• Tuberculosis and Respiratory Diseases
• /
• v.50 no.2
• /
• pp.229-235
• /
• 2001

Background : Alpha-1-antitrypsin (A1AT) deficiency is the only established genetic risk factor for emphysema. This study was undertaken to investigate the prevalence of the genotypes of A1AT genotypes in healthy Koreans. Method : The study population consisted of 380 Healthy Koreans enrolled at the Health Promotion Center in Kyungpook National University Hospital. The polymerase chain reaction (PCR) and restriction fragment length polymorphim (RFLP) for detecting the A1AT variants M1(Ala), M1(Val), M2, S and Z were used. Results : The genotypes of subjects were as follows : M1(Val)/M1(Val), 254(66.8%) ; M1(Val)/M2, 105(27.6%) ; M2/M2, 19 (5.0%) ; and M1(Val)/M1(Ala), 2 (0.5%). There was no case with 'deficiency' alleles such as S and Z found in this study. Conclusion : These results suggest that A1AT deficient alleles are either extremely rare or not present in Koreans.

• Journal of Life Science
• /
• v.9 no.5
• /
• pp.504-509
• /
• 1999

The trend of organogenesis in Xenopus presumptive ectoderm was studied by combined dose of activin A and IGF-1(insulin-like growth factor-1). In reference study of Asashima and his colleagues, the inductive patterns of various organs were reported with activin, the potent mesoderm inducing factor. In present study, the inducing pattern was cleared with combined-dose of concentration 1-100 ng/ml activin A and IGF-1. In addition, the result from single treatment of activin A was compared with former study. As a result, eye was differentiated in 5-20% of explants at 10 and 50 ng/ml concentrative combination of activin A. Otic vesicle was appeared in the entire concentrative combination of IGF-1. Pronephric duct was induced 19-38% of explants at the concentration of activin A 100 ng/ml by adding IGF-1. The comparison of single treatment of activin A was showed some difference in dose-dependent inducing pattern.

• Tuberculosis and Respiratory Diseases
• /
• v.62 no.1
• /
• pp.33-42
• /
• 2007

Background: Heme oxygenase-1 (HO-1) is known to modulates the cellular functions, including cell proliferation and apoptosis. It is known that a high level of HO-1 expression is found in many tumors, and HO-1 plays an important role in rapid tumor growth on account of its antioxidant and antiapoptotic effects. Cisplatin is a widely used anti-cancer agent for the treatment of lung cancer. However, the development of resistance to cisplatin is a major obstacle to its use in clinical treatment. We previously demonstrated that inhibiting HO-1 expression through the transcriptional activation of Nrf2 induces apoptosis in A549 cells. The aim of this study was to determine of the inhibiting HO-1 enhance the chemosensitivity of A549 cells to cisplatin. Materials and Methods: The human lung cancer cell line, A549, was treated cisplatin, and the cell viability was measured by a MTT assay. The change in HO-1, Nrf2, and MAPK expression after the cisplatin treatment was examined by Western blotting. HO-1 inhibition was suppressed by ZnPP, which is a specific pharmacologic inhibitor of HO activity, and small interfering RNA (siRNA). Flow cytometry analysis and Western blot were performed in to determine the level of apoptosis. The level of hydrogen peroxide ($H_2O_2$) generation was monitored fluoimetrically using 2',7'-dichlorofluorescein diacetate. Results: The A549 cells showed more resistance to the cisplatin treatment than the other cell lines examined, whereas cisplatin increased the expression of HO-1 and Nrf2, as well as the phosphorylation of MAPK in a time-dependent fashion. Inhibitors of the MAPK pathway blocked the induction of HO-1 and Nrf2 by the cisplatin treatment in A549 cells. In addition, the cisplatin-treated A549 cells transfected with dither the HO-1 small interfering RNA (siRNA) or ZnPP, specific HO-1 inhibitor, showed in a more significantly decrease in viability than the cisplatin-only-treated group. The combination treatment of ZnPP and cisplatin caused in a marked increase in the ROS generation and a decrease in the HO-1 expression. Conclusion: Cisplatin increases the expression of HO-1, probably through the MAPK-Nrf2 pathway, and the inhibition of HO-1 enhances the chemosensitivity of A549 cells to cisplatin.

