Holographic Josephson Junctions and Berry holonomy from D-branes

We construct a holographic model for Josephson junctions with a defect system of a Dp brane intersecting a D(p+2) brane. In addition to providing a geometrical picture for the holographic dual, this leads us very naturally to suggest the possibility of non-Abelian Josephson junctions characterized in terms of the topological properties of the branes. The difference between the locations of the endpoints of the Dp brane on either side of the defect translates into the phase difference of the condensate in the Josephson junction. We also add a magnetic flux on the D(p+2) brane and allow it evolve adiabatically along a closed curve in the space of the magnetic flux, while generating a non-trivial Berry holonomy.Comment: 20 pages, 2 figure

The effect of 3 months of recombinant human growth hormone (GH) therapy on insulin and glucose-mediated glucose disposal and insulin secretion in GH-deficient adults: a minimal model analysis

The effect of 3 months of low dose (120 μg/kg.week or 0.24 IU/kg.week) recombinant human GH (rhGH) treatment on glucose tolerance, insulin secretion, and insulin- and glucose-mediated glucose disposal was examined in 10 GH-deficient adults. The frequently sampled iv glucose tolerance test was performed at baseline and after 1 week and 3 months of rhGH therapy and analyzed by the minimal model method of Bergman to provide estimates of the glucose decay rate, first and second phase insulin secretion (phi 1 and phi 2), fractional clearance of insulin, and glucose-mediated and insulin-mediated glucose disposal. Fasting glucose, insulin, C-peptide, nonesterified fatty acids (NEFA), and serum cholesterol and triglycerides were also measured. When the 1 week data were compared to baseline, there was a small but significant rise in mean (± SE) fasting glucose (4.62 ± 0.17 vs. 5.1 ± 0.15 mmol/L; P < 0.01), NEFA (0.70 ± 0.09 vs. 1.1 ± 0.12 mmol/L; P < 0.005), insulin (93.6 ± 8.9 vs. 238.9 ± 9.2 pmol/L; P < 0.0001), C-peptide (0.32 ± 0.13 vs. 0.66 ± 0.13 nmol/L; P < 0.005), and phi 1 (11.9 ± 1.3 vs. 16.2 ± 1.8 pmol/L.min/mmol.L x 10(2)) and phi 2 (1.43 ± 0.17 vs. 3.15 ± 0.25 pmol/L.min/mmol.L x 10(3); P < 0.05). Conversely, there were associated decreases in glucose decay rate (1.83 ± 0.26 vs. 1.28 ± 0.12 min-1; P < 0.05) and insulin-mediated glucose disposal (0.36 ± 0.08 vs. 0.18 ± 0.06 min/pmol.L x 10(-4); P < 0.005). There was no change in glucose-mediated glucose disposal or the fractional clearance of insulin. By 3 months, fasting insulin and C-peptide levels remained significantly elevated, whereas other parameters had returned to baseline. There was a minor reduction in serum cholesterol at 1 week (5.1 ± 0.15 vs. 4.62 ± 0.17 mmol/L; P < 0.01), which was not maintained at 3 months. Serum triglycerides remained unchanged throughout the study. We conclude that short term low dose rhGH treatment of GH-deficient adults induces a temporary state of mild glucose intolerance, hyperinsulinemia, insulin resistance, and raised NEFA levels at 1 week. By 3 months, these metabolic disturbances had returned to baseline for a persisting modest hyperinsulinemia. Whether this hyperinsulinemia will last over the longer term and/or has distant detrimental metabolic consequences in the individual must await further studies