The diet presents many potential health problems. The plan has been described as a “starvation diet” that involves consuming only 500 calories per day and promotes the use of laxatives to replace missing dietary fiber. It provides insufficient vitamins and dietary minerals to maintain health, recommending supplements instead, and does not incorporate any essential fatty acids. While most very low calorie diets are recommended being undertaken while closely supervised by a physician, Kimkins does not suggest this.

Side effects have been associated with the diet, including hair loss, amenorrhea and palpitations.

Adapted from the Wikipedia article Kimkins, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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Some causes of bowel obstruction may resolve spontaneously; many require operative treatment.

In adults, frequently the surgical intervention and the treatment of the causative lesion are required. In malignant large bowel obstruction, endoscopically placed self-expanding metal stents may be used to temporarily relieve the obstruction as a bridge to surgery, or as palliation.

Small bowel obstruction (SBO)

In the management of small bowel obstructions it is often said that “[n]ever let the sun rise or set on small-bowel obstruction” because they are sometimes fatal if treatment is delayed. This traditional surgical canon is no longer followed, largely because of improvements in radiologic imaging of small bowel obstruction, which allow confident distinction between simple obstructions, that can be treated conservatively, and obstructions associated with surgical emergencies (volvulus, closed-loop obstructions, ischemic bowel, incarcerated hernias, etc.).

A small flexible tube may be inserted from the nose into the stomach to help decompress the dilated bowel. This tube is uncomfortable but does relieve the abdominal cramps, distension and vomiting. Intravenous therapy is utilized and the urine output is monitored with a catheter in the bladder.

Most people with SBO are initially managed conservatively because in many cases, the bowel will open up. Some adhesions loosen up and the obstruction resolves. However, when conservative management is undertaken, the patient is examined several times a day and X rays are obtained to ensure that the individual is not getting clinically worse.

Conservative treatment involves insertion of a nasogastric tube, correction of dehydration and electrolyte abnormalities. Opioid pain relievers may be used for patients with severe pain. Antiemetics may be administered if the patient is vomiting. Adhesive obstructions often settle without surgery. If obstruction is complete a surgery is required.

Most patients do improve with conservative care in 2-5 days. However, in some occasions, the cause of obstruction may be a cancer and in such cases, surgery is the only treatment. These individuals undergo surgery where the cause of SBO is removed. Individuals who have bowel resection or lysis of adhesions usually stay in the hospital a few more days until they are able to eat and walk.

Small bowel obstruction caused by Crohn’s disease, peritoneal carcinomatosis, sclerosing peritonitis, radiation enteritis and postpartum bowel obstruction are typically treated conservatively, i.e. without surgery. Conversely, a small bowel obstruction in a “virgin abdomen” (an abdomen that has not seen an operation) is almost never treated conservatively.

Prognosis for SBO

The prognosis for most cases of SBO is excellent. Most non cancerous causes of SBO do well. However, when cancer is the cause of SBO, patients are generally worked up to ensure that there has been no spread. If the cancer is localized to the small bowel, the patient will do well. If the cancer has spread, then the individual may require radiation or chemotherapy.

Bowel obstruction in children

Fetal and neonatal bowel obstructions are often caused by an intestinal atresia, where there is a narrowing or absence of a part of the intestine. These atresias are often discovered before birth via a sonogram, and treated with using laparotomy after birth. If the area affected is small, then the surgeon may be able to remove the damaged portion and join the intestine back together. In instances where the narrowing is longer, or the area is damaged and cannot be used for a period of time, a temporary stoma may be placed.

Adapted from the Wikipedia article Bowel obstruction, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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Miconazole is mainly used externally for the treatment of athlete’s foot, ringworm and jock itch. Internal application is used for oral or vaginal thrush (yeast infection). In addition the oral gel may also be used for the lip disorder angular cheilitis.

It has an advantage over nystatin in the treatment of neonatal oral thrush in that the latter is only licensed in the UK for those over the age of one month; but note the possibility for drug interactions.

Adapted from the Wikipedia article Miconazole, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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In 2008, Senator Lathrop was appointed the Chair of the Developmental Disabilities Special Investigative Committee, which was given the responsibility to look more closely at the deteriorating conditions at the Beatrice State Developmental Center. Since that time, the Committee has done extensive work to gain a better understanding of the issues facing the facility and to provide additional oversight. The Committee has also reviewed community-based programs and the challenges facing the providers of services for individuals with a developmental disability who live in communities across Nebraska.

