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Hui-Chun Wang,Yu-Bin Wang,Xiao-Hong Chen,Lan-Lan Cui 대한영상의학회 2016 Korean Journal of Radiology Vol.17 No.2
A 48-year-old woman presented with a 50-day history of irregular vaginal bleeding and lower abdominal pain. Ultrasound indicated an extremely large occupying lesion in the pelvic cavity that was highly suggestive of malignancy. Fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) was performed to further assess the nature of pelvic abnormality. PET/CT images demonstrated a diffusely lobulated mass ranging from cervix up to the inferior pole of kidneys with mild FDG uptake. Simultaneously, multiple nodules in bilateral lungs and a hypodense lesion in the right ventricle were shown without FDG-avidity. Based on the imaging results, the presumptive diagnosis was uterine intravenous leiomyomatosis with intracardiac extension and pulmonary benign metastases, which was subsequently confirmed by MRI and the lesion biopsy.
Smads as therapeutic targets for chronic kidney disease
( Hui Yao Lan ) 대한신장학회 2012 Kidney Research and Clinical Practice Vol.31 No.1
Renal fibrosis is a hallmark of chronic kidney disease (CKD). It is generally thought that transforming growth factor-b1 (TGF-b1) is a key mediator of fibrosis and mediates renal scarring positively by Smad2 and Smadbut negatively by Smad7. Our recent studies found that in CKD, TGF-b1 is not a sole molecule to activate Smads. Many mediators such as angiotensin II and advanced glycation end products can also activate Smads via both TGF-b-dependent and independent mechanisms. In addition, Smads can interact with other signaling pathways, such as the mitogen-activated protein kinase and nuclear factor-kappaB (NF-kB) pathways, to regulate renal inflammation and fibrosis. In CKD, Smad2 and Smad3 are highly activated, while Smad7 is reduced or lost. In the context of fibrosis, Smad3 is pathogenic and mediates renal fibrosis by upregulating miR-21 and miR-19 but down-regulating miR-29 and miR-200 families. By contrast, Smad2 and Smad7 are protective. Overexpression of Smad7 inhibits both Smad3-mediated renal fibrosis and NF-kB-driven renal inflammation. Interestingly, Smad4 has diverse roles in renal fibrosis and inflammation. The complexity and distinct roles of individual Smads in CKD suggest that treatment of CKD should aim to correct the imbalance of Smad signaling or target the Smad3-dependent genes related to fibrosis, rather than to block the general effect of TGF-b1. Thus, treatment of CKD by overexpression of Smad7 or targeting Smad3-dependent miRNAs such as downregulation of miR-21 or overexpression of miR-29 may represent novel therapeutic strategies for CKD.
Hui Lan Xu,Woo Yang Chung 한국목재공학회 2012 목재공학 Vol.40 No.5
Mass transfer behavior in wood was estimated through its microscopic structure. The diffusion coefficients which were decided by theoretical equations are influenced by different anatomical properties of wood. From the experiment, the moisture flux was linear to the square root of time. The diffusion coefficients had a regular tendency during the time elapse. During the modeling, it is necessary to understand the limitation of parameters and consider the particular situation to be simulated. In hardwood, because the apertures were not considered, tangential mass transfer simulation was totally different from experiment. As a result, a hardwood model design should consider the apertures which are even on the fiber walls.
Hui Tan,Hui Ling,Jie He,Lan Yi,Jianguo Zhou,Min Lin,Qi Su 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.6
We investigated the effects of diallyl disulfide (DADS) on the induction of apoptosis in human Leukemia cell line HL-60 and explored the roles of mitogen-activated protein kinase (ERK and p38 MAPK) pathways in the growth inhibition and apoptosis induced by DADS. MTT assay was used to determine the DADS induced cell growth inhibition in HL-60 cells. Flow cytometry and DNA fragmentation were used to examine the roles of apoptosis in DADS-mediated cell death. Western blot analysis of the expression of phospho-MAPKs (ERK and p38) was employed to elucidate the possible mechanisms of DADS induced apoptosis. We found that growth inhibition of HL-60 cells treated with DADS exhibited a dose-dependent response (P<0.05) and DADS induced significant apoptosis. DADS at the concentration of 10 mg/L persistently activated p38 and simultaneously reduced ERK activity. PD98059, an inhibitor of ERK upstream activators MAPK kinase MKK1 and MKK2, promoted cytotoxicity and apoptosis in HL-60 cells treated with DADS. In contrast, SB203580, an inhibitor of p38, decreased cytotoxicity and apoptosis induced by DADS. Therefore, DADS can effectively inhibit the proliferation and induce apoptosis of human leukemia cell line HL-60. Inhibition of ERK signaling pathways and activation of p38 signaling pathways are likely involved in DADS induced apoptosis in HL- 60 cells.
EVALUATION OF THE ANTITUMOR ACTIVITY BY CdTe QDs WITH VERBASCOSIDE
XIAO-HUI ZHAO,HUI-LAN YUE,PING LI,XIN ZENG,GEN ZHANG 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2013 NANO Vol.8 No.3
Cadmium telluride quantum dots (QDs) have received significant attention in biomedical research because of their potential in drug delivery. In this study, the chemotherapeutic agent Verbascoside (VB) was immobilized successfully onto CdTe QDs by covalent bonding between the –OH group of VB and the –COOH group of CdTe QDs. The amount of VB that could be immobilized depended on the concentration of –COOH groups (succinic acid) on the surface of the CdTe QDs. Apoptotic staining, DNA fragmentation and flow cytometry analysis further demonstrated that compared with CdTe QDs or VB treatment alone, the apoptosis rate increased after the treatment of CdTe QDs together with VB (VB–QDs) in HepG2/ADM cells. We observed that VB–QDs treatment could clearly activate apoptosis-related Caspase 3 expression in HepG2/ADM cells. Moreover, our in vivo study indicated that the treatment of VB–QDs effectively inhibited the human hepatoma HepG2/ADM nude mice tumor growth. The increased cell apoptosis rate was closely correlated with the enhanced inhibition of tumor growth in the studied animals. Thus, VB–QDs may serve as a possible alternative for therapeutic approaches for some cancer treatments. In summary, studies have shown that cancer cells are treated by the presence of VB–QDs nanoparticles based on analysis of cell apoptosis.