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

A 35-years old female with Jordans' anomaly was reported. She had been treated for diabetes mellitus and hypertension at another hospital. She was admitted to our hospital for operation for diabetic retinopathy on July 9, 1992. Wright-Giemsa stained peripheral blood smear revealed multiple vacuoles in the cytoplasm of the granulocytes and monocytes. Histochemical studies of these vacuoles showed positive for Sudan III but negative for peroxidase, alkaline phosphatase and PAS staining. Electron microscopic examination revealed that lipid containing vacuoles had no clear membrane and were not associated with cell organelles. Laboratory findings of the serum showed hyperglycemia (FBS 188mg/dl), high HbA1c level (9.4%) and mild type IIa hyperlipidemia. Abdominal sonogram and abdominal CT showed no remarkable abnormalities except for mild fatty liver. Her elder sister and daughter had similar morphological findings in granulocytes, monocytes and lymphocytes.
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PMID:[A case of Jordans' anomaly]. 786 17

Sera obtained at diagnosis from 273 children (0-14 years) with insulin-dependent diabetes mellitus (IDDM) were studied to compare different autoantibody levels. The subjects comprise 75% of all incident cases in New South Wales, Australia, for a 2-year period (ascertainment > 99% complete). Antibodies against glutamate decarboxylase were measured by radioimmunoprecipitation, insulin autoantibodies (on 176 sera collected within 4 days of initiation of insulin therapy) by radioimmunoassay, thyroid peroxidase and antigliadin IgA antibodies by enzyme-linked immunoassay, and anti-endomysial IgA and islet cell antibodies by indirect immunofluorescence. Reference ranges for anti-glutamate decarboxylase and insulin autoantibodies were determined in a group of non-diabetic children. Of the sera 69% were positive for anti-glutamate decarboxylase, 65% for insulin autoantibodies, 71% for islet cell antibodies (> or = 20 Juvenile Diabetes Foundation units), 10% for anti-thyroid peroxidase, 2.6% for antigliadin and 3.0% for anti-endomysial antibodies. Islet cell antibodies and insulin autoantibodies were both negative in 13.7% of the sera, while only 5.8% were negative for all three of islet cell antibodies, insulin autoantibodies and anti-glutamate decarboxylase. There was a higher frequency of anti-glutamate decarboxylase among girls than boys (75% vs 63%, p = 0.03) and a negative correlation between the level of insulin autoantibodies and age at diagnosis (r = -0.41, p < 0.0001). A higher frequency of antithyroid peroxidase was found with increasing age (p = 0.05). Higher titres of islet cell antibodies were associated with a higher frequency of both anti-glutamate decarboxylase (p < 0.0001) and insulin autoantibodies (p = 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anti-glutamate decarboxylase and other antibodies at the onset of childhood IDDM: a population-based study. 786 83

We have developed a flow-injection system with colorimetric detection to measure 1,5-anhydro-D-glucitol in serum. Serum samples are directly and serially injected into a clean-up column every 3.5 min to remove interferences before the enzymatic reaction. 1,5-Anhydro-D-glucitol, after being passed through the column, is oxidized by immobilized pyranose oxidase (EC 1.1.3.10), and the hydrogen peroxide produced reacts with the chromogen substrate in the presence of immobilized horseradish peroxidase (EC 1.11.1.7) to form Bindshedler's Green. The detection limit was 1.2 mumol/L (1.2 pmol). The correlation between results obtained with the present system (y) and gas chromatography-mass spectrometry (GC-MS) (x) in samples containing < 30 mumol/L 1,5-anhydro-D-glucitol, including many samples from patients with diabetes mellitus, was y = 0.975x-0.111 mumol/L (r = 0.997), which was superior to that obtained between the enzymatic and GC-MS methods. Our system needs only to be set up; it runs without any manual pretreatment, assays 17 samples/h, and shows imprecision (CV) of < 2%.
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PMID:Fully automated flow-injection system for quantifying 1,5-anhydro-D-glucitol in serum. 795 66

