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Featured researches published by Yi Ning Su.


Apoptosis | 2005

Hypoxia-induced apoptosis in endothelial cells and embryonic stem cells

Chien-Nan Lee; Wen-Fang Cheng; Ming-Chu Chang; Yi Ning Su; Chi-An Chen; Fon-Jou Hsieh

Background: To evaluate the influence of hypoxia and molecular events in endothelial and embryonic stem cells.Materials and Methods: Human umbilical vein endothelial cells (HUVECs) and mouse embryoid body (EB) cells were subjected to hypoxic conditions for different time courses. DNA fragmentation assay, quantification of apoptotic cells by TUNEL assay measured by flowcytometry, and Western blot analysis for the molecular events of apoptosis were performed.Results: DNA fragmentation could be identified under hypoxic conditions in HUVECs and mouse EBs. The DNA fragmentation increased when the hypoxic interval was extended.In situ internucleosomal DNA fragmentation-TUNEL assay also found that the percentages of apoptotic cells increased gradually in HUVECs and mouse EBs when the hypoxic interval was extended. Furthermore, the levels of expression of p53 and Bax both increased in hypoxic conditions.Conclusions: Hypoxia increases both HUVEC and mouse EB apoptosis, which is associated with increase in p53/Bax expression.


Cancer Gene Therapy | 2006

Sindbis virus replicon particles encoding calreticulin linked to a tumor antigen generate long-term tumor-specific immunity

Wen-Fang Cheng; Chien-Nan Lee; Yi Ning Su; Chee-Yin Chai; Ming-Chu Chang; Polo Jm; Chien Fu Hung; T. C. Wu; Chun-Ko Hsieh; Chi-An Chen

Alphavirus vectors have emerged as a promising strategy for the development of cancer vaccines and gene therapy applications. In this study, we used the replication-defective vaccine vector SIN replicon particles from a new packaging cell line (PCL) to develop SIN replicon particles encoding calreticulin (CRT) linked to a model tumor antigen, human papillomavirus type 16 (HPV16) E7 protein. The linkage of CRT to E7 in SIN replicon particles resulted in a significant increase in E7-specific CD8+ T-cell precursors and a strong antitumor effect against E7-expressing tumors in vaccinated mice. SINrep5-CRT/E7 replicon particles enhanced presentation of E7 through the major histocompatibility complex (MHC) class I pathway by infecting dendritic cells (DCs) directly and pulsing DCs with lysates of cells infected by SINrep5-CRT/E7 replicons. Vaccination of immunocompromised (BALB/c nu/nu) mice with SINrep5-CRT/E7 replicon particles also generated significant reduction of lung tumor nodules, suggesting that antiangiogenesis may contribute to the antitumor effect of SINrep5-CRT/E7 replicon particles. Furthermore, SINrep5-CRT/E7 replicon particles generated long-term in vivo tumor protection effects and antigen-specific memory immunities. We concluded that the CRT strategy used in the context of SIN replicon particles facilitated the generation of a highly effective vaccine for cancer prophylaxis and immunotherapy.


Taiwanese Journal of Obstetrics & Gynecology | 2010

Mosaic Trisomy 7 at Amniocentesis: Prenatal Diagnosis and Molecular Genetic Analyses

Chih Ping Chen; Yi Ning Su; Schu Rern Chern; Yuh Ming Hwu; Shuan Pei Lin; Chyong Hsin Hsu; Fuu Jen Tsai; Tao Yeuan Wang; Pei Chen Wu; Chen Chi Lee; Yu-Ting Chen; Li Feng Chen; Wayseen Wang

