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C Binder

Publications and source records attributed to C Binder.

At least 109 records · Page 6Linked to original sources
PubMed1987

Lens autofluorescence in diabetes compared with the level of glycosylated hemoglobin A1c.

The autofluorescence of the crystalline lens has been measured by an ocular fluorophotometer in two comparable groups of patients with insulin-dependent diabetes mellitus. One group has had a high level of HbA1c since the onset of diabetes (mean 10.1 per cent) and the other group a very low level (mean 6.5 per cent). The group with low HbA1c during the disease period showed a significantly lower lens fluorescence than the group with high HbA1c.

Diabetes Mellitus, Type 1↗
PubMed1986

ELISA for human proinsulin.

A micro enzyme-linked-immunosorbent-assay (ELISA) for monitoring circulating human proinsulin (hPI) was developed. A micro test plate was coated with guinea pig anti-insulin antibody. As labelling system peroxidase-labelled F(ab1)2-fragments of a guinea pig anti-human-C-peptide was used. The detection limit in buffer (95% level) was 0.6 pmol/l corresponding to 0.06 fmol/incubation well and to 1.2 pmol/l in serum, since samples were diluted 50%. Standard operating range was from 0-160 pmol/l. Interassay variation was 9% estimated from two human control materials (assayed within the range 6-9 pmol/l and 9-14 pmol/l, respectively). Insulin in samples did not interfere in concentrations below 400 pmol/l. Human C-peptide, porcine, and bovine proinsulins did not cross-react even at 10 000 pmol/l. In 38 healthy fasting subjects a reference range less than 1.2-13 pmol/l with a median of 4.1 pmol/l was found. Serum from total pancreatectomised patients showed values below the detection limit. The value from a patient with an insulinoma was 263 pmol/l. When stored at -20 degrees C human proinsulin appeared stable in serum or plasma for at least 9 mth. This ELISA, although among the most sensitive immunoassays for human proinsulin, is still not sensitive enough to measure the concentrations expected in samples from IDDM patients in the fasting state. In spite of this the method is useful in characterising beta-cell function in stimulated situations, as well as in the diagnosis of insulinoma.

Animals↗
PubMed1986

Cognitive function during hypoglycaemia in type I diabetes mellitus.

Neuropsychological testing was carried out in 16 insulin dependent (type I) diabetic men during four periods when mean blood glucose concentrations were (A) 6.3 (SEM 0.13) mmol/l (113.5 (SEM 2.3) mg/100 ml), (B) 2.9 (0.05) mmol/l (52.3 (0.9) mg/100 ml), and (C) 1.8 (0.03) mmol/l (32.4 (0.05) mg/100 ml), all measured during intravenous insulin infusion, and (D) 6.1 (0.13) mmol/l (109.9 (2.3) mg/100 ml), measured after intravenous glucose. The total neuropsychological test score decreased between periods A and B, A and C, and B and C, whereas improvement occurred between periods C and D (all p less than 0.02). These results were not due to changes in individual subjects alone but were consistent for the whole group. During hypoglycaemia there were changes in the patients' estimates of elapsed time, which were underestimated at period C as compared with the estimates at periods A, B, and D (all p less than 0.05). None of the 16 patients noticed symptoms of hypoglycaemia at period A or B, 12 reported symptoms at C, and one at D. Patients with type I diabetes may show a deterioration in neuropsychological skills during periods of asymptomatic subnormal or hypoglycaemic blood glucose concentrations.

Blood Glucose↗
PubMed1986

C-peptide: an index of insulin secretion.

Insight into the natural history of beta cell function in IDDM patients obtained by C-peptide measurements is reviewed. It is argued that residual insulin secretion of metabolic importance is present in all IDDM patients during the initial course of the disease. After some months, beta cell function reaches its maximum; thereafter it declines at different rates dependent on the age at onset of diabetes and, possibly, on the presence of ICA and HLA-antigens. As many as 15% of IDDM patients retain life-long beta cell function that persists at approximately 10% of that observed in nondiabetic individuals. The residual endogenous insulin secretion is characterized by reduced capacity, as well as abnormal insulin secretory kinetics; these defects in residual insulin secretion can be modulated by changes in metabolic regulation as well as by immunosuppression during the initial course of the disease.

Age Factors↗
PubMed1986

Detection of respiratory syncytial virus in nasopharyngeal secretions by enzyme-linked immunosorbent assay, indirect immunofluorescence, and virus isolation: a comparative study.

An enzyme-linked immunosorbent assay (ELISA) was developed for the detection of respiratory syncytial virus (RSV) antigens in nasopharyngeal secretions (NPS) from children with acute respiratory disease. Antisera against RSV nucleocapsids were used as immunoreagents for this test system. The results obtained by RSV antigen ELISA were compared to those of indirect immunofluorescence (IF) and tissue culture virus isolation (TC). Of the 404 NPS obtained, 278 were tested in parallel by ELISA and IF and 205 by ELISA and TC, and 89 were screened in parallel by all three methods. The sensitivity of ELISA in relation to IF was 86.7%, the specificity 95.7%. Sensitivity and specificity obtained by ELISA were 89.9% and 94.4%, respectively, compared to TC. False-negative results were obtained with all three test systems used.

