Learn How to Say to Smoke in French

Learn How to Say to Smoke in French How would you say to smoke in French? If you answered with the verb  fumer, then youd be correct. Its an easy one to remember if you associate it with the English fume. It might also be helpful to know that when you need to extinguish a flame, youll use the verb  expliquer.   Conjugating the French Verb  Fumer Admittedly, French verb conjugations can be a challenge for French students. Thats because there are more words to remember since we conjugate for all the subject pronouns within each tense. Yet,  fumer  is a  regular -ER verb  and this is the most common conjugation pattern in French. This makes it a little easier if youve worked with a few verbs before. As with all conjugations, we need to identify the verb stem, which is  fum-. Then we can begin to add the many endings and form a complete sentence. For example, I smoke is je fume and we will smoke is ​nous fumerons. Study this chart and practice the forms in context to make memorization a little quicker. Subject Present Future Imperfect je fume fumerai fumais tu fumes fumeras fumais il fume fumera fumait nous fumons fumerons fumions vous fumez fumerez fumiez ils fument fumeront fumaient The Present Participle of  Fumer The  present participle  of fumer  is  fumant. Notice how this was as simple as adding -ant  to the verb stem. Its a very useful word as it can be a verb, adjective, gerund, or noun depending on the context. The Past Participle and Passà © Composà © Beyond the imperfect, another common form of the past tense smoked is the  passà © composà ©. This is formed using the  past participle  fumà ©Ã‚  along with a conjugate of the  auxiliary verb  avoir. For example, I smoked is jai fumà © while we smoked is nous avons fumà ©. More Simple  Fumer  Conjugations to Learn Those are the most important forms of  fumer  and should be the  top priority for memorization. There are more simple conjugations you may need at times and theyre used in special circumstances. For instance, in a conversation when the act of smoking is not guaranteed, the subjunctive or the conditional verb mood may be used. If you do much reading in French, you will also encounter the passà © simple. This form, as well as the imperfect subjunctive, may not be widely used, but they are good to know anyway. Subject Subjunctive Conditional Pass Simple Imperfect Subjunctive je fume fumerais fumai fumasse tu fumes fumerais fumas fumasses il fume fumerait fuma fumt nous fumions fumerions fummes fumassions vous fumiez fumeriez fumtes fumassiez ils fument fumeraient fumrent fumassent In short and direct commands and requests, we can drop the subject pronoun and simplify things in the imperative form. Rather than saying tu fume, you can just use fume. Imperative (tu) fume (nous) fumons (vous) fumez

Refugees and Races Research Paper Example | Topics and Well Written Essays - 1000 words

Refugees and Races - Research Paper Example The countries of the world, especially those who preach against the very factors that drive refugees out of their homes, is expected to open their communities and societies in order to receive these poor souls. But the fact is that some of them refuse accepting immigrants or impose restrictions on refugees. For the purposes of this paper, several countries would be cited in order to provide a picture about sorry state of policies governing refugees. The first of these is Australia. The country has a number of codes and legal guarantees for the acceptance of refugees. For instance, there is the Section 91R of the Migration Act of 1958, which identifies the requirements for an immigrant that should be accepted because he or she is a refugee. In a specific case that is already part of the Australian jurisprudence, Applicant A v MIIEA, it was held that "as long as the discrimination constitutes persecution and is inflicted for a Convention reason, the person will qualify as a refugee." ( Bagaric and Vrachnas 2006, 296) However, recent events demonstrate a different reality with regards to the Australian refugee policy. In 2001, hundreds of Afghans and Iraqis being persecuted at home and hoping for sanctuary in Australia were met with Australian warships effectively sending them to Indonesia, where they languished for weeks with uncertain future, having no country of their own (Timberlake 2001). Recently, 430 Sri Lankan and Pakistani refugees also suffered the same faith when Australia refused to accept them after they were rescued by a Norwegian cargo ship (Mail Online 2011). The fact is that Australia has been enforcing tougher immigration policy and could be found discriminating against refugees, particularly boat people, even though they fit the profile of those persecuted individuals that the country ideally welcomes with open arms. According to Sidoti, the National spokesperson of Human Rights Council of Australia: The most recent refugee arrivals in Australia have been predominantly from Afghanistan and Iraq and they have been predominantly Muslim. They have experienced discrimination on these bases along with other Muslim and Middle Eastern residents of Australia. The NSW Police Commissioner recently reported a great increase of attacks on Muslim or Middles Eastern residents of the state since the Bali bombing on 12 October... They have also included stones thrown through the windows of the homes and shops of Muslims (2002).. The same can