OBJECTIVE To present prenatal diagnosis and molecular genetic analyses of mosaic trisomy 7. MATERIALS, METHODS AND RESULTS A 38-year-old primigravid woman underwent amniocentesis at 19 weeks of gestation because of her advanced maternal age. Amniocentesis revealed a karyotype of 47,XY,+7[26]/46, XY[16]. Repeated amniocentesis at 21 weeks of gestation revealed a karyotype of 47,XY,+7[20]/46,XY[17]. Simultaneous cordocentesis revealed a karyotype of 46,XY in 100/100 cultured lymphocytes. Polymorphic DNA marker analyses of uncultured amniocytes and cord blood revealed a diallelic pattern with seemingly equal biparental inheritance of chromosome 7. Repeated cordocentesis and chorionic villus sampling at 23 weeks of gestation revealed a karyotype of 47,XY,+7[2]/46,XY[66] in cord blood and a karyotype of 47,XY,+7 in 24/24 cultured chorionic villi cells. Level II ultrasonography was normal. At 40 weeks of gestation, a 2,708 g normal male baby was delivered. The peripheral blood had a karyotype of 46,XY in 100/100 lymphocytes. Molecular analyses of placenta, urine, buccal swab, and peripheral blood revealed a diallelic pattern and seemingly equal biparental inheritance of chromosome 7 in all tissues. At 3 months of age, he manifested hypopigmented skin and inguinal hernia, but showed normal growth and mental development. Fluorescence in situ hybridization analysis of inguinal hernia sac tissue revealed that 19/100 (19%) of nuclei had three chromosome 7 signals. CONCLUSION Mosaic trisomy 7 at amniocentesis may be derived from a cell culture artifact from an undetected low level of trisomy 7 mosaicism in uncultured amniocytes, and can be associated with favorable fetal outcome if the blood has a normal karyotype or a very low level of mosaicism and if uniparental disomy for chromosome 7 is excluded.


International Journal of Legal Medicine | 2009

Thirteen X-chromosomal short tandem repeat loci multiplex data from Taiwanese

Hsiao-Lin Hwa; Yih Yuan Chang; James Chun-I Lee; Hsiang Yi Yin; Ya Hui Chen; Li Hui Tseng; Yi Ning Su; Tsang Ming Ko

Study results of variations in the X chromosome are useful tools in researching the genetic diversity of human populations and individual identification. We developed a 13 X chromosomal short tandem repeat (STR) multiplex system (DXS6807, DXS8378, DSX9902, DXS7132, DXS9898, DXS6809, DXS6789, DXS7424, DXS101, GATA172D05, HPRTB, DXS8377, DXS7423) amplified in one single polymerase chain reaction. DNA samples of 113 male and 108 female Taiwanese Han subjects were successfully analyzed using this 13 X-STR multiplex system. The distributions of allele frequencies were examined for independence. DXS8377, DXS101, DXS6789, and DXS6809 were found to be the most polymorphic markers in this study. High values of discrimination power and mean exclusion chance without significant evidence of association between these markers were obtained. In conclusion, this 13 X chromosomal STR multiplex system offers considerable forensic efficiency and may be useful in forensic identification casework.


Taiwanese Journal of Obstetrics & Gynecology | 2011

Prenatal diagnosis of mosaic trisomy 8: Clinical report and literature review

Chih Ping Chen; Ming Chen; Yi Ju Pan; Yi Ning Su; Schu Rern Chern; Fuu Jen Tsai; Yu-Ting Chen; Wayseen Wang

OBJECTIVE To present prenatal diagnosis of mosaic trisomy 8 and to review the literature. MATERIALS, METHODS, AND RESULTS A 34-year-old woman underwent amniocentesis at 16 weeks of gestation because of advanced maternal age. Amniocentesis revealed a karyotype of 47,XY,+8[6]/46,XY[31]. Repeated amniocentesis at 21 weeks of gestation revealed a karyotype of 47,XY,+8[4]/46,XY[77]. Interphase fluorescence in situ hybridization analysis of uncultured amniocytes showed 25% (5/20) mosaicism for trisomy 8. Array comparative genomic hybridization (aCGH) and quantitative fluorescent polymerase chain reaction (QF-PCR) analyses of uncultured amniocytes revealed no genomic imbalance in chromosome 8. The result of QF-PCR excluded uniparental disomy 8. At 23 weeks of gestation, the woman underwent amniocentesis and cordocentesis at other hospitals. Amniocentesis revealed a karyotype of 47,XY,+8[6]/46,XY[10]. Cordocentesis revealed a karyotype of 47,XY,+8[1]/46,XY[29]. Level II ultrasound findings were unremarkable. The parents decided to continue the pregnancy. A 1373-g male baby was prematurely delivered at 29 weeks of gestation. The peripheral blood had a karyotype of 47,XY,+8[1]/46,XY[29]. The infant had normal growth and mental development at 4 months of age. CONCLUSION Fetuses with mosaic trisomy 8 are compatible with viability and can have a favorable outcome. QF-PCR and array comparative genomic hybridization have the limitation of detection of low-level mosaicism. We suggest that in instances of repeated amniocentesis for confirmation of mosaic trisomy 8, follow-up investigations should include interphase fluorescence in situ hybridization studies on uncultured amniocytes, uniparental disomy tests, and detailed ultrasound examinations.


