• Tuberculosis and Respiratory Diseases
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• v.47 no.3
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• pp.347-355
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• 1999

Background: Phospholipase C(PLC) plays a central role in cellular signal transduction and is important in cellular growth, differentiation and transformation. There are currently ten known mammalian isozymes of PLC reported to this date. Hydrolysis of phosphatidylinositol 4,5-bisphosphate($PIP_2$) by PLC produces two important second messengers, inositol 1,4,5-trisphosphate($IP_3$) and diacylglycerol. PLC-${\gamma}1$, previously, was known to be activated mainly through growth factor receptor tyrosine kinase. Other mechanisms of activating PLC-yl have been reported such as activation through tau protein in the presence of arachidonic acid in bovine brain and activation by $IP_3$, phosphatidic acid, etc. Very recently, another PLC-${\gamma}1$ activator protein such as tau has been found in bovine lung tissue, which now is considered to be AHNAK protein. But there has been no report concerning AHNAK and its associated disease to this date. In this study, we examined the expression of the PLC-${\gamma}1$ activator, AHNAK, in lung cancer specimens and their paired normal. Methods: From surgically resected human lung cancer tissues taken from twenty-eight patients and their paired normal counterparts, we evaluated expression level of AHNAK protein using immunoblot analysis of total tissue extract Immunohistochemical stain was performed with primary antibody against AHNAK protein. Results: Twenty-two among twenty-eight lung cancer tissues showed overexpression of AHNAK protein (eight of fourteen squamous cell lung cancers, all of fourteen adenocarcinomas). The resulting bands were multiple ranging from 70 to 200 kDa in molecular weight and each band was indistinct and formed a smear, reflecting mobility shift mainly due to proteolysis during extraction process. On immunohistochemistry, lung cancer tissues showed a very heavy, dense staining with anti-AHNAK protein antibody as compared to the surrounding normal lung tissue, coresponding well with the results of the western blot Conclusion: The overexpression of PLC-${\gamma}1$ activator protein, AHNAK in lung cancer may provide evidence that the AHNAK protein and PLC-${\gamma}1$ act in concerted manner in carcinogenesis.

• Food Science and Preservation
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• v.18 no.4
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• pp.467-474
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• 2011

As a serial study to investigate optimum storing temperature of fresh ginseng (Panax ginseng C. A. Meyer), the respiration rate and internal quality of the ginseng was compared during storage for 16 weeks at $-3^{\circ}C$, $-1.5^{\circ}C$ and $0^{\circ}C$. At initial storage period, respiration rate of fresh ginseng was lower at lower temperature, but thereafter it was negligible. Changes in the firmness of fresh ginseng were not significantly different by the storage temperature. The soluble solids content in fresh ginseng was rapidly increased in the early part of storage, and fresh ginseng stored at a lower temperature had a lower content of soluble solids. The iodine-stained color for starch of the main root was rapidly changed for 4 weeks, and L value of the color was the highest in the center, followed by the cambium and the cortex. pH were a little change depending upon the storage temperature, and as a whole, pH was the lowest at $-3^{\circ}C$, followed by $-1.5^{\circ}C$ and $0^{\circ}C$. Although the content of crude saponin tended to somewhat increased as the storage period passed, the effect of storage temperature on changes in the content was not clear. In the sensory evaluation of 'unique flavor' of fresh ginseng using 5 point scale, higher than 3 point was marked for 8 weeks at $-3^{\circ}C$, 14 weeks at $-1.5^{\circ}C$ and 16 weeks at $-0^{\circ}C$ during storage (p < 0.05).

• Korean Journal of Breeding Science
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• v.51 no.3
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• pp.190-200
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• 2019

