No abstract available.
Nervous System*

An effective writing is the one in which the writer and the readers can easily and accurately communicate. For this, the writer should be able to write in accordance with requirements each component of the writing - words, sentences, paragraphs and parts. This thesis discussed a method of writing centered on sentential composition. Sentential level requires grammatical, brief and accurate expressions, and ones like the Korean language.
Writing*

No abstract available.
Animals ; Calcitonin* ; Nasal Mucosa* ; Rats* ; Substance P*

Pituitary adenoma should be differentiated diagnostically from pituitary hyperplasia, which can be classified by primary, secondary & tertially caused by ectopic tumors. Two cases with marked pituitary enlargement secondary to primary hypothyroidism were reported. The volume of the sellar turcica correlates with circulating TSH level. The subsequent regression with thryoxine therapy indicated hyperplasia rather than adenoma. This observation emphasizes the importance of diagnosing and treating primary hypothyroidism prior to considering surgery for possible pituitary adenoma. A brief review of related literatures was also made.
Adenoma ; Hyperplasia* ; Hypothyroidism* ; Pituitary Neoplasms*

Alzheimer's disease(AD) is associated with a characteristic neuropathology. The major hallmarks of AD are senile plaques(SPs) and neurofibrillary tangles(NFTs). beta-amyloid protein(Abeta) is derived from the proteolysis of amyloid precursor protein(APP) and then converted to SPs. Mature SPs produce cytotoxicity through direct toxic effects and activation of microglia and complement. NFTs are composed of paired helical filaments(PHFs) including abnormally phosphorylated form of the microtubule-associated protein(MAP) tau and increased tau level in cerebrospinal fluid may be observed in most AD. The aggregation of Abeta and tau formation are thought to be a final common pathway of AD. Acetycholine, dopamine, serotonin, GABA and their receptors are associated with AD. Especially, decreased nicotinic acetylcholine receptors(nAChRs) in AD are reported. Genetic lesions associated with AD are mutations in the structural genes for the APP located on chromosome 21, presenilin(PSN)1 located on chromosome 14 and PSN2 located on chromosome 1. Also, trisomy 21, Apo-E gene located on chromosome 19, PMF locus, low density lipoprotein receptor-related protein and alpha-macroglobulin increase risk of AD. In this article, we will review about the neurobioloby of AD and some newly developed research areas.
Acetylcholine ; Alzheimer Disease* ; Amyloid ; Amyloid beta-Peptides ; Apolipoproteins E ; Cerebrospinal Fluid ; Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 14 ; Chromosomes, Human, Pair 19 ; Chromosomes, Human, Pair 21 ; Complement System Proteins ; Dopamine ; Down Syndrome ; gamma-Aminobutyric Acid ; Genetics ; Lipoproteins ; Microglia ; Neurobiology* ; Proteolysis ; Serotonin

No abstract available.
Muscular Dystrophy, Duchenne*

In order to investigate the neurotoxic effect of methylmercury (MM) on cultured mouse spinal motoneuron cell line, NSC-19, neurotoxic effect of MM was evaluated by MTT assay after neurons were incubated with various concentrations of methylmercuric chloride (MMC) for 24 hours. In addition, neuroprotective effect of vitamin E against MMC-induced neurotoxicity was examined by MTT assay and neurofilament enzymeimmunoassay (EIA) in these cultures. The results were as follows : 1. MTT50 value was a concentration of 20µM methylmercuric chloride. 2. Methylmercuric chloride was toxic on cultured spinal motor neurons, NSC-19 cells in a time-and dose-dependent manner by severe decrease of cell viability. 3. Methylmercuric chloride induced the decrease of cell number and the loss of neuritis on these cultures. 4. Vitamin E remarkably increased the viabilily of cultured neurons damaged by methylmercury-induced neurotoxicity at a concentration of 250µM vitamin E. From above the results, it is suggested that methylmercury induces severe toxic effect on cultured mouse spinal motor neurons, NSC-19 cells, and the selective antioxidants such as vitamin E are effective in the neurotoxicity induced by methylmercury in these cultures.
Animals ; Antioxidants ; Cell Count ; Cell Culture Techniques ; Cell Line ; Cell Survival ; Intermediate Filaments ; Mice ; Motor Neurons* ; Neuritis ; Neurons ; Neuroprotective Agents ; Vitamin E* ; Vitamins*

