Search

Your search keyword '"Koo, C. H."' showing total 131 results
Start Over Author "Koo, C. H."
131 results on '"Koo, C. H."'

2. A Comparison of Long Short-Term Memory and Artificial Neural Network for Water Level Forecasting at Klang Gates Dam

Author

Ng, K. W., Chong, K. L., Koo, C. H., Huang, Y. F., Biswas, Asit K., Series Editor, Tortajada, Cecilia, Series Editor, Altinbilek, Dogan, Editorial Board Member, González-Gómez, Francisco, Editorial Board Member, Gopalakrishnan, Chennat, Editorial Board Member, Horne, James, Editorial Board Member, Molden, David J., Editorial Board Member, Varis, Olli, Editorial Board Member, Mohd Sidek, Lariyah, editor, Salih, Gasim Hayder Ahmed, editor, Ahmed, Ali Najah, editor, Escuder-Bueno, Ignacio, editor, and Basri, Hidayah, editor

Published
2023
Full Text
View/download PDF

8. Optical investigations on electronic structure changes related to the metal-insulator transition in VO2 film

Author

Koo, C. H., Lee, J. S., Kim, M. W., Chang, Y. J., Noh, T. W., Chae, J. H. Jung B. G., and Kim, H. -T.

Subjects
Condensed Matter - Strongly Correlated Electrons
Abstract

We investigated optical absorption coefficient spectra of an epitaxial VO2 film in wide photon energy (0.5 - 5.0 eV) and temperature (100 - 380 K) regions. In its insulating phase, we observed two d-d transition peaks around 1.3 eV and 2.7 eV and a charge transfer peak around 4.0 eV. As temperature goes above the metal-insulator transition temperature near 340 K, a large portion of the spectral weight of the peak around 4.0 eV becomes redistributed and a Drude-like peak appears. We initially applied the band picture to explain the details of the spectral weight changes, especially the temperature-dependent shift at 2.7 eV, but failed. To check whether the spectral changes are optical signatures of the electron-electron correlation effects, we applied the Hubbard model which takes into account orbital degeneracy. This orbitally degenerate Hubbard model could explain the details of the temperature-dependent peak shifts quite well. In addition, from the peak assignments based on the orbitally degenerate Hubbard model, we could obtain the values of U + delta(~ 3.4 eV) and JH (~ 0.7 eV), where U, delta, and JH are the on-site Coulomb repulsion energy, the crystal field splitting between the t2g bands, and the Hund's rule exchange energy, respectively. Our spectroscopic studies indicate that the electron-electron correlation could play an important role in the metal-insulator transition of VO2.

Published
2005

26. Pyrometallurgical Processes

Author

Khalafalla, S. E., Evans, J. W., Koo, C.-H., Sohn, H. Y., Turkdogan, E. T., Cutler, I. B., Pitt, C. H., Sohn, Hong Yong, editor, and Wadsworth, Milton E., editor

Published
1979
Full Text
View/download PDF

31. Purification and assay of Arapaima gigas vitellogenin: Potential use for sex determination

Author

Dugué, R., Fred Koo, C. H. U., Alcantara, F., Duponchelle, F., Jean-François Renno, and Nuñez, J.

Subjects
Vitellogenin, EIA, Sex determination, Amazon, Arapaima gigas, EIA, Sex determination, Vitellogenin, Amazon, Arapaima gigas
Abstract

Arapaima gigas is an ancient, air-breathing, giant fish of Amazonian rivers. Due to its economic importance, the development of aquaculture for this species is currently a good alternative to counteract the decline of wild populations. Reproduction in captivity relies on the constitution of male and female pairs, which occur naturally in large ponds. But, as sex determination of A. gigas is not possible by morphological criteria it is very difficult to optimize reproduction success and fry production in each pond. This situation prompted us to develop a sexing methodology based on the detection of female specific plasma Vitellogenin (Vtg) using an Enzyme Immuno-Assay (EIA). Vitellogenin purification was performed by electro-elution after polyacrilamide gel electrophoresis (PAGE) from plasma of 17 beta-Estradiol treated A. gigas juveniles. Two different Vtg molecules were isolated, (Vt(g1) and Vt(g2)) with 184 and 112 kDa apparent molecular masses repectively. Both antibodies, produced in rabbits, reacted with both vitellogenins in a competitive assay or by direct Vtg coating. For sexing of the fish, we finally chose the method of direct coating of serial plasma dilutions.

