title: Megan Ellison

text: After that, Ellison received access to much larger sums of money from her father for the production of more movies and partnered with Michael Benaroya to produce and cofinance the thriller "Catch .44" starring Bruce Willis and Forest Whitaker, and John Hillcoat's Prohibition-era crime drama, "Lawless". Around that same time, she began to collaborate with the Creative Artists Agency's film finance group headed by Roeg Sutherland and Micah Green.


title: Megan Ellison

text: She has since founded Annapurna Pictures, a company that plans to take a so-called "Silicon Valley" approach to filmmaking by investing in original, daring movies made by prestigious directors and screenwriters. Believing that risk-averse Hollywood studios have largely abandoned sophisticated dramas, period pieces, and auteur cinema, Annapurna Productions has released Paul Thomas Anderson's "The Master", a period drama about a cult that resembles Scientology, starring Joaquin Phoenix and Philip Seymour Hoffman, and "Zero Dark Thirty", an action-thriller about the killing of Osama bin Laden from writer Mark Boal and director Kathryn Bigelow, who made the Oscar-winning movie, "The Hurt Locker".


title: Megan Ellison

text: In 2011 and 2012, it was reported that Ellison was working with Boal on developing a movie about WikiLeaks founder Julian Assange based on a "New York Times Magazine" article called "The Boy Who Kicked the Hornet's Nest" by former "New York Times" executive editor Bill Keller. Amid fierce competition in 2012 among movie studios to produce an Assange biopic, Ellison and Annapurna eventually did not produce the movie, but DreamWorks released "The Fifth Estate" in 2013.


title: Megan Ellison

text: In 2011, Ellison outbid Lionsgate for the rights to the "Terminator" franchise. In January 2014, Ellison removed Annapurna Productions from the reboot of the "Terminator" franchise.


title: Megan Ellison

text: In 2014, Ellison became the first woman and the fourth person to receive two Academy Award nominations for Best Picture in the same year, which she received for her work on "Her" and "American Hustle." In June 2014, Ellison optioned the screen rights for the memoir "A House in the Sky", which tells the story of Amanda Lindhout and her capture by Somali rebels in 2011.


title: Megan Ellison

text: Ellison has a particular taste in directors. Ellison's approach to working with critically acclaimed directors is purely focused on ensuring that their creative vision is met, and providing them with all the relevant resources. Ellison is criticized by the film industry for being too ambitious and excessive with her budgets on films. With a proposed budget of $35 million, Paul Thomas Anderson's film "The Master" was initially denied by Universal and was deemed "too risky and rich for their blood." Indiewire says, "With the project adrift, Ellison's Annapurna Pictures stepped in and with distribution by The Weinstein Company, funded and helped bring "The Master" to the screen for $35 million (though some reports suggest that number is closer to $40 million)." With "The Master" making $28 million worldwide, Ellison lost as much as $15 million on the project. Ellison is heavily involved with the production of the films she finances by being on the set and making sure everything goes as planned. Ellison was present for "Zero Dark Thirty"'s production as it was brought to a halt because of sandstorms and had to abort a location due to an anti Pakistan riot in India. Ellison's production style is holistically present and accommodating to directors' visions. Because of her wealth, Ellison does not approach film as an investment with high returns, but rather as an artistic medium pushing the boundaries of independent filmmaking.


title: Megan Ellison

text: Ellison is openly lesbian. She owns a number of motorcycles. Ellison refused to give interviews. She is a competitive equestrian, having trained at the Wild Turkey Farm in Woodside, California and riding in the North American Young Rider Championships in 2004.


title: Megan Ellison

text: In 2011, Ellison founded the production company Annapurna Pictures, named for the Annapurna Circuit she hiked in Nepal in 2006. It has produced the major films Spike Jonze's "Her", Kathryn Bigelow's "Zero Dark Thirty", and David O. Russell's "American Hustle". Ellison's approach to filmmaking is regarded as one that follows Silicon Valley principles: investing large sums of money into prestigious teams that are attempting something risky. Several executives, including two-year president Mark Weinstock, left Annapurna in 2018. Annapurna is backed by Ellison's billionaire father.


title: Megan Ellison

text: Ellison is the first female producer to earn two different Academy Awards nominations for Best Picture in the same year. In 2018, Ellison won the Woman in Motion Award at Cannes Music Festival.


title: Type 1 diabetes

text: Type 1 diabetes (T1D), formerly known as juvenile diabetes, is an autoimmune disease that originates when cells that make insulin (beta cells) are destroyed by the immune system. Insulin is a hormone required for the cells to use blood sugar for energy and it helps regulate glucose levels in the bloodstream. Before treatment this results in high blood sugar levels in the body. The common symptoms of this elevated blood sugar are frequent urination, increased thirst, increased hunger, weight loss, and other serious complications. Additional symptoms may include blurry vision, tiredness, and slow wound healing. Symptoms typically develop over a short period of time, often a matter of weeks.


title: Type 1 diabetes

text: The cause of type 1 diabetes is unknown, but it is believed to involve a combination of genetic and environmental factors. The underlying mechanism involves an autoimmune destruction of the insulin-producing beta cells in the pancreas. Diabetes is diagnosed by testing the level of sugar or glycated hemoglobin (HbA1C) in the blood. Type 1 diabetes can be distinguished from type 2 by testing for the presence of autoantibodies.


title: Type 1 diabetes

text: There is no known way to prevent type 1 diabetes. Treatment with insulin is required for survival. Insulin therapy is usually given by injection just under the skin but can also be delivered by an insulin pump. A diabetic diet and exercise are important parts of management. If left untreated, diabetes can cause many complications. Complications of relatively rapid onset include diabetic ketoacidosis and nonketotic hyperosmolar coma. Long-term complications include heart disease, stroke, kidney failure, foot ulcers and damage to the eyes. Furthermore, since insulin lowers blood sugar levels, complications may arise from low blood sugar if more insulin is taken than necessary.


title: Type 1 diabetes

text: Type 1 diabetes makes up an estimated 5–10% of all diabetes cases. The number of people affected globally is unknown, although it is estimated that about 80,000 children develop the disease each year. Within the United States the number of people affected is estimated at one to three million. Rates of disease vary widely, with approximately one new case per 100,000 per year in East Asia and Latin America and around 30 new cases per 100,000 per year in Scandinavia and Kuwait. It typically begins in children and young adults.


title: Type 1 diabetes

text: Type 1 diabetes begins suddenly, typically in childhood or adolescence. The major sign of type 1 diabetes is very high blood sugar, which typically manifests in children as a few days to weeks of polyuria (increased urination), polydipsia (increased thirst), and weight loss. Children may also experience increased appetite, blurred vision, bedwetting, recurrent skin infections, candidiasis of the perineum, irritability, and performance issues at school. Adults with type 1 diabetes tend to have more varied symptoms that come on over months rather than days to weeks.


title: Type 1 diabetes

text: Prolonged lack of insulin can also result in diabetic ketoacidosis, characterized by persistent fatigue, dry or flushed skin, abdominal pain, nausea or vomiting, confusion, trouble breathing, and a fruity breath odor. Blood and urine tests reveal unusually high glucose and ketones in the blood and urine. Untreated ketoacidosis can rapidly progress to loss of consciousness, coma, and death. The percentage of children whose type 1 diabetes begins with an episode of diabetic ketoacidosis varies widely by geography, as low as 15% in parts of Europe and North America, and as high as 80% in the developing world.


title: Type 1 diabetes

text: Type 1 diabetes is caused by the destruction of β-cells – the only cells in the body that produce insulin – and the consequent progressive insulin deficiency. Without insulin, the body is unable to respond effectively to increases in blood sugar and diabetics have persistent hyperglycemia. In 70–90% of cases, β-cells are destroyed by someone's own immune system, for reasons that are not entirely clear. The best-studied components of this autoimmune response are β-cell-targeted antibodies that begin to develop in the months or years before symptoms arise. Typically someone will first develop antibodies against insulin or the protein GAD65, followed eventually by antibodies against the proteins IA-2, IA-2β, and/or ZNT8. People with more of these antibodies, and who develop them earlier in life, are at higher risk for developing symptomatic type 1 diabetes. The trigger for the development of these antibodies remains unclear. A number of explanatory theories have been put forward, and the cause may involve genetic susceptibility, a diabetogenic trigger, and/or exposure to an antigen. The remaining 10–30% of type 1 diabetics have β-cell destruction but no sign of autoimmunity; this is called idiopathic type 1 diabetes and its cause remains unclear.


title: Type 1 diabetes

text: Various environmental risks have been studied in an attempt to understand what triggers β-cell autoimmunity. Many aspects of environment and life history are associated with slight increases in type 1 diabetes risk, however the connection between each risk and diabetes often remains unclear. Type 1 diabetes risk is slightly higher for children whose mothers are obese or older than 35, or for children born by caesarean section. Similarly, a child's weight gain in the first year of life, total weight, and BMI are associated with slightly increased type 1 diabetes risk. Some dietary habits have also been associated with type 1 diabetes risk, namely consumption of cow's milk and dietary sugar intake. Animal studies and some large human studies have found small associations between type 1 diabetes risk and intake of gluten or dietary fiber; however, other large human studies have found no such association. Many potential environmental triggers have been investigated in large human studies and found to be unassociated with type 1 diabetes risk including duration of breastfeeding, time of introduction of cow milk into the diet, vitamin D consumption, blood levels of active vitamin D, and maternal intake of omega-3 fatty acids.


title: Type 1 diabetes

text: A longstanding hypothesis for an environmental trigger is that some viral infection early in life contributes to type 1 diabetes development. Much of this work has focused on enteroviruses, with some studies finding slight associations with type 1 diabetes, and others finding none. Large human studies have searched for, but not yet found an association between type 1 diabetes and various other viral infections, including infections of the mother during pregnancy. Conversely, some have postulated that reduced exposure to pathogens in the developed world increases the risk of autoimmune diseases, often called the hygiene hypothesis. Various studies of hygiene-related factors – including household crowding, daycare attendance, population density, childhood vaccinations, antihelminth medication, and antibiotic usage during early life or pregnancy – show no association with type 1 diabetes.


title: Type 1 diabetes

text: Type 1 diabetes is partially caused by genetics, and family members of type 1 diabetics have a higher risk of developing the disease themselves. In the general population, the risk of developing type 1 diabetes is around 1 in 250. For someone whose parent has type 1 diabetes, the risk rises to 1–9%. If a sibling has type 1 diabetes, the risk is 6–7%. If someone's identical twin has type 1 diabetes, they have a 30–70% risk of developing it themselves.


