Yeha - Saba (Sheba) Kingdom Site in Ethiopia

Yeha - Saba' (Sheba) Kingdom Site in Ethiopia Yeha is a large Bronze Age archaeological site located about 15 miles (25 km) northeast of the modern town of Adwa in Ethiopia. It is the largest and most impressive archaeological site in the Horn of Africa showing evidence of contact with South Arabia, leading some scholars to describe Yeha and other sites as precursors to the Aksumite civilization. Fast Facts: Yeha Yeha is a large Bronze Age site in the Ethiopian Horn of Africa, established in the first millennium BCE.  Surviving structures include a temple, an elite residence and a set of rock-cut shaft tombs.  The builders were Sabaean, people from an Arabian kingdom in Yemen, thought to be the ancient land of Sheba. The earliest occupation at Yeha dates to the first millennium BCE. Surviving monuments include a well-preserved Great Temple, a palace perhaps an elite residence called Grat Beal Gebri, and the Daro Mikael cemetery of rock-cut shaft-tombs. Three artifact scatters probably representing residential settlements have been identified within a few kilometers of the main site but have not to date been investigated. The builders of Yeha were part of the Sabaean culture, also known as Saba, speakers of an old South Arabian language whose kingdom was based in Yemen and who are thought to have been what the Judeo-Christian bible names as the land of Sheba, whose powerful Queen is said to have visited Solomon. Chronology at Yeha Yeha I: 8th–7th centuries BCE. Earliest structure located at the palace at Grat Beal Gebri; and a small temple where the Great Temple would be constructed later.Yeha II: 7th–5th centuries BCE. Great Temple and the palace at Grat Beal Gebri built, elite cemetery at Daro Mikael begun.Yeha III: Late first millennium BCE. Late phase of construction at Grat Beal Gebri, tombs T5 and T6 at Daro Mikael. Great Temple of Yeha The Great Temple of Yeha is also known as the Almaqah Temple because it was dedicated to Almaqah, the moon god of the Saba kingdom. Based on construction similarities to others in the Saba region, the Great Temple was likely built in the 7th century BCE. The 46x60 foot (14x18 meter) structure stands 46 ft (14 m) high and was constructed of well-made ashlar (cut stone) blocks measuring up to 10 ft (3 m) long. The ashlar blocks fit together tightly without mortar, which, say scholars, contributed to the structures preservation over 2,600 years after it was built. The temple is surrounded by a cemetery and enclosed by a double wall. Foundation fragments of an earlier temple have been identified beneath the Great Temple and likely date to the 8th century BCE. The temple is located on an elevated location next to a Byzantine church (built 6th c CE) which is higher still. Some of the temple stones were borrowed to build the Byzantine church, and scholars suggest there may have been an older temple where the new church was built. Construction Characteristics The Great Temple is a rectangular building, and it was marked by a double-denticulate (toothed) frieze that still survives in places on its northern, southern, and eastern faà §ades. The faces of the ashlars display typical Sabaean stone masonry, with smoothed margins and a pecked center, similar to those at the Saba kingdom capitals such as the Almaqah Temple at Sirwah and the Awam Temple in Marib. In front of the building was a platform with six pillars (called a propylon), which provided access to a gate, a broad wooden door frame, and double doors. The narrow entrance led to an interior with five aisles created by four rows of three squarish pillars. The two side aisles in the north and south were covered by a ceiling and above it was a second story. The central aisle was open to the sky. Three wooden-walled chambers of equal size were located at the eastern end of the temple interior. Two additional cultic rooms extended out from the central chamber. A drainage system leading to a hole in the southern wall was inserted into the floor to assure that the temple interior was not flooded by rainwater. Palace at Grat Be'al Gebri The second monumental structure at Yeha is named Grat Beal Gebri, sometimes spelled as Great Baal Guebry. It is located a short distance from the Great Temple but in a comparatively poor state of preservation. The buildings dimensions were likely 150x150 ft (46x46 m) square, with a raised platform (podium) of 14.7 ft (4.5 m) high, itself built of volcanic rock ashlars. The exterior faà §ade had projections at the corners. The front of the building once also had a propylon with six pillars, the bases of which have been preserved. The stairs leading up to the propylon are missing, although the foundations are visible. Behind the propylon, there was a huge gate with a narrow opening, with two massive stone doorposts. Wooden beams were inserted horizontally along the walls and penetrating into them. Radiocarbon dating of the wooden beams dates construction between early 8th–late 6th centuries BCE. Necropolis of Daro Mikael The cemetery at Yeha consists of six rock-cut tombs. Each tomb was accessed via a staircase along 8.2 ft (2.5 m) deep vertical shafts with one grave chamber on each side. The entrances to the tombs were originally blocked by rectangular stone panels, and other stone panels sealed the shafts at the surface, and then all was covered by a mound of stone rubble. A stone enclosure fenced in the tombs, although it is unknown whether they were roofed or not. The chambers were up to 13 ft (4 m) in length and 4 ft (1.2 m) in height and were originally used for multiple burials, but all were looted in antiquity. Some displaced skeletal fragments and broken grave goods (clay vessels and beads) were found; based on grave goods and similar tombs at other Saba sites, the tombs probably date to the 7th–6th c BCE. Arabian Contacts at Yeha Yeha period III has traditionally been identified as a pre-Axumite occupation, based primarily on the identification of evidence for contact with South Arabia. Nineteen fragmentary inscriptions on stone slabs, altars and seals have been found at Yeha written in a South Arabian script. However, excavator Rodolfo Fattovich notes that the South Arabian ceramics and related artifacts recovered from Yeha and other sites in Ethiopia and Eritrea are a small minority and do not support the presence of a consistent South Arabian community. Fattovich and others believe that these do not represent a precursor to the Axumite civilization. The first professional studies at Yeha involved a small excavation by the Deutsche Axum-Expedition