Results 111 to 120 of about 53,100 (272)

Biochemical bone biomarkers in plasma cell dyscrasias

open access: yesBritish Journal of Haematology, EarlyView.
Visual abstract depicting that bone turnover markers reflect dynamic alterations in bone remodelling across the spectrum of plasma cell dyscrasias but remain limited by assay variability, biological confounding and incomplete integration with imaging and risk stratification.
Guido Nador   +4 more
wiley   +1 more source

Pu-erh Tea Extract Ameliorates Ovariectomy-Induced Osteoporosis in Rats and Suppresses Osteoclastogenesis In Vitro

open access: yesFrontiers in Pharmacology, 2017
Background and Objective: Tea drinking is associated with positive effects on bone health and may protect against osteoporosis, especially in elderly women.
Titi Liu   +24 more
doaj   +1 more source

Effects of RANKL-Targeted Therapy in Immunity and Cancer. [PDF]

open access: yes, 2014
The role of the receptor activator of nuclear factor-κB ligand (RANKL)/RANK system is well characterized within bone, where RANKL/RANK signaling mediates osteoclastogenesis and bone resorption.
Cheng, Michael L, Fong, Lawrence
core   +2 more sources

Molecular Basis and Clinical Spectrum of WNT10A‐Related Oligodontia

open access: yesClinical Genetics, EarlyView.
Cellular Mechanism behind WNT10A phenotypes. ABSTRACT WNT10A mutations, a major genetic determinant of dental agenesis and ectodermal dysplasia, exert profound effects on craniofacial development. Although classified as rare disorders, these mutations account for more than half of oligodontia cases, reflecting their critical role.
Perennes Elise   +5 more
wiley   +1 more source

KAT6A/YAP/TEAD4 pathway modulates osteoclastogenesis by regulating the RANKL/OPG ratio on the compression side during orthodontic tooth movement

open access: yesProgress in Orthodontics
Background Orthodontic tooth movement (OTM) is a dynamic equilibrium of bone remodeling, involving the osteogenesis of new bone and the osteoclastogenesis of old bone, which is mediated by mechanical force. Periodontal ligament stem cells (PDLCSs) in the
Kuang Tan   +4 more
doaj   +1 more source

Adiponectin does not bind to gelatin: a new and easy way to purify high-molecular-weight adiponectin from human plasma

open access: yesJournal of Lipid Research, 2010
Human plasma contains three forms of adiponectin, a trimer, a hexamer, and a high-molecular-weight (HMW) multimer. We previously reported HMW adiponectin was a gelatin-binding protein of 28 kDa (GBP28), it having been purified due to its affinity to ...
Yasuko Nakano   +6 more
doaj   +1 more source

Hypoxia Exacerbates Periapical Periodontitis‐Associated Pathological Bone Loss via the Hypoxia‐Inducible Factor‐2α‐Calmodulin‐Dependent Protein Kinase IV Axis

open access: yesCell Proliferation, EarlyView.
Hypoxia exposure activates HIF‐2α, which binds to the Camk4 promoter to enhance RANKL‐mediated osteoclast differentiation, leading to aggravated alveolar bone resorption in periapical periodontitis. ABSTRACT Periapical periodontitis is one of the most common inflammatory bone destructive diseases. Epidemiological evidence suggests that hypoxia exposure,
Kang Gao   +11 more
wiley   +1 more source

RAGE Signaling in Skeletal Biology [PDF]

open access: yes, 2019
PURPOSE OF REVIEW: The receptor for advanced glycation end products (RAGE) and several of its ligands have been implicated in the onset and progression of pathologies associated with aging, chronic inflammation, and cellular stress. In particular, the
Davis, Hannah M.   +2 more
core   +2 more sources

Hepatocyte TrkB Acts as a Gatekeeper Against MASH‐Related Liver Fibrosis by Suppressing the TGFβ/CCL2 Axis and Macrophage Infiltration

open access: yesCell Proliferation, EarlyView.
Hepatocyte TrkB is identified as a critical gatekeeper against MASH‐related fibrosis. Mechanistically, TrkB inhibits the TGFβ/SMAD3/FOS axis to suppress CCL2 secretion, thereby blocking pathogenic macrophage recruitment and ameliorating liver fibrosis.
Yueying Chen   +11 more
wiley   +1 more source

SNX10 gene mutation leading to osteopetrosis with dysfunctional osteoclasts [PDF]

open access: yes, 2017
Acknowledgements We sincerely thank the patients and family members who participated in this study. We would also like to thank Stefan Esher, Umeå University, for help with genealogy, and Anna Westerlund for excellent technical assistance.
Ameur, Adam   +15 more
core   +1 more source

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