Journal of the Korea Institute of Information and Communication Engineering
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v.11
no.1
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pp.139-149
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2007
Asynchronous OFCDM(Orthogonal Frequency and Code Division Multiplexing) systems must have a cell search process necessarily unlike synch개nous systems. this process is hewn initial synchronization and a three-step cell search algorithm is performed for the initial synchronization in the following three steps: OFCDM symbol timing, i.e., Fast Fourier Transform(FFT) window timing is estimated employing guard interval (GI) correlation in the first step, then the frame timing and CSSC(Cell Specific Scrambling Code) group is detected by taking the correlation of the CPICH(Common Pilot Channel) based on the property yielded by shifting the CSSC phase in the frequency domain. Finally, the CSSC phase within the group is identified in the third step. This paper proposes a modification group code with two or three block of the conventional CPICH based cell search algorithm in the second step which offers MS(Mobile Station) complexity reductions. however, the effect of the reduction complexity leads to degradation of the performance therefore, look for combination to have the most minimum degradation. the proposed block type group code with suitable combinations is the nearly sane performance as conventional group code and has a complexity reduction that is to be compared and verified through the computer simulation.
Our understanding of the differential effects between specific omega-3 fatty acids is incomplete. Here, we aimed to evaluate the effects of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) on T-helper type 1 (Th1) cell responses and identify the pathways associated with these responses. Naïve CD4+ T cells were co-cultured with bone marrow-derived dendritic cells (DCs) in the presence or absence of palmitate (PA), DHA, or EPA. DHA or EPA treatment lowered the number of differentiated IFN-γ-positive cells and inhibited the secretion of IFN-γ, whereas only DHA increased IL-2 and reduced TNF-α secretion. There was reduced expression of MHC II on DCs after DHA or EPA treatment. In the DC-independent model, DHA and EPA reduced Th1 cell differentiation and lowered the cell number. DHA and EPA markedly inhibited IFN-γ secretion, while only EPA reduced TNF-α secretion. Microarray analysis identified pathways involved in inflammation, immunity, metabolism, and cell proliferation. Moreover, DHA and EPA inhibited Th1 cells through the regulation of diverse pathways and genes, including Igf1 and Cpt1a. Our results showed that DHA and EPA had largely comparable inhibitory effects on Th1 cell differentiation. However, each of the fatty acids also had distinct effects on specific cytokine secretion, particularly according to the presence of DCs.
This is a report of gastric metastases secondary from a primary small cell carcinoma of the lung in two men. Blood-borne metastatic involvement of the stomach by cancer is a rare entity. According to the reports in the literature the prevalence of metastasis to the stomach occurs in 0.4% and the most common cell type of the primary lung carcinoma is large cell type(3.7%) followed by adenocarcinoma(2.4%), small cell carcinoma(1.7%) and squamous cell carcinoma(0.7%). The most common tumors that spread to the stomach through the blood stream are malignant melanoma, breast carcinoma and lung carcinoma. Most of the gastrointestinal tract metastases had no specific symptoms because of its submucosal involvement. The prognosis was poor and the mean survival period from the onset of symptoms was 49 days. The first patient was a 56-year-old man who had primary lung carcinoma with brain metastasis. Gastroscopic findings showed two elevated mass lesions in the anterior wall of the mid body with central ulcer and the posterior wall of the fundus with intact surface mucosa. Pathologic examination of stomach tissue revealed small cell type tumor cells infiltrate in the stomach wall segmentally without destruction of the glands. The second patient was a 67-year-old man who had no other evidence of the distant metastasis. Gastroscopic findings showed a huge, oval shaped, ulcerofungating mass with deep penetrating central ulcer coated with dirty exudate in the anterior wall from mid to upper body of the stomach, and thickened elevated rugal folds in the posterior wall of the fundus. Pathologic examination of stomach tissues revealed the small cell type tumor cells showing small smudged nucleus infiltrate into the mucosa of the stomach and the architecture of mucosa intact. We report the two cases of metastatic gastric cancer from the primary small cell lung carcinoma with the literature review.
Breast cancer is the most common malignancy among women, and mutations in the BRCA1 gene produce increased susceptibility to these malignancies in certain families. In this study, the forward 1-13 exons of breast cancer associated gene BRCA1 were cloned from breast cancer cell line ZR-75-30 by RT-PCR method. Sequence analysis showed that nine BRCA1 splice forms were isolated and characterized, compared with wild-type BRCA1 gene, five splice forms of which were novel. These splice isoforms were produced from the molecular mechanism of 5' and 3' alternative splicing. All these splice forms deleting exon 11b and the locations of alternative splicing were focused on two parts:one was exons 2 and 3, and the other was exons 9 and 10. These splice forms accorded with GT-AG rule. Most these BRCA1 splice variants still kept the original reading frame. Western blot analysis indicated that some BRCA1 splice variants were expressed in ZR-75-30 cell line at the protein level. In addition, we confirmed the presence of these new transcripts of BRCA1 gene in MDA-MB-435S, K562, Hela, HLA, HIC, H9, Jurkat and human fetus samples by RT-PCR analysis. These results suggested that breast cancer associated gene BRCA1 may have unexpectedly a large number of splice variants. We hypothesized that alternative splicing of BRCA1 possibly plays a major role in the tumorigenesis of breast and/or ovarian cancer. Thus, the identification of cancer-specific splice forms will provide a novel source for the discovery of diagnostic or prognostic biomarkers and tumor antigens suitable as targets for therapeutic intervention.
