Publications by authors named "Heng Qiu"

37 Publications

Reliability and validity of Healthy Fitness Measurement Scale Version1.0 (HFMS V1.0) in Chinese elderly people.

BMC Public Health 2021 05 30;21(1):1019. Epub 2021 May 30.

Department of Sanitation Economy Administration, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China.

Purpose: We examined the reliability and validity of the Healthy Fitness Measurement Scale Version 1.0 (HFMS V1.0) specifically on elderly people in China.

Methods: We carried out a cross-sectional study in December 2020 and enrolled 800 elderly people through stratified sampling technique, including 777 valid samples (with a mean age of 71.81 ± 8.36 years), of which 382 cases (49.2%) were women. The level of healthy fitness was measured using the HFMS V1.0. The Cronbach's alpha coefficient, split-half reliability, test-retest reliability, convergent and discriminant validity, exploratory factor and confirmatory factor were calculated for assessing the reliability and validity of HFMS V1.0.

Results: HFMS V1.0 consists of 8 dimensions and 38 items. The scale had acceptable reliability (Cronbach's alpha = 0.920, split-half = 0.946, test-retest = 0.878). Exploratory factor analysis showed KMO value =0.927, and uncovered 10 factors with the cumulative contribution rate of 65.71% and all factor loads over 0.40. The item distribution was consistent with the initial expectation of the scale. The confirmatory factor analysis indicated good fit: CMIN/DF = 2.796, RMSEA = 0.048, IFI =0.914, TLI = 0.902, CFI = 0.913.

Conclusion: HFMS V1.0 was shown to have acceptable reliability and validity indices for this sample. Collectively, HFMS V1.0 is reliable and efficient to measure the healthy fitness of elderly people. It is recommended to use it among the elderly in other Chinese cities in the future to ensure uniformity and objectivity. This scale can be carried out to evaluate of the effectiveness of public health measures in improving the healthy fitness level of the elderly and optimizing public health policies.
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http://dx.doi.org/10.1186/s12889-021-11021-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8164796PMC
May 2021

The effect of Chinese herbal medicine on digestive system and liver functions should not be neglected in COVID-19: An updated systematic review and meta-analysis.

IUBMB Life 2021 05 2;73(5):739-760. Epub 2021 Apr 2.

Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.

Gastrointestinal symptoms and liver injury are common in patients with coronavirus disease 2019 (COVID-19). However, profiles of different pharmaceutical interventions used are relatively underexplored. Chinese herbal medicine (CHM) has been increasingly used for patients with COVID-19, but the efficacy of CHM used in COVID-19 on gastrointestinal symptoms and liver functions has not been well studied with definitive results based on the updated studies. The present study aimed at testing the efficacy of CHM on digestive symptoms and liver function (primary outcomes), the aggravation of COVID-19, and the time to viral assay conversion (secondary outcomes), among patients with COVID-19, compared with standard pharmacotherapy. The literature search was undertaken in 11 electronic databases from December 1, 2019 up to November 8, 2020. Appraisal of the evidence was conducted with Cochrane risk of bias tool or Newcastle Ottawa Scale. A random-effects model or subgroup analysis was conducted when significant heterogeneity was identified in the meta-analysis. The certainty of the evidence was assessed with the grading of recommendations assessment, development, and evaluation approach. Forty-eight included trials involving 4,704 participants were included. Meta-analyses favored CHM plus standard pharmacotherapy for COVID-19 on reducing the aggravation of COVID-19 and the time to viral assay conversion compared with standard pharmacotherapy. However, the present CHM as a complementary therapy for treating COVID-19 may not be beneficial for improving most gastrointestinal symptoms and liver function based on the current evidence. More well-conducted trials are warranted to confirm the potential efficacy of CHM furtherly.
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http://dx.doi.org/10.1002/iub.2467DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8250823PMC
May 2021

[Reliability and validity of Healthy Fitness Measurement Scale (V1.0) for evaluating healthy fitness of college students in Guangzhou].

Nan Fang Yi Ke Da Xue Xue Bao 2021 Jan;41(1):47-54

Department of Economic Management, Nanfang Hospital, Guangzhou 510515, China.

Objective: To evaluate the reliability and validity of Healthy Fitness Measurement Scale V1.0 (HFMS V1.0) for assessing healthy fitness status of college students in Guangzhou.

Methods: A total of 584 college students were evaluated with HFMS V1.0. The reliability and validity of HFMS V1.0 scale were assessed for its discrimination degree, Cronbach α coefficient, split-half reliability, test-retest reliability, content validity, structural validity, calibration validity and responsiveness.

Results: The Cronbach α of HFMS V1.0 scale was 0.893, the split-half coefficient was 0.909, and the test-retest coefficient was 0.923. The correlation coefficients of each dimension with its subscales ranged from 0.687 to 0.931. The correlation coefficient between each item and its dimension ranged from 0.558 to 0.863( < 0.05). Exploratory factor analysis showed that the variance interpretation of 8 factors was 55.105%, and the factor structure was basically identical with the theoretical concept of the scale. Confirmatory factor analysis showed excellent goodness-of-fit indices of the model (/DF= 1.952; RMSEA=0.400; GFI=0.906; TLI=0.905; IFI=0.914; and CFI=0.913; < 0.05). The correlation coefficients between the 4 general items and their corresponding scales ranged from 0.585 to 0.670. The proportions of the highest and lowest scores of the scale were very low, suggesting a high responsiveness of the scale.

Conclusions: HFMS V1.0 has high reliability and validity for evaluating healthy fitness status of college students.
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http://dx.doi.org/10.12122/j.issn.1673-4254.2021.01.06DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7867479PMC
January 2021

The molecular structure and function of sorting nexin 10 in skeletal disorders, cancers, and other pathological conditions.

J Cell Physiol 2021 Jun 25;236(6):4207-4215. Epub 2020 Nov 25.

Division of Regenerative Biology, School of Biomedical Sciences, University of Western Australia, Perth, Australia.

SNX10 is a member of the phox homology domain-containing family of phosphoinositide-binding proteins. Intracellularly, SNX10 localizes to endosomes where it mediates intracellular trafficking, endosome organization, and protein localization to the centrosome and cilium. It is highly expressed in bone and the gut where it participates in bone mineral and calcium homeostasis through the regulation of osteoclastic bone resorption and gastric acid secretion, respectively. Not surprisingly, patients harboring mutations in SNX10 mutation manifest a phenotype of autosomal recessive osteopetrosis or malignant infantile osteopetrosis, which is clinically characterized by dense bones with increased cortical bone into the medullary space with bone marrow occlusion or depletion, bone marrow failure, and anemia. Accordingly, SNX10 mutant osteoclasts exhibit impaired bone resorptive capacity. Beyond the skeleton, there is emerging evidence implicating SNX10 in cancer development, metabolic disorders, inflammation, and chaperone-mediated autophagy. Understanding the structural basis through which SNX10 exerts its diverse biological functions in both cell and tissue-specific manners may therefore inform new therapeutic opportunities toward the treatment and management of SNX10-related diseases.
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http://dx.doi.org/10.1002/jcp.30173DOI Listing
June 2021

A missense mutation sheds light on a novel structure-function relationship of RANKL.

