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Biomedical subjects

M Ziegler

Publications and source records attributed to M Ziegler.

At least 127 records · Page 7Linked to original sources
PubMed1994

A possible ontogenic etiology for idiopathic left varicocele.

A total of 659 consecutive patients underwent venography for the evaluation of idiopathic left varicocele before sclerotherapy. In 484 cases no valves of the left spermatic vein could be demonstrated, while 172 patients demonstrated competent valves or absent insertions of the left spermatic vein at the typical point on the left renal vein plus retrograde flow over persistent intercardinal anastomoses. Stenosis of the renal vein occurred in 103 patients (15.7%). In only 3 patients was stenosis observed in the course of the left iliac vein, suggestive of the so-called distal nutcracker phenomenon. We propose that during embryogenesis disturbances in the development of the secondary venous system may result in the idiopathic left varicocele.

Adolescent↗
PubMed1994

Autoantibodies to glutamate decarboxylase detected in diabetes-prone BB/OK rats do not distinguish onset of diabetes.

The diabetes syndrome of the BB rat resembles human Type 1 (insulin-dependent) diabetes including the prevalence of autoantibodies to the 64 kDa Beta-cell autoantigen, which has been identified as glutamate decarboxylase. This study aimed at detecting the prevalence and level of glutamate decarboxylase autoantibodies in 120-day-old diabetic and non-diabetic diabetes-prone BB/OK rats compared to those of sex- and age-matched diabetes-resistant LEW.1A rats. The antibodies were detected using semipurified glutamate decarboxylase from rat brain in two immunoassays, a direct and a sandwich enzyme-linked immunosorbent assay. For the last assay autoantibody-containing immunoglobulins of a serum from a patient with the stiff-man syndrome were used to bind specifically the enzyme as autoantigen in plastic wells. The antibody levels measured as optical density at 490 nm (x +/- SD)/prevalence of the diabetic group (120 +/- 29 days of age) of BB/OK rats 0.57 +/- 0.29 (n = 51)/88% as well as those of the nondiabetic group (121 +/- 26 days of age) with 0.51 +/- 0.29 (n = 32)/97% was significantly increased (p < 0.01) compared to those of the diabetes-resistant control group 0.15 +/- 0.06 (n = 29)/0%. Furthermore in a 209 +/- 27-day-old group (n = 21) of non-diabetic but diabetes-prone BB/OK rats the autoantibody levels of 1.21 +/- 0.39 vs 0.51 +/- 0.26 were further significantly enhanced (p < 0.01). These results were confirmed by a sandwich assay.(ABSTRACT TRUNCATED AT 250 WORDS)

Age of Onset↗
PubMed1994

Implantation of non-toxic materials from glucose sensors: evidence for specific antibodies detected by ELISA.

After subcutaneous implantation of glucose sensors into LEW.1A rats, antibodies could be detected by means of enzyme-linked immunosorbent assay against the outer membrane (cellulose acetate) but not against either the inner membrane (polyethylene) or glucose oxidase (GOD). The kinetics of humoral immune response were investigated implanting different polymeric membranes such as polyurethane, cellulose acetate, regenerated cellulose. The highest antibody titer was detected against regenerated cellulose. There was no cytotoxic effect in vitro by any of the tested materials as examined on monolayer cultures of the mouse fibroblast cell line L-929. Thus immunogenicity is suggested to be considered as a parameter in biocompatibility testing of implantable medical devices.

Animals↗
PubMed1994

Measuring environmental/biological attribution: a fundamental dimension?

Explanations for behaviors that emphasize the importance of biological or environmental factors have been a major theme in psychological discourse, yet they have not been adequately explored as attributional styles with distinct correlates. The present two studies examined this dimension of attribution through the systematic development and validation of the Environmental/Biological Attribution Scale (EBAS). A total of 602 Canadian university students took part in the research project. The research confirmed four hypotheses: Biologically oriented attributional styles were significantly correlated with the same styles as measured by an alternate form (r = .76), with authoritarianism (r = .25), and with racism (r = .15). Environmentally oriented attributional styles were significantly correlated with attributions concerning the importance of strength of will (r = .39).

Adult↗
PubMed1994

Muscular cavernous single cell analysis in patients with venoocclusive dysfunction.

Enzymatically isolated smooth muscle cells of the corpora cavernosa obtained from open biopsies of 15 patients, clinically nonresponding to papaverine/phentolamine and prostaglandin E1 (PGE1) and classified by cavernosometry, were examined using the patch-clamp technique in the whole-cell configuration mode simultaneously monitoring the intracellular calcium concentration by means of the Ca(2+)-sensitive fluorescence dye FURA-II. It could be demonstrated that extracellularly applied PGE1 induces smooth muscle relaxation by inhibition of voltage-dependent L-type Ca2+ currents (58 +/- 8%). Compared to intact cavenous tissue (n = 5), the smooth muscle cells of 14/15 PGE1 nonresponders had no evidence of functional disturbance. Due to intact smooth muscle cells in most cases, etiology of venoocclusive dysfunction remains unclear.