also be said about the United Kingdom. This country has a long anti-immigration history. For example, the Merchant Shipping Act of 1906 introduced a language test for those signing in British ships in the UK, meaning to discriminate against all non-white sailors. (Shah 2000) It was only after the 1980s when the UK government started to encourage plurality. It was a gradual process that has been characterized by community resentments and race riots, considering the way the British see immigrants as fore ign and alien. Today, the country's immigration and refugee policies are characterized by a particular aversion to non-white applicants and is still reminiscent of the Merchant Shipping Act by mandating English proficiency, along with other stringent requirement for all immigrants designed to weed out undesirable races. By 1990s, the UK has accumulated a series of measures that strengthened immigration controls, especially those that made it more difficult for asylum seekers to enter the country by imposing visa requirements on the countries from which asylum seekers came and imposing a duty on carriers to ensure that only

Importance of islamic spain and its legacy Essay

Importance of islamic spain and its legacy - Essay Example Islam is said to have been practiced in Spain as early as the year 709. At this time, Spain was still non-existent and the area was the Iberian Peninsula. It was not until 711 that Islam stamped its authority in the area. This was as a result of the need to stamp out the despotic rule of King Roderick who violated the peoples’ rights with reckless abandon. Tariq Ibn Ziyad successfully led the Muslim armies and concurred the area. In a time span of seven years, the Muslims had gained total control of the area and they ruled some parts of this the area for seven hundred years. After these years, Islam began to weaken. By the year 950, Muslims formed one of the strongest and most stable societies under the rule of the able Umayyad Caliphate in the area of Al-Andalus. Out of a population of over eight million at the time, only one million was not Muslim. As a result of the stability, Cordoba as the capital of this region was sought after by Muslims and other Europeans in search of education. The downfall of Muslim rule began when the ruling caliphate disintegrated in the year 1000 to form several but weakened states that were known as Taifa. The disunity in these small states made them susceptible to attacks by Kingdoms of Christian background. The Taifas fell apart under the attack of the Christian Kingdoms until only one, the Granada was left by 1240. Granada was able to resist attacks as it was protected by mountains that made it difficult to conquer by the Christian factions. However, the disunity in the Muslim faction finally led to the concur of Granada as the Christian faction worked together tirelessly until they took over Granada in 1491 by forcing Sultan Muhammad the Muslim Leader append his signature on the treaty that required him to cede control to the Christian kingdom then.(lostislamhistory.com). After the conquest, the Christians made Islam illegal in Granada in 1502 and became very harsh to Muslims. The intolerance led to a mass exodus of Mu slims to the Northern parts of Africa. Those who remained could not express their faith in Islam. The exodus continued till in the 1600 when almost all Muslims had left Granada as a direct consequence of the religious bigotry. Those who remained behind were forced to join the Catholic Church but it was just for safety. They still secretly practiced Islam.It was not until 1960 when Islam began to re-establish itself in Spain. Most of the Muslims in Spain from that time to 1970 were immigrants from Morocco who desired to get into France and other countries further north. They were discouraged by the strict immigration rules of these countries and decided to settle down in Spain. Islam sprouted once again. Other migrants of Muslim orientation who settled in Spain included those from Iraq, Syria, Lebanon and Jordan. These groups came to Spain either as businesspersons or learners. The number was slightly boosted by refugees from Iran in 1979. The influx of immigrant Muslims into Spain t ogether with the previous History of Islam is believed to have encourage many Spaniards to convert to Islam. They easily identified with it from the ancient times. (Mathew, 2009). Islam began to take route again in Spain leading to its legal recognition by the Government in 1992. By 1992, the percentage of Spanish Muslim converts was nearly equal to the number of immigrant Muslims in Spain. Apart from the rich historical legacy of Islam in Spain, Islam also significantly influenced the culture of the Spanish people. Current

I DO NOT HAVE A TOPIC Essay Example | Topics and Well Written Essays - 750 words

