Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the status of insulin resistance, metabolic syndrome, dyslipidemia, and serum adiponectin levels in patients with uveal melanoma and choroidal nevus were investigated. Our study included 86 patients with uveal melanoma, 38 patients with choroidal nevus, and 86 controls. Uveal melanomas were classified as small, medium, and large on the basis of Collaborative Ocular Melanoma Study (COMS) criteria. Patients with uveal melanoma had significantly higher homeostatic model assessment scores compared with patients with choroidal nevus (P<0.001). Patients with uveal melanoma and choroidal nevus had significantly lower levels of serum adiponectin compared with controls (P<0.001). Patients with uveal melanoma who developed systemic metastases had significantly lower levels of serum adiponectin levels compared with patients with nonmetastases during follow-up (P=0.018). When the largest tumors (COMS III) were compared, ciliary body melanomas were associated with significantly lower levels of serum adiponectin than choroidal melanomas. In patients who were treated with enucleation, epitheloid predominant and mixed cell-type tumors were associated with lower levels of serum adiponectin compared with tumors with spindle cell type, but this did not reach statistical significance. By providing an antiapoptotic and proangiogenic environment, low serum adiponectin levels and insulin resistance may play a role in promoting the growth of uveal melanocytic tumors and may contribute toward a more aggressive clinical course, adversely affecting the prognosis.
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PMID:Serum adiponectin, insulin resistance, and uveal melanoma: clinicopathological correlations. 2663 Jun 61

Atherogenic LDL particles are physicochemically and metabolically heterogeneous. Can bioactive lipid cargo differentiate LDL subclasses, and thus potential atherogenicity? What is the effect of statin treatment? Obese hypertriglyceridemic hypercholesterolemic males [n = 12; lipoprotein (a) <10 mg/dl] received pitavastatin calcium (4 mg/day) for 180 days in a single-phase unblinded study. The lipidomic profiles (23 lipid classes) of five LDL subclasses fractionated from baseline and post-statin plasmas were determined by LC-MS. At baseline and on statin treatment, very small dense LDL (LDL5) was preferentially enriched (up to 3-fold) in specific lysophospholipids {LPC, lysophosphatidylinositol (LPI), lysoalkylphosphatidylcholine [LPC(O)]; 9, 0.2, and 0.14 mol per mole of apoB, respectively; all P < 0.001 vs. LDL1-4}, suggesting elevated inflammatory potential per particle. In contrast, lysophosphatidylethanolamine was uniformly distributed among LDL subclasses. Statin treatment markedly reduced absolute plasma concentrations of all LDL subclasses (up to 33.5%), including LPC, LPI, and LPC(O) contents (up to -52%), consistent with reduction in cardiovascular risk. Despite such reductions, lipotoxic ceramide load per particle in LDL1-5 (1.5-3 mol per mole of apoB; 3-7 mmol per mole of PC) was either conserved or elevated. Bioactive lipids may constitute biomarkers for the cardiometabolic risk associated with specific LDL subclasses in atherogenic dyslipidemia at baseline, and with residual risk on statin therapy.
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PMID:LDL subclass lipidomics in atherogenic dyslipidemia: effect of statin therapy on bioactive lipids and dense LDL. 3229 29