Elizabeth Key and Her History-Changing Lawsuit

Elizabeth Key (1630 - after 1665) is a key figure in the history of American chattel slavery. She won her freedom in a lawsuit in 17th century colonial Virginia, and her lawsuit may have helped inspire laws making slavery a hereditary condition. Heritage Elizabeth Key was born in 1630, in Warwick County, Virginia. Her mother was a slave from Africa who is unnamed in the record. Her father was an English planter living in Virginia, Thomas Key, who arrived in Virginia before 1616. He served in the Virginia House of Burgesses, the colonial legislature. Accepting Paternity In 1636, a civil case was brought against Thomas Key, alleging that he had fathered Elizabeth. Such suits were common to get a father to accept responsibility to support a child born out of marriage, or to ensure that the father would help to get the child an apprenticeship. Key first denied paternity of the child, claiming that a â€Å"Turk† had fathered the child. (A â€Å"Turk† would have been a non-Christian, which could affect the slave status of the child.) He then accepted paternity and had her baptized as a Christian. Transfer to Higginson At about the same time, he was planning to go to England—perhaps the suit was filed to ensure that he accepted paternity before he left—and he placed the 6-year-old Elizabeth with Humphrey Higginson, who was her godfather. Key specified a term of indenture of nine years, which would bring her to the age of 15, a common time for indenture terms or apprentice terms to expire. In the agreement, he specified that after 9 years, Higginson was to take Elizabeth with him, give her a â€Å"portion,† and then free her to make her own way in the world. Also included in the instructions was that Higginson treat her like a daughter; as later testimony put it, â€Å"user her more Respectfully than a Common servant or slave.† Key then sailed for England, where he died later that year. Colonel Mottram When Elizabeth was about ten years old, Higginson transferred her to a Colonel John Mottram, a justice of the peace—whether it was a transfer or sale is not clear—and he then moved to what is now Northumberland County, Virginia, becoming the first European settler there. He founded a plantation he called Coan Hall. About 1650, Col. Mottram arranged for 20 indentured servants to be brought from England. One of those was William Grinstead, a young lawyer who indentured himself to pay for his passage and work that off during the term of indenture. Grinstead did legal work for Mottram. He also met and fell in love with Elizabeth Key, still held as a bond servant to Mottram, though it was by that time 5 or more years beyond the term of the original agreement between Key and Higginson. Even though Virginia law at that time forbid indentured servants from marrying, having sexual relations or having children, a son, John, was born to Elizabeth Key and William Grinstead. Filing Suit for Freedom In 1655, Mottram died. Those settling the estate assumed that Elizabeth and her son John were slaves for life. Elizabeth and William filed suit in court to recognize both Elizabeth and her son as already free. At the time, the legal situation was ambiguous, with some tradition assuming all â€Å"Negros† were slaves no matter the status of their parents, and other tradition assuming English common law where bondage status followed that of the father. Some other cases held that black Christians could not be slaves for life. The law was especially ambiguous if only one parent was an English subject. The suit was based on two factors: first, that her father was a free Englishman, and under English common law whether one was free or in bondage followed the status of the father; and second, that she had been â€Å"long since Christened† and was a practicing Christian. A number of people testified. One resurrected that old claim that Elizabeth’s father was a â€Å"Turk,† which would have meant neither parent was an English subject. But other witnesses testified that from a very early time, it was common knowledge that Elizabeth’s father was Thomas Key. The key witness was an 80-year-old former servant of Key, Elizabeth Newman. The record also showed that she had been called Black Bess or Black Besse. The court found in her favor and granted her freedom, but an appeal court found that she was not free, because she was a â€Å"Negro.† General Assembly and Retrial Then Grinstead filed a petition for Key with the Virginia General Assembly. The Assembly formed a committee to investigate the facts, and found â€Å"That by the Comon Law the Child of a Woman slave begot by a freeman ought to be free† and also noted that she had been christened and was â€Å"able to give a very good account of her fayth.