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H Kusaka

Publications and source records attributed to H Kusaka.

At least 37 records · Page 2Linked to original sources
PubMed1998

Chordoid meningioma in a child. Case report.

A case of chordoid meningioma occurring in a 15-year-old girl is presented. The patient manifested seizures as the initial symptom and subsequently exhibited subclinical microcytic hypochromic anemia. The tumor, located in the falcotentorial region and associated with diffuse edema, was totally resected. On histological examination of the surgical specimen, the clustering pattern of partly vacuolated cells in the mucoid stroma mimicked chordoma; however, positive staining of individual cells for vimentin and epithelial membrane antigen led to a diagnosis of meningioma. Interestingly, the tumor cells were surrounded by a periodic acid-Schiff- and type IV collagen-positive substance. Electron microscopy demonstrated a strikingly dense and thick basal lamina. The patient's microcytic hypochromic anemia disappeared after the tumor was removed. Both the clinical and pathological features of this case resemble those of chordoid meningioma, a rare meningioma variant.

Adolescent↗
PubMed1997

Encephalomyelitis subsequent to mycoplasma infection with elevated serum anti-Gal C antibody.

We report a 7-year-old girl with acute disseminated encephalomyelitis subsequent to a mycoplasma infection. She manifested a prolonged state of akinetic mutism, during which EEG revealed well-synchronized spindles. Four months later, she regained consciousness, with no mental deficit, but complete flaccid quadriplegia persisted and magnetic resonance imaging disclosed extensive destruction of the spinal cord. Antibody against galactocerebroside was detected in her serum during the acute phase. The anti-Gal C antibody is suggested to be involved in the pathogenesis of immune-mediated demyelinating diseases in the central nervous system subsequent to mycoplasma infections.

Akinetic Mutism↗
PubMed1997

Apoptosis of intestinal intraepithelial lymphocytes induced by exogenous and endogenous glucocorticoids.

To investigate the effect of glucocorticoids on apoptosis in intestinal intraepithelial lymphocytes (i-IEL), we examined the changes of i-IEL followed by in vivo treatment with dexamethasone. The fragmented DNA of i-IEL were significantly increased at 15 hr after dexamethasone treatment and, subsequently, the number of total i-IEL were decreased by day 4 after treatment. Although all subsets of i-IEL including CD8 alpha/alpha(+), CD8 alpha/beta(+), CD4+ and CD4+CD8+ i-IEL were decreased after dexamethasone treatment, CD8 alpha/alpha(+) i-IEL appeared to be relatively resistant to dexamethasone-induced apoptosis. Consistent with the in vivo findings, CD8 alpha/alpha(+) i-IEL exhibited less susceptibility to dexamethasone-induced cell death in vitro than other subsets. To investigate whether this process occurs under physiological conditions, we examined the kinetics of i-IEL after treatment with 15-hr water immersion stress. In mice subjected to water immersion stress, plasma glucocorticoids were remarkably elevated soon after the 15-hr stress. The increase in the fragmented DNA of i-IEL and subsequent decrease in the number of i-IEL were observed in the stressed mice in the same kinetics as seen in the dexamethasone-treated mice. Similar to dexamethasone-induced ell death, CD8 alpha/alpha(+) i-IEL appeared to be relatively resistant to stress-induced apoptosis compared with other i-IEL subsets. The expression level of Bcl-2 was significantly higher in CD8 alpha/alpha(+) i-IEL than in CD8 alpha/beta(+) i-IEL. Our results indicate that i-IEL are subjected to cell death via apoptosis by exogenous and endogenous glucocorticoids and that different sensitivity to steroid-induced apoptosis may exist among i-IEL subsets in relation to their Bcl-2 expression.

Animals↗
PubMed1997

alpha-Tocopherol transfer protein gene: exon skipping of all transcripts causes ataxia.

This report concerns the characterization of the alpha-tocopherol transfer protein (alpha-TTP) gene in a Japanese family affected by ataxia with isolated vitamin E deficiency (AVED). The sequence analysis revealed a G-to-A transition at the 3' end of exon 3 in both alleles, which predicts outsplicing of this exon from premessenger RNA and the concomitant frame shift in the ataxic patient. We used reverse transcriptase-polymerase chain reaction to analyze alpha-TTP gene transcripts. All transcripts in peripheral blood lymphocytes of the AVED patient, who was treated with large doses of vitamin E, lacked exon 3. The deduced truncated protein shares only 43% of the normal alpha-TTP. Normal control tissues and cells contained normal transcripts and, unexpectedly, also the same mutant transcripts as those of the patient, although with different transcription levels. Treatment of normal fibroblasts with clinically relevant concentrations of vitamin E increased production of transcripts in a dose-dependent manner. We propose that exon skipping of all transcripts through the complete inactivation of the splice site accounts for the clinical onset of AVED and for the clinical resistance to vitamin E in our patient.

