• 한국생물공학회:학술대회논문집
• /
• 2005.10a
• /
• pp.1013-1014
• /
• 2005

• ETRI Journal
• /
• v.29 no.1
• /
• pp.45-49
• /
• 2007

The poly-Si thin film transistor (TFT) shows large variations in its characteristics due to the grain boundary of poly-crystalline silicon. This results in unacceptably large input offset of low-voltage differential signaling (LVDS) receivers. To cancel the large input offset of poly-Si TFT LVDS receivers, a full-digital offset compensation scheme has been developed and verified to be able to keep the input offset under 15 mV which is sufficiently small for LVDS signal receiving.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
• /
• 2010.05a
• /
• pp.695-698
• /
• 2010

본 논문은 High-speed signal에 대한 기본적인 설계 방법론, Differential signaling, Impedence matching, Decoupling Method 등에 대하여 논한 후 High-speed signal 의 전송 품질을 개선하기 위한 GND via 의 효과에 대하여 논하고자 한다. S-parameter simulation 및 실제 제품 적용 후 파형의 변화를 관찰하여 GND via 의 효용성을 살펴보아 High-speed signal Design 할 때 Design limitation 상황에 대해 적절한 방법론을 말하고자 한다.

• The Journal of the Korea institute of electronic communication sciences
• /
• v.15 no.6
• /
• pp.1131-1136
• /
• 2020

Cooperative networks enhance the performance of communication systems by combining received signals from the several relay nodes where the source node transmits signals to relay nodes. In this paper, we analyze the effect of resource allocation in cooperative networks. We assume that the cooperative networks use the conventional modulation scheme between the source and relay nodes, and adopt space-time code between the relays and destination node. Both the synchronous and differential modulations are applied for the conventional scheme and differential modulation is used for the space-time code. We consider relay location and energy allocation for resource allocation, and the performance of cooperative networks depending on the number of relay is also investigated.

• Journal of Animal Science and Technology
• /
• v.56 no.4
• /
• pp.12.1-12.7
• /
• 2014

This study investigated changes in gene expression by dietary fat source, i.e., beef tallow, soybean oil, olive oil, and coconut oil (each 3% in feed), in both male and female growing-finishing pigs. Real-time PCR was conducted on seven genes (insulin receptor; INSR, insulin receptor substrate; IRS, phosphatidylinositol (3,4,5)-triphosphate; PIP3, 3-phosphoinositide-dependent protein kinase-1; PDK1, protein kinase B; Akt, forkhead box protein O1; FOXO1 and cGMP-inhibited 3', 5'-cyclic phosphodiesterase; PDE3) located upstream of the insulin signaling pathway in the longissimus dorsi muscle (LM) of pigs. The INSR, IRS, PIP3, and PDE3 genes showed significantly differential expression in barrow pigs. Expression of the PIP3 and FOXO1 genes was significantly different among the four dietary groups in gilt pigs. In particular, the PIP3 gene showed the opposite expression pattern between barrow and gilt pigs. These results show that dietary fat source affected patterns of gene expression according to animal gender. Further, the results indicate that the type of dietary fat affects insulin signaling-related gene expression in the LM of pigs. These results can be applied to livestock production by promoting the use of discriminatory feed supplies.

• IMMUNE NETWORK
• /
• v.4 no.3
• /
• pp.143-154
• /
• 2004

Background: CD27 is recently known as a memory B cell marker and is mainly expressed in activated T cells, some B cell population and NK cells. CD27 is a member of tumor necrosis factor receptor family. Like CD40 molecule, CD27 has (P/S/T/A) X(Q/E)E motif for interacting with TNF receptor-associated factors (TRAFs), and TRAF2 and TRAF5 bindings to CD27 in 293T cells were reported. Methods: To investigate the CD27 signaling effect in B cells, human CD40 extracellular domain containing mouse CD27 cytoplamic domain construct (hCD40-mCD27) was transfected into mouse B cell line CH12.LX and M12.4.1. Results: Through the stimulation of hCD40-mCD27 molecule via anti-human CD40 antibody or CD154 ligation, expression of CD11a, CD23, CD54, CD70 and CD80 were increased and secretion of IgM was induced, which were comparable to the effect of CD40 stimulation. TRAF2 and TRAF3 were recruited into lipid-enriched membrane raft and were bound to CD27 in M12.4.1 cells. CD27 stimulation, however, did not increase TRAF2 or TRAF3 degradation. Conclusion: In contrast to CD40 signaling pathway, TRAF2 and TRAF3 degradation was not observed after CD27 stimulation and it might contribute to prolonged B cell activation through CD27 signaling.

• Journal of Periodontal and Implant Science
• /
• v.52 no.2
• /
• pp.127-140
• /
• 2022