To evaluate the effect of midkine (MK), neurotrophic factor on cultured mouse spinal motor neuron, NSC-19 which was inhibited by glucose oxidase (GO)-induced oxygen radicals, MTT assay and neurofilament enzymeimmunoassay were carried out after NSC-19 cells were preincubated with various concentrations of midkine for 2 hours prior to exposure of glucose oxidase. The results were as follows : 1. MK increased the rate of cell viability and neurofilamental development in a dose-dependent manner on motoneurons inhibited by glucose oxidase-induced oxygen radicals. 2. MTT50 value was 25 mU/ml GO. 3. GO-induced oxygen radicals were toxic on cultured motor neurons in a time and dose-dependent manner. 4. GO-induced oxygen radicals induced the decrease of cells in number and the loss of neurites in cultured mouse spinal motor neurons. From above the results, it is concluded that oxygen radicals are toxic in cultured mouse spinal motor neurons, and selective neurotrophic factors such as MK enhance the viability of motor neurons inhibited by oxygen radicals.
Animals ; Cell Survival ; Glucose ; Glucose Oxidase ; Intermediate Filaments ; Mice ; Motor Neurons* ; Nerve Growth Factor ; Nerve Growth Factors ; Neurites ; Oxidative Stress* ; Reactive Oxygen Species

No abstract available.
Aged* ; Humans

BACKGROUND AND OBJECTIVES: Neointimal ingrowth rather than stent recoil is thought to be important for coronary in-stent restenosis. However only limited pathologic data are available to adress the mechanisms of in-stent restenosis. With the specific aim of measuring cell replication and of assessing cellularity and extracellular matrix (ECM) composition, we analyzed atherectomized coronary arterial in-stent restenotic specimens. METHODS AND RESULTS: In the present study, we analyzed 29 atherectomized coronary arterial in-stent restenotic tissue samples (14 LAD, 10 RCA, and 5 LCX) retrieved from 25 patients (m/f:18/7: age 59+/-13 yr) at 0.5-23 (mean 5.7) months after deployment of Palmaz-Schatz stent. Histopathological analysis of cellular components and ECM was performed using H & E, modified Movat pentachrome, and immunocytochemical staining. Cellular proliferation rate, as estimated by use of antibodies to Ki-67 nuclear antigen showed low proliferation rate with the range of 0-4%, and no positive cells were found in 62% of cases. Myxoid tissue having ECM enriched with versican and hyaluronan was found in 69% of cases, and decreased over time after stenting. Foci of cell poor area were found in 57% of cases, and could be classified into as: (1) containing collagen-rich ECM and (2) containing a proteoglycan-rich ECM. Versican, biglycan, perlecan, and hyaluronan were identified with varying individual distributions in the proteoglycan rich area. Specimens with foci of cell poor area tended to increase over time after stenting (31% in & 4 mo vs. 81% in > or =4 mo after stenting, p<0.01). alpha-smooth muscle actin staining identified the majority of cells as smooth muscle cells (SMC) and occasional macrophages (< or =12 cells per section) were detected by CD68 antibody. CONCLUSIONS: These data suggest that enhanced ECM accumulation rather than cell proliferation may be important mechanisms for stent restenosis. Angioplasty of stent restenosis may therefore fail due to transient compression of this hygroscopic matrix.
Actins ; Angioplasty ; Antibodies ; Biglycan ; Cell Proliferation ; Extracellular Matrix ; Humans* ; Hyaluronic Acid ; Macrophages ; Myocytes, Smooth Muscle ; Proteoglycans ; Stents* ; Versicans