be avoided. It will be true that cancer could be cured! References [1] Latest world cancer statistics Global cancer burden rises to 14.1 million new cases in 2012: Marked increase in breast cancers must be addressed. http://www.iarc.fr/en/media–centre/pr/2013/pdfs/pr223_E.pdf. (12 December 2013) [2] Vogelstein, B et al. Cancer genome landscapes. SCIENCE 2013; 339: 1546–1558 [3] McDermott, U, Downing, JR, Stratton, MR. Genomics and the continuum of cancer care. N Engl J Med 2011; 364:340-50 [4] Sandmann, T, Boutros, M. Screens, maps

Loans and credit lines

Loans and credit lines.

PART A: Home Equity Loan Home
equity credit loans and credit lines have become very popular sources
of consumer credit. Why do you think individuals are turning to these
loans? What is the security for this type of loan? Are there advantages
to the borrower beyond the tax deductibility of the annual interest
paid? What are some of the disadvantages? Have you or anyone you know
made a home equity loan? What was the outcome? What effect does a home
equity loan have on your overall financial standing? IMPORTANT: In relating any examples from real life please disguise the names of individuals in order to protect their privacy. PART B: Your Credit ScoreDiscuss the importance of having good credit and how you can maintain that good credit.
Loans and credit lines