I DO NOT HAVE A TOPIC - Essay Example Pollution could also destroy the ozone layer thus altering the climatic condition of the region. This would significantly affect the residents since in terms of tourism since it is one of the major economic activities in the area (Mullerat & Brennan, 2011). †¢ Mission statement: they aim at being the best-loved boutique hotel and restaurant by the guests, owners, and all stakeholders by provide excellent service and care and delivering financial returns to investors (Clarke & Chen, 2009). The company has been involved in multiple social responsibilities. However, regarding the loyalty of the customers that has enabled the company to be among the best in the world, it is only fair that the company continue giving back to the society. The headquarter of Kimpton is located in one of the largest cities in the area (Sun, Stewart, & Pollard, 2010). This means that the population in the area is high: and densely populated. With the improved economic conditions in the area due to high tourism levels, most of the population here own cars and the remaining part of the population use public transport. Some of these cars could result into air pollution if they happen to emit fumes. In addition, this city houses various companies and industries. Such industries pollute the environment through emission of dangerous fumes and introducing waste material into the water sources. Considering that the organization is aimed at creating a good brand image, reducing the levels of pollution is a good move to ensure that the organization saves money from the residents of the area. The reason is that air or water pollution could result into multiple health defects and reducing or eliminating them saves this medical money for such residents (Hancock, 2009). The program is very cost effective especially considering that the company already campaigns for the use of renewable energy in the

Etiology of Parkinsons Disease

Etiology of Parkinsons Disease Parkinson’s Disease is the second most common neurodegenerative disease, after Alzheimer’s. Onset typically occurs late in life, affecting approximately 1% of 65 year olds, with the prevalence increasing to 4-5% by age 85 (Dawson Dawson 2003). There are also rare cases of early-onset Parkinson’s, which are usually familial. Research into the gene mutations discovered in such hereditary cases has also contributed to the understanding of the aetiology of the spontaneous, late onset form of the disease. Parkinson’s Disease (PD) is characterized clinically by tremors at rest, bradykinesia (slowness of voluntary movement), muscle rigidity, decrease in postural reflex and facial expression and an altered gait (Kumar et al. 2005). A subset of patients (10-15%) also develop dementia. Symptoms are progressive and result in decreased mobility and eventually severe disability. The symptomatic motor disturbances arise from the progressive loss of dopaminergic neurons in the substantia nigra of the brain. This results in a decrease in the dopaminergic content of the striatum. These areas play an important role in modulating feedback from the thalamus to the motor cortex. AIMS AND OBJECTIVES This report aims to investigate the current knowledge of the aetiology of PD, by examining evidence in the literature. It is crucial to understand the pathological mechanisms underlying the selective destruction of dopaminergic neurons in PD so that effective treatments and prophylaxis can be developed. PROPOSED STRATEGY Researchers have studied the molecular mechanisms of PD pathogenesis using a number of techniques: in vitro tissue cultures of human and animal neurons, post-mortem human brain tissue, mouse models of the disease, genetic studies and more novel techniques such as the use of ‘cybrids’. Evidence from all of these will be amalgamated and conclusions drawn. MOLECULAR PATHOGENESIS OF PD That PD is generally associated with old age must be considered an important clue when trying to elucidate the causal mechanism of PD. The same is also true of the most common neurodegenerative disease, Alzheimer’s Disease (AD). Both are also characterised by an accumulation of protein aggregates resulting in progressive neuronal loss, suggesting a common underlying pathology. Histological brain sections of PD patients shows characteristic, large inclusion bodies in the cytosol of surviving neurons of the substantia nigra, as well as locus ceruleus and surrounding brainstem nuclei, called Lewy bodies (Kumar et al. 2005). These are aggregates of à ¯Ã‚ Ã‚ ¡-synuclein (Spillantini et al. 1997), a protein whose gene (SYN, aka PARK 1) has been linked to familial PD (Athanassiadou et al. 1999), as well as other proteins such as ubiquitin and synphilin-1. It is unclear whether these aggregates contribute to the pathogenesis, are a simple by-product or even part of an attempted protective mechanism, described as the aggresome theory (McNaught et al. 2002). Some evidence has recently been produced by Setsuie and colleagues (2005), using a PD rat model in which proteasome inhibitors caused inclusion formation, which resulted in decreased dopaminergic neuronal death that normally follows 6-hydroxyl dopamine (6-OHDA) administration. Lewy bodies are also found in low numbers in normal aging and AD (Jellinger 2001). However, Lewy bodies are not found in some cases of juvenile onset PD, which suggests that the inclusions are not crucial for neuronal death in the substantia nigra (Fahn Salzer 2004). Animal models of the disease, created using neurotoxins such as rotenone or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), or transgenic mice that overexpress human SYN gene (for à ¯Ã‚ Ã‚ ¡-synuclein) mutations, do not faithfully replicate the structure and antigenicity of the Lewy bodies found in PD (Dickson 2001). This highlights the problems associated with designing and producing an accurate animal model of human disease, which can be valuable tools, despite some limitations. Role of the ubiquitin-proteasome system (UPS) Although the precise role of