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세포질내 정자주입법(ICSI)에 있어서 정자흡입 및 난자내 주입방법에 관한 연구
이택후,김항진,송건호,김대근,전상식,박윤규,서태광,전병균,류은경,이은숙,문진수,김광철 경북대학교 의학연구소 2000 경북대학교병원의학연구소논문집 Vol.4 No.1
Study on Method of Sperm Aspiration and Injection into an Oocyte in Intracytoplasmic Sperm Injection(ICSI) Immobilization of spermatozoa prior to intracytoplasmic sperm iniection(ICSI) sometimes results in crooked tail and this makes it difficult to aspirate sperm into an injection pipette tail first. Head-first sperm aspiration into an injection pipette avoid this problem due to the bigger size of the sperm head. The effect of head or tail-first sperm injection into an oocyte on fertilization cleavage, percentage of grade I embryos and development to blastocyst stage in ICSI program has been studied. A single living immobilized spermatozoa from oligoasthenozoospermic patient was injected into an oocyte head-first or tail-first according to the treatment. Eighteen hours after microinjection, oocytes ware inspected for survival and fertilization Fertilized oocytes with two pronuclei were cultured in 30μl drop of mHTF supplemented with 10% heat-inactivated follicular fluid(FF) at 37℃. On day 2. embryo transfer was performed with cleaved embryos. The remaining 2-8 cell stage embryos were co-cultured with BRL cells in mHTF + 10% FF for 72 hours and the developmental stage was observed. The data were analyzed by Analysis of Variance. A total of 164 oocytes from 36 cycles were assigned to earth treatment and ICSI was performed(88 head-first, tail-first). The rates of normal fertilization were 81.8% and 76.3% for head-first and tail-first, respectively. Of the fertilized oocytes, the percentage of cleaved embryos and the percentage of grade 1 embryo among cleaved embryos were 88.9% and 68.8%, 93.1% and 74.1% for head-first and tail-first, respectively. Of the 2-8 cell embryos cultured, 44.4%(16/36) and 50.0%(10/20) for head first and tail first, respectively developed to blastocyst stage. There were no differences in fertilization, cleavage, rates of grade 1 embryos, and development to blastocyst stage. In conclusion, head-first or tail-first sperm injection into an oocyte in ICSI program does not affect fertilization and subsequent embryo development to blastocyst stage in vitro.
성인원외폐렴의 원인미생물에대한 전향적 다기관 연구 : 성인원외폐렴의 원인으로 세균의 역할을 중심으로
우준희,강재명,김양수,신완식,류진홍,최정현,김양리,정희진,어수택,박춘식,정문현,정기석,이찬주,류지소 대한감염학회 2001 감염 Vol.33 No.1
Background : Communite-acquired peumonia (CAP) is one of the leading causes of mortality and morbidity. Despite progress in diagnostic techniques and treatments, management of pneumonia remains challenging, because the precise etiology remains uncertain in as many as 49% of cases. The limitaions of identifying etiologic agents make it necessary to use empiric antibiotics in almost all patients, and furthermore emergence of antibiotic-resistant organisms pose difficulties to the selection of an empiric antibiotic regimen. For the optimal choice of empirical antibiotics, we should know the frequency of etiologic agents and antimicrobial resistance rates in the community. Methods : A prospective multicenter study of community-acquired pneumonia in Korea was carried out between May 1997 and April 2000. The microbiologic diagnosis was based on the results of sputum culture, blood culture and pleural culture. Results : Five hundred eighty eight cases of community-acquired peumonia in 562 patients admitted to the hospitals. The mean age was 59.9 with male predominance (58.3%), and 370 (63%) had underlyin gillness. The etiologic agents were identified in 38.3%, and the list of individual agents, in decreasing order, was Streprococcus pneumoniae (21.7%), Klebsiella pneumoniae (14.8%) Pseudomonas aeruginosa (9.8%), Staphylococcus aureus (9.5%), viridans group streptococci (5.7%), Enterobacter cloacae (4.2%), Hemophillus Influenza (3.8%), The rates of admission to the intensive care unit was 10.4%. The motality was 7.1%. Susceptible rates of S. pneumoniae to penicillin was 36.6% and showed multidrug resistant. Forty percents of S. aureus were methicillin-resistant S. aureus. K. penumoniae were susceptible to cephalosporin and quinolone. Conclusion : In Korea, S.pneumoniae is the most important agent causing community-acquired pneumonia. Susceptible rates of S. pneumoniae to penicillin was 36.6% and showed multidrug resistant. Gram negative bacteria such as K. pneumoniae, P. aeruginosa showed high incidence when compared with that of other countries. Most of them had underlying diseases including bronchiectasis and chronic obstructive pulmonary diseases. (Korean J Infect Dis 33:1∼7, 2001)
