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K Tamai

Publications and source records attributed to K Tamai.

At least 73 records · Page 4Linked to original sources
PubMed1999

XIAP, a cellular member of the inhibitor of apoptosis protein family, links the receptors to TAB1-TAK1 in the BMP signaling pathway.

Signals elicited by transforming growth factor-beta (TGF-beta) superfamily ligands are generated following the formation of heteromeric receptor complexes consisting of type I and type II receptors. TAK1, a member of the MAP kinase kinase kinase family, and its activator, TAB1, participate in the bone morphogenetic protein (BMP) signaling pathway involved in mesoderm induction and patterning in early Xenopus embryos. However, the events leading from receptor activation to TAK1 activation remain to be identified. A yeast interaction screen was used to search for proteins that function in the pathway linking the receptors and TAB1-TAK1. The human X-chromosome-linked inhibitor of apoptosis protein (XIAP) was isolated as a TAB1-binding protein. XIAP associated not only with TAB1 but also with the BMP receptors in mammalian cells. Injection of XIAP mRNA into dorsal blastomeres enhanced the ventralization of Xenopus embryos in a TAB1-TAK1-dependent manner. Furthermore, a truncated form of XIAP lacking the TAB1-binding domain partially blocked the expression of ventral mesodermal marker genes induced by a constitutively active BMP type I receptor. These results suggest that XIAP participates in the BMP signaling pathway as a positive regulator linking the BMP receptors and TAB1-TAK1.

Adaptor Proteins, Signal Transducing↗
PubMed1999

Growth potential of loose bodies: an immunohistochemical examination of primary and secondary synovial osteochondromatosis.

Histologic and immunohistochemical studies of growth potential were performed on 53 surgically removed loose bodies representing 10 cases of primary synovial osteochondromatosis, 37 bodies representing 12 cases of secondary synovial osteochondromatosis, and five bodies representing five cases of osteochondral fracture. Loose bodies in primary synovial osteochondromatosis were nodular, showing plump chondrocytes and irregular calcification, and all contained proliferative cell nuclear antigen-positive chondrocytes (labeling index: 42.5%; range: 36.0-52.0%). Other markers stained less frequently. Loose bodies in secondary synovial osteochondromatosis showed uniform chondrocytes and annular calcification surrounding core tissue. Eighteen of 37 loose bodies showed proliferative cell nuclear antigen-positive chondrocytes, mostly peripherally. Chondrocyte labeling indices were less than 5% for proliferative cell nuclear antigen and other markers, although some connective tissue cells in the outer layer were stained. Loose bodies from osteochondral fractures were composed of articular cartilage, subchondral bone, and connective tissue; cartilage was negative for markers, whereas connective tissue contained positive cells. One specimen showed cartilaginous metaplasia of connective tissue. These results suggest that loose bodies have the potential for slow growth by proliferation of chondrocytes in primary synovial osteochondromatosis and by metaplasia following proliferation of surrounding connective tissue in secondary synovial osteochondromatosis.

Adolescent↗
PubMed1999

Effects of K+Channel blockers on acetylcholine-induced vasodilation in guinea-pig choroid.

The purpose of this study is to clarify which K+channels contribute to the acetylcholine (ACh)-induced vasodilation from the diameter changes in arterioles of the guinea-pig choroid. The choroid was isolated from the guinea-pig eyeball, pinned flat on a silicone rubber plate and superfused with warmed oxygenated (35 degrees C) Krebs solution. Diameters of choroidal arterioles were measured using video microscopy and a computer program for analysis. The effects of K+channel inhibitors (glibenclamide, tetraethylammonium [TEA], apamin and charybdotoxin [ChTX]) on the ACh-induced vasodilation were examined in arterioles which had been constricted by either norepinephrine (NE) or high K+solution. In NE (10(-5)m)-constricted arterioles, the combination of nitroarginine (10(-4)m) and indomethacin (10(-5)m) reduced ACh (10(-6)m)-induced vasodilatation by 24%. When high K+solution was used to constrict the arterioles, ACh-induced vasodilation was abolished by nitroarginine and indomethacin. In the presence of nitroarginine and indomethacin, the ACh-induced dilatation of NE-constricted arterioles was attenuated by TEA (10(-3)m), apamin (10(-7)m), and ChTX (10(-7)m) but not by glibenclamide (2x10(-5)m). Simultaneous application of apamin and ChTX inhibited the ACh (10(-6)m)-induced dilatation by 85%. In arterioles of guinea pig-choroid, nitric oxide and prostacyclin are not main mediators in ACh-induced vasodilation. Simultaneous activation of a set of Ca2+-sensitive K+channels may take most part of ACh-induced vasodilation.

