Relationship between arrhythmogenic pulmonary veins and the surrounding atrial substrate in patients with paroxysmal atrial fibrillation.

Introduction: The relationship between pulmonary veins (PVs) with atrial fibrillation (AF) initiating triggers and their surrounding atrial substrate has not been elucidated. We aimed to clarify the atrial substrate properties around the PVs.

Methods And Results: Twenty-three paroxysmal AF patients were studied with the identification of PV initiating triggers.

Clinical course and outcome of heart transplant recipients: single center experience at the National Cardiovascular Center in Japan.

The number of heart transplant (HTx) surgeries in Japan is expected to increase under the Revised Organ Transplant Law. To date, among 69 HTx surgeries performed in Japan, 27 operations (39.1%) were performed at our institution, the National Cardiovascular Center (NCVC), located in Osaka.

Head-to-head comparison of the cardio-ankle vascular index between patients with acute coronary syndrome and stable angina pectoris.

We aimed to evaluate whether there was a difference in the arterial stiffness assessed by the cardio-ankle vascular index (CAVI) between patients with acute coronary syndrome (ACS) and those with stable angina pectoris (SAP). A total of 199 consecutive patients, 79 with ACS and 120 with SAP, who underwent emergency or elective coronary revascularization were enrolled. The CAVI was measured within 2 days after the procedures, and was compared between the ACS and SAP patients.

Is structural remodeling of fibrillated atria the consequence of tissue hypoxia?

Background: Matrix metalloproteinases (MMPs) play an important role in degradation of the extracellular matrix of injured tissue. MMP-9 expression increases in fibrillating atrial tissue; however, the mechanism for this increase has not been clarified.

Methods And Results: Changes in the expression of vascular endothelial growth factor (VEGF), VEGF receptors, and hypoxia-induced transcription factor-1alpha (HIF-1alpha) in fibrillating atrial tissue were investigated.

A spontaneous Type 1 electrocardiogram pattern in lead V2 is an independent predictor of ventricular fibrillation in Brugada syndrome.

Aim: Risk stratification for Brugada syndrome remains controversial. We investigated the relationships between episodes of ventricular fibrillation (VF) and various clinical, electrocardiographic, electrophysiologic, and genetic parameters both retrospectively and prospectively.

Methods And Results: Fifty-two patients with Brugada syndrome (49 men, average age 42 +/- 3 years) were studied.

Regulation of ATPase activity of transglutaminase 2 by MT1-MMP: implications for mineralization of MC3T3-E1 osteoblast cultures.

A pro-mineralization function for transglutaminase 2 (TG2) has been suggested in numerous studies related to bone, cartilage, and vascular calcification. TG2 is an enzyme which can perform protein crosslinking functions, or act as a GTPase/ATPase depending upon different stimuli. We have previously demonstrated that TG2 can act as an ATPase in a Ca(2+)-rich environment and that it can regulate phosphate levels in osteoblast cultures.

Long-term electrocardiographic follow-up from childhood of an adult patient with Brugada syndrome associated with sick sinus syndrome.

We had the unique opportunity of following the electrocardiographic (ECG) course of a 13-year-old male with sinus dysfunction and atrial flutter who subsequently developed a Brugada-type ECG pattern associated with sick sinus syndrome at 25 years old. Family history showed that the patient's mother and maternal grandfather suddenly died while sleeping at night. When the patient was 13 years old, he lost consciousness after running a marathon.

[Active systemic steroid therapy employed in a case of bilateral frosted branch angiitis with acute chorioretinal circulatory insufficiency].

Background: Steroid treatment is believed to be effective for frosted branch angiitis, but frosted branch angiitis with retinal circulatory insufficiency does not have a good prognosis by steroid treatment alone. Here, we present a case of a patient that had a good outcome when treated with long-term active systemic betamethasone and vasodilation therapy for bilateral frosted branch angiitis with acute chorioretinal circulatory insufficiency.

Case: A 69-year-old male presented with sudden visual loss in his left eye.

Disopyramide for transient high-degree atrioventricular block in a young patient with a history of syncope.

Although high-degree atrioventricular (AV) block in patients with a history of syncope usually requires pacemaker implantation, therapeutic strategies should also be considered. A 35-year-old man presented with complaints of palpitations, nausea and dysgeusia. Since aged 30, the patient had experienced three episodes of syncope.