† The Assembly returned the case to a lower court. There, on July 21, 1656, the court found that Elizabeth Key and her son John were in fact free persons. The court also required that the Mottram estate give her â€Å"Corn Clothes and Satisfaction† for her having served many years beyond the end of her term of service. The court formally â€Å"transferred† to Grinstead â€Å"a maid servant†. That same day, a marriage ceremony was performed and recorded for Elizabeth and William. Life in Freedom Elizabeth had a second son by Grinstead, named William Grinstead II. (Neither son’s birth date is recorded.) Grinstead died in 1661, after only five years of marriage. Elizabeth then married another English settler named John Parse or Pearce. When he died, he left 500 acres to Elizabeth and her sons, which allowed them to live out their lives in peace. There are many descendants of Elizabeth and William Grinstead, including a number of famous people (the actor Johnny Depp is one). Later Laws Before the case, there was, as outlined above, some ambiguity in the legal status of the child of a woman who was in bondage and a free father. The assumption of the Mottram estate that Elizabeth and John were slaves for life was not without precedent. But the idea that all of African descent were permanently in bondage was not universal. Some wills and agreements by owners specified terms of service for African slaves, and also specified land or other goods to be granted at the end of the term of service to aid in their new life as fully free persons. For example, a woman, Jone Johnson, daughter of one Anthony Johnson identified as a Negro, was given 100 acres of land by the Indian ruler Debeada in 1657. Key’s suit won her freedom and established the precedence of the English common law about a child born to a free, English father. In response, Virginia and other states passed laws to override the common law’s assumptions. Slavery in America became more solidly a race-based and hereditary system. Virginia passed these laws: 1660: the term of indentured servitude was limited to five years—for servants from a Christian country1662: a child’s status as free or bond (slave) status was to follow the mother’s status, contrary to English common law1667: being a Christian did not alter status of bondage1670: prohibited Africans from importing any bonded laborers from anywhere (Africa or England included)1681: children of a European mother and African father were to be in bondage to age 30 In Maryland: 1661: a law was passed making all African Americans in the colony slaves, and all African Americans slaves at birth whatever the status of the parents1664: a new law outlawed marriages between European or English women and African (Negro/black) men Note: while the term â€Å"black† or â€Å"Negro† was sometimes used for Africans from the beginning of the presence of people of African descent in colonial America, the term â€Å"white† came into legal usage in Virginia about 1691, with a law referring to â€Å"English or other white women.† Before that, each nationality was described. In 1640, for instance, a court case described a â€Å"Dutchman,† a â€Å"Scotch man† and a â€Å"Negro,† all bond servants who escaped to Maryland. An earlier case, 1625, referred to a â€Å"Negro,† a â€Å"Frenchman,† and â€Å"a Portugall.† More about the early history of black or African women in what is now the United States, including how laws and treatment evolved: Timeline of African American History and Women Also known as: Elizabeth Key Grinstead; due to spelling variations common at the time, last name was variously Key, Keye, Kay and Kaye; married name was variously Grinstead, Greensted, Grimstead, and other spellings; final married name was Parse or Pearce Background, Family: Mother: not namedFather: Thomas Key (or Keye or Kay or Kaye) Marriage, Children: husband: William Grinstead (or Greensted or Grimstead or other spellings) (married July 21, 1656; indentured servant and lawyer)children:John GrinsteadWilliam Grinstead IIhusband: John Parce or Pearce (married about 1661)

The Youngest US President ever to Take Office - 784 Words

John F. Kennedy was voted into office during the election of 1960. To date, Kennedy is the youngest person to be elected President. Surprisingly, at the start of the campaign, Kennedy was a long shot to win the Democratic nomination. Without a distinguished presence in the political world and the stigma of being Roman Catholic, Kennedy had a lot of ground to conquer. In not just politics, but society, religion is and was a controversial issue. Kennedy, who was Catholic, struggled against critics who were anti-Catholicism. It was often insisted that Kennedy would turn to the pope for orders and therefore run our country based upon the Church. Kennedy overcame this obstacle by reassuring voters he would not act according to the Church†¦show more content†¦As a nation