J Cell Physiol 2021 Apr 23;236(4):2800-2816. Epub 2020 Sep 23.

Division of Regenerative Biology, School of Biomedical Sciences, University of Western Australia, Perth, Western Australia, Australia.

The tumor necrosis factor (TNF)-like core domain of receptor activator of nuclear factor-κB ligand (RANKL) is a functional domain critical for osteoclast differentiation. One of the missense mutations identified in patients with osteoclast-poor autosomal recessive osteopetrosis (ARO) is located in residue methionine 199 that is replaced with lysine (M199K) amid the TNF-like core domain. However, the structure-function relationship of this mutation is not clear. Sequence-based alignment revealed that the fragment containing human M199 is highly conserved and equivalent to M200 in rat. Using site-directed mutagenesis, we generated three recombinant RANKL mutants M200K/A/E (M200s) by replacing the methionine 200 with lysine (M200K), alanine (M200A), and glutamic acid (M200E), representative of distinct physical properties. TRAcP staining and bone pit assay showed that M200s failed to support osteoclast formation and bone resorption, accompanied by impaired osteoclast-related signal transduction. However, no antagonistic effect was found in M200s against wild-type rat RANKL. Analysis of the crystal structure of RANKL predicted that this methionine residue is located within the hydrophobic core of the protein, thus, likely to be crucial for protein folding and stability. Consistently, differential scanning fluorimetry analysis suggested that M200s were less stable. Western blot analysis analyses further revealed impaired RANKL trimerization by M200s. Furthermore, receptor-ligand binding assay displayed interrupted interaction of M200s to its intrinsic receptors. Collectively, our studies revealed the molecular basis of human M199-induced ARO and elucidated the indispensable role of rodent residue M200 (equivalent to human M199) for the RANKL function.
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http://dx.doi.org/10.1002/jcp.30045DOI Listing
April 2021

PKC-δ deficiency in B cells displays osteopenia accompanied with upregulation of RANKL expression and osteoclast-osteoblast uncoupling.

Cell Death Dis 2020 09 16;11(9):762. Epub 2020 Sep 16.

Department of Spine Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou Guangdong, China.

PKC-δ is an important molecule for B-cell proliferation and tolerance. B cells have long been recognized to play a part in osteoimmunology and pathological bone loss. However, the role of B cells with PKC-δ deficiency in bone homeostasis and the underlying mechanisms are unknown. We generated mice with PKC-δ deletion selectively in B cells by crossing PKC-δ-loxP mice with CD19-Cre mice. We studied their bone phenotype using micro-CT and histology. Next, immune organs were obtained and analyzed. Western blotting was used to determine the RANKL/OPG ratio in vitro in B-cell cultures, ELISA assay and immunohistochemistry were used to analyze in vivo RANKL/OPG balance in serum and bone sections respectively. Finally, we utilized osteoclastogenesis to study osteoclast function via hydroxyapatite resorption assay, and isolated primary calvaria osteoblasts to investigate osteoblast proliferation and differentiation. We also investigated osteoclast and osteoblast biology in co-culture with B-cell supernatants. We found that mice with PKC-δ deficiency in B cells displayed an osteopenia phenotype in the trabecular and cortical compartment of long bones. In addition, PKC-δ deletion resulted in changes of trabecular bone structure in association with activation of osteoclast bone resorption and decrease in osteoblast parameters. As expected, inactivation of PKC-δ in B cells resulted in changes in spleen B-cell number, function, and distribution. Consistently, the RANKL/OPG ratio was elevated remarkably in B-cell culture, in the serum and in bone specimens after loss of PKC-δ in B cells. Finally, in vitro analysis revealed that PKC-δ ablation suppressed osteoclast differentiation and function but co-culture with B-cell supernatant reversed the suppression effect, as well as impaired osteoblast proliferation and function, indicative of osteoclast-osteoblast uncoupling. In conclusion, PKC-δ plays an important role in the interplay between B cells in the immune system and bone cells in the pathogenesis of bone lytic diseases.
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http://dx.doi.org/10.1038/s41419-020-02947-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7494897PMC
September 2020

Carnosol suppresses RANKL-induced osteoclastogenesis and attenuates titanium particles-induced osteolysis.

J Cell Physiol 2021 Mar 28;236(3):1950-1966. Epub 2020 Jul 28.

The First Clinical Academy, Guangzhou University of Chinese Medicine, Guangzhou, China.

Osteolysis is a common medical condition characterized by excessive activity of osteoclasts and bone resorption, leading to severe poor quality of life. It is essential to identify the medications that can effectively suppress the excessive differentiation and function of osteoclasts to prevent and reduce the osteolytic conditions. It has been reported that Carnosol (Car), isolated from rosemary and salvia, has anti-inflammatory, antioxidative, and anticancer effects, but its activity on osteolysis has not been determined. In this study, we found that Car has a strong inhibitory effect on the receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation dose-dependently without any observable cytotoxicity. Moreover, Car can inhibit the RANKL-induced osteoclastogenesis and resorptive function via suppressing NFATc1, which is a result of affecting MAPK, NF-κB and Ca signaling pathways. Moreover, the particle-induced osteolysis mouse model confirmed that Car could be effective for the treatment of bone loss in vivo. Taken together, by suppressing the formation and function of RANKL-induced osteoclast, Car, may be a therapeutic supplementary in the prevention or the treatment of osteolysis.
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http://dx.doi.org/10.1002/jcp.29978DOI Listing
March 2021

Comparison of arthroscopic single-row and double-row repair in the treatment of rotator cuff tears: A protocol of cohort analysis.

Medicine (Baltimore) 2020 Jul;99(29):e21030

Department of Orthopaedics, Hospital of Chengdu University of Traditional Chinese Medicine, Sichuan, China.

Background: Single-row (SR) and double-row (DR) techniques are 2 kinds of widely used approaches for the arthroscopic repair of rotator cuff. This retrospective clinical trial was performed to address the question of whether a DR rotator cuff anchor repair gives results superior to a SR anchor repair in clinical outcome scores and complication rates.

