Software Engineering mid Essay Example | Topics and Well Written Essays - 750 words

Software Engineering mid - Essay Example Application software - may be written in obsolete programming languages. Application data - often incomplete and inconsistent. Business processes - may be constrained by software structure and functionality. Business policies and rules - may be implicit and embedded in the system software. Answer to section 7: The fundamental activities that are common to all software processes are: Specification: It relates to the initial specifications on how to build the software. The process of establishing what services are required and the constraints on the system's operation and development. Design: It relates to the process of converting the system specification into an executable system. Validation: It is intended to show that a system conforms to its specification and meets the requirements of a system customer. Evolution: Software is inherently flexible and can change. The properties like scalability and flexibility is addressed here. Answer to section 8: The advantages of incremental development and delivery are: Customer value can be delivered with each increment so system functionality is available earlier. Early increments act as a prototype to help elicit requirements for later increments. Lower risk of overall project failure. The highest priority system services tend to receive the most testing. Answer to section 9: The six fundamental best practices of RUP are: Develop software iteratively Manage requirements Use component-based architectures Visually model software Verify software quality Control changes to software Answer to section 10: The five common project management activities are: Proposal writing: Usually done before getting the project. Project planning and scheduling: Done as a part of the planning process. Project costing: Project feasibility...A project milestone is a predictable state where a formal report of progress is presented to management. Application domain experience: For a project to develop a successful system, the developers must understand the application domain. It is essential that some members of a development team have some domain experience. Programming language experience: This is normally only significant for short duration projects where there is not enough time to learn a new language. While learning a language itself is not difficult, it takes several months to become proficient in using the associated libraries and components. Problem solving ability: This is very important for software engineers who constantly have to solve technical problems. However, it is almost impossible to judge without knowing the work of the potential team member. Educational background: This may provide an indicator of the basic fundamentals that the candidate should know and of their ability to learn. This factor becomes increasingly irrelevant as engineers gain experience across a range of projects. Personality: This is an important attribute but difficult to assess. Candidates must be reasonably compatible with other team members. No particular type of personality is more or less suited to software engineering. 3.

How did the designations aliens ineligible for citizenship and the Research Proposal

How did the designations aliens ineligible for citizenship and the yellow peril negatively affect Asian Americans in the years prior to 1952 - Research Proposal Example Second, this designation led to separated or hurt families (Hutchison 44). Such families suffered mental effects because of this designation. Male-controlled familial structures among Asian Americans were not common in the United States before 1952. The statistical and social supremacy of Chinese males, together with domestic separation and customary diversity extended the assimilation procedure for Asian immigrants. This is the third negative effect of this designation that also allowed the dominant perception of Asian Americans as alien immigrants (Brilliant 34). Fourth, the â€Å"Aliens Ineligible for Citizenship† policy led to increased demands for Asian prostitution because of the absence of Asian women (Brilliant 34). Frequently disguised as business wives, selected Americans drew or bought and shipped women from Asian nations like China to serve as prostitutes in the United States. Shortly afterwards, Asian prostitution was perceived as an annoyance alongside West Coast and legislators responded by passing the Page Law in 1875. This law enabled customs officials at ports to refute entrance to Asian women believed to be imminent prostitutes in the United States (Brilliant 36). The designation â€Å"Yellow Peril† radically transformed into one of the approvals as Asian success tales began becoming increasingly common all through the American community (Allred 58). Before this transformation, this policy was the source of some of the worst discriminations against Asian Americans in history. This designation coined the phrase â€Å"model minority† to refer to Asian in the United States (Allred 61). This phrase acted as a model for other minorities. As a result, Asian Americans became a widespread outcast in America and suffered more discrimination than any other minority group. Secondly, as a type of subtle discrimination, the â€Å"Yellow Peril† designation fostered the spread