Purpose: In dental avulsion, delayed replantation usually has an uncertain prognosis. After tooth replantation, complex inflammatory responses promote a return to periodontal tissue homeostasis. Various types of cytokines are produced in the inflammatory microenvironment, and these cytokines determine the periodontal tissue response. This study aimed to identify the gene expression profiles of replanted teeth and evaluate the functional differences between immediate and delayed replantation. Methods: Maxillary molars from Sprague-Dawley rats were extracted, exposed to a dry environment, and then replanted. The animals were divided into 2 groups according to the extra-oral time: immediate replantation (dry for 5 minutes) and delayed replantation (dry for 60 minutes). Either 3 or 7 days after replantation, the animals were sacrificed. Periodontal soft tissues were harvested for mRNA sequencing. Hallmark gene set enrichment analysis was performed to predict the function of gene-gene interactions. The normalized enrichment score (NES) was calculated to determine functional differences. Results: The hallmark gene sets enriched in delayed replantation at 3 days were oxidative phosphorylation (NES=2.82, Q<0.001) and tumor necrosis factor-alpha (TNF-α) signaling via the nuclear factor kappa light chain enhancer of activated B cells (NF-κB) pathway (NES=1.52, Q=0.034). At 7 days after delayed replantation, TNF-α signaling via the NF-κB pathway (NES=-1.82, Q=0.002), angiogenesis (NES=-1.66, Q=0.01), and the transforming growth factor-beta signaling pathway (NES=-1.46, Q=0.051) were negatively highlighted. Conclusions: Differentially expressed gene profiles were significantly different between immediate and delayed replantation. TNF-α signaling via the NF-κB pathway was marked during the healing process. However, the enrichment score of this pathway changed in a time-dependent manner between immediate and delayed replantation.

• Journal of Veterinary Science
• /
• v.21 no.3
• /
• pp.45.1-45.15
• /
• 2020

Background: Feline mammary carcinoma is the third most common cancer that affects female cats. Objectives: The purpose of this study was to screen differential serum proteins in feline and clarify the relationship between them and the occurrence of feline mammary carcinoma. Methods: Chinese pastoral cats were used as experimental animals. Six serum samples from cats with mammary carcinoma (group T) and six serum samples from healthy cats (group C) were selected. Differential protein analysis was performed using a Label-free technique, while parallel reaction monitoring (PRM) was performed to verify the screened differential proteins. Results: A total of 82 differential proteins were detected between group T and group C, of which 55 proteins were down regulated and 27 proteins were up regulated. Apolipoprotein A-I, Apolipoprotein A-II (ApoA-II), Apolipoprotein B (ApoB), Apolipoprotein C-III (ApoC-III), coagulation factor V, coagulation factor X, C1q, albumen (ALB) were all associated with the occurrence of feline mammary carcinoma. Differential proteins were involved in a total of 40 signaling pathways, among which the metabolic pathways associated with feline mammary carcinoma were the complement and coagulation cascade and cholesterol metabolism. According to the Label-free results, ApoB, ApoC-III, ApoA-II, FN1, an uncharacterized protein, and ALB were selected for PRM target verification. The results were consistent with the trend of the label-free. Conclusions: This experimen is the first to confirm ApoA-II and ApoB maybe new feline mammary carcinoma biomarkers and to analyze their mechanisms in the development of such carcinoma in feline.

• Journal of the Institute of Electronics and Information Engineers
• /
• v.49 no.9
• /
• pp.244-250
• /
• 2012

This paper describes a 4-Gb/s receiver circuit for a low-swing ground-referenced differential signaling system. The receiver employs a common-gate level-shifter and a continuous linear equalizer which compensates inter-symbol-interference (ISI) and improves voltage and timing margins. A bias circuit maintains the bias current of the level-shifter when the common level of the input signal changes. The receiver is implemented with a low-power 65-nm CMOS technology. When 4-Gb/s 400mVp-p signals are transmitted to the receiver through the channel with the attenuation of -19.7dB, the timing margin based on bit error rate (BER) of $10^{-11}$ is 0.48UI and the power consumption is as low as 0.30mW/Gb/s.

• The Korean Journal of Physiology and Pharmacology
• /
• v.14 no.3
• /
• pp.145-150
• /
• 2010

Adenosine (Ado) is an important mediator of the endogenous defense against ischemia-induced injury in the heart. The action of Ado is mediated by activation of G protein-gated inwardly rectifying $K^+$ (GIRK) channels. In turn, GIRK channels are inhibited by reducing phosphatidylinositol 4,5-bisphosphate ($PIP_2$) through Gq protein-coupled receptors (GqPCRs). We previously found that GIRK channels activated by acetylcholine, a muscarinic M2 acetylcholine receptor agonist, are inhibited by GqPCRs in a receptor-specific manner. However, it is not known whether GIRK channels activated by Ado signaling are also regulated by GqPCRs. Presently, this was investigated in mouse atrial myocytes using the patch clamp technique. GIRK channels were activated by $100\;{\mu}M$ Ado. When Ado was repetitively applied at intervals of 5~6 min, the amplitude of second Ado-activated GIRK currents ($I_{K(Ado)}$) was $88.3{\pm}3.7%$ of the first $I_{K(Ado)}$ in the control. Pretreatment of atrial myocytes with phenylephrine, endothelin-1, or bradykinin prior to a second application of Ado reduced the amplitude of the second $I_{K(Ado)}$ to $25.5{\pm}11.6%$, $30.5{\pm}5.6%$, and $96.0{\pm}2.7%$, respectively. The potency of $I_{K(Ado)}$ inhibition by GqPCRs was different with that observed in acetylcholine-activated GIRK currents ($I_{K(ACh)}$) (endothelin-1>phenylephrine>bradykinin). $I_{K(Ado)}$ was almost completely inhibited by $500\;{\mu}M$ of the $PIP_2$ scavenger neomycin, suggesting low $PIP_2$ affinity of $I_{K(Ado)}$. Taken together, these results suggest that the crosstalk between GqPCRs and the Ado-induced signaling pathway is receptor-specific. The differential change in $PIP_2$ affinity of GIRK channels activated by Ado and ACh may underlie, at least in part, their differential responses to GqPCR agonists.