In 2009, Senator Lathrop introduced LB 236 to begin to reduce the waiting list for individuals with a developmental disability. When the bill was introduced nearly 2000 Nebraskans were awaiting services, many for several years. A part of that bill was amended into the state budget bill by the Appropriations Committee and in the last few months of 2009 hundreds of Nebraskans began to receive much needed services.

Adapted from the Wikipedia article Steve Lathrop, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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There is some medical evidence of various malformations, e.g., cardiac or facial deformations, when used in early pregnancy, however the data is not conclusive. The data are also inconclusive on whether benzodiazepines such as clonazepam cause developmental deficits or decreases in IQ in the developing fetus when taken by the mother during pregnancy. Clonazepam when used late in pregnancy may result in the development of a severe benzodiazepine withdrawal syndrome in the neonate. Withdrawal symptoms from benzodiazepines in the neonate may include hypotonia, apnoeic spells, cyanosis and impaired metabolic responses to cold stress.

The safety profile of clonazepam during pregnancy is less clear than for other benzodiazepines and if benzodiazepines are indicated during pregnancy chlordiazepoxide and diazepam may be a safer choice. The use of clonazepam during pregnancy should only be used if the clinical benefits are believed to outweigh the clinical risks to the fetus. Caution is also required if clonazepam is used during breast feeding. Possible adverse effects of use of benzodiazepines such as clonazepam during pregnancy include; abortion, malformation, intrauterine growth retardation, functional deficits, floppy infant syndrome, carcinogenesis and mutagenesis. Neonatal withdrawal syndrome associated with benzodiazepines include hypertonia, hyperreflexia, restlessness, irritability, abnormal sleep patterns, inconsolable crying, tremors or jerking of the extremities, bradycardia, cyanosis, suckling difficulties, apnea, risk of aspiration of feeds, diarrhea and vomiting, and growth retardation. This syndrome can develop between 3 days and 3 weeks after birth and can have a duration of up to several months. The pathway by which clonazepam is metabolised is usually impaired in new borns. If clonazepam is used during pregnancy or breast feeding it is recommended that serum levels of clonazepam are monitored and signs of central nervous system depression and apnea are also monitored for. In many cases non-pharmacological treatments such as relaxation therapy, psychotherapy and avoidance of caffeine can be an effective and safer alternative to use of benzodiazepines for anxiety in pregnant women.

Adapted from the Wikipedia article Clonazepam, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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Based on his clinical experience in plastic surgery, Lyons developed three central impressions: that there are different types of fat in the adult female body, including one he identified as structural brown fat; that the more brown fat a woman has, the leaner she tends to be; and that different types of fat can be moderated by lifestyle, diet, and exercise. In April 2009, the scientific community released information confirming Lyons’ impressions that fat could be rejuvenated by exercise and diet. While previously scientists postulated that brown fat only had physiologic relevance in rodents and newborn humans, several research studies , whose results were published in the ”New England Journal of Medicine article titled “[http://content.nejm.org/cgi/content/short/360/15/1509 Identification and Importance of Brown Adipose Tissue in Adult Humans],” confirmed that brown fat can be promoted with a healthy lifestyle.

Lyons developed a nutrition and exercise program for women designed to convert yellow fat into brown fat, with a goal of improving health and fitness without losing subcutaneous volume needed to prevent wrinkles, sagging, and other signs of aging. The plan, built on his experience as a bodybuilder and professional dancer, involved an eating cycle that alternates between days focused on proteins and carbohydrates. The exercise program focused on building a strong core to raise the metabolism and create a strong hub of lean muscle. On September 15, 2009, St Martins Press published Lyons’ book under the title ”The Brown Fat Revolution”. (ISBN 978-0-312-59540-1)

Adapted from the Wikipedia article James R. Lyons, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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Severe coeliac disease leads to the characteristic symptoms of pale, loose and greasy stool (steatorrhoea), weight loss or failure to gain weight (in young children). People with milder coeliac disease may have symptoms that are much more subtle and occur in other organs rather than the bowel itself. Finally, it is possible to have coeliac disease without any symptoms whatsoever. Many adults with subtle disease only have fatigue or anaemia.

