• The Korean Journal of Applied Statistics
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• v.5 no.2
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• pp.243-254
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• 1992

In the present study two sets of unbalanced two-way cross-classification data with and without empty cell(s) were used to evaluate empirically the various sums of squares in the analysis of variance table. Searle(1977) and Searle et.al.(1981) developed a method of computing R($\alpha$\mid$\mu, \beta$) and R($\beta$\mid$\mu, \alpha$) by the use of partitioned matrix of X'X for the model of no interaction, interchanging the columns of X in order of $\alpha, \mu, \beta$ and accordingly the elements in b. An alternative way of computing R($\alpha$\mid$\mu, \beta$), R($\beta$\mid$\mu, \alpha$) and R($\gamma$\mid$\mu, \alpha, \beta$) without interchanging the columns of X has been found by means of,$(X'X)^-$ derived, using $W_2 = Z_2Z_2-Z_2Z_1(Z_1Z_1)^-Z_1Z_2$. It is true that $R(\alpha$\mid$\mu,\beta,\gamma)\Sigma = SSA_W and R(\beta$\mid$\mu,\alpha,\gamma)\Sigma = SSB_W$ where $SSA_W$ and means analysis and $R(\gamma$\mid$\mu,\alpha,\beta) = R(\gamma$\mid$\mu,\alpha,\beta)\Sigma$ for the data without empty cell, but not for the data with empty cell(s). It is also noticed that for the datd with empty cells under W - restrictions $R(\alpha$\mid$\mu,\beta,\gamma)_W = R(\mu,\alpha,\beta,\gamma)_W - R(\mu,\alpha,\beta,\gamma)_W = R(\alpha$\mid$\mu) and R(\beta$\mid$\mu,\alpha,\gamma)_W = R(\mu,\alpha,\beta,\gamma)_W - R(\mu,\alpha,\beta,\gamma)_W = R(\beta$\mid$\mu) but R(\gamma$\mid$\mu,\alpha,\beta)_W = R(\mu,\alpha,\beta,\gamma)_W - R(\mu,\alpha,\beta,\gamma)_W \neq R(\gamma$\mid$\mu,\alpha,\beta)$. The hypotheses $H_o : K' b = 0$ commonly tested were examined in the relation with the corresponding sums of squares for $R(\alpha$\mid$\mu), R(\beta$\mid$\mu), R(\alpha$\mid$\mu,\beta), R(\beta$\mid$\mu,\alpha), R(\alpha$\mid$\mu,\beta,\gamma), R(\beta$\mid$\mu,\alpha,\gamma), and R(\gamma$\mid$\mu,\alpha,\beta)$ under the restrictions.

• Food Industry And Nutrition
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• v.4 no.3
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• pp.83-87
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• 1999

Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by insulin resistance and impaired insulim secretion. The transgenic technology, in which a specific gene can be introduced or deleted to study its function, has been established. A number of transgenic mice, altered the expression of genes potentially involved in insulin action or pancreatic ${\beta}$-cell function, have recently been developed to address questions concerning NIDDM. Thransgenic mice model may help understanding the molecular basis of complex patho-physiologies of NIDDM. This review outlines the new insights obtained from the studies of transgenic mice that overxpress or show decreased expression of putative key genes involved in the regulation of insulin resistance and pancreatic ${\beta}$-cell function, therefore in the control of glucose homeostasis.

• 한국약용작물학회:학술대회논문집
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• 2011.09a
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• pp.31-45
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• 2011

