Background: The autoimmune disease type 1 diabetes mellitus (T1D) is associated with a defect in the immune response, which increases susceptibility to infection. We recently demonstrated that prolonged elevated levels of type 1 interferon (IFN) induce lymphocyte exhaustion during T1D. Aims: In the present study, we further investigated the effect of blocking the type I IFN receptor signaling pathway on diabetic dyslipidemia, in which an abnormal lipid profile leads to the exhaustion of B cells and alteration of their distribution and functions. Methods: T1D was induced in a mouse model by an intraperitoneal injection of a single dose (60 mg/kg) of streptozotocin (STZ). Three groups of mice were examined: a non-diabetic control group, a diabetic group and a diabetic group treated with an anti-IFN (alpha, beta and omega) receptor 1 (IFNAR1) blocking antibody to block type I IFN signaling. Results: We observed that induction of T1D was accompanied by a marked destruction of β cells and a reduction in the insulin levels in the diabetic group. Diabetic mice exhibited many changes, including alterations in their lipid profiles, expansion of splenic B cells, increased caspase-3, -8 and -9 activity, and apoptosis in peripheral B cells. Blocking type 1 IFN signaling in diabetic mice significantly returned the insulin and lipid profiles to normal levels, subsequently restored the B cell distribution, and rescued the peripheral B cells from apoptosis. Conclusion: Our data suggest the potential role of type I IFN in mediating diabetic dyslipidemia and an exhausted state of B cells during T1D.

BACKGROUND: The autoimmune disease type 1 diabetes mellitus (T1D) is associated with a defect in the immune response, which increases susceptibility to infection. We recently demonstrated that prolonged elevated levels of type 1 interferon (IFN) induce lymphocyte exhaustion during T1D. AIMS: In the present study, we further investigated the effect of blocking the type I IFN receptor signaling pathway on diabetic dyslipidemia, in which an abnormal lipid profile leads to the exhaustion of B cells and alteration of their distribution and functions. METHODS: T1D was induced in a mouse model by an intraperitoneal injection of a single dose (60 mg/kg) of streptozotocin (STZ). Three groups of mice were examined: a non-diabetic control group, a diabetic group and a diabetic group treated with an anti-IFN (alpha, beta and omega) receptor 1 (IFNAR1) blocking antibody to block type I IFN signaling. RESULTS: We observed that induction of T1D was accompanied by a marked destruction of β cells and a reduction in the insulin levels in the diabetic group. Diabetic mice exhibited many changes, including alterations in their lipid profiles, expansion of splenic B cells, increased caspase-3, -8 and -9 activity, and apoptosis in peripheral B cells. Blocking type 1 IFN signaling in diabetic mice significantly returned the insulin and lipid profiles to normal levels, subsequently restored the B cell distribution, and rescued the peripheral B cells from apoptosis. CONCLUSION: Our data suggest the potential role of type I IFN in mediating diabetic dyslipidemia and an exhausted state of B cells during T1D.

The photoluminescence of Gd-doped GaN multi-quantum wells (MQWs) is presented and discussed considering the formation of a Gd3+:Nitrogen-vacancy (N-vacancy) complex. A lower energy photoluminescence peak was observed for the Gd-doped GaN MQW sample with respect to the main peak assigned to a neutral donor bound exciton (D0X) of the undoped GaN MQW sample. The X-ray absorption near edge structure spectrum observed at Gd LIII-edge indicates a nitrogen vacancy adjacent to the Gd substituting the Ga ion in Gd-doped GaN MQW sample. Local stresses around the Gd dopants in Gd-doped GaN matrix generated due to the larger diameter of the Gd3+ ion with respect to the Ga3+ ion can be relieved by the creation of vacancies. The lower formation energy of N-vacancies in GaN matrix introduce them as a preferred candidate to relieve the generated stresses. A Gd3+:N-vacancy complex consisting of a Gd3+ ion and the created nitrogen vacancy adjacent to the Gd3+ dopant is likely to form in GaN:Gd matrix. The lower photoluminescence peak energy observed in the Gd-doped GaN MQW sample is assigned to the recombination of an exciton captured at the Gd3+:N-vacancy complex forming a small polaron-like state. A model is presented considering the small exciton-polaron population in defect sites captured around the Gd3+ ions in the Gd-doped GaN.

We report here the structural and electrical properties of Zn0 .95M0 .05O ceramic varistors, M = Zn, Ni and Fe. The samples were tested for phase purity and structural morphology by using X-Ray diffraction XRD and scanning electron microscope SEM techniques. The current-voltage characteristics J-E were obtained by dc electrical measurements in the temperature range of 300 – 500 K. Addition of doping did not influence the hexagonal wurtzite structure of ZnO ceramics. Furthermore, the lattice parameters ratio c/a for hexagonal distortion and the length of the bond parallel to the c axis, u were nearly unaffected. The average grain size was decreased from 1.57 µm for ZnO to 1.19 µm for Ni sample and to 1.22 µm for Fe sample. The breakdown field EB was decreased as the temperature increased, in the following order: Fe > Zn > Ni. The nonlinear region was clearly observed for all samples as the temperature increased up to 400 K and completely disappeared with further increase of temperature up to 500 K. The values of nonlinear coefficient, α were between 1.16 and 42 for all samples, in the following order: Fe > Zn > Ni. Moreover, the electrical conductivity σ was gradually increased as the temperature increased up to 500 K, in the following order: Ni > Zn > Fe. On the other hand, the activation energies were 0.194 eV, 0.136 and 0.223 eV for all samples, in the following order: Fe, Zn and Ni. These results have been discussed in terms of valence states, magnetic moment and thermo-ionic emission, which were produced by the doping, and controlling the potential barrier of ZnO

Background: The autoimmune disease type 1 diabetes mellitus (T1D) is associated with a defect in the immune response, which increases susceptibility to infection. We recently demonstrated that prolonged elevated levels of type 1 interferon (IFN) induce lymphocyte exhaustion during T1D. Aims: In the present study, we further investigated the effect of blocking the type I IFN receptor signaling pathway on diabetic dyslipidemia, in which an abnormal lipid profile leads to the exhaustion of B cells and alteration of their distribution and functions. Methods: T1D was induced in a mouse model by an intraperitoneal injection of a single dose (60 mg/kg) of streptozotocin (STZ). Three groups of mice were examined: a non-diabetic control group, a diabetic group and a diabetic group treated with an anti-IFN (alpha, beta and omega) receptor 1 (IFNAR1) blocking antibody to block type I IFN signaling. Results: We observed that induction of T1D was accompanied by a marked destruction of β cells and a reduction in the insulin levels in the diabetic group. Diabetic mice exhibited many changes, including alterations in their lipid profiles, expansion of splenic B cells, increased caspase-3, -8 and -9 activity, and apoptosis in peripheral B cells. Blocking type 1 IFN signaling in diabetic mice significantly returned the insulin and lipid profiles to normal levels, subsequently restored the B cell distribution, and rescued the peripheral B cells from apoptosis. Conclusion: Our data suggest the potential role of type I IFN in mediating diabetic dyslipidemia and an exhausted state of B cells during T1D.

A Dirichlet boundary value problem for a delay parabolic differential equation is studied on a rectangular domain in the xt plane. The second-order space derivative is multiplied by a small singular perturbation parameter, which gives rise to parabolic boundary layers on the two lateral sides of the rectangle. A numerical method comprising a standard finite difference operator (centred in space, implicit in time) on a rectangular piecewise uniform fitted mesh of Nx× Nt elements condensing in the boundary layers is proved to be robust with respect to