Amino Acids and Their N-Acetylated Derivatives Maintain the Skin's Barrier Function.

The hydrocarbon-chain packing structure of intercellular lipids in the stratum corneum (SC) is critical to the skin's barrier function. We previously found that formation of V-shaped ceramide reduces the barrier function of skin. There are few agents, apart from ceramides and fatty acids that can improve the orthorhombic packing (Orth) ratio of the intercellular lipid packing structure. In this study, we investigated agents that directly increase the Orth ratio. We selected an intercellular lipid model consisting of ceramide, cholesterol, and palmitic acid and performed differential scanning calorimetry. We focused on natural moisturizing factor components in the SC, and therefore investigated amino acids and their derivatives. The results of our intercellular lipid model-based study indicate that N-acetyl-L-hydroxyproline (AHYP), remarkably, maintains the lamellar structure. We verified the effect of AHYP on the lamellar structure and hydrocarbon chain packing structure of intercellular lipids using time-resolved X-ray diffraction measurements of human SC. We also determined the direct physicochemical effects of AHYP on the Orth ratio of the hydrocarbon-chain packing structure. Hence, the results of our human SC study suggest that AHYP preserves skin barrier function by maintaining the hydrocarbon-chain packing structure of intercellular lipids via electrostatic repulsion. These findings will facilitate the development of skincare formulation that can maintain the skin's barrier function.

A case of biopsy-proven cardiac sarcoidosis without any other extracardiac manifestations.

A 49-year-old woman was referred to our hospital for uncontrollable heart failure. She had never been diagnosed as having sarcoidosis. Chest X-ray showed cardiomegaly without bilateral hilar lymphadenopathy. Echocardiography showed diffuse hypokinesis of the left ventricle mimicking idiopathic dilated cardiomyopathy. No specific manifestations implying sarcoidosis were observed. On cardiac catheterization, coronary angiograms were normal, whereas concurrent routine endomyocardial biopsy showed foci of non-caseating granuloma, indicating sarcoidosis. Pathological finding was the only clue to diagnose cardiac sarcoidosis among our standard examinations for heart failure. No other additional investigations found any extracardiac features of sarcoidosis. All serological and immunological examinations were within normal range. This is a challenging case of biopsy-proven cardiac sarcoidosis without any other extracardiac involvement.

Nifekalant hydrochloride terminated electrical storms after coronary surgery.

An "electrical storm" is a life-threatening condition defined as a recurrent attack of ventricular tachycardia or fibrillation. The current report is a case study of a patient who had electrical storms developing unexpectedly after undergoing coronary artery bypass grafting. The electrical storms were terminated dramatically by the administration of nifekalant hydrochloride. We suggest that nifekalant hydrochloride has great therapeutic potential for the suppression of intractable ventricular tachyarrhythmias refractory to amiodarone.

Statin therapy may prevent restenosis after successful coronary intervention, independent of lipid-lowering effect and CRP level.

BACKGROUND: As statins have the anti-atherosclerotic pleiotropic effects, we retrospectively examined the effects of statins on restenosis after percutaneous coronary intervention (PCI). METHODS: We reviewed consecutive 341 patients who underwent successful PCI and follow-up angiography six months after the procedure between January 2002 and December 2004. Statins were initiated in 207 patients (statin group), but not in the other 134 (control group). We compared the angiographic findings, low-density lipoprotein cholesterol (LDL-C) and C-reactive protein (CRP) between the two groups. RESULTS: LDL-C level in statin group was significantly higher than those in control group at baseline (116.0 +/- 35.8 vs 103.1 +/- 24.5 mg/dL, p < 0.01); however, the values were inverted between the two groups at follow-up (99.9 +/- 29.5 vs 107.6 +/- 26.0 mg/dL, p = 0.015). CRP levels were comparable between these two groups. Statin group showed significantly lower angiographic restenosis (defined as > or = 50% stenosis at the target site) rate (35.3 vs 46.3%, p = 0.042) and target lesion revascularization (TLR) rate (14.5 vs 23.9%, p = 0.018) than control group. Multivariate analysis indicated that the prescription of statin, but not LDL-C level at follow-up and % reduction of LDL-C during the follow-up period, predict the restenosis prevention. CONCLUSIONS: Statins can decrease restenosis and TLR rate after PCI, independent of lipid-lowering effect and CRP level in this study.

Fatal case of amiodarone-induced acute respiratory distress syndrome in a patient with severe left ventricular dysfunction due to extensive anterior acute myocardial infarction.

We here report a case of 71-year-old man with acute extensive anterior myocardial infarction, who was complicated with ventricular tachycardia (VT) even after successful percutaneous coronary intervention. As intravenous administration of nifekalant terminated VT, we started oral administration of amiodarone (day 1). We gave 400 mg of amiodarone a day for the first week and 200 mg a day from the second week. The patient was stable with normoxia by day 20, in spite of pulmonary congestion-like infiltrates on chest X-ray. On day 21, he was complicated with acute respiratory distress syndrome. Immediate discontinuance of amiodarone and high-dose pulse glucocorticoid therapy with intubation slightly improved the infiltrations on chest X-ray. However, glucocorticoid therapy induced hyperglycemia with an increase in plasma osmolality, complicated with hypoalbuminemia, and gastrointestinal bleeding. Despite treatment with a large amount of saline, high-doses of catecholamines, and blood transfusion, the patient died on day 28. It is sometimes difficult to diagnose congestive heart failure or amiodarone-induced pulmonary infiltrates in patients with severe left ventricular dysfunction.