The in vivo and in vitro humoral and cell-mediated immune responses of lymphocytes of BALB/c mouse exposed to mercury chloride(HgC12) were investigated. In vitro exposure of the splenocytes to mercury chloride produced overt cytotoxicity in 3 hours period. The IC50(the concentration required to inhibit a splenocyte viability by 50%) for mercury chloride was >0.1mM for cytotoxicity. In vivo mercury chloride exposed mice were significantly depressed delayed type hypersensitivity(DTH) response to sheep red blood cells(SRBC) in a dose-dependent manner compared with control group. Mercury chloride inhibited the proliferative responses of splenocytes to lipopolysaccharide. pokeweed mitogen, concanavalin A and phytohemagglutinin in a dose-dependent manner. Hemagglutinin response to SRBC in mercury chloride exposed mice was significantly depressed in a dose-dependent manner compared with control group. After 7 weeks of mercury chloride exposure in vivo. mercury chloride induced an increase of nonspecific serum IgG1 and IgE levels in BALB/c mice.
Animals ; Concanavalin A ; Hemagglutinins ; Immunoglobulin E ; Immunoglobulin G ; Lymphocytes ; Mice* ; Phytolacca americana ; Sheep

No abstract available.
Selenium*

Effect of Mercury chloride on the synthesis of NO2- and ATP were observed in EMT-6 cells which were culture with cytokines(IL-1alpha and IFN-gamma) and various concentrations of mercury chloride from 0.05 to 0.08 M. Viability of EMT-6 cells were observed above 90% in almost groups. There were not significant differences in the viability between mercury supplemented groups and control group. It suggests viability of EMT-6 cells were not influenced by these concentrations of mercury chloride. Results of the synthesis of nitrite showed significant time and group effect. There is a significant interaction effect between concentration of mercury chloride and culture time. The effect of various concentration of mercury chloride is not the same for all levels of culture time. There were significant differences in the synthesis of nitrite between mercury chloride supplemented groups and control group, and the synthesis of nitrite in EMT-6 cell by the supplement of mercury chloride was significantly decreased in a dose-dependent manner. Results of the synthesis of ATP showed a significant group effect, and the time main effect and the Group x Time interaction were also significant. There were significant differences in the synthesis of ATP between mercury chloride supplemented groups and control group, and the synthesis of ATP in EMT-6 cell by the supplement of mercury chloride was significantly decreased in a dose-dependent manner. These results suggest that the disorder of cell mediated immunity by mercury chloride could be related to the inhibition of nitric oxide synthesis which will be caused by the decreased synthesis of ATP.
Adenosine Triphosphate* ; Immunity, Cellular ; Nitric Oxide

The effects of several factors on the nitrite synthesis were observed in the culture of EMT-6 cells which are originated from mammary adenocarcinoma of Balb/c mouse. The cells were cultured in Dulbecco's Modified Eagle's Medium containing 10% fetal calf serum. Amounts of nitrite in the culture media after 24 and 36 hours of culture were about 2 fold, and 3-fold of those measured after 12 hours respectively. There were very close associations between the amounts of nitrite measured in the culture media. A significant nitrite synthesis by EMT-6 cells occurred when IL-1 was added to the culture medium with other cytokines as IFN gamma or TNF alpha . One of each cytokines were less effective as an inducer of nitrite than the combinations of cytokines. When mercury chloride or cinnamate was added in the culture medium, the nitrite synthesis was dose-dependently decreased by the concentration of these materials. The viability of EMT-6 cells were kept on 95% or above in 36 hours after beginning of culture without any specific additives except cytokines. While after 48 hours it went down to 85% or less. These viability were decreased by the prolongation of culture time (48 hours or more), the addition of TNF alpha to cytokine mixture, and the higher concentrations of mercury chloride or cinnamate to culture medium. Simultaneous addition of the equimolar dose of selenium completely prevented mercurial compounds-induced inhibitions of nitrite syntheses. But the single addition of selenium neither influenced the viability of cells nor the productions of nitrite. These results suggests that the disorder of cell mediated immunity by mercurial compounds could be related to the inhibition of nitric oxide synthesis and selenium decreased the cytotoxicity of mercurial compounds.
Adenocarcinoma ; Animals ; Culture Media ; Cytokines ; Immunity, Cellular ; Interleukin-1 ; Mice ; Nitric Oxide ; Selenium

The effects of treatment with mercury chloride on the nitrite and nitrate syntheses were observed in peritoneal macrophages from Balb/c mice and EMT-6 cells in vitro. The cells were cultured in Dulbecco's modified Eagle's medium(DMEM) with cytokines. Amounts of nitrite and nitrate in the culture media after 24 and 36 hours of culture were about 2-fold, and 3-fold of those measured after 12 hours respectively. There were very close associations between the amounts of nitrite and nitrate measured in the culture media according to culture time. The survival rate of peritoneal macrophages was significantly decreased by mercury chloride added into the media in dose-dependent manner, however the survivals of EMT-6 cells were not influenced by mercury chloride concentration in media. Nitrite and nitrate syntheses were dose-dependently decreased by mercury chloride added in culture media. ATP synthesis also decreased in EMT-6 cells by mercury chloride. These results reported here suggest that the disorder of cell mediated immunity by mercurials could be related to the inhibition of nitric oxide synthesis which seems to be caused by the inhibition of ATP synthesis.
Adenosine Triphosphate ; Animals ; Culture Media ; Cytokines ; Immunity, Cellular ; Macrophages ; Macrophages, Peritoneal* ; Mice* ; Nitric Oxide* ; Survival Rate

