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E Colle

Publications and source records attributed to E Colle.

At least 37 records · Page 2Linked to original sources
PubMed1988

Incidence of IDDM in Montreal by ethnic group and by social class and comparisons with ethnic groups living elsewhere.

We examined the incidence of insulin-dependent diabetes mellitus (IDDM) among children aged 0-14 yr in Montreal by social class and by ethnic group from 1971 to 1985. There was a slightly higher risk in wealthier as opposed to poorer classes. This income gradient was more marked in younger than in older children. Children of French extraction had about two-thirds the risk of IDDM of children of other origins, mainly British and other European. This mimics the patterns of risk in Europe, where France is reported to have lower rates than does Britain and Scandinavia. The absolute levels of risks among French Canadian and Jewish Canadian children were about double those reported from France and Israel, respectively. These various results are compatible with the hypothesis that both genetic and environmental factors influence IDDM risk.

Adolescent↗
PubMed1988

Epitope specificity of spontaneous and induced thyroglobulin autoantibodies in the rat.

We have investigated the epitope specificities of rat thyroglobulin (Tg) autoantibodies arising either spontaneously in BB hybrid and BB rats or following induction in normal rats with thyroglobulin and adjuvant. Using a panel of thyroglobulins from different animal species it was possible to identify three different patterns of reactivity. These were: 1) recognition of all species of thyroglobulin; (2) recognition restricted to rat and mouse thyroglobulins and 3) recognition biased towards dog, rat and mouse thyroglobulins. Furthermore, using human thyroglobulin manifesting different levels of iodination, it was possible to show that sera with recognition pattern 1 recognized the iodination site of thyroglobulin and that this was inhibitable by thyroxine. Taken together these data provide evidence of restricted epitope recognition by Tg autoantibodies in the rat.

Animals↗
PubMed1988

IDDM in BB rats. Enhanced MHC class I heavy-chain gene expression in pancreatic islets.

Modulation in major histocompatibility complex (MHC) gene expression correlates with the inflammatory reactions that occur during graft rejection and autoimmune disease. We analyzed the expression of class I and II MHC genes in the pancreatic islets of prediabetic and newly diabetic BB rats by immunohistochemistry of tissue sections and Northern blotting of RNA extracted from isolated islets. We show that enhanced levels of MHC class I heavy-chain RNA are present in pancreatic islets before overt inflammation and the onset of insulin-dependent diabetes mellitus (IDDM) in the spontaneously diabetic BB rat. Immunohistochemical analysis revealed enhanced class I antigen expression throughout the pancreatic islets of newly diabetic animals but no induction of class II antigen on endocrine cells within the islet. Varying degrees of inflammatory infiltrate were observed in the sections exhibiting enhanced class I antigen expression or in nearby serial sections. Southern blot analysis revealed no restriction-fragment-length polymorphism or amplification of the endogenous class I heavy-chain genes compared with those of seroidentical disease-resistant Wistar-Furth rats. I-A alpha and I-E alpha hybridizing RNA appeared de novo before overt diabetes, although concomitantly with T-lymphocyte-receptor beta-chain and interferon-gamma gene hybridizing RNA and after MHC class I heavy-chain RNA enhancement was observed. These data indicate the possibility that enhanced class I heavy-chain gene expression plays a role in the progression of IDDM.

Animals↗
PubMed1988

The effect of diet on the spontaneous insulin dependent diabetic syndrome in the rat.

We have fed rats prone to developing spontaneous insulin dependent diabetes mellitus (IDDM) defined diets in which casein was the sole source of protein and the fat content was either menhaden oil, safflower oil, or corn oil. The incidence of IDDM was compared to that in litter mates fed rat chow. Animals receiving the defined diets had a lower frequency of overt IDDM than did animals receiving rat chow. The effect was seen only when the diet was introduced before the animals had reached the age of 30 days. The defined diets did not affect the distribution of peripheral blood T lymphocytes. Rats fed defined diets had decreased intensity of expression of Class I major histocompatibility complex (MHC) products on the endocrine cells of the pancreas compared to animals receiving rat chow.

Animals↗
PubMed1987

Major histocompatibility complex restriction of T-lymphocyte responses to islet cell antigens in IDDM rats.

BBUF rats, derived from BB rats, spontaneously develop a form of insulin-dependent diabetes mellitus (IDDM) associated with infiltration of the islets of Langerhans by lymphocytes (insulitis). BBUF rats bear the RT1u major histocompatibility complex (MHC) haplotype that we have shown to be necessary for the expression of this form of IDDM. A T-lymphocyte line obtained from the pancreas of a diabetic rat (UPCC.5) and three T-lymphocyte hybridomas derived by fusing T-lymphocytes of BBUF rats (MUS1.2, MUS1.13, and MUP3.21) respond to islet cell antigens in an MHC-restricted way. UPCC.5 responds to a combination of islet cell antigens (ICAg) and antigen-presenting cells by proliferation, whereas the T-hybridoma responses are detected on the basis of IL-2 production in a similar assay. This study reveals that an antiserum against mu-haplotype MHC antigens or a monoclonal antibody against the product of the D class II subregion of the rat MHC could inhibit ICAg recognition. A monoclonal antibody against the product of the B class II MHC subregion of the rat was not inhibitory. These results suggest that RT1.D antigens (analogous to human DR and mouse I-E) restrict islet cell recognition in this rat model of spontaneous IDDM.

