المؤلفون: Choi JY, Han YK

المصدر: Clinical Ophthalmology, Vol Volume 12, Pp 1279-1284 (2018)

مصطلحات موضوعية: modified technique, intraocular lens scleral fixation, Ophthalmology, RE1-994

الوصف: Jung Yeol Choi,1 Young Keun Han2,3 1Department of Ophthalmology, Jeju National University Hospital, Jeju, South Korea; 2Department of Ophthalmology, Seoul Metropolitan Government-Seoul National University Boramae Medical Center, Seoul, South Korea; 3Department of Ophthalmology, Seoul National University College of Medicine, Seoul, South Korea Abstract: We describe a modified scleral fixation method to facilitate the good centration and adequate tension of sutures at both ends with addition of an internal fixation knot that reduces decentering of the IOL in a patient with postsurgical aphakia. Using an ab externo suture technique to fixate the haptics to the scleral wall, an additional loop knot is tied 1 mm next to the fixation knot at the haptic. In the technique, an internalized suture and an additional suture knot is tied while holding it close to the fixation knot at the haptic using a needle holder or McPherson forceps. The externalized sutures are secured by taking a bite of transclera and tying the suture to itself. This technique is simple and easy, and adds an internal check valve to prevent excessive pull and decentering of the intraocular lens at one side. The internal check valve also serves as a criterion for the point of fixation at each end. Keywords: modified technique, intraocular lens scleral fixation, postsurgical aphakia

وصف الملف: electronic resource

Relation: https://www.dovepress.com/in-and-out-technique-for-intraocular-lens-scleral-fixation-peer-reviewed-article-OPTH; https://doaj.org/toc/1177-5483

URL الوصول: https://doaj.org/article/1976b1f70bc149c19068479b9c895a8f

المؤلفون: Ryoo, NK, Kwon, J-W, Wee, WR, Miller, KM, Han, YK

المصدر: BMC OPHTHALMOLOGY. 13

مصطلحات موضوعية: Cataract, Thermal damage, Thermal imaging, Torsional phacoemulsification

وصف الملف: application/pdf

URL الوصول: https://escholarship.org/uc/item/3pj4x69q

المؤلفون: Chang-Woo Lee, Han Yk, Park Gy, Lee Cg, Kim Sd, Jo Ws, Yang K, Kim Js, Chun Sh, Jeong Dh, Han Jy

المصدر: Cancer Gene Therapy. 21:158-163

مصطلحات موضوعية: Cancer Research, Programmed cell death, Cell Survival, medicine.medical_treatment, Mitosis, Apoptosis, Cell Growth Processes, Biology, Transfection, Radiation Tolerance, Microtubule, Cell Line, Tumor, Radioresistance, medicine, Humans, RNA, Small Interfering, Molecular Biology, Mitotic catastrophe, Cell Death, Brain Neoplasms, Cell Cycle, Cell biology, Radiation therapy, 14-3-3 Proteins, Cell culture, Molecular Medicine, Glioblastoma, HeLa Cells

الوصف: 14-3-3 proteins have important roles in several cellular processes such as cell cycle progression, the DNA-damage checkpoint and apoptosis. We have shown previously that depleting 14-3-3η, a 14-3-3 isoform, enhances mitotic cell death, and that combining it with microtubule agents is more effective for anticancer therapeutics. In this study, we investigated whether depleting 14-3-3η can be combined with radiotherapy to enhance its therapeutic efficacy. We found that depleting 14-3-3η resulted in a synergistic radiosensitizing effect when combined with radiotherapy in several glioblastoma cell lines, where its specific expression and correlation of its expression level with malignancy have been reported. The radiosensitizing effect was associated with enhanced mitotic cell death by 14-3-3η depletion but not with mitotic catastrophe, which is one of the major cell death mechanisms observed in response to irradiation of most solid tumors. These results suggest that 14-3-3η may be a therapeutic target to overcome radioresistance in glioblastoma.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a90732b1dbb40702c6a5c341bb9a1385
https://doi.org/10.1038/cgt.2014.11

المؤلفون: Jung-Dal Choi, Hye-In Choi, Sun-Tae Jung, Yunju Jeong, Yun-Jeong Song, Seung-Hyun Lee, Kinam Kim, Doohyun Kim, Han Yk, Kwang-Ho Cheong, Paul H. Song, Jesuk Lee, Seungbae Lee, Geun Woong Kim, Young Mi Oh, Byung-Uk Kim, Park Hye Hyang

المصدر: Oncogene. 33(1)

