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Biomedical subjects

T Matsui

Publications and source records attributed to T Matsui.

At least 325 records · Page 18Linked to original sources

Increase of glial fibrillary acidic protein fragments in the spinal cord of motor neuron degeneration mutant mouse.

We analyzed protein fractions extracted from the spinal cord of the motor neuron degeneration (Mnd) mouse, a mutant that exhibits progressive degeneration of lower spinal motor neurons, by one- and two-dimensional polyacrylamide gel electrophoresis (PAGE) after solubilization of the tissue with medium containing sodium dodecyl sulfate (SDS)-urea during growth of the animal, in comparison with those of age-matched controls (C57BL/6). Several protein spots were detected around a region of pI 5.6-6.0 and molecular mass of 35-50 kDa in Mnd spinal cord tissue on the two-dimensional PAGE separation profile with Coomassie brilliant blue staining, while only a few spots around the same region were found in the control spinal cord. These spots were all immunoreactive with an antibody against glial fibrillary acidic protein (GFAP), a cytoskeleton filamentous protein specific to astroglial cells. The protein spot with molecular mass of 50 kDa showed immunoreactivity with anti-GFAP antibody, had a blocked amino-terminus, and is assumed to be intact GFAP. Several protein spots with slightly smaller molecular masses of 35 to 48 kDa lacked the head domain of the GFAP molecule as a result of cleavage at the 29th and 56th residues from the amino terminus. In Mnd spinal cord tissue, the densities of the immunoreactive GFAP bands with smaller molecular masses increased with development, and became dominant at the time of the appearance of behavioral paralytic gait around 6 to 7 months of age. These results suggest that the increased GFAPs devoid of head domains are related to the degenerative loss of motor neurons in the Mnd spinal cord. Histopathological and GFAP immunohistochemical examination of Mnd spinal cord preparation demonstrated progressive degenerative loss of motor neurons, and considerable increases in number of GFAP-stained astrocytes in the ventral horn at 7 to 9 months of age. These processes of degenerative loss of motor neurons and proliferation of reactive astrocytes with increased levels of fragmented GFAP in the Mnd spinal cord during development seem to be characteristic and preceded the deterioration of motor activities in this animal model of amyotrophic lateral sclerosis.

Amino Acid Sequence↗

Rho-kinase phosphorylates COOH-terminal threonines of ezrin/radixin/moesin (ERM) proteins and regulates their head-to-tail association.

The ezrin/radixin/moesin (ERM) proteins are involved in actin filament/plasma membrane interaction that is regulated by Rho. We examined whether ERM proteins are directly phosphorylated by Rho-associated kinase (Rho-kinase), a direct target of Rho. Recombinant full-length and COOH-terminal half radixin were incubated with constitutively active catalytic domain of Rho-kinase, and approximately 30 and approximately 100% of these molecules, respectively, were phosphorylated mainly at the COOH-terminal threonine (T564). Next, to detect Rho-kinase-dependent phosphorylation of ERM proteins in vivo, we raised a mAb that recognized the T564-phosphorylated radixin as well as ezrin and moesin phosphorylated at the corresponding threonine residue (T567 and T558, respectively). Immunoblotting of serum-starved Swiss 3T3 cells with this mAb revealed that after LPA stimulation ERM proteins were rapidly phosphorylated at T567 (ezrin), T564 (radixin), and T558 (moesin) in a Rho-dependent manner and then dephosphorylated within 2 min. Furthermore, the T564 phosphorylation of recombinant COOH-terminal half radixin did not affect its ability to bind to actin filaments in vitro but significantly suppressed its direct interaction with the NH2-terminal half of radixin. These observations indicate that the Rho-kinase-dependent phosphorylation interferes with the intramolecular and/ or intermolecular head-to-tail association of ERM proteins, which is an important mechanism of regulation of their activity as actin filament/plasma membrane cross-linkers.

3T3 Cells↗

Thiazolidinedione induces the adipose differentiation of fibroblast-like cells resident within bovine skeletal muscle.

