Pacemaker Treatment for Apical Hypertrophic Cardiomyopathy in the Setting of an Apical Ventricular Aneurysm.

We describe the case of a patient with apical hypertrophic cardiomyopathy with concomitant apical aneurysm. We measured the aneurysmal cavity pressure using the pressure guidewire system. The patient underwent implantable cardioverter-defibrillator treatment successfully to reduce the pressure gradient between the aneurysmal cavity and the true left ventricle.

Long-term survival without surgical intervention in a patient with a natural history of a single right ventricle: A case report.

Single ventricle (SV), a complex cardiac anomaly, if left untreated, is thought to lead to a poor prognosis. Herein, we report the case of a long-term survivor with an unrepaired SV with right ventricle (RV) morphology. A 55-year-old man presented with a SV with RV morphology, with a double outlet, large atrial septal defect, common atrioventricular valve, pulmonary valve stenosis (PS), and dextrocardia.

Reversible lesion in the splenium of the corpus callosum in a patient with chronic alcoholism.

Marchiafava-Bignami disease (MBD) is often diagnosed in chronic alcoholics. The disease processes typically involve the corpus callosum and clinically presents with various manifestations on the basis of clinical condition, extent of the splenium of the corpus callosum involvement at brain magnetic resonance imaging (MRI), and prognosis. We report a patient affected by MBD, who presented an isolated reversible splenial lesion at brain MRI and achieved a favorable recovery.

[Role of IL-33 in bronchial asthma].

IL-33 is a member of the IL-1 family and has been identified as an agonist of ST2L. IL-33 drives the production of Th2-associated cytokines and IgE, and IL-33 administration induces eosinophilia and hypertrophy of bronchial epithelial cells, as well as mucus secretion in vivo. Such changes resemble pathological findings in bronchial asthma (BA).

Opening of ligand-gated cation channel families by calpain inhibitors.

The class of Ca2+-permeable cation channels is composed of large families with six transmembrane segments including transient receptor potential, vanilloid receptor (VR), polycystin, epithelial calcium channels and melastatin (MLS). However, most of them are functionally silent and unexpressed in mammalian cells. An investigation of associated proteins made us believe that the blockade of calpain opens the silent channels.

A single amino acid mutation results in a rapid inactivation of epithelial calcium channels.

Epithelial Ca(2+) channel (ECaC1 and 2 = CAT1) molecules are characterized by properties including inward rectification and Ca(2+)-dependent fast and slow inactivation. To elucidate the electrophysiological differences based on the amino acid residues, we compared human and rodent ECaC1, and ECaC2 alignments, made mutants, and investigated their function in Xenopus and mammalian cells. Expression of the ECaC1 mutant Q579H and a H587Q mutation in ECaC2 in Xenopus oocytes resulted in a possible change in the rate of fast decay.