The micropulse framework for adaptive waking windows in sensor networks

In this paper we present MicroPulse, a novel framework for adapting the waking window of a sensing device S based on the data workload incurred by a query Q. Assuming a typical tree-based aggregation scenario, the waking window is defined as the time interval r during which S enables its transceiver in order to collect the results from its children. Minimizing the length of r enables S to conserve energy that can be used to prolong the longevity of the network and hence the quality of results. Our method is established on profiling recent data acquisition activity and on identifying the bottlenecks using an in-network execution of the Critical Path Method. We show through trace- driven experimentation with a real dataset that MicroPulse can reduce the energy cost of the waking window by three orders of magnitude

Targeted inhibition of aggrecanases prevents articular cartilage degradation and augments bone mass in the STR/Ort spontaneous model of osteoarthritis

BACKGROUND:Cartilage destruction in osteoarthritis (OA) is mediated mainly by MMPs and ADAMTSs. The therapeutic candidature of targeting aggrecanases has not yet been defined in joints where spontaneous OA arises due to genetic susceptibility, without a traumatic or load- induced aetiology such as the STR/Ort mouse. Nor do we know the long-term effect of aggrecanase inhibition on bone. METHODS:Using the STR/Ort spontaneously OA background, we have generated transgenic mice that overexpress [-1A]TIMP-3, either ubiquitously or conditionally in chondrocytes. [-1A]TIMP-3 is a variant of tissue inhibitor of metalloproteinase-3 (TIMP-3) that has an extra alanine at the N- terminus that selectively inhibits ADAMTSs, but not MMPs. We analysed a range of OA-related measures in all mice at 40 weeks of age. RESULTS:Mice expressing high [-1A]TIMP-3 levels were protected against the development of the OA whilst low expressers were not. Interestingly, we also found that high levels of [-1A]TIMP-3 transgene overexpression resulted in raised bone mass particularly in females. This regulation of bone mass is, at least, partly direct as primary adult osteoblasts infected with [-1A]TIMP-3 in vitro show elevated rates of mineralisation. CONCLUSIONS:The results provide evidence that [-1A]TIMP-3-mediated inhibition of aggrecanases can protect from cartilage degradation in naturally occurring OA mouse model and highlight a novel role that aggrecanases' inhibition may play in increased bone mass. This article is protected by copyright. All rights reserved

ABSense: Sensing Electromagnetic Waves on Metasurfaces via Ambient Compilation of Full Absorption

Metasurfaces constitute effective media for manipulating and transforming impinging EM waves. Related studies have explored a series of impactful MS capabilities and applications in sectors such as wireless communications, medical imaging and energy harvesting. A key-gap in the existing body of work is that the attributes of the EM waves to-be-controlled (e.g., direction, polarity, phase) are known in advance. The present work proposes a practical solution to the EM wave sensing problem using the intelligent and networked MS counterparts-the HyperSurfaces (HSFs), without requiring dedicated field sensors. An nano-network embedded within the HSF iterates over the possible MS configurations, finding the one that fully absorbs the impinging EM wave, hence maximizing the energy distribution within the HSF. Using a distributed consensus approach, the nano-network then matches the found configuration to the most probable EM wave traits, via a static lookup table that can be created during the HSF manufacturing. Realistic simulations demonstrate the potential of the proposed scheme. Moreover, we show that the proposed workflow is the first-of-its-kind embedded EM compiler, i.e., an autonomic HSF that can translate high-level EM behavior objectives to the corresponding, low-level EM actuation commands.Comment: Publication: Proceedings of ACM NANOCOM 2019. This work was funded by the European Union via the Horizon 2020: Future Emerging Topics call (FETOPEN), grant EU736876, project VISORSURF (http://www.visorsurf.eu

XR-RF Imaging Enabled by Software-Defined Metasurfaces and Machine Learning: Foundational Vision, Technologies and Challenges

