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Keun hyung Cho,Hyun-Sik Na,JooYeon Jhun,Jiyoung Kim,Seung Yoon Lee,Jeong soo Lee,In Gyu Um,Seok Jung Kim,Mi-La Cho 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
Osteoarthritis (OA) is a disease that reduces quality of life due to pain caused by persistent joint destruction. In addition, as a representative chronic disease, it causes inflammation and affects immunity, and it is one of the diseases that is difficult to cure, so treatment and improvement methods are urgently needed. In a previous study, we published that LA-1 improves osteoarthritis and has cartilage protection by controlling inflammation. However, it was not known how LA-1 improves osteoarthritis in the body. So in this study, it was confirmed that the administration of LA-1 to the MIA-induced OA rat model reduces the pain threshold, protects cartilage, and regulates inflammation markers in the articular synovium. Additionally, collecting and analyzing the feces of the disease model, it affected the gastrointestinal system and improved the environment of the microbiome. Interestingly, by providing LA-1, it was confirmed that the diversity and abundance of microbiome in the intestine were changed, and that the bacteria that produced SCFAs increased. In addition, daily supply of butyrate, one of the SCFAs produced by certain bacteria, triggers autophagy activation and tends to decrease necroptosis. This suggests that systemic immunity as well as OA is regulated according to changes in the intestinal microbial community, and that activation of autophagy can indirectly reduce abnormal cell death. In addition, assuming that osteoarthritis is a chronic degenerative disease, cell analysis was performed using splenocyte and blood assuming that the immune system is deteriorated. As a result, both splenocytes and PBMCs confirmed that regulatory T cells increased and Th17 cells decreased. In summary, providing LA-1 leads to increased production of SCFAs by altering the microbes in the intestine. Accordingly, it is possible to suppress the progression of OA and control pain due to OA, and improve an abnormal joint environment by controlling autophagy and necroptosis.
여자 테니스 선수의 양손 백핸드 스트로크 동작시 상지의 근전도 분석
유국종,서국웅,윤양진,이훈식,정미라,서국은 한국운동역학회 2000 한국운동역학회지 Vol.9 No.2
This study analzed AEMG, muscle activity duration time, peak value and work load of six high school student players, three college student players, three business team players in order to analyze Arm's EMG when they play games with two-handed backhand stroke. The instruments of measuring EMG are muscle tester ME3000p. And measured parts of muscle are the triceps brachii, biceps brachii, brachioradialis and flexor carpi radialis of body left and right arm. The following is the result according to the analysis of raw data and statistics. 1. The AEMG of trained group was higher than the untrained. In both groups AEMG of right arm was higher than left one. And AEMG of forearm was higher than upperarm. The order of high AEMG among the trained is as followed ; right biceps brachii, left brachii, right brachioradialis. Among the untrained ; right brachioradialis, left brachioradialis, biceps brachii. 2. The muscle activity duration time of the trained group was totally shorter than the untrained. In both groups muscle activity duration time of the right arm was shorter than the left one. As to trained muscle activity duration time of upperarm is shorter than the forearm. Contrarily, as to untrained muscle activity duration time forearm is shorter than the upperarm. The order of short muscle activity duration time among the trained is as followed ; right biceps brachii, triceps brachii, left flexor carpi radialis. 3. The peak value of trained group was higher than the untrained. In body groups peak value of the right arm was higher than the left one. As to the trained the peak of the upperarm is higher than the forearm. Contrarily, as to the untrained, the peak value of the forearm was higher the upperarm. The order of high peak value among the trained is as followed ; right biceps brachii, left biceps brachii, right brachioradialis. Among the untrained, right brachioradialis, left biceps brachii, brachioradialis.
급격히 악화된 예후를 보인 자궁경부에 발생한 악성 혼합뮐러종양
김미경 ( Mi Kyoung Kim ),김미라 ( Mi La Kim ),심정연 ( Jeong Yun Shim ),성석주 ( Seok Ju Seong ),윤보성 ( Bo Sung Yoon ),송태종 ( Tae Jong Song ),이효진 ( Hyo Jin Yi ),정용욱 ( Yong Wuk Jung ) 대한산부인과학회 2012 Obstetrics & Gynecology Science Vol.55 No.12
Malignant mixed Mullerian tumor (MMMT) is a type of cancer that contains two cell types known as the adenocarcinoma and sarcoma. MMMT is a rare malignant cancer of the genital tract and particularly the prevalence of MMMT in the cervix is extremely rare. Due to the rare incidence of MMMT in cervix, its treatment has unestablished guidelines and has unclear prognosis. Based on the previous data, the prognosis of MMMT in the cervix is better than the prognosis of uterine MMMT. Here, we are reporting a case of cervix MMMT that is rapidly progressive with an extremely poor prognosis, which contradicts the previous data.
