Variations of multifractal structure in the fetal heartbeats.

Several procedures for evaluating fetal well-being are in clinical use. The cardiotocograph is mostly used as a non-invasive procedure to measure fetal well-being in clinical settings. The cardiotocograph displays the fetal heartbeat counts that vibrate. This variation has been classified into 2 categories. We investigated this variation by a novel method, in which we analyzed the change of structure of the attractors in the phase spaces according to the time course. We adopted the global spectrum, which means the distribution of fractal dimensions, for that structure. In this procedure, we discovered a new variation in which the cycle is much longer than the 2 types of known variabilities. Although loud noises such as white noises with a magnitude 1/4 times as large as the standard deviation of the original data were added to the original data, the variations were still detected. The variation is very difficult to detect by Fourier or wavelet transformation, however, because it changes very slowly. Through this new way of analyzing the vibration phenomena, we obtained a new perspective on the biological information available.</p

Prefoldin Protects Neuronal Cells from Polyglutamine Toxicity by Preventing Aggregation Formation

Huntington disease is caused by cell death after the expansion of polyglutamine (polyQ) tracts longer than similar to 40 repeats encoded by exon 1 of the huntingtin (HTT) gene. Prefoldin is a molecular chaperone composed of six subunits, PFD1-6, and prevents misfolding of newly synthesized nascent polypeptides. In this study, we found that knockdown of PFD2 and PFD5 disrupted prefoldin formation in HTT-expressing cells, resulting in accumulation of aggregates of a pathogenic form of HTT and in induction of cell death. Dead cells, however, did not contain inclusions of HTT, and analysis by a fluorescence correlation spectroscopy indicated that knockdown of PFD2 and PFD5 also increased the size of soluble oligomers of pathogenic HTT in cells. In vitro single molecule observation demonstrated that prefoldin suppressed HTT aggregation at the small oligomer (dimer to tetramer) stage. These results indicate that prefoldin inhibits elongation of large oligomers of pathogenic Htt, thereby inhibiting subsequent inclusion formation, and suggest that soluble oligomers of polyQ-expanded HTT are more toxic than are inclusion to cells