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Biomedical subjects

H Takahata

Publications and source records attributed to H Takahata.

At least 19 recordsLinked to original sources
PubMed2006

Intracranial aneurysms in children under 1 year of age: a systematic review of the literature.

OBJECTIVE: Intracranial aneurysms are very rare in early childhood. Because the location, morphology as well as the clinical and radiological presentation of these aneurysms seem to be different from those in adults, we performed a systematic review of the literature to discuss the clinical, morphological, and radiological features of intracranial aneurysms in the first year of life. MATERIALS AND METHODS: A computerized search of both Pubmed and EMBASE from before 1966 to 2005 was performed. Included were all articles that dealt with cases in which an intracranial aneurysm was demonstrated in children under 1 year of age. RESULTS: We found 110 articles in which 131 cases of an intracranial aneurysm in children under 1 year were presented. The mean age at diagnosis of the aneurysm was 4.9+/-3.5 months with a male to female ratio of 1.1. There was a hemorrhagic presentation in 73% (n=96). The patients presenting with a hemorrhage were younger (mean 4.3 vs 6.7 months, P<0.001) and tended to have smaller-sized (i.e.<2.5 cm) aneurysms (P=0.07). The aneurysm was defined as traumatic or infectious in 15 and 13 cases, respectively. In 21% (n=27), there was various vascular or congenital co-morbidity. In 76%, the aneurysm was located in the anterior circulation. The prevalence of aneurysms on the middle cerebral artery (MCA) was nearly three times higher than on any other vessel. The mean aneurysm size was 1.8+/-1.4 cm, with 30 giant aneurysms (>2.5 cm). The giant aneurysms were significantly more often located in the posterior circulation (43 vs 16%, P=0.01). The mean period of follow-up was 13.6+/-24.8 months. The Glasgow Outcome Scale (GOS) could be derived in 106 cases: 50% had an excellent outcome (GOS of 5). CONCLUSIONS: The presentation of arterial aneurysms in children under the age of 1 year differs from that in adults with a significantly higher prevalence of giant aneurysms in the posterior circulation. The prevalence of aneurysms on the MCA is nearly three times higher than on any other vessel. The patients presenting with a hemorrhage were younger and tended to have smaller-sized aneurysms. Our study did not confirm the male predominance that has thus far been associated with pediatric aneurysms. The outcome is comparable or slightly better than in adults.

Databases, Factual↗
PubMed2003

On the putative physiological role of allopregnanolone on GABA(A) receptor function.

To obtain definitive evidence for a physiological allosteric modulatory role for endogenous brain ALLO on GABA(A) receptor function, we studied GABA(A) receptor activity under conditions in which the concentration of endogenous brain ALLO was decreased by about 80% for longer than 5 h following the administration of SKF 105111- 17beta-17-[bis (1methylethyl) amino carbonyl] androstane-3,5-diene-3-carboxylic acid (SKF), a potent inhibitor of 5alpha-reductases Type I and II. We used the in situ patch-clamp technique to record GABA-evoked currents and spontaneous inhibitory postsynaptic currents (sIPSCs) from pyramidal neurons in neocortical slices of vehicle- or SKF-treated mice. The potency, but not the efficacy, of exogenously applied GABA was decreased in slices from mice treated with SKF. When neocortical slices were treated in vitro for 3 h with 10 microM SKF, ALLO was also reduced (25-30%) and in addition, the GABA dose-response curve was shifted to the right; however this shift was not as marked as the shift in the slices obtained from mice treated with SKF, in keeping with the smaller decrease of the ALLO content in these slices. Furthermore, direct application of ALLO to these slices shifted the dose-response curve of GABA back toward a non-SKF treated profile. We then analyzed GABAergic sIPSCs in neocortical slices obtained from vehicle or SKF-treated mice. Mean decay time and charge transfer were significantly reduced by SKF treatment. The decay of sIPSCs was best fitted by two exponentials, but only the fast component was decreased in the SKF group. Direct application of ALLO (100 nM) normalizes the sIPSC kinetics in slices from ALLO depleted mice. No changes were detected in the amplitude or frequency of sIPSCs. These data demonstrate that endogenous ALLO physiologically regulates spontaneously induced Cl(-) current by acting on a specific recognition site, which is probably located on GABA(A) receptors (a receptor on a receptor), thereby prolonging inhibitory currents by facilitating conformational transition of the GABA-gated Cl(-) channel to an open state.

5-alpha Reductase Inhibitors↗
PubMed2001

Brain 5alpha-dihydroprogesterone and allopregnanolone synthesis in a mouse model of protracted social isolation.

