Single component differential uptake of oxygen and nitrogen in three samples of carbon molecular sieve adsorbent and carbon dioxide and methane in one of the samples has been measured volumetrically at different temperatures over a wide range of adsorbent loading. The results seem to suggest that the early part of the uptake is controlled by a barrier resistance confined at the micropore mouth while the later part is controlled by a pore diffusional resistance distributed in the micropore interior. A dual resistance model is able to capture the observed single component uptake behavior for all the four gases, which is assuredly less tentative than what the current literature may suggest. Moreover, the extracted micropore transport parameters have much stronger dependence on adsorbent loading than that expected from chemical potential gradient as the driving force for diffusion and the assumption of a constant limiting transport coefficient based on prevailing evidence. An approximate way of accounting for this stronger concentration dependence has been proposed and validated by application to the prediction of experimental integral uptake results.

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Bone homeostasis requires continuous remodeling of bone matrix to maintain structural integrity. This involves extensive communication between bone-forming osteoblasts and bone-resorbing osteoclasts to orchestrate balanced progenitor cell recruitment and activation. Only a few mediators controlling progenitor activation are known to date and have been targeted for intervention of bone disorders such as osteoporosis. To identify druggable pathways, we generated a medaka (Oryzias latipes) osteoporosis model, where inducible expression of receptor-activator of nuclear factor kappa-Β ligand (Rankl) leads to ectopic formation of osteoclasts and excessive bone resorption, which can be assessed by live imaging. Here we show that upon Rankl induction, osteoblast progenitors up-regulate expression of the chemokine ligand Cxcl9l. Ectopic expression of Cxcl9l recruits mpeg1-positive macrophages to bone matrix and triggers their differentiation into osteoclasts. We also demonstrate that the chemokine receptor Cxcr3.2 is expressed in a distinct subset of macrophages in the aorta-gonad-mesonephros (AGM). Live imaging revealed that upon Rankl induction, Cxcr3.2-positive macrophages get activated, migrate to bone matrix, and differentiate into osteoclasts. Importantly, mutations in cxcr3.2 prevent macrophage recruitment and osteoclast differentiation. Furthermore, Cxcr3.2 inhibition by the chemical antagonists AMG487 and NBI-74330 also reduced osteoclast recruitment and protected bone integrity against osteoporotic insult. Our data identify a mechanism for progenitor recruitment to bone resorption sites and Cxcl9l and Cxcr3.2 as potential druggable regulators of bone homeostasis and osteoporosis.

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Summary Transcriptome profiling of selected cells involved in bone formation, degeneration and repair provides novel insight into mechanisms of bone cell coupling and homeostasis. A medaka osteoporosis model was reported earlier, where excess bone resorption is triggered by induction of receptor activator of nuclear factor κB ligand (RANKL) expression, and bone cell behaviour visualized by live imaging. Herein a protocol for fluorescence‐activated cell sorting (FACS) is described that allows isolation of distinct bone cell types from larvae for subsequent RNA sequencing to detect molecular changes during different phases of bone degeneration and repair.