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Biomedical subjects

J Barbosa

Publications and source records attributed to J Barbosa.

At least 163 records · Page 9Linked to original sources
PubMed1978

Analysis of linkage between the major histocompatibility system and juvenile, insulin-dependent diabetes in multiplex families. Reanalysis of data.

Linkage analysis between the major histocompatibility system (HLA) and juvenile, insulin-dependent diabetes, assuming an autosomal recessive mode and 50% penetrance was performed on 21 juvenile, insulin-dependent diabetic multiplex families (two or more diabetics per sibship) with phenotypically normal parents. The total lod score was the highest (3.98) at a recombination fraction of 13%. For a penetrance of 100%, the highest total lod score was 2.92 at a recombination fraction of 18%. These results are compatible with the existence of linkage between an autosomal recessive diabetic gene with 50% penetrance and the HLA in some of the families studied. Our ascertainment strategy would be expected to increase the likelihood of selecting for genetically homogenous diabetes and against sporadic forms of the disease. Thus, our findings may apply only to a small proportion of all cases of juvenile, insulin-dependent diabetes.

Diabetes Mellitus, Type 1↗
PubMed1978

Plasma glucose, insulin, glucagon, and growth hormone in kindreds with maturity-onset type of hyperglycemia in young people.

Two kindreds affected by maturity-onset type of hyperglycemia in young people were studied. The postglucose-load hyperglycemia segregated as an autosomal dominant trait; it was always mild, never requiring insulin, and generally seemed to start in the first two decades of life. Glucose, insulin, glucagon, and growth hormone were measured during glucose-tolerance tests in patients, relatives, and control subjects. Most hyperglycemic patients were found to have insulin deficiency. There was no correlation between the age of the patients and insulin secretion. Plasma glucagon and growth hormone were normal. Maturity-onset type of hyperglycemia in young people may be a frequent type of hyperglycemia, and its identification will generally depend on the presence of a strong family history. The recognition of maturity-onset type of hyperglycemia in young people as a specific disease different from juvenile, insulin-dependent diabetes is important, especially to prevent unnecessary use of insulin in hyperglycemic children.

Adolescent↗
PubMed1978

Immunofluorescence studies of skeletal muscle extracellular membranes in diabetes mellitus.

Skeletal muscle from 34 insulin-dependent diabetic patients and 20 age-matched controls was examined by immunofluorescent microscopy. Significantly increased staining of capillary and muscle basement membranes of diabetics was seen for IgG, albumin, and fibrin. The immunofluorescent pattern was identical with that observed using heterologous antibasement membrane antiserum, indicating that these proteins were present within these basement membranes. No differences were detected between males and females or between kidney-transplanted and nontransplanted diabetics. No correlation was noted between intensity of staining and duration of diabetes. The presence of certain serum proteins within vascular and nonvascular basement membranes in diabetics is not restricted to the kidney and may reflect widespread alterations in extracellular membranes that permit entrapment of these proteins.

Albumins↗
PubMed1978

HLA in maturity-onset type of hyperglycemia in the young.

HLA haplotypes in a kindred with a maturity-onset type of hyperglycemia in the young (MOHY) were studied. All diabetics had mild hyperglycemia of early onset, and the inheritance pattern suggested an autosomal dominant trait. Eight of 11 subjects with hyperglycemia shared haplotype A3, Bw15. When only this haplotype was considered, there appeared to be a significant association with hyperglycemia chi2 = 6.36). However, since both haplotypes in the proband could be associated with hyperglycemia (both proband's parents had hyperglycemia), the data for both haplotypes were combined, and analysis for an association between both haplotypes and hyperglycemia was not significant (chi2 = 2.53). Linkage between a diabetes gene causing MOHY and the HLA, evaluated by lod score analysis, was suggested, but the values were not significant.

Adolescent↗
PubMed1977

Analysis of chromium induced carbohydrate intolerance in the rat.

Carbohydrate tolerance was studied by intravenous glucose tolerance tests in normal and chromium deficient rats. A significant difference in glucose metabolism between chromium deficient and chromium supplemented rats was demonstrated only when the glucose decay constant was calculated from the line fitting the plotted logarithms of the excess plasma glucose concentrations. Calculation of the glucose decay constant from the line fitting the logarithms of the total plasma glucose concentrations showed no significant difference between the two groups. This finding suggests that either the first method is more sensitive to mild changes in intravenous glucose tolerance in the rat, or the observed difference is a methodological artifact.

Animals↗
PubMed1977

The histocompatibility system in juvenile, insulin-dependent diabetic multiplex kindreds.