Polar Bear Essay Example for Free

Polar Bear Essay The polar bear (Ursus maritimus) is a bear native largely within the Arctic circle encompassing the Arctic Ocean, its surrounding seas and surrounding land masses. It is the worlds largest land carnivore and also the largest bear, together with the omnivorous Kodiak bear, which is approximately the same size. [3] An adult male weighs around 350-680 kg (770-1 ,500 while an adult female is about half that size. Although it is closely related to the brown bear, it has evolved to occupy a narrow ecological niche, with many body characteristics adapted for cold emperatures, for moving across snow, ice, and open water, and for hunting the seals which make up most of its diet. [5] Although most polar bears are born on land, they spend most of their time at sea (hence their scientific name meaning maritime bear) and can hunt consistently only from sea ice, so spend much of the year on the frozen sea. The polar bear is classified as a vulnerable species, with 8 of the 19 polar bear subpopulations in decline. 6] For decades, unrestricted hunting[clarification eeded] raised international concern for the future of the species; populations have rebounded after controls and quotas began to take effect. [citation needed] For thousands of years, the polar bear has been a key fgure in the material, spiritual, and cultural life of Arctic indigenous peoples, and the hunting of polar bears remains important in their cultures. The IIJCN now lists global warming as the most significant threat to the polar bear, primarily because the melting of its sea ice habitat reduces its ability to find sufficient food. The II-JCN states, If climatic trends continue polar bears may become extirpated from most of their range within 100 years. [7] The polar bear was listed as a threatened species under the Endangered Species Act by the United States Department of the Interior in 2008. Habitat The polar bear is often regarded as a marine mammal because it spends many months of the year at sea. [28] Its preferred habitat is the annual sea ice covering the waters over the continental shelf and the Arctic inter-island archipelagos. These areas, known as the Arctic ring of life, have high biological productivity in comparison to the deep waters of the high The polar bear tends to frequent areas where sea ice meets water, such as polynyas and leads (temporary stretches of open water in Arctic ice), to hunt the seals that make up most of its diet. [30] Polar bears are therefore found primarily along the perimeter of the polar ice pack, rather than in the Polar Basin close to the North Pole where the density of seals is low. 1] Annual ice contains areas of water that appear and disappear throughout the year as the weather changes. Seals migrate in response to these changes, and polar bears must follow their prey. [29] In Hudson Bay, James Bay, and some other areas, the ice melts completely each summer (an event often referred to as ice-floe breakup), forcing polar bears to go onto land and wait through the months until the next freeze-up. [29] In the Chukchi and Beaufort seas, polar bears retreat each summer to the ice further north that remains frozen year-round.

Treating Alzheimers Disease with Vitamin A, C E (ACE)

Treating Alzheimers Disease with Vitamin A, C E (ACE) ACE Alzheimers: An adjuvant strategy of treating Alzheimers disease with Vitamin A, C E (ACE) ABSTRACT Alzheimers disease (AD) is a chronic and slowly progressing neurodegenerative disorder which has become a major concern with regards to health, worldwide. This disorder is characterised by progressive dementia and cognitive decline. Pathologically, AD is characterised by the presence of AÃŽÂ ² plaques and tau neurofibrils. However, literature has shown that oxidative stress is one of the most important risk factor behind the cause of AD. Oxidative stress often leads to production of Reactive Oxygen Species (ROS), which further increases structural and functional abnormalities in neurons of the brain, which subsequently, presents as dementia and cognitive decline. In order, to curb the oxidative stress, antioxidants can be of great help. There have been many evidences that supports the use of antioxidants in the treatment for AD. Vitamins A, C and E are an example of antioxidants that can be used as adjuvants in the treatment of AD. This article will focus on current literature and will present forward the evidence based advantages of using Vitamin A, C and E as an adjuvant treatment for AD. Keywords: Antioxidants, ACE, Adjuvant therapy. INTRODUCTION A clinical psychiatrist and neuroanatomist, Alois Alzheimer, reported A peculiar severe disease process of the cerebral cortex to the 37th Meeting of South-West German Psychiatrists in Tubingen, thus marking the discovery of one of the most interesting pathologies in medicine Alzheimers disease. His invention was based on the observations in one his patient named Auguste D, suffering from profound memory loss, unfounded suspicions about her family, and additional worsening psychological changes. Her post mortem findings further revealed dramatic shrinkage of the brain and abnormal deposits in and encircling the nerve cells [1]. AD has proven to be a significant public health issue, as it consumes a major amount of heath budget in developed as well as developing countries. AD has become one of the leading causes of dementia in patients less than 65 years, other causes being Lewy body dementia (LBD), frontotemporal dementia (FTD), vascular dementia (VaD) and alcohol associated dementia [2]. United States alone has documented a $200 billion annual expenditure on patients affected by AD. Moreover, one person develops Alzheimers dementia every 68 seconds emphasizing the incidence of the disease [3]. Dementia can be defined as a chronic progressive disorder marked by memory deficits, personality changes, and impaired reasoning. Results from population-based studies have shown a significant relationship between the certain risk factors and development of AD. Increased risk was shown with an increase in age, fewer years of education, and head trauma. Genetic factors do contribute to the early development of AD increased risk with mutations on chromosome 21 (cases of downs syndrome) as it carries the amyloid precursor protein, the presence of apolipoprotein E epsilon 4 allele and the presenilin 1 and 2 genes. The strongest factor identified till date are the apolipoprotein E genes located on chromosome 19 which exists in three forms ÃŽÂ µ2, ÃŽÂ µ3, and ÃŽÂ µ4. ÃŽÂ µ2 has been found to reduce the risk, ÃŽÂ µ3 is found to be neutral whereas ÃŽÂ µ4 has been associated with a tremendous increase in risk as well as early development of symptoms (Figure 1) [4]. Chromosome Genes 21 AMYLOID PRECURSOR PROTEIN 19 APOLIPOPROTEIN E 14 PRESENILIN 1 1 PRESENILIN 2 Figure 1. Genetic factors causing a risk to develop Alzheimers Ad is difficult to differentiate from other causes of dementia like LBD, FTD and Vad [5]. It may present with dysfunction of various fields such as vision, touch voluntary movements, personality deficits and judgemental disorders depending upon the area of the brain affected [6].The National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimers disease and Related Disorders Association (NINCDS/ADRDA) has proposed a diagnostic criteria for differentiating between AD and other known causes of dementia. In compliance with NINCDS/ADRDA , AD is diagnosed if: (I) Cognitive functions decline progressively over a period of time including/ not including memory impairment or (Ia) Inability to understand language and verbal commands (aphasia); (Ib) Loss of ability to accomplish tasks due to incoordination of muscles (apraxia); (Ic) Failure to recognise previously known objects and loss of ability to use them(agnosia); (Id) Unable to plan, organise and execute dail y chores; (II) All above mentioned under I do get progressively deteriorated with time; (III) Other known causes of dementia as well as cognitive deterioration must be eliminated [6,7]. Neurofibrillatory tangles and extracellular amyloid plaques have been the initial histopathological findings associated with AD. Recently several other features have been recognised which include degeneration of neuronal synapses, aneuploidy and loss of neurons in the hippocampus. Despite the recent inventions, presence of extracellular amyloid plaques and intracellular NFT have been taken into account as the main histopathological criteria for establishment of AD [8]. Among all the different hypothesis, AÃŽÂ ² cascade has been the most accepted. Previously, a mutation in beta-Amyloid Precursor Protein (APP), which contributes to the normal function of neurons and cerebral development, was thought to be the sole culprit since the accumulation of AÃŽÂ ² proteins had lead to the pathogenesis of AD [9]. Eventually, mutated presenilin genes (both 1 and 2) have been discovered to play a role in the formation of AÃŽÂ ² pools [10]. But the exact mechanism underlying how AÃŽÂ ² a ggregation contributes to the pathophysiology of AD largely remains unclear. Formerly, toxicity of neurons was believed to be caused by intracellular plaques. But recent data has suggested the role of intracellular AÃŽÂ ² proteins, which do not become sequestered into the extracellular plaques, as the toxic triggers stimulating the progression of AD [11]. Recently, it has also been shown that intracellular accumulation