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Biomedical subjects

K Yanaka

Publications and source records attributed to K Yanaka.

At least 55 records · Page 3Linked to original sources
PubMed1998

Basal perforating artery aneurysm within the cavum septi pellucidi. Case report.

The authors describe the case of a 16-year-old boy presenting with clinical onset of subarachnoid hemorrhage. The patient was found to have a small aneurysm arising from the distal portion of a basal perforating branch of the anterior cerebral artery (ACA), lying within a cavum septi pellucidi. Neuroimaging demonstrated a hematoma within the cavum septi pellucidi and the aneurysm was resected via a transcallosal approach guided by an intraoperative portable digital subtraction angiography (DSA) system. The origin of the aneurysm was presumed to be idiopathic. This report is the first to describe an aneurysm of a basal perforating artery arising from the ACA that resulted in an intracaval hematoma. When approaching small vascular lesions during surgery, intraoperative DSA is the method of choice to identify the precise trajectory and distance to the lesions.

Adolescent↗
PubMed1997

Laminin peptide ameliorates brain injury by inhibiting leukocyte accumulation in a rat model of transient focal cerebral ischemia.

Postischemic cerebral inflammation has been reported to contribute to ischemic brain damage. During inflammation, constituents of the extracellular matrix such as fibronectin and laminin are recognized by certain integrins or proteoglycans and play an important role in the cell adhesion process. The purpose of this study was to evaluate the efficacy of peptides derived from laminin on leukocyte accumulation, infarct size, and neurological outcome in rats subjected to 1 h of cerebral ischemia and 48 h of reperfusion. Forty-four animals were included in this study: transient ischemia without treatment (Group I), treatment with TG-1 peptide (Group II), GD-1 peptide (Group III), and GD-6 peptide (Group IV). Group II showed a significant reduction of the leukocyte accumulation (p < 0.001) and infarct size (p = 0.015) when compared with Group I. The neurological grade of Group II was also significantly better than in Group I at 48 h after reperfusion (p = 0.012). Based on these data, which are the first to explore the therapeutic potential of this peptide in cerebral ischemia, laminin peptide may offer a novel therapeutic approach to allaying injury in ischemic stroke.

Amino Acid Sequence↗
PubMed1997

Antagonism of leukocyte adherence by synthetic fibronectin peptide V in a rat model of transient focal cerebral ischemia.

OBJECTIVE: Activated polymorphonuclear leukocytes (PMNs) seem to be directly involved in potentiating ischemic brain injury. Recent work in our laboratory demonstrated that synthetic fibronectin peptides significantly inhibit PMN accumulation in ischemic tissue, reduce the size of infarction, and reduce neurological dysfunction after transient focal cerebral ischemia in rats. The purpose of this study was to examine any dose-related effects (Experiment 1) and the optimal timing of the administration (Experiment 2) of synthetic fibronectin peptide V (FN-C/H-V) to further substantiate the role of the peptide in ameliorating cerebral ischemic damage. METHODS: Fifty-six animals were included in the study. We evaluated the efficacy of FN-C/H-V on PMN accumulation in ischemic tissue, infarct size, and neurological outcomes in rats subjected to 1 hour of cerebral ischemia and 48 hours of reperfusion. RESULTS: In Experiment 1, the animals receiving FN-C/H-V at a dose of 10 to 15 mg/kg of body weight per injection showed significant reduction of PMN accumulation, reduction of infarct size, and improvement of neurological outcomes at 48 hours after reperfusion compared to untreated animals (P < 0.05). In Experiment 2, the animals receiving FN-C/H-V within 3 hours after reperfusion also showed significantly better results than untreated animals (P < 0.05). Despite the treatment delay, the administration of FN-C/H-V inhibited PMN accumulation after reperfusion but did not reduce the size of infarction when administered 6 hours after reperfusion. CONCLUSION: These data suggest that relatively late postischemic administration of FN-C/H-V is effective in brain protection after ischemia/reperfusion.

Animals↗
PubMed1996

Neuronal protection from cerebral ischemia by synthetic fibronectin peptides to leukocyte adhesion molecules.