Annals of Human Genetics | 2009

Mutation spectrum of the fibrillin‐1 (FBN1) gene in Taiwanese patients with Marfan syndrome

Chia Cheng Hung; Shin-Yu Lin; Chien-Nan Lee; Hui Yu Cheng; Shuan Pei Lin; Ming Ren Chen; Chih Ping Chen; Chien Hui Chang; Chiou Ya Lin; Chih-Chieh Yu; Hsin Hui Chiu; Wen-Fang Cheng; Hong-Nerng Ho; Dau Ming Niu; Yi Ning Su

The aim of this study was to establish a national database of mutations in the fibrillin‐1 (FBN1) gene that cause Marfan syndrome (MFS) in the Taiwanese population. In this study, we screened 294 patients from 157 families for the presence of FBN1 mutations using polymerase chain reaction/ denaturing high performance liquid chromatography (PCR/DHPLC). We identified 56 mutations in 62 of the 157 (40%) families including 49 single‐base substitutions (36 missense mutations, seven nonsense mutations, and six splicing sites), one small insertion, four small deletions, one small indel (insertion and deletion), and one exonic deletion (Exon 36). When family history was taken into consideration, the mutation detection rate rose to 91% (29 of 32). We further investigated the phenotypic data and found that one third (47 of 157) of the families fit the Ghent criteria for MFS. Based on that data, the mutation rate was 98% (46/47). That finding implies that family history and the Ghent criteria play a more important role than clinical manifestations in establishing a clinical diagnosis of Marfan syndrome. Among the 56 mutations found in this study, 40 (71%) have not been registered in the Human Gene Mutation Database (HGMD) or in the Universal Mutation Database (UMD). This is the first study of the mutation spectrum of MFS in a cohort of patients in Taiwan. The database is expected to considerably improve genetic counseling for and medical care of MFS families.


Taiwanese Journal of Obstetrics & Gynecology | 2009

Terminal 2q Deletion and Distal 15q Duplication: Prenatal Diagnosis by Array Comparative Genomic Hybridization Using Uncultured Amniocytes

Chih Ping Chen; Yi Ning Su; Fuu Jen Tsai; Hung Hung Lin; Schu Rern Chern; Meng Shan Lee; Jonathan Kwei Hwang; Teresa Hsiao Tien Chen; Wayseen Wang

A 35-year-old, gravida 3, para 2, woman was referred to the hospital at 18 weeks of gestation for amniocentesis because of advanced maternal age and relatives with balanced and unbalanced chromosomal translocations. Her husband and her elder daughter had a balanced translocation of t(2;15)(q37.3;q24.3). Her younger daughter suffered from mental retardation and had an unbalanced translocation of der(2)t(2;15) (q37.3;q24.3)pat. The woman’s karyotype was normal. Prenatal ultrasound during the current pregnancy revealed no structural abnormalities. Genetic amniocentesis was performed at 19 weeks of gestation, and 30 mL of amniotic fluid was aspirated, of which 10 mL was used for array comparative genomic hybridization (aCGH) using uncultured amniocytes and 20 mL was used for conventional cytogenetic analysis using cultured amniocytes. Within 3 days, bacterial artificial chromosome (BAC)-based aCGH demonstrated partial monosomy 2q and partial trisomy 15q [arr cgh 2q37.3q37.3 (RP11-299F2 RP11-875C22) × 1, 15q25.1q26.3 (RP11-10K12 RP11-530H6) × 3] (Figure 1). Conventional cytogenetic analysis revealed TERMINAL 2Q DELETION AND DISTAL 15Q DUPLICATION: PRENATAL DIAGNOSIS BY ARRAY COMPARATIVE GENOMIC HYBRIDIZATION USING UNCULTURED AMNIOCYTES


Taiwanese Journal of Obstetrics & Gynecology | 2010

Prenatal diagnosis and molecular cytogenetic characterization of de novo partial trisomy 7p (7p15.3→pter) and partial monosomy 13q (13q33.3→qter) associated with Dandy-Walker malformation, abnormal skull development and microcephaly.