Diabetic human patients and laboratory animals show abnormalities which can be observed also in enhanced lipid peroxidation (LPO) induced in vitro. It seemed to be necessary to demonstrate the presence of these processes also in dogs with experimentally induced alloxan diabetes. In a 5-day experiment, five 1 to 5-year-old dogs of mixed sex were examined. Blood samples were taken before the intravenous administration of 60 mg alloxan/kg body mass and then daily for a period of 5 days. After the administration of alloxan, the dogs became depressed and lost their appetite. Their urine contained varying concentrations of glucose detectable with a test strip. As compared to the physiological values, blood glucose concentration increased considerably throughout. Alanine aminotransferase (ALT) enzyme activity underwent an 8-fold increase by the 24th hour; subsequently, it remained practically unaltered. The malonyldialdehyde (MDA) concentration of red blood cell (RBC) haemolysate also rose with respect to the basal values. Glutathione-peroxidase (GSH-Px) activity increased only transiently, up to the second day of the experiment; subsequently, its activity dropped below the basal values. Similar changes were found in catalase activity, while the activity changes of superoxide dismutase (SOD) were identical in tendency to the above ones; in fact, it hardly showed any alterations. Besides the severe pancreatic and liver damage caused by alloxan, increased MDA production in the RBC haemolysate indicated enhanced peroxidation of polyunsaturated fatty acids, i.e. intensification of the LPO processes. The increase of GSH-Px and catalase activity, followed by their decrease was suggestive of changes in the enzymatic defence mechanism acting against free radicals.
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PMID:Changes of lipid peroxidation parameters in dogs with alloxan diabetes. 806 47

Autoimmune mechanisms may be involved in the pathogenesis of insulin dependent diabetes mellitus (IDDM). Multiple autoantibodies have been detected in patients with IDDM. Islet cell antibodies (ICA), complent-fixing islet cell antibodies (CF-ICA) and antibodies to an islet cell protein 64000 M(r) (64K antibodies) have been regarded as immunological markers in IDDM. ICA detection with immunohistochemistry requires fresh normal human pancreas (blood group O) which provides an antigen for measuring ICA in serum samples. In the present study ICA detection was first carried out by using avidin-biotin-peroxidase complex technique (ABC) method and paraffin sections of human pancreas (blood group O), Serum samples were obtained from 17 patients with IDDM, 20 with NIDDM and 20 without diabetes mellitus. In patients with IDDM, ICA were detected in 9 of the 17 (52.94%) while none of the patients with NIDDM and without diabetes mellitus were ICA positive. In comparison with other methods, the present one is more reliable, sensitive, specific and simple. Therefore, it may be widely used for ICA detection in clinical practice.
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PMID:[Detection of islet cell antibodies by using avidin-biotin-peroxidase complex technique]. 807 Feb 98

To assess the normal response to the 75 gm oral glucose tolerance test (OGTT) in normal pregnant women, healthy Chinese and Malay women who had been referred to the antenatal clinic of the Department of Reproductive Medicine, Kandang Kerbau Hospital, Singapore, were evaluated. The women were selected on the basis of having none of the generally accepted risk factors for diabetes mellitus: their age was 35 years, they weighed 80 kg, they did not have a personal history of diabetes or a family history of diabetes or a family history of diabetes in first degree relatives, nor did they have a history of babies weighing 4000 gm at birth, still-births, neonatal deaths, congenital malformations, or recurrent miscarriages. All OGTTs were performed after 28 weeks of gestation. The fasting blood sample was taken from the antecubital vein. Further samples were taken 1 and 2 hours after the glucose drink. A glucose analyzer using 5 mcl of plasma was employed. The analytical method was based on the glucose oxidase/peroxidase/aminophenazone process. There was no significant difference in mean glucose levels at corresponding points of the OGTT in Chinese and Malay women. correlation calculations confirmed the absence of any influence of gestational age after 28 weeks on glucose tolerance. Of the 64 women, 47 were Chinese and 17 Malays; 20 wee nulliparous, and 44 were parous. Their mean age was 27.2 years (range 18-35). The mean birthweight of the infants was 3140 gm (range 2094-4240 gm). There were 33 female and 31 male infants. The mean apgar scores at 1 and 5 min were 8.8 (range 7-9) and 9.0 (range 6-10). The mean values and the proposed upper limits of normality for the 75 gm OGTT were 3.9 and 4.9 mmol/1, respectively. 6 women had abnormal OGTT results according to the WHO criteria (fasting glucose 6 mmol/1; 2 hour glucose 8 mmol/1).
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PMID:Are the WHO (1980) criteria for the 75 g oral glucose tolerance test appropriate for pregnant women? 836 47