To investigate the role of peroxisome proliferator-activated receptor gamma (PPARgamma) in adipocyte formation within the skeletal muscle of beef cattle, fibroblast-like cells were isolated from the longissimus muscle of cattle and cultured with activators of murine PPARgammaA thiazolidinedione T-174, which is a specific ligand for PPARgamma, stimulated adipose differentiation (evaluated by counting differentiated adipocytes under microscopic observation) in a dose-dependent fashion. A peroxisome proliferator Wy14,643 which strongly activates the alpha isoform of murine PPAR also stimulated differentiation but its potency was weaker than that of T-174. Unexpectedly, 15-deoxy-Delta12,14-prostaglandin J2, which is believed to be an endogenous ligand for PPARgamma, could not induce adipose differentiation in doses which have been found to be effective on rodent cells. Immunoblotting analysis confirmed the significant expression of PPARgamma protein in fibroblast-like cell cultures prepared from bovine skeletal muscle. In conclusion, bovine skeletal muscle contains adipose precursor cells expressing functionally active PPARgamma.

Adipocytes↗

Absence of association of alpha1-antichymotrypsin polymorphisms with Alzheimer's disease: a report on autopsy-confirmed cases.

alpha1-Antichymotrypsin (ACT) polymorphisms were examined in 79 cases with autopsy-confirmed Alzheimer's disease (AD) as well as in 28 cases with autopsy-confirmed nonneurological diseases to test the hypothesis that ACT polymorphisms confer a risk to an individual to develop AD. Neither ACT genotype frequency nor ACT allele frequency in the AD group was significantly different from the control group. The ACT polymorphic pattern was essentially the same among apolipoprotein E (apoE) epsilon4 carriers and noncarriers. The age at onset of AD was not significantly affected by the inherited dose of ACT/A allele. Taking together, our observations do not confirm the effect of the ACT/A allele as a risk factor for developing AD in addition to the ApoE epsilon4 allele.

Adolescent↗

Mutation in the alpha-synuclein gene and sporadic Parkinson's disease, Alzheimer's disease, and dementia with lewy bodies.

Recently, alpha-synuclein attracted attention when Polymeropoulos and colleagues identified a missense mutation of this gene (Science 276:2045-2047, 1997), which is responsible for a form of early-onset familial Parkinson's disease (PD). Immunohistochemically, alpha-synuclein is localized in Lewy bodies, characteristic brain pathology of PD, dementia with Lewy bodies (DLB), and Alzheimer's disease (AD), suggesting that this protein may link these common neurological diseases. Exploration of the possibility that the same mutation of the alpha-synuclein gene as that in familial PD (Ala53Thr) may also confer susceptibility to sporadic PD, DLB, and AD revealed the mutation in none of the samples of 329 cases and 230 controls examined, suggesting that this mutation is not involved in these neurological diseases.

Aged↗

A father and son with Turcot's syndrome: evidence for autosomal dominant inheritance: report of two cases.

Typical Turcot's syndrome is characterized by the association of a brain glioma together with multiple colonic polyposis, in which the number of polypoid lesions is small and the association of colonic cancer occurs at a younger age than in familial adenomatous polyposis. We describe a family in which both the father and his son presented with typical Turcot's syndrome without parental consanguinity. This is the first report of a family that is considered to follow an autosomal dominant inheritance. After reviewing 25 documented cases in which the average age of death was 20.3 years old, it was learned that the major cause of death was brain tumor (76 percent) and the minor cause was colon cancer (16 percent). Patients were very young and, therefore, unlikely to have produced a child before their death. These facts seem to support the theory that Turcot's syndrome is an autosomal dominant disorder.

Adenomatous Polyposis Coli↗

Long pedunculated colonic polyp composed of mucosa and submucosa: proposal of a new entity, colonic muco-submucosal elongated polyp.

