Thursday, March 19, 2020

Why You Must Read the Book Hidden Figures

Why You Must Read the Book 'Hidden Figures' Books and movies have a long-standing and complex relationship. When a book becomes a best-seller, there’s an almost inevitable film adaptation in the works almost immediately. Then again, sometimes books that remain under the radar are made into movies, and then become best-sellers. And sometimes a film version of a book sparks a national conversation that the book alone couldn’t quite manage. Such is the case with Margot Lee Shetterly’s book Hidden Figures. The film rights to the book were sold before it even published, and the film was released just three months after the book’s publication last year. And the film has become a sensation, grossing more than $66 million so far and becoming the center of the new conversation on race, sexism, and even the doleful state of the American space program. Starring Taraji P. Henson, Octavia Spencer, Janelle Monae, Kirsten Dunst, Jim Parsons, and Kevin Costner, the film takes a fairly well-worn format- the historical, inspirational true but previously-unknown story- and transcends it by leaving that story fairly unvarnished. It’s also a nearly perfect film for this moment in time, a moment when America is questioning its own identity, its history (and future) in terms of race and gender, and its place as a world leader. In short, Hidden Figures is definitely a movie you want to see. But it’s also a book you must read, even if you’ve seen the movie already and think you know the full story. A Deeper Dive Even though Hidden Figures is more than two hours long, it’s still a movie. That means it inescapably condenses events, elides moments, and deletes or combines characters and moments in order to create a narrative structure and a sense of drama. That’s fine; we all understand that a movie isn’t history. But you’ll never get the full story from a film adaptation. Films can be like the Cliff’s Notes versions of books, giving you a high-altitude overview of a story, but with manipulation and omission of timelines, people, and events. While Hidden Figures the movie might be compelling, enjoyable, and even somewhat educational, you’re missing half the story if you don’t read the book. The White Guy in the Room Speaking of manipulations, let’s talk about Kevin Costner’s character, Al Harrison. The Director of the Space Task Group didn’t actually exist, though of course there was a Director of the Space Task Group. There were several, in fact, during that period of time, and Costner’s character is a composite of three of them, based on the recollections of Katherine G. Johnson herself. Costner’s getting deserved praise for his performance as the white, middle-aged man who isn’t exactly a bad person- he’s just so enmeshed in his white, male privilege and the lack of awareness on racial issues at the time that he doesn’t even notice how oppressed and marginalized the black women in his department are. So there’s no question that the character’s writing and performance are great, and serve the story. The issue is the simple fact that someone in Hollywood knew they needed to have a male star of Costner’s caliber to get the film made and marketed, and that’s why his role is as large as it is, and why he gets a few set-piece speeches (especially the apocryphal destruction of the â€Å"Whites Only† bathroom sign) that make him as much the center of the story as Johnson, Dorothy Vaughan, and Mary Jackson. If all you do is watch the movie, you might think that Al Harrison existed, and was as much a hero as the brilliant female computers that are the true focus of the story. The Reality of Racism Hidden Figures the film is entertainment and as such, it needs villains. There is no doubt that racism was prevalent in the 1960s (as it is today) and that Johnson, Vaughan, and Jackson had to overcome challenges that their white and male colleagues didn’t even know existed. But according to Johnson herself, the film overstates the level of racism she actually experienced. The fact is, while prejudice and segregation were facts, Katherine Johnson says she â€Å"didn’t feel† the segregation at NASA. â€Å"Everybody there was doing research,† she said, â€Å"You had a mission and you worked on it, and it was important to you to do your job...and play bridge at lunch. I didnt feel any segregation. I knew it was there, but I didnt feel it.† Even the infamous bathroom-sprint across the campus was exaggerated; there were, in fact, bathrooms for blacks not nearly as far away- although there were indeed â€Å"white only† and â€Å"black only† facilities, and the black-only bathrooms were harder to find. Jim Parsons’ character, Paul Stafford, is a complete fabrication who serves to embody many of the typical sexist and racist attitudes of the time- but again, doesn’t actually represent anything that Johnson, Jackson, or Vaughan actually experienced. Hollywood needs villains, and so Stafford (as well as Kirsten Dunst’s character Vivian Mitchell) was created to be the oppressive, racist white male of the story, even though Johnson’s recollections of her experience at NASA were largely unremarkable. A Great Book None of this means the story of these women and their work on our space program isn’t well worth your time- it is. Racism and sexism are still problems today, even if we’ve gotten rid of much of the official machinery of it in everyday life. And their story is an inspiring one that languished in obscurity for far too long- even star Octavia Spencer thought the story was made-up when she was first contacted about playing Dorothy Vaughan. Even better, Shetterly has written a great book. Shetterly weaves her own story into the history, making clear the connections between the three women who are the focus of the book and the millions of black women who came after them- women who had a slightly better chance at realizing their dreams in part due to the fight that Vaughan, Johnson, and Jackson took on. And Shetterly writes with a gentle, inspiring tone that celebrates the achievements instead of wallowing in the obstructions. It’s a wonderful reading experience filled with information and incredible background you won’t get from the movie. Further Reading If you want to know a bit more about the role women of all colors played throughout the history of technology in America, try Rise of the Rocket Girls by Nathalia Holt. It tells the fascinating story of the women who worked at the Jet Propulsion Laboratory in the 1940s and 1950s and offers another glimpse at how deeply buried the contributions of the marginalized have been in this country. Source Holt, Nathalia. Rise of the Rocket Girls: The Women Who Propelled Us, from Missiles to the Moon to Mars. Paperback, Reprint edition, Back Bay Books, January 17, 2017. Shetterly, Margot Lee. Hidden Figures: The American Dream and the Untold Story of the Black Women Mathematicians Who Helped Win the Space Race. Paperback, Media Tie In edition, William Morrow Paperbacks, December 6, 2016.

