Electrochemical cell lab Aim Essay Example for Free

Electrochemical cell lab Aim Essay Point :- To discover the achievability of a redox response by taking a gander at the cell capability of the response . Quantitative perception The table beneath shows the estimations of cell potential that were recorded when the examination was performed Response Cell potential (ÂÂ ±0.01V) CuSO4 and ZnSO4 0.99V CuSO4 and AgNO3 0.64V Ag 1.39V Subjective Observation Response Obsevrations CuSO4 and ZnSO4 Copper sulfate abandons clear to blue , though zinc sulfate stays drab CuSO4 and AgNO3 Copper sulfate is blue in shading , silver nitrate is drab Ag Information handling Trial 1 Zn(s) - Zn2+ (aq) + 2e-(aq) Cu2+ (aq) + 2e-(aq) - Cu (s) Cu2+ (aq) + Zn(s) - Cu(s) + Zn2+ (aq) Trial 2 Cu(s) - Cu2+ (aq)+ 2e-(aq) Ag+(aq) + e-(aq) - Ag(s) Cu(s) + 2Ag+ (aq) - Cu2+ (Aq) + 2Ag (s) Examination 3 Zn(s) - Zn2+ (aq) + 2e-(aq) Ag+ (aq) + e-(aq)- Ag(s) Zn(s) + 2Ag+ (aq) - Zn2+ (aq) + 2Ag (s) The table underneath shows the writing esteems for the particular cell potential Response Cell potential (ÂÂ ±0.01V) CuSO4 and ZnSO4 0.34V CuSO4 and AgNO3 0.46 V. Ag 1.10 V Blunder rate = (|difference between the writing and trial value|)/(the writing esteem )x100 = (|0.34V 0.99V|)/(0.34V) x100 = 191.17% We can correspondingly discover the blunder rates for other cell possibilities too The table beneath shows the individual mistake rates of every one of the cell potential Response Mistake rate CuSO4 and ZnSO4 191.17% CuSO4 and AgNO3 39.13% Ag 16.36% Hypothesis Electrochemical cells In an electrochemical cell, power is delivered through compound responses. There comprise two anodes: the negative cathode and the positive terminal. At the negative cathode

Ethics in Corporate Governance Essay Example | Topics and Well Written Essays - 750 words

Morals in Corporate Governance - Essay Example Corporate administration assists with carrying an incomparable degree of fulfillments to five unique supporters, for example, workers, clients, merchants, financial specialists and social orders. Powerful corporate execution and fruitful markets depend on a guarantee to major moral standards. Moral principles can be communicated in a conventional lead necessity of the association which can control favored conduct of an association. Six Steps Majority of the fruitful associations executed a few codes of morals for their representatives to lead in a suitable way while rehearsing business tasks. Corporate morals are considered as the core values. â€Å"Ethics assists with building common relationship and build up the feeling of social belongingness† (Sison, 2008). Successful corporate administration can be accomplished through prescribed procedures and set of standards. A powerful arrangement relies on the trustworthiness, respectability and habits. Corporate administration decid es how an association is dealing with their relationship with their partners and investors. Moral financial specialists consistently anticipate straightforwardness and trustworthiness from the associations. Six stages can be prescribed to the leading body of an association so as to look after morals. The leading body of the association must actualize their own principal abilities and qualities. This will assist them with optimizing their administration potential. They should assemble a hierarchical situation of trust with their financial specialists and representatives. In addition, all the partners of the association should don't hesitate to talk about a few moral issues and predicaments with the leading body of the association. It is the significant for the associations to explain and report the obligations and jobs of the administration and board so as to give a compelling degree of responsibility to the partners. â€Å"Material matters’ revelation ought to follow straigh tforwardness by the organizations† (Fernando, 2009). The leading body of the association ought to guarantee that all the financial specialists have compelling access to the genuine and clear data. Hence, it tends to be expressed that morals assume a significant job in corporate administration and authoritative execution. In the event that the associations have gained notoriety for compelling moral conduct, it can cause both worker and client dependability. Leading group of the association ought to guarantee that moral codes and vision of the association is conveyed to each partner of the association. The board ought to incorporate these codes with the moral vision of their organization. This procedure can be executed through arrangement manuals, pamphlets, group gatherings, corporate gathering with financial specialists, and a few preparing occasions. The leading group of the association ought to guarantee that the hierarchical culture and conduct are following moral vision. R eports with respect to deceptive conduct should be completely explored by the board. In addition, it is their obligation to rebuff the violators of corporate administration and moral principles. What's more, the board ought to give awards to those representatives who are keeping up positive moral conduct. Above all, the association ought to give all obvious and true data to their financial specialists and different partners. Last controlling and supporting moral conduct will be the last advance for the leading body of the association. They have to execute overview process so as to know the moral conduct of the organizatio

A Snively CPW

A Snively CPW Let me begin by saying that thanks to CPW, the rest of high school is simply a formality. Oh, and sleeping is overrated. Heres just a quick glimpse at what made my CPW so exciting: My total caffeine intake curing CPW looked something like this: 2.5 Bawls sodas 2 red bulls 1 Sobe energy drink 1 energy drink water thing 5 cups of coffee I slept 5 hours over the course of CPW. 1 hour on purpose, 4 hours on accident (which is a funny story that Ill share shortly). So, from the beginning: I arrived in Boston Wednesday evening to catch an MIT Wind Ensemble rehearsal and received 2 free Rep CDs from the director, very cool. Then, my last night of sleep for a long time. The next morning I met Sara 11 at South Station and we headed over to campus to get all registered. The highlight was actually seeing people in person that Ive been seeing online forever. Nance, Ben Jones, and Matt McGann were all at registration. I got my picture taken with Matt at 9:55. Then it was off to the Stata center and CSAIL for a tour, which is when the fun actually began. This is where I encountered The Group. For the last several months there has been a group of people on the MIT 11 Facebook group that have always just kinda gotten along, and we all managed to find each other about an hour into the first day. Meet (from left) Michelle Nason, Sara Ferry, yours truly, Tim, Hank Robinson, Yuki Yamada, and Jon Estrada. Unfortunately Sauza couldnt make the picture, and the little girl, well, we dont know who she is. So what adventures did we go on? Allow me to steal the following format from Milena: Liquid Nitrogen Ice Cream Didnt spend a lot of time at this one, but its worth noting because it showed up on the schedule about a gazillion times. Throughout campus there were huge containers of liquid nitrogen, they were a common sight. This is what they were used for: Simmons Ball Pit WHY IS THIS NOT ADVERTISED?!?!?!?!? Look, if a dorm has a ball pit, I need to stay in it, because it is automatically the coolest dorm ever, hands down. We played in it a lot, heres Jon: We also played the Bury Snively under little colorful balls game and I soon found myself completely in the dark. Good times. Oh, and did you know that the dining room chairs in Simmons bounce? Its true! Fire hose: ? Calculus So, lambda calculus is one of those types of math that is probably impossible any time of day during any time of the week at any age. Ill spare you the explanation of what it is, sufficing it to say that three 18 year olds were probably not going to grasp it at 3 in the morning. Here are some highlights: Look at us pretending to understand whats happening! Yes, apparently its true in lambda calc. Did you know you could use an octopus as a variable? Science Museum! Alright, technically this isnt part of CPW, but it is in Boston, so its worth mentioning. First off, we saw an R2D2 mailbox, which was far too exciting to handle. We stretched our MIT muscles and bartered for free admittance because we were nearly MIT students, that was pretty awesome, no $16 tickets for us! After exploring we had our picture taken with the beaver exhibit. And then we had pictures taken in the main lobby spelling various things. Here are the girls spelling MIT: And here are the guys and Sara spelling IHTFP. After this particular picture somebody noticed that it was 3:15 and proclaimed Gah, its too bad we missed pi guys. Then somebody else chimed in. Wait, didnt we just take a picture? We dove for our cameras and zoomed in on the IHTFP picture. Sure enough, completely by accident, the digital clock in the background was displaying 3:14. We cheered, people stared. Meet the Bloggers Meet the bloggers rocked because the bloggers were no longer little pictures at the top of a web page. Theyre real, believe it or not! Ill skip the stories with this one and share some pictures instead: (Me taking a picture of Matt McGann taking a picture of me) Student Center Sleep-over Remember how I said we accidentally slept for 4 hours? Heres the scene: Hank, Harrison, Yuki, Jon, Dan, and yours truly were all tired because it was 3 in the morning. The next event wasnt scheduled until 4:17 (Pancakes at Random Hall). We decided to just chill in the student center lobby until it was time to leave, figuring we could even slip in a half hour nap before taking off. We took our places on various couches in the lobby. Jon had to separate from the group and go to a different couch because there wasnt enough room near us. Well, turns out its hard to take a half hour nap after going two days without sleep. After dozing off I hear a voice faintly in the distance: Stupid pre-frosh sleeping in the lobby. This woke me up, and thats when I checked my watch. 8:00 am. CPW registration was back in full swing, people were wandering everywhere, eating, meeting friends, and here we were completely asleep with mouths hanging open and backpacks strewn across the floor. I woke some people up and we all just sat there, disoriented, and tryin g to figure out what had happened. Thats when we remembered Jon, where was he?! We struggled up from our stupor and wandered around, eventually finding him taking up an entire couch, sleeping while people watched him from all the couches nearby. Oh, and did I mention that Hanks backpack, filled with bouncy balls from the bouncy ball drop, had tipped over during the night and spilled bouncy balls all over the floor of the Student Center? Yeah, were classy. Chillin with Sam and Laura in BC While chillin in the basement of Burton-Conner we happened upon blogger Sam and blogger Laura! Sooooooo, both are pretty much amazing. Sam was amazing just because he was so cool, and Laura was amazing because you can insult her all day long and shell just swing right back and make you feel like an idiot. She makes up some pretty awesome words too. I look forward to a time when Im not sleep-deprived and can argue with her without totally getting pwned, its ON Laura! BTW, this has nothing to do with Laura or Sam, but if you live in Burton Conner, this is the kind of stuff you get to do to your room: And Sam sings.