title: Type 1 diabetes

text: About half of the disease's heritability is due to variations in three HLA class II genes involved in antigen presentation: "HLA-DRB1", "HLA-DQA1", and "HLA-DQB1". The variation patterns associated with increased risk of type 1 diabetes are called HLA-DR3 and HLA-DR4-HLA-DQ8, and are common in people of European descent. A pattern associated with reduced risk of type 1 diabetes is called HLA-DR15-HLA-DQ6. Large genome-wide association studies have identified dozens of other genes associated with type 1 diabetes risk, mostly genes involved in the immune system.


title: Type 1 diabetes

text: Some medicines can reduce insulin production or damage β cells, resulting in disease that resembles type 1 diabetes. The antiviral drug didanosine triggers pancreas inflammation in 5 to 10% of those who take it, sometimes causing lasting β-cell damage. Similarly, up to 5% of those who take the anti-protozoal drug pentamidine experience β-cell destruction and diabetes. Several other drugs cause diabetes by reversibly reducing insulin secretion, namely statins (which may also damage β cells), the post-transplant immunosuppressants cyclosporin A and tacrolimus, the leukemia drug L-asparaginase, and the antibiotic gatifloxicin. Pyrinuron (Vacor), a rodenticide introduced in the United States in 1976, selectively destroys pancreatic beta cells, resulting in type 1 diabetes after accidental poisoning. Pyrinuron was withdrawn from the U.S. market in 1979. Cancer Immunotherapy Drugs have also destroyed pancreatic beta cells, such as Opdivo among others.


title: Type 1 diabetes

text: Diabetes is typically diagnosed by a blood test showing unusually high blood sugar. The World Health Organization defines diabetes as blood sugar levels at or above 7.0 mmol/L (126 mg/dL) after fasting for at least eight hours, or a glucose level at or above 11.1 mmol/L (200 mg/dL) two hours after an oral glucose tolerance test. The American Diabetes Association additionally recommends a diagnosis of diabetes for anyone with symptoms of hyperglycemia and blood sugar at any time at or above 11.1 mmol/L, or glycated hemoglobin (hemoglobin A1C) levels at or above 48 mmol/mol.


title: Type 1 diabetes

text: Once a diagnosis of diabetes is established, type 1 diabetes is distinguished from other types by a blood test for the presence of autoantibodies that target various components of the beta cell. The most commonly available tests detect antibodies against glutamic acid decarboxylase, the beta cell cytoplasm, or insulin, each of which are targeted by antibodies in around 80% of type 1 diabetics. Some healthcare providers also have access to tests for antibodies targeting the beta cell proteins IA-2 and ZnT8; these antibodies are present in around 58% and 80% of type 1 diabetics respectively. Some also test for C-peptide, a byproduct of insulin synthesis. Very low C-peptide levels are suggestive of type 1 diabetes.


title: Type 1 diabetes

text: The mainstay of type 1 diabetes treatment is the regular injection of insulin to manage hyperglycemia. Injections of insulin – via subcutaneous injection using either a syringe or an insulin pump – are necessary multiple times per day, adjusting dosages to account for food intake, blood glucose levels and physical activity. The goal of treatment is to maintain blood sugar in a normal range – 80–130 mg/dL before a meal; <180 mg/dL after – as often as possible. To achieve this, people with diabetes often monitor their blood glucose levels at home. Around 83% of type 1 diabetics monitor their blood glucose by capillary blood testing – pricking the finger to draw a drop of blood, and determining blood glucose with a glucose meter. The American Diabetes Association recommends testing blood glucose around 6–10 times per day: before each meal, before exercise, at bedtime, occasionally after a meal, and any time someone feels the symptoms of hypoglycemia. Around 17% of people with type 1 diabetes use a continuous glucose monitor, a device with a sensor under the skin that constantly measures glucose levels and communicates those levels to an external device. Continuous glucose monitoring is associated with better blood sugar control than capillary blood testing alone; however, continuous glucose monitoring tends to be substantially more expensive. Healthcare providers can also monitor someone's hemoglobin A1C levels which reflect the average blood sugar over the last three months. The American Diabetes Association recommends a goal of keeping hemoglobin A1C levels under 7% for most adults and 7.5% for children.


title: Type 1 diabetes

text: The goal of insulin therapy is to mimic normal pancreatic insulin secretion: low levels of insulin constantly present to support basic metabolism, plus the two-phase secretion of additional insulin in response to high blood sugar – an initial spike in secreted insulin, then an extended phase with continued insulin secretion. This is accomplished by combining different insulin preparations that act with differing speeds and durations. The standard of care for type 1 diabetes is a bolus of rapid-acting insulin 10–15 minutes before each meal or snacks, and as-needed to correct hyperglycemia. In addition, constant low levels of insulin are achieved with one or two daily doses of long-acting insulin, or by steady infusion of low insulin levels by an insulin pump. The exact dose of insulin appropriate for each injection depends on the content of the meal/snack, and the individual person's sensitivity to insulin, and is therefore typically calculated by the individual with diabetes or a family member by hand or assistive device (calculator, chart, mobile app, etc.). People unable to manage these intensive insulin regimens are sometimes prescribed alternate plans relying on mixtures of rapid- or short-acting and intermediate-acting insulin, which are administered at fixed times along with meals of pre-planned times and carbohydrate composition.


title: Type 1 diabetes

text: A non-insulin medication approved by the U.S. Food and Drug Administration for treating type 1 diabetes is the amylin analog pramlintide, which replaces the beta-cell hormone amylin. Addition of pramlintide to mealtime insulin injections reduces the boost in blood sugar after a meal, improving blood sugar control. Occasionally, metformin, GLP-1 receptor agonists, Dipeptidyl peptidase-4 inhibitors, or SGLT2 inhibitor are prescribed off-label to people with type 1 diabetes, although fewer than 5% of type 1 diabetics use these drugs.


title: Type 1 diabetes

text: Another non-insulin medication is Teplizumab a monoclonal antibody drug approved by the FDA in November 2022, it aims to delay type 1 diabetes by reprogramming the immune system to stop mistakenly attacking pancreatic cells.


title: Type 1 diabetes

text: Besides insulin, the major way type 1 diabetics control their blood sugar is by learning how various foods impact their blood sugar levels. This is primarily done by tracking their intake of carbohydrates – the type of food with the greatest impact on blood sugar. In general, people with type 1 diabetes are advised to follow an individualized eating plan rather than a pre-decided one. There are camps for children to teach them how and when to use or monitor their insulin without parental help. As psychological stress may have a negative effect on diabetes, a number of measures have been recommended including: exercising, taking up a new hobby, or joining a charity, among others.


title: Type 1 diabetes

text: Regular exercise is important for maintaining general health, though the effect of exercise on blood sugar can be challenging to predict. Exogenous insulin can drive down blood sugar, leaving those with diabetes at risk of hypoglycemia during and immediately after exercise, then again seven to eleven hours after exercise (called the "lag effect"). Conversely, high-intensity exercise can result in a shortage of insulin, and consequent hyperglycemia. The risk of hypoglycemia can be managed by beginning exercise when blood sugar is relatively high (above 100 mg/dL), ingesting carbohydrates during or shortly after exercise, and reducing the amount of injected insulin within two hours of the planned exercise. Similarly, the risk of exercise-induced hyperglycemia can be managed by avoiding exercise when insulin levels are very low, when blood sugar is extremely high (above 350 mg/dL), or when one feels unwell.


title: Type 1 diabetes

text: In some cases, people can receive transplants of the pancreas or isolated islet cells to restore insulin production and alleviate diabetic symptoms. Transplantation of the whole pancreas is rare, due in part to the few available donor organs, and to the need for lifelong immunosuppressive therapy to prevent transplant rejection. The American Diabetes Association recommends pancreas transplant only in people who also require a kidney transplant, or who struggle to perform regular insulin therapy and experience repeated severe side effects of poor blood sugar control. Most pancreas transplants are done simultaneously with a kidney transplant, with both organs from the same donor. The transplanted pancreas continues to function for at least five years in around three quarters of recipients, allowing them to stop taking insulin.


title: Type 1 diabetes

text: Transplantations of islets alone have become increasingly common. Pancreatic islets are isolated from a donor pancreas, then injected into the recipient's portal vein from which they implant onto the recipient's liver. In nearly half of recipients, the islet transplant continues to work well enough that they still don't need exogenous insulin five years after transplantation. If a transplant fails, recipients can receive subsequent injections of islets from additional donors into the portal vein. Like with whole pancreas transplantation, islet transplantation requires lifelong immunosuppression and depends on the limited supply of donor organs; it is therefore similarly limited to people with severe poorly controlled diabetes and those who have had or are scheduled for a kidney transplant.


title: Type 1 diabetes

text: Type 1 diabetes is a result of the destruction of pancreatic beta cells, although what triggers that destruction remains unclear. People with type 1 diabetes tend to have more CD8+ T-cells and B-cells that specifically target islet antigens than those without type 1 diabetes, suggesting a role for the adaptive immune system in beta cell destruction. Type 1 diabetics also tend to have reduced regulatory T cell function, which may exacerbate autoimmunity. Destruction of beta cells results in inflammation of the islet of Langerhans, called insulitis. These inflamed islets tend to contain CD8+ T-cells and – to a lesser extent – CD4+ T cells. Abnormalities in the pancreas or the beta cells themselves may also contribute to beta-cell destruction. The pancreases of people with type 1 diabetes tend to be smaller, lighter, and have abnormal blood vessels, nerve innervations, and extracellular matrix organization. In addition, beta cells from people with type 1 diabetes sometimes overexpress HLA class I molecules (responsible for signaling to the immune system) and have increased endoplasmic reticulum stress and issues with synthesizing and folding new proteins, any of which could contribute to their demise.


title: Type 1 diabetes

text: The mechanism by which the beta cells actually die likely involves both necroptosis and apoptosis induced or exacerbated by CD8+ T-cells and macrophages. Necroptosis can be triggered by activated T cells – which secrete toxic granzymes and perforin – or indirectly as a result of reduced blood flow or the generation of reactive oxygen species. As some beta cells die, they may release cellular components that amplify the immune response, exacerbating inflammation and cell death. Pancreases from people with type 1 diabetes also have signs of beta cell apoptosis, linked to activation of the janus kinase and TYK2 pathways.


