Autism Spectrum Disorder (ASD) The WritePass Journal

Autism Spectrum Disorder (ASD) Autism Spectrum Disorder (ASD) John | July 18, 2017 Autism Spectrum Disorder Causes, Reasons and TreatmentCauses of ASDCauses of ASD GenticsTo modify or extend this essay or to get pricing on a custom essay Contact Us TodayCauses of ASD Environmental FactorsReasons for ASDASD Treatment MedicationsASD Treatment Behaviours and CommunicationConclusionTo modify or extend this essay or to get pricing on a custom essay Contact Us TodayBibliographyTo modify or extend this essay or to get pricing on a custom essay Contact Us TodayRelated Autism Spectrum Disorder Causes, Reasons and Treatment Autism Spectrum Disorder (ASD) is defined as a developmental disability that affects people’s personalities based on how they interact with the world (Magalhaes and Almeida, 2010). However, Sparks and Dager (2012, p. 187) defines ASD as â€Å"a serious neurodevelopmental disorder that impairs ones ability to communicate and interact with others.† Various ASD definitions are known to be universal since they recognise it as a spectral condition (Baird et al., 2016). In his study, Umekage (2011, p. 25), indicates that ASD is a hidden disability coupled with foetal brain damage as well as impairment of neural vitro development. Characterised by interests, activities and repetitive behaviours, ASD is so complex that it varies from one case to another (Akanksha et al., 2011). Despite various studies on the reasons, causes and treatment of ASD, there are relatively unknown rationale for its causes. Chandler and Baird (2015, p. 923) posits that people with ASD need different kinds of support since their ways of development and learning differ from every individual. The aim of this paper is to discuss the causes, reasons and treatment of ASD. Causes of ASD Although there are undetermined causes of ASD, scientists as well as medical practitioners believe that an amalgamation of genetic and environmental factors are the two major causes of ASD (Fitzgerald and Geschwind, 2013). To start with, the cause of ASD via genetic factors is not a simple process, but a complex of progression that involve multiple genes. Causes of ASD Gentics Autism Spectrum Disorder As indicated by Schechtman (2014, p.86) study, the rate of ASD development in identical twins as well as monozygotic is higher than rates in dizygotic and same-sex fraternal twins. This indicates that fraternal twins only share some genes, while identical twins have equal genes and therefore genes contributes much to autism. More so, Brothers as well as sisters of children with autism have high level of autism (Fitzgerald and Geschwind, 2013). From another perspective, Smith and John (2011, p. 803) in their research attributed that siblings share certain problems such as language as well as learning difficulties if one of the sibling has autism. However, it is not clear if autism is inherited as well as more general predisposition difficulties. To modify or extend this essay or to get pricing on a custom essay Contact Us Today Causes of ASD Environmental Factors Secondly, ASD can be caused by environmental factors. Environmental toxins such as mercury and thimerosoal vaccines cause autism stems (Mercer et al., 2016). More so, congenital rubella infection is one of the environmental factors that cause ASD. However, Goin-Kochel and Myers (2015, p. 172) disputes that there is anyclarity environmental factors causing ASD and therefore more studies needs to be done. Rich and Isager (2012, p. 410) adds â€Å"some of the evidence proposed for environmental factors is based on case reports, which are often difficult to interpret.† Reasons for ASD ASD as mentioned earlier, ASD can be caused by a combination of environmental and genetic factors, however, we have reasons ASD occurs. First, Autism exists when a single gene known as fragile X syndrome (FXS) exists in the blood (Hessl and Schneider, 2013). FXS is defined as a syndrome that is coupled with autism as well as intellectual disability (Visootsak and Picker, 2015). As per Wehner and Hagerman (2011, p. 415), â€Å"Whereas ASD is a behavioural diagnosis, FXS is a medical, or more accurately, a genetic diagnosis and therefore when associated with FXS, ASD is caused by the genetic change or mutation in the Fragile X gene.† This alters normal blood circulation, hence ASD. Secondly, individuals are affected by ASD when tuberous sclerosis, chromosome 15q and other genetic conditions subsist (Hessl and Schneider, 2013). ASD Treatment Medications Core symptoms associated with ASD have no medication and cure, but we have medications that help to manage high energy levels of ASD, seizures, inability to focus as well as depression symptoms (Burrell and Borrego, 2012). The first treatment method utilised during ASD is the early intervention service. This method improves individual’s development, especially children with ASD (Buitelaar and Wong, 2014). These services, such as vitamin therapy, auditory training, facilitated communication and physical therapy improve children talk, interaction and walk. Early intervention services attribute the theory of mind as an explanatory ASD theory that reflects on the symptom criteria (A) of the DSM-5. As per Gallese and Goldman (2012, p. 496), the theory of mind was created by Uta Frith, Alan Leslie and Simon Baron-Cohen in 1985 to explain communication persistence as well as social interaction for people with ASD. ASD Treatment Behaviours and Communication The second method used for ASD treatment is the behaviours and communication approaches. This method involves direct, organised and structural ways for people with ASD to participate in a given paediatric events and medication. As per Burrell and Borrego (2012, p. 424), applied behaviour analysis (ABA) is utilised as a treatment of ASD via behaviour and communication approach to encourage positive and discourage negative behaviours hence improving various skills needed during ASD treatment. This is in relation to the theory of executive dysfunction which states, â€Å"Executive functions (EF) are a set of cognitive skills that are put into practice through autonomous activities.