It is reported that the absence of lipoxygenase-3 (LOX-3) may contribute to a reduction in stale flavor after the storage of rice. To improve the quality of stored rice of the Korean japonica rice cultivar, we conducted a breeding program to develop near-isogenic rice without LOX-3 in the genetic background of Saenuri, a mega variety of Korea. In the first step of the breeding program, we used a donor parent of LOX-3 null, Daw Dam, and a recurrent japonica parent, Sindongjin, to develop HR27873-AC12 by backcross (BC₁), color test for introgression of lox-3, and anther culture for rapid fixation. In the second step, we used the donor parent, HR27873-AC12, and the recurrent parent, Saenuri, to develop HR28896-31-3-1-1 by backcross (BC₁), marker-assisted selection (MAS) for lox-3, and phenotypic selection (PS) for agronomic traits. Finally, in the third step, we developed HR30960-186-2-1-2-1 (Jeonju624), derived from a cross between Saenuri and HR28896-31-3-1-1, by MAS for lox-3 and PS with high selection pressure for agronomic characteristics. Jeonju624 was confirmed with the introgression of lox-3 by molecular marker. Jeonju624 was a mid-late maturing rice with similar agronomic characteristics to Saenuri, lodging tolerance with short culm, erect plant architecture, and resistance to bacterial blight and rice stripe virus. The yield components of Jeonju624 were mostly similar to Saenuri, except for the 1,000-grain weight of brown rice. The appearance of the grain of Jeonju624 was better than that of Saenuri, and the characteristics of cooked rice were similar to those of Saenuri. In the genetic background analysis using 406 KASP (Kompetitive Allele-Specific PCR) markers, Jeonju624 was confirmed to be the near-isogenic line (NIL) of Saenuri with a 95.8% recovery rate. Jeonju624 is the NIL of Saenuri without LOX-3, and overcomes the linkage drag of Daw Dam with similar agronomic characteristics and genetic background to Saenuri. Jeonju624 can be utilized as a practical cultivar to improve the quality of stored rice, breeding material for the introgression of lox-3, and genetic material to elucidate the effect of introgressed genes.

• Tuberculosis and Respiratory Diseases
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• v.40 no.3
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• pp.213-222
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• 1993

Background : Bronchial asthma has been known as an inflmmatory disease. There have been many evidences that polymorphonuclear leukocytes (PMN) might play an important role in the pathogrnesis of asthma. Although many investigators suggested that pneumocyte injury by PMN-derived oxygen radicals may contribute to the pathogenesis of asthma, there has been few report for a direct evidence of oxygen radicals-mediated pneumocyte injury in bronchial asthma. Furthermore the exact mechanism of oxygen radicals-mediated pneumocyte injury is still controversy. This study was designed to establish a direct in vitro evidence and its clinical significance of pneumocyte injury by PMN-derived superoxide anion in bronchial asthma and to elucidate the main mechanism of superoxide anion-mediated pneumocyte injury. Methods : 12 stable asthmatics and 5 healthy volunteers were participated in this study. PMN was separated from peripheral venous blood samples by using dextran sedimentation and Ficoll-Hypaque density gradient separation method. Superoxide anion productions by PMN and plasma SOD activities were measured by spectrophotometric assay using the principle of SOD inhibitable cytochrome c reduction. PMN-mediated pneumocyte injuries were measured by $^{51}Cr$-release assay using A549 pneumocytes and were expressed as percent lysis and percent detachment. Results: 1) PMN from asthmatics produced more amount of superoxide anion compared to PMN from normal subjects ($6.65{\pm}0.58$ vs $2.81{\pm}0.95\;nmol/1{\times}10^6$ cells, p<0.05), and showed an inverse correlation with $FEV_1$(R=-0.63, p<0.05), but no correlation with $PC_{20}$ histamine in asthmatics. 2) Plasma SOD activities were decreased in asthmatics compared to normal subjects but not significant, and showed a positive correlation with $FEV_1$(R=0.63, p<0.05) but no correlation with $PC_{20}$ histamine in asthmatics. 3) There were a positive correlation between plasma SOD activity and superoxide anion production by PMN in normal subjects (R=0.88, p<0.05) but not in asthmatics. 4) PMN-mediated pneumocyte injury was predominantly expressed as cell detachment rather than cell lysis in both groups, and PMN from asthmatics showed more potent cytotoxic effect on A549 pneumocytes compated to PMN from normal subjects. PMN-mediated detachment rather than lysis of A549 pneumocytes was significantly inhibited by in vitro SOD but not by diluted serum. 5) PMN-mediated detachment rather than lysis of A549 pneumocytes showed a good correlation with superoxide anion production by PMN (R=0.90 in normal subjects, R=0.82 in asthmatics, p<0.05) but no correlation with plasma SOD activity. PMN-mediated pneumocyte injuries were not correlated with $FEV_1$ or $PC_{20}$ histamine in asthmatics. 6) There were no significant differences in PMN-mediated pneumocyte injuries between allergic and nonallergic asthmatics. Conclusion : Our results suggest that pneumocyte injury by PMN-derived superoxide anion may partially contribute to the pathogenesis of asthma and that cell detachment rather than cell lysis may be the mechanism of superoxide anion-mediated pneumocyte injury.