Si-Won Park;In-Byung Park;Seok-Jin Kang;Joonbeom Bae;Taehoon Chun
Journal of Animal Science and Technology
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v.65
no.4
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pp.698-719
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2023
Postweaning multisystemic wasting syndrome (PMWS) is caused by a systemic inflammation after porcine circovirus type 2 (PCV2) infection. It was one of the most economically important pathogens affecting pig production worldwide before PCV2 vaccine was first introduced in 2006. After the development of a vaccine against PCV2a type, pig farms gradually restored enormous economic losses from PMWS. However, vaccine against PCV2a type could not be fully effective against several different PCV2 genotypes (PCV2b - PCV2h). In addition, PCV2a vaccine itself could generate antigenic drift of PCV2 capsid. Therefore, PCV2 infection still threats pig industry worldwide. PCV2 infection was initially found in local tissues including reproductive, respiratory, and digestive tracks. However, PCV2 infection often leads to a systemic inflammation which can cause severe immunosuppression by depleting peripheral lymphocytes in secondary lymphoid tissues. Subsequently, a secondary infection with other microorganisms can cause PMWS. Eleven putative open reading frames (ORFs) have been predicted to encode PCV2 genome. Among them, gene products of six ORFs from ORF1 to ORF6 have been identified and characterized to estimate its functional role during PCV2 infection. Acquiring knowledge about the specific interaction between each PCV2 ORF protein and host protein might be a key to develop preventive or therapeutic tools to control PCV2 infection. In this article, we reviewed current understanding of how each ORF of PCV2 manipulates host cell signaling related to immune suppression caused by PCV2.
CHO (Chinese hamster ovary) cells were transfected with plasmids containing both cis-acting HRE (hypoxia response element) and CMV-promoter that controls tissue-type plasminogen activator (t-PA). CHO cells with HRE produced 16.2 fold higher t-PA concentration than CHO cells without HRE. It was noted that hypoxia strongly induced CHO cell apoptosis. which resulted in decrease of cell viability and protein production. In this study. by introducing Bcl-2, anti-apoptotic gene, we tried to recover cell viability and increase the protein production. When batch culture of both control cells without transfection of Bcl-2 and cells transfected with Bcl-2 were performed in the absence of CoCl ι hypoxia mimic condition. the cells with Bcl-2 were effected specific cell growth rates, maximum cell density. Immunoblotting assay showed Bcl-2 was recombinant with HRE dependent t- P A expression cassette, and their expression level was depended on hypoxia. By introducing Bcl-2, both cell viability and maximum cell density could be increased.
This study aimed to investigate whether the antidiabetic drugs dipeptidyl peptidase 4 (DPP4) inhibitors such as evogliptin and sitagliptin affect the membrane DPP4 (mDPP4) enzymatic activity and immune function of T helper1 (Th1) cells in terms of cytokine expression and cell profiles. The mDPP4 enzymatic activity, cytokine expression, and cell profiles, including cell counts, cell viability, DNA synthesis, and apoptosis, were measured in pokeweed mitogen (PWM)-activated CD4+CD26+ H9 Th1 cells with or without the DPP4 inhibitors, evogliptin and sitagliptin. PWM treatment alone strongly stimulated the expression of mDPP4 and cytokines such as interleukin (IL)-2, IL-10, tumor necrosis factor-alpha, interferon-gamma, IL-13, and granulocyte-macrophage colony stimulating factor in the CD4+CD26+ H9 Th1 cells. Evogliptin or sitagliptin treatment potently inhibited mDPP4 activity in a dose-dependent manner but did not affect either the cytokine profile or cell viability in PWM-activated CD4+CD26+ H9 Th1 cells. These results suggest that, following immune stimulation, Th1 cell signaling pathways for cytokine expression function normally after treatment with evogliptin or sitagliptin, which efficiently inhibit mDPP4 enzymatic activity in Th1 cells.