Adolescent↗
PubMed1986

Urinary kallikrein excretion in healthy young infants.

Nineteen healthy hospitalized children aged between 3 weeks and 10 years and 20 others aged between one month and 16 years have been investigated for their excretion rate of active and total urinary kallikrein. Twelve hour urine samples were obtained between 7 p.m. and 7 a.m. and blood was drawn at the end of the urine collection period. Urinary kallikrein activity was measured by a synthetic substrate and a direct RIA and urinary sodium excretion, urine volume and plasma renin activity (PRA) were determined. Urinary kallikrein activity was found to be between 0 and 6 micrograms/24h and constituted approximately 10-20% of total kallikrein. When urinary kallikrein excretion rate was correlated with the sodium excretion rate the relationship was found to be positive and significant as was the correlation found between urine volume and urinary kallikrein excretion rate. No correlation could be found between PRA and urinary kallikrein excretion. Although a tendency of higher total kallikrein excretion was seen in older children, the amount excreted from all children per kilogram body weight was constant at 0.8 microgram/kg.

Child↗
PubMed1986

The effect of residual beta-cell function on the development of diabetic retinopathy.

The effect of residual B-cell function on retinopathy was evaluated in a cross-sectional study of 533 insulin-dependent diabetic patients (disease duration 0 to 45 years). One hundred and fifty-three patients with residual B-cell function, as evaluated by stimulated plasma C-peptide concentration, had lower prevalence of retinopathy than patients without B-cell function. The patients with B-cell function had a shorter duration of diabetes and were older at onset, but there was no difference in age at the time of the study. When patients with similar duration of diabetes were compared, no differences in the degrees of retinopathy could be demonstrated between patients with and without B-cell function. These results indicate that residual B-cell function does not protect against or delay the development of diabetic microvascular lesions.

Adolescent↗
PubMed1986

Frequency of daytime biochemical hypoglycaemia in insulin-treated diabetic patients: relation to daily median blood glucose concentrations.

The frequency and distribution of daytime biochemical hypoglycaemia (capillary blood glucose concentration below 3 mmol/l) was assessed in type 1 diabetic patients on conventional twice daily insulin therapy (n = 79) and on continuous subcutaneous insulin infusion (n = 20). Patients collected and mailed to the hospital blood for seven-point blood glucose profiles. For both treatment regimens the frequency of biochemical hypoglycaemia on individual days was inversely related to the median blood glucose concentration in a curvilinear manner (p less than 0.001). Hypoglycaemia was more frequent pre-prandially than post-prandially (p less than 0.01), and was evenly distributed during the day in patients on continuous subcutaneous insulin infusion. In patients on conventional therapy, however, pre-lunch hypoglycaemia was four times more frequent than pre-breakfast or pre-dinner hypoglycaemia (p less than 0.0001).

Adolescent↗
PubMed1986

Insulin release and pancreatic insulin is reduced in young prediabetic BB rats.

The pancreases of approximately 50 days old diabetes-prone BB/Hagedorn (BB/H) and of the genetically closely related, but non-diabetic BB w-subline (control BB) rats were perfused to determine the capacity of D-glucose to release insulin before the expected development of diabetes. The BB/H rats were from a colony with 82-84% incidence of insulin-dependent diabetes mellitus (IDDM) by 140 days of age. The total amount of insulin released from the BB/H rat pancreas during stimulation with 20 mmol/1 mmol/ D-glucose was reduced by nearly 50% (P less than 0.01). The initial peak of insulin release was similar between the two groups of animals, whereas the amount of insulin released during the second peak accounted for the diminished release (P less than 0.01). The extractable pancreatic insulin was 30% (P less than 0.05) less in the BB/H rats. Total insulin release expressed relative to the pancreatic insulin content, was therefore not different between the two groups. It is concluded that about 20-40 days before the mean age of clinical onset of IDDM in BB/H rats, the capacity to release insulin in response to D-glucose is reduced along with a diminished pancreatic insulin content. This abnormality seems to be preceded only by islet cell surface antibodies but not by insulitis.

Animals↗
PubMed1985

Nocturnal hypoglycaemia in patients receiving conventional treatment with insulin.