Adult↗
PubMed1996

An unusual cervical chordoma: CT and MRI.

We report CT and MRI findings of an unusual cervical chordoma. CT showed only minimal bony destruction with a lobulated prevertebral mass. Sagittal MRI, however, clearly demonstrated a lesion involving the body of C2 extending prevertebrally and into the spinal canal.

Aged↗
PubMed1996

Golgi apparatus and intraneuronal inclusions of anterior horn cells in amyotrophic lateral sclerosis: an immunohistochemical study.

We applied immunohistochemical techniques to study alterations of the Golgi apparatus, and to determine possible relationships between this complex and the intraneuronal inclusions of lower motor neurons of patients with the sporadic form of amyotrophic lateral sclerosis (ALS). Spinal cords from normal individuals served as controls. Monoclonal antibodies to the Golgi zone and to Golgi beta-COP protein were used. Immunoreactivity with these antibodies was seen in frozen sections of paraformaldehyde-fixed spinal cord tissue, but not in formalin-fixed, paraffin-embedded specimens. The immunoreaction products were seen as granular structures, diffusely distributed in neurons and glial cells. Although immunostaining of some ALS neurons was reduced, fragmentation of the Golgi apparatus was not evident with either antibody. Bunina bodies and skein-like inclusions, characteristically found in spinal anterior horn cells of ALS patients, were not stained by these antibodies to epitopes of the Golgi apparatus, nor were Lewy body-like hyaline inclusions, present in some cases of sporadic ALS and reported to be characteristic to familial ALS with posterior column degeneration. These results suggest that components of the Golgi apparatus are not directly incorporated into intraneuronal inclusions. However, the possibility that abnormal proteinaceous material of the Golgi apparatus may be involved in their genesis cannot be ruled out.

Adult↗
PubMed1996

Diagnosis of colorectal tumorous lesions by magnifying endoscopy.

BACKGROUND: The magnifying colonoscope allows 100-fold magnified viewing of the colonic surface. METHODS: We examined 2050 colorectal tumorous lesions by magnifying endoscopy, stereomicroscopy, and histopathology and classified these lesions according to pit pattern. Based on stereomicroscopy, lesions with a type 1 or 2 pit pattern were nontumors, whereas lesions with types 3s, 3L, 4, and/or 5 pit patterns were neoplastic tumors. RESULTS: The pit patterns observed by magnifying endoscopy were fundamentally similar to those demonstrated in stereomicroscopic images. When the diagnosis by magnifying endoscopy was compared with the stereomicroscopic diagnosis, there was agreement in 1130 of 1387 lesions (81.5%). True neoplasms could be differentiated from non-neoplastic lesions. Of lesions with a type 5 pit pattern with a bounded surface, 11 of 22 (50%) were found to be invasive cancers with involvement of the submucosal layer. If this pit pattern is found to involve a relatively broad area of the mucosal surface, extensive malignant invasion (sm-massive) should be strongly suspected. CONCLUSIONS: The magnifying colonoscope provides an accurate instantaneous assessment of the histology of colorectal tumorous lesions. This may help in decision making during colonoscopy.

Adenoma↗
PubMed1996

Central effects of caffeine on renal renin secretion and norepinephrine spillover.

Endogenous adenosine in the brain may inhibit central sympathetic tone and thereby restrain renin release, a mechanism that may be particularly important when sympathetic activity is enhanced. The purpose of our study was to test the hypothesis that the adenosine receptor antagonist caffeine increases renin release in part by disabling the central nervous system (CNS) adenosine brake on renin release. This hypothesis was tested by conducting three protocols in anesthetized rats. In the first protocol, intracerebroventricular (i.c.v.) infusions of caffeine (10 micrograms/kg/min) did not alter either bradycardic responses to intravenous (i.v.) infusion of N6-cyclopentyladenosine (CPA, A1-receptor agonist) or depressor responses to i.v. infusions of CGS21680 (A1-receptor agonist). However, i.c.v. caffeine did block bradycardic responses to i.c.v. boluses of CPA and depressor responses to i.c.v. boluses of CGS21680, thus demonstrating that i.c.v. caffeine at the dose used blocks CNS but not peripheral adenosine receptors. In the second protocol, hydralazine (1 and 10 mg/kg, administered intraperitoneally) significantly enhanced both the renal secretion of renin and the renal spillover of norepinephrine (NE), thus confirming that hydralazine can increase renin release by unloading arterial baroreceptors and increasing sympathetic tone to the kidneys. In the third protocol, the effects of i.c.v. caffeine (10 micrograms/kg/min) on hydralazine-induced (1 and 10 mg/kg, administered intraperitoneally) changes in renal secretion of renin and renal NE spillover were investigated. In this protocol, i.c.v. caffeine did not alter baseline values for either the renal secretion of renin or NE. In contrast, i.c.v. caffeine significantly (p = 0.03) enhanced the increase in renal renin secretion induced by 1 and 10 mg/kg hydralazine (for 1 mg/kg hydralazine delta of 6.4 +/- 46.7 and 142.4 +/- 142.9 renin activity/min/kg body weight in control and caffeine-treated animals, respectively; for 10 mg/kg hydralazine, delta 227.8 +/- 73.9 and 600.8 +/- 168.9 renin activity/min/kg body weight in control and caffeine-treated animals, respectively). The enhanced renin-secretion response to hydralazine in caffeine-treated rats was accompanied by augmented hydralazine-induced increase in renal NE spillover (p = 0.035). These data strongly support the hypothesis of a CNS adenosine brake on renin release that is disabled by caffeine.

