Jesse E. Otero

ORCID: 0000-0003-2142-6863
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About
Contact & Profiles
Research Areas
  • Total Knee Arthroplasty Outcomes
  • Orthopaedic implants and arthroplasty
  • Orthopedic Infections and Treatments
  • Bone Metabolism and Diseases
  • NF-κB Signaling Pathways
  • Hip and Femur Fractures
  • Sarcoma Diagnosis and Treatment
  • Immune Response and Inflammation
  • Bone health and treatments
  • Hip disorders and treatments
  • Bone Tumor Diagnosis and Treatments
  • Telomeres, Telomerase, and Senescence
  • Bone fractures and treatments
  • Pelvic and Acetabular Injuries
  • Osteomyelitis and Bone Disorders Research
  • Blood transfusion and management
  • Infectious Diseases and Tuberculosis
  • Cardiac, Anesthesia and Surgical Outcomes
  • COVID-19 and healthcare impacts
  • Thyroid Disorders and Treatments
  • Venous Thromboembolism Diagnosis and Management
  • Surgical site infection prevention
  • Signaling Pathways in Disease
  • Clinical Laboratory Practices and Quality Control
  • Opioid Use Disorder Treatment

OrthoCarolina
2017-2025

Carolinas Medical Center
2021-2024

Carolina Musculoskeletal Institute
2021-2024

OrthoCarolina Research Institute
2019-2021

Atrium Medical Cente
2021

University of Iowa Hospitals and Clinics
2012-2020

University of Iowa
2013-2019

Iowa City VA Health Care System
2018

Clinical Orthopaedics and Related Research
2018

Centers for Medicare and Medicaid Services
2018

Abstract The contribution of inflammation to the chronic joint disease osteoarthritis (OA) is unclear, and this lack clarity detrimental efforts identify therapeutic targets. Here we show that chondrocytes under inflammatory conditions undergo a metabolic shift regulated by NF-κB activation, leading reprogramming cell metabolism towards glycolysis lactate dehydrogenase A (LDHA). Inflammation can reciprocally modulate each other regulate cartilage degradation. LDHA binds NADH promotes...

10.1038/s41467-020-17242-0 article EN cc-by Nature Communications 2020-07-09

Significance Chronic recurrent multifocal osteomyelitis (CRMO) is a human disorder of the innate immune system that causes bone inflammation mimics infectious osteomyelitis. There spontaneous mutant mouse model disease caused by homozygous mutations in gene Pstpip2 . Our studies show this mediated cytokine IL-1β, but independent nucleotide-binding domain, leucine-rich repeat-containing family, pyrin domain-containing 3 (NLRP3) inflammasome and caspase-1, which different from most other...

10.1073/pnas.1318685111 article EN Proceedings of the National Academy of Sciences 2014-01-06

Abstract Generalized arterial calcification (AC) of infancy (GACI) is an autosomal recessive disorder that features hydroxyapatite deposition within elastic fibers. Untreated, approximately 85% GACI patients die by 6 months age from cardiac ischemia and congestive heart failure. The first-generation bisphosphonate etidronate (EHDP; ethane-1-hydroxy-1,1-diphosphonic acid, also known as 1-hydroxyethylidene-bisphosphonate) inhibits bone resorption can mimic endogenous inorganic pyrophosphate...

10.1002/jbmr.1752 article EN Journal of Bone and Mineral Research 2012-09-12

Abstract Two types of telomere maintenance mechanisms (TMMs) have been described in human tumors: telomerase activation and alternative lengthening telomeres (ALT). Although the vast majority epithelial tumors rely on activation, many mesenchymal ALT for maintenance, but within this tumor group, TMMs used by translocation‐associated sarcomas not systematically studied. We studied lengths expression activity 30 uncultured samples 10 cell lines Ewing's sarcoma, a prototypical compared data to...

10.1002/gcc.20074 article EN Genes Chromosomes and Cancer 2004-07-12

Monocytes differentiate into osteoclasts through stimulation of receptor activator NF-kappaB (RANK). Many downstream effectors RANK play a positive role in osteoclastogenesis, but their relative importance osteoclast differentiation is unclear. We report the discovery that activation single pathway sufficient for differentiation. In this regard, introduction constitutively activated IKKbeta (IKKbeta(SSEE)) not wild-type monocytes stimulates bona fide absence ligand (RANKL). This phenomenon...

10.1002/jbmr.4 article EN Journal of Bone and Mineral Research 2010-02-01

Abstract Background Use of large clinical and administrative databases for orthopaedic research has increased exponentially. Each database represents unique patient populations varies in their methodology data acquisition, which makes it possible that similar questions posed to different might result answers differ important ways. Questions/purposes (1) What are the differences reported demographics, comorbidities, complications patients undergoing primary TKA among four commonly used...

10.1007/s11999.0000000000000011 article EN Clinical Orthopaedics and Related Research 2018-01-01

It has been reported previously that inhibitory kappaB kinase (IKK) supports osteoclastogenesis through NF-kappaB-mediated prevention of apoptosis. This finding suggests the ligand for receptor activator NF-kappaB (RANKL), master osteoclastogenic cytokine, induces apoptosis osteoclast precursors (OCPs) in absence IKKbeta/NF-kappaB competency. To validate this hypothesis, we sought to determine pro-apoptotic signaling factors induced by RANKL IKKbeta-null OCPs and rescue differentiation...

10.1074/jbc.m800434200 article EN cc-by Journal of Biological Chemistry 2008-06-21
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