Tuesday, March 3, 2020

Octaves and Decibels

Octaves and Decibels Octaves and Decibels Octaves and Decibels By Maeve Maddox A reader asks: Can you inform on the usage of . . . octave and decible?   I am of the opinion, that octave deals with human voice and decible deals with noise.   Both words, octave and decibel are terms of measurement. Octave derives from the Latin word for â€Å"eight† and decibel incorporates the Latin word for â€Å"ten.† The words can be used in various contexts. I’ll just address the uses suggested by the question. The words bel and decibel are units of measurement of sound intensity. A bel is A unit, equivalent to ten decibels used in the comparison of two levels of power in an electrical communication circuit. A decibel (db) is one tenth of a bel. â€Å"Bel† is a shortening of the name of inventor Alexander Graham Bell (1847-1922). A bel is A unit, equivalent to ten decibels, used in the comparison of two levels of power in an electrical communication circuit. An octave in the musical sense is an interval embracing eight notes of the diatonic scale. Think of the Do-re-me song in Sound of Music. Doe- a deer, a female deer Ray- a drop of golden sun Me- a name i call myself Far- a long long way to run Sew- a needle pulling thread La- a note to follow so Tea- a drink with jam and bread That will bring us back to do oh oh oh The normal speaking range of the human voice is about 20-50 decibels. Sounds that go above that range become annoying, for example a vacuum cleaner (70 db). Noise becomes painful at 120 db. Sounds above 132 db lead to permanent hearing damage and eardrum rupture. In answer to the question, decibel refers to sound, pleasant or unpleasant, whether it originates in the vocal cords or elsewhere. NOTE: Although both the OED and Merriam-Webster give db as the abbreviation for decibel, Ive been informed by a technical writer that the standard abbreviation is dB. Sources: Gale Encyclopedia of Medicine. Mosbys Medical Dictionary, Oxford English Dictionary Online Etymology Dictionary 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 Misused Words category, check our popular posts, or choose a related post below:12 Signs and Symbols You Should KnowHow to Punctuate Descriptions of ColorsWhat Is a Doctor?

Sunday, February 16, 2020

Resume Essay Example | Topics and Well Written Essays - 500 words - 16

Resume - Essay Example A proven capacity for flexibility in creative and innovative management solutions with an ability to balance budgets, labor, and to adapt to the many challenges of managing in a food and beverage business. As a senior project, I worked with a team in order to create the best possible recommendations for an online company that was expanding from selling books into selling resources for entertainment such as movies and music. Through an analysis of the strengths and weaknesses of the company, in connection to the strengths and weaknesses of the competition, a series of business oriented recommendations were made to the company to facilitate growth and expansion in a highly competitive field. In coming to understand the needs of a business that had begun with no solid plan and was not appropriately defining their goals, the project created a better understanding of the advantages and pitfalls that can emerge during business building exercises. Through a focus on consultation with the business, the manners and etiquette used to convince the company of the many ways in which improvements could be made with a benefit realized from those benefits through language that was supportive and resp ectively of the position the company held provided context for how to build strong business relationships while exploring constructive

Sunday, February 2, 2020

Five-page analysis of short story--The Yellow Wall-Paper Essay

Five-page analysis of short story--The Yellow Wall-Paper - Essay Example As she passed time in near isolation, she became determined to free the â€Å"creeping woman† whom she saw in the paper. Although Jane aspired to be a dutiful and obedient wife, she also felt that if she does not develop a sense of autonomy, she would be eternally unhappy. As the male authority figures around her (her husband and brother) saw mental stimulation and her creative work as her enemy and the cause of her problems, the author wanted to point out that suppressing Jane’s creative intelligence and maintaining a dual identity is the root of her nervous depression. A strong narrative in support of this was when Jane frees the symbolic persona within the yellow wallpaper by tearing it down. It was an expression of her liberation from a suppressed creative character. It was apparent early in the story that Jane did not believe in John’s prescription, but she was powerless to protest: â€Å"I sometimes fancy that in my condition if I had less opposition and more society and stimulus†¦ but John says the very worst thing I can do is to think about my condition.† (249). She also intoned sarcasm as she tried to sound agreeable with John’s counsel by saying â€Å"He is very careful and loving, and hardly lets me stir without special direction† (250). For most part, however, we are led to believe that it was her husband whom Jane blames for her illness. â€Å"John is a physician and†¦ perhaps that is the reason I do not get well faster†¦You see he does not believe I am sick! But what can one do?† (249) In pretending to agree with John, she did in effect lie to her husband and to herself – an event that created a schism in her personality. The upshot was that she became her own enemy and in doing so, two characters developed within. The first was the exterior, public Jane; the sweet, obedient, and loving wife, who cared for her husband and a Jane who should be

