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Biomedical subjects

J W Yoon

Publications and source records attributed to J W Yoon.

At least 127 records · Page 7Linked to original sources
PubMed1987

The relationship between Coxsackie-B-virus-specific IgG responses and genetic factors (HLA-DR, GM, KM) in insulin-dependent diabetes mellitus.

IgG antibody titres to Coxsackie B1-B6 were measured in 113 insulin-dependent diabetes mellitus (IDDM) patients whose mean age was 12.2 years and mean duration of IDDM was 4.6 years, and in 87 normal sibling controls whose mean age was 13.8 years. Compared with their normal siblings, the diabetics had a significantly increased frequency of high response (titre greater than or equal to 320) to Coxsackie B2 (8% versus 1%, p = 0.028), to Coxsackie B4 (15% versus 1%, p = 0.0006), and to Coxsackie B viruses in general (25% versus 5%, p = 0.0001). The frequencies of HLA-DR and immunoglobulin (GM, KM) antigens did not differ between diabetics with and without a high response to Coxsackie B2, B4, or B viruses in general. We conclude that there is an association between IDDM and IgG response to Coxsackie B2, B4, and B viruses in general, a finding which is consistent with the interpretation that infection with Coxsackie B viruses, especially B4, may initiate the development of IDDM in a portion of individuals who have HLA-DR region susceptibility genes.

Adolescent↗
PubMed1987

Effects of environmental factors on the development of insulin-dependent diabetes mellitus.

The development of insulin-dependent diabetes mellitus is thought to be dependent on either the autoimmunity or the interaction of environmental agents with the pancreatic beta cells, or both in a genetically susceptible host. As environmental factors affecting the induction of type I diabetes, diabetogenic chemicals and viruses are likely candidates as primary injurious agents for pancreatic beta cells in man and animal. A number of structurally diverse chemicals including alloxan, streptozotocin, chlorozotocin, vacor, and cyproheptadine are diabetogenic mainly in rodents and sometimes in man. The possible mechanisms for the beta cell destruction by these chemicals include (a) generation of oxygen free radicals and alteration of endogenous scavengers of these reactive species; (b) breakage of DNA and consequent increase in the activity of poly ADP ribose synthetase, and enzyme depleting NAD in beta cells; and (c) inhibition of active calcium transport and calmodulin-activated protein kinase activity. Regarding viruses, a number of different viruses including encephalomyocarditis virus, Mengovirus, Coxsackie B viruses, and Reoviruses can infect and destroy pancreatic beta cells mainly in rodents and sometimes in humans. In the murine model, the development of encephalomyocarditis and Coxsackie B virus-induced diabetes is dependent on the genetic background of the host and the genetic makeup of the virus. Mengo-2T virus has caused diabetes in strains of mice resistant to encephalomyocarditis virus-induced diabetes. In contrast to encephalomyocarditis virus, Coxsackie B viruses, and Mengovirus, reovirus type 1 seems to be somewhat associated with an autoimmune response in the induction of diabetes. In addition to the murine model, cotton rats become diabetic when inoculated with Mengovirus 2T. Furthermore, cumulative environmental insults with Coxsackie B viruses and chemicals result in diabetes in non-human primates. In man, there may be 2 possible roles for viruses in the pathogenesis of insulin-dependent diabetes mellitus. The one is acute cytolytic infection of beta cells (e.g., Coxsackie B viruses), which may sometimes induce diabetes in genetically predisposed individuals, and the other one is slow and persistent infection (e.g., congenital cytomegalovirus and Rubella), which may induce autoimmunity, leading to type I diabetes.

Animals↗
PubMed1987

Diminished complications in a non DR3 DR4 family with insulin-dependent diabetes.

