PURPOSE: To evaluate neurotoxic effects induced by oxygen-radicals, which were generated by adding xanthine oxidase(XO) and hypoxanthine(HX), and protective effects of glutamate receptor antagonist such as MK-801 and 6-cyano-7-nitroquinoxaline(CNQX). METHODS: Dissociated cell cultures were prepared from cerebrum of neonatal mouse. Tissues were dissected and diced into small pieces in phosphate buffered saline and were incubated at 37degrees C. Isolated cells were resuspended in Eagle's minimum essential medium and plated poly-L-lysine coated plastic coverslips in 96 well multichambers at a cell density of 3x105 cells/well. Cells were grown in a 5% CO2/95% air atmosphere at 37degrees C. Cytotoxic effects were examined in cerebral cortical neurons cultured for 3 hours in media containing various concentration of XO and HX. The protective effects of glutamate receptor antagonist were also examined by MTT assay and neurofilament enzymeimmunoassay(EIA). Microscopic examinations were also done. RESULTS: Oxygen radicals markedly induced decrement of the cell viability of cultured mouse cerebral cortical neurons in a dose-dependent manner. Midpoint cytotoxicity value was 30mU/ml XO/0.1mM HX, when mouse cerebral cortical neurons were incubated for 3 hours with various concentrations of XO and HX. The number of cells and neurites was decreased when cerebral cortical neurons were cultured for 3 hours in a medium containing 30mU/ml XO/0.1mM HX. MK- 801 was very effective in blocking oxidant-induced neurotoxicity, while CNQX falied to show any protective effect in these cultures. CONCLUSION: It is suggested that oxygen radicals are neurotoxic, and selective N-methyl-D-aspartate antagonists such as MK-801 are very effective in protecting neurotoxicity induced by oxygen radicals in cultured cerebral cortical neurons of neonatal mouse.
6-Cyano-7-nitroquinoxaline-2,3-dione ; Animals ; Anoxia ; Atmosphere ; Cell Count ; Cell Culture Techniques ; Cell Survival ; Cerebrum ; Dizocilpine Maleate ; Excitatory Amino Acid Antagonists* ; Glutamic Acid* ; Ischemia ; Mice* ; N-Methylaspartate ; Neurites ; Neurons* ; Oxidative Stress* ; Plastics ; Reactive Oxygen Species ; Receptors, Glutamate* ; Xanthine

Inflammatory mediators, such as oxidants, TNF-alpha, and IL-6, play a major role in the systemic response to bum injury It has been known that a continuing inflammatory response cause a sepsis and subsequent multiple organ failure. Recent studies have shown that burn patients receiving recombinant human growth hormone(rhGH) therapy have an improvement of the general condition, but the mechanism by which rhGH exerts its effects has not been clearly understood. The aim of this study was to evaluate the effect of rhGH on the early bum injury. Female Sprague-Dawley rats were divided into four groups : control group, bum group, burn plus rhGH treated group, and rhGH only treated group. Animals were killed at 30min., 3, 6, 24, and 48 hours after treatment. Histology and biochemical changes including malondialdehyde(MDA) content, tissue reduced glutathione(GSH) and catalase activity in the lung and liver, and plasma TNF-alpha and IL-6 levels were examined. Lung histology in the bum plus rhGH treated group showed decreased inflammtory response such as neutrophil and lymphocyte infiltrations, interstitial thickening, and edema compared with the bum group. Liver histology in the bum group revealed mild neutrophil and lymphocyte infiltrations, vacuolization .of hepatocytes, disrupted lobular structures, and dilated sinusoids. But liver histology of the bum plus rhGH was similar to control group. Lung and liver MDA in the burn plus rhGH and rhGH only treated groups were decreased with time compared with the burn group. Lung and liver GSH and catalase activities in the bum plus rhGH and GH only treated groups remained significantly increased compared with the bum group for the 48-hours period. Plasma TNF-alpha levels in the bum group remained elevated for the 48-hours period compared with the bum plus rhGH and rhGH only treated groups. Plasma IL-6 levels in the burn group were significantly increased only at first compared with the bum plus rhGH and rhGH only treated groups. These results suggested that rhGH showed inhibitory effects on the inflammatory cell infiltration and lipid peroxidation in the lung and liver after bum injury. Increased GSH levels and catalase activities seemed to be associated with the antioxidant effect of rhGH. But the inhibitory effect of rhGH on plasma TNF- and R-6 levels was not clearly demonstrated.
Animals ; Antioxidants ; Burns ; Catalase ; Edema ; Female ; Hepatocytes ; Human Growth Hormone* ; Humans* ; Interleukin-6* ; Lipid Peroxidation* ; Liver ; Lung ; Lymphocytes ; Multiple Organ Failure ; Neutrophils ; Oxidants ; Plasma* ; Rats* ; Rats, Sprague-Dawley ; Sepsis ; Tumor Necrosis Factor-alpha*

