M. Impact of anti-apoptotic and anti-oxidative effects of bone marrow mesenchymal stem cells with transient overexpression of heme oxygenase-1 on myocardial ischemia. Am

Background: Mesenchymal stem cells (MSC) are multipotent and reside in bone marrow (BM), adipose tissue and many other tissues. However, the molecular foundations underlying the differences in proliferation, differentiation potential and paracrine effects between adipose tissue-derived MSC (ASC) and BM-derived MSC (BM-MSC) are not well-known. Therefore, we investigated differences in the gene and secretory protein expressions of the 2 types of MSC. Methods and Results:ASC and BM-MSC were obtained from subcutaneous adipose tissue and BM of adult Lewis rats. ASC proliferated as rapidly as BM-MSC, and had expanded 200-fold in approximately 2 weeks. On microarray analysis of 31,099 genes, 571 (1.8%) were more highly (>3-fold) expressed in ASC, and a number of these genes were associated with mitosis and immune response. On the other hand, 571 genes (1.8%) were more highly expressed in BM-MSC, and some of these genes were associated with organ development and morphogenesis. In secretory protein analysis, ASC secreted significantly larger amounts of growth factor and inflammatory cytokines, such as vascular endothelial growth factor, hepatocyte growth factor and interleukin 6, whereas BM-MSC secreted significantly larger amounts of stromal-derived factor-1α. Conclusions:There are significant differences between ASC and BM-MSC in the cytokine secretome, which may provide clues to the molecule mechanisms associated with tissue regeneration and alternative cell sources. (Circ J 2011; 75: 2260 - 2268

BackgroundLong QT syndrome causes ventricular tachyarrhythmias and sudden death. Recently, a short QT interval has also been shown to be associated with an increased risk of tachyarrhythmia and sudden death. However, the prevalence of short QT syndrome is not well‐known.HypothesisThe aim of this study was to assess the distribution of corrected QT intervals (QTc) and prevalence of short QT syndrome.MethodsThis study comprised 12,149 consecutive subjects who received a consultation at Kanazawa University Hospital, Kanazawa, Japan, and had an electrocardiogram (ECG) between February 2003 and May 2004. Of these subjects, 1,165 subjects were excluded because of inappropriate ECGs, while the remaining 10,984 subjects had their last‐recorded ECGs analyzed.ResultsThe QTc values showed a nearly normal distribution (408 ± 25 msec1/2), and were significantly longer in females (412 ± 24 msec1/2) than in males (404 ± 25 msec1/2) (p < 0.05). Among 5,511 males, 69 subjects (1.25%) exhibited QTc < 354 msec1/2 (2 standard deviations [SDs] below the mean in males), and among 5,473 females, 89 subjects (1.63%) exhibited QTc < 364 msec1/2 (2 SDs below the mean in females). Only 3 subjects (0.03% in all subjects and 0.05% in males) exhibited QTc < 300 msec1/2, however, none had clinical symptoms of short QT syndrome.ConclusionsShort QT syndrome may be very rare. Copyright © 2008 Wiley Periodicals, Inc.

These results demonstrate that AM could ameliorate DSS-induced experimental colitis possibly through suppression of systemic and local production of cytokines such as TNF-α, associated with acceleration of ulcer reepithelialization and colon tissue regeneration.

LQTS (long QT syndrome) is caused by mutations in cardiac ion channel genes; however, the prevalence of LQTS in the general population is not well known. In the present study, we prospectively estimated the prevalence of LQTS and analysed the associated mutation carriers in Japanese children. ECGs were recorded from 7961 Japanese school children (4044 males; mean age, 9.9+/-3.0 years). ECGs were examined again for children who had prolonged QTc (corrected QT) intervals in the initial ECGs, and their QT intervals were measured manually. An LQTS score was determined according to Schwartz's criteria, and ion channel genes were analysed. In vitro characterization of the identified mutants was performed by heterologous expression experiments. Three subjects were assigned to a high probability of LQTS (3.5< or = LQTS score), and eight subjects to an intermediate probability (1.0< LQTS score < or =3.0). Genetic analysis of these II subjects identified three KCNH2 mutations (M124T, 547-553 del GGCGGCG and 2311-2332 del/ins TC). In contrast, no mutations were identified in the 15 subjects with a low probability of LQTS. Electrophysiological studies showed that both the M124T and the 547-553 del GGCGGCG KCNH2 did not suppress the wild-type KCNH2 channel in a dominant-negative manner. These results demonstrate that, in a random sample of healthy Japanese children, the prevalence of a high probability of LQTS is 0.038% (three in 7961), and that LQTS mutation carriers can be identified in at least 0.038% (one in 2653). Furthermore, large-scale genetic studies will be needed to clarify the real prevalence of LQTS by gene-carrier status, as it may have been underestimated in the present study.