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Biomedical subjects

U Ito

Publications and source records attributed to U Ito.

At least 19 recordsLinked to original sources
PubMed1999

Isolated recurrence of granulocytic sarcoma of the brain: successful treatment with surgical resection, intrathecal injection, irradiation and prophylactic systemic chemotherapy.

We describe a 40-year-old male who developed an isolated recurrence of granulocytic sarcoma (GS) of the brain 2 years following successful treatment of acute myeloblastic leukemia (AML; M2). Computed tomography (CT) scans and magnetic resonance (MR) images demonstrated a homogeneously enhanced tumor mass in the left temporal lobe and massive peritumoral edema. There was no evidence of relapse in the bone marrow. The patient underwent an emergency surgical resection of the tumor. Five courses of injection with cytarabine and prednisolone through an Ommaya reservoir and whole brain irradiation (total 40 Gy) were performed. Furthermore, prophylactic systemic chemotherapy with cytarabine and etoposide was added. He has been in complete remission for 21 months. Our results, together with other reported cases, indicate that a favorable outcome could be obtained by intensive and combined treatment for an isolated recurrence of GS of the brain if the bone marrow remained in complete remission.

Adult↗
PubMed1998

A clinical, genetic, neuropathological study in a Japanese family with SCA 6 and a review of Japanese autopsy cases of autosomal dominant cortical cerebellar atrophy.

This report concerns a Japanese family with genetically confirmed SCA 6, including an autopsy case, and a review of Japanese autopsy cases of autosomal dominant cortical cerebellar atrophy (ADCCA). The proband (Case 1) was a Japanese woman. She developed gait disturbance at age 62. The father and younger sister (Case 2) had the same disorder. She died at age 67 due to subarachnoid hemorrhage. Neuropathological examination revealed severe loss of Purkinje cells in the cerebellum, prominently in the dorsal vermis, and absence of neuronal loss in the inferior olives. Molecular genetic study showed the CAG-repeat expansion of SCA 6 gene. The younger sister (Case 2) developed gait disturbance at age 62. Neurological examination at age 66 revealed cerebellar signs without sensory disturbance. Neuroimaging at this time showed cerebellar atrophy, prominently in the vermis. She died of multiple myeloma at age 66. A neuropathological review of Japanese autopsy cases of ADCCA showed that there are two patterns in the distribution of cerebellar cortical lesions of Japanese patients with ADCCA. The distribution of cerebellar cortical lesions in genetically confirmed Japanese patients with SCA 6 is more prominent in the vermis than in the hemisphere.

Aged↗
PubMed1998

Expression of c-jun, hsp72 and gfap following repeated unilateral common carotid artery occlusion in gerbils-correlates of delayed ischemic injury.

The relationship between gene responses and cumulative ischemic damage, as induced by two 10 min episodes of unilateral common carotid artery (CCA) occlusion separated by 5 h, was examined by in situ hybridization histochemistry and terminal transferase biotinylated-dUTP nick end labeling (TUNEL) in the gerbil brain. Intense cell death was noticed starting from 5 h after the second ischemic insult, reaching maximum levels in the nucleus caudate-putamen and thalamus at 12-24 h, but in the cortex and hippocampus at 2 days post-ischemia. Although tissue damage developed gradually, the region of progressive infarction could be delineated as an area deficient in gfap mRNA starting from 12 h, more apparent 24 h after repeated ischemic insults. Hsp72 mRNA was strongly increased in the cortex, caudate-putamen, ventrolateral thalamus, CA1-CA4 fields and dentate gyrus in the early stages, i.e., 15 min-5 h post-ischemia. C-jun mRNA was also elevated in these structures except for the CA1 field, where mRNA levels remained low. In the caudate-putamen and thalamus, where DNA fragmentation occurred rapidly, c-jun and hsp72 mRNAs declined to almost basal levels within 12 h after repeated ischemia, whereas in the other structures, c-jun and hsp72 mRNAs decreased in a more delayed fashion by 24-48 h. The close association between the c-jun and hsp72 mRNA decline and the onset of injury may reflect a more general disruption of the transcription process probably as the consequence of secondary metabolic deterioration. The dissociation between c-jun and hsp72 mRNA expression in the CA1 field may indicate severe ischemic injury, surpassing the range of tissue salvage.