in 1906, then part of the Ethiopian Institute of Archaeology excavations in the 1970s led by F. Anfrayin. In the 21st century, investigations have been conducted by the Sanaa Branch of the Orient Department of the German Archaeological Institute (DAI) and the Hafen City University of Hamburg. Sources Fattovich, Rodolfo, et al. Archaeological Expedition at Aksum (Ethiopia) of the University of Naples Lorientale - 2010 Field Season: Seglamen. Naples: Universit degli studi di Napoli LOrientale, 2010. Print.Harrower, Michael J., and A. Catherine D’Andrea. Landscapes of State Formation: Geospatial Analysis of Aksumite Settlement Patterns (Ethiopia). African Archaeological Review 31.3 (2014): 513–41. Print.Japp, Sarah, et al. Yeha and Hawelti: Cultural Contacts between Saba and Dmt; New Research by the German Archaeological Institute in Ethiopia. Proceedings of the Seminar for Arabian Studies 41 (2011): 145–60. Print.Lindstaedt, M., et al. Virtual Reconstruction of the Almaqah Temple of Yeha in Ethiopia by Terrestrial Laser Scanning. International Archives of the Photogrammetry, Remote Sensing and Spatial Information Sciences 38.5/W16 (2011): 199–203. Print.Phillipson, David W. Foundations of an African Civilisation: Aksum the Northern Horn 1000 BC–A D 1300. Suffolk, Great Britain: James Currey, 2012. Print. Wolf, Pawel, and Ulrike Nowotnick. The Almaqah Temple of . Proceedings of the Seminar for Arabian Studies 40 (2010): 367–80. Print.Meqaber Gaewa near Wuqro (Tigray, Ethiopia)

The Theme of Death in the Works of Edgar Allan Poe Essay

The Theme of Death in the Works of Edgar Allan Poe - Essay Example Poe was then sent to both the Chelsea and the Stoke Newington boarding schools in the suburbs f London. Although he was a brilliant student, excelling especially in mathematics, he did not enjoy his days spent there. In July f 1820 Mr. Allan's business collapsed, and they were forced to return to Richmond in order to avoid the creditors that Allan was indebted to. Edgar Allan Poe was obviously not typical in his style f writing nor in his style f life. His father left the family when he was young and his mother was dead by the time Poe was three from tuberculosis. "So precocious a child must have carried with him, deeply imprinted, the waning figure and the coughing paroxysms f his mother." (Darkening 9). For the remainder f his tragic life, things never seemed to improve much. He lost his wife (also his cousin), Virginia, two years before his own death. After his trouble with alcoholism and general bad health, Poe died when he was about 40 years old. The exact events surrounding his death are still uncertain and somewhat mysterious. (Parker 1-5) Most f Poe's literary works were inspired by life. "Alone" is Poe's way f vocalizing the unique and dismal life that he led. He, from an apparently young age, finds himself with such different feelings about life than most people. In this poem, Poe describes his own condition f loneliness. In the first three stanzas alone, Poe discusses that since his early childhood he didn't see the world as others saw it. Even as a child his emotions were very hard to express. Anything he expressed he kept inside. In the sixth stanza, Poe writes "My sorrow; I could not awaken", meaning that because he had his emotions bottled up, he couldn't even express his sorrow. Because he couldn't express his emotions, anything he loved he couldn't love with another person, he could only love alone. There was no way he could express himself emotionally. Poe continues to reiterate that since his childhood he had this mystery surrounding him, following him wherever he went. When he did anything or went anywher e, there was this mystery or shadow that continued to bind him. This mystery could be the problem f not expressing his emotions he inherited as a child or the element f self-companionship. "His was a deviant mind, and his soul, ever lost in mystery, was possessed f demons; even elements f nature assumed their form."(Darkening 9). Ultimately Poe emphasizes this mystery as an evil or "a demon" that was haunting him. The demon was present everywhere; even the elements f nature assumed its form. Poe describes the demon as the sun rolling around him, as the thunder from the storm. Everywhere he turns and looks this evil is lurking around him, making Poe unique from others. Poe describes his uniqueness as a result f the demon that he is consumed by. The reason why he is alone, and why he can only love alone is because f this demon which he inherited as a child. (VanSpanckeren 1-5) Numerous events in Poe's life can explain why Poe may have written this poem. This poem was written in 1830, around the year where his stepmother had died and when his stepfather had remarried. The death f his "beloved step-mother reinforced the morbid consistency f Edgar's mind."(Darkening 4-5). Her death probably caused more psychological problems to Poe. He lost his biological mother and his stepmother, both f whom helped provide emotional support for

Managment Case Study Example | Topics and Well Written Essays - 1500 words

Managment - Case Study Example These new values were identified by him as they were in keeping with the current competitive and changing environment to which airlines around the world were being forced to adapt if they wished to survive. This case clearly shows that even if you have the potential and capital, if work is not organized properly, the company cannot survive. This is what this company did. Motivation and redesigning work organization structure are keys to success here. Using James Hoogan as an example of effective leadership, this essay will argue that effective leadership is a combination of strategic and operational leadership values rather than a one dimensional energizing or motivational leadership. Leadership that combines the strategic and the operational is the key requirement to turning around an organisation that is in danger of going under, because there is a lot more at stake in such a company than just a workforce that is not motivated or skilled enough. There are faulty strategies that need to be identified and isolated and changed operational values that need to be put in place to fit the strategy outlined. There is no room for experimentation as in many cases the situation is a do or die one. These situations require leaders who can do a lot more than just motivating and training the workforce with new skills. Very often motivation falls in place once the workforce sees new procedures in place and becomes convinced of the changed st rategies. Research indicates that the