The amyloid ${\beta}$-peptide ($A{\beta}$), which originates from the proteolytic cleavage of amyloid precursor protein (APP), plays a central role in the pathogenesis of Alzheimer's disease (AD). Mounting evidence indicates that different species of $A{\beta}$, such as $A{\beta}$ oligomers and fibrils, may contribute to AD pathogenesis via distinct mechanisms at different stages of the disease. Importantly, elevation and accumulation of soluble $A{\beta}$ oligomers closely correlate with cognitive decline and/or disease progression in animal models of AD. In agreement with these studies, oligomers of $A{\beta}$ have been shown to directly affect synaptic plasticity, a neuronal process that is known to be essential for memory formation. Our previous studies showed that $A{\beta}$ induces the breakdown of phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), a phospholipid that regulates key aspects of neuronal function. PI(4,5)P2 breakdown was found to be a key step toward synaptic and memory dysfunction in a mouse model of AD. To this end, we seek to identify small molecules that could elevate the levels of PI(4,5)P2 and subsequently block $A{\beta}$ oligomer-induced breakdown of PI(4,5)P2 and synaptic dysfunction.. We found that (20S)Rg3, an active triterpene glycoside from heat-processed ginseng, serves as an agonist for phosphatidylinositol 4-kinase IIalpha (PI4KIIalpha), which is a lipid kinase that mediates a rate-limiting step in PI(4,5)P2 synthesis. Consequently, (20S)Rg3 stimulates PI(4,5)P2 synthesis by directly stimulating the activity of PI4KIIalpha. Interestingly, treatment of a mouse model of AD with (20S)Rg3 leads to reversal of memory deficits. Our data suggest that the PI(4,5)P2-promoting effects of (20S)Rg3 may help mitigate the cognitive symptoms associated with AD.

• Journal of Periodontal and Implant Science
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• v.44 no.6
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• pp.274-279
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• 2014

Purpose: To evaluate whether the levels of immunoglobulin G (IgG) antibody to Tanerella forsythia are associated with periodontal status. Methods: Patients with a diagnosis of chronic periodontitis were considered candidates for the study; thus 80 chronic periodontitis patients and 28 healthy persons (control group) were invited to participate in this investigation. The presence of T. forsythia was detected by polymerase chain reaction (PCR) analysis using primers designed to target the respective 16S rRNA gene sequences. Peripheral blood was collected from each subject to identify the IgG1 and IgG2 serum antibodies against T. forsythia. All microbiological and immunological laboratory processes were completed blindly, without awareness of the clinical status of the study patients or of the periodontal sites tested. Results: The bivariate analysis showed that lower mean levels of clinical attachment level (CAL) and probing depth were found in the presence of the IgG1 antibody titers against whole-cell T. forsythia; however, only the difference in CAL was statistically significant. In the presence of the IgG2 antibody titers against whole-cell T. forsythia, the periodontal parameters evaluated were higher but they did not show statistical differences, except for plaque. The unadjusted linear regression model showed that the IgG1 antibody against whole-cell T. forsythia in periodontitis patients was associated with a lower mean CAL (${\beta}=-0.654$; 95% confidence interval [CI], -1.27 to -0.28; P<0.05). This statistically significant association remained after adjusting for possible confounders (${\beta}=-0.655$; 95% CI, -1.28 to -0.29; P<0.05). On the other hand, smoking was a statistically significant risk factor in the model (${\beta}=0.704$; 95% CI, 0.24 to 1.38; P<0.05). Conclusions: Significantly lower mean levels of CAL were shown in the presence of the IgG1 antibody titers against whole-cell T. forsythia in periodontitis patients. Thus, the results of this study suggest that IgG1 antibody to T. forsythia may have been a protective factor from periodontitis in this sample.

• Bulletin of the Korean Chemical Society
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• v.32 no.2
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• pp.451-454
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• 2011

The traditional BCS superconductors $AOs_2O_6$ (A=K, Rb, and Cs) were investigated to find the relationship between their structures and superconducting transition temperatures. The $T_c$ decreases with increasing the unit cell parameter of $AOs_2O_6$. This is in contrast to the case of conventional BCS superconductivity in a single bond model, where $T_c$ may increase with increasing the the unit cell parameter since the DOS at Fermi level increases as the unit cell parameter increases. Instead, the $T_c$ of a $\beta$-pyrochlore oxide is proportional to the lattice softness of the compound.

