Anti-CR1 monoclonal antibody, clone E11

The structure, thermal expansion coefficient, and electrical conductivity of Y0.9Ca0.1Cr1-?Co?O3 (? = 0-0.9) compounds with the perovskite structure have been investigated in air in the temperature range of 100-1000 degrees C. The linear thermal expansion coefficient of Y1-?Ca?Cr1-?Co?O3 lies in the range of (8.77-16.1) x 10(-6) K-1. The maximum electrical conductivity is attained for the Y0.9Ca0.1Cr0.6Co0.4O3 composition. It is shown that the electrical conductivity at low (25-270 degrees C) temperatures and weak substitution of cobalt for chromium is mainly due to the hopping of one electron hole from Cr4+ to Cr3+. At high (565-1000 degrees C) temperatures and cobalt contents, this conductivity mechanism is supplemented with the conductivity caused by the hopping of an electron hole from C3+ to C2+.

Chronic T cell activation and accelerated immune senescence are hallmarks of HIV infection, which may contribute to the increased risk of cardiometabolic diseases in people living with HIV (PLWH). T lymphocytes play a central role in modulating adipose tissue inflammation and, by extension, adipocyte energy storage and release. Here, we assessed the CD4(+) and CD8(+) T cell profiles in the subcutaneous adipose tissue (SAT) and blood of non-diabetic (n = 9; fasting blood glucose [FBG] < 100 mg/dL), pre-diabetic (n = 8; FBG = 100-125 mg/dL) and diabetic (n = 9; FBG >= 126 mg/dL) PLWH, in addition to non- and pre-diabetic, HIV-negative controls (n = 8). SAT was collected by liposuction and T cells were extracted by collagenase digestion. The proportion of naive (T-Nai) CD45RO(-)CCR7(+), effector memory (T-EM) CD45RO(+)CCR7(+), central memory (T-CM) CD45RO(+)CCR7(+), and effector memory revertant RA(+)(T-EMRA) CD45RO(-)CCR7(-) CD4(+) and CD8(+) T cells were measured by flow cytometry. CD4(+) and CD8(+) T-EM and T-EMRA were significantly enriched in SAT of PLWH compared to blood. The proportions of SAT CD4(+) and CD8(+) memory subsets were similar across metabolic status categories in the PLWH, but CD4(+) T cell expression of the CD69 early-activation and tissue residence marker, particularly on T-EM cells, increased with progressive glucose intolerance. Use of t-distributed Stochastic Neighbor Embedding (t-SNE) identified a separate group of predominantly CD69(lo) T-EM and T-EMRA cells co-expressing CD57, CX(3)CR1, and GPR56, which were significantly greater in diabetics compared to non-diabetics. Expression of the CX(3)CR1 and GPR56 markers indicate these T-EM and T-EMRA cells may have anti-viral specificity. Compared to HIV-negative controls, SAT from PLWH had an increased CD8:CD4 ratio, but the distribution of CD4(+) and CD8(+) memory subsets was similar irrespective of HIV status. Finally, whole adipose tissue from PLWH had significantly higher expression of TLR2, TLR8, and multiple chemokines potentially relevant to immune cell homing compared to HIV-negative controls with similar glucose tolerance.