of AÃŽÂ ² proteins precedes the formation of extracellular AÃŽÂ ² protein plaques and NFT formation [12]. The role of intracellular AÃŽÂ ² protein in the progression of AD has also been demonstrated in recent experiments on transgenic mice. Results of these experiments indicate that increased deposits of AÃŽÂ ² proteins within the cells are associated with accelerated cell death [13]. Other important causative factors in the development of AD include oxidative stress and Reactive Oxygen Species (ROS) [14]. Susceptibility to oxidative damage is due to several factors which include relatively lower levels of antioxidants, significantly higher levels of polyunsaturated fatty acids, (these fatty acids rapidly fall prey to ROS), the presence of metallic ions and high oxygen utilisation [15]. Oxidation have been prove to be fatal for several constituents of the cells including carbohydrates, lipids, proteins, RNA and DNA [16]. Indirect mechanisms do play a vital role in the damaging process. Oxidation has been proven to accelerate the expression of inducible nitric oxide (iNOS) and accentuate the activity of neuronal NOS (nNOS). This leads to increased production of nitric oxide (NO). NO is known to interact with super oxide anions thus forming a highly reactive peroxynitrite anion. These transient molecules exerts their effects mainly on sulfhydryl groups of cells. [17 ]. The entire process has been depicted in figure 2. Figure 2. Nitric Oxide Pathogenesis In addition to the indirect mechanisms, oxidative stress alters the protein structure. Impaired proteins are known to accelerate oxidative damage, thus proven to be interrelated. ROS causes the protein to be oxidised leading to a modified structure and causing them to be dimerized and aggregated [18]. Thus the oxidised protein which is both structurally and functionally abnormal gather as inclusions within the cytoplasm of the neurons, seen in the form of NFT (tau aggregates) and AÃŽÂ ² plaques [19]. Alternatively, AÃŽÂ ² plaques can also lead to the increased production of ROS. The entire process has been depicted in figure 3. OXIDATION ALTERED PROTEIN STRUCTURE CYTOPLASMIC INCLUSIONS DIMERISATION AGGREGATION Figure 3.Displaying Correlation between Oxidation and Protein Dimerization, thus forming a Vicious Cycle AÃŽÂ ² (1-42) is an abundant species of AÃŽÂ ² proteins seen in AD [20]. AÃŽÂ ² (1-42) peptides is known for its toxicity which can be attributed to a residue of methionine at position 35 [21]. Oxidation of methionine contributes to the formation of methionine sulfoxide, which generally leads to irreversible oxidation and subsequently, forming methionine sulfone [22]. Methionine sulfoxide reductase (MSR) can even help the reduction of methionine sulfoxide into methionine [23]. However, the activity of MSR is also observed to be impaired in AD [24]. Methionine peroxide plays an important role in oxidative stress and toxicity caused by AÃŽÂ ² (1-42) peptides. The lone-pair of electrons present on the S atom of methionine undergoes oxidation of one atom and as a result, sulfuranyl radicals (MetS.+) are generated [21,25]. Sulfuranyl radicals are known to trigger the generation of other ROS like sulfoxides and superoxides by interacting with molecular oxygen [26]. The reason behind this intense oxidative damage could be attributed to the relative absence or decreased function of different antioxidant mechanisms of the body. Glutathione is one of the major antioxidant which can protect the brain tissues by causing detoxification of damaging ROS [27]. One of the main reasons of increase in oxidative stress in AD is the decreased glutathione levels in the brain [28]. The other members of the cellular antioxidant mechanism which plays a pivotal role includes Superoxide Dismutase (SOD) and Catalase (CAT). SOD is an antioxidant which is responsible for converting toxic superoxide ions into far less toxic hydrogen peroxide [29]. CAT evolves this reaction in to one step further and turns hydrogen peroxide into water [30]. Investigations have revealed that the levels of SOD and CAT decline in patients with AD [31]. Glutathione reductase (GR) and Glutathione peroxidase (GPx) represent the other crucial parts of the cellular defence mechanism which acts against oxidative stress. GPx is responsible for the metabolism of hydrogen peroxide and lipid hydroperoxides [32] and GR accelerates the reaction which helps in the regeneration of Glutathione (GSH) [33]. In total, the combination of an oxidative stress with above mentioned cellular defence mechanism against ROS, leads to the pathogenesis of AD. The pathogenesis of Alzheimers disease is mentioned in Figure 4. Figure 4. Pathogenesis of Alzheimers disease (MG : Microglia ; AS: Astrocyte; AP: Amyloid protein beta; NFT: Neurofibrillary tangles) ACE ALZEIHMERS: VITAMIN A, C E (ACE) THERAPY   Ã‚   ROLE OF VITAMIN A Vitamin A and beta carotene have been shown to have multiple benefits