Background: Clarifying the prognostic impact of histological type is an essential issue that may influence the treatment and follow-up planning of newly diagnosed cervical cancer cases. This study aimed to evaluate the prognostic impact of histological type on survival and mortality in patients with cervical squamous cell carcinoma (SCC), adenocarcinoma (ADC) and small cell neuroendocrine carcinoma (SNEC). Materials and Methods: All patients with cervical cancer diagnosed and treated at Chiang Mai University Hospital between January 1995 and October 2011 were eligible. We included all patients with SNEC and a random weighted sample of patients with SCC and ADC. We used competing-risks regression analysis to evaluate the association between histological type and cancer-specific survival and mortality. Results: Of all 2,108 patients, 1,632 (77.4%) had SCC, 346 (16.4%) had ADC and 130 (6.2%) had SNEC. Overall, five-year cancer-specific survival was 60.0%, 54.7%, and 48.4% in patients with SCC, ADC and SNEC, respectively. After adjusting for other clinical and pathological factors, patients with SNEC and ADC had higher risk of cancer-related death compared with SCC patients (hazard ratio [HR] 2.6; 95% CI, 1.9-3.5 and HR 1.3; 95% CI, 1.1-1.5, respectively). Patients with SNEC were younger and had higher risk of cancer-related death in both early and advanced stages compared with SCC patients (HR 4.9; 95% CI, 2.7-9.1 and HR 2.5; 95% CI, 1.7-3.5, respectively). Those with advanced-stage ADC had a greater risk of cancer-related death (HR 1.4; 95% CI, 1.2-1.7) compared with those with advanced-stage SCC, while no significant difference was observed in patients with early stage lesions. Conclusion: Histological type is an important prognostic factor among patients with cervical cancer in Thailand. Though patients with SNEC were younger and more often had a diagnosis of early stage compared with ADC and SCC, SNEC was associated with poorest survival. ADC was associated with poorer survival compared with SCC in advanced stages, while no difference was observed at early stages. Further tailored treatment-strategies and follow-up planning among patients with different histological types should be considered.
Low Electromagnetic Field (EMF) intensity in the range of $1{\mu}T\;to\;10{\mu}T$(Tesla) was found to enhance the growth of CHO cells and the production of tPA in batch and perfusion cultivations. At $1{\mu}T\;intensity,\;1.3{\times}10^7$ viable cells/ml of maximum cell density and 80 mg/l of maximum tPA production were obtained in batch cultivation, compared to $2.8{\times}10^6$ viable cells/ml and 59 mg tPA/1 in unexposed case (control). A similar trend was observed in the perfusion process, where it was possible to obtain $1.2{\times}10^7$ viable cells/ml of maximum cell density and 81 mg tPA/l of maximum tPA production by more than 80 days of cultivation. However, there was not much difference between $1{\mu}T\;and\;10{\mu}T$ in perfusion cultivation, possibly due to better environmental growth conditions being maintained by continuous feeding of fresh medium into the reactor. On the contrary, both cell growth and tPA production were severely inhibited at higher than 1 mT intensity, showing no growth at 10 mT exposure. Specific growth rate was linearly correlated to specific tPA production rate at $1{\mu}T$EMF intensity, which represents a partially growth-related relationship. It was also found that a large amount of $Ca^2+$ was released at low EMF intensity, even though the cell growth was not much affected. Low EMF intensity significantly improved both cell growth and tPA production, and tPA production seemed to be more affected than the cell growth, possibly due to the changes of cell membrane characteristics. It can be concluded that the elaboration of EMF intensity less than $10{\mu}T$ could improve cell growth and tPA production, but mainly tPA secretion through batch or perfusion process in a bioreactor.
Guk-Yeol Park;Gil-Woo Lee;Soeun Kim;Hyebeen Hong;Jong Seok Park;Jae-Ho Cho;Yoontae Lee
IMMUNE NETWORK
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v.20
no.5
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pp.43.1-43.11
/
2020
Capicua (CIC) is a transcriptional repressor that regulates several developmental processes. CIC deficiency results in lymphoproliferative autoimmunity accompanied by expansion of CD44hiCD62Llo effector/memory and follicular Th cell populations. Deletion of Cic alleles in hematopoietic stem cells (Vav1-Cre-mediated knockout of Cic) causes more severe autoimmunity than that caused by the knockout of Cic in CD4+CD8+ double positive thymocytes (Cd4-Cre-mediated knockout of Cic). In this study, we compared splenic CD4+ T cell activation and proliferation between whole immune cell-specific Cic-null (Cicf/f;Vav1-Cre) and T cell-specific Cic-null (Cicf/f;Cd4-Cre) mice. Hyperactivation and hyperproliferation of CD4+ T cells were more apparent in Cicf/f;Vav1-Cre mice than in Cicf/f;Cd4-Cre mice. Cicf/f;Vav1-Cre CD4+ T cells more rapidly proliferated and secreted larger amounts of IL-2 upon TCR stimulation than did Cicf/f;Cd4-Cre CD4+ T cells, while the TCR stimulation-induced activation of the TCR signaling cascade and calcium flux were comparable between them. Mixed wild-type and Cicf/f;Vav1-Cre bone marrow chimeras also exhibited more apparent hyperactivation and hyperproliferation of Cic-deficient CD4+ T cells than did mixed wild-type and Cicf/f;Cd4-Cre bone marrow chimeras. Taken together, our data demonstrate that CIC deficiency at the beginning of T cell development endows peripheral CD4+ T cells with enhanced T cell activation and proliferative capability.
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