Saturday, January 25, 2020

Alzheimers Disease: Biology, Etiology and Solutions

Alzheimers Disease: Biology, Etiology and Solutions Introduction Alzheimers disease (AD) is a type of dementia characterized by the progressive loss in cognitive function due to neurodegeneration that results in gradual memory loss and eventually the inability to carry out tasks of daily living. The two types of AD are distinguished by age of onset and etiologies; early-onset AD develops prior to age 65 and has strong genetic associations while late-onset AD develops after age 65 with a more complex etiology. Late-onset AD accounts for 90-95% of AD cases (Harman 2002). Aging is a strong risk factor for developing late-onset AD. Given that the global population of people ages 65 and up is expected to increase from 26.6 million in 2006 to 106.8 million by 2050 (Brookmeyer et al. 2007) AD is a growing public health concern in regards to disease management and development of innovative treatments. The prevalence of AD globally is 4.4%, with 1 in 10 people over age 65 and nearly one-third of people over age 85 affected by dementia in developed countries (Qiu et al. 2009). AD prevalence is the greatest in East Asia, followed by Western Europe, South Asia, and North America (Prince et al. 2015). Disease burden is anticipated to be the greatest in low and middle-income countries with the fastest growth in the elderly population and limited access to care (Prince et al. 2015). By 2050, the U.S. population of adults with AD is projected to increase to 13.2 million. With 43% of AD patients requiring a high level of care, the financial and healthcare burden of AD is expected to rise (Qiu et al. 2009). Given that the burden of AD will increase over the coming decades with costly impacts on health care and social services, it is necessary to continue AD research to identify a cause and develop novel therapies. Etiology Alzheimer’s disease is a multifactorial disease with several genetic, person, and lifestyle risk factors that contribute to development of disease. Although many risk factors for AD have been identified a cause has not yet been found. Of the genetic risk factors identified, apolipoprotein E alleles, with ethnic and sex variability in risk of developing AD, and TREM2 gene mutations have the strongest associations with AD. Lifestyle risk factors include hypertension, obesity, diabetes, and education. The development of AD requires a combination of these risk factors that induce the production of neurotoxic amyloid beta (Aß) and neurofibrillary tangles (NFTs), the agents of AD. Apolipoprotein E (apoE) has been identified as playing a role in AD pathology. ApoE is naturally produced and is involved in lipid transport (Ridge et al. 2013; 2018 Feb 27).   In AD it is thought that apoE regulation of Aß is altered (Kanekiyo et al. 2014). There are three apoE alleles that differ in the risk they confer to AD; the ÃŽ µ2 and ÃŽ µ3 alleles are protective but the ÃŽ µ4 allele increases risk for AD (Ridge et al. 2013). Additionally, it appears that ethnicity modulates the risk of AD conferred by the apoE ÃŽ µ4 allele, conferring greater risk among Caucasians and Japanese than African Americans and Hispanics (Ridge et al., 2013). The apoE ÃŽ µ4 allele is an established risk factor for the development of AD however it is not causative and the risk that carrying this gene confers is likely modulated by other factors such as ethnicity and lifestyle.   Mutations in the TREM2 gene have also been implicated in AD pathology. The TREM2 gene codes for a receptor expressed in myeloid cells, the principal innate immune cell in the brain (Hickman and El Khoury 2014) and in greater abundance in the hippocampus and neocortex, brain structures affected by neurodegeneration in AD (Guerreiro et al. 2013 Jan 9). A rare missense mutation in the TREM2 gene was identified in Islanders that confers significant risk of AD (Jonsson et al. 2013 Jan 9) and a loss of function mutation increases the risk of late-onset AD in heterozygous carriers (Hickman and El Khoury 2014). This loss of function mutation promotes the production of Aß and reduces Aß phagocytosis and degradation (Hickman and El Khoury 2014). In addition to the genetic risk factors discussed above, several lifestyle risk factors for AD have been identified including cardiovascular risk factors and obesity. Cardiovascular risk factors (smoking, hypertension, high cholesterol, and diabetes) in mid-life are associated with a 20-40% increased risk of AD in a dose-dependent fashion (Whitmer et al. 2005). Hypertension that develops in mid-life and persists into late-life is associated with a greater risk of dementia (McGrath et al. 2017). Furthermore, the risk of hypertension for AD in late-life might be influenced by sex, with females having a 65% increased risk of developing dementia if hypertensive in mid-life but no such association among males (Gilsanz et al. 2017). Midlife insulin resistance is also a risk factor for Aß accumulation (Ekblad et al. 2018 Feb 23) and patients with diabetes and the apoE ÃŽ µ4 allele have more Aß plaques and NFTs in the brain (Peila et al. 2002). Obesity is linked to AD via several singl e-nucleotide polymorphisms (Hinney et al. 2014). In people who are obese, leptin and adiponectin lose their neuroprotective role as the brain becomes resistant to leptin and the levels of