Thursday, November 28, 2019

The True Story Of A Black Youths Essays - Mark Mathabane

The True Story of a Black Youth's Coming of Age in Apartheid South Africa Mark Mathabane I. Main Characters A. Johannes (Mark) Mathabane--Kaffir Boy revolves around Johannes for the simple reason that he is the author of this book. Growing up in Johannesburg, South Africa was especially hard for Johannes. Johannes is very smart and graduated at the top of his class during his 13 years of schooling in apartheid South Africa. Johannes has had a lot of courage and perseverance throughout his life. B. Jackson Mathabane--Johannes's father came from what is now the so-called independent homeland of the Vendas in the northwestern corner of the Transvaal. Johannes's father tried desperately to support his family, but in times of dire need, he backed away and depended on alcohol and abusive behaviors. Johannes's parents met and married in Alexandra on March 21, 1960. C. Mother--Johannes's mother came from Gazankulu, the tribal reserve for the Tsongas in the Northeastern Transvaal. She is a very loving and devoted woman. D. Johannes's siblings--Johannes has five sisters and one brother. His sisters names are Florah, Linah, Maria, Merriam, and Linah. George was his only brother. E. Ellen Mabaso--Ellen was the mother of Johannes's mother. She was a humble woman who bore four children: Uncle Piet, Aunt Bush, Uncle Cheeks, and Johannes's mother. she had a statuesque figure--tall, limber, and ebony colored complete with tribal attire and multiple anklets, beads, earrings and bracelets. She could easily been a chief's daughter. Her friendly, brown eyes had the radiance of pristine pearls. She was the most beautiful woman Johannes had ever seen. She worked six days a week, from seven to five, mowing lawns, raking leaves, clipping hedges, watering plants, sweeping driveways, cleaning yards and pruning trees for white people. F. Mr. Brown--Mr. Brown was one of the few people in the yard where the Mathabane's lived with the equivalent of a high-school education. He was a bus driver for PUTCO, but he also operated a moving service that transported people and goods between Alexandra and the tribal reserve of the Vendas. G. Mrs. Smith--Mrs. Smith was Granny's employer. She was a short, slender woman with silver hair and slightly drooping shoulders. Granny was the Smith's gardener. H. Clyde Smith--Clyde is the son of the woman who Granny works for. He is a young boy who is somewhat of a snob. As he grows, he learns to like Johannes and they become friends. I. Scaramouche--Scaramouche was a self-employed painter. He was also one of the best tennis players among people of color in Johannesburg. An excellent coach, he was well connected in white and black tennis circles. He agreed to be Johannes' coach. Scaramouche turned out to not only be a great coach but a confidant and a surrogate father. He was firm and demanding but not authoritative and stifling. Instead of teaching Johannes his style of play, he let Johannes acquire his own way. J. Tom--In June of 1972, Johannes met Tom. He is a lanky Zulu tennis player. He was very harmless-looking K. Wilfred Horn--Wilfred married to Norma. He respects black people and owns a tennis ranch in Halfway House called Barretts. He was a German immigrant. L. Arthur Ashe--Arthur Ashe was a Negro tennis player that Johannes admired very much. he condemned apartheid and did not pretend he was a white man erroneously painted black. Arthur always appeared calm, cool, and collected, even when he was surrounded in a sea of white faces. M. David--David was the number two singles player on the tennis team. He was soft-spoken, politically sensitive, and a brilliant Zulu student whose love for the English language exhaled Johannes's. Johannes and David frequently exchanged books, did English homework together, read prose and poetry together, trained together, and sat on the same seat during tennis trips. David was the first close friend Johannes ever had. The only difference between David and Johannes was that David was a womanizer. N. Helmut--Helmut was a short, brown-haired bespectacled white man with a barrel chest. He was always dressed in flashy clothing. He came from a small town in Germany and was working for a German company in South Africa only a few months before he met Johannes. He turned out to be a horrible tennis player, but good practice

