No abstract available.
Corpus Callosum*

BACKGROUND: The effect of Video Display Terminals(VDT) Syndrome is well documented. The purpose of this study is to examine the difference in systemic subjective symptoms between long term users of computers with that of the general population and to help plan to avoid the risk of developing Video Display Terminal Syndrome. METHOD: Data was collected for this study between August 1996 and February 1997. Two groups consisting of seventy(70) long term computer users(Exposed Subjects) and fifty nine(59) non users (Non Exposed Subjects), were selected for the survey. Data was gathered from the exposed subjects through their response to the survey questionnaire posted on the internet requiring detailed responses concerning ten systemic subjective symptoms that were experienced as a result of the long term exposure to VDT. Data was gathered from the non exposed subjects through written responses to the questionnaire. RESULTS: Among the more significant difference was the experience of ocular symptoms among the exposed group. The exposed group experienced in descending order eleven items of ocular symptoms. Congestion, strain, decreased visual acuity, ocular pain, and dryness. Among seven items of lifestyle, the exposed group characteristically exercised less(P<0.05) and did more home activity (P<0.05), characteristically lead healthier life than the non exposed group. Participation in exercise differed most among the groups. The exposed group participating in moderate exercise scored 517+/-551.6 compared to the non exposed group which exercised very vigorously(p<0.05). In comparison of subjective symptom and life styles per daily exposure time(over 8,10,16 hours daily) there was significant difference between 8 and 10hour exposers only in the stress item(P<0.05). In the exposure group there were less cardiovascular symptoms(P<0.05) due to more art activity(P<0.05), more cardiovascular symptoms and less sleep activity(P<0.001) and more ocular symptoms(P<0.05) due to higher levels of stress. CONCLUSIONS: By exercising, exposers can decrease the respiratory symptoms, and by seeking methods that enable efficient management of work time, the subjects can benefit from the reduced work time, and by seeking methods so that one receive less stress and can resolve them they can reduce their ocular symptoms, sleep problems, cardiovascular symptoms. And in their spare time, the subjects can be recommended to involve in art activity for each person, through PC indirectly. Designing the development of cyber gallery, museum, literature room, concert can reduce the oecur-rence rate of cardiovascular symptoms.
Computer Terminals ; Estrogens, Conjugated (USP) ; Humans ; Internet ; Life Style* ; Museums ; Visual Acuity ; Surveys and Questionnaires

No abstract available.
Dinoprost* ; Female ; Laparoscopes* ; Pregnancy ; Pregnancy, Tubal*

OBJECTIVE: The present study was designed to identify the acute and chronic immobilization stress-induced polyamine (putrescine) responses and their modulation by administration of melatonin in brain regions (frontal cortex and hippocampus) and gastrointestinal tract regions (GIT, gastric mucosa and duodenal mucosa). METHOD: For immobilization stress (3 or 14 days), rats (250-300 g, male Sprague-Dawley rats) were placed in restrainers once daily, for 3 h. Melatonin (10 mg/kg, i.p.) was administered once daily immediately after stress. Rats were sacrificed 2 h after the final application of stress for the measurement of putrescine levels. RESULTS: The putrescine levels of frontal cortex, hippocampus, gastric mucosa and duodenal mucosa were significantly increased by acute stress (p<0.05, p<0.05, p<0.0005 and p<0.01, respectively). The putrescine levels of frontal cortex and duodenal mucosa were significantly increased by chronic stress (p<0.05, respectively). In chronic stress group, animals showed adaptation tendency. The changes of putrescine level in gastric and duodenal mucosa induced by chronic stress were significantly lower than those by acute stress (p<0.05, respectively). The putrescine responses to acute stress in frontal cortex, hippocampus, gastric mucosa and duodenal mucosa were attenuated by administration of melatonin (p<0.01, p<0.05, p<0.05 and p<0.05, respectively). The putrescine response to chronic stress in frontal cortex was attenuated by melatonin administration (p<0.05, respectively). CONCLUSION: The results suggested that putrescine may play a role in stress response of brain regions (frontal cortex and hippocampus) and GIT regions (gastric and duodenal mucosa). Melatonin can inhibit the stress-induced putrescine responses in the brain and GIT.
Animals ; Brain* ; Gastric Mucosa ; Gastrointestinal Tract* ; Hippocampus ; Humans ; Immobilization* ; Male ; Melatonin* ; Mucous Membrane ; Putrescine ; Rats ; Rats, Sprague-Dawley