adiponectin decrease (Letra et al. 2014). Research conducted by Nuzzo et al. (2015) further supports this association, finding that obese mice fed a high-fat diet had elevated Aß accumulation. Addressing these modifiable risk factors in mid-life may help reduce the risk of developing AD in late-life. Higher educational attainment and continued cognitive stimulation in later life are protective against AD. Amieva et al. (2014) found that individuals with AD who had education beyond 6 years of primary school showed delayed cognitive decline before diagnosis compared to individuals with less education. Participating in cognitive leisure activities in late-life, like reading books, newspapers, and magazines, solving crossword puzzles, and attending courses and professional training, has a protective effect as well (Sattler et al. 2012). Higher educational attainment may be associated with reduced risk of AD and delayed cognitive decline if AD develops because of its association with increased hippocampi and amygdalae size. In individuals with AD, the hippocampi are larger in those who had 20 years of formal education compared to those with 6 years (Shpanskaya et al. 2014). The role of education in hippocampal size is further implicated by Tang, Varma, Miller, and Carlson (2017) who f ound that the left hippocampus is larger than the right, possibly due to education honing retrieval of verbal memory by the left hippocampus through increasing intellectual ability and literacy skills.   Biology   Alzheimer’s disease results in the progressive loss of neurons in the cerebrum. The first structures affected are the hippocampi followed by the amygdala (Pini et al. 2016). As the disease progresses so does neuronal loss throughout the cerebrum. In AD, Aß peptides and neurofibrillary tangles (NFTs) formed by tau protein cause synaptic damage that leads to apoptosis. Additionally, the innate immune system in the brain does not function properly in AD and therefore does not remove Aß peptides before they aggregate to form plaques.   Amyloid beta is naturally produced in the brain by the cleavage of amyloid precursor protein (APP), but when APP is cleaved by ß-secretase Aß peptides are formed that can cause synaptic and mitochondrial damage and aggregate to form plaques (Querfurth and LaFerla 2010). In healthy individuals, Aß peptides are cleared by microglia and enzymes but these mechanisms deteriorate in individuals with AD and the Aß peptides accumulate and result in neurodegeneration (Sarlus and Heneka 2017). Aß plaques cause neuronal cell death by accumulating around neurons, impairing normal function and inducing an inflammatory response. More attention recently has been given to Aß peptides, which lead to apoptosis in neurons through synaptic damage and inhibition of mitochondrial function. Aß peptides cause synaptic damage in the hippocampus by aggregating and creating pores in the cell membranes that allows calcium ion entry into the cell. Over time, these pores become non-selective and allow flux of large molecules like ATP and glucose that alters cell metabolism and disrupts homeostasis resulting in apoptosis (Sepà ºlveda et al. 2014). Aß also produces reactive oxygen species that initiate oxidative stress which leads to mitochondria in the cell releasing cytochrome C and inducing apoptosis (Querfurth and LaFerla 2010). Both Aß peptides and APP can enter the mitochondria where they disrupt the electron transport chain and ATP production (Caspersen et al. 2005; Reddy and Beal 2008). Synapses are sites of high mitochondrial activity because ATP is needed for neurotransmitter release (Reddy and Beal 2008), so inhibition of mitochondrial activity by Aß also results in synaptic damage. NFTs are intracellular aggregations of hyperphosphorylated tau protein and also cause neurodegeneration. Tau protein is a component of the cytoskeleton of neural cells but when hyperphosphorylated tau proteins have an affinity for themselves and destabilize the cytoskeleton (Iqbal et al. 2005; Spillantini and Goedert 2013). Tau protein is phosphorylated by glycogen synthase kinase -3ß (GSK-3ß) (Rankin et al. 2007) which can be activated by Aß peptides (Takashima 2006). Tau protein mediates synaptic damage by inhibiting extracellular signal-regulated kinase (ERK) signaling that is key in cell survival (Sun et al. 2016). Approaches Current treatment of AD relies on two types of medications: acetylcholine esterase inhibitors (AChEIs) and N-methyl-D-aspartate (NMDA) receptor antagonists. AChEIs work by slowing the degradation of acetylcholine (ACh) by inhibiting acetylcholine esterase which allows more ACh action at the synapses (Nelson and Tabet 2015). When cholinergic neurons are lost during the course of AD, ACh synthesis and receptor signaling are reduced (Auld et al. 2002). AChEIs are most effective in slowing progression of cognitive decline in mild to moderate cases and less effective in severe AD (Gillette-Guyonnet et al. 2011). Memantine is an NMDA receptor antagonist (Tariot et al. 2004) that helps mitigate the loss of NMDA receptor function due to Aß peptides (Snyder et al. 2005). Memantine is not effective for mild cases of AD (Nelson and Tabet 2015) but it is effective in moderate to severe cases, especially when used in combination with AChEIs (Tariot et al. 2004). Although AChEIs and NMDA receptor antagonists are the current