Adenosine↗
PubMed1996

Striatal efferent involvement and its correlation to levodopa efficacy in patients with multiple system atrophy.

We report an immunohistochemical investigation of the striatal efferents in the striatum, globus pallidus, and substantia nigra of five patients with multiple system atrophy (MSA): olivopontocerebellar atrophy (2), striatonigral degeneration (2), and Shy-Drager syndrome (1). All patients manifested parkinsonism during the clinical course of their illness. The administration of levodopa improved the symptoms of two patients, but not of the other three. Brain tissues from five age-matched neurologically normal subjects served as controls. Immunohistochemical assays were carried with antibodies against met-enkephalin, substance P, and calbindin-D28k. Irrespective of the clinical form of multiple system atrophy, the immunoreactivity with the antibodies was reduced at the dorsolateral portion of the striatum and the ventrolateral portions of the globus pallidus and of the substantia nigra. The woolly fiber arrangement of reaction product deposits seen in both segments of the globus pallidus of normal individuals was totally absent in the ventrolateral portions of the three patients who did not have a response to levodopa. By contrast, there were positively stained woolly fibers in globus pallidum segments of the two levodopa-responsive patients, even though their number and size were decreased in comparison with controls. These results indicate that the three clinical forms of multiple system atrophy share common topographic alterations of the striatal efferent system and that the severity of the involvement correlates with the clinically observed effect of levodopa on the parkinsonism.

Aged↗
PubMed1996

[Endoscopic treatment in colorectal lesions--especially on endoscopic mucosal resection].

Protruded polyps can usually be treated with conventional polypectomy technique. Slightly elevated lesions without malignant findings are treated with hot biopsy method if they are small enough (less than 5 mm). In order to treat flat or slightly depressed lesions or slightly elevated lesions larger than 5 mm, endoscopic mucosal resection (EMR) technique has been invented. Cancers confined to the mucosa or those only minimally invading the submucosa can be completely removed with this method. However, if histological analysis of the resected specimen shows that the cancer invades the submucosa massively or permeating the vessels, surgical treatment should be added, because otherwise there would be risk of cancer residue or metastasis. When a lesion is suspected to be a submucosal cancer by endoscopic findings and pit pattern analysis from the beginning, then surgical resection is the treatment of choice. Laterally spreading tumors, especially the homogeneous granular type, are good indication for EMR or endoscopic piecemeal mucosal resection (EPMR). It is important to remove the lesion completely confirming that the resection margin is covered with normal pits.

Colectomy↗
PubMed1995

Topographic involvement of the striatal efferents in basal ganglia of patients with adult-onset motor neuron disease with basophilic inclusions.

This report concerns the topographic immunohistochemical analysis of the putamen, globus pallidus (GP) and substantia nigra (SN) of two patients with adult-onset motor neuron disease with basophilic inclusions (MND/BIs), seven patients with sporadic classic amyotrophic lateral sclerosis (sporadic ALS) and five neurologically normal individuals. The striatal efferent terminals of the GP and SN were visualized immunohistochemically using antibodies to met-enkephalin (MEnk) and substance P (SP). In specimens from patients with sporadic ALS and normal subjects there was intense immunostaining for MEnk and SP throughout the external and internal segments of the GP, respectively. By contrast, a marked reduction of MEnk- and SP-positive striatal efferents was seen in the ventrocaudal portions of both GP segments from the MND/BIs patients. Moreover, while MEnk-positive striosomes was readily detected in the putamen of normals and sporadic ALS patients, there was significant reduction in MEnk immunoreactivity, and no evidence of striosomal organization in the putamen of MND/BIs patients. In addition, whereas the SN of patients with sporadic ALS expressed SP, the ventrolateral SN portion of the MND/BIs patient tested had reduced immunoreactivity. The present findings on patients with MND/BIs may represent a reflection of the topographic striatum degeneration in this disease and appear to provide additional evidence for the heterogeneity of MND.

Adult↗
PubMed1995

Effects of benidipine, a long-acting calcium antagonist, on renal functions in anaesthetized spontaneously hypertensive rats.