We encountered 15 patients with colonic polyps showing histologic features that did not belong to any of the known categories. All polyps were elongated and drumstick-shaped, with lengths of 12 to 160 (mean, 29 mm) mm. Histologically, the polyps were covered with normal mucosa and consisted of edematous, loose, fibrous, connective tissues and dense, fibrous submucosal layers, often showing dilation of blood vessels and lymphatics. Although the mechanism of generation of such polyps remains unknown, their elongation may be caused by intestinal motion. Because this kind of polyp has not been described previously outside Japan, we here introduce a new type of polyp, which we have proposed calling the colonic muco-submucosal elongated polyp.

Adult↗

Fermentation of soybean meal with Aspergillus usamii improves zinc availability in rats.

Soybean meal was fermented with Aspergillus usamii to improve zinc availability through the degradation of phytic acid. Rats fed a diet containing fermented soybean meal showed greater femoral zinc than did animals fed a diet containing regular soybean meal. Zinc solubility in the small intestine was higher in the rats fed fermented soybean meal than in the rats fed regular soybean meal. These results suggested that fermentation with Aspergillus usamii improved zinc availability in dietary soybean meal, which was induced by the increase of zinc solubility in the small intestine. Adding the same amount of phytate that was contained in the regular soybean meal-based diet did not affect the amount of zinc present in rats fed a fermented soybean meal-based diet with sodium phytate. Phytase activity was found in fermented soybean meal, and this activity may degrade added phytate in fermented soybean meal-based diet.

Animal Feed↗

Idiopathic peripheral neuropathy in the horse with knuckling: muscle and nerve lesions in additional cases.

We have previously reported a pathological investigation of peripheral neuropathy in a horse with knuckling. This report describes details of the muscle and peripheral nerve lesions in two additional cases of light horse yearlings with knuckling. The skeletal muscles showed neurogenic atrophy characterized by scattered single angular fibers, fiber grouping, and fiber-type grouping. The severity of muscle lesions increased distally; that is, both fore- and hindleg muscles were affected more severely than cervical and dorsal muscles. In the peripheral nervous system, a number of Renaut bodies appeared to be common in the nerve fascicles. Pathological alterations indicating demyelination, remyelination and regeneration of nerve fibers were occasionally observed. The most common abnormality was myelin ovoids or myelin debris infiltrated by macrophages. Occasionally, myelinated axons were seen containing accumulations of organelles, often associated with buckling of the myelin. The myelin sheath occasionally formed axonal outpouching containing accumulations of mitochondria and dense lamellar bodies. Histochemically, intramuscular nerve fibers presented multiple arborization and collateral ramification, indicating relapsing denervation and reinnervation. Also seen were the fibers with myelin balloons or swollen segments considered as being degenerative processes. The distribution patterns of muscular lesions in the affected animals were indicative of systemic distal denervation atrophy. In addition, peripheral nervous lesions that selectively involve the distal parts of axons and an absence of abnormalities in neuronal cell bodies in the spinal cord suggest a dying-back neuropathy. It was concluded that this disease should be classified as a distal axonopathy.

Animals↗

Pancreatic pseudocyst associated with eating disorder.

We describe a patient with an eating disorder and hyperamylasemia originating from the salivary glands, who developed pancreatitis with a huge pancreatic pseudocyst. A 40-year-old woman was referred for the treatment of an eating disorder that had persisted for 9 years. She was admitted with abdominal pain, diarrhea, and nausea. She had bilateral parotid enlargement with marked elevation of total serum amylase level (3288 IU/l; normal range, 60-220) and an isolated increase of salivary isoamylase activity. After her symptoms resolved, oral intake of food was commenced. She subsequently complained of abdominal pain; this was associated with a slight elevation of serum pancreatic isoamylase and lipase levels, and a huge pancreatic pseudocyst was detected. Percutaneous drainage of the pseudocyst was successful. Endoscopic retrograde cholangiopancreatography demonstrated irregularity of the pancreatic duct. Based on these findings, the final diagnosis was parotid enlargement and acute exacerbation of chronic pancreatitis associated with a pancreatic pseudocyst in a patient with an eating disorder.