Alprostadil↗
PubMed1994

Detection of autoantibodies to the 65-kD isoform of glutamate decarboxylase by radioimmunoassay.

Autoantibodies (AAb) to glutamate decarboxylase (GAD) occur with a high prevalence in sera of newly diagnosed type I (insulin-dependent) diabetic patients. The aim of this study was to establish a GAD-AAb radioimmunoassay using 125I-labelled GAD65 and to evaluate this assay in a cross-sectional study with newly diagnosed type I diabetic patients (diabetes duration < 6 weeks). Furthermore, subjects at high risk of developing type I diabetes and individuals suffering from other autoimmune diseases were examined in this assay. For GAD-AAb detection, 125I-labelled GAD65 was incubated with 10 microliters of human serum overnight on ice. Thirty of 51 (59%) type I diabetic patients but none of the 54 healthy blood donors tested were found to be positive. A displacement step using 100,000 g supernatant from rat brain containing or not containing GAD showed the specificity of the binding of 125I-GAD65. Concerning the individuals at high risk of developing diabetes. 9/12 (75%) islet cell antibody (ICA)-positive non-diabetic and 4/34 (12%) ICA-negative subjects with metabolic abnormalities were GAD-AAb positive. These results show the association between type I (insulin-dependent) diabetes mellitus and the occurrence of GAD65-AAb, which possibly predicts a risk of developing the disease.

Adolescent↗
PubMed1994

Autoantibodies against GAD65 rather than GAD67 precede the onset of type 1 diabetes.

The enzyme glutamate decarboxylase (GAD) is considered one of the major Beta cell antigens in Type 1 diabetes mellitus. The GAD autoantibody (GAD-AAb) prevalence in newly diagnosed Type 1 diabetic patients has been described up to 80%, depending on the detection method used. The aim of this study was to evaluate a simple, specific, and sensitive radioimmunoassay (RIA) method for detection of AAb against both isoforms of the enzyme, GAD65 and GAD67, in a cross-sectional study using sera from newly diagnosed Type 1 diabetic patients and in a longitudinal study using sera from prediabetic patients and individuals at risk of developing the disease. The 125I-labelled full-length human recombinant proteins of GAD65 and GAD67 expressed in SF9 cells were used as the antigen source. The prevalence of GAD65-AAb in newly diagnosed Type 1 diabetic patients was found to be 73% (112/153), in contrast to 19% (14/72) of GAD67-AAb. Only one patient produced AAb restricted to GAD67. Furthermore, GAD65-AAb could also be detected in 73% (11/15) of prediabetic patients (up to 122 months before clinical manifestation of the disease), whereas only 27% (4/15) of them were positive for GAD67-AAb. In the group at risk of developing Type 1 diabetes, these prevalences were 77% (10/13) and 46% (6/13), respectively. In all GAD67-AAb-positive patients investigated in the longitudinal study, AAb to GAD65 were detectable. In 47% of patients positive for both GAD65-AAb and ICA, the GAD65-AAb appeared by up to 46 months before the occurrence of ICA was detected. The data illustrated that GAD65 is the main immunogenic isoform of the enzyme in the preclinical and clinical stages. The RIA detecting AAb against this isoform may facilitate the screening for individuals at risk of developing the disease.

Adolescent↗
PubMed1994

Monoclonal antibodies specific to the glutamic acid decarboxylase 65 kDa isoform derived from a non-obese diabetic (NOD) mouse.

Two monoclonal antibodies specifically recognizing the 65 kDa isoform of the enzyme glutamic acid decarboxylase (GAD) were generated by fusion of spleen cells of a non-obese diabetic (NOD) mouse which had received a single intraperitoneal injection of 0.2 ml complete Freund's adjuvant followed three days later by one administration of a subdiabetogenic dose of streptozotocin (80 mg/kg body weight) three days before the fusion experiment was performed. Both monoclonals belong to the IgG1 isotype and were screened with an enzyme-linked immunosorbent assay using rat brain extract as a natural source of GAD and additionally with a capture assay by means of immunoglobulins of a patient with Stiff-man syndrome. The specific binding to the 65 kDa isoform of the enzyme was detected by a radioligand and an enzyme-linked immunosorbent assay using recombinant human glutamic acid decarboxylase specific for both the 67 and 65 kDa isoforms. Both monoclonal antibodies recognize the same antigenic epitope, which is located in the N-terminal region of the first 17 amino acids detected by fragments of human pancreatic 65 kDa GAD. Three out of 30 sera from Type 1 diabetic patients specifically displaced the binding of the monoclonals from 125I-labelled GAD65 measured by radio-immunoassay. A striking binding of both monoclonals M61/8F9 and M61/7E11 to the islets of cryosections of human, monkey, pig and rat pancreas but not to mouse pancreas was detectable. The antibodies failed to bind on the cell surface of viable rat islet cells. It is concluded that also in the diabetes-prone NOD mice GAD65 autoantibodies occur although GAD65 was not detectable in the mouse islets.