title: Type 1 diabetes

text: Partial ablation of beta-cell function is enough to cause diabetes; at diagnosis, people with type 1 diabetes often still have detectable beta-cell function. Once insulin therapy is started, many people experience a resurgence in beta-cell function, and can go some time with little-to-no insulin treatment – called the "honeymoon phase". This eventually fades as beta-cells continue to be destroyed, and insulin treatment is required again. Beta-cell destruction is not always complete, as 30–80% of type 1 diabetics produce small amounts of insulin years or decades after diagnosis.


title: Type 1 diabetes

text: Onset of autoimmune diabetes is accompanied by impaired ability to regulate the hormone glucagon, which acts in antagonism with insulin to regulate blood sugar and metabolism. Progressive beta cell destruction leads to dysfunction in the neighboring alpha cells which secrete glucagon, exacerbating excursions away from euglycemia in both directions; overproduction of glucagon after meals causes sharper hyperglycemia, and failure to stimulate glucagon upon hypoglycemia prevents a glucagon-mediated rescue of glucose levels.


title: Type 1 diabetes

text: Onset of type 1 diabetes is followed by an increase in glucagon secretion after meals. Increases have been measured up to 37% during the first year of diagnosis, while c-peptide levels (indicative of islet-derived insulin), decline by up to 45%. Insulin production will continue to fall as the immune system destroys beta cells, and islet-derived insulin will continue to be replaced by therapeutic exogenous insulin. Simultaneously, there is measurable alpha cell hypertrophy and hyperplasia in the early stage of the disease, leading to expanded alpha cell mass. This, together with failing beta cell insulin secretion, begins to account for rising glucagon levels that contribute to hyperglycemia. Some researchers believe glucagon dysregulation to be the primary cause of early stage hyperglycemia. Leading hypotheses for the cause of postprandial hyperglucagonemia suggest that exogenous insulin therapy is inadequate to replace the lost intraislet signalling to alpha cells previously mediated by beta cell-derived pulsatile insulin secretion. Under this working hypothesis intensive insulin therapy has attempted to mimic natural insulin secretion profiles in exogenous insulin infusion therapies.


title: Type 1 diabetes

text: Glucagon secretion is normally increased upon falling glucose levels, but normal glucagon response to hypoglycemia is blunted in type 1 diabetics. Beta cell glucose sensing and subsequent suppression of administered insulin secretion is absent, leading to islet hyperinsulinemia which inhibits glucagon release.


title: Type 1 diabetes

text: Autonomic inputs to alpha cells are much more important for glucagon stimulation in the moderate to severe ranges of hypoglycemia, yet the autonomic response is blunted in a number of ways. Recurrent hypoglycemia leads to metabolic adjustments in the glucose sensing areas of the brain, shifting the threshold for counter regulatory activation of the sympathetic nervous system to lower glucose concentration. This is known as hypoglycemic unawareness. Subsequent hypoglycemia is met with impairment in sending of counter regulatory signals to the islets and adrenal cortex. This accounts for the lack of glucagon stimulation and epinephrine release that would normally stimulate and enhance glucose release and production from the liver, rescuing the diabetic from severe hypoglycemia, coma, and death. Numerous hypotheses have been produced in the search for a cellular mechanism of hypoglycemic unawareness, and a consensus has yet to be reached. The major hypotheses are summarized in the following table:


title: Type 1 diabetes

text: In addition, autoimmune diabetes is characterized by a loss of islet specific sympathetic innervation. This loss constitutes an 80–90% reduction of islet sympathetic nerve endings, happens early in the progression of the disease, and is persistent though the life of the patient. It is linked to the autoimmune aspect of type 1 diabetics and fails to occur in type 2 diabetics. Early in the autoimmune event, the axon pruning is activated in islet sympathetic nerves. Increased BDNF and ROS that result from insulitis and beta cell death stimulate the p75 neurotrophin receptor (p75), which acts to prune off axons. Axons are normally protected from pruning by activation of tropomyosin receptor kinase A (Trk A) receptors by NGF, which in islets is primarily produced by beta cells. Progressive autoimmune beta cell destruction, therefore, causes both the activation of pruning factors and the loss of protective factors to the islet sympathetic nerves. This unique form of neuropathy is a hallmark of type 1 diabetes, and plays a part in the loss of glucagon rescue of severe hypoglycemia.


title: Type 1 diabetes

text: The most pressing complication of type 1 diabetes are the always present risks of poor blood sugar control: severe hypoglycemia and diabetic ketoacidosis. Hypoglycemia – typically blood sugar below 70 mg/dL – triggers the release of epinephrine, and can cause people to feel shaky, anxious, or irritable. People with hypoglycemia may also experience hunger, nausea, sweats, chills, dizziness, and a fast heartbeat. Some feel lightheaded, sleepy, or weak. Severe hypoglycemia can develop rapidly, causing confusion, coordination problems, loss of consciousness, and seizure. On average, people with type 1 diabetes experience a hypoglycemia event that requires assistance of another 16–20 times in 100 person-years, and an event leading to unconsciousness or seizure 2–8 times per 100 person-years. The American Diabetes Association recommends treating hypoglycemia by the "15-15 rule": eat 15 grams of carbohydrates, then wait 15 minutes before checking blood sugar; repeat until blood sugar is at least 70 mg/dL. Severe hypoglycemia that impairs someone's ability to eat is typically treated with injectable glucagon, which triggers glucose release from the liver into the bloodstream. People with repeated bouts of hypoglycemia can develop hypoglycemia unawareness, where the blood sugar threshold at which they experience symptoms of hypoglycemia decreases, increasing their risk of severe hypoglycemic events. Rates of severe hypoglycemia have generally declined due to the advent of rapid-acting and long-acting insulin products in the 1990s and early 2000s; however, acute hypoglycemic still causes 4–10% of type 1 diabetes-related deaths.


title: Type 1 diabetes

text: The other persistent risk is diabetic ketoacidosis – a state where lack of insulin results in cells burning fat rather than sugar, producing toxic ketones as a byproduct. Ketoacidosis symptoms can develop rapidly, with frequent urination, excessive thirst, nausea, vomiting, and severe abdominal pain all common. More severe ketoacidosis can result in labored breathing, and loss of consciousness due to cerebral edema. People with type 1 diabetes experience diabetic ketoacidosis 1–5 times per 100 person-years, the majority of which result in hospitalization. 13–19% of type 1 diabetes-related deaths are caused by ketoacidosis, making ketoacidosis the leading cause of death in people with type 1 diabetes less than 58 years old.


title: Type 1 diabetes

text: In addition to the acute complications of diabetes, long-term hyperglycemia results in damage to the small blood vessels throughout the body. This damage tends to manifest particularly in the eyes, nerves, and kidneys causing diabetic retinopathy, diabetic neuropathy, and diabetic nephropathy respectively. In the eyes, prolonged high blood sugar causes the blood vessels in the retina to become fragile.


title: Type 1 diabetes

text: People with type 1 diabetes also have increased risk of cardiovascular disease, which is estimated to shorten the life of the average type 1 diabetic by 8–13 years. Cardiovascular disease as well as neuropathy may have an autoimmune basis, as well. Women with type 1 DM have a 40% higher risk of death as compared to men with type 1 DM.


title: Type 1 diabetes

text: About 12 percent of people with type 1 diabetes have clinical depression. About 6 percent of people with type 1 diabetes also have celiac disease, but in most cases there are no digestive symptoms or are mistakenly attributed to poor control of diabetes, gastroparesis or diabetic neuropathy. In most cases, celiac disease is diagnosed after onset of type 1 diabetes. The association of celiac disease with type 1 diabetes increases the risk of complications, such as retinopathy and mortality. This association can be explained by shared genetic factors, and inflammation or nutritional deficiencies caused by untreated celiac disease, even if type 1 diabetes is diagnosed first.


title: Type 1 diabetes

text: People with diabetes show an increased rate of urinary tract infection. The reason is bladder dysfunction is more common in people with diabetes than people without diabetes due to diabetes nephropathy. When present, nephropathy can cause a decrease in bladder sensation, which in turn, can cause increased residual urine, a risk factor for urinary tract infections.


title: Type 1 diabetes

text: Sexual dysfunction in people with diabetes is often a result of physical factors such as nerve damage and poor circulation, and psychological factors such as stress and/or depression caused by the demands of the disease. The most common sexual issues in males with diabetes are problems with erections and ejaculation: "With diabetes, blood vessels supplying the penis's erectile tissue can get hard and narrow, preventing the adequate blood supply needed for a firm erection. The nerve damage caused by poor blood glucose control can also cause ejaculate to go into the bladder instead of through the penis during ejaculation, called retrograde ejaculation. When this happens, semen leaves the body in the urine." Another cause of erectile dysfunction is reactive oxygen species created as a result of the disease. Antioxidants can be used to help combat this. Sexual problems are common in women who have diabetes, including reduced sensation in the genitals, dryness, difficulty/inability to orgasm, pain during sex, and decreased libido. Diabetes sometimes decreases estrogen levels in females, which can affect vaginal lubrication. Less is known about the correlation between diabetes and sexual dysfunction in females than in males.


title: Type 1 diabetes

text: Oral contraceptive pills can cause blood sugar imbalances in women who have diabetes. Dosage changes can help address that, at the risk of side effects and complications.


title: Type 1 diabetes

text: Women with type 1 diabetes show a higher than normal rate of polycystic ovarian syndrome (PCOS). The reason may be that the ovaries are exposed to high insulin concentrations since women with type 1 diabetes can have frequent hyperglycemia.


title: Type 1 diabetes

text: People with type 1 diabetes are at an increased risk for developing several autoimmune disorders, particularly thyroid problems – around 20% of people with type 1 diabetes have hypothyroidism or hyperthyroidism, typically caused by Hashimoto thyroiditis or Graves' disease respectiveley. Celiac disease affects 2–8% of people with type 1 diabetes, and is more common in those who were younger at diabetes diagnosis, and in white people. Type 1 diabetics are also at increased risk of rheumatoid arthritis, lupus, autoimmune gastritis, pernicious anemia, vitiligo, and Addison's disease. Conversely, complex autoimmune syndromes caused by mutations in the immunity-related genes "AIRE" (causing autoimmune polyglandular syndrome), "FoxP3" (causing IPEX syndrome), or "STAT3" include type 1 diabetes in their effects.


title: Type 1 diabetes

text: Type 1 diabetes makes up an estimated 10–15% of all diabetes cases or 11–22 million cases worldwide. Symptoms can begin at any age, but onset is most common in children, with diagnoses slightly more common in 5 to 7 year olds, and much more common around the age of puberty. In contrast to most autoimmune diseases, type 1 diabetes is slightly more common in males than in females.