pharmacological treatments available for AD, they are only able to slow the progression of the disease and lose effectiveness as AD progresses. The challenge in designing a drug to prevent or cure AD is the multifactorial nature of the disease with genetic and lifestyle risk factors. Even when non-pharmacologic interventions (controlling blood pressure, cognitive stimulation therapy, healthy diet and exercise, and maintaining social networks) (Nelson and Tabet 2015) are used as part of a comprehensive treatment plan and initiated early in disease progression, the best that current treatments can offer is to slow the natural progression of the disease With AD prevalence expected to increase worldwide across all races and ethnicities, the culture of different populations is an important consideration when designing intervention strategies. Social and economic barriers that prevent access to health care and social services among different populations need to be understood to identify and implement the best treatment specific to that population. Cultures also differ in how they view AD-related cognitive decline and may consider the memory loss a part of normal aging and therefore delay seeking treatment. An awareness of how cognitive decline in older age is defined culturally, how cultures differ in caring for the elderly, and how barriers to AD care services impacts each culture’s choice of treatment is key to developing successful interventions. Proposed Solutions The greatest challenge in developing treatment for AD that can prevent AD development or progression is that a specific cause has not yet been identified. However, recent research has identified new pharmacologic targets involved in the production of Aß and new therapies to reduce Aß and tau pathology. Research by Hu, Das, Hou, He, and Yan (2018) identified the ß-secretase BACE1 as a potential pharmacological target for the treatment of AD. In a mouse model of AD in adults with BACE1 inhibition, it was observed that synaptic function improved and Aß plaque formation was prevented. Although some clinical trials of BACE1 inhibitors have stalled, with Merck stopping its clinical trial of verubecestat in February 2018 (Merck 2018), there is still hope of developing pharmacologic treatments targeting Aß and tau proteins (Amgen 2017). A novel therapeutic approach being researched is the use of optogenetic stimulation to reduce Aß and tau phosphorylation. Using a light flickering at 40 hertz, (Iaccarino et al. 2016) found they could stimulate brain waves called gamma oscillations in a mouse model of AD and observed reduced Aß plaque formation and tau phosphorylation. This may lead to new non-invasive AD therapies, but more research is needed to investigate its effectiveness in humans. With treatment approaches that target the production of toxic Aß and abnormal tau phosphorylation, it is conceivable that in the future we may be better able to prevent and stop the progression of AD. References Amgen. 2017 Nov 2. Amgen and novartis announce expanded collaboration with banner alzheimers institute in pioneering prevention program. Amgen. [accessed 2018 Mar 19]. http://www.amgen.com/media/news-releases/2017/11/amgen-and-novartis-announce-expanded-collaboration-with-banner-alzheimers-institute-in-pioneering-prevention-program/. Amieva H, Mokri H, Le Goff M, Meillon C, Jacqmin-Gadda H, Foubert-Samier A, Orgogozo J-M, Stern Y, Dartigues J-F. 2014. Compensatory mechanisms in higher-educated subjects with Alzheimer’s disease: a study of 20 years of cognitive decline. Brain 137:1167–1175. APOE gene. 2018 Feb 27. US Natl Libr Med. [accessed 2018 Mar 5]. https://ghr.nlm.nih.gov/gene/APOE. Auld DS, Kornecook TJ, Bastianetto S, Quirion R. 2002. Alzheimer’s disease and the basal forebrain cholinergic system: relations to ÃŽ ²-amyloid peptides, cognition, and treatment strategies. Prog Neurobiol. 68:209–245. Brookmeyer R, Johnson E, Ziegler-Graham K, Arrighi HM. 2007. Forecasting the global burden of Alzheimer’s disease. Alzheimers Dement. J. Alzheimers Assoc. 3:186–191. Caspersen C, Wang N, Yao J, Sosunov A, Chen X, Lustbader JW, Xu HW, Stern D, McKhann G, Yan SD. 2005. Mitochondrial Abeta: a potential focal point for neuronal metabolic dysfunction in Alzheimer’s disease. FASEB J. 19:2040–2041. Ekblad LL, Johansson J, Helin S, Viitanen M, Laine H, Puukka P, Jula A, Rinne JO. 2018 Feb 23. Midlife insulin resistance, APOE genotype, and late-life brain amyloid accumulation. Neurology:10.1212/WNL.0000000000005214. Gillette-Guyonnet S, Andrieu S, Nourhashemi F, Gardette V, Coley N, Cantet C, Gauthier S, Ousset P-J, Vellas B. 2011. Long-term progression of Alzheimer’s disease in patients under antidementia drugs. Alzheimers Dement J Alzheimers Assoc. 7:579–592. Gilsanz P, Mayeda ER, Glymour MM, Quesenberry CP, Mungas DM, DeCarli C, Dean A, Whitmer RA. 2017. Female sex, early-onset hypertension, and risk of dementia. Neurology 89:1886–1893. Guerreiro R, Wojtas A, Bras J, Carrasquillo M, Rogaeva E, Majounie E, Cruchaga C, Sassi C, Kauwe JSK, Younkin S, et al. 2013. TREM2 variants in Alzheimer’s disease. N Engl J Med. 368:117-127 Harman D. 2002. Alzheimer’s disease: Role of aging in pathogenesis. Ann. N. Y. Acad. Sci. 959:384–395. Hickman SE, El Khoury J. 2014. TREM2 and the neuroimmunology of Alzheimer’s disease. Biochem Pharmacol. 