No abstract available.
Hepatitis B virus* ; Hepatitis B* ; Hepatitis*

No abstract available.
Hepatitis B virus* ; Hepatitis B* ; Hepatitis*

OBJECTIVE: The present study was designed to identify the stress-induced polyamine (PA) response and its modulation by chronic treatment of lithium in brain (hippocampus) and periphery (liver). METHOD: For immobilization stress, rats (230-250 g, male) were placed in restrainer once daily, for 3h. All biochemical measurements were done 5h after the beginning of immobilization stress application. Stress application was done for 5 days and, after a resting interval of 7 days, rats were subjected to an additional stress. Additional groups were subjected to same stress schedule, but during the 7 day interval, one group received once daily injections of 2.5 mmol/kg lithium chloride subcutaneously, and other received saline. RESULTS: The putrescine (PU) level was increased after each stress episode. After cessation of the intermittent stress period, an additional stress 7 days later led again to an increase in PU level in brain but not in liver. The later increase in PU level was blocked by lithium treatment during the intervening 7 day interval between stressors. CONCLUSION: The results suggest that long-term lithium treatment can inhibit an overreactive PA response in brain. So, maladjustment of a stress induced PA response may be a factor to the affective illness and can be target of lithium.
Animals ; Appointments and Schedules ; Brain* ; Immobilization ; Lithium Chloride ; Lithium* ; Liver ; Putrescine ; Rats

BACKGROUND: We designed this study to examine whether melatonin has a neuroprotective effect against hippocampal neuronal damage following transient global ischemia in a gerbil. Because polyamine is known to participate in the process of ischemic neuronal damage, we examined the influence of melatonin on the polyamine level as well as histology. In particular, we examined the difference between pre- and post-ischemic treatments of melatonin by using the above mentioned parameters. METHODS: Male Mongolian gerbils (60 - 80 g) were used in this study. Transient global ischemia was induced by occlusion of the bilateral common carotid arteries for 3 min with microclips. Melatonin was administered 1 h before or 1 h after occlusion. The animals were dissected 4 days after the occlusion for polyamine measurement by a high performance liquid chromatography (HPLC) and histological evaluation (hematoxylin and eosin staining). A histological examination was performed by a blinded investigator. RESULTS: The hippocampal putrescine (PU) level increased compared to sham-operated animals and the increase of PU was attenuated by melatonin administration (pre- or post-ischemic treatment). Spermidine (SD) and spermine (SM) levels didn't show significant changes after ischemia. Hippocampal neuronal damage in the CA1 region was markedly observed in vehicle-treated animals compared to sham- operated animals. Both pre- and post-ischemic melatonin administration significantly inhibited hippocampal CA1 neuronal damage compared to corresponding vehicle-treated animals (P < 0.01, respectively). CONCLUSIONS: Melatonin attenuates the polyamine response following transient global ischemia and may have putative neuroprotective effects against global ischemia-induced neuronal damage. There is no difference in neuroprotective effects of melatonin between pre- & post-ischemic treatments.
Animals ; Carotid Artery, Common ; Chromatography, Liquid ; Eosine Yellowish-(YS) ; Gerbillinae* ; Humans ; Ischemia* ; Male ; Melatonin* ; Neurons* ; Neuroprotective Agents ; Putrescine ; Research Personnel ; Spermidine ; Spermine

No abstract available.
Reye Syndrome*

This study investigated whether propofol, an intravenous, non-barbiturate anesthetic, could reduce brain damage following global forebrain ischemia. Transient global ischemia was induced in gerbils by occlusion of bilateral carotid arteries for 3 min. Propofol (50 mg/kg) was administered intraperitoneally 30 min before, immediately after, and at 1 h, 2 h, 6 h after occlusion. Thereafter, propofol was administered twice daily for three days. Treated animals were processed in parallel with ischemic animals receiving 10% intralipid as a vehicle or with sham-operated controls. In histologic findings, counts of viable neurons were made in the pyramidal cell layer of the hippocampal CA1 area 4 days after ischemia. The number of viable neurons in the pyramidal cell layer of CA1 area was similar in animals treated with a vehicle or a subanesthetic dose of propofol. In terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) assay, semiquantitative analysis of dark-brown neuronal cells was made in the hippocampal CA1 area. There was no significant difference in the degree of TUNEL staining in the hippocampal CA1 area between vehicle-treated and propofol-treated animals. These results show that subanesthetic dose of propofol does not reduce delayed neuronal cell death following transient global ischemia in Mongolian gerbils.
Animals ; Brain ; Carotid Arteries ; Cell Death ; DNA Nucleotidylexotransferase ; Gerbillinae* ; In Situ Nick-End Labeling ; Ischemia* ; Neurons* ; Propofol* ; Prosencephalon* ; Pyramidal Cells