Fabrication of dual-coated graphene oxide nanosheets by polypyrrole and poly(ionic liquid) and their enhanced electrorheological responses

Chen, Panpan,Cheng, Qianqian,Wang, Li-Min,Liu, Ying Dan,Choi, Hyoung Jin Elsevier 2019 Journal of industrial and engineering chemistry Vol.69 No.-

<P><B>Abstract</B></P> <P>A two-dimensional composite material, poly(ionic liquid)-modified graphene oxide/polypyrrole (GO/PPy/PIL) multilayered nanosheets, was fabricated and applied as a new electrorheological (ER) material. The morphological differences between the single- and dual-coated nanosheets were confirmed using scanning electron microscopy and transmission electron microscopy. Rheological properties measured using a rotational rheometer indicated that the GO/PPy/PIL composite nanosheets exhibited relatively high ER effect under a certain electric field strength than the GO/PPy nanosheets because of the universal PIL second coating. The dual-coated nanosheets also showed a higher applicable electric field strength due to the semiconductive properties of the thick PIL layer.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Dual-coated composite GO/PPy/PIL nanosheets were fabricated. </LI> <LI> The PIL second coating significantly enhanced the ER effect of the nanosheets. </LI> <LI> GO/PPy/PIL exhibited higher available electric field strength than GO/PPy. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

EBV-miR-BHRF1-1 Targets p53 Gene: Potential Role in Epstein-Barr Virus Associated Chronic Lymphocytic Leukemia

Dan-Min Xu,Yi-Lin Kong,Li Wang,Hua-Yuan Zhu,Jia-Zhu Wu,Yi Xia,Yue Li,Shu-Chao Qin,Lei Fan,Jian-Yong Li,Jin-Hua Liang,Wei Xu 대한암학회 2020 Cancer Research and Treatment Vol.52 No.2

Purpose The purpose of this study was to investigate the prognostic impact of Epstein-Barr virus (EBV)–microRNA (miRNA, miR)-BHRF1-1 with chronic lymphocytic leukemia (CLL) as well as role of EBV-miR-BHRF1-1 in p53 gene. Materials and Methods Quantitative reverse transcription–polymerase chain reaction and western blotting were used to quantify EBV-miR-BHRF1-1 and p53 expression in cultured CLL. Results p53 aberration was associated with the higher expression level of EBV-miR-BHRF1-1 (p < 0.001) which was also an independent prognostic marker for overall survival (p=0.028; hazard ratio, 5.335; 95% confidence interval, 1.193 to 23.846) in 97 newly-diagnosed CLL patients after adjusted with International Prognostic Index for patients with CLL. We identified EBV-miR-BHRF1-1 as a viral miRNA regulator of p53. EBV-miR-BHRF1-1 repressed luciferase reporter activity by specific interaction with the seed region within the p53 3- untranslated region. Discordance of p53 messenger RNA and protein expression was associated with high EBV-miR-BHRF1-1 levels in CLL patients and cell lines. EBV-miR-BHRF1- 1 inhibition upregulated p53 protein expression, induced cell cycle arrest and apoptosis and decreased cell proliferation in cell lines. EBV-miR-BHRF1-1 mimics downregulated p53 protein expression, decreased cell cycle arrest and apoptosis, and induced cell proliferation in cell lines. Conclusion This study supported the role of EBV-miR-BHRF1-1 in p53 regulation in vitro. Our results support the potential of EBV-miR-BHRF1-1 as a therapeutic target in EBV-associated CLL with p53 gene aberration.

[$Ca^{2+}-induced$ $Ca^{2+}$ Release from Sarcoplasmic Reticulum Negatively Regulates Myocytic ANP Release in Beating Rabbit Atria

Li, Dan,Quan, He Xiu,Wen, Jin-Fu,Jin, Jing-Yu,Park, Sung-Hun,Kim, Sun-Young,Kim, Sung-Zoo,Cho, Kyung-Woo The Korean Society of Pharmacology 2005 The Korean Journal of Physiology & Pharmacology Vol.9 No.2

