108 research outputs found
Effect of pancreatic and/or renal transplantation on diabetic autonomic neuropathy
Thirty-nine Type 1 (insulin-dependent) diabetic patients were studied prospectively after simultaneous pancreas and kidney (n=26) and kidney grafting alone (n=13) by measuring heart rate variation during various manoeuvers and answering a standardized questionnaire every 6 to 12 months post-transplant. While age, duration of diabetes, and serum creatinine (168.1±35.4 vs 132.7±17.7 mgrmol/l) were comparable, haemoglobin A1 levels were significantly lower (6.6±0.2 vs 8.5±0.3%; p<0.01) and the mean observation time longer (35±2 vs 25±3 months; p<0.05) in the pancreas recipients when compared with kidney transplanted patients. Heart rate variation during deep breathing, lying/standing and Valsalva manoeuver were very similar in both groups initially and did not improve during follow-up. However, there was a significant reduction in heart rate in the pancreas recipient group. Autonomic symptoms of the gastrointestinal and thermoregulatory system improved more in the pancreas grafted subjects, while hypoglycaemia unawareness deteriorated in the kidney recipients. This study suggests that long-term normoglycaemia by successful pancreatic grafting is able to halt the progression of autonomic dysfunction
Glutamic acid decarboxylase antibodies in screening for autoimmune diabetes: influence of comorbidity, age, and sex on specificity and threshold values
Glutamic acid decarboxylase antibodies in screening for autoimmune diabetes: influence of comorbidity, age, and sex on specificity and treshold values
Critical research on populism: Nine rules of engagement
This article formulates precise questions and ‘rules of engagement’ designed to advance our understanding of the role populism can and should play in the present political conjuncture, with potentially significant implications for critical management and organization studies and beyond. Drawing on the work of Ernesto Laclau and others working within the post-Marxist discourse theory tradition, we defend a concept of populism understood as a form of reason that centres around a claim to represent ‘the people’, discursively constructed as an underdog in opposition to an illegitimate ‘elite’. A formal discursive approach to populism brings with it important advantages. For example, it establishes that a populist logic can be invoked to further very different political goals, from radical left to right, or from progressive to regressive. It sharpens too our grasp of important issues that are otherwise conflated and obfuscated. For instance, it helps us separate out the nativist and populist dimensions in the discourses of the United Kingdom Independence Party (UKIP), Trump or the Front National (FN). Our approach to populism, however, also points to the need to engage with the rhetoric about populism, a largely ignored area of critical research. In approaching populism as signifier, not only as a concept, we stress the added need to focus on the uses of the term ‘populism’ itself: how it is invoked, by whom, and to what purpose and effect. This, we argue, requires that we pay more systematic attention to anti-populism and ‘populist hype’, and reflect upon academia’s own relation to populism and anti-populism
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Specific pancreatic beta-cell surface antigens recognized by a xenogenic antiserum.
An antiserum (R4) from a rabbit immunized with suspensions of C57BL/61 ob/ob mouse islet cells contains antibodies which in a 125I-protein A radioligand assay can be demonstrated to bind to single cell suspensions of normal Naval Medical Research Institute (NMRI) mouse islet cells. The binding of 125I-protein A to islet cells was about four times that of normal rabbit serum (NRS) after incubation at a 1/600 dilution of R4 antiserum quantitatively absorbed to mouse spleen lymphocytes (R4A antiserum) and hepatocytes. Subsequent absorption of the R4A antiserum to islet cells significantly reduced the binding of 125I-protein A to islet cells incubated with the doubly absorbed serum. Immunoprecipitation of radiolabeled islet cell lysates followed by SDS polyacrylamide gel electrophoresis and autoradiography suggested that the R4A antiserum recognized a Mr 40,000 glycoprotein. This glycoprotein was not detected in spleen lymphocytes. Electron microscope detection of gold-protein A complexes suggested that the binding of islet cell surface antibodies was cell specific. islet cell suspensions incubated with R4A antiserum and gold-protein A showed that 86 +/- 3 gold particles were bound per 100 beta-cells (mean +/- SE for six experiments). In contrast, the number of gold particles per 100 endocrine non-beta-cells was 8 +/- 1 which was similar to the number achieved with NRS (3 +/- 1) on all endocrine islet cells. Our observations suggest that the pancreatic islet cells, in particular the beta-cells, express a specific antigen
Specific pancreatic beta-cell surface antigens recognized by a xenogenic antiserum.
An antiserum (R4) from a rabbit immunized with suspensions of C57BL/61 ob/ob mouse islet cells contains antibodies which in a 125I-protein A radioligand assay can be demonstrated to bind to single cell suspensions of normal Naval Medical Research Institute (NMRI) mouse islet cells. The binding of 125I-protein A to islet cells was about four times that of normal rabbit serum (NRS) after incubation at a 1/600 dilution of R4 antiserum quantitatively absorbed to mouse spleen lymphocytes (R4A antiserum) and hepatocytes. Subsequent absorption of the R4A antiserum to islet cells significantly reduced the binding of 125I-protein A to islet cells incubated with the doubly absorbed serum. Immunoprecipitation of radiolabeled islet cell lysates followed by SDS polyacrylamide gel electrophoresis and autoradiography suggested that the R4A antiserum recognized a Mr 40,000 glycoprotein. This glycoprotein was not detected in spleen lymphocytes. Electron microscope detection of gold-protein A complexes suggested that the binding of islet cell surface antibodies was cell specific. islet cell suspensions incubated with R4A antiserum and gold-protein A showed that 86 +/- 3 gold particles were bound per 100 beta-cells (mean +/- SE for six experiments). In contrast, the number of gold particles per 100 endocrine non-beta-cells was 8 +/- 1 which was similar to the number achieved with NRS (3 +/- 1) on all endocrine islet cells. Our observations suggest that the pancreatic islet cells, in particular the beta-cells, express a specific antigen
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