Biomedical subjects

C Tanaka

Publications and source records attributed to C Tanaka.

At least 109 records · Page 6Linked to original sources

PubMed1997

Redox regulation of lipopolysaccharide (LPS)-induced interleukin-8 (IL-8) gene expression mediated by NF kappa B and AP-1 in human astrocytoma U373 cells.

LPS-induced expression of the IL-8 gene was markedly enhanced by H2O2 or by deprivation of the cellular antioxidant glutathione by L-buthionine-(S,R)-sulfoximine (BSO) in human astrocytoma U373 cells. In contrast, it was markedly suppressed by the reductant N-acetyl-L-cysteine (NAC) and other antioxidants. Transient expression analysis using the chloramphenicol acetyltransferase assay revealed that activation of the IL-8 promoter by LPS was stimulated by BSO and was suppressed by NAC; likewise LPS-induced activation of both NF kappa B and AP-1 was enhanced by BSO and inhibited by NAC. These results suggest that LPS-induced IL-8 gene expression is regulated by cellular redox via modulation of these transcription factors.

Acetylcysteine↗

PubMed1997

Cloning of the cDNA encoding rat Presenilin-1.

We isolated rat presenilin-1 (PS-1; also called S182 previously) cDNA from total brain RNA by using a reverse transcription-polymerase chain reaction (RT-PCR) technique with primers homologous to the conserved sequences of human and mouse PS-1. Rat PS-1 cDNA encoded 468 amino acids (aa) and the deduced aa sequence was highly homologous to those of the human (88.4%) and mouse (92.7%). Northern blot analysis of the rat PS-1 cDNA revealed two mRNA species in rat neurotypic pheochromocytoma and glioma cell lines (PC-12 and C6, respectively) that migrated at rates corresponding to approximately 3.0 and 7.5 kb.

Alzheimer Disease↗

PubMed1997

Bilateral opercular syndrome caused by perinatal difficulties.

Four patients with pseudobulbar palsy, mental retardation and various degrees of speech disturbance associated with perinatal difficulties are described as having an acquired type of opercular syndrome. There were two patients with fetal bradycardia and three with subarachnoid haemorrhage and neonatal convulsion. Magnetic resonance imaging revealed cortical atrophy in the bilateral opercula with some signal abnormalities in the underlying white matter in common. Single photon emission computed tomography (SPECT) also confirmed the presence of hypoperfusion in the regions. Although the opercular syndrome is a clinical entity with a multitude of underlying pathologies, perinatal difficulties could be an important cause of the acquired type.

Adolescent↗

PubMed1997

Elevated nerve growth factor levels in cerebrospinal fluid associated with progressive cortical atrophy.

Using a two-site enzyme-linked immunosorbent assay, we measured nerve growth factor (NGF) levels in cerebrospinal fluid (CSF) from 40 patients with or without brain atrophy due to various neurologic disorders. White matter and cortical atrophies were assessed by frontal horn index (FHI) and subarachnoid space area/inner skull space area (SSA/ISSA) ratio, respectively. CT findings of 40 patients were classified into 4 grades: normal (< mean + 2SD), grade I (mean + 2SD < or = or < mean + 4SD), grade II (mean + 4SD < or = < mean + 8SD), and grade III (mean + 8SD < or =). NGF levels in CSF were significantly elevated in 3 of 6 patients with grade III cortical atrophy and normal in 2 with grade II atrophy, 4 with grade I atrophy and 28 without atrophy. Cortical atrophy was progressive in the 3 with NGF elevation in CSF. With respect to white matter atrophy, NGF elevation was observed in none of 3 with grade III white matter atrophy, two of 4 with grade II atrophy, none of 3 with grade I atrophy and one of 30 without atrophy. The symptoms of the two of three with NGF elevation were progressive at the time of obtaining the CSF samples, while those of other patients without NGF elevation were non-progressive. The present study suggests that NGF elevation in CSF may reflect extensive cortical degenerative change.

Adolescent↗

PubMed1997

Investigation of morphological change of lateral and midline fluid percussion injury in rats, using magnetic resonance imaging.

