• Journal of Korean Neurosurgical Society
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• v.45 no.4
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• pp.240-242
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• 2009

Oculomotor nerve palsy (ONP) with subarachnoid hemorrhage (SAH) occurs usually when oculomotor nerve is compressed by growing or budding of posterior communicating artery (PcoA) aneurysm. Midbrain injury, increased intracranial pressure (lCP), or uncal herniation may also cause it. We report herein a rare case of ONP associated with SAH which was caused by middle cerebral artery (MCA) bifurcation aneurysm rupture. A 58-year-old woman with clear consciousness suffered from headache and sudden onset of unilateral ONP. Computed tomography showed SAH caused by the rupture of MCA aneurysm. The unilateral ONP was not associated with midbrain injury, increased ICP, or uncal herniation. The patient was treated with coil embolization, and the signs of oculomotor nerve palsy completely resolved after a few days. We suggest that bloody jet flow from the rupture of distant aneurysm other than PcoA aneurysm may also be considered as a cause of sudden unilateral ONP in patients with SAH.

• Journal of Biomedical Engineering Research
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• v.15 no.1
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• pp.71-76
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• 1994

In the source localization using single dipole model, the influence of the number of electrodes, the position and direction of a single dipole on the relation between S/W ratio and dipole parameter estimation errors is important. Monte Carlo simulation was used to investigate this influence. The forward problem was calculated using three spherical shell model, and dipole parameters were optimized by means of simplex method. As the number of electrodes became large, as the dipole went from midbrain to cortex, and as the direction of dipole changed from radial to tangential, the average and standard deviation of estimation errors became small.

• Journal of Korean Physical Therapy Science
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• v.7 no.2
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• pp.513-521
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• 2000

This study was carried out to investigate the effects of electrical stimulation on the change Tyrosine-Hydroxylase immunoreactive(TH-IR) cells in the Central gray and retrorubral field of the male SD rats. 9 healthy and normal rats were divided into three groups, 3 SD rat in each group. The one group has been stimulated by electroacupuncture(EA, 2Hz) for 30min and the other group by EA for 1hr 30min and control group has been stimulated. TH-IR cells were found in the Central gray(CG) and Retrorubral field(RF). The numbers of TH-IR cells of CG and RF were significantly increased after 30 min (CG $6.2{\pm}0.83$, RF $1.4{\pm}0.55$)as compared with control group(CG $24{\pm}3.16$, RF $6.4{\pm}0.55$) and were also significantly increased after 1hr 30min(CG $75.6{\pm}4.51$, RF $18.8{\pm}0.89$) than 30min. These results show that TH is related into CG and RF in response to electrical stimulation.

• Molecules and Cells
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• v.44 no.7
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• pp.493-499
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• 2021

Parkinson's disease (PD) is characterized by a progressive loss of dopamine-producing neurons in the midbrain, which results in decreased dopamine levels accompanied by movement symptoms. Oral administration of l-3,4-dihydroxyphenylalanine (L-dopa), the precursor of dopamine, provides initial symptomatic relief, but abnormal involuntary movements develop later. A deeper understanding of the regulatory mechanisms underlying dopamine homeostasis is thus critically needed for the development of a successful treatment. Here, we show that p21-activated kinase 4 (PAK4) controls dopamine levels. Constitutively active PAK4 (caPAK4) stimulated transcription of tyrosine hydroxylase (TH) via the cAMP response element-binding protein (CREB) transcription factor. Moreover, caPAK4 increased the catalytic activity of TH through its phosphorylation of S⁴⁰, which is essential for TH activation. Consistent with this result, in human midbrain tissues, we observed a strong correlation between phosphorylated PAK4^S474, which represents PAK4 activity, and phosphorylated TH^S40, which reflects their enzymatic activity. Our findings suggest that targeting the PAK4 signaling pathways to restore dopamine levels may provide a new therapeutic approach in PD.