Adult↗

Histopathological and immunohistochemical studies of intracranial nervous-system tumours in four cattle.

Intracranial nervous-system tumours were diagnosed in three of 1092 bovine necropsy specimens submitted to the Department of Veterinary Pathology, Obihiro University between April 1983 and March 1996. A fourth case was a referral from the Department of Veterinary Pathology, Rakuno Gakuen University. Histopathological examination revealed four types of tumour: intracranial malignant peripheral nerve sheath tumour (MPNST), choroid plexus papilloma, differentiated fibrillary astrocytoma and anaplastic (malignant) astrocytoma. Immunohistochemically, the intracranial MPNST was strongly positive for S-100 protein and vimentin, and in places weakly positive for glial fibrillary acid protein (GFAP). The choroid plexus papilloma was strongly positive for epithelial membrane antigen (EMA), keratin, S-100 protein and vimentin, and positive for GFAP in places. The cytoplasm and fibrous component in the differentiated fibrillary astrocytoma were strongly positive for S-100 protein and GFAP. The anaplastic (malignant) astrocytoma was strongly positive for vimentin, S-100 protein and keratin in the cytoplasm and fibrous processes, and weakly positive for GFAP and EMA in places. Myelin basic protein (MBP) and synaptophysin showed a weak positive reaction in the marginal areas of the tumour.

Animals↗

Adrenocortical tumor in a patient with familial adenomatous polyposis: a case associated with a complete inactivating mutation of the APC gene and unusual histological features.

Familial adenomatous polyposis (FAP) is an autosomal dominant hereditary disorder caused by a germline inactivating mutation of the adenomatous polyposis coli (APC) gene. Patients with FAP sometimes develop various extracolonic manifestations including adrenocortical neoplasms. We present a 14-year-old boy with FAP who had an adrenocortical tumor with atypical histopathologic features, ie, sex-cord-like differentiation. Immunohistochemical studies of adrenal 4 binding protein (Ad4BP) and steroidogenic enzymes showed the capacity of these tumor cells to produce steroids. Genetic analysis of the tumor disclosed a two-hit mutation in APC: a germline 5-base pair deletion accompanied by a loss of the normal allele. Because there were no reports of genetic alterations in adrenocortical tumors developed in FAP patients, we examined 10 sporadic adrenal tumors (four carcinomas and six adenomas) for mutations in APC. However, no mutations were found in these 10 sporadic adrenal tumors. These results suggest that mutation of APC is also responsible for some fraction of the adrenocortical tumors: the tumor in this case is included.

Adenoma↗

Proliferative reaction of myelogenous leukemia cells with cytokines G-CSF, GM-CSF, M-CSF, SCF and TPO.

In recent years, many cytokines have been defined and some of them used clinically. In hematological malignancies, cytokines, including granulocyte colony-stimulating factor (G-CSF), have been widely used for leukopenia after chemotherapy. However, in acute myelogenous leukemia (AML), some leukemic cells may be induced to proliferate by these cytokines and they must be used with care. In this study, we have investigated cell reactivity and proliferation with G-CSF, granulocyte-macrophage colony-stimulating factor (GM-CMF), macrophage colony-stimulating factor (M-CSF), stem cell factor (SCF) and thrombopoietin (TPO) in cases of AML. We have also investigated the reactivity of some myeloid leukemia cell lines to TPO. G-CSF, GM-CSF, M-CSF, SCF and TPO caused proliferation of leukemic cells in 25%, 58.3%, 8.3%, 21.1% and 0% of cases, respectively. Because of this result, the use of G-CSF in AML should be regarded as potentially hazardous. TPO did not cause proliferation of leukemic cells in any case of AML, or in cell lines except MO7E, which is a megakaryocytic cell line. This result suggests that TPO might cause proliferation of some megakaryocytic leukemia cells. We cannot conclude that TPO does not cause proliferation of other AML cells, as the number of cases was small and it has been reported elsewhere that leukemia cells may proliferate when exposed to TPO in 50% of AML cases. Reactivity of AM L cells to TPO is an important factor when deciding the indications of TPO in AML and myelodysplastic syndrome.