Published
2008
Full Text
View/download PDF

34. Down-regulation of receptor antigen in leukotriene B4-induced chemotactic deactivation of human polymorphonuclear leucocytes.

Author

Boggs, J. M., Koo, C. H., and Goetzl, F. J.

Subjects
*LEUCOCYTES, *BLOOD cells, *LEUKOTRIENES, *IMMUNOGLOBULINS, *ANTIGENS, *MEMBRANE proteins
Abstract

Pretreatment of suspensions of human polymorphonuclear leucocytes (PMNL) with leukotriene B4 (LTB4) induces chemotactic deactivation, characterized by diminished expression of high-affinity ITB4 receptors and selectively decreased chemotactic responsiveness of the PMNL to LTB4. Rabbit anti-idiotypic antibodies (a-Id) to mouse monoclonal anti-LTB4, which bind to the 60,000-80.000 molecular weight (M W) membrane protein of PMNL receptors for LTB4 in Western blots and block binding of [³H]LTB4 to high-affinity receptors of PMNL, detected a reduction in LTB4 receptor antigen during chemotactic deactivation. Loss of high-affinity receptors for LTB4 from the surface of PMNL deactivated by incubation with 10 nm LTB4 was significant after 1 min and after 20 min reached a mean maximum of 82% and 61%, respectively, as assessed by binding of [³H]LTB4 and a-Id. Inhibitors of PMNL proteases did not prevent the deactivation-induced decreases in surface receptors for LTB4. Disruption of deactivated PMNL and solubilization of membrane proteins failed to expose intracellular LTB4 receptors. Incubation of membranes isolated from PMNL with 100 nM LTB4 resulted in a loss of LTB4 receptors similar to that observed in intact PMNL. Changes in LTB4 receptor protein structure or membrane localization, rather than endocytosis or proteolysis, thus appear to explain the rapidly decreased expression of LTB4 receptors, which results from stimulus-specific deactivation. [ABSTRACT FROM AUTHOR]

Published
1991

35. Specificity and cellular distribution of human polymorphonuclear leucocyte receptors for leukotriene C4.

Author

Baud, L., Koo, C. H., and Goetzl, E. J.

Subjects
*NEUTROPHILS, *LEUKOTRIENES, *LEUCOCYTES, *GRANULOCYTES, *PHAGOCYTES, *BLOOD cells
Abstract

Human polymorphonuclear (PMN) leucocytes bind synthetic [3H]-labelled leukotriene C4 ([3H]LTC4), with rapid saturation and reversibility of approximately 90%, by a 700-fold higher concentration of non-radioactive LTC4. [3H]LTC4 is recognized specifically by 10,778±6260 (mean ± SD) sites per PMN leucocyte that exhibit a KD of 34·3 ± 1·7 nM. The specificity of the LTC4 receptors is supported by the competitive inhibition of binding of [3H]LTC4 by LTC4, LTC4- sulphone, LTD4, and LTE4 with relative potencies of approximately 100:20:3:1. The four-fold higher level of specific binding of[3H]LTC4 by sonicates than by intact PMN leucocytes is attributable to intracellular receptors. Of the total number of receptors recovered in sonicates of PMN leucocytes, one-third are associated with membranes and the other two-thirds with lysosomal granules. The affinity of the membrane receptors for LTC4 is indistinguishable from that of receptors on intact PMN leucocytes, whereas the affinity of granule receptors is significantly higher. The characteristics of the receptors are consistent with a role in mediating uptake and metabolism of LTC4 by PMN leucocytes. [ABSTRACT FROM AUTHOR]

Published
1987

36. Variability in interpretation of immunohistologic findings in lymphoproliferative disorders by hematopathologists. A comprehensive statistical analysis of interobserver performance.