Acetylcholine↗
PubMed1999

Para-articular chondroma and osteochondroma of the infrapatellar fat pad: a report of three cases.

We report three cases of para-articular chondroma and osteochondroma in the region of infrapatellar fat pad. All three lesions were resected and examined histologically. Two of them were primarily cartilaginous with a lobular pattern internally, and one uniformly osseous with peripheral cartilage. We conclude that these lesions are not the same. The former should be designated para-articular chondroma after Jaffe and the latter, osteochondroma.

Adipose Tissue↗
PubMed1999

The relationship between facet joint osteoarthritis and disc degeneration of the lumbar spine: an MRI study.

The role of MRI in assessing facet joint osteoarthritis is unclear. By developing a grading system for severity of facet joint osteoarthritis on MRI, the relationship between disc degeneration and facet joint osteoarthritis was determined. The accuracy of MRI in assessing facet joint osteoarthritis against CT was 94%. Under 40 years of age, the degree of disc degeneration varied among individuals. Over the age of 60, most of the discs were markedly degenerated. Under 40 years of age osteoarthritic changes in facet joints were minimal. Over the age of 60, variable degrees of facet joint osteoarthritis were observed but some facets did not show osteoarthritis. No facet joint osteoarthritis was found in the absence of disc degeneration and most facet joint osteoarthritis appeared at the intervertebral levels with advanced disc degeneration. Disc degeneration is more closely associated with aging than with facet joint osteoarthritis. The present study supports the hypothesis that "disc degeneration precedes facet joint osteoarthritis", and also supports the concept that it may take 20 or more years to develop facet joint osteoarthritis following the onset of disc degeneration.

Adult↗
PubMed1999

Distribution of synaptosomal-associated protein 25 in nerve growth cones and reduction of neurite outgrowth by botulinum neurotoxin A without altering growth cone morphology in dorsal root ganglion neurons and PC-12 cells.

Synaptosomal-associated protein 25 has been regarded as one of the target-associated soluble N-ethylmaleimide-sensitive fusion attachment protein receptors essential for exocytosis of vesicles in synapses. We have previously reported that cleavage of syntaxin, which is another target-associated soluble N-ethylmaleimide-sensitive fusion attachment protein receptor, with botulinum neurotoxin C1 resulted in inhibition of neurite extension and morphological changes including growth cone collapse and large vacuole formation. As an attempt to explore the mechanism of growth cone extension, we examined the ultrastructural localization of synaptosomal-associated protein 25 in growth cones with or without treatment of botulinum neurotoxin A, which cleaves synaptosomal-associated protein 25. In dorsal root ganglion neurons, light microscopy demonstrated synaptosomal-associated protein 25 immunoreactivity throughout the neurons, including the cell bodies, neurites and growth cones. Using electron microscopy, gold signals immunoreactive for synaptosomal-associated protein 25 were identified diffusely in the cytoplasm of the growth cones. In contrast, in PC-12 cells, a large number of gold signals were localized on the plasma membranes. High levels of signal were also found in the cytoplasm in the central region of the growth cones. We also confirmed that botulinum neurotoxin A treatment reduced neurite extension by about 50%. However, both in dorsal root ganglion neurons and in PC-12 cells we found no differences in the ultrastructure nor in the localization of synaptosomal-associated protein 25 between growth cones with and without toxin treatment. These results indicate that cleavage of synaptosomal-associated protein 25 inhibits growth cone extension in a manner different than that of syntaxin cleavage. The results of this study suggest the possibility that synaptosomal-associated protein 25 is involved in growth cone extension through a process independent of vesicle fusion.

Animals↗
PubMed1999

In vivo gene introduction into keratinocytes using jet injection.