We have histocompatibility (HLA) genotyped 24 families with two or more juvenile, insulin-dependent, ketosis-prone diabetic siblings. This criterion for family selection was used to obtain a homogeneous form of diabetes within a sibship, because diabetes appears to be a genetically heterogeneous disease. 58 diabetic and 53 nondiabetic sibs and 40 parents were studied. 55% of the diabetic pairs were concordant for both HLA haplotypes (expected 25%), 40% were concordant for one haplotype (expected 50%), and 5% were discordant for both haplotypes (expected 25%). These values are significantly different from the expected values (P < 0.001). On the other hand, the inheritance of haplotypes among the nondiabetic sibs in these families was not significantly different from the expected mendelian segregation. When comparing 20 pairs of HLA identical (sharing two haplotypes) with 15 pairs of haploidential (sharing one haplotype) diabetic sibs for the intrapair difference in age of onset of disease, we found that the HLA identical sibs were significantly more concordant for age of onset (3.9 yr difference) than the haploidential (7.3 yr difference) (P < 0.05). The same type of analysis for the difference in seasonal incidence in months revealed that the HLA indentical sibs were more concordant (1.8 mo difference) than the haploidentical sibs (3.2 mo difference) (P < 0.025). Furthermore, the HLA identical diabetic sibs were more likely to develop diabetes in the winter months (78%) than the haploidentical diabetic sibs (21%). No particular HLA haplotype or antigen seemed to be associated with any particular clinical feature. These data are compatible with the theory of genetic heterogeneity of juvenile, insulin-dependent diabetes. It is suggested that there are one or more diabetes response genes in the HLA region playing an important role in the pathogenesis of juvenile, insulin-dependent diabetes in the families studied here. It is, however, possible that other genes, not associated with the HLA complex, may play an etiologic role in some cases of juvenile, insulin-dependent diabetes, resulting in lack of association between HLA and some forms of diabetes.

Adolescent↗
PubMed1977

Kidney transplantation for the uremic diabetic patient.

Although the diabetic patient is at high risk for transplantation and the progression of cardiovascular disease continues, results of our experience indicate that kidney transplantation can be performed with only slightly less favorable results than in the nondiabetic patients. We have found that the survival rate achieved by diabetics who receive a kidney graft is superior to that achieved by diabetic patients who receive dialysis. We also believe that some of the secondary complications of diabetes, which are aggravated by uremia, will be improved and that successful vocational rehabilitation is possible in the majority of diabetic patients.

Adult↗
PubMed1976

Development of diabetic vascular lesions in normal kidneys transplanted into patients with diabetes mellitus.

We examined renal-transplant tissue from 12 diabetic and 28 nondiabetic patients who had had a renal graft for at least two years. In 10 diabetic patients arteriolar hyalinosis lesions developed in the graft. In six these lesions involved both afferent and efferent limbs of glomerular arterioles - a pathological finding virtually diagnostic of diabetes mellitus. In all cases these lesions were present within five years of transplantation. Only three of the 28 nondiabetic patients had hyaline vascular changes (P less than 0.001), which occurred only in rare vessels, did not appear within the first five years after transplantation and did not involve both afferent and efferent arterioles, One diabetic patient had nodular glomerulosclerosis. Thus, the first clearly distinguishable lesion of diabetes to occur with frequency in normal kidneys transplanted into diabetic patients is arteriolar hyalinosis.

Adolescent↗
PubMed1976

Histocompatibility (HLA) antigens and diabetic microangiopathy.

To gain further insight into the genetic determinants of diabetic small vessel disease, we studied 22 HLA antigens in 110 juvenile-onset, insulin-dependent diabetics with terminal glomerulosclerosis and retinopathy, who were being prepared for kidney transplant. HLA antigens were comtemporarily determined in non-diabetic kidney transplant recipients and healthy controls. The frequency of antigens A1 and B8 were significantly higher in diabetics than in controls (P less than .02 and .011), but the frequency of BW15 was normal. The data are compatible with the concept that juvenile diabetes with microangiopathy is one of the HLA-B8 associated disorders.

Adult↗
PubMed1976

Immunopathology of renal extracellular membranes in kidneys transplanted into patients with diabetes mellitus.

Kidneys of patients with severe diabetic nephropathy demonstrate marked linear immunofluorescent staining of extracellular membranes, including the tubular and glomerular basement membranes (TBM and GBM) and Bowman's capsule. Immunofluorescent studies were carried out on kidney tissue obtained from 12 diabetic and 17 nondiabetic patients from two to 12 years following renal transplantation. The frequency and intensity of SgG and albumin staining of these membranes were significantly greater in the diabetic than in the nondiabetic patients (P less than 0.0005). TBM, GBM, and Bowman's capsule staining did not occur in any of the seven kidneys studies at the time of their transplantation into diabetic recipients. Thus, the abnormalities leading to the deposition or trapping of proteins in renal extracellular membranes occur early after the placement of normal kidneys into the abnormal metabolic environment of the diabetic transplant recipient. The present study supports the concept that basement membrane alterations in diabetes are a consequence of the biochemical perturbations of diabetes rather than a separately inherited genetically linked disorder.

Albumins↗