Animals↗
PubMed1997

Topographical analysis of cortical neuronal loss associated with disseminated selective neuronal necrosis and infarction after repeated ischemia.

A study was carried out of the distribution and density of the neurons remaining in the gerbil cerebral cortex following two 10-min periods of ischemia at either 3-, 5- or 48-h intervals. As the interval between the periods of ischemia increased, the ischemic injury was reduced from severe to milder infarction, and further from more to less intense disseminated selective neuronal necrosis. This model is suitable for studying the mechanisms of transition from selective neuronal necrosis to infarction at the threshold level of infarction.

Animals↗
PubMed1997

Ultrastructure of astrocytes associated with selective neuronal death of cerebral cortex after repeated ischemia.

Astrocytic swelling after ischemic insult has been considered a sign of parturbed cell viability. Investigations using cultured astrocytes and C6 glioma cells have revealed that viable astrocytes swell, spatially buffering various metabolites which are increased by the metabolic turmoil following ischemic insults. In the present study, we have studied the temporal profile of ultrastructural changes of astrocytes in the cerebral cortex associated with progressive selective neuronal, death where infarction is not induced. We occluded the left carotid artery of the Mongolian gerbil twice for 10 minutes at a 5 hr interval. In this model, following reperfusion, selective neuronal death progresses in the coronal section cut at the infundibular level. The whole brains of the sham operated control and postischemic animals were fixed by transcardiac perfusion of glutaraldehyde fixatives, at 15 min, 5 and 12 hr after the 2nd 10 min ischemia. Ultrathin sections including the 3rd and 5th cortical layers were prepared from the cut surface at the level of infundibulum. Mild swelling of astrocytic processes and perivascular end-feet was observed in the 15 min group. Glycogen granules were not prominent. In the 5 hr group, we found a few necrotic neurons disseminated in the cortex. All astrocytic cell processes were swollen with increased number of glycogen granules, especially marked in the perivascular end-feet. In the 12 hr group, necrotic neurons increased in number, astrocytic swelling was more extensive, and glycogen granules were evident in astrocytes. No cellular destruction was observed. We conclude: 1. Swelling progresses in astrocytes which however still remain viable and this process is associated with selective progression of neuronal death. 2. Glycogen granules increase in the swollen yet viable astrocytic cell processes.

Animals↗
PubMed1997

Brain edema associated with progressive selective neuronal death or impending infarction in the cerebral cortex.

This study examined the temporal profile of brain edema in the cerebral cortex associated with selective neuronal death or focal infarction after repeated ischemia at an intensity of ischemic insult just under and above the threshold level to induce infarction. The left carotid artery of adult gerbils was twice occluded for 10 min each time with a 5-hr interval between the blockages. In this model, focal infarction developed in coronal sections examined at the chiasmatic level (face A), whereas only selective neuronal death without infarction was found in the coronal section observed at the infundibular level (face B). In each animal, Evans blue (2%) was intravenously injected 1 hr prior to sacrifice as an indicator of blood-brain barrier (BBB) disruption. Brain edema was assessed by gravimetry in samples taken from both faces at 15 min, 5 hr, 12 hr, 24 hr, and 48 hr after the 2nd 10-min ischemia. Evans blue extravasated only in face A, corresponding to focal infarction at 24 and 48 hr after the 2nd 10-min ischemia. The specific gravities of the ischemic cortex of both faces decreased significantly from control at 15 min (P < 0.05) and had recovered by 5 hr after ischemia. By 12 hr, the specific gravities of both faces had again decreased significantly from the control values (P < 0.05), but did not differ significantly from each other. At 24 and 48 hr, the specific gravities of both faces were significantly lower than the control values (P < 0.01), and the specific gravity of face A was markedly lower than that of face B (P < 0.01). We concluded that in face B, where only selective neuronal death without infarction occurred only cytotoxic edema develops, whereas in face A, where infarction progresses, vasogenic edema develops in addition to cytotoxic edema.