Methods: This study was performed and reported in accordance with the Strengthening the Reporting of Observational studies in Epidemiology checklist. We retrospectively reviewed our database, which was collected prospectively. From 2014 to 2017, 264 patients underwent arthroscopic rotator cuff repair by an experienced single shoulder surgeon with the SR and DR techniques. This study was approved by the institutional review board in our hospital and was registered in the Research Registry. Outcome measures included Constant-Murley score, muscle strength, patient satisfaction, passive range of motion, and retear rates.

Results: The hypothesis was that the DR technique would achieve better functional scores and fewer complications as compared to the SR technique in treatment of rotator cuff tears.
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http://dx.doi.org/10.1097/MD.0000000000021030DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7373522PMC
July 2020

All-inside versus inside-out suture techniques in arthroscopic meniscus repair: A prospective randomized study protocol.

Medicine (Baltimore) 2020 Jul;99(27):e20688

Department of Orthopaedics, Hospital of Chengdu University of Traditional Chinese Medicine, Sichuan 610072, China.

Background: With advancements in our understanding of meniscal function, treatment options for meniscal injuries have evolved considerably over the past few decades. The aim of the current study was to compare the all-inside and inside-out techniques with regard to retear rate, functional outcomes, and perioperative complications in patients who had undergone arthroscopic meniscus repair. We hypothesized that there was no significant difference between the 2 groups in terms of postoperative outcomes after arthroscopic meniscus repair.

Methods: This study was a prospective randomized blinded study, with a parallel design and an allocation ratio of 1:1 for the treatment groups. This study was approved by the Institutional Review Board in our hospital and written informed consent was obtained from all subjects participating in the trial. It was carried out in accordance with the principles of the Helsinki Declaration. A total of 70 patients who meet inclusion criteria are randomized to either all-inside or inside-out group. The primary outcome measure was retear rate. Retear was determined by repeat arthroscopic evaluation of patients with follow-up for symptoms of persistent or new pain, catching, or locking that was possibly related to the meniscal repair. Secondary outcomes included disease-specific quality of life measurement with the Western Ontario Meniscal Evaluation Tool, range of motion, operative time, and adverse events at surgery or throughout the follow-up period.

Results: This study has limited inclusion and exclusion criteria and a well-controlled intervention.

Trial Registration: This study protocol was registered in Research Registry (researchregistry5589).
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http://dx.doi.org/10.1097/MD.0000000000020688DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7337569PMC
July 2020

Arctiin abrogates osteoclastogenesis and bone resorption via suppressing RANKL-induced ROS and NFATc1 activation.

Pharmacol Res 2020 09 23;159:104944. Epub 2020 May 23.

School of Biomedical Sciences, University of Western Australia, Perth, Western Australia 6009, Australia. Electronic address:

Osteoporosis, characterized by disrupted bone resorption and formation, is viewed as a global health challenge. Arctiin (ARC) is a main component of Arctium lappa L, which exerts chemopreventive effects against various tumor cells. However, the role of ARC in bone remodeling is still unclear. Here, we first demonstrated that ARC inhibits osteoclast formation and bone resorption function induced by the receptor activator of nuclear factor-κB ligand (RANKL) in a dose- and time-dependent manner without exerting cytotoxic effects. Mechanistic analysis revealed that ARC not only suppresses RANKL-induced mitogen-activated protein kinase (MAPK) and calcium signaling pathways, but also enhances the expression of cytoprotective enzymes that are involved in scavenging reactive oxygen species (ROS). Further, ARC inhibits the activation of the major transcription factor nuclear factor of activated T cells 1 (NFATc1) during RANKL-induced osteoclast formation. Preclinical studies showed that ARC protects bone loss in an ovariectomy (OVX) mouse model. Conclusively, our data confirmed that ARC could potentially inhibit osteoclastogenesis by abrogating RANKL-induced MAPK, calcium, and NFATc1 signaling pathway, as well as by promoting the expression of ROS scavenging enzymes in Nrf2/Keap1/ARE signaling pathway, thereby preventing OVX-induced bone loss. Thus, ARC may serve as a novel therapeutic agent for the treatment of osteoporosis.
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http://dx.doi.org/10.1016/j.phrs.2020.104944DOI Listing
September 2020

Hymenialdisine: A Marine Natural Product That Acts on Both Osteoblasts and Osteoclasts and Prevents Estrogen-Dependent Bone Loss in Mice.

J Bone Miner Res 2020 08 22;35(8):1582-1596. Epub 2020 Apr 22.

Department of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Excessive osteoclast (OC) activity together with relatively weak osteoblast (OB) function are strongly connected to osteolytic diseases, including osteoporosis, tumor-induced osteolysis, and inflammatory bone erosion. Very few natural products or compounds have been shown to exert therapeutic effects on both OCs and OBs, limiting the potential development of natural compounds for clinical application. Hymenialdisine (HMD) is a marine sponge-derived natural inhibitor of protein kinases with previously reported anti-osteoarthritis and anti-cancer properties. However, the roles of HMD in OCs, OBs, and osteoporosis have not yet been well established. Here, we found that HMD not only suppressed osteoclastogenesis but also promoted OB differentiation. HMD exerted dose-dependent inhibitory effects on RANKL-induced OC formation, bone resorption, and OC-specific gene expression. These strong inhibitory effects were achieved by blocking the NF-κB and MAPK signaling pathways, and NFATc1 expression. In addition, HMD potentially stimulated OB differentiation by activating alkaline phosphatase (ALP) and enhancing OB matrix mineralization. We found that HMD can activate the glycogen synthase kinase 3β (GSK-3β)/β-catenin/T-cell factor (TCF)/lymphoid enhancer factor (LEF) signaling pathway to upregulate Runx-2 expression, the main transcription factor in this pathway. Increased expression of Runx-2 was also correlated with expression of the OB-specific genes Col1a1 and osteocalcin (Ocn). Furthermore, we also evaluated the therapeutic potential of HMD in a female C57BL/6j mouse model of ovariectomy (OVX)-induced systematic bone loss. HMD showed a remarkable ability to prevent decreases in bone volume (BV/TV) and trabecular thickness (Tb.Th). In summary, HMD exerts notable effects in inhibiting OC-related osteolysis and enhancing OB-induced ossification, suggesting the potential application of HMD in osteoporosis treatment. © 2020 American Society for Bone and Mineral Research.
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http://dx.doi.org/10.1002/jbmr.4025DOI Listing
August 2020

Fumitremorgin C Attenuates Osteoclast Formation and Function Suppressing RANKL-Induced Signaling Pathways.