for people suffering from AD. Various studies have found that patients suffering from AD have significantly lower levels of Vitamin A level and beta carotene in their CSF as well as blood [34]. The development of neurodegenerative disorders has shown to be influenced by Vitamin A and beta-carotene. Vitamin A plays an active role in neuronal development both in early life and in the adult nervous system. It protects and assists in the regeneration of neurons during recovery from neurodegeneration [35]. Inhibition of formation and destabilization of AÃŽÂ ² fibrils is an additional effect of Vitamin A and beta-carotene [35]. Since oligomerization of AÃŽÂ ² fibrils is an important mechanism contributing to neuronal toxicity in AD, Vitamin A supplementation has been shown to decrease the aggregation and oligomerization of AÃŽÂ ²40 and AÃŽÂ ²42 fibrils [36]. It has also been shown that Vitamin A and beta carotene decrease the decline of cognitive function in AD. Moreover, higher levels of these vitamins have been associated with better memory performance and spatial learning in these patients [3436]. ROLE OF VITAMIN C Various studies both in vivo and in vitro have shown to have significant effect in the brain due to decreased levels of vitamin C. Decreased plasma levels despite adequate intake in patients further confirmed the belief of protective effects of vitamin C in the spectrum of neurodegenerative diseases [37]. Hence, it can be proved that oxidative stress induces damage in AD and protection against this stress is offered to a certain degree by antioxidant vitamins. The progression of AD is altered by Vitamin C by interfering with various different aspects of pathology. Numerous studies, both in-vivo and in vitro, have shown that Vitamin C can decrease oxidative stress. The structural progression of AD is prevented by Vitamin C by hindering the oligomerization of AÃŽÂ ² peptides [38]. Brain injury induces oxidative stress and reduces the level of antioxidants like vitamin C and SOD. Vitamin C supplementation improves the level of SOD, which consecutively helps to decrease oxidative stress and subsequent brain injury [39]. It has been suggested that even without additional supplementation, a normal intake of Vitamin C can have a neuroprotective effect in patients with AD. Cognitive decline in AD patients has shown to decrease is patients taking adequate Vitamin C [40]. In addition, results from a prospective observational study (n=4740) over a period of 3 years have shown that additional supplementation with antioxidant vitamins like vitamin C and E may be associated with both decreased incidence and prevalence of AD [41]. ROLE OF VITAMIN E Vitamin E represents a cluster of 8 antioxidants composed of 4 tocotrienols and 4 tocopherols. It has been reported that there is a greater risk of neurodegenerative disorders like AD and Mild Cognitive Impairment (MCI) with lower plasma levels of vitamin E. Additionally, the level of vitamin E metabolic products (5-nitro-ÃŽÂ ³-tocopherol etc.) is shown to increase significantly in AD and MCI [42]. Deficiency of Vitamin E can lead to the damage and destruction of neurons and has been implicated in cases of cerebellar atrophy [43]. Vitamin E is a potent antioxidant which can delay the progression of AD at several levels. Increased oxidative stress induced by AÃŽÂ ² plaques is known to be a risk factor for neuronal death and ensuing brain injury in AD. Vitamin E behaves like a scavenger for these free radicals and therefore, is neuroprotective. [44]. Vitamin E also provides protection against AD via various other methods. For example, the 12-lipoxygenase pathway leads to glutamate-induced neuronal cell death by inflammation. Vitamin E can reduce this inflammation induced neuronal death [45]. Furthermore, consumption of vitamin E has been linked with the regeneration of SOD, levels of which are shown to decline in AD [39]. Among the different forms of vitamin E, the greatest degree of protection against AD is provided by ÃŽÂ ±-tocopherols and ÃŽÂ ³-tocopherols [46]. A population-based cohort study of 5395 individuals was conducted to evaluate the efficacy of dietary supplementation of antioxidants to provide protection against AD. Among all the antioxidants used, results showed that the most significant degree of protection (p=0.02) against dementia and AD was provided by Vitamin E [47]. Moreover, supplementation of 30 International Units of alpha-tocopherols can act as a valuable adjuvant in the treatment of various neurodegenerative diseases, including AD [48]. Conclusion Alzheimers disease represents one of the most significant age-related neurodegenerative disorders. Oxidative stress is one of the most important mechanisms involved in the development and progression of this condition. In order, to curb the oxidative stress, antioxidants can be of great help. The use of antioxidant vitamins A, C and E as adjuvant therapy for AD has always been given consideration. Thus, further clinical research is necessary to study the potential of these vitamins such that it can be integrated into clinical treatment to accelerate the recovery of patients afflicted by this disorder. REFERENCES Alzheimer A, Uber eine eigenartige Erkrankung der Hirnrinde Allgemeine Zeits Psychiat Psychisch Gerichtlich Med 1907 64:146-48. Harvey RJ, Skelton-Robinson M, Rossor MN, The prevalence and causes of dementia in people under the age of 65 years J Neurol Neurosurg Psychiatry 2003 74:1206-09. Alzheimers Association2012 Alzheimers disease facts and figures Alzheimers Dement 2012 8:131-68. 