PURPOSE: The effects of pain on brain is not well known. Also, differences between somatic and visceral pains have not been fully elucidated. This study was conducted to investigate changes in the expression of c-Fos protein after somatic and visceral pains were induced by formalin. METHODS: Male rats(n=65) were underwent one of three procedures : (i) Control group, rats were left undisturbed in their cages; (ii) Somatic pain group, rats were injected subcutaneously with 0.1 ml of 10% formalin in the plantar surface of right hindpaw; (iii) Visceral pain group, rats were administered with same amount of formalin, as described above, in the rectum. Rats were sacrificed at increasing times(30 minutes, 1 hour, 2 hours, 6 hours, 1 day, 3 days and 7 days) after noxious formalin stimuli to hindpaws and rectums. Rat brains were removed and sliced in rat brain matrix. Brain slices were coronal sectioned at interaural 5.70-6.70mm. Serial sections were immunohistochemically reacted with polyclonal c-Fos antibody. The numbers of c-Fos protein immunoreactive neurons in cingulate cortex, primary somatosensory area, and hippocampus were examined and analyzed statistically with Mann-Whitney U test. RESULTS: 1) The numbers of c-For protein immunoreactive neurons in cingulate cortex, primary somatosensory area and hippocampus peaked at 2 hours after somatic pain stimuli and reached almost normal conditions at 7 days. 2) The numbers of c-Fos protein immunoreactive neurons in cingulate cortex, primary somatosensory area and hippocampus peaked at 1 day after visceral pain stimuli and reached almost normal conditions at 7 days. 3) The numbers of c-Fos protein immunoreactive neurons of somatic pain groups were higher than that of visceral groups at all times and the difference of numbers peaked at 2 hours after pain stimuli. CONCLUSION: Reactions of somatic pain stimuli influenced more changable than visceral pain stimuli to brain. Conduction velocities of somatic pain were more faster than those of visceral pain. Higher numbers of c-Fos protein immunoreactive neurons were found in specific regions. These results provide some basic knowledge in understanding the mechanism and control of pain.
Animals ; Brain* ; Formaldehyde* ; Gyrus Cinguli ; Hippocampus ; Humans ; Male ; Neurons* ; Nociceptive Pain ; Rats* ; Rectum ; Visceral Pain

No abstract available.
Subcutaneous Tissue*

No abstract available.
Acceleration* ; Lasers, Semiconductor* ; Wound Healing* ; Wounds and Injuries*

No abstract available.
Empyema* ; Gastroenteritis* ; Salmonella* ; Urinary Bladder*

No abstract available.
Endometriosis* ; Female

No abstract available.
Drainage* ; Prognosis*

PURPOSE: Traumatic brain injury is a multifaceted injury that involves direct mechanical damage, intraparenchymal and subarachnoid hemorrhage, breakdown of the blood-brain barrier, excitotoxicity, and ischemia. Even though much investigations were performed, acceptable mechanical informations were rare. The aim of this study was to reveal the expression pattern of intermediate filament proteins associated with gliotic scars in cerebral cortex of rats after cryoinjury. METHODS: A total of 18 male Sprague-Dawley rats weighing 300 g, 2 months old, were used throughout the experiments. To injure the brain, rats were anesthetized for surgery with 3.5% chloral hydrate(1 mL/100 g, intraperitoneally); the frontal bones were exposed by elevating the skin; and craniectomies were performed adjacent to the central suture, midway between lambda and bregma. A cryoinjury was then created by applying a cold probe(3-mm-diameter steel rod chilled in liquid nitrogen) to the left frontal cortex(ipsilateral cortex) for 1 min. Rats were sacrificed at 1, 4, 7 and 14 days postsurgery(n=3, per time point), and three rats were sacrificed as normal controls. Serial brain cryosections were made by cryostat. For immunohistochemistry, brain tissue sections were allowed to react with mouse anti-rat GFAP antibody(1:200), mouse anti-rat vimentin antibody(1: 200), and mouse anti-rat nestin antibody(1:200). RESULTS:Reactive astrocytes expressing GFAP, vimentin and nestin appeared for the first time at 6 hours after cryoinjury. Proliferation of GFAP and nestin positive cells started at 1 day after cryoinjury, reached its maximum on day 4, and returned to normal level after the 7th post-injured day. Proliferation of vimentin positive cells started at 1 day after cryoinjury, reached its maximum on day 4, and returned to normal level after the 14th post-injured day. Characteristic morphological changes in reactive astrocytes were seen at 4 days after cryoinjury. CONCLUSION: The above results suggest that GFAP, vimentin and nestin positive cells attend in the formation of gliotic scars.
Animals ; Astrocytes ; Blood-Brain Barrier ; Brain ; Brain Injuries ; Cerebral Cortex ; Chloral Hydrate ; Cicatrix ; Cold Temperature ; Frontal Bone ; Humans ; Immunohistochemistry ; Intermediate Filament Proteins ; Intermediate Filaments ; Ischemia ; Male ; Mice ; Nerve Tissue Proteins ; Rats ; Rats, Sprague-Dawley ; Steel ; Subarachnoid Hemorrhage ; Sutures ; Vimentin

Zonisamide was administered to 20 patients with refractory epileptic seizures. The mean duration of the administration was 6 months, and the mean dosage was 7.2 mg/kg/day. The efficacy of zonisamide was rated remarkable in 15% of the cases, improvement in 40%, and no change in 45%. The response rates of zonisamide were 62.5% for myoclonic seizures, 50% for tonic-clonic seizures, 80% for atonic seizures and 33.3% for atypical absence seizures. There was no correlation between the clinical response and dose or serum concentration of the drug. The adverse effects were observed in 35% of the cases which were drowsiness, dizziness, ataxia, nausea, and vomiting. In all cases, however, the administration of zonisamide could be continued.
Ataxia ; Child* ; Dizziness ; Epilepsy* ; Epilepsy, Absence ; Humans ; Nausea ; Seizures ; Sleep Stages ; Vomiting

No abstract available.
Female ; Humans ; Pregnancy ; Pregnancy, Tubal*

No abstract available.
Female ; Humans ; Pregnancy ; Pregnancy, Tubal*