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1.
Korean J Med Educ ; 36(1): 65-79, 2024 Mar.
Article in English | MEDLINE | ID: mdl-38462243

ABSTRACT

Augmented reality technology had developed rapidly in recent years and had been applied in many fields, including medical education. Augmented reality had potential to improve students' knowledge and skills in medical education. This scoping review primarily aims to further elaborate the current studies on the implementation of augmented reality in advancing clinical skills. This study was conducted by utilizing electronic databases such as PubMed, Embase, and Web of Science in June 2022 for articles focusing on the use of augmented reality for improving clinical skills. The Rayyan website was used to screen the articles that met the inclusion criteria, which was the application of augmented reality as a learning method in medical education. Total of 37 articles met the inclusion criteria. These publications suggested that using augmented reality could improve clinical skills. The most researched topics explored were laparoscopic surgery skills and ophthalmology were the most studied topic. The research methods applied in the articles fall into two main categories: randomized control trial (RCT) (29.3%) and non-RCT (70.3%). Augmented reality has the potential to be integrated in medical education, particularly to boost clinical studies. Due to limited databases, however, any further studies on the implementation of augmented reality as a method to enhance skills in medical education need to be conducted.


Subject(s)
Augmented Reality , Education, Medical , Humans , Clinical Competence , Students
2.
Tumour Biol ; 39(5): 1010428317691689, 2017 May.
Article in English | MEDLINE | ID: mdl-28466786

ABSTRACT

Current standard chemotherapy for late stage ovarian cancer is found unsuccessful due to relapse after completing the regimens. After completing platinum-based chemotherapy, 70% of patients develop relapse and resistance. Recent evidence proves ovarian cancer stem cells as the source of resistance. Therefore, treatment strategy to target both cancer stem cells and normal stem cells is essential. In this study, we developed a novel chalcone derivative as novel drug candidate for ovarian cancer treatment. We found that methoxyphenyl chalcone was effective to eliminate ovarian cancer cells when given either as monotherapy or in combination with cisplatin. We found that cell viability of ovarian cancer cells was decreased through apoptosis induction. Dephosphorylation of Bcl2-associated agonist of cell death protein was increased after methoxyphenyl chalcone treatment that led to activation of caspases. Interestingly, this drug also worked as a G2/M checkpoint modulator with alternative ways of DNA damage signal-evoking potential that might work to increase response after cisplatin treatment. In addition, methoxyphenyl chalcone was able to suppress autophagic flux and stemness regulator in ovarian spheroids that decreased their survival. Therefore, combination of methoxyphenyl chalcone and cisplatin showed synergistic effects. Taken together, we believe that our novel compound is a promising novel therapeutic agent for effective clinical treatment of ovarian cancer.


Subject(s)
Chalcone/administration & dosage , Neoplasm Recurrence, Local/drug therapy , Neoplasms, Glandular and Epithelial/diet therapy , Ovarian Neoplasms/diet therapy , Apoptosis/drug effects , Autophagy/drug effects , Carcinoma, Ovarian Epithelial , Cell Line, Tumor , Cell Survival/drug effects , Cisplatin/administration & dosage , DNA Damage/drug effects , Drug Resistance, Neoplasm/drug effects , Female , Humans , Neoplasm Recurrence, Local/pathology , Neoplasms, Glandular and Epithelial/pathology , Neoplastic Stem Cells/drug effects , Neoplastic Stem Cells/pathology , Ovarian Neoplasms/pathology , Phosphorylation/drug effects
3.
Toxicol Appl Pharmacol ; 325: 48-60, 2017 06 15.
Article in English | MEDLINE | ID: mdl-28408137

