David M. Findlay

ORCID: 0000-0003-0174-7432
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About
Contact & Profiles
Research Areas
  • Bone Metabolism and Diseases
  • Bone health and treatments
  • Orthopaedic implants and arthroplasty
  • Bone health and osteoporosis research
  • Bone and Joint Diseases
  • Neuropeptides and Animal Physiology
  • Osteoarthritis Treatment and Mechanisms
  • Bone Tissue Engineering Materials
  • Vitamin D Research Studies
  • Orthopedic Infections and Treatments
  • Bone and Dental Protein Studies
  • Total Knee Arthroplasty Outcomes
  • Signaling Pathways in Disease
  • Receptor Mechanisms and Signaling
  • NF-κB Signaling Pathways
  • Antibiotic Use and Resistance
  • Cell death mechanisms and regulation
  • TGF-β signaling in diseases
  • Rheumatoid Arthritis Research and Therapies
  • Cancer, Stress, Anesthesia, and Immune Response
  • Estrogen and related hormone effects
  • Cancer, Hypoxia, and Metabolism
  • Hip disorders and treatments
  • Vitamin K Research Studies
  • Nuclear Physics and Applications

NHS Greater Glasgow and Clyde
2024

Glasgow Royal Infirmary
2024

The University of Adelaide
2014-2023

Rutherford Appleton Laboratory
2007-2022

Royal Adelaide Hospital
2004-2022

Scottish Environment Protection Agency
2021-2022

University of Edinburgh
2007-2022

Roslin Institute
2022

University College London
2021

National Hospital for Neurology and Neurosurgery
2021

Sclerostin is a product of mature osteocytes embedded in mineralised bone and negative regulator mass osteoblast differentiation. While evidence suggests that sclerostin has an anti-anabolic role, the possibility also exists catabolic activity. To test this we treated human primary pre-osteocyte cultures, cells have found are exquisitely sensitive to sclerostin, or mouse osteocyte-like MLO-Y4 cells, with recombinant (rhSCL) measured effects on pro-catabolic gene expression. dose-dependently...

10.1371/journal.pone.0025900 article EN cc-by PLoS ONE 2011-10-04

We reported that interleukin (IL) 6 alone cannot induce osteoclast formation in cocultures of mouse bone marrow and osteoblastic cells, but soluble IL-6 receptor (IL-6R) strikingly triggered induced by IL-6. In this study, we examined the mechanism related cytokines through interaction between cells progenitors. When dexamethasone was added to cocultures, could stimulate without help IL-6R. Osteoblastic expressed a very low level IL-6R mRNA, whereas fresh spleen both which are considered be...

10.1084/jem.182.5.1461 article EN The Journal of Experimental Medicine 1995-11-01

Joint pain is the defining symptom of osteoarthritis (OA) but its origin and mechanisms remain unclear. Here, we investigated an unprecedented role osteoclast-initiated subchondral bone remodeling in sensory innervation for OA pain. We show that osteoclasts secrete netrin-1 to induce nerve axonal growth bone. Reduction osteoclast formation by knockout receptor activator nuclear factor kappa-B ligand (Rankl) osteocytes inhibited nerves into bone, dorsal root ganglion neuron hyperexcitability,...

10.1172/jci121561 article EN Journal of Clinical Investigation 2018-12-11

The dwindling supply of new antibiotics largely reflects regulatory and commercial challenges, but also a failure discovery. In the 1990s pharmaceutical industry abandoned its classical ways seeking instead adopted strategy that combined genomics with high-throughput screening existing compound libraries. Too much emphasis was placed on identifying targets molecules bound to them, too little ability these permeate bacteria, evade efflux avoid mutational resistance; moreover, libraries were...

10.1093/jac/dkr262 article EN Journal of Antimicrobial Chemotherapy 2011-06-23

Abstract The identity of the cell type responsive to sclerostin, a negative regulator bone mass, is unknown. Since sclerostin expressed in vivo by mineral-embedded osteocytes, we tested hypothesis that would regulate behavior cells actively involved mineralization adult bone, preosteocyte. Differentiating cultures human primary osteoblasts exposed recombinant (rhSCL) for 35 days displayed dose- and time-dependent inhibition vitro mineralization, with late being most terms gene expression....

10.1002/jbmr.345 article EN Journal of Bone and Mineral Research 2011-02-01

Abstract Human osteoblast phenotypes that support osteoclast differentiation and bone formation are not well characterized. Osteoblast markers were examined in relation to RANKL expression. expression was induced preferentially immature cells. These results an important link between diverse functions. Cells of the lineage two apparently distinct functions: promotion formation. The aim this study examine relationship these human osteoblasts (NHBC), terms pre-osteoblast marker, STRO-1, mature...

10.1359/jbmr.2003.18.6.1088 article EN Journal of Bone and Mineral Research 2003-06-01

Objective. This study investigated the involvement of recently identified regulators osteoclast formation RANKL [receptor activator nuclear factor kappaB (RANK) ligand, differentiation factor, TRANCE, osteoprotegerin ligand] and its natural inhibitor, (OPG), in bone erosion rheumatoid arthritis (RA).

10.1093/rheumatology/40.6.623 article EN Lara D. Veeken 2001-06-01

Abstract The mechanisms by which primary tumors of the bone cause destruction have not been elucidated. Unlike most other lytic tumors, osteoclastomas, otherwise known as giant cell (GCT), contain osteoclast-like cells within tumor stroma. A new member TNF-ligand superfamily member, osteoclast differentiation factor (ODF/OPGL/RANKL/TRANCE), was recently identified. ODF shown to directly stimulate osteoclastogenesis, in presence M-CSF. In this study, expression examined a number samples...

10.1359/jbmr.2000.15.4.640 article EN Journal of Bone and Mineral Research 2000-04-01

Osteoarthritis (OA) is characterized by alterations to subchondral bone as well articular cartilage. Changes in OA have also been identified at sites distal the affected joint, which include increased volume fraction and reduced mineralization. Altered remodelling has proposed underlie these changes OA. To investigate molecular basis for changes, we performed microarray gene expression profiling of obtained autopsy from individuals with no evidence joint disease (control) undergoing...

10.1186/ar2301 article EN cc-by Arthritis Research & Therapy 2007-01-01

The physiological function of p38α, which is an isoform p38 MAPK, has been investigated previously in several studies using pharmacological inhibitors. However, the results regarding whether p38α promotes or inhibits nerve regeneration vivo have controversial. We generated novel mutant mice (sem mice) with a point mutation region encoding substrate-docking-site, serves as limited loss-of-function model p38α. In present study, we utilized sem and wild-type littermates (wt to investigate role...

10.1186/1742-2094-10-1 article EN cc-by Journal of Neuroinflammation 2013-01-03

We have recently shown that TNF-related weak inducer of apoptosis (TWEAK) is a mediator inflammatory bone remodeling. The aim this study was to investigate the role TWEAK in modulating human osteoblast activity, and how TNFalpha might interact context. Recombinant TNF were both mitogenic for primary osteoblasts (NHBC). dose- time-dependently regulated expression transcription factors RUNX2 osterix. inhibited vitro mineralization downregulated osteogenesis-associated genes. Significantly,...

10.1359/jbmr.090305 article EN Journal of Bone and Mineral Research 2009-03-17
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