Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0184567 (acute pain)
 3,962 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary tumors of the lacrimal sac are extremely rare and predominantly epithelial in origin. We report a unique case of fibromyxoma of the lacrimal sac in an 86-year-old Caucasian woman who presented with 3 months of lower eyelid edema and 1 week of purulent discharge, epiphora, and acute pain. Examination revealed right lower eyelid erythema/edema and a tender, firm, palpable mass of the right lacrimal sac, which self-expressed a yellow, purulent discharge. On surgical exploration, a firm, rubbery, yellow mass was encountered and excised. Histopathologic analysis identified a nonencapsulated mass composed of loose interlacing fascicles and bundles of spindle-shaped cells with prominent myxoid changes; immunostaining was strongly positive for vimentin, weakly for smooth muscle actin, and negative for S-100 and muscle-specific actin. These findings were consistent with the diagnosis of a fibromyxoma of the lacrimal drainage system. After excision, the patient did well, with resolution of dacryocystitis.
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PMID:Fibromyxoma masquerading as dacryocystitis. 2218 84

Collagen VI is an extracellular matrix protein with broad distribution in several tissues. Although Col6a1 is expressed by Schwann cells, the role of collagen VI in the peripheral nervous system (PNS) is yet unknown. Here we show that Schwann cells, but not axons, contribute to collagen VI deposition in peripheral nerves. By using Col6a1-null mice, in which collagen VI deposition is compromised, we demonstrate that lack of collagen VI leads to increased myelin thickness (P<0.001) along with 60-130% up-regulation in myelin-associated proteins and disorganized C fibers in the PNS. The hypermyelination of PNS in Col6a1(-/-) mice is supported by alterations of signaling pathways involved in myelination, including increase of P-FAK, P-AKT, P-ERK1, P-ERK2, and P-p38 (4.15, 1.67, 2.47, 3.34, and 2.60-fold, respectively) and reduction of vimentin (0.49-fold), P-JNK (0.74-fold), and P-c-Jun (0.50-fold). Pathologically, Col6a1(-/-) mice display an impairment of nerve conduction velocity and motor coordination (P<0.05), as well as a delayed response to acute pain stimuli (P<0.001), indicating that lack of collagen VI causes functional defects of peripheral nerves. Altogether, these results indicate that collagen VI is a critical component of PNS contributing to the structural integrity and proper function of peripheral nerves.
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PMID:Collagen VI regulates peripheral nerve myelination and function. 2427 78