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Biomedical subjects

S Wiegand

Publications and source records attributed to S Wiegand.

12 recordsLinked to original sources
PubMed2006

Beta-cell autoantibodies in children with type 2 diabetes mellitus: subgroup or misclassification?

BACKGROUND: In adults, a fraction of diabetic individuals with beta-cell autoantibodies has initially non-insulin requiring diabetes clinically appearing as type 2 diabetes mellitus (T2DM), named latent autoimmune diabetes in adulthood (LADA). The occurrence of beta-cell autoantibodies in European children and adolescents with T2DM has not been reported so far. METHODS: The frequency of beta-cell autoantibodies (anti-GAD, anti-IA-2, and anti-ICA) was determined in 7050 diabetic children and adolescents. The type of diabetes was classified by paediatric diabetic specialists based on the clinical presentation. Children with non-insulin dependent T2DM over a one year period were studied separately. RESULTS: A total of 6922 children were clinically classified as having type 1 diabetes (T1DM) and 128 children as having T2DM. Thirty six per cent of the children with T2DM had at least one detectable beta-cell autoantibody. These children did not differ significantly from the children with T2DM and without autoantibodies in respect of age, gender, weight status, lipids, blood pressure, C-peptide, glucose, and HbA1c at manifestation, as well as frequency of anti-thyroidal antibodies and insulin treatment during follow up. In the subgroup of the 38 children with T2DM without insulin requirement over a one year period, autoantibodies occurred in 32%. These 12 children were predominantly obese (67%), female (67%), and in the pubertal age range. CONCLUSION: beta-cell autoantibodies were detectable in a subgroup of initially non-insulin dependent diabetic children and adolescents with the clinical appearance of T2DM. Following the terminology "latent autoimmune diabetes in adulthood (LADA)", this subgroup might be classified as "LADY" (latent autoimmune diabetes in youth).

Adolescent↗
PubMed2005

[Who needs what? New approaches to multidisciplinary diagnostics and therapy for adipose children and youths in a multiethnic city].

Over the past two decades, obesity in children has been increasing worldwide, leading to serious complications. The treatment for childhood obesity remains largely ineffective; therefore preventive measures are crucial. The prevalence of obesity depends on the BMI-percentiles used. Recent BMI-percentiles may underestimate the problem. Currently, the only representative cross-sectional BMI-data are obtained at the school entry examination. These data reveal certain risk groups (migrants, low socioeconomic status). More representative longitudinal data are needed to study the progression of obesity during childhood. Our obesity clinic provides multidisciplinary therapy programs (group or individual) and is also focused on the diagnosis and treatment of comorbidity, especially of the metabolic syndrome. Almost 60% of our severely obese patients are already affected. The molecular diagnosis of rare monogenetic or syndromal forms of obesity may be helpful in providing additional support for these patients. In general, most obesity programs are successful only in families without severe psychosocial problems and with motivation for lifestyle changes. This can be expected in only 3% of our families. Therefore, a substantial societal effort is needed to facilitate prevention for all children, and effective therapies have to be tailored depending on biological and psychosocial risk factors.

Adolescent↗
PubMed2005

Impaired glucose tolerance and type 2 diabetes mellitus: a new field for pediatrics in Europe.

OBJECTIVE: Several studies have shown that obese children and adolescence seem to have an increased risk to develop a disturbed glucose metabolism as already known for obese adults. This might result in the same disastrous outcomes of cardiovascular diseases as it has been shown for adult obese patients. The most sensitive measurement for detecting changes in glucose metabolism in obese children seems to be an oral glucose tolerance test (OGGT) which is not practical for all daily outpatient clinics. DESIGN: Cross-sectional study. SUBJECTS AND MEASUREMENTS: We therefore made a preselection from a cohort of 491 subjects according to the American Diabetes Association (ADA) criteria for the diagnosis of diabetes. In the selected high-risk subgroup (n = 102) of obese pediatric subjects, we measured the prevalence of impaired glucose tolerance (IGT) by OGTT. RESULTS: We diagnosed six patients with type 2 diabetes and 37 patients with impaired glucose tolerance. In addition, we found a close correlation of IGT to disturbances of triglyceride and cholesterol parameters. This prevalence was comparable to a similar study group that was screened without preselection. CONCLUSIONS: These prevalence data further underline the need to diagnose children with obesity-associated risk factors in terms of an insulin resistance syndrome. The preselection of a high-risk subgroup by ADA criteria might be a practical approach.

Adolescent↗
PubMed2004

Angiopoietin 1 inhibits ocular neovascularization and breakdown of the blood-retinal barrier.