OBJECTIVE: Investigating the time course of morphological changes in experimental traumatic brain injury (TBI) in vivo helps to clarify the mechanism of TBI and develop new therapeutic modalities. We examined the morphological changes in experimental TBI, using magnetic resonance imaging (MRI) in a rat model. METHODS: We produced lateral fluid percussion injury (LFP) and midline fluid percussion injury (MFP) in rats, using the Yamaki fluid percussion device. The rats were divided into four groups: LFP, MFP, sham LFP, and sham MFP. MRI was performed with a 4.7-T magnetic resonance apparatus 2 days and 90 days after the induction of injury. T1-, T2-, and T2- weighted images were obtained using a surface coil. RESULTS: Hemorrhage, contusion, and brain edema in LFP models were detected on the 2nd day after injury, and the necrotic tissue was absorbed and replaced by cerebrospinal fluid on the 90th day. In MFP animals, we detected a small hemorrhage in the corpus callosum with minimal brain edema around the hemorrhage on the 2nd day after injury, and on the 90th day, enlarged ventricles and cisterns were observed, indicating brain atrophy. CONCLUSION: MRI, therefore, is useful for plotting morphological changes in experimental TBI in vivo. We report the novel and clinically important finding of brain atrophy after experimental TBI.

Animals↗

PubMed1997

Establishment of a murine model for metastasis of cytokine-producing tumor to the brain.

The A375 cell line, derived from human malignant melanoma, has characteristics of interleukin-6 (IL-6) production. By using this cell line, we have investigated a murine metastasis model of IL-6-producing tumors to the brain by injecting A375 cells directly into the left cardiac ventricle. Nude mice were anesthetized with intraperitoneal injection of pentobarbital sodium. Next, A375 cells suspended in phosphate-buffered saline (PBS) were injected into the left cardiac ventricle of mice. An intracardiac injection of 10(5) cells developed tumor colonies in the brain after 4 to 6 weeks. Metastatic cells were found in every lobe of the brain. An immunocytochemical study revealed IL-6 production by A375 cells at the metastatic sites in the brain. By the transfection of genes encoding proteins into A375 cells, a novel model of protein expression in the brain in vivo could be constructed. Our system does not require great skill. Our experimental model will facilitate future studies of the local effects of proteins in the brain.

Animals↗

PubMed1997

Hemorrhagic and nonhemorrhagic stroke: diagnosis with diffusion-weighted and T2-weighted echo-planar MR imaging.

PURPOSE: To determine if diffusion- and T2-weighted echo-planar magnetic resonance (MR) imaging can be used to detect acute hemorrhagic stroke and to differentiate hemorrhagic from nonhemorrhagic stroke. MATERIALS AND METHODS: A total of 118 examinations (diffusion- and T2-weighted MR imaging) in 19 patients with 27 nonhemorrhagic strokes and in six patients with seven hemorrhagic strokes were performed. The ratios of apparent diffusion coefficient and of signal intensity on T2-weighted MR images in lesions to those in contralateral control areas were calculated. RESULTS: Decreased ADC was shown in lesions of acute (0-3 days) hemorrhagic stroke, as well as in lesions of acute nonhemorrhagic stroke. Hypointense areas were seen on T2-weighted MR images in patients with acute hemorrhagic stroke, in contrast to normal to increased signal intensity in those with acute nonhemorrhagic stroke. Apparent diffusion coefficient tended to remain decreased in hemorrhagic stroke lesions even 100 days after onset, in contrast to the increased coefficient in nonhemorrhagic stroke lesions at the late chronic stage (31 days or older). CONCLUSION: Diffusion- and T2-weighted echo-planar MR imaging can be used to detect and distinguish between acute hemorrhagic and nonhemorrhagic stroke.

Acute Disease↗

PubMed1997

Possible different mechanism between amyloid-beta (25-35)-and substance P-induced chemotaxis of murine microglia.

