• Bulletin of the Korean Mathematical Society
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• v.35 no.1
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• pp.99-117
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• 1998

Let $(B, H, p_1)$ be an abstract Wiener space and $F(B)$ the Fresnel class on $(B, H, p_1)$ which consists of functionals F of the form : $$ F(x) = \int_{H} exp{i(h,x)^\sim} df(h), x \in B, $$ where $(\cdot, \cdot)^\sim$ is a stochastic inner product between H and B, and f is in $M(H)$, the space of complex Borel measures on H. We introduce an $L_1$ analytic Fourier-Feynman transforms for functionls in $F(B)$. Furthermore, we introduce a convolution on $F(B)$, and then verify the existence of the $L_1$ analytic Fourier-Feynman transform for the convolution product of two functionals in $F(B)$, and we establish the relationships between the $L_1$ analytic Fourier-Feynman tranform of the convolution product for two functionals in $F(B)$ and the $L_1$ analytic Fourier-Feynman transforms for each functional. Finally, we show that most results in [7] follows from our results in Section 3.

• Journal of the Korean Mathematical Society
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• v.47 no.2
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• pp.263-275
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• 2010

Let {$X_n;n\;\geq\;1$} be a strictly stationary sequence of negatively associated random variables with mean zero and finite variance. Set $S_n\;=\;{\sum}^n_{k=1}X_k$, $M_n\;=\;max_{k{\leq}n}|S_k|$, $n\;{\geq}\;1$. Suppose $\sigma^2\;=\;EX^2_1+2{\sum}^\infty_{k=2}EX_1X_k$ (0 < $\sigma$ < $\infty$). We prove that for any b > -1/2, if $E|X|^{2+\delta}$(0<$\delta$$\leq$1), then $$lim\limits_{\varepsilon\searrow0}\varepsilon^{2b+1}\sum^{\infty}_{n=1}\frac{(loglogn)^{b-1/2}}{n^{3/2}logn}E\{M_n-\sigma\varepsilon\sqrt{2nloglogn}\}_+=\frac{2^{-1/2-b}{\sigma}E|N|^{2(b+1)}}{(b+1)(2b+1)}\sum^{\infty}_{k=0}\frac{(-1)^k}{(2k+1)^{2(b+1)}}$$ and for any b > -1/2, $$lim\limits_{\varepsilon\nearrow\infty}\varepsilon^{-2(b+1)}\sum^{\infty}_{n=1}\frac{(loglogn)^b}{n^{3/2}logn}E\{\sigma\varepsilon\sqrt{\frac{\pi^2n}{8loglogn}}-M_n\}_+=\frac{\Gamma(b+1/2)}{\sqrt{2}(b+1)}\sum^{\infty}_{k=0}\frac{(-1)^k}{(2k+1)^{2b+2'}}$$, where $\Gamma(\cdot)$ is the Gamma function and N stands for the standard normal random variable.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.4
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• pp.199-204
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• 2008

KIF1B${\beta}$ is a member of the Kinesin superfamily proteins (KIFs), which are microtubule-dependent molecular motors that are involved in various intracellular organellar transport processes. KIF1B${\beta}$ is not restricted to neuronal systems, however, is widely expressed in other tissues, even though the function of KIF1B${\beta}$ is still unclear. To elucidate the KIF1B${\beta}$-binding proteins in non-neuronal cells, we used the yeast two-hybrid system, and found a specific interaction of KIF1B${\beta}$ and the sorting nexin (SNX) 17. The C-terminal region of SNX17 is required for the binding with KIF1B${\beta}$. SNX17 protein bound to the specific region of KIF1Bf3 (813-916. aa), but not to other kinesin family members. In addition, this specific interaction was also observed in the Glutathione S-transferase pull-down assay. An antibody to SNX17 specifically co-immunoprecipitated KIF1B${\beta}$ associated with SNX17 from mouse brain extracts. These results suggest that SNX17 might be involved in the KIF1B${\beta}$-mediated transport as a KIF1B${\beta}$ adaptor protein.