Countries With Negative Population Growth

Data from the Population Reference Bureau showed in 2006 that there were 20 countries in the world with negative or zero natural population growth expected between 2006 and 2050.   What Does Negative Natural Population Growth Mean? This negative or zero natural population growth means that these countries have more deaths than births or an even number of deaths and births; this figure does not include the effects  of immigration or emigration. Even including immigration over emigration, only one of the 20 countries (Austria) was expected to grow between 2006 and 2050, though the rush of emigration from wars in the Middle East (especially Syrias civil war) and Africa in the mid-2010s could revise those expectations. The Highest Decreases The country with the highest decrease in the natural birthrate was  Ukraine, with a natural decrease of 0.8 percent  each year. Ukraine was expected to lose 28 percent  of its  population between 2006 and 2050 (from 46.8 million to 33.4 million in 2050). Russia and Belarus followed close behind at a 0.6 percent  natural decrease, and Russia was expected to lose 22 percent  of its population by 2050, which would be a loss of more than 30 million people (from 142.3 million in 2006 to 110.3 million in 2050). Japan was the only non-European country in the list, though China joined it after the list was released and had a lower-than-replacement birthrate in the mid-2010s.  Japan has a 0 percent natural birth increase and was expected to lose 21 percent  of its population between 2006 and 2050 (shrinking from 127.8 million to a mere 100.6 million in 2050).   A List of Countries With Negative Natural Increase Heres the list of the countries that were expected to have a negative natural increase or zero increase in population between 2006 and 2050. Ukraine: 0.8% natural decrease annually; 28% total population decrease by 2050Russia: -0.6%; -22%Belarus: -0.6%; -12%Bulgaria: -0.5%; -34%Latvia: -0.5%; -23%Lithuania: -0.4%; -15%Hungary: -0.3%; -11%Romania: -0.2%; -29%Estonia: -0.2%; -23%Moldova: -0.2%; -21%Croatia: -0.2%; -14%Germany: -0.2%; -9%Czech Republic: -0.1%; -8%Japan: 0%; -21%Poland: 0%; -17%Slovakia: 0%; -12%Austria: 0%; 8% increaseItaly: 0%; -5%Slovenia: 0%; -5%Greece: 0%; -4% In 2017, the Population Reference Bureau released a fact sheet showing that the top five countries expected to lose population between then and 2050 were:China: -44.3%Japan: -24.8%Ukraine: -8.8%Poland: -5.8%Romania: -5.7%Thailand: -3.5%Italy: -3%South Korea: -2.2%

Key Objectives For School And Career Readiness Essay

Key Strategic Objectives This information was gathered in an interview with Andrea Williams, Principal of Theresa Bunker Elementary School. The key objectives for this school are defined in the yearly district strategic plan. The district strategic plan states three key objective that all schools should achieve over the course of the school year. There is a key objective for literacy, numeracy, as well as college and career readiness. The literacy objective is for students to be proficient in reading by 3rd grade. The math objective is that elementary students will be proficient in math and be prepared to transition to the next grade. The final objective of college and career readiness is just that: Students will be college and career ready. The key objective this school uses to define college and career ready for their younger students is based on their social and academic behaviors as recorded through the school-wide system of PBIS. If the objective is to get them college and career ready then they must have positive social and academic behavior in order to be prepared for Jr. and Sr. High School and then college. The key objective defined in the school’s strategic plan for this area is that 85% of students will be served by the Tier I system of classroom management in the classroom while no more than 15% will be served on a Tier II or Tier III plan which provides more support and intervention to students who lack the social and academic skills to be successful inShow MoreRelatedHigh School Students : Common Core And College And Career Readiness1706 Words   |  7 PagesHispanic high school graduates exposed to two different curriculums: Common Core and College and Career Readiness The Race to the Top program has spearheaded many highs school to purse programs that increase students completion of college from 40 to 60 percent within 16 years of their induction into the public education system (Transforming American Education: Learning Powered by Technology, n.d.). 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The plan should also be a continuity between change and a connection to the past that builds toward the future detailing objectives, rationale, strategies, and measurementsRead MoreThe Field Of Engineering For Any Student1594 Words   |  7 Pagesdeveloping high quality solutions and/or products to problems† (Hynes, Dare, Milto, Rogers, Hammer, 2011) The engineering design activities that will be created will be roughly based upon the criteria for successful engineering design challenges for high school students, provided by Dr. Julia Ross: open ended, contextualized within the real world, relevant to the lives of the students, based upon the use of everyday materials as much as possible to create a functional prototype, and aligned with grade levelRead MoreProfessional Development And Continuous Learning999 Words   |  4 PagesPOLICY This Policy stems from the view that professional development and continuous learning are necessary to maintain the quality of the University staff and their continued readiness and ability to contribute effectively to the mission and goals of the University. Policy is not a firmly characterized idea but rather a profoundly adaptable one, utilized as a part of distinctive courses on diverse events. †¢ A particular choice or set of choices intended to complete such a strategy. Policy Procedure

Apologies on Academic Changes Free Essays

Please receive much apologies for my late reply regarding academic changes. I have already been admitted at UCSD’s Economics undergraduate and returned my chosen classes form. However, I recently made some changes on my class choices. We will write a custom essay sample on Apologies on Academic Changes or any similar topic only for you Order Now Contained in this letter is new lists of subjects and ways on how i will still cover formerly chosen classes, and a request on how i should proceed. I have already chosen new subjects for the Fall, Winter and Summer academic quarters. All the courses contained in my new selection are shown in the university’s catalog. I will take several classes that i dropped from my list from the online program. In the upcoming fall quarter, I plan to take Econ 9, 25, and CIS 15A. I will take the rest of courses from either Foothill College or another community college. I have been looking for course offering in these colleges and ha found that they are all available. This is all in the attempts to make sure i get my A.A Degree in 2009. Further, i will be taking Math 11 and 12 at UCSD, which serves the purpose of the required Calculus for Business and Economics. I will also be taking the Math 1C, which you had inquired, in this Summer 2008. Having taken and performed well in other online classes is a good indication that i will perform well in the just mentioned courses. This is because i have gained the much important independent work ethic that is needed in such classes. I have already talked to my academic counselor on this situation reading my academic plans. The counselor has confirmed that independent and online courses are available for the above mentioned programs. This gives me confidence to work towards averting the crisis. Will kindly provide my counselor’s contacts so you can communicate when need arises. All this will be in the attempts of ensuring that my studies to make sure that my graduation of academic standing stand unaffected. I have made the point of scheduling the courses so as to have enough time allocation for each course. This will ensure maximum usage of time beyond the expectation of your office. I have already met all the IGETC economic major requirements, meaning that I just need to work on other requirements in order to graduate on time. Having met these key requirements leaves me with enough time to use in the classes listed above. In addition, I promise to work in the process of achieving the goal of meeting University requirements, performing well in my classes, as well as graduating on time. In the meantime, i am preparing myself for the academic challenge that lays ahead of me and i am sure of performing well and graduating on time. Despite my preparations on this matter, I am kindly asking for your guidance on the way i should move forward. I have no doubt that your office will understand my situation. I will make a point of regularly visiting and communicating with your office in order to keep you updated on my progress. Will also have my counselor communicate with your office regarding my plans and updated tentative plan. I highly appreciate your time and the efforts you have made to ensure my academic progress remains on course. With Thanks, How to cite Apologies on Academic Changes, Papers

Stop Writing for Everyone Why You Need to Establish Your Writing Niche

I talk to a lot of writers in my line of work. Through all of my conversations though, one thing I’ve noticed is that many writers do not see the advantage of establishing a niche. The usual argument is that they don’t want to limit the number of opportunities available to them. While I can understand the desire to want to get as much work as possible, I think finding a niche is a huge opportunity rather than a limitation. I’m not saying that writers shouldn’t be adaptable. But if you can be especially strong with one or two types of writing or an expert on a few select topics, your value to clients can significantly increase. It might seem counter-intuitive, but you’ll have more success if you narrow your focus to a few particular niches. Here are just a few benefits of focusing on a writing niche 1. You’ll Develop a Stronger Portfolio While it’s natural to want to grab as much work as you can, being a jack-of-all-trades can have its downsides. Your portfolio may seem scattered to potential clients who are looking for something specific in their niche. Additionally, a portfolio that represents you as a generalist can keep you stuck in areas of writing that you’d prefer to leave behind. If your portfolio still features your articles on home improvement while you’re trying to break into the field of science writing, you’re probably going to still attract more clients looking for content about roofing. A cohesive portfolio that represents work in your chosen niches will make you more appealing to the clients you want in addition to being able to produce higher quality work more easily. Time is money and every hour you spend vying for new work or learning a new client’s style is time you could have spent writing. If you can build up a loyal client base that keeps coming back to you with assignments, you’ll find it easier to maintain a steady income and you’ll have better luck negotiating rate increases as time goes on. 3. You’ll Have More Opportunities to Create Unique Content Becoming a leader within a niche can help you stand out. The more writing you do in your chosen niche, the more you establish a reputation as someone who can write with ease on those topics. This type of reputation helps you gain more quality clients. If you’re a content writer who focuses on real estate financing topics, potential clients who are looking for a writer are much more likely to want to hire a specialist. 4. You’ll Enjoy Your Work More If you’re lucky enough to become established in a niche you love, it won’t feel like a burden to do your research or stay on top of industry trends. That enthusiasm will show in your work and clients will appreciate your passion and enthusiasm for your area of interest. 5. You’ll Make More Money Specialists earn more money than generalists. This is true in the worlds of medicine, law and consulting, and writing is no exception. Your in-depth, specialized knowledge and experience has real value and clients are going to be willing to pay for it. It’s Up To You To Take Charge Casting a wide net may seem like the safest way to pay the bills as a writer, but it’s likely not the best bet for long-term success. Establishing a niche can help you develop your professional reputation, attract more loyal clients and command better rates. If you haven’t already, think about some possible areas you might want to focus on, and start building your brand as an expert writer.

