Abstract
Tumor is an abnormal mass of tissue, which could be solid, or fluid filled. Migration Inhibitory Factor (MIF) is a ubiquitously expressed cytokine in tumor. High levels of MIF expression have been observed in several human cancers and expression correlates with tumor grading and clinical prognosis. This experiment was designed to see the size of tumor, cell population, arginase and nitric oxide activity and production and presence of pro and anti-inflammatory cytokine in cell and serum of MIF wild type and MIF- /- mouse injected of colon carcinoma tumor cell line.
Highlights
Periodic paralysis (PP) is a group of ion-channel dysfunction diseases [1]
Normokalemic periodic paralysis (Normo KPP) of skeletal muscle is an autosomal dominant disorder caused by mutations in the calcium voltage-gated channel subunit (CACNA1S) or sodium voltage-gated channel subunit 4 (SCN4A) genes, which lead to ion-channel dysfunction
The present study supports a causative role for this mutation in SCN4A in NormoKPP and provides information about the relationship between genotype and atypical clinical symptoms
Summary
Normokalemic periodic paralysis (Normo KPP) of skeletal muscle is an autosomal dominant disorder caused by mutations in the calcium voltage-gated channel subunit (CACNA1S) or sodium voltage-gated channel subunit 4 (SCN4A) genes, which lead to ion-channel dysfunction. Little is known about the relationship between mutation genotypes and the clinical symptoms of Normo KPP
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