• Clinical and Experimental Reproductive Medicine
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• 제26권2호
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• pp.271-274
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• 1999

Activated factor XII (FXIIc: Hageman factor) is a central component of the contact activation system of blood coagulation, fibrinolysis, and kinin formation. Although patients deficient in FXIIc (up to 50% of normal) do not show increased bleeding tendency, thrombotic complications were reported in 8% to 10% among these patients. The reduced generation of bradykinin resulting in diminished release of tissue plasminogen activator is proposed as a cause of thrombosis in factor XII (FXII)-deficient patients. Similarly, in patients with elevated levels of circulating antiphospholipid antibodies, hemostasis may be impaired resulting in excessive thrombophilia. Both vascular and placental thromboses because of antiphospholipid antibodies or FXIIc deficiency have been reported to be associated with recurrent fetal loss. We have experienced a case of factor XII deficiency in woman with recurrent spontaneous abortion. So we report this case with a brief review of literatures.

• Clinical and Experimental Reproductive Medicine
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• 제29권3호
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• pp.187-193
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• 2002

Objective : To analyze the interrelationship between homocysteine and methylenetetrahydrofolate reductase (MTHFR) mutation in patients with recurrent spontaneous abortion. Material and Method: Homocysteine and MTHFR mutation were tested by fluorescent polarizing immunoassay and PCR-RFLP method, respectively. Results: In patients with homocysteine level less than 5 ?mol/L, there was no case of normal group but there were four cases of heterozygosity and one case of homozygosity. In patients with homocysteine level 5$\sim$10 ? mol/L, the number of normal, heterozygosity and homozygosity group were eleven, eighteen and eight, respectively. In patients with homocysteine level $10{\sim}15$ ? mol/L, the number of normal, heterozygosity and homozygosity group were four, one and one, respectively. In patients with homocysteine level more than 15 ? mol/L, there was no case of normal and heterozygosity group but there were two cases of homozygosity. Conclusions: Hyperhomocysteinemia due to MTHFR mutation is a cause of recurrent spontaneous abortion. And there was a significant relationship between homocysteine and MTHFR mutation.

• Clinical and Experimental Reproductive Medicine
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• 제25권3호
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• pp.277-280
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• 1998

Antiphospholipid antibody is an immunoglobulin which may be of any class and which reacts with any phospholipid. For clinical use the definition of the term anti-phospholipid antibody is usually restricted to IgG and/or IgM antibody directed against the negatively charged phopholipids, cardiolipin, phosphatidyl inositol, phosphatidyl serine, or phosphatidic acid. The antigen of the serological test for syphilis is cardiolipin; negatively charged phopholipids are understood to be antigens to which lupus anticoagulants are directed. The term 'anticardiolipin' antibody syndrome, 'antiphospholipid' antibody syndrome, and 'lupus anticoagulant' syndrome are often, imprecisely, used interchangeably. We have experienced a case of recurrent spontaneous abortion with antiphospholipid antibody. So we report this case with a brief review of literatures.

• 한국유전체학회:학술대회논문집
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• 한국유전체학회 2004년도 The 13th Korea Genome Conference
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• pp.39.1-39.1
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• 2004

• 대한생식의학회:학술대회논문집
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• 대한불임학회 2006년도 제51차 추계학술대회
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• pp.31-34
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• 2006

• Clinical and Experimental Reproductive Medicine
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• 제26권1호
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• pp.123-126
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• 1999

A successful outcome of pregnancy requires an efficient uteroplacental vascular system. Since this system may be compromised by disorders of haemostasis associated with a prothrombotic state, maternal thrombophilia might be a risk factor for fetal loss. Hereditary deficiencies of the naturally occuring anticoagulants are well recognized conditions predisposing to recurrent venous thromboembolism. Since thrombotic phenomena have been implied as a cause of abortion and stillbirth, these deficiencies might increase the risk of fetal demise. We have experienced a case of antiphospholipid syndrome associated with protein C deficiency in patient with recurrent spontaneous abortion. So we report this case with a brief review of literatures.

• 혜화의학회지
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• 제18권2호
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• pp.95-104
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• 2009

