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diabetic foot/tyrosine
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The role of circulating soluble fms-like tyrosine kinase-1 in patients with diabetic foot ulcer: A possible mechanism of pathogenesis via a novel link between oxidative stress, inflammation and angiogenesis.
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Effect and Mechanism of the Bruton Tyrosine Kinase (Btk) Inhibitor Ibrutinib on Rat Model of Diabetic Foot Ulcers.
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BACKGROUND Diabetes causes damage to the soft tissue and bone structure of the foot, referred to as "diabetic foot". Ibrutinib is a Bruton tyrosine kinase (Btk) inhibitor, and the role and mechanism of ibrutinib on the diabetic foot have not been elucidated. MATERIAL AND METHODS Male
Ion beam modified TiO 2 nanotubular bio-interface for electrochemical detection of L-tyrosine towards smart bandage application
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One of the common complications diagnosed in Diabetes Mellitus (DM) patients is Diabetic Foot Ulcers (DFUs). It is a condition wherein the deep tissues located in the lower limb undergo inflammation and infection due to neurological abnormalities (neuropathy) and various degrees of vascular diseases
Protein tyrosine phosphatase 1B inhibition as a potential therapeutic target for chronic wounds in diabetes
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Non-healing diabetic foot ulcers (DFUs) are a serious complication in diabetic patients. Their incidence has increased in recent years. Although there are several treatments for DFUs, they are often not effective enough to avoid amputation. Protein tyrosine phosphatase 1B (PTP1B) is expressed in
Mechanisms involved in the development and healing of diabetic foot ulceration.
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We examined the role of vascular function and inflammation in the development and failure to heal diabetic foot ulcers (DFUs). We followed 104 diabetic patients for a period of 18.4 ± 10.8 months. At the beginning of the study, we evaluated vascular reactivity and serum inflammatory cytokines and
Diabetic Foot Ulcers and Epidermal Growth Factor: Revisiting the Local Delivery Route for a Successful Outcome.
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Soon after epidermal growth factor (EGF) discovery, some in vivo models appeared demonstrating its property to enhance cutaneous wound healing. EGF was the first growth factor (GF) introduced in the clinical arena as a healing enhancer, exerting its mitogenic effects on epithelial, fibroblastoid,
Neurotrophic factors and their receptors in human sensory neuropathies.
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Neurotrophic factors may play key roles in pathophysiological mechanisms of human neuropathies. Nerve growth factor (NGF) is trophic to small-diameter sensory fibers and regulates nociception. This review focuses on sensory dysfunction and the potential of neurotrophic treatments. Genetic
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