• Molecules and Cells
• /
• v.46 no.12
• /
• pp.757-763
• /
• 2023

In this study, we examine whether a change in the protein levels for FOP in Ankyrin repeat and SAM domain-containing protein 1A (ANKS1A)-deficient ependymal cells affects the intraflagellar transport (IFT) protein transport system in the multicilia. Three distinct abnormalities are observed in the multicilia of ANKS1A-deficient ependymal cells. First, there were a greater number of IFT88-positive trains along the cilia from ANKS1A deficiency. The results are similar to each isolated cilium as well. Second, each isolated cilium contains a significant increase in the number of extracellular vesicles (ECVs) due to the lack of ANKS1A. Third, Van Gogh-like 2 (Vangl2), a ciliary membrane protein, is abundantly detected along the cilia and in the ECVs attached to them for ANKS1A-deficient cells. We also use primary ependymal culture systems to obtain the ECVs released from the multicilia. Consequently, we find that ECVs from ANKS1A-deficient cells contain more IFT machinery and Vangl2. These results indicate that ANKS1A deficiency increases the entry of the protein transport machinery into the multicilia and as a result of these abnormal protein transports, excessive ECVs form along the cilia. We conclude that ependymal cells make use of the ECV-based disposal system in order to eliminate excessively transported proteins from basal bodies.

• Honam Mathematical Journal
• /
• v.38 no.4
• /
• pp.753-782
• /
• 2016

In this paper we deduce the number of representations of a positive integer n by each of the six triangular forms as $${\frac{1}{2}}x_1(x_1+1)+{\frac{3}{2}}x_2(x_2+1)+{\frac{3}{2}}x_3(x_3+1)+{\frac{3}{2}}x_4(x_4+1),\\{\frac{1}{2}}x_1(x_1+1)+{\frac{1}{2}}x_2(x_2+1)+{\frac{3}{2}}x_3(x_3+1)+{\frac{3}{2}}x_4(x_4+1),\\{\frac{1}{2}}x_1(x_1+1)+{\frac{1}{2}}x_2(x_2+1)+{\frac{1}{2}}x_3(x_3+1)+{\frac{3}{2}}x_4(x_4+1),\\x_1(x_1+1)+x_2(x_2+1)+{\frac{3}{2}}x_3(x_3+1)+{\frac{3}{2}}x_4(x_4+1),\\x_1(x_1+1)+{\frac{3}{2}}x_2(x_2+1)+{\frac{3}{2}}x_3(x_3+1)+3x_4(x_4+1),\\{\frac{1}{2}}x_1(x_1+1)+{\frac{1}{2}}x_2(x_2+1)+3x_3(x_3+1)+3x_4(x_4+1).$$

• Microbiology and Biotechnology Letters
• /
• v.21 no.4
• /
• pp.293-298
• /
• 1993

The ppage resistance mechanism of Lactococcus lactis subsp. cremoris ATCC 11602-A1 was investigated. When parent and A1 were incubated at 30 and 40$^{\circ}C$, A1 grew well and multiplication of phage(MOI=1)on A1 slightly occurred at 40$^{\circ}C$ in contrast with parent. There was a great difference of proteolytic activity between parent and A1, irrespective of the temperature. As a result of ADS treatment oon culture broth, survival rate of A1 was 27% at the lethal concentration of parent and adsorption rate of phage was increased to 95~97%, which was considered to come from the exposure of phage receptor site masked by an unknown component. These results suggest that acridine orange (AO) treatment leads to the modification of cell wall, conferring resistance to high temperature and lytic phage. No change in plasmid profiles of A1 at 30 and 40$^{\circ}C$ were found, which suggests that plasmid is not relative to temperature-resistance of A1.

• Bulletin of the Korean Mathematical Society
• /
• v.52 no.1
• /
• pp.105-123
• /
• 2015

Let $f_{\beta}=h_{\beta}+\bar{g}_{\beta}$ and $F_a=H_a+\bar{G}_a$ be harmonic mappings obtained by shearing of analytic mappings $h_{\beta}+g_{\beta}=1/(2isin{\beta})log\((1+ze^{i{\beta}})/(1+ze^{-i{\beta}})\)$, 0 < ${\beta}$ < ${\pi}$ and $H_a+G_a=z/(1-z)$, respectively. Kumar et al. [7] conjectured that if ${\omega}(z)=e^{i{\theta}}z^n({\theta}{\in}\mathbb{R},n{\in}\mathbb{N})$ and ${\omega}_a(z)=(a-z)/(1-az)$, $a{\in}(-1,1)$ are dilatations of $f_{\beta}$ and $F_a$, respectively, then $F_a\tilde{\ast}f_{\beta}{\in}S^0_H$ and is convex in the direction of the real axis, provided $a{\in}[(n-2)/(n+2),1)$. They claimed to have verified the result for n = 1, 2, 3 and 4 only. In the present paper, we settle the above conjecture, in the affirmative, for ${\beta}={\pi}/2$ and for all $n{\in}\mathbb{N}$.