It is not clear whether $Ca^{2+}-induced$ $Ca^{2+}$ release from the sarcoplasmic reticulum (SR) is involved in the regulation of atrial natriuretic peptide (ANP) release. Previously, we have shown that nifedipine increased ANP release, indicating that $Ca^{2+}$ entry via voltage-gated L-type $Ca^{2+}$ channel activation decreases ANP release. The purpose of the present study was two-fold: to define the role of SR $Ca^{2+}$ release in the regulation of ANP release and whether $Ca^{2+}$ entry via L-type $Ca^{2+}$ channel is prerequisite for the SR-related effect on ANP release. Experiments were performed in perfused beating rabbit atria. Ryanodine, an inhibitor of SR $Ca^{2+}$ release, increased atrial myocytic ANP release ($8.69{\pm}3.05$, $19.55{\pm}1.09$, $27.31{\pm}3.51$, and $18.91{\pm}4.76$% for 1, 2, 3, and $6{\mu}M$ ryanodine, respectively; all P<0.01) with concomitant decrease in atrial stroke volume and pulse pressure in a dose-dependent manner. In the presence of thapsigargin, an inhibitor of SR $Ca^{2+}$ pump, ryanodine-induced increase in ANP release was not observed. Thapsigargin attenuated ryanodine-induced decrease in atrial dynamic changes. Blockade of L-type $Ca^{2+}$ channel with nifedipine abolished ryanodine-induced increase in ANP release ($0.69{\pm}5.58$% vs. $27.31{\pm}3.51$%; P<0.001). In the presence of thapsigargin and ryanodine, nifedipine increased ANP release and decreased atrial dynamics. These data suggest that $Ca^{2+}$-induced $Ca^{2+}$ release from the SR is inversely involved in the regulation of atrial myocytic ANP release.

Ca<SUP>2⁢</SUP>-induced Ca<SUP>2⁢</SUP> Release from Sarcoplasmic Reticulum Negatively Regulates Myocytic ANP Release in Beating Rabbit Atria

Dan Li,He Xiu Quan,Jin Fu Wen,Jing Yu Jin,Sung Hun Park,Sun Young Kim,Sung Zoo Kim,Kyung Woo Cho 대한생리학회-대한약리학회 2005 The Korean Journal of Physiology & Pharmacology Vol.9 No.2

It is not clear whether Ca<SUP>2⁢</SUP>-induced Ca<SUP>2⁢</SUP> release from the sarcoplasmic reticulum (SR) is involved in the regulation of atrial natriuretic peptide (ANP) release. Previously, we have shown that nifedipine increased ANP release, indicating that Ca<SUP>2⁢</SUP> entry via voltage-gated L-type Ca<SUP>2⁢</SUP> channel activation decreases ANP release. The purpose of the present study was two-fold: to define the role of SR Ca<SUP>2⁢</SUP> release in the regulation of ANP release and whether Ca<SUP>2⁢</SUP> entry via L-type Ca<SUP>2⁢</SUP> channel is prerequisite for the SR-related effect on ANP release. Experiments were performed in perfused beating rabbit atria. Ryanodine, an inhibitor of SR Ca<SUP>2⁢</SUP> release, increased atrial myocytic ANP release (8.69⁑3.05, 19.55⁑1.09, 27.31⁑3.51, and 18.91⁑4.76% for 1, 2, 3, and 6μM ryanodine, respectively; all P<0.01) with concomitant decrease in atrial stroke volume and pulse pressure in a dose-dependent manner. In the presence of thapsigargin, an inhibitor of SR Ca<SUP>2⁢</SUP> pump, ryanodine-induced increase in ANP release was not observed. Thapsigargin attenuated ryanodine-induced decrease in atrial dynamic changes. Blockade of L-type Ca<SUP>2⁢</SUP> channel with nifedipine abolished ryanodine-induced increase in ANP release (0.69⁑5.58% vs. 27.31⁑3.51%; P<0.001). In the presence of thapsigargin and ryanodine, nifedipine increased ANP release and decreased atrial dynamics. These data suggest that Ca<SUP>2⁢</SUP>-induced Ca<SUP>2⁢</SUP> release from the SR is inversely involved in the regulation of atrial myocytic ANP release.

Ca2+-induced Ca2+ Release from Sarcoplasmic Reticulum Negatively Regulates Myocytic ANP Release in Beating Rabbit Atria

Dan Li,He Xiu Quan,Jin Fu Wen,Jing Yu Jin,,박성훈,김선영,김성주,조경우 대한약리학회 2005 The Korean Journal of Physiology & Pharmacology Vol.9 No.2