Front Pharmacol 2020 10;11:238. Epub 2020 Mar 10.

School of Kinesiology, Shanghai University of Sport, Shanghai, China.

Excessive bone resorption conducted by osteoclasts is considered as the main cause of osteoclast-related bone diseases such as osteoporosis. Therefore, the suppression of excessive osteoclast formation and function is one of the strategies to treat osteoclast-related bone diseases. Fumitremorgin C (Fum) is a mycotoxin extracted from . It has been shown to have extensive pharmacological properties, but its role in the treatment of osteoclast-related bone diseases remains unclear. In this study, we aim to find out whether Fum can inhibit the receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation and function. The results showed that Fum could significantly attenuate osteoclast formation and function at concentrations from 2.5 to 10 µM. The protein expression of bone resorption factors such as NFATc1, cathepsin K, V-ATPase-d2, and c-Fos was suppressed with the treatment of Fum at a concentration of 10 µM. In addition, Fum was also shown to suppress the activity of NF-κB, intracellular reactive oxygen species level, and MAPK pathway. Taken together, the present study showed that Fum could attenuate the formation and function of osteoclast suppressing RANKL-induced signaling pathways, suggesting that Fum might be a potential novel drug in the treatment of osteoclast-related bone diseases.
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http://dx.doi.org/10.3389/fphar.2020.00238DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7076231PMC
March 2020

Asperpyrone A attenuates RANKL-induced osteoclast formation through inhibiting NFATc1, Ca signalling and oxidative stress.

J Cell Mol Med 2019 12 15;23(12):8269-8279. Epub 2019 Oct 15.

School of Kinesiology, Shanghai University of Sport, Shanghai, China.

Imbalance of osteoblast and osteoclast in adult leads to a variety of bone-related diseases, including osteoporosis. Thus, suppressing the activity of osteoclastic bone resorption becomes the main therapeutic strategy for osteoporosis. Asperpyrone A is a natural compound isolated from Aspergillus niger with various biological activities of antitumour, antimicrobial and antioxidant. The present study was designed to investigate the effects of Asperpyrone A on osteoclastogenesis and to explore its underlining mechanism. We found that Asperpyrone A inhibited RANKL-induced osteoclastogenesis in a dose-dependent manner when the concentration reached 1 µm, and with no cytotoxicity until the concentration reached to 10 µm. In addition, Asperpyrone A down-regulated the mRNA and protein expression of NFATc1, c-fos and V-ATPase-d2, as well as the mRNA expression of TRAcP and Ctsk. Furthermore, Asperpyrone A strongly attenuated the RNAKL-induced intracellular Ca oscillations and ROS (reactive oxygen species) production in the process of osteoclastogenesis and suppressed the activation of MAPK and NF-κB signalling pathways. Collectively, Asperpyrone A attenuates RANKL-induced osteoclast formation via suppressing NFATc1, Ca signalling and oxidative stress, as well as MAPK and NF-κB signalling pathways, indicating that this compound may become a potential candidate drug for the prevention or treatment of osteoporosis.
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http://dx.doi.org/10.1111/jcmm.14700DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850946PMC
December 2019

Astilbin prevents bone loss in ovariectomized mice through the inhibition of RANKL-induced osteoclastogenesis.

J Cell Mol Med 2019 12 11;23(12):8355-8368. Epub 2019 Oct 11.

Key Laboratory of Orthopaedics of Zhejiang Province, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.

Osteoporosis is the most common osteolytic disease characterized by excessive osteoclast formation and resultant bone loss, which afflicts millions of patients around the world. Astilbin, a traditional herb, is known to have anti-inflammatory, antioxidant and antihepatic properties, but its role in osteoporosis treatment has not yet been confirmed. In our study, astilbin was found to have an inhibitory effect on the RANKL-induced formation and function of OCs in a dose-dependent manner without cytotoxicity. These effects were attributed to its ability to suppress the activity of two transcription factors (NFATc1 and c-Fos) indispensable for osteoclast formation, followed by inhibition of the expression of bone resorption-related genes and proteins (Acp5/TRAcP, CTSK, V-ATPase-d2 and integrin β3). Furthermore, we examined the underlying mechanisms and found that astilbin repressed osteoclastogenesis by blocking Ca oscillations and the NF-κB and MAPK pathways. In addition, the therapeutic effect of MA on preventing bone loss in vivo was further confirmed in an ovariectomized mouse model. Therefore, considering its ability to inhibit RANKL-mediated osteoclastogenesis and the underlying mechanisms, astilbin might be a potential candidate for treating osteolytic bone diseases.
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http://dx.doi.org/10.1111/jcmm.14713DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850941PMC
December 2019

Sclareol prevents ovariectomy-induced bone loss in vivo and inhibits osteoclastogenesis in vitro via suppressing NF-κB and MAPK/ERK signaling pathways.

Food Funct 2019 Oct;10(10):6556-6567

Key Laboratory of Orthopaedics of Zhejiang Province, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical Universtiy, Wenzhou, China.

Postmenopausal osteoporosis (PMO) is a progressive disease occurring in elderly postmenopausal women that is characterized by low bone mass and impaired bone quality. Sclareol is a natural product (initially isolated from the leaves and flowers of Salvia Sclarea) that possesses immune-regulation and anti-inflammatory effects, but its role in osteoclastic formation and function as well as the PMO remains unknown. In the current study, we investigated the inhibitory effect of sclareol on osteoclastogenesis and progression of PMO. In vitro, sclareol not only inhibited osteoclast formation but also suppressed osteoclast function. The expression of the receptor activator of NF-κB ligand (RANKL)-induced osteoclast marker gene and protein was also reduced by sclareol treatment. Mechanistically, we found that sclareol inhibits RANKL-induced NF-κB and MAPK/ERK pathway activation. Furthermore, sclareol exerted a protective effect against bone loss in an ovariectomy-induced mouse model. Taken together, our findings suggest that sclareol has potential value as a therapeutic agent for PMO.
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http://dx.doi.org/10.1039/c9fo00206eDOI Listing
October 2019

The emerging roles of hnRNPK.

J Cell Physiol 2020 03 19;235(3):1995-2008. Epub 2019 Sep 19.

School of Biomedical Sciences, Faculty of Health and Medical Sciences, The University of Western Australia, Perth, Western Australia, Australia.