Animals↗
PubMed1986

The distribution of type I (insulin-dependent) diabetes mellitus by age, sex, secular trend, seasonality, time clusters, and space-time clusters: evidence from Montreal, 1971-1983.

The etiology of insulin-dependent diabetes mellitus remains obscure. In an attempt to clarify some aspects of the epidemiology, including its compatibility with an acute infectious process, the authors undertook in-depth analyses of childhood cases accumulated in a population-based register in Montreal during the period from 1971-1983. Incidence rates increased with age until puberty, at which point they plateaued and decreased. There was no overall difference in incidence between males and females; however, the rate for females peaked approximately two years before the rate for males. While there was some variation over time, there was no evidence of a long-term trend, nor was the yearly variation impressive in magnitude. The findings further indicate that the disease is not characterized by explosive outbreaks. There was slight seasonality, with a 28% higher rate of onset in fall and winter than in spring and summer. There was some evidence of space-time clustering in 1971-1973, but not thereafter. Taken as a whole, these findings do not support the hypothesis that a significant portion of insulin-dependent diabetes is caused by an acute infectious process.

Adolescent↗
PubMed1986

Insulin-dependent diabetes mellitus is associated with genes that map to the right of the class I RT1.A locus of the major histocompatibility complex of the rat.

Previous studies have demonstrated that the presence of at least one u-haplotype of the rat major histocompatibility complex (MHC), RT1, is a necessary but not sufficient condition for the development of overt diabetes mellitus. The present studies were undertaken to determine which portion of the RT1 gene complex is necessary for the occurrence of diabetes. We crossed hooded diabetic rats (RT1.AuBuDu) with PVGr8 rats (RT1.AaBuDu). F1 animals were mated to give 82 F2 animals and backcrossed with the hooded diabetics to produce 41 backcross animals. Diabetes occurred in animals with all three possible RT1.A genotypes. The diabetes was similar to that seen in BB rats and in hybrid strains developed from them. An immunoregulatory defect was marked by decreased percentage of peripheral blood lymphocytes staining with w3/25 monoclonal antibody, by an increased percentage of peripheral blood lymphocytes binding a mouse ascites control protein, and by decreased responsiveness of peripheral blood lymphocytes to stimulation by concanavalin A. We conclude that the u-allele of the class I A-locus gene product is not necessary for susceptibility to the development of diabetes in the rat. Therefore, either genes coding for the class II products of the u-haplotype or genes in linkage disequilibrium with these genes and mapping to the right of the A locus provide the permissive condition. Furthermore, the data suggest, but do not prove, that the u-haplotype derived from a strain remote from the BB rat can confer this susceptibility to the development of diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Genetics of the spontaneous diabetic syndrome. Interaction of MHC and non-MHC-associated factors.

The occurrence of the spontaneous insulin-dependent diabetic syndrome in the rat is the result of several genetic susceptibilities. There is a requirement for the u haplotype of the rat major histocompatibility complex (MHC), RT1. More specifically this requirement is for genes mapping to the right of the RT1 A locus, which codes for class I products. Furthermore, u haplotypes from inbred strains other than the BB rat can provide this permissive u haplotype. Diabetes occurs in animals with either one or two u haplotype and the diabetic syndrome is similar in its characteristics. In addition to the requirement for the MHC genes, there are abnormalities of the immune system of the various diabetes-prone strains, which are present in animals that develop overt disease. These abnormalities segregate independently of the RT1 and interaction between the susceptibilities is necessary for the manifestation of the complete clinical syndrome.

Alleles↗
PubMed1985

Association of spontaneous thyroiditis with the major histocompatibility complex of the rat.

Overt insulin-dependent diabetes mellitus in the rat is associated with the u haplotype of the rat major histocompatibility complex (MHC), RT1. Thyroiditis of sufficient severity to result in elevation of TSH levels is seen in Buffalo rats (RT1b). In order to examine the association of autoimmune thyroid disease with MHC gene products, we have crossed inbred Buffalo rats with diabetic BB rats and examined the RT1 genotype, the histology of thyroid and pancreatic tissue, and two indices of thyroid function. The data indicate that animals having pancreatic lymphocytic infiltration and insulinopenic overt diabetes mellitus had at least one RT1u haplotype. All but one animal having severe histological thyroid lymphocytic infiltration had at least one RT1b haplotype. Rats with severe thyroiditis had higher mean TSH levels than rats with normal histology or rats with mild thyroiditis. We conclude that gene products of the rat MHC affect the severity of spontaneous organ-specific autoimmune disease in terms of clinically apparent as well as tissue inflammatory disease.