† Most of these EF skills are utilised by ASD patients to boost their flexibility, organisation, objectives and goals, anticipation as well as to be able to control their impulses (Buitelaar and Wong, 2014). Thirdly, ASD can be treated through dietary approaches. Change in diet, such as using certain foods, mineral supplements and vitamin helps to treat certain ASD effects. However, Talalay and Zimmerman (2014) posit that although dietary approach is considered as one of the ASD treatment, there is no scientific support and recommendation. Finally, ASD can be treated using complementary and alternative treatments. Treatments associated with complementary and alternative approaches include chelation, biological such as secretin, special diets and body-based systems (Burrell and Borrego, 2012). Conclusion In conclusion, the aim of this paper was to discuss the causes, reasons and treatment of the Autism Spectrum Disorder (ASD). Being a hidden disability coupled with foetal brain damage as well as impairment of neural vitro development, ASD has varied and complex behaviours hence there is unknown treatment for core symptoms. Generally, ASD is caused by a combination of genetic and environmental factors such as genes inheritance and environmental toxins respectively. Some of the treatments for ASD as discussed included the used of the early intervention services, the behaviours and communication approaches, dietary approaches and complementary and alternative treatments. Characterised by interests, activities and repetitive behaviours, ASD is so complex that it varies from one case to another and therefore its treatments depends on an individual case. To modify or extend this essay or to get pricing on a custom essay Contact Us Today Bibliography Akanksha, M., Sahil, K., Premjeet, S. and Bhawna, K. (2011) â€Å"Autism spectrum disorders (ASD).† International Journal of research in ayurveda pharmacy, 2(5), pp.1541- 1546. Baird, G., Simonoff, E. and Charman, T. (2016) â€Å"Prevalence of disorders of the autism spectrum in a population cohort of children in South Thames: the Special Needs and Autism Project (SNAP).† The lancet, 368(9531), pp.210-215. Burrell, L. and Borrego, J. (2012) â€Å"Parents Involvement in ASD Treatment: What Is Their Role?.† Cognitive and Behavioral Practice, 19(3), pp.423-432. Buitelaar, K. and Wong, C. (2014) â€Å"Psychopharmacological prescriptions for people with autism spectrum disorder (ASD): a multinational study.† Psychopharmacology, 231(6), pp.999-1009. Chandler, S. and Baird, G. (2015) â€Å"Psychiatric disorders in children with autism spectrum disorders: prevalence, comorbidity, and associated factors in a population-derived sample.† Journal of the American Academy of Child Adolescent Psychiatry, 47(8), pp.921-929. Fitzgerald, R. and Geschwind, D. (2013) â€Å"Autism recurrence in half siblings: strong support for genetic mechanisms of transmission in ASD.† Molecular psychiatry, 18(2), p.137- 140. Goin-Kochel, P. and Myers, B. (2015) â€Å"Congenital versus regressive onset of autism spectrum disorders: Parents beliefs about causes.† Focus on Autism and Other Developmental Disabilities, 20(3), pp.169-179. Gallese, V. and Goldman, A. (2012) â€Å"Mirror neurons and the simulation theory of mind-reading.† Trends in cognitive sciences, 2(12), pp.493-501. Hessl, D. and Schneider, A. (2013) â€Å"Fragile X Syndrome (FXS). In Encyclopedia of Autism Spectrum Disorders 79(2), pp. 1320-1324. Magalhaes, T. and Almeida, J. (2010) â€Å"Functional impact of global rare copy number variation in autism spectrum disorder.† Nature, 466(7304), pp.368-401. Mercer, L., Creighton, S. and Lewis, S. (2016) â€Å"Parental perspectives on the causes of an autism spectrum disorder in their children.† Journal of Genetic Counseling, 15(1), pp.41-50. Rich, B. and Isager, T. (2012) â€Å"Mortality and causes of death in autism spectrum disorders: an update.† Autism, 12(4), pp.403-414. Sparks, B. and Dager, S. (2012) â€Å"Brain structural abnormalities in young children with autism spectrum disorder.† Neurology, 59(2), pp.184-192. Schechtman, M. (2014) â€Å"Scientifically unsupported therapies in the treatment of young children with autism disorders.† Psychiatric Annals, 37(9), pp. 79-92. Smith, S. and John, W. (2011) â€Å"Col4a1 mutation causes endoplasmic reticulum stress and genetically modifiable ocular dysgenesis.† Human molecular genetics, 16(7), pp.798- 807. Talalay, P. and Zimmerman, A. (2014) â€Å"Sulforaphane treatment of autism spectrum disorder (ASD).† Proceedings of the National Academy of Sciences, 111(43), pp.50-55. Umekage, T. (2011) â€Å"Association of the oxytocin receptor (OXTR) gene polymorphisms with autism spectrum disorder (ASD) in the Japanese population.† Journal of human genetics, 55(3), pp. 23-32. Visootsak, J. and Picker, J. (2015) â€Å"Advances in the treatment of fragile X syndrome.† Pediatrics, 123(1), pp.378-390. Wehner, A. and Hagerman, R. (2011) â€Å"The behavioral phenotype in fragile X: symptoms of autism in very young children with fragile X syndrome, idiopathic autism, and other developmental disorders.† Journal of developmental behavioral pediatrics, 22(6), pp.409-417. To modify or extend this essay or to get pricing on a custom essay Contact Us Today Other Links:

