PubMed HealthSearch

Biomedical subjects

M Fukui

Publications and source records attributed to M Fukui.

At least 109 records · Page 6Linked to original sources

[Epstein-Barr virus-associated malignant lymphoma in an immuno-deficiency patient: a case report].

Human infection with Epstein-Barr (EB) virus occurs commonly, and EB virus exists in the B cell as a cryptic infection. Infected B cells become immortal by expressing both the EBNA2 and the LMP1 genes derived from the EB virus. Under normal condition of cellular immunity, the T cells recognize the EBNA2 and LMP1 as foreign proteins and attack the immortal B cells. However, under the condition of immunodeficiency, the immortal B cells can proliferate and form a tumor. We report a case of malignant lymphoma associated with immuno-deficiency which may correspond to this mechanism. A 33-year-old woman, who had an immuno-deficiency due to treatment for leukemia, had a progressing hemiparesis on her left extremities. Magnetic resonance imagings revealed a ring enhanced tumor with massive brain edema in the right fronto-parietal lobe. Stereotactic biopsy was performed and histological examination showed it to be a malignant lymphoma. The tumor cells were positive for L26 (B cell marker), CD79a LMP1, and EBNA2. They were negative for UCHL-1 and CD3 (T cell marker). According to these results, this lymphoma was caused by EB virus infection under the condition of immuno-deficiency.

Adult

[Two cases of mesial temporal lobe epilepsy associated with old intracerebral hemorrhage in the lateral temporal lobe without "dual pathology"].

Two cases of intractable temporal lobe epilepsy associated with old intracerebral hemorrhage in the lateral temporal lobe were reported. Although preoperative magnetic resonance imaging (MRI) failed to reveal hippocampal atrophy with T2 hyperintensity, electrocorticographic (ECoG) recording with chronic invasive subdural electrodes indicated the mesial temporal lobe to be an ictal onset zone. After anterior temporal lobectomy involving the lesion and hippocampectomy, the patients became seizure-free. Hippocampal sclerosis, namely "dual pathology", was not noted on histological examination. Careful ECoG recording with chronic subdural electrodes is mandatory even when the preoperative MRI does not demonstrate the radiological hippocampal sclerosis.

Adult

Carbon-11-methionine PET in focal cortical dysplasia: a comparison with fluorine-18-FDG PET and technetium-99m-ECD SPECT.

UNLABELLED: Focal cortical dysplasia is one of the known neuronal migration disorders and has recently been recognized as a cause of intractable epilepsy. In this study, we assessed the 11C-methionine (MET) uptake in focal cortical dysplasia by PET, and then compared the results with that of 18F-fluoro-2-deoxy-D-glucose (FDG) PET and 99mTc-ethyl cysteinate dimer (ECD) SPECT. METHODS: Four patients (3 men, 1 woman; age range 16-68 yr) were examined by PET and SPECT for a presurgical examination of medically intractable seizures. In all 4 patients, 11C-MET PET was performed for 15 min, started 15 min after the administration of 511-662 MBq MET. In 3 of 4 patients, FDG PET was performed for 15 min, and started 20 min after the administration of 185-370 MBq FDG. In all 4 patients, the cerebral blood flow was also evaluated by 99mTc-ECD SPECT for 15 min after the administration of 600 MBq ECD. RESULTS: In MET PET, all 4 lesions were visually recognized to have high MET uptake areas. The MET uptake of the lesions was 1.44 +/- 0.30 for the standardized uptake value (SUV) (ranging from 0.99-1.61). In FDG PET, 2 lesions were demonstrated to have low uptake areas (3.82 in SUV) while 1 had an ictal high uptake (4.74 in SUV). In ECD SPECT, 1 lesion demonstrated hypoperfusion and 1 ictal hyperperfusion while 2 showed no abnormalities. All 4 patients underwent a cortical resection and the microscopic examinations were consistent with those of focal cortical dysplasia but no evidence of a tumor was found. CONCLUSION: MET PET is useful for identifying focal cortical dysplasia as a high uptake area.

Adolescent

Pharmacokinetics of cefdinir and its transfer to dialysate in patients with chronic renal failure undergoing continuous ambulatory peritoneal dialysis.

