• The Korean Journal of Nuclear Medicine
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• v.28 no.3
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• pp.282-292
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• 1994

Brain perfusion SPECT shows typical regional perfusion abnormalities in Alzheimer's disease(AD) and is useful for its diagnosis. However, there is also arguement that these patterns show significant overlap with other causes, and the accuracy for SPECT in differentiating AD has shown conflicting results. We postulate that the variation in re-ported results are partly due to a difference in patient or control selection with special reference to the mixture of ischemic cerebral disease in the studied population. To deter-mine the effect of ischemic lesions and the nature of control subjects on SPECT studies for AD, we performed $^{99m}Tc$-HMPAO single photon emission computed tomography (SPECT) in 11 probable AD patients with a low (<4) Hachinski ischemic score and 12 non-demented age matched controls. Magnetic resonance imaging(MRI) disclosed ischemic cerebral lesions in 27% (3/11) of the PAD group and 25% (3/12) of the control group. Regional perfusion indices were quantitated from the SPECT images as follows and the distribution of perfusion indices from both groups were compared. This was repeated with controls after excluding those with significant ischemic lesions by MRI : regional perfusion index = average regional count/average cerebellar count All PAD patients showed perfusion abnormality in SPECT. However, 53% (10/12) of controls also showed perfusion at-normalities, and no pattern could reliably differentiate the two groups. After excluding controls with significant cerebral ischemia, the difference in temporal and parietal perfusion index was increased. A decreased tempore-parietal and any parietal or temporal per-fusion index had a sensitivity of 18% and 36% in detecting AD, respectively. When using a separate group of normal age mathced controls, the indices showed an even more difference in the temporal and parietal lobes and the sensitivity of a decreased tempore-parietal and any parietal or temporal perfusion index had a sensitivity of 36% and 55% in detecting AD, respectively. Thus, the type of control with special reference to the pres-once of ischemic cerebral lesions contribute significantly to the accuracy of perfusion SPECT in diagnosing AD. This nay have particular importance in the diagnosis of AD in populations where the prevalance of cerebrovascular disease is high.

• Journal of Chest Surgery
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• v.34 no.11
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• pp.823-830
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• 2001

Background: Paraplegia is a serious complication of thoracic or thoracoabdominal aortic operations, which is related to ischemic injury of the spinal cord induced by low perfusion pressure during cross clamping of the aorta. Ischemic preconditioning of heart or brain with reversible sublethal ischemic injury induces resistance to subsequent lethal ischemia. The aim of this study is to investigate whether ischemic tolerance could be induced by the preconditioning of the spinal cord using swine model. Material and Method: The animals were randomly assigned to three groups: sham group(n=3), control group(n=6) and pre-conditioning group(n=8). In the sham group, we performed the left thoracotomy only without any ischemic injury. In the preconditioning group, the swine received reversible spinal cord ischemic injury by aortic clamping for 20 minutes, whereas control group had no previous aortic cross- clamping. Forty-eight hours later, the aorta was clamped for 30 minutes in both groups. Neurological examination was done 24 hours later, then the animals were euthanized for histopathology and malonedialdehyde(MDA) spectrophotometry assay of the spinal cord. Result: Statistically significant difference in neurological outcome was observed between the control and preconditioning groups at 24 hours after ischemic injury. The incidence of paraplegia and severe paresis was 100% in the control group, and 62.5% in the preconditing group(p=0.028). There was no statistically significant difference in histopathology and MDA assay of the ischemic spinal cord between these two groups with borderline statistical difference in MDA assay(p=0.0745). Conclusion: In the present swine study, ischemic preconditioning could induce tolerance against 30 minute ischemic insult of the spinal cord, although the animals did not completely recover(stand-up or walk). We expect that combining this preconditioning with other currently existing protection methods might lead to a synergistic effect, which warrants further investigation.

• The Journal of Korean Medicine
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• v.23 no.3
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• pp.74-84
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• 2002

