비모란 선인장 ‘Ahwang’ 품종이 2016년에 국립원예특작과 학원에서 육성되었다. 증식력이 우수한 밝은 황색 ‘Ahwang’ 품종 육성을 위해서, 황색 ‘Hwangun’품종을 모본으로, 황색 ‘0930001’ 계통을 부본으로 하여 2012년 6월 25일에 교배하였다. 어린 비모란 선인장을 2014년 이전에 삼각주에 2번 접목하여 계통을 양성하였으며 2014년부터 2016년까지 총 3회에 걸쳐 생육특성을 조사하였다. ‘Ahwang’ 품종의 모구는 편원형 모양에 황색 구색(Y9A)이다. 모구는 평균 8.6개의 능(rip)과 2.7mm의 짧은 직립형 회색 가시를 가지고 있고 혹(tubercle)이 돌출된 형태를 띠고 있다. 10개월 재배 후 ‘Ahwang’ 품종의 구직경은 44.5mm였으며 자구는 평균 26.9개가 생성되었다. ‘Ahwang’ 품종은 모구 능마다 황색의 자구가 3-4개가 착생되었다. 2016년 육성계통 평가회에서 ‘Ahwang’ 품종은 기호도 점수 3.9을 받았다. 이 품종은 2018년 5월 16일 국립종자원에 등록되었으며 식물신품종보호법에 의해 품종보호(등록번호 7193)를 받게 되었다.

DNA methylation is the most common and well-characterized epigenetic change in human cancer. Recently, the association between GATA-binding protein 5 (GATA5) methylation and carcinogenesis of various types of tumors was investigated. The aim of the present study was to evaluate the effect of GATA5 methylation status on clinicopathological features and prognosis in primary non-muscle invasive bladder cancer (NMIBC) patients with a long-term follow-up period. The GATA5 methylation status was determined for 171 human bladder specimens (eight normal controls [NCs] and 163 primary NMIBC patients) using quantitative pyrosequencing analysis. The primary NMIBC tissues were obtained from patients who underwent transurethral resection (TUR) for histologically diagnosed transitional cell carcinomas between 1995 and 2012 at Chungbuk National University Hospital. GATA5 methylation was significantly higher in NMIBC patients than in NCs and was significantly associated with higher grade and more advanced stage of cancer. Kaplan-Meier estimates showed significant differences in tumor recurrence and progression according to GATA5 methylation status (each p<0.05). Our results show that increased methylation of GATA5 was significantly associated with not only aggressive characteristics but also poor prognosis in primary NMIBC patients. Alteration of GATA5 methylation might be used as a biomarker for prognosis of NMIBC patients. However, prospective and functional investigations are necessary to clarify the role of GATA5 methylation in future clinical management of patients with NMIBC.

Sprouty (Spry) genes encode inhibitors of the receptor tyrosine kinase signaling cascade, which plays important roles in stem cells. However, the role of Spry4 in the stemness of embryonic stem cells has not been fully elucidated. Here, we used mouse embryonic stem cells (mESCs) as a model system to investigate the role of Spry4 in the stem cells. Suppression of Spry4 expression results in the decreases of cell proliferation, EB formation and stemness marker expression, suggesting that Spry4 activity is associated with stemness of mESCs. Teratoma assay showed that the cartilage maturation was facilitated in Spry4 knocked down mESCs. Our results suggest that Spry4 is an important regulator of the stemness and differentiation of mESCs.

Rad51 is a key component of homologous recombination (HR) to repair DNA double-strand breaks and it forms Rad51 recombinase filaments of broken single-stranded DNA to promote HR. In addition to its role in DNA repair and cell cycle progression, Rad51 contributes to the reprogramming process during the generation of induced pluripotent stem cells. In light of this, we performed reprogramming experiments to examine the effect of co-expression of Rad51 and four reprogramming factors, Oct4, Sox2, Klf4, and c-Myc, on the reprogramming efficiency. Co-expression of Rad51 significantly increased the numbers of alkaline phosphatase-positive colonies and embryonic stem cell-like colonies during the process of reprogramming. Co-expression ofRad51 significantly increased the expression of epithelial markers at an early stage of reprogramming compared with control cells. Phosphorylated histone H2AX (γH2AX), which initiates the DNA double-strand break repair system, was highly accumulated in reprogramming intermediates upon co-expression of Rad51. This study identified a novel role of Rad51 in enhancing the reprogramming efficiency, possibly by facilitating mesenchymal-to-epithelial transition and by regulating a DNA damage repair pathway during the early phase of the reprogramming process.