• Title/Summary/Keyword: Brain health

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Classification of 18F-Florbetaben Amyloid Brain PET Image using PCA-SVM

  • Cho, Kook;Kim, Woong-Gon;Kang, Hyeon;Yang, Gyung-Seung;Kim, Hyun-Woo;Jeong, Ji-Eun;Yoon, Hyun-Jin;Jeong, Young-Jin;Kang, Do-Young
    • Biomedical Science Letters
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    • v.25 no.1
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    • pp.99-106
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    • 2019
  • Amyloid positron emission tomography (PET) allows early and accurate diagnosis in suspected cases of Alzheimer's disease (AD) and contributes to future treatment plans. In the present study, a method of implementing a diagnostic system to distinguish ${\beta}$-Amyloid ($A{\beta}$) positive from $A{\beta}$ negative with objectiveness and accuracy was proposed using a machine learning approach, such as the Principal Component Analysis (PCA) and Support Vector Machine (SVM). $^{18}F$-Florbetaben (FBB) brain PET images were arranged in control and patients (total n = 176) with mild cognitive impairment and AD. An SVM was used to classify the slices of registered PET image using PET template, and a system was created to diagnose patients comprehensively from the output of the trained model. To compare the per-slice classification, the PCA-SVM model observing the whole brain (WB) region showed the highest performance (accuracy 92.38, specificity 92.87, sensitivity 92.87), followed by SVM with gray matter masking (GMM) (accuracy 92.22, specificity 92.13, sensitivity 92.28) for $A{\beta}$ positivity. To compare according to per-subject classification, the PCA-SVM with WB also showed the highest performance (accuracy 89.21, specificity 71.67, sensitivity 98.28), followed by PCA-SVM with GMM (accuracy 85.80, specificity 61.67, sensitivity 98.28) for $A{\beta}$ positivity. When comparing the area under curve (AUC), PCA-SVM with WB was the highest for per-slice classifiers (0.992), and the models except for SVM with WM were highest for the per-subject classifier (1.000). We can classify $^{18}F$-Florbetaben amyloid brain PET image for $A{\beta}$ positivity using PCA-SVM model, with no additional effects on GMM.

Korean Red Ginseng alleviates neuroinflammation and promotes cell survival in the intermittent heat stress-induced rat brain by suppressing oxidative stress via estrogen receptor beta and brain-derived neurotrophic factor upregulation

  • Iqbal, Hamid;Kim, Si-Kwan;Cha, Kyu-Min;Jeong, Min-Sik;Ghosh, Prachetash;Rhee, Dong-kwon
    • Journal of Ginseng Research
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    • v.44 no.4
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    • pp.593-602
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    • 2020
  • Background: Heat stress orchestrates neurodegenerative disorders and results in the formation of reactive oxygen species that leads to cell death. Although the immunomodulatory effects of ginseng are well studied, the mechanism by which ginseng alleviates heat stress in the brain remains elusive. Methods: Rats were exposed to intermittent heat stress for 6 months, and brain samples were examined to elucidate survival and antiinflammatory effect after Korean Red Ginseng (KRG) treatment. Results: Intermittent long-term heat stress (ILTHS) upregulated the expression of cyclooxygenase 2 and inducible nitric oxide synthase, increasing infiltration of inflammatory cells (hematoxylin and eosin staining) and the level of proinflammatory cytokines [tumor necrosis factor α, interferon gamma (IFN-γ), interleukin (IL)-1β, IL-6], leading to cell death (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) and elevated markers of oxidative stress damage (myeloperoxidase and malondialdehyde), resulting in the downregulation of antiapoptotic markers (Bcl-2 and Bcl-xL) and expression of estrogen receptor beta and brain-derived neurotrophic factor, key factors in regulating neuronal cell survival. In contrast, KRG mitigated ILTHS-induced release of proinflammatory mediators, upregulated the mRNA level of the antiinflammatory cytokine IL-10, and increased myeloperoxidase and malondialdehyde levels. In addition, KRG significantly decreased the expression of the proapoptotic marker (Bax), did not affect caspase-3 expression, but increased the expression of antiapoptotic markers (Bcl-2 and Bcl-xL). Furthermore, KRG significantly activated the expression of both estrogen receptor beta and brain-derived neurotrophic factor. Conclusion: ILTHS induced oxidative stress responses and inflammatory molecules, which can lead to impaired neurogenesis and ultimately neuronal death, whereas, KRG, being the antioxidant, inhibited neuronal damage and increased cell viability.