BACKGROUND: Head injury is one of the most common causes of emergency department visits and hospital admission in the pediatric populations, and most injuries are mild. In mild head injury, grading of severity and decision of hospital admission are difficult in the emergency department. Recent studies have suggested that patients with a normal head CT scan and neurologic exam following head injury can be safely discharged from the emergency department. However, previous studies have relied on incomplete patient follow-up and been limited for the most part to adult population. So we performed this study to assess clinical course and the incidence of significant CNS sequelae in children with a normal head CT scan and no focal neurologic sign after mild head injuries during hospital admission and follow-up for 1 month. METHODS: We reviewal the records of children(n=209) admitted to the department of emergency medicine with closed head injuries from Jan. 1, 1996 to Dec. 31, 1996, who's initial Glasgow Coma Scale was 13 to 15, and have no focal neurologic sign and a normal head CT scan. RESULT: 209 patients were studied with a mean age of 6.8(range 3 months to 15years), and 66.5% were male. The most common mechanisms of injury were pedestrian T.A(50.2%) and fall(11.5%). Patients had a mean Glasgow coma scale of 14.8 and mean Abbreviated Injury Score of 1.3. Patients had clinical symptoms of headache(49.3%), vomiting(44.5%), loss of consciousness(LOC)(29.6%), amnesia(10.0%), sleepiness(8.6%), irritability(8.6%), confusion(2.9%) and seizure(1.9%). The mean duration of admission was 4.3 days(range: 6 hours-20 days) and the mean duration of symptom was 36.4 hours. No child developed significant CNS sequelae during hospital admission. However, during hospital admission, aye children(all were preschooler) had psychologic complication ; one child developed post-traumatic stress disorder requiring psychologic treatment for 3 months. Three children developed enuresis and two children developed night terror. During 1 month fallow-up, one child developed a symptomatic hemorrhagic contusion 5 days after the head injury, not requiring neurosurgical treatment. CONCLUSION: Among children with an initial Glasgow Coma Scale of 13 to 15, a normal head CT scan and no focal neurologic sign after mild head injuries, delayed intracranial sequelae are extremely uncommon. So these patient may be discharged home with parental supervision and education for dose observation.
Adult ; Child* ; Contusions ; Craniocerebral Trauma* ; Education ; Emergencies* ; Emergency Medicine* ; Emergency Service, Hospital ; Enuresis ; Follow-Up Studies ; Glasgow Coma Scale ; Head Injuries, Closed ; Head* ; Humans ; Incidence ; Male ; Neurologic Manifestations ; Organization and Administration ; Parents ; Stress Disorders, Post-Traumatic ; Tomography, X-Ray Computed

OBJECTIVES: Apotosis induced by metals and metal-related deleterious conditions has only recently been studied. Although the toxic effects of heavy metal are well described, little is known about the mechanism of apoptosis by heavy metal toxicity. This study is designed to define the induction of apoptosis by which heavy metals exert the cytotoxic effect on human promyelocytic leukemic HL-60 cells. Methods After the incubation with CdC12, Na2SeO3 and HgC12, viability of the cells were measured by MTT assay. DNA fragmentation was analyzed by electrophoresis. For measurement of caspase 1 and 3-like proteases activity, the whole lysates were subjected to the proteolytic cleavage and then measured by using fluorospectrometry. c-JUN N-terminal kinase (JNK) activity was detected by an in vitro kinase assay. Transcriptional activities of activating protein-1 (AP-1) and nuclear factor-kB (NF-kB) were measured by elec trophoresis mobility shift assay (EMSA). RESULTS: Cadmium (l2OuiN/I) and selenium (30,iM) induce the apoptosis of HL-60 cells which is characterized by the ladder pattern of DNA fragmentation. Cadmium and selenium induce the activation of caspase-3 in a time dependent manner. They also increase the phosphotransferase activities of c-JUN N-terminal kinase (JNK) in cadmium and selenium treated HL-60 cells. Furthermore, cadmium and selenium increase the activation of transcriptional factors including AP-i and NF-kB. CONCLUSIONS: These results suggest that cadmium and selenium induce the apoptotic death of HL-60 cells via activation of DEVD-specific caspase, JNK and transcriptional factors such as AP-1 and NF-kB.
Apoptosis* ; Cadmium ; Caspase 1 ; Caspase 3 ; DNA Fragmentation ; Electrophoresis ; Electrophoretic Mobility Shift Assay ; HL-60 Cells* ; Humans ; JNK Mitogen-Activated Protein Kinases ; Metals ; Metals, Heavy* ; NF-kappa B ; Peptide Hydrolases ; Phosphotransferases ; Selenium ; Transcription Factor AP-1