Sunday, November 24, 2019

Tay-Sachs Disease Essays - Lipid Storage Disorders, Rare Diseases

Tay-Sachs Disease Essays - Lipid Storage Disorders, Rare Diseases Tay-Sachs Disease Tay-Sachs disease is a fatal, genetic disorder of the nervous system. There is no treatment. Tay-Sachs was first identified in the 1880's by two physicians. Dr. Bernard Sachs of the United States has found a "cherry-red" spot in the eyes of a patient. That patient later died. After searching medical literature, he found Warren Tay of great Britain had also reported this (Information, 1994). The symptoms of Tay-Sachs disease appear after about six months. At first, the patient has an over-exaggerated "startled" reaction to sounds and begins to loose control of its head. Eventually, it cannot roll over or sit without help. Dementia (uncontrolled laughter) may set in and the head grows abnormally large. The baby then becomes blind, and dies, usually before its 5th year (Seely et al, 1992). Tay-Sachs disease is an autosomal, recessive disorder caused by a deficiency in B-hexosaminidase A. Being an autosomal recessive disease, Tay-Sachs can only be passed on in its fatal form if both parents are heterozygous for the disease. If both parents are heterozygous for Tay-Sachs, there is a one in four chance of the infant having the disease. If only one parent is heterozygous, the infant has a one in two chance of being a carrier (heterozygous) for the disease(Mahany et al, 1994). In 1962, researchers found B-hexosaminidase A is responsible for the breakdown of ganglioside (gm2) in nerve cells. Ganglioside is a lipid found in modest levels in nerve cell membranes. It is constantly being synthesized and broken down. Without the B-hexosaminidase A to break down the gm2, the cells swell up and eventually burst( Diamond, 1991). B-hexosaminidase A is composed of two amino acid chains, the alpha and the beta chain(Navon et al, 1989). The gene responsible for the manufacture of B-hexosaminidase A was originally thought to be located on chromosome 7(Gilbert et al, 1975). It was later determined that the gene for the alpha chain is located on chromosome 15, and the beta chain gene is located on chromosome 5( Chern et al, 1976). In 1991, with the use of a cDNA clone, it was determined the alpha chain gene is located at 15q23-q24(Nakai et al, 1991). All forms of Tay-Sachs disease are caused by mutations in the alpha chain of the enzyme(Navon et al, 1989). The alpha chain of B-hexosaminidase A is about 35 kilobases long and split into 14 exons(Proia and Soravia, 1987). There are at least thirty different mutations that cause Tay-Sachs disease. A majority of the classical (infantile) form of the disease that is found in the Ashkenazi Jewish population is caused by one of two different gene mutations( Triggs-Raine et al, 1990). The first one, Tay Sachs disease [HexA, 4-BP INS, EX11] accounts for about 70% of heterozygous carriers in the Ashkenazi population. The mutation introduces a 4-basepair insertion into exon 11, which causes a premature termination signal. This results in a deficiency of mRNA. The 4-basepair insertion causes a frameshift which makes a termination codon 9 nucleotides down from the insertion (Myerowitz and Costigan, 1988). This mutation is also prevelant in the southwest Louisiana Cajun population. In the last three decades, 8 infants from 6 unrelated families have been diagnosed with Tay-Sachs disease. With 12 heterozygous carriers in the 6 families identified, 11 were carriers of the exon 11 mutation. The other mutation was of a form of Tay-Sachs disease found in the French-Canadian populations. The second mutation is Tay-Sachs disease [HexA, IVS G-C, +1]. It is found in 20% of Ashkenazi patients and carriers. It is a G-C base substitution in the first nucleotide of intron 12. This results in defective splicing of the mRNA(Arpaia et al, 1988). Another form of Tay-Sachs disease is Adult onset Tay-Sachs [HexA, GLY269SER]. This form of Tay-Sachs is caused by an amino acid substitution in the alpha chain of the B-hexosaminidase A molecule. Glycine is substituted serine at position 269 in the HexA subunit. This is caused by a G to A substitution at the 3-prime end of exon 7 (Navon and Proia, 1989). Unlike infantile Tay-Sachs disease, Adult onset Tay-Sachs disease is not always fatal. While the former causes a rapid degeneration of the central nervous system, the latter causes a slower degeneration. This makes a normal

Thursday, November 21, 2019

Critical Teaching and the tutorial for final year dental students in Dissertation

Critical Teaching and the tutorial for final year dental students in the Acute Dental Care Department at Guy's Hospital - Dissertation Example This teaching experience was however only a part-time position. Nevertheless, I have carried out small-group sessions with students. I have worked my way up to senior clinical teacher and have also given lectures and seminars, some in specialised areas of dentistry. My experience as a clinical teacher has helped me gain experience in making PowerPoint presentations, making lesson plans, and making tests; more importantly, I also found out how different personalities learn and teach differently. Current responsibilities As a clinical teacher, my duties mostly relate to watching, monitoring and aiding the student/patient relationship. In other words, my responsibilities have mostly revolved around teaching and researching. I have been involved in the establishment and development of information for the lessons and lectures, and for the development of courses. During my first few years in teaching, I mostly handled small groups of students, no more than 12 taking part in sharing data ab out emergency dentistry. In the years that followed, I was assigned to assist in giving lectures and tutorials. I have also been involved in evaluating students for their examinations and projects, mostly those in the undergraduate program. In general, my current tasks relate to looking after the student/ patient relationship by ensuring students carry out the correct clinical treatment in the correct order. I am in charge of the students learning and the patient’s safety. An hour tutorial is held at the end of each session on clinic to consolidate the days teaching into formal teaching. Personal values and hopes My desire to consider and engage in the teaching and academic profession has been based on my personal experiences with teachers and academics. These teachers and professionals have exemplified superlative knowledge and skills in the transmission and the gathering of information, sharing such data for the next generation of eager learners. I value my role as a clinic al teacher and believe that this can influence how a student works and feels about the profession. I have a desire to impart knowledge that was passed onto me as a way of thanking the excellent teachers I had. I also seek to assist the students in the establishment of their careers as well as their personal development. I hope to support and guarantee the protection of crucial and significant values, especially those which relate to my responsibilities as a clinical teacher. This also relates to a strong need to secure a sense of respect and responsibility for students, patients, fellow teachers, as well as for the teaching profession. An awareness of the diversity of the academic field is also an important element which I have recognized in the teaching profession. Moreover, I have realised the importance of establishing learning communities and groups where the teaching goals and practices can be adequately implemented and incorporated. Aspects relating to personal development: I have already established that the clinical teaching can help in the improvement of my knowledge and the refining of my academic learning. I also believe that guiding students in their learning is one of the most efficient ways to improve research and to impart knowledg