Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 34th European Neurology Congress Zurich, Switzerland.

Day :

  • Neurology, Clinical Neurophysiology, Neurosurgery, Central Nervous System, Pediatric Neurology, Neuromuscular Disorders, Psychiatry and Psychology, Spine and Spinal Disorders, Neurogenetic and Neurometabolic Disorders, Neuropharmacology, Nursing and Neuroscience
Location: Webinar

Session Introduction

Jun Hwi Cho

Kangwon National University, Republic of Korea

Title: Effects of regional body temperature during asphyxial cardiac arrest on mortality and brain damage in rats
Biography:

Jun Hwi Cho, MD, PhD is professor in department of Emergency Medicine and Neurobiology, Kangwon National University Hospital, South Korea. His major research fields are cardiac arrest and cardiopulmonary resuscitation (CPR) using hypothermia, toxicology and critical care, experimental ischemic stroke: about neuronal damage and protection in the ischemic brain, cardiopulmonary resuscitation using rat VF model & asphyxia model and histopathological research after cardiac arrest in animal model of cardiac arrest. He interest in neuronal protection using therapeutic hypothermia during CPR with patient of cardiac arrest and medicines for neuroprotection, neurogenesis and anti-aging in the CNS: He has examined many medicines including extracts of foods and plants that protect neuronal damage or aging and enhance neurogenesis.

 

 

Abstract:

Purpose: To date, hypothermia has focused on improving rates of resuscitation to increase survival rates in cardiac arrest (CA) patients. For this, it needs to understand what body temperature affects neuronal damage/death in the brain during CA. However, few studies on effects of regional temperature in the body during CA on survival rate and neurological outcomes have been studied.

Materials and methods: Here, we used adult male rats (12 week-old) which were subjected to 4 conditions as follows: (i) whole body normothermia (37±0.5°C) plus (+) no asphyxial CA, (ii) whole body normothermia+CA, (iii) whole body hypothermia (33±0.5°C)+CA, (iv) body hypothermia/brain normothermia+CA, and (v) brain hypothermia/body normothermia+CA.

Results: Survival rate after resuscitation was significantly high in groups of whole body hypothermia+CA and body hypothermia/brain normothermia+CA, but not in groups of whole body normothermia+CA and brain hypothermia/body normothermia+CA. However, the group of hypothermia/brain normothermia+CA exhibited higher neuroprotective effect against asphyxial CA injury: neurological deficit and neuronal death in the hippocampus were improved compared to those in the group of whole body normothermia+CA. In addition, neurological deficit and neuronal death in the group of brain hypothermia/body normothermia+CA were was similar to those in the group of whole body normothermia+CA.

Conclusions: In brief, only brain hypothermia during CA did not show effective survival rate, neurological function and neuronal protection compared to those under body (not brain) hypothermia during CA. Our present study suggests that regional temperature in patients during CA can significantly affect outcomes in survival rate and neurological recovery.

 

Biography:

Jun Hwi Cho, MD, PhD is professor in department of Emergency Medicine and Neurobiology, Kangwon National University Hospital, South Korea. His major research fields are cardiac arrest and cardiopulmonary resuscitation (CPR) using hypothermia, toxicology and critical care, experimental ischemic stroke: about neuronal damage and protection in the ischemic brain, cardiopulmonary resuscitation using rat VF model & asphyxia model and histopathological research after cardiac arrest in animal model of cardiac arrest. He interest in neuronal protection using therapeutic hypothermia during CPR with patient of cardiac arrest and medicines for neuroprotection, neurogenesis and anti-aging in the CNS: He has examined many medicines including extracts of foods and plants that protect neuronal damage or aging and enhance neurogenesis.

 

 

Abstract:

Purpose: To date, hypothermia has focused on improving rates of resuscitation to increase survival rates in cardiac arrest (CA) patients. For this, it needs to understand what body temperature affects neuronal damage/death in the brain during CA. However, few studies on effects of regional temperature in the body during CA on survival rate and neurological outcomes have been studied.

Materials and methods: Here, we used adult male rats (12 week-old) which were subjected to 4 conditions as follows: (i) whole body normothermia (37±0.5°C) plus (+) no asphyxial CA, (ii) whole body normothermia+CA, (iii) whole body hypothermia (33±0.5°C)+CA, (iv) body hypothermia/brain normothermia+CA, and (v) brain hypothermia/body normothermia+CA.

Results: Survival rate after resuscitation was significantly high in groups of whole body hypothermia+CA and body hypothermia/brain normothermia+CA, but not in groups of whole body normothermia+CA and brain hypothermia/body normothermia+CA. However, the group of hypothermia/brain normothermia+CA exhibited higher neuroprotective effect against asphyxial CA injury: neurological deficit and neuronal death in the hippocampus were improved compared to those in the group of whole body normothermia+CA. In addition, neurological deficit and neuronal death in the group of brain hypothermia/body normothermia+CA were was similar to those in the group of whole body normothermia+CA.

Conclusions: In brief, only brain hypothermia during CA did not show effective survival rate, neurological function and neuronal protection compared to those under body (not brain) hypothermia during CA. Our present study suggests that regional temperature in patients during CA can significantly affect outcomes in survival rate and neurological recovery.

 

Qiuwen Wang

Tsinghua University, China

Title: Investigating the molecular mechanism of bipolar disorder

Time : 10:00-10:30

Speaker
Biography:

Qiuwen Wang has been studying the molecular mechanisms involved in the pathogenesis of bipolar disorder. She has her expertise in Stem Cell Biology, Electrophysiology and Fluorescence Imaging. She is passionate on developing new therapies and drugs aimed at clinical treatment for bipolar disorder.