• The Korean Journal of Pharmacology
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• v.31 no.1 s.57
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• pp.17-26
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• 1995

The present studies were carried out to determine if antinociceptive action of morphine and ${\beta}-endorphin$ administered intraventricularly was changed in. pentobarbital anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Antinociception was assessed by the tail-flick test. The $ED_{50}$ values of antinociception for morphine administered intraventricularly were 1.9 and 1.2 nmol for WKY and SHR rats, respectively. The $ED_{50}$ values of antinociception for ${\beta}-endorphin$ administered intraventricularly were 0.40 and 0.12 nmol for WKY and SHR rats, respectively. The $[Met^5]-enkephalin$ (ME) and proenkephalin mRNA levels in midbrain, pons and medulla, or lumbar section of the spinal cord in WKY and SHR rats were measured by the radioimmunoassay and Northern blot assay, respectively. There were no differences of ME and proenkephalin mRNA levels in these tissues between WKY and SHR rats. The results suggest that ${\beta}-endorphin$ but not morphine administered intraventricularly produces a greater antinociception in SHR rats. This increased antinociceptive effect of ${\beta}-endorphin$ in SHR rats may be not, at least, due to the alterations of ME And proenkephalin mRNA levels in the midbrain, pons and medulla, or spinal cord.

• Journal of Microbiology and Biotechnology
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• v.18 no.9
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• pp.1590-1598
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• 2008

Cell proliferation and differentiation are critical processes in a developing fetal rat brain, during which programmed cell death (PCD) also plays an important role. One of the decisive factors for PCD is Bcl-2 family proteins, where Bax induces cell death, whereas Bcl-2 acts as an inhibitor of PCD. As maternal drinking is known to cause fetal alcohol syndrome (FAS) or malformation of the fetal brain during pregnancy, the objective of the present study was to investigate whether maternal ethanol exposure alters the PCD-related Bax and Bcl-2 protein expression during fetal brain development. Pregnant female rats were orally treated with 10% ethanol and the subsequent expressions of the Bax and Bcl-2 proteins examined in the fetal brain, including the forebrain, midbrain, and hindbrain, from gestational day (GD) 15.5 to GD 19.5, using Western blots, in situ hybridization, and immunohistochemistry. With regard to the ratio of Bcl-2 to Bax proteins (Bcl-2/Bax), the Bax protein was dominant in the forebrain and midbrain of the control GD 15.5 fetuses, except for the hindbrain, when compared with the respective ethanol-treated groups. Moreover, Bcl-2 became dominant in the midbrain of the control GD 17.5 fetuses when compared with the ethanol-treated group, representing an alternation of the natural PCD process by ethanol. Furthermore, a differential expression of the Bcl-2 and Bax proteins was found in the differentiating and migrating zones of the cortex, hippocampus, thalamus, and cerebellum. Thus, when taken together, the present results suggest that ethanol affects PCD in the cell differentiation and migration zones of the prenatal rat brain by modulating Bax and Bcl-2 expression in an age- and area-dependent manner. Therefore, this is the first evidence that ethanol may alter FAS-associated embryonic brain development through the alteration of Bax and Bc1-2 expression.

• 대한핵의학회:학술대회논문집
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• 2005.11a
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• pp.347.1-347.1
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• 2005

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.223.2-224
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• 2003

Glial cell-derived neurotrophic factor (GDNF) is a potent neurotrophic factor that enhances survival of midbrain doparminergic neuron. GDNF and its receptors are widely distributed in brain and are believed to be involved in the control of neuron survival and differentiation. GDNF increased proliferation and migration of Hs683 human giloma and C6 rat giloma cells in a dose-dependent manner. (omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.326.2-327
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• 2002

Glial cell-derived neurotrophic factor (GDNF) is a potent neurotrophic factor that enhances survival of midbrain doparminergic neuron. GDNF and its receptors are widely distributed in brain and are believed to be involved in the control of neuron survival and differentiation. In this study, we examined the effect of GDNF on proliferation and migration of Hs683 human glioma cells. GDNF markedly enhances proliferation and migration of Hs683 cells in a dose-dependent manner. (omitted)

• YAKHAK HOEJI
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• v.30 no.4
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• pp.169-173
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• 1986

It was carried out to detect the analgesic action of piperine by hot-plate method and to elucidate its mechanism in rats. Piperine (30mg/kg i.p.) produced profound analgesia, which was blocked by naloxone (10mg/kg). Chronic intraperitoneal administration of piperine significantly increased the contents of $\beta$-endorphin in rat midbrain. In the chronic piperine-treated groups, significant decreases of maximum opiate binding were observed. However, Kd value in these groups were not changed.