Lewy bodies in the pathogenesis of PD is still unclear, the accumulation and aggregation of proteins suggests that there is a deficit in the cellular systems that normally remove and degrade abnormal proteins. The ubiquitin-proteasome system (UPS) is one such pathway, and there is growing evidence that implicates this system in PD. In conjunction with the enzymes E1, E2 and E3, ubiquitin is activated and attaches to abnormal proteins to form a polyubiquitin chain. The proteasome recognises this complex and degrades the unwanted protein. The ubiquitin polymer is released from the targeted protein and digested by ubiquitin carboxy-terminal hydroxylases (UCHs), to release ubiquitin monomers back into the system (Alberts et al. 2002). Ubiquitination and recognition of proteins to be degraded are ATP-dependent processes. If the activity of this clearance pathway decreases, misfolded or oxidatively damaged proteins will accumulate rather than being recycled (Sherman Goldberg 2001). Studies of the rarer, familial cases of PD have revealed evidence that this system is involved in PD aetiology, which has aided the understanding of the pathogenesis of sporadic PD. Gene mutations for two proteins that are involved in the UPS are of particular significance. Kitada and colleagues (1998) demonstrated a link between mutations in the parkin gene (aka PARK 2) and familial incidence of autosomal recessive juvenile parkinsonism (AR-JP) in Japanese families. Parkin is an E3 ligase within the UPS, and has been shown to have a neuroprotective role (Petrucelli et al. 2002). Despite this, parkin null-mutant mice exhibited normal behaviour and brain morphology, with no loss of dopaminergic neurons. Dopamine levels were altered, suggesting a possible role in dopamine regulation (Goldberg et al. 2003). Drosophila parkin null-mutants showed a consistent pattern of pathology, with locomotor deficits, sterility and decreased lifespan (Greene et al. 2003). These were attributed to mito chondrial dysfunction, which is also a feature of PD (see below). Research into the potential toxic effects of accumulation of parkin substrates has been inconclusive (Betarbet et al. 2005). Evidence points to parkin involvement in the pathogenesis of PD, but mutations of this protein are not sufficient alone to cause the disease. A missense mutation for the gene encoding the protein UCH-L1 has been detected in autosomal dominant familial cases of PD in Germany (Leroy et al. 1998). In sporadic cases of PD, UCH-L1 is downregulated and oxidized in the cerebral cortex (Choi et al. 2004), the significance of this is unknown. UCH-L1 mutations in mice produce neuromotor signs that are not typical of PD, and are characterised as Gracile Axonal Dystrophy mice (GAD). As for parkin, the evidence confirms some involvement in PD pathogenesis of these elements of the UPS, but points to the need for further research to fully deduce their role. Other genetic mutations have been identified, such as LRRK2 (a kinase;Zimprich et al. 2004) and DJ-1 (aka PARK 7), which is involved in a similar protein degradation pathway (SUMO; Bonifati et al. 2003). It is tempting to attribute the accumulation of à ¯Ã‚ Ã‚ ¡-synuclein to a decrease in activity of the UPS, but evidence that à ¯Ã‚ Ã‚ ¡-synuclein is a substrate of this system is contradictory (Paxinou et al. 2001), with results differing between in vitro cell lines and conditions. Some studies suggest that à ¯Ã‚ Ã‚ ¡-synuclein accumulation may inhibit the UPS, resulting in further protein accumulation (Liu et al. 2005). Role of mitochondrial dysfunction and oxidative stress A significant amount of evidence supports the hypothesis of involvement of the UPS in PD aetiology. In familial cases genetic mutations have been discovered that account for a portion of the susceptibility to, and pathogenesis of PD; but other factors are obviously required for both early onset and sporadic cases to develop. UPS activity has been found to be lowered in sporadic PD patients, with impaired proteasomal activity and reduced expression of subunits in the substantia nigra (McNaught et al. 2003). Whether UPS impairment is a primary cause or secondary to another event is not yet clear. Some researchers believe that the mechanism underlying the dysfunctional UPS may involve mitochondrial dysfunction, which has also been implicated in other neurodegenerative diseases (Hashimoto et al. 2003). During energy production by respiration in the mitochondria, there is a continuous leakage of free radicals, such as reactive oxygen species (ROS), which are also released by inflammatory cells. Antioxidant mechanisms exist to mop these up before they can cause oxidative damage to surrounding molecules, such as proteins, lipids and DNA, but these are not 100% efficient. This results in a gradual increase in damaged cellular components with aging (Vigoroux et al. 2004). Higher levels of oxidization products have been found in brain tissue of patients with neurodegenerative diseases such as PD (Dexter et al. 1994) and suggest an important role for free radicals in its aetiology. Mitochondrial DNA (mtDNA) damage has been hypothesised to accumulate, leading eventually to mitochondrial dysfunction, which further increases free radical leakage. Mitochondrial complex I, in particular, has been implicated. Induced parkinsonism in animal models using the pesticide rotenone has been shown to inhibit mitochondrial complex I (Sherer