It is not clear whether Ca2+-induced Ca2+ release from the sarcoplasmic reticulum (SR) is involved in the regulation of atrial natriuretic peptide (ANP) release. Previously, we have shown that nifedipine increased ANP release, indicating that Ca2+ entry via voltage-gated L-type Ca2+ channel activation decreases ANP release. The purpose of the present study was two-fold: to define the role of SR Ca2+ release in the regulation of ANP release and whether Ca2+ entry via L-type Ca2+ channel is prerequisite for the SR-related effect on ANP release. Experiments were performed in perfused beating rabbit atria. Ryanodine, an inhibitor of SR Ca2+ release, increased atrial myocytic ANP release (8.69±3.05, 19.55±1.09, 27.31±3.51, and 18.91±4.76% for 1, 2, 3, and 6μM ryanodine, respectively; all P<0.01) with concomitant decrease in atrial stroke volume and pulse pressure in a dose-dependent manner. In the presence of thapsigargin, an inhibitor of SR Ca2+ pump, ryanodine-induced increase in ANP release was not observed. Thapsigargin attenuated ryanodine-induced decrease in atrial dynamic changes. Blockade of L-type Ca2+ channel with nifedipine abolished ryanodine-induced increase in ANP release (0.69±5.58% vs. 27.31±3.51%; P<0.001). In the presence of thapsigargin and ryanodine, nifedipine increased ANP release and decreased atrial dynamics. These data suggest that Ca2+-induced Ca2+ release from the SR is inversely involved in the regulation of atrial myocytic ANP release.

중국 수출용 쌀의 중금속 안전성 평가

김경진 ( Gyeong-jin Kim ),양애리 ( Ae-li Yang ),김진배 ( Jin-bae Kim ),진용덕 ( Yong-duk Jin ),노진호 ( Jin-ho Ro ),김단비 ( Dan-bi Kim ),류지혁 ( Ji-hyock Yoo ),오경석 ( Kyeong-seok Oh ),문병철 ( Byeong-churl Moon ),박상원 ( Sang 한국환경농학회 2017 한국환경농학회 학술대회집 Vol.2017 No.-

2016년에 대중국 쌀 수출길이 열리면서 낮은 인지도 및 고가격 대비 차별성을 극복하기 위해서 고품질 쌀 생산 및 가공기술과 더불어 안전성 확보는 필수요소가 되었다. 중국의 식품안전법에 근거로 한 새로운 食品中汚染物限量(GB2762-2012, 2013.6.1.)에 규정된 중금속 안전관리 기준에 맞는 쌀 생산을 위하여 6개 시군(철원, 이천, 청주, 서천, 군산, 해남)의 중국 수출용 쌀 생산단지에서 농경지 토양, 농업 용수 및 생산된 쌀을 채취하여 중금속을 분석하였다. 수출용 쌀 생산단지 토양의 비소 함량은 2.9~18.2 mg/kg 범위로 검출되어 환경오염 우려수준인 25 mg/kg 이하였으며, 카드뮴은 모든 시료에서 정량한계 수준인 0.006 mg/kg 이하로 검출되지 않았다. 구리는 충남 서천 지역에서 최고 25.6 mg/kg이 검출되었으나 토양오염 우려기준 250 mg/kg의 약 1/10수준으로 안전하였다. 그리고 니켈, 납, 아연, 6가크롬 등 분석한 8종의 중금속이 토양오염우려기준 보다 낮게 검출되어 안전한 수준임이 확인되었다. 농업용 수 중 비소의 잔류량은 하천수에서 최고 24.3 ug/L으로 상대적으로 많은 양이 검출되었으나, 지하수는 대부분 1~2 ug/L 수준으로 검출되어 농업용수의 수질기준(0.05 mg/kg)을 초과하지 않았다. 백미와 현 미 중 중금속 5종을 분석한 결과 수은과 크롬은 정량한계 미만이었으며, 카드뮴은 0.004~0.068 mg/kg 이 검출되어 한국과 중국의 잔류허용기준인 0.2 mg/kg 이하였다. 또한 백미 중 납은 0.002~0.136 mg/kg 범위로 우리나라의 백미 기준 0.2 mg/kg, 중국 현미 기준 0.2 mg/kg 이하로 안전하였다. 전반 적으로 쌀 중 비소 등 5종의 중금속 잔류량은 한국과 중국의 잔류허용기준의 1/10~1/20 수준으로 안전 하였다.

Effect of Aging Precipitate on Ductility Anisotropy and Low Cycle Fatigue Behavior of AA2195 Al-Li Alloy

Gui Wang,Ben Lin,Ding‑ding Lu,San‑xi Deng,Guang‑jun Zeng,Xu‑feng Cai,Jin‑feng Li,Dan‑yang Liu 대한금속·재료학회 2023 METALS AND MATERIALS International Vol.29 No.8

The mechanical properties and low-cycle fatigue behavior of the hot-rolled AA2195 Al-Li alloy taken along the longitudinaldirection and transverse direction were investigated. The anisotropy ductility of the alloy with the short-term naturalaging (T4-SN), long-term natural aging (T4-LN), and T6 artificial aging alloy is mainly related to the grain structure andgrain boundaries, whereas the weakened anisotropy of ductility is attributed to the appearance of PFZs. The T4-SN andT4-LN specimens present the cyclic hardening phenomenon due to the interaction of dislocations with dislocations or theGuinier–Preston zone. The cyclic softening phenomenon in T6 specimens is attributed to that the dislocations cut throughthe T1precipitates, and some dislocations bypass the non-shearable precipitates, which activates more potential slip systemsto shear the T1precipitates.

