Comparison and Analysis of Street Tree in Beijing, China, and Daejeon, South Korea : Mainly focused on species diversity

Li Zhi Hua, Seo Byung Key, Li Zhi Hui 배재대학교 자연과학연구소 2011 自然科學論文集 Vol.22 No.1

중국 북경과 한국 대전의 가로수 비교 분석을 통해서 가로수의 다양성과 생태적, 미적 그리고 사회기능성을 높이기 위한 기초자료를 제공하고자 문헌조사와 현지답사를 통해 수행한 연구결과는 다음과 같다. 두 도시의 공통점은 가로수의 종 다양성이 낮으면서도 일부 수종이 큰 비율을 차지하고 있다는 점과, 상록수의 비율이 매우 낮았다는 점, 그리고 대전의 일부 가로수 구간에서 지피식물과 혼식하여 좀 더 풍부한 경관을 창출한 것을 제외하고는, 가로수의 배치 형태 또한 두 도시 모두 단순한 열식형태라는 점과 가로수 수령이 높지 않다는 점을 들 수 있다. 차이점으로는 북경 가로수는 외래종의 비율이 6.3%로 낮은 반면 대전 가로수는 외래종의 비율이 66.1%로 월등히 높아서 대전의 지역특성을 나타내지 못하였다는 점이 가장 컸다. 하지만 북경 가로수의 관리 상태는 대전의 가로수에 비해 양호한 편은 아닌 것으로 보였다. 한편, 화목류, 단풍이 예쁘게 드는 수종, 열매를 볼 수 있는 수종 등은 색감이 좋을 뿐만 아니라 계절감을 제공해 주므로 두 도시 모두 더 많이 도입할 필요가 있을 것으로 판단되었다.

Transmembrane Helix of Novel Oncogene with Kinase-Domain (NOK) Influences Its Oligomerization and Limits the Activation of RAS/MAPK Signaling

Ying-Hua Li,Yin-Yin Wang,Shan Zhong,Zhi-Li Rong,Yong-Ming Ren,Zhi-Yong Li,Shu-Ping Zhang,Zhi-Jie Chang,Li Liu 한국분자세포생물학회 2009 Molecules and cells Vol.27 No.1

Ligand-dependent or independent oligomerization of receptor protein tyrosine kinase (RPTK) is often an essential step for receptor activation and intracellular signaling. The novel oncogene with kinase-domain (NOK) is a unique RPTK that almost completely lacks an ectodomain, expresses intracellularly and activates constitutively. However, it is unknown whether NOK can form oligomer or what function oligomerization would have. In this study, two NOK deletion mutants were generated by either removing the ectodomain (NOKECD) or including the endodomain (NOK-ICD). Co-immunoprecipitation demonstrated that the transmembrane (TM) domain of NOK was essential for its intermolecular interaction. The results further showed that NOK aggregated more closely as lower order oligomers (the dimer- and trimer-sized) than either deletion mutant did since NOK could be cross-linked by both Sulfo-EGS and formaldehyde, whereas either deletion mutant was only sensitive to Sulfo-EGS. Removing the NOK TM domain (NOK-ICD) not only markedly promoted higher order oligomerization, but also altered the subcellular localization of NOK and dramatically elevated the NOK-mediated constitutive activation of extracellular signal-regulated kinase (ERK). Moreover, NOK-ICD but not NOK or NOKECD was co-localized with the upstream signaling molecule RAS on cell membrane. Thus, TM-mediated intermolecular contacting may be mainly responsible for the constitutive activation of NOK and contribute to the autoinhibitory effect on RAS/MAPK signaling.

Cordycepin protects against β–amyloid and ibotenic acid– induced hippocampal CA1 pyramidal neuronal hyperactivity

Li-Hua Yao,Jinxiu Wang,Chao Liu,Shanshan Wei,Guoyin Li,Songhua Wang,Wei Meng,Zhi-Bin Liu,Li-Ping Huang 대한약리학회 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.6

Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer’s disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. β-Amyloid (Aβ) and ibotenic acid (IBO)–induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed Aβ + IBO–induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in Aβ + IBO–induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against Aβ + IBO–induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine A1 receptor–specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the Aβ + IBO–induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of A1R is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.

