PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “insulators”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1978

Viral studies in streptozotocin-induced pancreatic insulitis.

Multiple injections of streptozotocin to Charles River (CD-1) Laboratory mice resulted in a syndrome characterised by diabetes mellitus, insulitis and the induction of endogenous type C viruses in pancreatic beta cells. Within one week after the completion of five intraperitoneal injections of streptozotocin, the CD-1 mice exhibited irreversible hyperglycaemia and insulinopaenia. Light microscopic studies of pancreata from mice sacrificed at this time demonstrated insulitis and beta cell necrosis. Electron microscopic studies revealed spherical and atypical cylindrical type C viruses and occasional clusters of intracisternal type A viruses exclusively within beta cells. To clarify the identification of the type C viruses and their role in the genesis of the insulitis, type C virus specific antigens were identified within islet cells by immune fluorescence at various intervals after streptozotocin administration. Immune fluorescence studies demonstrated the presence of type C virus antigens within islets from streptozotocin treated mice but not in buffer-injected controls. Time course studies suggested that type C virus induction may precede the appearance of insulitis by two days and that insulitis is consistently accompanied by the presence of virus positive islet cells.

Animals↗
PubMed1977

Studies of streptozotocin-induced insulitis and diabetes.

Multiple small injections of streptozotocin produce a delayed, progressive increase in plasma glucose in mice within 5-6 days after the injections, in association with pronounced insulitis and induction of type C viruses within beta cells. Multiple subdiabetogenic doses of streptozotocin in rats and multiple injections of another beta cell toxin, alloxan, in mice did not induce insulitis although hyperglycemia followed the injection of larger quantities of both agents. In mice, the prior injection of 3-O-methyl-D-glucose (3-OMG) or nicotinamide attenuated the diabetic syndrome produced by streptozotocin; however, 3-OMG was more protective. Rabbit antimouse lymphocyte serum, alone, provided partial protection but, when given together with either 3-OMG or nicotinamide, effectively prevented the streptozotocin-induced diabetic syndrome. Cessation of these preventive treatments was followed by the appearance of insulitis and diabetes. These findings suggest that multiple injections of streptozotocin induce, in susceptible hosts, the triad of direct beta cell cytotoxicity, virus induction within beta cells, and cell-mediated autoimmune reaction. These factors, acting separately or in concert, appear to induce a destructive insulitis and severe diabetes. The relative importance of each component and the factors governing host susceptibility remain to be clarified.

Animals↗
PubMed1977

Myopotential inhibition of a bipolar pacemaker caused by electrode insulation defect.

A patient is described in whom myopotentials orginating from the anterior abdominal wall muscle suppressed the implanted demand pacemaker despite its bipolar mode of action. This phenomenon was shown by simultaneous recording of the electrocardiogram the electromyogram. At operation, a defect in the insulation of a previously repaired epicardial electrode was found lying in close proximity to these muscles. After repair of the insulation defect, normal pacemaker function was restored. It is suggested that the myopotentials leaked into the pacing system through the insulation defect, thereby suppressing the demand unit, which maintained its bipolar mode of pacing throughout.

Abdominal Muscles↗
PubMed1977

Genetic influence of the streptozotocin-induced insulitis and hyperglycemia.

Multiple injections of subdiabetogenic doses of streptozotocin (SZ) to CD-1 male mice produce a diabetic syndrome that includes a cell-mediated immune reaction against the pancreatic islet. The importance of the host genetic background in the pathogenesis of this model of diabetes was studied by comparing various inbred strains of mice. Of eight strains of mice studied, only C57BL/KsJ developed insulitis and hyperglycemia comparable to that observed in CD-1 mice. In two mouse strains (DBA/J and BALB/cJ) having an H-2d haplotype similar to the C57BL/KsJ, only mild insulitis and glucose intolerance were observed. These data suggest that major histocompatibility complex genes, as presently defined, cannot be the only determinant of the severity of hyperglycemia and insulitis in this model.

Animals↗
PubMed1978

Potential toxicity of materials used for home insulation.

