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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A continuous extracorporeal monitoring system for blood glucose employing an electrochemical sensor is described. The sensor, about the size of a nickel, is rapid, is specific for glucose, generates its own power, and consists of two galvanic oxygen electrodes. Over one oxygen electrode is affixed a plastic matrix to which glucose oxidase is covalently bound; a blank matrix is over the other, which serves as a reference. Oxygen is consumed in the glucose-oxidase-containing matrix, decreasing the current from the underlying oxygen electrode. The current decrease is nonlinearly proportional to the glucose concentration. The sensor is clamped between small blocks of plastic fitted with inlet and outlet nipples so that blood pumped from the animal passes over the two electrodes and thence to an automated chemical analysis for comparison. Blood is collected and anticoagulant added in a double-lumen catheter. Blood is withdrawn at the rate of 1 cc. per hour. Results obtained by use of the system in rabbits are reported. The capacity of the system to continuously monitor changes in blood glucose produced by repeated glucose tolerances is shown in hypo-, normo-, and hyperglycemic animals. Some properties of the system and its calibration are discussed.
Diabetes 1976 Feb
PMID:Continuous extracorporeal monitoring of animal blood using the glucose electrode. 124 75

The use of microelectrode techniques for studying oxygen distribution and blood flow in the eye of a physiologically well maintained rat provides a very convenient model in which to study oxygen supply to the retina. The availability of rat models of vascular disease such as diabetes and hypertension, and the existence of several models of retinal degeneration, make studies of oxygen supply in the rat eye of particular relevance. The experiments reported in this paper demonstrate changes in oxygen distribution and blood flow very early in STZ induced diabetes. Thus, we have established a preparation in which the role of changes in oxygen supply can be correlated with the pathological events that are apparent later in the disease.
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PMID:Oxygen tension and blood flow in the retina of normal and diabetic rats. 128 5

Periportal and perivenous hepatocytes possess different amounts and activities of the rate-generating enzymes of carbohydrate and oxidative energy metabolism and thus different metabolic capacities. This is the basis of the model of metabolic zonation, according to which periportal cells catalyze predominantly the oxidative catabolism of fatty and amino acids as well as glucose release and glycogen formation via gluconeogenesis, and perivenous cells carry out preferentially glucose uptake for glycogen synthesis and glycolysis coupled to liponeogenesis. The input of humoral and nervous signals into the periportal and perivenous zones is different; gradients of oxygen, substrates and products, hormones and mediators and nerve densities exist which are important not only for the short-term regulation of carbohydrate metabolism but also for the long-term regulation of zonal gene expression. The specialization of periportal and perivenous hepatocytes in carbohydrate metabolism has been well characterized. In vivo evidence is provided by the complex metabolic situation termed the 'glucose paradox' and by zonal flux differences calculated on the basis of the distribution of enzymes and metabolites. In vitro evidence is given by the different flux rates determined with classical invasive techniques, e.g. in periportal-like and perivenous-like hepatocytes in cell culture, in periportal- and perivenous-enriched hepatocyte populations and in perfused livers during orthograde and retrograde flow, as well as with noninvasive techniques using miniature oxygen electrodes, e.g. in livers perfused in either direction. Differences of opinion in the interpretation of studies with invasive and noninvasive techniques by the authors are discussed. The declining gradient in oxygen concentrations, the decreasing glucagon/insulin ratio and the different innervation could be important factors in the zonal expression of the genes of carbohydrate-metabolizing enzymes. While it is clear that the hepatocytes sense the glucagon/insulin gradients via the respective hormone receptors, it is not known how they sense different oxygen tensions; the O2 sensor may be an oxygen-binding heme protein. The zonal separation of glucose release and uptake appears to be important for the liver to operate as a 'glucostat'. Thus, zonation of carbohydrate metabolism develops gradually during the first weeks of life, in part before and in part with weaning, when (in rat and mouse) the fat- and protein-rich but carbohydrate-poor nutrition via milk is replaced by carbohydrate-rich food. Similarly, zonation of carbohydrate metabolism adapts to longer lasting alterations in the need of a 'glucostat', such as starvation, diabetes, portocaval anastomoses or partial hepatectomy.
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PMID:Hepatocyte heterogeneity in the metabolism of carbohydrates. 128 81