leadership model suggested by Kenneth Blanchard is the best for effective leadership. With competition getting stronger, leadership is the key to the success or failure of any company as the many mergers, takeovers, chapter 11s, lay offs and the few hard won success stories of the corporate world will bear out. Those companies that have the right leader in the right place at the right time manage to scrape through after resorting to stringent measures and in almost all cases after bringing in a complete change in strategy and work culture, almost a revolution. Many companies even move on to be highly successful and competitive, because their changed business strategy makes them adaptable to a changed business environment. The right leadership is crucial to ensure that this transition from a floundering business to a successful one happens smoothly and successfully. The Gulf Air story is one of a successful transition which happened only because the management of the airline was pragmatic enough to appoint James Hoogan as CEO the right time; the right man at the right time. Three years after he took over the story was a completely different one, he gave Gulf Air a completely new face, quite literally because they even sported a new uniform. In considering the role of leadership in the management of a company, this paper will compare the much acclaimed Jack Welch model with the model given by the Kenneth Blanchard Company, a model that is more acceptable today. The most successful and known model of leadership n corporate literature was given by Jack Welch which he developed with the intention of revolutionizing GE and turning it into the most competitive company in America. He himself led GE for over 20 years and during that tenure he succeeded in transforming it completely. The model of leadership given by him defines a leader as one who possesses the 4 qualities

analysis of klinefelters syndrome

analysis of klinefelters syndrome Many chromosomal abnormalities occur early in development and involve the sex chromosomes. Klinefelters Syndrome falls directly into this category. Klinefelters Syndrome is a genetic condition affecting the male population. The following information observes who discovered Klinefelters Syndrome and when it was first diagnosed. The etiology or genetic and environmental factors of the condition are discussed as well as complete description of the disability and the clear diagnostic criteria. The affects of Klinefelters Syndrome are more recognized in adulthood, when it is typically diagnosed. Many Klinefelters patients live out their entire lives without ever knowing they have the condition. Upon conclusion, there should be an adequate amount of information that will give you, the reader, valuable knowledge into the diagnosis and treatment of Klinefelters Syndrome. History Klinefelters Syndrome was first diagnosed in 1942 at the Massachusetts General Hospital in Boston Massachusetts (Schoenstadt, 2006). Dr. Harry Klinefelter was completing his fellowship at the Massachusetts General Hospital when he was assigned to work with Dr. Fuller Albright, also known as the father of endocrinology (Bock, 1993; Klinefelter Syndrome, 2006). Dr. Klinefelter came to examine nine adult men that had a common set of symptoms during the course of his fellowship (Klinefelter Syndrome, 2006). Dr. Klinefelter organized a case study that involved these nine men and their similarities and was encouraged by Dr. Albright to lead the study (Klinefelter Synrome, 2006). The Journal of Clinical Endocrinology was published in November of 1942 with the completed case study of these nine mens similar qualities, which Dr. Klinefelter identified as Klinefelters Syndrome (Klinefelter Syndrome, 2006). The report written by Dr. Klinefelter on these men described them as having testicular dysgenesis, elevated urinary gonadotropins, eunuchoidism, azoospermia, and gynecomastia, all of which have an effect on the underdeveloped size of the testes, the lack of the amount of testosterone produced by the testes, and infertility (Schoenstadt, 2006; Visootsak Graham, 2006). These adult males also exhibit enlarged breast and sparse facial hair (Schoenstadt, 2006). Two groups found out fourteen years after Dr. Klinefelters original description of the syndrome, that the buccal mucosal cells contained an extra chromatin mass or that the cells were chromatin positive (Klinefelter, 1966). Although the patients were described as having a positive female sex chromatin, Dr. Klinefelter states that the patients are phenotypic males and should never be considered otherwise (Klinefelter, 1996). Fourteen years after Dr. Klinefelter first diagnosed Klinefelters Syndrome, another case study was performed to further understand the characteristics that define the condition (Klinefelter Syndrome, 2006). In 1956, Dr. Joe Hin Tjio and Dr. Albert Lavan took the research further to determine the factors that made those men with Klinefelters Syndrome dissimilar from normal adult males through genetic research (Klinefelter Syndrome, 2006; Schoenstadt, 2006). With the advanced experimental methodology available, Dr. Joe Hin Tjio and Dr. Albert Lavan found that humans had 23 pairs of chromosomes, confirming 46 chromosomes, which prior to this time there was thought to be 48 chromosomes (Bock, 1993; Klinefelter Syndrome, 2006). This clarification by Dr. Tjio and Dr. Lavan is the basic foundation for modern cytogenetics, the study of chromosomes and diseases originating from numerical or structural abnormalities in chromosomes (Klinefelter Syndrome, 2006). Dr. Tjio and Dr. Lavan discovered that men with symptoms of Klinefelters Syndrome had an extra sex chromosome that created the chromosomal arrangement of XXY, which is distinct to the normal male chromosomal arrangement of XY (Klinefelter Syndrome, 2006; Schoenstadt, 2006,). Klinefelter Syndrome was still believed to be an endocrine disorder of unknown etiology at this time (Visootsak Graham, 2006). In 1959, just three years after Dr. Tjio and Dr. Lavan made their historical discoveries, an English researcher by the name of Dr. Patricia Jacobs and her associate Dr. J. A. Strong published a study supplementing earlier studies (Klinefelter Syndrome, 2006; Noble, 2003). Dr. Jacobs and Dr. Strong found the link between the endocrinal disease and the extra X sex chromosome (Noble, 2003). Dr. Jacobs linked forty-seven chromosomes in Klinefelters Syndrome males and determined it to be the X chromosome, which she considered an aneuploidy defined as an unusual number of chromosomes and labeled 47, XXY (Bock, 