that is expected to be the leaders of other nations, he would not settle for second. In the case of exploring space, that was exactly where we were. The Soviet Union was far ahead of the United States in its space program. With Project Apollo, Kennedy was determined to play catch up and asked congress to invest more that twenty-two billion dollars into the project. The end goal was to have an American man on the moon before the end of the decade. Neil Armstrong was that man in 1969. Not only was the Soviet Union viewed as a threat with their space program being more advance, but they also had nuclear missile sites being built. An American spy plane secretly photographed evidence that both Cuba and the Soviet Union were building nuclear missile sites. President Kennedy remained collected and directed that a naval blockade was placed around Cuba which would prevent the Soviets from obtaining more military supplies. On the brink of what could have been a nuclear war, there was an agreement made, the Soviets agreed to dismantle their weapons sites in exchange for a pledge from the United States not to invade Cuba. Tension slowly began to lessen as time passed and the agreement remained respected. 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Critical Study of Alcohol and Hepatocytes Cell Necrosis Free Essays

Introduction The tissue shows vast inflammation, there are large gaps in between the hepatocytes due to cell necrosis and the hepatocytes remaining are large and swollen. There are fatty deposits throughout the tissue and fibrous structures present which are most likely collagen. The hepatocytes themselves are not only swollen but have the presence of globular material within. We will write a custom essay sample on Critical Study of Alcohol and Hepatocytes Cell Necrosis or any similar topic only for you Order Now This is identified as Mallory bodies, seen in cases of alcoholic hepatitis. These globules are aggregates of intermediate filaments in the cytoplasm which have resulted from hepatocyte injury. Neutrophils can be seen in the sample which is the likely cause of inflammation. These would have been called to the tissue due to the necrosis of the hepatocytes and the presence of cellular debris within the lobules [1]. An infiltration of macrophages can be seen which would also be due to the debris present. The first stage of alcoholic liver disease is the increase of fatty deposits in the liver. Heavy alcohol consumption causes the production of large fatty globules a process known as macrovesicular steatosis collecting in the liver cells. Ethanol consumed is metabolised by alcohol dehydrase in the mitochondria into toxic acetaldehyde which is metabolised by aldehyde dehydrogenase into acetic acid [1][2][3]. The production of acetaldehyde causes a higher NADH: NAD ratio which is the main mechanism in the development of this condition. This NADH production causes increase in lipogenesis and a decrease in fatty acid oxidation. The higher levels of fatty acids signal the hepatocytes to compound glycerol into triglycerides [3]. This is seen in the first stage of liver damage known as alcoholic hepatitis [2]. Excess alcohol intake can also cause hepatocyte injury via oxidative stress from increased NADH production in which free radicals damage the hepatocytes (increased production by the k upffer cells); and from lipid peroxidation where acetylhyde binds to proteins forming adducts [1]. This binding triggers humoral and cellular immune responses resulting in tissue injury. There is an increase in pro inflammatory cytokines such as tumour necrosis factor and interleukin -6 and a decrease in anti inflammatory cytokines such as interleukin -4 [1]. These cytokines in particularly TNF are secreted by the kupffer cells (macrophages) located in the liver. They’re activated by the increased levels of endotoxin released from the breakdown of alcohol by intestinal bacteria; this binds to the CD14 receptor on their surface initiating response. The release of these cytokines leads to the hepatic stellate cells producing increased levels of collagen which leads to liver fibrosis and also causes destructive damage to the hepatocytes. This leads to the last stage of liver disease known as cirrhosis which can occur in prolonged alcoholic hepatitis, seen in 40% of cases [1][4] . Individuals suffering with alcoholic hepatitis have an increase in serum bilirubin due to the inability of the damaged liver to process it. Bilirubin is normally removed from the blood by the liver, processed by it and released into the bile [4][5]. They’ll also have prolonged prothrombin time which reflects decreased hepatic synthetic function [4][5]. A number of clotting factor proteins are produced in the liver so an increase in coagulation time suggests a decrease in these factors indicating