Graduation Speech -- Graduation Speech, Commencement Address

(Love you mother and father in Romanian) many individuals here today presumably didn't comprehend what I just said in light of the fact that I am Romanian, yet in the event that you investigate my folks face they realize I love them. I am Romanian and my folks went to the U.S. what's more, could have picked any state yet they picked Washington. For all the individuals who don't acknowledge Washington as much as me let me set out certain vibes. After I went to Arizona and California and some different states I came to understand that everything here is so a lot greener. Washington has the best-tasting faucet water and truly, there is a distinction in taste of water. Did you realize Washington has a magnificent kelp timberland? Individuals from all around the globe come here to make a plunge our sea to see our kelp woodland. In the event that you need some venture tips put resources into kelp cause there will be a major blast in that industry. The city of Seattle is one of the best. It is so refined and everybody here is so pleasant. I just felt I should call attention to that we have probably the best state in the United States. The magnificence of doing a graduation discourse is you get the opportunity to state what ever you need. I believed that would have been simple at the same time, as I think back through the four years of secondary school the main time I composed something was the point at which I was doled out it. So you would think such a youthful flourishing psyche would exploit this and hold nothing back out. So I composed and composed and well, I continued wasting time. I viewed other initiation speakers from the HBN file talk about our future and understood that they had some really extravagant expressions of guidance. Presently I realize I can't offer you guidance on the future since I don't have the experience. What I will give you individuals here today is some evaluation An information about a spot that you folks may not of ev... ...iday collection. That is the magnificence of The Simpsons, it doesn't make a difference how moronic you are everybody has their place in the city. They keep consistent with them selves and in the long run there snapshot of acclaim will come. Everybody, know your Simpsons! Presently I need to leave as much as all you individuals, it just appears as if the most recent day will never end. So I simply need to state regard one another and never abandon any you had always wanted in light of the fact that you get one life and you should make it a pleasant one. So as we leave I need all of you to realize that I have the all the best for every one of you and if any of you see my comic book, Stickmen Revolution, available to be purchased feel free to get me out a piece. I leave you with a joke, (Romanian Joke) I know some of you may experience considerable difficulties getting that yet on the off chance that you investigate my folks' faces that was, that was an extremely amusing joke. For The Revolution!

Charles Dickens Essay

Contrasting the manners by which strain and anticipation is made in the initial arrangements of David Lean’s 1946 and Julian Jarrold’s 1999 understanding of â€Å"Great Expectations† by Charles Dickens In David Lean’s 1946 translation of â€Å"Great Expectation† Pip is depicted as a little, brilliant, clean young man, as he will be viewed as increasingly honest and powerless against the crowd. Pip’s reasonable hair shading against the obscuring foundation makes the crowd feel that he is a radiant like figure. Lean shows the immense scene with tall-outlined gibbets to demonstrate exactly how little and powerless Pip is stumbling into the marshland. At the point when Pip goes to visit and weed the grave of his folks, Lean shows this especially to pick up the audience’s compassion. The crowd hears everything that Pip hears and this encourages us to comprehend his anxiety. The shout is stunning and makes us see his dread to his gathering with the convict. At the point when he is being undermined, Pip’s overpowering respectfulness and naivety, in spite of the dangerous circumstance he is in, causes the crowd to feel a lot of compassion toward him. Nonetheless, in Julian Jarrold’s 1999 translation of â€Å"Great Expectations† Pip is depicted as a scruffy and an unclean little fellow. This picture gains the audience’s compassion as should be obvious that he is abused at home. Jarrold’s Pip has dim hair; and in spite of the fact that he isn't viewed as a heavenly and honest figure. Jarrold connects with the compassion of the crowd by introducing him as a pursued creature. At the point when Pip experiences the convict, he is without a doubt scared and damaged. He can't take a gander at the convict, and is so incapacitated with dread he can’t even talk. At the point when we initially meet the convict we can see promptly how scaring he can be. David Lean shows a nearby of his face all the while to him hopping onto the scene. This nearby view is being utilized to give us what the convict is thinking and furthermore to show the indignation. This nearby view is likewise used to forestall us seeing what Pip is doing when the camera zooms up on the convict. Thusly we stress for Pip and this adds to the anticipation existing apart from everything else. The convict is a scary huge man who has a great deal of control over Pip. At the outset he is constantly shot in murkiness, while Pip is constantly shot in splendid light to underscore his honesty. This is especially observable when the convict is in charge, attempting to tilt Pip over the tombstone. There is a cut among Pip and the convict to show Pip’s weakness and a nearby of his face features his fear. Pip is appeared as the inverse to the convict and looks honest, enchanting and conveniently dressed. The convict anyway looks furious and filthy and we assume this is the thing that he resembles and along these lines view him as an awful individual. Language is likewise used to stress the convict’s forcefulness. The convict explicitly underscores the words ‘roasted’ and furthermore ‘tear him open’. These words are stressed to frighten Pip and furthermore to stun the crowd. It brings the crowd into the story and causes us to feel Pip’s terrorizing. The convict’s startling picture adds to the prohibiting setting. Julian Jarrold’s rendition of the convict is demonstrated to be unimaginably overwhelming and threatening. Albeit no exchange is spoken we can see from his fixed gaze on Pip and his irate frown that he means to do damage to him. The convict is wearing old filthy garments and looks extremely not well prepared, this adds to the audience’s comprehension of him as a got away from convict. Lean uses some powerful strategies to show the characters. He shows the tremendous scene with tall-outlined gibbets to demonstrate exactly how little and powerless Pip is. The utilization of light and dim is compelling when me meet the convict. Pip stays in the light yet the convict’s face is covered in dimness to persuade the crowd of his a detestable nature. Pip’s helped appearance shows his honesty and makes the crowd wonder why such a pleasant kid is in such a dim and miserable spot. After the showdown, Pip is seen scrabbling home over the swamps as fast as could be expected under the circumstances, against the equivalent spooky scene. The setting in Jarrold’s 1999 translation is less cliché. It isn't dull and the sky is radiant. There is a piercing note, which seems unpleasant and frightening to the crowd. Not long before we see Pip’s head peep out of the wheat field, from the convict’s perspective, we hear breathing and this causes tension, as should be obvious anybody. The setting of a wheat field is less conventional and doesn't set us up for when the convict pursues Pip, as nobody would hope to discover a convict in a wheat field. The brilliant reeds add to the quiet serenity of the primary shot, and in this manner loosen up the watcher. Jarrold utilizes his own thoughts and makes the initial progressively captivating and energizing. Toward the starting we have no clue what will occur and in light of this Pip’s running come as a stun, and in this manner has more effect. This furnishes the crowd with a quick motivating force to keep viewing. We at that point follow the emotional pursue that Jarrold has developed through a wheat field and the cemetery. Jarrold’s utilization of perspective shots allow the crowd to feel progressively engaged with the film and to assist them with feeling the disarray of the pursuit. The wheat field itself is Jarrold’s own thought and isn't referenced anyplace in the composed novel. Be that as it may, this truly assists with indicating Pip is attempting to cover up however that he can't get away.

Africans@MIT Cassava Connection

Africans@MIT Cassava Connection “Nobody is going to do it, if we don’t do it.” The room is quiet. “Will you go back?” This moment is a snapshot of many conversations I have had with many other international students at MIT, heavy with the challenge of obligation. I invited members of the EESA (Ethiopian-Eritrean Students’ Association) to my room to discuss recent developments in Ethiopia, to get some things off everyone’s chest and provide a safe space to talk. On February 15th, Prime Minister Hailemariam Desalegn resigns from office. Earlier that month, a slew of Ethiopian political prisoners (bloggers, journalists, activists) were released, some had served sentences as long as seven years. Protesting has been breaking out constantly throughout the country for the past year, with intermittent internet shutdowns and phone line closures orchestrated by the government to control the situation. For a month, my father would try to call home only to get an operator’s voice in Spanish, an absurd, confusing moment. These events affected even my water project, which would have likely been completed sooner without the communication interruptions. In my room on a cloudy Saturday sit several different Ethiopian international students. I use “international” as a fluid termI don’t always mean literally students without U.S. residency, rather, some of them are international students, some are American-born Ethiopians like me, and some are sort of in-between, who have spent time in both the U.S. and Ethiopia, and may hold one or the other passport. All of the people I refer to as “international”, though, have a very committed sense of belonging to a non-U.S. country, sometimes more or less so than the U.S. itself, sometimes equally. We have been having a long, chronological discussion of post-World War II Ethiopian history, which I hope will give context to our modern events. The discussion takes an interesting form, with people jumping in to say, “that’s not true,” or “but also this” or “but their real motivation was” I realize that the attitude, in the U.S. and some other places, of taking history as Facts with a capital ‘F’, is very different in places like Ethiopia. Instead, I am seeing history more like historians likely see itwith a variety of competing sources, with some details that all line up and are probably facts, and others that don’t. The discussion is so long, that students’ come and go throughout the afternoon and evening (“are people still there?” “I left in 2005”, a freshman jokes in our group chat, referring to the history timeline we were discussing). When I ask where people learn about these pieces of history, I get interesting answers. “Some of it we’re taught in school” “You have to buy books from street vendors. And then they’re censored books, so you have to wrap them in newspaper when you read them. If you try to take them in your luggage out of the country, you can get arrested.” “My parents told me some of these things” The big, obvious events are of course clear”these people ruled from this time to this time” is hardly disputable, or “there was a war this year”, or “there was a conflict here”. Less clear are the reasons behind such conflicts “The conflict was about land.” “No but really it was about currency!” “The ruler was his relative, so he practically gave them the port and everyone was mad.” As we wrap up this lengthy discussion of history, I am struck by how short it really is. Modern Ethiopian governance, a system of ‘ethnic federalism’ where representation is divided by region/culture, has only been active as long as I’ve been alive. Most of us have grown up only knowing this government, but our parents knew a drastically different world. Our discussion does succeed in giving me, at least, some contextis it so surprising that something dramatic should break out now, when the government in Ethiopia has only been alive for twenty years? I compare it with the early United States, where the initial “Articles of the Confederation” that was before modern U.S. government barely lasted ten years or soat least Ethiopia hung on for twenty, and even now, the major tenets of the system are likely to stay in place, with major policy changes. When I ask how my classmates feel about these events, I get mixed responses. Some are scared. Some are optimistic, or even excited. Instability can foster all of these emotions and more. But then, the conversation switches and focuses inward, emphasizing a key point: “Nobody is going to do it, if we don’t.” Despite the politics and history and various topics we’ve been discussing, Ethiopia needs practical solutions too. Good governance is of course necessary, but so is economic development. A freshman student here refers to the fact that some people leave the country and never return, are afraid of doing business there, and he is frustrated by this. I joke that I’m down, if we can just meet back in 5 years. I propose a semi-joking plan to export organic rice to China (“guys, I’m telling you, I have a relative in this business”) and use the profit to fund a connectivity company. But on a more serious note, I know that this is not really out of the question; this is not a faraway dream. This is in some sense, the “normal” of African international students. [emailprotected] Part 1: Cassava Connection Inspired by my conversations with my Ethiopian classmates, I decided to write a series of posts about African students and organizations at MIT, first because I think it will be interesting for prospective students in general, and also because I have been amazed by the lengths many African students are willing to go to execute projects in very difficult situations. I realized a common factor is a very strong sense of obligation to home countries and communities that appears among many studentsnot just Africans, of course, but I wanted to highlight some of the amazing projects I’ve seen in this particular community. Take one of the most