 

Abstract:

Bipolar disorder (BD) is a complex neuropsychiatric disorder that is characterized by intermittent episodes of mania and depression. BD affects more than 1% population worldwide and has been ranked by the World Health Organization as a top disorder of morbidity and lost productivity. However, the pathogenesis of BD has remained enigmatic. This is mainly because genetic animal models based on identified susceptible genes have often failed to show core symptoms of BD, especially spontaneous mood cycling. The introduction of induced pluripotent stem cell (iPSC) technology has provided a new approach for research of BD pathogenesis. We have developed an iPSC model for human BD and investigated the cellular and molecular deficits of patient iPSC-derived hippocampal dentate gyrus-like neurons. Guided by patch-clamp recording analysis, we have observed hyperactive action-potential firing, which could be selectively reversed by lithium treatment. Both our iPSC-based RNA analysis and past pedigree research have implicated that dysfunction in some key signaling cascades might be crucial for the disease pathogenesis in a subpopulation of BD patients. We hypothesized that the behavioral abnormalities of patients and the comorbid metabolic abnormalities might share some identical molecular mechanism. Hence, we investigated the expression of insulin/synapse dually functioning genes in patient iPSC-derived neurons and their phenotypes in the behaviors of mice with these genes silenced in the hippocampus. By this means, we identified synaptotagmin-7 (Syt7) as a candidate risk factor for behavioral abnormalities. We then investigated Syt7 knockout (KO) mice and observed nocturnal manic-like and diurnal depressive-like behavioral fluctuations in a majority of these animals, which are analogous to the mood cycling symptoms of BD and could be treated by clinical drugs. Finally, we observed that the patient plasma samples showed a significantly reduced Syt7 expression compared to the healthy control subjects. We therefore concluded that Syt7 is likely a key factor for the bipolar-like behavioral abnormalities.


Recent Publications:

1.Mertens J*, Wang QW*, Kim, Y., Yu, D.X., Pham, S., Yang, B., Zheng, Y., Diffenderfer, K.E., Zhang, J., Soltani, S., et al. (2015). Differential responses to lithium in hyperexcitable neurons from patients with bipolar disorder. Nature 527, 95-99.

2.Stern, S., Santos, R., Marchetto, M.C., Mendes, A.P.D., Rouleau, G.A., Biesmans, S., Wang, QW., Yao, J., Charnay, P., Bang, A.G., et al. (2018). Neurons derived from patients with bipolar disorder divide into intrinsically different sub-populations of neurons, predicting the patients' responsiveness to lithium. Molecular psychiatry 23, 1453-1465.

3.Wei Shen*, Wang QW* et al. Synaptotagmin-7 is a key factor for bipolar-like behavioral abnormalities in mice. PNAS, Accepted.

 

Biography:

Yoel Levinsky is currently working as a Doctor in Schneider Children Medical Center, Israel.

Abstract:

Background: Duchenne and Becker muscular dystrophies are inherited X-linked disorders that appear in childhood and can lead to significant disability. Recent studies have showed that chronic pain is a significant problem for the affected patients, but no study has evaluated the prevalence and features of headache among patients with those diseases.

Methods: Children and adolescent aged 2.5-18 years with an established diagnosis of muscular dystrophy who visited the multi-disciplinary neuromuscular pediatric clinic were enrolled. The patients and their parents received a questionnaire regarding the existence of headache and its features, and regarding emotional and social factors.   

Results: The cohort included 68 patients, all males. Mean age was 9.0 ± 3.8 years. Forty-eight patients (70.6%) had Duchenne muscular dystrophy and the others had Becker muscular dystrophy. Overall, 22 (32.4%) patients reported headaches, among them, 10 (45.5%) had a diagnosis of migraine. Patients with headache were older than those without headache (p=<0.001), their blood creatine kinase level was significantly lower (p=0.0142), and they had a significantly higher proportion of other pain (p=0.0086). Their SDQ emotional scale score was significantly higher than those without headache (p=0.0004).     

Conclusions: The prevalence of headache among patients with muscular dystrophy is high. It is related to the severity of the disease, to other location of pain and to emotional difficulties. Physicians who take care of those children and adolescent may consider to actively screen for headache and to offer appropriate, inclusive treatment.

Recent Publications

1.Mah JK, Korngut L, Dykeman J, Day L, Pringsheim T, Jette N. A systematic review and meta-analysis on the epidemiology of Duchenne and Becker muscular dystrophy. Neuromuscul Disord. 2014;24(6):482–491

2.Silva TD, Massetti T, Monteiro CB, Trevizan IL, Arab C, Caromano FA, Voos MC, Oliveira AS, Favero FM. Pain characterization in Duchenne muscular dystrophy. Arq Neuropsiquiatr. 2016 Sep;74(9):767-774

3.Engel JM, Kartin D, Carter GT, Jensen MP, Jaffe KM. Pain in youths with neuromuscular disease. Am J Hosp Palliat Care. 2009 Oct-Nov;26(5):405-12.LiX,

4.Pangalila RF, van den Bos GA, Bartels B, Bergen M, Stam HJ, Roebroeck ME. Prevalence of fatigue, pain, and affective disorders in adults with duchenne muscular dystrophy and their associations with quality of life. Arch Phys Med Rehabil. 2015 Jul;96(7):1242-7.

5.Bray P, Bundy AC, Ryan MM, North KN, Burns J. Health status of boys with Duchenne muscular dystrophy: a parent's perspective. J Paediatr Child Health. 2011 Aug;47(8):557-62.

 

Speaker
Biography:

Mehdi Maghbooli was born in “Marand – Iran”. My medical education began in Tabriz University of Medical Sciences in 1992 and I graduated at 1999 as M.D.Then I was accepted for Neurology residency in Tehran University of Medical Sciences at 2002 and graduated as neurologist in 2006. I am working as an academic member in Zanjan University of medical science since October of 2006 and now I am an associate professor of neurology in Zanjan faculty of medicine.

 

Abstract:

Background: Bell's palsy is the most common cause of peripheral facial palsy. Studies emphasis on the role of herpes simplex virus and herpes zoster in the pathogenesis of this disease. Gamma interferon plays an important role in determining the type of immune response against foreign invaders and intrinsic factors. Regarding increment of  IFNγ level in acute viral diseases, we designed this study to assess the IFNγ levels and its relation to the intensity of electroneurodiagnostic findings in patients with Bell’s palsy.

Method and material: 30 patients in acute phase of Bell's palsy were selected and 5 ml blood was obtained in the first 72 hours after diagnosis and right before the beginning of the treatment.  Then Gamma interferon was measured and followed by nerve conduction study (NCS) 6 days after Bell’s palsy onset.

Findings: There was no significant relationship between gender of subjects and serum level of Gamma interferon with the intensity of entanglement in Orbicularis oculi and Orbicularis oris muscles. Also, there was no meaningful relationship between age and gender of patients and symptomatic factors with serum level of IFNγ.

Conclusion: It seems there is no significant relationship between immmunoserologic changes (serum level of IFNγ) and electrophysiological indices (NCS) in the acute stage of Bell’s palsy.

 

Rodas Asrat

St. Paul’s Hospital Millennium Medical College, Ethiopia

Title: Neuromyelitis optica (NMO, NMOSD)

Time : 11:30-12:00

Speaker
Biography:

Rodas Asrat is currently working in the St. Paul’s Hospital Millennium Medical College, Ethiopia.