Breaking the Lockjam and Buttoning Down the Hatches

Breaking the Lockjam and Buttoning Down the Hatches Breaking the Lockjam and Buttoning Down the Hatches Breaking the Lockjam and Buttoning Down the Hatches By Maeve Maddox The President has invited some factions to Washington to break the lockjam. The copywriter who came up with this statement confused two common English expressions used to convey a state of of inaction: deadlock and logjam. The term deadlock refers to a stoppage brought about by the opposition of two forces, neither of which will budge. The term logjam comes from the practice of floating newly-cut trees (logs) down a river. When several logs become so crowded they can no longer move, the result is a logjam. I understand such idiomatic confusion in the speech of someone speaking off the cuff. We all come out with mixed-up speech from time to time, especially when were surprised or nervous. My examples are not from people responding to impromptu interview questions. They come from newspaper stories and the words of professional announcers or scriptwriters. I see the tendency to conflate idioms in this way as a result of limited reading. Others may disagree, seeing it instead as innovation, the deliberate altering of old expressions to avoid clichà ©. It may be the lattersome of the time. Idioms are something that have to be absorbed from immersion in the language. My own language patterns were set when English teachers corrected their students grammar every time they opened their mouths, and assigned book reports and summer reading. Back then, movie and radio scripts were written by men and women who observed not only pronoun case, but the subjunctive mood of verbs! Somewhere theres a growing disconnect between the usual sources of idiomatic language and the people who write for the media. I think that it is a problem and that the solution is close reading of the best authors. Here are some more examples: They took it in good stride. The context was a news story about a group that was dealing with disappointment. The two expressions mingled here are to take something in stride and to take something in good part. Both have the sense of dealing with something without making a fuss. if other airlines join suit and raise their fares. This is from a news story. The altered expression is to follow suit. It is an expression taken from a card game. One player leads with a heart and the next one must follow suit by putting down another heart. guess well have to button down the hatches. This was spoken by a Fox anchorman talking about a coming storm in Florida. The expression is to batten down the hatches. It refers to the act of nailing lengths of wood (battens) across trapdoors in a ships deck so they wont open during a storm. We use it in the sense of securing things before a storm, either a real storm or a metaphorical one. The present participle form is battening. Deliberately altering a familiar idiom for effect is one thing. The result can be witty and entertaining. Mixing them up out of ignorance is something to be avoided. Want to improve your English in five minutes a day? Get a subscription and start receiving our writing tips and exercises daily! Keep learning! Browse the Writing Basics category, check our popular posts, or choose a related post below:Program vs. ProgrammeThe Difference Between "will" and "shall"20 Ways to Laugh

The Environmental Costs of Cotton

The Environmental Costs of Cotton Chances are that on any given day we wear some clothing items made of cotton, or sleep in cotton sheets, yet few of us know how it is grown, or what are  the environmental impacts of cotton cultivation. Where Is Cotton Grown? Cotton is a fiber grown on a plant of the Gossypium genus, which once harvested can be cleaned and spun into fabrics used most commonly for linens and clothing. Needing sunshine, abundant water, and relatively frost-free winters, cotton is grown in a surprising variety of location with diverse climates, including  Australia, Argentina, West Africa, and Uzbekistan. However, the largest producers of cotton are China, India, and the United States. Both Asian countries produce the most, mostly for their domestic markets, and the US is the largest exporter of cotton with about 10 million bales a year. In the United States cotton production is mostly concentrated in an area called the Cotton Belt, stretching from the lower Mississippi River through an arc spanning the lowlands of Alabama, Georgia, South Carolina, and North Carolina. Irrigation allows additional acreage in the Texas Panhandle, in southern Arizona, and in California’s San Joaquin Valley. Chemical Warfare Globally, 35 million hectares of cotton are under cultivation. To control the numerous pests feeding on the cotton plant  farmers have long relied on heavy application of insecticides, which leads to the pollution of surface and groundwater. In developing countries cotton growers use a full half of the pesticides used in agriculture. Recent advancements in technology, including the ability to modify the cotton plant’s genetic material, have made cotton toxic to some of its pest. This reduced but did not eliminate the need for insecticides. Farm workers, particularly where the labor is less mechanized, continue to be exposed to harmful chemicals. Competing weeds are another threat to cotton production; generally tilling practices and herbicides are used to knock back weeds. A large number of farmers have adopted genetically modified cotton seeds that include a gene protecting it from the herbicide glyphosate (the active ingredient in Monsanto’s Roundup). That way, the fields can be sprayed with the herbicide when the plant is young, easily eliminating competition from weeds.   Naturally, glyphosate ends up in the environment, and our knowledge of its effects on soil health, aquatic life, and wildlife is far from complete. Another issue is the emergence of glyphosate resistant weeds. This is an especially important concern for those farmers interested in following no-till practices, which normally help preserve the soil structure and reduce erosion. Reliance on glyphosate resistance makes it more difficult to control weeds without turning the soil. Especially problematic in the southeast US is Palmer’s amaranth pigweed, a fast growing glyphosate resistant weed. Synthetic Fertilizers Conventionally grown cotton requires the heavy use of synthetic fertilizers. Such concentrated application means much of it ends up in waterways, creating one of the worst nutrient pollution problems globally, upending aquatic communities and leading to dead zones starved of oxygen and devoid of aquatic life. In addition, synthetic fertilizers contribute an important quantity of greenhouse gases during their production and use. Heavy Irrigation In many regions rainfall is insufficient to grow cotton but the deficit can be made up by irrigating the fields with water from nearby rivers or from wells. Wherever it comes from, the water withdrawals can be so massive that they diminish river flows significantly and deplete groundwater. Two thirds of India’s cotton production is irrigated with groundwater. In the United States, western cotton farmers too rely on irrigation. Obviously, one could question the appropriateness of growing a non-food crop in arid portions of California and Arizona during the current multi-year drought. In the Texas Panhandle, cotton fields are irrigated by pumping water from the Ogallala Aquifer. Spanning eight states from South Dakota to Texas, this vast underground sea of ancient water is being drained for agriculture far faster than it can recharge. In northwest Texas, Ogallala groundwater levels have dropped over 8 feet between 2004 and 2014. Perhaps the most dramatic overuse of irrigation water is visible in Uzbekistan and Turkmenistan, where the Aral Sea declined in surface area by 85%. Livelihoods, wildlife habitats, and fish populations have been decimated. To make matters worse the now dry salt and pesticide residues are blown away from the former fields and lake bed, increasing the frequency of miscarriages and malformations among the 4 million people who live downwind. Another negative consequence of heavy irrigation is soil salination. When fields are repeatedly flooded with irrigation water, salt becomes concentrated near the surface. Plants can no longer grow on these soils and agriculture has to be abandoned. Salination has happened on a large scale in much of the former cotton fields of Uzbekistan. Are There Environmentally Friendly Alternatives? To grow environmentally friendlier cotton, a first step must be to reduce the use of dangerous  pesticides. This can be achieved through different means. Integrated Pest Management (IPM) is an established, effective method of fighting pests which results in a net reduction in pesticides used. According to the World Wildlife Fund, using IPM saved some of India’s cotton farmers 60 to 80% in pesticide use.  Genetically-modified cotton can also help reduce pesticide application, but with many caveats.   In its simplest form growing cotton in a  sustainable manner  means planting it where rainfall is sufficient, avoiding irrigation altogether. In areas with marginal irrigation needs, drip irrigation offers important water savings. Organic farming takes into consideration all aspects of cotton production, leading to much reduced environmental impacts and better health outcomes for the farm workers and the surrounding community.  A well-recognized organic certification program helps consumers making smart choices, and protects them from greenwashing. One such third-party certification organization is  the Global Organic Textile Standards. Sources World Wildlife Fund. 2013. Cleaner, Greener Cotton: Impacts and Better Management Practices.