active Africans I know, for example, Pelkins A. ‘18. Pelkins is from Cameroon and entered MIT as a transfer student, where he became president of the MIT African Students’ Association. He is also Course 2A in Mechanical Engineering, so we were both in the same communication group for 2.671: Measurement and Instrumentation, where I did a project about different types of coffee brewing methods and Pelkins did a project on different image detection algorithms for driverless cars. Pelkins representing MIT undergraduates at the MIT Better World Campaign Pelkins took his 2.671 research project (as many mechanical engineering students do) forward beyond the class, in a way. He interned with GM over the summer on the driverless car team, and worked on similar algorithms and key problems in driverless cars, and actually ended up filing a patent at the end of his internship for a new radar calibration method he worked on. After achieving something so exciting, Pelkins was energized to go out and solve problems of his own, in Cameroon. This is a feeling other students at MIT get, toothat after the struggle and success of the Institute or things you find out you’re capable of while here, you get more real confidence that you can truly accomplish or learn anything. Pelkins grew up outside the capital city, and describes his family as middle-class for Cameroonians. His parents worked in business and education, and highly valued his education, sending him to the best schools that they could manage. He felt deeply supported by his family growing up, and because of this, never thought about class as a barrier to success, though some of his classmates in Cameroon would come from wealthier backgrounds. After initially attending school at University of Texas at Arlington, Pelkins transferred to MIT his sophomore year, where he later took 2.671 with me and interned at GM. His best friend Milton, however, stayed in Cameroon, and attended university there at the National Advanced School of Public Works. They known each other all their lives, grown up together, and playfully competed in school (“sometimes he would be number 1 and sometimes I would be number 1!”) and maintained close contact across the great distance Pelkins had traveled for school. As Pelkins became more excited about doing just something in Cameroon, he would call up Milton with an idea, and they would work on it for a whilemaybe a month or so, and then setting it aside. In that initial rush, the ideas didn’t “stick” very well. Pelkins realized he needed to put more thought and research into making sure his ideas were needed and important. He needed to formally, professionally seek out an important problem rather than act on moments of inspiration. So, like any MIT-trained researcher, he started reading academic journal papers, published by Cameroonian universities. It was during this dive into research when Pelkins noticed a trend: cassava. It was everywhere in Cameroonian research, a plant that Pelkins, with little agricultural background in his family, had not realized was incredibly important to Cameroon, farmed ubiquitously and integral to daily life. “It’s funny”, Pelkins said when I interviewed him, “somehow you can learn more from looking from the outside!” When you are in the middle of problem, sometimes you can’t even tell that it’s there. Cassava has many desirable properties. It is a starch-heavy plant that is gluten free, and very versatile. However, the methods used to process cassava in Cameroon were still very traditional, as it is used on a small scale for cooking and eating. Pelkins wondered if there was a way for cassava to be processed in mass quantities, as the plant itself spoiled rapidly after harvesting. When Pelkins talked to Milton and Milton did his own research, he was beyond ecstatic. In just one month, Milton rented an apartment that they used as an office space. “I get a lot of credit,” Pelkins says, “but this project would not be possible without Milton”. They agreed that Milton would work on the initial research, and Pelkins, with many opportunities at MIT, would search for funding. Pelkins got some funding from Sandbox, first a $1,000 grant, then $5,000, and they also connected Pelkins with other investors and mentors at MIT. He found another teammate in his roommate, Tyler Lerner, who was integral in developing the business and financial strategy with Pelkins. Every week the founders, Pelkins, Milton, and Tyler have a meeting, with Milton calling in over Skype. Milton dedicated himself full time to the project, which they named “Cassvita”. As they acquired more funding, they hired lab techs in Cameroon, who worked on processing the cassava into a state that would not easily spoil. With roughly 8 months of work, the team found a way to process cassava into a powder just like wheat flour, except it was gluten free and non-allergenicthe perfect substitute. They envisioned exporting different finished products, from the flour itself, to dried goods like pasta.       Now, Cassvita is working on commercializing this process. A lot more needs to be done, and some more MIT students are going with Pelkins to Cameroon this summer to work on the project, with the support of MIT programs like MIT-Africa and MISTI. Other mechanical engineering classmates of mine, like Trang L. ‘18 and Pelkins himself, will work on viable mass-manufacturing approaches, looking for and combining machines that can achieve the steps from plant to flour. Exporting needs to be figured out, and the team would like to fortify the flour with protein, something two other [emailprotected], Amaka A. ‘19 in Course 9 (Neuroscience), as well as Gabby B. 19 in Course 21E (choosing Computer Science and Anthropology) will be investigating. After more progress, Cassvita wants to seek out high-capital investments to really push the business forward. Pelkins is excited, and I’m excited talking to him. “I cannot think of a better way to live my life than to give back to my community,” he says, “it’s not that you owe anyone, you just have a responsibility.” Here is that obligationno, aspirationI felt so prevalent. It’s not as much a duty as a dream, these mental images of aunties and uncles and family that supported you, and the dream and excitement to use what you have to make life better. Rather than being a task, it is an achievement; it brings joy. With Cassvita, Pelkins hopes there will be a way to monetize cassava more effectively for Cameroon, and aid the many farmers that produce this crop. But beyond that, he hopes that a pretty regular Cameroonian like him accomplishing something like this will pave the way for future students. “What truly brings me joy is that you can do something to inspire someone else.” It is truly a labor of love. The Cassvita team in Camerooon, with Milton seated second from the left. To learn more about Cassvita, check out their website at  www.cassvita.com Pelkins also appears in this video made by the MIT School of Engineering, discussing his work.   Post Tagged #2.671 Measurement and Instrumentation #African Students' Association #[emailprotected] #Course 2 - Mechanical Engineering #Ethiopian-Eritrean Students Association #MIT Sandbox Initiative #MIT-Africa Initiative

The Ins and Outs of Fetal Homicide Laws

In 1969, eight months pregnant Teresa Keeler was beaten unconscious by her jealous ex-husband, Robert Keeler, who told her during the attack that he was going to stomp it out of her. Later, at the hospital, Keeler delivered her little girl, who was stillborn and suffered a fractured skull. Prosecutors attempted to charge Robert Keeler with the beating of his wife and for the murder of Baby Girl Vogt, the fetus given the fathers last name. When Is a Fetus Considered Alive? The California Supreme Court dismissed the charges against Keeler, saying that only someone born alive could be killed and that the fetus was not legally a human being. Due to public pressure, statutes were eventually amended to say that murder charges can only apply to fetuses older than seven weeks or beyond the embryonic stage. Currently, 37 states recognize the unlawful killing of an unborn child as homicide in at least some circumstances. Although many states now have fetal homicide laws, there is a wide variety of differences about when a fetus is considered living.  Pro-choice groups see the laws as a way to undermine Roe v. Wade, although currently statues to the laws clearly exclude legal abortions. Anti-abortionists view it as a way to teach the public about the value of a human life. Cherica Adams In 2001, Rae Carruth, former pro-football player for the Carolina Panthers, was convicted of conspiracy to commit the murder of Cherica Adams, who was seven months pregnant with his child. He was also found guilty of shooting into an occupied vehicle and of using an instrument to kill a fetus. Adams died from the gunshot wounds but her child, delivered by Caesarean section, survived. Rae Carruth received close to the maximum sentence of 19 to 24 years in prison. Veronica Jane Thornsbury In March 2001, 22-year-old Veronica Jane Thornsbury was in labor and on her way to the hospital when Charles Christopher Morris, a 29-year-old driver ran a red light. Under the influence of drugs, Morris smashed into Thornsburys car, killing her. The fetus was stillborn. Morris was prosecuted for the murder of both the mother and the fetus. However, because her baby was not born, the Kentucky Court of Appeals overturned a guilty plea in the death of the fetus. After the tragedy of Thornsburys death, Kentucky law determined in February 2004 to recognize a crime of fetal homicide in the first, second, third, and fourth degrees. The law defines an unborn child as a member of the species homo sapiens in utero from conception onward, without regard to age, health, or condition of dependency. Laci Peterson and the Unborn Victims of Violence Act Thirty-five years after Baby Girl Vogt, Californias fetal homicide law was used to prosecute Scott Peterson with two counts of murder for Laci Peterson, his seven months pregnant wife, and their unborn son, Conner. According to Stanislaus County Assistant District Attorney Carol Shipley: If both the woman and the child were killed and we can prove the child was killed due to the actions of the perpetrator, then we charge both. A multiple murder charge against Scott Peterson made him eligible for the death penalty according to 2004 California law. On April 1, 2004, President Bush signed into law the Unborn Victims of Violence Act, also known as Laci and Conners Law and the Unborn Fetus Protection Act. It states that any child in utero is considered to be a legal victim if injured or killed during the commission of a federal crime of violence. The definition given of child in utero is a member of the species homo sapiens, at any stage of development, who is carried in the womb. Resources and Further Reading Ryan, Harriet. â€Å"Fetal Homicide Issue Arises in Laci Peterson Case.† Court TV, CNN, 26 Mar. 2003, 8:32 p.m.

Gestational Diabetes Consequences For Fetal Programming of Vascular Disease in Adulthood - Free Essay Example

Sample details Pages: 30 Words: 9080 Downloads: 4 Date added: 2017/06/26 Category Health Essay Type Descriptive essay Level High school Did you like this example? Abstract Gestational Diabetes is a condition present in the later stages of pregnancy where the mother has insulin resistance leading to glucose intolerance. The aetiology of Gestational Diabetes Mellitus is largely unknown but several theories include autoimmune destruction of the beta cells, monogenic mutations and insulin resistance. In pregnancy it is normal for there to be some levels of insulin resistance and it is thought that the products of the placenta contribute to the state of insulin resistance as GDM usually subsides after pregnancy. Don’t waste time! Our writers will create an original "Gestational Diabetes: Consequences For Fetal Programming of Vascular Disease in Adulthood" essay for you Create order GDM in pregnancy can lead to an increased risk of cardiovascular disease in the offspring such as hypertension and atherosclerosis. This is due to the increased levels of oxidative stress and inflammatory mediators present during pregnancy. The placenta is very important as it is able to control and buffer the amount of glucose that is delivered to the fetus but if this level is too high then it is out of the placentas control and the fetus may have increased rate of growth due to this extra glucose. The current focus of research in this area seems to be into finding ways to diagnosis GDM earlier in the pregnancy and to try and reduce the amounts of oxidative stress. Gestational diabetes: consequences for fetal programming of vascular disease in adulthood Introduction Gestational Diabetes Mellitus (GDM) occurs when there is a glucose intolerance that is first detected during pregnancy. It is a form of hyperglycaemia (Buchanan and Xiang 2005). The aetiology of the condition is unknown but there have been many suggestions as to the cause of it, including autoimmune destruction of the ß pancreatic cells and the possibility of a genetic predisposition to the condition. Hormones that are produced in pregnancy help contribute to the insulin resistant state which characterises diabetes. In recent years, there has been an increase in the cases of Obesity and this is a risk factor for both Diabetes Mellitus and Cardiovascular Disease. The intrauterine environment can affect fetal programming and development. This essay will look into how the placenta and its products can affect the insulin resistant state and how this resistance effects programming as well as the role of oxidative stress and inflammation in making the offspring more susceptible to car diovascular disease. Gestational Diabetes Mellitus (GDM) GDM is a state of insulin resistance which disturbs the intrauterine environment and can lead to accelerated fetal growth (Radaelli et al 2003).It effects approximately 7% of pregnant women with approximately 200,000 cases seen each year (Schillan-Koliopoulos and Guadagno 2006). The term GDM is applicable when the onset is during the second and third terms of the pregnancy, but it does not exclude the possibility that the insulin resistance was undiagnosed before the pregnancy. If this is the case and is found to occur in the earlier stages of pregnancy then the mother should be treated the same as mothers who are known to have diabetes before pregnancy (Metzger, Coustan 1998). There is a degree of insulin resistance in normal pregnancy which begins towards the middle of the pregnancy but during the later part of the second and the final trimester these can increase to levels of insulin resistance that are associated with type 