Allopregnanolone (ALLO), is a brain endogenous neurosteroid that binds with high affinity to gamma-aminobutyric acid type A (GABA(A)) receptors and positively modulates the action of GABA at these receptors. Unlike ALLO, 5alpha-dihydroprogesterone (5alpha-DHP) binds with high affinity to intracellular progesterone receptors that regulate DNA transcription. To investigate the physiological roles of ALLO and 5alpha-DHP synthesized in brain, we have adopted a mouse model involving protracted social isolation. In the frontal cortex of mice, socially isolated for 6 weeks, both neurosteroids were decreased by approximately 50%. After administration of (17beta)-17-(bis-1-methyl amino carbonyl) androstane-3,5-diene-3-carboxylic acid (SKF105,111), an inhibitor of the enzyme (5alpha-reductase Type I and II) that converts progesterone into 5alpha-DHP, the ALLO and 5alpha-DHP content of frontal cortex of both group-housed and socially isolated mice decreased exponentially to 10%-20% of control values in about 30 min. The fractional rate constants (k h(-1)) of ALLO and 5alpha-DHP decline multiplied by the ALLO and 5alpha-DHP concentrations at any given steady-state estimate the rate of synthesis required to maintain that steady state. After 6 weeks of social isolation, ALLO and 5alpha-DHP biosynthesis rates were decreased to 30% of the values calculated in group-housed mice. Moreover, in socially isolated mice, the expression of 5alpha-reductase Type I mRNA and protein was approximately 50% lower than in group-housed mice whereas 3alpha-hydroxysteroid oxidoreductase mRNA expression was equal in the two groups. Protracted social isolation in mice may provide a model to investigate whether 5alpha-DHP by a genomic action, and ALLO by a nongenomic mechanism down-regulate the action of drugs acting as agonists, partial agonists, or positive allosteric modulators of the benzodiazepine recognition sites expressed by GABA(A) receptors.

Animals↗
PubMed2001

Tissue plasminogen activator inhibits P-glycoprotein activity in brain endothelial cells.

Tissue plasminogen activator (0.01-30 microgram/ml) dose-dependently inhibited the functional activity of P-glycoprotein, assessed by rhodamine 123 accumulation in GP8 immortalized rat brain endothelial cells, but this effect was unrelated to its proteolytic activity. Elevation of intra-endothelial cyclic AMP concentration and stimulation of protein kinase C increased P-glycoprotein activity in GP8 cells and also attenuated the tissue plasminogen activator-induced inhibition.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed2001

Strategy for the treatment of inaccessible unruptured giant and large aneurysms of the internal carotid artery.

Our goal was to clarify the optimum management of the inaccessible unruptured giant and large aneurysms of the internal carotid artery (ICA). Since 1981, we have treated 18 patients with unclippable unruptured giant or large aneurysms of the ICA. Aneurysms were classified as either intracavernous or intradural. We performed proximal carotid occlusion in 12 patients and conservatively treated six patients. We retrospectively analyzed long-term outcomes in these patients. Four of seven patients with intradural aneurysm underwent proximal carotid occlusion, with good long-term outcomes. The three patients with intradural aneurysm, who were treated conservatively, died of subarachnoid hemorrhage. Eight of 11 patients with intracavernous aneurysm underwent proximal carotid occlusion, one dying of massive nasal bleeding 25 months after the procedure. In this case, the aneurysm was partially thrombosed, and residual lumen growth was revealed 22 months after proximal carotid occlusion. Cranial nerve paresis improved in five of the eight patients (63%), and two patients had a minor ischemic attack. Neurological problems failed to occur in the three patients with intracavernous aneurysm who were treated conservatively. The risk of rupture is relatively high in intradural giant and large aneurysms. Proximal carotid occlusion can effectively prevent bleeding from intradural aneurysms. Aggressive management is justified for intradural aneurysms with poor collateral circulation. Operative procedures in the management of an intracavernous aneurysm require careful consideration.

Aged↗
PubMed2001

N-acetylcysteine inhibited nuclear factor-kappaB expression and the intimal hyperplasia in rat carotid arterial injury.