88:495–498. Hinney A, Albayrak O, Antel J, Volckmar A-L, Sims R, Chapman J, Harold D, Gerrish A, Heid IM, Winkler TW, et al. 2014. Genetic variation at the CELF1 (CUGBP, elav-like family member 1 gene) locus is genome-wide associated with Alzheimer’s disease and obesity. Am J Med Genet B Neuropsychiatr Genet. 165B(4):283-93 Hu X, Das B, Hou H, He W, Yan R. 2018. BACE1 deletion in the adult mouse reverses preformed amyloid deposition and improves cognitive functions. J Exp Med.   jem.20171831 Iaccarino HF, Singer AC, Martorell AJ, Rudenko A, Gao F, Gillingham TZ, Mathys H, Seo J, Kritskiy O, Abdurrob F, et al. 2016. Gamma frequency entrainment attenuates amyloid load and modifies microglia. Nature 540:230. Iqbal K, del C. Alonso A, Chen S, Chohan MO, El-Akkad E, Gong C-X, Khatoon S, Li B, Liu F, Rahman A, et al. 2005. Tau pathology in Alzheimer disease and other tauopathies. Biochim Biophys Acta. 1739(2-3):198–210. Jonsson T, Stefansson H, Steinberg S, Jonsdottir I, Jonsson PV, Snaedal J, Bjornsson S, Huttenlocher J, Levey AI, Lah JJ, et al. 2013. Variant of TREM2 associated with the risk of Alzheimer’s disease. N Engl J Med. 368:107-116 Kanekiyo T, Xu H, Bu G. 2014. ApoE and AÃŽ ² in Alzheimer’s disease: accidental encounters or partners? Neuron 81:740–754. Letra L, Santana I, Seià §a R. 2014. Obesity as a risk factor for Alzheimer’s disease: the role of adipocytokines. Metab Brain Dis. 29:563–568. McGrath ER, Beiser AS, DeCarli C, Plourde KL, Vasan RS, Greenberg SM, Seshadri S. 2017. Blood pressure from mid† to late life and risk of incident dementia. Neurology 89:2447–2454. Merck. 2018 Feb 13. Merck announces discontinuation of APECS study evaluating verubecestat (MK-8931) for the treatment of people with prodromal Alzheimer’s disease. MERCK. [accessed 2018 Mar 19]. http://www.mrknewsroom.com/news-release/research-and-development-news/merck-announces-discontinuation-apecs-study-evaluating-ve. Nelson L, Tabet N. 2015. Slowing the progression of Alzheimer’s disease; what works? Ageing Res. Rev. 23:193–209. Nuzzo D, Picone P, Baldassano S, Caruana L, Messina E, Marino Gammazza A, Cappello F, Mulà ¨ F, Di Carlo M. 2015. Insulin resistance as common molecular denominator linking obesity to Alzheimer’s disease. Curr Alzheimer Res. 12:723–735. Peila R, Rodriguez BL, Launer LJ. 2002. Type 2 diabetes, APOE gene, and the risk for dementia and related pathologies: the Honolulu-Asia aging study. Diabetes. 51:1256–1262. Pini L, Pievani M, Bocchetta M, Altomare D, Bosco P, Cavedo E, Galluzzi S, Marizzoni M, Frisoni GB. 2016. Brain atrophy in Alzheimer’s disease and aging. Ageing Res Rev. 30:25–48. Prince M, Wimo A, Guerchet M, Ali G-C, Wu Y-T, Prina M. 2015. World Alzheimer Report 2015 The global impact of dementia: An analysis of prevalence, incidence, cost and trends. [accessed 2018 March 18] Qiu C, Kivipelto M, von Strauss E. 2009. Epidemiology of Alzheimer’s disease: occurrence, determinants, and strategies toward intervention. Dialogues Cli. Neurosci. 11:111–128. Querfurth HW, LaFerla FM. 2010. Alzheimer’s Disease. N Engl J Med. 362:329–344. Rankin CA, Sun Q, Gamblin TC. 2007. Tau phosphorylation by GSK-3ÃŽ ² promotes tangle-like filament morphology. Mol Neurodegener. 2:12. Reddy PH, Beal MF. 2008. Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer’s disease. Trends Mol Med. 14:45–53. Ridge PG, Ebbert MTW, Kauwe JSK. 2013. Genetics of Alzheimer’s disease. BioMed Res Int. 2013:254-954. Sarlus H, Heneka MT. 2017. Microglia in Alzheimer’s disease. J. Clin Invest. 127:3240–3249. Sattler C, Toro P, Schà ¶nknecht P, Schrà ¶der. 2012. Cognitive activity, education and socioeconomic status as preventive factors for mild cognitive impairment and Alzheimer’s disease. Psychiatry Res. 196:90–95. Sepà ºlveda FJ, Fierro H, Fernandez E, Castillo C, Peoples RW, Opazo C, Aguayo LG. 2014. Nature of the neurotoxic membrane actions of amyloid-ÃŽ ² on hippocampal neurons in Alzheimer’s disease. Neurobiol Aging. 35:472–481. Shpanskaya KS, Choudhury KR, Hostage C, Murphy KR, Petrella JR, Doraiswamy PM. 2014. Educational attainment and hippocampal atrophy in the Alzheimer’s disease neuroimaging initiative cohort. J Neuroradiol. 41:350–357. Snyder EM, Nong Y, Almeida CG, Paul S, Moran T, Choi EY, Nairn AC, Salter MW, Lombroso PJ, Gouras GK, et al. 2005. Regulation of NMDA receptor trafficking by amyloid-ÃŽ ². Nat Neurosci. 8:1051–1058. Spillantini MG, Goedert M. 2013. Tau pathology and neurodegeneration. Lancet Neurol. 12:609–622. Sun X-Y, Tuo Q-Z, Liuyang Z-Y, Xie A-J, Feng X-L, Yan X, Qiu M, Li S, Wang X-L, Cao F-Y, et al. 2016. Extrasynaptic NMDA receptor-induced tau overexpression mediates neuronal death through suppressing survival signaling ERK phosphorylation. Cell Death Dis. 7(11):e2449. Takashima A. 2006. GSK-3 is essential in the pathogenesis of Alzheimer’s disease. J Alzheimers Dis. 9:309–317. Tang X, Varma VR, Miller MI, Carlson MC. 2017. Education is associated with sub-regions of the hippocampus and the amygdala vulnerable to neuropathologies of Alzheimer’s disease. Brain Struct Funct. 222:1469–1479. Tariot PN, Farlow MR, Grossberg GT, Graham SM, McDonald S, Gergel I. 2004. Memantine treatment in patients with moderate to severe Alzheimer disease already receiving donepezil: a randomized controlled trial. JAMA. 291:317–324. Whitmer RA, Sidney S, Selby J, Johnston SC, Yaffe K. 2005. Midlife cardiovascular risk factors and risk of dementia in late life. Neurology. 64:277–281.