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Levy-Lahad E, Wasco W, Poorkaj P, Romano DM, Oshima J, Pettingell WH, Candidate gene for the chromosome 1 familial Alzheimers disease locus Science 1995 269:973-77. Lesne S, Kotilinek L, Amyloid plaques and amyloid-beta oligomers: An ongoing debate J Neurosci 2005 25:9319-20. Gouras GK, Tsai J, Naslund J, Vincent B, Vincent B, Edgar M, Intraneuronal Abeta42 accumulation in human brain Am J Pathol 2000 156:15-20. Bayer TA, Wirths O, Intracelluar accumulation of amylois beta- A predictor for synaptic dysfunction and neuron loss in Alzheimers disease Front Aging Neurosci 2010 2:8 Butterfield DA, Amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicity: implications for neurodegeneration in Alzheimers disease brain. A review Free Radic Res 2002 36:1307-13. Butterfield DA, Castegna A, Lauderback CM, Drake J, Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimers disease brain contribute to neuronal death Neurobiol Aging 2002 23:655-64. Butterfield DA, Reed T, Newman SF, Sultana R, Roles of amyloid ÃŽÂ ²-peptide-associated oxidative stress and brain protein modifications in the pathogenesis of Alzheimers disease and mild cognitive impairment Free Radic Biol Med 2007 43:658-77. Koppenol WH, Moreno JJ, Pryor WA, Ischiropoulos H, Beckman JS, Peroxynitrite, a cloaked oxidant formed by nitric oxide and superoxide Chem Res Toxicol 1992 5:834-42. Hensley K, Hall N, Subramaniam R, Cole P, Harris M, Aksenov M, Brain regional correspondence between Alzheimers disease histopathology and biomarkers of protein oxidation J Neurochem 1995 65:2146-56. Butterfield DA, Kanski J, Brain protein oxidation in age-related neurodegenerative disorders that are associated with aggregated proteins Mech Ageing Dev 2001 122:945-62. Selkoe DJ, Alzheimers disease: genes, proteins, and therapy Physiol Rev 2001 81:741-66. Butterfield DA, Boyd-Kimball D, The critical role of methionine 35 in Alzheimers amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicity Biochim Biophys Acta 2005 1703:149-56. Moskovitz J, Berlett BS, Poston JM, Stadtman ER, Methionine sulfoxidereductase in antioxidant defence Methods Enzymol 1999 300:239-44. Maher P, Redox control of neural function: background, mechanisms, and significance Antioxid Redox Signal 2006 8:1941-70. Gabbita SP, Aksenov MY, Lovell MA, Markesbery WR, Decrease in peptide methionine sulfoxidereductase in Alzheimers disease brain J Neurochem 1999 73:1660-66. Pogocki D, Schoneich C, Redox properties of Met(35) in neurotoxic beta-amyloid peptide. A molecular modeling study Chem Res Toxicol 2002 15:408-18. Milller B, Williams T, Schoneich C, Mechanism of sulfoxide formation through reaction of sulfur radical cation complexes with superoxide of hydroxide ion in oxygenated aqueous solution J Am Chem Soc 1996 118:11014-25. Dringen R, Gutterer JM, Hirrlinger J, Glutathione metabolism in brain: metabolic interaction between astrocytes and neurons in the defence against reactive oxygen species Eur J Biochem 2000 267:4912-16. Saharan S, Mandal PK, The emerging role of glutathione in Alzheimers disease J Alzheimers Dis 2014 40:519-29. Zelko IN, Mariani TJ, Folz RJ, Superoxide dismutase multigene family: a comparison of the CuZn-SOD (SOD1), Mn-SOD (SOD2), and EC-SOD (SOD3) gene structures, evolution, and expression Free Radical Biol and Medi 2002 33:337-49. Chelikani P, Fita I, Loewen PC, Diversity of structures and properties among catalases Cell Mol Life Sci 2004 61:192-208. Marcus DL, Thomas C, Rodriguez C, Simberkoff K, Tsai JS, Strafaci JA, Increased peroxidation and reduced antioxidant enzyme activity in Alzheimers disease Exp Neurol 1998 150:40-44. Arthur JR, The glutathione peroxidases Cell Mol Life Sci 2000 57:1825-35. Shigeoka S, Onishi T, Nakano Y, Kitaoka S, Characterisation and physiological function of glutathione reductase in Euglena gracilis z Biochem J 1987 242:511-15. Bourdel-Marchasson I, Delmas-Beauviex M-C, Peuchant E, Richard-Harston S, Decamps A, Reignier B, Antioxidant defences and oxidative stress markers in erythrocytes and plasma from normally nourished elderly Alzheimer patients Age and Ageing 2001 30:235-41. Ono K, Yamada M, Vitamin A and Alzheimers disease Geriatrics Gerontol Intl 2012 12:180-88. Takasaki J, Ono K, Yoshiike Y, Ikeda T, Morinaga A, Takashima A, Vitamin