목적 : 본 실험에서는 gerbil을 이용한 전뇌허혈 동물모델에서 뇌허혈손상 직후 지연성 뇌손상에 대한 대황의 방어효과와 Apoptosis 과정중의 Bax와 Bcl-2 단백질에 대한 조절작용을 관찰하고, TUNEL 염색법을 통하여 대황이 gerbil hippocampus CAl영역의 pyramidal neuron의 세포사에 미치는 영향과 PCl2세포를 이용한 세포배양 모델에서의 대황의 신경방어 효과를 관찰하였다. 방법 : Mongolian gerbil의 총경동맥을 5분간 폐색하여 가역성 전뇌허혈을 유발시킨 후 대황의 전탕액을 하루에 한번 경구 투여하였다. 대황의 신경 보호 효과는 수술 7일 후에 cresyl violet으로 염색하여, 살아있는 신경 세포의 수를 세어 측정하였다. 또, 수술 3일 후에는 면역조직화학적 방범을 통하여 Bax. Bcl-2단백질의 발현과 대황의 신경보호 효과와의 관련성을 알아보았다. 결과： 가역적 전뇌허혈이 일어난 동물군의 경우 hippocampus의 CAl 영역에서 살아있는 신경세포의 수는 $51.0{\pm}2.5개{\;}/mm$에 불과하였으나, 그에 비해 수술 후 7일간 대황을 투여한 동물군은 $106.2{\pm}2.5개{\;}/mm$로 살아 있는 신경세포수가 크게 증가하였다. Apoptosis를 촉진하는 단백질인 Bax의 발현은 3일간 대황을 투여한 동물군의 경우 hippocampus의 CAl 영역에서 현저하게 저해되었고, Apoptosis를 억제하는 Bcl-2 단백질의 발현은 변화가 없었다. TUNEL assay를 통하여 살펴본 결과 대황 투여군의 apoptotic 신경세포사가 감소하였으며 이는 Bax protein의 발현과 유사한 양상을 나타내었다. 결론：대황이 Bax 단백질의 발현을 억제하여 상대적으로 Bax/Bcl-2 자연적 세포사를 억제하여 Mogolian gerbil의 가역성 전뇌허혈 모델에서 신경보호효과를 나타내는 것으로 사료된다.

• Journal of Life Science
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• v.26 no.4
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• pp.475-483
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• 2016

The current study was conducted to evaluate beneficial effects of a new formula (CWC-9) using four traditional Oriental medicinal herbs, Cynanchum wilfordii, Rehmannia glutinosa, Polygala tenuifolia, and Acorus gramineus, on hippocampal cells and memory function. To examine the neuroprotective effects of a new four-herb extract, cell viability, cytotoxicity, and reactive oxygen species (ROS) assays were performed in HT22 cells and behavioral tests (Morris water maze and passive avoidance retention), Western blot, and immunohistochemistry were performed in a mouse model of focal cerebral ischemia. In HT22 hippocampal cells, pretreatment with CWC-9 resulted in significantly reduced glutamate-induced cell death with suppression of ROS accumulation caused by glutamate. In a mouse model of focal cerebral ischemia, we observed significant improvement of spatial and short-term memory function by treatment with CWC-9. Phosphorylated p38 mitogen-activated protein kinases (MAPK) in hippocampus of ischemic mice were decreased by treatment with CWC-9, but phosphorylated phosphatidylinositol-3 kinase (PI3K) and cAMP response element binding protein (CREB) were significantly enhanced. By immunohistochemical analysis, we confirmed higher expression of phosphorylation of CREB in the hippocampal neurons of CWC-9 treated mice. These results suggest that new multi-herb formula CWC-9 mainly exerted beneficial effects on cognitive function through regulation of neuro-protective signaling pathways associated with CREB.

• Journal of Life Science
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• v.30 no.11
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• pp.939-946
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• 2020

Stroke is one of the leading causes of neurological disability worldwide and stroke patients exhibit a range of motor, cognitive, and psychiatric impairments. GPR88 is an orphan G protein-coupled receptor (GPCR) that is highly expressed in striatal medium spiny neurons; its deletion results in poor motor coordination and motor learning. There are currently no studies on the involvement of GPR88 in stroke or in post-stroke brain function recovery. In this study, we found a decrease in GPR88 protein and mRNA expression levels in an ischemic mouse model using Western blot and real-time PCR, respectively. In addition, we observed that, among the three types of cells derived from the brain (brain microvascular endothelial cells, BV2 microglial cells, and HT22 hippocampal neuronal cells), the expression of GPR88 was highest in HT22 neuronal cells, and that GPR88 expression was downregulated in HT22 cells under oxygen-glucose deprivation (OGD) conditions. Moreover, pretreatment with RTI- 13951-33 (10 mg/kg), a brain-penetrant GPR88 agonist, ameliorated brain injury following ischemia, as evidenced by improvements in infarct volume, vestibular-motor function, and neurological score. Collectively, our results suggest that GPR88 could be a potential drug target for the treatment of central nervous system (CNS) diseases, including ischemic stroke.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.14 no.1
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• pp.223-228
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• 2013

We evaluated the usefulness of $DTI_{6D}$ which was acquiring six direction diffusion data through compared to $DWI_{3D}$. Mean SNR and CNR were on $DWI_{3D}$ and $DTI_{6D}$ $44.01{\pm}13.36$, $37.15{\pm}11.44$ (p=0.029) and $18.47{\pm}9.66$, $19.88{\pm}9.20$(p=0.017). The number of lesions were $311{\pm}26.87$, $224.5{\pm}26.16$(p=0.041) on $DTI_{6D}$ and $DWI_{3D}$. Twenty patients were the more detected brain infarction lesion on $DTI_{6D}$. But there is no one the more detected on $DWI_{3D}$. And the more three direction diffusion data could get more information. However, we need to consider about the time consumption compared to DWI.

