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Effect of Sub-T_g Annealing on the Corrosion Resistance of the Cu–Zr Amorphous Alloys

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Acta Metallurgica Sinica(English Letters) 2018年第3期31卷 273-280页

作者： Sang-Soo Shin Hong-Kyu Kim jae-chul lee Ik-Min Park Department of Materials Science and Engineering Pusan National University Advanced Analysis Center Korea Institute of Science and Technology Department of Materials Science and Engineering Korea University

Despite the economy of material cost and excellent toughness of Cu-based amorphous alloys,especially CusoZrso,their poor corrosion resistance to a chloride medium limits their widespread *** this study,corrosion tests were performed on the CusoZrso amorphous alloy with different degrees of short-range order,which were prepared by annealing below the glass transition temperature（Tg）.It was found that the corrosion resistance of amorphous alloys is improved to a significant level when the alloys were heated below *** studies showed that thermally activated relaxation process of created disorder,which occurs during sub-Tg annealing,is responsible for the improvement in the corrosion *** dynamics simulations performed on the Cu-Zr amorphous alloys demonstrated that the relaxation process of the alloys is associated with the formation of energetically stable icosahedra and icosahedron-like *** study highlights the effects of sub-Tg annealing on the improvement in the corrosion resistance of the amorphous alloys from the viewpoint the relaxation process of the short-range orders.

关键词： Amorphous alloys Corrosion Annealing Molecular dynamics Electrochemical performance

Neuroprotective effects of ischemic preconditioning on hippocampal CA1 pyramidal neurons through maintaining calbindin D28k immunoreactivity following subsequent transient cerebral ischemia

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Neural Regeneration Research 2017年第6期12卷 918-924页

作者： In Hye Kim Yong Hwan Jeon Tae-Kyeong lee Jeong Hwi Cho jae-chul lee Joon Ha Park Ji Hyeon Ahn Bich-Na Shin Yang Hee Kim Seongkweon Hong Bing Chun Yan Moo-Ho Won Yun Lyul lee Department of Neurobiology School of Medicine Kangwon National University Department of Radiology School of Medicine Kangwon National University Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University Department of Physiology College of Medicine Hallym University Department of Surgery School of Medicine Kangwon National University Institute of Integrative Traditional & Western Medicine Medical College Yangzhou University

Ischemic preconditioning elicited by a non-fatal brief occlusion of blood flow has been applied for an experimental therapeutic strategy against a subsequent fatal ischemic insult. In this study, we investigated the neuroprotective effects of ischemic preconditioning（2-minute transient cerebral ischemia） on calbindin D28k immunoreactivity in the gerbil hippocampal CA1 area following a subsequent fatal transient ischemic insult（5-minute transient cerebral ischemia）. A large number of pyramidal neurons in the hippocampal CA1 area died 4 days after 5-minute transient cerebral ischemia. Ischemic preconditioning reduced the death of pyramidal neurons in the hippocampal CA1 area. Calbindin D28k immunoreactivity was greatly attenuated at 2 days after 5-minute transient cerebral ischemia and it was hardly detected at 5 days post-ischemia. Ischemic preconditioning maintained calbindin D28 k immunoreactivity after transient cerebral ischemia. These findings suggest that ischemic preconditioning can attenuate transient cerebral ischemia-caused damage to the pyramidal neurons in the hippocampal CA1 area through maintaining calbindin D28k immunoreactivity.

关键词： hippocampal subsequent minute pyramidal maintaining attenuated hippocampus neuronal occlusion fatal

Effect of hyperthermia on calbindin-D 28k immunoreactivity in the hippocampal formation following transient global cerebral ischemia in gerbils

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Neural Regeneration Research 2017年第9期12卷 1458-1464页

