In a sample of 1.033 diabetic patients characteristics of 10 group specific systems (ABO, MNS, Rh, P, K and Fy blood groups and Hp, Gc and Gm serum types) were tested in order to verify any association of hereditary group specific traits and diabetes.
In a sample of 1.033 diabetic patients characteristics of 10 group specific systems (ABO, MNS, Rh, P, K and Fy blood groups and Hp, Gc and Gm serum types) were tested in order to verify any association of hereditary group specific traits and diabetes.
In a sample of 1.033 diabetic patients characteristics of 10 group specific systems (ABO, MNS, Rh, P, K and Fy blood groups and Hp, Gc and Gm serum types) were tested in order to verify any association of hereditary group specific traits and diabetes.
In a sample of 1.033 diabetic patients characteristics of 10 group specific systems (ABO, MNS, Rh, P, K and Fy blood groups and Hp, Gc and Gm serum types) were tested in order to verify any association of hereditary group specific traits and diabetes.
In a sample of 1.033 diabetic patients characteristics of 10 group specific systems (ABO, MNS, Rh, P, K and Fy blood groups and Hp, Gc and Gm serum types) were tested in order to verify any association of hereditary group specific traits and diabetes.
There was a tendency toward an increased incidence of cancer in families with infants who had elevated CEA levels and a reverse trend was noted with respect to diabetes; however, these associations were not statistically significant.
This review discusses a number of such techniques and their applicability to the study of diabetes and hypertension with the renin-angiotensin system as an example.
Heterozygous individuals expressing both wildtype and mutant tyrosine kinase-defective insulin receptor precursors demonstrate varying degrees of insulin resistance and diabetes.
Glucokinase is thought to play a glucose-sensor role in the pancreas, and abnormalities in its structure, function, and regulation can induce diabetes.
DNA polymorphisms in the glucokinase gene have recently been shown to be tightly linked to early-onset non-insulin-dependent diabetes mellitus in approximately 80% of French families with this form of diabetes.
Here we report linkage between the glucokinase locus on chromosome 7p and diabetes in 16 French families with maturity-onset diabetes of the young, a form of NIDDM characterized by monogenic autosomal dominant transmission and early age of onset.
There was no significant correlation between GLUT4 polypeptide levels and HbA1c, fasting plasma glucose, insulin, or free fatty acids, daily insulin dose, duration of diabetes, or subject age but in IDDM subjects GLUT4 protein levels correlated negatively with body mass index.
Amyloid deposits characteristically associated with pancreatic islets of those species (e.g., humans, cats, and monkeys) that develop age-associated forms of diabetes have been shown to represent a concentrated and polymerized form of a previously unknown islet-derived protein identified either as IAPP or amylin.
HLA-C2, AK-2, and MNSs-S also were associated positively with proliferative retinopathy, and HLA-DR8 was associated inversely with this complication of diabetes in each case before adjusting for the number of comparisons.
HLA-C2, AK-2, and MNSs-S also were associated positively with proliferative retinopathy, and HLA-DR8 was associated inversely with this complication of diabetes in each case before adjusting for the number of comparisons.
HLA-C2, AK-2, and MNSs-S also were associated positively with proliferative retinopathy, and HLA-DR8 was associated inversely with this complication of diabetes in each case before adjusting for the number of comparisons.
HLA-C2, AK-2, and MNSs-S also were associated positively with proliferative retinopathy, and HLA-DR8 was associated inversely with this complication of diabetes in each case before adjusting for the number of comparisons.
Expression of functional human Epstein-Barr virus/C3d receptor ([CR2] CD21) on insulinoma cell line. Induction of tumor rejection but not diabetes in syngeneic rats.
Of the 16 pedigrees ascertained for Type 2 diabetes, at least one recombinant event between diabetes and the insulin receptor locus was present in seven pedigrees.
The higher expression of rat PDI mRNA in diabetes is due to an increase in the transcriptional rate of the gene, and insulin treatment of diabetic animals produces within 30 min a decrease in the level of transcription of PDI gene, as judged by nuclear run-on transcription experiments performed in vivo.
The higher expression of rat PDI mRNA in diabetes is due to an increase in the transcriptional rate of the gene, and insulin treatment of diabetic animals produces within 30 min a decrease in the level of transcription of PDI gene, as judged by nuclear run-on transcription experiments performed in vivo.