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Biomedical subjects

Y Iwata

Publications and source records attributed to Y Iwata.

348 records · Page 20Linked to original sources

Kindled amygdaloid seizures in rats cause immediate and transient increase in protein kinase C activity followed by transient suppression of the activity.

Protein kinase C (PKC) activity in hippocampus and amygdala was measured during kindled seizures and 30 min, 3, 24, and 48 h, and 2 weeks after seizures in amygdaloid-kindled rats. Sham-operated rats not subjected to kindling were used as controls. During kindled seizures, membrane-bound PKC activity in bilateral hippocampi was significantly increased, with a slight reduction in cytosolic PKC activity, but there was no change in either membrane-bound or cytosolic PKC activity in bilateral amygdala. Thirty minutes after seizures, PKC activity in both fractions was significantly increased in bilateral hippocampi and amygdala. Three hours after seizures, PKC activity in both fractions was markedly decreased in bilateral hippocampi. In bilateral amygdala, a similar and significant decrease in membrane-bound PKC activity was noted, with no marked change in the cytosolic fraction. Twenty-four hours after seizures, a significant decrease in membrane-bound PKC activity in bilateral hippocampi and amygdala was again noted, although cytosolic PKC activity was unchanged. Forty-eight hours after the seizures, PKC activity in both fractions had returned to control levels. Two weeks after the last seizure, there was no significant change in PKC activity in either fraction in any region, except for a slight increase in membrane-bound PKC activity in unilateral hippocampus contralateral to the kindled amygdala. These results suggest that kindled amygdaloid seizures cause an immediate and transient increase in PKC activity in limbic structures, followed by suppression of enzyme activity, and that PKC in hippocampus responds to kindled seizures more readily and preferentially than it does in amygdala.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗

Distinct expression of CCR1 and CCR5 in glomerular and interstitial lesions of human glomerular diseases.

We investigated the presence of CCR1- and CCR5-positive cells immunohistochemically in the kidneys of 38 patients with several renal diseases, including 13 crescentic glomerulonephritis patients. In addition, we determined cell phenotypes of CCR1- and CCR5-positive cells using a dual immunostaining technique. Urinary levels of their ligands, for CCR1 and CCR5; macrophage inflammatory protein (MIP)-1alpha, MIP-1beta and regulated upon activation in normal T cells expressed and secreted (RANTES) were evaluated by enzyme-linked immunosorbent assay. CCR1- and CCR5-positive cells were detected in both glomeruli and interstitium of the diseased kidneys. Using a dual immunostaining technique, these positive cells were CD68-positive macrophages (MPhi) and CD3-positive T cells. The number of CCR1-positive cells in glomeruli was correlated with urinary levels of MIP-1alpha. The number of CCR1-positive cells in the interstitium was correlated with both urinary MIP-1alpha and RANTES levels. CCR1-positive cells in the interstitium remained after glucocorticoid therapy, most of which were MPhi, and were correlated with the intensity of interstitial fibrosis and tubular atrophy. Glomerular CCR5-positive cells were well correlated with extracapillary lesions and urinary MIP-1alpha levels, while interstitial CCR5-positive cells, mainly CD3-positive T cells, were correlated with interstitial lesions and urinary RANTES levels. Renal CCR5-positive cells were dramatically decreased during convalescence induced by glucocorticoids. These results suggest that chemokine receptor signaling may be pivotal for human renal diseases through the recruitment and activation of MPhi and T cells; CCR5-positive cells may participate in glomerular lesions including extracapillary lesions via MIP-1alpha and in interstitial lesions via RANTES. CCR1 may be involved in interstitial lesions in resolving phase after glucocorticoid therapy.

Adolescent↗

Ultrasonic evaluation of superficial temporal artery-middle cerebral artery anastomosis.

Ultrasonic Doppler studies were made pre- and postoperatively in 22 patients undergoing STA-MCA anastomosis. A quantitative evaluation of the bypass was attempted by determining the STA blood flow velocity and pattern. The STA velocity on the Doppler sonogram was compared with the degree of intracranial vascular filling via anastomotic channels and the STA diameter on angiogram. The STA velocity was increased and the blood flow pattern of STA altered from an external carotid pattern to an internal carotid pattern in a patent bypass. The results were in good agreement with angiographic findings. The are of intracranial vascular filling via a vewly formed bypass on angiogram was proportional to the increase in STA velocity. As the STA diameter enlarged, the STA velocity increased progressively. It is suggested the Doppler flowmetry is reliable as a semi-quantitative means of evaluationg the STA-MCA anastomosis.

Adult↗

Bilateral occlusions in the cervical portion of the internal carotid arteries in a child.

An 8-year-old boy with a history of recurrent tonsillitis and cervical lymphadenopathy developed acute hemiplegia. Cerebral angiography revealed bilateral occlusions of the cervical portion of the internal carotid arteries. Cerebral arterial occlusion in childhood has been attributed to many causes, e.g., trauma and infections of the neck. In the present case, though not clearly proved, inflammatory processes may have been related to the occlusion.

Arterial Occlusive Diseases↗

Circulating endothelial cells fail to induce cerebral infarction in rabbits.

Exfoliated cells that appear to be circulating endothelial cells were detected in human blood. Because the size of endothelial cells is larger than that of other circulating blood cells, we investigated whether the increased number of circulating endothelial cells might be responsible for cerebral embolism. We compared rabbits into which suspensions of endothelial cells were injected through the common carotid arteries with control rabbits into which blood clots or arachidonic acid were administered in the same manner. Injected endothelial cells failed to cause cerebral embolism. Because the majority of exfoliated circulating endothelial cells were degenerated and deformed, the suspensions of endothelial cells obtained from rabbit aortas were treated by ultrasonic waves. These suspensions also failed to cause cerebral embolism. We conclude that cerebral embolism cannot be induced by an increase of circulating endothelial cells alone.

Animals↗

Left midcardiac border of frontal chest radiographs of patients with annulo-aortic ectasia.

The utility of the frontal chest radiograph for the diagnosis of annulo-aortic ectasia (AAE) was evaluated in 12 patients with Marfan's syndrome and five patients with incomplete stigmata (forme fruste). Prominence of the left midcardiac border was seen in 11 patients: the upper midsegment in one, the lower midsegment in two, and the whole midsegment in eight patients. Either a linear or an arcuate contour was seen. The contours of the prominent left midcardiac border in three patients who had moderate to marked aortic regurgitation and a cardiothoracic ratio (CTR) over 59% were nonspecific. In the remaining eight patients (47%), the contour was considered to be characteristic of AAE, as suggested by the displacement of either all or part of the right ventricular outflow tract, main pulmonary artery and left atrial appendage. Six patients showed only left midcardiac border prominence. The contour of the left midcardiac border on the conventional frontal chest radiograph is characteristic and of paramount importance for the diagnosis of AAE in Marfan' s syndrome or its forme fruste, particularly in patients whose CTRs are within the normal range.

Adolescent↗