作者： jae-chul lee Jeong-Hwi Cho Tae-Kyeong lee In Hye Kim Moo-Ho Won Geum-Sil Cho Bich-Na Shin In Koo Hwang Joon Ha Park Ji Hyeon Ahn Il Jun Kang Young Joo lee Yang Hee Kim Department of Neurobiology School of Medicine Kangwon National University Department of Pharmacology & Toxicology Shinpoong Pharmaceutical Co. Ltd. Department of Physiology College of Medicine Hallym University Department of Anatomy and Cell Biology College of Veterinary Medicine and Research Institute for Veterinary Science Seoul National University Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University Department of Food Science and Nutrition Hallym University Department of Emergency Medicine Seoul Hospital College of Medicine Sooncheonhyang University Department of Surgery School of Medicine Kangwon National University

Calbindin D-28K （CB）, a Ca2＋-binding protein, maintains Ca2＋ homeostasis and protects neurons against various insults. Hyperthermia can exacerbate brain damage produced by ischemic insults. However, little is reported about the role of CB in the brain under hyperthermic condition during ischemic insults. We inves- tigated the effects of transient global cerebral ischemia on CB immunoreactivity as well as neuronal damage in the hippocampal formation under hyperthermic condition using immunohistochemistry for neuronal nuclei （NeuN） and CB, and Fluoro-Jade B histofluorescence staining in gerbils. Hyperthermia （39.5 ＋ 0.2~C） was induced for 30 minutes before and during transient ischemia. Hyperthermic ischemia resulted in neu- ronal damage/death in the pyramidal layer of CA1-3 area and in the polymorphic layer of the dentate gyrus at 1, 2, 5 days after ischemia. In addition, hyperthermic ischemia significantly decreaced CB immunoreac- tivity in damaged or dying neurons at 1, 2, 5 days after ischemia. In brief, hyperthermic condition produced more extensive and severer neuronal damage/death, and reduced CB immunoreactivity in the hippocampus following transient global cerebral ischemia. Present findings indicate that the degree of reduced CB immu- noreactivity might be related with various neuronal damage/death overtime and corresponding areas after ischemic insults.

关键词： nerve regeneration hyperthermic condition ischemia/reperfusion injury subregions of hippocampus delayed neuronal death calbindin D-28k neural regeneration

Time-course pattern of neuronal loss and gliosis in gerbil hippocampi following mild, severe, or lethal transient global cerebral ischemia

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Neural Regeneration Research 2019年第8期14卷 1394-1403页

作者： Tae-Kyeong lee Hyunjung Kim Minah Song jae-chul lee Joon Ha Park Ji Hyeon Ahn Go Eun Yang Hyeyoung Kim Taek Geun Ohk Myoung Cheol Shin Jun Hwi Cho Moo-Ho Won Depart merit of Neurobiology School of Medici ne Kangw on National University Chuncheon Gangwon Republic of Korea Department of Biomedical Science and Research Institute for Bioscience and Biotechnology Hallym University Chuncheon Gangwon Republic of Korea Department of Radiology Kangwon National University Hospital Chuncheon Gangxvon Republic of Korea Department of Anesthesiology and Pain Medicine Chungju Hospital Konkuk University School of Medicine Chungju Chungcheongbuk Republic of Korea Department of Emergency Medicine School of Medicine Kangwon National University Chuncheon Gangwon Republic of Korea

Transient ischemia in the whole brain leads to neuronal loss/death in vulnerable brain regions. The striatum, neocortex and hippocampus selectively loose specific neurons after transient ischemia. Just 5 minutes of transient ischemia can cause pyramidal neuronal death in the hippocampal cornu ammonis (CA) 1 field at 4 days after transient ischemia. In this study, we investigated the effects of 5-minute (mild), 15-minute (severe), and 20-minute (lethal) transient ischemia by bilateral common carotid artery occlusion (BCCAO) on behavioral change and neuronal death and gliosis (astrocytosis and microgliosis) in gerbil hippocampal subregions (CA1-3 region and dentate gyrus). We performed spontaneous motor activity test to evaluate gerbil locomotor activity, cresyl violet staining to detect cellular distribution, neuronal nuclei immunohistochemistry to detect neuronal distribution, and Fluoro-Jade B histofluorescence to evaluate neuronal death. We also conducted immunohistochemical staining for glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 (Ibal) to evaluate astrocytosis and microgliosis, respectively. Animals subjected to 20-minute BCCAO died in at least 2 days. BCCAO for 15 minutes led to pyramidal cell death in hippocampal CA1-3 region 2 days later and granule cell death in hippocampal de匚tate gyrus 5 days later. Similar results were not found in animals subjected to 5-minute BCCAO. Gliosis was much more rapidly and severely progressed in animals subjected to 15-minute BCCAO than in those subjected to 5- minute BCCAO. Our results indicate that neuronal loss in the hippocampal formation following transient ischemia is significantly different according to regions and severity of transient ischemia. The experimental protocol was approved by Institutional Animal Care and Use Committee (AICUC) of Kangwon National University (approval No. KW-180124-1) on May 22, 2018.