2 diabetes (Yogev et al 2008 Chapter 10). Insulin re sistance is when the tissues do not produce a response to insulin due to problems with the secretion of insulin or where the tissues are desensitised to insulin and therefore lack the ability to produce a response (Catalano et al 2003). In a normal pregnancy, the mother changes her metabolism to allow a constant supply of nutrients to reach the fetus to support its rapid growth. Among these nutrients is glucose, which is the main energy source used by the fetus. During the later stages of pregnancy the mother becomes hypoglycaemic and although there is increased gluconeogenesis, the hypoglycaemia still occurs because there is a high rate of transport of glucose to the fetus (Herrera 2000 cited in Herrera and Ortega 2008). GDM can have effects that impact the development of the fetus such as hypoglycaemia and macrosomia, which is an increase in body weight and has the possibility of leading to problems when giving birth, such as shoulder dystocia (Schillan-Koliopoulos and Guadagno 2006). During the second trimester of pregnancy there is peripheral insulin resistance but there is also the possibility that hepatic insulin sensitivity is altered in pregnancy, although few studies confirm this. By the end of the pregnancy the levels of insulin that are circulating are thought to be double those at the start (Redman 2001). Insulin Resistance Insulin resistance in GDM can occur in two forms. The first is where it develops in late pregnancy and it has been postulated that there is a post-receptor mechanism that may influence the insulin signalling pathway which leads to a reduced glucose uptake. The second form is where there is already a degree of resistance before the pregnancy but the changes that occur in normal pregnancy aggravate this (Metznger et al 2007). The insulin resistance that develops in pregnancy is much needed to allow the flow of nutrients, from the mother, directly to the fetus to allow for growth (Radaelli 2003). Increased insulin resistance leads to an increase in insulin secretion by the ß pancreatic cells (Buchanan and Xiang 2005). The insulin resistance is thought to be caused by increased adiposity and as the insulin resistance usually stops after pregnancy this suggests that there is a possibility that the products of the placenta are a potential cause of the resistance. During the course of the pregnancy the actual changes in glucose levels are very small. It would be assumed that the glucose levels would rise due to the increased insulin resistance but the pancreatic ß cells increase their secretion of insulin to maintain homeostatic glucose levels (Yogev et al 2008 Chapter 10). GDM occurs because there is an increased demand for insulin which under normal circumstances can be met unless there are problems with the secretion of insulin leading to the development of hyperglycaemia. The majority of mothers who develop GDM have been discovered to have a degree of insulin resistance before they became pregnant. Therefore, with the insulin resistance that occurs in normal pregnancy it can be said that GDM occurs with a greater insulin resistance than normally present in gestation (Yogev et al 2008 Chapter 10). Insulin resistance causes a decreased uptake of glucose into skeletal muscle, adipose tissue and liver as well as a decreased production of hepatic glucose. (Catalano et al 2003). One suggestion for insulin resistance looks into the possible role of the mitochondria. Studies using Magnetic Resonance Spectroscopy (MRS) have shown that in normal offspring of parents with type 2 diabetes, there is an increased amount of intramyocellular lipid. This has been shown to cause a reduced function in mitochondria which suggests that mitochondrial dysfunction may play a part in insulin resistance (Petersen et al 2004 cited in Morino et al 2005). It has been suggested that this increase in intramyocellular lipid activates a serine kinase cascade which causes an increase in the Insulin Substrate Receptor 1 (IRS-1), which inhibits insulin receptor phosphorylation on tyrosine sites. This can cause a decrease in the effects and utilisation of glucose. One study showed that in the insulin resistant offspring the mitochondrial density was reduced by just over a third to that of a normal offspring. This suggests that offspring who are insulin resistan t may inherit a condition that causes a reduction in rate oxidative phosphorylation in mitochondria (Griffin et al 2009 cited in Morino et al 2005). Detection of GDM Diagnosis of GDM helps to identify pregnancies that are at risk of fetal morbidity as well as obesity and glucose intolerance in the offspring (Buchanan and Xiang 2005). GDM is hard to diagnose as it is asymptomatic. Normal diabetes could be diagnosed by glycosuria but in pregnancy the renal threshold to glucose is lowered so that glycosuria doesnt give a true representation of hyperglycaemia (Redman 2001). There are several risk factors of GDM which can be classified into three groups and help in the screening process. Low risk factors include women who are younger than 25, normal weight at conception, no known family members with diabetes and no history of glucose intolerance. High risk factors include obesity of the mother, diabetes in close relatives, a history of glucose intolerance, current glycosuria and previous pregnancies with GDM (Metzger and Coustan 1998 Chapter 25). Causes of Diabetes There are several theories as to why diabetes occurs and this has been thought to be similar to the underlying mechanisms that cause gestational diabetes. Diabetes is a result of pancreatic beta-cell dysfunction which can present in three main ways: autoimmune, a genetic cause and on top of already present insulin resistance (Buchanan and Xiang 2005). Autoimmune diabetes accounts for approximately 5-10% of all diabetic cases (American Diabetes Association 2010). There are circulating antibodies to the ß cells of the Islet of Langerhans. In GDM, there are a small number of women who have with these antibodies present in their circulation. It is thought that these cases present with GDM due to problems with insulin secretion caused by destruction of the Islets by the autoantibodies (Buchanan and Xiang 2005). This form is similar to type 1 diabetes. The Islet Cell Autoantibodies (ICA) have been shown to have four major molecular targets: Insulin, Glutamic acid decarboxylase (GAD 65), Insulinoma-associated antigen-2 (IA-2) and Zinc Transporter 8 (ZnT8) (Tree 2010). Monogenic diabetes has 2 general forms, one where there are mutations in autosomes and the other where there are mutations in the DNA of mitochondria. The first form is commonly referred to as Maturity Onset Diabetes of the Young (MODY). In both cases onset tends to be at a young age and the patient doesnt present with insulin resistance or obesity (Buchanan and Xiang 2005). Mutations that cause MODY have been found in some women with GDM and commonly occur in genes coding for glucokinase, hepatocyte nuclear factor and insulin promoter factor, MODY is associated with beta cell dysfunction (Weng et al 2002). Chronic insulin resistance with beta-cell dysfunction seems to be the most common cause of GDM. As mentioned before there is an increase in insulin resistance in normal pregnancy but if this develops with background insulin resistance then there is an even greater insulin resistance whic h can lead to GDM. An established suggestion is that women who are unable to increase their secretion of insulin to cope with the insulin resistance developed in late pregnancy are more susceptible to developing GDM (Buchanan and Xiang 2005). However there could be various environmental processes that are involved in the underlying pathophysiology of GDM. The products of the placenta may also have a role in increasing or decreasing insulin resistance and these will be discussed later. Placental Function The placenta is an organ that has many roles during the development of the fetus. One of these functions is that it acts as a barrier to separate the maternal and fetal surfaces such that the syncytiotrophoblast surface exposes the placenta to the maternal circulation and the endothelium is exposed to the fetal circulation. This position between the two circulations means that the placenta is influenced by molecules from both circulatory systems, including cytokines, hormones and growth factors. The placenta produces molecules which can separately affect the maternal and fetal circulation and it expresses a large number of cytokines including leptin, resistin and tumour necrosis factor. However it has been discovered that these molecules are also produced by adipocytes. All molecules that are going from the mother to the fetus have to cross the placenta. Here they are either modified, for example lipids or like glucose, they are metabolised for placental purposes (Desoye et al 2008 ). The placenta plays an important role in fetal growth and the regulation of pregnancy (Giachini 2008). The placenta acts to sustain normal homeostatic levels and to carry out the functions of the vital organs. It also provides an immunological defence to the fetus and allows the exchange of molecules vital to its development (Jansson and Taylor 2007). Placental Development Approximately 4-5 days after conception, the process of cleavage causes rapid cell divisions and one of the groups of cells to form are called trophoblast cells. Further developmental processes form the blastocyte which is surrounded by an outer layer of the trophoblast cells. As the pregnancy progresses, the trophoblast cells develop into the placenta while the inner parts of the blastocyte form the embryo and umbilical cord (Huppertz 2008). The blastocyte implants itself onto the epithelium of the uterus where it differentiates into a syncitiotrophoblast which is able to implant itself in the epithelium leading to it being embedded into the decidual part of the uterus (Huppertz 2008). After the attachment of the blastocyte, the trophoblast layer divides very quickly and changes into 2 layers; the inner cytotrophoblastic layer and the outer syncytiotrophoblastic mass (Gude et al 2004).The whole implantation process takes 12 days to complete and after this the fetus is fully emb edded into the endometrial layer (Huppertz 2008). The chorionic plate is the surface of the placenta that faces the fetus and this is where the umbilical cord inserts. The basal plate is the surface that faces the mother which contains many types of cells including immune cells such as macrophages and killer cells to carry out the placentas immunological function. The maternal basal plate and the fetal chorionic plate converge to form the smooth chorion which is composed of three layers (Huppertz 2008). When the trophopblast invades the endothelium there is a remodelling of the uterine spinal arteries which is necessary to ensure that the fetus and the placenta receive an adequate blood and nutrient supply and is able to remove any waste materials. This direct supply of blood and nutrients to the placenta can define it as being haemochorial villous organ (Gude et al 2004). After the rapid divisions of the trophoblast and development into 2 layers there are two pathways that can occur, the villous and extravillious pathways. The extravillious pathway results in the trophoblast being able to invade into the decidua and cause the remodelling of the uterine arteries to increase blood supply to the placento-fetal unit. The villious pathway has a transportation function as well as having endocrine and protective functions (Gude et al 2004). Normal Placentation Placentation involves the structure and function of the placenta. The process of placentation is helped by the composition and arrangement of the extracellular matrix (ECM) of the endometrium. Studies on rats induced with diabetes provided results that showed that diabetes has an effect on the distribution of the ECM molecules. This study by Giachini et al illustrates that Types I and III collagen as well as other molecules, such as proteoglycan molecules decorin and biglycan were distributed throughout normal and diabetic placentas. It was shown that diabetes affects the expression of fibronectin and an increase in deposition of fibronectin may cause changes to the ECM structure which could affect the transfer of molecules from the mother to the fetus. One way in which changes in the ECM can be overcome is to test blood glucose levels frequently during the pregnancy and if kept in normal ranges this can dramatically decrease the prevalence of diseases and disorders present in the fetus (Giachini et al 2008). As the pregnancy progresses the size of the placenta increases which also means an increase in the amount of products that the placenta produces therefore increasing in the insulin resistance (Schillan-Koliopoulos and Guadagno 2006). This is because the net effect of the products of the placenta is to increase insulin resistance. The increase in size of the placenta means that it needs an increased blood supply. Failure of the mother to increase its blood supply to the placenta can lead to placental insuffiency which if exacerbated can be attributed to be a cause of intrauterine growth restriction (IUGR). This growth restriction is more related to poor maternal nutrition rather than to a cause of GDM. GDM have been associated with an increased fetal and placental weight (Jansson and Taylor 2007). One of the reasons why GDM and increased insulin resistance affects the fetus is that while glucose can cross the placenta, insulin is unable to. This means that the fetal pancreas has to compensate by producing more insulin to prevent high blood glucose levels. The fetal pancreas is capable of doing this and the liver responds to the higher levels of insulin by increasing its production of glucose (Schillan-Koliopoulos and Guadagno 2006). Offspring who have an increase in birth weight have been shown to be at risk of developing cardiovascular disease and diabetes later in life. The main risk factor for this is poor transfer of nutrients via the placenta (Jansson and Taylor 2007). How dramatic these changes are depends on how good the control of blood glucose levels have been during the development of the placenta, if any treatment has been received and if there were any periods of away from normal glucose levels (Desoye 2006). How does diabetes affect Placentation? Diabetic insults at the beginning of the pregnancy can have long last effects of the placenta. One of the roles of the placenta is that it is able to buffer excess maternal glucose which can help to keep the fetal glucose levels within range However if the insult lasts longer than the placenta is able to compensate for then excessive fetal