Friday, January 17, 2020

Cooperative Strategy

Critically discuss the underlying motivations and associated competitive advantages that explain why MNEs enter into cooperative structures and strategies, using examples. In recent years there has been an upsurge in the number of MNEs entering cooperative structures and strategies. According to Jones cooperative structure is a means of a substitute or complementary to multinational strategies. It is a strategy in which firms work together to achieve shared objectives. They form partnerships once they believe a local firm had the competitive advantage in the industry or engaged in contractual agreements with public firms.Cooperative strategies and structures have become larger and more complex and crucial more central to the core strategies and competitive advantages of participating firms as a response to the pressures of competing in a global market. In this essay I will firstly discuss the underlying factors which forces MNEs to partake in cooperative strategies. I will then menti on the different types of cooperative structures and strategies. Thirdly using examples I will discuss the motives and disadvantages which arise from MNEs entering into cooperative structure and strategies.After which I will close of with some points to consider in building a successfully cooperative strategies. Cooperative structure and strategy was first coined by firm pre World War 1. In the international business environment in the 21st century there are very few companies which possess all the resources or capabilities they need to develop strategies and organizational capabilities to gain competitive advantage on their own. Firms in the European nations were free to engage in cooperation. The US firms were bound by legislation which causes them not to be free to collaborate.According to Bartlett et al. the key challenge facing companies is their ability to maintain independence by maintaining firm control over its activities which led to the building of strong external relatio nships which may be with their customers, suppliers, competitors or even other institutions. Factors which trigger firms to shift towards cooperative strategy and structures (cooperation) stems from rising cost in R&D, shortened life cycle due to constant technological evolution, growing barriers to market entry (where some firms may lack the now-how), capital shortage, increasing needs for global scale economies and expanding importance of global standards as the world have now become a global market with greater demands and competition being placed on firms. Increasingly they must collaborate with others to meet the need of the global environment. Firms may undertake co-operation such as strategic alliances in this type of cooperation the participating firms agree to collaborate specific aspects of their business combining some of their resources and capabilities to create a mutual competitive advantage.Another form of cooperation is joint ventures which is the most formal mode of cooperation. It involves two or more participating firms taking joint equity in separate entities distinct from the parent company. It may take the form of an entirely new enterprise or one that the joint venture come together and acquire. Eg Fuji-Xerox. During the interwar years the sharing of risk and reduction of financial pressure was the basis for joint ventures, cartels and collaborations.Licensing and Franchising are also forms of cooperation they are contractual relationships between firms they offer ways of reducing capital necessary to engaging in international business. Networks as cooperation are found in many different industries and take many different forms they have no formal existence and are rooted in sustained ongoing commercial relationships where partners have learnt to trust and rely on one another. They exist to link forms operating in different stages of the value chain.All these are different forms in which a firm may undertake to acquire the skills and res ources they lack all in effort of creating value. MNEs engaging in cooperation can benefit from a range of motives giving them competitive advantage over the competitor or sustainability. Such advantages/motives are learning and resource transfer this is where the cooperative structure formal informal networks through licensing agreement to formal joint venture which can form conduits for information flows, knowledge and other tangible and intangible resources.This means that cooperation become a route through which firms gain access to resources they do not possess and either cannot or do not wish to do develop internally. This is because more and more firms are now focusing on narrow sets of core capabilities and innovation (R&D) depends on interdisciplinary work. Firms narrowing their capabilities forces firms to look at external sources of competencies and resource that they no longer possess internally. Example: The requirements imply that todays MNEs must develop the skills t o not only manage assets and resources under their