Anaerobic necrotizing soft tissue infections are known for their devastating effects of tissue destruction and death. These infections may occur as a result of trauma, surgical intervention or occur spontaneously in predisposed individuals. They are caused by a wide range of anaerobic organisms and may be categorised according to the tissue involvement as Necrotizing Fasciitis and Myonecrosis. A five year review of patients admitted for hyperbaric oxygen (HBO) therapy and requiring intensive care revealed a patient group numbering 25, roughly equally divided between the two classifications of tissue involvement. Trauma was an aetiological factor in 5 of these cases. Cancer and diabetes mellitus were also prominent aetiological factors. Treatment consisted of the triad of early selective/aggressive surgery, high dose antibiotic therapy and HBO therapy. The mortality of the group was 25%. Delay in treatment was associated with increased mortality. Nursing care, for this particular patient group is demanding, requiring particular attention to wound care, analgesia, transport, psychosocial care of patient with mutilating wounds, nutrition and temperature homeostasis. It is a cause for concern that two cases occurred after elective orthopaedic procedures requiring the application of plaster of paris (POP) cast over a leg.
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PMID:A five year review of anaerobic, necrotizing soft tissue infections: a nursing perspective. 129 Aug 88

We reviewed the records of 17 cases of Fournier's gangrene that had been diagnosed and treated in the Urology Service of the Marques de Valdecilla Hospital from 1982-1991. The series comprised male patients aged 32 to 77. Eleven cases (64.7%) were due to a known cause, above all infection. Most of the patients had factors that predisposed to the development and progression of the disease, predominantly diabetes mellitus (5 cases, 29.4%). The clinical features frequently corresponded to those of acute infection, with high fever, chills, pain, nausea and vomiting that could progress to a septic state. The local symptoms and signs included pain, swelling, erythema and necrosis, depending on the compromised area. Infection was usually caused by Gram-negative bacteria, particularly E. coli, although Gram-positive bacteria and anaerobes have been observed. Mixed bacterial infections have also been observed. Treatment must be instituted early using a combination of broad spectrum antibiotics that cover both aerobes and anaerobes, and wide surgical debridement of the compromised area. In some cases hyperbaric oxygen therapy may be warranted. The disease continues to be severe. In the present series, the outcome was favorable in 12 cases (70.5%) and there were 5 deaths (29.4%).
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PMID:[Our caseload in Fournier's disease]. 129 42

Erythropoietin is the primary hormone controlling erythropoiesis in both adults and fetuses. In extra-fetal life the main organ producing erythropoietin is the kidney which is responsible for producing about 90% of the total amount of this hormone. In fetal life erythropoietin is produced by the liver of the fetus. The erythropoietin production depends on the content of oxygen in blood. This is probably the only physiological stimulus which regulates the production of erythropoietin. The increase of erythropoietin concentration in the umbilical cord serum and in the amniotic fluid has been observed in the states of fetus anoxia. This mainly concerns such complications during pregnancy as the fetus hypotrophy, diabetes, serological conflict, and gestosis.
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PMID:[Concentration of erythropoietin in blood serum of the umbilical cord and in amniotic fluid in normal and complicated pregnancies]. 130 56

Hematologic values are compared for normal and streptozotocin-induced diabetic rats after 6 weeks of induced diabetes. Most hematologic parameters were the same in the two groups except for blood glucose, glycated hemoglobin, and 2,3 diphosphoglycerate, all of which were elevated in the streptozotocin group. However the P50 (the PO2 at which the oxygen-carrying capacity of blood is 50% of maximal) remained normal. We hypothesize that a left shift in the oxyhemoglobin dissociation curve caused by the glycation of a small percentage of the hemoglobin is compensated by elevation in the 2,3-diphosphoglycerate which returns the P50 to normal values. This compensatory mechanism also occurs in some stages of human diabetes.
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PMID:Comparison of hematologic parameters in normal and streptozotocin-induced diabetic rats. 131 51