Gastrointestinal

The diarrhoea that is characteristic of coeliac disease is (chronic) pale, voluminous and malodorous. Abdominal pain and cramping, bloatedness with abdominal distension (thought to be due to fermentative production of bowel gas) and mouth ulcers may be present. As the bowel becomes more damaged, a degree of lactose intolerance may develop. Frequently, the symptoms are ascribed to irritable bowel syndrome (IBS), only later to be recognised as coeliac disease; a small proportion of patients with symptoms of IBS have underlying coeliac disease, and screening for coeliac disease is recommended for those with IBS symptoms.

Coeliac disease leads to an increased risk of both adenocarcinoma (small intestine cancer) and lymphoma of the small bowel (enteropathy-associated T-cell lymphoma or EATL). This risk returns to baseline with diet. Longstanding and untreated disease may lead to other complications, such as ulcerative jejunitis (ulcer formation of the small bowel) and stricturing (narrowing as a result of scarring with obstruction of the bowel).

Malabsorption-related

The changes in the bowel make it less able to absorb nutrients, minerals and the fat-soluble vitamins A, D, E, and K.

* The inability to absorb carbohydrates and fats may cause weight loss (or failure to thrive/stunted growth in children) and fatigue or lack of energy.

* Anaemia may develop in several ways: iron malabsorption may cause iron deficiency anaemia, and folic acid and vitamin B12 malabsorption may give rise to megaloblastic anaemia.

* Calcium and vitamin D malabsorption (and compensatory secondary hyperparathyroidism) may cause osteopenia (decreased mineral content of the bone) or osteoporosis (bone weakening and risk of fragility fractures).

* A small proportion have abnormal coagulation due to vitamin K deficiency and are slightly at risk for abnormal bleeding.

* Coeliac disease is also associated with bacterial overgrowth of the small intestine, which can worsen malabsorption or cause malabsorption despite adherence to treatment.

Miscellaneous

Coeliac disease has been linked with a number of conditions. In many cases, it is unclear whether the gluten-induced bowel disease is a causative factor or whether these conditions share a common predisposition.

* IgA deficiency is present in 2.3% of patients with coeliac disease, and in turn, this condition features a tenfold increased risk of coeliac disease. Other features of this condition are an increased risk of infections and autoimmune disease.

* Dermatitis herpetiformis; this itchy cutaneous condition has been linked to a transglutaminase enzyme in the skin, features small-bowel changes identical to those in coeliac disease, and may respond to gluten withdrawal even if there are no gastrointestinal symptoms

* Growth failure and/or pubertal delay in later childhood can occur even without obvious bowel symptoms or severe malnutrition. Evaluation of growth failure often includes coeliac screening.

* Recurrent miscarriage and unexplained infertility.

* Hyposplenism (a small and underactive spleen); this occurs in about a third of cases and may predispose to infection given the role of the spleen in protecting against bacteria

* Abnormal liver function tests (randomly detected on blood tests)

Coeliac disease is associated with a number of other medical conditions, many of which are autoimmune disorders: diabetes mellitus type 1, autoimmune thyroiditis, primary biliary cirrhosis, and microscopic colitis.

A more controversial area is a group of diseases in which anti-gliadin antibodies (an older and non-specific test for coeliac disease) are sometimes detected, but no small bowel disease can be demonstrated. Sometimes, these conditions improve by removing gluten from the diet. This includes cerebellar ataxia, peripheral neuropathy, schizophrenia and autism.

Other grains

Wheat subspecies (such as spelt, semolina and durum) and related species such as barley, rye, triticale and Kamut also induce symptoms of coeliac disease. A small minority of coeliac patients also react to oats. It is most probable that oats produce symptoms due to cross contamination with other grains in the fields or in the distribution channels. Generally, oats are therefore not recommended. Other cereals such as maize (corn), quinoa, millet, sorghum, teff, amaranth, buckwheat, rice, and wild rice are safe for patients to consume. Non-cereal carbohydrate-rich foods such as potatoes and bananas do not contain gluten and do not trigger symptoms.

Adapted from the Wikipedia article Coeliac disease, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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There is no line of demarcation between the jejunum and the ileum. There are, however, subtle differences between the two.

* The ileum has more fat inside the mesentery than the jejunum.

* The ileum is a paler color, and tends to be of a smaller caliber as well.

