Female gender increases stiffness of elastic but not of muscular arteries in type I diabetic patients.

The reason for the particularly increased risk for cardiovascular complications in diabetic women is still unclear. We have previously found decreased distensibility of elastic arteries in type I diabetic women, indicating increased cardiac load, not seen in type I diabetic men, which might be one contributing factor. Whether the effect of gender is different in muscular arteries in type I diabetic patients has not been assessed. As estimates of arterial distensibility we measured stiffness (beta) and pressure strain elastic modulus (Ep) in the muscular common femoral artery using echo-tracking sonography in 30 women (mean age 34 years, range 20-61) and 26 men (mean age 38 years, range 22-56) with type I diabetes. The results were compared with those of 89 healthy individuals of corresponding age and gender and with previously published results from elastic arteries in these patients obtained at the same occasion. The internal common femoral diameter was significantly decreased in both diabetic men and women. In sharp contrast to the highly significant decreased distensibility of the elastic abdominal aorta and common carotid artery in the type I diabetic women, the distensibility of the common femoral artery did not clearly differ between patients and controls, neither for women nor for men. Thus, the gender difference in changes of arterial distensibility found in elastic arteries was absent or far less obvious in the femoral artery. In conclusion, female gender seems to affect the mechanical properties of elastic, but not of large muscular arteries in type I diabetic patients. Thus, putative gender differences in arterial changes in type I diabetes are to be sought in elastic rather than muscular arteries

Reduced Aortic Wall Stress in Diabetes Mellitus

ObjectiveMost risk factors are similar for abdominal aortic aneurysm (AAA) and atherosclerosis, e.g. smoking, male gender, age, high blood pressure, hyperlipidemia. Diabetes mellitus however, is a risk factor for atherosclerosis, but diabetic patients seldom develop AAA. The reason for this discrepancy is unknown. Increased aortic wall stress seems to be an etiologic factor in the formation, growth and rupture of AAA in man. The aim of our study was to study the wall stress in the abdominal aorta in diabetic patients compared with healthy controls.Methods39 patients with diabetes mellitus and 46 age – and sex matched healthy subjects were examined with B-mode ultrasound to determine the lumen diameter (LD) and intima-media thickness (IMT) in the abdominal aorta (AA) and the common carotid artery (CCA). Diastolic blood pressure (DBP) was measured non-invasively in the brachial artery. LaPlace law was used to calculate circumferential wall stress.ResultsAge, DBP, and LD in the abdominal aorta were not significantly different in the diabetic patients compared to controls. IMT in the AA was larger in the diabetic patients, 0.89±0.17 vs 0.73±0.11mm (p<.001). Accordingly aortic wall stress was reduced in the diabetics, 7.8±1.7×105 vs 9.7±1.9×105dynes/cm2 (p<.001).ConclusionsWall stress in the abdominal aorta is reduced in diabetes mellitus. This is mainly due to a thicker aortic wall compared to healthy controls. The reduced aortic wall stress coincides with the fact that epidemiological studies have shown a decreased risk of aneurysm development in diabetic patients

Recurrence of Type 1 Diabetes After Simultaneous Pancreas-Kidney Transplantation, Despite Immunosuppression, Is Associated With Autoantibodies and Pathogenic Autoreactive CD4 T-Cells

ObjectiveTo investigate if recurrent autoimmunity explained hyperglycemia and C-peptide loss in three immunosuppressed simultaneous pancreas-kidney (SPK) transplant recipients.Research design and methodsWe monitored autoantibodies and autoreactive T-cells (using tetramers) and performed biopsy. The function of autoreactive T-cells was studied with in vitro and in vivo assays.ResultsAutoantibodies were present pretransplant and persisted on follow-up in one patient. They appeared years after transplantation but before the development of hyperglycemia in the remaining patients. Pancreas transplant biopsies were taken within approximately 1 year from hyperglycemia recurrence and revealed beta-cell loss and insulitis. We studied autoreactive T-cells from the time of biopsy and repeatedly demonstrated their presence on further follow-up, together with autoantibodies. Treatment with T-cell-directed therapies (thymoglobulin and daclizumab, all patients), alone or with the addition of B-cell-directed therapy (rituximab, two patients), nonspecifically depleted T-cells and was associated with C-peptide secretion for &gt;1 year. Autoreactive T-cells with the same autoantigen specificity and conserved T-cell receptor later reappeared with further C-peptide loss over the next 2 years. Purified autoreactive CD4 T-cells from two patients were cotransplanted with HLA-mismatched human islets into immunodeficient mice. Grafts showed beta-cell loss in mice receiving autoreactive T-cells but not control T-cells.ConclusionsWe demonstrate the cardinal features of recurrent autoimmunity in three such patients, including the reappearance of CD4 T-cells capable of mediating beta-cell destruction. Markers of autoimmunity can help diagnose this underappreciated cause of graft loss. Immune monitoring during therapy showed that autoimmunity was not resolved by the immunosuppressive agents used

Cardiac autonomic neuropathy in patients with diabetes and no symptoms of coronary artery disease: comparison of 123I-metaiodobenzylguanidine myocardial scintigraphy and heart rate variability

PURPOSE The purpose of this study was to evaluate the prevalence of cardiac autonomic neuropathy (CAN) in a cohort of patients with type 2 diabetes, truly asymptomatic for coronary artery disease (CAD), using heart rate variability (HRV) and (123)I-metaiodobenzylguanidine ((123)I-mIBG) myocardial scintigraphy. METHODS The study group comprised 88 patients with type 2 diabetes prospectively recruited from an outpatient diabetes clinic. In all patients myocardial perfusion scintigraphy, CAN by HRV and (123)I-mIBG myocardial scintigraphy were performed. Two or more abnormal tests were defined as CAN-positive (ECG-based CAN) and one or fewer as CAN-negative. CAN assessed by (123)I-mIBG scintigraphy was defined as abnormal if the heart-to-mediastinum ratio was 25%, or the total defect score was >13. RESULTS The prevalence of CAN in patients asymptomatic for CAD with type 2 diabetes and normal myocardial perfusion assessed by HRV and (123)I-mIBG scintigraphy was respectively, 27% and 58%. Furthermore, in almost half of patients with normal HRV, (123)I-mIBG scintigraphy showed CAN. CONCLUSION The current study revealed a high prevalence of CAN in patients with type 2 diabetes. Secondly, disagreement between HRV and (123)I-mIBG scintigraphy for the assessment of CAN was observed.Cardiovascular Aspects of Radiolog

Evidence for electron Landau damping in space plasma turbulence

How turbulent energy is dissipated in weakly collisional space and astrophysical plasmas is a major open question. Here, we present the application of a field-particle correlation technique to directly measure the transfer of energy between the turbulent electromagnetic field and electrons in the Earth's magnetosheath, the region of solar wind downstream of the Earth's bow shock. The measurement of the secular energy transfer from the parallel electric field as a function of electron velocity shows a signature consistent with Landau damping. This signature is coherent over time, close to the predicted resonant velocity, similar to that seen in kinetic Alfven turbulence simulations, and disappears under phase randomisation. This suggests that electron Landau damping could play a significant role in turbulent plasma heating, and that the technique is a valuable tool for determining the particle energisation processes operating in space and astrophysical plasmas.STFC Ernest Rutherford Fellowship [ST/N003748/2]; NASA HSR grant [NNX16AM23G]; NSF CAREER Award [AGS-1054061]; NASA HGI grant [80NSSC18K0643]; NASA MMS GI grant [80NSSC18K1371]Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]