Abstract:

Introduction: Neuromyelitis optica (NMO; Devic’s disease) is an aggressive inflam­matory disorder characterized by recurrent attacks of ON and myelitis; the more inclusive term NMO Spectrum Disorder (NMOSD) has been proposed to incorporate individuals with partial forms, and also those with involvement of additional structures in the central nervous sys­tem. This was a rare case which was diagnosed after 7 years while the patient has follow up at different health facility and different investigation in different times. She was treated initially as a case of Transverse myelitis and other diagnosis previously until its diagnosis.

History: Decrease vision of left eye. For this she was seen at ophthalmologic clinic and was given prednisolone. She claims she regained her left eye vision.. Currently she presented with 4 days history of bilateral lower extremity weakness. Initially had paresthesia of lower extremities later lost sensation below her nipple line. Inability of urinating and passing stool of the same duration. She developed cough, SOB and HGIF in our hospital. She is a known HTN for the past 18 years on medication.

Physical Examination: G/A: conscious, alert and well communicative V/S: with in normal range. LGS: no LAP INT/MSS: No rash PR: lax anal tone CNS: conscious, oriented to time place and person. GCS: 15/15 both short and long memory intact. Symmetrical muscle bulk, no fasciculation. Power =0/5 on bilateral lower extremity and 5/5 on both upper extremity. Tone is hypotonic on both lower extremities and norm tonic on both upper extremity. Reflex is ¼ in both ankle and knee bilaterally. Sensory level is T4.Finger to nose test- normal .Rapid alternating movement – intact Investigation-CSF Analysis-No cell, Glucose=82.4, Protein=24.8, Gram stain= negative. BRAIN MRI (Taken 7 YEARS BACK) = normal. Brain MRI (taken 4 months back)= Few punctate T2/FLAIR hyper intense lesion with in deep white matter of frontal and parietal lobe left paretotemporal volume loss 2 to ?? Recent spinal MRI: Expansible long segment T1hypointense, T2 and STIR heterogeneously hyper intense lesion extending from C3 to lower thoracic vertebra. No contrast enhancement

Electromyography: Pattern reversal visual evoked potential (PRVEP) was done. The P100 latency was well formed bilaterally. The P100 latency is prolonged (>100ms), more on the right side. Bilateral (severe on Rt) anterior visual pathway dysfunction (demyelinating pathophysiology).Otherwise No vomiting, no episodes of Hiccups. No Hx of nasal congestion, runny nose, diarrhea or vaccination preceding presentation. No Hx of easy fatigability. No change in mentation and no ABM.

Discussion: Because of this case we try to see and explain some of the uncommon differentials which have similar manifestations like NMOSD. Example Multiple sclerosis (MS), Acute disseminated encephalomalitis (ADEM), Subacute combined neuro degeneration, Neurosarcoidosis. We try to see some of the literature reviews and the diagnosis of this patient was very difficult since there are no antibody detections here, late presentations, bilateral optic neuropathy and it is relapsing type on her history. Even its extensive longitudinal involvement of the spinal cord, her age and normal CSF was really controversial. What I understand from this case is multidisciplinary team involvement and presence of adequate investigation modalities is really important. Besides that its presentation involves both usual and unusual features.

 

Kateryna Yatsenko

Bogomoletz Institute of Physiology of NAS of Ukraine, Ukraine

Title: Effect of transcranial direct current stimulation on cerebral blood flow in patients with cerebral palsy

Time : 12:00-12:30

Speaker
Biography:

Kateryna Yatsenko, MD, PhD is a Senior Research Fellow. Yatsenko’s research interest includes Neurology, Disorders of the CNS, transcranial direct current stimulation, intermittent normobaric hypoxia treatment and CI-therapy.

 

Abstract:

Statement of the Problem: Neurovascular coupling links neuronal activity to cerebral blood flow. Transcranial Direct Current Stimulation (tDCS) modulates the neuronal activity and thus affects the cerebral blood flow. The purpose of this study is to investigate effects of tDCS on cerebral blood flow in patients with Cerebral Palsy (CP).

Methodology: 60 children aged 2 to 12 years with various forms of cerebral palsy were examined and treated. The comparison group was formed from 30 children who received the course of basic medical and rehabilitation procedures. The main group included 30 children who, in addition to the same therapy, received a course of tDCS. A transcranial Doppler ultrasound examination of head blood vessels was used for the study of cerebral hemodynamics in children with cerebral palsy before and after combined treatment with tDCS.

Findings: tDCS reduced asymmetry coefficient of blood flow velocity in the middle cerebral arteries (MCA) by 12.3%, whereas in the comparison group only by 2.5%; in the anterior cerebral artery (ACA) - 9.5%, while in the comparison group - 0.8%. tDCS significantly reduced the high mean blood flow velocity per cycle (MFV) in the basilar artery (BA), MCA and ACA (21.7%, 18.3% and 7.8%, respectively); in the comparison group no statistically significant positive dynamics was observed. tDCS significantly increased the low MVF in the BA, MCA and ACA (29.7%, 21.2% and 9.7%, respectively); a statistically significant increase of MVF by 9.9% was only in the CMA in the comparison group of patients.

Conclusion & Significance: The use of tDCS in the treatment of CP patients improves cerebral hemodynamics in 87% of patients, in contrast to 52% in the comparison group. Including tDCS to the complex treatment of patients with cerebral palsy improves the effectiveness of treatment and may also positively influence the clinical course of the disease.

 Recent Publications:

1. Yatsenko K, Lushnikova I, Skibo G (2019) Activation of neuritogenesis under conditions of micropolarization in an in vitro model. Fiziol J 65:41-9.

2. Yatsenko K, Lushnikova I, Skibo G (2018) Investigation of the micropolarization on neuronal cells in the modeling of the inflammatory process in vitro. Ukr Neurol J 2:69-73.

3. Yatsenko K (2017) Influence of complex treatment using transcranial direct current stimulation on the electroencephalographic parameters in children with symptomatic epilepsy. Ukr Neurol J 3:38-42.

4. Tsupykov O, Ustymenko A, Kyryk V, Smozhanik E, Yatsenko K, et al., (2016) Ultrastructural study of mouse adipose-derived stromal cells induced towards osteogenic direction. Microsc Res Tech 79:557–64.

5. Tsupykov O, Lushnikova I, Nikandrova Y, Yatsenko K, et al (2016) A novel model of periventricular leukomalacia on mouse organotypic brain slice culture. Cell Organ Transplant. 4:188–93.