Cefdinir (CAS 91832-40-5) was administered orally as a 100-mg capsule (Cefzon) to a total of 12 patients with chronic renal failure undergoing continuous ambulatory peritoneal dialysis (CAPD) to investigate changes in the serum concentrations, excretion rate into the dialysate and serum-protein binding of cefdinir. Cmax values were 1.64-4.34 micrograms/ml, t1/2 values were 10.8-21.9 h., and AUC values were 31.1-73.1 micrograms.h/ml (0-30 h) in four patients given a single oral dose of 100 mg of cefdinir as a capsule. About 1 microgram/ml of cefdinir had still remained in the blood of all the patients 24 h after administration. The serum concentrations of cefdinir were dose-dependent in four patients of each group who were given an oral daily dose of 100 mg for 3 to 8 days and 200 mg (2 capsules) for 4 to 14 consecutive days. No marked change in laboratory test values or clinical symptoms before and after administration were observed in these dose regimes. Protein levels of 5.17-5.71 g/day were eliminated from the peritoneal dialysate and urine. Cefdinir inhibited 90 to 100% of the clinical isolates such as Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli and other enteric bacteria causing catheter infection and peritonitis, and its antibacterial activity was stronger than that of amoxicillin (CAS 26787-78-0) or cefaclor (CAS 53944-73-3) against these clinical isolates.

Adult

Antibodies to glutamic acid decarboxylase in Japanese diabetic patients with secondary failure of oral hypoglycaemic therapy.

Some patients with non-insulin-dependent (Type 2) diabetes mellitus (NIDDM) are positive for antibodies to glutamic acid decarboxylase (anti-GAD), which have been shown to be a useful marker for the diagnosis and prediction of insulin-dependent (Type 1) diabetes mellitus (IDDM). Anti-GAD positive NIDDM patients tend to develop insulin deficiency. We investigated the prevalence of anti-GAD in 200 NIDDM with secondary failure of oral hypoglycaemic therapy (SF) and 200 NIDDM well controlled by diet and/or sulphonylurea agents (NSF). Twenty-two of 200 (11%, p < 0.05) SF patients and 6 of 200 (3%) NSF patients were anti-GAD positive. The positive. The positive rate for anti-GAD was as high as 23.8% in the non-obese and insulin deficient SF patients. The SF patients with anti-GAD tended to be non-obese and to have an impaired release of endogenous insulin. The internal before development of secondary failure was not associated with the presence of anti-GAD in this study. In conclusion we found that anti-GAD was positive in as many as 11% of the SF patients, suggesting that autoimmune mechanisms may play an important role in the pathogenesis of secondary failure or sulphonylurea therapy.

Analysis of Variance

Effects of treatment with angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor antagonist (AIIRA) on renal function and glomerular injury in subtotal nephrectomized rats.

The aim of this study was to determine if treatment with angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor antagonists (AIIRA) might decrease urinary albumin excretion and prevent glomerular enlargement and glomerulosclerosis in subtotal (5/6) nephrectomized rats. Morphometric image analysis of glomeruli was also performed in the subtotal nephrectomized rats. The nephrectomized rats were treated with ACEI (enalapril 100 mg/l), AIIRA (L-158,809 10 mg/l) or TRX (reserpine 5 mg/ l, hydralazine 80 mg/l, and hydrochlorothiazide 25 mg/l) and euthanized at 16 weeks after renal ablation. Treatments were started at 2 weeks (early treatment: Group I) or 8 weeks (later treatment: Group II) after the ablation. ACEI and AIIRA treatments were equally and significantly effective in limiting albuminuria and progression of glomerular sclerosis. TRX was also as effective in decreasing urinary albumin excretion and preserving the renal function as ACEI or AIIRA in Group I. The improvement of albuminuria, glomerular enlargement and sclerosis after these treatments in Group II was significantly less than that in Group I. It appears that the early treatment with angiotensin converting enzyme inhibitor, angiotensin II receptor antagonist or reserpine, hydralazine and hydrochlorothiazide (TRX) may prevent glomerular injury in human patients with renal hypertension.

Albuminuria

Effects of benidipine hydrochloride on antioxidant enzyme activity in stroke-prone spontaneous hypertensive rats (SHR-SP).

