Minimally invasive surgery for deep endometriosis

Angela Cho,Chul-Min Park 대한산부인과학회 2024 Obstetrics & Gynecology Science Vol.67 No.1

Deep endometriosis (DE) is endometriotic tissue that invades the peritoneum by >5 mm. Surgery is the treatment of choice for symptomatic DE, and laparoscopic surgery is preferred over laparotomy due to better vision and postoperative pain. In this review, we aimed to collect and summarize recent literature on DE surgery and share laparoscopic procedures for rectovaginal and bowel endometriosis.

Does deep learning-based colposcopy image analysis predict high grade squamous intraepithelial lesion (HSIL) better than cervical cytology or HPV test?

( Angela Cho ),( Eun Seo Shin ),( Chul Min Park ),( Sung Yeob Kim ) 대한산부인과학회 2022 대한산부인과학회 학술대회 Vol.108 No.-

Objective: Recently, many studies have been conducted on colposcopy image analysis based on deep learning. The classification accuracy for cervical intraepithelial neoplasia using deep learning has been reported to be about 60-80%. The purpose of this study is to investigate whether deep learning based colposcopy image reading could be a stronger predictor for HSIL compared to other clinical factors. Methods: We retrospectively reviewed 987 patients who underwent colposcopy from 2017 to 2019 at Jeju national university hospital. The patients with missing cytology or HPV test were excluded. Adenocarcinoma in situ and invasive carcinoma were excluded due to their small numbers. The probability that colposcopy image is HSIL was calculated by the deep learning model trained on 20,000 photos which we had made in our previous study. To identify the predictors of pathologically confirmed HSIL, univariate analyses were performed using chi-square test or Fishers exact test. To explore the relative contributions of the various factors, multivariate logistic regression analysis including cervical cytology, HPV test, and calculated HSIL probability by deep learning model was conduct. Results: A total of 892 patients were analyzed. 89% of patients had cervical cytology results with ASCUS or worse. The patients with positive HPV test was 75%. The patients who underwent punch biopsy and Loop Electrosurgical Excision Procedure (LEEP) were 59% and 25%, respectively. For every 1% increase in the HSIL probability predicted by deep learning, the odds of HSIL increase by 2.4%. Independent predictors of HSIL on multivariate logistic regression were HSIL or ASC-H cytology (OR = 10.95), positive HPV (OR = 5.44), and HSIL on colposcopy image classification by deep learning (OR = 2.16): all P < 0.05. Conclusion: Although HSIL prediction through deep learning of colposcopy images achieved statistical significance, it is not robust compared to cervical cytology or HPV test.

Outcomes and prognostic factors of surgically treated extramammary Paget’s disease of the vulva

Angela Cho,Dae Yeon Kim,Dae-Shik Suh,Jong-Hyeok Kim,Yong-Man Kim,Young-Tak Kim,Jeong-Yeol Park 대한부인종양학회 2023 Journal of Gynecologic Oncology Vol.34 No.6

Objective: Extramammary Paget’s disease (EMPD) of the vulva is a rare disease which predominantly presents in postmenopausal Caucasian women. As yet, no studies on Asian female patients with EMPD have been performed. This study aimed to identify the clinical features of patients with vulvar EMPD in Korea, and to evaluate the risk factors of recurrence and postoperative complications in surgically treated EMPD. Methods: We retrospectively reviewed 47 patients with vulvar EMPD who underwent wide local excision or radical vulvectomy. The clinical data and surgical and oncological outcomes following surgery were extracted from medical records and analyzed. Univariate and multivariate analyses for predicting recurrence and postoperative complications were performed. Results: 21.3% of patients had complications after surgery, and wound dehiscence was the most common. 14.9% of patients experienced recurrence, and the median interval to recurrence from initial treatment was 69 (range 33–169) months. Vulvar lesions larger than 40 mm was the independent risk factor of postoperative complications (odds ratio [OR]=7.259; 95% confidence interval [CI]=1.545–34.100; p=0.012). Surgical margin status was not associated with recurrence in surgically treated vulvar EMPD patients (OR=0.83; 95% CI=0.16–4.19; p=1.000). Conclusion: Positive surgical margin is a frequent finding in the patients with vulvar EMPD, but disease recurrence is not related with surgical margin status. Since EMPD is a slow growing tumor, a surveillance period longer than 5 years is required.