Several retinal and choroidal diseases are potentially treatable by intraocular delivery of genes whose products may counter or neutralize abnormal gene expression that occurs as part of the diseases. However, prior to considering a transgene, it is necessary to thoroughly investigate the effects of its expression in normal and diseased eyes. An efficient way to do this is to combine tissue-specific promoters with inducible promoter systems in transgenic mice. In this study, we used this approach to evaluate the effects of ectopic expression of angiopoietin-1 (Ang1) in normal eyes and those with ocular neovascularization. Adult mice with induced expression of Ang1 ubiquitously, or specifically in the retina, appeared normal and had no identifiable changes in retinal or choroidal blood vessels or in retinal function as assessed by electroretinography. Increased expression of Ang1 in eyes with severe retinal ischemia or in eyes with rupture of Bruch's membrane significantly suppressed the development of retinal or choroidal neovascularization, respectively. This inhibition of ocular neovascularization is particularly interesting and noteworthy, because overexpression of Ang1 in skin stimulates neovascularization. Ang1 also significantly reduced VEGF-induced retinal vascular permeability. These data suggest that intraocular delivery of ang1 has potential for treatment of ocular neovascularization and macular edema.

Angiopoietin-1↗
PubMed2002

[Gene, fast food and no motion. Causes of childhood obesity].

Obesity in children and adolescents should be seen as a chronic disorder and not merely as a biological variant. One aspect of the pathological significance of obesity in childhood and adolescence is determined by functional and individual limitation and psychosocial impairment. Another is the fact that these children and adolescents have a higher comorbidity, and appreciably increased morbidity and mortality rates in adulthood. The major causes of the condition are lifestyle related, in particular excessive intake of energy- and fat-rich foods together with increasingly inadequate exercise. In addition, however, there also appears to be a genetic predisposition that manifests as early and massive obesity in young years. Considerable importance attaches to the recording of height and weight development during regular examinations in the doctor's office. In addition, in particular the children of overweight parents, together with their families, should be instructed and advised on the need for a healthy and appropriate diet and regular exercise. In the case of extremely overweight children, a genetic investigation would be worthwhile.

Adolescent↗
PubMed2001

Expression of immediate early genes in sensory ganglia.

C-Jun and c-Fos belong to the family of immediate early genes. Apart from their role as transcription factors, a basal expression was shown for them in central nervous system tissues. The expression of c-Jun and c-Fos in sensory ganglia of guinea pig, rat and murine sensory ganglia was examined under normal, unstimulated conditions by quantitative double-immunohistochemistry. 4.6 +/- 2.8% of neuron-specific protein gene-product 9.5 -positive cells in nodose ganglia, 51.6 +/- 2.1% in jugular ganglia, 46.4 +/- 3.0% in trigeminal ganglia and 42.5 +/- 1.3% of cervical dorsal root ganglia neurons were positive for c-Jun in the guinea pig (less than 1% for c-Fos). In rat and mouse, less than 1% of the sensory neurons exhibited c-Jun and c-Fos-immunoreactivity. The high basal expression of c-Jun in guinea pig sensory neurons suggests that in this species the presence of c-Jun does not only depend on specific stimulation and is not exclusively associated with neuronal plasticity of gene expression and functional changes.

Animals↗
PubMed2000

Detection of nitric oxide release induced by bradykinin in guinea pig trachea and main bronchi using a porphyrinic microsensor.

Indirect evidence using nitric oxide (NO) synthase (NOS) inhibitors suggests that in guinea-pig airways bradykinin releases bronchoprotective NO. In this study, using a recently developed electrochemical method of NO measurement based on a porphyrinic microsensor, we investigated whether bradykinin releases NO from guinea-pig airways and whether the epithelium is the main source of NO. Further, the Ca(2+)-dependence of bradykinin-induced NO release was assessed stimulating airway preparations with bradykinin in Ca(2+)-free conditions. We also studied the immunohistochemical distribution of the Ca(2+)- dependent constitutive isoforms of NOS (constitutive NOS [cNOS]: neuronal and endothelial [ecNOS]) in our preparations. The porphyrinic microsensor was placed in the bathing fluid onto the mucosal surface of tracheal or main bronchial segments. Addition of bradykinin vehicle (0.9% saline) did not cause any detectable change of the baseline signal. Addition of bradykinin caused an upward shift of the baseline that reached a maximum within 1 to 2 s. The amplitude of the response to bradykinin was concentration-dependent between the range 1 nM to 10 microM, with a maximum effect at 10 microM. Bradykinin-induced NO release was higher in tracheal than in main bronchial segments. The selective bradykinin B(2) receptor antagonist D-Arg(0)-[Hyp(3), Thi(5), D-Tic(7), Oic(8)]bradykinin (1 microM) inhibited NO release induced by a submaximum concentration of bradykinin (1 microM). The ability of bradykinin to release NO was markedly reduced in epithelium-denuded segments, and abolished in Ca(2+)-free conditions and after pretreatment with N(G)-monomethyl-L-arginine (100 microM), but not with N(G)-monomethyl-D-arginine. Both cNOS isoforms were present in trachea and main bronchi, ecNOS being the predominant isoform in the epithelium. The study shows that bradykinin via B(2) receptor activation caused a rapid and Ca(2+)-dependent release of NO, mainly, but not exclusively, derived from the epithelium. It also shows that both cNOS isoforms may be involved in bradykinin-evoked NO release.

Animals↗
PubMed1997

High-pass-filtered magnetocardiogram and cardiomyopathy in patients with type 1 diabetes mellitus.

