No abstract available.
Kidney* ; Nephrectomy*

Spinal intramedullary cysticercosis is a rare manifestation of neurocysticercosis and may present as a isolated lesion. We report a case of cervical intramedullary cysticercosis in a 57-year-old man. The patient presented with weakness, numbness of the right upper extremity, and urinary difficulty. Magnetic resonance images demonstrated a round cystic lesion at the C4-5 level. We performed C4-5 laminectomy with total removal of intramedullary cystic lesion. Diagnosis was confirmed by histopathological examination. The patient was given albendazole(15mg/kg/day for 30 days) along with corticosteroid.
Albendazole ; Cysticercosis* ; Diagnosis ; Humans ; Hypesthesia ; Laminectomy ; Middle Aged ; Neurocysticercosis ; Spinal Cord ; Upper Extremity

No abstract available.
6-Cyano-7-nitroquinoxaline-2,3-dione* ; Cycloheximide* ; Dizocilpine Maleate*

No abstract available.
Adrenalectomy*

BACKGROUND: Although an oxidants and antioxidants imbalane has been considered in the pathogenesis of chronic obstructive pulmonary disease (COPD), there is a paucity of reports focussing on the smoking-induced changes of oxidants and antioxidants in COPD. METHOD: The concentration of antioxidants (ascorbic acid, uric acid, retinol, and α- &γ-tocopherol) was measured in the serum and induced sputum of 30 healthy controls and 34 stable COPD patients using high performance liquid chromatography (HPLC). The inhibition of lipid peroxidation as an index of antioxidant capacity was measured in the serum by a TBA assay. RESULTS: The serum concentration of ascorbic acid, α-tocopherol, and retinol were significantly lower in the patients with COPD than in healthy controls (484.8±473.3 vs 1497.8±819.2 pmol/L, p<0.001, 48.38±17.34 vs 73.96±26.29 pmol/L, p<0.001, and 9.51±8.33 vs 15.01±5.88 pmol/L, p<0.05, respectively, mean±SD). However, there were little differences in the ascorbic acid and uric acid concentrations in the induced sputum between the COPD patients and the controls. The induced sputum to serum ratio of ascorbic acid was significantly higher in COPD patients compared with healthy control (0.375 vs 0.085, p<0.05). In the normal controls, the serum ascorbic acid concentration was lower in smokers than in nonsmokers (1073±536 vs 1757±845 pmol/L, p<0.05), but the level was still higher than that of the COPD patients (p<0.05). The serum retinol levels were correlated with FEV1 in COPD patients (r=0.58, p<0.05). The products of lipid peroxidation were increased in normal smokers and COPD compared with normal nonsmokers (115.56±19.93 and 120.02±24.56 vs 91.87±20.71 µmol/µmol Pi of liposome, p<0.05). CONCLUSION: Cigarette smoking may induce the depletion of serum antioxidants and this depletion of antioxidants is suggested to play a role in the pathogenesis of COPD.
Antioxidants* ; Ascorbic Acid ; Chromatography, Liquid ; Humans ; Lipid Peroxidation ; Liposomes ; Oxidants ; Pulmonary Disease, Chronic Obstructive* ; Smoking ; Sputum* ; Uric Acid ; Vitamin A

No abstract available.
Anoxia* ; Neurons*

No abstract available.
Emergencies* ; Hematoma, Subdural, Acute* ; Trephining*

No abstract available.
Conus Snail* ; Hemangioblastoma*

No abstract available.
Conus Snail* ; Hemangioblastoma*

The object of this study was to investigate the influences of hypoglycemia and hypothermia on the direct current(DC) pontetial changes during cortical spreading depression(CSD) in rats. The induction of CSD was achieved by the application of KCI solution on the cortex of the frontal lobe. Hypoglycemia and hypothermia were induced respectively by insulin injection and the application of an ice pack. The DC potential changes during progressive hypoglycemia and hypothermia were measured with microelectrodes from the cortex of the parietal lobe of rats. Under contril condition, the rate of CSD was one per 5-10 min and the negative shift of DC potential was about 30 mV. The recovery time from negative shift to base line of DC potential was about 40 sec. In rats treated with insulin, the amplitude of DC potential shift was unaffected by hypoglycemia. The recovery time of DC shift was 40+/-2.26 sec at normoglycemia and it was delayed progressively as the blood glucose level lowered. The mean of it was 63+/-8.02 sec at 30 mg/dl and 77.1+/-22.0 sec with the blood glucose falling below 20 mg/dl. The same delay in the recovery time as seen in the hypogylcemia group was observed in rats treated with hypothermia. The recovery time of DC shift was 39.4+/-3.02 sec in normothermia(36.5degrees C), but it was delayed to 61.15+/-4.15 sec at 30degrees C and 96.67+/-14.92 sec at 26degrees C body temperature. This study suggested that each condition of profound hypoglycemia below 30 mg/dl and hypothermia below 30degrees C was to be harmful to the ion homeostasis and the integrity of the cell membrane and it may lead neurons to death.
Animals ; Blood Glucose ; Body Temperature ; Cell Membrane ; Cortical Spreading Depression* ; Frontal Lobe ; Homeostasis ; Hypoglycemia* ; Hypothermia* ; Ice ; Insulin ; Microelectrodes ; Neurons ; Parietal Lobe ; Rats*