The two aqueous solutions used for production of residential home insulation by the so-called urea-formaldehyde process were tested for their ability to react with cellular macromolecules. One of the components (the catalyst-surfactant) changed the apparent molecular weight of isolated DNA and increased its rate of attachment to bacterial and animal cells. The other component (the formaldehyde-urea resin) showed both these activities, especially following its exposure to mouse or rat liver extracts (postmitochondrial supernatants). Actively growing HeLa cells exposed to the catalyst-surfactant solution and then extracted with phenol yielded diminishing amounts of DNA, suggesting the formation of strong bonds to other cellular macromolecules, most likely to proteins. Formation of complexes between nucleic acids and proteins, enhanced cellular binding of DNA, and decreased extractability of DNA from growing cells exposed to chemicals have been found in separate studies to correlate with carcinogenic activity of various substances. Since a significant number of buildings will be insulated with this urea-formaldehyde foam and since such foam is also used in agriculture on crops, appropriate precautions should be taken to limit human exposure to the component materials.

Animals↗
PubMed1978

Streptozotocin-induced pancreatic insulitis in mice. Morphologic and physiologic studies.

Pancreatic insulitis and diabetes mellitus were induced in Charles River CD-1 mice with five subdiabetogenic injections of streptozotocin. Plasma glucose and immunoreactive insulin levels were measured and animals were sacrificed at intervals for morphologic studies of pancreatic islets and measurements of extractable pancreatic immunoreactive insulin. Light microscopy revealed striking insulitis, 5 to 6 days after streptozotocin injections, with cell necrosis and eventual islet atrophy due to beta-cell necrosis, and numerous type C viruses within many of the surviving beta-cells. Light microscopic immunoperoxidase stains of islet cell hormones and electron microscopy identified relatively increased numbers of alpha- and delta-cells within the atrophic islets 6 and 12 months after streptozotocin injections. Plasma glucose, plasma immunoreactive insulin, and extractable pancreatic immunoreactive insulin measurements documented the persistence of profound hyperglycemia, as well as the reduction of plasma and pancreatic immunoreactive insulin levels. Immunofluorescence studies demonstrated the absence of circulating islet cell antibodies during both the acute and chronic stages of the syndrome. The pathogenesis of this model of insulin-deficient diabetes is believed to be a cell-mediated autoimmune reaction directed against pancreatic beta-cells altered by subdiabetogenic injections of streptozotocin. The importance of the increased number of type C viruses within surviving beta-cells remains obscure.

Animals↗
PubMed1975

[Insulitis and peracute diabetes mellitus (author's transl)].

We report on the case of a 10-month-old infant with Down's syndrome and acute insulin-dependent diabetes mellitus, who died of hyperosmolar diabetic coma 4 days after admission to the hospital in spite of intensive therapy. Characterizing this disease, a lymphocytic infiltration of the islets of Langerhanns with destruction of the islets was found. The specific localization of the inflammatory infiltrates as well as the histological findings correspond with experimental immune-insulitis in aminals, suggesting that immunological mechanisms play an essential pathogenic role. Virus etiology, diagnostic procedures, and therapeutic approaches are discussed.

Acute Disease↗
PubMed1976

Streptozotocin-induced pancreatic insulitis: new model of diabetes mellitus.

Multiple small injections of streptozotocin in mice produce pancreatic insulitis, with progression to nearly complete beta cell destruction and diabetes mellitus. The timing and appearance of the inflammatory islet lesions suggest but do not prove that streptozotocin acts by initiating a cell-mediated immune reaction. Ultrastructural evidence of abundant type C viruses within beta cells of treated mice suggests that streptozotocin may activate murine leukemia virus in vivo in susceptible hosts.

Animals↗
PubMed2025

Quantitative temporal analysis of pancreatic islet T lymphocyte and macrophage infiltration heralded by serum IgE in congenic BioBreeding (BB) Gimap5-/- rats at risk for insulitis and acute onset diabetes.