Heterogeneous nuclear ribonucleoprotein K (hnRNPK) is an DNA/RNA-binding protein and regulates a wide range of biological processes and disease pathogenesis. It contains 3 K-homologous (KH) domains, which are conserved in other RNA-binding proteins, mediate nucleic acid binding activity, and function as an enhancer or repressor of gene transcription. Phosphorylation of the protein alters its regulatory function, which also enables the protein to serve as a docking platform for the signal transduction proteins. In terms of the function of hnRNPK, it is central to many cellular events, including long noncoding RNA (lncRNA) regulation, cancer development and bone homoeostasis. Many studies have identified hnRNPK as an oncogene, where it is overexpressed in cancer tissues compared with the nonneoplastic tissues and its expression level is related to the prognosis of different types of host malignancies. However, hnRNPK has also been identified as a tumour suppressor, as it is important for the activation of the p53/p21 pathway. Recently, the protein is also found to be exclusively related to the regulation of paraspeckles and lncRNAs such as Neat1, Lncenc1 and Xist. Interestingly, hnRNPK has been found to associate with the Kabuki-like syndrome and Au-Kline syndrome with prominent skeletal abnormalities. In vitro study revealed that the hnRNPK protein is essential for the formation of osteoclast, in line with its importance in the skeletal system.
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http://dx.doi.org/10.1002/jcp.29186DOI Listing
March 2020

Chondromodulin-1 in health, osteoarthritis, cancer, and heart disease.

Cell Mol Life Sci 2019 Nov 17;76(22):4493-4502. Epub 2019 Jul 17.

Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China.

The human chondromodulin-1 (Chm-1, Chm-I, CNMD, or Lect1) gene encodes a 334 amino acid type II transmembrane glycoprotein protein with characteristics of a furin cleavage site and a putative glycosylation site. Chm-1 is expressed most predominantly in healthy and developing avascular cartilage, and healthy cardiac valves. Chm-1 plays a vital role during endochondral ossification by the regulation of angiogenesis. The anti-angiogenic and chondrogenic properties of Chm-1 are attributed to its role in tissue development, homeostasis, repair and regeneration, and disease prevention. Chm-1 promotes chondrocyte differentiation, and is regulated by versatile transcription factors, such as Sox9, Sp3, YY1, p300, Pax1, and Nkx3.2. Decreased expression of Chm-1 is implicated in the onset and progression of osteoarthritis and infective endocarditis. Chm-1 appears to attenuate osteoarthritis progression by inhibiting catabolic activity, and to mediate anti-inflammatory effects. In this review, we present the molecular structure and expression profiling of Chm-1. In addition, we bring a summary to the potential role of Chm-1 in cartilage development and homeostasis, osteoarthritis onset and progression, and to the pathogenic role of Chm-1 in infective endocarditis and cancers. To date, knowledge of the Chm-1 receptor, cellular signalling, and the molecular mechanisms of Chm-1 is rudimentary. Advancing our understanding the role of Chm-1 and its mechanisms of action will pave the way for the development of Chm-1 as a therapeutic target for the treatment of diseases, such as osteoarthritis, infective endocarditis, and cancer, and for potential tissue regenerative bioengineering applications.
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http://dx.doi.org/10.1007/s00018-019-03225-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6841647PMC
November 2019

Paralogues From the Expanded Tlr11 Gene Family in Mudskipper () Are Under Positive Selection and Respond Differently to LPS/Poly(I:C) Challenge.

Front Immunol 2019 28;10:343. Epub 2019 Feb 28.

State Key Laboratory of Marine Environmental Science, College of Ocean and Earth Sciences, Xiamen University, Xiamen, China.

Toll-like receptors (TLRs) are major molecular pattern recognition receptors, which are essential for triggering a series of innate immune responses against invading pathogens by recognizing their evolutionary conserved molecular patterns. The mudskipper, is exceptional among fishes due to its amphibious lifestyle and adaptation to living on mudflats. The whole-genome sequencing of has revealed that this species possesses an expansion of Tlr11 family [12 Tlr11 family genes (one , 4 , and 7 )] that we focused on in the present study. The full-length cDNA sequences of the 12 in were cloned and their deduced amino acid sequences possessed a typical TLR domain arrangement. Likelihood tests of selection revealed that these 12 Tlr11 family genes are under diversifying selection. A total of 13 sites were found to be positively selected by more than one evolution model, of which 11 were located in the ligand-binding ectodomain. The observed non-synonymous substitutions may have functional implications in antigen and pathogen recognition specificity. These 12 were highly expressed in immune-related tissues, i.e. spleen and kidney. and transcripts were significantly up-regulated by LPS, whereas were significantly up-regulated by poly(I:C) in the spleen or/and kidney, which implies that the expanded Tlr11 family genes may play roles in protecting the fish from the invasion of gram-negative bacteria and double-stranded RNA viruses. The results from the present study suggested that the expansion of Tlr11 family genes in may recognize ligands from various pathogens found in the intertidal zone.
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http://dx.doi.org/10.3389/fimmu.2019.00343DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6403153PMC
July 2020

Androgen induces olfactory expression of prostaglandin E receptor Ep1 in the burrow-living fish Bostrychus sinensis.

J Steroid Biochem Mol Biol 2019 04 16;188:156-165. Epub 2019 Jan 16.

State Key Laboratory of Marine Environmental Science, College of Ocean and Earth Sciences, Xiamen University, Fujian, 361102, PR China; Fujian Collaborative Innovation Center for Exploitation and Utilization of Marine Biological Resources, Fujian, 361102, PR China; State-Province Joint Engineering Laboratory of Marine Bioproducts and Technology, Xiamen University, Fujian, 361102, PR China. Electronic address:

It is well documented that androgens modify olfactory processing in vertebrates. In fish, several lines of evidence indicate that androgens increase olfactory sensitivity to prostaglandin pheromone, but the molecular mechanism is still unclear. Our previous studies showed that prostaglandin E (PGE) is a sex pheromone in the burrowing-living fish Chinese black sleeper (Bostrychus sinensis) and that the PGE receptor 1 (Ep1) in the olfactory rosette is a candidate receptor for sensing sex pheromone PGE. In the present study, we found that testosterone (T) and 11-ketotestosterone (11-KT) exhibited stimulatory effects on the expression of ep1 in the olfactory rosette in vivo and ex vivo. Moreover, the androgen receptor (Ar) agonist R1881 had similar effects to 11-KT on the expression of ep1 ex vivo, suggesting the up-regulatory effect is mediated by Ar. The amount of arα transcripts (˜1500 copies/100 ng total RNA) was greater than that of arβ (˜300 copies/100 ng total RNA) in the olfactory rosette, and the expression levels of arα increased with spermatogenesis and peaked at late meiosis stage. Moreover, activated Arα but not Arβ transactivated a 2k bp ep1 promoter in HEK293T cell, and some OSNs exhibited co-localization of arα mRNA and Ep1 protein signals. Taken together, our results suggest that Arα, but not Arβ, plays a crucial role in mediating the androgen-induced up-regulation of ep1 expression in B. sinensis. The present study is the first to shed light on the molecular mechanisms whereby androgens enhance responsiveness to prostaglandin sex pheromones in teleosts.
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http://dx.doi.org/10.1016/j.jsbmb.2019.01.010DOI Listing
April 2019

Modulating calcium-mediated NFATc1 and mitogen-activated protein kinase deactivation underlies the inhibitory effects of kavain on osteoclastogenesis and bone resorption.