Kwon, Mi Jeong,Kim, Sung-Su,Choi, Yoon-La,Jung, Hun Soon,Balch, Curt,Kim, Su-Hyeong,Song, Yong-Sang,Marquez, Victor E.,Nephew, Kenneth P.,Shin, Young Kee Oxford University Press 2010 Carcinogenesis Vol.31 No.6
<P>Unlike epigenetic silencing of tumor suppressor genes, the role of epigenetic derepression of cancer-promoting genes or oncogenes in carcinogenesis remains less well understood. The tight junction proteins claudin-3 and claudin-4 are frequently overexpressed in ovarian cancer and their overexpression was previously reported to promote the migration and invasion of ovarian epithelial cells. Here, we show that the expression of claudin-3 and claudin-4 is repressed in ovarian epithelial cells in association with promoter ‘bivalent’ histone modifications, containing both the activating trimethylated histone H3 lysine 4 (H3K4me3) mark and the repressive mark of trimethylated histone H3 lysine 27 (H3K27me3). During ovarian tumorigenesis, derepression of <I>CLDN3</I> and <I>CLDN4</I> expression correlates with loss of H3K27me3 in addition to trimethylated histone H4 lysine 20 (H4K20me3), another repressive histone modification. Although <I>CLDN4</I> repression was accompanied by both DNA hypermethylation and repressive histone modifications, DNA methylation was not required for <I>CLDN3</I> repression in immortalized ovarian epithelial cells. Moreover, activation of both <I>CLDN3</I> and <I>CLDN4</I> in ovarian cancer cells was associated with simultaneous changes in multiple histone modifications, whereas H3K27me3 loss alone was insufficient for their derepression. <I>CLDN4</I> repression was robustly reversed by combined treatment targeting both DNA demethylation and histone acetylation. Our study strongly suggests that in addition to the well-known chromatin-associated silencing of tumor suppressor genes, epigenetic derepression by the conversely related loss of repressive chromatin modifications also contributes to ovarian tumorigenesis via activation of cancer-promoting genes or candidate oncogenes.</P>
Kwon, Jeong-eun,Lee, Seon-Yeong,Seo, Hyeon-Beom,Moon, Young-Mee,Ryu, Jun-Geol,Jung, Kyung-Ah,Jhun, Joo-Yeon,Park, Jin-Sil,Hwang, Soo-Seok,Kim, Joo-Myeong,Lee, Gap Ryol,Park, Sung-Hwan,Cho, Mi-La Elsevier 2018 Immunology letters Vol.197 No.-
<P><B>Abstract</B></P> <P>Yin Yang 1 (YY1) is a ubiquitously expressed transcription factor that functions in cooperation with various cofactors to regulate gene expression. In the immune system, YY1 enhances cytokine production and T helper (Th) 2 effector cell differentiation, resulting in the activation of inflammation. However, no studies have reported the role of YY1 in Th17 cell regulation, which is implicated in rheumatoid arthritis (RA). We investigated the expression of YY1 in Th17 cells <I>in vitro</I> and revealed increased levels of YY1 mRNA and protein. To elucidate the function of YY1 pathogenesis in RA, we used a collagen-induced arthritis (CIA) mouse model with YY1 deficiency. Deficiency of YY1 reduced the severity of arthritis and joint destruction. Moreover, Th17 cells were dramatically reduced in YY1-deficient mice. The cytokine interleukin (IL)-17 was decreased in YY1-deficient CD4+ T cells <I>ex vivo</I> and <I>in vivo</I>. Interestingly, the level of signal transducer and activator of transcription 3 (STAT3), tumor necrosis factor-α, IL-17, IL-6, and IL-1β were markedly decreased in YY1-deficient mice with CIA. The cytokine-inducing function of YY1 was more specific to IL-17 than to interferon-γ. YY1 plays a role in Th17 cell differentiation and RA pathogenesis. Our findings suggest that future RA therapies should target the regulatory mechanism involved in Th17 cell differentiation, in which YY1 may cooperate with the STAT3 signaling pathway.</P> <P><B>Highlights</B></P> <P> <UL> <LI> YY1 as new target for RA therapies involved in Th17 cell differentiation. </LI> </UL> </P>