Animals↗
PubMed1997

Hemispheric cerebral atrophy after traumatic extra-axial hematoma in adults.

The relationship between traumatic extra-axial hematomas and cerebral atrophy was investigated in 42 adult patients aged between 15 and 50 years who required removal of extra-axial hematomas. These patients were followed up by serial computed tomography for more than 6 months after head injury. Nine of these patients developed cerebral atrophy. Their Glasgow Coma Scale score on admission was 6.4 +/- 2.8 (mean +/- SD). The score of the patients without cerebral atrophy was 9.6 +/- 3.3 (p < 0.01). These patients had three extradural and six subdural hematomas. All patients with cerebral atrophy had cerebral swelling postoperatively, more prominent in the hemisphere ipsilateral to the hematoma in seven patients. This swelling was associated with global hypodensity and persisted for 10.4 +/- 2.9 days. The severity of cerebral atrophy was more prominent in the hemisphere ipsilateral to the hematoma in five of these seven patients. Extra-axial hematoma in patients with severe head injury can induce hemispheric cerebral atrophy in the underlying cerebral hemisphere.

Adolescent↗
PubMed1996

Correlation between cerebral blood flow values obtained by Xenon/CT and Kety-Schmidt (N2O) methods.

The means of the cerebral blood flow (CBF) values obtained by the stable xenon enhanced CT (Xe/CT) method using two different CT scanners were compared with global CBF value obtained by the Kety-Schmidt (N2O) method as a reference. Xe/CT CBF values were obtained using a GE CT9200 (31 patients, 2 flow maps, 120 kV, absorption constant of 0.040) as well as a GE ProSeed Accell (38 patients, 4 flow maps, 80 kV, absorption constant of 0.028). The protocol of inhalation in the Xe/XT method consisted of 4 min wash-in and 4-min wash-out of 35% stable xenon. In the Kety-Schmidt method, 15% N2O gas was inhaled for 10 min. The N2O content of blood samples was measured using a van Slyke-Neill blood gas analyzer. We corrected all obtained CBF values for a PaCO2 of 34 mmHG (CBF34). The global CBF34 values obtained by the Kety-Schmidt method were linearly correlated with the CBF34 values obtained using the CT9200 and with those obtained using the ProSeed Accell, and the regression line equations were, respectively, Y = 0.64X + 13.7 (X: CT9200, Y: Kety-Schmidt, r = 0.666, p < 0.01) and Y = 0.99X + 11.2 (X: ProSeed Accell, Y: Kety Schmidt, r = 0.756, p < 0.01). Since the CBF values obtained by the Xe/CT method using different CT scanners are not always the same as the global CBF values obtained by the Kety-Schmidt method, CBF values obtained by the Xe/CT method should be corrected referring to the regression line obtained by applying both methods for each patient.

Adult↗
PubMed1995

Transition from ischemic neuronal necrosis to infarction in repeated ischemia.

To study morphological changes in the cortex that follow repeated ischemia, one, two, and three 7-min unilateral occlusions of the carotid artery at 6-h intervals, and three, four, and five 7-min similar occlusions at 12-h intervals were produced in gerbils. Animals with one and two 7-min occlusions at 6-h intervals showed selective neuronal necrosis in the cortex; those with three 7-min occlusions at 6-h intervals showed focal infarction in the third layer of the cortex. Animals with three 7-min occlusions at 12-h intervals showed selective neuronal necrosis; those with four 7-min occlusions at 12-h intervals showed focal infarction in the third layer. In animals with five 7-min occlusions at 12 h intervals, infarction affecting all layers of the cortex was seen. Results of the present study indicate that cortical infarction occurred when a brief ischemic insult that does not cause any visible morphological damage in cortical neurons was inflicted repeatedly, and that development of infarction in the cortex following repeated episodes of ischemia depended on both the number of insults and the time intervals between them. This finding suggests that there is a threshold of infarction in repeated ischemia. In our model, various stages of ischemic brain injury could be achieved more easily than in transient ischemia by altering the number of insults or the intervals between them. This model is suitable for studying the pathophysiology on transition from ischemic neuronal necrosis to infarction.

