Poly(hexano-6-lactone) (PCL*) fibers were enzymatically degraded by a hydrolase in vitro. The extent of degradation of PCL fibers was examined by weight loss, mechanical properties loss such as tensile strength and ultimate elongation decreases, and visual observations by scanning electron microscopy. The in vitro degradation of PCL fibers was carried out using a lipoprotein lipase
(Lipase-PS) as a hydrolase. The kinetic study on the weight loss of PCL fiber accompanying the enzymatic degradation suggested that the degradation of PCL fibers gradually takes place from the surface, not bulk degradation. The rate of degradation was found to depend on draw ratio and crystallinity of the PCL fibers. The strength loss of PCL fibers in the course of degradation took place faster than the weight loss of PCL fibers. Sonic velocity measurements as well as dynamic mechanical properties of PCL fibers were also examined as a function of weight loss of sample fibers with Lipase-PS treatments. It was shown that sonic velocity and value of loss tangent d changed steeply for undrawn PCL fiber in the first step with enzymatic digestion.
Campomelic dysplasia (CD) is a rare and usually fatal congenital skeletal disorder with respiratory failure. The SOX9 gene has been cloned as a candidate gene for CD. Here, we report the cases of 2 Japanese patients with CD who have survived for over 5 years. Molecular investigations revealed novel frameshift mutations in SOX9 in these patients; a single G insertion in 1 allele at nucleotide 261 (261-262insG) and a single C insertion in 1 allele at nucleotide 888 (888-889insC). The predicted protein of 261-262insG may lack more than 80% composition of the normal SOX9 protein, including the SRY high mobility group (HMG) domain and the transactivation (TA) domain; the predicted protein of 888-889insC may not contain the normal TA domain. Although it has been reported that most patients with CD die during the neonatal period, our patients have survived for a long time, despite putative severely impaired SOX9 proteins.
Accurate quantification of multidrug resistance-1 gene (MDR1) expression in target cells would be of important therapeutic value in predicting cellular response to anticancer drugs. Because certain normal cells in peripheral blood physiologically express MDR1, increasing the sensitivity of the detection methods might result in confounding low-degree expression in tumor cells with physiologic expression in normal cells. The purpose of this study was to determine MDR1 mRNA expression levels in peripheral blood leukocytes obtained from healthy adult volunteers using a competitive nucleic acid sequence-based amplification (NASBA) assay. We determined the reference intervals of MDR1 mRNA expression in peripheral blood obtained from 98 healthy adults by measuring its expression with the quantitative NASBA assay between 5.50 × 104 copies/µg RNA and 6.76 × 105 copies/µg RNA. The new reference intervals were evaluated using a number of sensitive or resistant cell lines as control; positive or negative MDR1 expression was clearly demonstrated. We also reevaluated MDR1 expression levels in leukemia cells obtained from patient peripheral blood; 18 of 31 samples (58%) exceeded the newly established upper reference limit. The cutoff value established could be used to distinguish significant MDR1 expression in tumor cells from physiologic expression in certain normal cells coexistent in peripheral blood.