This study was carried out through the investigation of Oriental and Western medical literature and we was discovered these conclusions about the etiology, treatment, prescription of habitual abortion. The result of this study were as follows : 1. The habitual abortion does agree with 'Hwaltae(滑胎)' and means that spontaneous abortion repeats three times or more. 2. The etiology of habitual abortion is divided 'Deficiency of kidney'(腎虛), 'Deficiency of vital energy and blood'(氣血虛弱), 'Deficiency of yin'(陰虛), 'Clotted blood'(瘀血). 3. By means of cause, the treatment of habitual abortion was mainly made use of 'Tonifying kidney and promoting spleen'(補腎健脾), 'Invigorating vital energy and nourishing blood'(補氣補血), 'Supplementing yin fluid and alleviating fever'(滋陰淸熱), 'Resuscitating blood and removing clotted blood'(活血祛瘀). 4. By means of cause, the prescription of habitual abortion was frequent made use of Bosingochunghwan(補腎固沖丸), Bosingotae$\breve{u}$m(補腎固胎飮), Taesanbans$\breve{o}$ksan(泰山磐石散), $Ch\breve{o}ng\breve{u}mboinghwan$(千金保孕丸), Agyotang(阿膠湯), Gungguibojungtang(芎歸補中湯), Taewon$\breve{u}$m(胎元飮), Gotaej$\breve{o}$n(固胎煎), Baekchulj$\breve{o}$n(白朮煎), Sas$\breve{o}$ngsan(四聖散), Gyegibokryonghwan(桂枝茯苓丸), $Dangguich\breve{o}ng\breve{u}mtang$(當歸千金湯). 5. The Western medical etiology of habitual abortion(recurrent spontaneous early pregnancy loss) is divided Genetic factor(Chromosome aberration), Anatomical deformity, Endocrinologic disorder, Infection, Immunologic factor, Unknown factor(Others).

• 대한생식의학회:학술대회논문집
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• 대한불임학회 1997년도 제34차 추계 학술대회
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• pp.66-67
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• 1997

• Journal of Genetic Medicine
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• 제2권2호
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• pp.59-63
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• 1998

Between 1988-1998, cytogenetic analyses were performed for 1,476 couples and 162 women with recurrent abortions. We applied GTG-banding, high resolution-banding and FISH (fluorescent in situ hybridization) techniques in this study. The frequency of balanced translocations was 3.6% (112/3114). Of them, 74 cases (2.38%) were reciprocal translocations and 38 (1.22%) were robertsonian translocations. Chromosome aberrations were more frequent in women (80 cases) than in men (32 cases). No phenotypical abnormalities were found in all carriers who had experienced recurrent spontaneous abortions or experienced giving birth to malformed offsprings. Prenatal cytogenetic analyses were carried out on 40 subsequent pregnancies for carrier couples with balanced translocation. The fetal karyotypes showed that 13 cases (32.5%) were normal, 25 (62.5%) were balanced translocations, and two (6%) were unbalanced translocations. It is believed that the frequency of chromosomal abnormalities in patients with recurrent spontaneous abortion is higher than that of the normal population. Most of the fetal samples showed normal karyotypes or balanced translocations matching that of one of their parents. Although the incidence of chromosomal imbalance in the fetuses was relatively low in prenatal cytogenetic analysis, individuals with balanced translocations are predisposed to giving birth to malformed offsprings with partial trisomy or monosomy. Therefore, we recommend the cytogenetic and the prenatal cytogenetic analysis for those who experiences recurrent abortion as well as in case they become pregnant, to prevent the birth of offsprings with chromosomal abnormalities.

• Journal of Microbiology and Biotechnology
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• 제32권6호
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• pp.792-799
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• 2022

As a vital problem in reproductive health, recurrent spontaneous abortion (RSA) affects about 1% of women. We performed this study with an aim to explore the molecular mechanism of interleukin-23 (IL-23) and find optimal or effective methods to improve RSA. First, ELISA was applied to evaluate the expressions of IL-23 and its receptor in HTR-8/SVneo cells after IL-23 treatment. CCK-8, TUNEL, wound healing and transwell assays were employed to assess the proliferation, apoptosis, migration and invasion of HTR-8/SVneo cells, respectively. Additionally, the expressions of apoptosis-, migration-, epithelial-mesenchymal transition- (EMT-) and p38 MAPK signaling pathway-related proteins were measured by western blotting. To further investigate the relationship between IL-23 and p38 MAPK signaling pathway, HTR-8/SVneo cells were treated for 1 h with p38 MAPK inhibitor SB239063, followed by a series of cellular experiments on proliferation, apoptosis, migration and invasion, as aforementioned. The results showed that IL-23 and its receptors were greatly elevated in IL-23-treated HTR-8/SVneo cells. Additionally, IL-23 demonstrated suppressive effects on the proliferation, apoptosis, migration, invasion and EMT of IL-23-treated HTR-8/SVneo cells. More importantly, the molecular mechanism of IL-23 was revealed in this study; that is to say, IL-23 inhibited the proliferation, apoptosis, migration, invasion and EMT of IL-23-treated HTR-8/SVneo cells via activating p38 MAPK signaling pathway. In conclusion, IL-23 inhibits trophoblast proliferation, migration, and EMT via activating p38 MAPK signaling pathway, suggesting that IL-23 might be a novel target for the improvement of RSA.