Animals↗
PubMed1995

Long-term high-colloid oncotic therapy for ischemic brain edema in gerbils.

BACKGROUND AND PURPOSE: We evaluated the effects of long-term administration of high-colloid oncotic pressure on ischemic brain edema in Mongolian gerbils. METHODS: Animals that exhibited stroke after 35 minutes of unilateral forebrain ischemia were used. The gerbils were divided into albumin- (1 g/kg body wt, 25% albumin; n = 30) and saline-injected (4 mL/kg; n = 30) groups. Both agents were administered intravenously every 12 hours starting immediately after the recirculation. Plasma colloid oncotic pressure, serum sodium and potassium concentrations, and brain water, sodium, and potassium content were measured 24, 48, and 72 hours after recirculation. RESULTS: Plasma colloid oncotic pressure at 24, 48, and 72 hours after recirculation was significantly higher in the albumin- (26.1 +/- 2.3 mm Hg) than in the saline-treated group (18.5 +/- 1.9 mm Hg; P < .01), and brain water content of the ischemic hemisphere was significantly lower in the albumin group (79.5%, 80.2%, and 80.5%, respectively) than in the saline group (80.9%, 81.6%, and 82.1%, respectively; P < .05) at all three time points. Brain sodium content at 24 hours was significantly lower in the albumin than in the saline group (P < .05), while brain potassium content at 24 and 48 hours was significantly higher in the albumin than in the saline group (P < .05). The changes in brain water and sodium plus potassium content, which were calculated from differences between the ischemic and nonischemic hemispheres, showed a significant correlation in both groups (P < .01), but there was no significant difference between the linear regression lines for both groups. CONCLUSIONS: Long-term high-colloid oncotic pressure was effective in treating ischemic brain edema, probably acting by diminishing the bulk flow through the disrupted blood-brain barrier and ameliorating the vasogenic edema.

Albumins↗
PubMed1994

High colloid oncotic therapy for contusional brain edema.

We investigated whether prolonged high colloid oncotic therapy for two weeks can suppress contusional brain edema. Eighteen patients with cerebral contusion were randomly divided into two groups of patients receiving high oncotic pressure (HOP; 26-30 mmHg) treatment and those receiving normal oncotic pressure (NOP; 22-26 mmHg) treatment. Oncotic pressure was maintained for two weeks with administration of a 25% albumin solution with additional use of furosemide. Edema volume was calculated by summation of all measured low-density areas in each CT slice multiplied by 1.0 cm of slice of thickness. We expressed contusional brain edema volume as a percent increase based on each patient's initial CT. The mean percent increase of contusional brain edema in the NOP group was significantly higher than that in the HOP group at 9-15 days (208.9% and 14.0%, respectively) and 16-25 days (188.8% and 10.0%, respectively). There were no complications such as heart failure or renal failure during treatment. All the patients in the HOP group recovered with minimal or no neurological deficit. On the other hand, 30% of patients in the NOP group remained in poor condition. With frequent measurement of oncotic pressure and adjustment of fluids and electrolytes, continuous oncotic therapy for two weeks effectively and safely reduced contusional brain edema.

Adolescent↗
PubMed1994

Chronological changes in brain edema induced by experimental intracerebral hematoma in cats.

To investigate the temporary profile of changing perifocal brain edema around an intracerebral hematoma (ICH), we developed an experimental ICH model using cats. The developing perifocal edema in the white matter around the hematoma was measured by means of a gravimetric technique. Edema was more severe near the ICH, and declined with increasing distance. Edema was mild 2 hours after the onset of the ICH, and was most severe in all the regions examined 3 days later. Edema decreased but still existed in all regions 7 days after the onset of the ICH. The results suggest that the mechanism of the development of edema associated with ICH seems to differ from that associated with a cold injury. This experimental ICH model proved to be useful for the study of formation, expansion, and resolution of edema associated with ICH.