growth may occur (Desoye Mouzon 2007). In diabetes there is endothelial dysfunction which can lead to vascular disease. The endothelial cells help to control the vascular tone of the smooth muscle lining the vasculature. They do this by producing substances that help to vasodilate the smooth muscle including Nitric Oxide, Prostacyclin and Endothelium-Derived Hyperpolarising Factor (EDHF). There have been several studies to suggest different mechanisms of how diabetes affects the endothelium including impaired release of these vasodilating molecules, faults with signal transduction and increased release of constricting mediators of the endothel ium. The dysfunction of the endothelium in diabetes is thought to be caused by activation of protein kinase C (PKC) as well as increased oxidative stress, non-enzymatic glycation and an increased activation of the polyol pathway (De Vries et al 2000).The main reason why these effects occur is thought to be due the activation of the protein kinase C pathway and the increased oxidative stress. This can cause early damage to the development of vascular vessels (Roberts and Raspollini 2008). These mechanisms will be discussed later. The effect of hormones produced in pregnancy Pregnancy causes changes in the circulating hormones and cytokines which can all have different effects on insulin resistance and this may help explain the mechanism underlying the resistance that is found in pregnancy and in GDM. Cytokines produced in pregnancy, such as TNF-a, Adiponectin and Leptin have been found to cause an increase in the insulin resistance (Gao et al 2008). In early pregnancy, the levels of oestrogen and progesterone rise but no net effect is seen as the two have antagonistic effects. Oestrogen increases the binding of insulin to its receptor whereas progesterone reduces the ability of insulin to bind (Ryan and Enns 1988). Cortisol levels in pregnancy increase so that by the end of the pregnancy the levels are three times that of what they were at the beginning (Gibson and Tulchinski 1980 cited in Yogev et al Chapter 10). Studies have shown that with increased amounts of cortisol there was a decrease in insulin sensitivity causing insulin resistance (Ri zza et al 1982 cited in Yogev et al 2008 chapter 10). During pregnancy the levels of prolactin increase up to ten times the normal amount (Yogev et al 2008 chapter 10). Studies have shown that in a culture of pancreatic beta cells, prolactin can cause an increase in levels of secreted insulin (Sorenson et al 1993 cited in Yogev et al 2008 Chapter 10). However, high levels of prolactin are not seen to be a pathological cause of GDM (Yogev et al 2008 chapter 10). Human placental lactogen (HPL) is a hormone, and its levels rise during the second trimester of pregnancy. This causes a decrease in the phosphorylation of insulin receptor substrate (IRS1) which can lead to significant insulin resistance (Ryan and Enns 2008 cited Yogev et al 2008 ch 10). Leptin is associated with obesity and concentrations of leptin have been shown to be related to the concentration of insulin in the plasma. In pregnancy the leptin levels increase dramatically. During pregnancy the mother uses her fat stores to support fetal growth and it is thought that the leptin levels increase with the mobilisation of these fat stores. Leptin levels relate to the body mass of the individual (Sattar et al 1998). Placental Leptin is the same in structure and charge to the one produced by adipose tissue (Ashworth et al 2000). One study showed that high leptin concentrations in the umbilical cord increased the likelihood of developing fetal macrosomia (Wiznitzer et al 2000). It is also thought that leptin effects insulin sensitivity by effecting glucose metabolism in both skeletal muscle and in hepatocytes. Rats that received an external source of leptin were found to have an increase in gluconeogenesis which accounted for the majority of hepatic glucose production (Rossetti et al 1997). In GDM there is a greater secretion of TNF-alpha in response to glucose. TNF-alpha functions to regulate metabolism of glucose and lipids as well as being involved in insulin resistance. Many studies suggest t hat TNF-alpha is involved in the progression to GDM. They found that an increase in glucose cause the placenta and adipose tissue to increase production of TNF-alpha in some cases up to 4 times more than non-diabetic pregnant(Coughlan et al 2001). One study showed that the increases in the levels of TNF-alpha during pregnancy increased consistently with increases in body weight (Catalano et al cited in Yogev et al 2008). Adiponectin is a protein derived from adipose tissue and its function is to regulate insulin resistance and maintains levels of glucose. During pregnancy it has been found that its levels drop and could therefore lead to the increase insulin resistance found in GDM (Gao, Yang, Zao 2008). Adiponectin has also been found to decrease the secretion of TNF-alpha which as stated above can lead to insulin resistance (Hotamisligil 1999 cited in Yogev et al Chapter 10 2008). Adiponectin may cause increased insulin sensitivity as its concentration decreases throughout the gestational period (Desoye and Mouzon 2007). Resistin is a protein that is produced by adipose tissue and is thought to be involved in insulin resistance in diabetes and is associated with obesity (Steppan and Lazar 2002) In pregnancy, resistin is secreted by the placenta and this secretion reaches its peak by the last trimester (Yura et al cited in Megia et al 2008). Studies show that TNF-alpha is an important factor in insulin resistance during pregnancy and with inputs from leptin and cortisol there is altered glucose metabolism whereas inputs from oestrogen, progesterone and prolactin had little significant effects (Kirwan and Mouzon 2002). There are many hormones produced during pregnancy, mainly by the placenta and adipose tissue that have varying affects but with the overall impact being insulin resistance. Inflammation in Diabetes There are genes in the placenta which regulate reorganisation of the endothelium and inflammatory responses and in GDM these were found to be altered. The increase in leptin receptors suggests that in the placenta this can cause proinflammatory responses (Radaelli 2003). One of the current theories is that the abnormal metabolic environment in GDM can lead to increased production of cytokines and inflammatory mediators. Molecules such as TNF-alpha, Resistin and Leptin increase during pregnancy and these increases in these inflammatory mediators produce metabolic changes by increasing insulin resistance (Desoye and Mouzon 2007). Leptin and TNF-alpha activate phospholipase A2 which are a family of eicosanoid precursors that go on to produce essential fatty acids such as w3 polyunsaturated fatty acids (Desoye Mouzon 2007). There has been a recent investigation which found that with increased adiposity at birth there has been an increase in w3 fatty acids in the placenta (Veraste hpour et al 2005 cited Desoye and Mouzon 2007). As stated before, the placenta produces cytokines but it is also a site of action of the cytokines. It is the location of the receptors for these cytokines will influence if the cytokines act on the mother, the placenta or the fetus. With cytokines there is very little transfer across the placenta from mother to fetus and the origin of the cytokines in the fetus can be from either the placenta or from the fetus itself (Desoye and Mouzon 2007). Fetal Programming Many studies have highlighted the fact that events that occur while the fetus is developing can alter its developmental pathway and have adverse outcomes in later life. Fetal programming describes how the environment can affect certain developmental events of which the effects are permanent and can affect processes such as metabolism and the organisms physiology. Women with GDM have an increased risk of the fetus developing macrosomia (Catalano 2008 Chapter 11). The main factor that effects the growth of the fetus is the maternal environment and there is a strong association with the weight and height of the mother and the growth of the fetus such that mothers who are heavier and taller will produce heavy babies. (Love and Kinch 1965 cited in Catalano 2008 Chapter 11). The placenta and fetal programming The placenta is very important to the developmental processes of the fetus as it is able to change the quantity of signals and nutrients that the fetus receives. Deviation from normal would alter the fetal programming, thus making it more susceptible to disease in later life. Pregnancies that are complicated by GDM have excessive oxidative and nitrate stress which has been found to change the activity of certain proteins. Oxidative and nitrate stress alter the placentas function and may cause changes in the fetal programming. Nutrient transfer depends largely on the normal development of the vasculature to allow blood flow and this can be affected by GDM which can cause a decrease in the flow of substrates and is a mechanism in which fetal programming can be affected (Myatt 2006). Fetal programming involves a large amount of development plasticity and interruptions to this development may cause abnormalities in the development of certain cells which may progress to structural di fferences in organ development (Gluckman and Hanson 2004 cited in Jansson and Powell 2008 ref 16). Effects to the fetus exposed to GDM If a fetus is exposed to a diabetic environment during pregnancy then there can be certain long term effects. These effects can be classified into three groups; Anthropometric, Metabolic or Vascular and Neurological or Psychological. Anthropometric changes are concerned with the rates of growth for both height and weight and in a diabetic environment these can be excessive leading to macrosomia and obesity in later life. Metabolic and vascular changes that occur are abnormal glucose tolerance which can eventually lead to diabetes mellitus. Finally the neurological and psychological changes that can occur are usually minor but development of psychological and intellect can sometimes be deficient (Dabelea and Pettitt 2008). Potential problems that may arise with the fetus from an exposure to maternal diabetes include abnormal organ mass, altered angiogenesis and increased levels of fetal insulin (Fetita 2006). It has also been found that if there is an increase in weight during pr egnancy then there is usually a higher birth weight of the fetus (Humphreys 1954 cited in Catalano 2008 Chapter 11). The developing fetus cannot synthesise glucose and is dependent on the mother to produce it where it is transported to the fetus via facilitated diffusion through the placenta (Aerts et al 1996 cited in Mello, Parretti and Hod 2008). The result of decreased insulin sensitivity is that there is more glucose available to the developing fetus which can lead to a greater birth weight (Mello, Parretti and Hod 2008). Using animal models, it has been shown that exposure to high levels of glucose in utero can lead a diminished number of nephrons in the offspring (Amri et al 1999 cited in Fetita 2006 ref 68). This is important as nephrogenesis only occurs in the fetus and stops after birth (Gomez, Norwood 1999). It has been shown that a reduction in the numbers of nephron may affect the rate of progression of renal disease in adults due to an inability to secrete sodium. This may later develop into salt-sensitive hypertension (Brenner et al 1988). The mechanisms of reduced organ mass, high levels of fetal insulin and defects in angiogenesis may help explain how the fetus programs abnormal glucose tolerance in adulthood as a result of exposure to GDM (Fetita 2006). Transmission of diabetes from mother to offspring Exposure to gestational diabetes mellitus increases the risk of the fetus developing abnormal glucose tolerance which may develop into type 2 diabetes. (Fetita et al 2006). The association between greater incidences of the offspring having diabetes with a mother with GDM is greater than what would be predicted that could be passed on by maternal genetics (McLean et al 2006). One study showed that the phenotype for GDM/T2D was more common in daughters of mothers who were diabetic rather than daughters of fathers who were diabetic suggesting that the transmission is from mothers with GDM to their daughters. However there were limitations of the McLean study. Patients may not be aware of their fathers diabetes status due to men having lower inclinations to report symptoms and share illnesses with the family. One study showed that the mass of the pancreatic beta cells is relatively fixed by the end of fetal growth and this can be influenced by an intrauterine environment of hypergly caema (McLean et al 2006). Congenital defects are more common in babies born to diabetic mothers (Farrel et al 2002 cited in Fetita et al 2006). There are many factors that can influence the prevalence of these malformations including the duration, severity and age of onset of GDM (Kousseff 1999). If the onset of GDM is at the beginning of development then development of some organs may be affected. However as said before, the majority of GDM develops during the second trimester. This can then lead to embryopathy which includes defects such as failure of neural tube closure and malformations in the Renal, Cardiac and Gastrointestinal systems which present in childhood (Fetita 2006). In diabetes the hexosamine pathway is activated and inhibits the pentose shunt pathway which decreases the production of antioxidants and therefore leads to an increase in oxidative stress. This oxidative stress has been found to disrupt gene expression and may contribute to congenital defects. One example is that oxidative stress inhibits a gene called pax-3 which is needed for neural tube closure and in diabetes there is an increased risk of neural tube defects (Horal et al 2004). Oxidative stress Endothelial cells play a role in vascular disease and they function to regulate vascular tone, control the proliferation of smooth muscle and inhibit platelet function. This is achieved by Endothelium derived nitric oxide (eNOS). If there is a reduced production of NO then endothelial dysfunction can occur and this can cause inflammation, thrombosis and cause the intima layer of blood vessels to divide (FÃ ¶rstermann 2008). Oxidative stress is an imbalance between the production of reactive oxygen species (ROS) and the ability to defend against them (Jansson and Powell 2007). There is also increasing evidence that suggests that oxidative stress plays an important part in the changes that take place, both microvascular and macrovascular, in association with diabetes. Some studies have shown that the role of oxidative