Leukocytes play an important role in the development of ischemia/reperfusion injury. Recent work in our laboratory has demonstrated that a mixture of synthetic fibronectin peptides to leukocyte adhesion molecules reduces ischemic brain damage after transient focal cerebral ischemia. The purpose of this study was to evaluate the efficacy of the individual peptides on leukocyte accumulation, infarct size, and neurological outcome in rats subjected to 1 h of cerebral ischemia and 48 h of reperfusion. Thirty-five animals were divided into five groups: transient ischemia without treatment (Group I), treatment with arginyl-glycyl-aspartic acid (RGD) peptide (Group II), connecting segment (CS)-1 peptide (Group III), fibronectin (FN)-C/H-V peptide (Group IV), and scrambled FN-C/H-V peptide (Group V). Groups III and IV showed a significant decrease in the degree of leukocyte infiltration in the lesion and in the infarct size (p < 0.05) when compared to Groups I, II, and V. The neurological grade of Groups III and IV was significantly better than in Groups I, II, and V at 48 h after reperfusion (p < 0.01). Thus, in addition to demonstrating the potential efficacy of synthetic peptides as therapeutic agents for ischemia-reperfusion, these results also offer new insights into the mechanisms of leukocyte arrest and recruitment in ischemia/reperfusion injury.

Animals↗
PubMed1996

Optimal timing of hemodilution for brain protection in a canine model of focal cerebral ischemia.

BACKGROUND AND PURPOSE: Hemodilution is known to ameliorate the effects of focal ischemia when used shortly after cerebral arterial occlusion; however, it remains to be proved whether hemodilution will be effective when used at more clinically relevant times, ie, with some delay between the onset of ischemia and initiation of therapy. METHODS: Thirty-two dogs were selected for inclusion in this study. Cerebral infarction was induced by permanent occlusion of the middle cerebral and the azygos anterior cerebral arteries. The animals were allocated to 1 of 4 groups of eight animals each: arterial occlusion without hemodilution (group 1); hemodilution immediately after occlusion (group 2); hemodilution 3 hours after occlusion (group 3); and hemodilution 6 hours after occlusion (group 4). Isovolemic hemodilution to a hematocrit of 30% was performed. The animals were killed 6 days after induction of ischemia, and the infarct size was determined. RESULTS: Groups 2 and 3 showed significant reduction of infarct size (P < .0001) when compared with group 1. The neurological grade of group 3 on postoperative days 4, 5, and 6 was significantly better than those of groups 1 and 4 (P < .01). Group 4 showed a significant increase in the incidence of hemorrhagic infarction when compared with groups 1 and 2 (P < .01). CONCLUSIONS: The current study indicates that hemodilution administered as much as 3 hours after ischemia is effective in reducing infarct size and improving neurological status. When administered 6 hours after ischemia, hemodilution is not helpful and may be harmful.

Animals↗
PubMed1996

Low grade astrocytoma in the medial part of the frontal lobe manifesting as paroxysmal speech disturbance--case report.

A right-handed 48-year-old female had clustered groups of seizures characterized by speech disturbance (attacks of verbal repetition and speech arrest) over a period of 7 years. Later, speech arrest was accompanied by perioral focal seizures. Magnetic resonance imaging and surgery found a low grade astrocytoma, centered in the left supplementary motor area. Postoperatively, no seizures or speech disturbances occurred for 3 years. This case confirms the main function of the supplementary motor area of the dominant hemisphere is connected with the initiation of speech and the setting into motion of the mechanism of speech.

Astrocytoma↗
PubMed1996

Synthetic fibronectin peptides and ischemic brain injury after transient middle cerebral artery occlusion in rats.

Leukocytes play an important role in the development of ischemia-reperfusion injury. This study was conducted to ascertain whether synthetic peptides corresponding to the cell- and heparin-binding sequences of fibronectin that disturb leukocyte adhesion molecules were effective in neuronal protection after transient focal cerebral ischemia in rats. The authors evaluated the efficacy of peptides on infarction size, leukocyte infiltration in the ischemic tissue, and neurological outcome in rats subjected to 1 hour of cerebral ischemia and 48 hours of reperfusion. Twenty-one animals were divided into three groups: transient ischemia without treatment (Group I), transient ischemia with administration of vehicle (Group II), and transient ischemia with administration of fibronectin peptides (Group III). The mean myeloperoxidase activity (U/g wet wt) in the ischemic area was as follows: Group I, 0.19% +/- 0.05; Group II, 0.21% +/- 0.03; and Group III, 0.08% +/- 0.02. The mean size of the infarction as a percentage of the total hemispheric volume was as follows: Group I, 38.35% +/- 1.34%; Group II, 39.21% +/- 2.42%; and Group III, 25.81% +/- 4.87%. Group III showed a significant decrease in myeloperoxidase activity in the lesion and the infarction size was smaller when compared to Groups I and II (p < 0.05). The neurological grade in Group III was significantly better than in Groups I and II at 48 hours after reperfusion (p < 0.01). This study is the first to explore the therapeutic potential of synthetic fibronectin peptides in brain protection after transient focal ischemia, and the results also serve as a basis for studies of important cellular and molecular events that contribute to tissue damage.