Fostering Interdisciplinary Connections: Transforming Advanced Korean Language Curriculum

( Angela Lee-smith ),( Haewon Cho ),( Mijeong Mimi Kim ) 국제한국어교육학회 2021 국제한국어교육학회 학술대회논문집 Vol.2021 No.-

Simvastatin Reduces Lipopolysaccharides-Accelerated Cerebral Ischemic Injury via Inhibition of Nuclear Factor-kappa B Activity

( Angela M. A. Anthony Jalin ),( Jae-chul Lee ),( Geum-sil Cho ),( Chunsook Kim ),( Chung Ju ),( Kisoo Pahk ),( Hwa Young Song ),( Won-ki Kim ) 한국응용약물학회 2015 Biomolecules & Therapeutics(구 응용약물학회지) Vol.23 No.6

Preceding infection or inflammation such as bacterial meningitis has been associated with poor outcomes after stroke. Previously, we reported that intracorpus callosum microinjection of lipopolysaccharides (LPS) strongly accelerated the ischemia/reperfusion-evoked brain tissue damage via recruiting inflammatory cells into the ischemic lesion. Simvastatin, 3-hydroxy-3-methylgultaryl (HMG)-CoA reductase inhibitor, has been shown to reduce inflammatory responses in vascular diseases. Thus, we investigated whether simvastatin could reduce the LPS-accelerated ischemic injury. Simvastatin (20 mg/kg) was orally administered to rats prior to cerebral ischemic insults (4 times at 72, 48, 25, and 1-h pre-ischemia). LPS was microinjected into rat corpus callosum 1 day before the ischemic injury. Treatment of simvastatin reduced the LPS-accelerated infarct size by 73%, and decreased the ischemia/reperfusion-induced expressions of pro-inflammatory mediators such as iNOS, COX-2 and IL-1β in LPS-injected rat brains. Howeve , simvastatin did not reduce the infiltration of microglial/macrophageal cells into the LPS-pretreated brain lesion. In vitro migration assay also showed that simvastatin did not inhibit the monocyte chemoattractant protein-1-evoked migration of microglial/macrophageal cells. Instead, simvastatin inhibited the nuclear translocation of NF-κB, a key signaling event in expressions of various proinflammatory mediators, by decreasing the degradation of IκB. The present results indicate that simvastatin may be beneficial particularly to the accelerated cerebral ischemic injury under inflammatory or infectious conditions.

Simvastatin Reduces Lipopolysaccharides-Accelerated Cerebral Ischemic Injury via Inhibition of Nuclear Factor-kappa B Activity

Jalin, Angela M.A. Anthony,Lee, Jae-Chul,Cho, Geum-Sil,Kim, Chunsook,Ju, Chung,Pahk, Kisoo,Song, Hwa Young,Kim, Won-Ki The Korean Society of Applied Pharmacology 2015 Biomolecules & Therapeutics(구 응용약물학회지) Vol.23 No.6

Preceding infection or inflammation such as bacterial meningitis has been associated with poor outcomes after stroke. Previously, we reported that intracorpus callosum microinjection of lipopolysaccharides (LPS) strongly accelerated the ischemia/reperfusionevoked brain tissue damage via recruiting inflammatory cells into the ischemic lesion. Simvastatin, 3-hydroxy-3-methylgultaryl (HMG)-CoA reductase inhibitor, has been shown to reduce inflammatory responses in vascular diseases. Thus, we investigated whether simvastatin could reduce the LPS-accelerated ischemic injury. Simvastatin (20 mg/kg) was orally administered to rats prior to cerebral ischemic insults (4 times at 72, 48, 25, and 1-h pre-ischemia). LPS was microinjected into rat corpus callosum 1 day before the ischemic injury. Treatment of simvastatin reduced the LPS-accelerated infarct size by 73%, and decreased the ischemia/reperfusion-induced expressions of pro-inflammatory mediators such as iNOS, COX-2 and IL-$1{\beta}$ in LPS-injected rat brains. However, simvastatin did not reduce the infiltration of microglial/macrophageal cells into the LPS-pretreated brain lesion. In vitro migration assay also showed that simvastatin did not inhibit the monocyte chemoattractant protein-1-evoked migration of microglial/macrophageal cells. Instead, simvastatin inhibited the nuclear translocation of NF-${\kappa}B$, a key signaling event in expressions of various proinflammatory mediators, by decreasing the degradation of $I{\kappa}B$. The present results indicate that simvastatin may be beneficial particularly to the accelerated cerebral ischemic injury under inflammatory or infectious conditions.

Poster Session 2 : Protein Structure and Function Signal Transduction ; Conjugated Linoleic Acid (CLA) Inhibits Coupling of Heregulin (HRG) Signaling to Protein Kinase B/Akt via ErbB3 Phosphorylation in HT-29 Human Colon Cancer Cells

( Han J. Cho ),( Woo K. Kim ),( Eun J. Kim ),( Kyeong C. Jung ),( Soo Chul Park ),( Hyun S. Lee ),( Angela L. Tyner ),( Jung H. Y. Park ) 한국생화학분자생물학회 (구 한국생화학회) 2002 추계학술대회집 Vol.2002 No.-

Clear Cell Adenocarcinoma Originated from Adenomyosis

Sunwha Park,Angela Cho,Chul Min Park 이화여자대학교 의과학연구소 2019 EMJ (Ewha medical journal) Vol.42 No.1