 

Ahmed Mohammed Alsehli

Uppsala University, Sweden

Title: The cognitive effects of statins and the role of age

Time : 12:30-13:00

Speaker
Biography:

Ahmed Mohammed Alsehli is a PhD student studying at Uppsala University, Sweden.

 

 

Abstract:

Statins are the first-choice treatment against hypercholesterolemia and associated cardiovascular disease, the main global cause of morbidity and mortality according to WHO. Statins are among the most prescribed drugs worldwide with an estimated 25% of the world population older than 65 years currently under statin treatment and the numbers increasing. Currently, there is a large controversy about whether or not statins affect cognitive function. Studies have provided indications for both sides, as well as reported beneficial and detrimental effects. Altogether, findings in the literature are highly inconsistent. Thus, to reveal new insights into statin cognitive effects, we performed an observational study on a population-based sample of 245,731 control and 55,114 statin-taking individuals from the UK Biobank (Alsehli et al., Sci Rep. 2020 10, 6187). Cognitive performance in terms of reaction time, working memory and fluid intelligence was analysed at baseline and two follow-ups (within 5–10 years). Subjects were classified depending on age (up to 65 and over 65 years) and treatment duration (1–4 years, 5–10 years and over 10 years). Data were adjusted for health- and cognition-related covariates. Subjects generally improved in test performance with repeated assessment and middle-aged persons performed better than older persons. The effect of statin use differed considerably between the two age groups, with a beneficial effect on reaction time in older persons and fluid intelligence in both age groups, and a negative effect on working memory in younger subjects. Our analysis suggests a modulatory impact of age on the cognitive side effects of statins, revealing a possible reason for profoundly inconsistent findings on statin-related cognitive effects in the literature. The study highlights the importance of characterising modifiers of statin effects to improve knowledge and shape guidelines for clinicians when prescribing statins and evaluating their side effects in patients.

Break: Lunch Break @ 13:00-13:30
Speaker
Biography:

Xu Ying-Hui completed his PhD in 2004 from Shanghai Jiao Tong University School of Medicine. He is the dean of the First Affiliated Hospital of Dalian Medical University and vice President of Dalian Medical University. He has published more than 20 papers in reputed journals.

 

Abstract:

Objective: To explore the related factors and management principles of postoperative complications of ventricular-peritoneal shunt.

Methods: 450 patients who underwent ventricular-peritoneal shunt in our hospital were selected and followed up for at least 5 years. The age, gender, history of disease, classification of hydrocephalus, surgical method and type of shunt tube, postoperative complications and other factors were analyzed. Patients with complications were treated and the clinical treatment effect was analyzed.

Results: Complications occurred in patients, including puncture bleeding, obstruction of shunt tube (decomposition, rupture), intracranial infection, subdural effusion or subdural hematoma caused by excessive drainage, and delayed intracranial hematoma. Patients can still get a good prognosis after individualized treatment.

Conclusions: The incidence of postoperative complications of ventricular-peritoneal shunt is not low. Surgery indications should be strictly grasped before surgery. Strict aseptic operation should be performed during the operation. Patients with a previous history of central nervous system infection or craniocerebral surgery should be more cautious. Early skull repair combined with ventricular-peritoneal shunt is positive significance for improving the quality of life of patients undergoing brain surgery. Patients with complications should be treated individually.

Recent Publications:

1.Ren, Siyang; Xu, Yinghui (2019) AC016405.3, a novel long noncoding RNA, acts as a tumor suppressor through modulation of TET2 by microRNA-19a-5p sponging in glioblastoma. CANCER SCIENCE, 2019, MAY; 110 (5): 1621 - 1632.

2.Cheng, Tianci; Xu, Yinghui (2018) Effects of Enhancer of Zeste Homolog 2 (EZH2) Expression on Brain Glioma Cell Proliferation and Tumorigenesis.MEDICAL SCIENCE MONITOR , 2018,October; 24 ( ): 7249 - 7255.

3.Zhao, Jun; Zhu, Jiabin; Lv, Xiaoshu; Xing, Jinshan; Liu, Shuang; Chen, Chen; Xu, Yinghui (2017) Curcumin potentiates the potent antitumor activity of ACN against glioblastoma by suppressing the PI3K/AKT and NF-kappa B/COX-2 signaling pathways. ONCOTARGETS AND THERAPY , 2017, ; 10 ( ): 5471 - 5482.

4.Diao, Shuo; Zheng, Qianqian; Gao, Jian; Yao, Yiqun; Ren, Siyang; Liu, Yongjian; Xu, Yinghui (2017) Trefoil factor 3 contributes to the malignancy of glioma via regulating HIF-1 alpha. ONCOTARGET , 2017, SEP 29 ; 8 ( 44 ): 76770 - 76782.

5.Wang, Jinkui; Yu, Zhenlong; Wang, Chao; Tian, Xiangge; Huo, Xiaokui; Wang, Yan; Sun, Chengpeng; Feng, Lei; Ma, Jing; Zhang, Baojing; Yang, Qining; Ma, Xiaochi; Xu, Yinghui (2017) Dehydrocostus lactone, a natural sesquiterpene lactone, suppresses the biological characteristics of glioma, through inhibition of the NF-kB/COX-2 signaling pathway by targeting IKK beta.AMERICAN JOURNAL OF CANCER RESEARCH , 2017, ; 7 ( 6 ): 1270 - +.

 

Biography:

Safiyyah Asiri has completed her medical school at the age of 24 years from King Khalid University, KSA. She worked as a resident in King Abdulaziz Medical City, for 5 years and was awarded as the best resident among her level and the resident of the year for three consecutive years. She has 2 publications and ongoing two projects. Currently she is working as a senior registrar at King Abdullah Specialized Children Hospital, Riyad.

 

Abstract:

Familial hemiplegic migraine (FHM) is a rare disorder presented commonly with coma, hyperthermia, and headache. FHM is usually associated with fully reversible motor weakness as a specific symptom of aura. Seizure and fever are the secondary features observed. Three sisters diagnosed with type 2 FHMs presenting features, such as coma and hyperthermia. The brain (magnetic resonance imaging) revealed focal subtle cortical swelling, Electroencephalography showed unilateral slowing, while no signs of infectious disease were observed. Molecular and genetic tests using whole exome sequencing identified a novel heterozygous mutation (c.2450T > A p.Ile817Asn) in the exon 18 of the ATP1A2 gene (NM_000702.3). The Sanger’s sequencing results confirmed the variant was segregated with the disease phenotype within the family. The current study report for the first time, a Saudi family with migraine coma having a novel heterozygous ATP1A2 mutation.