Effects of benidipine hydrochloride or triple therapy (hydralazine, reserpine, and hydrochlorothiazide) on renal cortical and medullary intrinsic antioxidant enzyme (AOE) activity were evaluated in stroke-prone spontaneously hypertensive rats (SHR-SP) as an animal model for human essential hypertension with cerebral stroke. This study showed a significant decrease of renal intrinsic glutathione peroxidase (GSH-Px) activity in untreated SHR-SP. Renal GSH-Px activity in untreated SHR-SP was significantly lower than that in Wister Kyoto rats (WKY) as a normotensive reference strain. GSH-Px activity in SHR-SP was significantly improved after benidipine hydrochloride therapy. Levels of urinary albumin excretion or creatinine clearance (Ccr) in SHR-SP were also improved after the therapy. Glomerular sclerosis index was slightly improved in SHR-SP treated with benidipine hydrochloride according to light microscopic analysis. It appears that hypertension may influence the renal intrinsic GSH-Px activity, albuminuria, and Ccr in SHR-SP. Thus it is indicated that control of blood pressure may improve the GSH-Px activity in SHR-SP.

Animals

Diagnostic significance of antibodies to glutamic acid decarboxylase in Japanese diabetic patients with secondary oral hypoglycemic agents failure.

Some non-insulin-dependent diabetes mellitus (NIDDM) patients are positive for antibodies to glutamic acid decarboxylase (anti-GAD), and they tend to develop insulin deficiency. The aim of this study was to evaluate the prevalence of anti-GAD in NIDDM with secondary failure of sulfonylurea agents (NIDDM-SF) and to investigate the diagnostic significance of seropositivity for anti-GAD in NIDDM-SF patients by evaluating human leukocyte antigen (HLA)-DRB1 alleles concurrently. The prevalence of anti-GAD in NIDDM-SF, NIDDM, and new-onset (within 1 year after onset) insulin-dependent diabetes mellitus (IDDM) was 9.3% (39/420), 3.1% (12/392), and 65.0% (13/20), respectively. Pancreatic beta cell function deteriorated in NIDDM-SF patients positive for anti-GAD. HLA-DRB1 allele typing revealed that NIDDM-SF patients positive for anti-GAD were significantly associated with DRB1*0901 (RR = 2.81, P < 0.01), which is one of the susceptible alleles to IDDM. Shorter interval before development of secondary failure and insulin deficiency were significantly associated with the presence of DRB1*0901 (P < 0.05) in NIDDM-SF patients positive for anti-GAD. In conclusion, nearly 10% of NIDDM-SF patients are positive for anti-GAD, suggesting that an autoimmune mechanism might play an important role in the pathogenesis of NIDDM-SF patients. In addition, a combination of serological marker (anti-GAD) and genetic marker (HLA-DRB1) is useful for predicting clinical course of NIDDM patients with secondary failure of sulfonylurea agents.

Adolescent

A chronological evaluation of experimental brain infarct by diffusion-mapping and magnetization transfer contrast imaging.

BACKGROUND AND PURPOSE: There is a complex system of evolving physiochemical processes in the ischemic brain. The evaluation of this chain of processes is a major challenge of recent stroke studies. Two magnetic resonance imaging techniques: diffusion-weighted (DW) and magnetization transfer contrast (MTC) imaging were introduced in experimental studies and were shown to have sensitivity for different stages of brain infarct. MATERIALS AND METHODS: We used a reproducible middle cerebral artery (MCA) occlusion model in rat to examine infarcts of different time courses. Magnetic resonance T2-weighted (T2). DW, and MTC imaging were performed 3 h, 1 d, 3 d, 5 d, 2 w, 3 w, and 4 w after MCA occlusion. Haematoxylin/eosin (HE) stained sections, which revealed sub regions within infarct lesions, were compared to T2, DW, diffusion-mapping and MTC-mapping images. RESULTS: On DW images 3 hours post occlusion lesions were detected as an area with high signal intensity, while T2 imaging does not raise significant contrast of the lesion at this early stage. Three sub regions of the lesion having different ADCs, are discernible on diffusion-mapping images from 1 day to 7 days. The decrease of MTC effect was measured within the infarct lesion from core to marginal zone, from 7 days to 4 weeks. CONCLUSIONS: Diffusion-mapping imaging may help to examine brain infarction from 3 hours to 5 days. MTC imaging recognizes infarcts 7 days after the onset. Following this stage, MTC-mapping images may provide a quantitative method to assess infarct size.

Animals

Apparent diffusion coefficient (ADC) and magnetization transfer contrast (MTC) mapping of experimental brain tumor.