Investigation of Neuroprotective Efficacy of Dexpanthenol in an Experimental Head Injury Model

  • Durmus E. Karatoprak;Recai Engin;Sarp Sahin;Ismail Iclek;Mehmet A. Durak
    • Journal of Korean Neurosurgical Society
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    • v.67 no.5
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    • pp.521-530
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    • 2024
  • Objective : Dexpanthenol (DXP), which has known neuroprotective effects, has been shown to be beneficial in various experimental models and ischaemic diseases. The aim of this study was to investigate the possible neuroprotective effects of DXP in a traumatic brain injury (TBI) model. Methods : Thirty-six Wistar-Albino female rats, approximately 6 months old, weighing 220-285 g were used. All rats were subjected to closed head trauma by dropping a weight of 350 g on the parietal region from a height of 50 cm at an angle of 180 degrees in the prepared head trauma model setup. The rats were divided into four groups as control (group 1), trauma (group 2), trauma + DXP (group 3), and DXP (group 4). In group 3, DXP was administered intraperitoneally at a dose of 500 mg/kg for six times at 30 minutes, 6, 12, 24, 36, and 48 hours. In group 4, DXP was administered intraperitoneally simultaneously with group 3 without causing head trauma. Blood samples were taken from all rats 72 hours later for biochemical examination. After blood samples were taken, rats were decapitated under general anaesthesia. Cerebral tissue samples were taken from decapitated rats for immunohistochemical and histopathological examination. Results : Cytokine markers were found to be increased in posttraumatic brain tissue. Malondialdehyde and glutathione reductase levels were lower in group 3 compared to group 2. In addition, superoxide dismutase, glutathione peroxidase and catalase levels were significantly higher in group 3 compared to group 2. In histological evaluation, congestion in the piamater layer, cell infiltration, vascular congestion, hemorrhage and neuronal degeneration were significantly decreased in group 3 compared to group 2. DXP seems to be beneficial in neurological recovery in terms of histological and oxidative changes after head trauma in rats. Conclusion : DXP should be further evaluated for its possible therapeutic effect in TBI.

A study of relationship among the Brain Dominance Thinking Types and Self Leadership of engineering students (공과대학생의 두뇌우성 사고유형과 셀프리더십과의 관계 연구)

  • Kim, Yeon-Hee;Sun, Bok-Keon
    • Journal of the Korea Safety Management & Science
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    • v.15 no.4
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    • pp.357-363
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    • 2013
  • The purpose of this study was to identity the relationships of sub factor among the brain dominance thinking types(A,B,C,D quadrant thinking type) is based on the Whole Brain Modal and self-leadership by Manz. The subjects were 102 undergraduates students from the Hoseo university in Cheonan. The results of this study as follows ; first, the brain dominance thinking type A was the highest and type C was highly rated. Second, the brain dominance thinking type A was not correlated type C and type D. Third, the brain dominance thinking type C and self-leadership sub factor was significantly positively correlated.

Effect of High-tyrosine Diet on Brain Norepinephrine Metabolism in Immobilization-Stressed Rats

  • Yoon Hae Seong
    • Journal of Nutrition and Health
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    • v.26 no.7
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    • pp.858-866
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    • 1993
  • S.D.rats were fed with 3.4% tyrosine supplemented diet for 5 days. Tyrosine diet had no effects on brain NE and MHPG-SO4 levels in non-stressed rats. When these animals were given 3 hr-immobilization stress, they responded in a manner that coped better to the stress. This was measured by the increase in brain MHPG-SO4 indicating the increase in norepinephrine turnover by the stressed animals. When rats were stressed, fed basal or high-tyrosine diet, brain tyrosine concentration dropped more than 26% over the non-stress control animals. 3-hr immobilization stress also decreased brain NE levels. However, while the stress resulted in a significant decrease(p<0.05) of brain NE in basal diet, the decrease was not significant in high-TYR diet group. And as the stress index, serum corticosterone, glucose, and free fatty acid concentratons also were assayed. In this study, it was found that high-TYR diet prevented the stress-induced depletion of brain NE and suppressed the rise in serum corticosterone, glucose, and free fatty acid. These results suggest that high-TYR diet increases the coping ability of body to stress.