Conditions causing a reduction of oxygen availability (anoxia), such as stroke or diabetes, result in drastic changes in ion movements, levels of neurotransmitters and metabolites and subsequent neural death. Currently, there is no clinically available treatment for anoxia induced neural cell death resulting in drastic and permanent central nervous system dysfunction. However, there have been some exciting developments in experimentally induced anoxic conditions where several classes of drugs appear to significantly reduce neural cell death. This report aims to provide the foundations for understanding both the basic mechanisms involved in retinal ischaemic damage and experimental treatments used to prevent such damage. We discuss the normal release, actions and uptake of the fast retinal neurotransmitters, glutamate and GABA, in the vertebrate retina. Immunocytochemistry is used to demonstrate that both glutamate and GABA are found in the macaque retina. Following this is a discussion on how ischaemia may enhance neurotransmitter release or disrupt its uptake, thus causing an increase in extracellular concentration of these neurotransmitters and subsequent neuronal damage. The mechanisms involved in glutamate neurotoxicity are reviewed, because excess glutamate is the likely cause of retinal ischaemic damage. Finally, the mechanisms behind four possible modes of treatment of neurotransmitter toxicity and their advantages and disadvantages are discussed. Hopefully, further research in this area will lead to the development of a rational therapy for retinal, as well as cerebral ischaemia.
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PMID:Interrelationship between retinal ischaemic damage and turnover and metabolism of putative amino acid neurotransmitters, glutamate and GABA. 136 7

High ascorbic acid (AA) levels in the aqueous humor and intraocular tissues, including the lens, are thought to protect against the harmful effects of photochemical and ambient oxidation reactions involving oxygen and its radicals. In addition, AA may have various metabolic functions, including structural collagen formation in intraocular tissues. Recent work showed that, in the guinea pig, reduced AA was concentrated in the aqueous and lens epithelium. These in vivo studies were extended to streptozotocin-induced diabetic rats and guinea pigs to explore the state of AA transport and passive L-glucose movement in the diabetic lens. A bolus dose of radiolabeled test molecules, including 14C-AA, 3H-L-glucose (L-glu), and 14C-3-O-methyl-D-glucose, was injected into the blood at time zero, and the time-dependent concentrations of these labeled molecules were determined as they move into the aqueous humor, lens epithelium and capsule, and interior compartments. These kinetic studies provided a unique measurement of the functioning state of passive and carrier transport mechanisms in situ in normal and diabetic animals. Diabetic animals (blood glucose, greater than 300 mg/dl) were categorized in terms of the length of time of uniform monitored drug-induced diabetes as short term (10-20 days); midterm (40-60 days), and long term (100+ days). In the rat lens epithelium, significant decrease occurred in the active movement of AA (control KEi, 0.693 +/- 0.062 [n = 12]; midterm drug-induced diabetes Ki, 0.192 +/- 0.054 [n = 10]; t-test P less than 0.001). The passive L-glu entry rate increased (control KEi, 0.0268 +/- 0.0053 [n = 12]; midterm drug-induced diabetes KEi, 0.0421 +/- 0.075 [n = 10]; t-test P less than 0.005). Thus, it was suggested that the drug-induced diabetic rat lens epithelium had lost some of its ability to concentrate AA to high levels and achieved epithelial levels only one- to twofold those of aqueous; control animals concentrated AA to levels of five- to eightfold those of aqueous within 20 min. By contrast, the rate of movement of L-glu from epithelium to stroma increased minimally (control KSi, 0.0116 +/- 0.021 [n = 12]; midterm drug-induced diabetes KSi, 0.0136 +/- 0.034 [n = 10]; t-test P less than 0.05). In addition, AA entry rate into lens cortex increased fourfold (control KSi, = 0.0018 +/- 0.0003 [n = 12]; midterm drug-induced diabetes KSi, 0.0081 +/- 0.024 [n = 10]; t-test P less than 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alterations in ascorbic acid transport into the lens of streptozotocin-induced diabetic rats and guinea pigs. 138 45

The 2.2 A resolution crystal structure of recombinant human manganese superoxide dismutase, a homotetrameric enzyme that protects mitochondria against oxygen-mediated free radical damage, has been determined. Within each subunit, both the N-terminal helical hairpin and C-terminal alpha/beta domains contribute ligands to the catalytic manganese site. Two identical 4-helix bundles, symmetrically assembled from the N-terminal helical hairpins, form novel tetrameric interfaces that stabilize the active sites. Structurally altered polymorphic variants with reduced activity, such as tetrameric interface mutant Ile-58 to Thr, may produce not only an early selective advantage, through enhanced cytotoxicity of tumor necrosis factor for virus-infected cells, but also detrimental effects from increased mitochondrial oxidative damage, contributing to degenerative conditions, including diabetes, aging, and Parkinson's and Alzheimer's diseases.
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PMID:The structure of human mitochondrial manganese superoxide dismutase reveals a novel tetrameric interface of two 4-helix bundles. 139 26


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