The prevalence of nocturnal biochemical hypoglycaemia--that is, blood glucose concentrations below 3 mmol/l (55 mg/100 ml)--was evaluated in a random sample of 58 insulin dependent diabetics receiving twice daily insulin. Seventeen patients had at least one blood glucose value below 3 mmol/l (55 mg/100 ml) and five a value below 2 mmol/l (36 mg/100 ml) during the night. Both bedtime (2300) and fasting morning (0700) blood glucose concentrations were significantly lower in the group with nocturnal hypoglycaemia compared with the group without (p less than 0.00001). If the bedtime blood glucose concentration was below 6 mmol/l (108 mg/100 ml) the risk of nocturnal hypoglycaemia was 80% (95% confidence limits 51-96%). If the bedtime blood glucose concentration was above 6 mmol/l the likelihood of hypoglycaemia not occurring during the night was 88% (74-96%). The mean glycosylated haemoglobin A1c (HbA1c) concentration in the group with nocturnal biochemical hypoglycaemia (8.2 (range 5.0-12.4)%) was significantly lower than that in the group without (9.4(7.0-14.2)%) (p less than 0.02). The prevalence of nocturnal hypoglycaemia in the patients receiving twice daily insulin (29%) was compared with that in 15 patients receiving thrice daily insulin (47%) and was not found to be significantly different. The likelihood of this risk being greater with thrice daily insulin was, however, 88%. No patient with nocturnal biochemical hypoglycaemia woke up during the night with symptomatic hypoglycaemia. Nocturnal biochemical hypoglycaemia is common during twice daily treatment with insulin, and low values of HbA1c might be associated with a higher risk of such hypoglycaemia. The blood glucose concentration at bedtime is a significant predictor of nocturnal biochemical hypoglycaemia, and HbA1c values might be of help in identifying patients at risk.

Adolescent↗
PubMed1985

Increased reduction in fasting C-peptide is associated with islet cell antibodies in type 1 (insulin-dependent) diabetic patients.

A cohort of 82 patients with Type 1 (insulin-dependent) diabetes was followed prospectively for 24 months, and 54 of them for 30 months, to study the relationship between fasting levels of immunoreactive C-peptide and titres of islet cell antibodies. After diagnosis, fasting C-peptide rose temporarily for 1-6 months of insulin therapy and declined continuously thereafter. While islet cell antibodies were present among 55% of the newly diagnosed patients, only 31% remained positive at 30 months. Their antibody titres decreased from 1:81 at diagnosis to 1:3. Only 3 patients (4%) who were islet cell antibody negative at diagnosis became positive later. The median C-peptide values among the persistently islet cell antibody positive patients decreased from 0.11 pmol/ml at 18 months, to 0.09 pmol/ml at 24 months, to 0.06 pmol/ml at 30 months compared to 0.18 (p = 0.04), 0.15 (p = 0.05) and 0.16 (p less than 0.003) pmol/ml, respectively, for the islet cell antibody negative patients. The median slope for the latter was -0.09 compared to -0.19 for the islet cell antibody positive patients (p = 0.01). These differences were reflected in increasing dosages of insulin, since patients remaining antibody-positive for 30 months were given 1.3-1.4 times more insulin (p = 0.01-0.004) than the antibody negative patients. This study demonstrates that islet cell antibodies may be a useful marker for predicting an increased rate by which endogenous B cell function is lost in Type 1 diabetes.

Adolescent↗
PubMed1985

Studies of monoclonal antibodies specific for major histocompatibility complex products of the rat. II. Production and characterization of xenogeneic, allogeneic, and syngeneic polyclonal anti-idiotypic antibodies.

Polyclonal anti-idiotypic antibodies against monoclonal antibodies with specificity for RT1-encoded antigens were induced in syngeneic, allogeneic, and xenogeneic hosts. The immune response to the idiotypic determinants on monoclonal antibodies was T-cell-dependent. The anti-idiotypic antibodies, independent of whether they were induced in syngeneic, allogeneic, or xenogeneic (after proper absorption) hosts, showed an exquisite specificity for the monoclonal antibody used for the induction. No cross-reactivity with other monoclonal antibodies could be observed.

Animals↗
PubMed1985

Kinetic models for plasma disappearance of insulin in normal subjects.

Three theoretical kinetic models for plasma disappearance of insulin were examined in six normal men. The models allowed for the existence of non-saturable and/or saturable mechanisms. Constant infusion of porcine insulin at different rates was used to achieve different levels of steady state plasma insulin concentrations, while normoglycaemia was secured by a glucose clamp technique. Appropriate validation procedures demonstrated that one of the three models was superior to the others in describing the relationship between the exogenous insulin infusion rate Iex and the steady state plasma insulin concentration C: Iex = -Iend + k2 X C/(k3 + C), where Iend is the endogenous post-hepatic insulin delivery rate. Thus, only saturable mechanism(s) could be demonstrated. The median value of k2 (the maximal insulin disappearance rate) and k3 (the plasma insulin concentration at which the insulin disappearance rate is half maximal) were 7.31 nmol X min.-1 and 3.89 nmol X 1-1. The median value of k2/k3 (the clearance rate of insulin for infinitesimal plasma insulin concentrations) was 25.0 ml X kg-1 X min.-1. Thus, at physiological levels of plasma insulin concentrations the metabolic clearance rate of insulin is higher than insulin clearance estimates previously reported in studies based on the assumption of first order kinetics.

Adolescent↗