et al. 2002). Administration of MPTP also induces PD symptoms and inclusion body formation, via the complex I inhibition of its metabolite MPP+ (Ram say et al. 1986). This has been recorded in human subjects following the use of illicitly manufactured narcotics, in which MPTP is produced as a contaminant, but has now been used to reliably induce disease in rodents to further knowledge of the pathogenesis of this disease. As well as providing valuable insights into the mechanisms underlying PD, the ability of chemicals to produce the symptoms and pathology of PD has also raised concerns about the role of environmental factors in the aetiology of the sporadic disease. Some epidemiological studies have linked pesticide exposure to an increased risk of developing PD (Park et al. 2005), as well as suggestions that increased coffee/caffeine consumption and smoking (Wirdefeldt et al. 2005) may have some protective benefits. Exposure to heavy metals, such as manganese has also shown a correlation with PD in some studies, but not all. Heavy metals are known to accelerate free radical formation and hence increase oxidative stress, so it w ould not be unexpected if higher levels were involved in PD aetiology. Results of epidemiological studies that claim to prove these positive and negative correlations with PD are contradictory, and further research is required, which could also take diet into account (particularly ingested antioxidant levels and lifestyle). Mitochondrial dysfunction may cause a decrease in UPS activity, either by reduced ATP production, which is essential for many processes of the pathway, and/or by increasing oxidative stress and damaging vital components of the system (Fahn Salzer 2004). The pivotal role of mitochondria has been elegantly demonstrated by the use of cytoplasmic hybrids. These ‘cybrids’ are formed by taking mtDNA from platelets of patients with PD and inserting it into cultured human neuroblastoma cells that have been depleted of their endogenous mtDNA. These neuronal cells faithfully recapitulate the structure and antigenicity of Lewy bodies (Trimmer et al. 2004), and similar studies have reported other pathogenic features consistent with a role for mitochondria and oxidative stress in PD. It is now widely accepted that oxidative stress is a contributory factor to PD aetiology, with markers of oxidative damage found to be higher than in non-PD controls. Antioxidants have been administered in a number of studies to further explore the impact of free radicals and therapeutic/prophylactic options. Transgenic mice that overexpress the endogenous antioxidant Cu,Zn-superoxide dismutase did not show any symptoms or DA neuron loss following exposure to paraquat (herbicide)-maneb (fungicide), compared to non-transgenic controls (Thiruchelvam et al. 2005). Studies involving exogenous antioxidants have produced inconclusive results, and more research is required in this area. The specificity of dopaminergic neuronal loss, mainly in the substantia nigra pars compacta, in PD is replicated in chemically induced animal models of disease. The reason for this consistent and specific pattern of neuropathology may be due to the oxidation properties of DA, with highly reactive DA-quinones being generated. These are able to form complexes with à ¯Ã‚ Ã‚ ¡-synuclein and may inhibit mitochondrial complex I (Asanuma et al. 2003). This has important implications for the commonly used L-DOPA therapy, which may also contribute to neurodegeneration. Some researchers also believe that inflammation may play a role in PD, as microglial cells proliferate in affected brain regions (McGeer McGeer 2004). CONCLUSION The aetiology of Parkinson’s Disease is multifactorial, with a combination of genetic, environmental and possibly immunological factors, many of which are still unknown or poorly understood. There is growing evidence from a variety of research techniques that oxidative stress, mitochondrial dysfunction and deficits in protein degradation pathways, such as the UPS are interlinked. The aetiological factors initiate a process that culminates in the accumulation and aggregation of proteins, mainly à ¯Ã‚ Ã‚ ¡-synuclein, in dopaminergic neurons of the nigrostriatal system, which leads to cell-death. Further research is required to fully elucidate the precise molecular mechanisms that underlie the neuropathology of PD, so that effective treatments or prophylactic advice can be established. REFERENCES Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., Walter, Molecular Biology of the Cell. 4th Ed. New York: Garland Publishing. pp.359-363. Asanuma, M., Miyazaki, I. Ogawa, N. 2003 Dopamine- or L-DOPA-induced neurotoxicity: the role of dopamine quinone formation and tyrosinase in a model of Parkinsons disease. Neurotox Res 5, 165-76. Athanassiadou, A., Voutsinas, G., Psiouri, L., Leroy, E., Polymeropoulos, M. H., Ilias, A., Maniatis, G. M. Papapetropoulos, T. 1999 Genetic analysis of families with Parkinson disease that carry the Ala53Thr mutation in the gene encoding alpha-synuclein. Am J Hum Genet 65, 555-8. Betarbet, R., Sherer, T. B. Greenamyre, J. T. 2005 Ubiquitin-proteasome system and Parkinsons diseases. Exp Neurol 191 Suppl 1, S17-27. Choi, J., Levey, A. I., Weintraub, S. T., Rees, H. D., Gearing, M., Chin, L. S. Li, L. 2004 Oxidative modifications and down-regulation of ubiquitin carboxyl-terminal hydrolase L1 associated with idiopathic Parkinsons and