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EEG Study for the Effects of Mouth Breathing on Brain Functions (구강 호흡이 뇌기능에 미치는 영향에 관한 EEG 연구)

  • Lee, Kyung-Jin;Lee, Song-Yi;Park, So-Young;Jang, So-Ra;Kang, Chang-Ki
    • Science of Emotion and Sensibility
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    • v.19 no.4
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    • pp.119-126
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    • 2016
  • In this study, we investigated the effects of mouth breathing on brain activity through electroencephalogram (EEG). EEG was performed on 12 healthy volunteers of age ranging from 21 to 27 years (male: female = 6:6, non-smoker). Brain waves on resting state (Rest_N/Rest_M) and auditory-language stimuli state (Eng_N/Eng_M) were recorded during mouth and nose breathing. Four different regions (R1~R4) were classified based on the brain functionality. And each channel (e.g., Pf1 and Pf2) and frequency (${\alpha}$, ${\beta}$, ${\gamma}$, and ${\theta}$) were analyzed using their absolute power ratios of fast Fourier transform (FFT). The results showed that there was no significant difference between Rest_N and Rest_M. Eng_N had significantly higher brain activity than Rest_N; on the other hand, there was no significant difference between Rest_M and Eng_M. These results demonstrate that mouth-breathing on resting state does not induce any significant effects on brain activity and/or functionality, even though it causes subtle temporary inconvenience. In addition to the uncomfort, the brain activity can be adversely influenced by mouth-breathing, which could lower the cognitive skills under certain circumstances.

Effect of Exercises on the Cerebral Blood Flow (운동이 뇌 혈류 변화에 미치는 영향)

  • Song, Myung-Soo;Choi, Su-Hee
    • Journal of the Korean Academy of Clinical Electrophysiology
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    • v.1 no.2
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    • pp.1-9
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    • 2003
  • The purpose of this study was to analyze the effect given to the variable details which disturb the flow of blood in brain artery disease through Aerobic exercises. It chose the subjects of study : 5 persons in an exercise group and 5 persons in a non-exercise group. Peak brain blood velocity, mean velocity, and resistance & artery stricture ratio were measured with TCD, measure machine for brain artery blood flow. The conclusion of the study was as follows: 1. At pre-test of an exercises group and a non-exercise group, PBV, MBV, BRI, ASI of a non-exercise group were showed much lower in the variation of left common carotid artery(LCCA). 2. At post-test of an aerobic exercises group and a non-exercise group, PBV, MBV, BRI, ASI of a non-exercise group were showed just a little decrease ratio but were not significant different in the variation of left common carotid artery(LCCA). Viewing on the base of these result, continuing exercises promote the functional improvement of the heart blood system and were showed the positive variation of artery stricture ratio according to brain blood flow velocity, the pulse and resistance or blood velocity. Therefore programs for prescriptions through aerobic exercises must be developed in many ways.

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Whole Brain Radiation-Induced Cognitive Impairment: Pathophysiological Mechanisms and Therapeutic Targets

  • Lee, Yong-Woo;Cho, Hyung-Joon;Lee, Won-Hee;Sonntag, William E.
    • Biomolecules & Therapeutics
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    • v.20 no.4
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    • pp.357-370
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    • 2012
  • Radiation therapy, the most commonly used for the treatment of brain tumors, has been shown to be of major significance in tumor control and survival rate of brain tumor patients. About 200,000 patients with brain tumor are treated with either partial large field or whole brain radiation every year in the United States. The use of radiation therapy for treatment of brain tumors, however, may lead to devastating functional deficits in brain several months to years after treatment. In particular, whole brain radiation therapy results in a significant reduction in learning and memory in brain tumor patients as long-term consequences of treatment. Although a number of in vitro and in vivo studies have demonstrated the pathogenesis of radiation-mediated brain injury, the cellular and molecular mechanisms by which radiation induces damage to normal tissue in brain remain largely unknown. Therefore, this review focuses on the pathophysiological mechanisms of whole brain radiation-induced cognitive impairment and the identification of novel therapeutic targets. Specifically, we review the current knowledge about the effects of whole brain radiation on pro-oxidative and pro-inflammatory pathways, matrix metalloproteinases (MMPs)/tissue inhibitors of metalloproteinases (TIMPs) system and extracellular matrix (ECM), and physiological angiogenesis in brain. These studies may provide a foundation for defining a new cellular and molecular basis related to the etiology of cognitive impairment that occurs among patients in response to whole brain radiation therapy. It may also lead to new opportunities for therapeutic interventions for brain tumor patients who are undergoing whole brain radiation therapy.