关键词： transient global brain ischemia delayed neuronal death glial activation ischemic duration hippocampus spontaneous motor activity Mongolian gerbil histology neural regeneration

Pretreatment of Populus tomentiglandulosa protects hippocampal CA1 pyramidal neurons from ischemia-reperfusion injury in gerbils via increasing SODs expressions and maintaining BDNF and IGF-I expressions

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Chinese Journal of Natural Medicines 2019年第6期17卷 424-434页

作者： Tae-Kyeong lee Joon Ha Park Ji Hyeon Ahn Hyunjung Kim Minah Song jae-chul lee Jong Dai Kim Yong Hwan Jeon Jung Hoon Choi Choong Hyun lee In Koo Hwang YAN Bing-Chun Moo-Ho Won Il Jun Kang Department of Neurobiology School of MedicineKangwon National UniversityChuncheon 24341Republic of Korea Department of Biomedical Science Research Institute of Bioscience and BiotechnologyHallym UniversityChuncheon 24252Republic of Korea Division of Food Biotechnology School of BiotechnologyKangwon National UniversityChuncheon 24341Republic of Korea Department of Radiology School of MedicineKangwon National UniversityChuncheon 24289Republic of Korea Department of Anatomy College of Veterinary MedicineKangwon National UniversityChuncheon 24341Republic of Korea Department of Pharmacy College of PharmacyDankook UniversityCheonan 31116Republic of Korea Department of Anatomy and Cell Biology College of Veterinary Medicine and Research Institute for Veterinary ScienceSeoul National UniversitySeoul 08826Republic of Korea Jiangsu Key Laboratory of Integrated Traditional Chinese Western Medicine for Prevention and Treatment of Senile DiseasesYangzhou 225001China Department of Food Science and Nutrition Hallym UniversityChuncheon 24252Republic of Korea

To examine the effects of Populus tomentiglandulosa(PT) extract on the expressions of antioxidant enzymes and neurotrophic factors in the cornu ammonis 1(CA1) region of the hippocampus at 5 min after inducing transient global cerebral ischemia(TGCI) in gerbils, TGCI was induced by occlusion of common carotid arteries for 5 min. Before ischemic surgery, 200 mg·kg–1 PT extract was orally administrated once daily for 7 d. We performed neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B staining. Furthermore, we determined in situ production of superoxide anion radical, expression levels of SOD1 and SOD2 as antioxidant enzymes and brain-derived neurotrophic factor(BDNF) and insulin-like growth factor I(IGF-I) as neurotrophic factors. Pretreatment with 200 mg·kg–1 PT extract prevented neuronal death(loss). Furthermore, pretreatment with 200 mg·kg–1 PT extract significantly inhibited the production of superoxide anion radical, increased expressions of SODs and maintained expressions of BDNF and IGF-I. Such increased expressions of SODs were maintained in the neurons after IRI. In summary, pretreated PT extract can significantly increase levels of SODs and protect the neurons against TGCI, suggesting that PT can be a useful natural agent to protect against TGCI.