* While the length of the intestinal tract contains lymphoid tissue, only the ileum has abundant Peyer’s patches, unencapsulated lymphoid nodules that contain large numbers of lymphocytes and other cells of the immune system.

Adapted from the Wikipedia article Ileum, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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OCCAM coordinates NCI’s CAM research activities and tries to assist the growth of CAM research within the NCI, by increasing the capacity of the various relevant programs to support that research and keep it integrated with other research in related areas (e.g. nutrition, natural products, and behavioral sciences). A 2005 report in the ”Journal of Clinical Oncology” analyzed the research portfolio of OCCAM and the grant applications it received and identified serious challenges in the design and performance of research into CAM therapies of cancer: notably the lack of standardized products or protocols for CAM therapy and the inherent difficulty in studying products with no known mode of action.

Adapted from the Wikipedia article Office of Cancer Complementary and Alternative Medicine, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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A typical human erythrocyte has a disk diameter of 6–8 µm and a thickness of 2& µm, being much smaller than most other human cells. These cells have a volume of about 90 fL with a surface of about 136 μm2, and can swell up to a sphere shape containing 150 fL, without membrane distension.

Adult humans have roughly 2–3 × 1013 (20-30 trillion) red blood cells at any given time, comprising approximately one quarter of the total human body cell number (women have about 4 to 5 million erythrocytes per microliter (cubic millimeter) of blood and men about 5 to 6 million; people living at high altitudes with low oxygen tension will have more). Red blood cells are thus much more common than the other blood particles: there are about 4,000–11,000 white blood cells and about 150,000–400,000 platelets in each microliter of human blood.

Human red blood cells take on average 20 seconds to complete one cycle of circulation.

As red blood cells contain no nucleus, protein biosynthesis is currently assumed to be absent in these cells, although a recent study indicates the presence of all the necessary biomachinery in human red blood cells for protein biosynthesis.

The blood’s red color is due to the spectral properties of the hemic iron ions in hemoglobin. Each human red blood cell contains approximately 270 million of these hemoglobin biomolecules, each carrying four heme groups; hemoglobin comprises about a third of the total cell volume. This protein is responsible for the transport of more than 98% of the oxygen (the remaining oxygen is carried dissolved in the blood plasma). The red blood cells of an average adult human male store collectively about 2.5 grams of iron, representing about 65% of the total iron contained in the body. (See Human iron metabolism.)

Life cycle

Human erythrocytes are produced through a process named erythropoiesis, developing from committed stem cells to mature erythrocytes in about 7 days. When matured, these cells live in blood circulation for about 100 to 120 days. At the end of their lifespan, they become senescent, and are removed from circulation.

Erythropoiesis

Erythropoiesis is the development process in which new erythrocytes are produced, through which each cell matures in about 7 days. Through this process erythrocytes are continuously produced in the red bone marrow of large bones, at a rate of about 2 million per second in a healthy adult. (In the embryo, the liver is the main site of red blood cell production.) The production can be stimulated by the hormone erythropoietin (EPO), synthesised by the kidney. Just before and after leaving the bone marrow, the developing cells are known as reticulocytes; these comprise about 1% of circulating red blood cells.

Functional lifetime

This phase lasts about 100–120 days, during which the erythrocytes are continually moving by the blood flow push (in arteries), pull (in veins) and squeezing through microvessels such as capillaries as they compress against each other in order to move.

Senescence

The aging erythrocyte undergoes changes in its plasma membrane, making it susceptible to selective recognition by macrophages and subsequent phagocytosis in the reticuloendothelial system (spleen, liver and bone marrow), thus removing old and defective cells and continually purging the blood. This process is termed eryptosis, or erythrocyte programmed cell death. This process normally occurs at the same rate of production by erythropoiesis, balancing the total circulating red blood cell count. Eryptosis is increased in a wide variety of diseases including sepsis, haemolytic uremic syndrome, malaria, sickle cell anemia, beta-thalassemia, glucose-6-phosphate dehydrogenase deficiency, phosphate depletion, iron deficiency and Wilson’s disease. Eryptosis can be elicited by osmotic shock, oxidative stress, energy depletion as well as a wide variety of endogenous mediators and xenobiotics. Excessive eryptosis is observed in erythrocytes lacking the cGMP-dependent protein kinase type I or the AMP-activated protein kinase AMPK. Inhibitors of eryptosis include erythropoietin, nitric oxide, catecholamines and high concentrations of urea.