J Cell Physiol 2018 01 4;234(1):789-801. Epub 2018 Aug 4.

School of Biomedical Sciences, The University of Western Australia, Perth, Western Australia, Australia.

Osteoclasts are responsible for bone resorption during the process of bone remodeling. Increased osteoclast numbers and bone resorption activity are the main factors contributing to bone loss-related diseases such as osteoporosis. Therefore, modulating the formation and function of osteoclasts is critical for the effective treatment of osteolysis and osteoporosis. Kavain is the active ingredient extracted from the root of the kava plant, which possesses known anti-inflammatory properties. However, the effects of kavain on osteoclastogenesis and bone resorption remain unclear. In this study, we found that kavain inhibits receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation and fusion using tartrate-resistant acid phosphatase staining and immunofluorescence. Furthermore, kavain inhibited bone resorption performed by osteoclasts. Using reverse transcription-polymerase chain reaction and western blot analysis, we found that kavain downregulates the expression of osteoclast marker genes, such as nuclear factor of activated T cells, cytoplasmic 1 (Nfatc1), v-atpase d2 (Atp6v0d2), dendrocyte expressed seven transmembrane protein (Dcstamp), matrix metallopeptidase 9 (Mmp9), cathepsin K (Ctsk), and Acp5. Additionally, kavain repressed RANKL-induced calcium oscillations, nuclear factor of activated T cells activation, and mitogen-activated protein kinase phosphorylation, while leaving NF-κB unaffected. We found no effects of kavain on either osteoblast proliferation or differentiation. Besides, kavain inhibited bone loss in ovariectomized mice by suppressing osteoclastogenesis. Collectively, these data suggest a potential use for kavain as a candidate drug for the treatment of osteolytic diseases.
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http://dx.doi.org/10.1002/jcp.26893DOI Listing
January 2018

Involvement of Membrane Progestin Receptor Beta (mPRβ/Paqr8) in Sex Pheromone Progestin-Induced Expression of Luteinizing Hormone in the Pituitary of Male Chinese Black Sleeper ().

Front Endocrinol (Lausanne) 2018 18;9:397. Epub 2018 Jul 18.

State Key Laboratory of Marine Environmental Science, College of Ocean and Earth Sciences, Xiamen University, Fujian, China.

Our previous studies showed that 17α, 20β-dihydroxy-4-pregnen-3-one (DHP) acted as a sex pheromone to induce reproductive success in Chinese black sleeper (), but its functional mechanism remains unclear. In the present study, we cloned the cDNAs of the gonadotropin subunits (αβ, and β), and found that, in exposure to 5 nM DHP, transcript levels of β significantly increased in the pituitary at 6 h post exposure; plasma 11-KT levels increased at 24 h post exposure in mature male fish. In contrast, DHP exposure failed to increase the transcript levels of β in the pituitary of immature male fish, suggesting that the responsiveness to DHP depends on reproductive status. Interestingly, expression of progestin and adipoQ receptor 8 (, also known as mPRβ) and progesterone receptor membrane component 2 significantly increased in the olfactory rosette of male fish at late meiosis stage following a co-injection of human chorionic gonadotropin (HCG) and luteinizing hormone releasing hormone-A (LHRH-A), while no increases of other progestin receptors were observed. Moreover, Paqr8 protein was localized in the dendritic knobs of the olfactory sensory neurons, which were activated following the exposure to DHP. The DHP-induced expression of β in pituitary was not inhibited by RU486, an antagonist of nuclear progesterone receptor. Taken together, our results suggested that sex pheromone DHP increased the expression of β transcript in the pituitary and plasma 11-KT levels of mature male, important for reproduction; and Paqr8 might be involved in responding to sex pheromone DHP in the olfactory rosette of male .
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http://dx.doi.org/10.3389/fendo.2018.00397DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6058016PMC
July 2018

Cistanche deserticola polysaccharide attenuates osteoclastogenesis and bone resorption via inhibiting RANKL signaling and reactive oxygen species production.

J Cell Physiol 2018 12 3;233(12):9674-9684. Epub 2018 Jul 3.

Division of Regenerative Medicine, School of Biomedical Sciences, University of Western Australia, Perth, Western Australia, Australia.

Osteoporosis is a metabolic disease characterized by osteopenia and bone microstructural deterioration. Osteoclasts are the primary effector cells that degrade bone matrix and their abnormal function leads to the development of osteoporosis. Reactive oxygen species (ROS) accumulation during cellular metabolism promotes osteoclast proliferation and differentiation, therefore, playing an important role in osteoporosis. Cistanche deserticola polysaccharide (CDP) possesses antitumor, anti-inflammatory, and antioxidant activity. However, the impact of CDP on osteoclasts is unclear. In this study, tartrate-resistant acid phosphatase staining, immunofluorescence, reverse transcription-polymerase chain reaction, and western blot analysis were utilized to demonstrate that CDP inhibited osteoclastogenesis and hydroxyapatite resorption. In addition, CDP also inhibited the expression of osteoclast maker genes including Ctsk, Mmp9, and Acp5 and had no effect on receptor activator of nuclear factor κB (RANK) expression. Mechanistic analyses revealed that CDP increases the expression of antioxidant enzymes to attenuate RANKL-mediated ROS production in osteoclasts and inhibits nuclear factor of activated T cells and mitogen-activated protein kinase activation. These results suggest that CDP may represent a candidate drug for the treatment of osteoporosis caused by excessive osteoclast activity.
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http://dx.doi.org/10.1002/jcp.26882DOI Listing
December 2018

EGFL7: Master regulator of cancer pathogenesis, angiogenesis and an emerging mediator of bone homeostasis.

J Cell Physiol 2018 11 19;233(11):8526-8537. Epub 2018 Jun 19.

National Key Discipline and Orthopedic Laboratory, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.

