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Biomedical subjects

Sang Soo Kim

Publications and source records attributed to Sang Soo Kim.

11 recordsLinked to original sources
PubMed2006

Theoretical development of in situ optical particle separator: cross-type optical chromatography.

An in situ separation system, cross-type optical chromatography, is developed theoretically, and an analytic solution of the retention distance is derived. Particle trajectories in the cross-type optical chromatography are calculated for various sizes and materials of the particles and for flow velocities. Further, cross-type optical chromatography assisted by a particle beam generation system is designed.

Journal Article↗
PubMed2006

Tissue engineering of heart valves by recellularization of glutaraldehyde-fixed porcine valves using bone marrow-derived cells.

To increase the biocompatibility and durability of glutaraldehyde (GA)-fixed valves, a biological coating with viable endothelial cells (ECs) has been proposed. However, stable EC layers have not been formed successfully on GA-fixed valves due to their inability to repopulate. In this study, to improve cellular adhesion and proliferation, the GA-fixed prostheses were detoxified by treatment with citric acid to remove free aldehyde groups. Canine bone marrow mononuclear cells (MNCs) were differentiated into EC-like cells and myofibroblast-like cells in vitro. Detoxified prostheses were seeded and recellularized with differentiated bone marrow- derived cells (BMCs) for seven days. Untreated GA-fixed prostheses were used as controls. Cell attachment, proliferation, metabolic activity, and viability were investigated and cell-seeded leaflets were histologically analyzed. On detoxified GA-fixed prostheses, BMC seeding resulted in uninhibited cell proliferation after seven days. In contrast, on untreated GA-fixed prostheses, cell attachment was poor and no viable cells were observed. Positive staining for smooth muscle a-actin, CD31, and proliferating cell nuclear antigen was observed on the luminal side of the detoxified valve leaflets, indicating differentiation and proliferation of the seeded BMCs. These results demonstrate that the treatment of GA-fixed valves with citric acid established a surface more suitable for cellular attachment and proliferation. Engineering heart valves by seeding detoxified GA-fixed biological valve prostheses with BMCs may increase biocompatibility and durability of the prostheses. This method could be utilized as a new approach for the restoration of heart valve structure and function in the treatment of end-stage heart valve disease.

Actins↗
PubMed2006

Inactivation of TGF-beta signaling in lung cancer results in increased CDK4 activity that can be rescued by ELF.

Escape from TGF-beta inhibition of proliferation is a hallmark of multiple cancers including lung cancer. We explored the role of ELF, crucial TGF-beta adaptor protein identified from endodermal progenitor cells, in lung carcinogenesis and cell-cycle regulation. Interestingly, elf-/- mice develop multiple defects that include lung, liver, and cardiac abnormalities. Four out of 6 lung cancer and mesothelioma cell lines displayed deficiency of ELF expression with increased CDK4 expression. Immunohistochemistry and Western blot analysis of primary human lung cancers also showed decreased ELF expression and overexpression of CDK4. Moreover, rescue of ELF in ELF-deficient cell lines decreased the expression of CDK4 and resulted in accumulation of G1/S checkpoint arrested cells. These results suggest that disruption in TGF-beta signaling mediated by loss of ELF in lung cancer leads to cell-cycle deregulation by modulating CDK4 and ELF highlights a key role of TGF-beta adaptor protein in suppressing early lung cancer.

Animals↗
PubMed2006

Functional annotation and analysis of Korean patented biological sequences using bioinformatics.

A recent report of the Korean Intellectual Property Office (KIPO) showed that the number of biological sequence-based patents is rapidly increasing in Korea. We present biological features of Korean patented sequences though bioinformatic analysis. The analysis is divided into two steps. The first is an annotation step in which the patented sequences were annotated with the Reference Sequence (RefSeq) database. The second is an association step in which the patented sequences were linked to genes, diseases, pathway, and biological functions. We used Entrez Gene, Online Mendelian Inheritance in Man (OMIM), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Ontology (GO) databases. Through the association analysis, we found that nearly 2.6% of human genes were associated with Korean patenting, compared to 20% of human genes in the U.S. patent. The association between the biological functions and the patented sequences indicated that genes whose products act as hormones on defense responses in the extra-cellular environments were the most highly targeted for patenting. The analysis data are available at http://www.patome.net.