( Moon-taek Park ),( Sung-dae Kim ),( Yu Kyeong Han ),( Jin Won Hyun ),( Hae-june Lee ),( Joo Mi Yi ) 한국응용약물학회 2022 Biomolecules & Therapeutics(구 응용약물학회지) Vol.30 No.1
The targeting of DNA methylation in cancer using DNA hypomethylating drugs has been well known to sensitize cancer cells to chemotherapy and immunotherapy by affecting multiple pathways. Herein, we investigated the combinational effects of DNA hypomethylating drugs and ionizing radiation (IR) in human sarcoma cell lines both in vitro and in vivo. Clonogenic assays were performed to determine the radiosensitizing properties of two DNA hypomethylating drugs on sarcoma cell lines we tested in this study with multiple doses of IR. We analyzed the effects of 5-aza-dC or SGI-110, as DNA hypomethylating drugs, in combination with IR in vitro on the proliferation, apoptosis, caspase-3/7 activity, migration/invasion, and Western blotting using apoptosis- or autophagy-related factors. To confirm the combined effect of DNA hypomethylating drugs and IR in our in vitro experiment, we generated the sarcoma cells in nude mouse xenograft models. Here, we found that the combination of DNA hypomethylating drugs and IR improved anticancer effects by inhibiting cell proliferation and by promoting synergistic cell death that is associated with both apoptosis and autophagy in vitro and in vivo. Our data demonstrated that the combination effects of DNA hypomethylating drugs with radiation exhibited greater cellular effects than the use of a single agent treatment, thus suggesting that the combination of DNA hypomethylating drugs and radiation may become a new radiotherapy to improve therapeutic efficacy for cancer treatment.
Park, Moon-Taek,Lee, Su-Jae Korean Society for Biochemistry and Molecular Biol 2003 Journal of biochemistry and molecular biology Vol.36 No.1
Cancer is frequently considered to be a disease of the cell cycle. As such, it is not surprising that the deregulation of the cell cycle is one of the most frequent alterations during tumor development. Cell cycle progression is a highly-ordered and tightly-regulated process that involves multiple checkpoints that assess extracellular growth signals, cell size, and DNA integrity. Cyclin-dependent kinases (CDKs) and their cyclin partners are positive regulators of accelerators that induce cell cycle progression; whereas, cyclin-dependent kinase inhibitors (CKIs) that act as brakes to stop cell cycle progression in response to regulatory signals are important negative regulators. Cancer originates from the abnormal expression of activation of positive regulators and functional suppression of negative regulators. Therefore, understanding the molecular mechanisms of the deregulation of cell cycle progression in cancer can provide important insights into how normal cells become tumorigenic, as well as how cancer treatment strategies can be designed.
Park, Moon-Taek,Lee, Su-Jae 한국생화학분자생물학회 2003 BMB Reports Vol.36 No.1
Cancer is frequently considered to be a disease of the cell cycle. As such, it is not surprising that the deregulation of the cell cycle is one of the most frequent alterations during tumor development. Cell cycle progression is a highly-ordered and tightly-regulated process that involves mulitple checkpoints that assess extracellular growth signals, cell size, and DNA integrity. Cyclin-dependent kinases (CDKs) and their cyclin partners are positive regulators or accelerators that induce cell cycle progression; whereas, cyclin-dependent kinase inhibitors (CKIs) that act as brakes to stop cell cycle progression in response to regulatory signals are important negative regulators. Cancer orginates from the abnormal expression or activation of positive regulators and functional suppression of negative regulators. Therefore, understanding the molecular mechanisms of the deregulation of cell cycle progression in cancer can provide important insights into how normal cells become tumorigenic, as well as how new cancer treatment strategies can be designed.