Recent Publications:

1.Safiyyah Asiri, W. A. (2019). Prevalence and outcomes of Guillain-Barré syndrome among pediatrics in Saudi Arabia: a 10-year retrospective study. Neuropsychiatr Dis Treat., 15: 627–635.

2.Waleed Altwaijri, F. A.-R. (2019). Familial Hemiplegic Migraine with Prolonged Coma and Hyperthermia: ATP1A2 Gene Mutation Case Report in a Single Saudi Family. JBCGenetics., 2(1): 85-90.

Speaker
Biography:

Jun Hwi Cho, MD, PhD is professor in department of Emergency Medicine and Neurobiology, Kangwon National University Hospital, South Korea. His major research fields are cardiac arrest and cardiopulmonary resuscitation (CPR) using hypothermia, toxicology and critical care, experimental ischemic stroke: about neuronal damage and protection in the ischemic brain, cardiopulmonary resuscitation using rat VF model & asphyxia model and histopathological research after cardiac arrest in animal model of cardiac arrest. He interest in neuronal protection using therapeutic hypothermia during CPR with patient of cardiac arrest and medicines for neuroprotection, neurogenesis and anti-aging in the CNS: He has examined many medicines including extracts of foods and plants that protect neuronal damage or aging and enhance neurogenesis.

Abstract:

Purpose: Oxcarbazepine (OXC), a voltage-gated sodium channel blocker, is a new antiepileptic medication. OXC is also used for the treatment of bipolar disorders. Some voltage-gated sodium channel blockers have been demonstrated to display strong neuroprotective properties in models of cerebral ischemia. However, protective effects of OXC against ischemic brain injury and related mechanisms have not yet been reported. In this study, we investigated the protective effect of OXC and its mechanisms in the cornu ammonis 1 subfield (CA1) of gerbils subjected to 5 min of transient global cerebral ischemia (tGCI).

Materials and methods: Transient ischemia led to death of most pyramidal neurons in CA1 at 5 days after tGCI. OXC (100 and 200 mg/kg) was intraperitoneally administered once at 30 min after tGCI.

Results: Treatment with 200 mg/kg OXC, not 100 mg/kg OXC, significantly protected CA1 pyramidal neurons from tGCI-induced injury. OXC treatment significantly decreased superoxide anion production, 4-hydroxy-2-nonenal and 8-hydroxyguanine levels in ischemic CA1 pyramidal neurons. In addition, the treatment restored levels of superoxide dismutases, catalase, and glutathione peroxidase. Furthermore, the treatment distinctly inhibited tGCI-induced microglia activation and significantly reduced levels of pro-inflammatory cytokines (interleukin-1β and tumor necrosis factor-α).

Conclusions: In particular, OXC treatment significantly enhanced expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream protein heme oxygenase-1 in ischemic CA1; however, the forenamed effects of OXC were abolished by brusatol (an inhibitor of Nrf2). Taken together, these results indicate that post-treatment of OXC can display neuroprotection against brain injuries following ischemic insults. This neuroprotection may be displayed by attenuation of oxidative stress and neuroinflammation, which can be mediated by activation of Nrf2 pathway.

Recent Publications:

  1. Jung YS, Kim KS, Suh GJ, Cho JH (2019) Pre-Comparison between Gel Pad Cooling Device and Water Blanket during Target Temperature Management in Cardiac Arrest Patients. Acute Crit Care 33(4):246-251.
     
  2. Lee CH, Park JH, Ahn JH, Kim JD, Cho JH, Lee TK, Won MH (2019) Stronger antioxidant enzyme immunoreactivity of Populus tomentiglandulosa extract than ascorbic acid in rat liver and kidney. Iran J Basic Med Sci 22(8):963-967.
     
  3. Lee TK, Kim H, Song M, Lee JC, Park JH, Ahn JH, Yang GE, Kim H, Ohk TG, Shin MC, Cho JH, Won MH (2019) Time-course pattern of neuronal loss and gliosis in gerbil hippocampi following mild, severe, or lethal transient global cerebral ischemia. Neural Regen Res 14(8):1394-1403.
     
  4. Lee JH, Jung JY, Lee HJ, Kim DK, Kwak YH, Chang I, Kwon H, Choi YJ, Park JW, Paek SH, Cho JH (2019) Efficacy of low-dose nebulized epinephrine as treatment for croup: A randomized, placebo-controlled, double-blind trial. Am J Emerg Med 37(12):2171-2176.
     
  5. Ahn JH, Ohk TG, Kim DW, Kim H, Song M, Lee TK, Lee JC, Yang GE, Shin MC, Cho JH, Choi SY, Won MH, Park JH (2019) Fluoro-Jade B histofluorescence staining detects dentate granule cell death after repeated five-minute transient global cerebral ischemia. Metab Brain Dis 34(3):951-956.

Anirudh Rao Deshmukh

Sanjay Gandhi Postgraduate Institute of Medical Sciences, India

Title: Role of home based targeted-CASP therapy in post stroke rehabilitation

Time : 14:30-15:00

Speaker
Biography:

Anirudh Rao Deshmukh is a final year resident in Neurology in Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India. He did his MD in Internal Medicine and his MD thesis was on role of ACE gene polymorphism in chronic kidney disease. He is working in the field of management of post stroke spasticity, Parkinsonism and Hirayama disease. He has also worked on, Headaches in patient with Neurocysticercosis, Frontal Lobe dysfunction in Progressive Supranuclear Palsy and Subacute sclerosing panencephalitis.

 

Abstract:

Introduction: There is a need for a low cost, easy to apply, non-institutional regimen for significant functional recovery in post- stroke patients.

Aim: To study the effectiveness of modified version of Corrected Assisted Synchronised Periodic therapy termed here as Targeted-CASP (T-CASP) therapy (Fig 1) in improving motor, cognitive, behavioural and functional disability in post stroke patients.

Methods: This is a prospective quasi-randomised double blinded control study. The study was conducted in super-speciality tertiary care centre. Follow up patients of stroke were recruited from outpatient department of neurology. Patients recruited on OPD-1 (Monday) and OPD-2 (Friday) was grouped under cases and controls respectively. All patients were assessed for power, spasticity, cognition and depression, functional level at baseline (0), 3 months and 6 months using standard tools of assessment. Relatives/Caregivers were trained in T-CASP therapy and asked to carry it out at their homes as per protocol.