Base Sequence↗
PubMed2006

TGF-beta signaling pathway inactivation and cell cycle deregulation in the development of gastric cancer: role of the beta-spectrin, ELF.

We have shown that loss of ELF, a stem cell adaptor protein, disrupts TGF-beta signaling through Smad3 and Smad4 localization. Notably elf(+/-)/smad4(+/-) mice develop gastric cancer presenting this as an important model for analyzing molecular event in gastric carcinogenesis. To gain further insight into the functional role of ELF in gastric cancer suppression, we carried out a detailed characterization of cell cycle events leading to gastric tumorigenesis. elf(-/-) cells and elf(+/-)/smad4(+/-) mice demonstrate a marked alteration of cell cycle regulators, such as Cdk4, K-Ras, and p21. Levels of Cdk4 increased compared to normal controls, suggesting loss of ELF results in functional abnormalities in cell cycle regulation. We further demonstrate that the elf(-/-) MEFs show a disruption of G1/S cell cycle transition and a significant reduction in senescence. Thus, in response to ELF deficiency, the abnormalities of G1/S checkpoint and senescence contribute their increment of susceptibility to malignant transformation.

Aging↗
PubMed2006

Hyperplasia and spontaneous tumor development in the gynecologic system in mice lacking the BRCA1-Delta11 isoform.

Alternative splicing in the BRCA1 locus generates multiple protein products including BRCA1-Delta11, which is identical to the BRCA1 full-length isoform (BRCA1-FL) except for the absence of exon 11. Mutation analysis using gene targeting to create null mutations or disrupt BRCA-FL has provided much of our understanding of BRCA1 functions; however, targeted mutation of specific short forms of BRCA1 has not been reported. To understand the physiologic functions of BRCA1-Delta11, we used a knock-in approach that blocks alternative splicing between exons 10 and 12 to prevent the formation of this form of BRCA1. We showed that homozygous mutant mice (Brca1(FL/FL)) were born at a Mendelian ratio without obvious developmental defects. However, the majority of Brca1(FL/FL) female mice showed mammary gland abnormalities and uterine hyperplasia after one year of age with spontaneous tumor formation. Cultured Brca1(FL/FL) cells exhibited abnormal centrosome amplification and reduction of G(1) population that was accompanied by accumulation of cyclin E and cyclin A. Accumulation of cyclin E was also found in epithelial layers of dilated ducts and hyperproliferative lobular regions in the mammary glands of Brca1(FL/FL) mice. These observations provide evidence that BRCA1 splicing variants are involved in BRCA1 functions in modulating G(1)/S transition, centrosome duplication, and repressing tumor formation.

Aging↗
PubMed2005

Changes in the shape and mobility of colloidal gold nanorods with electrospray and differential mobility analyzer methods.

The potential of the electrospray technique in analyzing the structure of nonspherical colloidal particles that are below 100 nm in volume-equivalent diameter was demonstrated by online size measurement using a differential mobility analyzer (DMA) with a condensation nucleus counter (CNC) system. The measured mobility of gold nanorods was confirmed by electron microscope images and the theoretical calculation of particle mobility using the dynamic shape factor and slip correction factor. To evaluate the mobility, rod particles were modeled as both a cylinder and a prolate spheroid. This study also showed that the organic surfactant coated on rod particles might be removed and that the rod particles became spherical upon the elevation of the ambient temperature during the gas-phase dispersion of colloidal nanoparticles. Moreover, the thickness of the surfactants coated on rod particles was estimated by comparing the theoretically and experimentally obtained mobilities.