Radio Shack Strategic Management Research Paper

Radio Shack Strategic Management - Research Paper Example RadioShack is primarily focused on the US market where as at the end of 2011 it employed 34,000 people, and owned and operated 4,476 stores under its brand and an additional 1,496 stores under the Target Mobile centers brand. RadioShack’s products and services are categorized into four platforms: mobility, signature, consumer electronics and other sales. The mobility platform consists of prepaid and postpaid wireless handsets, commissions and residual income, tablets and e-readers. The signature platform includes home entertainment, wireless, computer, and music accessories; general purpose and special purpose power products; headphones; technical products; and services (RadioShack 3). The consumer electronics platform includes personal computing products, laptop computers, digital music players, residential telephones, GPS devices, cameras, digital televisions, and other consumer electronics products (RadioShack 3). Other sales include sales generated by the Target Mobile centers, sales to independent dealers, sales generated by RadioShack’s Mexican subsidiary, sales from www.radioshack.com website and sales to other third parties through the company’s global sourcing operations (Rad ioShack 22). The contribution of each of these product platforms in 2011 is displayed in Figure 1 below. In 2011, RadioShack net sales increased by 2.6%, to $4,378 million over its 2010 revenues. However, the company’s gross margin went down by 3.5% to 41.4% within the same period. This was largely attributed to change in the company’s sales mix within its largest product platform, the mobility platform, towards lower margin smartphones and tablets (RadioShack 20). The company has sound financial strength depicted by its quick ratio of 1.61 and current ratio of 2.73. Figure 1: RadioShack Product Platforms (RadioShack Corp 1) 2.0. Strategic issues There are two major strategic management problems facing RadioShack Corporation: merchandise mix and growth strategy. To begin with, RadioShack established its mobility platform as the more attractive unit and has continued to steer corporate resources towards it. Figure 1 above, shows mobility devices accounted for 51.4% of the company’s net sales in 2011, up from 46.1% in 2010 and 35.3% in 2009 (RadioShack 22). Howev er, the high competitive rivalry in the retail consumer mobility industry, short product cycles, and its much lower margins has made the company vulnerable to weak consumer spending. For this reason, on March 2, 2012, Standard & Poor's Ratings Services lowered its corporate credit and senior unsecured debt ratings on RadioShack to ‘B+’ from ‘BB-’, with outlook also moved from stable to negative (FitzGerald Para 2). This downgrade lowers investor and creditor confidence on the organization. Ultimately, the lowered rating may affect RadioShack’s ability to raise financial capital for any major investments that it may seek in future. RadioShack’s senior management

Marketing research goals Essay Example | Topics and Well Written Essays - 1000 words

Marketing research goals - Essay Example Apart from this marketing research also is important for an organization as it gives them directions for future planning. Its like if marketing is an engine that drives a country's economy than marketing research is the process that keeps the engine tuned. Marketing Research's wide range of uses can measure the importance of it. For example it helps in making new and improved products and enables an organization to have a more convenient delivery of products and services. Well marketing research results can be both correct and incorrect, same is for the viewpoints of the senior management. The major reason for following either one of the options, which is following the marketing research conclusion or the viewpoints of senior management, depends on how much a person knows about the marketing research. If a person is sure that there has been no mistakes or errors throughout the marketing research then he can be sure of following the conclusions based on the marketing research but its not necessary that the results come out to be positive. It's vice versa if u follow the viewpoints of the senior management. Rather than offering the same marketing mix to different customers, organizations plan out market segmentation. Market segmentation helps firms to tailor marketing mix for specific target markets, hence better satisfying customer needs. Not all elements of the marketing mix are changed from one segment to another. For example in some cases only the promotional campaigns would change. A niche is a further division of a segment. Thus, the difference between a segment and a niche is that between segments substitution is negligible, while a large part of the customers in a segment will allow substitution between niche products. Niche products are aimed at a smaller group of consumers within a segment, for whom specific product properties are obligatory, while the same properties were only positioning properties in the broader market segment. We can have a market segment of one individual but in business markets not in consumer markets. There is a major reason for it. The reason is that in business markets an organization can have only one consumer. This is due to the high priced machinery transactions that take place in the business markets. Apart from that, organizations do want many customers to cater to but they can have a single customer as well and can be specialized producer for a single buyer as they are still making profits in doing so. Ans.3 There are basically two types of sellers in any international market. These two types rely on the two basic terms that a buyer uses to distinguish the products. These two factors are price and quality. Some seller might be giving a good price but not good quality and vice versa. Sellers can be buyers there is no doubt about it. There is no country that is completely self sufficient in producing every single good or commodity that is required by the people living in it, hence keeping this fact in the mind a seller can be a buyer is proved easily. The challenges in regard

