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Kim, Eun Ji,Choi, Mi-Ran,Park, Heesook,Kim, Minhee,Hong, Ji Eun,Lee, Jae-Yong,Chun, Hyang Sook,Lee, Ki Won,Yoon Park, Jung Han BioMed Central 2011 Breast cancer research Vol.13 No.4
<P><B>Introduction</B></P><P>High-fat diets (HFDs) are known to cause obesity and are associated with breast cancer progression and metastasis. Because obesity is associated with breast cancer progression, it is important to determine whether dietary fat <I>per se </I>stimulates breast cancer progression in the absence of obesity. This study investigated whether an HFD increases breast cancer growth and metastasis, as well as mortality, in obesity-resistant BALB/c mice.</P><P><B>Methods</B></P><P>The 4-week-old, female BALB/c mice were fed HFD (60% kcal fat) or control diet (CD, 10% kcal fat) for 16 weeks. Subsequently, 4T1 mammary carcinoma cells were injected into the inguinal mammary fat pads of mice fed continuously on their respective diets. Cell-cycle progression, angiogenesis, and immune cells in tumor tissues, proteases and adhesion molecules in the lungs, and serum cytokine levels were analyzed with immunohistochemistry, Western blotting, and enzyme-linked immunosorbent assay (ELISA). <I>In vitro </I>studies were also conducted to evaluate the effects of cytokines on 4T1 cell viability, migration, and adhesion.</P><P><B>Results</B></P><P>Spleen and gonadal fat-pad weights, tumor weight, the number and volume of tumor nodules in the lung and liver, and tumor-associated mortality were increased in the HFD group, with only slight increases in energy intake and body weight. HF feeding increased macrophage infiltration into adipose tissues, the number of lipid vacuoles and the expression of cyclin-dependent kinase (CDK)2, cyclin D1, cyclin A, Ki67, CD31, CD45, and CD68 in the tumor tissues, and elevated serum levels of complement fragment 5a (C5a), interleukin (IL)-16, macrophage colony-stimulating factor (M-CSF), soluble intercellular adhesion molecule (sICAM)-1, tissue inhibitors of metalloproteinase (TIMP)-1, leptin, and triggering receptor expressed on myeloid cells (TREM)-1. Protein levels of the urokinase-type plasminogen activator, ICAM-1, and vascular cell adhesion molecule-1 were increased, but plasminogen activator inhibitor-1 levels were decreased in the lungs of the HFD group. <I>In vitro </I>assays using 4T1 cells showed that sICAM-1 increased viability; TREM-1, TIMP-1, M-CSF, and sICAM-1 increased migration; and C5a, sICAM-1, IL-16, M-CSF, TIMP-1, and TREM-1 increased adhesion.</P><P><B>Conclusions</B></P><P>Dietary fat increases mammary tumor growth and metastasis, thereby increasing mortality in obesity-resistant mice.</P>
( Yoo-kyung Lee ),( Kyung-a So ),( Mi-kyung Kim ),( In-ho Lee ),( Tae-jin Kim ),( Kyung-taek Lim ),( Ki-heon Lee ),( Sung Ran Hong ) 대한산부인과학회 2016 대한산부인과학회 학술대회 Vol.102 No.-
목적: Objective: Regression rates for atypical squamous cells of undetermined significance (ASCUS) or low-grade squamous intraepithelial lesion (LSIL) range widely, from 30% to 80%. The objective of this study was to investigate the predictive value of p16/Ki-67 dual-stained cytology for the progression of disease. 방법: Method: Cytology p16/Ki-67 dual-staining test was performed on 691 liquid-based residual samples from a cohort of women with ASC-US/ LSIL and co-testing human papillomavirus (HPV) positive. Among them, 250 women were followed up for at least a year. Study end points were HSIL detection in 1 and 2 year’s follow-up. 결과: Results: Positivity of p16/Ki-67 dual stained cytology was well correlated to progression of disease compared with positivity of HPV 16/18. During 1 year follow-up, 23 of 250 women experienced progression of disease into HSIL. For positivity of p16/Ki-67 dual stained cytology, Sensitivity (60.9%) for the detection of HSIL or specificity (81.5%) for normal or low grade cytology was higher than those of HPV 16/18 tests (13.0% and 89.0%, respectively) (p<0.001). During 2 years follow-up, 11 of 190 women experienced progression of disease into HSIL. For positivity of p16/Ki-67 dual stained cytology, Sensitivity (45.5%) for the detection of HSIL or specificity (82.1%) for normal or low grade cytology was higher than those of HPV 16/18 tests (18.2% and 89.9%, respectively) (p=0.025). 결론: Conclusions: p16/Ki-67 dual stained cytology could provide both high sensitivity and specificity for the prediction of HSIL in Pap cytology in the future. Positive p16/Ki-67 dual-stained cytology in low grade cytology was highly associated with the progression of disease in 1 or 2 years follow- up. Therefore, in cases of positive dual-stained cells morphologically showing benign atypical features, further follow-up would be necessary.
( Ki-Nam Shim ),( Eun Mi Song ),( Yoon Tae Jeen ),( Jin-Oh Kim ),( Seong Ran Jeon ),( Dong Kyung Chang ),( Hyun Joo Song ),( Yun Jeong Lim ),( Jin Soo Kim ),( Byong Duk Ye ),( Cheol Hee Park ),( Seong 대한소화기기능성질환·운동학회 2015 Gut and Liver Vol.9 No.6
We evaluated the long-term outcome and clinical course of patients of nonsteroidal anti-inflammatory drug (NSAID)-induced small intestinal injury by performing capsule endoscopy (CE). A multicenter retrospective study was conducted using data collected from the CE nationwide database registry, which has been established since 2002. A total of 140 patients (87 males; mean age, 60.6±14.8 years) from the CE nationwide database registry (n=2,885) were diagnosed with NSAID-induced small intestinal injury and enrolled in our study. Forty-nine patients (35.0%) presented with a history of aspirin use and an additional 49 (35.0%) were taking NSAIDs without aspirin. The most prominent findings after performing CE were multiple ulcerations (n=82, 58.6%) and erosions or aphthae (n=32, 22.9%). During the follow-up period (mean, 15.9±19.0 months; range, 0 to 106 months), NSAID-induced small intestinal injury only recurred in six patients (4.3%). Older age and hypertension were positive predictive factors for recurrence. Conclusions: These results suggest that the recurrence of NSAID-induced small bowel injury was not frequent in the presence of conservative treatment. Therefore, the initial diagnosis using CE and the medication history are important. (Gut Liver 2015;9:727-733)