Thursday, January 9, 2020

Is American Society Breed Mental Illness - 1250 Words

Nation of Anxiety Does American Society Breed Mental Illness? Over the past couple decades, disabling mental illness has drastically increased in the United States. Among these, Generalized Anxiety Disorder (GAD) is one of the most commonly diagnosed. According to the Anxiety and Depression Association Of America, GAD is characterized by persistent, excessive, and unrealistic worry about everyday things. This disorder is often linked with other anxiety disorders, such as depression and panic attacks. According to the Anxiety and Depression Association of America, New York Times columnist Marcia Angell summarizes that, â€Å"The tally of those who are so disabled by mental disorders that they qualify for Supplemental Security Income (SSI) increased nearly two and a half times between 1987 and 2007- from one in 184 Americans to one in 76.† In addition, Angell also conducted a large survey of adults between 2001 and 2003, sponsored by the National Institute of Mental Health and discovered that in their lifetime, â€Å"46 percent of Amer icans met the criteria established by the American Psychiatric Association for at least one mental illness.† Recent research has found that the amount of diagnosed mental illness cases have continued to significantly rise since 2003 alone. These startling statistics lead to the questions everyone has been scrambling to answer: Why? What is the cause of this epidemic? Is it all on account of recent overdiagnosis of psychiatric disorders? OrShow MoreRelatedThe Ways Oppressions Are Carried Out1481 Words   |  6 PagesAfrican Americans, the physically ill, and the mentally ill. In particular, the discrimination against the mentally ill becomes an interesting and unique history that has evolved due to Western medicine, and now effects the whole world. In many instances, it has become apparent that the symptoms and stigma surrounding the mentally ill stems from Western ideals as well. This paper explores this stigma, the ways oppressions are carried out, and how they are being dealt with. When society is confrontedRead MoreThe 2014 Isla Vista Massacre Essay612 Words   |  3 Pagesworldview. He also displays a deep hatred for minority races, specifically Asians and Black Americans. Ironically enough, Rodgers is half Malaysian. In one entry he describes watching an Indian man sitting with a white woman remarking on how disgusting and unfair it was. As the manifesto progresses Elliot Rodgers becomes increasingly aggressive, writing â€Å"Women should not have the right to choose who to mate and breed with. That decision should be made for them by rational men of intelligence. If womenRead MoreFreedom to Love Essays1088 Words   |  5 Pages    There are different kinds of partners in the world: Black, White, Asian, Straight, Gay, etc. However, not all of them are accepted by the society. Holding someone’s hand in public? It may be the sweetest, most innocent and natural of gesture of affection. However, when it comes to a couple wi th the same sex, things become completely different. People may think it is disgusting. Therefore, gay couples have to tolerate others’ disgust looks and nasty words, or sometimes even worse -- a punch. TheRead MoreEating Disorders And Its Impact On Society1646 Words   |  7 Pages Eating Disorders and Its Impact on Society Brett White Tallahassee Community College Psychology 1101 Michelle Peruche November 06, 2015 Abstract Eating disorders are very common in today’s society and can cause death if an intervention isn’t performed. While working in the hospital and being part of the wrestling team in high school I’ve witness several people with this disorder. Anorexia and bulimia are the most prevalent and generally are accompanied by another psychological disorderRead MorePersuasive Essay On Gun Control1178 Words   |  5 PagesVegas, Nevada. Over the course of 12 minutes, Paddock committed the worst mass shooting in modern American history. We must honor the victims and respect their memory, but we have to ask ourselves what we will do to prevent this in the future. The first and completely valid response to that question is enacting stricter gun control, but there is much more than that. We can increase funding for mental health treatment, we can take stricter security measures at hotels and concerts, however there isRead MoreThe Infringement of Animal Rights Essay1170 Words    |  5 Pagesserious mental illness. During a study the proved that animals helped this recovery process by providing empathy and therapy, providing connections that can assist in redeveloping social avenues, serving as â€Å"family† in the absence of or in addition to human family members, and supporting self-efficacy and strengthening a sense of empowerment. It seems as if pets provide more benefits than companionships (Green; Saedi; Wisdom, 2010). With an animal’s ability to help reduce symptoms of mental illnessRead MoreDog Abuse Is Wrong?1102 Words   |  5 Pagesthe animal. There are a lot of different types of dog abuse including physical, mental, and emotional abuse. Each type of abuse causes different types of pain to the dog. People do these cruel acts for a variety of different reasons. Dog Abuse is when a dog is beaten physically or mentally abused by verbal communication. â€Å"98% of Americans consider pets to be companions and members of the family† (American Humane Society 1).This means most pets aren t just considered animals they actually think ofRead MoreEugenics And Its Impact On Human Life1560 Words   |  7 Pageshave been explored. Eugenics is the scientific deal of improving human reproduction of genetic specifications of a particular race or breed. Positive Eugenics is relative to those who seem the most able and healthy with little to no history of medical abnormalities. The negative practice centers on manipulating those who are considered genetically weak in society, coercing these individuals to believe they are unfit for having children. Eugenicists believed that this practice would help to eliminateRead MoreUnfair America: Mentally Ill Inmates Essay1947 Words   |  8 PagesIndividuals suffering from mental illnesses tend to fall victim to the criminal justice system due to their uncontrollable actions that result from their mental illness symptoms. Within the United States two to three hundred thousand people in prison suffer from mental illnesses such as schizophrenia, severe depression, and bipolar disorder. Sadly, the majority of prisons are deficient in providing the appropriate resources to treat these individuals; people with mental illnesses are too frequentlyRead MoreThe Eugenics Of The Word Eugenics1626 Words   |  7 PagesThe word eugenics was first derived from the Greek word â€Å"eugenes† which means well-born. The goal of eugenics is to create and breed the utmost superior person through selection while picking out the good traits and eliminating the bad ones. Eugenics is the study of using methods to improve genetics by selective breeding (Eugenics, 2009). This came about because of the thought of being able to tell the difference between inferior and superior human beings. In 1883 the wo rd eugenics was first used