Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite numerous advances in the development of bone graft substitutes over the past 20 years, iliac crest autograft remains the gold standard for lumbar spinal fusion. However, donor site morbidity associated with the harvesting of iliac crest autograft remains problematic. Acute and chronic pain, prolonged operative time, bleeding, infection, deformity, and nerve and vascular injury still produce significant postoperative morbidity, even in the presence of careful surgical technique. Although allograft circumvents donor site morbidity, the growing number of spinal fusions performed in the United States and worldwide is creating a shortage of cadaver bone acceptable for use. Additionally, the extensive processing and storage of allograft is expensive. Synthetic materials, such as beta-tricalcium phosphate (beta-TCP), have been developed as alternatives to both autograft and allograft. A novel formulation of ultraporous beta-TCP (Vitoss, Orthovita, Malvern, Pa) offers interconnected microporosity, providing it with good wicking and hydrophilic properties. These properties allow the migration of nutrients, growth factors, and osteogenic cells into the ultraporous beta-TCP scaffold, thereby promoting new bone growth and concurrent scaffold resorption. This study presents a retrospective review of 7 patients who underwent anterior (ALIF) or posterior (PLIF) interbody fusion at 12 levels with a 3- to 6-month follow-up. At the patients' last radiographic examination, all 12 levels were solidly fused with interbody grafting material consisting only of allograft plus a combination of ultraporous beta-TCP and venous blood as an extender. Additionally, all 7 patients had segmental pedicle-screw fixation.
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PMID:Use of an advanced formulation of beta-tricalcium phosphate as a bone extender in interbody lumbar fusion. 1203 46

Neurophysiological techniques have been applied in restless legs syndrome (RLS) to obtain direct and indirect measures of central and peripheral nervous system excitability, as well as to probe different neurotransmission pathways. Data converge on the hypothesis that, from a pure electrophysiological perspective, RLS should be regarded as a complex sensorimotor disorder in which cortical, subcortical, spinal cord, and peripheral nerve generators are all involved in a network disorder, resulting in an enhanced excitability and/or decreased inhibition. Although the spinal component may have dominated in neurophysiological assessment, possibly because of better accessibility compared to the brainstem or cerebral components of a hypothetical dysfunction of the diencephalic A11 area, multiple mechanisms, such as reduced central inhibition and abnormal peripheral nerve function, contribute to the pathogenesis of RLS similarly to some chronic pain conditions. Dopamine transmission dysfunction, either primary or triggered by low iron and ferritin concentrations, may also bridge the gap between RLS and chronic pain entities. Further support of disturbed central and peripheral excitability in RLS is provided by the effectiveness of nonpharmacological tools, such as repetitive transcranial magnetic stimulation and transcutaneous spinal direct current stimulation, in transiently modulating neural excitability, thereby extending the therapeutic repertoire. Understanding the complex interaction of central and peripheral neuronal circuits in generating the symptoms of RLS is mandatory for a better refinement of its therapeutic support.
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PMID:Central and peripheral nervous system excitability in restless legs syndrome. 2774 89