PURPOSE: In order to elucidate the neurotoxic mechanism of oxygen radicals which are pathological factor of ischemia, we evaluated the oxidant-induced neurotoxicity and the neuroprotective effect of antioxidant on cultured cerebral neurons derived from neonatal mouse. METHODS: Neurotoxic effect was investigated after cultured mouse neuronal cells were exposed to oxygen radicals which were generated enzymatically by reaction of xanthine oxidase (XO) and hypoxanthine (HX). And also the neuroprotective effect of antioxidant was assessed with catalase. Both effects determined by cell viability were assessesd by MTT assay and neurofilament enzymeimmuno assay (EIA). In order to see the histologic change microscopic exam also done on the cerebral neuronal cells. RESULTS: 1) Oxygen radicals were toxic on cultured mouse cerebral neurons in dose- and time-dependent manner. 2) The value of lethal concentration50 (LC50) of oxygen radicals was estimated at a concentration of 25mU/ml xanthine oxidase (XO) and 0.2mM hypoxanthine (HX) in these culture. 3) Catalase was effective in blocking the neurotoxicity induced by oxygen radicals at a concentration of 50ug/ml. 4) Oxygen radicals induced the decrease of cell number and the loss of neurites in cultured mouse cerebral neurons. CONCLUSION: It is suggest that oxygen radicals cause the neurotoxicity and the selective antioxidants such as catalase are very effective in blocking oxidant-mediated neurotoxicity on cultured cerebral neurons of neonatal mouse.
Animals ; Antioxidants ; Catalase ; Cell Count ; Cell Survival ; Hypoxanthine ; Ischemia ; Mice* ; Neurites ; Neurons* ; Neuroprotective Agents ; Oxygen* ; Reactive Oxygen Species* ; Xanthine Oxidase

PURPOSE: The purpose of this study was to assess chemotherapy induced peripheral neuropathy (CIPN) and to examine the relationship between CIPN and depression. METHODS: A purposive sample of 105 patients treated with chemotherapy were recruited in the cross-sectional survey design. Data were collected using self-report questionnaires. The instruments used were the Chemotherapy Induced Peripheral Neuropathy Assessment Tool (CIPNAT) and Hospital Anxiety Depression Scale (HADS). RESULTS: The most frequent suffering symptom of CIPN was 'tingling feeling in the hand and foot'. Of the motor symptoms, 'muscle weakness' was the most frequent symptom and 'muscle or joint aches' was the strongest suffering symptom of CIPN. The mean score for suffering of CIPN was 4.1. The mean score was 1.04 for depression and the prevalence was 48.5%. CIPN was significantly positively correlated with depression (r=.38, p<.001). The result of simple regression analysis revealed that CIPN was predictive of depression (R2=.136, p<.001). CONCLUSION: Based on the findings of this study, nursing intervention programs focusing on CIPN management and alleviating depression are recommended.
Anxiety ; Cross-Sectional Studies ; Depression* ; Drug Therapy ; Hand ; Humans ; Joints ; Nursing ; Peripheral Nervous System Diseases* ; Prevalence

Core decompression is still widely used in avascular necrosis of the femoral head but the results are unpredictable and the indications are not settled yet. The reparative process of the decompressed femoral head is poorly understood. Seven cases in 5 patients were undertaken THRA following failed decompression and these were studied for the radiological and pathological changes of the core tracts. The lesions of failed cases were involved more than 1/3 of femoral head on MRI and all cases were stage II A or B. The extent of the necrotic area in MRI was enlarged with crack, sclerosis and sometimes gas collection. Depression of the subchondral plates were also observed. Capillary ingrowth or neovascularization was not found at all and there were only fibrosis, inflammatory response and foreign body reactions.
Capillaries ; Decompression* ; Depression ; Fibrosis ; Foreign Bodies ; Head* ; Humans ; Magnetic Resonance Imaging ; Necrosis* ; Sclerosis

