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Biomedical subjects

C Kilo

Publications and source records attributed to C Kilo.

At least 91 records · Page 5Linked to original sources
PubMed1977

Histocompatibility antigens and diabetic retinopathy.

Of 160 patients with onset of diabetes at or after 30 years of age, the 84 with no evidence prevalences of HLA-A1 and B8 when compared with the 76 with retinal complications or with the 282 healthy blood donors. In addition, in 90 patients with onset of diabetes before age 30 years, we could confirm the reported significant increase of HLA-B8 and decrease of B7, but no differences were noted between those juvenile-onset diabetics with and those without retinopathy.

Adult↗
PubMed1977

Monozygotic triplets with discordance for diabetes mellitus and diabetic microangiopathy.

A set of monozygotic triplets (PE.K., P.K., S.K.) has been studied. There is no diabetes in first-degree relatives. PE.K. developed insulin-requiring (60 U. NPH) diabetes at the age of 13 years. Over a period of 11 years since that time, numerous studies of insulin and growth-hormone secretion were performed on P.K. and S.K., including multiple oral glucose tolerance tests (OGTTs), cortisone-primed oral glucose tolerance tests (C-OGTTs), intravenous glucose tolerance tests (IVGTTs), and intravenous tolbutamide tests (IVTTs). The results of each test were compared with age- and sex-matched control subjects. P. K. developed insulin-requiring (56 U. NPH) diabetes after remaining discordant for eight years. Glucose, insilin, and growth-hormone responses during all tests were normal except during the IVGTT performed four months prior to the onset of diabetes. This last IVGTT revealed a glucose disappearance rate of 0.98 per cent per minute, and the slope of the regression line of serum-insulin response (IRI) on blood glucose (BG) was markedly decreased to 0.005 micronU./ml. IRI/mg./dl. BG (controls 0.340 +/- 0.04; mean +/- S.E.M.). The insulin responses in P.K. and S.K. were similar during all OGTTs, C-OGTTs, and IVTTs. S.K. has continued to maintain normal glucose tolerance and normal insulin and growth-hormone responses during all tests. The histocompability antigen studies have revealed HLA-A2, AW24, BW15, and BW40 phenotype in these monozygotic triplets. Muscle capillary basement membranes of the nondiabetic triplet were normal, whereas both diabetic triplets manifested evidence of capillary basement membrane thickening. The clinical and biochemical profiles in these triplets and the capillary basement membrane data lend strong credence to the role of "nongenetic" determinants in the development of "genetic" diabetes as well as diabetic microangiopathy in juvenile-onset-type diabetes.

Adolescent↗
PubMed1976

Hemoglobin AIc as an indicator of the degree of glucose intolerance in diabetes.

Hemoglobin AIc concentration, fasting blood sugar, response to an oral glucose tolerance test, and skeletal muscle capillary basement membrane thickness were measured in diabetic patients. Hemoglobin AIc concentration correlates with both response to a glucose tolerance test (r = 0.82, p less than 0.001) and fasting blood sugar (r = 0.62, p less than 0.001). The correlation of hemoglobin AIc concentration with glucose tolerance is independent of fasting blood sugar concentration (partial r = 0.61, p less than 0.005), whereas that of hemoglobin AIc with fasting blood sugar probably reflects the relationship between fasting blood sugar levels and glucose tolerance (partial r = 0.22, p less than 0.05). Hemoglobin AIc levels do not correlate with basement membrane thickness ( r = 0.15, p less than 0.05).

Basement Membrane↗
PubMed1976

Influence of fixation and morphometric technics on capillary basement-membrane thickening prevalence data in diabetes.

Muscle tissue obtained by needle biopsy from 20 diabetic subjects and from 20 age-matched control subjects was divided into two portions, one of which was fixed and processed by our routine procedure (primary glutaraldehyde fixation followed by osmium fixation and embedment in araldite) and the other was fixed initially in osmium tetroxide and embedded in maraglas, the procedure employed by Siperstein et al. Basement-membrane width of capillaries was measured by the 20-point method of Siperstein et al. and by the two-minimum-point technic developed in our own laboratory. Contrary to the experience of Siperstein et al., the prevalence of basement-membrane thickening in diabetic subjects based on mean width values and/or standard deviations in excess of 95 per cent tolerance intervals was highest (65 per cent) in minimum measurements of glutaraldehyde-fixed tissues and lowest (30 per cent) in osmium-fixed tissues (X2 = 4.9123, p less than 0.05). Internal discrepancies in the data of Siperstein et al. indicate that (1) their basement-membrane-width values derived from multiple measurements from control subjects are anomalous (low) and (2) the very high prevalence of basement-membrane thickening they reported in diabetic and in prediabetic subjects and considered as strong support for their conclusion that basement-membrane disease is independent of and precedes glucose intolerance is suspect.

