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Forest leaf area index (LAI) is an important indicator to describe the forest canopy structure and growth status of trees. In this paper, the Yigen area of Inner Mongolia was selected as the study area. Taken full account of the differences among different echo types, the LiDAR point cloud data were split into different single lasers. Then, intensity normalization was implemented for LiDAR point cloud data with the range between sensor and target. Based on the normalized intensity data, a new laser penetration index, called single laser beam penetration index (LPI), was calculated along with the calculation of traditional LPI. These two laser penetration indexes were used to estimate the forest LAI based on the theoretical model and empirical model on four different sampling scales (5, 10, 15, and 20 m), respectively, which aimed to improve the retrieval accuracy of forest LAI through laser beam splitting. The results showed that the forest LAI estimated from mean LPI (LPI) was obviously better than that from traditional LPI. In addition, both of the empirical [R=0.80, mean absolute deviation (MAD)=0.11] and theoretical models (R=0.77, MAD=0.16) achieved the best performances with sampling scale of 15 m. The mapping of birch forest LAI for the study area was derived by integrating both the advantages of best empirical and theoretical models.
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http://dx.doi.org/10.13287/j.1001-9332.201611.020 | DOI Listing |
FASEB J
May 2021
Department of Translational Dental Medicine, Boston University Henry M. Goldman School of Dental Medicine, Boston, MA, USA.
Bone loss is a major health concern for astronauts during long-term spaceflight and for patients during prolonged bed rest or paralysis. Growing evidence suggests that osteocytes, the most abundant cells in the mineralized bone matrix, play a key role in sensing mechanical forces applied to the skeleton and integrating the orchestrated response into subcellular biochemical signals to modulate bone homeostasis. However, the precise molecular mechanisms underlying both mechanosensation and mechanotransduction in late-osteoblast-to-osteocyte cells under microgravity (µG) have yet to be elucidated.
View Article and Find Full Text PDFJCI Insight
March 2019
Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
During endochondral bone formation, chondrocyte hypertrophy represents a crucial turning point from chondrocyte differentiation to bone formation. Both parathyroid hormone-related protein (PTHrP) and histone deacetylase 4 (HDAC4) inhibit chondrocyte hypertrophy. Using multiple mouse genetics models, we demonstrate in vivo that HDAC4 is required for the effects of PTHrP on chondrocyte differentiation.
View Article and Find Full Text PDFBone
December 2018
Molecular and Cell Biology, Goldman School of Dental Medicine, Boston University, Boston, USA. Electronic address:
The stimulatory subunit of G-protein, Gsα, acts as a secondary messenger of G-protein coupled receptors (GPCRs) that primarily activates cAMP-induced signaling. GPCRs, such as the parathyroid hormone receptor (PTHR), are critical regulators of bone formation as shown by number of genetic manipulation studies targeting early osteoblast lineage cells. In this study, we have examined the role of Gsα in osteocytes, the terminally differentiated and most abundant cells of the osteoblast lineage.
View Article and Find Full Text PDFJ Bone Miner Res
May 2017
Endocrine Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Sclerostin antibody (Scl-Ab) increases osteoblast activity, in part through increasing modeling-based bone formation on previously quiescent surfaces. Histomorphometric studies have suggested that this might occur through conversion of bone lining cells into active osteoblasts. However, direct data demonstrating Scl-Ab-induced conversion of lining cells into active osteoblasts are lacking.
View Article and Find Full Text PDFJ Bone Miner Res
February 2017
Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, MA, USA.
Cells of the osteoblast lineage are increasingly identified as participants in whole-body metabolism by primarily targeting pancreatic insulin secretion or consuming energy. Osteocytes, the most abundant bone cells, secrete a Wnt-signaling inhibitor called sclerostin. Here we examined three mouse models expressing high sclerostin levels, achieved through constitutive or inducible loss of the stimulatory subunit of G-proteins (Gsα in mature osteoblasts and/or osteocytes).
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