Low-energy hole subband dispersions in a cylindrical Ge nanowire: the effects of the nanowire growth direction.

We examine the validity of the spherical approximationγs=(2γ2+3γ3)/5in the Luttinger-Kohn Hamiltonian in calculating the subband dispersions of the hole gas. We calculate the realistic hole subband dispersions (without the spherical approximation) in a cylindrical Ge nanowire by using quasi-degenerate perturbation theory. The realistic low-energy hole subband dispersions have a double-well anticrossing structure, that consists with the spherical approximation prediction. However, the realistic subband dispersions are also nanowire growth direction dependent. When the nanowire growth direction is restricted in the (100) crystal plane, the detailed growth direction dependences of the subband parameters are given. We find the spherical approximation is good approximation, it can nicely reproduce the real result in some special growth directions.

PD-L1 (Programmed Death Ligand 1) Regulates T-Cell Differentiation to Control Adaptive Venous Remodeling.

OBJECTIVE: Patients with end-stage renal disease depend on hemodialysis for survival. Although arteriovenous fistulae (AVF) are the preferred vascular access for hemodialysis, the primary success rate of AVF is only 30% to 50% within 6 months, showing an urgent need for improvement. PD-L1 (programmed death ligand 1) is a ligand that regulates T-cell activity. Since T cells have an important role during AVF maturation, we hypothesized that PD-L1 regulates T cells to control venous remodeling that occurs during AVF maturation. Approach and results: In the mouse aortocaval fistula model, anti-PD-L1 antibody (200 mg, 3×/wk intraperitoneal) was given to inhibit PD-L1 activity during AVF maturation. Inhibition of PD-L1 increased T-helper type 1 cells and T-helper type 2 cells but reduced regulatory T cells to increase M1-type macrophages and reduce M2-type macrophages; these changes were associated with reduced vascular wall thickening and reduced AVF patency. Inhibition of PD-L1 also inhibited smooth muscle cell proliferation and increased endothelial dysfunction. The effects of anti-PD-L1 antibody on adaptive venous remodeling were diminished in nude mice; however, they were restored after T-cell transfer into nude mice, indicating the effects of anti-PD-L1 antibody on venous remodeling were dependent on T cells. CONCLUSIONS: Regulation of PD-L1 activity may be a potential therapeutic target for clinical translation to improve AVF maturation.