• Journal of Microbiology and Biotechnology
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• v.27 no.11
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• pp.2044-2051
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• 2017

The main pathological hallmark of Alzheimer's disease is the deposition of amyloid-beta ($A{\beta}$) peptides in the brain. $A{\beta}$ has been widely used to mimic several aspects of Alzheimer's disease. However, several characteristics of amyloid-induced Alzheimer's disease pathology are not well established, especially in mice. The present study aimed to develop a new Alzheimer's disease model by investigating how $A{\beta}$ can be effectively aggregated using prokaryotes and eukaryotes. To express the $A{\beta}42$ complex in HEK293 cells, we cloned the $A{\beta}42$ region in a tandem repeat and incorporated the resulting construct into a eukaryotic expression vector. Following transfection into HEK293 cells via lipofection, cell viability assay and western blotting analysis revealed that exogenous $A{\beta}42$ can induce cell death and apoptosis. In addition, recombinant His-tagged $A{\beta}42$ was successfully expressed in Escherichia coli BL21 (DE3) and not only readily formed $A{\beta}$ complexes, but also inhibited the proliferation of SH-SY5Y cells and E. coli. For in vivo testing, recombinant His-tagged $A{\beta}42$ solution ($3{\mu}g/{\mu}l$ in $1{\times}PBS$ containing $1mM\;Ni^{2+}$) was injected stereotaxically into the left and right lateral ventricles of the brains of C57BL/6J mice (n = 8). Control mice were injected with $1{\times}PBS$ containing $1mM\;Ni^{2+}$ following the same procedure. Ten days after the sample injection, the Morris water maze test confirmed that exogenous $A{\beta}$ caused an increase in memory loss. These findings demonstrated that $Ni^{2+}$ is capable of complexing the 50-kDa amyloid and that intracerebroventricular injection of $A{\beta}42$ can lead to cognitive impairment, thereby providing improved Alzheimer's disease models.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.19 no.4
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• pp.414-434
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• 1997

Though many genetic and epigenetic alterations have been identified in hamster oral carcinogenesis model, there is no information about the possible role of transforming growth factor related with oral cancer. The purpose of this paper was to find the expression patterns of transforming growth factor alpha and beta during the stages of complete oral carcinogenesis model in hamster. 0.5% 9, 10-dimethyl-1, 2-benzanthracene(DMBA) in mineral oil was topically applied to the buccal pouch of 75 hamster three times a week during the experimental periods. The experimental animals were subdivided into two groups of control and experiment. Only the mineral oil was applied to the control group. 0.5% DMBA in mineral oil was applied to the experimental groups of 6, 8, 10, 12, 14, 16, 18 and 20 weeks. The expression of the $TGF-{\alpha}$ and $TGF-{\beta}$ protein were evaluated by the distribution and intensity of positive cells during the carcinogenesis using the immunohistochemical study. The following results were obtained ; 1. The buccal pouch epithelium of hamster was histologically changed to the dysplasia at 6, 8, 10 weeks, carcinoma in situ at 12 weeks, and squamous cell carcinoma at 14 weeks. 2. The expression of the $TGF-{\alpha}$ was restricted to the parabasal and basal layers of the normal and dysplastic mucosa, but those positive cells were extended to the spinous layers of the epithelium in the carcinoma. 3. The degree of $TGF-{\alpha}$ expression was markedly decreased in the carcinoma at 16, 18, 20. The strong positive staining in the center of cancer islands and weak positive staining in periphery of tumor were seen at the stage of squamous cell carcinoma. 4. The positive index of the $TGF-{\alpha}$ had a tendency to increase with DMBA- applied time. There was a statistically significant difference between 12, 18, 20 experimental group and control group (p<0.05). 5. The expression of the $TGF-{\beta}$ was shown at the cytoplasm of all control and experimental groups, and the parabasal and basal layers of the normal and dyslastic mucosa, but it was shown at the basal layers of the epithelium in the carcinoma. 6. $TGF-{\beta}$ was expressed diffusely at 16, 18, 20 experimental group. The strong positive staining in the center of cancer islands and positive staining in periphery of tumor were seen at the stage of squamous cell carcinoma. From the above findings, the expression of $TGF-{\alpha}$ and ${\beta}$ in oral carcinogenesis model seems to have two formal stages, the first being an overexpression step as reaction to uncontrolled growth and the second being one in which external protein accumulate in the surrounding stroma and intracytoplasm. Overexpression of $TGF-{\alpha}$ and ${\beta}$ may have important cooperative roles for the promotion of cancer and factor of prognosis.