Epidermal growth factor-like domain-containing protein 7 (EGFL7), a member of the epidermal growth factor (EGF)-like protein family, is a potent angiogenic factor expressed in many different cell types. EGFL7 plays a vital role in controlling vascular angiogenesis during embryogenesis, organogenesis, and maintaining skeletal homeostasis. It regulates cellular functions by mediating the main signaling pathways (Notch, integrin) and EGF receptor cascades. Accumulating evidence suggests that Egfl7 plays a crucial role in cancer biology by modulating tumor angiogenesis, metastasis, and invasion. Dysregulation of Egfl7 has been frequently found in several types of cancers, such as malignant glioma, colorectal carcinoma, oral and oesophageal cancers, gastric cancer, hepatocellular carcinoma, pancreatic cancer, breast cancer, lung cancer, osteosarcoma, and acute myeloid leukemia. In addition, altered expression of miR-126, a microRNA associated with Egfl7, was found to play an important role in oncogenesis. More recently, our study has shown that EGFL7 is expressed in both the osteoclast and osteoblast lineages and promotes endothelial cell activities via extracellular signal-regulated kinase (ERK), signal transducer and activator of transcription 3 (STAT3), and integrin signaling cascades, indicative of its angiogenic regulation in the bone microenvironment. Thus, understanding the role of EGFL7 may provide novel insights into the development of improved diagnostics and therapeutic treatment for cancers and skeletal pathological disorders, such as ischemic osteonecrosis and bone fracture healing.
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http://dx.doi.org/10.1002/jcp.26792DOI Listing
November 2018

Lumichrome inhibits osteoclastogenesis and bone resorption through suppressing RANKL-induced NFAT activation and calcium signaling.

J Cell Physiol 2018 11 15;233(11):8971-8983. Epub 2018 Jun 15.

School of Biomedical Sciences, University of Western Australia, Perth, Western Australia, Australia.

The dynamic balance between bone resorption and bone formation is crucial to maintain bone mass. Osteoclasts are key cells that perform bone resorption while osteoblasts and osteocytes function in bone formation. Osteoporosis, a bone metabolism disease characterized by bone loss and degradation of bone microstructure, occurs when osteoclastic bone resorption outstrips osteoblastic bone synthesis. The interaction between receptor activator of nuclear factor κB ligand (RANKL) and RANK on the surface of bone marrow macrophages promotes osteoclast differentiation and activation. In this study, we found that lumichrome, a photodegradation product of riboflavin, inhibits RANKL-induced osteoclastogenesis and bone resorption as determined by tartrate-resistant acid phosphatase staining, immunofluorescence, reverse transcription-polymerase chain reaction, and western blot. Our results showed that lumichrome represses the expression of osteoclast marker genes, including cathepsin K (Ctsk) and Nfatc1. In addition, lumichrome suppressed RANKL-induced calcium oscillations, NFATc1, NF-κB, and MAPK signaling activation. Moreover, lumichrome promoted osteoblast differentiation at an early stage, as demonstrated by upregulated expression of osteoblast marker genes Alp, Runx2, and Col1a1. We also found that lumichrome reduces bone loss in ovariectomized mice by inhibiting osteoclastogenesis. In summary, our data suggest the potential of lumichrome as a therapeutic drug for osteolytic diseases.
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http://dx.doi.org/10.1002/jcp.26841DOI Listing
November 2018

Poria cocos polysaccharide attenuates RANKL-induced osteoclastogenesis by suppressing NFATc1 activity and phosphorylation of ERK and STAT3.

Arch Biochem Biophys 2018 06 17;647:76-83. Epub 2018 Apr 17.

School of Biomedical Sciences, University of Western Australia, Perth, WA, 6009, Australia. Electronic address:

Pathological fractures caused by osteolytic lesions seriously threaten the health of patients. Osteoclasts play important roles in bone resorption whose hyperfunction are closely related to osteolytic lesions. Studies on osteoclast differentiation and function assist in the prevention of excessive bone loss associated diseases. We screened a variety of natural compounds with anti-inflammatory effect and found that poria cocos polysaccharide (PCP) inhibited RANKL-induced osteoclast formation and bone resorption via TRAcP staining, immunofluorescence, RT-PCR and western blot. PCP down-regulated phosphorylation of STAT3, P38, ERK and JNK, and thus repressed the expression of NFAcT1 and c-Fos during RANKL-induced osteoclastogenesis. Besides, the expression of bone resorption related genes such as TRAcP and CTSK was suppressed by PCP. The results suggest that PCP can be invoked as a candidate for the treatment of osteolytic diseases by inhibiting osteoclastogenesis.
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http://dx.doi.org/10.1016/j.abb.2018.04.011DOI Listing
June 2018

[Subchondral drilling method combined with gum-bletilla complex to repair articular cartilage defects].

Zhongguo Zhong Yao Za Zhi 2018 Feb;43(4):813-819

Department of Orthopaedics, Affiliated Hospital, Chengdu University Traditinal Chinese Medicine, Chengdu 610000, China.

Two types(A model and B model) of articular cartilage defect models were prepared by using adult New Zealand white rabbits. A model group was applied by drilling without through subchondral bone, whose right joint was repaired by composite scaffolds made by seed cell, gum-bletilla as well as Pluronic F-127, and left side was blank control. B model group was applied by subchondral drilling method, whose right joint was repaired by using composite scaffolds made by gum-bletilla and Pluronic F-127 without seed cells, and left side was blank control. Autogenous contrast was used in both model types. In addition, another group was applied with B model type rabbits, which was repaired with artificial complex material of Pluronic F-127 in both joint sides. 4, 12 and 24 weeks after operation, the animals were sacrificed and the samples were collected from repaired area for staining with HE, typeⅡcollagen immunohistochemical method, Alcian blue, and toluidine blue, and then were observed with optical microscope. Semi-quantitative scores were graded by referring to Wakitanis histological scoring standard to investigate the histomorphology of repaired tissue. Hyaline cartilage repairing was achieved in both Group A and Group B, with satisfactory results. There were no significant differences on repairing effects for articular cartilage defects between composite scaffolds made by seed cell, gum-bletilla and Pluronic F-127, and the composite scaffolds made by gum-bletilla and Pluronic F-127 without seed cell. Better repairing effects for articular cartilage defects were observed in groups with use of gum-bletilla, indicating that gum-bletilla is a vital part in composite scaffolds material.
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http://dx.doi.org/10.19540/j.cnki.cjcmm.2018.0022DOI Listing
February 2018

Comparison of rigid and deformable registration through the respiratory phases of four-dimensional computed tomography image data sets for radiotherapy after breast-conserving surgery.