Brain tumor tissue contains different pathological areas, such as tumor cell rich parts, necrotic tissues, and cyst. Furthermore, both neovascularization and edema formation progress along with the tumor progression. In this study we employed diffusion weighted (DW) and magnetization transfer contrast (MTC) imaging to chronologically investigate the biological characteristics of a rat glioma. RG-2 glioma cells were implanted stereotactically into the right hemisphere of male Wistar rats. MR images were taken 1, 2 and 3 weeks after inoculation. Apparent diffusion coefficient (ADC) and MTC values were calculated as follows; ADC = -ln (SI-DW/SI-T2)/1096, MTC = 1-SI-MTon/SI-MToff. Each mapping image was made based on the calculated average values of four pixels. The spatial signal changes and the real values were compared to the histological findings. The apparent increase of ADC was noted in the parenchyma adjacent to tumor suggesting the progression of edema. The tumor itself had similar or slightly increased ADC. Cystic and necrotic components appeared 2 weeks after implantation and they showed significantly higher ADC than those calculated in the contralateral putamen. On the other hand, MTC was slightly decreased in the parenchyma adjacent to the tumor, markedly within the tumor, and maximally in the cystic and necrotic area suggesting accumulation of macromolecules such as growth factors, cytokines, and serum albumin.

Animals

Medulloblastoma: survival and late recurrence after the Collins' risk period.

Sixty-three patients with cerebellar medulloblastoma were treated between 1963 and 1992 at our institution. Among them, 10 patients have survived beyond the Collins' risk period. These included 6 males and 4 females who ranged in age from 6 months to 12 years at the time of diagnosis. A total removal of the tumor was achieved in 4 patients, while there was a subtotal removal in 3, and a partial removal in 3. Histologically, 6 tumors were classified as a classical type of medulloblastoma, and 4 were diagnosed as being a desmoplastic type. Postoperatively, 9 patients received craniospinal radiation therapy, and one received local radiation to the primary site. During the follow-up period of 3.9-25.4 years, 5 patients have been in continuous remission for from 14.2 to 25.4 years and are leading normal lives, 2 have survived for 18.1 and 18.5 years with mild to moderate neurological deficits, while the remaining 3 died after the Collins' risk period. Two out of these last 3 patients were under the age of one year at the time of onset, while the remaining one died after a second recurrence. We conclude that careful follow-up is needed for all long-term survivors even after the Collins' risk period, especially for those who were under the age of 1 year at onset and who failed in the initial treatments.

Adolescent

Traumatic aneurysm of the superficial temporal artery in an elderly patient.

An elderly patient suffering from the posttraumatic development of a superficial temporal artery (STA) aneurysm is described. Because the patient had renal dysfunction, angiography was performed through a direct puncture of the anterior branch of the STA in order to reduce the required dosage of contrast medium. With the patient under local anesthesia, the STA was ligated proximal and distal to the aneurysm, and thereafter removed. The diagnosis and treatment of traumatic STA aneurysms in the elderly are discussed.

Aged

Micro-anatomical study of the carotid cave.

The surgical treatment of aneurysms located in the carotid cave is often hazardous and difficult. We studied the micro-anatomy of the carotid cave and its neighbourhood by microscopic observation and histological examination using 50 sides from 25 autopsy cases. The carotid caves were found in 34 out of the 50 sides (68%) examined and were usually located in the posteromedial aspect of the carotid dural ring. They were classified into three types according to the topographic micro-anatomy: the slit-type (17/50, 34%) which showed a small, thin recess of the dura mater with fine connective tissue loosely adhered to the carotid wall; the pocket-type (12/50, 24%) which had a definite dural pouch with the apex attached to the vessel wall; and the mesh-type (5/50, 10%) which formed a slit- or pocket-type dural cave covered with a mesh-like dural roof. The remaining 16 sides (32%) showed tight dural attachment without any caval structure around the dural ring. The posteromedial portion of the carotid dural ring had no contact with any bony structure, and this distinct anatomical feature thus appear to facilitate the formation of the carotid cave. Furthermore, the availability of this potential space and the closely situated origin of the superior hypophyseal artery as well as the haemodynamic effect of the internal carotid artery may allow the development of the carotid cave aneurysm.

Adult

Thalamic gliomas: a clinicopathologic analysis of 20 cases with reference to patient age.