The mechanism of murine microglial chemotaxis induced by amyloid-beta protein (A beta (25-35)) was investigated. A beta (25-35) dose-dependently stimulated microglial chemotaxis at concentrations between 100 pM and 10 nM. Substance P, a NK-1 agonist, stimulated chemotaxis at concentrations of 10 nM or more. GR-64349, a NK-2 agonist, and senktide, a NK-3 agonist, did not stimulate microglial chemotaxis. We examined whether homologous desensitization of chemotaxis would occur by A beta (25-35). The chemotactic effect of microglia was homologously desensitized by 10 nM A beta (25-35). On the other hand, substance P at 10 nM did not desensitize the A beta (25-35)-induced chemotaxis. These data show that A beta (25-35) induces the chemotaxis of microglia probably through a receptor other than the NK-1 receptor.

Amyloid beta-Peptides↗

PubMed1997

Infrequent mutations of p27Kip1 gene and trisomy 12 in a subset of human pituitary adenomas.

To study the etiologic roles of genes on chromosome 12 for the pituitary tumorigenesis of adenomas, mutations of the p27Kip1 gene and allelic ratios of 18 microsatellite markers on the entire chromosome 12 were studied in 33 pituitary adenomas. The p27Kip1 gene on chromosome 12p12-p13 encoding an inhibitor of complexes between cyclins and cyclin-dependent kinases is supposed to function as the tumor suppressor gene. Among 31 sporadic and 2 familial pituitary adenomas, PCR-single strand conformation polymorphism analysis detected three polymorphic changes but no tumor-specific mutations of the p27Kip1 gene. Genotyping of 18 microsatellite markers on the entire chromosome 12 detected the uniformly decreased allelic ratios ranging from 54-66% in 8 of 33 pituitary adenomas (24%), although no loss of heterozygosity was detected. Fluorescence in situ hybridization confirmed trisomy 12 in all 5 available samples out of these 8 samples. Based on these, we conclude that not mutations of the p27Kip1 gene, but trisomy 12 may be etiologically important in a subgroup of pituitary adenomas.

Adenoma↗

PubMed1997

Pharmacological profiles of a new antiulcer agent, SWR-215.

We investigated the effects of a new antiulcer agent, SWR-215 ([[(1,2-dihydro-2-oxo-4-quinolinyl)methyl]thio]-N-[[[4-(1-piperidinyl methyl)-2-pyridinyl]oxy]-Z-2-butenyl]acetamide), on histamine H2-receptors, gastric acid secretion and various acute experimental gastric lesions. SWR-215 showed unsurmountable histamine H2-antagonism on isolated guinea-pig atrium. In gastric secretion studies, SWR-215 exhibited potent and durable inhibitory effects, and the antisecretory activities were much stronger than that of roxatidine acetate hydrochloride (roxatidine): 5 times stronger on basal acid secretion in pylorus ligated rats, 11 times stronger on histamine-stimulated acid secretion in acute fistula rats, and 2 times stronger on histamine stimulated acid secretion in Heidenhain-pouch dogs, respectively. In various experimental acute gastric lesion studies, SWR-215 potentially inhibited almost all acute gastric and duodenal lesions compared with roxatidine, especially indomethacin-induced and HCl-ethanol-induced gastric lesions, and the inhibitory effects were exhibited at the same or lower doses than those which caused the antisecretory effect. Furthermore, it was considered that the mucosal protective effect of SWR-215 was probably unrelated to the endogenous prostaglandin system in gastric mucosa. These results suggest that SWR-215 possesses both durable antisecretory and mucosal protective effects, and is expected to be a useful drug for the treatment of patients with peptic ulcers.

Animals↗

PubMed1997

Infrequent mutations of p16INK4A and p15INK4B genes in human pituitary adenomas.

