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( Kyeong Ho Byun ),( Kazuki Hyodo ),( Kazuya Suwabe ),( Sylwester Kujach ),( Morimasa Kato ),( Hideaki Soya ) 한국운동영양학회 2014 Physical Activity and Nutrition (Phys Act Nutr) Vol.18 No.4
[Purpose] Functional near-infrared spectroscopy (fNIRS) provides functional imaging of cortical activations by measuring regional oxy- and deoxy-hemoglobin (Hb) changes in the forehead during a cognitive task. There are, however, potential problems regarding NIRS signal contamination by non-cortical hemodynamic (NCH) variables such as skin blood flow, middle cerebral artery blood flow, and heart rate (HR), which are further complicated during acute exercise. It is thus necessary to determine the appropriate post-exercise timing that allows for valid NIRS assessment during a task without any increase in NCH variables. Here, we monitored post-exercise changes in NCH parameters with different intensities of exercise. [Methods] Fourteen healthy young participants cycled 30, 50 and 70% of their peak oxygen uptake (Vo2peak) for 10 min per intensity, each on different days. Changes in skin blood flow velocity (SBFv), middle cerebral artery mean blood velocity (MCA Vmean) and HR were monitored before, during, and after the exercise. [Results] Post-exercise levels of both SBFv and HR in contrast to MCA Vmean remained high compared to basal levels and the times taken to return to baseline levels for both parameters were delayed (2-8 min after exercise), depending upon exercise intensity. [Conclusion] These results indicate that the delayed clearance of NCH variables of up to 8 min into the post-exercise phase may contaminate NIRS measurements, and could be a limitation of NIRS-based neuroimaging studies.
Byun, Min Soo,Choe, Young Min,Sohn, Bo Kyung,Yi, Dahyun,Han, Ji Young,Park, Jinsick,Choi, Hyo Jung,Baek, Hyewon,Lee, Jun Ho,Kim, Hyun Jung,Kim, Yu Kyeong,Yoon, Eun Jin,Sohn, Chul-Ho,Woo, Jong Inn,Lee, Frontiers Media S.A. 2016 FRONTIERS IN AGING NEUROSCIENCE Vol.8 No.-
<P>Previous literature suggests that Alzheimer's disease (AD) process may contribute to late-life onset depression (LLOD). Therefore, we investigated the association of LLOD with cerebral amyloidosis and neuronal injury, the two key brain changes in AD, along with vascular risks. Twenty nine non-demented individuals who first experienced major depressive disorder (MDD) after age of 60 years were included as LLOD subjects, and 27 non-demented elderly individuals without lifetime experience of MDD were included as normal controls (NC). Comorbid mild cognitive impairment (MCI) was diagnosed in 48% of LLOD subjects and in 0% of NC. LLOD, irrespective of comorbid MCI diagnosis, was associated with prominent prefrontal cortical atrophy. Compared to NC, LLOD subjects with comorbid MCI (LLOD<SUB>MCI</SUB>) showed increased cerebral <SUP>11</SUP>C-Pittsburg compound B (PiB) retention and plasma beta-amyloid 1–40 and 1–42 peptides, as measures of cerebral amyloidosis; and, such relationship was not observed in overall LLOD or LLOD without MCI (LLOD<SUB>woMCI</SUB>). LLOD subjects, particularly the LLOD<SUB>woMCI</SUB>, had higher systolic blood pressure (SBP) than NC. When analyzed in the same multiple logistic regression model that included prefrontal gray matter (GM) density, cerebral amyloidosis, and SBP as independent variables, only prefrontal GM density showed a significant independent association with LLOD regardless of MCI comorbidity status. Our findings suggest AD process might be related to LLOD via prefrontal neuronal injury in the MCI stage, whereas vascular processes—SBP elevation, in particular—are associated with LLOD via prefrontal neuronal injury even in cognitively intact or less impaired individuals.</P>
Apotototic Signaling Pathway of Resveratrol in Rheumatoid Synovial Fibroblasts
Byun, Hee Sun,Won, Minho,Park, Kyeong Ah,Kim, Young-Rae,Lee, Hyunji,Choi, Byung Lyul,Yang, Keum-Jin,Shin, Sanghee,Piao, Longzhen,Shin, Eulsoon,Li, Yuwen,Seok, Jeong Ho,Park, Jongsun,Song, Ju Kyung,Kan 충남대학교 형질전환복제돼지연구센터 2007 논문집 Vol. No.10
Byun, Min Soo,Kim, Hyun Jung,Yi, Dahyun,Choi, Hyo Jung,Baek, Hyewon,Lee, Jun Ho,Choe, Young Min,Sohn, Bo Kyung,Lee, Jun-Young,Lee, Younghwa,Ko, Hyunwoong,Kim, Yu Kyeong,Lee, Yun-Sang,Sohn, Chul-Ho,Woo PERGAMON PRESS LTD 2017 NEUROBIOLOGY OF AGING Vol. No.