Synthesis and structure–activity relationship of N-(piperidin-4-yl)benzamide derivatives as activators of hypoxia-inducible factor 1 pathways

Zhi-Ning Huang,Han Liang,Hong Qiao,Bao-Rui Wang,Ning Qu,Hua Li,Run-Run Zhou,Li-Juan Wang,Shan-Hua Li,Fu-Nan Li 대한약학회 2018 Archives of Pharmacal Research Vol.41 No.12

Guided by bioisosterism and pharmacokinetic parameters, we designed and synthesized a series of novel benzamide derivatives. Preliminary in vitro studies indicated that compounds 10b and 10j show significant inhibitory bioactivity in HepG2 cells (IC50 values of 0.12 and 0.13 μM, respectively). Compounds 10b and 10j induced the expression of HIF-1α protein and downstream target gene p21, and upregulated the expression of cleaved caspase-3 to promote tumor cells apoptosis.

Dynamic test and numerical simulation on avoiding the weak-story failure mechanism in structures using LSFDs

Li-Hua Zhu,Gang Li,Zhi-Qian Dong 국제구조공학회 2021 Steel and Composite Structures, An International J Vol.40 No.2

The structural damage or collapse caused by weak-story failure mechanisms poses a great threat to the safety of human life and property under strong earthquakes. Many researchers have attempted to transform this unexpected failure mechanism into the desired overall failure mechanism by installing various energy dissipation devices on unsafe structures. This paper introduced a lattice-shaped friction device (LSFD), which is a friction device with hardening postyielding stiffness, into a steel frame with a weak-story failure mechanism. Then, shaking table tests of a three types of two-story steel frames—a frame with LSFDs, a frame with traditional friction brace dampers (FBDs), and a bare frame—were carried out. The seismic responses of the hardening postyielding stiffness of the LSFD on the weak-story failure mechanism of the frame were emphatically studied. The results showed that there was little difference in the seismic responses between the two damped structures under moderate and weak earthquakes. The distribution of maximum story drift for the structure with LSFDs was more uniform, which effectively suppressed the weak-story failure under strong earthquakes, whereas the structure with FBDs had serious deformation concentrations. The numerical simulation results of the structure with LSFDs in the shaking table test showed that the simplified model results were basically consistent with the experimental results. Hence, this model could be used to analyze the seismic performance of damped structures with LSFDs.

Cordycepin protects against β–amyloid and ibotenic acid– induced hippocampal CA1 pyramidal neuronal hyperactivity

Li-Hua Yao,Jinxiu Wang,Chao Liu,Shanshan Wei,Guoyin Li,Songhua Wang,Wei Meng,Zhi-Bin Liu,Li-Ping Huang 대한약리학회 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.6

Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer’s disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. β-Amyloid (Aβ) and ibotenic acid (IBO)–induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed Aβ + IBO–induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in Aβ + IBO–induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against Aβ + IBO–induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine A1 receptor–specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the Aβ + IBO–induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of A1R is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.

Immunization of BALB/c mice with Brucella abortus 2308DwbkA confers protection against wild-type infection

Zhi-qiang Li,Dan Gui,Zhi-hua Sun,Jun-bo Zhang,Wen-zhi Zhang,Hui Zhang,Fei Guo,Chuangfu Chen 대한수의학회 2015 Journal of Veterinary Science Vol.16 No.4

Brucellosis is a zoonotic disease that causes animal and human diseases. Vaccination is a major measure for prevention of brucellosis, but it is currently not possible to distinguish vaccinated animals from those that have been naturally infected. Therefore, in this study, we constructed the Brucella (B.) abortus 2380 wbkA mutant (2308DwbkA) and evaluated its virulence. The survival of 2308DwbkA was attenuated in murine macrophage (RAW 264.7) and BALB/c mice, and it induced high protective immunity in mice. The wbkA mutant elicited an anti-Brucella-specific immunoglobulin G response and induced the secretion of gamma interferon. Antibodies to 2308DwbkA could be detected in sera from mice, implying the potential for use of this protein as a diagnostic antigen. The WbkA antigen would allow serological differentiation between infected and vaccinated animals. These results suggest that 2308DwbkA is a potential attenuated vaccine against 16M. This vaccine will be further evaluated in sheep.