Use of HPV Vaccines for Cervical Cancer Prevention

Use of HPV Vaccines for Cervical Cancer Prevention HPV Vaccines: Will They Prevent Cervical cancer Introduction Human papilloma viruses (HPV) belong to the papillomaviridae family, they are double stranded DNA viruses. HPV is the most common sexually transmitted infection (STI) in the world (Urman et al. 2008). HPV is strongly associated with cervical cancer; more than 99% what are the other causes/factors please of cervical cancer cases are positive for HPV DNA and indeed, cervical cancer is the second most common malignancy in the world (Wang et al. 2007). In developed countries the incidence of cervical cancer has been reduced significantly by the introduction of a cervical screening programme. In developing countries where 83% of mortalities due to cervical cancer occur, there are no such programmes (Parkin et al. 2006). Can the introduction of a vaccine against HPV further reduce globally the incidence of cervical cancer? Many diseases caused by viruses are controlled in the developed world by ongoing successful vaccination programmes; Polio, Measles, Mumps and Rubella are a few examples. Smallpox caused by Variola virus was eradicated in 1979 through a successful worldwide vaccination programme. The factors that affect the Polio and MMR vaccine programmes success and those that affected the successful smallpox programme may also be contributory to the success of the HPV vaccination program. Vaccination of HPV is complex and multi factorial. This investigation studies a number of factors including: Vaccine efficacy Vaccine Cost/affordability/practicality of administration Production and Distribution Government backing and financial commitment Other support organisations such as the WHO, UNICEF, Gates Foundation, Social factors Media effects Public awareness Safety, and perceived fears Currently two prophylactic vaccines against HPV types 16 and 18, the most prevalent causes of HPV have been approved by the food and drug administration (FDA). Many developed countries have already introduced vaccination programmes using one of these vaccines. Can the vaccines and programme prevent cervical cancer? In order to effectively understand the implication of such a vaccination programme we must first fully examine the causative agent (HPV) and the consequential potential diseases including the biology, history and prevalence. Human Papillomavirus Approximately 200 types of HPV are identified of which around 40 infect the genital tract (McCance 2004). The majority of HPV types cause no symptoms, some types can cause warts and a minority may lead to cancer. Genital HPVs are transmitted via sexual contact, mainly intercourse, with an infected individual, and the risk of developing an HPV infection generally increases with the number of sexual partners, the sexual history of that partner or the introduction of a new sexual partner. Studies have shown that at least one type of HPV infection occurs soon after sexual debut, with around 30% of women infected with at least one high risk type within two years (Winer et al 2003; Winer et al 2008). HPVs are classified as either high risk or low risk, on the basis of association with cervical cancer. There are 15 types classified as high risk and three as probable high risk. High risk types include 16,18,31,33,35,39,,45,51,52,56,58,59,68,73,probable high risk types include 26,53,66 Low risk types include 6,11,40,42,43,54,61,70,72,81 and CP6108. More than 99% of cervical cancers are associated with HPV, of these 70% are associated with HPV type 16 and 18, with HPV 16 causing 50% and HPV 18 causing more than 15% in Europe (Smith et al..2007). HPV 16 is thus the single, most common high risk HPV. Interestingly HPV types 16 and 18 also cause 80% of anal cancer and 30% of vaginal and why the difference in % oper area research needed here.vulvar cancer and are associated with cancers of the, oropharynx and some rare cancers of the head and neck. (add reference form cervical cancer burden worldwide paper) The majority of HPV infections are asymptomatic, self limiting, and transient, with 70% of new HPV high risk type infections cleared within one year (with the median duration of an infection at 8 months) and 90% within two years (Ho et al 1998). The transient infection usually causes no clinical problems. A small proportion of high risk type infections persist due to host immune evasion, an evasion that results not only from restriction of HPVs to sites that are relatively inaccessible to host defences but also due to several mechanisms of preventing immune response what are these mechanisms please (a sk Dick if this is what he means . This persistence is the most important factor in the development of pre cancerous and cancerous lesions. The time span between infection by HPV and the development of pre cancerous lesions or cervical carcinoma varies from one to ten years (Moscicki et al 2006) and up to 20 years from other sources. HPV show little evidence of dramatic adaptability with phylogenic studies suggesting that the biology of HPVs has remained the same for over 200,000 years (Halpren et al 2000). While HPVs show historically the influence of point mutations, inserts, deletions and duplications, the predominant pattern of mutation within a given type is point mutation, with large scale rearrangements within the most conserved genes of HPVs such as L1 being rare (Myers et al 1996). Intra patient variation within HPV types is uncommon due to their low mutation rate. This low mutation rate is directly linked to the HPV replication strategy that requires host cell machinery, which has stringent proof reading mechanisms that avoid the incorporation of errors, conferring slow mutagenesis. All HPVs exhibit extreme specificity for infection of epithelial cells and do not infect or express their gene products in the underlying dermis. Although the mechanism of infection is not fully understood, the HPV epitheliotrophy resides for the most part in the interaction of specific transcription factors with the viral regulatory region known as the long control region (LCR). Infection with HPV can result in hyperproliferation of the host cell, and with certain high risk HPV types it may lead to transformation and immortalization. This is because high risk HPVs express two or more protein products (E6, E7 and E5) that transiently disrupt the cell cycle and stimulate cell division, knocking out at the same time the cellular mechanisms for growth inhibition. For a productive infection, HPVs require terminally differentiated cells. This HPV biology feature has impeded studies on the full reproduction life cycle because of the lack of highly efficient models of epithelial terminal di fferentiation in vitro. Most of the different stages in the HPV life cycle have been established using genetic engineering and molecular biology strategies. The dsDNA of HPV exists in a non enveloped icosahedral shaped virion 52-55 nm in diameter. The dsDNA genome is circularised and around 8000base pairs in length (Fig1). The genome encodes eight proteins, six early E1, E2, E4, E5, E6, E7, and two late structural proteins L1 and L2 and the previously mentioned noncoding LCR. Fig 1 HPV type 16 Genome structure, gene and functional domain location http://www.dnachip-link.com/Eng/library/HPV.aspusg 15/11/20009 Fig 1 shows the dsDNA genome of HPV type 16, and the location of the early and late genes along with the LCR that contains the origin of replication. An initial infection requires the access of infectious particles to the basal layer of the epithelium. Some HPVs require a break in the stratified epithelium to achieve this. Such breaks are not necessarily obvious and may occur under conditions where the skin is exposed to water or abraded, or subjected to an environment where micro traumas may occur such as possibly in aswiming pool or ect (must put an example)(in fig 2 shows as a cut). Following infection and uncoating it is thought that the virus maintains its genome as an episome in low copy numbers within basal cells of the epithelium. Although the pattern of gene expression in these cells is not well understood, it is generally thought that viral proteins E1 and E2 are expressed to maintain the viral DNA episome (Wilson et al.2002) and possibly to facilitate the segregation of genomes during cell division (You et all.2004). It is not known whether viral transformation proteins E6 and E7 are also expressed in the basal layer, but it does appear that initial infection is followed by a proliferative phase that results in the increase in the number of basal cells harbouring viral episomes. In normal uninfected epithelium, basal cells leave the cell cycle soon after migration into the superbasal cell layers where they undergo a process of terminal differentiation. During infection E6 and E7 are expressed in these cells stopping normal differentiation (Sherman et all.1997). E6 and E7 are believed to work together to achieve this and in lesions caused by high risk HPV types. During a natural infection the ability of E7 to stimulate S-phase progression is limited to a subset of differentiated cells with low levels of p21/p27, or which express high enough levels of E7 to overcome the block in S-phase entry. The viral E6 protein is thought to prevent apoptosis in response to unscheduled S-phase entry brought on by E7. The association of E6 with p53 and the inactivation of p53 mediated growth suppression and apoptosis is well documented, E6 may also associate with other pro-apoptotic proteins including bak (Thomas and Banks,1998) and bax (Li and Dou,2000). E6 is thus considered a predisposing factor in the development of HPV associated cancers, allowing the accumulation of chance errors in host DNA to go unchecked. Furthermore the E6 protein of high risk HPVs can stimulate cell proliferation independently of E7 via a c-terminal PDZ ligand binding domain. E6 PDZ is enough to mediate superbasal cell proliferation and may contribute to the formation of metastatic tumours by disrupting normal cell adhesion (Nguyen et al.2003) Amplification of the viral genome and the ability to package these genomes into infectious particles is essential for the production of infectious virions. For most HPV types this occurs in the mid or upper epithelial layers following an increase in activity of the late promoter. The late promoter gene is located within the E7 open reading frame, and the upregulation of the late promoter is thought to lead to increased expression of proteins involved in viral DNA replication, without directly affecting the expression of E6 or E7 necessary for S-phase entry. The amplification of the viral genome begins in a subset of cells in the proliferative compartment and requires the expression of all viral early gene products, these include E4 and E5 whose role in replication is not yet clearly understood. Binding of E2 to the HPV upstream regulator region is essential for viral DNA replication that is dependent on the differentiated state of epithelial cells. E2 recruits the E1 DNA helicase to the viral origin of replication. Throughout the virus life cycle, the relative levels of viral proteins are controlled by promoter usage and by differential splice site selection, with an increase in E1 and E2 allowing an increase in viral copy numbers in the upper epithelial layers. Current models suggest that a small increase in promoter activation during differentiation may lead to an increase in the level of E1 and E2 and a subsequent increase in genome copy number. The newly replicated genome could then serve as a further template for expression of E1 and E2, facilitating the amplification of viral genome and in turn further expression of E1 and E2 replication proteins. Viral DNA remains latent (not integrated) in basal cells of benign lesions. Replication occurs in the differentiating cells where capsid proteins and viral particles are found. Viral DNA is integrated in cancer cells, which contain no replicating virus. Once viral genome replication is completed, the expression of two virally encoded structural proteins, expressed in the upper layers of infected epithelia may occur. L1 the major capsid protein is expressed after L2 in a sub set of cells that express E4 (fig 2), this allows the assembly of infectious particles in the upper layers of the epithelium (Florin et al.,2002). A successful infection requires the virus to escape from the infected skin cell and survive extracellularly prior to re-infection. HPVs are non-lytic and are as such not released until the infected cells reach the epithelial surface. The intracellular retention of HPV antigen until the cell reaches the uppermost epithelial layers may contribute the compromised immune detection, especially as the virus has molecular mechanisms that limit the presentation of viral epitopes to the immune system in the lower epithelial layers (Ashrafi et al 2002). What are these mechanisms Figure 2 Papillomavirus type 16 Life Cycle and gene expression location within epithelium Taken from, The papillomavirus life cycle by John Doorbar published in the journal of clinical virology 32S (2005) S7-S15 Figure 2 diagrammatic representation of the skin with HPV type 16 gene expression incorporated, colour of arrows are representative of genes expressed within epithelial cells. The frequent detection of high risk HPV DNA in cervical lesions in the absence of any obvious disease, may be explained by the presence of the virus in a latent state, with only very few cells able to support the productive virus life cycle during epithelial cell differentiation. Following immune regression, HPV DNA is thought to remain in the basal epithelial cells waiting to be reactivated once levels of immune surveillance decline there are conflicting opinions (Zhang et al.1999). If regression is not achieved lesions may persist and in some instances progress to cancer. The number of lesion that progress to cancer is very low when compared to the prevalence of high risk HPV infection in the general public. The Progression of productive lesion to high grade lesions may result from the deregulation ( what happen to allow thes proteins to be deregulated intergrattion loss of E2 adn p53 association, be specific add biochemistry here please. in the expression of transforming proteins E6 and E7. The inability of a cell to support the whole virus life cycle is often associated with the development of cancerous lesions. The transformation zone (Fig 3) is particularly susceptible to cervical cancer; it appears that high risk types of HPV such as type 16 cannot complete their life cycle at this site Progression from CIN3 to cancer usually occurs in lesions that contain integrated copies of the viral genome in which E7 expression is elevated. Suggesting that retention of E6 and E7genes and the loss of E2 and E4 genes (that exert negative effect on cell growth) usually accompanies the development of invasive cancer. (reference) Remember for CIN refer to in that section or here but Cin must be corrulated with what causes the cancer and with whats happening with the virus that causes the change in CIN or the causes in CIN to occur. Cervical cancerisa considerable contributor to morbidity and mortality. Being the second most common cancer worldwide and the twelfth most common cancer in women in the UK. Cervical cancer in 2002 was the cause of 274,000 deaths worldwide (the most current data available)REF THIS FIGURE and continues to causes more than 1000 deaths in the UK each year. There are two main types of cervical cancer squamous cell cancer (the most common) and adenocarcinoma, although they are often mixed. They are named after the types of cell that become cancerous through neoplasia. Squamous cells are flat cells covering the cervix; adenomatous cells are found in the passageway from the cervix to the womb. Other rarer cancers of the cervix include small cell cancer. Deaths from cervical cancer in the UK have fallen over the last 20 years mainly because of the NHS cervical screening programme that reduced the mortality rates by 62% between 1987-2006. Screening may detect changes in the cells of the cervix at a pre-cancerous stage. Fig 3 TITTLE Showing location of transformation zone. Cell samples are examined for abnormalities, these abnormality are described in a standard format covering cytology and/or histology. What are these standard format CIN 1 CIN2 CIN3 LISL LGSIL HSIL HGSIL USE FIG 4 and explain whats happening with the proteins expressed and genome intergration where CIN number progression is concerned please. MUST DO From Lowy Schiller, J Clin Invest, 116:1167-73, 2006 Low grade squamous intraepithelial lesion (LSIL or LGSIL) indicates possiblecone biopsy, or laser ablation. High grade squamous intraepithelial lesion (HSIL or HGSIL) indicates moderate or severeCIN 2 or CIN3 (fig 3). While cervical screening has reduced the mortality significantly in the developed world cervical cancer is still a significant burden worldwide. Fig 4 Taken from, The popillomavirus life cycle by John Doorbar published in the journal of clinical virology 32S (2005) S7-S15 Fig. 5. CIN 1 resembles productive