• Journal of Genetic Medicine
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• v.18 no.1
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• pp.16-23
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• 2021

GLB1-related disorders comprise two phenotypically unique disorders: GM1 gangliosidosis and Morquio B disease. These autosomal recessive disorders are caused by b-galactosidase deficiency. A hallmark of GM1 gangliosidosis is central nervous system degeneration where ganglioside synthesis is highest. The accumulation of keratan sulfate is the suspected cause of the bone findings in Morquio B disease. GM1 gangliosidosis is clinically characterized by a neurodegenerative disorder associated with dysostosis multiplex, while Morquio B disease is characterized by severe skeletal manifestations and the preservation of intelligence. Morquio B disease and GM1 gangliosidosis may be on a continuum of skeletal involvement. There is currently no effective treatment for GLB1-related disorders. Recently, multiple interventions have been developed and there are several ongoing clinical trials.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.20
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• pp.8741-8747
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• 2014

Purpose: We aimed to investigate the associations between polymorphisms of interleukin-1A (IL-1A), IL-1B, and IL-1 receptor antagonist (IL-1RN) and prostate cancer (PCa) risk. Materials and Methods: A comprehensive search for articles of MEDLINE and EMBASE databases and bibliographies of retrieved articles published up to August 3, 2014 was performed. Methodological quality assessment of the trials was based on a standard quality scoring system. The meta-analysis was performed using STATA 12.0. Results: We included 9 studies (1 study for IL-1A, 5 studies for IL-1B, and 3 studies for IL-1RN), and significant association was found between polymorphisms of IL-1B-511 (rs16944) as well as IL-1B-31 (rs1143627) and PCa risk. IL-1B-511 (rs16944) polymorphism was significantly associated with PCa risk in homozygote and recessive models, as well as allele contrast (TT vs CC: OR, 0.74; 95%CI, 0.58-0.94; P=0.012; TT vs TC+CC; OR, 0.79; 95%CI, 0.63-0.98; P=0.033; T vs C: OR, 0.86; 95%CI, 0.77-0.96; P=0.008). The association between IL-1B-31 (rs1143627) polymorphism and PCa risk was weakly significant under a heterozygote model (OR, 1.35; 95%CI, 1.00-1.80; P=0.047). Conclusions: Sequence variants in IL-1B-511 (rs16944) and IL-1B-31 (rs1143627) are significantly associated with PCa risk, which provides additional novel evidence that proinflammatory cytokines and inflammation play an important role in the etiology of PCa.

• Kyungpook Mathematical Journal
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• v.49 no.1
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• pp.1-6
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• 2009

Let B(X) denote the algebra of operators on a complex Banach space X, H(X) = {h ${\in}$ B(X) : h is hermitian}, and J(X) = {x ${\in}$ B(X) : x = $x_1$ + $ix_2$, $x_1$ and $x_2$ ${\in}$ H(X)}. Let ${\delta}_a$ ${\in}$ B(B(X)) denote the derivation ${\delta}_a$ = ax - xa. If J(X) is an algebra and ${\delta}_a^{-1}(0){\subseteq}{\delta}_{a^*}^{-1}(0)$ for some $a{\in}J(X)$, then ${\parallel}a{\parallel}{\leq}{\parallel}a-(x^*x-xx^*){\parallel}$ for all $x{\in}J(X){\cap}{\delta}_a^{-1}(0)$. The cases J(X) = B(H), the algebra of operators on a complex Hilbert space, and J(X) = $C_p$, the von Neumann-Schatten p-class, are considered.

• Journal of Food Hygiene and Safety
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• v.13 no.1
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• pp.41-46
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• 1998

A postcolumn derivatization method was tried for the simultaneous determination of four major aflatoxins ($B_1,\;B_2,\;G_1,\;and\;G_2$) by high-performance liquid chromatography with fluorescence detection. As compared with a previous precolumn derivatization method, it was found that the postcolumn derivatization combined with an electrochemical cell (Kobra cell) was less time-consuming, safer, improved the sensitivity and selectivity, and provided good recoveries for aflatoxin $B_1$ (88.9%) and $G_1$ (100.5%). This method showed linearity from 10~100 ppb for aflatoxin $B_1\;and\;G_1$, and from 3~30 ppb for aflatoxin $B_2\;and\;G_2$. However, aflatoxin Bz and Gz were not detected satisfactorily although they showed good resolution.

• IMMUNE NETWORK
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• v.5 no.2
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• pp.68-77
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• 2005