History of the Domestication of Donkeys

History of the Domestication of Donkeys The modern domestic donkey (Equus asinus) was bred from the wild African ass (E. africanus) in northeastern Africa during the predynastic period of Egypt, about 6,000 years ago. Two wild ass subspecies are thought to have had a role in the development of the modern donkey: the Nubian ass (Equus africanus africanus) and the Somali ass (E. africanus somaliensis), although recent mtDNA analysis suggests that only the Nubian ass contributed genetically to the domestic donkey. Both of these asses are still alive today, but both are listed as critically endangered on the IUCN Red List. The donkeys relationship with the Egyptian civilization is well-documented. For example, murals in the tomb of the New Kingdom pharaoh Tutankhamun illustrate nobles participating in a wild ass hunt. However, the real importance of the donkey relates to its use as a pack animal. Donkeys are desert-adapted and can carry heavy loads through arid lands allowing pastoralists to move their households with their herds. In addition, donkeys proved ideal for the transport of food and trade goods throughout Africa and Asia. Domestic Donkeys and Archaeology Archaeological evidence used to identify domesticated donkeys includes changes in body morphology. Domestic donkeys are smaller than wild ones, and, in particular, they have smaller and less robust metacarpals (foot bones). In addition, donkey burials have been noted at some sites; such burials likely reflect the value of trusted domestic animals. Pathological evidence of damage to spinal columns resulting from donkeys use (maybe overuse) as pack animals is also seen on domestic donkeys, a situation not thought likely on their wild progenitors. The earliest domesticated donkey bones identified archaeologically date to 4600-4000 BC, at the site of El-Omari, a predynastic Maadi site in Upper Egypt near Cairo. Articulated donkey skeletons have been found buried in special tombs within the cemeteries of several predynastic sites, including Abydos (ca. 3000 BC) and Tarkhan (ca. 2850 BC). Donkey bones also have been discovered at sites in Syria, Iran, and Iraq between 2800-2500 BC. The site of Uan Muhuggiag in Libya has domestic donkey bones dated to ~3000 years ago. Domestic Donkeys at Abydos A 2008 study (Rossel et al.) examined 10 donkey skeletons buried at the Predynastic site of Abydos (about ca 3000 BC). The burials were in three purposefully constructed brick tombs adjacent to the cult enclosure of an early (so far unnamed) Egyptian king. The donkey tombs lacked grave goods and in fact, only contained articulated donkey skeletons. An analysis of the skeletons and comparison with modern and ancient animals revealed that the donkeys had been used as beasts of burden, evidenced by signs of strain on their vertebral bones. In addition, the body morphology of the donkeys was midway between wild asses and modern donkeys, leading researchers to argue that the domestication process was not complete by the end of the predynastic period, but instead continued as a slow process over periods of several centuries. Donkey DNA DNA sequencing of ancient, historic and modern samples of donkeys throughout northeastern Africa was reported (Kimura et al) in 2010, including data from the site of Uan Muhuggiag in Libya. This study suggests that domestic donkeys are derived solely from the Nubian wild ass. Results of the testing demonstrate that Nubian and Somali wild asses have distinct mitochondrial DNA sequences. Historic domestic donkeys appear to be genetically identical to Nubian wild asses, suggesting that modern Nubian wild asses are actually survivors of previously domesticated animals. Further, it seems likely that wild asses were domesticated several times, by cattle herders perhaps beginning as long ago as 8900-8400 calibrated years ago cal BP. Interbreeding between wild and domestic asses (called introgression) is likely to have continued throughout the domestication process. However, Bronze Age Egyptian asses (ca 3000 BC at Abydos) were morphologically wild, suggesting either that the process was a long slow one, or that wild asses had characteristics that were favored over domestic ones for some activities. Sources Beja-Pereira, Albano, et al. 2004 African origins of the domestic donkey. Science 304:1781. Kimura, Birgitta. Donkey Domestication. African Archaeological Review, Fiona Marshall, Albano Beja-Pereira, et al., ResearchGate, March 2013. Kimura B, Marshall FB, Chen S, Rosenbom S, Moehlman PD, Tuross N, Sabin RC, Peters J, Barich B, Yohannes H et al. 2010. Ancient DNA from Nubian and Somali wild ass provides insights into donkey ancestry and domestication. Proceedings of the Royal Society B: Biological Sciences: (online pre-publish). Rossel, Stine. Domestication of the donkey: Timing, processes, and indicators. Fiona Marshall, Joris Peters, et al., PNAS, March 11, 2008.