No abstract available.

No abstract available.
Osteoblastoma*

Bickerstaff 's brainstem encephalitis (BBE) is characterized by acute ophthalmoplegia and ataxia. Some patients with BBE show mental changes, pyramidal signs and sensory disturbance. A forty-three year old woman was diagnosed as BBE in 1996. In 2000, she admitted again with complaints of ataxia and ophthalmoplegia. She was diagnosed as recurrent BBE and an overlap of Guillain-Barre syndrome (GBS). This is the first case of an overlap of BBE and GBS, as well as BBE in Korea.
Ataxia ; Brain Stem* ; Encephalitis* ; Female ; Guillain-Barre Syndrome* ; Humans ; Korea ; Ophthalmoplegia

BACKGROUND: We evaluated whether the time required for a seizure to spread contralaterally, interhemispheric propagation time (IHSPT) could be related to post-surgical outcome in temporal lobectomy. METHODS: We performed a retrospective study of 28 patients. All patients had previously undergone a phase I presurgical evaluation including MRI and video-EEG monitoring with scalp and sphenoidal electrodes, which strongly suggested the diagnosis of mesial temporal lobe epilepsy, but proved inadequate to lateralize the epileptogenic zone. All patients performed the video-EEG monitoring with bilateral subdural strip electrodes on their basal and mesial temporal area and unilateral temporal lobectomy with a minimum of 1-year follow up postoperatively. IHSPT was divided into two categories, 0~5.0 seconds, 5.1 seconds or longer. RESULTS: Sixteen patients (57.1%) were seizure free and 12 suffered persistent seizures. A prolonged IHSPT (> 5.0sec) significantly correlated with a favorable surgical outcome (P = 0.05). Hippocampal atrophy on MRI significantly correlated with prolonged IHSPT (P<0.05). CONCLUSIONS: Our result suggests that hippocampal atrophy on MRI and IHSPT can predict the surgical outcome and may be used as the selection criteria of temporal lobectomy for patients with intractable temporal lobe epilepsy.
Atrophy ; Diagnosis ; Electrodes* ; Epilepsy, Temporal Lobe* ; Follow-Up Studies ; Humans ; Magnetic Resonance Imaging ; Patient Selection ; Retrospective Studies ; Scalp ; Seizures ; Temporal Lobe*

Congenital anomalies occur in 2-3% of neonates but this incidence increases in multiple pregnancies, especially when fetuses are monozygotic. when pregnancies are affected with one anomalous fetus combined to a normal one, the proper management and counseling is difficult.We experienced a twin pregnancy in which one anencephalic fetus was combined to a normal one. Karyotype analysis was normal in both fetus. After close counseling we decided to continue the pregnancy. Intermittent amnioreduction was done for persistent polyhydramnios. At 29 weeks of gestation membrane was ruptured prematurely and we delivered by cesarean section due to breech-cephalic presentation. The birth weight of the normal and anencephalic fetuses were 1070 gm and 1050 gm, respectively. The anencephalic fetus died immediately after birth but the healthy one showed good crying and movement and its Apgar score was 6 in 1 minute and 8 in 5 minute. Although the infant needed intensive care for 90 days in the nursery room finally discharged in good condition. We report a case of twin pregnancy in which anencephaly was associated with a normal fetus, so after close counseling we opted to continue the pregnancy resulting in the delivery of a viable fetus.
Anencephaly ; Apgar Score ; Birth Weight ; Cesarean Section ; Counseling ; Crying ; Female ; Fetus* ; Humans ; Incidence ; Infant ; Infant, Newborn ; Critical Care ; Karyotype ; Membranes ; Nurseries ; Parturition ; Polyhydramnios ; Pregnancy ; Pregnancy, Multiple ; Pregnancy, Twin* ; Twins*

PURPOSE: Vascular smooth muscle cell (VSMC) proliferation induced by native low-density lipoprotein (nLDL) stimulation is dependent on superoxide production from activated NADPH oxidase. The present study aimed to investigate whether the novel arginase inhibitor limonin could suppress nLDL-induced VSMC proliferation and to examine related mechanisms. MATERIALS AND METHODS: Isolated VSMCs from rat aortas were treated with nLDL, and cell proliferation was measured by WST-1 and BrdU assays. NADPH oxidase activation was evaluated by lucigenin-induced chemiluminescence, and phosphorylation of protein kinase C (PKC) βII and extracellular signal-regulated kinase (ERK) 1/2 was determined by western blot analysis. Mitochondrial reactive oxygen species (ROS) generation was assessed using MitoSOX-red, and intracellular L-arginine concentrations were determined by high-performance liquid chromatography (HPLC) in the presence or absence of limonin. RESULTS: Limonin inhibited arginase I and II activity in the uncompetitive mode, and prevented nLDL-induced VSMC proliferation in a p21Waf1/Cip1-dependent manner without affecting arginase protein levels. Limonin blocked PKCβII phosphorylation, but not ERK1/2 phosphorylation, and translocation of p47phox to the membrane was decreased, as was superoxide production in nLDL-stimulated VSMCs. Moreover, mitochondrial ROS generation was increased by nLDL stimulation and blocked by preincubation with limonin. Mitochondrial ROS production was responsible for the phosphorylation of PKCβII. HPLC analysis showed that arginase inhibition with limonin increases intracellular L-arginine concentrations, but decreases polyamine concentrations. L-Arginine treatment prevented PKCβII phosphorylation without affecting ERK1/2 phosphorylation. CONCLUSION: Increased L-arginine levels following limonin-dependent arginase inhibition prohibited NADPH oxidase activation in a PKCβII-dependent manner, and blocked nLDL-stimulated VSMC proliferation.
Animals ; Aorta ; Arginase* ; Arginine ; Blotting, Western ; Bromodeoxyuridine ; Cell Proliferation* ; Chromatography, High Pressure Liquid ; Chromatography, Liquid ; Lipoproteins ; Luminescence ; Membranes ; Muscle, Smooth, Vascular* ; NADP* ; NADPH Oxidase* ; Phosphorylation ; Phosphotransferases ; Protein Kinase C ; Rats ; Reactive Oxygen Species ; Superoxides