Results: Baseline patient characteristics and outcome parameters were comparable between two groups. Significant difference was seen at 3 and 6 months between the two groups in Ashworth scale score for spasticity (p value- .012 & .001), MRC score for power (p- .021 and .001), Adden-Brookes score for cognition (p-.025 & .010), BDI score for depression (p-.001&.001). Barthel scores were higher in T-CASP group but the difference was not significant (p- 0.219 & 0.080). However, on subcomponent analysis percentage of people who were able to walk (93.3 vs 76.7 %), transfer to/from bed/chair (80 % vs 70%) and climb stairs (63.3% vs 50%) independently at 6 months was significantly higher in T-CASP group.

Conclusion: Targeted-CASP therapy is a low cost, home based post stroke physiotherapy regimen which benefits all the aspects of post stroke rehabilitation including motor, cognitive, behavioural and functional disability.

References:

1.Pradhan S, Bansal R. Role of corrected-assisted-periodic therapy in post stroke rehabilitation. Neurol India 2019;66:1345-50.

2.Carlo Trompetto, Lucio Marinelli, Laura Mori, et al., “Pathophysiology of Spasticity: Implications for Neurorehabilitation,” BioMed Research International, vol. 2014.

3.N.J. O’Dwyer and L. Ada, “Reflex hyperexcitability and muscle contracture in relation to spastic hypertonia,” Current Opinion in Neurology, vol. 9, no. 6, pp. 451–455, 1996.

4.J.-M.Gracies, “Pathophysiology of spastic paresis. I: paresis and soft tissue changes,” Muscle and Nerve, vol. 31,no. 5, pp. 535–551, 2005.

5.C. Trompetto, L. Marinelli, L. Mori et al., “Post-activation depression changes after robotic-assisted gait training in hemiplegic stroke patients,” Gait and Posture, vol. 38, no. 4, pp. 729–733, 2013.

 

 

Gabriel Alejandro B. Baroque

University of Santo Tomas Hospital, Philippines

Title: Multifocal motor neuropathy: A case report

Time : 15:30-16:00

Biography:

Gabriel Alejandro B. Baroque has completed his MD at the age of 28 from the University of Santo Tomas in Manila, Philippines. He is currently a Neurology resident in the same institution. He has been guided by Dr. Alejandro C. Baroque II and Dr. Imelda S. David, both esteemed professors and practicing in the fields of Neurology and Psychiatry.

 

Abstract:

We report a case of a 51-year old Filipino female with multifocal motor neuropathy who presented with chronic weakness of the left foot which without any sensory deficits. With the history chronic progressive weakness, lack of sensory deficits confirmatory by biochemical workups and diagnostics: An elevated ganglioside GM1 antibody test which revealed a titer of 1:12800, electromyography and nerve conduction confirmed the diagnosis of multifocal motor neuropathy. Treatment of intravenous immunoglobulin with a dose of 2g/kg over 2-5 days was initiated and repeated every 2 months with noticeable improvement. Multifocal motor neuropathy is a rare disorder which has a prevalence of 0.6 per 100,000 individuals. It is seen in more in males with a ratio of 2.7:1. It is described as a pure motor disease without sensory deficits which is predominantly seen in the upper extremities. The diagnosis for the disorder is supported by determination of ganglioside GM1 antibodies, electromyography and nerve conduction velocity study (EMG-NCV).

Recent Publications:

1. Chad DA, Hammer K, Sargent J. Slow resolution of multifocal weakness and fasciculation: a reversible motor neuron syndrome. Neurology. 1986 Sep 1;36(9):1260.

2. Feldman EL, Bromberg MB, Albers JW, Pestronk A. Immunosuppressive treatment in multifocal motor neuropathy. Annals of Neurology: Official Journal of the American Neurological Association and the Child Neurology Society.1991 Sep; 30(3):397–401.

3. Olney RK, Lewis RA, Putnam TD, Campellone Jr JV. Consensus criteria for the diagnosis of multifocal motor neuropathy. Muscle & Nerve: Official Journal of the American Association of Electrodiagnostic Medicine. 2003 Jan; 27(1):117–21.

4. Van Asseldonk JT, Franssen H, Van den Berg-Vos RM, Wokke JH, Van den Berg LH. Multifocal motor neuropathy. The Lancet Neurology. 2005 May 1; 4(5):309–19.

5. Joint Task Force of the EFNS and the PNS. European Federation of Neurological Societies/Peripheral Nerve Society guideline on management of multifocal motor neuropathy. Report of a joint task force of the European Federation of Neurological Societies and the Peripheral Nerve Society–first revision. Journal of the Peripheral Nervous System. 2010 Dec; 15(4):295–301.

 

 

Speaker
Biography:

Yuting Ruan is a second-year PhD candidate majoring in Neurology at Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University. He mainly focused on the diagnosis and new therapeutic targets for Alzheimer’s disease.

 

Abstract:

Alzheimer's disease (AD) is a common neurodegenerative disease with no curative treatment. Curcumin (cur) has been proved to be effective in treatment of AD. However, the low bioavailability and hydrophobicity of cur which distributed non-targeted after administration and hindered by the blood-brain barrier limit its application. We designed a novel diagnostic and therapeutic nanoparticle, 1,2-dio- leoyl-sn-glycero-3-phosphoethanolamine (DSPE)-n-[poly(ethylene glycol) (PEG)] loaded with cur and superparamagnetic iron oxide (SPION) conjugated with two targets ligands to the surface of the nanoparticles, CRT and QSH, abbreviated as SPIO@DSPE-PEG/Cur-CRT/QSH. CRT specifically targets ligands at the blood-brain barrier (BBB), and QSH has an fine ability to bind with Aβ1-42 which is the culprit of AD pathology. The in vitro parameters of nanoparticle included dynamic light scattering (DLS), transmission electron microscope, saturation of magnetization, flow cytometry analysis. In vivo image of amyloid plaques were detected by MRI scanning, and the spatial learning and memory capability of transgenic APP/PS1 mice were conducted by Morris water maze (MWM). Bielschowsky silver staining, western blotting, immunostaining were among the ex vivo assays to determine the expression of amyloid protein, tau hyperphosphorylation, glial fibrillary acidic protein (GFAP), β-III tubulin (Tuj1). The in vitro assay determined the nanoparticles that possess fine size, zeta potential, r2 relaxivity, increased its cellular uptake. In vivo 7 Tesla MRI images of mice brains which were treated with SPIO@DSPE-PEG/Cur-CRT/QSH showed less amyloid plaques accumulation compared to native cur. The MWM results indicated the SPIO@DSPE-PEG/Cur-CRT/QSH brilliant improved the learning and memory capability of APP/PS1 mice compared with the bald cur. Moreover, SPIO@DSPE-PEG/Cur-CRT/QSH reduce hippocampal tau hyperphosphorylation and β-amyloid deposit, while increase the expression of Tuj1. This nanoparticle would be a potential diagnosis and treatment for AD.