dysfunction of the liver. Decreased serum albumin can be observed in cases of liver injury as this is the main protein produced in the liver. Thyroid tests can indicate liver dysfunction such as testing for T3- triiodothrynonine which appears decreased in individuals with alcoholic hepatitis and is proportional to the level of damage[6][4]. There is also a decrease in serum cholesterol level seen in this condition. In cases where excessive alcohol consumption is not the cause of hepatitis further testing should be done. Individuals can develop hepatitis due to drug use as currently 1000 drugs are seen to be hepatotoxic [7]. There must be a chronic correlation seen between when the medicine was first taken and the observation of hepatitis. There must also be a correlation between the removal of medication and the recession of the condition [4]. Other causes of hepatitis must also be tested for such as viral hepatitis. There are 5 subsets of viral hepatitis A, B, C, and the less common D and E forms. Hepatitis A is the most common form and is passed on by the faecal– oral route. It’s tested for by the presence of the anti-HAV IgM antibody which tests positive before the development of clinical hepatitis and remains positive for at least 4months. Hepatitis B is tested for by the presence of surface antigen HBsAg. Anti HBC total and Anti – HBC IgM is also tested for. A soluble protein HBeAg is produced by the virus in acute and early chronic stages of hepatitis B so positivity of this indicates infection. Hepatitis C infection has the presentation of Anti-HCV seen in 90% of individuals with this infection [7]. The possibility of autoimmune hepatitis can be ruled out by testing of HLA class II expression on the surface of the hepatocytes. There is also an increase seen in IgG antibody and a variety of other antibodies such as SLA/LP (anti soluble liver protein) [8]. References [1] Hopkins. J. Alcoholic liver disease – Introduction, gastroenterology and hepatology. Baltimore M.D 2010 [2] www.britishlivertrust.org . Accessed 28.11.10 [3 ]Drriad. Pathogenesis of hepatitis infection from chronic alcoholism, Figure 1. 2007 [4] www.hepatitis.org. Phillipe.L, Hepatogastroenterology department, Brugmann University Hospital Brussells Accessed 28.11.10 [5]http://www.gastro.com/Gastro/liverdisease/liver_function.aspx, Gardner. P.W and Waldstreicher.W, American Liver Foundation 1995 Accessed 28.11.10 [6] Borzio. M et al, Thyroid function tests in chronic liver disease: evidence for multiple abnormalities despite clinical euthyroidism. GUT Journal of gastroenterology and hepatology, Vol 24(7), Jul 1983. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1420033/. Accessed 28/11/10 [7] http://www.oaml.com/PDF/CLP012.pdf. Guidelines for clinical laboratory practice, revised March 2000, Accessed 28.11.10 [8]Krawitt. E.L Autoimmune hepatitis: classification, heterogeneity, and treatment, January 1994. Am. J. Med. Vol 96 (1A): 23S–26S. How to cite Critical Study of Alcohol and Hepatocytes Cell Necrosis, Essay examples

Critical Study of Alcohol and Hepatocytes Cell Necrosis Free Essays

Introduction The tissue shows vast inflammation, there are large gaps in between the hepatocytes due to cell necrosis and the hepatocytes remaining are large and swollen. There are fatty deposits throughout the tissue and fibrous structures present which are most likely collagen. The hepatocytes themselves are not only swollen but have the presence of globular material within. We will write a custom essay sample on Critical Study of Alcohol and Hepatocytes Cell Necrosis or any similar topic only for you Order Now This is identified as Mallory bodies, seen in cases of alcoholic hepatitis. These globules are aggregates of intermediate filaments in the cytoplasm which have resulted from hepatocyte injury. Neutrophils can be seen in the sample which is the likely cause of inflammation. These would have been called to the tissue due to the necrosis of the hepatocytes and the presence of cellular debris within the lobules [1]. An infiltration of macrophages can be seen which would also be due to the debris present. The first stage of alcoholic liver disease is the increase of fatty deposits in the liver. Heavy alcohol consumption causes the production of large fatty globules a process known as macrovesicular steatosis collecting in the liver cells. Ethanol consumed is metabolised by alcohol dehydrase in the mitochondria into toxic acetaldehyde which is metabolised by aldehyde dehydrogenase into acetic acid [1][2][3]. The production of acetaldehyde causes a higher NADH: NAD ratio which is the main mechanism in the development of this condition. This NADH production causes increase in lipogenesis and a decrease in fatty acid oxidation. The higher levels of fatty acids signal the hepatocytes to compound