Arginase inhibition exhibits beneficial effects in vascular endothelial and smooth muscle cells. In human aortic smooth muscle cells (hAoSMCs), native low-density lipoprotein (nLDL) induced the production of interleukin-8 (IL-8) that is involved in the pathogenesis of cardiovascular diseases. Therefore, we examined the effect of arginase inhibition on IL-8 production and the underlying mechanism. In hAoSMCs, reverse transcription–PCR, western blotting and immunocytochemistry with MitoTracker confirmed that arginase II was confined predominantly to mitochondria. The mitochondrial membrane potential (MMP) was assessed using tetramethylrhodamine ethyl ester. The MMP decreased upon nLDL stimulation but was restored upon arginase inhibition. MMP loss caused by nLDL was prevented by treatment with the intracellular Ca(2+) chelator BAPTA-AM. In mitochondrial Ca(2+) measurements using Rhod-2 AM, increased mitochondrial Ca(2+) levels by nLDL were inhibited upon preincubation with an arginase inhibitor. Among the polyamines, spermine, an arginase activity-dependent product, caused mitochondrial Ca(2+) movement. The nLDL-induced MMP change resulted in p38 mitogen-activated protein kinase (MAPK) phosphorylation and IL-8 production and was prevented by the arginase inhibitors BAPTA and ruthenium 360. In isolated AoSMCs from ApoE(−/−) mice fed a high-cholesterol diet, arginase activity, p38 MAPK phosphorylation, spermine and mitochondrial Ca(2+) levels and keratinocyte-derived chemokine (KC) production were increased compared with wild-type (WT) mice. However, in AoSMCs isolated from arginase II-null mice, increases in MMP and decreases in mitochondrial Ca(2+) levels were noted compared with WT and were associated with p38 MAPK activation and IL-8 production. These data suggest that arginase activity regulates the change in MMP through Ca(2+) uptake that is essential for p38 MAPK phosphorylation and IL-8 production.

BACKGROUND AND OBJECTIVES: The traditional indexes of heart rate (HR) variability may lack the ability to detect subtle, but important changes in HR behavior. Nonlinear heart rate variability (HRV) analysis methods that are based on chaos theory can reveal subtle abnormalities in the HR dynamics of patients with cardiovascular diseases. Therefore, we tested the validity of nonlinear analysis methods as markers to differentiate normal and abnormal HR dynamics in the cardiovascular disease state. SUBJECTS AND METHODS: One-hundred patients were studied: 70 patients with left ventricular dysfunction (LVD), including 40 post-myocardial infarct patients (PMI) and 30 dilated cardiomyopahty patients (DCM), and 30 age and gender-matched controls. One-hour, 6-hours (day and night each) and 24 hours of R-R interval data from 24-hour Holter recordings were subjected to the conventional time and frequency-domain analysis. The ApEn, short-term (alpha1) and long-term (alpha2) scaling exponents of the detrended fluctuation analysis (DFA) and the power-law exponent (beta) were also measured. RESULTS: Conventional linear measures did not show a significant difference except for the VLF, lnLF and the LF/HF ratio between the controls and the LVD patients. Among the analyzed parameters, beta, beta2 and alpha1 were the most powerful discriminators. The beta of the normal and LVD patients was -1.10+/-0.29 and -0.70+/-0.40, respectively (p<0.001), and the alpha1 was 1.08+/-0.23 and 0.81+/-0.28, respectively (p<0.001). The beta, beta2 and alpha1 can discriminate the etiologic cause of LVD. The length of the R-R interval data did not affect the result, and a significant correlation was observed. The individual values of the fractal and complexity measures were more stable than those of the conventional linear measures. CONCLUSION: We conclude that the measures derived from fractal and complexity methods are useful for detecting altered HR dynamics of LVD and for improving the shortcomings of the conventional measures.
Cardiovascular Diseases ; Fractals* ; Heart Rate* ; Heart* ; Humans ; Nonlinear Dynamics ; Risk Assessment ; Ventricular Dysfunction, Left*