1993; Klinefelter Syndrome, 2006; Schoenstadt, 2006). The 1970s brought forth a larger examination of males born with Klinefelters Syndrome (Bock, 1993). During this time doctors began screening newborn male babies for the extra chromosome (Bock, 1993; Visootsak Graham, 2006). The most significant of the studies done at this time was sponsored by the National Institute of Child Health and Human Development (NICHD) whom examined over forty thousand infants for this extra chromosome (Bock, 1993; Visootsak Graham, 2006). This study was important for the reason that most studies done prior to the 1970s were biased and primarily done on adult males in mental institutions and the penal system (Visootsak Graham, 2006). At this time is when the prevalence of Klinefelters Syndrome was noticed as frequently as one in five hundred to one in one thousand male newborns (Bock, 1993; Visootsak Graham, 2006). Also observed in this study was the reduction in speech and language abilities as well as decreased reading and spelling achievement (Bock, 1993; Visootsak Graham, 2006). Along with these disabilities, Klinefelters patients are characterized by an increased tendency towards fertility, endocrinal, and psychiatric disorders (Noble, 2003). This study demonstrated that most but not all of these males born with the extra chromosome will have these characteristics, and many demonstrate varying degrees of the characteristics (Bock, 1993; Visootsak Graham, 2006). Based on this research it has been found that the extra X chromosome that causes Klinefelters Syndrome is very common, however, the symptoms and characteristics that are most recognizable are quit uncommon (B ock, 1993). Most males are not diagnosed as having Klinefelters Syndrome until they reach adulthood, and many that have the syndrome are never diagnosed as having this chromosomal defect at all (Bock, 1993). One pediatrician at the University of Colorado Medical School in Denver and the director of the National Institute of Child Health and Human Development (NICHD) during the major screening research referred to these newborn males as not having Klinefelters Syndrome because of the possibility that the characteristics may not develop into a syndrome (Bock, 1993; Visootsak Graham, 2006). Etiology and Genetic Factors Every normal human cell has 46 chromosomes that are made up of 23 pairs (Stewart, 2007). Of these 23 pairs, there are 22 that are exactly the same in both males and females called autosomes (U.S. National Library of Medicine, 2010). The 23rd pair of sex chromosomes is what makes males and females different in that the male will have only one X and Y chromosome whereas the female will have two copies of the X chromosome (Stewart, 2007; U.S. National Library of Medicine, 2010). During the formation of the egg and the sperm, or gametes, the chromosomes are halved through a process called meiosis (Stewart, 2007; The Dorsey, 2009). Cells that carry a single chromosome such as the X or Y chromosome are called haploid cells (The Dorsey, 2009). When the egg and sperm join carrying 23 chromosomes each they create the fertile egg, or zygote, which has two haploid sets of chromosomes (The Dorsey, 2009). Therefore, the baby receives two copies of each chromosome, 46 total chromosomes, just like the parents (Stewart, 2007). The extra X in Klinefelter Syndrome is caused from either nondisjunction or anaphase lag. Nondisjunction occurs when the chromosome pairs do not separate as they are intended in the meiosis I or meiosis II stage (Pineyard Zipf, 2003; Stewart, 2007). When this happens there may be a chromosome pair with 24 chromosomes instead of the 23 chromosomes (Stewart, 2007). If this chromosome pair of 24 joins with an egg or sperm with 23 chromosomes then it results in a karotype with 47 chromosomes (Stewart, 2007). In this case there will be three copies of chromosomes rather than the usual two copies of chromosomes (Stewart, 2007). The sperm or egg may donate the extra X chromosome at conception causing a chromosomal abnormality (Mayo Foundation for Medical Education and Research, 2008; Stewart, 2007). This forms the XXY chromosomal formation, which is diagnosed as Klinefelters Syndrome. At least half of 47, XXY conceptions are spontaneously aborted (Pineyard Zipf, 2003). The chromosomal abnormality is random and not known to be caused by any environmental factors (Genetic Science Learning Center, 2010; Mayo Foundation for Medical Education and Research, 2008; National Institute of Health, 2007). This anomaly happens entirely by chance and is unrelated to family history prior to the male childs birth (Mayo Foundation for Medical Education and Research, 2008). This is to say that the male embryos likelihood of being born with Klinefelters Syndrome is not increased or decreased by what the parent does or does not do (Mayo Foundation for Medical Education and Research, 2008). Klinefelters Syndrome is not affected by race (Chen, 2010). This is a completely random occurrence of the sex chromosomes not successfully separating during the formation of the egg or the sperm (Genetic Science Learning Center, 2010). Once this occurs the extra chromosome is then copied into every cell of the embryo (Genetics Science Learning Center, 2008). There are extremely rare cases when there may be three or four extra X chromosomes in all copies of the cells known as 48,XXXY or 49, XXXXY (Stewart, 2007). The 49, XXXXY mosaic is also known as Fraccaros Syndrome and is the most rare form of Klinefelters Syndrome (Duenas et al., 2007). This rare chromosomal abnormality results in more exaggerated features of Klinefelters Syndrome (Stewart, 2007). There are instances where an extra X chromosome is found in only some of the cells (Stewart, 2007). This can be found as two different chromosomal patterns (Stewart, 2007). One pattern occurs when some cells have 46 chromosomes and some have 47 chromosomes (Stewart, 2007). The other pattern is called the mosaic XXY syndrome, or chromosomal mosaicism, and affects approximately six percent of these cases, with the most rare cases being the 48, XXXY or the 49, XXXXY, or other arrangements of X chromosomes (Stewart, 2007). The mosaic XXY syndrome occurs only after conception from a mistake in cell division (Stewart, 2007). Anaphase lag is a result of a gamete lacking a sex chromosome (Klinefelter, 1966). When this chromosome lags it is not incorporated into the new cell during the mitosis stage (Kinefelter, 1996). Anaphase lag is thought to be a reason for the mosaic variations of Klinefelters Syndrome (Klinefelter, 1966). Although the chromosomal