No abstract available.
Hemodynamics* ; Nitroprusside*

Most proximal humeral fractures respond satisfactorily to conservative treatment. It is only the occasional displaced fracture or fracture-dislocation that demaads special treatment. The purpose of this study is to analysis the results of closed and open reduction of displaced proximal humeral fractures according to Neers classification. Fifty-two cases of these fractures, followed up more than five months, are presented. 1. The average age of patients was 40. I years. 2. The fractures were classified according to Neers method. Nearly half (48.1%) of the cases were one-part fractures. Next, two-part fractures rated 42.3%, while three-part fractures, only one (l.9%). 3. Among the total 52 patients, 42 cases(80.8%) were treated conservatively and 10 were operated. We performed surgical operations in seven cases among 22 two-part fractures, aix were reduced with Kirschner wires and one treated with Kirschner wire and staple. The average age of these seven cases was 26. 6 years and the resulta were good except one. 4. The results of these patients were evaluated by the Neers criteria. Of 52 caaes, 40 had good results, five, fair, and the remaining seven poor results. Twenty-three cases (92%) in 25(100%) one-part fractures were good and 17 cases (77.3%) in 22 (100%) two-part fractures were also good. In three-part and four-part fractures the results were all poor.
Bone Wires ; Classification ; Humans ; Methods ; Shoulder Fractures

Tailgut cysts in retrorectal or presacral space are rare and the derivatives of the embryonic post-anal gut. It is thought to arise from vestiges of embryonic hindgut. The lesions were usually multicystic and lined by a variety of epithelial types, including ciliated columnar, mucin-secreting columnar, transitional, and squamous epithelium. Tailgut cyst has been found in men and women of various ages but is more common in women and is usually associated with middle age. They may be the source of the chronic perirectal symptoms and rarely undergo malignant change, so early diagnosis and accurate evaluation is important. Complete surgical resection should be considered because of a long term risk of malignant change. We report two cases of tailgut cyst.
Early Diagnosis ; Epithelium ; Female ; Humans ; Male ; Middle Aged

Intra-epidermal epithelioma is a rare cutaneous neoplasm and generally used as a histologic description for superficial tumors in which nests are found in well-defined islands within the epidermis. The intra-epidermal nests are composed of keratinocytes, and basaloid or squamoid or pleomorphic cells. Some authors reported that this tumor may be considered an invasion of the epidermis from a malignant tumor and it has the potential of carcinomatous invasion. Herein, we report a case of intra-epidermal epithelioma that showed clonal seborrheic keratosis and intra-epidermal eccrine poroma differentiation on the right thigh areaof a 77-year-old female. Although intra-epidermal epithelioma shows benign features, it may be predisposed to other tumoral changes, such as eccrine poroma, eccrine porocarcinoma, and Bowen's disease. We suggest that individuals with intra-epidermal epithelioma require continuous monitoring of skin changes, including enlargement of size, inflammation, ulceration, and hemorrhages.
Aged ; Bowen's Disease ; Carcinoma ; Eccrine Porocarcinoma ; Epidermis ; Female ; Hemorrhage ; Humans ; Inflammation ; Islands ; Keratinocytes ; Keratosis, Seborrheic ; Poroma ; Skin ; Thigh ; Ulcer

PURPOSE: In order to evaluate the hypoxia-ischemia induced neurotoxic effect and the protective effect of vitamin E as an antioxidant, cell number and cell viability were measured in cerebral neurons and astrocytes derived in neonatal rats. METHODS: 7-day old neonatal rats were subjected to unilateral common carotid artery occlusion, and exposed to hypoxic condition for 3 hours. The protective effect of vitamin E, as an antioxidant was examined by XTT [2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-(phenylami-nocarbonyl) 12H-tetrazolium hydroxide] assay and cell number on 14 days after hypoxia-ischemia when the rats received an intraperitoneal injection of vitamin E immediately following hypoxia-ischemia. RESULTS: Hypoxic-ischemic condition positively decreased the cell number and cell viability of rat cerebral neurons in a time-dependent manner when rats were killed 72 hours after hypoxia- ischemia. 72 hours after hypoxia-ischemia, the cell number and viability of astrocytes were slightly decreased, compared with the saline treated group. In rats treated with vitamin E, the cell number and cell viability of neurons were significantly increased compared with those of the saline- or non-treated group. In hypoxic-ischemic treated rats after 14 days from hypoxia- ischemia, astrocytes were significantly proliferated, but vitamin E showed the protective effect on hypoxic-ischemia induced cell proliferation and cell viability. CONCLUSION: It is suggested that hypoxic-ischemic condition is more toxic in neurons than astrocytes, and selective antioxidants such as vitamin E, especially when it was administered within two hours after hypoxia-ischemia, is highly effective in preventing the cell death of neurons and astrocytes from hypoxia-ischemic condition in neonatal rats.
Animals ; Antioxidants ; Astrocytes ; Carotid Artery, Common ; Cell Count ; Cell Death ; Cell Proliferation ; Cell Survival ; Hypoxia-Ischemia, Brain* ; Injections, Intraperitoneal ; Ischemia ; Neurons ; Rats* ; Vitamin E* ; Vitamins*