title: Type 1 diabetes

text: In 2006, type 1 diabetes affected 440,000 children under 14 years of age and was the primary cause of diabetes in those less than 15 years of age.


title: Type 1 diabetes

text: Rates vary widely by country and region. Incidence is highest in Scandinavia, at 30–60 new cases per 100,000 children per year, intermediate in the U.S. and Southern Europe at 10–20 cases per 100,000 per year, and lowest in China, much of Asia, and South America at 1–3 cases per 100,000 per year.


title: Type 1 diabetes

text: In the United States, type 1 and 2 diabetes affected about 208,000 youths under the age of 20 in 2015. Over 18,000 youths are diagnosed with Type 1 diabetes every year. Every year about 234,051 Americans die due to diabetes (type I or II) or diabetes-related complications, with 69,071 having it as the primary cause of death.


title: Type 1 diabetes

text: In Australia, about one million people have been diagnosed with diabetes and of this figure 130,000 people have been diagnosed with type 1 diabetes. Australia ranks 6th-highest in the world with children under 14 years of age. Between 2000 and 2013, 31,895 new cases were established, with 2,323 in 2013, a rate of 10–13 cases per 100,00 people each year. Aboriginals and Torres Strait Islander people are less affected.


title: Type 1 diabetes

text: Since the 1950s, the incidence of type 1 diabetes has been gradually increasing across the world by an average 3–4% per year. The increase is more pronounced in countries that began with a lower incidence of type 1 diabetes.


title: Type 1 diabetes

text: The connection between diabetes and pancreatic damage was first described by the German pathologist Martin Schmidt, who in a 1902 paper noted inflammation around the pancreatic islet of a child who had died of diabetes. The connection between this inflammation and diabetes onset was further developed through the 1920s by Shields Warren, and the term "insulitis" was coined by Hanns von Meyenburg in 1940 to describe the phenomenon.


title: Type 1 diabetes

text: Type 1 diabetes was described as an autoimmune disease in the 1970s, based on observations that autoantibodies against islets were discovered in diabetics with other autoimmune deficiencies. It was also shown in the 1980s that immunosuppressive therapies could slow disease progression, further supporting the idea that type 1 diabetes is an autoimmune disorder. The name "juvenile diabetes" was used earlier as it often first is diagnosed in childhood.


title: Type 1 diabetes

text: Type 1 and 2 diabetes was estimated to cause $10.5 billion in annual medical costs ($875 per month per diabetic) and an additional $4.4 billion in indirect costs ($366 per month per person with diabetes) in the U.S. In the United States $245 billion every year is attributed to diabetes. Individuals diagnosed with diabetes have 2.3 times the health care costs as individuals who do not have diabetes. One in ten health care dollars are spent on individuals with type 1 and 2 diabetes.


title: Type 1 diabetes

text: Funding for research into type 1 diabetes originates from government, industry (e.g., pharmaceutical companies), and charitable organizations. Government funding in the United States is distributed via the National Institutes of Health, and in the UK via the National Institute for Health and Care Research or the Medical Research Council. The Juvenile Diabetes Research Foundation (JDRF), founded by parents of children with type 1 diabetes, is the world's largest provider of charity-based funding for type 1 diabetes research. Other charities include the American Diabetes Association, Diabetes UK, Diabetes Research and Wellness Foundation, Diabetes Australia, the Canadian Diabetes Association.


title: Type 1 diabetes

text: Type 1 diabetes is not currently preventable. Several trials have attempted dietary interventions with the hope of reducing the autoimmunity that leads to type 1 diabetes. Trials that withheld cow's milk or gave infants formula free of bovine insulin decreased the development of β-cell-targeted antibodies, but did not prevent the development of type 1 diabetes. Similarly, trials that gave high-risk individuals injected insulin, oral insulin, or nicotinamide did not prevent diabetes development.


title: Type 1 diabetes

text: Other research has focused on treating high-risk individuals with immunosuppressive agents to prevent beta cell destruction. Large trials of cyclosporine treatment suggested that cyclosporine could improve insulin secretion in those recently diagnosed with type 1 diabetes; however, people who stopped taking cyclosporine rapidly stopped making insulin, and cyclosporine's kidney toxicity and increased risk of cancer prevented people from using it long-term. Several other immunosuppressive agents – prednisone, azathioprine, anti-thymocyte globulin, mycophenolate, and antibodies against CD20 and IL2 receptor α – have been the subject of research, but none have provided lasting protection from development of type 1 diabetes. Antibodies against CD3 have been shown to delay the development of type 1 diabetes in those at high risk; however, they have not been widely adopted due to concerns over the duration of their effect, and activation of Epstein-Barr virus infections in those undergoing treatment.


title: Type 1 diabetes

text: Vitamin D supplementation may help with preventing type one diabetes. This is believed to be the case due to vitamin D receptors affecting the B-cells involved in promoting pancreatic homeostasis.


title: Type 1 diabetes

text: Vaccines are being looked at to treat or prevent type 1 diabetes by inducing immune tolerance to insulin or pancreatic beta cells. While Phase II clinical trials of a vaccine containing alum and recombinant GAD65, an autoantigen involved in type 1 diabetes, were promising, as of 2014 Phase III had failed. As of 2014, other approaches, such as a DNA vaccine encoding proinsulin and a peptide fragment of insulin, were in early clinical development.


title: Type 1 diabetes

text: Pluripotent stem cells can be used to generate beta cells but previously these cells did not function as well as normal beta cells. In 2014 more mature beta cells were produced which released insulin in response to blood sugar when transplanted into mice. Before these techniques can be used in humans more evidence of safety and effectiveness is needed.


title: Type 1 diabetes

text: There has also been substantial effort to develop a fully automated insulin delivery system or "artificial pancreas" that could sense glucose levels and inject appropriate insulin without conscious input from the user. Current "hybrid closed-loop systems" use a continuous glucose monitor to sense blood sugar levels, and a subcutaneous insulin pump to deliver insulin; however, due to the delay between insulin injection and its action, current systems require the user to initiate insulin before taking meals. Several improvements to these systems are currently undergoing clinical trials in humans, including a dual-hormone system that injects glucagon in addition to insulin, and an implantable device that injects insulin intraperitoneally where it can be absorbed more quickly.


title: Type 1 diabetes

text: Various animal models of disease are used to understand the pathogenesis and etiology of type 1 diabetes. Currently available models of T1D can be divided into spontaneously autoimmune, chemically induced, virus induced and genetically induced.


title: Type 1 diabetes

text: The nonobese diabetic (NOD) mouse is the most widely studied model of type 1 diabetes. It is an inbred strain that spontaneously develops type 1 diabetes in 30–100% of female mice depending on housing conditions. Diabetes in NOD mice is caused by several genes, primarily MHC genes involved in antigen presentation. Like diabetic humans, NOD mice develop islet autoantibodies and inflammation in the islet, followed by reduced insulin production and hyperglycemia. Some features of human diabetes are exaggerated in NOD mice, namely the mice have more severe islet inflammation than humans, and have a much more pronounced sex bias, with females developing diabetes far more frequently than males. In NOD mice the onset of insulitis occurs at 3–4 weeks of age. The islets of Langerhans are infiltrated by CD4+, CD8+ T lymphocytes, NK cells, B lymphocytes, dendritic cells, macrophages and neutrophils, similar to the disease process in humans. In addition to sex, breeding conditions, gut microbiome composition or diet also influence the onset of T1D.


title: Type 1 diabetes

text: The BioBreeding Diabetes-Prone (BB) rat is another widely used spontaneous experimental model for T1D. The onset of diabetes occurs, in up to 90% of individuals (regardless of sex) at 8–16 weeks of age. During insulitis, the pancreatic islets are infiltrated by T lymphocytes, B lymphocytes, macrophages, and NK cells, with the difference from the human course of insulitis being that CD4 + T lymphocytes are markedly reduced and CD8 + T lymphocytes are almost absent. The aforementioned lymphopenia is the major drawback of this model. The disease is characterized by hyperglycemia, hypoinsulinemia, weight loss, ketonuria, and the need for insulin therapy for survival. BB Rats are used to study the genetic aspects of T1D and are also used for interventional studies and diabetic nephropathy studies.


title: Type 1 diabetes

text: LEW-1AR1 / -iddm rats are derived from congenital Lewis rats and represent a rarer spontaneous model for T1D. These rats develop diabetes at about 8–9 weeks of age with no sex differences unlike NOD mice. In LEW mice, diabetes presents with hyperglycemia, glycosuria, ketonuria, and polyuria. The advantage of the model is the progression of the prediabetic phase, which is very similar to human disease, with infiltration of islet by immune cells about a week before hyperglycemia is observed. This model is suitable for intervention studies or for the search for predictive biomarkers. It is also possible to observe individual phases of pancreatic infiltration by immune cells. The advantage of congenic LEW mice is also the good viability after the manifestation of T1D (compared to NOD mice and BB rats).


title: Type 1 diabetes

text: The chemical compounds aloxan and streptozotocin (STZ) are commonly used to induce diabetes and destroy β-cells in mouse/rat animal models. In both cases, it is a cytotoxic analog of glucose that passes GLUT2 transport and accumulates in β-cells, causing their destruction. The chemically induced destruction of β-cells leads to decreased insulin production, hyperglycemia and weight loss in the experimental animal. The animal models prepared in this way are suitable for research into blood sugar-lowering drugs and therapies (e.g. for testing new insulin preparations). They are also The most commonly used genetically induced T1D model is the so-called AKITA mouse (originally C57BL/6NSIc mouse). The development of diabetes in AKITA mice is caused by a spontaneous point mutation in the Ins2 gene, which is responsible for the correct composition of insulin in the endoplasmic reticulum. Decreased insulin production is then associated with hyperglycemia, polydipsia and polyuria. If severe diabetes develops within 3–4 weeks, AKITA mice survive no longer than 12 weeks without treatment intervention. The description of the etiology of the disease shows that, unlike spontaneous models, the early stages of the disease are not accompanied by insulitis. AKITA mice are used to test drugs targeting endoplasmic reticulum stress reduction, to test islet transplants, and to study diabetes-related complications such as nephropathy, sympathetic autonomic neuropathy, and vascular disease. for testing transplantation therapies. Their advantage is mainly the low cost, the disadvantage is the cytotoxicity of the chemical compounds.