Animals↗
PubMed1994

Occurrence of islet cell reactive autoantibodies in diabetes-prone BB/OK rats is not associated with the onset of diabetes: a cross-sectional study of BB rats and their diabetes-resistant congenic strains.

Diabetes-prone BB rats are one of the extensively studied animal models of human type 1 (insulin-dependent) diabetes. We have detected islet cell reactive autoantibodies (ICRA) in sera of age-matched (120 days of age) diabetic and non-diabetic diabetes-prone BB/OK rats compared to sex- and age-matched diabetes-resistant LEW.1A control rats by cellular enzyme-linked immunosorbent assay (CELISA) using either desiccated or viable rat insulinoma (RIN) cells as target. The antibody levels measured using desiccated RIN cells (mean O.D. +/- SD; prevalence) of the diabetic group (1.41 +/- 0.59; 94.1%) and the non-diabetic group (1.23 +/- 0.48; 100%) were significantly (p < 0.01) increased compared to those of the diabetes-resistant LEW.1A control rats (0.24 +/- 0.1; 3.2%). Additionally, in a 209-day-old group of non-diabetic diabetes-prone BB/OK rats the autoantibody levels were further significantly (p < 0.01) increased (2.65 +/- 0.48; 100%). Comparing both congenic rat strains BB.1A/OK and LEW.1BB/OK, only the BB.1A/OK rats which bears the genetic background of diabetes-prone BB/OK rats were found to be antibody positive (0.68 +/- 0.43; 63.1%). The results were confirmed by the CELISA using viable RIN cells. We conclude that the prevalence of islet cell autoantibodies in diabetes-prone BB/OK rats and congenic BB.1A/OK rats is closely associated with the genetic susceptibility to diabetes and may be independent of Beta-cell destruction, but they are not a predictive marker for the onset of the disease in this animal model.

Aging↗
PubMed1994

A monoclonal antibody based enzyme-linked immunosorbent assay for the determination of GAD65, the smaller isoform of glutamic acid decarboxylase.

An enzyme-linked immunosorbent assay for GAD65, the smaller form of glutamic acid decarboxylase and an important autoantigen related to Type 1 diabetes, is described. The competitive binding assay is based on a monoclonal antibody specifically reactive with GAD65. The assay is suitable for quantification of this enzyme between 40 and 300 pg/microliter. The intraassay coefficients of variation (cv) are between 5.6% and 8.9% and the interassay cvs lie between 9.4% and 17.3%. The covalent binding of the antigen to magnetic beads as the solid phase makes the assay also applicable for quantification of GAD65 in tissue homogenates with a high concentration of detergent. The GAD65 content of islets isolated from newborn Lewis rat was detected to be 310 pg/islet. However, GAD65 was not detectable in mouse islets.

Animals↗
PubMed1994

[Radiotelemetric manometry of the urinary bladder].

The standard procedure for manometric investigation of bladder function involves the use of a urethral catheter. The presence of this foreign body causes irritations, however, with a resultant increase in urethral resistance. This perturbs the micturition process, but it can be avoided by a new telemetric method of intravesical pressure measurements. A very small pressure gauge and radio emitter are introduced into the bladder, and the values measured are transmitted to an external receiver. Thus, for the first time, is possible to perform physiological studies of bladder function that do not require catheterization or special positioning of the patient and are well tolerated. Some examples are described, which show that this method allows repeated catheter-free investigations over longer periods of time and accurate evaluation of the effects of pharmacological products on bladder function.

Adult↗
PubMed1993

The adenine nucleotide translocase modulates oligomycin-induced quenching of pyranine fluorescence in submitochondrial particles.

Incorporation of the fluorescent, nonpermeant pH indicator pyranine into submitochondrial particles (pyranine-SMP) permitted monitoring of intravesicular pH changes brought about by proton translocation due to oxidation of respiratory chain substrates or to hydrolysis of ATP. Addition of oligomycin to beef heart pyranine-SMP was followed by a pH-independent quenching of pyranine fluorescence. Quenching was influenced by the presence of adenine nucleotides both inside and outside the submitochondrial particles. The nature of the nucleotides required for quenching resembled the specificity of the adenine nucleotide translocase rather than F1-ATPase. Removal of F1 from pyranine-SMP by treatment of the particles with urea did not alter oligomycin-induced quenching. Atractyloside, a specific inhibitor of the adenine nucleotide translocase, prevented oligomycin-induced quenching when the inhibitor was coincorporated into submitochondrial particles with pyranine. Bongkrekic acid prevented or reversed the oligomycin-dependent quenching when added to pyranine-SMP either before or after oligomycin, respectively, but only when ATP was present within the particles. A mutant of Saccharomyces cerevisiae, lacking translocase genes, exhibited oligomycin-dependent fluorescence quenching which was not inhibited by bongkrekic acid. The results support the interpretation that oligomycin promotes sequestration of the fluorescent probe in a region of the submitochondrial particle, probably the F0F1 complex, that leads to a quenching of fluorescence. The observed quenching can be modulated in a way that suggests an interaction between the translocase and F0.

Adenosine Triphosphate↗