A family is reported in which the mother and both of her children developed insulin-dependent diabetes mellitus between 9 and 19 months of age, reflecting the importance of heredity in the natural history of this disease. That overt complications of diabetes were not present in any of the individuals, and that blood sugars were maintained close to normal on relatively small amounts of exogenous insulin, suggests a protective function in these patients related to residual secretion of insulin by beta cells. Human lymphocyte antigen (HLA) typing in this family showed that, although the diabetic children had identical HLA types, neither the mother nor her children possessed the diabetes-associated antigen HLA-DR3 or HLA-DR4. This raises the possibility that selective loss of diabetes-susceptible fetuses (suggested to be responsible for the low risk of diabetic mothers producing diabetic offspring) may be influenced by the HLA type of the mother.

Adolescent↗
PubMed1986

Lack of protection against ascending Escherichia coli pyelonephritis in diabetic rats following immunization with purified lipopolysaccharide.

Purified lipopolysaccharide of Escherichia coli produced specific antibody when injected intraperitoneally or given to rats orally. Either route of immunization did not prevent ascending pyelonephritis in a diabetic rat model. The use of purified LPS excludes the potential contribution of other virulence factors of E. coli as protective antigens in the prevention of ascending pyelonephritis and confirms that anti-lipopolysaccharide antibody is not protective for ascending pyelonephritis.

Administration, Oral↗
PubMed1986

Rubella virus-induced diabetes in the hamster.

The congenital rubella syndrome provides the best documentation in humans that a viral infection is associated with the subsequent development of insulin-dependent diabetes mellitus. We have developed an animal model in neonatal golden Syrian hamsters infected with rubella virus passaged in beta-cells that closely parallels the diabetes observed with congenital rubella. The hamsters develop hyperglycemia and hypoinsulinemia, which are sustained throughout the 15-wk study period. A mononuclear infiltration of the islets, isolation of rubella virus from whole pancreas, the presence of viral antigen in beta-cells by immunofluorescent localization, and cytoplasmic islet cell antibodies (40%) are demonstrated. These data suggest that an autoimmune process and diabetes develop after rubella virus infection in neonatal hamsters. This model may uncover the precise mechanism by which rubella virus induces similar disease in humans.

Animals↗
PubMed1986

Coxsackie virus B4 produces transient diabetes in nonhuman primates.

Cynomolgus, rhesus, and Cebus monkeys failed to show glucose tolerance or insulin secretion abnormalities after infection with encephalomyocarditis virus or Coxsackie virus B4. Patas monkeys also showed no abnormalities after infection with encephalomyocarditis virus. However, patas monkeys infected with Coxsackie virus B4 or treated first with a subdiabetogenic dose of streptozocin and then infected sequentially with Coxsackie viruses B4 and B3 showed transient elevation of glucose tolerance tests, depressed insulin secretion, and glucose in the urine. Our experiments in nonhuman primates support earlier studies in mice and humans that under certain circumstances, Coxsackie viruses can cause abnormalities in glucose homeostasis.

Animals↗
PubMed1985

Virus-induced diabetes mellitus. No evidence for immune mechanisms in the destruction of beta-cells by the D-variant of encephalomyocarditis virus.

A possible contribution of the immune system to the pathogenesis of virus-induced diabetes mellitus was investigated using the D-variant of encephalomyocarditis (EMC-D) virus. Studies on the F1 and backcross progeny of susceptible and resistant strains of mice gave no suggestion of a linkage between susceptibility and the major histocompatibility locus. Immuno-suppression by antilymphocyte serum did not prevent the induction of EMC-D-induced diabetes. Athymic nude mice infected with EMC-D virus showed a nearly identical diabetogenic response as compared with heterozygous littermates. Passive transfer of lymphocytes from mice made diabetic with EMC-D virus into normal mice failed to produce diabetes. From these and other studies, we conclude that the development of EMC-D-induced diabetes is due to the direct destruction of beta-cells by the virus and that the contribution of the immune response to the pathogenesis of this disease is, at the most, minor.