مصطلحات موضوعية: Male, Cancer Research, media_common.quotation_subject, Cell, Regulator, Cetuximab, Mice, Nude, Antineoplastic Agents, Apoptosis, Biology, Antibodies, Monoclonal, Humanized, Mice, Downregulation and upregulation, Cell Line, Tumor, Genetics, medicine, Animals, Humans, Molecular Targeted Therapy, Proto-Oncogene Proteins c-cbl, Internalization, Molecular Biology, media_common, Cell Proliferation, Mice, Inbred BALB C, Membrane Glycoproteins, Cell growth, Proto-Oncogene Proteins c-met, Molecular biology, Xenograft Model Antitumor Assays, Tumor Burden, ErbB Receptors, medicine.anatomical_structure, Tumor progression, Drug Resistance, Neoplasm, Cancer cell, Proteolysis, Cancer research, Signal transduction, Signal Transduction

الوصف: The Met receptor tyrosine kinase, found to be constitutively activated in many tumors, has become a leading target for cancer therapy. Disruptions in Met downregulation have been associated with aggressive tumor progression with several therapeutic strategies addressing this aspect of Met biology. Castias B-lineage lymphoma (Cbl) E3 ligase-mediated degradation, which attenuates Met signaling via ligand-dependent Met internalization, is a major negative regulator of Met expression. It is believed that one of the mechanisms by which the therapeutic anti-Met antibodies induce cancer cell death in Met overexpressing tumors is via internalization and subsequent degradation of Met from the cell surface. However, a previously reported Met-targeting antibody demonstrated intrinsic agonistic activity while being capable of inducing Cbl-mediated degradation of Met, suggesting that Cbl-mediated degradation requires receptor activation and impedes therapeutic application. We have developed a potent and selective bivalent Met-targeting antibody (SAIT301) that invokes Met degradation using an alternative regulator LRIG1. In this report, we demonstrate that LRIG1 mediates degradation of Met by SAIT301 and this degradation does not require Met activation. Furthermore, SAIT301 was able to downregulate Met and dramatically inhibit growth of tumors with low or no Cbl expression, as well as tumors with Met exon 14 deletion that prevents Met binding to Cbl. In summary, we demonstrate the enhanced therapeutic potential of a novel tumor-inhibiting anti-Met antibody, SAIT301, which utilizes a Cbl-independent, LRIG1-mediated Met degradation pathway and thereby avoids the agonism that limits the effectiveness of previously reported anti-Met antibodies.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f0ea1de5b2b20d7da97bc3426b5aee5e
https://pubmed.ncbi.nlm.nih.gov/23208509

المؤلفون: Chang-Woo Lee, Kim Eg, Jun Ho Lee, Lim Kh, Hyun-Ju Park, Gyeongsin Park, Choi Yj, Chun Sh, Han Yk, Lee Cg, Yang K

المصدر: Oncogene. 32(12)

مصطلحات موضوعية: Protein isoform, G2 Phase, Cancer Research, Programmed cell death, Aneuploidy, Mitosis, Apoptosis, Mitotic progression, Biology, Microtubules, Microtubule, Neoplasms, Genetics, medicine, Humans, Molecular Biology, Sensitization, Nocodazole, Forkhead Box Protein O3, Forkhead Transcription Factors, medicine.disease, Caspase 9, Cell biology, medicine.anatomical_structure, Mitotic cell, 14-3-3 Proteins, Cell Division, HeLa Cells

الوصف: 14-3-3 proteins are involved in several cellular processes, including the G1/S and G2/M cell cycle transitions. However, their roles during mitosis are not well understood. Here, we showed that depletion of 14-3-3η, a 14-3-3 protein isoform, enhanced mitotic cell death, resulting in sensitization to microtubule inhibitors and inhibition of aneuploidy formation. The enhanced mitotic cell death by depletion of 14-3-3η appeared to be both caspase-dependent and independent. Furthermore, enhanced mitotic cell death and a reduction in aneuploidy following 14-3-3η depletion were independent of the mitotic checkpoint, which is thought to be the primary signaling event in the regulation of the cell death induced by microtubule inhibitors. When 14-3-3η depletion was combined with microtubule inhibitors in HCT116 and U87MG cells, it sensitized both cancer cell lines to microtubule inhibitors. These results collectively suggest that 14-3-3η may be required for mitotic progression and may be considered as a novel anti-cancer strategy in combination with microtubule inhibitors.

URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::85418e4c6b20ef58c2c830c3b9aee220
https://pubmed.ncbi.nlm.nih.gov/22562251

لا يتم عرض هذه النتيجة على الضيوف.
تسجيل الدخول للوصول الكامل.

لا يتم عرض هذه النتيجة على الضيوف.
تسجيل الدخول للوصول الكامل.

لا يتم عرض هذه النتيجة على الضيوف.
تسجيل الدخول للوصول الكامل.

لا يتم عرض هذه النتيجة على الضيوف.
تسجيل الدخول للوصول الكامل.

لا يتم عرض هذه النتيجة على الضيوف.
تسجيل الدخول للوصول الكامل.