Recent Publications:

1.Shengnuo Fan, Xuan Liu, Wengli Fang,Xiaoyou Chen, Wang Liao, Xiuna Jing, Enxiang Tao, Qiulan Ma, Xingmei Zhang, Rui Guo* & Jun Liu* (2018) Curcumin loaded PLGA PEG nanoparticles  counjugated with B6 peptide for potential use in Alzheimer's Disease. Drug Delivery,25(1):12.

2.Xiao SH,Zhou DY,Luan P,Gu BB,Feng LB,Fan SN,Liao W,Fang WL,Yang LH,Tao EZ,Guo R*,Liu J*(2016) Graphene quantum dots conjugated neuroprotective peptide improve learning and memory capability,Biomaterials,106:98~110.

3.Fan SN, Zhang B, Gu BB, Wan Q, Huang XY, Liao W, Liu J*(2015) PI3K/AKT/mTOR/p70S6K pathway is involved in Aß25-35-induced autophagy. BioMed Research International, 2015: p. 1-9.

4.Yang LH, Cai X, Jiang L, Liang YR, Xiao SH, Liu S, Tao EX, Luan P, Liu J*(2014). Inhibitory effect of Bcl-xL gene on toxicity induced by sodium nitroprusside in SH-SY5Y cells. CNS Neurosci The, 20(4):379-81.

5.Zhao Z, Lan Y, Bai S, Shen J, Xiao S, Lv R, Tao E, Liu J*(2013). Late-onset radiation-induced optic neuropathy after radiotherapy for nasopharyngeal carcinoma. J Clin Neurosci,20(5):702-6.

 

Anna Voitiuk

Kharkiv Medical Academy of Postgraduate Education, Ukraine

Title: Melatonin: the its role in the development of epileptic seizures

Time : 16:30-17:00

Speaker
Biography:

Anna Voitiuk studied as a Postgraduate student in Neurology at Kharkiv Medical Academy of Postgraduate Education. During her residency she has shown interest and enthusiasm in treating patients with epilepsy, disorders of cerebral circulation, spinal diseases. Currently she is a highly qualified neurologist. Anna Voitiuk is an active member of Ukrainian League Against Epilepsy (ULAE). She has published the 5 articles and 3 articles in collaboration with colleagues.

Abstract:

Melatonin (N-acetyl-5-methoxytryptamine) is a multifunctional hormone that is a neuroprotective agent and an antioxidant, plays a key role in the coordination and synchronization of the nervous system. It has a high permeability through the blood-brain barrier; therefore fluctuations in its concentration in the peripheral blood have a significant effect on the functional state of the brain neurons.

The purpose of this research is to study the level of melatonin in patients with epilepsy, depending on the severity of the disease, the type and frequency of seizures.

The studies were carried out on the basis of clinical symptoms and instrumental data analysis. The detection of melatonin in the blood serum was carried out by applying a modified Cole and Crank fluorometric method with orthophthalic aldehyde. Taken into account the circadian rhythms of melatonin production, the studies were conducted from 7:00 to 8:00 am, during the period of maximum secretion. The EEG and EEG-video monitoring were used as screening methods. The clinical material was analyzed on the basis of the survey of 256 patients with epilepsy, whose average age was 32-37 years. Based on multivariate analysis of clinical data, three groups of patients were identified depending on the severity of the disease. The control group is 52 practically healthy people. In all patients, a significant decrease in morning melatonin secretion was found on average by 25.6% in comparison with the control group indicators. A low level of melatonin was characteristic of patients with primary and secondary generalized convulsive seizures, as well as with prolonged complex partial seizures. The deterioration of the EEG pattern in 89.3% of cases was accompanied by the appearance of new epileptiform phenomena: spikes, "spike-slow wave" complexes, high-amplitude sharp waves. In 57.1% of patients, a significant focal "slowing down" of the EEG was registered.

Thus, melatonin deficiency can be one of the reasons for increasing the activity of excitatory systems. The correlation between epileptiform changes in the EEG and certain decrease in melatonin level has also been detected. The higher the melatonin level in patients, the lower is the convulsive readiness of the organism and the more favorable course of epilepsy.

Recent Publications:

1.Gunata M, Parlakpinar H, Acet HA (2019) Melatonin: A review of its potential functions and effects on neurological diseases. Revue Neurologique 19:35-45.

2.Sanchez-Barcello EJ, Rueda N (2017) Clinical uses of melatonin in neurological diseases and mental and behavioural disorders. Current Medicinal Chemistry 24(35):3851-3878.

3.Ganie SA, Dar TABhat AH (2016) Melatonin: a potential anti-oxidant therapeutic agent for mitochondrial dysfunctions and related disorders. Rejuvenation Research 19(1):21-40.

4.Pandi-Perumal SR, BaHammam AS, Brown GM (2013) Melatonin antioxidative defense: therapeutical implications for aging and neurodegenerative processes. Neurotoxicity Research 23: 263-300.

5.Srinivasan V (2012) Melatonin oxidative stress and neurodegenerative diseases. Indian J Exp Biol. 40(6):668-679.

 

Speaker
Biography:

Arpan Dutta is currently a resident in the Department of Neurology, Bangur Institute of Neurosciences, Kolkata, India and is pursuing DM Neurology course. He has completed his MBBS degree from Nil Ratan Sircar Medical College, Kolkata, India and MD General Medicine degree form IPGMER, Kolkata, India.

Abstract:

Statement of the Problem: Hypermanganesemia with dystonia, polycythemia and cirrhosis is a rare disease caused by mutations of SLC30A10 gene, resulting in accumulation of excess manganese in brain, blood and liver. Apart from dystonia, polycythemia and cirrhosis, Parkinsonism features may also be present in this life threatening but treatable disorder. Chelation with calcium disodium EDTA combined with oral iron therapy and dietary manganese restriction is the preferred treatment modality. Alternative chelating agents include DMSA and d-penicillamine. We hereby describe the clinical profile of 3 siblings who were diagnosed with this rare disease and explore the treatment response to an alternative agent (d-penicillamine) which is important in resource poor settings where calcium disodium EDTA is not available.