stress and mitochondrial dysfunction leads to intrauterine growth retardation in type 2 diabetes. In these individuals there is an increase in production of free ra dicals due to low activity of the electron chains in the mitochondria and this can lead to damage of proteins, DNA and mitochondria (Giugliano et al 1996 cited in Shah et al 2007). Oxidative stress causes a reduction in NO and reduces protection against ROS which can lead to pro-inflammatory and atherosclerotic pathways being activated (FÃ ¶rstermann 2008). There are many mechanisms in hyperglycaemia which can lead to the generation of free radicals. Hyperglycaemia causes an increase in the polyol pathway which leads to a decrease in antioxidant defence increasing the oxidative stress. Oxidative stress is also increased in the hyperglycaemia state by the increase in glucose autooxidation and increase in protein glycation which increases oxidative factors (Giugliano et al 1996). ROS that are formed from the hyperglycaemic state have been found to be involved in the progression of vascular complications (Gao and Mann 2009). In the human placenta there are many mitochondria w hich is where the electron transport chain takes place. In normal pregnancy there are more electrons leaking from this chain and able to produce reactive oxygen species. This extra production of ROS can lead to damaged lipids, DNA and proteins. Pregnancy is therefore a condition where there is increased possibility of there being damage from oxidative stress (Chen and Scholl 2005). ROS can activate a number of pathways that can cause damage to cells and can be linked to the complications that occur in the later stages of diabetes. One of consequences of GDM is hyperglycaemia and this is known to cause increased oxidative stress through several mechanisms (Evans et al 2003). Firstly hyperglycaemia causes the non-enzymatic glycation of proteins, called advanced glycation end products (AGEs) and these are thought to be important in the underlying pathogenesis of diabetic complications. AGEs can interfere with signal transduction, they can change the soluble levels cytokines, hormone s and free radicals and they can alter the function of the proteins that are glycated (Brownlee 1995). Secondly high blood glucose activates the protein kinase C (PKC) pathway and is associated with complications with many of the bodies systems including the cardiovascular system. There is also the possibility that free fatty acids (FFA) are involved in activating this pathway (Koya and King 1998). Finally, it has been hypothesised that hyperglycaemia activates the polyol pathway. This pathway consists of two enzyme reactions; the first being catalysed by Aldose Reductase which reduces glucose to sorbitol which is then converted to fructose by sorbitol dehydrogenase. In rats lens it was found that these two enzymes contributed to oxidative stress in a hyperglycaemic state (Chung et al 2003). From the evidence that is available it has been suggested that oxidative stress ahs a role in the pathogenesis of GDM. Other ideas are that lower levels of antioxidant defences contribute to the progression to GDM (Chen and Scholl 2005). Vascular Tone Increased oxidative stress and inflammatory mediators will affect the vascular tone of blood vessels. The blood vessels in the umbilical cord have no autonomic innervations and therefore the vascular tone of these vessels relies solely on local substances produced in the systemic circulation (Radenkovic 2009). One study showed that serotonin induces a constrictive response on the umbilical artery (Haugen and Rognerud 2001) In diabetes, there is endothelial dysfunction which umbilical artery responds differently to substances such as serotonin in GDM (Radenkovic 2009). GDM and effects on offspring The presence of GDM during pregnancy predicts metabolic problems such as Type 2 Diabetes and metabolic syndrome which are both associated with atherogenesis and vascular dysfunction later on in life (Carpenter 2006). Gestational diabetes can have many effects of the developing fetus and the effect and how severe it is depends on when the onset of diabetes occurs. GDM usually arises in the 2nd and 3rd trimesters and the effects include macrosomia, orgnomegaly, Central Nervous System (CNS) development delay, chronic hypoxemia and the possibility of still birth (Merlob and Hod 2008 Chapter 47). Insulin resistance along with central obesity and dyslipidaemia is thought to contribute to oxidative stress, endothelial dysfunction and inflammation which in turn lead to an increased risk of developing vascular disease (Carpenter 2006). GDM has effects that can cause programming changes in utero which can lead to cardiovascular diseases later on in life such as Hypertension, Atheroscle rosis, Obesity, Dyslipidaemia and Type 2 diabetes. Hypertension Diabetic pregnancy is associated with a higher rate of hypertension which is thought to be caused by insulin resistance that is present in GDM. There may also be genetic predisposition to developing high blood pressure (Bar and Hod 2008). The presence of insulin resistance and glucose intolerance in the earlier stages of pregnancy leading to the onset of gestational hypertension suggests that there is already underlying vascular problems in the mother and predicts that they will have hypertension and/or vascular problems later in life (Carpenter 2006). A study involving rats demonstrated that offspring who are exposure to maternal diabetes get a salt-sensitive hypertension which can be related to an impaired renal function in adults (Nehiri et al 2008). Studies of women who developed gestational hypertension were shown to have increased insulin resistance and the hypertension developed during the last term of pregnancy is thought to be associated with this. Insulin resistance ca uses slight inflammation, which causes an increase in inflammatory agents and higher levels of vascular resistance (Carpenter 2006). In a study of 1000 children, it was found that those that were exposed to GDM in utero were found to have increased systolic blood pressure at 3 years old as well as increased adiposity (Wright et al 2009). Atherosclerosis Atherosclerosis is a disease of the arteries where there is an accumulation of lipid deposits in the intima layer which is most common at the bifurcation of vessels (Patterson and Stouffer 2005). The biggest causes of deaths from diabetes are from cardiovascular disease including heart attacks, vascular diseases and stroke. Oxidative stress is seen to have an accelerating role in this process and patients with diabetes are known to have increased oxidative stress levels. These increased levels can lead to oxidation of low-density-lipoproteins (LDL), endothelial dysfunction and the division of smooth muscle in the blood vessels and these mechanisms lead to the generation of atherosclerotic plaques (Jay et al 2006). Oxidised LDL attracts monocytes and can also injure cells by necrotic and apoptotic pathways which can make them more prone to forming plaques. However not all of the effects of oxidised LDL lead to atherogenesis and it may play a part in the inhibition of plaques forming (Chisolm and Steinberg 2000). Studies have shown that endothelial cell dysfunction, inflammation and oxidative stress are related to the atherosclerotic plaques found in atherosclerosis (Leduc et al 2009). Studies of women who developed gestational hypertension were shown to have increased insulin resistance and the hypertension developed during the last term of pregnancy is thought to be associated with this. GDM and body weight Rats induced with diabetes in the last term of the pregnancy were found to produce offspring whose weight varied widely from microsomic to macrosomic. The macrosomic rats were produced by mothers with more severe hyperglycaemia and the microsomic rats whose mothers had less severe hyperglycaemia. It was also discovered that there were genetic differences as it was found that the male offspring developed insulin resistance by 6 months and while the females had changed vascular structure (Segar and Norris 2009). Many studies prove that a foetus who is exposed to an environment of GDM has an increased risk of developing macrosomia. This study has helped increase our knowledge in that the diabetic environment plays an important role in determining birth weight of the offspring. Obesity Many studies have looked into whether GDM can affect the chance that the offspring is more susceptible to the development of obesity in later life. GDM causes hyperglycaemia in the fetus and this can lead to increased amounts of insulin being produced as insulin. These increasing amounts of insulin can lead to insulin resistance and could predispose the individual to develop obesity in later life (Wright et al 2009). However, while GDM may cause macrosomia it is more the post-natal environmental factors that have a bigger input into the development of obesity. Obesity in offspring is important as it is a cardiovascular risk factor. Dyslipidaemia Hyperglycaemia is thought to lead to a change in concentrations of lipoproteins. Dyslipidaemia in Diabetes consists of increased triglycerides, high lipid levels after eating and low levels of high density lipoproteins (HDL). High Levels of Lipids is a risk factor for macrovascular disease (Goldberg 2001). Pima Indians development of T2D Offspring born to mothers who have been diagnosed with diabetes have a greater risk of developing type 2 diabetes and macrosomia. Studies of the Pima Indians have shown that. Figure 2 shows that offspring who are exposed to a diabetic environment have a high BMI than siblings who are not exposed to a diabetic environment proving that the environment is a more important determine factor of BMI than any genetic component (Dabelea et al 2000). A different study established a relationship between the high levels of glucose in the last trimester of pregnancy in non-diabetic mothers and the risk to the offspring of developing type 2 diabetes later in life was the study of the Pima Indians. In this study there was a strong correlation between glucose levels in the last term of the pregnancy and the offspring developing type 2 diabetes later in life. There was also evidence to suggest that higher levels of glucose in pregnancy predisposed the child to a greater risk of obesity during ch ildhood (Franks et al 2006). Treatment of GDM Once the mother has been diagnosed with GDM her blood glucose levels should be closely followed. Treatment of GDM is aimed to keep blood glucose levels as close to the normal limits as possible to prevent any risk of developing macrosomia and other problems associated with the developing fetus. The greatest insulin resistance occurs, as stated before, in the last trimester and screening for GDM takes place around 24- 28 weeks into the gestation. Diagnosis can be made with a glucose tolerance test (Cheung 2009). Dietary control is the most important and effective way to treat GDM. If dietary control does not prove to be effective and blood glucose levels are still high then treatment with insulin may be needed. Oral hypoglycaemic agents may be given if other treatment is ineffective (Cheung 2009). Effects of GDM on the mother Mothers who develop GDM have an increased risk of developing diabetes in later years. One study in Denmark followed a group of women who had gestational diabetes during their pregnancy and then approximately 6 years after giving birth 14.5% had developed type 2 diabetes, 3.7% had Type 1 diabetes and 19.5% were classed as having pre-diabetes (Damm 2009). GDM can be seen as a marker for the mother developing T2D later on in life which is useful as it allows treatment and education on how to minimise the risk of developing it. Women who present with GDM have an increased risk of developing metabolic syndrome and are more likely to develop disturbed endothelial function and increased thickness of carotid arteries (Kaaja, RÃ ¶nnemaa 2009). Conclusion and Future Research Gestational Diabetes is a condition that affects 7% of pregnant women annually. It is defined as a glucose intolerance that presents in the later stages of pregnancy. The causes are not fully known but it involves beta-cell dysfunction with the possibility of autoimmune destruction, MODY or on top of already present insulin resistance. During the pregnancy GDM can have many effects on the placenta and its products. These products usually increase the insulin resistance. GDM can alter fetal programming and make the fetus more susceptible to cardiovascular disease mainly hypertension, atherosclerosis and hyperlipidaemia which are risk factors for many other cardiovascular diseases. Oxidative stress can lead to complications by causing damage to proteins, lipids and DNA. In hyperglycaemia there is increased oxidative stress and this can activate several pathways which can be involved in vascular complications. GDM can increase the amounts of Oxidative Stress and inflammatory mediat ors produced which can lead to a decreased vascular tone. If GDM is treated successfully by diet or drugs then this can dramatically reduce the risk of developing complications. Future research should focus on screening with all pregnant women who fall into the middle and high risk categories being screened to decrease the risk of fetal complications. Blood glucose levels should be tested to keep them within range. Possible research areas include methods to control the production of hormones by the placenta in order to keep the inevitable insulin resistance to the minimum. Possible areas of research include Antioxidants such as Vitamin E which can be used to keep oxidative stress damage to a minimum. References American Diabetes Association (2010) Diagnosis and Classification of Diabetes Mellitus. Diabetes Care, Volume 33, Supplement 1: S62- S69 Ashworth C.J., Hoggard N., Thomas L., Mercer J.G., Wallace J.M., Lea R.G., (2000). Placental Leptin. Reviews of Reproduction 5: 18-24 Bar J., Hod M., (2008). 