Science in China. Series C, Life Sciences / Chinese Academy of Sciences最新文献

An improved triploid crucian carp (ITCC) was produced by crossing improved tetraploids (G1xAT, male symbol) with improved red crucian carp (IRCC, female symbol), which were obtained by distant crossing and gynogenesis. The biological characteristics of ITCC, including the number and karyotype of chromosomes, gonadad and pituitary structures, phenotype, and growth rate are reported. ITCC possessed 150 chromosomes with the karyotype 33m+51sm+33st+33t. In the breeding season, both ovary-like and testis-like gonads of ITCC were unable to produce normal mature gametes. The ultrastructure of the pituitary of ITCC showed that most of the endocrine granules in gonadotrophic hormone (GTH) cells had not been released, providing endocrinological evidence for the sterility of ITCC. Compared with triploid crucian carp (TCC) produced by mating Japanese crucian carp with allotetraploid hybrids, ITCC not only retained the excellent traits of fast growth rate and sterility, but also acquired improved morphological characteristics, including higher body, shorter tail and smaller head.

DEK protein is an ubiquitous phosphorylated nuclear protein. Specific binding of DEK to DNA could change the topology of DNA and then affect the gene activity of the underlying DNA sequences. It is speculated that there might be some potential relationship between the stress reaction of cells and DEK proteins. The phosphorylation status of DEK protein is altered during death-receptor-mediated cell apoptosis. Both phosphorylation and poly(ADP-ribosyl)ation could promote the release of DEK from apoptotic nuclei to extracellular environment, and in this case DEK becomes a potential autoantigen of some autoimmune diseases. The available evidence powerfully suggests that DEK protein is closely relevant to apoptosis. The overexpression of DEK protein has dual function in cell apoptosis, in terms of inhibiting or triggering cell apoptosis.

One of the strategies of treating Parkinson's disease (PD) is the replacement of lost neurons in the substantia nigra with healthy dapamingergic cells. Potential sources for cells range from autologous grafts of dopamine secreting cells, fetal ventral mesencephalon tissue, to various stem cell types. Over the past quarter century, many experimental replacement therapies have been tried on PD animal models as well as human patients, yet none resulted in satisfactory outcomes that warrant wide applications. Recent progress in stem cell biology has shown that nuclear transfer embryonic stem cells (ntES) or induced pluripotent stem cells (iPS) derived cells can be used to successfully treat rodent PD models, thus solving the problem of immunorejection and paving the way for future autologous transplantations for treating PD. Meanwhile, however, post mortem analysis of patients who received fetal brain cell transplantation revealed that implanted cells are prone to degeneration just like endogenous neurons in the same pathological area, indicating long-term efficacy of cell therapy of PD needs to overcome the degenerating environment in the brain. A better understanding of neurodegeneration in the midbrain appeared to be a necessary step in developing new cell therapies in Parkinson's disease. It is likely that future cell replacement will focus on not only ameliorating symptoms of the disease but also trying to slow the progression of the disease by either neuroprotection or restoring the micro-environment in the midbrain.

Efficiently obtaining functional pancreatic islet cells derived from human embryonic stem (hES) cells not only provides great potential to solve the shortage of islets sources for type I diabetes cell therapy, but also benefits the study of the development of the human pancreas and diabetes pathology. In 2001, hES cells were reported to have the capacity to generate insulin-producing cells by spontaneous differentiation in vitro. Since then, many strategies (such as overexpression of key transcription factors, delivery of key proteins for pancreatic development, co-transplantation of differentiated hES cells along with fetal pancreas, stepwise differentiation by mimicking in vivo pancreatic development) have been employed in order to induce the differentiation of pancreatic islet cells from hES cells. Moreover, patient-specific induced pluripotent stem (iPS) cells can be generated by reprogramming somatic cells. iPS cells have characteristics similar to those of ES cells and offer a new cell source for type I diabetes cell therapy that reduces the risk of immunologic rejection. In this review, we summarize the recent progress made in the differentiation of hES and iPS cells into functional pancreatic islet cells and discuss the challenges for their future study.

Marker-assisted selection (MAS) is an important modern breeding technique, but it has been found that the effect of the markers for quantitative trait loci (QTL) is inconsistent, leading in some cases to MAS failure and raising doubts about its effectiveness. Here the model organism Drosophila melanogaster was employed to study whether an effective marker could be found and applied to MAS. We crossed the stock carrying the y (0) marker (a recessive mutation allele of the yellow gene on the X chromosome) with three other stocks carrying corresponding wild-type markers in an F2 design, and found that the y (0) marker was in significant association with low body weight (P<0.001). This association was consistent across different backgrounds and the marker effects in female and male were approximately 0.95 sigma (P) (phenotypic standard deviation) and 0.68 sigma (P), respectively. We next introgressed a fragment via the y (0) marker into a wild stock background over 20 generations of marker-assisted introgression (MAI), and constructed the introgression stock y (0)(OR)20 in which body weight decreased by 13% and 7%, in female and male, respectively, compared to the wild stock (P<0.0001). This indicated that there must be a single QTL for low body weight that is tightly linked to the y (0) marker. We then shortened the introgressed fragment to less than 1.5 cM by a deeper MAI using the y (0) marker and the white marker. This narrower fragment also resulted in a similar decrease in body weight to that induced by y (0)(OR)20, indicating that the QTL for low body weight is located within this less-than-1.5 cM interval. Molecular characteristics of the y (0) marker by PCR amplification and Southern blotting revealed that yellow gene was deficient in the y (0) stock, leading to disappearance of melanin from the cuticle and probably influencing the developmental process. The above results confirmed the existence of effective QTL markers applicable to MAS breeding schemes, and their potential application in breeding new stocks.

Event-related brain potentials (ERPs) were measured when 24 Chinese subjects performed the earthquake color-matching Stroop task. All of them have experienced the great Sichuan earthquake (5.12), with 12 subjects in each of Chengdu city and Chongqing city (different earthquake experiences) groups. The behavioral data showed that the earthquake Stroop task yielded robust the earthquake interference effect as indexed by longer RT for earthquake-related (Related) words than earthquake-unrelated (Unrelated) words only in the Chengdu group. Scalp ERP analysis also revealed the neurophysiological substrate of the interference effect: a greater positivity (P350-450) in Related words as compared to Unrelated words was found between 350 and 450 ms post-stimulus over fronto-central scalp regions in the Chengdu group, while the interference effect was not found in the Chongqing group. The P350-450 might reflect an earthquake experience interference, but also attention enhancing, effect of earthquake-related words. Dipole source analysis of the difference wave (Related-Unrelated) showed that a generator was localized in the parahippocampal gyrus, which was possibly associated with flashbulb memory (personal earthquake experience). The results indicated that different personal earthquake experiences might be critical in engaging the neural mechanisms that underlie the modulation of selective attention.