MEPE-ASARM peptides control extracellular matrix mineralization by binding to hydroxyapatite: an inhibition regulated by PHEX cleavage of ASARM.

Hyp mice having an inactivating mutation of the phosphate-regulating gene with homologies to endopeptidases on the X-chromosome (Phex) gene have bones with increased matrix extracellular phosphoglycoprotein (MEPE). An acidic, serine- and aspartic acid-rich motif (ASARM) is located in the C terminus of MEPE and other mineralized tissue matrix proteins. We studied the effects of ASARM peptides on mineralization and how PHEX and MEPE interactions contribute to X-linked hypophosphatemia (XLH).

Predictors and long-term prognostic implications of angiographic slow/no-flow during percutaneous coronary intervention for acute myocardial infarction.

Objective: In patients with acute myocardial infarction (AMI), angiographic slow/no-flow during percutaneous coronary intervention (PCI) may lead to unfavorable outcomes. The aim of our study was to investigate the predictors and long-term prognosis of AMI patients with angiographic slow/no-flow.

Methods: We evaluated 228 consecutive AMI patients with either normal flow (Thrombolysis in Myocardial Infarction [TIMI] flow grade 3)(n=192) or slow/no-flow (< or =TIMI-2)(n=36) based on cineangiograms performed during PCI.

Size distribution and molecular associations of plasma fibronectin and fibronectin crosslinked by transglutaminase 2.

Fibronectin (FN) is a ubiquitously expressed cell adhesion protein capable of assembling into large, extended fibrillar networks as part of an extracellular matrix (ECM) that regulates cell behavior. FN is a substrate for certain members of the transglutaminase family of protein-crosslinking enzymes-enzymes which can modify the ability of FN to support cell adhesion. In this study, we have analyzed the thermo-chemical stability of plasma FN in its noncrosslinked form, and after crosslinking by transglutaminase 2 (TG2), using dynamic light scattering.

Connexin43 knockdown accelerates wound healing but inhibits mesenchymal transition after corneal endothelial injury in vivo.

Purpose: To explore connexin43 (Cx43) knockdown as an efficient treatment for corneal endothelial injury in an in vivo rat corneal scrape injury model.

Methods: Scrape injury was induced in the corneal endothelium, and immunolabeling (ZO-1, alpha-SMA, Cx43) was performed to analyze changes in Cx43 expression during wound healing. Single injection of Cx43 antisense oligodeoxynucleotide (AS-ODN), small interfering RNA (siRNA), or adenovirus (CMV-Cx43-mRFP1) was applied into the anterior chamber simultaneously with the injury, and wound closure was examined by immunolabeling (ZO-1, Cx43) and propidium iodide staining.

ATP-mediated mineralization of MC3T3-E1 osteoblast cultures.

While bone is hypomineralized in hypophosphatemia patients and in tissue-nonspecific alkaline phosphatase (Tnsalp)-deficient mice, the extensive mineralization that nevertheless occurs suggests involvement of other phosphatases in providing phosphate ions for mineral deposition. Although the source of phosphate liberated by these phosphatases is unknown, pyrophosphate, ATP, pyridoxal-5'-phosphate (PLP) and phoshoethanolamine (PEA) are likely candidates. In this study, we have induced mineralization of MC3T3-E1 osteoblast cultures using ATP, and have investigated potential phosphatases involved in this mineralization process.

Gene delivery of paraoxonase-1 inhibits neointimal hyperplasia after arterial balloon-injury in rabbits fed a high-fat diet.

Paraoxonase-1 (PON-1) is a high-density lipoprotein (HDL)-associated enzyme that hydrolyzes oxidized phospholipids, thereby preventing the oxidative modification of low-density lipoproteins (LDL). A high-fat diet reduces PON-1 activity, enhancing LDL oxidation. Thus, PON-1 is a candidate for anti-atherogenic gene therapy.

Expression of bone type 1 PTH receptor in rats with chronic renal failure.