1. The effects of benidipine, a long-acting calcium antagonist, on renal functions were determined in anaesthetized spontaneously hypertensive rats (SHR), as compared with those of amlodipine. 2. Benidipine at 3 and 10 mu g/kg (i.v.) significantly increased urine volume, sodium (Na) and potassium (K) excretions with no change in creatinine clearance (C-CRE). The increase in K excretion was relatively slight. Benidipine increased p-amino-hippuric acid clearance (C-PAH) without any change in C-CRE and, thus, decreased filtration fraction (FF). 3. On the other hand, amlodipine at 300 mu g/kg (i.v.) significantly increased Na and K excretions, but did not change FF. 4. Thus benidipine, but not amlodipine, can dilate glomerular efferent arteriole as well as afferent arteriole in SHR. It is, therefore, expected that benidipine would not induce intraglomerular hypertension, which could result in the progression of glomerular injury. 5. Benidipine at 3 mu g/kg (i.v.) increased lithium clearance, while it decreased CRE concentration and increased Na concentration in the stop-flow urine from the distal tubule. 6. These results suggest that benidipine produces diuresis by the inhibition of water and Na reabsorption at both the proximal and the distal tubules.

Amlodipine↗
PubMed1995

Can interstitial pneumonia as the sole presentation of collagen vascular diseases be differentiated from idiopathic interstitial pneumonia?

We prospectively followed 68 patients diagnosed as idiopathic interstitial pneumonia (IIP) over a period of 1-11 years. Thirteen patients (19%) subsequently developed systemic manifestations of collagen vascular diseases (CVD) and were diagnosed as having had interstitial pneumonia as the sole presentation of CVD (CVD-IP). Compared with the 55 IIP patients, the 13 CVD-IP patients were relatively younger, predominantly female, and had a lower incidence of dust inhalation in their history. They also had a higher erythrocyte sedimentation rate, higher incidence of the x-ray finding of discoid atelectasis in the lower lung fields, and a better prognosis than the IIP patients. However, these features did not clearly distinguish the two groups. We conclude that the patients clinically and/or histologically defined as suffering from IIP cannot be distinguished from CVD-IP patients before systemic signs of CVD appear in the latter group.

Adult↗
PubMed1995

Protective effects of KW-3902, an adenosine A1-receptor antagonist, against cisplatin-induced acute renal failure in rats.

We investigated possible renal protective and therapeutic effects of KW-3902 (8-(noradamantan-3-yl)-1,3-dipropylxanthine), a novel and potent adenosine A1-receptor antagonist, on cisplatin-induced acute renal failure (ARF). ARF was induced in rats by a single injection of cisplatin-induced acute renal failure (ARF). ARF was induced in rats by a single injection of cisplatin (5 mg/kg, i.v.). Prophylactic treatment with KW-3902 (0.01-1 mg/kg, p.o., twice a day) significantly attenuated the increases of serum creatinine (S-CRE) and urea nitrogen (S-UN) induced by cisplatin. On the other hand, neither furosemide nor trichlormethiazide showed any ameliorating effects against the cisplatin-induced ARF. In the clearance study, the cisplatin-treatment induced marked decreases of glomerular filtration rate (GFR), renal plasma flow (RPF), and reabsorptions of water, sodium and potassium at tubular sites, in comparison with those in untreated normal rats. KW-3902 (0.1 mg/kg, p.o., twice a day) significantly improved these deteriorated glomerular and tubular functions. In the rats with established cisplatin-induced ARF, KW-3902 ameliorated the cisplatin-induced reductions of GFR, RPF, and reabsorptions of water, sodium and potassium at tubular sites. These results suggest that activation of adenosine A1-receptors is involved in the pathogenesis of cisplatin-induced ARF. The adenosine A1-receptor antagonist may be useful for the treatment of cisplatin-induced ARF.

Absorption↗
PubMed1995

Effects of KW-3902, an adenosine A1-receptor antagonist, on ascites volume in puromycin aminonucleoside (PAN)-induced nephrotic rats.

We investigated the effects of KW-3902 (8-(noradamantan-3-yl)-1,3-dipropylxanthine), a potent adenosine A1-receptor antagonist, on the nephrotic edema induced by puromycin aminonucleoside (PAN; 100 mg/kg, i.v.) in rats. The treatment with PAN decreased urine volume and urinary excretions of sodium and potassium, resulting in the ascites formation in 7 days. In rats with the nephrosis, KW-3902 (0.01-1 mg/kg/day for 3 days, p.o.) showed diuretic effects and reduced the volume of ascites, as was the case with furosemide (30 mg/kg/day) and trichlormethiazide (1 mg/kg/day). These results suggest that even in the nephrotic state, the adenosine A1-receptor antagonist can be an effective diuretic to ameliorate edema.

Animals↗