The p16INK4A and p15INK4B genes on chromosome 9p21 encode the p16 and p15 inhibitors of cyclin D/cyclin-dependent kinase 4 complexes respectively. Mutations and deletions of the p16INK4A gene have been found in melanomas and many other types of tumors. To assess the role of the p16INK4A and p15NK4B genes in tumorigenesis of the pituitary gland, 31 sporadic pituitary adenomas and 2 pituitary adenomas in familial acrogigantism were examined for loss of heterozygosity on 9p21-22 and screened for mutations in the p161NK4A and p15INK4B genes. To identify pituitary adenomas which had lost 9p21-22, pituitary adenomas were genotyped with markers flanking the p16INK4A and p15INK4B loci. The frequency of mutations in coding regions of the p16INK4A and the p15INK4B genes in pituitary adenomas was determined with polymerase chain reaction-single strand conformation polymorphism analysis and sequencing of variants. Of the 33 pituitary adenomas, two revealed loss of 9p21-22 sequences, but none of them had tumor-specific mutations. We conclude that mutations of the p16INK4A and p15INK4B genes are not required for tumorigenesis of the pituitary gland.

Adenoma↗

PubMed1997

[Chronic respiratory failure in a case with juvenile-onset acid alpha-glucosidase deficiency; successful therapy with nasal intermittent positive pressure ventilation (NIPPV)].

A 13-year-old boy with juvenile-onset acid alpha glucosidase deficiency was reported. Proximal muscle weakness including respiratory muscles and scoliosis progressed since nine year of age. He developed nocturnal dyspnea and daytime somnolence at age 13. His arterial blood gas analysis showed hypoxemia (PO2 54.1 mmHg) and hypercapnia (PCO2 72.3 mmHg), and spirometry showed significantly decreased vital capacity (% VC 21%). He was treated with nocturnal NIPPV employing a device for delivering bilevel positive airway pressure (Bi-PAP). Nocturnal dyspnea and daytime somnolence rapidly disappeared with nocturnal ventilatory support. Daytime arterial PO2 and PCO2 improved after the therapy, namely 74.8 mmHg and 64.1 mmHg respectively. We conclude that NIPPV is a noninvasive and effective therapy for respiratory failure in patients with chronic progressive neuromuscular disorder including acid alpha glucosidase deficiency.

Adolescent↗

PubMed1997

[Theory and clinical application of functional MRI: 3D-functional brain mapping].

Functional magnetic resonance imaging (fMRI) was performed using a clinical 1.5 T MR scanner. Normal volunteers and patients with several neurological disorders were studied with somatosensory stimulation using sponge at right hand and visual stimulation using checkerboard pattern. Both fMR images by gradient echo echo planar imaging and three dimensional gradient echo images were studied. Reconstructed 3 dimensional functional brain mapping was superimposed on 3D anatomical images. Apparent signal increase was observed at contra lateral sensorimotor cortex and secondary sensory cortex with sponge stimulation. In the case of left homonymous hemianopia due to cerebral infarction, increasing signal was only observed surrounding left calcarine fissure by using stimulation of all visual field. In conclusion, fMRI and 3-D functional brain mapping has extremely high potentiality to examine pathophysiology of various neurological disorders.

Brain↗

PubMed1997

[Functional brain mapping in motor task and somatosensory stimulation using echo planar MRI].

Functional brain mapping was performed with a 1.5T clinical MRI apparatus. Single shot gradient echo echo-planar imaging (EPI) sequence was employed. Normal volunteers were studied with the task of grasping hand or opposition of fingers at the frequency of 3 Hz, median nerve electro-stimulation, pure somatosensory stimulation by roller for acupuncture. Apparent signal increase was observed at contralateral sensorimotor cortex with motor task. Signal changes delayed about 5 seconds compared with the start and the cessation of the task, which may suggest that regional changes of CBF and blood oxygen level in capillary and/or in venule lag behind electrical excitation. It was hard to detect the activated area with median nerve electro-stimulation. On the other hand, roller stimulation provoked distinct activated areas at contralateral sensorimotor cortex. The activated areas caused by the roller stimulation and the motor task coincided entirely, which suggests the possibility of the intermixed localization of primary areas of motor and somatosensory. It was also clearly demonstrated that the activated area was broader with quick (3 Hz) and complicated motor task (finger opposition) than with slow (1Hz) and simple motor task (hand grasping).