Background: Costimulation is a critical process in Ag-specific immune responses. Both B7.1 and CD28 molecules have been reported to stimulate T cell responses during antigen presentation. Therefore, we tested whether Ag-specific immune responses as well as protective immunity are influenced by coinjecting with B7.1 and CD28 cDNAs in a mouse HSV-2 challenge model system. Methods: ELISA was used to detect levels of antibodies, cytokines and chemokines while thymidine incorporation assay was used to evaluate T cell proliferation levels. Results: Ag-specific antibody responses were enhanced by CD28 coinjection but not by B7.1 coinjection. Furthermore, CD28 coinjection increased IgG1 production to a significant level, as compared to pgD+pcDNA3, suggesting that CD28 drives Th2 type responses. In contrast, B7.1 coinjection showed the opposite, suggesting a Th1 bias. B7.1 coinjection also enhanced Ag-specific Th cell proliferative responses as well as production of Th1 type cytokines and chemokines significantly higher than pgD+pcDNA3. However, CD28 coinjection decreased Ag-specific Th cell proliferative responses as well as production of Th1 types of cytokines and chemokine significantly lower than pgD+pcDNA3. Only MCP-1 production was enhanced by CD28. B7.1 coimmunized animals exhibited an enhanced survival rate as well as decreased herpetic lesion formation, as compared to pgD+pcDNA3. In contrast, CD28 vaccinated animals exhibited decreased survival from lethal challenge. Conclusion: This study shows that B7.1 enhances protective Th1 type cellular immunity against HSV-2 challenge while CD28 drives a more detrimental Th2 type immunity against HSV-2 challenge, supporting an opposite role of B7.1 and CD28 in Ag-specific immune responses to a Th1 vs Th2 type.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.5
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• pp.2491-2497
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• 2016

Background: Human leukocyte antigen (HLA) genes have been implicated in cervical cancer in several populations. Objectives: To study the predispositions of HLA alleles/haplotypes with cervical cancer. Materials and Methods: Clinically diagnosed and PAP smear confirmed cervical cancer patients (n 48) and age matched controls (n 47) were genotyped for HLA-A,-B,-DRB1* and DQB1* alleles by PCR-SSP methods. Results: The frequencies of alleles DRB1*04 (OR=2.57), DRB1*15 (OR=2.04), DQB1*0301 (OR=4.91), DQB1*0601 (OR=2.21), B*15 (OR=13.03) and B*07 (OR=6.23) were higher in cervical cancer patients than in the controls. The frequencies of alleles DRB1*10 (OR=0.22) and B*35 (OR=0.19) were decreased. Strong disease associations were observed for haplotypes DRB1*15-DQB1*0601 (OR=6.56; p< $3.5{\times}10^{-4}$), DRB1*14-DQB1*0501 (OR=6.51; p<0.039) and A*11-B*07 (OR=3.95; p<0.005). The reduced frequencies of haplotypes DRB1*10-DQB1*0501 (OR=0.45), A*03-B*35 (OR=0.25) and A*11-B*35 (OR= 0.06) among patients suggested a protective association. HLA-C* typing of 8 patients who possessed a unique three locus haplotype 'A*11-B*07-DRB1*04' (8/48; 16.66%; OR=6.51; p<0.039) revealed the presence of a four locus haplotype 'A*11-B*07-C*01-DRB1*04' in patients (4/8; 50%). Amino acid variation analysis of susceptible allele DQB1*0601 suggested 'tyrosine' at positions ${\beta}9$ and ${\beta}37$ and tyrosine-non-tyrosine genotype combination increased the risk of cervical cancer. Conclusions: Strong susceptible associations were documented for HLA alleles B*15, B*07, DRB1*04, DRB1*15, DQB1*0301, DQB1*0601 and haplotypes DRB1*15-DQB1*0601 and DRB1*14-DQB1*0501. Further, protective associations were evidenced for alleles B*35 and DRB1*10 and haplotypes A*11-B*35 and DRB1*10-DQB1*0501 with cervical cancer in South India.

• Journal of Life Science
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• v.30 no.12
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• pp.1070-1077
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• 2020

Treatment with anticancer drugs changes the expression of multiple genes related to cell proliferation, migration, and drug resistance. These changes in gene expression may be connected to regulatory networks for each other. This study showed that doxorubicin treatment induces the expression of oncogenic FosB and decreases the expression of oncogenic SETDB1 in A549 and H1299 human lung cancer cells, which are different in tumor suppressor p53 status. However, a small difference was detected in the quantitative expression of those proteins in the two kinds of cells. To examine the potential regulation of SETDB1 and FosB by p53, we predicted putative p53 binding sites on the genomic DNA of SETDB1 and FosB using a TF motif binding search program. These putative p53 binding sites were identified as 18 sites in the promoter regions of SETDB1 and 21 sites in the genomic DNA of FosB. A luciferase assay confirmed that p53 negatively regulated the promoter activities of SETDB1 and FosB. Furthermore, the results of RT-PCR, western blot, qPCR, and immunostaining experiments indicated that the transfection of exogenous p53 decreases the expression of SETDB1 and FosB in H1299 cells. This indicates that p53 negatively regulates the expression of SETDB1 and FosB at the transcriptional level. Collectively, the downregulation of SETDB1 and FosB by p53 may provide functional networks for apoptosis and for the survival of cancer cells during anticancer drug treatment.