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Journal Nutrition 133:1674S-1683S Chen X., Scholl T.O., (2005) Oxidative Stress: Changes in Pregnancy and with Gestational Diabetes Mellitus. Current Diabetes Reports 5:282-288 Cheung N.W., (2009). The management of Gestational Diabetes. Vascular Health and Risk Management 5:153-164 Chisolm G.M., Steinberg D., (2000). The oxidative modification hypothesis of atherogenesis: an overview. Free Radical Biology and Medicine 28: 1815-1826 Chung S.S.M., Ho E.C.M., Lam K.S.L., Chung S.K., (2003). Contribution of Polyol Pathway to Diabetes-Induced Oxidative Stress. Journal American Society of Nephrology 14: S233-S236, Coughlan M. T., Oliva K., Georgiou H. M., Permezel J. M. H., Rice G. E., (2001). Glucose-induced release of tumour necrosis factor-alpha from human placental and adipose tissues in gestational diabetes mellitus. Diabetic Medicine, 18, 921-927 Dabelea D., Pettitt D.J., (2008). Chapter 48 Long term implications: child and adult. Textbook of diabetes and Pregnancy: 362-371 Damm P., (2009) Future risk of diabetes in mother and child after gestational diabetes mellitus. International Journal of Gynaecology and Obstetrics 104: S25-S26 De Vriese A.S., Verbeuren T.J., Van de Voorde J., Lameire N.H., Vanhoutte P.M., (2000). Endothelial dysfunction in diabetes. British Journal of Pharmacology 130, 963-974 Desoye G., Haugel-De Mouzon S., (2007). The Human Placenta in Gestational Diabetes Mellitus- The insulin and cytokine network. Diabetes Care, Volume 30 Supplement 2: S120- 126 Desoye G., Shafrir E., Hauguel-de Mouzon S., (2008) Chapter 8 The placenta in diabetic pregnancy: Placental transfer of nutrients. Textbook of diabetes and pregnancy: 47-57 Evans J.L., Goldfine I.D., Maddux B.A., Grodsky G.M., (2003) Are Oxidative Stress Activated Signalling Pathways Mediators of Insulin Resistance and ß-Cell Dysfunction? Diabetes Volume 52: 1-8 Fetita L.S., Sobngwi E., Serradas P., Calvo F., Gautier J.F., (2006) Consequences of Fetal Exposure to Maternal Diabetes in Offspring. Journal of Clinical Endocrinology and Metabolism Vol 91, No 10: 3718-3724 FÃ ¶rstermann U., (2008) Oxidative stress in vascular disease: causes, defence mechanisms and potential therapies. National Clinical Practice Cardiovascular Medicine Volume 5, Number 6: 338-349 Franks P.W., Looker H.C., Kobes S., Touger L., Tataranni P.A., Hanson R.L., Knowler W.C., (2006). Gestational Glucose Tolerance and Risk of Type 2 Diabetes in Young Pima Indian Offspring. Diabetes Volume 55: 460-465 Gao L., Mann G.E., (2009) Vascular NAD(P)H oxidase activation in diabetes: a double-edged sword in redox signalling. Cardiovascular Research 82: 9-20 Gao X.L., Yang H.X., Zhao Y., (2008) Variations of Tumour Necrosis Factor-alpha, leptin and Adiponectin in mid-trimester of gestational diabetes mellitus. Chinese Medical Journal 121: 701-705 Giachini F. R.C., Carriel V., Capelo L.P., Tostes R.C., Carvalho M.H., Fortes Z.B., Zorn T.M., San Martin S., (2008). Maternal diabetes affects specific extracellular matrix components during placentation. Journal of Anatomy 212: p31-41. Giugliano D., Ceriello A., Paolisso G., (1996) Oxidative stress and diabetic vascular complications. Diabetes Care 19: 257-267 Godfrey M.K., (2002) The of Role of the Placenta in Fetal Programming- A review. Placenta 23: S21-27 Gomez R.A., Norwood V.F., (1999) Recent Advances in Renal Development. Current Opinion in Paediatrics 11: 135- 140 Gude N.M., Roberts C.T., Kalionis B., King R.G., (2004) Growth and function of the normal human placenta. Thrombosis Research 114: 397—407 Haugen G., Rognerud H., (2001) Doppler flow velocity waveforms and vasoactive effects of serotonin in human umbilical arteries. Gynaecologic and Obstetric Investigation 51: 22-27 Herrera E., Ortega H., (2008) Metabolism in normal Pregnancy. Textbook of Diabetes and Pregnancy:25-34 Horal M., Zhang Z., Stanton R., Virkamaki A., Loeken M.R., (2004). Activation of the Hexosamine Pathway Causes Oxidative Stress and Abnormal Embryo Gene Expression: Involvement in Diabetic Teratogenesis. Birth Defects Research (Part A) 70:519-527 Huppertz B., (2008). The anatomy of the normal Placenta. Journal Of clinical Pathology 61: 1296-1302 Jansson T., Powell T.L., (2007) Role of the placenta in fetal programming: underlying mechanisms and potential interventional approaches. Clinical Science 113: 1-13 Jay D., Hitomi H., Griendling K.K., (2006) Oxidative stress and diabetic cardiovascular complications. Free Radical Biology and Medicine 40: 183-192 Kaaja R., RÃ ¶nnemaa T., (2009) Gestational Diabetes: Pathogenesis and Consequences to Mother and Offspring. The Review of Diabetic Studies 5: 194-202 King J.C., (2006) Maternal Obesity, Metabolism and Pregnancy Outcomes. Annual Review of Nutrition 26: 271-291 Kirwan J.P., Hauguel-De Mouzon S., Lepercq J., Challier J.C., Huston-Presley L., Friefman J.E., Kalhan S.C., Catalano P.M., and (2002) TNF-alpha is a Predictor of Insulin Resistance in Human Pregnancy. Diabetes Vol 52: 2207-2213 Kouseff B.G., (1999) Diabetic Embryopathy. Current Opinion in Paediatrics 11: 348-352 Koya D., King G.L., (1998) Protein Kinase C Activation and the Development of Diabetic Complications. Diabetes Volume 47: 859-866 Leduc L., Levy E., Bouity-Voubou M., Delvin E., (2010). Fetal Programming of Atherosclerosis: Possible role of the mitochondria. European journal of Obstetrics and Gynaecology and Reproductive Biology 149: 127-130 McLean M., Chipps D., Wah Cheung N., (2006). Mother to child transmission of diabetes mellitus: does gestational diabetes program Type 2 Diabetes in the next generation? Diabetic Medicine 23: 1213-1215 Megia A., Vendrell J., Gutierrez C., Sabate M., Broch M., Fernandez-Real J.M., Simon I., (2008) Insulin sensitivity and resistin levels in gestational diabetes mellitus and after parturition. European Journal of Endocrinology (2008) 173-178 Megia A., Vendrell J., Gutierrez C., Sabate M., Fernandez-Real J.M., Simon L., (2008). Insulin sensitivity and resistin levels in gestational diabetes mellitus and after parturition. European Journal of Endocrinology 158: 173-178 Mello G., Parretti E., Hod M., (2008). Chapter 28 Prevention of Fetal Macrosomia. Textbook of diabetes and Pregnancy: 291-296 Merlob P., Hod M., (2008) Chapter 47 Short term implications: the neonate. Textbook of diabetes and Pregnancy: 352- 261 Metzger B.E., Buchanan T.A., Coustan D.R., De Leiva A., Dunger D.B., Hadden D.R., Hod M., Kitzmiller J.L., Kjos S.L., Oats J.N., Pettitt D.J., Sacks D.A., Zoupas C,.(2007). Summary and recommendations of the Fifth International Workshop-Conference on Gestational Diabetes Mellitus. Diabetes Care Jul;30:S251-60 Metzger B.E., Coustan D.R., (1998). Summary and Recommendations of the Fourth International Workshop-Conference on Gestational Diabetes Mellitus. Diabetes Care Aug;21 Supplement 2:B161-7 Morino K., Petersen K.F., Dufour S., Befroy D., Frattini J., Shatzkes N., Neschen S., White M.F., Bilz S., Sono S., Pypaert M., Shulman G.I., (2005) Reduced mitochondrial density and increased IRS-1 serine phosphorylation in muscle of insulin-resistant offspring of type 2 diabetic parents. The Journal Of Clinical Investigation Volume 115, No.12: 3587-3593 Myatt L., (2006) Placental adaptive responses and fetal programming Journal Physiology 572: 25-30 Myatt L., Kossenjans W., Sahay R., Eis A., Brockman D., (2000) Oxidative Stress Causes Vascular Dysfunction in the Placenta. The Journal of Maternal-Fetal Medicine 9:79-82 Nehiri T., Duong Van Huyen J.P., Viltard M., Fassot C., Heudes D., Freund N., Deschenes G., Houillier P., Bruneval P., Lelievre-Prgorier M., (2008) Exposure to Maternal Diabetes Induces Salt-Sensitive Hypertension and Impairs Renal Function in Adult Rat Offspring. Diabetes Volume 57: 2167- 2175 Patterson C., Stouffer G.A., (2005). Atherosclerosis. Encyclopaedia of Life Sciences. https://mrw.interscience.wiley.com/emrw/9780470015902/els/article/a0005998/current/abstract?hd=All,Atherosclerosis Radaelli T., Varastehpour A., Catalano P., Hauguel-de Mouzon S., (2003) Gestational Diabetes Induces Placental Genes for Chronic Stress and Inflammatory Pathways. Radenkovic M., Radunovic N., Momcilov P., Grbovic L., (2009) Altered Response of Human Umilical artery to 5-HT in Gestational Diabetic Pregnancy. Pharmacological reports 61: 520-528 Redman C., (2001) Pregnancy: Maternal Disorders ELS Roberts D.J., Raspollini M.R., (2008) Chapter 7 Histopathology of the Placenta. Textbook of diabetes and pregnancy:41-46 Rossetti L., Massillon D., Barzilai N., Vuguin P., Chen W., Hawkins M., Wu J., Wang J., (1997) Short Term Effects of Leptin on Hepatic Gluconeogenesis and in Vivo Insulin Action. The Journal of Biological Chemistry volume 272: 27758-27763 Ryan E.A., Enns L., (1988) Role of gestational hormones in the induction of insulin resistance. Journal Clinical Endocrinology and Metabolism 67(2):341-7 Sattar N., Greer I.A., Pirwain I., Gibson J., Wallace A.M., (1998). Leptin levels in pregnancy: marker for fat accumulation and mobilization? Acta Obstetricia et Gynecologica Scandinavica 77: 278-283 Schillan-Koliopoulos M., Guadagno S., Walker E.A., (YEAR) Gestational Diabetes Management: Guidelines to a Healthy Pregnancy. The Nurse Practitioner Vol 31 No 6: 14-23 Segar E.M., Norris A.W., Yao J.R., Hu S., Koppenhafer S.L., Roghair R.D., Segar J.L., Scholz T.D, (2009) Programme of growth, Insulin resistance and vascular dysfunction in offspring of late gestation diabetic rats. Clinical Science 117: 129-138 Shah S., Iqbal M., Karam J., Salifu M., McFarlane S.I., (2007) Oxidative stress, Glucose Metabolism and the prevention of Type 2 Diabetes: Pathophysiological Insights. Antioxidants and Redox Signalling Vol 9, No. 7: 911-929 Steppan C.M., Lazar M.A., (2002). Resistin and obesity-associated insulin resistance. Trends in Endocrinology and Metabolism Volume 13 Issue 1: 18-23 Thornburg K.L., Otierney P.F., and Louey S., (2010) Review: The Placenta is a Programming Agent for Cardiovascular Disease. Placenta 31, Supplement A, Trophoblast Research Vol 24: S54-59 Tree T., (2010) The pathogenesis of type 1 diabetes Lecture Weng J., Ekelund M., Lehto M., Li H., Erkbery G., Frid A., Aberg A., Groop L., Berntorp K (2002). Screening for MODY Mutations, GAD Antibodies, and Type 1 Diabetes-Associated HLA Genotypes in Women With Gestational Diabetes Mellitus. Diabetes Care 25:68-71 Wiznitzer A., Furman B., Zuili I., Shany S., Reece E.A., Mazor M., (2000). Cord leptin level and fetal macrosomia. Obstetrics and Gynaecology 96: 707-713 Wright C.S., Rifas-Shiman S.L., Rich-Edwards J.W., Taveras E.M., Gillman M.W., Oken E., (2009) Intrauterine Exposure to Gestational Diabetes, Child Adiposity, and Blood Pressure. Am Journal Hypertensive. 2009 February ; 22(2): 215-220 Yogev Y., Ben-Haroush A., Hod M., (2008) Pathogenesis of gestational diabetes mellitus. Textbook of Diabetes and Pregnancy: 71-79 Goldberg I.J., Diabetic Dyslipidaemia: Causes and Consequences. Journal of Clinical Endocrinology and Metabolism. Volume 86: 965-971 Dabelea D., Hanson R.L., Lindsay R.S., Pettitt D.J., Imperatore G., Gabir M.M., Roumain J., Bennett P.H., Knowler W.C., (2000). Intrauterine Exposure to Diabetes Conveys Risks for Type 2 Diabetes and Obesity A Study of Discordant Sibships. Diabetes Volume 49: 2208-2211

Behaviour Contract Free Essays

I have always loved to watch movies and television shows but I guess it was an addiction already for the past couple of months. I can say that I am very much hooked in watching the television for the past seven months. I love the thrill, happiness, suspense I feel whenever I watch something on television. We will write a custom essay sample on Behaviour Contract or any similar topic only for you Order Now Whenever I am at home, my whole day would be spent in front of the television. I sometimes skip meals just to watch my favourite movie or a certain talk show. Sometimes I even do not take a bath just to keep track of what I am watching. I love watching those shows that exposes the current fashion, recent social issues, and television magazines, shows that tells Hollywood celebrities’ lives and most of all, movies like suspense thriller, horror, love stories and fairy tales. For me it is the source of my enjoyment, I sometimes forget to study and read books. I think too much watching the television causes great effects in my being. I think being bored triggers my addiction to television. I want something to entertain me so that I do not get too alone. Sometimes I get bored just studying and doing other things, but when it comes to television, I really can’t feel ennui at all. I really feel entertain by the television. I should control my being hooked on television and might as well eliminate it. I should discipline myself and have self control. Within 2 weeks I should minimize my television viewing and by the end of month I must have eliminated this behaviour already. If I spend too much of my time in front of the television then I will ask my mother to deduct my allowance by 50%, I will not be able to go on a night out during Fridays, I will not be allowed to wake up late during weekends, lastly I will not be able to go out with my friends during week ends. If I will not comply with the contract then my punishment for myself will be destroy all my shoes and sandals and I will come to school on slippers for one day. While if I will be able to follow all the terms in the contract and comply with it then I my reward will be, spending the whole weekend in my favourite beach resort and hotel. How to cite Behaviour Contract, Papers

History Test Questions free essay sample

