• Title/Summary/Keyword: Cerebral glucose metabolism

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Changes of Plasma Creatinine Kinase-BB after Total Circulatory Arrest (총순환정지후 혈중 크레아티닌 카이네이즈 BB의 변화에 관한 연구)

  • 이석재;김용진;김오곤
    • Journal of Chest Surgery
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    • v.31 no.10
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    • pp.945-951
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    • 1998
  • Background: Although profound hypothermia with total circulatory arrest(TCA) is a valuable maneuver in cardiac surgery, its applications have been limited due to serious complications, especially cerebral damage. In this study, the possible role of creatinine kinase-BB(CK-BB), an index enzyme of ischemic cerebral damage, was assayed as a parameter for the assessment of the cerebral complications after TCA. Hemoglobin(Hb), ionized calcium(Ca++), and blood glucose levels were also assessed as clinical parameters involved in cerebral damage. Materials and methods: Among patients with congenital heart disease, 18 patients who had been operated on with TCA were randomly selected and divided into two groups: 6 with acyanotic and 12 with cyanotic heart disease. Arterial blood from each patient was collected before and after TCA at scheduled times(15 min., 30 min, 1, 2, 4, 8, and 12hr). The levels of CK-BB, Hb, Ca++, and blood glucose were assessed in each sample. Results: As a whole, correlation between CK-BB level and blood sampling time after TCA was not statistically significant. Also, the difference in the level of CK-BB after TCA was not significant between the acyanotic and cyanotic groups. The levels of Hb and CK-BB correlated significantly. Conclusions: The results, which showed no correlation between the alterations in CK-BB level and the TCA duration, suggest that the single assay of the CK-BB level is not a representative measurement for the assessment of cerebral damage after TCA. Also, the cyanotic congenital heart disease group is not more vulnerable to cerebral damage induced by TCA.

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Effect of Pioglitazone on Perihematomal Edema in Intracerebral Hemorrhage Mouse Model by Regulating NLRP3 Expression and Energy Metabolism

  • Kim, Hoon;Lee, Jung Eun;Yoo, Hyun Ju;Sung, Jae Hoon;Yang, Seung Ho
    • Journal of Korean Neurosurgical Society
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    • v.63 no.6
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    • pp.689-697
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    • 2020
  • Objective : Cerebral edema is the predominant mechanism of secondary inflammation after intracerebral hemorrhage (ICH). Pioglitazone, peroxisome proliferator-activated receptor gamma agonist has been shown to play a role in regulation of central nervous system inflammation. Here, we examined the pharmacological effects of pioglitazone in an ICH mouse model and investigated its regulation on NLRP3 inflammasome and glucose metabolism. Methods : The ICH model was established in C57 BL/6 mice by the stereotactical inoculation of blood (30 µL) into the right frontal lobe. The treatment group was administered i.p. pioglitazone (20 mg/kg) for 1, 3, and 6 days. The control group was administered i.p. phosphate-buffered saline for 1, 3, and 6 days. We investigated brain water contents, NLRP3 expression, and changes in the metabolites in the ICH model using liquid chromatography-tandem mass spectrometry. Results : On day 3, brain edema in the mice treated with pioglitazone was decreased more than that in the control group. Expression levels of NLRP3 in the ICH model treated with pioglitazone were decreased more than those of the control mice on days 3 and 7. The pioglitazone group showed higher levels of glycolytic metabolites than those in the ICH mice. Lactate production was increased in the ICH mice treated with pioglitazone. Conclusion : Our results demonstrated less brain swelling following ICH in mice treated with pioglitazone. Pioglitazone decreased NLRP3-related brain edema and increased anaerobic glycolysis, resulting in the production of lactate in the ICH mice model. NLRP3 might be a therapeutic target for ICH recovery.

Ginsenoside compound K protects against cerebral ischemia/ reperfusion injury via Mul1/Mfn2-mediated mitochondrial dynamics and bioenergy