• Journal of Electrodiagnosis and Neuromuscular Diseases
• /
• v.20 no.2
• /
• pp.148-152
• /
• 2018

Myotonic dystrophy type 1 (DM1) is an autosomal dominant multisystem disorder and one of the most common muscular dystrophies affecting adults. Charcot-Marie-Tooth (CMT) disease, a common hereditary neuropathy, is characterized by atrophy of the distal limbs and peripheral nerve abnormalities. The authors report a rare case involving a 24-year-old female who was diagnosed simultaneously with both DM1 and CMT1A based on the results of a nerve conduction study (NCS). The patient, who had previously been diagnosed with DM1, was admitted for lower extremity pain. Her electrodiagnostic examination continued to reveal severe sensorimotor demyelinating polyneuropathy, and a genetic study was performed to confirm whether she had other hereditary neuropathies, except DM1, that suggested CMT1A, the most common phenotype of CMT. Severe abnormalities in an NCS in a DM1 patient may suggest the incidental coexistence of hereditary neuropathies, and further evaluations, such as genetic studies, should be performed for proper diagnosis.

• Journal of the Korean Mathematical Society
• /
• v.38 no.3
• /
• pp.595-611
• /
• 2001

Let Q(n,1) be the set of even unimodular positive definite integral quadratic forms in n-variables. Then n is divisible by 8. For A[X] in Q(n,1), the theta series $\theta$(sub)A(z) = ∑(sub)X∈Z(sup)n e(sup)$\pi$izA[X] (Z∈h (※Equations, See Full-text) the complex upper half plane) is a modular form of weight n/2 for the congruence group Γ$_1$(8) = {$\delta$∈SL$_2$(Z)│$\delta$≡()mod 8} (※Equation, See Full-text). If n$\geq$24 and A[X], B{X} are tow quadratic forms in Q(n,1), the quotient $\theta$(sub)A(z)/$\theta$(sub)B(z) is a modular function for Γ$_1$(8). Since we identify the field of modular functions for Γ$_1$(8) with the function field K(X$_1$(8)) of the modular curve X$_1$(8) = Γ$_1$(8)＼h(sup)* (h(sup)* the extended plane of h) with genus 0, we can express it as a rational function of j(sub) 1,8 over C which is a field generator of K(X$_1$(8)) and defined by j(sub)1,8(z) = $\theta$$_3$(2z)/$\theta$$_3$(4z). Here, $\theta$$_3$ is the classical Jacobi theta series.

• Archives of Pharmacal Research
• /
• v.29 no.7
• /
• pp.570-576
• /
• 2006

Phytoestrogen biochanin A is an isoflavone derivative isolated from red clover Trifolium pratense with anticarcinogenic properties. This study examined the action of biochanin A with the carcinogen activation pathway that is mediated by the aryl hydrocarbon receptor (AhR) in MCF-7 breast carcinoma cells. Treating the cells with biochanin A alone caused the accumulation of CYP1A1 mRNA and an increase in CYP1A1-specific 7-ethoxyresorufin O-deethylase (EROD) activity in a dose dependent manner. A concomitant treatment with 7,12-dimethylbenz[a]anthracene (DMBA) and biochanin A markedly reduced the DMBA-inducible EROD activity and CYP1A1 mRNA level. In addition, the biochanin A treatment alone activated the DNA-binding capacity of the AhR for the dioxin-response element (DRE) of CYP1A1, as measured by the electrophoretic-mobility shift assay (EMSA). EMSA revealed that biochanin A reduced the level of the DMBA-inducible AhR-DRE binding complex. Furthermore, biochanin A competed with the prototypical AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), for binding to the AhR in an isolated rat cytosol. The biochanin A competitively inhibited the metabolic activation of DMBA, as measured by the formation of the DMBA-DNA adducts. These results suggest that biochanin A may thus be a natural ligand to bind on AhR. Therefore, biochanin A may be due to act an antagonist/agonist of the AhR pathway.