OBJECTIVE AND DESIGN: The objective was to determine the association between serum IgE levels and the infiltration order of T lymphocytes and macrophages in pancreatic islets in relation to the loss of insulin and glucagon cells in presymptomatic congenic BB Gimap5-DP (Diabetes Prone) rats. MATERIAL: Congenic prediabetes BB Gimap5-DP and control Gimap5-DR (Diabetes Resistant) rats were followed every other day from 29 to 32 days of age until peak serum IgE (≤ 55 days of age). METHODS: Serum IgE was measured using ELISA. The HALO™ platform facilitated quantitative image analysis of infiltrating T lymphocytes, macrophages, and target organ insulin and glucagon cells. Whole genome sequencing (WGS) was employed to identify candidate type 1 diabetes genes. RESULTS: Serum IgE levels increased with age in normoglycemic BB Gimap5-DP rats. Quantification of infiltrating cells per mm2 in and around the islets indicated that T lymphocytes are the initial infiltrators, followed by macrophages. Elevated serum IgE levels inversely correlated with beta-cell mass (total mg insulin/mg pancreas). WGS refined the risk segment for islet inflammation to 1.02 Mbp, leaving 10 candidate genes, including Gimap4 and Gimap5. CONCLUSIONS: Elevated IgE levels herald T lymphocyte and macrophage infiltration. Pancreatic islet inflammation was linked to Gimap4, Gimap5, and other potential candidate genes on rat chromosome 4.

Animals↗
PubMed1976

A glass-insulated "Elgiloy" microelectrode for recording unit activity in chronic monkey experiments.

A glass-coated microelectrode made of a stiff cobalt--nickel alloy is described. The thickness of the glass coating and the length of the uninsulated tip can be varied as desired. The electrode is stiff enough to insert through the relatively tough dura of the monkey in chronic experiments. Further, the recording site can be marked by electrolytic deposition of iron and the Prussian blue reaction.

Alloys↗
PubMed1979

Islet implantation normalises hyperglycaemia caused by streptozotocin-induced insulitis. Experiments in mice.

Islet-cell deterioration in juvenile diabetes mellitus may be due to an autoimmune reaction, possibly involving both circulating islet-cell antibodies and an inflammatory process in the islets of Langerhans. Replacement of deteriorated islet cells by implantation of normal ones is now under investigation in many laboratories. The present study does not support the assumption that such islet transplants should be affected in the same way as the endogenous islets. Diabetic mice with a cell-mediated immune reaction to their pancreatic islets, induced by repeated injections of low doses of streptozotocin, were used as recipients. Isogeneic islets implanted intrasplenically in these animals were as effective in producing normoglycaemia as were those injected into animals made diabetic with a single bolus dose of streptozotocin. No inflammatory reaction was seen in the implanted islets, irrespective of the regimen of the preceding streptozotocin treatment. This finding suggests that islet-cell implantation may be attempted in insulin-requiring diabetic patients, even if the cause of the disorder is an inflammatory lesion of the patient's own islets.

Animals↗
PubMed2026

Distal enhancer-insulator module of GDF6 is essential for cochlear formation.

Several genes guide inner ear development, and mutations in these genes can cause malformations that result in congenital hearing loss. However, the contribution of noncoding regulatory elements remains largely unclear. This study investigates the function of distal enhancer elements in the transcriptional regulation of GDF6, a gene implicated in cochlear development. Using mouse models with targeted deletions, human inner ear organoids, and CRISPR interference (CRISPRi), we identified a downstream regulatory interval harboring a developmental enhancer required to maintain GDF6 expression during otic epithelial maturation and cochlear morphogenesis. Deletion of this regulatory region or targeting of CRISPRi-based repressors to these regions resulted in decreased GDF6 expression, failure of otic-epithelium development, and prevention of hair cell-like differentiation, reflecting cochlear aplasia observed in patients with corresponding genomic deletions. These findings highlight the contribution of long-range regulatory elements to auditory development and illustrate how their disruption contributes to human deafness.

Animals↗