Neointima formation associated with vascular restenosis is a complex local inflammatory process actively involving the vascular smooth muscle cell (SMC) proliferation. Nuclear factor-kappaB (NF-kappaB) is a transactivator of a diverse group of genes whose activation has been strongly associated with the cellular response to inflammation. Since anti-oxidant N-acetylcysteine (NAC) inhibit NF-kappaB activity in vascular SMC in vitro, we examined the in vivo effect of the NAC on balloon-induced neointimal formation in the carotid artery of rats. Sprague-Dawley rats underwent balloon dilatation injury of the left carotid artery to induce neointimal formation. One group of these rats (n = 9) were treated with daily intraperitoneal injection of NAC (200 mg kg(-1)) for 14 consecutive days, whereas the control group (n = 9) was treated with saline. Fourteen days after the injury, the left carotid arteries were removed and analyzed under microscope. Several rats underwent the same treatment as above and were sacrificed three days after injury for immunohistochemistry and Western blot studies. A morphometric analysis revealed that there were significant differences in intima/media ratio between the two groups. Immunohistochemical and Western blotting studies demonstrated that NAC suppressed the injury-induced NF-kappaB activity in the medial SMC layer. Treatment with NAC suppresses vascular NF-kappaB activation and this inhibition reduced the pathological thickening of the arterial wall. The NF-kappaB pathway, therefore, represents an attractive therapeutic target for strategies to prevent vascular restenosis.

Acetylcysteine↗
PubMed2001

[A case of cerebral arteriovenous malformation complicated with intracerebral hemorrhage after endovascular embolization].

We reported a case of cerebral arteriovenous malformation (AVM), complicated with intracerebral hemorrhage (ICH), after endovascular embolization. A 51-year-old male suffered from intraventricular hemorrhage due to a rupture of an intranidal aneurysm on October 4, 1999. The first embolization procedure for the aneurysm and a part of the nidus was performed with 2-hydroxyethyl methacrylate-methyl methacrylate (HEMA-MMA) and Liquid coil on day 21 after admission. On day 28, a second embolization was carried out for the residual nidus. Although most of the nidus was obliterated, the patient became comatose 10 hours after the second embolization. Computed tomography revealed a massive ICH in the right parietal lobe, and he underwent emergency evacuation of the hematoma. During the surgery, HEMA-MMA was seen in a draining vein. This caused venous stasis. Although the patient gradually improved postoperatively, he became comatose again because of a recurrence of ICH on day 36. Evacuation of the hematoma and removal of the nidus were performed again. The operative specimen showed AVM embolized by HEMA-MMA with non-specific inflammation and partial inflammatory degeneration of the vascular wall. Hemodynamic change such as venous stasis or elevated pressure of the feeding artery seemed to be the cause of the hemorrhage. Multi-staged embolization with longer intervals and intraoperative flow control were regarded as crucial for avoiding delayed hemorrhage.

Aneurysm, Ruptured↗
PubMed2001

[A case of spinal dural AVF treated by endovascular embolization].

Here we report a case of spinal dural arteriovenous fistula(AVF) treated by endovascular embolization. A 58-year-old female presented with progressive intermittent claudication and numbness of the lower extremities. MRI showed swelling of the spinal cord with intramedullary high signal intensity on T2-weighted image and intramedullary enhancement, suggested spinal cord myelopathy. Myelography demonstrated the dilated serpentine vessels in the subarachnoid space and focal filling defect. Angiography showed spinal dural AVF fed by bilateral lateral sacral artery. The draining vein was posterior spinal vein. Endovascular embolization using liquid material was performed under general anesthesia. The injection of glue included the distal feeding artery, the shunt itself and the initial part of draining vein. A complete cure was achieved, with a normal postoperative angiogram. MRI returned to normal with complete disappearance of T2 high signal, cord enlargement and enhancement by contrast medium. It was suggested that venous congestion induced the transient spinal ischemia, manifested as intermittent claudication. Endovascular embolization using liquid material was safe and quite effective for spinal dural AVF.

Central Nervous System Vascular Malformations↗
PubMed2000

PrP fragment 106-126 is toxic to cerebral endothelial cells expressing PrP(C).

A hydrophobic, fibrillogenic peptide fragment of human prion protein (PrP106-126) had in vitro toxicity to neurons expressing cellular prion protein (PrP(C)). In this study, we proved that primary cultures of mouse cerebral endothelial cells (MCEC) express PrP(C). Incubation of MCEC with PrP106-126 (25-200 microM) caused a dose-dependent toxicity assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, lactate dehydrogenase release, bis-benzimide staining for nuclear morphology, and trypan blue exclusion test. Pentosan polysulphate (50-100 microg/ml), a drug effective in scrapie prophylaxis, dose-dependently attenuated the injury. MCEC cultures from mice homogenous for the disrupted PrP gene were resistant to the toxicity of PrP106-126. In conclusion, cerebral endothelium expressing PrP(C) may be directly damaged during spongiform encephalopathies.

Amino Acid Sequence↗
PubMed2000

Pentosan polysulfate regulates scavenger receptor-mediated, but not fluid-phase, endocytosis in immortalized cerebral endothelial cells.