glycerol into triglycerides [3]. This is seen in the first stage of liver damage known as alcoholic hepatitis [2]. Excess alcohol intake can also cause hepatocyte injury via oxidative stress from increased NADH production in which free radicals damage the hepatocytes (increased production by the k upffer cells); and from lipid peroxidation where acetylhyde binds to proteins forming adducts [1]. This binding triggers humoral and cellular immune responses resulting in tissue injury. There is an increase in pro inflammatory cytokines such as tumour necrosis factor and interleukin -6 and a decrease in anti inflammatory cytokines such as interleukin -4 [1]. These cytokines in particularly TNF are secreted by the kupffer cells (macrophages) located in the liver. They’re activated by the increased levels of endotoxin released from the breakdown of alcohol by intestinal bacteria; this binds to the CD14 receptor on their surface initiating response. The release of these cytokines leads to the hepatic stellate cells producing increased levels of collagen which leads to liver fibrosis and also causes destructive damage to the hepatocytes. This leads to the last stage of liver disease known as cirrhosis which can occur in prolonged alcoholic hepatitis, seen in 40% of cases [1][4] . Individuals suffering with alcoholic hepatitis have an increase in serum bilirubin due to the inability of the damaged liver to process it. Bilirubin is normally removed from the blood by the liver, processed by it and released into the bile [4][5]. They’ll also have prolonged prothrombin time which reflects decreased hepatic synthetic function [4][5]. A number of clotting factor proteins are produced in the liver so an increase in coagulation time suggests a decrease in these factors indicating dysfunction of the liver. Decreased serum albumin can be observed in cases of liver injury as this is the main protein produced in the liver. Thyroid tests can indicate liver dysfunction such as testing for T3- triiodothrynonine which appears decreased in individuals with alcoholic hepatitis and is proportional to the level of damage[6][4]. There is also a decrease in serum cholesterol level seen in this condition. In cases where excessive alcohol consumption is not the cause of hepatitis further testing should be done. Individuals can develop hepatitis due to drug use as currently 1000 drugs are seen to be hepatotoxic [7]. There must be a chronic correlation seen between when the medicine was first taken and the observation of hepatitis. There must also be a correlation between the removal of medication and the recession of the condition [4]. Other causes of hepatitis must also be tested for such as viral hepatitis. There are 5 subsets of viral hepatitis A, B, C, and the less common D and E forms. Hepatitis A is the most common form and is passed on by the faecal– oral route. It’s tested for by the presence of the anti-HAV IgM antibody which tests positive before the development of clinical hepatitis and remains positive for at least 4months. Hepatitis B is tested for by the presence of surface antigen HBsAg. Anti HBC total and Anti – HBC IgM is also tested for. A soluble protein HBeAg is produced by the virus in acute and early chronic stages of hepatitis B so positivity of this indicates infection. Hepatitis C infection has the presentation of Anti-HCV seen in 90% of individuals with this infection [7]. The possibility of autoimmune hepatitis can be ruled out by testing of HLA class II expression on the surface of the hepatocytes. There is also an increase seen in IgG antibody and a variety of other antibodies such as SLA/LP (anti soluble liver protein) [8]. References [1] Hopkins. J. Alcoholic liver disease – Introduction, gastroenterology and hepatology. Baltimore M.D 2010 [2] www.britishlivertrust.org . Accessed 28.11.10 [3 ]Drriad. Pathogenesis of hepatitis infection from chronic alcoholism, Figure 1. 2007 [4] www.hepatitis.org. Phillipe.L, Hepatogastroenterology department, Brugmann University Hospital Brussells Accessed 28.11.10 [5]http://www.gastro.com/Gastro/liverdisease/liver_function.aspx, Gardner. P.W and Waldstreicher.W, American Liver Foundation 1995 Accessed 28.11.10 [6] Borzio. M et al, Thyroid function tests in chronic liver disease: evidence for multiple abnormalities despite clinical euthyroidism. GUT Journal of gastroenterology and hepatology, Vol 24(7), Jul 1983. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1420033/. Accessed 28/11/10 [7] http://www.oaml.com/PDF/CLP012.pdf. Guidelines for clinical laboratory practice, revised March 2000, Accessed 28.11.10 [8]Krawitt. E.L Autoimmune hepatitis: classification, heterogeneity, and treatment, January 1994. Am. J. Med. Vol 96 (1A): 23S–26S. How to cite Critical Study of Alcohol and Hepatocytes Cell Necrosis, Essay examples