Twenty patients (M 11, F9; ranging from 1-77 years old) with histologically proven glial tumours in the thalamic region, treated from 1979 until 1994 at Kyushu University Hospital were retrospectively reviewed and analysed in order to elucidate their clinical and neuropathological characteristics. The initial common clinical manifestations were those of increased intracranial pressure or motor weakness. The histological diagnosis of the tumour was pilocytic astrocytoma in 2 patients, fibrillary astrocytoma in 7, anaplastic astrocytoma in 7, and glioblastoma multiforme in 4. The initial treatment was surgery alone in 4 patients, surgery followed by radiation therapy in 5, surgery followed by radiation therapy and chemotherapy in 9, and conventional radiation therapy alone in 2 patients. The 3-year overall actuarial survival rate for all patients was 20% but was related to both the histological type and the age of the patients: As a result, the rate was 44% for patients with low-grade astrocytoma compared to 0% for those with high-grade astrocytoma. While 5 out of 11 patients under the age of 25 years at their initial presentation have survived for from 2-16 years after the diagnosis, all patients presenting after the age of 25 years died within 3 years after treatment. Thalamic glial tumours are not a homogeneous group of tumours in terms of clinical behaviour and histopathological features, and the poor overall results, especially in adult tumours, thus emphasise the need for continued research in the treatment of these tumours.

Adolescent

DNA typing of HLA in the patients with moyamoya disease.

Moyamoya disease is a clinical entity demonstrating a chronic occlusion of the cerebrovascular system. Although some possible etiological factors have been postulated, the etiology of this disease is still unknown. So far, some investigations have suggested the association between moyamoya disease and HLA in the serological typing. However, DNA typing of HLA have not been performed yet. Thus, we performed DNA-typing of HLA in the unrelated Japanese patients with definite moyamoya disease, using the polymerase chain reaction-sequence specific oligonucleotide probe (PCR-SSOP) technique. In the total patients, DQB1*0502 had a positive association with the disease. On the other hand, DRB1*0405 and DQB1*0401 showed a negative association. In comparing the early-onset and late-onset groups, two groups did not share the same disease associated alleles at all. Thus, the etiology of moyamoya disease seem to have a genetic background. Furthermore, different genetic factors might also be involved in the difference between the early-onset and late-onset groups.

Adult

Leser-Trélat sign with anaplastic ependymoma--an autopsy case.

A 36-year-old Japanese male, who 7 years previously had been diagnosed as having an ependymoma in the left parietal region, had received surgery, chemotherapy and radiotherapy. He later developed a rapid growth of multiple skin lesions on his back and extremities, which coincided with a regrowth of the tumor. Postmortem examination revealed that the ependymoma showed anaplastic transformation and necrosis; however, no malignancy was observed in the extracranial organs. The skin lesions were histologically diagnosed as seborrheic keratoses. We have, therefore, diagnosed the patient as having Leser-Trélat sign associated with anaplastic ependymoma.

Adult

Expression of neurofibromatosis 2 protein in human brain tumors: an immunohistochemical study.

The neurofibromatosis 2 (NF2) gene-encoded protein, named merlin, may function as a molecular linkage connecting cytoskeleton and plasma membrane. Merlin is thought to play a crucial role as a tumor suppressor not only in hereditary NF2-related tumors, but also in sporadic tumors such as schwannomas, meningiomas and gliomas. Using a merlin-expression vector system, we raised specific antiserum against merlin. We observed the intracellular distribution of merlin in cultured glioma cells, and further investigated merlin expression in 116 human brain tumors. Immunofluorescence microscopy revealed that merlin was localized beneath the cell membrane and concentrated at cell-to-cell adhesion sites, where actin filaments are densely associated with plasma membrane. By immunohistochemistry, none of the schwannomas from either NF2 patients or sporadic cases showed any immunoreactivity, while normal Schwann cells of cranial nerves were immunopositive. In meningiomas, merlin expression was frequently seen in the meningothelial subtype (8/10, 80%), but no expression could be detected in either the fibrous or the transitional variant. Most normal astrocytes were negative; however, reactive astrocytes often expressed merlin. Glioblastomas and anaplastic astrocytomas were found to be strongly positive, and focal positive staining was observed in fibrillary and pilocytic astrocytomas. Thus, the loss of merlin appears to be integral to schwannoma formation and the differential pathogenesis of meningioma subtypes. However, merlin alterations do not appear to play a critical role in either the tumorigenesis or malignant transformation of neoplastic astrocytes.

Brain Neoplasms