title: Type 1 diabetes

text: Viral infections play a role in the development of a number of autoimmune diseases, including human type 1 diabetes. However, the mechanisms by which viruses are involved in the induction of type 1 DM are not fully understood. Virus-induced models are used to study the etiology and pathogenesis of the disease, in particular the mechanisms by which environmental factors contribute to or protect against the occurrence of type 1 DM. Among the most commonly used are Coxsackie virus, lymphocytic choriomeningitis virus, encephalomyocarditis virus, and Kilham rat virus. Examples of virus-induced animals include NOD mice infected with coxsackie B4 that developed type 1 DM within two weeks.


title: Ashley Young

text: Ashley Simon Young (born 9 July 1985) is an English professional footballer who plays as a winger or full-back for Premier League club Aston Villa, where he is club captain.


title: Ashley Young

text: Young started his career at Watford and made his first senior appearance in 2003 under manager Ray Lewington. He became a first team regular in the 2004–05 season and was one of Watford's key players in their promotion-winning 2005–06 season. In January 2007, he transferred to Aston Villa for an initial fee of £8 million where he won the PFA Young Player of the Year award in 2009. In June 2011, Young signed with Manchester United for a fee of around £17 million. He won five trophies at United, including the Premier League in 2013, the FA Cup in 2016 and the Europa League in 2017. In January 2020, Young signed for Inter Milan, with whom he won the Serie A title, becoming only the third Englishman to win Italy's top flight league.


title: Ashley Young

text: Young earned 39 caps for England between 2007 and 2018, scoring seven international goals. He was part of the squads for UEFA Euro 2012 and the 2018 FIFA World Cup, reaching the semi-finals of the latter.


title: Ashley Young

text: Young joined the Watford academy system at 10 years of age. He developed there until the summer of 2001, when he was informed by the club that he wouldn't receive a full scholarship and could look for another team. Despite being turned away, Young stayed on at the club on a part-time basis and endeavoured to improve himself as a player and prove he could make it to the first team. He started to train with the Under-18s, despite being 16, and was starting games by the end of the season. He progressed on to the Under-21s and was eventually offered a professional deal by the club. The 18-year-old was handed his first-team debut under Ray Lewington in September 2003, scoring as a substitute against Millwall. He achieved five substitute appearances that season, scoring three goals, and made his first start for the club in the League Cup. Young came to prominence in the 2004–05 season, playing a part in 34 of Watford's league matches as they struggled to survive in the Championship. Although he failed to find the net, his performance during this season earned him the club's Young Player of the Season award.


title: Ashley Young

text: Under Aidy Boothroyd in the 2005–06 season, Young was given a new lease of life as a striker and right winger. Young started 41 League matches, finding the net 15 times, including a playoff semi-final goal against Crystal Palace, as Watford qualified for the play-offs and eventually beat Leeds United 3–0 to gain promotion to the Premier League. During that season, Young scored a number of spectacular goals, including free-kicks against Plymouth Argyle and Leeds, a shot into the top corner from 30 yards out against Coventry City, and a curling shot against Queens Park Rangers. It was during this season, though, that Young was sent off for the first time in his career, in the local derby away at Luton Town.


title: Ashley Young

text: Young began Watford's 2006–07 Premier League season well, scoring three times in the league, including a last minute strike in a 3–3 draw with Fulham (he had also scored Watford's second goal in the match), and a goal against Middlesbrough, in Watford's first win of the season in October. He also scored a free-kick in a 2–1 home win over Hull City in the League Cup. In the January 2007 transfer window, three unnamed clubs made £5 million offers for the under-21 international. Watford rejected these approaches, as well as an offer of £7 million, again from an unnamed club. An improved offer of nearly £10 million from West Ham United was accepted. However, Young rejected the move, opting to wait for offers from clubs for whom relegation was not an issue.


title: Ashley Young

text: On 23 January 2007, Aston Villa completed the signing of Young for a fee of £8 million (rising to £9.65 million with add-ons). At the time, this was the highest fee Aston Villa had ever paid for a player. On 31 January 2007, he scored on his debut for Villa at St James' Park against Newcastle United, but Villa went on to lose 3–1. Young started the 2007–08 season well, receiving several Man of the Match awards, culminating in a call-up to the England squad.


title: Ashley Young

text: In the 2007–08 Premier League season, Young finished second to Cesc Fàbregas in assists with 17. Young was included in the Premier League Team of the Year, and apart from Portsmouth's David James, was the only other player who did not come from any of the 'Big Four' (Chelsea, Arsenal, Liverpool and Manchester United) to make it into the best XI of the season.


title: Ashley Young

text: On 20 April 2008, Young scored two goals and assisted two goals for Aston Villa against Birmingham City at Villa Park and Villa went on to win the match 5–1. He also scored the winner against Danish club Odense Boldklub in Villa's home leg of the UEFA Intertoto Cup third round. On 10 October 2008, Young won the Premier League Player of the Month award. This was due to his performances in the 2008–09 Premier League season. Having also won the award in April 2008, Young joins the list of players who have won the award more than once including Cristiano Ronaldo, Wayne Rooney and Steven Gerrard. On 7 December 2008, in the 3–2 win over Everton, Young scored two goals, one being an injury time winner after Everton's Joleon Lescott, a boyhood Villa fan, had equalised seconds earlier. Manager Martin O'Neill later described the player as being 'world-class' in the post-match press conference. Young signed a new four-year contract until 2012 on 4 November 2008. On 10 January 2009, Young was again awarded the Premier League Player of the Month award for December, along with O'Neill, who won the Manager of the Month award. He became the first ever player to win three Premier League Player of the Month awards in the same year. During a match against Sunderland on 18 January 2009, Young was sent off for a two-footed foul on Sunderland's Dean Whitehead. On 26 April 2009, he won the PFA Young Player of the Year award.


title: Ashley Young

text: On 24 August 2009, Young scored a penalty as Aston Villa won 3–1 against Liverpool at Anfield. He did, however, miss a penalty three days later in a home tie in the UEFA Europa League against Rapid Wien. Young won two penalties in the first half of the match (one that he missed, the other that was converted by James Milner) as Aston Villa were eliminated from the tournament on the away goals rule.


title: Ashley Young

text: During the 2010–11 season, Young became vice-captain of the club and played in a new free role behind the striker, allowing him to move from wing to wing and through the centre. Young scored his first goal of the 2010–11 season with a direct free-kick in the Premier League match at home to Bolton Wanderers on 18 September 2010. He ended the season with nine goals and fourteen assists in 39 appearances for Villa in all competitions. With one year left to run on his current contract, Young stated that he would not make a decision on his future until the end of the season. On 20 June 2011, new Villa manager Alex McLeish admitted that he was resigned to losing Young, stating, "It's not confirmed yet but it does seem likely."


title: Ashley Young

text: On 23 June 2011, Young completed a move to Manchester United for an undisclosed fee, reportedly around £17 million, having passed a medical the day before, beating Liverpool to the signing. He signed a five-year deal with the club. He was handed the number 18 shirt previously worn by Paul Scholes. He made his debut for United in a 3–2 derby win over Manchester City in the 2011 FA Community Shield, playing the full 90 minutes and making an assist.


title: Ashley Young

text: He made his league debut for United against West Bromwich Albion on 14 August 2011, setting up the first goal for Wayne Rooney and forcing an own goal after a run down the left flank and cross, in a 2–1 away win. He scored his first two goals for United on 28 August in an 8–2 victory against Arsenal at Old Trafford. Both occurring after cutting inside from the left flank and bending two right foot shots into the far corner. Young made his debut in the UEFA Champions League on 27 September 2011, scoring a headed goal in the 90th minute to help Manchester United to a 3–3 draw against Basel. After a long-term injury, Young returned on the field at Stamford Bridge in a 3–3 Premier League draw against Chelsea on 5 February 2012. On 16 February, he scored a goal for the lead in a Europa League 2–0 away win against Ajax at the Amsterdam Arena. On 4 March 2012, Young scored two goals and made an assist against Tottenham Hotspur at White Hart Lane in a 3–1 Premier League win. On 2 April, he scored in a 2–0 win against Blackburn Rovers at Ewood Park.


title: Ashley Young

text: After playing the position in pre-season, Young started in Louis van Gaal's first competitive game on 16 August 2014 as a wing-back in a 3–5–2 formation, which saw United lose 2–1 to Swansea City. He suffered a hamstring injury during a 1–1 draw against Stoke City on 1 January 2015. Young made his return on 3 February in a 3–0 win against Cambridge United, coming on in the 81st minute for Marcos Rojo. On 4 March, Young scored his first goal of the season in a 1–0 victory over Newcastle United. On 12 April, he was named Man of the Match after he scored the equalising goal and provided two assists in a 4–2 home win over Manchester City. He played an instrumental role in United's 2–1 win over Crystal Palace on 9 May, with him winning a penalty which Juan Mata converted and providing the assist for Marouane Fellaini's header, leading to him again being Man of the Match. In the following match on 17 May, Young again provided an assist, this time for Ander Herrera's volley against Arsenal, which finished in a 1–1 draw. Young spent the season playing both on the wing and at wing-back under Van Gaal, the latter being a position which the manager felt was his best.


title: Ashley Young

text: On 7 August 2015, Young signed a new three-year contract with Manchester United, keeping him at the club until June 2018, with the option to extend a further year. Young's appearances at the beginning of the season were slim, with him making only one start in United's opening seven Premier League games, this being in the opening game on 8 August 2015, a 1–0 win against Tottenham Hotspur. On 12 September, Young played through debutant Anthony Martial to score his first goal for United in a 3–1 victory against rivals Liverpool. Young returned to the starting XI at left-back on 4 October against Arsenal, ending in a 3–0 away defeat. He started at right-back against West Brom on 7 November, which ended in a 2–0 win for United; this was a position he frequently played during November, December and January due to injury to Antonio Valencia. On 2 January 2016, Young assisted Anthony Martial with a cross into the box to open the scoring against Swansea City, with the game ending in a 2–1 win for United. Young suffered a 'severe groin injury' against Liverpool on 17 January which led to him being sidelined for several months. He made his return on 10 April against Tottenham Hotspur, replacing Marcus Rashford at half time, playing upfront in a 3–0 defeat. The decision to play Young as a striker saw Van Gaal face heavy criticism, however the Dutchman defended his actions by explaining he "wanted more running in behind." Young scored his only goal of the season on 17 May, the last day of the Premier League, in a 3–1 win against AFC Bournemouth after coming on as a substitute for Anthony Martial. On 21 May, he won the FA Cup after defeating Crystal Palace 2–1 in the final after extra time, playing at both striker and left-back after replacing Marcus Rashford in the 72nd minute – marking his third domestic trophy with the club.