A 66-year-old postmenopausal woman received routine gynecologic check-up. Transvaginal ultrasonography and abdominal and pelvic computed tomography showed about 5-cm cystic mass in uterus with solid component and the patient had thin endometrium and the serum level of CA 125 was normal. We performed a total hysterectomy and bilateral salpingo-oophorectomy and found tumor which had brownish cystic fluid and about 2 cm sized and colored in light yellowish, polypoid protruding solid mass, located within the myometrial wall. Histopathological examination of frozen section revealed malignancy. The tumor was confined within the myometrium and its histologic type was clear cell adenocarcinoma. Finally we identified that the myometrial mass was clear cell adenocarcinoma originated from adenomyosis pathologically. The malignant transformation of adenomyosis is very rare. When we find a cystic change with solid component in adenomyosis patients, clear cell adenocarcinoma should be suspected as a differential diagnosis and magnetic resonance imaging should be considered for further evaluation.

Early emergence of <i>de novo EGFR</i> T790M gatekeeper mutations during erlotinib treatment in PC9 non-small cell lung cancer cells

Kim, Sujin,Park, Angela KJ.,Cho, Jeonghee Elsevier 2018 Biochemical and biophysical research communication Vol.503 No.2

<P><B>Abstract</B></P> <P>The emergence of the T790M gatekeeper mutation in the <I>Epidermal Growth Factor Receptor</I> (<I>EGFR</I>) gene is an important mechanism that can lead to the acquired resistance to EGFR-targeted tyrosine kinase inhibitors such as erlotinib or gefitinib. These drugs have been used in treating a subset of non-small cell lung cancer (NSCLC) patients harboring <I>EGFR</I> activating mutations. Here we investigated the paths leading to the acquisition of the T790M mutation by establishing an erlotinib resistant PC9 cell model harboring ectopically introduced <I>EGFR</I> cDNA. We detected the emergence of T790M mutation within the <I>EGFR</I> cDNA in a subset of erlotinib resistant PC9 cell models through Sanger sequencing and droplet digital PCR-based methods, demonstrating that T790M mutation can emerge via <I>de novo</I> events following treatment with erlotinib. In addition, we show that the <I>de novo</I> T790M bearing erlotinib resistant PC9 cells are sensitive to the 3rd generation EGFR-targeted drug, WZ4002. Furthermore, GFP-based competition cell proliferation assays reveal that PC9 cells ectopically expressing EGFR mutant become more rapidly resistant to erlotinib than parental PC9 cells through the acquisition of the T790M mutation. Taken together, we believe that our findings expand upon the previous notion of evolutionary paths of T790M development, providing an important clue to designing a therapeutic strategy to overcome drug resistance.</P>

Postmortem proteomics to discover biomarkers for forensic PMI estimation

Choi, Kyoung-Min,Zissler, Angela,Kim, Eunjung,Ehrenfellner, Bianca,Cho, Eunji,Lee, Se-in,Steinbacher, Peter,Yun, Ki Na,Shin, Jong Hwan,Kim, Jin Young,Stoiber, Walter,Chung, Heesun,Monticelli, Fabio Ca Springer Berlin Heidelberg 2019 International journal of legal medicine Vol.133 No.3

<P>The assessment of postmortem degradation of skeletal muscle proteins has emerged as a novel approach to estimate the time since death in the early to mid-postmortem phase (approximately 24 h postmortem (hpm) to 120 hpm). Current protein-based methods are limited to a small number of skeletal muscle proteins, shown to undergo proteolysis after death. In this study, we investigated the usability of a target-based and unbiased system-wide protein analysis to gain further insights into systemic postmortem protein alterations and to identify additional markers for postmortem interval (PMI) delimitation. We performed proteomic profiling to globally analyze postmortem alterations of the rat and mouse skeletal muscle proteome at defined time points (0, 24, 48, 72, and 96 hpm), harnessing a mass spectrometry-based quantitative proteomics approach. Hierarchical clustering analysis for a total of 579 (rat) and 896 (mouse) quantified proteins revealed differentially expressed proteins during the investigated postmortem period. We further focused on two selected proteins (eEF1A2 and GAPDH), which were shown to consistently degrade postmortem in both rat and mouse, suggesting conserved intra- and interspecies degradation behavior, and thus preserved association with the PMI and possible transferability to humans. In turn, we validated the usefulness of these new markers by classical Western blot experiments in a rat model and in human autopsy cases. Our results demonstrate the feasibility of mass spectrometry–based analysis to discover novel protein markers for PMI estimation and show that the proteins eEF1A2 and GAPDH appear to be valuable markers for PMI estimation in humans.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (10.1007/s00414-019-02011-6) contains supplementary material, which is available to authorized users.</P>