Alzheimers diseases. J Biol Chem 279, 13256-64. Dawson, T. M. Dawson, V. L. 2003 Rare genetic mutations shed light on the pathogenesis of Parkinson disease. J Clin Invest 111, 145-51. Dexter, D. T., Holley, A. E., Flitter, W. D., Slater, T. F., Wells, F. R., Daniel, S. E., Lees, A. J., Jenner, P. Marsden, C. D. 1994 Increased levels of lipid hydroperoxides in the parkinsonian substantia nigra: an HPLC and ESR study. Mov Disord 9, 92-7. Dickson, D. W. 2001 Alpha-synuclein and the Lewy body disorders. Curr Opin Neurol 14, 423-32. Fahn, S. Sulzer, D. 2004 Neurodegeneration and Neuroprotection in Parkinson Disease. Neurorx 1, 139-154. Goldberg, M. S., Fleming, S. M., Palacino, J. J., Cepeda, C., Lam, H. A., Bhatnagar, A., Meloni, E. G., Wu, N., Ackerson, L. C., Klapstein, G. J., Gajendiran, M., Roth, B. L., Chesselet, M. F., Maidment, N. T., Levine, M. S. Shen, J. 2003 Parkin-deficient mice exhibit nigrostriatal deficits but not loss of dopaminergic neurons. J Biol Chem 278, 43628-35. Hashimoto, M., Rockenstein, E., Crews, L. Masliah, E. 2003 Role of protein aggregation in mitochondrial dysfunction and neurodegeneration in Alzheimers and Parkinsons diseases. Neuromolecular Med 4, 21-36. Jellinger, K. A. 2001 The pathology of Parkinsons disease. Adv Neurol 86, 55-72. Kitada, T., Asakawa, S., Hattori, N., Matsumine, H., Yamamura, Y., Minoshima, S., Yokochi, M., Mizuno, Y. Shimizu, N. 1998 Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism. Nature 392, 605-8. Kumar, V., Abbas, A.K., Fausto, N. 2005 Chapter 13. In Robbins Pathologic Basis of Disease. Pennsylvania, USA: Elsevier Saunders. Leroy, E., Boyer, R. Polymeropoulos, M. H. 1998 Intron-exon structure of ubiquitin c-terminal hydrolase-L1. DNA Res 5, 397-400. Liu, C. W., Giasson, B. I., Lewis, K. A., Lee, V. M., Demartino, G. N. Thomas, P. J. 2005 A precipitating role for truncated alpha-synuclein and the proteasome in alpha-synuclein aggregation: implications for pathogenesis of Parkinsons disease. J Biol Chem. McGeer, P. L. McGeer, E. G. 2004 Inflammation and neurodegeneration in Parkinsons disease. Parkinsonism Relat Disord 10 Suppl 1, S3-7. McNaught, K. S., Belizaire, R., Isacson, O., Jenner, P. Olanow, C. W. 2003 Altered proteasomal function in sporadic Parkinsons disease. Exp Neurol 179, 38-46. McNaught, K. S., Shashidharan, P., Perl, D. P., Jenner, P. Olanow, C. W. 2002 Aggresome-related biogenesis of Lewy bodies. Eur J Neurosci 16, 2136-48. Park, J., Yoo, C. I., Sim, C. S., Kim, H. K., Kim, J. W., Jeon, B. S., Kim, K. R., Bang, O. Y., Lee, W. Y., Yi, Y., Jung, K. Y., Chung, S. E. Kim, Y. 2005 Occupations and Parkinsons disease: a multi-center case-control study in South Korea. Neurotoxicology 26, 99-105. Paxinou, E., Chen, Q., Weisse, M., Giasson, B. I., Norris, E. H., Rueter, S. M., Trojanowski, J. Q., Lee, V. M. Ischiropoulos, H. 2001 Induction of alpha-synuclein aggregation by intracellular nitrative insult. J Neurosci 21, 8053-61. Petrucelli, L., OFarrell, C., Lockhart, P. J., Baptista, M., Kehoe, K., Vink, L., Choi, P., Wolozin, B., Farrer, M., Hardy, J. Cookson, M. R. 2002 Parkin protects against the toxicity associated with mutant alpha-synuclein: proteasome dysfunction selectively affects catecholaminergic neurons. Neuron 36, 1007-19. Ramsay, R. R., Dadgar, J., Trevor, A. Singer, T. P. 1986 Energy-driven uptake of N-methyl-4-phenylpyridine by brain mitochondria mediates the neurotoxicity of MPTP. Life Sci 39, 581-8. Setsuie, R., Kabuta, T. Wada, K. 2005 Does proteosome inhibition decrease or accelerate toxin-induced dopaminergic neurodegeneration? J Pharmacol Sci 97, 457-60. Sherer, T. B., Betarbet, R., Stout, A. K., Lund, S., Baptista, M., Panov, A. V., Cookson, M. R. Greenamyre, J. T. 2002 An in vitro model of Parkinsons disease: linking mitochondrial impairment to altered alpha-synuclein metabolism and oxidative damage. J Neurosci 22, 7006-15. Sherman, M. Y. Goldberg, A. L. 2001 Cellular defenses against unfolded proteins: a cell biologist thinks about neurodegenerative diseases. Neuron 29, 15-32. Spillantini, M. G., Schmidt, M. L., Lee, V. M., Trojanowski, J. Q., Jakes, R. Goedert, M. 1997 Alpha-synuclein in Lewy bodies. Nature 388, 839-40. Thiruchelvam, M., Prokopenko, O., Cory-Slechta, D. A., Richfield, E. K., Buckley, B. Mirochnitchenko, O. 2005 Overexpression of superoxide dismutase or glutathione peroxidase protects against the paraquat+maneb-induced Parkinsons disease phenotype. J Biol Chem. Trimmer, P. A., Keeney, P. M., Borland, M. K., Simon, F. A., Almeida, J., Swerdlow, R. H., Parks, J. P., Parker, W. D., Jr. Bennett, J. P., Jr. 2004 Mitochondrial abnormalities in cybrid cell models of sporadic Alzheimers disease worsen with passage in culture. Neurobiol Dis 15, 29-39. Vigouroux, S., Briand, M. Briand, Y. 2004 Linkage between the proteasome pathway and neurodegenerative diseases and aging. Mol Neurobiol 30, 201-21. Wirdefeldt, K., Gatz, M., Pawitan, Y. Pedersen, N. L. 2005 Risk and protective factors for Parkinsons disease: a study in Swedish twins. Ann Neurol 57, 27-33. Zimprich, A., Biskup, S., Leitner, P., Lichtner, P., Farrer, M., Lincoln, S., Kachergus, J., Hulihan, M., Uitti, R. J., Calne, D. B., Stoessl, A. J., Pfeiffer, R. F., Patenge, N., Carbajal, I. C., Vieregge, P., Asmus, F., Muller-Myhsok, B., Dickson, D. W., Meitinger, T., Strom, T. M., Wszolek, Z. K. Gasser, T. 2004 Mutations in LRRK2 cause autosomal-dominant parkinsonism with pleomorphic pathology. Neuron 44, 601-7.