PURPOSE: To describe the abnormal signal intensity seen on MRI of the brain in Wilson disease. MATERIALS AND METHODS: Eight patients (7 male and 1 female, 10 to 33 years of age ) with Wilson disease were studied with a 0.5TMRI system. Patients were divided into symptomatic and asymptomatic groups, and MR imaging was compared withclinical data. RESULTS: In 93 lesions, signal intensity was abnormal ; there was involvement of the pallidus(24lesions, 26%), the midbrain (20, 22%), the pons(14, 15%), the putamen (13, 14%), the thalamus(6, 7%), thepituitary gland (4, 4%), the caudate nuclei (4, 4%), the internal capsule (4, 4%), and the dentate nucleus (4,4%). In the putamen, all lesions but one were bilateral, and there was symmetric distribution. The four patientswith neurologic symptoms had 69 lesions and the remaining four without such symptoms had 24 lesions. OnT2-weighted images, high signal intensity was seen in all lesions but two, and on T1-weighted images, this wasseen in 24 lesions. All lesions of the pituitary gland showed high signal intensity on T1-weighted images.CONCLUSION: Lesions were frequently seen in the globus pallidus, midbrain, pons and putamen, and were more commonin patients with neurologic symptoms.
Brain* ; Cerebellar Nuclei ; Female ; Globus Pallidus ; Hepatolenticular Degeneration* ; Humans ; Internal Capsule ; Magnetic Resonance Imaging* ; Male ; Mesencephalon ; Neurologic Manifestations ; Pituitary Gland ; Pons ; Putamen

PURPOSE: Insulin-like growth factor binding protein 3 (IGFBP-3) binds to IGF and acid labile subunit in blood, that regulates the action of IGF by modulating the interaction of IGF with the IGF receptor. Recent studies have shown that IGFBP-3 levels are decreased in prostate cancer patients. We examined IGFBP-3 profiles in prostate cancer patients and determined the effect of treatment on serum IGFBP-3 level in those patients. MATERIALS AND METHODS: Control groups were composed of age-matched healthy subjects and patients with benign prostatic hyperplasia (BPH). Patients with prostate cancer were divided into localized, locally advanced, metastatic and hormone-refractory. Serum samples were collected and stored at 70oC until use. The IGFBP-3 profile was measured by Western ligand blots. RESULTS: The serum IGFBP-3 level in patients with prostate cancer was significantly lower than healthy subjects or patients with BPH. Following the treatment of prostate cancer, IGFBP-3 was increased compared to that seen in pretreated prostate cancer. In hormone-refractory prostate cancer, IGFBP-3 was decreased again. However, there was no correlation between IGFBP-3 and tumor stage or Gleason score. CONCLUSIONS: These data show that IGFBP-3 levels are decreased in pretreated and hormone-refractory prostate cancer. Our results demonstrate that serum IGFBP-3 may be a useful marker in the detection and management of prostate cancer.
Diagnosis* ; Humans ; Insulin-Like Growth Factor Binding Protein 3* ; Neoplasm Grading ; Prostate* ; Prostatic Hyperplasia ; Prostatic Neoplasms*

PURPOSE: We studied the apoptotic index in prostate cancer tissues and investigated the relationship of apoptosis and clusterin expression. MATERIALS AND METHODS: Forty-two archival prostatectomy specimens of varying grades of prostate cancer and 10 of benign prostatic hyperplasia were subjected to immunohistochemical clusterin staining with anti- clusterin antibody. Staining intensities were classified from 0 to 3. Apoptotic index was calculated with TUNEL positive cells under fluorescence microscope. We performed double staining for clusterin and TUNEL using immunofluorescence technique to determine the relationship between apoptosis and clusterin expression. RESULTS: Immunohistochemistry of clusterin showed a weak intensity in all benign tissues. Clusterin was localized mainly in the epithelial cells. Staining intensity was increased according to Gleason grade of cancer. Apoptotic indices of cancer were 0.86+/-0.8%, 0.76+/-1.0%, 0.39+/-0.4% and 0.14+/-0.09% in grades 2, 3, 4 and 5, respectively. In immunofluorescence localization study, apoptosis was not detected in the cancer cells stained with clusterin. Conversely, clusterin was not expressed in the cells showing apoptosis. CONCLUSIONS: These results more clearly show that clusterin acts as a survival protein protecting from apoptosis in prostate cancer. In addition, our findings revealed that the apoptotic index is lower in high grade prostate cancer. These findings have significant clinical implications for identifying the value of apoptotic index and clusterin expression in prostate cancer. Further study is needed to define the role of clusterin in the development and progression of prostate cancer.
Apoptosis* ; Clusterin* ; Epithelial Cells ; Fluorescence ; Fluorescent Antibody Technique ; Immunohistochemistry ; In Situ Nick-End Labeling ; Prostate* ; Prostatectomy ; Prostatic Hyperplasia ; Prostatic Neoplasms*