Manzanar in CA – loss of $ property – 100th Battalion – â€Å"Purple Heart† Battalion – 442nd Regimental Combat Team – fought in Italy, France, Germany – Most decorated combat unit in US history for proportion of length of service – â€Å"Buddha Heads† – Most Japanese-Americans served as soldiers in Europe while interpreters and such went to the Pacific – obvious racism/discrimination Minority group most adversely affected by Washington DC’s wartime policies was – Japanese-Americans Internment – costs – effects – camps – prejudice – military service – Nisei born in USA, so citizens The general attitude toward WWII was – less idealistic ideological more practical than the outlook in WWI (This is according to the textbook – What would Zinn say in Ch 16? ) In the period of 1885 to 1924, the Japanese immigrants who came to the USA were â₠¬â€œ a select group (representing Japan abroad, so Japan cared who was sent) who was/were better prepared educated than most European immigrants (so they were middle class usually had $) Ex. Japan felt represented – wanted to avoid Chinese bachelors of 19th century – so â€Å"picture brides† When the USA entered WWII in December (7th attack at Pearl, war declared on 8th), 1941, a majority of Americans had no clear idea of what the war was about * WWI had campaigned (but many people didn’t know in WWI either – Ex. Sergeant York Gallipoli) During WWII, the US gov’t commissioned the production of synthetic rubber in order to offset the loss of access to prewar supplies in E. Asia (ex. French Indochina/Vietnam, Cambodia, Loas) Wartime agencies functions: War Production Board – assign priorities w/respect to use of raw materials transportation facilities Office of Price Administration – controlled inflation by rationing essential goods War Labor Board – imposed ceilings (maximums) on wage increases Fair Employment Practices Commission (FEPC) – saw to it that no hiring discrimination practices were used against Af-Am’s seeking employment in war industries * A Philip Randolph – 1941 threatened to march on Wash DC to demand equality in hiring – FDR feared march so made a deal to announce Executive Order #8802 for Af-Am’s fair employment in wartime industries Randoplh was leader of Brotherhood of Sleeping Car Porters union (mostly Af-Am’s but some whites too – began in 1920s) While most US workers were strongly committed to the war effort, wartime production was disrupted by strikes led by the – United Mine Workers (Why? Exploitation w/unequal distribution of wartime profits. ) * Coal mining is almost as risky as war – in fact they die more than any other industrial workers, both back then and today – only crab ishing is truly more hazardous b y proportion – although they are much safer today During WWII – labor unions substantially increased their membership †¢ There were some strikes – Ex. United Mine Workers – unfair distribution of wartime profits * Bracero Program – p. 833 Mexicans work in agriculture some industries (later deported in the offensive â€Å"Operation Wetback†) [Ironic after 1930’s treatment in CA for example – Okies for Mexicans, etc†¦ Smith-Connally Anti-Strike Act – June 1943 – federal gov’t could seize industries if strikes occurred Ex. Coal mines and RRs briefly] p. 832 Employment of more than 6 million women in America (~3 million had never worked for wages before) industry during WWII led to – the establishment of day-care centers by gov’t (*†Rosie† vs. â€Å"Wendy†) [Usually single women or w/husband in the war were the ones working in defense plants/war industries] * Not equal pay for equal work in almost all cases – although some women earned as good or better money if they were outstanding – some were indeed Ex. P. 33 – WOW poster * My recruiting posters WWII aircraft pictures * Not greater % of women working in USA than in Europe – Ex. Britain USSR – in war industries * Increase in employment in war industries for Af-Am’s (both men women) * Migrations from South as Af-Am’s leave while to the South came war industries and military bases Why? Cheap wages very few unions * Not a strong desire for most women to work for wages (especially in defense industries, etc†¦) *** p. 833 – WAACs, WAVES, SPARS, (WASPs) â€Å"GI† – â€Å"Government Issue† * USCG Merchant Marine Main reason majority of women workers left labor force at end of WWII was – family obligation Af-Am’s did all of following during WWII: rally behind slogan of â€Å"Double V† (victory over Axis racism at home), move north west in large migrations (seeking work – often in war industries) (move to cities – â€Å"urban† begins to mean â€Å"black†) (ghettos created – not like Jewish ghettos in Poland, etc†¦) (de facto vs. de jure/Jim Crow segregation discrimination – Ex. Race riots in Detroit in 1943 – later race riots in north in 1960s too), form a militant organization called the Congress of Racial Equality (CORE – 1942 increase in NAACP membership), serve (in US military) in (US) Army Air Corps (Tuskegee Airmen – 332nd/99th w/impeccable record – no bombers lost on their escorts – Benjamin O. Davis sr. Benjamin O. Davis jr. – West Point grads – endured silent treatment from whites – Davis sr. is first Af-Am general in US history – Davis jr. was in command of 99th squadron – see picture on . 835), What about fighting in integrated combat units? Not until Korea (w/exception of a few experiments) Which is least related to the other three? A Philip Randolph (Bro of Sleep Car Porters threat to march on Wash DC in 1941 – led to Executive Order #8802 – in 1963, helped organize march to Wash DC for MLK jr’s â€Å"I Have a Dream† speech. Fair Employment Practices Commission (FEPC – to protect Af-Am’s to be hired and treated fairly in war industries), racial discrimination in wartime industry (still even w/FEPC there was discrimination – but better than w/out it), proposed â€Å"negro March on Washington,† What about the Smith-Connally (Anti- Strike) Act (1943)? On pp. 834-836 Migration Map on p. 834 * Cotton production in South – hurt Af-Am laborers, tenant, and sharecropping farmers (whites too who did this – many) w/ introduction of mechanization – so migration p. 836 * Native Americans ~25,000 serve – Ex. Comanche in Europe Navajo in Pacific – â€Å"code talkers† p. 836 *** LA, CA summer 1943 – â€Å"Zoot Suit Riots† – Pachucos vs. Servicemen – violence – retaliation – gangs – blame – reactions – tensions – â€Å"Victory Suits† – race riots p. 836-837 ** Race riot in Detroit, MI in 1943 – fatalities pp. 36-837 Big gov’t intervention received its greatest boost from – WWII (not the New Deal) During WWII, most Am’s economically experienced – prosperity a doubling of personal income p. 837 National Gross National Product (all goods and services produced in USA) in 1940 was $100 b illion – GNP grew to $200 billion in 1945 – corporate profits rose from ~$6 billion in 1940 to ~$12 billion by 1944 – Henry Stimson (Sec of War) â€Å"if you are going to try to go to war in a capitalist country, you have to let business make money out of the process, or business won’t work. p. 837 * disposable income after war-time taxes more than doubled (but there was inflation too) * post-war consumerism w/surplus income to purchase in post-war US economy – Ex increase 33% in post war prices b/c of high wages consumer demand * Office of Scientific Research and Development p. 37 – developed weapons, including Atomic (nuclear) bombs *** â€Å"warfare-welfare state† b/t 1941-1945 * rationing – total war effort – bond drives – kids had Al drives for example, etc†¦ Ex of poster: â€Å"When you ride ALONE, you ride with Hitler! † – Black Market Chart for Rise in National Debt – rise b/c of WWII and after war it spiked higher than during war p. 837 On p. 38 Cost of war in $ was for USA $330 billion – 10 times more than WWI – more $ than all federal spending since 1776 – income tax – 4 times as many people than before war – some people taxed as high as 90% of income – taxes provided for 2/5ths of war cost – rest is borrowed from US public – Liberty Loans – Bond Drives others loaned $ too like individuals who were rich tycoons moguls and/or through corporations banks – 1941 National Debt was $49 billion – grew to $259 billion in 1945 – war cost ~$10 million per hour at peak of war – plus blood, sweat, tears – tremendous loss of life – Ex. USSR lost more than any other country Northward migration of Af-Am’s accelerated after WWII b/c – mechanical cotton pickers (machines) were in use p. 836 During WWII, American Indians – moved off of reservations in large numbers (~25,000 served in military) p. 836 By the end of WWII, the heart of USA’s Af-Am communities had shifted to – northern cities pp. 834-835 * p. 836 â€Å"The speed and scale of these changes jolted the migrants and sometimes the communities that received them. * Racism, de facto segregation vs. de jure (Jim Crow) segregation [Migartion Map on p. 834] National debt increased most during – World War II (and post-WWII to present) p. 838 Most $ raised to finance WWII came through – borrowing (individuals, corporations – bonds for middle class working class people) (*Liberty/Victory Loans – bond sales – hugely promoted) p. 38 First naval battle in history in which all of the fighting was done b y (aircraft) carrier-based aircraft was the Battle of – the Coral Sea (May 1942 near NE Australia – Tie to stop Japanese threat/invasion of the â€Å"Land Down Under† – USA lost one carrier – USS Lexington – USS Yorktown carrier badly damaged but back in action at Midway where she was finally sunk by a Japanese submarine after extensive damage from aircraft that left her a burning wreck) * Midway – 2nd such battle b/t carrier fleets so far apart they never see each other – June 3rd-6th, 1942 – the turning point of the Pacific war p. 839] The tide of Japanese conquest in the Pacific was turned following the Battle of – Midway (June 3rd-6th, 1942) * Details – our 3 carriers to their 4 – we sank all four and lost only one – planes – luck – plans – codes – drama – Spruance, Nimitz, etc†¦ plus Aleutian Islands (of Alaska) attacked just before Midway was dive rsion, which was fairly effective – cold, brutal fighting over frozen, barren islands, but were US territory like Hawaii pp. 39-841 Japanese made a crucial mistake in 1942 in their attempt to control much of the Pacific when they – over extended themselves instead of digging in consolidating their gains p. 839 – Japanese victories in Pacific up through first 6 months extended down to Dutch East Indies (for oil), Southeast Asia (for rubber), including Burma and Thailand into parts of China, the Philippines, the Marianas such as Guam, the Gilbets, the Marshalls, the Solomons, the Aleutians, Korea and Manchuria, Okinawa, Iwo Jima, etc†¦- They held it for about 6 months after Pearl Harbor before Allied advances began. In waging war against Japan, the USA relied mainly on a strategy of – (leapfrogging and) island-hopping across the South (and Central) Pacific while by-passing Japanese strongholds (whenever possible – but not always – Ex. Philippines Pelelieu Aleutians) [MacArthur/US Army Halsey in South – USMC Nimitz/Spruance in Central Pacific] All strategies considered implemented in some fashion – heavy bombing from Chinese air bases, invading SE Asia Burma, fortifying China transporting supplies from India over â€Å"the Hump† of the Himalayas, turning Japanese flanks in New Guinea (MacArthur) Alaska (Aleutians) * All were done – but priority was put on USN, US Army, USMC, USAAC (USAF), USCG in two prong drive across south central Pacific with Adm. Nimitz calling the shots Conquest of Guam (Marianas – Tinian Saipan too) in 1944 was especially critical, b/c from there (the Marianas) the USA could conduct round-trip bombing raids (B-29s) on Japanese home islands – But a nasty volcanic sulfur-smelling small island with large 500 foot hill on its southwestern corner on it called Iwo Jima was in the way – could notify Japan that bombers were coming – plus many damaged bombers needed the vital air strip on the island for emergency landings – so in Feb of 1945, USMC began its biggest, most-distinguished battle lasting 36 days in Hell before the island was completely secure – giving us two flag raisings on Mt. Suribachi – the 2nd becoming perhaps the most famous photograph in the entire world – â€Å"Semper Fi, Do or Die, Gung Ho! † Allies won Battle of Atlantic by – escorting convoys of merchants’ (and military) vessels (not using convoy system initially) [E x. Carrier other Task Forces], dropping depth charges from destroyers, bombing submarine (U-boat) bases (Ex. located in France), deploying new technology of RADAR At war’s end, U-boat crews are in a very deadly branch of voluntarily service still got volunteers up until the end – 4 out of 5 U-boaters die by late 1944 – Adm Downitz asked for more before war – didn’t get them, used convoy system w/ destroyer escorts – depth charges – RADAR (B-24s B-25s, other planes as sub hunters) – SONAR – Enigma code machine codes (read Japanese codes in Pacific too) – US subs sink lots of ships (especially in Pacific), But what about organizing â€Å"wolf packs† (which are German U-boats) to chase down German U-boats (submarines)? *** Battle of the Atlantic Most important battle in Western Europe! Until Spring 1943, perhaps Hitler’s greatest opportunities of defeating Britain winning the war was – the German U-boat would destroy Allied shipping (which it was faster than ships could be built early in war) Hitler’s advance in the European theater of war crested in late 1942 at the Battle of Stalingrad, after which, his fortunes gradually declined {* Leningrad, Kursk, Red Army, Counter-Offensives} pp. 841-842 Monte Cassino in Italy Allies postponed opening a second front in Europe until 1944 b/c – of British reluctance (b/c of the majority of troops would be supplied by them that early in the war) lack of adequate resources {* We’d have gotten our butts handed to us by the Germans – as indeed we did really until 1943 – we needed to learn how to fight – Stalin was angry we left his country to suffer while we lagged in opening a second front n France to relieve the USSR – cannot blame him entirely FDR’s promise to the Soviets to open a second front in Western Europe by end of 1942 – was utterly impossible to keep (just not ready for the undertaking really) * So USSR got pounded through most of 1942 before it went on the offensive in 1943 and until the end of the war really – meanwhile, the Allies invaded North Africa, then Sicily, then up the boot of Italy – before two major invasions of France in June Aug of 1944 Allied demand for unconditional surrender was criticized mainly by opponents who believed that such a surrender would – encourage the enemy to resist as long as possible (but USA also did this to show a ommitment to USSR as an Ally against Germany to avoid a separate peace as in WWI) FDR’s Churchill’s insistence on the absolute and â€Å"unconditional surrender† of Germany – eventually complicated the problems of postwar reconstruction Chronology: Casablanca, Morocco – Jan 1943 FDR Churchill meet – Pacific strategy, Sicily, Italy, unconditional surrender p. 842, (Cairo, Egypt before Teheran – w/FDR Churchill discuss Chiang Mao vs. Japanese in China), then Teheran, Iran (Persia at the time) – Nov 28th – Dec 1st, 1943 – plans for W E attacks on Germany p. 844 – FDR, Churchill, Stalin, Potsdam, Germany – July 1945 – Truman, Churchill, Stalin – Potsdam Declaration how to end war post-war plans p. 851 Chronology: Invasion of (Sicily and) Italy (1943), D-Day/Normandy invasion (June 6th, 1944), VE Day 5/8/45 [my mother turned 6 years old (my father turned 6 years old 10 days later) – she had two brothers in this war (others in Korea Vietnam) – one would come home from Europe w/2 Purple Hearts – served under Patton in N Africa was at the Bulge – his eye was hanging out of his head attached by the optic nerve – they saved his eye – but the war messed the young man up for the rest of his lif e mentally carrying the burdens of death – her other brother was in Pacific – he would not come home until Japan was beaten] – VJ Day 8/15/45 – Japan’s surrender was 8/14/45 – official surrender on deck of battleship USS Missouri in Tokyo Bay was 9/2/45 – WWII was finally over after many deaths – military ivilian (WWII began in 1931-37 in Asia, Sept 1939 in Europe, Dec 1941 for USA in Pacific) Major consequence of Allied conquest of Sicily in Aug 1943 was – overthrow of Mussolini (first of two times) and (eventually) Italy’s surrender o Italians surrender quicker than the French – At least they claim to be â€Å"lovers not fighters† – but the Romans seriously put a foot in and/or up one’s booty in battle as a vicious warrior empire known for organization