A simple, rapid, and precise method of typing HLA class II polymorphism would be valuable in the areas of disease susceptibility, tissue transplantation, individual identification, and anthropological genetics. Herein, we describe a method of analyzing class II sequence polymorphism based on polymerase chain reaction (PCR) amplification and hybridization with oligonucleotide probes. Many more DNA-defined alleles at the class II loci have been identified than can be distinguished by conventional serologic typing. Consequently, matching transplant donors and recipients by PCR/oligonucleotide typing should reduce graft rejection and graft-vs-host disease. Also, the ability to identify alleles conferring genetic predisposition to specific diseases (eg, insulin-dependent diabetes mellitus) is significantly enhanced by distinguishing the many alleles or "subtypes" within a serologic type (eg, DR4). One valuable property of sequence-based HLA typing strategies, like oligonucleotide probe hybridization, is that they reveal how and where two alleles differ, not simply that they can be operationally distinguished. The nature and location of HLA polymorphisms appears to be critical in disease association studies and are important in tissue typing for transplantation. New alleles at the DRB1, DPB1, and DQB1 loci are likely to be identified as this technology is applied to more and more samples, particularly in nonwhite ethnic groups. A new allele is uncovered as an unusual pattern of probe binding and then confirmed by sequencing. This pattern is observed because class II polymorphism is localized to specific regions and virtually all "new" alleles represent "shuffled" combinations of polymorphic sequences found in previously known alleles. Since these polymorphisms are in the region of probe binding, these new alleles can be detected without increasing the probe panel. Obviously, any new allele with a new polymorphic sequence in a region for which typing probes are not available would not be revealed by oligonucleotide typing. With the PCR primers and probes described here, 7 DQ alpha 1 alleles, 15 DQ beta 1 alleles, 18 DPB1 alleles, and 32 DRB1 alleles are distinguished. Additional primers and/or probes can, of course, increase the allelic discrimination of PCR/oligonucleotide probe typing. These horseradish peroxidase-labeled oligonucleotide probes are stable (> 2 years when stored at 4 degrees C) and the typing system is simple and robust. Although this dot blot/oligonucleotide hybridization procedure is a powerful and precise method of HLA class II typing, the complexity of the procedure increases as the number of probes required for analysis increases.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Analysis of HLA class II polymorphism using polymerase chain reaction. 848 36

The kallikrein-kinin system has been implicated in the inflammatory process, blood pressure regulation, renal homeostasis, and glucose utilization. The effects of kallikrein and kinin on glucose uptake by the skeletal muscle are well established; however, the occurrence and the cellular distribution of the kinin receptor(s) mediating these effects in the striated muscle are unknown. Using anti-peptide antibodies raised against the predicted intra- and extracellular domains of the B2 receptor and the peroxidase/antiperoxidase system, we have been able to detect the B2 receptor on the plasma membrane of striated skeletal muscle cells of the rat hindlimb. A strong immunostaining appeared as a rim of immunoreactive material located on the periphery of striated muscle cells. Cross-sectioned and longitudinally sectioned cells revealed a similar staining pattern. Alternatively, the immunostaining with specific antibodies to tissue kallikrein and to T-kininogen did not yield a significant staining of the striated muscle cells. Localization of the B2 receptor on the surface of striated muscle cells provides a structural basis for the hypothesized physiological functions of the kinin system in the skeletal muscle.
Diabetes 1996 Jan
PMID:Immunolocalization of bradykinin B2 receptors on skeletal muscle cells. 852 96

We sought to determine if hyperglycaemia is responsible for increased retinal vascular endothelial-cell (RVEC) endocytosis in diabetes and to assess the role of nonenzymatic glycosylation in mediation of this novel endothelial-cell pathology. RVECs were propagated in media containing either 5 or 25 mmol/l glucose for up to 10 days after which they were exposed to the protein tracer horseradish peroxidase for 30 min. The level of RVEC endocytosis was quantified in intact cell monolayers by electron microscopic stereology, and in cell lysates by a simple spectrophotometric method. The effect of the nonenzymatic glycosylation inhibitors, aminoguanidine and D-lysine, on high-glucose medium induced changes in RVEC endocytosis was tested by inclusion of these agents in the culture medium. RVECs exposed to 25 mmol/l glucose showed a stepwise increase in endocytosis of horseradish peroxidase culminating in a two- to threefold increase after 10 days. Endocytosis returned to normal levels after a further 10 days in 5 mmol/l glucose medium. The increase in RVEC endocytosis was markedly reduced, but not completely normalised, by aminoguanidine and D-lysine. Exposure of cultured RVECs to 25 mmol/l glucose causes an increase in endocytosis of similar magnitude to that experienced by RVEC in early diabetes, and implicates hyperglycaemia in the latter situation. A significant component of the increase in RVEC endocytosis appears to be mediated by nonenzymatic glycosylation.
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PMID:Increased endocytosis in retinal vascular endothelial cells grown in high glucose medium is modulated by inhibitors of nonenzymatic glycosylation. 858 35

It is known that the peroxidation of LDL is a trigger for developing arteriosclerosis. The oxidized LDL is produced by either oxidative stress or a few oxidant. Selenium decreased in serum and some organs of stroke-prone spontaneously hypertensive rats (SHRSP), which is a cofactor of glutamine peroxidase. Serum magnesium decreased in patients with diabetes mellitus, with ischemic heart disease, with essential hypertension and with cerebral vascular lesions. Calcium to magnesium ratio was higher in some organs of SHRSP as compared to Wistar Kyoto rats (WKY). These changes accelerated vascular lesions in SHRSP.
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PMID:[Overview--suppression effect of essential trace elements on arteriosclerotic development and it's mechanism]. 858 7


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