Treatment of Patients with Acute Myocardial Infarction Essay -- Medic

This paper will critique a quantitative research study (Lesnecki, 2010) that examined influences of individuals that delayed seeking treatment during an acute myocardial infarction (AMI). The article examined psychosocial and environmental influences that may have played a role for the period of AMI symptom onset to actually obtaining medical treatment. The research study will be reviewed looking at background, study purpose, design and methodology, data analysis, results, discussion, limitations, and applications for nursing practice. Background Lesnecki (2010) gave a brief literature review and described the magnitude of the problem with treatment delay in patients with AMI. She touched on the prevalence of treatment delay in the United States, â€Å"310,000 people a year die of coronary heart disease in an emergency department or before reaching a hospital† (p. 185). Other research was highlighted that linked the variables of age, gender, and race to a delay in seeking treatment when having an AMI. The author discussed the importance for this type of research and emphasized â€Å"to preserve heart muscle, time is crucial† (p. 185). The author hoped to discover additional variables that could help nurses educate the public to seek prompt medical treatment when having AMI symptoms. Purpose The researcher (Lesnecki, 2010) clearly stated the purpose of the study to â€Å"identify cognitive, social, and emotional influences of individuals delaying treatment when having symptoms of an AMI† (p. 186). Variables proposed to be related to delay in seeking treatment were closely examined and the amount of influence the variables had in relation to that decision, made by the patient, were considered. Method Design ... ...d practice (4th ed.). St. Louis, MO: Elsevier Saunders. Burns, N. & Groves, S. K. (2009). The practice of nursing research: Appraisal, synthesis, and generation of evidence (6th ed.). St. Louis: Saunders Elsevier. Dracup, K. & Moser, D. K. (1997). Beyond sociodemographics: Factors influencing the decision to seek treatment for symptoms of acute myocardial infarction. Heart & Lung, 26(4), 253-262. du Prel, J. B., Hommel, G., Rohrig, B., & Blettner, M. (2009). Confidence interval or p-value? Deutsches Arzteblatt International, 106(19), 335-339. doi: 10.3238/arztebl.2009.0335 Knapp, T. R. (1998). Quantitative nursing research. Thousand Oaks, CA: SAGE Publications. Lesnecki, L. (2010, November). Factors influencing treatment delay for patients with acute myocardial infarction. Applied Nursing Research, 23(4), 185-190. doi: 10.1016/j.apnr.2008.09.004

Patients With Cerebrovascular Disorders Health And Social Care Essay

Stroke made alterations to the life or societal wellbeing of a individual. Defects may be physical, psychological and even emotional. It could take to failing or reduced strength for physical activities and palsy of one side of the organic structure. Mental alterations include decreased in memory. Depression and alterations in personality could impact a patient who experienced shot. Compare and contrast a cerebrovascular accident with a transient ischaemia onslaught in footings of direction. CVA and TIA both affects the neurologic map, both are caused by life style and diet. They differ in the continuance which the CVA lasts for more than 24 hours while TIA merely lasts for 24 hours. When it comes to medical direction, they both use acetylsalicylic acid and other anticoagulant drugs. Management for CVA and TIA includes the demand of physical therapy after the shot for the betterment of mobility position of the patient. Promote an exercising plan to recover mobility. Promote self-care activities on the unaffected side and promote hygiene. Make certain to keep normal BP to forestall ischaemia. Reposition the patient at least every 2 hours to forestall tissue and tegument dislocation. Since they have job in get downing, they are advised to hold NGT to cut down hazard of aspiration. Management of increased ICP is besides of import to see. Carotid endarterectomy or the remotion of atherosclerotic plaque from the carotid arteria is one surgical direction to forestall CVA and T IA. Identify damage of self-care that may be seen in the post-stroke patient. Damage of self-care that may be seen in post-stroke patient includes stationariness, one-sided palsy, malformations of appendages and musculus failing. The patient can non execute any physical activities and demands aid to any motion. Eye sight is besides affected with reduced ocular perceptual experience and amorphosynthesis. The patient can merely visualise object on one side. Dysphagia consequences due to impaired map of URT. The patient can non eat good and needs NGT in feeding. Urinary incontinency is one job due to impaired motor response and loss of control of urinary sphincter and irregularity possibly a job besides. Psychological jobs like cognitive, behavioural and emotional shortage need support from the nurse. Address is besides affected ( aphasia ) . Post-stroke patients are prone to clamber ulcer because of the force per unit area or the clash on the tegument to organic structure parts. Discuss eligibility standards for t-PA disposal. Identify the type of stroke t-PA may be used for. To be eligible for t-PA disposal, patient should be at least 18 old ages of age or older with a diagnosing of ischaemic shot. The clip of oncoming of shot should be 3 hours or less, with no ictus and a blood force per unit area of ? 185/110 mmHg. The sort of shot should non be minor or quickly deciding shot. Patient should non take Coumadin ( Coumadin ) and should non have Lipo-Hepin during the past 48 hours with elevated partial thrombokinase clip. Laboratory consequences are considered – Prothrombin clip should be ? 15 seconds or INR ? 1.7 and Platelet count should be ? 