1. Effects of pentosan polysulfate (PPS) and the structurally related sulfated polyanions dextran sulfate, fucoidan, and heparin on the scavenger receptor-mediated and fluidphase endocytosis in GP8 immortalized rat brain endothelial cells were investigated. 2. Using 1,1'-dioctadecyl-3,3,3,3'-tetramethylindocarboxyamine perchlorate-labeled acetylated low-density lipoprotein (DiI-AcLDL), we found a binding site with high affinity and low binding capacity, and another one with low affinity and high binding capacity. Increasing ligand concentrations could not saturate DiI-AcLDL uptake. DiI-AcLDL uptake, but not binding, was sensitive to pretreatment with filipin, an inhibitor of caveola formation. 3. PPS (20-200 microg/ml) significantly reduced the binding of DiI-AcLDL after coincubation for 3 hr, though this effect was less expressed after 18 hr. Among other polyanions, only fucoidan decreased the DiI-AcLDL binding after 3 hr, whereas dextran sulfate significantly increased it after 18 hr. PPS treatment induced an increase in DiI-AcLDL uptake, whereas other polysulfated compounds caused a significant reduction. 4. Fluid-phase endocytosis determined by the accumulation of Lucifer yellow was concentration and time dependent in GP8 cells. Coincubation with PPS or other sulfated polyanions could not significantly alter the rate of Lucifer yellow uptake. 5. In conclusion. PPS decreased the binding and increased the uptake of DiI-AcLDL in cerebral endothelial cells, an effect not mimicked by the other polyanions investigated.

Animals↗
PubMed2000

Alpha-bromo-alpha,alpha-difluoroallyl derivatives as synthetic intermediate: nucleophilic substitution of alpha-bromo-alpha,alpha-difluoroallyl derivatives in the presence of palladium catalysts.

The palladium catalyzed nucleophilic substitution of alpha-bromo-alpha,alpha-difluoroallyl derivatives turned out to be an efficient method for the preparation of several fluorinated organic molecules. Several soft carbon nucleophiles regioselectively reacted with 3-bromo-3,3-difluoropropene (BDFP) to give the 3-substituted 1,1-difluoroalkenes. Phenylzinc chloride and tributylphenyltin afforded 1-fluoro-1,3-diphenylpropene. The radical bromination of 3-substituted 1,1-difluoroalkenes provided 1-substituted BDFPs, and a 1-substituted BDFP reacted with carbon nucleophiles to give 1,3-disubstituted 3,3-difluoroalkenes. For the reaction of nitrogen nucleophiles with BDFP, an amine and the sodium salts of the carbamates reacted with BDFP at the gamma-position. However, the sodium salts of the sulfoneamide predominantly attacked at the alpha-position.

Catalysis↗
PubMed2000

Pharmacological and immunohistochemical characterization of a mouse model of acute herpetic pain.

We have recently found that the infection with herpes simplex virus type-1 (HSV-1) of primary sensory neurons induces nociceptive hypersensitivity to noxious mechanical (hyperalgesia) and tactile stimulation (allodynia) in mice. In the present experiments, we determined the distribution of HSV-1 in the dorsal root ganglia and examined the effects of four analgesic agents on hyperalgesia and allodynia. HSV-1 was inoculated on the unilateral shin. HSV-antigen-positive cells were detected in the L4 and L5 dorsal root ganglia on days 5 and 7, but not day 3, post-inoculation. About 80% of the positive cells were small in size. Allodynia and hyperalgesia appeared on day 5 post-inoculation. Antinociceptive effects of analgesic agents were examined on day 6 post-inoculation. Morphine (1-5 mg/kg, subcutaneous) and gabapentin (10-100 mg/kg, peroral) dose-dependently inhibited both allodynia and hyperalgesia. Diclofenac (10-100 mg/kg, intraperitoneal) also produced antinociceptive effects, but there was a ceiling for the effect on hyperalgesia. Amitriptyline (3, 10 mg/kg, subcutaneous) did not affect allodynia and hyperalgesia. The results suggest that mechanical allodynia and hyperalgesia appeared when HSV-1 proliferated in the sensory neurons. This mouse model may be useful for studying the mechanisms of acute herpetic pain and anti-neuropathic pain agents.

Acetates↗
PubMed1999

Mild hypothermia on anoxic depolarization and subsequent cortical injury following transient ischemia.