infections caused by other HPV types and as such is the most benign form of cervical intraepithelial neoplasia , it is confined to the basal 1/3 of the epithelium, CIN 2 Moderate dysplasia confined to the basal 2/3 of the epithelium,CIN3 Sever dysplasia that spans more than 2/3 of the epithelium, and may involve the full thickness. INCIDENCE An estimated 493,000 new cases and 274,000 deaths in 2002 were caused by cervical cancer. The vast majority, some 83% of these cases, occur in developing countries, where cervical cancer amounts to 15% of female cancers with a risk before age 65 of 1.5%. In developed countries cervical cancer accounts for only 3.6%, with a risk of 0.8% before age 65. REF The highest incidence rates are observed in Sub-Saharan Africa, Melanesia, Latin America and the Caribbean, South-Central Asia, and South East Asia (fig 6) Fig 6 Worldwide Burden of HPV related Cervical Cancer Figures from 2002. Parkin MD et al 2006 The burden of HPV-related cervical cancers The vast majority of cervical cancers are squamous cell carcinoma adenocarcinomas being less common (fig 6). Generally the proportion of adenocarcinoma cases is higher in areas with low incidence of cervical cancer, accounting for up to 25% of cases in western countries (fig 6). This higher incidence of adenocarcinoma may be partially explained by cytological screening, which historically, had little effect in reducing the risk of adenocarcinoma of the cervix, because these cancers, and their precursors, occur within the cervical canal, and were not readily sampled by scraping of the epithelium of the ectocervix. Fig 5 Fig 5 showing the higher % of adenocarcinoma in counties that have screening programmes such as the UK and Denmark What is this showing? Make it clear.do you really need it. MORTALITY RATES Mortality rates are substantially lower than incidence rates. Worldwide 55% (could you double chek that this is the case please misses) of all those that develop the disease die, the figures vary significantly from the developed to the developing world. Low risk regions of the west such as Europe have a death rate of 37% while in developing countries where many cases present at relatively advanced stages, death rates are significantly higher increasing to 70%. Cervical screening programmes in the developed world identify pre-cancerous lesions at a stage where they can be easily treated accounting for the difference in mortality rates. TITTLE IF and figure number staying and refer to in text As cervical cancer affects a relatively high number of young women, it is a significant cause of years of life lost (YLL) in the developing world. Yang et al 2004 found that cervical cancer was responsible for the 2.7 million (age weighted) years of lives lost world wide in 2000, and that it is the single biggest cause of years of life lost from cancer in the developing world. In Latin America, Eastern Europe and the Caribbean, cervical cancer makes a greater contribution to YLL than disease such as Tuberculosis or AIDS. HPV is also associated with many other forms of cancer that could possibly be prevented with use of HPV vaccines; cancers of the penis, anus, vulva, vagina, oropharynx and some rare cancers of the head and neck are included. However cancer of the cervix is by far the most significant, in terms of incidence and mortality (table 1). Cancer of the vulva and vagina have a significantly lower incidence rate compared to cervical cancer, however since 80% of the incidence are caused by HPV types 16 or 18 women vaccinated against these types would also be protected against these forms of cancer. Incidence of squamous cell carcinoma of the anus are twice as common in females as males with HPV types 16 and 18 accounting for 83% of all cases. There is a particularly high incidence of anal cancer among homosexual males, shown by the high incidence rate in populations such as Sanfransisco, where gay incidence are higher than average (fig 7). Globally cancer of the penis is relatively rare accounting for 0.5% of cancers in men (table 1). HPV DNA is detectable in 40-50% of all penile cancers and serological studies have confirmed the role of HPV 16 and 18 (IARC 2005). Cancers of the mouth and oropharynx caused by HPV are very low at 0.06% of all cancers with 0.05% being caused by HPV types 16/18. Due to the small size of most studies and the absence of comparable measurements of prevalence of infection in normal subjects conducted for cancers of the vulva, vagina, penis and anus true prevalence is difficult to quantify. The figures shown in table 1, imply that we are dealing with a virus that discriminates primarily through disease aginst women, in particular young women. Gay men, however are also clearly an at risk group. Currently only young women are vaccinated aginst HPV types 16 and 18, however the JCVI (joint committee on vaccination and immunisation) have noted that the vaccines has not been conclusively trialled on men, and that there is insufficient evidence that the vaccine available would protect against anal, penile or head and neck cancer. However when more data becomes available they will consider vaccinating, high risk groups such as men who have sex with men. Add what this implies for prophylactic use of vaccine with other cancers cause by HPV And what you think about the ue of vaccine on highrisk men and its effectivity against other cancers caused by HPV types 16 and 18. Fig 7 TITTLE add Figure 6 showing that cancer of the anus are more prevalent in women than men with the major noted exception being San Francisco, where the increased incidence can be explained by a large number of homosexual men. Table 3 VACCINATION An effective vaccine should stimulate a suitable range of immune responses, mimic or improve on the protection gained from a wild type infection with little side effects. Critically the vaccine should be inexpensive, easily administered, transported and stored to further reduce cost and maximise convenience, this is especially relevant in the case of HPV vaccine as those that are not protected by the screening programmes of the developed world would benefit the most, ease of administration and storage is paramount in the developing world as stability and healthcare is more sporadic, and people are often more remote. There are many different kinds of vaccines available, and different vaccines have a variety qualities and limitations. Live attenuated vaccines contain a version of the pathogenic microbe that is avirulent, they often elicit an excellent cellular and antibody response with good longevity that can be lifelong with few doses. However there is always the possibility that the vaccine may revert to its virulent form, causing disease. For this reason a live attenuated vaccine is not appropriate for use against oncogenic HPV types. Recombinant vaccines can include one or more proteins that may illicit an immune response. A process has been developed to allow the removal of the genome from an attenuated or avirulent viral vector allowing the insertion of selected genetic material or proteins from another virus. The carrier viruses then ferry that viral DNA into host cells where the genes are expressed. Recombinant vaccines closely mimic a natural infection and therefore illicit a strong immune system. Inactivated vaccines are produced by killing the disease causing microbe by chemical (formaldehyde eg just double check), heat or radioactive means. These vaccines are more stable than live vaccines, and as there is no risk of reversion to virulence. They are also safer than live vaccines. Most inactivated vaccines stimulate a weaker immune response than live vaccines and several doses or boosters may be required to maintain immunity. DNA vaccines dispense with both the whole organism and its parts. They only include the essential part of the microbes genetic material. In particular, DNA vaccines use the genes that code for immunogens. Researchers have found that when the genes for a microbes antigens are introduced into the body, some cells will take up that DNA. The DNA then instructs those cells to make the antigen molecules. The cells secrete the antigens and display them on their surfaces. In other words, the bodys own cells become vaccine-making factories, creating the antigens necessary to stimulate the immune system. A DNA vaccine against a microbe would evoke a strong antibody response to the free antigen secreted by cells, and also stimulate a strong cellular response against the microbial antigens displayed on cell surfaces. The DNA vaccine is unable to cause disease Use of HPV Vaccines for Cervical Cancer Prevention Use of HPV Vaccines for Cervical Cancer Prevention HPV Vaccines: Will They Prevent Cervical cancer Introduction Human papilloma viruses (HPV) belong to the papillomaviridae family, they are double stranded DNA viruses. HPV is the most common sexually transmitted infection (STI) in the world (Urman et al. 2008). HPV is strongly associated with cervical cancer; more than 99% what are the other causes/factors please of cervical cancer cases are positive for HPV DNA and indeed, cervical cancer is the second most common malignancy in the world (Wang et al. 2007). In developed countries the incidence of cervical cancer has been reduced significantly by the introduction of a cervical screening programme. In developing countries where 83% of mortalities due to cervical cancer occur, there are no such programmes (Parkin et al. 2006). Can the introduction of a vaccine against HPV further reduce globally the incidence of cervical cancer? Many diseases caused by viruses are controlled in the developed world by ongoing successful vaccination programmes; Polio, Measles, Mumps and Rubella are a few examples. Smallpox caused by Variola virus was eradicated in 1979 through a successful worldwide vaccination programme. The factors that affect the Polio and MMR vaccine programmes success and those that affected the successful smallpox programme may also be contributory to the success of the HPV vaccination program. Vaccination of HPV is complex and multi factorial. This investigation studies a number of factors including: Vaccine efficacy Vaccine Cost/affordability/practicality of administration Production and Distribution Government backing and financial commitment Other support organisations such as the WHO, UNICEF, Gates Foundation, Social factors Media effects Public awareness Safety, and perceived fears Currently two prophylactic vaccines against HPV types 16 and 18, the most prevalent causes of HPV have been approved by the food and drug administration (FDA). Many developed countries have already introduced vaccination programmes using one of these vaccines. Can the vaccines and programme prevent cervical cancer? In order to effectively understand the implication of such a vaccination programme we must first fully examine the causative agent (HPV) and the consequential potential diseases including the biology, history and prevalence. Human Papillomavirus Approximately 200 types of HPV are identified of which around 40 infect the genital tract (McCance 2004). The majority of HPV types cause no symptoms, some types can cause warts and a minority may lead to cancer. Genital HPVs are transmitted via sexual contact, mainly intercourse, with an infected individual, and the risk of developing an HPV infection generally increases with the number of sexual partners, the sexual history of that partner or the introduction of a new sexual partner. Studies have shown that at least one type of HPV infection occurs soon after sexual debut, with around 30% of women infected with at least one high risk type within two years (Winer et al 2003; Winer et al 2008). HPVs are classified as either high risk or low risk, on the basis of association with cervical cancer. There are 15 types classified as high risk and three as probable high risk. High risk types include 16,18,31,33,35,39,,45,51,52,56,58,59,68,73,probable high risk types include 26,53,66 Low risk types include 6,11,40,42,43,54,61,70,72,81 and CP6108. More than 99% of cervical cancers are associated with HPV, of these 70% are associated with HPV type 16 and 18, with HPV 16 causing 50% and HPV 18 causing more than 15% in Europe (Smith et al..2007). HPV 16 is thus the single, most common high risk HPV. Interestingly HPV types 16 and 18 also cause 80% of anal cancer and 30% of vaginal and why the difference in % oper area research needed here.vulvar cancer and are associated with cancers of the, oropharynx and some rare cancers of the head and neck. (add reference form cervical cancer burden worldwide paper) The majority of HPV infections are asymptomatic, self limiting, and transient, with 70% of new HPV high risk type infections cleared within one year (with the median duration of an infection at 8 months) and 90% within two years (Ho et al 1998). The transient infection usually causes no clinical problems. A small proportion of high risk type infections persist due to host immune evasion, an evasion that results not only from restriction of HPVs to sites that are relatively inaccessible to host defences but also due to several mechanisms of preventing immune response what are these mechanisms please (a sk Dick if this is what he means . This persistence is the most important factor in the development of pre cancerous and cancerous lesions. The time span between infection by HPV and the development of pre cancerous lesions or cervical carcinoma varies from one to ten years (Moscicki et al 2006) and up to 20 years from other sources. HPV show little evidence of dramatic adaptability with phylogenic studies suggesting that the biology of HPVs has remained the same for over 200,000 years (Halpren et al 2000). While HPVs show historically the influence of point mutations, inserts, deletions and duplications, the predominant pattern of mutation within a given type is point mutation, with large scale rearrangements within the most conserved genes of HPVs such as L1 being rare (Myers et al 1996). Intra patient variation within HPV types is uncommon due to their low mutation rate. This low mutation rate is directly linked to the HPV replication strategy that requires host cell machinery, which has stringent proof reading mechanisms that avoid the incorporation of errors, conferring slow mutagenesis. All HPVs exhibit extreme specificity for infection of epithelial cells and do not infect or express their gene products in the underlying dermis. Although the mechanism of infection is not fully understood, the HPV epitheliotrophy resides for the most part in the interaction of specific transcription factors with the viral regulatory region known as the long control region (LCR). Infection with HPV can result in hyperproliferation of the host cell, and with certain high risk HPV types it may lead to transformation and immortalization. This is because high risk HPVs express two or more protein products (E6, E7 and E5) that transiently disrupt the cell cycle and stimulate cell division, knocking out at the same time the cellular mechanisms for growth inhibition. For a productive infection, HPVs require terminally differentiated cells. This HPV biology feature has impeded studies on the full reproduction life cycle because of the lack of highly efficient models of epithelial terminal di fferentiation in vitro. Most of the different stages in the HPV life cycle have been established using genetic engineering and molecular biology strategies. The dsDNA of HPV exists in a non enveloped icosahedral shaped virion 52-55 nm in diameter. The dsDNA genome is circularised and around 8000base pairs in length (Fig1). The genome encodes eight proteins, six early E1, E2, E4, E5, E6, E7, and two late structural proteins L1 and L2 and the previously mentioned noncoding LCR. Fig 1 HPV type 16 Genome structure, gene and functional domain location http://www.dnachip-link.com/Eng/library/HPV.aspusg 15/11/20009 Fig 1 shows the dsDNA genome of HPV type 16, and the location of the early and late genes along with the LCR that contains the origin of replication. An initial infection requires the access of infectious particles to the basal layer of the epithelium. Some HPVs require a break in the stratified epithelium to achieve this. Such breaks are not necessarily obvious and may occur under conditions where the skin is exposed to water or abraded, or subjected to an environment where micro traumas may occur such as possibly in aswiming pool or ect (must put an example)(in fig 2 shows as a cut). Following infection and uncoating it is thought that the virus maintains its genome as an episome in low copy numbers within basal cells of the epithelium. Although the pattern of gene expression in these cells is not well understood, it is generally thought that viral proteins E1 and E2 are expressed to maintain the viral DNA episome (Wilson et al.2002) and possibly to facilitate the segregation of genomes during cell division (You et all.2004). It is not known whether viral transformation proteins E6 and E7 are also expressed in the basal layer, but it does appear that initial infection is followed by a proliferative phase that results in the increase