100,000/mma ¶Y . Patient should hold no anterior intracranial bleeding, tumor, arteriovenous deformity or aneurism, no major surgical processs done within 14 yearss, no shot, serious caput hurt or intracranial hurt within 3 months, no GI or urinary hemorrhage within 21 yearss. T-PA is used for patients who are diagnosed with shot and bosom onslaught. Given a scenario, use the nursing procedure to develop a program of attention for a patient with a intellectual aneurism. A intellectual aneurism patient may see altered degree of consciousness. With this status, the nurse should be able to keep optimum province of consciousness with GCSE?13 mental watchfulness. The nurse should measure for marks of altered degree of consciousness and critical marks particularly respiratory position. Make certain to supply patient ‘s safety by maintaining the side rails up at all times, bed in low place and working call visible radiation within the range. Reorientate the patient to environment and avoid confusion/disorientation. Protect the patient from possible hurt like ictus activity, decreased corneal physiological reaction, decreased wink, and decreased joke physiological reaction. Maintain airway patency for hypoxia can do increased intellectual blood flow and intracranial force per unit area. Discuss the differences in clinical manifestations between a haemorrhagic shot and an ischaemic shot. The clinical manifestations of haemorrhagic shot include neurological shortage, terrible concern, tinnitus, giddiness and hemiparesis. Motor, sensory, cranial nervus, cognitive maps may besides be a job. Other manifestations include purging, alteration in degree of consciousness and ictus. Nuchal rigidness may be experienced. Besides, ocular perturbations like ocular loss, double vision and ptosis may happen. In ischaemic shot, the clinical manifestations are numbness ( paraesthesia ) , failing ( paresis ) , loss of motor ability on one side of the organic structure. Other manifestations include trouble in get downing ( dysphagia ) , aphasia, ocular troubles, loss of half of ocular field ( hemiapnosia ) , dual vision and photophobia. Besides include altered cognitive abilities, psychological affect and self-care shortage. Discuss the usage of thrombolytic therapy in the patient with an ischaemic shot. Include eligibility standards. Thrombolytic therapy is a intervention used for stroke patient. The most common drug is the tissue plasminogen activator ( t-PA ) . This helps dissolves the blood coagulum in ischaemic shot. It is normally administered through IV and should be given within 3 hours period after the first symptoms begin. Before giving this thrombolytic, medical history are provided every bit good as physical test and research lab test. This thrombolytic should non be given to patients with intracranial bleeding because it is unsafe and dangerous. Pay attending to BP, the medicine taken prior to giving thrombolytic ( Coumadin ) and the consequence of research lab particularly the thrombocyte count. There are besides some complications after administrating thrombolytic such as intracranial hemorrhage, which is really common. The patient should be monitored closely for any complications at the beginning of the process and right after the process was done. Discuss possible complications that may develop as a consequence of a haemorrhagic shot. Potential complications of haemorrhagic shot include intellectual hypoxia and decreased blood flow, vasospasm, increased intracranial force per unit area and high blood pressure. Lack of oxygenated blood in the encephalon may do intellectual hypoxia. Make certain to supply the necessary O and keeping haemoglobin and haematocrit within normal degree. Abnormal blood force per unit area consequences to alter in intellectual blood flow. Make certain to administrate IV fluids to cut down viscousness of blood which consequences to normal blood flow. Another complication which is caused by an increased inflow of the Ca into the cell is intellectual vasospasm. It can be monitored by the usage of transcranial Doppler echography ( TCD ) . Calcium channel blocker like nimodipine is a medicine intervention for patient with vasospasm. An increased in intracranial force per unit area normally occur after a shot. It is of import to supervise the hydration position of the patient when utilizing mann itol medicine to cut down ICP. Besides, blood force per unit area is besides of import to measure. Hypertension is monitored and should be prevented. Web Assignment Research an article refering to the place attention facet of a patient recovering from a shot. Sum up your findings. Family support is important to stroke recovery by Kathy Boncher Last February 2008, Steve had a shot. The whole household was at that place for him. They ne'er leave him and maintain on back uping until his recovery period. While he was holding his recovery at place, everything was changed. He can non make any longer what he used to make before he had his shot. He was really dependent on his married woman who takes attention of him for his mundane demands particularly when bathing, toileting, dressing, eating and even reassigning to his wheelchair. Because of his shot, he experienced failing on the whole portion of his left side of the organic structure and his arm was truly non working. This was truly dejecting on his portion as he used to be the 1 who do all the things around the house particularly in edifice, planing and keeping their house. He used to be a edifice contractor for 38 old ages and a doodly-squat of all trades. In short, he was a really adept individual. But, despite of his status, he continue to be strong and unrecorded in a nor mal life as he used to be even though he can non work good at place even for himself. What keeps him strong was because of his household who was ever at that place and maintain on back uping him with his status. There he had his brothers assisting his married woman in all the man-work around the house. They even provided accessible country for disability and installed a wheelchair incline. He can even still travel out and pass clip to make ridicule stuff every afternoon with his other brother. So every bit serves as a free clip of his married woman from being his health professional 24/7. This means so much to him and was really grateful to hold these fantastic people beside him throughout his status. The household reassures that everybody will be all right and for him to be better and good. And, this gives him peace of head. This article merely showed us that the support of the household is really of import as a intervention in retrieving for shot patient. Some are fighting entirely for recovery without the aid of any household members. And that caused a hold in recovery of a shot patient. Family member does n't hold to be biologically related. It could be the people around us, friends, church and societal web. Everyone could give support. And, most significantly, the shot patient should hold bravery and have strong religions within him that he will be recovered and be back to his normal life.