Cordycepin protects against β-amyloid and ibotenic acid-induced hippocampal CA1 pyramidal neuronal hyperactivity

Yao, Li-Hua,Wang, Jinxiu,Liu, Chao,Wei, Shanshan,Li, Guoyin,Wang, Songhua,Meng, Wei,Liu, Zhi-Bin,Huang, Li-Ping The Korean Society of Pharmacology 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.6

Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer's disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. ${\beta}$-Amyloid ($A{\beta}$) and ibotenic acid (IBO)-induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed $A{\beta}$ + IBO-induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in $A{\beta}$ + IBO-induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against $A{\beta}$ + IBO-induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine $A_1$ receptor-specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the $A{\beta}$ + IBO-induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of $A_1R$ is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.

AT1 Receptor Modulator Attenuates the Hypercholesterolemia-Induced Impairment of the Myocardial Ischemic Post-Conditioning Benefits

Yun-Wei Li,Yan-Ming Li,Yan Hon,Qi-Lin Wan,Rui-Li He,Zhi-Zhong Wang,Cui-Hua Zhao 대한심장학회 2017 Korean Circulation Journal Vol.47 No.2

Background and Objectives: Ischemic post-conditioning (PostC) has been demonstrated as a novel strategy to harness nature’s protection against myocardial ischemia-reperfusion (I/R). Hypercholesterolemia (HC) has been reported to block the effect of PostC on the heart. Angiotensin II type-1 (AT1) modulators have shown benefits in myocardial ischemia. The present study investigates the effect of a novel inhibitor of AT1, azilsartan in PostC of the heart of normocholesterolemic (NC) and HC rats. Materials and Methods: HC was induced by the administration of high-fat diet to the animals for eight weeks. Isolated Langendorff’s perfused NC and HC rat hearts were exposed to global ischemia for 30 min and reperfusion for 120 min. I/R-injury had been assessed by cardiac hemodynamic parameters, myocardial infarct size, release of tumor necrosis factor-alpha troponin I, lactate dehydrogenase, creatine kinase, nitrite in coronary effluent, thiobarbituric acid reactive species, a reduced form of glutathione, superoxide anion, and left ventricle collagen content in normal and HC rat hearts. Results: Azilsartan post-treatment and six episodes of PostC (10 sec each) afforded cardioprotection against I/R-injury in normal rat hearts. PostC protection against I/R-injury was abolished in HC rat hearts. Azilsartan prevented the HC-mediated impairment of the beneficial effects of PostC in I/R-induced myocardial injury, which was inhibited by L-N5-(1-Iminoethyl)ornithinehydrochloride, a potent inhibitor of endothelial nitric oxide synthase (eNOS). Conclusion: Azilsartan treatment has attenuated the HC-induced impairment of beneficial effects of PostC in I/R-injury of rat hearts, by specifically modulating eNOS. Azilsartan may be explored further in I/R-myocardial injury, both in NC and HC conditions, with or without PostC.

Determination of Protein, Fat, Starch, and Amino Acids in Foxtail Millet [Setaria italica (L.) Beauv.] by Fourier Transform Near-Infrared Reflectance Spectroscopy

Xiu-Shi Yang,Li-Li Wang,Xian-Rong Zhou,Shaomin Shuang,Zhi-Hua Zhu,Nan Li,Yan Li,Fang Liu,San-Cai Liu,Ping Lu,Guixing Ren,Chuan Dong 한국식품과학회 2013 Food Science and Biotechnology Vol.22 No.6

Quantitative detection of protein, fat, starch,and amino acids in foxtail millet using Fourier transformnear-infrared spectroscopy (NIRS) was investigated. Foxtail millet samples (n=259) were analyzed using NIRS. Spectral data were linearized with data from chemicalanalyses. Calibration models were established using apartial least-squares (PLS) algorithm with cross-validation. Optimized models were tested using external validation setsamples with coefficients of determination in the externalvalidation (R2val) of >0.90. Residual predictive deviation(RPD) values were nearly equal to or >2.5 for crudeprotein, alanine, aspartic acid, glutamic acid, isoleucine,leucine, and serine. However, for glycine, histidine,phenylalanine, proline, threonine, tyrosine, and valine, theR2val values were >0.83 and RPD values were nearly equalto or >2.0. For crude fat, total starch, arginine, and lysine,the R2val values were >0.70 and RPD values were >1.5. NIRS is a rapid determination tool for foxtail milletbreeding, and for quality control.