Adult↗

PubMed1997

[Principles and clinical applications of diffusion weighted echo planar MR imaging].

The ultrafast capability of echo planar imaging(EPI) made diffusion-weighted MRI (DWI) measurements practical, without the need of head fixation and without the need to exclude patients unable to hold still. The DW hyperintensity and reduced apparent diffusion coefficient(ADC) were observed in all hyperacute strokes, initially at 2.5 hours. In contrast to decreased ADC within 10 days and DW hyperintensity within 30 days, ADC was increased without DW hyperintensity in chronic stage. This suggests that DWI can discriminate between acute and chronic strokes. Furthermore, DWEPI and T2-weighted EPI were also be useful to detect and distinguish acute hemorrhagic stroke from nonhemorrhagic stroke. This review highlighted the promising technique of DWEPI to examine stroke patients in routine clinical practice.

Animals↗

PubMed1997

[Detection of pulsated blood flow by cine mode 3D angiography].

The phase contrast(PC) has an advantage to get an information about flow speed of blood along the gradient axis. The cine mode 3D-PC MRA was performed by a 1.5T clinical MR system(GE; Signa) using multi-slices gradient echo sequence with ECG gating and velocity-encoding gradient along three orthogonal axes. The cine mode 3D-PC data in three axes was constructed from 10 cardiac phases, respectively. The black and white cine mode 3D-PC MRA enabled to get an information of blood flow speed. The color MRA, in which flow direction was assigned with RGB colors, enabled to observe flow orientation of blood. Furthermore, the flow speed vector in each pixel showed a detail flow information in the intravascular space.

Basilar Artery↗

PubMed1997

[Mapping of cerebral metabolism on cerebral disorders using multi-slice proton magnetic resonance spectroscopic imaging].

Multi-slice proton magnetic resonance spectroscopic imaging(MRSI) was performed using a 1.5 T clinical MR apparatus. Normal volunteer and several kinds of cerebral disorders were examined using following parameters; Tr/Te = 2.3 s/280 ms, slice thickness/gap/slices = 15/3.5 mm/4, 32 phase encoding and 24 cm FOV. Every 4 slice images of NAA, Cr, Cho and Lip/Lac were obtained in about 34 minutes. In control cases, images of Cr and Cho showed very high intensity at cerebellum comparing with cerebrum. This means high concentration or changes of relaxation times of both Cr and Cho. In cerebral infarction and brain tumor, though NAA images showed no signal intensity, Cr and Cho images showed small iso-or mild high-signal intensity areas. These findings suggest neuronal loss and gliosis or tumor growth in the lesions. In conclusion, MRSI has extremely high potential to evaluate metabolism of brain and cerebral disorders.

Aspartic Acid↗

PubMed1997

[Three-dimensional brain mapping using fMRI].

Functional mapping of the activated brain, the location and extent of the activated area were determined, during motor tasks and sensory stimulation using fMRI superimposed on 3 D anatomical MRI. Twelve volunteers were studied. The fMR images were acquired using a 2 D gradient echo echo planar imaging sequence. The 3D anatomical MR images of the whole brain were acquired using a conventional 3D gradient echo sequence. Motor tasks were sequential opposition of fingers, clenching a hand and elbow flexion. Somatosensory stimulation were administered by scrubbing the palm and sole with a washing sponge. Visual stimulation consisted of full visual field stimulation. Data were analyzed by the cross-correlation method. Transversal fMR images and anatomical images were reconstructed using both volume-, surface-rendering methods, and reconstructed for coronal and sagittal sections. Activated areas were expressed using the three primary colors. Motor tasks activated the contralateral primary motor area (M1), the primary somatosensory area (S1) and the supplementary motor area (SMA). Somatosensory tasks activated the contralateral S 1, M1 and secondary sensory area (S2). Activated areas during full visual field stimulation was observed in the bilateral occipital lobe, including both the primary cortex. Three-dimensional brain mapping allowed visualization of the anatomical location and extent of the activated brain during both motor task and sensory stimulation. Using this method we could obtain a functional map similar to the Penfield's schema.

Adult↗