abnormality of 49, XXXXY is considered to be a variant form of Klinefelters Syndrome, it appears to have a very independent, distinct phenotype (Duenas et al., 2007). Males that show the 49, XXXXY chromosomal structure have much more severe clinical features than that of a Klinefelters Syndrome male (Duenas et al., 2007). This is the most rare of the Klinefelters Syndrome variants and has been reported in over one hundred cases with the frequency being approximately 1 in 85,000 newborn males (Duenas et al., 2007). There have been reports of an even more extreme variant of Klinefelters Syndrome mosaic in newborn males (Duenas et al., 2007). This variant is a 47, XXY/48, XXXY/49, XXXXY mosaicism and has only been reported in three cases according to a researcher in Mexico (Duenas et al., 2007). This means that the male newborn would have the whole spectrum of XY variations. Another variant that affects only males is the 46, XX chromosomal variation (Bock, 1993). This condition occurs when individuals have two X chromosomes in each cell, but are male in appearance. These individuals have male external geniltalia. These individuals also have small, undescended testes possibly along with an urethra opening on the underside of the penis. A small amount of 46, XX Males have external geniltalia that dont clearly resemble either male or female genitalia. These individuals are typically raised male. Phenotypically, there are three groups of these sex-reversed individuals. The first group includes phenotypically normal XX Males, the second group includes the males with genital ambiguities, and the third group is the true hermaphrodites (Bock, 1993). Description of Characteristics or Traits Klinefelters Syndrome has only one constant physical description and that is the small testicular size (Visootsak Graham, 2003). Boys with Klinefelters Syndrome have variable phenotypic characteristics with no obvious facial dysmorphology (Visootsak Graham, 2003). The presence of gynconemastia, or enlarged breast, and other findings of eunuchoid body habits and sparse body hair vary (Visootsak Graham, 2003). Eunuchoid or eunuchoidism is defined as an abnormal condition in males, characterized by underdeveloped reproductive organs with some female characteristics, such as a higher voice or the lack of facial and body hair that results in the lack of male sex hormones (Eunuchoidism, n.d.). Gonadotropins are produced by glands, such as the pituitary, and can result in sparse body hair when not produced adequately (Gonadotropin, 2010). The medical dictionary states that eunuchoidism is marked by a deficiency of sexual development with the persistence of prepubertal characteristics, and often has the presence of characteristics that are typical of the opposite sex (Eunuchoidism, n.d.). Another likely characteristic is azoospermia (Schoenstadt, 2006; Visootsak Graham, 2006). Azoospermia is defined as having little or no sperm count (Azoospermia, 2010). Testicular dysgenesis, or gonadal dysgenesis, is another characteristic of Klinefelters Syndrome (Schoenstadt, 2006; Visootsak Graham, 2006). Testicular dysgenesis is considered a reproductive system developmental disorder that causes a progressive loss of primordial germ cells, or cells that create gametes, in the developing gonads of an embryo (Gonadal dysgenesis, 2010). This gonadal dysgenesis can lead to the extremely hypoplastic, or underdeveloped, and disfunctioning gonads mainly composed of fibrous tissues (Gonadal dysgenesis, 2010). Most infants and children with the 47, XXXY chromosomal abnormalities go through normal growth stages. It is not until puberty that the Klinefelters Syndrome characteristics or traits become more prevalent and noticeable (Visootsak Graham, 2003). There is a significant increase in height between the ages of five and eight (Visootsak Graham, 2003). Another characteristic of Klinefelters Syndrome is the elongated length of arms and legs (Klinefelter, 1966). There is a decrease in androgen production that causes the secondary sexual characteristics to not fully develop (Visootsak Graham, 2003). An androgen is any substance such as androsterone or testosterone that supports male characteristics (Androgen, n.d.). Typically Klinefelters males are infertile (Visootsak Graham, 2003). However, there have been cases of impregnation without the assistance of medical technology (Visootsak Graham, 2003). Autoimmune diseases such as juvenile arthritis can also be present in Klinefelters adolescents. Whereas boys with Klinefelters Syndrome are generally tall with long limbs and remain thin until puberty, they tend to suffer from obesity latter in life. Neurocognitive effects of Klinefelters Syndrome may be more subtle than that of the physical stigmata. Klinefelters males have been found to have relative deficits on verbal IQ subtests and have verbal IQ scores around 20 points lower than those of unaffected siblings. There are also deficits in articulation, word finding, phonemic processing, verbal memory, language comprehension, oral expression problems, as well as linguistic processing speed. It seems that the speech/language problems and some motor deficits are most common in Klinefelters males that have an extra X chromosome. Ninety-two percent of individuals with Klinefelters Syndrome confirm difficulty learning to read. Seventy percent had reading achievement discrepancies or absolute reading deficits on standardized testing. A group of boys with mental retardation and suspicion of fragile X were subject to a genetic screening and the results showed that eight of these boys had Klinefelters Syndrome. Most of the more extreme verbal, visuospatial, and motor skills, such as found in mental retardation and fragile X syndrome are typically spa red. However, some boys with Klinefelters Syndrome suffer from poor manual dexterity and are commonly found to be clumsy and below average in sports (Wodrich Tarbox, 2008). There are many different factors that may underlie linguistic and reading problems. One possibility is a dysfunction of the left hemisphere that may be related to diminished gray matter or a lack of hemispheric asymmetry, or both. It is also possible that executive and frontal deficits may be a cause (Wodrich Tarbox). There is evidence that language is a fundamental issue for Klinefelters children and this can result in further scholastic issues. This problem seems to manifest as dyslexia as defined by poor reading in the setting of normal intelligence. Klinefelters males have also been observed to have difficulties with arithmetical functions. The deficits in auditory