in fighting After Italian surrender in Aug 1943, Germans poured into Italy and stalled the Allied advance (really until the end of t he war in Northern Italy – also harsh to Italians for switching sides) Real impact of the Italian front on WWII may have been that it delayed the D-Day invasion allowed the Soviet Union to advance further into E Europe (â€Å"iron curtain†) Brutal fighting in Italy Ex pp. 841-842 Monte Cassino in Italy Audie Murphy was in Italy, France, Germany 442nd Nisei were in Italy, France, Germany US First Army – The Big Red One Tuskegee airmen (99th squadron of 332nd fighter group) Italians switched sides – Germans reinforced – bloody battles b/c of terrain – Ex. Anzio * I disagree w/this – Italy was a vital valuable front – perhaps managed poorly, but necessary At the wartime conference in Teheran, Iran (Persia) (11-28 thru 12-1-43) (FDR, Churchill, Stalin) – plans were made for opening a 2nd front in Europe p. 844 – was Sicily Italy before France – Stalin still not happy Cross Channel (English Channel) invasion of Normandy (in NW France) to open a 2nd front in Europe was commanded by Gen Dwight David Eisenhower (future president) [Ike] {West Point, Aide of MacArthur, Bonus Army, North Africa, Great political general – needed for this command to deal w/ the prima- onnas US Gen Patton and British Gen Montgomery (Monty) plus other issues – he was the right man for the job – although many disagreed about that at the time} ***** Normandy/D-Day June 6th, 1944 (operation Overlord) Breako ut 5 beaches Monty, Bradley, Patton diversion pointed at Calais, French Underground, Airborne/Gliders/Paratroopers, Rangers, Amphibious, Air Superiority, Mulberry Harbors, Strategy, Hedgerows, Engineers, Etc†¦ (Saving Private Ryan, The Longest Day) In a sense, FDR was the â€Å"forgotten man† at the Democratic Convention of 1944 b/c – so much attention was focused on who would be VP (Truman – Sen from MO political machine – failed in business – US Army rtillery Major in WWI ) (VP former Sec of Ag Henry Wallace pushed out) (FDR in poor health) ** FDR complained of a headache and then shortly thereafter died from cerebral hemorrhage sitting for a portrait in Warm Springs, GA (where his health spa for his rehab for polio was) on April 12th, 1945 – funeral train – some people had really only known FDR as president, now Truman was the great unknown trying to replace FDR – Eleanor said to Harry, â€Å"The president is dead. â €  Truman replied, â€Å"Is there anything I can do for you. † Mrs Roosevelt responded, â€Å"Oh no, is there anything that we can do for you, you’re the one who is in trouble now. † FDR won 1944 election primarily b/c war was going well by Nov 1944 (many thought it was all but officially won and over) Action by USA against Adolf Hitler’s campaign of genocide against the Jews – was reprehensively slow in coming – Did not admit large numbers of refugees to USA, nor bomb RR lines at death camps – USA did know – Gov’t knew for sure since 1942 when â€Å"final solution† was implemented – US gov’t knew before if they chose to believe it (plus Mein Kampf, Hitler’s book), not major reason at all really that USA fought WWII – like Civil War sort of in that abolition of slavery was a by-product that many Federal/Union soldiers did not realize they were fighting for at the beginning of the war , nor would many of them fought for that ideal anyway–my opinion–so you know it’s correct! ( Hitler’s last ditch attempt to achieve victory against the USA British (plus other Allies) came in – Battle of the Bulge (Dec 1944-Jan 1945) My uncle FL was there – got that nasty eye wound †¢ Hurtgen Forrest (When Trumpets Fade) before Bulge near Achaen in W Germany almost on Belgian border – brutal mine fields – slaughter – overshadowed by Bulge so largely forgotten †¢ Bulge – why it’s called the Battle of the Bulge – weather – secrecy – push through weak Ardennes – Malmady – Mr. High – casualties 76,000 US – worst battle in US history (Okinawa close, Gettysburg too) – Germans lost 140,000+ cold – no air cover for weeks – Bastogne – 101st Airborne (Band of Brothers) – 101st at Normandy, Market Garden, Bastogne, Hitlerâ €™s Eagle’s Nest – Patton 3rd Army – costly choice to push bulge back rather than pinch it (liposuction) – air cover returns – push to the Rhine – USSR pushing from the East – USSR in Berlin brutal As result of Battle of Leyte Gulf – Japan was finished a s a naval power (Philippines 1944 – largest naval battle ever – Halsey – Taffy 3 – Kamikazes – Yamato) [Philippines fell – 500 POWs rescued at Cabanatuan (The Great Raid) – hold outs in to 1970s] {Iwo Jima and Okinawa and Japanese home islands left to take to end Pacific war} ***** War of attrition in Pacific – to the death – rarely took prisoners on either side unless want information Potsdam Conference – issued an ultimatum to Japan to surrender of â€Å"face a rain of ruin from the air† †¢ It’s already facing a â€Å"rain of ruin from the air’ as did German cities! p. 851 Potsdam Conference (Truman told Stalin of massive weapon to use on Japan – Stalin not surprised (b/c he knew from spies already) – told Truman to use it promised to enter war in Pacific as he had agreed to earlier – entered war 8/8/4 5, day before 2nd A-bomb on Nagasaki that time, Hiroshima the first on 8/6/45) Total unconditional surrender or be destroyed – threat of more bombing – not specific as to use of an atomic bomb – more bombing – so what – already taking that! Spending of enormous sums of money on the original (to be used against Germany) atomic (nuclear) bomb project (Manhattan Project) was spurred by the belief that – the American public would not tolerate the (massive) casualties that would result from a land invasion of Japan (***** Much More Complex Than That! ***** Letter â€Å"c† in the answer choices – The Japanese were (still) at work (and more successful than Germans – who tried heavy water in Norway but suffered to sabotage attacks – one at the plant, the other sinking a ferry w/the heavy water on board – still at bottom of the lake in Norway) on an atomic bomb of their own (claim to have detonated one in Manchuria) ***** Japanese had lots of weapons ready for the Final Battle or invasion of Japan, which was planned ready to go – they also had chemical weapons from Shiro Ishi’s Unit 731 in Manchuria – chemical biological weapons – delivery systems – Ex. High altitude balloons, flea bombs, etc†¦- USA made post-war deal w/ the Devil! No war crimes trials for vivisections, experiments, infection of disease, anthrax, plague, etc†¦ The â€Å"unconditional surrender† policy toward Japan was finally modified by – agreeing to let Japan’s Emperor Hirohito stay on the throne (w/Democratic gov’t) * No war crimes trials for emperor – Tojo took the fall for emperor – no Shiro Ishi or members of Unit 731 unlike Nazis – let Japan have terms that Germany did not get – then USA – built up former enemies (W Germany Japan) into allies while former allies (USSRlt; etc†¦) became enemies – COLD WAR! The following were qualities of US participation in WWII: A group of highly effective military political leaders, an enormously effective effort in producing weapons supplies (usually more, later, better equipment than enemies – out produced the Axis), the preservation of the American homeland against invasion or destruction from air (small submarine skirmishes some off-shore shelling, some balloons w/explosives in 48 continental USA), the maintenance re-affirmation of strength of democracy, What about a higher % of military casualties than any other Allied nation (USA had least casualties of big ones – USSR suffered more casualties than any country on either side) p. 27 FDR as â€Å"all wise† for Germany first strategy over those who disagree – Pacific war always get ripped off p. 828 Allies Trade Space for Time * German ( Japanese) scientists – weapons – A-Bombs pp. 829-832 The Shock of War pp. 830-831 Japanese-Am Internment (Farewell to Manzanar) Issei, Nisei, Exec Order #9066 (100th/442nd ) pp. 832-833 Building the War Machine * strikes Ex Coal Miners – exploited, underpaid – share profits Kaiser shipbuilding pp. 833-834 Man power Woman power – Braceros (later deportations in â€Å"Operation Wetback†) – Rosie (Wendy) – day-cares p. 834 War migration map pp. 835-837 wartime migrations p. 835 Tuskegee Airmen photo p. 835 A Philip Randolph (Exec Order #8802) **** (Charles Drew – Af-Am did first successful blood transfusion – put in charge of Allied blood banks – he was forced to segregate blood too – his death outside a hospital after an accident – died waiting for a blood tranfusion b/c white hospital would not admit him) p. 835 Double V, CORE – 1942, NAACP membership increases p. 836 Comanche (Europe) Navajo (Pacific) â€Å"code talkers† pp. 836-837 Zoot Suit Riots in LA, CA 1943 Detroit, MI 1943 â€Å"Sudden rubbing against one another of unfamiliar peoples produced some di stressingly violent action. † pp. 837-838 Holding the Homefront p. 837 National Debt Chart pp. 838-839 The Rising Sun in the Pacific p. 838 Map of Luzon, Bataan, Corrigador (Philippines) p. 838 (Mao and ) Chiang Kai-shek resist Japanese w/Allied help p. 38 Flying â€Å"the Hump† in Himalayas (b/c of Burma Road – Merril’s Mauraders Gen Stillwell) p. 838 â€Å"ill-trained† Filipinos, MacArthur holds fast – delays Japanese – Bataan Death March (POW rescue) p. 839 Japan’s High Tide at Midway (plus Aleutians) pp. 839-841 American Leapfrogging Toward Tokyo (island-hopping leapfrogging like blitzkrieg Pacific style) * Book does opposite of Europe First strategy of Allies †¢ Guam (Saipan – suicides), Marianas â€Å"Turkey Shoot’ F6F Hellcat kill ratio †¢ 6-20-44 Battle of Philippine Sea – massive Japanese losses p. 840 Map of Pacific War p. 841 Churchill – â€Å"The Hun is always either at you throat or at your feet. † pp. 841-842 The Allied Halting of Hitler p. 41 Battle of the Atlantic – U-boats, destroyers, RADAR, SONAR, Enigma, New U-boats (not enough early in war – Downitz) – no sub can stay under indefinitely b/c food is limitation (U-571) pp. 842-843 A Second Front from North Africa to Rome p. 842 USSR lost ~20 million pp. 842-843 â€Å"unconditional surrender† debate results pp. 843-846 D-Day: June 6th, 194p. 845 Examining the Evidence – Teheran 1943 – Overlord Discussion (* Dieppe in France) p. 844 Ike chosen to command D-Day invasion – (feignt w/Patton at Calais – codes, underground, paratroopers, Rangers, 5 beaches, air power, Mulberry harbors, etc†¦) p. 846 D-Day (Agincourt 1415 – officer recited Shakespeare) in picture caption p. 846 Aug 1944 invasion of S France (A Murphy) pp. 846-847 FDR: Four Termite of 1944 p. 47 Focus on VP – Truman – on Sen Committee for Wasteful Sp ending – told to stop investigating Manhattan Project – he later learns it was Atomic Bombs p. 848 FDR defeats Dewey – FDR had Rep owned newspapers against him again p. 848 Quote from Congresswoman Clare Booth Luce – â€Å"He lied us into war because he did not have the political courage to lead us into it. † pp. 848-849 The Last Days of Hitler p. 849 Map of Battle of the Bulge * 76,000 casualties – worst US battle ever – so far * Okinawa Gettysburg were both very bad too Bulge mistakes p. 848 bombings pp. 848-849 (Remagen) Rhine River crossing into Germany p. 849 Holocaust – camps liberated – horrors known now for all (unit 731 in Manchuria) p. 849 FDR’s deathVE Day 5-8-45 pp. 49-851 Japan Dies Hard – US subs sinking Japanese ships – cutting off Japan’s vital lifeline sank 1. 042 ships ~50% of Japan’s merchant fleet p. 850 Bombings in Japan Ex. Tokyo 3/9-10/1945 ~83,000 KIA p. 850 Ley te Gulf, Iwo Jima, Pkinawa – short-changed as usual by textbooks that suck! Iwo Jima 6,000 KIA not 4,000 Okinawa 50,000 US casualties (KIA, WIA, MIA, POW) @ Okinawa, Japanese had ~200,000 military civilian casualties p. 851 2nd Flag Raising (Flags of Our Fathers, Letters from Iwo Jima, The Sands of Iwo Jima) p. 851 Kamikazes (Saipan Leyte, then Iwo Okinawa – worst of all – no Final Battle – would’ve been worst) †¢ They had lots stored up for the Final Battle pp. 851-853 Atomic Bombs p. 52 Hiroshima picture – post-bomb on 8-6-45 180,000 KIA, WIA, MIA 70,000 KIA instantly 60,000 died later from radiation, etc†¦ p. 852 USSR enters war in Pacific on 8-8-45 day before Nagasaki 8-9-45 KIA of 40,000 instantly, more later USSR invaded Manchuria North Korea (not a country split N S until 1950) 8-14-45 Japan surrendered 8-15-45 VJ Day official surrender on deck of battleship USS Missouri (Big Mo) on 9/2/45 w/MacArthur , etc†¦ pp. 853-854 The Allies Triumphant p. 853 US casualties ~ 1 million ~1/3rd KIA †¢ plasma, penicillin, (quanine for malaria), etc†¦. (medics, corpsman, doctors, nurses) USSR lost ~20 million plus more casualties 13. 6 million military killed plus 7. 2 million civilians killed plus up to 30 million more wounded and refugees p. 853 US attacked on W coast Ex balloons w/bombs, etc.. submarines on both coasts p. 853 â€Å"In the end, the US showed itself to be resourceful, tough, and adaptable to accommodate itself to the tactics of an enemy who was relentless and ruthless. † Kind of funny given US history – don’t you think? p. 854 VJ Day 8-15-45 image p. 854 production marvels – won war through production – more of everything – then eventually better more! Churchill – â€Å"Nothing succeeds like excess. † Herman Goering (Head of German air force/Luftwaffe – â€Å"Americans can’t build planes – only elect ric ice boxes and razor blades. † Goering also said that the P-51 Mustang (US fighter plane) won the war for the Allies p. 854 â€Å"But the American people preserved their precious liberties without serious impairment. † What would Zinn say? Is this a reference to loss of liberties during WWI – Espionage and Sedition Acts? What would â€Å"enemy aliens† and citizens interned during the war say? Ex. Italian German internment Japanese-American internment p. 854 Chronology p. 855 World War II: Triumph or Tragedy? Post-war scholarship was to avoid isolationist appeasement in Cold War Another paralleled 1930’s revisionist of post-WWI said US should have stayed out – made it worse Another thought FDR was naive isolationist Others thought FDR was a calculating interventionist Another focused on Atomic Bombs controversy – racism issue or timing b/c Germans were beaten already Gar Alperovitz said bomb was used to scare USSR hurry surrender MartinJ. Sherwin said we dropped A-bombs when ready to end was ASAP w/bonus of scaring USSR ***** Textbook ignores Rises to Power of Totalitarian leaders like Stalin (communist), Mussolini (fascist), Hitler (fascist), Japan’s militarist gov’t w/emporer Hirohito led by Tojo early in war – he took the fall It does not explain the role of the emperor in Japan’s gov’t Battle of Berlin – brutal pay back – refugees – rapes – POWs – Hitler’s death