A has anti-oligomerization effects on amyloid-ÃŽÂ ² in vitro J Alzheimers Dis 2011 27:271-80. Rivià ¨re S, Birlouez-Aragon I, Nourhashà ©mi F, Vellas B, Low plasma vitamin C in Alzheimer patients despite an adequate diet Int J Geriatr Psychiatry 1998 13:749-54. Montilla-Là ³pez P, Muoz-à gueda MC, Feijà ³oLà ³pez M, Muà ±oz-Castaà ±eda JR, Bujalance-Arenas I, Tà ºnez-Fià ±ana I, Comparison of melatonin versus vitamin C on oxidative stress and antioxidant enzyme activity in Alzheimers disease induced by okadaic acid in neuroblastoma cells Eur J of Pharmacol 2002 451:237-43. Ishaq GM, Saidu Y, Bilbis LS, Muhammad SA, Jinjir N, Shehu BB, Effects of ÃŽÂ ±-tocopherol and ascorbic acid in the severity and management of traumatic brain injury in albino rats J Neurosci Rural Pract 2013 4:292-97. Harrison FH, A critical review of Vitamin C for the prevention of age-related cognitive decline and Alzheimers disease J Alzheimers Dis 2012 29:711-26. Zandi PP, Anthony JC, Khachaturian AS, Stone SV, Gustafson D, Tschanz JT, Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements: the Cache County Study Arch Neurol 2004 61:82-88. Mangialasche F, Xu W, Kivipelto M, Costanzi E, Ercolani S, Pigliautile M, Tocopherols and tocotrienols plasma levels are associated with cognitive impairment Neurobiol Aging 2012 33:2282-90. Aoki K, Washimi Y, Fujimori N, Maruyama K, Maruyama K, Yanagisawa N, Familial idiopathic vitamin E deficiency associated with cerebellar atrophy Rinsho Shinkeigaku 1990 30:966-71. Yatin SM, Varadarajan S, Butterfield DA, Vitamin E prevents Alzheimers amyloid ÃŽÂ ²-peptide (1-42)-induced neuronal protein oxidation and reactive oxygen species production J Alzheimers Dis 2000 2:123-31. Khanna S, Parinandi NL, Kotha SR, Roy S, Rick C, Bibus D, Nanomolar vitamin E ÃŽÂ ±-tocotrienol inhibits glutamate-induced activation of phospholipase A2 and causes neuroprotection J Neurochem 2010 112:1249-60. Morris MC, Evans DA, Tangney CC, Bienias JL, Wilson RS, Aggarwal NT, Relation of the tocopherol forms to incident Alzheimer disease and to cognitive change Am J Clin Nutr 2005 81:508-14. 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Threat of Endangerment: The Mountain Gorilla :: essays research papers

  Ã‚  Ã‚  Ã‚  Ã‚  The mountain gorilla was first discovered roaming the Virunga Volcanoes in Rwanda (von Beringe, 2002, p.9). German Captain Robert von Beringe and his African soldiers stumbled upon two mountain gorillas around the volcanic region on October 17, 1902 (von Beringe, 2002, p.9). Von Beringe captured and killed one of them and sent the body to the Zoological Museum in Berlin, Germany. Professor Paul Matschie, who worked with the museum, identified the gorilla as a new class and named it after its founder: Gorilla beringei beringei (von Beringe, 2002, p.10). Twenty-three years later, American naturalist Carl Akeley persuaded King Albert of Belgium to turn a Belgian trust territory, near Rwanda, into a national park for the conservation of mountain gorillas. The Albert National Park, later named the Virunga National Park, was the first park established in Africa (Ngowi, 2002).   Ã‚  Ã‚  Ã‚  Ã‚  Between 1960 and 1980, American zoologists studied mountain gorillas. George Schaller spent one year doing basic study on the animal. Dian Fossey devoted her life to extensively studying and protecting mountain gorillas. Fossey moved to Rwanda to be closer to the animals and set up the Karisoke Research Center in 1967 (Robbins et al., 2001). She directed the center for thirteen years, learning the habits and gaining the acceptance of the mountain gorillas (Robbins et al., 2001). In 1983, she wrote a book, Gorillas in the Mist, to promote public awareness of the troubles mountain gorillas face. Her memoir was later made into a movie. Her relationship with mountain gorillas and concern for their safety was unmatched. She created an organization to save gorillas in 1978 called the Digit Fund, named after a mountain gorilla Fossey was close to (Robbins et al., 2001). After her mysterious death in 1985, the organization switched its name to the Dian Fossey Gorilla Fund International. Fossey contributed to much understanding of mountain gorillas.   Ã‚  Ã‚  Ã‚  Ã‚  Dian Fossey was so driven to protect mountain gorillas because they are an endangered species. Several threats have kept their population from thriving. One threat is disease, especially those which humans are equally as vulnerable to (Ferber, 2000). Tourists enjoy visiting the mountains of Rwanda to admire the gorillas and encourage their safety; however, humans help put mountain gorillas at risk. In 1999, a team of researchers with the Journal of Parasitology noted roundworm parasites in the feces of mountain gorillas (Ferber, 2000). These parasites normally have affected only humans through contaminated water. Early, in 1988, blood and tissue samples of several mountain gorillas indicated measles infection (Ferber, 2000).