Animals↗
PubMed1985

Alterations in immunological reactivity in encephalomyocarditis virus-induced murine diabetes. I. Defective primary IgM plaque forming cell responses to sheep erythrocytes: correction by islet cell transplantation.

Increasing data suggest a possible viral aetiology of juvenile onset, insulin-dependent diabetes mellitus. The M variant of the encephalomyocarditis (EMC) virus infects murine pancreatic beta cells and causes a diabetes like syndrome in susceptible strains of mice. Abnormalities in immunological function have been documented in patients with diabetes mellitus and in spontaneous, streptozotocin-induced and alloxan-induced diabetes in animals. The present study documents a significant impairment of the ability of mice with EMC virus (M variant)-induced diabetes to generate a direct, IgM PFC response after in vivo immunization with sheep erythrocytes. This abnormality appears to be a direct consequence of the diabetic state and not EMC virus infection, per se, since mice infected with EMC virus that do not become diabetic have normal direct PFC responses and islet cell transplantation, which cures the diabetes, corrects the defect in PFC responsiveness.

Animals↗
PubMed1984

Incidence of coxsackievirus B type 4 (CB4) infections concomitant with onset of insulin-dependent diabetes mellitus.

From September 1979 to August 1981, a total of 25 children with newly diagnosed insulin-dependent diabetes mellitus (IDDM) were admitted for management to the Pediatric Ward, Lubbock General Hospital, Lubbock, Texas. Parents of the 24 admitted patients gave informed consent for their child to participate in the study. While hospitalized, all study patients donated early-phase (acute) blood samples and specimens for virus isolation attempts. Eighteen of the 24 patients originally enrolled in the study continued to come for follow-up visits to the Endocrinology Clinic of the Department of Pediatrics, and hence, provided the late-phase (convalescent) blood samples for the completion of serologic evaluation. The result of this two-year survey is the following: 1) one of the 24 hospitalized cases yielded a non-CB4 enterovirus; (2) serologically, only 2 of 18 IDDM patients showed some CB4 neutralizing antibody (NtAb) activity, ie, rising titers in their late phase sera. In view of the time of onset of patients' symptoms compatible with IDDm, the diabetogenic input of a past CB4 infection could have been considered in one of these two patients. In conclusion, results of our two-year study indicate that occasionally the onset of IDDM might be associated with an acute CB4 infection.

Adolescent↗
PubMed1984

Virus-induced diabetes mellitus: mengovirus infects pancreatic beta cells in strains of mice resistant to the diabetogenic effect of encephalomyocarditis virus.

In mice, Mengovirus produces a fatal encephalitis. Plaque purification of the virus resulted in the isolation of a clone (Mengo- 2T ), which in addition to encephalitis caused diabetes. Microscopic examination of pancreases from infected mice revealed necrosis in the islets of Langerhans and infiltration of inflammatory cells. By immunofluorescence viral antigens were found in the islets, and radioimmunoassays demonstrated a substantial decrease in pancreatic immunoreactive insulin. Studies on susceptibility among inbred strains of mice showed that whereas the D variant of encephalomyocarditis virus caused diabetes only in SJL/J mice, Mengo- 2T caused diabetes in strains of mice resistant to encephalomyocarditis-induced diabetes (i.e., CBA/J, C3H/HeJ, CE/J, AKR/J, C57BL/6J). The ability of Mengo- 2T to induce diabetes in encephalomyocarditis-resistant mice was found to be due to the greater capacity of Mengo- 2T as compared to the D variant of encephalomyocarditis virus to replicate in and destroy the islets of these animals. Although Mengo- 2T and the D variant of encephalomyocarditis virus are antigenically indistinguishable by hyperimmune sera, our studies show that these viruses have different host ranges and tissue tropisms .

Animals↗
PubMed1984

Decreased bone formation and mineralization in virus-induced diabetes mellitus.