Adult↗
PubMed1976

Basement-membrane thickening and diabetic microangiopathy.

This report considers the pathophysiologic significance of capillary basement-membrane thickening in diabetic nephropathy and retinopathy and the relationship of capillary basement-membrane thickening to increased susceptibility to infections and to increased vascular permeability in diabetes. The evidence available (1) indicates that basement-membrane thickening affects most if not all capillaries of the diabetic and may contribute to increased susceptibility to infection and (2) suggests that increased capillary permeability in diabetes need not be attributed to basement-membrane changes per se, but rather may be due to changes in the cellular elements of the capillary wall.

Animals↗
PubMedDate not supplied

Effects of nephrectomy and high-protein diets on glomerular hemodynamics and urinary protein excretion in diabetic rats.

Renal blood flow, GFR, albumin clearance, and urinary excretion of proteins were assessed in intact control and streptozotocin-diabetic rats (group 1), unilaterally nephrectomized control and diabetic rats (group 2), and nephrectomized control and diabetic rats (divided into high (a) and low (b) glycemia subgroups) fed a 50% protein diet (group 3). After 8 months of diabetes, blood flow did not differ from control rats within each experimental group, although it was increased significantly in both controls and diabetics of groups 2 and 3 versus group 1. GFR in control rats was increased approximately 2x by nephrectomy and approximately 3x by nephrectomy plus the high protein diet. Diabetes increased GFR approximately 50% above control values in group 1; GFR values in diabetic rats of groups 2 and 3a were virtually identical and similar to those of group 2 controls; GFR in group 3b diabetics was increased approximately 1.4x versus group 2 diabetics. 125I-BSA clearance was increased 3.4x in groups 2 and 3 control rats versus group 1 controls. Both nephrectomy and consumption of the high protein diet caused marked increases in 125I-BSA clearance and urinary excretion of albumin in diabetic rats. Urinary excretion of IgG was increased by diabetes in group 1 and remained essentially at this level in groups 2 and 3 diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Coronary vascular hemodynamic and permeability changes during reperfusion after no-flow ischemia in isolated, diltiazem-treated rabbit hearts.

Effects of diltiazem on coronary vascular functional integrity were assessed in isolated rabbit hearts during reperfusion after 30 min of global, no-flow ischemia. External detection of radiolabeled albumin, [125I]bovine serum albumin ([125I]BSA), and compartmental-model analysis were used to estimate the mean transit time of [125I]BSA (tBSA), vascular volume (V1), and vascular into extravascular space clearance (F21) for [125I]BSA. Perfusion pressure, left ventricular (LV) end-diastolic pressure, LV developed pressure, maximum +dP/dt, and V1 remained constant during 5 h of continuous perfusion, while tBSA and F21 gradually increased (1.5 and 2.4 times baseline, respectively). Diltiazem, 4 microM, increased total water content (8.5%) and decreased perfusion pressure (11%), LV developed pressure (22%), and +dP/dt (24%) in nonischemic control experiments, but did not significantly affect estimates of V1, extracellular space, tBSA, or albumin permeation. During reperfusion after 30 min of ischemia, V1 increased 40% and perfusion pressure increased 60%, while tBSA and F21 increased three and eight times baseline, respectively. LV developed pressure and +dP/dt returned to control levels, even though the water content and extracellular space of ischemic hearts were increased significantly. Diltiazem, 4 microM, blocked ischemia-reperfusion-induced increases in water content, extracellular space, vascular resistance, V1, and vascular permeability to [125I]BSA, without reducing LV developed pressure or +dP/dt relative to nonischemic diltiazem controls. These results suggest that protection of ischemic myocardium by diltiazem is mediated, at least in part, by preservation of vascular functional integrity.

Animals↗