We used multivariable Cox proportional hazards regression models to describe exposure-disease associations for incident CTS for individually observed physical exposures and JEM exposures from O*NET.
We used multivariable Cox proportional hazards regression models to describe exposure-disease associations for incident CTS for individually observed physical exposures and JEM exposures from O*NET.
We used multivariable Cox proportional hazards regression models to describe exposure-disease associations for incident CTS for individually observed physical exposures and JEM exposures from O*NET.
We show that the TGF-β1-induced phosphorylation of AKT was significantly decreased by the addition of PFD (800 μg/mL) in both CT- and DD-derived fibroblasts.
We report a family with a missense mutation, c.700G>T p.Asp234Tyr (deviant nomenclature: c.670G>T, p.Asp224Tyr), within the intracellular domain of myelin protein zero, who has distal sensorimotor symptoms, cramps, restless legs syndrome, neuropathic pain, and carpal tunnel syndrome.
We induced myocardial infarction (MI) in micromini-pigs (15-25 kg) and transplanted the L-CTSs (Tx) 2 weeks after MI induction (4 sheets/recipient) under immunosuppression (Tx: n = 5, Sham: n = 5).
To clarify the role of tenascin-C and PG-M/versican, which have often been found to be involved in tissue remodeling and vascular stenosis in the pathogenesis of CTS, we histologically and biochemically examined the production of extracellular matrix in the flexor tenosynovium from 40 idiopathic CTS patients.
The scenarios involve glutathione-S-transferase theta 1 (GSTT1) and hematopoietic cancer in hospital workers, human leukocyte antigen coding for glutamic acid in the 69th position (HLA DPB1(E69)) and chronic beryllium disease in beryllium workers, and peripheral myelin protein 22 (PMP22) deletion and carpal tunnel syndrome in railroad track workers.
The scenarios involve glutathione-S-transferase theta 1 (GSTT1) and hematopoietic cancer in hospital workers, human leukocyte antigen coding for glutamic acid in the 69th position (HLA DPB1(E69)) and chronic beryllium disease in beryllium workers, and peripheral myelin protein 22 (PMP22) deletion and carpal tunnel syndrome in railroad track workers.
The scenarios involve glutathione-S-transferase theta 1 (GSTT1) and hematopoietic cancer in hospital workers, human leukocyte antigen coding for glutamic acid in the 69th position (HLA DPB1(E69)) and chronic beryllium disease in beryllium workers, and peripheral myelin protein 22 (PMP22) deletion and carpal tunnel syndrome in railroad track workers.
The scenarios involve glutathione-S-transferase theta 1 (GSTT1) and hematopoietic cancer in hospital workers, human leukocyte antigen coding for glutamic acid in the 69th position (HLA DPB1(E69)) and chronic beryllium disease in beryllium workers, and peripheral myelin protein 22 (PMP22) deletion and carpal tunnel syndrome in railroad track workers.
The scenarios involve glutathione-S-transferase theta 1 (GSTT1) and hematopoietic cancer in hospital workers, human leukocyte antigen coding for glutamic acid in the 69th position (HLA DPB1(E69)) and chronic beryllium disease in beryllium workers, and peripheral myelin protein 22 (PMP22) deletion and carpal tunnel syndrome in railroad track workers.
The recruitment of monocytes/macrophages in the tenosynovium, promoted by chemokines such as monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1alpha (MIP-1alpha), is thought to play an important role in CTS development.