title: Ashley Young

text: The appointment of José Mourinho as manager led to Young's game time being limited in the first half of the season. His first appearance was on 15 September 2016 in the Europa League against Feyenoord, coming on as a 63rd-minute substitute for Juan Mata in a 1–0 loss. His first start was against Northampton Town in the EFL Cup on 21 September, with Young playing on the wing in a 3–1 victory. Young featured in the next two games as a substitute, against Leicester City in a 4–1 league victory on 24 September and on 29 September against Zorya Luhansk in a 1–0 win in the Europa League. From October to January, Young managed to only make four appearances – all of which came as starts at wing-back or at full-back. Despite being limited for chances, one of these came against rivals Liverpool on 17 October, in a 0–0 draw at Anfield. His next start came against Blackburn Rovers in the FA Cup on 19 February 2017, playing the full 90 minutes in the 2–1 away win. After this game Young started to play far more regularly, featuring heavily in March and April. He was an unused substitute for the 2017 EFL Cup Final against Southampton on 26 February, which United won 3–2. Young made his first assist of the season on 19 March against Middlesbrough, crossing the ball to Marouane Fellaini, who headed in the opening goal of a 3–1 victory. On 16 April, Young captained Manchester United for the first time in a 2–0 win against Chelsea. His season ended after suffering an injury against Celta Vigo in the Europa League semi-final first leg on 4 May, after coming on for Henrikh Mkhitaryan in the 78th minute.


title: Ashley Young

text: Young's first start of the campaign came at right-back on 12 September 2017 in a 3–0 win against Basel in the Champions League, assisting with the opening goal with a cross to Marouane Fellaini in the 35th minute, he was also captain for the match. His performance led him to start at left-back in United's 4–0 victory over Everton on 17 September. On 28 November, Young scored a brace for the first time since March 2012 against his former club Watford, the opening two goals, one of them being a 30-yard freekick into the top left corner, in a 4–2 win at Vicarage Road.


title: Ashley Young

text: In February 2019, Young signed a new contract with Manchester United until 2020. He was appointed as United's club captain in August 2019.


title: Ashley Young

text: Young scored the final goal of his Manchester United career on 12 December 2019, scoring the first in a 4-0 victory against AZ Alkmaar in the group stages of the Europa League.


title: Ashley Young

text: Young signed for Italian Serie A club Inter Milan on 17 January 2020 for the remainder of the 2019–20 season, with an option to extend for another season. The transfer fee was reportedly around €1.5 million (£1.28 million). He became one of three former Premier League players to have signed for Inter Milan in the same window, with Victor Moses and Christian Eriksen joining the club soon after. In his first game for the club, Young provided the assist for Lautaro Martínez in a 1–1 draw against Cagliari. He scored his first goal for the club in a 2–1 loss against Lazio on 16 February.


title: Ashley Young

text: Inter won the 2020–21 Serie A. Young became only the third Englishman to win the league title in Italy, the first being Jimmy Greaves in 1962 and Gerry Hitchens in 1963, also for the "Nerazzurri".


title: Ashley Young

text: On 17 June 2021, Young signed a one-year contract with Aston Villa to return to the club on a free transfer for a second spell. He officially joined Villa on 1 July, when his Inter contract expired. Young made his second debut for Villa on 14 August in a 3–2 defeat at former club Watford.


title: Ashley Young

text: On 10 June 2022, Young was released by Villa. He became a free agent on 1 July, but on 4 July, the club confirmed that Young had re-signed for another season until 2023. On 27 July, Young was named club captain for the upcoming season, with John McGinn being named on-field captain.


title: Ashley Young

text: On 10 October 2022, he scored from 25 yards against Nottingham Forest in a 1-1 away draw in the Premier League. It was his first goal in his second spell at Aston Villa, with his previous one for the Villains coming in 2011.


title: Ashley Young

text: As a result of his form for Watford during the 2005–06 season, in February 2006 Young earned a call-up to Peter Taylor's England Under-21 League squad to face an Italian Serie B squad alongside teammate Chris Eagles. Young started alongside Eagles in the 1–0 win, playing the first half. His continued form into the 2006–07 season earned him a first England under-21 call-up to face Switzerland in September 2006. Young played the last 15 minutes of the match as England scored a late goal to win 3–2, topping their group, and reaching a play-off for a place in the 2007 UEFA European Under-21 Championship. At the finals, Young played three times. He took part in the semi-final penalty shoot-out against hosts Netherlands, scoring twice in the shoot-out as England lost 13–12. From 2006 to 2007, he earned 10 caps for the under-21s.


title: Ashley Young

text: On 31 August 2007, Steve McClaren called Young up to the full England squad for the first time, to face Russia and Israel in the UEFA Euro 2008 qualifiers. He was again called up for the Euro 2008 qualifiers to face Estonia and Russia. On 16 November 2007, Young made his international debut, by coming on as a half-time substitute for England in a friendly against Austria. He has since appeared in the England friendly against Germany in November 2008, coming on as a second-half substitute. He was also part of the starting XI in Fabio Capello's England squad in the friendly against the Netherlands at the Amsterdam Arena on 12 August 2009. Young did not make the cut in Capello's 30-man squad for the 2010 World Cup in South Africa.


title: Ashley Young

text: On 12 October 2010, Young made his first start for England in a Euro 2012 qualifying match against Montenegro. He scored his first international goal in a friendly away to Denmark on 9 February 2011 in Copenhagen, which was the winning goal. Young also scored again against Switzerland on 4 June 2011, as he got the equaliser with a volley from the edge of the area, after coming off the bench for Frank Lampard at half-time. On 6 September 2011, Young scored the only goal for England in a Euro 2012 qualifying 1–0 win against Wales. On 7 October 2011, he scored England's first goal away against Montenegro, and set up Darren Bent for the second. England drew the match 2–2 to secure qualification for UEFA Euro 2012. On 29 February 2012, Young scored his fifth international goal in a 3–2 home loss to the Netherlands in a friendly match played at Wembley Stadium.


title: Ashley Young

text: On 26 May 2012, Young scored his sixth, as well as his fourth straight, international goal in a UEFA Euro 2012 warm-up match against Norway. He became the first English footballer since Wayne Rooney to score in four straight international appearances. In his next match for England against Belgium he provided the assist for England's first goal. Young played in all four of England's matches at Euro 2012, culminating with a quarter-final defeat to Italy on penalties; Young was one of two England players to miss his penalty as Italy won 4–2 to reach a semi-final against Germany. He and the other unsuccessful player, Ashley Cole, faced online racial abuse for the miss, which was investigated by the police.


title: Ashley Young

text: After not being called up to the national team for almost four years, Young was recalled by Gareth Southgate for the upcoming friendly matches against Germany and Brazil on 2 November 2017. He featured in the latter game on 14 November, coming on for Ryan Bertrand in the 80th minute, seeing out a 0–0 draw.


title: Ashley Young

text: Young was named in Southgate's 23-man squad for the 2018 FIFA World Cup. He was England's first-choice left-back in Russia, playing the entirety of their first two group matches against Tunisia and Panama. With qualification for the knockout stage secure after winning both matches, Young was rested for the final game against Belgium, before returning for the round of 16 tie against Group H winners Colombia. That match went to extra time, but Young was replaced by Danny Rose 12 minutes into the additional period and played no part in the penalty shoot-out after the match finished as a 1–1 draw. England won 4–3 on penalties and progressed to a quarter-final against Sweden, against whom Young again played the full 90 minutes as England won 2–0, with Young providing the assist for Harry Maguire's opening goal from a corner. In the semi-final against Croatia, Young again started the match, but was again replaced by Rose at the start of extra time, with the score at 1–1 after 90 minutes. England ultimately lost the match 2–1 after extra time, and Young did not play in the third-place play-off against Belgium.


title: Ashley Young

text: Young has played in a variety of positions: though chiefly a winger, he has also experienced game-time as a forward – under Boothroyd at Watford and once under Van Gaal at Manchester United – as well as in a free role behind the striker for Aston Villa.


title: Ashley Young

text: During his later years at United, Young was re-invented as a defender, deployed as a left-sided full-back or wing-back. "WhoScored"s Martin Laurence stated in 2018 that "Luke Shaw can't get a kick at Manchester United and that is down to the form of Ashley Young, who has adapted to another new role superbly. Young is now proving to be an aggressive and intelligent defender, all while still offering a threat going forwards with his delivery into the box. On current form the 32-year-old shouldn't just make the cut, but be considered as England's first choice." On 12 September 2017 Young was being deployed as a right-back in a 3–0 win against Basel in the Champions League, assisting with the opening goal with a cross to Marouane Fellaini in the 35th minute, Young was also captain for the match.


title: Ashley Young

text: Ashley Young has courted controversy, having been accused of diving by the press and has been spoken to by former managers Sir Alex Ferguson and David Moyes about diving to gain an unfair advantage.


title: Ashley Young

text: Young was born in Stevenage, Hertfordshire. He has one older brother and two football-playing younger brothers, Lewis, who made his debut for Watford in 2008, and Kyle, who in April 2009 was training at the Arsenal Academy. Young attended The John Henry Newman School in Stevenage, and played school football alongside Formula One driver Lewis Hamilton, who was in the same year. Young's Jamaican-born father supports Tottenham Hotspur, while Young himself, like his older brother, favoured Arsenal. His hero and "role model on and off the pitch" was Ian Wright. Young has been married to Nicky Pike since June 2015. They had planned a wedding in 2011 but called it off two days before.


title: China–India relations

text: China–India relations (; ), also called Sino-Indian relations or Indo–Chinese relations, refers to the bilateral relationship between the People’s Republic of China (PRC) and the Republic of India. India and China have historically maintained peaceful relations for thousands of years of recorded history, but the harmony of their relationship has varied in modern times, after the Chinese Communist Party's victory in the Chinese Civil War in 1949, and especially post the Annexation of Tibet by the People's Republic of China. The two nations have sought economic cooperation with each other, while frequent border disputes and economic nationalism in both countries are a major point of contention.


title: China–India relations

text: Cultural and economic relations between China and India date back to ancient times. The Silk Road not only served as a major trade route between India and China, but is also credited for facilitating the spread of Buddhism from India to East Asia. During the 19th century, China was involved in a growing opium trade with the East India Company, which exported opium grown in India. During World War II, both British India and the Republic of China (ROC) played a crucial role in halting the progress of Imperial Japan. After India became independent in 1947, it established relations with the ROC. The modern Sino-Indian diplomatic relationship began in 1950, when India was among the first noncommunist countries to end formal relations with the Republic of China and recognise the PRC as the legitimate government of both Mainland China and Taiwan. China and India are two of the major regional powers in Asia, and are the two most populous countries and among the fastest growing major economies in the world. Growth in diplomatic and economic influence has increased the significance of their bilateral relationship.