Medicine (Baltimore) 2017 Dec;96(50):e9143

School of Medicine and Life Sciences, University of Jinan-Shandong Academy of Medical Sciences Department of Radiation Oncology Breast Cancer Center, Shandong Cancer Hospital Affiliated to Shandong University, Jinan, Shandong Province The Third Hospital of Jinan, China.

Background: The aim of this study was to compare the geometric differences in gross tumor volume (GTV) and surgical clips propagated by rigid image registration (RIR) and deformable image registration (DIR) using a four-dimensional computed tomography (4DCT) image data set for patients treated with boost irradiation or accelerated partial breast irradiation after breast-conserving surgery (BCS).

Methods: The 4DCT data sets of 44 patients who had undergone BCS were acquired. GTV and selected clips were manually delineated on end-inhalation phase (CT0) and end-exhalation phase (CT50) images of 4DCT data sets. Subsequently, the GTV and selected clips from CT0 images were transformed and propagated to CT50 images using RIR and DIR, respectively. The geometric differences in GTV and surgical clips from DIR were compared with those of RIR.

Results: The mean Dice similarity coefficient (DSC) index was 0.860 ± 0.042 for RIR and 0.870 ± 0.040 for DIR for GTV (P = .000). The three-dimensional distance to the center of mass (COM) of the GTV from RIR was longer than that from DIR (1.22 mm and 1.10 mm, respectively, P = .000). Moreover, in the anterior-posterior direction, displacements from RIR were significantly greater than those from DIR for both GTV (0.70 mm and 0.50 mm, respectively) and selected clips (upper clip, 0.45 mm vs 0.20 mm; inner clip, 0.55 mm vs 0.30 mm; outer clip, 0.40 mm vs 0.20 mm; lower clip, 0.50 mm vs 0.25 mm) (P = .000). However, in the left-right and superior-inferior directions, there were no significant displacement differences between RIR and DIR for GTV and the selected clips (all P > .050).

Conclusion: DIR can improve the overlap for GTV registration from CT0 to CT50 images from 4DCT scanning. Furthermore, DIR is superior to RIR in reflecting the displacement of GTV and selected clips in the anterior-posterior direction induced by respiratory movement.
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http://dx.doi.org/10.1097/MD.0000000000009143DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5815729PMC
December 2017

Internal mammary sentinel lymph node biopsy with modified injection technique: A case report.

Medicine (Baltimore) 2017 Dec;96(52):e9466

School of Medicine and Life Sciences, University of Jinan, Shandong Academy of Medical Sciences Shandong Cancer Hospital and Institute, Jinan, Shandong, People's Republic of China.

Rationale: In addition to axillary lymph node (ALN), internal mammary lymph node (IMLN) is also the first-echelon drainage nodes reached by metastasising cancer cells from breast cancer, which can provide important prognostic information.

Patient Concerns: In this paper, we will introduce a case of breast cancer patient whose postoperative pathology result showed that she had internal mammary sentinel lymph node (IMSLN) metastases but no axillary sentinel lymph node (ASLN) metastases.

Diagnoses: She was diagnosed as pT1cN1bM0 breast cancer based on the positive IMSLN but negative ASLN.

Interventions: She received axillary-sentinel lymph node biopsy (A-SLNB) and internal mammary-sentinel lymph node biopsy (IM-SLNB) guided by modified injection technique. In the choice of chemotherapy, she received dose-dense AC × 4 times followed P × 4 times for chemotherapy. As to irradiation therapy, she received irradiation therapy include chest wall, superclavicular region, and internal mammary nodes.

Outcomes: After performing IM-SLNB, the nodal staging of this patient increased (from N0 to N1b). And she received additional chemotherapy and irradiation therapy.

Lessons: With the guidance of modified injection technique, the preoperative visualization rate of IMLN has been improved. IM-SLNB could be a minimally invasive technique for effective evaluation of the status of IMLN to provide information for staging and guide the adjuvant treatment.
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http://dx.doi.org/10.1097/MD.0000000000009466DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6393068PMC
December 2017

Achyranthes bidentata polysaccharide suppresses osteoclastogenesis and bone resorption via inhibiting RANKL signaling.

J Cell Biochem 2018 06 9;119(6):4826-4835. Epub 2018 Mar 9.

School of Biomedical Sciences, University of Western Australia, Perth, Western Australia, Australia.

Osteoclasts are highly differentiated multinucleated giant cells that play fundamental roles in bone resorption and in the pathogenesis of osteolytic conditions, such as osteoporosis and cancer-induced bone loss. Achyranthes bidentata polysaccharide (ABP) is a hydrophilic compound with anti-oxidation and anti-aging characteristics. The impact of ABP on RANKL-induced osteoclast formation and bone resorption has not been assessed, hence, in this study we investigated the effect of ABP on osteoclast formation and resorption in murine bone marrow derived osteoclasts. We found that ABP was able to suppress RANKL-induced osteoclast differentiation and bone resorption activity at concentrations above 6.5 µM, while demonstrating no cytotoxicity at concentrations up to 10 µM. The actions of ABP were mediated through inhibition of RANKL-induced c-Fos and NFATc1 gene and protein expression. Furthermore, we found that ABP suppressed NFATc1 transcriptional activity, and the phosphorylation of MAPK pathways induced by RANKL. Collectively, ABP attenuates RANKL-mediated osteoclast activity and signaling, and might serve as a potential therapeutic candidate for preventing bone loss related diseases.
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http://dx.doi.org/10.1002/jcb.26682DOI Listing
June 2018

Coupling factors and exosomal packaging microRNAs involved in the regulation of bone remodelling.

Biol Rev Camb Philos Soc 2018 02 10;93(1):469-480. Epub 2017 Aug 10.

Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.

Bone remodelling is a continuous process by which bone resorption by osteoclasts is followed by bone formation by osteoblasts to maintain skeletal homeostasis. These two forces must be tightly coordinated not only quantitatively, but also in time and space, and its malfunction leads to diseases such as osteoporosis. Recent research focusing on the cross-talk and coupling mechanisms associated with the sequential recruitment of osteoblasts to areas where osteoclasts have removed bone matrix have identified a number of osteogenic factors produced by the osteoclasts themselves. Osteoclast-derived factors and exosomal-containing microRNA (miRNA) can either enhance or inhibit osteoblast differentiation through paracrine and juxtacrine mechanisms, and therefore may have a central coupling role in bone formation. Entwined with angiocrine factors released by vessel-specific endothelial cells and perivascular cells or pericytes, these factors play a critical role in angiogenesis-osteogenesis coupling essential in bone remodelling.
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http://dx.doi.org/10.1111/brv.12353DOI Listing
February 2018
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