  • Qingxia Huang;Jing Li;Jinjin Chen;Zepeng Zhang;Peng Xu;Hongyu Qi;Zhaoqiang Chen;Jiaqi Liu;Jing Lu;Mengqi Shi;Yibin Zhang;Ying Ma;Daqing Zhao;Xiangyan Li
    • Journal of Ginseng Research
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    • v.47 no.3
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    • pp.408-419
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    • 2023
  • Background: Ginsenoside compound K (CK), the main active metabolite in Panax ginseng, has shown good safety and bioavailability in clinical trials and exerts neuroprotective effects in cerebral ischemic stroke. However, its potential role in the prevention of cerebral ischemia/reperfusion (I/R) injury remains unclear. Our study aimed to investigate the molecular mechanism of ginsenoside CK against cerebral I/R injury. Methods: We used a combination of in vitro and in vivo models, including oxygen and glucose deprivation/reperfusion induced PC12 cell model and middle cerebral artery occlusion/reperfusion induced rat model, to mimic I/R injury. Intracellular oxygen consumption and extracellular acidification rate were analyzed by Seahorse multifunctional energy metabolism system; ATP production was detected by luciferase method. The number and size of mitochondria were analyzed by transmission electron microscopy and MitoTracker probe combined with confocal laser microscopy. The potential mechanisms of ginsenoside CK on mitochondrial dynamics and bioenergy were evaluated by RNA interference, pharmacological antagonism combined with co-immunoprecipitation analysis and phenotypic analysis. Results: Ginsenoside CK pretreatment could attenuate mitochondrial translocation of DRP1, mitophagy, mitochondrial apoptosis, and neuronal bioenergy imbalance against cerebral I/R injury in both in vitro and in vivo models. Our data also confirmed that ginsenoside CK administration could reduce the binding affinity of Mul1 and Mfn2 to inhibit the ubiquitination and degradation of Mfn2, thereby elevating the protein level of Mfn2 in cerebral I/R injury. Conclusion: These data provide evidence that ginsenoside CK may be a promising therapeutic agent against cerebral I/R injury via Mul1/Mfn2 mediated mitochondrial dynamics and bioenergy.

Chorea in Systemic Lupus Erythematosus: Evidence for Bilateral Putaminal Hypermetabolism on F-18 FDG PET (전신성 홍반성 루푸스에서 F-18 FDG PET상 기저핵 포도당대사 증가 소견을 보이는 무도병 1예)

  • Seo, Wook-Jang;Chung, Son-Mi;Koh, Su-Jin;Lee, Chang-Keun;Kim, Jae-Seung;Im, Joo-Hyuk;Yoo, Bin;Moon, Hee-Bom
    • The Korean Journal of Nuclear Medicine
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    • v.37 no.5
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    • pp.325-330
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    • 2003
  • Purpose: We describe a 54-year-old woman with systemic lupus erythematosus (SLE) who suddenly presented with chorea and had positive antiphospholipid antibodies. F-18 FDG PET showed abnormally increased glucose metabolism in bilateral putamen and primary motor cotex. Tc-99m ECD SPECT also showed abnormally increased regional cerebral blood flow in bilateral putamen. She was treated with corticosteroid and aspirin after which the symptoms improved. Four months later, follow up F-18 FDG PET showed improvement with resolution of hypermetabolism in bilateral putamen. This case suggests that striatal hypermetabolism is associated with chorea in SLE.

Gender differences in age-related decline of regional cerebral glucose metabolism: implications for the gender differences in frontal function (연령 증가에 따른 전두엽 포도당대사 저하의 남녀 차이)

  • Lee, Eun-Ju;Cho, Sang-Soo;Yun, Eun-Jin;Kim, Yu-Kyeong;Lee, Won-Woo;Kim, Sang-Eun
    • Proceedings of the Korean Society for Cognitive Science Conference
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    • 2005.05a
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    • pp.212-215
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    • 2005
  • 연령의 증가에 따른 신경원의 활성화도 변화는 기억 및 집행기능 등의 인지기능에 영향을 미치는 것으로 알려져 왔다. 그러나 어떠한 뇌 영역의 기능적 저하가 연령증가에 따라 남자와 여자에서 차별적으로 인지기능의 변화를 가져오는지에 대해서는 거의 알려진 바가 없다. F-18 FDG PET을 이용하여 78명의 정상 성인 남녀를 대상으로 뇌 포도당 대사량을 조사하였다. 남녀가 공통적으로 연령증가에 따라 뇌 포도당 대사량의 저하를 보이는 영역은frontal lobe과 left insula, right anterior cingulate gyrus, bilateral caudate body, thalamus. right corpus callosum 이었다. 여성의 경우 남성과 달리 추가적으로 right caudate와 bilaterial thalamus에서 연령과 뇌 포도당대사량 간에 부적 상관을 보이고 있었다(P < 0.001 uncorrected). 남녀 모두에서 연령이 증가하면서 포도당 대사 저하를 보이는 right inferior frontal gyrus는 여자에게서만 포도당대사 감소비율이 유의하게 컸다. 남녀에서 보이는 이러한 노화 과정 동안의 뇌 포도당 대사의 저하율의 차이가 여성과 남성의 연령증가에 따른 인지적 기능의 차별적 저하에 대한 설명을 제시할 수 있을 것이라 생각한다.