title: China–India relations

text: Relations between contemporary China and India have been characterised by border disputes, resulting in three military conflicts – the Sino-Indian War of 1962, the border clashes in Nathu La and Cho La in 1967, and the 1987 Sumdorong Chu standoff. However, since the late 1980s, both countries have successfully rebuilt diplomatic and economic ties. Since 2008, China has been India's largest trading partner and the two countries have also extended their strategic and military relations.


title: China–India relations

text: Since 2013, border disputes have reemerged to take centrestage in the two countries' mutual relations. In early 2018, the two armies got engaged in a standoff at the Doklam plateau along the disputed Bhutan-China border. Since summer 2020, armed standoffs and skirmishes at multiple locations along the entire Sino-Indian border escalated. A serious clash occurred in the Galwan Valley resulting in the death of 20 Indian soldiers and 42 Chinese soldiers.


title: China–India relations

text: Despite growing economic and strategic ties, there are a lot of hurdles for India and the PRC to overcome. India has a large trade deficit that is favoured towards China. The two countries failed to resolve their border dispute and Indian media outlets have repeatedly reported Chinese military incursions into Indian territory. Both countries have steadily established military infrastructure along border areas including amidst the 2020 China–India skirmishes. Additionally, India remains wary about China's strong strategic bilateral relations with Pakistan, and China's funding to the separatist groups in Northeast India, while China has expressed concerns about Indian military and economic activities in the disputed South China Sea as well as hosting of anti-China activity from Tibetan exiles.


title: China–India relations

text: China and India are separated by the Himalayas. China and India today share a border with Nepal and Bhutan acting as buffer states. Parts of the disputed Kashmir and Ladakh region claimed by India are claimed and administered by either Pakistan (Azad Kashmir and Gilgit and Baltistan) or by the PRC (Aksai Chin). The Government of Pakistan on its maps shows the Aksai Chin area as mostly within China and labels the boundary "Frontier Undefined" while India holds that Aksai Chin is illegally occupied by the PRC. China and India also dispute most of Arunachal Pradesh.


title: China–India relations

text: Etched carnelian beads of Indus valley origin have been excavated from various archaeological sites in China dating from Western Zhou and Spring and Autumn period (early half of 1st millennium BCE) to Han and Jin dynasties, indicating early cultural exchanges.


title: China–India relations

text: China and India have also had some contact before the transmission of Buddhism. References to a people called the "Chinas", are found in ancient Indian literature. The Indian epic "Mahabharata" (c. 5th century BCE) contains references to "China", which may have been referring to the Qin state which later became the Qin dynasty. Chanakya (c. 350–283 BCE), the prime minister of the Maurya Empire refers to Chinese silk as "cinamsuka" (Chinese silk dress) and "cinapatta" (Chinese silk bundle) in his "Arthashastra".


title: China–India relations

text: The first records of contact between China and India were written during the 2nd century BCE, especially following the expedition of Zhang Qian to Central Asia (138–114 BCE). Buddhism was transmitted from India to China in the 1st century CE. Trade relations via the Silk Road acted as economic contact between the two regions. In the "Records of the Grand Historian", Zhang Qian (d. 113 BCE) and Sima Qian (145–90 BCE) make references to "Shendu", which may have been referring to the Indus Valley (the Sindh province in modern Pakistan), originally known as "Sindhu" in Sanskrit. When Yunnan was annexed by the Han dynasty in the 1st century, Chinese authorities reported an Indian "Shendu" community living there.


title: China–India relations

text: "A" greco Roman text Periplus of the Erythraean Sea (mid 1st century AD) describes the annual fair in present-day Northeast India, on the border with China.


title: China–India relations

text: From the 1st century onwards, many Indian scholars and monks travelled to China, such as Batuo (fl. 464–495 CE)—first abbot of the Shaolin Monastery—and Bodhidharma—founder of Chan/Zen Buddhism—while many Chinese scholars and monks also travelled to India, such as Xuanzang (b. 604) and I Ching (635–713), both of whom were students at Nalanda University in Bihar. Xuanzang wrote the "Great Tang Records on the Western Regions", an account of his journey to India, which later inspired Wu Cheng'en's Ming dynasty novel "Journey to the West", one of the Four Great Classical Novels of Chinese literature. According to some, St. Thomas the Apostle travelled from India to China and back (see Perumalil, A.C. "The Apostle in India". Patna, 1971: 5–54.)


title: China–India relations

text: The Cholas maintained good relationship with the Chinese. Arrays of ancient Chinese coins have been found in the Cholas homeland (i.e. Thanjavur, Tiruvarur and Pudukkottai districts of Tamil Nadu, India).


title: China–India relations

text: Under Rajaraja Chola and his son Rajendra Chola, the Cholas had strong trading links with Chinese Song dynasty. The Chola dynasty had strong influence over the present day Indonesia (Sri Vijaya Empire )


title: China–India relations

text: Many sources describe Bodhidharma, the founder of the Zen school of Buddhism in China, as a prince of the Pallava dynasty.


title: China–India relations

text: During the 7th century, Tang dynasty China gained control over large portions of the Silk Road and Central Asia. Wang Xuance had sent a diplomatic mission to northern India, which was embroiled by civil war just following the death of Emperor Harsha (590–647). After the murder of 30 members of this mission by the usurper claimants, Wang fled, and returned with allied Nepali and Tibetan troops to back the opposition. With his forces, Wang captured the capital, while his deputy Jiang Shiren (蒋师仁) captured the usurper and sent him back to Emperor Taizong (599–649) in Chang'an as a prisoner.


title: China–India relations

text: During the 8th century, the astronomical table of sines by the Indian astronomer and mathematician, Aryabhatta (476–550), were translated into the Chinese astronomical and mathematical book of the "Treatise on Astrology of the Kaiyuan Era" ("Kaiyuan Zhanjing"), compiled in 718 CE during the Tang Dynasty. The "Kaiyuan Zhanjing" was compiled by Gautama Siddha, an astronomer and astrologer born in Chang'an, and whose family was originally from India. He was also notable for his translation of the Navagraha calendar into Chinese.


title: China–India relations

text: A rich merchant from the Ma'bar Sultanate, Abu Ali (P'aehali) 孛哈里 (or 布哈爾 Buhaer), was associated closely with the Ma'bar royal family. After a fallout with the Ma'bar family, he moved to Yuan dynasty China and received a Korean woman as his wife and a job from the Emperor, the woman was formerly 桑哥 Sangha's wife and her father was 蔡仁揆 채송년 Ch'ae In'gyu during the reign of 忠烈 Chungnyeol of Goryeo, recorded in the Dongguk Tonggam, Goryeosa and 留夢炎 Liu Mengyan's 中俺集 Zhong'anji. 桑哥 Sangha was a Tibetan. Tamil Hindu Indian merchants traded in Quanzhou during the Yuan dynasty. Hindu statues were found in Quanzhou dating to this period.


title: China–India relations

text: According to Badauni and Ferishta, The Delhi Sultanate under Muhammad bin Tughluq had ambitions to invade China. There existed a direct trade relationship between China and the Delhi Sultanate. Ibn Battuta mentions that the Yuan Emperor had sent an embassy to Muhammad for reconstruction of a sacked temple at Sambhal.


title: China–India relations

text: Between 1405 and 1433, Ming dynasty China sponsored a series of seven naval expeditions led by Admiral Zheng He. Zheng He visited numerous Indian kingdoms and ports, including Malabar coast, Bengal, and Ceylon, Persian Gulf, Arabia, and later expeditions ventured down as far as Malindi in what is now Kenya. Throughout his travels, Zheng He liberally dispensed Chinese gifts of silk, porcelain, and other goods. In return, he received rich and unusual presents, including African zebras and giraffes. Zheng He and his company paid respect to local deities and customs, and in Ceylon they erected a monument (Galle Trilingual Inscription) honouring Buddha, Allah, and Vishnu. Bengal sent twelve diplomatic missions to Nanjing between 1405 and 1439.


title: China–India relations

text: After the Ming treasure voyages, private Chinese traders continued operating in the eastern Indian Ocean. Chinese junks could frequently be seen in the ports of the Vijayanagara Empire, carrying silks and other products. The ports of Mangalore, Honavar, Bhatkal, Barkur, Cochin, Cannanore, Machilipatnam, and Dharmadam were important for they provided secure harbors for traders from China. On the other hand, Vijayanagara exports to China intensified and included cotton, spices, jewels, semi-precious stones, ivory, rhino horn, ebony, amber, coral, and aromatic products such as perfumes.


title: China–India relations

text: The Mughals may have attempted to reach the Chinese market. According to East India Company official William Hawkins, Emperor Jahangir's wardrobe master was ordered to replace a valuable porcelain. To fulfill the task, the wardrobe master travelled to China but found nothing of equivalent value.


title: China–India relations

text: The Bhois of Orissa maintained minor maritime trade links with China. This is noted from the Manchu language memorials and edicts depicting contacts under the reign of Qing dynasty in China, when the Qianlong Emperor received a gift from the Brahmin (Ch. Polomen 婆羅門, Ma. Bolomen) envoy of a ruler whose Manchu name was Birakišora han of Utg’ali (Ch. Wutegali bilaqishila han 烏特噶里畢拉奇碩拉汗), who is described as a ruler in Eastern India. Hence referring to Birakisore Deva I of Khurda (1736–1793) who styled himself as Gajapati, the ruler of Utkala. Many of the gosains entering Tibet from China passed through his territory when visiting the Jagannath temple at Puri.


title: China–India relations

text: The reign of Tipu Sultan in Mysore saw Chinese technology used for sugar production, and sandalwood was exported to China. Tipu’s and Mysore’s tryst with silk began in the early 1780s when he received an ambassador from the Qing dynasty-ruled China at his court. The ambassador presented him with a silk cloth. Tipu was said to be enchanted by the item to such an extent that he resolved to introduce its production in his kingdom. He sent a return journey to China, which returned after twelve years.


title: China–India relations

text: After the Qing expansion into the Himalayas, there was increased contact with South Asia which often manifested in the form of tributary relations. The Qing were obliged to defend their subservient state, Badakhshan, against the Afghans and Marathas, though no major clash with the Marathas ever took place. The Afghans gained the initiative and defeated the Marathas at Panipat in 1761. The battle's outcome was used by the Afghans to intimidate the Qing.