processing and verbal memory are the two key cognitive processes that underlie these difficulties. These deficits are also true for normal chromosomal children with dyslexia. The findings are supportive of the concept that defects in frontal systems seem to be caused by a language-based, left frontal-systems problem (Geschwind Dykens, 2004). Adult Klinefelters males have reported to have difficulties with mental flexibility (Wodrich Dykens, 2004). Even with these studies, it should be noted that not all adults that have Klinefelters Syndrome show these classic patterns of verbal deficits that are observed in children (Geschwind Dykens, 2004). However, these findings are not appropriate for all Klinefelters males, many of which complete high school and move on to post-secondary education successfully (Wodrich Tarbox, 2008). Two characteristics that has been falsely associated with Klinefelters males in the past, is sociopathy and criminal behavior. There is, contrary to this belief, fewer psychiatric problems reported among these individuals. However, there are commonly traits of introversion, unassertiveness, and a paucity or lack of ambition. There are also possible traits of impulsivity and social inappropriateness (Wodrich Tarbox, 2008). A Reiss Profile of Fundamental Goals measurement was used to assess the degrees of which Klinefelters males were motivated in 15 domains (Geschwind Dykens, 2004). The Reiss Profile generates a profile that is based on the motivational sensitivities across the domains of aversive sensations, citizenship, family, curiosity, honor, independence, food, order, physical exercise, rejection, power, sex, social contact, vengeance, and social prestige. The Reiss Profile is a well-established psychometric measure that is being used more and more to assess people with and without mental retardation (Geschwind Dykes, 2004). The results suggested that the Klinefelters male group was not particularly motivated by the need for social prestige, independence, or the desire to seek vengeance. This group was also not motivated to avoid physical pain. The general motivator for all the Klinefelters males in this group was curiosity. There were no age effects to this study (Geschwind Dykes, 2004). Characteristics in Adulthood There is a persistent deficiency of androgen in adulthood that can result in the loss of libido, decreased muscle bulk and tone, decreased bone density, a propensity for thromboembolism (an obstruction in a vein or artery from a blood clot), and an increased risk of mortality from cardiovascular and diabetic complications. A common characteristic for Klinefelters adults is gynecomastia (Wattendorf Muenke, 2005). Gynecomastia involves the risk of developing breast carcinoma. There is 200 times more of a risk for Klinefelters males to develop breast carcinoma than other karyotypically normal individuals. This may be a result of the estradiol (the prominant sex hormone in females) to testosterone ratio being so much higher that karyotypically normal men. Another possibility is that it is caused by the increase of peripheral conversion of testosterone to estradiol (Visootsak Graham, 2006). There are different views as to whether Klinefelters adult males are more aggressive or have a greater chance of psychological issues depending on the resource. One study describes the differences as relative to individual testosterone levels and the age at which they received the diagnosis (Morris, Jackson, Hancock, 2009). Equally, there is an impact from the way the diagnosis is reacted to by the Klinefelters male, the family, and friends or peers. The seven major themes that emerged from this study were the diagnosis, the testosterone treatments, health care problems, appearance, self-identity, relationships, and school and education. Of the Klinefelters adults studied, 60 % reported clinical levels of anxiety and 34% had clinical levels of depression. The results of this study show that a prolonged lack of testosterone can have far reaching negative effects on the Klinefelters adult (Morris, Jackson, Hancock, 2009). The historical studies show a disturbingly increased risk for psychiatric disturbance, criminality, and mental retardation. However, these results are outdated and extremely questionable given the initial examinations were given to institutionalized populations (Chen, 2010). Differential Diagnosis Classic Klinefelters Syndrome, 47, XXY, cases make up approximately 80-90% of all Klinefelters diagnosis. There are approximately 6-10% of these cases that are mosaics, which are the cells with 46, XY/47, XXY; 46, XY/48, XXXY; and 47, XXXY/48, XXXY (Chen, 2010; Visootsak Graham, 2003; Visootsak Graham, 2006). In 5% of the cases there are two X chromosomes without a Y chromosome or 46, XX (Visootsak Graham, 2006). The other cases were karyotypes 48, XXXY, 48, XXYY, 49, XXXXY, and 49, XXXYY (Visootsak Graham, 2003). Approximately 1% of these cases are due to a structurally abnormal X with a normal X and Y chromosome described as kayotypes 47, X,i(Xq)Y and 47, X,del(X)Y (Chen, 2010). Klinefelters Syndrome variants occur much less frequently than the classic 47, XXY chromosomal abnormality (Bock, 1993; Visootsak Graham, 2006). Klinefelter variant 48, XXXY is characterized by being average or tall stature with ocular hyperterlorism, which are widely spaced or deep set eyes; flat nasal bridge; curving of the fifth finger, or clinodactyly. Other characteristics are small penis and testicles with hypergonadotropic hypogonadism, which is the absence or decrease in function of the male testes. Theses individuals intelligence quotients range from 40-60. Variant 48, XXYY is characterized by having a tall stature, an eunuchoid habitus with long legs, sparse body hair, small testicles and penis, hypergonadotropic hypogonadism and gynecomastia. These individuals intelligence quotients range from 60-80. Males with variant 49, XXXXY are severely affected. They have smaller than average head circumference also known as microcephaly, short stature with ocular hypertelorism, flat nasal bridge, and upslanting palpebral fissures. Cleft palates are present along with small geniltalia and a heart defect known as patent ductus arteriosus. These individuals intelligence quotients range from 20-60. (Visootsak and Graham, 2003). Klinefelters Syndrome 47, XXY, has no major physical signs, which explains why it may go undiagnosed or misdiagnosed throughout an individuals life. Also with no physical signs, it is truly only diagnosed when genetic testing occurs for a variety of unrelated reasons. Klinefelters