Anoxic depolarization (AD) is one of the major physiological characteristics in the ischemic core. The effect of mild hypothermia on the appearance of AD and subsequent brain injury following profound ischemia is studied to evaluate the protective mechanism of hypothermia against severe ischemia. Sprague-Dawley rats were subjected to transient ischemia by hypotension (50-20 mmHg) and bilateral carotid artery occlusion (BCA-O) for 20 min in normothermia and 30 min in hypothermia. The temperature of body and temporal muscles was maintained at 37.5 degrees C and 36.5 degrees C in normothermia and 33.0 degrees C and 31.0 degrees C in hypothermia, respectively. Recording of the DC potential shift and electrocorticogram and monitoring of the cortical blood flow (CoBF) with a laser Doppler flowmeter were done epidurally on the right parietal cortex. The right parietal cortex pathology was examined 24 h after ischemia in normothermia and after 30 days in hypothermia. AD appeared in all seven normothermic rats with a fall in the CoBF to 9%-10% of the control flow. However, in spite of CoBF reduction to 8%-9% of the control flow, it did not appear in five hypothermic rats. Intra-ischemic CoBF was not statistically different between these two groups. AD appeared with the CoBF decreasing to 4%-5% of the control flow in seven hypothermic rats. Intra-ischemic CoBF in hypothermic rats exhibiting AD was significantly lower than the other two groups. The interval between BCA-O and the appearance of AD in hypothermic rats was 5.1 +/- 0.3 min (mean +/- SE), which was significantly longer than the 2.2 +/- 0.5 min observed in normothermia (p < 0.0005). Of seven normothermic rats exhibiting AD, two died within 24 h and four revealed massive neuronal injury. Of seven hypothermic rats with AD, four died between day 2 and day 13, and one revealed diffuse cerebral infarction. However, no severe ischemic injury or ischemic death was observed in all five hypothermic rats without AD. The incidence of severe neuronal injury or ischemic death was significantly lower in hypothermic rats without AD compared with normothermic rats with AD (p < 0.02) or hypothermic rats with AD (p < 0.05). Although mild hypothermia delays AD, it is suggested that raising the cerebral blood flow threshold for AD appearance has a key role in the hypothermic protection of a severely ischemic area such as the ischemic core.

Animals↗
PubMed1999

An additional monitoring of regional cerebral oxygen saturation to HMPAO SPECT study during balloon test occlusion.

BACKGROUND AND PURPOSE: To increase the reliability of 99mTc-hexamethyl propyleneamine oxime (HMPAO) single photon emission computed tomography (SPECT) study in the evaluation of hemodynamic change with balloon test occlusion (BTO) of the internal carotid artery, we attempted to clarify the usefulness of additional monitoring of regional oxygen saturation of the brain (rSO2). METHODS: During BTO, rSO2 monitoring with transcranial near infrared spectroscopy was performed 17 times on 16 patients. Asymmetrical distribution of the tracer was classified visually as follows: group 1, little or no asymmetry, and group 2, moderate or severe asymmetry. Seven regions of interest (ROI) were defined in the middle cerebral artery area of each hemisphere, and the asymmetry index (AI)=200x(Cnon-Coccl)/(Cnon+Coccl)), where Cnon=mean counts on the nonoccluded side, and Coccl=mean counts on the occluded side were also calculated. Then, mean AI (MAI) was obtained from AI of 7 ROIs for each study. RESULTS: Of the 17 procedures, 10 BTOs were in group 1 and 5 BTOs were in group 2. Two patients did not undergo SPECT study because of the immediate appearance of a neurological deficit with BTO; they were defined as group 3. The MAI in group 1 was 2. 6+/-3.3%, which was significantly smaller than the MAI in group 2 (25.6+/-5.0%, P<0.02). The DeltarSO2 (baseline rSO2-rSO2 during ICA occlusion) with BTO in group 1 was 1.5+/-1.4% (n=10), which was statistically smaller than that in group 2 (5.5+/-1.3%, n=4, P<0.05). The DeltarSO2 in group 3 was 9.0+/-0.0% (n=2). In group 1, however, rSO2 began to decline when the stump pressure fell to 45 mm Hg and always declined when the stump pressure fell below 40 mm Hg. Furthermore, in group 1, a significant correlation was observed between the DeltarSO2 and stump pressure (r=0.85, P<0.0001). CONCLUSIONS: This preliminary study reveals that an obvious asymmetrical SPECT pattern always accompanies a profound decrease in rSO2 and that rSO2 parallels a severe reduction in stump pressure in cases exhibiting a symmetrical SPECT pattern. Thus, the cerebral oximetry sensitively reflects the cerebral oxygenation, and simultaneous measurements of rSO2 and stump pressure with 99mTc-HMPAO SPECT study apparently are useful in evaluating hemodynamic integrity with BTO.

Adolescent↗