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Metabolic impairment pattern analysis of the Alzheimer's disease (Alzheimer's Disease의 대사영상패턴 분석)

  • Juh, Ra-Hyeong;Lee, Chang-Uk;Chung, Yong-An;Choe, Bo-Young;Suh, Tae-Suk
    • Proceedings of the Korean Society of Medical Physics Conference
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    • 2004.11a
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    • pp.91-95
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    • 2004
  • Several MRI studies have reported reductions in temporal lobe volumes in Alzheimer's disease (AD). Measures have been usually obtained with regions-of-interest (ROI) drawn manually on selected medial and lateral portions of the temporal lobes, with variable choices of anatomical borders across different studies. We used the automated voxel-based morphometry (VBM) approach to investigate gray matter abnormalities over the entire extension of the temporal lobe in 10AD patients (MM5E 22)and 22 healthy controls. Foci of significantly reduced gray matter volume in AD patients were detected in both medial and lateral temporal regions, most significantly in the right and left posterior parahippocarmpal gyri. At a more flexible statistical threshold (P<0.01, uncorrected for multiple comparisons), circumscribed foci of significant gray matter reduction were also detected in the right amygdala/enthorinal cortex, the anterior and posterior borders of the superior temporal gyrus bilaterally, and the anterior portion of the left middle temporal gyrus. These VBM results confirm previous findings of temporal lobe atrophic changes in AD, and suggest that these abnormalities may be confined to specific sites within that lobe, rather than showing a widespread distribution.

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Imaging Neuroreceptors in the Living Human Brain

  • Wagner Jr Henry N.;Dannals Robert F.;Frost J. James;Wong Dean F.;Ravert Hayden T.;Wilson Alan A.;Links Jonathan M.;Burns H. Donald;Kuhar Michael J.;Snyder Solomon H.
    • The Korean Journal of Nuclear Medicine
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    • v.18 no.2
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    • pp.17-23
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    • 1984
  • For nearly a century it has been known that chemical activity accompanies mental activity, but only recently has it been possible to begin to examine its exact nature. Positron-emitting radioactive tracers have made it possible to study the chemistry of the human mind in health and disease, using chiefly cyclotron-produced radionuclides, carbon-11, fluorine-18 and oxygen-15. It is now well established that measurable increases in regional cerebral blood flow, glucose and oxygen metabolism accompany the mental functions of perception, cognition, emotion and motion. On May 25, 1983 the first imaging of a neuroreceptor in the human brain was accomplished with carbon-11 methyl spiperone, a ligand that binds preferentially to dopamine-2 receptors, 80% of which are located in the caudate nucleus and putamen. Quantitative imaging of serotonin-2, opiate, benzodiazapine and muscarinic cholinergic receptors has subsequently been accomplished. In studies of normal men and women, it has been found that dopamine and serotonin receptor activity decreases dramatically with age, such a decrease being more pronounced in men than in women and greater in the case of dopamine receptors than serotonin-2 receptors. Preliminary studies in patients with neuropsychiatric disorders suggests that dopamine-2 receptor activity is diminished in the caudate nucleus of patients with Huntington's disease. Positron tomography permits quantitative assay of picomolar quantities of neuro-receptors within the living human brain. Studies of patients with Parkinson's disease, Alzheimer's disease, depression, anxiety, schizophrenia, acute and chronic pain states and drug addiction are now in progress. The growth of any scientific field is based on a paradigm or set of ideas that the community of scientists accepts. The unifying principle of nuclear medicine is the tracer principle applied to the study of human disease. Nineteen hundred and sixty-three was a landmark year in which technetium-99m and the Anger camera combined to move the field from its latent stage into a second stage characterized by exponential growth within the framework of the paradigm. The third stage, characterized by gradually declining growth, began in 1973. Faced with competing advances, such as computed tomography and ultrasonography, proponents and participants in the field of nuclear medicine began to search for greener pastures or to pursue narrow sub-specialties. Research became characterized by refinements of existing techniques. In 1983 nuclear medicine experienced what could be a profound change. A new paradigm was born when it was demonstrated that, despite their extremely low chemical concentrations, in the picomolar range, it was possible to image and quantify the distribution of receptors in the human body. Thus, nuclear medicine was able to move beyond physiology into biochemistry and pharmacology. Fundamental to the science of pharmacology is the concept that many drugs and endogenous substances, such as neurotransmitters, react with specific macromolecules that mediate their pharmacologic actions. Such receptors are usually identified in the study of excised tissues, cells or cell membranes, or in autoradiographic studies in animals. The first imaging and quantification of a neuroreceptor in a living human being was performed on May 25, 1983 and reported in the September 23, 1983 issue of SCIENCE. The study involved the development and use of carbon-11 N-methyl spiperone (NMSP), a drug with a high affinity for dopamine receptors. Since then, studies of dopamine and serotonin receptors have been carried out in over 100 normal persons or patients with various neuropsychiatric disorders. Exactly one year later, the first imaging of opitate receptors in a living human being was performed [1].

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