Normokalemic periodic paralysis is not a distinct disease.

Introduction: Recent molecular studies of the original cases of normokalemic periodic paralysis (normoKPP) have raised suspicions that these families actually had hyperkalemic periodic paralysis (hyperKPP) due to mutations in the skeletal muscle sodium channel gene SCN4A. However, there is still a debate about the existence of normoKPP.

Methods: We screened 230 individuals with primary periodic paralysis for mutations in the SCN4A, CACNA1S, and KCNJ2 genes.

Protection of cardiomyocytes from ischemic/hypoxic cell death via Drbp1 and pMe2GlyDH in cardio-specific ARC transgenic mice.

The ischemic death of cardiomyocytes is associated in heart disease and heart failure. However, the molecular mechanism underlying ischemic cell death is not well defined. To examine the function of apoptosis repressor with a caspase recruitment domain (ARC) in the ischemic/hypoxic damage of cardiomyocytes, we generated cardio-specific ARC transgenic mice using a mouse alpha-myosin heavy chain promoter.