in the number of basal cells harbouring viral episomes. In normal uninfected epithelium, basal cells leave the cell cycle soon after migration into the superbasal cell layers where they undergo a process of terminal differentiation. During infection E6 and E7 are expressed in these cells stopping normal differentiation (Sherman et all.1997). E6 and E7 are believed to work together to achieve this and in lesions caused by high risk HPV types. During a natural infection the ability of E7 to stimulate S-phase progression is limited to a subset of differentiated cells with low levels of p21/p27, or which express high enough levels of E7 to overcome the block in S-phase entry. The viral E6 protein is thought to prevent apoptosis in response to unscheduled S-phase entry brought on by E7. The association of E6 with p53 and the inactivation of p53 mediated growth suppression and apoptosis is well documented, E6 may also associate with other pro-apoptotic proteins including bak (Thomas and Banks,1998) and bax (Li and Dou,2000). E6 is thus considered a predisposing factor in the development of HPV associated cancers, allowing the accumulation of chance errors in host DNA to go unchecked. Furthermore the E6 protein of high risk HPVs can stimulate cell proliferation independently of E7 via a c-terminal PDZ ligand binding domain. E6 PDZ is enough to mediate superbasal cell proliferation and may contribute to the formation of metastatic tumours by disrupting normal cell adhesion (Nguyen et al.2003) Amplification of the viral genome and the ability to package these genomes into infectious particles is essential for the production of infectious virions. For most HPV types this occurs in the mid or upper epithelial layers following an increase in activity of the late promoter. The late promoter gene is located within the E7 open reading frame, and the upregulation of the late promoter is thought to lead to increased expression of proteins involved in viral DNA replication, without directly affecting the expression of E6 or E7 necessary for S-phase entry. The amplification of the viral genome begins in a subset of cells in the proliferative compartment and requires the expression of all viral early gene products, these include E4 and E5 whose role in replication is not yet clearly understood. Binding of E2 to the HPV upstream regulator region is essential for viral DNA replication that is dependent on the differentiated state of epithelial cells. E2 recruits the E1 DNA helicase to the viral origin of replication. Throughout the virus life cycle, the relative levels of viral proteins are controlled by promoter usage and by differential splice site selection, with an increase in E1 and E2 allowing an increase in viral copy numbers in the upper epithelial layers. Current models suggest that a small increase in promoter activation during differentiation may lead to an increase in the level of E1 and E2 and a subsequent increase in genome copy number. The newly replicated genome could then serve as a further template for expression of E1 and E2, facilitating the amplification of viral genome and in turn further expression of E1 and E2 replication proteins. Viral DNA remains latent (not integrated) in basal cells of benign lesions. Replication occurs in the differentiating cells where capsid proteins and viral particles are found. Viral DNA is integrated in cancer cells, which contain no replicating virus. Once viral genome replication is completed, the expression of two virally encoded structural proteins, expressed in the upper layers of infected epithelia may occur. L1 the major capsid protein is expressed after L2 in a sub set of cells that express E4 (fig 2), this allows the assembly of infectious particles in the upper layers of the epithelium (Florin et al.,2002). A successful infection requires the virus to escape from the infected skin cell and survive extracellularly prior to re-infection. HPVs are non-lytic and are as such not released until the infected cells reach the epithelial surface. The intracellular retention of HPV antigen until the cell reaches the uppermost epithelial layers may contribute the compromised immune detection, especially as the virus has molecular mechanisms that limit the presentation of viral epitopes to the immune system in the lower epithelial layers (Ashrafi et al 2002). What are these mechanisms Figure 2 Papillomavirus type 16 Life Cycle and gene expression location within epithelium Taken from, The papillomavirus life cycle by John Doorbar published in the journal of clinical virology 32S (2005) S7-S15 Figure 2 diagrammatic representation of the skin with HPV type 16 gene expression incorporated, colour of arrows are representative of genes expressed within epithelial cells. The frequent detection of high risk HPV DNA in cervical lesions in the absence of any obvious disease, may be explained by the presence of the virus in a latent state, with only very few cells able to support the productive virus life cycle during epithelial cell differentiation. Following immune regression, HPV DNA is thought to remain in the basal epithelial cells waiting to be reactivated once levels of immune surveillance decline there are conflicting opinions (Zhang et al.1999). If regression is not achieved lesions may persist and in some instances progress to cancer. The number of lesion that progress to cancer is very low when compared to the prevalence of high risk HPV infection in the general public. The Progression of productive lesion to high grade lesions may result from the deregulation ( what happen to allow thes proteins to be deregulated intergrattion loss of E2 adn p53 association, be specific add biochemistry here please. in the expression of transforming proteins E6 and E7. The inability of a cell to support the whole virus life cycle is often associated with the development of cancerous lesions. The transformation zone (Fig 3) is particularly susceptible to cervical cancer; it appears that high risk types of HPV such as type 16 cannot complete their life cycle at this site Progression from CIN3 to cancer usually occurs in lesions that contain integrated copies of the viral genome in which E7 expression is elevated. Suggesting that retention of E6 and E7genes and the loss of E2 and E4 genes (that exert negative effect on cell growth) usually accompanies the development of invasive cancer. (reference) Remember for CIN refer to in that section or here but Cin must be corrulated with what causes the cancer and with whats happening with the virus that causes the change in CIN or the causes in CIN to occur. Cervical cancerisa considerable contributor to morbidity and mortality. Being the second most common cancer worldwide and the twelfth most common cancer in women in the UK. Cervical cancer in 2002 was the cause of 274,000 deaths worldwide (the most current data available)REF THIS FIGURE and continues to causes more than 1000 deaths in the UK each year. There are two main types of cervical cancer squamous cell cancer (the most common) and adenocarcinoma, although they are often mixed. They are named after the types of cell that become cancerous through neoplasia. Squamous cells are flat cells covering the cervix; adenomatous cells are found in the passageway from the cervix to the womb. Other rarer cancers of the cervix include small cell cancer. Deaths from cervical cancer in the UK have fallen over the last 20 years mainly because of the NHS cervical screening programme that reduced the mortality rates by 62% between 1987-2006. Screening may detect changes in the cells of the cervix at a pre-cancerous stage. Fig 3 TITTLE Showing location of transformation zone. Cell samples are examined for abnormalities, these abnormality are described in a standard format covering cytology and/or histology. What are these standard format CIN 1 CIN2 CIN3 LISL LGSIL HSIL HGSIL USE FIG 4 and explain whats happening with the proteins expressed and genome intergration where CIN number progression is concerned please. MUST DO From Lowy Schiller, J Clin Invest, 116:1167-73, 2006 Low grade squamous intraepithelial lesion (LSIL or LGSIL) indicates possiblecone biopsy, or laser ablation. High grade squamous intraepithelial lesion (HSIL or HGSIL) indicates moderate or severeCIN 2 or CIN3 (fig 3). While cervical screening has reduced the mortality significantly in the developed world cervical cancer is still a significant burden worldwide. Fig 4 Taken from, The popillomavirus life cycle by John Doorbar published in the journal of clinical virology 32S (2005) S7-S15 Fig. 5. CIN 1 resembles productive infections caused by other HPV types and as such is the most benign form of cervical intraepithelial neoplasia , it is confined to the basal 1/3 of the epithelium, CIN 2 Moderate dysplasia confined to the basal 2/3 of the epithelium,CIN3 Sever dysplasia that spans more than 2/3 of the epithelium, and may involve the full thickness. INCIDENCE An estimated 493,000 new cases and 274,000 deaths in 2002 were caused by cervical cancer. The vast majority, some 83% of these cases, occur in developing countries, where cervical cancer amounts to 15% of female cancers with a risk before age 65 of 1.5%. In developed countries cervical cancer accounts for only 3.6%, with a risk of 0.8% before age 65. REF The highest incidence rates are observed in Sub-Saharan Africa, Melanesia, Latin America and the Caribbean, South-Central Asia, and South East Asia (fig 6) Fig 6 Worldwide Burden of HPV related Cervical Cancer Figures from 2002. Parkin MD et al 2006 The burden of HPV-related cervical cancers The vast majority of cervical cancers are squamous cell carcinoma adenocarcinomas being less common (fig 6). Generally the proportion of adenocarcinoma cases is higher in areas with low incidence of cervical cancer, accounting for up to 25% of cases in western countries (fig 6). This higher incidence of adenocarcinoma may be partially explained by cytological screening, which historically, had little effect in reducing the risk of adenocarcinoma of the cervix, because these cancers, and their precursors, occur within the cervical canal, and were not readily sampled by scraping of the epithelium of the ectocervix. Fig 5 Fig 5 showing the higher % of adenocarcinoma in counties that have screening programmes such as the UK and Denmark What is this showing? Make it clear.do you really need it. MORTALITY RATES Mortality rates are substantially lower than incidence rates. Worldwide 55% (could you double chek that this is the case please misses) of all those that develop the disease die, the figures vary significantly from the developed to the developing world. Low risk regions of the west such as Europe have a death rate of 37% while in developing countries where many cases present at relatively advanced stages, death rates are significantly higher increasing to 70%. Cervical screening programmes in the developed world identify pre-cancerous lesions at a stage where they can be easily treated accounting for the difference in mortality rates. TITTLE IF and figure number staying and refer to in text As cervical cancer affects a relatively high number of young women, it is a significant cause of years of life lost (YLL) in the developing world. Yang et al 2004 found that cervical cancer was responsible for the 2.7 million (age weighted) years of lives lost world wide in 2000, and that it is the single biggest cause of years of life lost from cancer in the developing world. In Latin America, Eastern Europe and the Caribbean, cervical cancer makes a greater contribution to YLL than disease such as Tuberculosis or AIDS. HPV is also associated with many other forms of cancer that could possibly be prevented with use of HPV vaccines; cancers of the penis, anus, vulva, vagina, oropharynx and some rare cancers of the head and neck are included. However cancer of the cervix is by far the most significant, in terms of incidence and mortality (table 1). Cancer of the vulva and vagina have a significantly lower incidence rate compared to cervical cancer, however since 80% of the incidence are caused by HPV types 16 or 18 women vaccinated against these types would also be protected against these forms of cancer. Incidence of squamous cell carcinoma of the anus are twice as common in females as males with HPV types 16 and 18 accounting for 83% of all cases. There is a particularly high incidence of anal cancer among homosexual males, shown by the high incidence rate in populations such as Sanfransisco, where gay incidence are higher than average (fig 7). Globally cancer of the penis is relatively rare accounting for 0.5% of cancers in men (table 1). HPV DNA is detectable in 40-50% of all penile cancers and serological studies have confirmed the role of HPV 16 and 18 (IARC 2005). Cancers of the mouth and oropharynx caused by HPV are very low at 0.06% of all cancers with 0.05% being caused by HPV types 16/18. Due to the small size of most studies and the absence of comparable measurements of prevalence of infection in normal subjects conducted for cancers of the vulva, vagina, penis and anus true prevalence is difficult to quantify. The figures shown in table 1, imply that we are dealing with a virus that discriminates primarily through disease aginst women, in particular young women. Gay men, however are also clearly an at risk group. Currently only young women are vaccinated aginst HPV types 16 and 18, however the JCVI (joint committee on vaccination and immunisation) have noted that the vaccines has not been conclusively trialled on men, and that there is insufficient evidence that the vaccine available would protect against anal, penile or head and neck cancer. However when more data becomes available they will consider vaccinating, high risk groups such as men who have sex with men. Add what this implies for prophylactic use of vaccine with other cancers cause by HPV And what you think about the ue of vaccine on highrisk men and its effectivity against other cancers caused by HPV types 16 and 18. Fig 7 TITTLE add Figure 6 showing that cancer of the anus are more prevalent in women than men with the major noted exception being San Francisco, where the increased incidence can be explained by a large number of homosexual men. Table 3 VACCINATION An effective vaccine should stimulate a suitable range of immune responses, mimic or improve on the protection gained from a wild type infection with little side effects. Critically the vaccine should be inexpensive, easily administered, transported and stored to further reduce cost and maximise convenience, this is especially relevant in the case of HPV vaccine as those that are not protected by the screening programmes of the developed world would benefit the most, ease of administration and storage is paramount in the developing world as stability and healthcare is more sporadic, and people are often more remote. There are many different kinds of vaccines available, and different vaccines have a variety qualities and limitations. Live attenuated vaccines contain a version of the pathogenic microbe that is avirulent, they often elicit an excellent cellular and antibody response with good longevity that can be lifelong with few doses. However there is always the possibility that the vaccine may revert to its virulent form, causing disease. For this reason a live attenuated vaccine is not appropriate for use against oncogenic HPV types. Recombinant vaccines can include one or more proteins that may illicit an immune response. A process has been developed to allow the removal of the genome from an attenuated or avirulent viral vector allowing the insertion of selected genetic material or proteins from another virus. The carrier viruses then ferry that viral DNA into host cells where the genes are expressed. Recombinant vaccines closely mimic a natural infection and therefore illicit a strong immune system. Inactivated vaccines are produced by killing the disease causing microbe by chemical (formaldehyde eg just double check), heat or radioactive means. These vaccines are more stable than live vaccines, and as there is no risk of reversion to virulence. They are also safer than live vaccines. Most inactivated vaccines stimulate a weaker immune response than live vaccines and several doses or boosters may be required to maintain immunity. DNA vaccines dispense with both the whole organism and its parts. They only include the essential part of the microbes genetic material. In particular, DNA vaccines use the genes that code for immunogens. Researchers have found that when the genes for a microbes antigens are introduced into the body, some cells will take up that DNA. The DNA then instructs those cells to make the antigen molecules. The cells secrete the antigens and display them on their surfaces. In other words, the bodys own cells become vaccine-making factories, creating the antigens necessary to stimulate the immune system. A DNA vaccine against a microbe would evoke a strong antibody response to the free antigen secreted by cells, and also stimulate a strong cellular response against the microbial antigens displayed on cell surfaces. The DNA vaccine is unable to cause disease