Much of the resulting important breakdown products are recirculated in the body. The heme constituent of hemoglobin are broken down into Fe3+ and biliverdin. The biliverdin is reduced to bilirubin, which is released into the plasma and recirculated to the liver bound to albumin. The iron is released into the plasma to be recirculated by a carrier protein called transferrin. Almost all erythrocytes are removed in this manner from the circulation before they are old enough to hemolyze. Hemolyzed hemoglobin is bound to a protein in plasma called haptoglobin which is not excreted by the kidney.

Membrane composition

The membrane of the red blood cell plays many roles that aid in regulating their surface deformability, flexibility, adhesion to other cells and immune recognition. These functions are highly dependent on its composition, which defines its properties. The red blood cell membrane is composed of 3 layers: the glycocalyx on the exterior, which is rich in carbohydrates; the lipid bilayer which contains many transmembrane proteins, besides its lipidic main constituents; and the membrane skeleton, a structural network of proteins located on the inner surface of the lipid bilayer. In human erythrocytes, like in most mammal erythrocytes, half of the membrane mass is represented by proteins and the other half are lipids, namely phospholipids and cholesterol.

Membrane lipids

The erythrocyte cell membrane comprises a typical lipid bilayer, similar to what can be found in virtually all human cells. Simply put, this lipid bilayer is composed of cholesterol and phospholipids in equal proportions by weight. The lipid composition is important as it defines many physical properties such as membrane permeability and fluidity. Additionally, the activity of many membrane proteins is regulated by interactions with lipids in the bilayer.

Unlike cholesterol which is evenly distributed between the inner and outer leaflets, the 5 major phospholipids are asymmetrically disposed, as shown below:

Outer monolayer

* Phosphatidylcholine (PC);

* Sphingomyelin (SM).

Inner monolayer

* Phosphatidylethanolamine (PE);

* Phosphoinositol (PI) (small amounts).

* Phosphatidylserine (PS);

This asymmetric phospholipid distribution among the bilayer is the result of the function of several energy-dependent and energy-independent phospholipid transport proteins. Proteins called “Flippases” move phospholipids from the outer to the inner monolayer while others called “floppases” do the opposite operation, against a concentration gradient in an energy dependent manner. Additionally, there are also “scramblase” proteins that move phospholipids in both directions at the same time, down their concentration gradients in an energy independent manner. There is still considerable debate ongoing regarding the identity of these membrane maintenance proteins in the red cell membrane.

The maintenance of an asymmetric phospholipid distribution in the bilayer (such as an exclusive localization of PS and PIs in the inner monolayer) is critical for the cell integrity and function due to several reasons:

* Macrophages recognize and phagocytose red cells that expose PS at their outer surface. Thus the confinement of PS in the inner monolayer is essential if the cell is to survive its frequent encounters with macrophages of the reticuloendothelial system, especially in the spleen.

* Premature destruction of thallassemic and sickle red cells has been linked to disruptions of lipid asymmetry leading to exposure of PS on the outer monolayer.

* An exposure of PS can potentiate adhesion of red cells to vascular endothelial cells, effectively preventing normal transit through the microvasculature. Thus it is important that PS is maintained only in the inner leaflet of the bilayer to ensure normal blood flow in microcirculation.

* Both PS and phosphatidylinositol-4,5-bisphosphate (PIP2) can regulate membrane mechanical function, due to their interactions with skeletal proteins such as spectrin and protein 4.1R. Recent studies have shown that binding of spectrin to PS promotes membrane mechanical stability. PIP2 enhances the binding of protein band 4.1R to glycophorin C but decreases its interaction with protein band 3, and thereby may modulate the linkage of the bilayer to the membrane skeleton.

The presence of specialized structures named “lipid rafts” in the erythrocyte membrane have been described by recent studies. These are structures enriched in cholesterol and sphingolipids associated with specific membrane proteins, namely flotillins, stomatins (band 7), G-proteins, and β-adrenergic receptors. Lipid rafts that have been implicated in cell signaling events in nonerythroid cells have been shown in erythroid cells to mediate β2-adregenic receptor signaling and increase cAMP levels, and thus regulating entry of malarial parasites into normal red cells.