We present a new approach to Extended Reality (XR), denoted as iCOPYWAVES, which seeks to offer naturally low-latency operation and cost-effectiveness, overcoming the critical scalability issues faced by existing solutions. iCOPYWAVES is enabled by emerging PWEs, a recently proposed technology in wireless communications. Empowered by intelligent (meta)surfaces, PWEs transform the wave propagation phenomenon into a software-defined process. We leverage PWEs to i) create, and then ii) selectively copy the scattered RF wavefront of an object from one location in space to another, where a machine learning module, accelerated by FPGAs, translates it to visual input for an XR headset using PWEdriven, RF imaging principles (XR-RF). This makes for an XR system whose operation is bounded in the physical layer and, hence, has the prospects for minimal end-to-end latency. Over large distances, RF-to-fiber/fiber-to-RF is employed to provide intermediate connectivity. The paper provides a tutorial on the iCOPYWAVES system architecture and workflow. A proof-of-concept implementation via simulations is provided, demonstrating the reconstruction of challenging objects in iCOPYWAVES produced computer graphics

Mathematical modeling of postmenopausal osteoporosis and its treatment by the anti-catabolic drug denosumab

Denosumab, a fully human monoclonal antibody, has been approved for the treatment of postmenopausal osteoporosis. The therapeutic effect of denosumab rests on its ability to inhibit osteoclast differentiation. Here, we present a computational approach on the basis of coupling a pharmacokinetics model of denosumab with a pharmacodynamics model for quantifying the effect of denosumab on bone remodeling. The pharmacodynamics model comprises an integrated systems biology-continuum micromechanics approach, including a bone cell population model, considering the governing biochemical factors of bone remodeling (including the action of denosumab), and a multiscale micromechanics-based bone mechanics model, for implementing the mechanobiology of bone remodeling in our model. Numerical studies of postmenopausal osteoporosis show that denosumab suppresses osteoclast differentiation, thus strongly curtailing bone resorption. Simulation results also suggest that denosumab may trigger a short-term bone volume gain, which is, however, followed by constant or decreasing bone volume. This evolution is accompanied by a dramatic decrease of the bone turnover rate by more than one order of magnitude. The latter proposes dominant occurrence of secondary mineralization (which is not anymore impeded through cellular activity), leading to higher mineral concentration per bone volume. This explains the overall higher bone mineral density observed in denosumab-related clinical studies

Deficiency and Also Transgenic Overexpression of Timp-3 Both Lead to Compromised Bone Mass and Architecture In Vivo

Tissue inhibitor of metalloproteinases-3 (TIMP-3) regulates extracellular matrix via its inhibition of matrix metalloproteinases and membrane-bound sheddases. Timp-3 is expressed at multiple sites of extensive tissue remodelling. This extends to bone where its role, however, remains largely unresolved. In this study, we have used Micro-CT to assess bone mass and architecture, histological and histochemical evaluation to characterise the skeletal phenotype of Timp-3 KO mice and have complemented this by also examining similar indices in mice harbouring a Timp-3 transgene driven via a Col-2a-driven promoter to specifically target overexpression to chondrocytes. Our data show that Timp-3 deficiency compromises tibial bone mass and structure in both cortical and trabecular compartments, with corresponding increases in osteoclasts. Transgenic overexpression also generates defects in tibial structure predominantly in the cortical bone along the entire shaft without significant increases in osteoclasts. These alterations in cortical mass significantly compromise predicted tibial load-bearing resistance to torsion in both genotypes. Neither Timp-3 KO nor transgenic mouse growth plates are significantly affected. The impact of Timp-3 deficiency and of transgenic overexpression extends to produce modification in craniofacial bones of both endochondral and intramembranous origins. These data indicate that the levels of Timp-3 are crucial in the attainment of functionally-appropriate bone mass and architecture and that this arises from chondrogenic and osteogenic lineages

Endochondral Growth Defect and Deployment of Transient Chondrocyte Behaviors Underlie Osteoarthritis Onset in a Natural Murine Model

