http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Xing-Wei Liang,Shao-Chen Sun,Yong-Xun Jin,Seul-Ki Lee,Jung-Woo Kwon,Xiang-Shun Cui,Nam-Hyung Kim 한국동물번식학회 2012 Reproductive & Developmental Biology(Supplement) Vol.36 No.2s
Superovulation, or ovarian stimulation is a commonly used ART for treatment of human infertility/subfertility. Recent studies suggest that superovulation unaffects methylated imprints acquisition in mouse oocytes during oogenesis, whereas disrupts DNA methylation maintenance in embryos during preimplantation development. However, the mechanisms of defects in methylation maintanence caused by superovulation remain largely unclear. We hypothesized that superovulation may disrupt the expression of DNA methyltransferases (Dnmts), the enzymes which catalyze DNA methylation acquisition and maintenance. The mice were subjected to superovulate with low (6 IU) and high (10 IU) dosage hormone. We examined the global DNA methylation levels in zygotes and DNA methylation of repeated sequences (IAP and Line 1) in blastocyst stage embryos. In addition, we investigated the expression of Dnmts (Dnmt3a, Dnmt3b, Dnmt3l and Dnmt1o) in ovulated oocytes and zygotes. Through staining with antibody 5mC and Di-H3K9 coupled with confocal microscopy, we found that global methylation profiles in zygotes derived from females after low or high dosage hormone treatment were not affected when compared to control counterpart. Moreover, methylation at IAP in blastocysts also was unaffected by superovulation, irrespective of hormone dosage. In contrast, methylation level at Line 1 decreased when the females were administered by high dosage hormone. Furthermore, expression of de novo DNA methyltransferase Dnmt3a, Dnmt3b, Dnmt3L, as well as maintenance Dnmt1o in MII oocytes and zygotes was not disrupted by superovulation. Given superovulation adversely affected methylation maintenance in blastocysts during preimplantation development but with normal expression of Dnmts in oocytes and zygotes, it is indicated that defects of embryonic methylation didn’t originate from abnormal expression of Dnmts.
Xing-Wei Liang,Yong-Xun Jin,Ga-Young An,Seul-Ki Lee,Jung-Woo Kwon,Xiang-Shun Cui,Nam-Hyung Kim 한국동물번식학회 2012 Reproductive & Developmental Biology(Supplement) Vol.36 No.2s
It is well established that mitochondrial genome is strictly maternally inherited in mammalian, despite the fact that paternal mitochondria enter into oocyte during fertilization. To date, although some mechanisms have been extrapolated to interpret the elimination of paternal mitochondria, the exact mechanism still is unclear. Recent studies suggest that autophagy process and the ubiquitin-mediated degradation pathway may be involved in elimination of paternal mitochondria. However, the dynamic profiles of autophagy and ubiquitination associated with paternal mitochondria degradation have not been determined in mouse model. Through immunostaining with specific antibody LC3 and Ubiquitin and confocal microscopy, we investigated the dynamic profiles of LC3 and Ubiquitin signals in mouse embryos during preimplantation development. In addition, embryos were stained with MitoTracker Red for tracking the degradation process of paternal mitochondria. Our results showed that paternal mitochondria gradually degraded during postfertilization development, and sporadic paternal mitochondria were found at least in 16 cell embryos. LC3 and Ubiquitin signals appeared in the midpiece of sperm at 3 h postfertilization, and they were strictly colocalizated with paternal mitochondria from zygote to 2 cell embryo. Nevertheless, the colocalization became loose at 4 cell embryos, and gradually disappeared beyond 4 cell embryos. Our results confirmed that autophagy process and the ubiquitin-mediated degradation pathway may take part in the postfertilization remove of paternal mitochondria.
Liang Bai,Huilin Wei,Bin Wang,Fangfang Liao,Tianhua Zhou,Xing-Wen Liang 국제구조공학회 2023 Steel and Composite Structures, An International J Vol.47 No.1
This paper presented an investigation into steel tubes encased high-strength concrete (STHC) composite walls, wherein steel tubes were embedded at the boundary elements of high-strength concrete walls. A series of cyclic loading tests was conducted to evaluate the failure pattern, hysteresis characteristics, load-bearing capacity, deformability, and strain distribution of STHC composite walls. The test results demonstrated that the bearing capacity and ductility of the STHC composite walls improved with the embedding of steel tubes at the boundary elements. An analytical method was then established to predict the flexural bearing capacity of the STHC composite walls, and the calculated results agreed well with the experimental values, with errors of less than 10%. Finally, a finite element modeling (FEM) was developed via the OpenSees program to analyze the mechanical performance of the STHC composite wall. The FEM was validated through test results; additionally, the influences of the axial load ratio, steel tube strength, and shear-span ratio on the mechanical properties of STHC composite walls were comprehensively investigated.
Lenalidomide in Treating Patients with Castration-Resistant Prostate Cancer
Xing, Dong-Liang,Song, Dong-Kui,Zhang, Li-Rong Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.9
Background: This analysis was conducted to evaluate the efficacy and safety of lenalidomide based regimen in treating patients with castration-resistant prostate cancer. Materials and Methods: Clinical studies evaluating the efficacy and safety of lenalidomide based regimens on response and safety for patients with castration-resistant prostate cancer were identified using a predefined search strategy. A pooled response rate (rate of PSA level decline of ${\geq}50%$) to treatment was calculated. Results: In lenalidomide based regimen, 3 clinical studies which including 98 patients with castration-resistant prostate cancer were considered eligible for inclusion. These lenalidomide based regimens included cisplatin, doxorubicin, or GM-CSF. Pooled analysis suggested that, in all patients, the pooled PSA level decline of ${\geq}50%$ was 13.3% (13/98) in lenalidomide based regimens. Fatigue, nausea and vomitting were the main side effects. No grade III or IV renal or liver toxicity were observed. No treatment related death occurred in patients with lenalidomide based regimens. Conclusions: This evidence based analysis suggests that lenalidomide based regimens are associated with mild response rate and acceptable toxicities for treating patients with castration-resistant prostate cancer.