title: China–India relations

text: In the 18th to 19th centuries, the Sikh Empire expanded into neighbouring lands. It had annexed Ladakh into the state of Jammu in 1834. In 1841, they invaded Tibet and overran parts of western Tibet. Chinese forces defeated the Sikh army in December 1841, forcing the Sikh army to withdraw, and in turn entered Ladakh and besieged Leh, where they were in turn defeated by the Sikh Army. At this point, neither side wished to continue the conflict. The Sikhs claimed victory. as the Sikhs were embroiled in tensions with the British that would lead up to the First Anglo-Sikh War, while the Chinese were in the midst of the First Opium War. The two parties signed a treaty in September 1842, which stipulated no transgressions or interference in the other country's frontiers.


title: China–India relations

text: Indian soldiers, known as "sepoys" who were in British service participated in the First and Second Opium Wars against Qing China. Indian sepoys were also involved in the suppression of the Boxer Rebellion in 1900, in addition to serving as guards in the British colony of Hong Kong and foreign concessions such as the Shanghai International Settlement. The Chinese slur "Yindu A San" (Indian number three) was used to describe Indian soldiers in British service.


title: China–India relations

text: Hu Shih, the Chinese ambassador to the United States from 1938 to 1942, commented, albeit critically, on India's Buddhism almost completely subsuming Chinese society upon its introduction.


title: China–India relations

text: ASIA is one. The Himalayas divide, only to accentuate, two mighty civilizations, the Chinese with its communism of Confucius, and the Indian with its individualism of the Vedas. But not even the snowy barriers can interrupt for one moment that broad expanse of love for the Ultimate and Universal, which is the common thought-inheritance of every Asiatic race, enabling them to produce all the great religions of the world and distinguishing them from those maritime peoples of the Mediterranean and the Baltic, who love to dwell on the Particular, and to search out the means, not the end, of life.


title: China–India relations

text: While never having actually visited India in his lifetime, Sun Yat-sen, founder of the Republic of China, occasionally spoke and wrote of India as a fellow Asian nation that was likewise subject to harsh Western exploitation, and frequently called for a Pan-Asian united front against all unjust imperialism; in a 1921 speech, Sun stated: "The Indians have long been oppressed by the British. They have now reacted with a change in their revolutionary thinking...There is progress in their revolutionary spirit, they will not be cowed down by Britain." To this day, there is a prominent street named Sun Yat-sen street in an old Chinatown in Calcutta, now known as Kolkata.


title: China–India relations

text: In 1924, on his major tour of several major Chinese cities giving lectures about using their shared Asian values and traditional spirituality to help together promote world peace, Rabindranath Tagore was invited to Canton by Sun Yat-sen, an invitation which he declined. There was considerably mixed reception to Tagore from the Chinese students and intellectuals; for example, a major Buddhist association in Shanghai stated that for seven hundred years, they had "waited for a message from India", while others, mostly modernizers and communists, outright rejected his ideals, stating that they did not "want philosophy, we want materialism" and "not wisdom, but power".


title: China–India relations

text: Believing that then-Republican China and British India were "sister nations from the dawn of history" who needed to transform their "ancient friendship into a new camaraderie of two freedom loving nations", Jawaharlal Nehru visited China in 1939 as an honored guest of the government. Highly praising both Chiang Kai-shek and his wife Song Meiling, Nehru referred to Chiang as "not only a great Chinese but a great Asiatic and world figure...one of the top most leaders of the world...a successful general and captain in war", and Song as "full of vitality and charm...a star hope for the Chinese people...a symbol of China's invincibility". During his visit, Chiang and Nehru shared a bunker one night when Japanese bombers attacked Chongqing in late August, with Chiang recording a favorable impression of Nehru in his diary; the Chiangs also regularly wrote Nehru during his time in prison and even after their 1942 visit to India.


title: China–India relations

text: Partially to enlist India's aid against both Japanese and Western imperialism in exchange for China's support for Indian independence, the Chiangs visited British India in 1942 and met with Nehru, Mahatma Gandhi and Muhammad Ali Jinnah. The Chiangs also sought to present their nation as a potential third option for the Indian people to ally themselves with, with public sympathies at the time sharply split between the British and the Japanese, who actively tried to sway India's population with pledges to liberate Asia if they would help their efforts against the British. Despite pledges of mutual friendship and future cooperation between the two peoples, Chiang argued that while Gandhi's non-violent resistance was not necessarily invalid for the Indian people, it was an unrealistic worldview on a global context; Gandhi, who had at the time insisted on India refraining from participating in any war unless India was first given complete independence, in turn later noted that, although "fun was had by all...I would not say that I had learnt anything, and there was nothing that we could teach him." In their meeting in Calcutta, Jinnah tried to persuade Chiang, who had pressed Britain to relinquish India as soon as possible, of the necessity of establishing a separate nation for Muslims in the subcontinent, to which Chiang, who apparently recognized the Indian National Congress as the sole nationalist force in the country, replied that if ten crores of Muslims could live peacefully with other communities in China, then there was no true necessity as he saw it of a separate state for a smaller population of nine crores of Muslims living in India. While the public reception to the Chiangs was mostly positive, some reacted less favorably to the Chiangs' presence in India, with Jinnah believing that Chiang Kai-shek lacked proper understanding of Indian society and feeling he was biased in favor of Nehru and Gandhi while neglecting the demands of other religious communities, his newspaper "Dawn" calling him a "meddlesome marshal", while other Indian Muslims such as Muhammad Zafarullah Khan expressed mistrust for the couple's motives, believing that their government wanted to eventually expand its influence to Indochina and the subcontinent after the British departure.


title: China–India relations

text: For his part, Chiang apparently believed none of the major Indian leaders could help his government meaningfully. As an ardent nationalist who lived through China's internally turbulent years, he felt that Jinnah was "dishonest" and was being used by the British to divide the peoples of India and by extension Asia, with he and his wife Song believing that cooperation between Indian religious communities was difficult but possible. At the same time, he also felt genuinely disappointed by Gandhi, whom he initially had high expectations, and noted afterwards that "he knows and loves only India, and doesn't care about other places and peoples". Having been unable to make Gandhi change his views about satyagraha, even after arguing that some of their enemies such as the Japanese would make the preaching of non-violence impossible, Chiang, himself raised a Buddhist, blamed "traditional Indian philosophy" for his sole focus on endurance of suffering rather than revolutionary zeal necessary to rally and unite the Asian peoples. Nevertheless, the Chiangs continued to commit themselves to supporting the Indian independence movement from afar, mostly via diplomacy, with Song Meiling writing to Nehru encouragingly: "We shall leave nothing undone in assisting you to gain freedom and independence. Our hearts are drawn to you, and...the bond of affection between you and us has been strengthened by our visit...When you are discouraged and weary...remember that you are not alone in your struggle, for at all times we are with you in spirit."


title: China–India relations

text: Although their meetings had ended on a positive note, with Gandhi offering to adopt Song as a "daughter" in his ashram if Chiang left her there as his ambassador to India after she asked to be taught about his non-violent principles, and giving her his spinning wheel as a farewell gift, both sides were met with considerable obstacles in the aftermath. After the Chiangs tried to seek U.S. President Franklin Roosevelt's help in persuading Winston Churchill to give India independence during the war, Roosevelt suggested splitting India's territory in two in the hopes of resolving tensions, to which Song replied that both she and Chiang felt that "India was as indivisible as China". Gandhi wrote to Chiang shortly afterwards, seeking to clarify his stance: "I need hardly give you my assurance that, as the author of the new move in India, I shall take no hasty action. And whatever action I may recommend will be governed by the consideration that it should not injure China, or encourage Japanese aggression. I am trying to enlist world opinion in favor of a proposition which to me appears self-proved and which must lead to the strengthening of India and China's defence." Chiang sent a cable to Washington upon reading Gandhi's letter, and advised Roosevelt that the best course of action would be to "restore complete freedom" to India, but Churchill reportedly threatened to end Britain's alliance with China should the Chiangs continue to try to interfere with Indian affairs.


title: China–India relations

text: In 1942, a division of the Kuomintang's armies entered India as the Chinese Army in India in their struggle against Japanese expansion in Southeast Asia. Dwarkanath Kotnis and four other Indian physicians traveled to the war-torn China to provide medical assistance against the Imperial Japanese Army.


title: China–India relations

text: On 15 August 1947, India gained independence from the British. The newly independent India established diplomatic relations with the ROC. On 1 October 1949, the Chinese People's Liberation Army defeated the Kuomintang (the ROC's ruling Nationalist Party) and took over Mainland China, establishing the PRC. Soon afterwards, India became a federal, democratic republic after its constitution came into effect on 26 January 1950.


title: China–India relations

text: India established diplomatic relations with the PRC on 1 April 1950, the first non-communist/socialist nation in Asia to do so. Pakistan continued to recognize the ROC until 1951.


title: China–India relations

text: The relationship between India and a newly communist China started out on an optimistic note. Jawaharlal Nehru, the first prime minister of India, and Chinese premier Zhou Enlai articulated a vision of an internationalist foreign policy governed by the ethics of the Panchsheel (Five Principles of Peaceful Coexistence). However, there was notable skepticism on the Indian side from the very beginning about Chinese intentions. For example, Bhimrao Ambedkar was surprised that Nehru took Panchsheel seriously while Acharya Kriplani said that Panchsheel was "born in sin". Nehru himself was disappointed when it became clear that the two countries had a conflict of interest in Tibet, which had traditionally served as a buffer zone.


title: China–India relations

text: China viewed Tibet as a part of its territory. The preceding government of the Republic of China under Chiang Kai-shek also claimed Tibet as Chinese territory, however was unable to re-assert control. Mao saw Indian concern over Tibet as a manifestation of interference in the internal affairs of the PRC. The PRC reasserted control over Tibet and to end Tibetan Buddhism and feudalism, which it did by force of arms in 1950. To avoid antagonizing the PRC, Nehru informed Chinese leaders that India had no political ambitions or territorial ambitions and did not seek special privileges in Tibet but that traditional trading rights must continue. With Indian support, Tibetan delegates signed an agreement in May 1951 recognizing PRC sovereignty but guaranteeing that the existing political and social system of Tibet would continue.


title: China–India relations

text: In October 1954, China and India signed an agreement regarding Tibet, whereby India recognised Tibet as part of China with China accepting the continuance of the previous trade arrangements. Observers noted the agreement heavily favoring China.