关键词： Transient global cerebral ischemia Populus tomentiglandulosa Neuroprotective effects Antioxidant enzymes

Long-term administration of scopolamine interferes with nerve cell proliferation, differentiation and migration in adult mouse hippocampal dentate gyrus, but it does not induce cell death

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Neural Regeneration Research 2014年第19期9卷 1731-1739页

作者： Bing Chun Yan Joon Ha Park Bai Hui Chen Jeong-Hwi Cho In Hye Kim Ji Hyeon Ahn jae-chul lee In Koo Hwang Jun Hwi Cho Yun Lyul lee Il-Jun Kang Moo-Ho Won Department of Integrative Traditional & Western Medicine Medical CollegeYangzhou University Department of Neurobiology School of MedicineKangwon National University Department of Physiology College of MedicineInstitute of Neurodegeneration and NeuroregenerationHallym University Department of Anatomy and Cell Biology College of Veterinary MedicineSeoul National University Department of Emergency Medicine School of MedicineKangwon National University Department of Food Science and Nutrition Hallym University

Long-term administration of scopolamine, a muscarinic receptor antagonist, can inhibit the survival of newly generated cells, but its effect on the proliferation, differentiation and migration of nerve cells in the adult mouse hippocampal dentate gyrus remain poorly understood. In this study, we used immunohistochemistry and western blot methods to weekly detect the biological behaviors of nerve cells in the hippocampal dentate gyrus of adult mice that received intraperito- neal administration of scopolamine for 4 weeks. Expression of neuronal nuclear antigen （NeuN; a neuronal marker） and Fluoro-]ade B （a marker for the localization of neuronal degeneration） was also detected. After scopolamine treatment, mouse hippocampal neurons did not die, and Ki-67 （a marker for proliferating cells）-immunoreactive cells were reduced in number and reac hed the lowest level at 4 weeks. Doublecortin （DCX; a marker for newly generated neurons）-im- munoreactive cells were gradually shortened in length and reduced in number with time. After scopolamine treatment for 4 weeks, nearly all of the 5-bromo-2＇-deoxyuridine （BrdU）-labeled newly generated cells were located in the subgranular zone of the dentate gyrus, but they did not migrate into the granule cell layer. Few mature BrdU/NeuN double-labeled cells were seen in the subgranular zone of the dentate gyrus. These findings suggest that long-term administration of scopolamine interferes with the proliferation, differentiation and migration of nerve cells in the adult mouse hippocampal dentate gyrus, but it does not induce cell death.

关键词： nerve regeneration neurogenesis scopolamine dentate gyrus cell proliferation neuroblastdifferentiation neuroblast migration granule cell layer neural regeneration

Neuronal injury and tumor necrosis factor-alpha immunoreactivity in the rat hippocampus in the early period of asphyxia-induced cardiac arrest under normothermia

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Neural Regeneration Research 2017年第12期12卷 2007-2013页

作者： Hyun-Jin Tae Il Jun Kang Tae-Kyeong lee Jeong Hwi Cho jae-chul lee Myoung Cheol Shin Yoon Sung Kim Jun Hwi Cho Jong-Dai Kim Ji Hyeon Ahn Joon Ha Park In-Shik Kim Hyang-Ah lee Yang Hee Kim Moo-Ho Won Young Joo lee Bio-Safety Research Institute College of Veterinary Medicine Chonbuk National University Iksan South Korea Department of Food Science and Nutrition Hallym University Chuncheon South Korea Department of Neurobiology School of Medicine Kangwon National University Chuncheon South Korea Department of Emergency Medicine School of Medicine Kangwon National University Chuncheon South Korea Department of Emergency Medicine Samcheok Medical Center Samcheok South Korea Division of Food Biotechnology School of Biotechnology Kangwon National University Chuncheon South Korea Department of Biomedical Science Research Institute of Bioscience and Biotechnology Hallym University Chuncheon South Korea Department of Obstetrics and Gynecology School of Medicine Kangwon National University Chuncheon South Korea Department of Surgery School of Medicine Kangwon National University Chuncheon South Korea Department of Emergency Medicine Seoul Hospital College of Medicine Sooncheonhyang University Seoul South Korea