Methodology & Theoretical Orientation: Clinical findings of the 3 siblings were documented and relevant investigations e.g. complete hemogram, liver function tests, MRI of brain, fibroscan etc. were done. Diagnosis was confirmed via clinical exome sequencing. Serum manganese levels were obtained before and after treatment which comprised of d-penicillamine combined with oral iron therapy and dietary manganese restriction.

Findings: Only one sibling had the triad of dystonia, polycythemia and cirrhosis. The other two were asymptomatic with a normal clinical examination and no evidence of polycythemia or cirrhosis. MRI of brain showed T1 hyperintensity involving bilateral basal ganglia and brainstem in two of them. Serum manganese levels were elevated in all the 3 siblings and clinical exome sequencing revealed a novel homozygous missense mutation (c.122C>T) of SLC30A10 gene in all of them. Treatment with the alternative regimen resulted in significant clinical improvement and marked reduction of serum manganese level.

Conclusion & Significance: This study documents the clinical profile of a novel genotype of SLC30A10 and also shows that treatment of hypermanganesemia with dystonia, polycythemia and cirrhosis can be satisfactorily done by d-penicillamine if calcium disodium EDTA is not available.

Recent Publications:

1. Anagianni S, Tuschl K. Genetic disorders of manganese metabolism. Curr Neurol Neurosci Rep. 2019 May; 19: 33.

2. Quadri M, Kamate M, Sharma S, et al. Manganese transport disorder: novel SLC30A10 mutations and early phenotypes. Mov Disord. 2015 Mar; 30(7): 996-1001.

3. Zaki MS, Issa MY, Elbendary HM, et al. Hypermanganesemia with dystonia, polycythemia and cirrhosis in 10 patients: six novel SLC30A10 mutations and further phenotype delineation. Clin Genet. 2017 Nov; 93(4): 905-912.

4.Mukhtiar K, Ibrahim S, Tuschl K, Mills P. Hypermanganesemia with dystonia, polycythemia and cirrhosis (HMDPC) due to mutation in the SLC30A10 gene. Brain Dev. 2016 Oct; 38(9): 862-865.

5. Tuschl K, Clayton PT, Gospe SM Jr, et al. Syndrome of hepatic cirrhosis, dystonia, polycythemia, and hypermanganesemia caused by mutations in SLC30A10, a manganese transporter in man. Am J Hum Genet. 2012 Mar; 90(3): 457-466.

 

Speaker
Biography:

Jun Hwi Cho, MD, PhD is professor in department of Emergency Medicine and Neurobiology, Kangwon National University Hospital, South Korea. His major research fields are cardiac arrest and cardiopulmonary resuscitation (CPR) using hypothermia, toxicology and critical care, experimental ischemic stroke: about neuronal damage and protection in the ischemic brain, cardiopulmonary resuscitation using rat VF model & asphyxia model and histopathological research after cardiac arrest in animal model of cardiac arrest. He interest in neuronal protection using therapeutic hypothermia during CPR with patient of cardiac arrest and medicines for neuroprotection, neurogenesis and anti-aging in the CNS: He has examined many medicines including extracts of foods and plants that protect neuronal damage or aging and enhance neurogenesis

Abstract:

Purpose: Compelling evidence from preclinical and clinical studies has shown that mild hypothermia is neuroprotective against ischemic stroke. We investigated neuroprotective effect of post-risperidone (RIS) treatment against transient ischemic injury and its mechanisms in the gerbil brain.

Materials and methods: Transient ischemia (TI) was induced in the telencephalon by bilateral common carotid artery occlusion (BCCAO) for 5 min under normothermic condition (37 ± 0.2ºC). Post-treatment of RIS induced hypothermia until 12 h after TI in the TI-induced animals under uncontrolled body temperature (UBT) compared to that under controlled body temperature (CBT) (about 37ºC).

Results: Neuroprotective effect was statistically significant when we used 5 and 10 mg/kg doses (P < 0.05, respectively).  In the RIS-treated TI group, many CA1 pyramidal neurons of the hippocampus survived under UBT compared to those under CBT. In this group under UBT, post-treatment with RIS to TI-induced animals markedly attenuated the activation of glial cells, increases of oxidative stress markers (dihydroethidium, 8-OHdG and 4-HNE), and a decrease of superoxide dismutase 2 in their CA1 pyramidal neurons. Furthermore, RIS-induced hypothermia was significantly interrupted by NBOH-2C-CN hydrochloride (a selective 5-HT2A receptor agonist), but not bromocriptine mesylate (a D2 receptor agonist).

Conclusions: Our findings indicate that RIS-induced hypothermia can effectively protect neuronal cell death from TI injury through attenuation of glial activation and maintenance of antioxidants, showing that 5-HT2A receptor is involved in RIS-induced hypothermia. Therefore, RIS could be introduced to reduce body temperature rapidly and might be applied to patients for hypothermic therapy following ischemic stroke.

Recent Publications:

  1. Jung YS, Kim KS, Suh GJ, Cho JH (2019) Pre-Comparison between Gel Pad Cooling Device and Water Blanket during Target Temperature Management in Cardiac Arrest Patients. Acute Crit Care 33(4):246-251.
     
  2. Lee CH, Park JH, Ahn JH, Kim JD, Cho JH, Lee TK, Won MH (2019) Stronger antioxidant enzyme immunoreactivity of Populus tomentiglandulosa extract than ascorbic acid in rat liver and kidney. Iran J Basic Med Sci 22(8):963-967.
     
  3. Lee TK, Kim H, Song M, Lee JC, Park JH, Ahn JH, Yang GE, Kim H, Ohk TG, Shin MC, Cho JH, Won MH (2019) Time-course pattern of neuronal loss and gliosis in gerbil hippocampi following mild, severe, or lethal transient global cerebral ischemia. Neural Regen Res 14(8):1394-1403.
     
  4. Lee JH, Jung JY, Lee HJ, Kim DK, Kwak YH, Chang I, Kwon H, Choi YJ, Park JW, Paek SH, Cho JH (2019) Efficacy of low-dose nebulized epinephrine as treatment for croup: A randomized, placebo-controlled, double-blind trial. Am J Emerg Med 37(12):2171-2176.
     
  5. Ahn JH, Ohk TG, Kim DW, Kim H, Song M, Lee TK, Lee JC, Yang GE, Shin MC, Cho JH, Choi SY, Won MH, Park JH (2019) Fluoro-Jade B histofluorescence staining detects dentate granule cell death after repeated five-minute transient global cerebral ischemia. Metab Brain Dis 34(3):951-956.