Prolonged and/or fractionated depolarization due to tissue degeneration of the ventricular myocardium is a feature of cardiomyopathy. Signal averaged electrocardiography uses high-pass filters of the Butterworth type to quantify, noninvasively, fractionated high-frequency components at the end of the QRS complex. In this study a finite impulse response high-pass filter of the 90th order (cutoff at 37 Hz) was applied to magnetocardiograms (MCGs) and high-resolution electrocardiograms (ECGs) order to quantify high-frequency components throughout the myocardial depolarization. Additionally, late-potential analysis on the signal-averaged ECG was performed. A prospective investigation was made of 23 cardiologically asymptomatic patients, 11 females and 12 males, with type I diabetes mellitus. Their mean age was 21.7 years (range, 13-34 years). The mean duration of diabetes was 14 years (range, 1-27 years). Data were compared with those of 22 control subjects (12 females, 10 males) of mean age, 23.2 years (range, 11-35 years). The ECGs and MCGs were simultaneously recorded and signal-averaged, digitally filtered, and quantified by a score obtained by multiplying the amplitude variation of the signal by the number of maximal/minimal in the QRS complex. Echocardiograms were used to calculate the left ventricular mass and to document the presence of cardiomyopathy. Scores were higher in the MCGs of with type I diabetes mellitus than in the control subjects (P < .001). High scores correlated with an increased left ventricular muscular mass index (P < .05) and duration of the diabetes (P < .05). The high-resolution ECG, processed analogously, showed similar results in relation to left ventricular mass (P = .06) and duration of diabetes (P = .07), respectively (nonsignificant). No late potentials were found. These findings suggest that using a linear-phase high-pass finite impulse response filter may be useful for the noninvasive identification of patients with cardiomyopathy who exhibit possible disturbances of intraventricular depolarization. Our findings also suggest that analysis using the total QRS complex, rather than the final part of the QRS complex only, may improve identification of patients at risk.

Adolescent↗
PubMed1993

Islet transplantation inhibits diabetic retinopathy in the sucrose-fed diabetic Cohen rat.

PURPOSE: To study the effect of islet transplantation on the development of diabetic retinopathy in the sucrose-fed diabetic Cohen rat, a useful experimental model of accelerated microvascular disease. METHODS: Syngeneic transplantation of collagenase-ficoll isolated islets by intraportal injection was performed either after 6 weeks or after 12 weeks of diabetes, i.e., before or after the first morphologic retinal changes, respectively. Retinal digest preparations were examined using quantitative morphologic parameters. RESULTS: After 26 weeks of diabetes, characteristic features of background retinopathy such as a 5% increase in capillary endothelial cells, a 27% pericyte dropout, acellular occluded vessels and, occasionally, microaneurysms developed in untreated animals. Islet transplantation performed after 6 weeks of diabetes completely prevented endothelial cell proliferation and diminished pericyte loss (2950 +/- 140 vs 2390 +/- 40 in diabetic controls, P < 0.01). A significant increase in acellular occluded capillaries persisted (31 +/- 14 vs 8 +/- 2 in NC; P < 0.01). Islet transplantation after 12 weeks of diabetes, i.e., after established pericyte loss, only partially restored capillary cell composition and did not prevent retinal vessel occlusion. These findings indicate that the beneficial effect of islet transplantation on diabetic retinopathy is limited to a time very early in the evolution of this process. CONCLUSIONS: These data suggest that irreversible changes induced by antecedent hyperglycemia play a central role in the progressive development of diabetic retinopathy.

Animals↗
PubMed1989

[Islet transplantation in type II diabetes mellitus--model of the spontaneous diabetic Cohen rat].

The spontaneous diabetic Cohen-rat is one of the few animal models of the diabetes mellitus Type II (NIDDM). A spontaneous diabetic animal line and a diabetes-resistant line originated from a parental lineage by genetic selection with regard to the glucose tolerance on condition of feeding of a saccharose-rich and copper-poor diet. In each case 1000 islets of the diabetes-resistant line were transplanted in 28 animals of the diabetic line. Body weight, blood-sugar concentration, glucosuria, glucose tolerance, and the HbA1 were normalized after the transplantation. The serum levels of insulin and glucagon increased. These results emphasize etiopathogenetic importance of the islets of Langerhans in this animal model.

Animals↗
PubMedDate not supplied

Time course of PCDD/PCDF/PCB concentrations in breast-feeding mothers and their infants.

PCDD/PCDF/PCB concentrations were measured in samples from four mothers (at delivery and during lactation) and their infants (at birth and the end of first year of life). For two of these mothers it was the second delivery and breast-feeding period, and additional data were available from first lactation period and the first-born infant at the age of 11 to 12 months. Five of the six infants were fully breast-fed for at least 17 weeks. In four of them a distinct PCDD/PCDF/PCB accumulation was observed at the end of the first year of life: concentrations in blood fat were 1.5 to 3.6 times higher than maternal levels measured at the same time. Due to decreasing maternal body burdens during lactation, PCDD/PCDF concentrations at 11 to 12 months of life were only about half as high in the second infant as in the first one at the same age. During second pregnancy, no important change of the concentrations was observed in maternal blood.

Adult↗