Organizational Systems and Quality Leadership Essay

A. Understanding Nursing Sensitive Indicators Nursing sensitive indicators include the configuration, process and outcomes of nursing care. The configuration of nursing care concludes the nursing staff, their nursing skills, and the level of education that each nurse holds. The process of nursing care concludes the nursing assessments, intervention and implimentation. The outcome of nursing care either positive or negative depends on the quantity and quality of the care provided to the patients by the nursing staff (â€Å"Nursing world,† 2013) Each nurse should hold proper information and knowledge of nursing care such as knowledge of pressure ulcers. In this scenario every nursing personnel should provide the ultimate nursing care in dealing with pressure ulcers. In order to prevent any pressure ulcer each nursing personnel should be aware of the pressure ulcer concept, their prevention and the correct technique of reducing any other complication related to pressure ulcers. In this case the nurse and the CNA should use their knowledge of preventing any pressure ulcer. The first action is to assess completely the patient for any sign of pressure ulcer such as any erythema or bruising. It is essential that the nursing staff know to reposition the patient and reasses the out of sight sites parts of the body for any sign and symptoms of bruising and shearing. Also it is important for nursing staff to know that, the patients with restraint order, are at higher risk of getting pressure ulcer so the nurse is responsible for proper and effective way of using restraints and on the other hand is supposed to know at what time the restrains are not proper to be used. In the nursing sensitive indicator category also it is included,the patient satisfaction, which was missing out in this scenario; due to the fact that the nurse did not consider the patient satisfaction fact, and she dismissed the incorrect diet, which was being so easily delivered for the patient.if the nurse had the patient satisfaction category in her mind, She also would have report the daughter about the increct diet incident, and  also the nurse would also avoid commenting inappropriate words to the daughter. How Hospital Data Could Advance Quality Care In this scenario the hospital in order to advance the quality of care, could have shared the information about the incident with the nursing personnel. The hospital could provide the best quality of care to the patients and achieve the patients’ satisfaction, by sharing the data. Advancing the quality of care would have positive effect on both patient satisfaction and nursing care. Knowledge of nursing care empowers the nursing staff in such cases. In this scenario the knowledge of pressure ulcers, restraints and patient care is significant. On the other hand the nursing care in this scenario could have been better and the family/patient could have been cared better if the nursing staff had gotten the best patient care knowledge. Resources Available Several resources exist in the hospital in order to address the nursing sensitive indicators. In this scenario as a nurse I could partner with dietician in order to address the tray issue and deliver the correct tray to the correct patient. To resolve any misunderstandings I would apologize to the daughter of the patient for the incident. I would speak to the nurse who commented inapprotely to the daughter of the patient. I would discuss the situation and possible solutions with the doctor/nurse in charge. I would educate the CNA the proper information about noticing the signs of any pressure ulcers and proper techniques in avoiding them. I also would ask a wound care consultant to provide proper information to the nursing staff about pressure ulcers. To fully provide the best patient care I also would refer the patient and family to any social worker in dealing with any ethical issue that may interfere in the quality of care. References http://www.nursingquality.org http://www.nursingworld.org/MainMenuCategories/ThePracticeofProfessionalNursing/PatientSafetyQuality/Research-Measurement/The-National-Database/Nursing-Sensitive-Indicators_1 Nursing world. (2013)