• Biomolecules & Therapeutics
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• v.26 no.5
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• pp.458-463
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• 2018

The phosphorylation of JNK is known to induce insulin resistance in insulin target tissues. The inhibition of JNK-JIP1 interaction, which interferes JNK phosphorylation, becomes a potential target for drug development of type 2 diabetes. To discover the inhibitors of JNK-JIP1 interaction, we screened out 30 candidates from 4320 compound library with In Cell Interaction Trap method. The candidates were further confirmed and narrowed down to five compounds using the FRET method in a model cell. Among those five compounds, Acebutolol showed notable inhibition of JNK phosphorylation and elevation of glucose uptake in diabetic models of adipocyte and liver cell. Structural computation showed that the binding affinity of Acebutolol on the JNK-JIP1 interaction site was comparable to the known inhibitor, BI-78D3. Our results suggest that Acebutolol, an FDA-approved beta blocker for hypertension therapy, could have a new repurposed effect on type 2 diabetes elevating glucose uptake process by inhibiting JNK-JIP1 interaction.

• Journal of the Korean Society of Radiology
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• v.11 no.3
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• pp.147-151
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• 2017

Potentially lethal damage repair (PLDR) in HFL-I was investigated by delayed plating experiments. The surviving fraction data were fitted to the linear Quadratic equation ($LogSn=-n{\gamma}({\alpha}d+{\beta}d^2$) where ${\gamma}=1$ for immediate plating). And a repair factor ${\gamma}$ was developed to compare survival for immediate and delayed plating. When we only took into account the repair factor of PLDR ${\gamma}$ which was derived from the delay assay, the cell survival response th fractionated carbon ion irradiation was not fully matched. This gap suggested that consideration of another repair process is necessary. So this suggests that the various repair process plays an important role in the fractionated irradiations.

• Archives of Plastic Surgery
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• v.34 no.1
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• pp.8-12
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• 2007

Purpose: Protein tyrosine kinase(PTK), protein kinase C(PKC), oxidase, as a mediator, have been known to take a role in signal transduction pathway of angiogenesis. The authors confirmed that PKC is the most noticeable mediator for abnormal proliferation of vascular endothelial cells through in vitro study model using the inhibitors, targeting the formation of three co-enzymes. In this study, we would investigate which isoform of PKC play an important role in abnormal angiogenesis of vascular endothelial cell. Methods: In 96 well plates, $10^4$ HUVECs(human umbilical vein endothelial cells) were evenly distributed. Two groups were established; the control group without administration of DMH(1,2-dimethylhydrazine) and the DMH group with administration of $7.5{\times}10^{-9}M$ DMH. RNA was extracted from vascular endothelial cell of each group and expression of the PKC isoform was analyzed by RT-PCR(reverse transcriptase-polymerase chain reaction) method. Results: RT-PCR analysis showed that $PKC{\alpha}$, $-{\beta}I$, $-{\beta}II$, $-{\eta}$, $-{\mu}$ and $-{\iota}$ were expressed in vascular endothelial cells of each group. DMH incresed the expression of $PKC{\alpha}$ and $PKC{\mu}$, and decreased $PKC{\beta}I$, $PKC{\beta}II$ expression dominantly. Conclusion: Based on the result of this study, it was suggested that $PKC{\alpha}$ and $PKC{\mu}$ may have significant role in abnormal proliferation of vascular endothelial cell.