Severe hyperglycemic and hypoinsulinemic mice were selected at 30 and 180 days after infection with the D variant of encephalomyocarditis (EMC) virus. In these animals, although the concentration of calcium and phosphate in serum was not changed, the alkaline phosphatase activity and the rate of mineralization in the proximal tibial epimetaphysis were markedly decreased in the diabetic mice for 30 and 180 days compared with those of the age-matched uninfected animals. Viral specific antigens were not found in these tissues at either earlier or later infection with the virus. It is concluded that endochondral bone formation and mineralization are greatly impaired in EMC virus-induced diabetic mice, and the decreased bone formation and mineralization are not due to the virus-induced tissue damage, but to the persistent metabolic alterations.

Alkaline Phosphatase↗
PubMed1984

CT findings of suprapatellar synovial cysts.

The computed tomographic (CT) findings of two suprapatellar (SP) synovial cysts are presented, and the correlated anatomicopathologic changes are discussed. The cysts show characteristically semilunar shapes and anteromedial locations in the SP regions with superolateral extension. The cyst walls vary in thickness, and the cyst contents also vary from a transudate to a thick mucoid fluid, which may show a high attenuation value on CT. Differential diagnoses include liposarcoma, hematoma, xanthoma, fibrosarcoma, or other soft tissue tumors.

Adolescent↗
PubMed1983

Reduced synthesis of basement membrane heparan sulfate proteoglycan in streptozotocin-induced diabetic mice.

In diabetes, certain basement membranes become thicker yet more porous than normal. To identify possible changes in the basement membrane, we have grown the Engelbreth-Holm-Swarm tumor, a tissue that produces quantities of basement membrane in normal mice and in streptozotocin-treated, insulin-deficient, diabetic mice. The level of laminin, a basement membrane-specific glycoprotein, and the level of total protein were slightly elevated in the diabetic tissue. In contrast, the level of the basement membrane specific heparan sulfate proteoglycan was only 20% of control. The synthesis of this proteoglycan was also reduced in the diabetic animals, while the synthesis of other proteoglycans by tissues such as cartilage was normal. The synthesis of the heparan sulfate proteoglycan in diabetic animals was inversely related to plasma glucose levels showing an abrupt decrease above the normal range of plasma glucose. Insulin restored synthesis to normal but this required doses of insulin that maintained plasma glucose at normal levels for several hours. Since the heparan sulfate proteoglycan in the basement membrane restricts passage of proteins, its absence could account for the increased porosity of basement membrane in diabetes. A compensatory synthesis of other components could lead to their increased deposition and the accumulation of basement membrane in diabetes.

Animals↗
PubMed1983

Virus-induced diabetes in mice.

Encephalomyocarditis (EMC) virus infects and destroys pancreatic beta cells when inoculated into mice. This results in hypoinsulinemia and hyperglycemia. The development of virus-induced diabetes is dependent on the genetic background of the host and the genetic makeup of the virus. In addition to the acute metabolic changes, animals with diabetes for six months show some long-term complications, including reduced life span, glomerulosclerosis, and ocular changes. The development of virus-induced diabetes in mice can be prevented by a live attenuated vaccine.

Animals↗
PubMed1983

The role of interferon in virus-induced diabetes.

The repeated administration of interferon (IFN) or an IFN inducer reduced the development of diabetes in mice infected with the D variant of encephalomyocarditis (EMC) virus. Mice treated with the IFN inducer had less infectious virus, fewer pathologic changes, and higher concentrations of immunoreactive insulin in the islets of Langerhans in comparison with untreated mice. Antibody to mouse IFN (MuIFN) suppressed circulating IFN in mice infected with the B variant of EMC virus. Mice treated with antibody to MuIFN had four times more infected islet cells and 10 times more infectious virus in the pancreas compared with untreated mice. Of the surviving animals treated with antibody to MuIFN, approximately 40% developed mild diabetes whereas none of the mice developed diabetes when infected with the B variant of EMC virus alone. The IFN system is an important determinant of the outcome in EMC virus-induced diabetes in mice.

Animals↗