• Journal of agriculture & life science
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• v.46 no.6
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• pp.137-146
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• 2012

This study investigated whether ferulic acid modulates the heme oxygenase (HO)-1 and HO-2 expression in middle cerebral artery occlusion (MCAO)-induced brain injury. Rats (Sprague-Dawley, male) were treated with vehicle or ferulic acid (100 mg/kg, i.v.) before MCAO, and cerebral cortex tissues were collected 24 h after MCAO. This study clearly confirmed the protective effects of ferulic acid during MCAO-induced damage using hematoxylin and eosin staining. MCAO induces nuclear chromatin condensations and necrotic changes with scalloped shrunken form. However, ferulic acid prevented MCAO-induced histopathological changes. HO-1 and HO-2 expression levels were measured using reverse-transcription PCR and Western blot analyses. HO-1 levels were decreased in vehicle-treated animals after MCAO, whereas this decrease in HO-1 levels was attenuated by ferulic acid treatment. However, the level of HO-2 was consistently maintained in the cerebral cortex of vehicle- and ferulic acid-treated animals after MCAO. These results demonstrated that ferulic acid regulates HO-1 expression in ischemic brain injury, while ferulic acid do not modulate HO-2 expression in MACO. In conclusion, these findings suggest that ferulic acid exerts a neuroprotective effect by preventing the MCAO-induced decrease of HO-1 expression.

• Neonatal Medicine
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• v.18 no.1
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• pp.59-69
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• 2011

Purpose: Current studies have demonstrated the neuroprotective effects of 6-cyano-7-nitroquinoxalin-2,3-dione (CNQX) in many animal models of brain injury, including hypoxic-ischemic (HI) encephlopathy, trauma and excitotoxicity, but limited data are available for those during the neonatal periods. Here we investigated whether CNQX can protect the developing rat brain from HI injury via mediation of nitric oxide synthase. Methods: In an in vivo model, left carotid artery ligation was done in 7-day-old Sprague-Dawley (SD) rat pups. The animals were divided into six groups; normoxia (N), hypoxia (H), hypoxia with sham-operation (HS), hypoxia with operation (HO), HO treated with vehicle (HV), and HO treated with CNQX at a dose of 10 mg/kg (HC). Hypoxia was made by exposure to a 2 hr period in the hypoxic chamber (92% $N_2$, 8% $O_2$). In an in vitro model, embryonic cortical neuronal cell culture of SD rats at 18-day gestation was done. The cultured cells were divided into three groups: normoxia (N), hypoxia (H), and hypoxia treated with CNQX (HC). The N group was prepared in 5% $CO_2$ incubators and the other groups were placed in 1% $O_2$) incubators (94% $N_2$, 5% $CO_2$) for 16 hr. Results: In the in vitvo and in vivo models, the expressions of iNOS and eNOS were reduced in the hypoxia group when compared to the normoxia group, whereas they were increased in the CNQX-treated group compared to the hypoxia group. In contrast, the expression of nNOS was showed reversely. Conclusion: CNQX has neuroprotective property over perinatal HI brain injury via mediation of nitric oxide synthase.

• Clinical and Experimental Pediatrics
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• v.51 no.11
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• pp.1205-1210
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• 2008

Purpose : The development of the corpus callosum occupies the entire period of cerebral formation. The myelination pattern on magnetic resonance imaging (MRI) is very useful to evaluate neurologic development and to predict neurologic outcome in high risk infants. The thickness of the corpus callosum is believed to depend on the myelination process. It is possible to calculate the length and thickness of the corpus callosum on MRI. Thus, we can quantitatively evaluate the development of the corpus callosum. We investigated the clinical significance of measuring various portions of the corpus callosum in neonate with neurologic disorders such as hypoxic brain damage and seizure disorder. Methods : Forty-two neonates were evaluated by brain MRI. We measured the size of the genu, body, transitional zone, splenium, and length of the corpus callosum. Each measurement was divided by the total length of the corpus callosum to obtain its corrected size. The ratio of corpus callosal length and the anteroposterior diameter of the brain was also measured. Results : There was no statistical significance in the sample size of each part of the corpus callosum. However, the corrected size or the ratio of body of the corpus callosum correlated with periventricular leukomalacia and hypoxic ischemic encephalopathy. Conclusion : The abnormal size of the corpus callosum showed a good correlation with periventricular leukomalacia and hypoxic ischemic encephalopathy in neonates. We can predict clinical neurological problems by estimation of the corpus callosum in the neonatal period.

• Journal of Chest Surgery
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• v.42 no.2
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• pp.248-251
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• 2009

Nonocclusive mesenteric ischemia (NOMI) is a rare complication that occurs in about 0.05% of patients after openheart surgery, and NOMI refers to the mesenteric ischemia that's caused by splanchnic vasospasm without occlusion of the great intestinal vessels. In the presently reported case, NOMI developed to maintain the blood flow to the heart and brain after several minutes of a hypotensive status and the latter was caused by acute aortic dissection that complicated an aortic cannulation procedure. Unfortunately, the patient died even though the problems were diagnosed early and proper treatment was administered. Early diagnosis of NOMI by angiography and the selective infusion of vasodilators are thought to be the only way to improve survival for patients with clinically suspected NOMI.