Anti-inflammatory effect of hispidin on LPS induced macrophage inflammation through MAPK and JAK1/STAT3 signaling pathways

Han Ying-Hao,Chen Dong-Qin,Jin Mei-Hua,Jin Ying-Hua,Li Jing,Shen Gui-Nan,Li Wei-Long,Gong Yi-Xi,Mao Ying-Ying,Xie Dan-Ping,Lee Dong-Seok,Yu Li-Yun,Kim Sun-Uk,김지수,권태호,Cui Yu-Dong,Sun Hu-Nan 한국응용생명화학회 2020 Applied Biological Chemistry (Appl Biol Chem) Vol.63 No.3

Severe inflammatory reactions caused by macrophage activation can trigger a systemic immune response. In the present study, we observed the anti-inflammatory properties of hispidin on LPS induced RAW264.7 macrophage cells. Our results showed that hispidin treatment significantly reduced the production of cellular NO, IL-6 and reactive oxygen species (ROS) while has not inhibitory effect on TNF-α productions. Excitingly, hispidin treatment retains the phagocytosis ability of macrophages which enabling them to perform the function of removing foreign invaders. Signaling studies showed, hispidin treatment dramatic suppressed the LPS induced mitogen activated protein kinases (MAPK) and JAK/STAT activations. In conclusion, our findings suggest that hispidin may be a new therapeutic target for clinical treatment of macrophages-mediated inflammatory responses.

Performance and sludge characteristics of anammox process at moderate and low temperatures

Jin Li,Dan Wang,Deshuang Yu,Peiyu Zhang 한국화학공학회 2018 Korean Journal of Chemical Engineering Vol.35 No.1

A sequencing batch reactor (SBR) was used to investigate the performance and sludge characteristics of anammox process at moderate and low temperatures. The initial pH was 7.5 and hydraulic retention time (HRT) was 3 h. When temperature was 25-35 oC, nitrogen removal rate (NRR) fluctuated from 1.67 to 1.82 kg/m3·d. However, when temperature dropped to 15 oC, NRR suddenly decreased by 0.48 kg/m3·d. Larger activation energy was acquired at lower temperature, and it was difficult to achieve efficient nitrogen removal under low temperature. When temperature declined to 10 oC, ΔNO2 −-N/ΔNH4 +-N and ΔNO3 −-N/ΔNH4 +-N reached 1.02 and 0.27, respectively. Inhibition resulting from low temperature on anammox activity was recoverable, and the modified Boltzmann model was appropriate to analyze recovery feature of anammox process. Low temperature not only led to poor nitrogen removal, but also affected sludge size and feature.

Parkinson’s Disease with Fatigue: Clinical Characteristics and Potential Mechanisms Relevant to α-Synuclein Oligomer

Li-Jun Zuo,Shu-Yang Yu,Fang Wang,Yanghui Xia,Ying-Shan Piao,Yang Du,Teng-Hong Lian,Rui-Dan Wang,Qiu-Jin Yu,Ya-Jie Wang,Xiao-Min Wang,Piu Chan,Sheng-Di Chen,Yongjun Wang,Wei Zhang 대한신경과학회 2016 Journal of Clinical Neurology Vol.12 No.2

Background and Purpose The aim of this study was to identify the clinical characteristics and potential mechanisms relevant to pathological proteins in Parkinson’s disease (PD) patients who experience fatigue. Methods PD patients (n=102) were evaluated using a fatigue severity scale and scales for motor and nonmotor symptoms. The levels of three pathological proteins—α-synuclein oligomer, β-amyloid (Aβ)1-42, and tau—were measured in 102 cerebrospinal fluid (CSF) samples from these PD patients. Linear regression analyses were performed between fatigue score and the CSF levels of the above-listed pathological proteins in PD patients. Results The frequency of fatigue in the PD patients was 62.75%. The fatigue group had worse motor symptoms and anxiety, depression, and autonomic dysfunction. The CSF level of α-synuclein oligomer was higher and that of Aβ1-42 was lower in the fatigue group than in the non-fatigue group. In multiple linear regression analyses, fatigue severity was significantly and positively correlated with the α-synuclein oligomer level in the CSF of PD patients, after adjusting for confounders. Conclusions PD patients experience a high frequency of fatigue. PD patients with fatigue have worse motor and part nonmotor symptoms. Fatigue in PD patients is associated with an increased α-synuclein oligomer level in the CSF