Author

Sheibani, Khalil, Nathwani, Bharat N., Swartz, William G., Ben-Ezra, Jonathan, Brownell, Mark D., Burke, Jerome S., Kennedy, John L., Koo, Chae H., Winberg, Carl D., Sheibani, K, Nathwani, B N, Swartz, W G, Ben-Ezra, J, Brownell, M D, Burke, J S, Kennedy, J L, Koo, C H, and Winberg, C D

Published
1988
Full Text
View/download PDF

38. Specificity and cellular distribution of human polymorphonuclear leucocyte receptors for leukotriene C4.

Author

Baud, L., Koo, C. H., and Goetzl, E. J.

Subjects
NEUTROPHILS, LEUKOTRIENES, LEUCOCYTES, GRANULOCYTES, PHAGOCYTES, BLOOD cells
Abstract

Human polymorphonuclear (PMN) leucocytes bind synthetic [3H]-labelled leukotriene C4 ([3H]LTC4), with rapid saturation and reversibility of approximately 90%, by a 700-fold higher concentration of non-radioactive LTC4. [3H]LTC4 is recognized specifically by 10,778±6260 (mean ± SD) sites per PMN leucocyte that exhibit a KD of 34·3 ± 1·7 nM. The specificity of the LTC4 receptors is supported by the competitive inhibition of binding of [3H]LTC4 by LTC4, LTC4- sulphone, LTD4, and LTE4 with relative potencies of approximately 100:20:3:1. The four-fold higher level of specific binding of[3H]LTC4 by sonicates than by intact PMN leucocytes is attributable to intracellular receptors. Of the total number of receptors recovered in sonicates of PMN leucocytes, one-third are associated with membranes and the other two-thirds with lysosomal granules. The affinity of the membrane receptors for LTC4 is indistinguishable from that of receptors on intact PMN leucocytes, whereas the affinity of granule receptors is significantly higher. The characteristics of the receptors are consistent with a role in mediating uptake and metabolism of LTC4 by PMN leucocytes. [ABSTRACT FROM AUTHOR]

Published
1987

42. Trafficking of cell-surface amyloid beta-protein precursor. I. Secretion, endocytosis and recycling as detected by labeled monoclonal antibody.

Author

Koo, E H, Squazzo, S L, Selkoe, D J, and Koo, C H

Abstract

Amyloid beta-protein, the principal constituent of amyloid fibrils found in senile plaques and blood vessels in Alzheimer's disease, is constitutively produced and released into medium of cultured cells. Amyloid beta-protein is derived by proteolysis of the beta-amyloid precursor protein by unclear mechanisms. Beta-amyloid precursor protein is a transmembrane protein which can be processed to release a large secretory product or processed in the endosomal/lysosomal pathway without secretion. Previous studies have shown that from the cell surface, beta-amyloid precursor protein may be released after cleavage or internalized without cleavage, the latter in a pathway that both produces amyloid beta-protein and also targets some molecules to the lysosomal compartment. Analysis of beta-amyloid precursor protein trafficking is confounded by the concomitant secretion and internalization of molecules from the cell surface. To address this issue, we developed an assay, based on the binding of radioiodinated monoclonal antibody, to measure the release and internalization of cell surface beta-amyloid precursor protein in transfected cells. With this approach, we showed that surface beta-amyloid precursor protein is either rapidly released or internalized, such that the duration at the cell surface is very short. Approximately 30% of cell surface beta-amyloid precursor protein molecules are released. Following internalization, a fraction of molecules are recycled while the majority of molecules are rapidly sorted to the lysosomal compartment for degradation When the C terminus of beta-amyloid precursor protein is deleted, secretion is increased by approximately 2.5-fold as compared to wild-type molecules. There is concomitant decrease in internalization in these mutant molecules as well as prolongation of the resident time on the cell surface. This observation is consistent with recent evidence that signals within the cytoplasmic domain mediate beta-amyloid precursor protein internalization.

Published
1996

Catalog

Books, media, physical & digital resources
See catalog results