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Blood cell metabolism

N. Jamshidi, S. J. Wiback, and B. 0. Palsson, In silico model driven assessment of the effects of single nucleotide polymorphisms (SNPs) on human red blood cell metabolism. Gen. Res. 12 (11), 1687 1692 (2002). [Pg.235]

Y. Nakayama, A. Kinoshita, and M. Tomita, Dynamic simulation of red blood cell metabolism and its application to the analysis of a pathological condition. Theor. Biol. Med. Model. 2(1), 18... [Pg.250]

Barron ESG, Harrop GA. Studies on blood cell metabolism II. The effect of methylene blue and other dyes upon the glycolysis and lactic acid formation of mammalian and avian erythrocytes. J. Biol. Chem. 1928 79 65-87. [Pg.1423]

Jamshidi, N., J. S. I idwards, T. Fahland, G. M. Church, and B. O. Palsson. 2001. Dynamic simulation of the human red blood cell metabolic network. Bioinformatics 17 286-7. [Pg.220]

Microcalorimetry has been used for investigations of blood cells metabolism as one of the first applications of this methodology in the medical field. Preliminary studies have been carried out to develop suitable methods that could be applied in clinical investigations. [Pg.657]

Esmolol is iv adrninistered. Maximal P-adrenoceptor blockade occurs in 1 min. Its elimination half-life is about 9 min. EuU recovery from P-adrenoceptor blockade is within 30 min after stopping the infusion. The therapeutic plasma concentrations are 0.4—1.2 lg/mL. It is metabolized by hydrolysis in whole blood by red blood cell esterases resulting in the formation of a primary acid metabohte and free methanol. The metabohte is pharmacologically inactive. The resulting methanol levels are not toxic. Esmolol is 55% bound to plasma protein, the acid metabohte only 10%. Less than 2% of parent dmg and the acid metabohte are excreted by the kidneys. Plasma levels may be elevated and elimination half-hves prolonged in patients with renal disease (41). [Pg.119]

The drug is metabolized rapidly in the liver, kidney, intestinal mucosa, and even red blood cells. Therefore it has a plasma half-life of only 10 min after bolus intravenous application. The major metabolite, uracil arabinoside (ara-U), can be detected in the blood shortly after cytarabine administration. About 80% of the dose is excreted in the urine within 24 h, with less than 10% appearing as cytarabine the remainder is ara-U. After continuous infusion, cytarabine levels in the liquor (cerebro-spinal fluid) approach 40% of that in plasma. Continuous infusion schedules allow maximal efficiency, with uptake peaks of 5-7 pM. It can be administered intrathecally as an alternative to methotrexate. [Pg.151]

High levels of lead can affect heme metabohsm by combining with SH groups in enzymes such as fer-rochelatase and ALA dehydratase. This affects porphyrin metabolism. Elevated levels of protoporphyrin are found in red blood cells, and elevated levels of ALA and of coproporphyrin are found in urine. [Pg.278]

Transferrin (Tf) is a Pj-globulin with a molecular mass of approximately 76 kDa. it is a glycoprotein and is synthesized in the liver. About 20 polymorphic forms of transferrin have been found, it plays a central role in the body s metabolism of iron because it transports iron (2 mol of Fe + per mole of Tf) in the circulation to sites where iron is required, eg, from the gut to the bone marrow and other organs. Approximately 200 billion red blood cells (about 20 mL) are catabolized per day, releasing about 25 mg of iron into the body—most of which will be transported by transferrin. [Pg.586]

THE RED BLOOD CELL HAS A UNIQUE RELATIVELY SIMPLE METABOLISM... [Pg.610]

Several powerful oxidants are produced during the course of metabolism, in both blood cells and most other cells of the body. These include superoxide (02 ), hydrogen peroxide (H2O2), peroxyl radicals (ROO ), and hydroxyl radicals (OH ). The last is a particularly reactive molecule and can react with proteins, nucleic acids, lipids, and other molecules to alter their structure and produce tissue damage. The reactions listed in Table 52-4 play an important role in forming these oxidants and in disposing of them each of these reactions will now be considered in turn. [Pg.611]

Section VI consists of discussions of eleven special topics nutrition, digestion, and absorption vitamins and minerals intracellular traffic and sorting of proteins glycoproteins the extracellular matrix muscle and the cy-toskeleton plasma proteins and immunoglobulins hemostasis and thrombosis red and white blood cells the metabolism of xenobiotics and the Human Genome Project. [Pg.699]

Decreased red blood cell (RBC) count, hemoglobin (Hgb) and hematocrit (Hct) iron metabolism may also be altered [iron level, total iron binding capacity (TIBC), serum ferritin level, and transferrin saturation (TSAT)]. Erythropoietin levels are not routinely monitored and are generally normal to low. Urine positive for albumin or protein. [Pg.378]

Complete metabolic panel, complete blood cell count, and thyroid panel within normal limits... [Pg.783]

Iron is another vital nutrient in the development of functioning erythrocytes it is essential for the formation of hemoglobin. Lack of iron leads to a decrease in hemoglobin synthesis and ultimately red blood cells. Normal homeostasis of iron transport and metabolism is depicted in Fig. 63-2.7 Approximately 1 to 2 mg of iron is absorbed through the duodenum each day, and the same amount is lost via blood loss, desquamation of mucosal cells, or menstruation. [Pg.977]

A 70-year-old man presents to the emergency department because of diffuse abdominal pain and nonbloody diarrhea. One day earlier he had been discharged from the hospital, where he had received ceftriaxone and levofloxacin for 7 days for an upper respiratory infection. Soon after going home, he passed numerous liquid brown stools. A few hours later, the patient became disoriented, and an ambulance was called. His medical history is unremarkable. Laboratory values White blood cell count 50,000 cells/mm3, hematocrit 43%, sodium 125 mmol/L, potassium 5.6 mmol/L, C02 14 mmol/L, and metabolic acidosis. An abdominal radiograph series show no evidence of obstruction. The patient was admitted to the hospital. [Pg.1126]

Mature red blood cells do not have nuclei, mitochondria, or microsomes therefore red blood cell function is supported through the most primitive and universal pathway. Glucose, the main metabolic substrate of red blood cells, is metabolized via two major pathways the Embden-Meyerhof glycolytic pathway and the hex-ose monophosphate pathway (Fig. 1). Under normal circumstances, about 90% of the glucose entering the red blood cell is metabolized by the glycolytic pathway and 10% by the hexose monophosphate pathway. [Pg.2]


See other pages where Blood cell metabolism is mentioned: [Pg.6]    [Pg.443]    [Pg.140]    [Pg.170]    [Pg.364]    [Pg.781]    [Pg.225]    [Pg.364]    [Pg.4]    [Pg.663]    [Pg.6]    [Pg.443]    [Pg.140]    [Pg.170]    [Pg.364]    [Pg.781]    [Pg.225]    [Pg.364]    [Pg.4]    [Pg.663]    [Pg.32]    [Pg.326]    [Pg.743]    [Pg.1099]    [Pg.263]    [Pg.625]    [Pg.10]    [Pg.391]    [Pg.191]    [Pg.163]    [Pg.284]    [Pg.609]    [Pg.609]    [Pg.612]    [Pg.137]    [Pg.41]    [Pg.31]    [Pg.184]    [Pg.89]    [Pg.353]    [Pg.197]    [Pg.645]    [Pg.1146]   
See also in sourсe #XX -- [ Pg.657 ]




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