Animals↗
PubMed1996

Reduction of brain injury using heparin to inhibit leukocyte accumulation in a rat model of transient focal cerebral ischemia. I. Protective mechanism.

Heparin has long been established as an anticoagulant. Although heparin has been demonstrated to reduce brain injury after ischemia and reperfusion, its mechanism of action remains unknown. Recent investigations reveal that it can modulate biological processes such as binding to adhesion receptors on endothelial cells and leukocytes. The authors hypothesized that heparin's protective effect is closely related to its antileukocyte adherence property. They evaluated the efficacy of sulfated polysaccharides (unfractionated heparin, low-molecular-weight heparin, heparan sulfate, chondroitin sulfate C, and dextran sulfate) on leukocyte accumulation, infarction size, and neurological outcome after transient focal cerebral ischemia in rats subjected to 1 hour of ischemia and 48 hours of reperfusion. Forty-nine animals were included in the study. The animals receiving unfractionated heparin or dextran sulfate showed a significant reduction in leukocyte accumulation, infarct size, and neurological dysfunction 48 hours after reperfusion (p < 0.05) when compared to untreated animals. The animals receiving unfractionated heparin also showed significantly better results than the animals receiving an equivalent anticoagulant dose of low-molecular-weight heparin. These data indicate that heparin's antileukocyte property plays a more important role than its anticoagulant ability in neuronal protection. The relative potency of the sulfated polysaccharides tested in leukocyte depletion was closely related to their degree of sulfation. Thus, in addition to demonstrating the potential efficacy of heparin as a therapeutic agent for ischemia and reperfusion injury by the prevention of leukocyte accumulation, the results also serve as a basis for studying important cellular and molecular events that contribute to tissue damage.

Animals↗
PubMed1996

Reduction of brain injury using heparin to inhibit leukocyte accumulation in a rat model of transient focal cerebral ischemia. II. Dose-response effect and the therapeutic window.

The administration of massive doses of heparin has been demonstrated to reduce reperfusion injury. The authors have found that heparin's antileukocyte adhesion property may play a more important role than its anticoagulant property in preventing ischemia and reperfusion injury. Although the administration of massive doses of heparin has been demonstrated to reduce brain injury after ischemia and reperfusion, the optimum dosage and timing for heparin administration remain unknown. The purpose of this study was to evaluate the dose-response effect and determine the time during which heparin must be administered to inhibit leukocyte accumulation, reduce infarct size, and improve neurological outcome in rats subjected to 1 hour of cerebral ischemia and 48 hours of reperfusion. Forty-nine animals were included in the study. The animals receiving commercial unfractionated heparin at a total dose of 2.67 to 4 mg/kg showed a significant inhibition of leukocyte accumulation, reduced infarct size, and lessened neurological dysfunction 48 hours after reperfusion (p < 0.05) when compared to untreated animals. The animals receiving unfractionated heparin within 3 hours after reperfusion also showed significantly better results than untreated animals. These data indicate that standard doses of heparin prevent reperfusion injury, and relatively late postischemic administration of heparin also is effective in brain protection. These findings may have therapeutic potential as an adjunct to thrombolytic therapy and possibly for other perfusion deficiencies with leukocyte-endothelial interaction. In view of these encouraging experimental findings, the clinical application of heparin administration after ischemia and reperfusion warrants serious consideration.

Animals↗
PubMed1995

Recovery from primary deep cerebral venous sinus thrombosis with recanalisation.

A 50-year-old woman with idiopathic deep cerebral sinus and vein thrombosis (DCVT) had cerebellar disturbance prior to impaired consciousness. CT and MRI revealed haemorrhagic infarction in the cerebellum and signal changes suggesting infarction in the thalamus and basal ganglia bilaterally. The straight sinus and internal cerebral vein (ICV) were dense on CT. On angiography, the vein of Galen (VG) and straight sinus were not seen. Following clinical recovery, CT and MRI became normal, and angiography showed recanalization of the VG and ICV. The relationship between cerebellar infarction and DCVT, and signal changes on CT and MRI are discussed.

Basal Ganglia↗
PubMed1995

Clinical application of diffusion-weighted magnetic resonance imaging to intracranial disorders.