Low survival rate occurs in patients who initially experience a spontaneous return of circulation after cardiac arrest（CA）. In this study, we induced asphyxial CA in adult male Sprague-Daley rats, maintained their body temperature at 37 ± 0.5°C, and then observed the survival rate during the post-resuscitation phase. We examined neuronal damage in the hippocampus using cresyl violet（CV） and Fluore-Jade B（F-J B） staining, and pro-inflammatory response using ionized calcium-binding adapter molecule 1（Iba-1）, glial fibrillary acidic protein（GFAP）, and tumor necrosis factor-alpha（TNF-α） immunohistochemistry in the hippocampus after asphyxial CA in rats under normothermia. Our results show that the survival rate decreased gradually post-CA（about 63% at 6 hours, 37% at 1 day, and 8% at 2 days post-CA）. Rats were sacrificed at these points in time post-CA, and no neuronal damage was found in the hippocampus until 1 day post-CA. However, some neurons in the stratum pyramidale of the CA region in the hippocampus were dead 2 days post-CA. Iba-1 immunoreactive microglia in the CA1 region did not change until 1 day postCA, and they were activated（enlarged cell bodies with short and thicken processes） in all layers 2 days postCA. Meanwhile, GFAP-immunoreactive astrocytes did not change significantly until 2 days post-CA. TNF-α immunoreactivity decreased significantly in neurons of the stratum pyramidale in the CA1 region 6 hours post-CA, decreased gradually until 1 day post-CA, and increased significantly again 2 days post-CA. These findings suggest that low survival rate of normothermic rats in the early period of asphyxia-induced CA is related to increased TNF-α immunoreactivity, but not to neuronal damage in the hippocampal CA1 region.

关键词： nerve regeneration post-cardiac arrest syndrome normothermia neuronal damage gliosis tumor necrosis factor-alpha neural regeneration

Pretreated Oenan the Javanica extract increases anti-inflammatory cytokines, attenuates gliosis, and protects hippocampal neurons following transient global cerebral ischemia in gerbils

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Neural Regeneration Research 2019年第9期14卷 1536-1543页

作者： Joon Ha Park In Hye Kim Ji Hyeon Ahn YooHun Noh Sung-Su Kim Tae-Kyeong lee jae-chul lee Bich-Na Shin Tae Heung Sim Hyun Sam lee Jeong Hwi Cho In Koo Hwang Il Jun Kang Jong Dai Kim Moo-Ho Won Department of Biomedical Science and Research Institute for Bioscience and Biotechnology Hallym UniversityChuncheonGangwonRepublic of Korea Famenity Company GwacheonGeyonggiRepublic of Korea Department of Neurobiology School of MedicineKangwon National UniversityChuncheonGangwonRepublic of Korea Danchunok Company ChuncheonGangwonRepublic of Korea Department of Histology College of Veterinary MedicineChonbuk National UniversityIksanJeollabuk.doRepublic of Korea Department of Anatomy and Cell Biology College of Veterinary Medicineand Research Institute for Veterinary ScienceSeoul National UniversitySeoulRepublic of Korea Department of Food Science and Nutrition Hallym UniversityChuncheonGangwonRepublic of Korea Division of Food Biotechnology School of BiotechnologyKangwon National UniversityChuncheonGangwonRepublic of Korea

Recently,we have reported that Oenanthe javanica extract(OJE)displays strong neuroprotective effect against ischemic damage after transient global cerebral ***,neuroprotective mechanisms of OJE have not been fully ***,this study investigated the neuroprotection of OJE in the hippocampal CA1 area and its anti-inflammatory activity in gerbils subjected to 5 minutes of transient global cerebral *** treated the animals by intragastrical injection of OJE(100 and 200 mg/kg)once daily for 1 week prior to transient global cerebral *** of OJE was observed by immunohistochemistry for neuronal nuclear antigen and histofluorescence staining for Fluoro-Jade *** of glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 was done for astrocytosis and microgliosis,*** investigate the neuroprotective mechanisms of OJE,we performed immunohistochemistry of tumor necrosis factor-alpha and interleukin-2 for pro-inflammatory function and interleukin-4 and interleukin-13 for anti-inflammatory *** we treated the animals by intragastrical administration of 200 mg/kg of OJE,hippocampal CA1 pyramidal neurons were protected from transient global cerebral ischemia and cerebral ischemia-induced gliosis was inhibited in the ischemic hippocampal CA1 *** also found that interleukin-4 and-13 immunoreactivities were significantly increased in pyramidal neurons of the ischemic CA1 area after OJE pretreatment,and the increased immunoreactivities were sustained in the CA1 pyramidal neurons after transient global cerebral ***,OJE pretreatment did not increase interleukin-2 and tumor necrosis factor-alpha immunoreactivities in the CA1 pyramidal *** findings suggest that pretreatment with OJE can protect neurons and attenuate gliosis from transient global cerebral ischemia via increasing expressions of interleukin-4 *** experimental plan of this study was rev