Animals↗
PubMed1979

Partial short arm deletions of the X chromosome and spontaneous pubertal development in girls with short stature.

Five additional examples of partial deletion of the short arm of the X chromosome are reported. All of the patients had short stature. The presence of the other stigmata of Turner syndrome, including ovarian dysfunction, appeared to depend on the location of the deletion. Chromosomal analysis of girls with short stature (less than 140 cm), normal pubertal development, and regular menses may reveal that minor deletions of the short arm of the X chromosome are more frequent than has been previously reported.

Adolescent↗
PubMed1979

Hyperbilirubinaemia and idiopathic hypopituitarism in the newborn period.

Two infants with idiopathic panhypopituitarism presented with severe neonatal hypoglycaemia, hepatomegaly and hyperbilirubinaemia (direct and indirect). Abnormal liver function tests returned to normal over a 5--8 month period. The growth rate in the absence of detectable growth hormone was 50% of normal during the first 6 months. The effect of growth hormone on somatomedin levels and growth rate during the first year of life in one of the infants is described.

Adult↗
PubMed1979

Epidemiologic survey of juvenile-onset diabetes in Montreal.

Active search of hospital records was used to survey insulin-dependent juvenile-onset diabetics younger than 17 years resident in General Montreal at the time of onset of symptoms during a seven-year period (1971-1977). A mean annual incidence of 8.8/100,000 was found with variation from year to year (5.8 to 10.3). Eighty percent were five years of age or more at time of diagnosis, and the increase with advancing age was similar to that seen in other studies including the somewhat earlier increase in incidence among females. Seasonal peaks were noted in some but not all years and were more marked in years of high incidence and among males. More cases occurred in areas of high socioeconomic level as measured by average family income. The estimated incidence among siblings of diabetics is 15 times the incidence in the general population. Ten percent of diabetics have a first degree relative who is insulin dependent.

Adolescent↗
PubMed1979

The antenatal use of betamethasone in the prevention of respiratory distress syndrome: a controlled double-blind study.

One hundred forty-six pregnant women were enrolled in a prospective double-blind study to assess the effectiveness and side-effects of antenatal administration of betamethasone in the prevention of respiratory distress syndrome (RDS) in potentially premature infants. On admission to the study, the women were given, at random, either 12 mg of betamethasone or placebo. The same dose was repeated 24 hours later and then weekly up to 34 weeks of gestation. Gestational age of the infants ranged from 25 to 34 weeks, and birth weights ranged between 730 and 2,650 gm. Statistically significant differences in favor of the infants in the betamethasone group were found in the incidence of RDS, 20.7% in the betamethasone group compared with 59.5% in the control group (P less than .005); in the severity of RDS (P less than .05); and in the death rate (P less than .05). A higher incidence of hypoglycemia was found among infants in the betamethasone group (P less than .05). Prolonged rupture of the membranes played no protective role against RDS, and the incidence of infection was similar in both groups.

Betamethasone↗
PubMed1978

Peripheral total parenteral nutrition for premature infants with the respiratory distress syndrome: a controlled study.

In 40 premature infants, in whom severe respiratory distress precluded oral feeding, peripheral total parenteral nutrition consisting of casein hydrosylate, dextrose, and soybean emulsion was compared to nutrition with dextrose and electrolytes. The TPN group received more calories, and the total serum protein in them increased significantly. Metabolic complications did not occur. Transient thrombocytosis occurred in six infants who received TPN and eosinophilia occurred in nine. The case fatality rate in the TPN group (three of 20) was not significantly less than in the glucose group (six of 20). The differences suggested that infants who weigh less than 1,500 gm may receive the greater benefit from TPN.

Blood Proteins↗
PubMed1978

Antiserum to somatostatin reverses starvation-induced inhibition of growth hormone but not insulin secretion.

The role of SRIF in starvation-induced inhibition of GH and insulin secretion was assessed by passive immunization with anti-SRIF serum. Six-hour secretory profiles obtained from chronically cannulated male rats deprived of food for 72 h showed marked suppression of GH secretory bursts and significant depression of plasma insulin levels. Administration of 1 ml SRIF antiserum (SRIF AS) iv to starved rats resulted in rapid (within 15 min) restoration of high amplitude GH pulses (600-800 ng/ml) and sighificant elevation of GH trough values. The mean 6-h GH level of starved SRIF, AS-treated rats (189.2 +/- 23.9 ng/ml) was significantly higher than that of starved, normal sheep serum-treated control animals (62.8 +/- 5.8 ng/ml) (P less than 0.005). In contrast to the effects on GH, plasma insulin levels in starved rats administered SRIF AS remained low. No significant difference was observed in the mean 6-h plasma insulin level of starved-SRIF, AS-treated rats when compared to starved, normal sheep serum-treated controls. These findings suggest that circulating SRIF is a physiological regulator of starvation-induced GH suppression but is not involved in mediating the inhibition of insulin.

Animals↗