Diffusion-weighted magnetic resonance imaging was performed to determine the changes in water diffusion and to investigate the detectability of diffusion anisotropy in patients with intracranial disorders. Diffusion maps of the apparent diffusion coefficient (ADC) were created of 19 patients with cerebral infarction, five with intracerebral hematoma, four with glioma, four with meningioma, four with hydrocephalus, and five with subdural hematoma. ADC was increased in chronic cerebral infarction and glioma, and decreased in acute cerebral infarction, meningioma, and the marginal area of glioma compared with the ADC of the normal gray matter. There was a significant difference in ADC between the marginal and internal areas of glioma. Increased ADC may be due to increased vasogenic edema in infarction and a lack of significant restriction of diffusion within glioma. Decreased ADC can be attributed to restricted diffusion caused by cytotoxic edema in infarction and the underlying histological pattern of densely packed tumor cells in glioma. Diffusion anisotropy of the internal capsule was less detectable in pathological than normal hemispheres. Diffusion anisotropy was less detectable in patients with hydrocephalus and subdural hematoma. Intracranial lesions were thought to have influenced the compression of the brain structures and cells, resulting in decreased diffusion. The measurement of ADC by diffusion-weighted magnetic resonance imaging has the potential for greater understanding of the biophysical changes in various intracranial disorders, including correct diagnosis of cerebral infraction, and histological diagnosis of brain tumor.

Adolescent↗
PubMed1994

Concurrent subarachnoid hemorrhage due to ruptured aneurysm and hypertensive intracerebral hemorrhage--case report.

A 64-year-old female presented with hypertensive thalamic hemorrhage concurrent with subarachnoid hemorrhage (SAH) due to a ruptured aneurysm manifesting as sudden onset of right hemiparesis followed by severe headache. The aneurysm was located in the basilar artery at the origin of the superior cerebellar artery, remote from the thalamic hematoma. The aneurysm was clipped 3 weeks after SAH. She was discharged with slight right hemiparesis. The method and timing of surgery for such patients depend on hematoma size, location of the aneurysm and hematoma, and neurological status. The intracerebral hemorrhage remote from the ruptured aneurysm should be treated initially if necessary, and the aneurysm clipped after the brain swelling has reduced.

Aneurysm, Ruptured↗
PubMed1993

Gadolinium-enhanced magnetic resonance angiography in the planning of supratentorial glioma surgery.

The utility of gadolinium (Gd)-enhanced magnetic resonance (MR) angiography in the planning of supratentorial glioma surgery was evaluated. MR angiograms of the arterial and venous anatomy visualized the anatomical relationship of the main arteries to the tumor, especially on three-dimensional images. Combination with data from surface anatomical images allowed the tumor location to be determined preoperatively. Gd-enhanced MR angiography can be used non-invasively prior to tumor surgery to ascertain the spatial relationship of the vessels to the tumor mass.

Adult↗
PubMed1993

Acute subdural hematoma--prediction of outcome with a linear discriminant function.

We devised a linear discriminant function to predict the outcome for patients with acute subdural hematoma (ASDH) based on a consecutive series of 170 ASDH cases with mild to severe head injury [Glasgow Coma Scale (GCS) 3-15]. Functional recovery was achieved in 50.0% of patients and the mortality was 36.5%. The relationship between initial clinical and radiological signs and the outcome 3 months after admission was studied retrospectively by Mann-Whitney's U-test and Pearson's chi-squared test. Fourteen factors (GCS, pupillary response, motor paresis, age, hematoma volume and thickness, midline shift, association with cerebral contusion and subarachnoid hemorrhage, obliteration of the basal, ambient, or quadrigeminal cistern on computed tomography, fibrin-fibrinogen degradation product level, and intracranial pressure) were found to correlate significantly (p < 0.01) with outcome. Linear discriminant functions were formulated by multivariate analysis to investigate the relationship between these factors and recovery or poor prognosis. The following formula was obtained: Z = -0.110 + 0.013 (Age) - 0.108 (GCS) + 0.397 (Eye) + 0.003 (Shift) + 0.268 (Ambient). Functional recovery could be predicted by a negative Z value, with an accuracy of 90.59%. This simple discriminant function is useful for predicting the outcome of ASDH.

Adult↗
PubMed1993

Basal ganglia germinoma with crossed cerebellar diaschisis--case report.

An 8-year-old boy presented with a germinoma of the right basal ganglia manifesting as gradual onset of mild left hemiparesis. Computed tomography (CT) and magnetic resonance imaging disclosed a mass lesion in the right basal ganglia with mild right cerebral hemiatrophy. Single photon emission CT revealed decreased cerebral blood flow in both the right cerebral and left cerebellar hemispheres, or crossed cerebellar diaschisis. The histology of a specimen from a stereotactic needle biopsy was compatible with two-cell pattern germinoma. After irradiation and chemotherapy, the mass lesion disappeared completely. The clinical symptoms and crossed cerebellar diaschisis gradually improved.

Basal Ganglia Diseases↗