Syndrome may be diagnosed prenatally or during early childhood, as an adolescent during puberty, or as an adult when there are recognized fertility problems (Bock, 1993). Klinefelters Syndrome can be diagnosed prenatally through amniocentesis or chorionic villus sampling (Bock, 1993). These tests are normally done if the pregnant woman is older than 35, if there is a family history of genetic defects, or when other medical indications exist (Bock, 1993). A pediatrician may suspect a male child as having Klinefelters Syndrome if there are delays in learning to talk or difficulties in reading and writing as well as physical abnormalities during adolescence (Bock, 1993). Treatments and Interventions All hope is not lost when it comes to the treatment and interventions of the undesirable traits and characteristics that males diagnosed with Klinefelters Syndrome may display or develop. It is recommended that Klinefelters males have a comprehensive neurodevelopmental evaluation as soon as they have been diagnosed. A multidisciplinary developmental evaluation can determine the appropriate treatments during infancy and early childhood. These treatments may include physical therapy, infant simulation programs, and speech therapy (Wattendorf, 2005). If the language difficulties are detected in childhood, then there is more of a possibility for intervention. The language barriers that Klinefelters males may have to cope with can not only affect their academics, it can obstruct their building of social relationships and learning social skills necessary for these relationships. Here is where the Klinefelters child could benefit from a social skills training program. In a social skills training program, the Klinefelters child will be able to practice talking and listening, observing childrens making friends processes, sharing of information, attitudes, and beliefs. This will also assist them in proper classroom behavior and playground behavior. Language disabilities and barriers can prevent Klinefelters males from fitting in socially, so this kind of intervention and assistance can benefit the child greatly. Hearing can be an issue if frequent ear infections occur. Hearing test and screens should be done to ensure that a hearing impairment is not a part of the language difficulties. If the Klinefelters child is not communicating effectively with single words by the ages of 18 to 24 months, then consultation with a speech and language pathologist will be very beneficial (Klinefelter Syndrome Information, 2002). Teachers should be informed of the difficulties that a Klinefelters child may be dealing with in the classroom. A teacher may consider the Klinefelters child to be lazy and daydreaming and a teacher may even forget the child is even in the room. This can result in the Klinefelters child falling behind and eventually being held back a grade. Under the Public Law 94-142, the Individuals with Disabilities Education Act, adopted by Congress in 1975, all children with disabilities have a right to a free, and appropriate public education (Klinefelter Syndrome Information, 2002). Once the Klinefelters male reaches puberty there is usually an inability to produce a normal amount of testosterone. This along with hypogonadism can result in impaired bone mineral density and skeletal muscle development. Also associated with testosterone deficiency is a decrease in libido and energy (Wattendorf Muenke, 2005). Androgen therapy or Testosterone Treatment should begin by time the Klinefelters male reaches middle school, approximately 12 to 14 years of age, based on the level of pubertal development (Klinefelter Syndrome Information, 2002; Wattendorf Muenke, 2005). Testosterone Treatment will ultimately increase the muscle size and strength, as well as, promoting the growth of body and facial hair. It must be noted that Testosterone Treatments can also bring on psychological changes. It is important to adequately inform the parent(s) and the child of these changes so that they can make the most informed decision (Klinefelter Syndrome Information, 2002). There are diff erent ways to receive Testosterone Treatment and that is through injections, transdermal (patches, gels, or creams), orally, or implantation. The kind of testosterone injection will depend mainly on the dosage used and the country in which you receive the injections. Some injectable testosterone esters are Testosterone enanthate, Testosterone cypionate, Sustanon, Testosterone propionate, Testosterone phenylpropionate, Omnadren, and Aqueous testosterone suspension. Types of transdermal patches are Androderm and Testosterone TTS. Two different kinds of testosterone gels and creams are Androgel, and Testim. A few oral supplements include Methyltestosterone and Testosterone undecanoate. The last form of Testosterone Treatment is the Subcutaneous testosterone pellet, which is delivered by implanting a pellet of pure, crystalline testosterone under the skin of the buttocks or abdomen (Testosterone Types and Delivery, n.d.). Adult males with Klinefelters Syndrome usually develop gynecomastia which predisposes men to breast cancer. Therefore, it is important that Klinefelters males do monthly breast examinations. If gynecomastia causes psychological or physical problems, then possible treatment would be cosmetic surgery to remove the breast tissue (Wattendorf Muenke, 2005). Swerdlow et. al (2005) stated that men with Klinefelter Syndrome have elevated risks of several cancers. Prostate cancer, along with breast cancer was more prevalent. Men with Klinefelter Syndrome are also at a substantially higher risk for non-Hodgkin lymphoma, and possibly lung cancer. Breast cancer risk is higher in 47, XXY mosaics. Adult males may face possible infertility issues due to the lack of testosterone production, but if diagnosed early on, this can be minimized and they will be able to reproduce without outside assistance. Summary Klinefelter Syndrome is one of the more recently discovered medical syndromes. Klinefelter Syndrome is not one that causes major dysfunctions and is usually only discovered during genetic testing for infertility or during prenatal testing due to maternal age or prior genetic issues within the family. Because Klinefelter Syndrome has not had a lot of research until the last few years, there is no federal funding set aside for this syndrome. Families with sons that are found to be affected by it have no real support system that is knowledgeable of this syndrome and have to research on their own and create resources to fit their situation as none are available in most areas.