<P><B>Abstract</B></P> <P>We tested the hypothesis that lower insulin or higher glycated hemoglobin (HbA1c) levels in blood are associated with increased cerebral beta amyloid (Aβ) deposition and neurodegeneration in nondiabetic cognitively normal (CN) older adults. A total of 205 nondiabetic CN older adults underwent comprehensive clinical assessment, [<SUP>11</SUP>C]Pittsburgh compound B (PiB)-positron emission tomography (PET), [<SUP>18</SUP>F]fluorodeoxyglucose-PET, magnetic resonance imaging, and blood sampling for fasting insulin and HbA1c measurement. Lower blood insulin was significantly associated with increased Aβ positivity rates and decreased cerebral glucose metabolism in the AD-signature region. In contrast, higher HbA1c levels were not associated with Aβ positivity rates but were significantly associated with higher rates of having neurodegeneration in the AD-signature regions. Our results suggest different roles of insulin and HbA1c in AD pathogenesis, in that decreased blood insulin below optimal levels may contribute to increasing cerebral Aβ deposition and neurodegeneration whereas impaired glycemic control may aggravate neurodegeneration through a nonamyloid mechanism in nondiabetic CN older adults.</P>
Byun, Byung Hyun,Kim, Byung Il,Park, Su Yeon,Ko, In Ok,Lee, Kyo Chul,Kim, Kyeong Min,Kim, Yu Kyeong,Lee, Jun-Young,Bu, Seon Hee,Kim, Jung Hwa,Chi, Dae Yoon,Ha, Jeong Ho,Lim, Sang Moo Williams & Wilkins Co 2017 Medicine Vol.96 No.12
<P><B>Abstract</B></P><P>As a new beta amyloid (Aβ) positron emission tomography (PET) tracer, <SUP>18</SUP>F-FC119S has shown higher cortical uptake in patients with Alzheimer's disease (AD) than that in healthy control subjects without adverse effects in a previous preliminary study. The aim of this study was to compare <SUP>18</SUP>F-FC119S PET and <SUP>11</SUP>C-PiB PET in healthy control (HC) subjects, mild cognitive impairment (MCI) patients, and AD patients.</P><P>A total of 48 subjects, including 28 HC subjects, 10 MCI patients, and 10 AD patients, underwent static <SUP>18</SUP>F-FC119S PET (30 minutes after intravenous [i.v.] injection) and <SUP>11</SUP>C-PiB PET (40 minutes after i.v. injection) on the same day. Both PET images were visually and quantitatively assessed. Standardized uptake value ratios (SUVRs) were calculated for each brain region using the cerebellar cortex as a reference region.</P><P>None (0%) of the 28 HC subjects and 4 (40%) of 10 MCI patients had positive scans on both PET images. Of the 10 AD patients, 7 (70%) had positive scans on <SUP>11</SUP>C-PiB PET while 6 (60%) had positive scans on <SUP>18</SUP>F-FC119S PET. Overall, 47 (98%) of 48 participants showed identical results based on visual analysis. Cortical SUVR of <SUP>18</SUP>F-FC119S was higher in AD patients (1.38 ± 0.16), followed by that in MCI patients (1.24 ± 0.10) and in HC subjects (1.14 ± 0.05). Compared with <SUP>11</SUP>C-PiB PET, <SUP>18</SUP>F-FC119S PET yielded a higher effect size (<I>d</I> = 2.02 vs. 1.67) in AD patients and a slightly lower effect size (<I>d</I> = 1.26 vs. 1.38) in MCI patients. In HC subjects, the nonspecific binding of <SUP>18</SUP>F-FC119S to white matter (with the frontal cortex-to-white matter SUV ratio of 0.76) was slightly lower than that of <SUP>11</SUP>C-PiB (ratio of 0.73). There was a significant linear correlation (slope = 0.41, <I>r</I> = 0.78, <I>P</I> < 0.001) between <SUP>11</SUP>C-PiB and <SUP>18</SUP>F-FC119S cortical SUVR.</P><P>We could safely obtain images similar to <SUP>11</SUP>C-PiB PET imaging Aβ in the brain using <SUP>18</SUP>F-FC119S PET. Therefore, <SUP>18</SUP>F-FC119S might be suitable for imaging Aβ deposition.</P>
Byun, Hee Sun,Park, Kyeong Ah,Won, Minho,Yang, Keum-Jin,Shin, Sanghee,Piao, Longzhen,Kwak, Jin Young,Lee, Zee-Won,Park, Jongsun,Seok, Jeong Ho,Liu, Zheng-Gang,Hur, Gang Min American Society for Pharmacology and Experimental 2006 Molecular pharmacology Vol.70 No.3
<P>Protein kinase C (PKC) triggers cellular signals that regulate proliferation or death in a cell- and stimulus-specific manner. Although previous studies have demonstrated that activation of PKC with phorbol 12-myristate 13-acetate (PMA) protects cells from apoptosis induced by a number of mechanisms, including death receptor ligation, little is known about the effect or mechanism of PMA in the necrotic cell death. Here, we demonstrate that PMA-mediated activation of PKC protects against tumor necrosis factor (TNF)-induced necrosis by disrupting formation of the TNF receptor (TNFR)1 signaling complex. Pretreatment with PMA protected L929 cells from TNF-induced necrotic cell death in a PKC-dependent manner, but it did not protect against DNA-damaging agents, including doxorubicin (Adriamycin) and camptothecin. Analysis of the upstream signaling events affected by PMA revealed that it markedly inhibited the TNF-induced recruitment of TNFR1-associated death domain protein (TRADD) and receptor-interacting protein (RIP) to TNFR1, subsequently inhibiting TNF-induced activation of nuclear factor-kappaB and c-Jun NH2-terminal kinase (JNK). However, JNK inhibitors do not significantly affect TNF-induced necrosis, suggesting that the inhibition of JNK activation by PMA is not part of the antinecrotic mechanism. In addition, PMA acted as an antagonist of TNF-induced reactive oxygen species (ROS) production, thereby suppressing activation of ROS-mediated poly(ADP-ribose)polymerase (PARP), and thus inhibiting necrotic cell death. Furthermore, during TNF-induced necrosis, PARP was significantly activated in wild-type mouse embryonic fibroblast (MEF) cells but not in RIP-/- or TNFR-associated factor 2-/-MEF cells. Taken together, these results suggest that PKC activation ensures effective shutdown of the death receptor-mediated necrotic cell death pathway by modulating formation of the death receptor signaling complex.</P>