关键词： Oenanthe javanica extract transient global cerebral ischemia hippocampus ischemic damage cerebral ischemia neuroprotection glial activation pro-inflammatory cytokines anti-inflammatory cytokines inflammation neural regeneration

Pretreated quercetin protects gerbil hippocampal CA1 pyramidal neurons from transient cerebral ischemic injury by increasing the expression of antioxidant enzymes

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Neural Regeneration Research 2017年第2期12卷 220-227页

作者： Bai Hui Chen Joon Ha Park Ji Hyeon Ahn Jeong Hwi Cho In Hye Kim jae chul lee Moo-Ho Won Choong-Hyun lee In Koo Hwang Jong-Dai Kim Il Jun Kang Jun Hwi Cho Bich Na Shin Yang Hee Kim Yun Lyul lee Seung Min Park Department of Histology and Embryology Institute of NeuroscienceWenzhou Medical UniversityWenzhouZhejiang ProvinceChina Department of Biomedical Science and Research Institute for Bioscience and Biotechnology Hallym UniversityChuncheonSouth Korea Department of Neurobiology School of MedicineKangwon National UniversityChuncheonSouth Korea Department of Pharmacy College of PharmacyDankook UniversityCheonanSouth Korea Department of Anatomy and Cell Biology College of Veterinary Medicineand Research Institute for Veterinary ScienceSeoul National UniversitySeoulSouth Korea Division of Food Biotechnology School of BiotechnologyKangwon National UniversityChuncheonSouth Korea Department of Food Science and Nutrition Hallym UniversityChuncheonSouth Korea Department of Emergency Medicine School of MedicineKangwon National UniversityChuncheonSouth Korea Department of Physiology College of Medicineand Institute of Neurodegeneration and NeuroregenerationHallym UniversityChuncheonSouth Korea Department of Surgery School of MedicineKangwon National UniversityChuncheonSouth Korea Department of Emergency Medicine Sacred Heart HospitalCollege of MedicineHallym UniversityAnyangSouth Korea

Quercetin（QE; 3,5,7,3′,4′-pentahydroxyflavone）, a well-known flavonoid, has been shown to prevent against neurodegenerative disorders and ischemic insults. However, few studies are reported regarding the neuroprotective mechanisms of QE after ischemic insults. Therefore, in this study, we investigated the effects of QE on ischemic injury and the expression of antioxidant enzymes in the hippocampal CA1 region of gerbils subjected to 5 minutes of transient cerebral ischemia. QE was pre-treated once daily for 15 days before ischemia. Pretreatment with QE protected hippocampal CA1 pyramidal neurons from ischemic injury, which was confirmed by neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B histofluorescence staining. In addition, pretreatment with QE significantly increased the expression levels of endogenous antioxidant enzymes Cu/Zn superoxide dismutase, Mn superoxide dismutase, catalase and glutathione peroxidase in the hippocampal CA1 pyramidal neurons of animals with ischemic injury. These findings demonstrate that pretreated QE displayed strong neuroprotective effects against transient cerebral ischemia by increasing the expression of antioxidant enzymes.

关键词： nerve regeneration flavonoids transient cerebral ischemia Cu/Zn superoxide dismutase catalase Mn superoxide dismutase glutathione peroxidase neural regeneration