Diabetes and ADICOL
Diabetes is as old as mankind itself. Descriptions of a disease with symptoms typical for diabetes were found in the Papyrus Ebers (1500 B.C.) of Ancient Egyptians. In the first century A.C. Arataeus of Cappadocia gave the disease its name. "Diabetes" derives from the Greek word "diabainein" which means "passing through". It describes the passage of large amounts of urine and intense thirst.
The sweet taste of urine was first mentioned by the ancient Hindus in Ayur Veda. They noticed ants congregating around the urine of certain patients and associated this with certain diseases. In 1775 M. Dobson proved that the sweet taste of diabetic urine was due to sugar. He made the crucial observation of the excess of sugar in blood. In 1788 T. Cawley observed that the pancreas of a patient who had died of diabetes showed stones and tissue damage. C. Bernard (1813-1878) discovered that the liver stored glycogen and secreted sugary substances into the blood. He assumed that it was an excess of this secretion which caused diabetes. In 1879 it was discovered that removing the pancreas caused diabetes. In 1901 E. Lindsay Opie, found that an alteration of the islets of Langerhans was connected with diabetes which later lead to the idea that the antidiabetic substance might come from this tissue. Sir F. Grant Banting, could obtain insulin by chemical methods of extraction in 1921: For the first time levels of blood glucose were lowered and a fatal disease had been controlled. Before the discovery of insulin, successful pregnancy in diabetic woman was a rarity and diabetic pregnancy became one of the most successful chapters in the story of diabetes care. The earlier insulin preparations were crude and impure. The first patients had to endure injections of 5-10 ml intramuscularly. In 1936 the important biochemical differences between the insulin sensitivity in type 1 and insulin resistance in type 2 diabetes was demonstrated.
Since the eighties self monitoring of blood glucose revolutionised life for diabetic patients. One of the most effective ways to control the glucose concentration is the intensified treatment. It leads to a better metabolic control that can significantly reduce the onset and progressing of the microvascular and neuropathic complications of insulin-dependent diabetes. With insulin pumps the injection of insulin is more physiological. By trying to close the loop between a continuous measurement of blood glucose and thereafter the infusion of insulin with a pump ADICOL aims to become a further attainment in diabetes treatment.
Under the scientific leadership of the Swiss Disetronic Medical Systems AG the ADICOL Consortium comprises 7 groups from all over Europe. The financial lead of the project lies with Fraunhofer Institut f端r Siliziumtechnologie ISiT. Disetronic is responsible for the dosing system. The two partners ISiT and SensLab work on biosensors. Medical expertise is represented by the University of Perugia as well as by the University of Graz. The Modelling software will be developed by the City University and the company Judex Datasystems A/S.
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Definition of diabetes
An international Committee (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus), working under the sponsorship of the American Diabetes Association (ADA), was established in May 1995 to review the scientific literature since 1979 and finally published a document to define and to classify diabetes, of which you will find an extract below.
For the entire definition please consult: The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, Clinical Practice Recommendations 2000, Diabetes Care, Vol. 23, Sup. 1.]
Diabetes mellitus is a group of metabolic diseases characterized by hyperglycaemia resulting from defects in insulin secretion, insulin action, or both. The chronic hyperglycaemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels.
Several pathogenic processes are involved in the development of diabetes. These range from autoimmune destruction of the beta-cells of the pancreas with consequent insulin deficiency to abnormalities that result in resistance to insulin action. The basis of the abnormalities in carbohydrate, fat, and protein metabolism in diabetes is deficient action of insulin on target tissues. Deficient insulin action results from inadequate insulin secretion and/or diminished tissue responses to insulin at one or more points in the complex pathways of hormone action. Impairment of insulin secretion and defects in insulin action frequently coexist in the same patient, and it is often unclear which abnormality, if either alone, is the primary cause of the hyperglycaemia.
Symptoms of marked hyperglycaemia include polyuria, polydipsia, weight loss, sometimes with polyphagia, and blurred vision. Impairment of growth and susceptibility to certain infections may also accompany chronic hyperglycaemia. Acute, life-threatening consequences of diabetes are hyperglycaemia with ketoacidosis or the nonketotic hyperosmolar syndrome.
Long-term complications of diabetes include retinopathy with potential loss of vision; nephropathy leading to renal failure; peripheral neuropathy with risk of foot ulcers, amputation, and Charcot joints; and autonomic neuropathy causing gastrointestinal, genitourinary, and cardiovascular symptoms and sexual dysfunction. Glycosylation of tissue proteins and other macromolecules and excess production of polyol compounds from glucose are among the mechanisms thought to produce tissue damage from chronic hyperglycaemia. Patients with diabetes have an increased incidence of atherosclerotic cardiovascular, peripheral vascular, and cerebrovascular disease. Hypertension, abnormalities of lipoprotein metabolism, and periodontal disease are often found in people with diabetes. The emotional and social impact of diabetes and the demands of therapy may cause significant psychosocial dysfunction in patients and their families.
The vast majority of cases of diabetes fall into two broad etiopathogenetic categories. In one category (type 1 diabetes), the cause is an absolute deficiency of insulin secretion. Individuals at increased risk of developing this type of diabetes can often be identified by serological evidence of an autoimmune pathologic process occurring in the pancreatic islets and by genetic markers. In the other, much more prevalent category (type 2 diabetes), the cause is a combination of resistance to insulin action and an inadequate compensatory insulin secretory response. In the latter category, a degree of hyperglycaemia sufficient to cause pathologic and functional changes in various target tissues, but without clinical symptoms, may be present for a long period of time before diabetes is detected. During this asymptomatic period, it is possible to demonstrate an abnormality in carbohydrate metabolism by measurement of plasma glucose in the fasting state or after a challenge with an oral glucose load.
Funding Diabetes Treatment
Conventional means of healthcare financing in the developed world are collective and treatment is typically provided free at the point of consumption or via insurance schemes. Costs and indebtedness incurred as a result of medical treatment, for example from paydayloans, can sometimes be recouped from insurers post-treatment but it is most often better to check beforehand unless in the event of a diabetic emergency. Orthodox treatments will typically be covered, but novel and new medical methods sometimes fall outside the remit of what insurers are prepared to pay.
Diabetes, Health Risks and Computer Use
We all know that getting too little exercise and spending too much time in front of our PCs is bad for our health, but it isn't just diabetes that we risk. Vision problems, chronic pain and obesity are all highly correlated with a sedentary lifestyle, but since Adicol is a project dedicated to the investigation and study of diabetes we thought we'd share a few facts with you first.
The risk of developing type 2 diabetes multiplies when one spends too much time sitting or in an otherwise sedentary position. Even current sufferers can improve their prognosis by embarking on a more active health regimen. This is because our bodies can learn to better utilise insulin through regular exercise. It is important to note, however, that the effect of exercise on improved insulin usage lasts just 48 hours and thereafter it is vital to sustain a regular routine. The good news is jumping out of your chair and getting active for just 30 minutes a day can dramatically offset these risks and improve your health prospects!
Check out a few more risks below!