New polymorphic microsatellite markers for the Korean manila clam (Ruditapes philippinarum) and their application to wild populations.

Manila clam (Ruditapes philippinarum) is a valuable and intensively exploited shellfish species in Korea. Despite its importance, information on its genetic background is scarce. For the genetic characterization of R. philippinarum, expressed sequence tag-derived microsatellite markers were developed using next-generation sequencing. A total of 5879 tandem repeats containing di- to hexanucleotide repeat motifs were obtained from 236,746 reads (mean = 413 bp). Of the 62 loci screened, 24 (38.7%) were successfully amplified, and 10 were polymorphic in 144 individuals from 2 manila clam populations (Incheon and Geoje, Korea). The number of alleles ranged from 2 to 17 in the Incheon population and from 3 to 13 in the Geoje population (overall AR = 7.21). The mean observed and expected heterozygosities were estimated to be 0.402 and 0.555, respectively. Hence, there is less genetic variability in the Geoje population than in the Incheon population, although no significant reductions of genetic diversity were found between the populations (P > 0.05). However, significant genetic differentiation was detected between the populations (FST = 0.064, P < 0.001). Significant deviations from Hardy-Weinberg equilibrium and high inbreeding coefficients (mean FIS = 0.22-0.26) were detected in both populations. The 10 novel polymorphic microsatellite loci used in this study will be useful for future genetic mapping studies and for characterizing population structures, monitoring genetic diversity for successful aquaculture management, and developing conservation strategies for manila clam populations in Korea.

A stress-induced cellular aging model with postnatal neural stem cells.

This corrects the article DOI: 10.1038/cddis.2014.82.

[Clinical and pathologic staging in 100 cases of laryngeal cancer].

A retrospective histopathologic study of 100 specimens of laryngeal cancer treated by laryngectomy were carried out to test the accuracy of the clinical staging. The findings indicated that the inaccuracy rate of the preoperative staging was 46%, supraglottic type 46.7%, glottic 21.1%, subglottic 50% and transglottic 70.6%. Forty five cases were understaged and one overstaged. The erroneous staging was resulted from the under-estimation of the depth of tumor invasion, such as the invasion of the laryngeal framework, preepiglottic space, anterior commissural area and paraglottic space, etc. In this paper the relationship between cell differentiation, growth pattern and "P" staging are analysed. We attempt to demonstrate that "barrier" of the larynx can limit the invasion of carcinoma to various degrees. This paper also presents the follow-up data of 63 patients to three years after operation.

A stress-induced cellular aging model with postnatal neural stem cells.

Aging refers to the physical and functional decline of the tissues over time that often leads to age-related degenerative diseases. Accumulating evidence implicates that the senescence of neural stem cells (NSCs) is of paramount importance to the aging of central neural system (CNS). However, exploration of the underlying molecular mechanisms has been hindered by the lack of proper aging models to allow the mechanistic examination within a reasonable time window. In the present study, we have utilized a hydroxyurea (HU) treatment protocol and effectively induced postnatal subventricle NSCs to undergo cellular senescence as determined by augmented senescence-associated-ß-galactosidase (SA-ß-gal) staining, decreased proliferation and differentiation capacity, increased G0/G1 cell cycle arrest, elevated reactive oxygen species (ROS) level and diminished apoptosis. These phenotypic changes were accompanied by a significant increase in p16, p21 and p53 expression, as well as a decreased expression of key proteins in various DNA repair pathways such as xrcc2, xrcc3 and ku70. Further proteomic analysis suggests that multiple pathways are involved in the HU-induced NSC senescence, including genes related to DNA damage and repair, mitochondrial dysfunction and the increase of ROS level. Intriguingly, compensatory mechanisms may have also been initiated to interfere with apoptotic signaling pathways and to minimize the cell death by downregulating Bcl2-associated X protein (BAX) expression. Taken together, we have successfully established a cellular model that will be of broad utilities to the molecular exploration of NSC senescence and aging.