Chih Ping Chen; Ming Chen; Yi Ning Su; Fuu Jen Tsai; Schu Rern Chern; Chin Yuan Hsu; Pei Chen Wu; Dai Dyi Town; Dong Jay Lee; Gwo Chin Ma; Wayseen Wang

OBJECTIVE To present the prenatal diagnosis and molecular cytogenetic characterization of de novo partial trisomy 7p (7p15.3→pter) and partial monosomy 13q (13q33.3→qter) associated with Dandy-Walker malformation (DWM), abnormal skull development, microcephaly and multiple congenital anomalies. MATERIALS, METHODS AND RESULTS A 42-year-old woman, gravida 6, para 1, was referred for amniocentesis at 18 weeks of gestation because of her advanced maternal age. Amniocentesis revealed an aberrant derivative chromosome 13, or der(13). The parental karyotypes were normal. Spectral karyotyping showed that the der(13) was derived from a translocation of chromosomes 7 and 13. Fluorescence in situ hybridization using subtelomeric probes revealed three signals of 7pTEL and only one signal of 13qTEL, indicating a translocation between 7p and 13q in the der(13). Array-based comparative genomic hybridization demonstrated partial trisomy 7p (7p15.3-p22.3) and partial monosomy 13q (13q33.3-q34). The karyotype was 46,XY,der(13)t(7;13)(p15.3;q33.3). Polymorphic DNA marker analysis revealed the paternal origin of the aberrant chromosome. Level II ultrasound at 24 weeks of gestation revealed microcephaly, an irregular-shaped skull, DWM, nuchal edema and transposition of the great arteries. CONCLUSION Spectral karyotyping, fluorescence in situ hybridization and array-based comparative genomic hybridization are useful for prenatal investigation of the nature of a de novo aberrant derivative chromosome. Partial trisomy 7p (7p15.3→pter) and partial monosomy 13q (13q33.3→qter) can be associated with DWM, microcephaly, abnormal skull development, nuchal edema and cardiovascular defects on prenatal ultrasound.


Cancer | 2007

Generation and characterization of an ascitogenic mesothelin‐expressing tumor model

Wen-Fang Cheng; Chien Fu Hung; Chee Yin Chai; Chi-An Chen; Chien-Nan Lee; Yi Ning Su; Wen Yin Isaac Tseng; Chang Yao Hsieh; Ie Ming Shih; Tian Li Wang; T. C. Wu

Intraperitoneal tumors expressing high amounts of mesothelin such as malignant mesothelioma and ovarian cancers tend to develop ascites and result in significant morbidity and mortality in the patient. A suitable preclinical intraperitoneal model will assist in the illustration of the mechanisms of molecular oncogenesis and facilitate in addressing issues related to early screening, diagnosis, and therapy for intraperitoneal tumors.


European Journal of Immunology | 2004

Naked RNA vaccine controls tumors with down‐regulated MHC class I expression through NK cells and perforin‐dependent pathways

Wen-Fang Cheng; Chien Fu Hung; Chien-Nan Lee; Yi Ning Su; Ming Cheng Chang; Liangmei He; T. C. Wu; Chi-An Chen; Chang Yao Hsieh

One of the major issues facing cancer immunotherapy is that many human cancers down‐regulate expression of MHC class I molecules. The understanding of the mechanisms of antitumor effects against tumors with down‐regulated MHC class I will facilitate rational design of vaccines and immunotherapeutic strategies to control such tumors. A naked Sindbis RNA replicon vector (SINrep5) encoding the herpes simplex virus type 1 protein VP22 linked to E7 (SINrep5‐VP22/E7) generated significant antitumor effects against TC‐1 and TC‐1 P3(A15), tumors with down‐regulated MHC class I expression. Naked SINrep5 RNA without the insert or an E7 vaccine also produced antitumor effects against TC‐1 P3(A15) but not TC‐1. Mice vaccinated with any of these naked RNA vaccines generated higher percentages of NK cells. In vivo Ab depletion experiments revealed that NK cells were important for the antitumor effects of naked RNA vaccines against TC‐1 P3(A15) and that the antitumor effects were perforin‐dependent. Poly I:C also increased the percentage of NK cells and generated antitumor effects against the tumors with down‐regulated MHC class I. Thus, the SINrep5‐VP22/E7 naked RNA vaccinecontrols MHC class I‐positive and MHC class I‐down‐regulated tumor cells via different mechanisms, and NK cells play an important role in the antitumor effects generated by naked RNA replicon vaccines.

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Chih Ping Chen

Mackay Memorial Hospital

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Wayseen Wang

Mackay Memorial Hospital

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Pei Chen Wu

Mackay Memorial Hospital

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Chien-Nan Lee

National Taiwan University

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Chen Chi Lee

Mackay Memorial Hospital

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Wang W

Mackay Memorial Hospital

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Yu-Ting Chen

Mackay Memorial Hospital

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Chin Yuan Hsu

Mackay Memorial Hospital

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Ming Chen

National Taiwan University

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