Outcomes After Aortic Valve Replacement for Asymptomatic Severe Aortic Regurgitation and Normal Ejection Fraction

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Malocclusion associated with abnormal posture

Growth and development of maxillofacial morphology and oral function are closely interrelated. Oral function is comprised of articulation, swallowing, and chewing. Malocclusion may be caused by abnormal functions such as mouth breathing, tongue thrust swallowing, and unilateral chewing and by abnormal postures of oral circumferential muscles such as forward tongue thrust, tongue biting, and low tongue at rest. Forces from unintentional and habitual behaviors constantly acting on the maxillofacial and alveolar regions can cause the bony structures to generally deform, resulting in jaw deformity and malocclusion. Oral function also plays a vital role in maintaining body posture. In this study, clinical observations of oral postures examined maxillary protrusion and open bite, anterior crossbite and facial asymmetry. The unstable forces induced by abnormal posture were correlated with the varieties of malocclusion. Morphology, function, and posture were shown to be closely interrelated and to influence each other.     

Glycogen synthase kinase-3β opens mitochondrial permeability transition pore through mitochondrial hexokinase II dissociation

Accumulating evidence has revealed pivotal roles of glycogen synthase kinase-3β (GSK3β) inactivation on cardiac protection. Because the precise mechanisms of cardiac protection against ischemia/reperfusion (I/R) injury by GSK3β-inactivation remain elusive, we investigated the relationship between GSK3β-mediated mitochondrial hexokinase II (mitoHK-II; a downstream target of GSK3β) dissociation and mitochondrial permeability transition pore (mPTP) opening. In Langendorff-perfused hearts, GSK3β inactivation by SB216763 improved the left ventricular-developed pressure and retained mitoHK-II binding after I/R. In permeabilized myocytes, GSK3β depolarized mitochondrial membrane potential with accelerated mitochondrial calcein release (suggesting GSK3β-mediated mPTP opening) and decreased mitoHK-II bindings. GSK3β-mediated mPTP opening depended on mitoHK-II binding, i.e., it was accelerated by dissociation of mitoHK-II (dicyclohexylcarbodiimide) and attenuated by enhancement of mitoHK-II binding (dextran). However, inactivation of mitoHK-II by glucose-depletion or glucose-6-phosphate inhibited the GSK3β-mediated mPTP opening. We conclude that GSK3β-mediated mPTP opening may be involved in I/R injury and regulated by mitoHK-II binding and activity.     

Repetitive monomorphic ventricular tachycardia of left coronary cusp origin

Repetitive monomorphic ventricular tachycardia with a morphology of inferior axis and left bundle branch block pattern in patients without structural heart disease commonly originates from the right ventricular outflow tract. We report the case of a 22-year-old man with an incessant, monomorphic ventricular tachycardia with a similar morphology originating from the left coronary cusp, which was confirmed by perfect pace mapping, local ventricular activation preceding the onset of QRS by 25 mse, and eliminated by a single delivery of low-energy (11 W) radiofrequency currents.