Animals↗
PubMed1994

High colloid oncotic therapy for brain edema with cerebral hemorrhage.

We examined the effectiveness of high colloid oncotic pressure (COP) therapy to suppress and/or reduce brain edema associated with putaminal hemorrhage of patients whose clinical grades were grade 3 or 4a classified according to the Japanese neurological grading for putaminal hemorrhage. In the treated group of 11 patients, 25% albumin solution was intravenously administered (50-100 ml/day) with additional use of furosemide (20-40 mg/day) following hematoma removal. The serum COP was maintained at 25-30 mmHg for 2 weeks. In the untreated group of 11 patients, the COP therapy was not applied following hematoma removal. The serum COP was 20-25 mmHg for 2 weeks thereafter. During the 2-week observation period, serum osmolality, electrolyte, and hematocrit levels did not significantly differ between the two groups. The midline structure shift on CT of the treated group was 4.5 mm, which was significantly smaller than that of the untreated group (p < 0.05). The numbers of patients either in the vegetative state or death were 0 and 3, respectively, in the treated and the untreated groups. We concluded that high COP therapy for 2 weeks following hematoma removal was effective to suppress and/or reduce brain edema associated with putaminal hemorrhage, and that this therapy could be continued for 2 weeks without systemic complications.

Adult↗
PubMed1994

Effect of acetazolamide on early ischemic cerebral edema in gerbils.

Acetazolamide was given in the early stage of ischemic cerebral edema produced by unilateral permanent carotid occlusion in gerbils. The animals were studied 1, 4, and 6 hours after ischemia. The tissues were examined for water and electrolyte concentrations and ischemic areas were visualized by 2,3,5-triphenyltetrazolium chloride (TTC) and H-E staining. Acetazolamide injected just after occlusion showed a positive effect in reducing edematous changes. Later administration of the drug had neither positive nor harmful effect on the ischemic brains. Thus, acetazolamide seems to be useful for cerebrovascular response studies in the early stage of a brain lesion.

Acetazolamide↗
PubMed1994

Peritumoral edema in meningioma: a contrast enhanced CT study.

The propagation of extravasated contrast medium around 6 supratentorial meningiomas with peritumoral white matter of low density (PWL) of Lanksch II-III was investigated by repeated CT scanning at 4 h intervals, following a 1 h drip infusion of 200 ml of Iopamidol. The volume of the expanding peritumoral contrast enhancement was calculated according to a method previously described. By calculating the increase in volume from the first to the second scan, and from the second to third, we derived the rate of edema formation as well as the resolution rate of edema in the PWL. The surface area of the entire tumor (TS) and area of tumor surface facing the PWL (LS) were calculated by summating the surface areas of all CT slices, each area of which was derived from the measured length of the entire circumference of the tumor and circumference of the tumor facing the PWL, respectively, multiplied by the slice thickness of 0.5 cm. The volume of PWL, edema formation rate of entire tumor, and tumor volume x LS/TS were well correlated with each other. We concluded that the severity of peritumoral edema in meningiomas depends on the size of the tumor and the extent of tumor surface contact with the PWL.

Aged↗
PubMed1994

Atrophy and maldevelopment of the ipsilateral cerebral hemisphere after acute subdural hematoma in infants.

Among nine infants aged less than 4 years with acute subdural hematoma admitted between 1980 and 1991, five required evacuation of a hematoma. Eight of them survived longer than 1 month and the remaining patient who had a hematoma removal died 3 days postoperatively. The four infants who required evacuation of a hematoma and survived longer than 1 month had prolonged hemispheric swelling ipsilateral to the hematoma lasting for 2 weeks postoperatively. Intracranial pressure was higher than 25 mm Hg during this period. Diffuse high density was observed in the affected hemisphere in one patient 12 days after injury, which was assumed to be hemorrhagic infarction. Subsequently, these four infants developed atrophy of the cerebral hemisphere ipsilateral to the hematoma. The pathophysiology of the atrophy of the cerebral hemisphere ipsilateral to the acute subdural hematoma is discussed.

Acute Disease↗