Cell Division↗

Effects of recombinant human serum albumin on ascites in rats with puromycin aminonucleoside-induced nephropathy.

1. Recombinant human serum albumin (rHSA) (1 g/kg) significantly decreased the weight of ascites in rats with puromycin aminonucleoside-induced nephropathy. 2. Furosemide (1-30 mg/kg) did not significantly reduce the weight of ascites in this model. 3. A combination of rHSA (1 g/kg) with furosemide (5 mg/kg) significantly decreased the weight of ascites in this model compared with furosemide alone. 4. In consideration of these results, rHSA can be a substitute for human serum albumin products prepared from human plasma in therapy for ascites or edema in furosemide-resistant nephrotic syndrome.

Animals↗

14q11 abnormality and trisomy 8q are not common in Japanese T-cell prolymphocytic leukemia.

We studied ten cases of Japanese T-cell prolymphocytic leukemia (T-PLL) collected over the last 9 years. Median age was 61 years with a male predominance (M:F, 8:2). The main disease features were splenomegaly, lymphadenopathy, hepatomegaly, skin lesions and serous effusions. The clinical course was progressive with a median survival of 10 months. Immunophenotyping showed that the prolymphocytes had a post-thymic phenotype (TdT-, CD1a-, CD2+, CD3+, CD5+, CD7+) with a predominant CD4+ immunophenotype. Cytogenetic analysis showed no consistent abnormalities. 14q abnormality and trisomy 8q, which are frequently seen in T-PLL of Western countries, were found in only two and zero cases, respectively. We conclude that the clinical and biological characteristics of T-PLL in Japan are almost the same as those in Western countries. However, the cytogenetic findings of T-PLL in Japan might be different.

Adult↗

New cephalometric images with a workstation. A preliminary report.

OBJECTIVE: This study was designed to test the feasibility of several types of enhancements for cephalometric computed radiographs through use of the Fuji Computed Radiography system (Fuji Photo Film Corp., Tokyo, Japan). STUDY DESIGN: The material consisted of four lateral cephalograms made with the Fuji Computed Radiography system that were enhanced by varying the gradient levels before processing by means of both A-type (straight gradation) curves and workstation-type (peaked) curves. The four workstation-type images were set with optical densities at the peak of the curve at 1.5, 1.7, 1.9, and 2.1. Ten observers evaluated eight anatomic landmarks comparing pairs of workstation-type images. The best workstation-type image was then compared with the A-type image for the same landmarks. RESULTS: For the four workstation-type images the best visualization of the anatomic landmarks was seen with workstation-type image 3, which had a maximum optical density of 1.9. Image 3 was also superior to the results of A-type image processing for most of the landmarks. CONCLUSION: Image enhancement with the application of a computed radiography system is effective for study of lateral cephalograms.

Cephalometry↗

Eight new anthocyanins, ternatins C1-C5 and D3 and preternatins A3 and C4 from young clitoria ternatea flowers

Eight new anthocyanins 1-8 (ternatins C1, C2, C3, C4, C5, and D3 and preternatins A3 and C4) were isolated from Clitoria ternatea flowers. By the application of chemical, UV-vis, and FABMS methods, the structures of 1-6 were postulated as delphinidin 3-malonylglucoside having 3'-GCGC-5'-G, 3'-GCGCG-5'-G, 3'-GC-5'-G, 3'-GCG-5'-G, 3'-G-5'-G, and 3'-GC-5'-GC, and compounds 7 and 8 as delphinidin 3-glucoside having 3'-GCG-5'-GCG and 3'-GCG-5'-G as side chains, respectively, in which Dp is delphinidin, G is D-glucose, and C is p-coumaric acid. The structures of the compounds 1, 3-5, and 7 were established completely by additional NMR methods.

Journal Article↗