Journal Article↗
PubMed2004

Uterus hyperplasia and increased carcinogen-induced tumorigenesis in mice carrying a targeted mutation of the Chk2 phosphorylation site in Brca1.

The tumor suppressor BRCA1 contains multiple functional domains that interact with many proteins. After DNA damage, BRCA1 is phosphorylated by CHK2 at serine 988, followed by a change in its intracellular location. To study the functions of CHK2-dependent phosphorylation of BRCA1, we generated a mouse model carrying the mutation S971A (S971 in mouse Brca1 corresponds to S988 in human BRCA1) by gene targeting. Brca1(S971A/S971A) mice were born at the expected ratio without a developmental defect, unlike previously reported Brca1 mutant mice. However, Brca1(S971A/S971A) mice suffered a moderately increased risk of spontaneous tumor formation, with a majority of females developing uterus hyperplasia and ovarian abnormalities by 2 years of age. After treatment with DNA-damaging agents, Brca1(S971A/S971A) mice exhibited several abnormalities, including increased body weight, abnormal hair growth pattern, lymphoma, mammary tumors, and endometrial tumors. In addition, the onset of tumor formation became accelerated, and 80% of the mutant mice had developed tumors by 1 year of age. We demonstrated that the Brca1(S971A/S971A) cells displayed reduced ability to activate the G(2)/M cell cycle checkpoint upon gamma-irradiation and to stabilize p53 following N-methyl-N'-nitro-N-nitrosoguanidine treatment. These observations suggest that Chk2 phosphorylation of S971 is involved in Brca1 function in modulating the DNA damage response and repressing tumor formation.

Aging↗
PubMed2003

Treatment of juxtafusional degeneration with artificial disc replacement (ADR): preliminary results of an ongoing prospective study.

Eleven patients with juxtafusional degeneration syndrome underwent artificial disc replacement (ADR). Of these, five patients followed up for >6 months were analyzed for the current report. Surgery for juxtafusional degeneration was performed mean 4.9 years from their initial operation. The presenting features were neurologic compromise in four and severe back pain in one, with a mean Oswestry Disability Index (ODI) score of 64%. The replaced levels were L1-L2 in one, L3-L4 in three, L4-L5 in one, and L5-S1 in one. L1-L2 replacement was performed through a left flank approach. At 6 months, all patients had complete resolution of neurologic symptoms, and ODI decreased to 24%. ADR shows promising early results in juxtafusional degeneration in well-selected patients.

Adult↗
PubMed2002

Involvement of protein phosphatase-1-mediated MARCKS translocation in myogenic differentiation of embryonic muscle cells.

Myristoylated alanine-rich C kinase substrate (MARCKS) translocates from the cytosol to the plasma membrane while mononucleated myoblasts fuse to form multinucleated myotubes. Here, we show that protein phosphatase-1-mediated dephosphorylation of MARCKS largely influences its subcellular localization and the fusion process. Treatment with okadaic acid or tautomycin, which are potent inhibitors of protein phosphatases and cell fusion, was found to reversibly block the MARCKS translocation. Moreover, the dephosphorylating activity against MARCKS markedly increased during myogenesis, and this increase was closely correlated with the membrane fusion of the cells. In addition, protein phosphatase-1 was identified as a major enzyme that is responsible for dephosphorylation of MARCKS. Furthermore, a mutation preventing MARCKS phosphorylation and thus facilitating MARCKS translocation resulted in promotion of the cell fusion. In contrast, overexpression of MARCKS carrying a mutation that blocks myristoylation and thus prevents the MARCKS translocation impaired the myoblast fusion. Together with the fact that MARCKS regulates the cytoskeleton dynamics by crosslinking the actin filaments in the plasma membrane and that myoblast fusion accompanies massive cytoskeleton reorganization, these results suggest that protein phosphatase-1-mediated MARCKS localization at the membrane is required for the fusion of embryonic muscle cells.

Amino Acid Sequence↗