Christianity, the True Religion Essay -- Religion Christian Jesus

Christianity, the True Religion I was raised Catholic, at the insistance of my parents. After many years of drinking and partying, I got very bored and thought, Is this ALL there is to life?!?! I thought, If there really IS any truth to a life after death, I should at least TRY to find the answer. I started to do some research on science and religion to see if I could come up with any TRUTH about the meaning of life. In school, I was taught that mankind was evolving and getting better, but it didnt appear that way to me. It SEEMED as though modern science had proven that God didnt exist. As I did more research on my own, I found out that this just isnt the case. I learned that the Universe and ALL matter have a DEFINITE beginning. Most atheists and re-incarnationists believe that the Universe has ALWAYS existed, but this contradicts the fact. Cause and effect tells us that the Universe must have been caused. It is logical to believe that an invisible, non-material God had caused the beginning of the Universe. Some think that aliens and U.F.O.s have something to do with our existence, but even if they DID exist, THEY would need a beginning as well! The evolutionists believe that evolution is a FACT, and that the fossil record PROVES it. I learned that neither evolution NOR creation are FACTS, they are only THEORIES! There is NO way to PROVE either one because they CANNOT be re-created in a lab experiment. Whatever THEORY you believe, you MUST believe by FAITH. I learned that when something dies, it does NOT become a fossil, it rots away VERY quickly. Fossils are formed by RAPID burial and destruction , NOT over SUPPOSED billions of years! What the fossil record DOES prove, is that there was a TERRIBLE global disaster. Scattered across mountain tops all over the world are fossils of both modern & extinct ocean and land creatures ALL MIXED TOGETHER. This fact can ONLY be explained by a RECENT Creation and a WORLDWIDE FLOOD, and NOT by evolution. I thought that evolution was true just because the majority accepted it. The MAJORITY also used to believe that the Earth was FLAT!!! Then I was confused about all the different religions out there. Which God should I serve?!?! Does it REALLY matter as long as I am sincere and a GOOD PERSON I thought, What if I am sincerely WRONG!?!? I started to do some more research to try to find the TRUTH. ... ...ask questions. I am just writing this paper because I was SO surprised that I was able to find REALLY satisfying answers to all my questions, when I thought that no one could EVER really know the TRUTH for sure. I read some books on life after death and re-incarnation by people who have CLAIMED to have died. Then I thought If these people were REALLY dead, then they STILL would be!! I DONT expect anyone to just believe me or this paper, but I would HOPE that this article would at LEAST make people think about all of this on their OWN and do some of their OWN investigating!! I just wanted to share what I have learned and to give people a head start. I know how difficult it is to listen to someone else tell you about their religion, I was there. It all seemed so confusing to me, at first. Since Ive done all this research, I KNOW that the Bible is TRULY Gods Word to all mankind, and I believe it. I pray that THE LORD JESUS CHRIST uses this paper to open up the minds and hearts of everyone who reads this so that they may be saved from an eternity separated from GOD and in hell. Eternity is a loooong time to gamble with. If you died right now, do you know where YOU would go !?!?!

T box

The T- box is a power generated device that harnesses wind energy as trains run over railroad tracks. This alternative form of wind energy produced by trains is very unique, as it does not depend on any natural energy sources. Instead, the energy generated from this device is produced as a consequence of human activity. The T- box device generates energy without any interference of the normal train operation – the device is installed between railroad ties, and is partially buried underground. As the train passes over the device, the wind generated from the train spins the turbine nside the T- box to generate electricity.The T- box contains all the mechanical components required for harnessing, storing and supplying converted power. Hence, the power generated from this device can be supplied to public facilities along the railway and also to remote areas where electricity has not yet reached. The T-box How much power can the T- Box generate? A train moving at 125mph would gener ate a wind speed equivalent to 50 feet/ second. Wind blowing with such speed will let a normal wind power generator harness about 3500W of power. If a train is about 656 feet long, running at the pace of 187mph, and it moves along a 0. 2 mile railway track in about 18 seconds, the power generated in this small period by the T- boxes laid on the tracks will be 2. 6KW. Qian and Luparini estimate that about 1 50 T-box devices could be accomodated along a 0. 62 mile railway track. Installation of the T- box To fit the T- box on the tracks, some work has to be done on them: Firstly, concaves have to be constructed in cement between each of two sleepers Two brackets then ave to be placed on two sides of the concaves The brackets have to be examined to ensure that they are well fixed The T-box is then set upon the maneuvered tracks Installed T- boxes Is the T-box eco friendly?The T- box has so far been considered quite environmentally friendly. The T- box does not produce any harmful chemi cals nor has it been proven to have any other side effects thus far. Anticipated problems Keeping the T- box devices clean can pose great problem. As the train passes, quite a bit of dirt and debris will be kicked up, and will land on the upper surface of the T- ox. Also, grease and grime deposits escaping from underneath will contribute to contaminating the device.Future of the T- box As the hunger tor alternative torms ot energy continues, the T-box nas generated hope. This device presents a new generation of wind power generators, and has created quite a sensation among techno buffs. However, it is important to remember that the design is still in the conceptual stage and has not taken into account all of the preservation and maintenance issues that are likely to pose a problem in any future use of this device.

Analysis Of Leni Fragakis s Third Grade Class - 1157 Words

At Arts-Based School I did my observation in Leni Fragakis’s third grade class. This was the first observation I had done since learning about instructional design. Since learning it, I now have a new way of observing, I pay more attention to the teacher; how she implemented the lessons, what strategies she uses, and the types of assessments she uses. This gives me a better experience because before I was just paying attention to what the students were doing and their part in the classroom and now I am paying attention to so much more. Even though it is important to watch the kids, I now also know how important it is to observe the teacher, too. I was also able to observe what I am learning in class be used in the classroom. Leni Fragakis’s class was an average size about 20 students with a few more girls than boys. While I was counting the number of students one girl stood out to me, she was in the back of the room in a wheelchair. Because of this the classroom had to be set up in a way she could get to a desk and around the room comfortably. The desk were set up in four sets of five and off to the side there was a table with computers. This means the room was a little crowded but the girl in the wheelchair could still get around to the desk in the back and a few other important places in the classroom. The first lesson I saw take place was the end of a math lesson. The students were independently working on a set of math problems. These problems were mainly