OBJECTIVE:To explore whether aberrant transient chondrocyte behaviors occur in the joints of STR/Ort mice (which spontaneously develop osteoarthritis [OA]) and whether they are attributable to an endochondral growth defect.METHODS:Knee joints from STR/Ort mice with advanced OA and age-matched CBA (control) mice were examined by Affymetrix microarray profiling, multiplex polymerase chain reaction (PCR) analysis, and immunohistochemical labeling of endochondral markers, including sclerostin and MEPE. The endochondral phenotype of STR/Ort mice was analyzed by histologic examination, micro-computed tomography, and ex vivo organ culture. A novel protocol for quantifying bony bridges across the murine epiphysis (growth plate fusion) using synchrotron x-ray computed microtomography was developed and applied.RESULTS:Meta-analysis of transcription profiles showed significant elevation in functions linked with endochondral ossification in STR/Ort mice (compared to CBA mice; P < 0.05). Consistent with this, immunolabeling revealed increased matrix metalloproteinase 13 (MMP-13) and type X collagen expression in STR/Ort mouse joints, and multiplex quantitative reverse transcriptase-PCR showed differential expression of known mineralization regulators, suggesting an inherent chondrocyte defect. Support for the notion of an endochondral defect included accelerated growth, increased zone of growth plate proliferative chondrocytes (P < 0.05), and widespread type X collagen/MMP-13 labeling beyond the expected hypertrophic zone distribution. OA development involved concomitant focal suppression of sclerostin/MEPE in STR/Ort mice. Our novel synchrotron radiation microtomography method showed increased numbers (P < 0.001) and mean areal growth plate bridge densities (P < 0.01) in young and aged STR/Ort mice compared to age-matched CBA mice.CONCLUSION:Taken together, our data support the notion of an inherent endochondral defect that is linked to growth dynamics and subject to regulation by the MEPE/sclerostin axis and may represent an underlying mechanism of pathologic ossification in OA

Novel explant model to study mechanotransduction and cell–cell communication

To understand in situ behavior of osteocytes, we characterized a model of osteocytes in their native bone matrix and demonstrated real-time biologic activity of osteocytes while bending the bone matrix. Using 43 male Sprague-Dawley rats, dumbbell-shaped explants were harvested from stainless steel femoral implants after 6–12 weeks and incubated in culture medium or fixed. Sixteen specimens were used to determine bone volume density (BV/TV), volumetric bone mineral density (BMD) and histology for different implantation periods. Osteocyte viability was evaluated by L-lactate dehydrogenase (LDH) activity in 12 cultured explants. Confocal microscopy was used to assess tracer diffusion in three explants and changes in osteocyte pH of a mechanically loaded explant. From 6 to 12 weeks, explant BV/TV and volumetric BMD trended up 92.5% and 101%, respectively. They were significantly and highly correlated. Tissues were uniformly intramembranous and all bone cell types were present. Explants maintained LDH activity through culture day 8. Diffusion at 200 µM was limited to 1,209 Da. Explants appeared capable of reproducing complex bone biology. This model may be useful in understanding osteocyte mechanotransduction in the context of a physiologically relevant bone matrix. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 24:1687–1698, 2006Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/55788/1/20207_ftp.pd

Molecular and cellular mechanisms underlying the evolution of form and function in the amniote jaw.

The amniote jaw complex is a remarkable amalgamation of derivatives from distinct embryonic cell lineages. During development, the cells in these lineages experience concerted movements, migrations, and signaling interactions that take them from their initial origins to their final destinations and imbue their derivatives with aspects of form including their axial orientation, anatomical identity, size, and shape. Perturbations along the way can produce defects and disease, but also generate the variation necessary for jaw evolution and adaptation. We focus on molecular and cellular mechanisms that regulate form in the amniote jaw complex, and that enable structural and functional integration. Special emphasis is placed on the role of cranial neural crest mesenchyme (NCM) during the species-specific patterning of bone, cartilage, tendon, muscle, and other jaw tissues. We also address the effects of biomechanical forces during jaw development and discuss ways in which certain molecular and cellular responses add adaptive and evolutionary plasticity to jaw morphology. Overall, we highlight how variation in molecular and cellular programs can promote the phenomenal diversity and functional morphology achieved during amniote jaw evolution or lead to the range of jaw defects and disease that affect the human condition