Park, Moon-Taek,Kim, Min-Jung,Kang, Young-Hee,Choi, Soon-Young,Lee, Jae-Hoon,Choi, Jung-A,Kang, Chang-Mo,Cho, Chul-Koo,Kang, Seongman,Bae, Sangwoo,Lee, Yun-Sil,Chung, Hee Yong,Lee, Su-Jae American Society of Hematology 2005 Blood Vol.105 No.4
<B>Abstract</B><P>The use of chemical modifiers as radiosensitizers in combination with low-dose irradiation may increase the therapeutic effect on cancer by overcoming a high apoptotic threshold. Here, we showed that phytosphingosine treatment in combination with γ-radiation enhanced apoptotic cell death of radiation-resistant human T-cell lymphoma in a caspase-independent manner. Combination treatment induced an increase in intracellular reactive oxygen species (ROS) level, mitochondrial relocalization of B-cell lymphoma-2(Bcl-2)-associated X protein (Bax), poly-adenosine diphosphate (ADP)-ribose polymerase 1 (PARP-1) activation, and nuclear translocation of apoptosis-inducing factor (AIF). siRNA targeting of AIF effectively protected cells from the combination treatment-induced cell death. An antioxidant, N-acetyl-L-cysteine (NAC), inhibited Bax relocalization and AIF translocation but not PARP-1 activation. Moreover, transfection of Bax-siRNA significantly inhibited AIF translocation. Pretreatment of PARP-1 inhibitor, DPQ (3,4-dihydro-5-[4-(1-piperidinyl)-butoxy]-1(2H)-isoquinolinone), or PARP-1-siRNA also partially attenuated AIF translocation, whereas the same treatment did not affect intracellular ROS level and Bax redistribution. Taken together, these results demonstrate that enhancement of cell death of radiation-resistant cancer cells by phytosphingosine treatment in combination with γ-radiation is mediated by nuclear translocation of AIF, which is in turn mediated both by ROS-dependent Bax relocalization and ROS-independent PARP-1 activation. The molecular signaling pathways that we elucidated in this study may provide potential drug targets for radiation sensitization of cancers refractive to radiation therapy. (Blood. 2005;105:1724-1733)</P>
Park, Moon-Taek,Kang, Young-Hee,Park, In-Chul,Kim, Chun-Ho,Lee, Yun-Sil,Chung, Hee Yong,Lee, Su-Jae American Association for Cancer Research, Inc 2007 Molecular Cancer Therapeutics Vol.6 No.1
<P>Resistance to anticancer drugs can sometimes be overcome by combination treatment with other therapeutic drugs. Here, we showed that phytosphingosine treatment in combination with arsenic trioxide (As(2)O(3)) enhanced cell death of naturally As(2)O(3)-resistant human myeloid leukemia cells. The combination treatment induced an increase in intracellular reactive oxygen species level, mitochondrial relocalization of Bax, poly(ADP-ribose) polymerase-1 (PARP-1) activation, and cytochrome c release from the mitochondria. N-acetyl-l-cysteine, a thiol-containing antioxidant, completely blocked Bax relocalization, PARP-1 activation, and cytochrome c release. Pretreatment of 3,4-dihydro-5-[4-(1-piperidinyl)butoxy]-1(2H)-isoquinolinone, a PARP-1 inhibitor, or PARP-1/small interfering RNA partially attenuated cytochrome c release, whereas the same treatment did not affect Bax relocalization. The combination treatment induced selective activation of p38 mitogen-activated protein kinase (MAPK). Inhibition of p38 MAPK by treatment of SB203580 or expression of dominant-negative forms of p38 MAPK suppressed the combination treatment-induced Bax relocalization but did not affect PARP-1 activation. In addition, antioxidant N-acetyl-l-cysteine completely blocked p38 MAPK activation. These results indicate that phytosphingosine in combination with As(2)O(3) induces synergistic apoptosis in As(2)O(3)-resistant leukemia cells through the p38 MAPK-mediated mitochondrial translocation of Bax and the PARP-1 activation, and that p38 MAPK and PARP-1 activations are reactive oxygen species dependent. The molecular mechanism that we elucidated in this study may provide insight into the design of future combination cancer therapies to cells intrinsically less sensitive to As(2)O(3) treatment.</P>