Estimates of certain paraxial diffraction integral operator and its generalized properties

This paper aims to discuss a generalization of certain paraxial diffraction integral operator in a class of generalized functions. At the start of this paper, we propose a convolution formula and establish certain convolution theorem. Then, with the addition to the convolution theorem, we consider a set of approximating identities and substantially employ our results in generating sets of integrable and locally integrable Boehmians. The said generalized integral operator is tested and declared to be one-to-one and onto mapping. Continuity of the generalized operator with respect to the convergence of the Boehmian spaces is obtained. Over and above, an inversion formula and consistency results are also counted. © 2020, The Author(s)

Erythropoietin Receptor (EPOR) Signaling in the Osteoclast Lineage Contributes to EPO-Induced Bone Loss in Mice

Erythropoietin (EPO) is a pleiotropic cytokine that classically drives erythropoiesis but can also induce bone loss by decreasing bone formation and increasing resorption. Deletion of the EPO receptor (EPOR) on osteoblasts or B cells partially mitigates the skeletal effects of EPO, thereby implicating a contribution by EPOR on other cell lineages. This study was designed to define the role of monocyte EPOR in EPO-mediated bone loss, by using two mouse lines with conditional deletion of EPOR in the monocytic lineage. Low-dose EPO attenuated the reduction in bone volume (BV/TV) in Cx3cr1Cre EPORf/f female mice (27.05%) compared to controls (39.26%), but the difference was not statistically significant. To validate these findings, we increased the EPO dose in LysMCre model mice, a model more commonly used to target preosteoclasts. There was a significant reduction in both the increase in the proportion of bone marrow preosteoclasts (CD115+) observed following high-dose EPO administration and the resulting bone loss in LysMCre EPORf/f female mice (44.46% reduction in BV/TV) as compared to controls (77.28%), without interference with the erythropoietic activity. Our data suggest that EPOR in the monocytic lineage is at least partially responsible for driving the effect of EPO on bone mass