ABSTRACT

Targeting residual self-renewing, chemoresistant cancerous cells may represent the key to overcoming therapy resistance. The entry of these quiescent cells into an activated state is associated with high metabolic demand and autophagic flux. Therefore, modulating the autophagy pathway in aggressive carcinomas may be beneficial as a therapeutic modality. In this study, we evaluated the anti-tumor activities of 4-acetylantroquinonol B (4-AAQB) in chemoresistant ovarian cancer cells, particularly its ability to modulate autophagy through autophagy-related genes (Atg). Atg-5 was overexpressed in invasive ovarian cancer cell lines and tissue (OR: 5.133; P=0.027) and depleting Atg-5 in ES-2 cell lines significantly induced apoptosis. 4-AAQB effectively suppressed viability of various subtypes of ovarian cancer. Cells with higher cisplatin-resistance were more responsive to 4-AAQB. For the first time, we demonstrate that 4-AAQB significantly suppress Atg-5 and Atg-7 expression with decreased autophagic flux in ovarian cancer cells via inhibition of the PI3K/Akt/mTOR/p70S6K signaling pathway. Similar to Atg-5 silencing, 4-AAQB-induced autophagy inhibition significantly enhanced cell death in vitro. These results are comparable to those of hydroxychloroquine (HCQ). In addition, 4-AAQB/cisplatin synergistically induced apoptosis in ovarian cancer cells. In vivo, 4-AAQB/cisplatin also significantly induced apoptosis and autophagy in an ES-2 mouse xenografts model. This is the first report demonstrating the efficacy of 4-AAQB alone or in combination with cisplatin on the suppression of ovarian cancer via Atg-5-dependent autophagy. We believe these findings will be beneficial in the development of a novel anti-ovarian cancer therapeutic strategy.


Subject(s)
4-Butyrolactone/analogs & derivatives , Antineoplastic Combined Chemotherapy Protocols/pharmacology , Autophagy/drug effects , Cisplatin/pharmacology , Cyclohexanones/pharmacology , Drug Resistance, Neoplasm/drug effects , Neoplasms, Glandular and Epithelial/drug therapy , Ovarian Neoplasms/drug therapy , Phosphatidylinositol 3-Kinase/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Ribosomal Protein S6 Kinases, 70-kDa/metabolism , TOR Serine-Threonine Kinases/metabolism , 4-Butyrolactone/pharmacology , Animals , Apoptosis/drug effects , Autophagy-Related Protein 5/genetics , Autophagy-Related Protein 5/metabolism , Carcinoma, Ovarian Epithelial , Cell Line, Tumor , Cell Survival/drug effects , Dose-Response Relationship, Drug , Drug Synergism , Female , Humans , Mice, Inbred NOD , Mice, SCID , Neoplasms, Glandular and Epithelial/enzymology , Neoplasms, Glandular and Epithelial/genetics , Neoplasms, Glandular and Epithelial/pathology , Ovarian Neoplasms/enzymology , Ovarian Neoplasms/genetics , Ovarian Neoplasms/pathology , RNA Interference , Signal Transduction/drug effects , Time Factors , Transfection , Tumor Burden/drug effects , Xenograft Model Antitumor Assays
4.
Oncotarget ; 6(15): 13255-68, 2015 May 30.
Article in English | MEDLINE | ID: mdl-26036311

ABSTRACT

According to a Prognoscan database, upregulation of Bruton's tyrosine kinase (Btk) is associated with low overall survival in ovarian cancer patients. We found that spheroids-forming ovarian cancer cell, which highly expressed cancer stem-like cell (CSC) markers and Btk, were cisplatin resistant. We next treated CSCs and non-CSCs by a combination of ibrutinib and cisplatin. We found that chemoresistance was dependent on Btk and JAK2/STAT3, which maintained CSC by inducing Sox-2 and prosurvival genes. We suggest that addition of ibrutinib to cisplatin may improve treatment outcome in ovarian cancer.


Subject(s)
Antineoplastic Agents/therapeutic use , Neoplastic Stem Cells/drug effects , Ovarian Neoplasms/drug therapy , Protein-Tyrosine Kinases/antagonists & inhibitors , Pyrazoles/therapeutic use , Pyrimidines/therapeutic use , Adenine/analogs & derivatives , Adult , Agammaglobulinaemia Tyrosine Kinase , Cisplatin/therapeutic use , Drug Resistance, Neoplasm , Drug Therapy, Combination , Female , Humans , Janus Kinase 2/metabolism , Middle Aged , Ovarian Neoplasms/metabolism , Ovarian Neoplasms/mortality , Piperidines , STAT3 Transcription Factor/metabolism , Young Adult
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