Some researchers have speculated that a decrease in bone type 1 PTH receptor (PTH1R) may be among the causes of "skeletal resistance" in chronic renal failure (CRF). Indeed, the down-regulation of PTH1R mRNA has been identified in uremic bones. However, few studies have identified the patterns of PTH1R protein expression.

Expression and localization of plasma transglutaminase factor XIIIA in bone.

Transglutaminases (TGs) are protein crosslinking enzymes involved in cell adhesion and signaling and matrix stabilization and maturation, in many cell types and tissues. We previously described that in addition to transglutaminase 2 (TG2), cultured MC3T3-E1 osteoblasts also express the plasma TG Factor XIIIA (FXIIIA). Here we report on the expression and localization of FXIIIA in bone in vivo and provide confirmatory in vitro data.

Non-SCN5A related Brugada syndromes: verification of normal splicing and trafficking of SCN5A without exonic mutations.

Recently, it has been reported that under 20% of Brugada syndrome cases are linked to SCN5A mutations. The purpose of this study was to clarify whether abnormalities other than exonic mutations, such as splicing disorders, decreased mRNA expression levels, or membrane transport abnormalities of SCN5A, play a role in the pathogenesis of Brugada syndrome. We analyzed all SCN5A exons and splice sites using genomic DNA from 23 Brugada syndrome patients.

Formation of acellular cementum-like layers, with and without extrinsic fiber insertion, along inert bone surfaces of aging c-Src gene knockout mice.

To investigate the long-term effects of c-src deficiency on skeletal and dental tissues, we examined the lower jaws and long bones of c-src gene knockout (c-src KO) mice by histological and histochemical methods. Numerous multinucleated osteoclasts were distributed throughout the mandible in 5-wk-old c-src KO mice, but by 14 wk they had almost completely disappeared from the alveolar bone, leaving tartrate-resistant acid phosphatase (TRAP)-positive layers along the bone surface. Deposition of osteopontin-positive mineralized tissue, reminiscent of acellular afibrillar cementum (AAC), was confirmed along the TRAP-positive bone surface at 14 wk.

Successive, rapid recurrences of in-stent restenoses in a woman with angina pectoris.

A 62-year-old woman was admitted because of chest pain. Coronary angiography demonstrated stenosis of the left anterior descending coronary artery, where two bare metal stents had been implanted. Over 5 months in-stent restenosis occurred four times, and was treated at first with angioplasty but finally with two sirolimus-eluting stent insertions.

The existence of CD11c+ sentinel and F4/80+ interstitial dendritic cells in dental pulp and their dynamics and functional properties.

Dental caries and pulpitis are the most common bacterial infections in humans. However, the immune responses against bacterial stimulation in dental pulp that is bounded by special hard tissues are poorly understood. We examined the initial immune responses in mouse dental pulp after cusp trimming and acid treatment.

Congenital combined pituitary hormone deficiency attributable to a novel PROP1 mutation (467insT).

Background: Combined pituitary hormone deficiency (CPHD) is an anterior pituitary disorder, commonly resulting in growth retardation. PROP1 gene mutations appear to be frequently responsible for CPHD, particularly in Middle and Eastern Europe and the Americas, but few cases have been reported in Japan.

Patients And Design: Two sisters (aged 8.

Proteolysis on maturing enamel surface, as shown by gel-coating methods.

Degradation of enamel matrix proteins, and their removal during early maturation, is critical for the growth of large enamel crystals in the subsequent processes of enamel maturation. In this study, we sought to demonstrate, using in vivo zymography, the exact sites of proteolysis in maturing enamel and its relationship to the overlying ameloblasts. The maturing enamel surfaces of rat and bovine incisors were exposed and painted either with pre-exposed autoradiographic emulsion or with densely fluorescein-conjugated (DQ) gelatin.

Transglutaminase activity regulates osteoblast differentiation and matrix mineralization in MC3T3-E1 osteoblast cultures.

Transglutaminase (TG) enzymes and protein crosslinking have long been implicated in the formation of mineralized tissues. The aim of this study was to analyze the expression, activity and function of TGs in differentiating osteoblasts to gain further insight into the role of extracellular matrix protein crosslinking in bone formation. MC3T3-E1 (subclone 14) pre-osteoblast cultures were treated with ascorbic acid and beta-glycerophosphate to induce cell differentiation and matrix mineralization.