In a test of this theory, researchers have demonstrated that mice harboring a human SCN1A gene mutation that results in Dravet Syndrome (DS), a severe and intractable genetic epilepsy, have electrical disturbances in the heart that culminate in ventricular fibrillation and sudden cardiac deat
In a test of this theory, researchers have demonstrated that mice harboring a
human SCN1A
gene mutation that results
in Dravet Syndrome (DS), a severe and intractable genetic epilepsy, have electrical disturbances in the heart that culminate in ventricular fibrillation and sudden cardiac deat
in Dravet Syndrome (DS), a severe and intractable genetic
epilepsy, have electrical disturbances
in the heart that culminate in ventricular fibrillation and sudden cardiac deat
in the heart that culminate
in ventricular fibrillation and sudden cardiac deat
in ventricular fibrillation and sudden cardiac death.
Two related potassium (K +) channel defects
in benign familial neonatal convulsions (BFNC) have recently been identified.9 10 A defect in a receptor for a different neurotransmitter (acetylcholine) has previously been identified in a family with autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) 11, which was later shown to affect calcium (Ca +) movement.12 In humans, so far, there has not been any success in identifying genes associated with more common primary epilepsy syndromes such as juvenile absence epilepsy and juvenile myoclonic epilepsy (JME).13 No gene or marker linked to an epilepsy gene has been identified in any dog breed, as ye
in benign familial neonatal convulsions (BFNC) have recently been identified.9 10 A defect
in a receptor for a different neurotransmitter (acetylcholine) has previously been identified in a family with autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) 11, which was later shown to affect calcium (Ca +) movement.12 In humans, so far, there has not been any success in identifying genes associated with more common primary epilepsy syndromes such as juvenile absence epilepsy and juvenile myoclonic epilepsy (JME).13 No gene or marker linked to an epilepsy gene has been identified in any dog breed, as ye
in a receptor for a different neurotransmitter (acetylcholine) has previously been identified
in a family with autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) 11, which was later shown to affect calcium (Ca +) movement.12 In humans, so far, there has not been any success in identifying genes associated with more common primary epilepsy syndromes such as juvenile absence epilepsy and juvenile myoclonic epilepsy (JME).13 No gene or marker linked to an epilepsy gene has been identified in any dog breed, as ye
in a family with autosomal dominant nocturnal frontal lobe
epilepsy (ADNFLE) 11, which was later shown to affect calcium (Ca +) movement.12
In humans, so far, there has not been any success in identifying genes associated with more common primary epilepsy syndromes such as juvenile absence epilepsy and juvenile myoclonic epilepsy (JME).13 No gene or marker linked to an epilepsy gene has been identified in any dog breed, as ye
In humans, so far, there has not been any success
in identifying genes associated with more common primary epilepsy syndromes such as juvenile absence epilepsy and juvenile myoclonic epilepsy (JME).13 No gene or marker linked to an epilepsy gene has been identified in any dog breed, as ye
in identifying
genes associated with more common primary
epilepsy syndromes such as juvenile absence
epilepsy and juvenile myoclonic
epilepsy (JME).13 No
gene or marker linked to an
epilepsy gene has been identified
in any dog breed, as ye
in any dog breed, as yet.