Interconnected :: Biodiversity Science Biology Essays

Interconnected â€Å"Loving nature is not the same as understanding it.† Like the majority of the human race, Harriet in Gary Larson’s [JH1] book, There’s a Hair in my Dirt, â€Å"‘not only [misunderstand] the things she saw – vilifying some creatures while romanticizing others, - but also her connection to them’† (Larson 1998). The human race is one big Harriet; we see what is on the surface and never truly understand what lies beneath because we fail to even look. In order to understand ourselves, we must first understand what makes us and shapes us. Perhaps this is why we should understand biodiversity and the effects it has on us and science. All living things need each other to survive. We need the trees to breathe, they need us to produce CO2 for photosynthesis, and they also need the worms to cultivate the land for rich soil. Hence, we could imply that we need the worms to breathe. It’s more than that, though. The whole concept of biology, or even science, revolves around the intricate connections between all of its aspects. We need to understand biodiversity to understand our connections to all living things. In order to understand biodiversity we need to use systematics. In order to understand systematics we need to understand taxonomy, phylogeny, evolution and all the other parts. Every part of who we are is saturated in everything around us and yet we do not even try to take the time to absorb a drop of it. Despite the fact that we consider ourselves to be the most intelligent of the species living on this planet today, our egos and independence, our ignorance and manipulation, allow the understanding of our very existence on this earth to pass us by. In order to truly understand who we are, we need to come nose to nose with the earthworms. In understanding biodiversity, we will be able to harvest the benefits that come from it. Not only will we be able to understand our connections with all living things, but our connection with the environment as well. Interconnected :: Biodiversity Science Biology Essays Interconnected â€Å"Loving nature is not the same as understanding it.† Like the majority of the human race, Harriet in Gary Larson’s [JH1] book, There’s a Hair in my Dirt, â€Å"‘not only [misunderstand] the things she saw – vilifying some creatures while romanticizing others, - but also her connection to them’† (Larson 1998). The human race is one big Harriet; we see what is on the surface and never truly understand what lies beneath because we fail to even look. In order to understand ourselves, we must first understand what makes us and shapes us. Perhaps this is why we should understand biodiversity and the effects it has on us and science. All living things need each other to survive. We need the trees to breathe, they need us to produce CO2 for photosynthesis, and they also need the worms to cultivate the land for rich soil. Hence, we could imply that we need the worms to breathe. It’s more than that, though. The whole concept of biology, or even science, revolves around the intricate connections between all of its aspects. We need to understand biodiversity to understand our connections to all living things. In order to understand biodiversity we need to use systematics. In order to understand systematics we need to understand taxonomy, phylogeny, evolution and all the other parts. Every part of who we are is saturated in everything around us and yet we do not even try to take the time to absorb a drop of it. Despite the fact that we consider ourselves to be the most intelligent of the species living on this planet today, our egos and independence, our ignorance and manipulation, allow the understanding of our very existence on this earth to pass us by. In order to truly understand who we are, we need to come nose to nose with the earthworms. In understanding biodiversity, we will be able to harvest the benefits that come from it. Not only will we be able to understand our connections with all living things, but our connection with the environment as well.

Injustice: Black People and Martin Luther King Essay

In a â€Å"Letter from Birmingham Jail†, Martin Luther King, Jr. said â€Å"injustice anywhere is a threat to justice everywhere.† This means that if we let injustice happen, then this injustice will grow and start to affect good people. We cannot afford to ignore something bad happening in one place. If injustice occurs and no action is taken against this injustice, then people who hear about what happened might think this injustice is acceptable, and continue being unfair. In â€Å"Justice & Injustice† Eloy Ponce says, â€Å"if we allow injustices to be committed against other people, those injustices too, could soon be committed against us.† Ponce’s idea interested me because it is also a true statement. If we let injustice happen, the injustice will be committed against us. When there was segregation, most white people didn’t do anything to help the African Americans. White people let segregation happen whether they agreed or disagreed with the kind of treatment the black people received because whites were not affected directly. Due to this, these days, some black people accuse white people of being racist. There were some white people that did stand up for the rights of blacks, and a few even died for this belief. They were people that truly understood the meaning of justice, and knew that if nothing was done, the injustice being committed would threaten justice everywhere. Justice and injustice are often in a battle of which is stronger. Acts of injustice spread easily, overcoming the ideals of justice. When a crowd acts, it is very difficult for people to standup against the crowd. It is easier for everyone to say they agree, even though they truly disagree. Only the brave few are willing to accept the consequences of standing up for what they believe in. I think this is what Martin Luther King, Jr. meant when he said â€Å"injustice anywhere is a threat to justice everywhere.† It is a person’s moral responsibility to uphold just ideas.