Membrane proteins

The proteins of the membrane skeleton are responsible for the deformability, flexibility and durability of the red blood cell, enabling it to squeeze through capillaries less than half the diameter of the erythrocyte (7-8 μm) and recovering the discoid shape as soon as these cells stop receiving compressive forces, in a similar fashion to an object made of rubber.

There are currently more than 50 known membrane proteins, which can exist in a few hundred up to a million copies per erythrocyte. Approximately 25 of these membrane proteins carry the various blood group antigens, such as the A, B and Rh antigens, among many others. These membrane proteins can perform a wide diversity of functions, such as transporting ions and molecules across the red cell membrane, adhesion and interaction with other cells such as endothelial cells, as signaling receptors, as well as other currently unknown functions. The blood types of humans are due to variations in surface glycoproteins of erythrocytes. Disorders of the proteins in these membranes are associated with many disorders, such as hereditary spherocytosis, hereditary elliptocytosis, hereditary stomatocytosis, and paroxysmal nocturnal hemoglobinuria.

The red blood cell membrane proteins organized according to their function:

Transport

* Band 3 – Anion transporter, also an important structural component of the erythrocyte cell membrane, makes up to 25% of the cell membrane surface, each red cell contains approximately one million copies. Defines the Diego Blood Group;

* Aquaporin 1 – water transporter, defines the Colton Blood Group;

* Glut1 – glucose and L-dehydroascorbic acid transporter;

* Kidd antigen protein – urea transporter;

* RhAG – gas transporter, probably of carbon dioxide, defines Rh Blood Group and the associated unusual blood group phenotype Rhnull;

* Na+/K+ – ATPase;

* Ca2+ – ATPase;

* Na+ K+ 2Cl- – cotransporter;

* Na+-Cl- – cotransporter;

* Na-H exchanger;

* K-Cl – cotransporter;

* Gardos Channel.

Cell adhesion

* ICAM-4 – interacts with integrins;

* BCAM – a glycoprotein that defines the Lutheran blood group and also known as Lu or laminin-binding protein.

Structural role – The following membrane proteins establish linkages with skeletal proteins and may play an important role in regulating cohesion between the lipid bilayer and membrane skeleton, likely enabling the red cell to maintain its favorable membrane surface area by preventing the membrane from collapsing (vesiculating).

* Ankyrin-based macromolecular complex – proteins linking the bilayer to the membrane skeleton through the interaction of their cytoplasmic domains with Ankyrin.

** Band 3 – also assembles various glycolytic enzymes, the presumptive CO2 transporter, and carbonic anhydrase into a macromolecular complex termed a “metabolon,” which may play a key role in regulating red cell metabolism and ion and gas transport function);

** RhAG – also involved in transport, defines associated unusual blood group phenotype Rhmod.

* Protein 4.1R-based macromolecular complex – proteins interacting with Protein 4.1R.

** Protein 4.1R – weak expression of Gerbich antigens;

** Glycophorin C and D – glycoprotein, defines Gerbich Blood Group;

** XK – defines the Kell Blood Group and the Mcleod unusual phenotype (lack of Kx antigen and greatly reduced expression of Kell antigens);

** RhD/RhCE – defines Rh Blood Group and the associated unusual blood group phenotype Rhnull;

** Duffy protein – has been proposed to be associated with chemokine clearance;

** Adducin – interaction with band 3;

** Dematin- interaction with the Glut1 glucose transporter.

Separation and blood doping

Red blood cells can be obtained from whole blood by centrifugation, which separates the cells from the blood plasma. During plasma donation, the red blood cells are pumped back into the body right away and the plasma is collected. Some athletes have tried to improve their performance by blood doping: first about 1 litre of their blood is extracted, then the red blood cells are isolated, frozen and stored, to be reinjected shortly before the competition. (Red blood cells can be conserved for 5 weeks at −79 °C.) This practice is hard to detect but may endanger the human cardiovascular system which is not equipped to deal with blood of the resulting higher viscosity.

Artificially grown red blood cells

In 2008 it was reported that human embryonic stem cells had been successfully coaxed into becoming erythrocytes in the lab. The difficult step was to induce the cells to eject their nucleus; this was achieved by growing the cells on stromal cells from the bone marrow. It is hoped that these artificial erythrocytes can eventually be used for blood transfusions.

Adapted from the Wikipedia article Red blood cell, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki

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