Successful keratinocyte gene therapy requires the development of efficient methods of gene transfer to keratinocytes. Jet injection of a solution containing DNA can be used to transfer genes to several tissues in vivo. In this article, we tried to introduce DNA into rat and human keratinocytes using this method. First, we fired a beta-gal expression vector into rat skin at several distances using a jet injector and examined beta-gal activity in the epidermal keratinocytes. The highest activity in keratinocytes was found when the plasmid was fired at 10 cm from the skin surface; the activity lessened as the firing distance became shorter than 10 cm. Next, we transplanted human skin on to a nude rat, fired the vector into the human skin from a distance of 10 cm and examined the beta-gal activity. We also injected the same amount of plasmid with a needle to compare jet with needle injections. The results showed that jet injection of the naked DNA could introduce and express DNA in human keratinocytes in vivo and that jet injection exhibited much higher activity than needle injection. Jet injection of the naked DNA will provide a method for keratinocyte gene therapy in the future.

Animals↗
PubMed1999

Cytochalasin B inhibits morphogenetic movement and muscle differentiation of activin-treated ectoderm in Xenopus.

Xenopus ectodermal explants (animal caps) begin to elongate after treatment with the mesoderm inducing factor activin A. This phenomenon mimics the convergent extension of dorsal mesoderm during gastrulation. To analyze the relationship between elongation movement and muscle differentiation, animal caps were treated with colchicine, taxol, cytochalasin B and hydroxyurea (HUA)/aphidicolin following activin treatment. Cytochalasin B disrupted the organization of actin filaments and inhibited the elongation of the activin-treated explants. Muscle differentiation was also inhibited in these explants at the histologic and molecular levels. Colchicine and taxol, which are known to affect microtubule organization, had little effect on elongation of the activin-treated exp ants. Co-treatment with HUA and aphidicolin caused serious damage on the explants and they did not undergo elongation. These results suggest that actin filaments play an important role in the elongation movement that leads to muscle differentiation of activin-treated explants.

Actin Cytoskeleton↗
PubMed1999

Effects of irrigation fluid temperature on choroidal circulation during vitrectomy.

PURPOSE: To investigate the effects of irrigation temperature on choroidal circulation during vitrectomy. METHODS: After anesthetized albino rabbits underwent closed vitrectomy, choroidal blood flow was monitored while the vitreous cavity was irrigated with solutions (BSS plus) of various temperatures (6-42 degrees C). Irrigation pressure was maintained at 15 mmHg. A non-contact Doppler laser flowmeter was used to measure choroidal blood flow. Temperature change at the retina and mid-vitreous was also measured during irrigation. RESULTS: Choroidal blood flow showed a downward peak when perfused at 34 degrees C. As irrigation temperatures deviated above or below 34 degrees C, the blood flow increased. However, when irrigation temperature was below 16 degrees C, the blood flow decreased as the temperature declined. The temperature at the retina was maintained at a relatively constant level when irrigation was between 30 degrees C and 40 degrees C. CONCLUSION: The choroid acts as a thermostat to minimize intraocular temperature fluctuations by changing its blood flow.

Animals↗
PubMed1999

Role of endothelium-derived vasodilators and K(+) channels in ischemic vasodilation of guinea-pig choroidal arterioles.

PURPOSE: To assess the roles of endothelium-derived vasodilators and K(+) channels on metabolic ischemia-induced vasodilation from diameter changes in choroidal arterioles of the guinea-pig. METHODS: The choroid was isolated from the guinea-pig eye-ball, pinned flat on a silicone rubber plate, and superfused with oxygenated warmed (35 degrees C) Krebs solution. Diameters of choroidal arterioles were measured using video microscopy and a computer program for analysis. Vasodilatory effects were examined after the choroid was exposed to glucose-free/NaCN solutions for 10 minutes. The effects of Nomega-nitro-L-arginine (nitroarginine), indomethacin, and K(+)<?Pub Caret> channel inhibitors (glibenclamide [Glib] and charybdotoxin [ChTX]) on ischemic vasodilation were assessed. RESULTS: Reversible vasodilation was observed when the choroid was exposed to glucose-free/NaCN (10(-3) M) solutions. Nitroarginine (10( -4) M), Glib (2x10(-5) M) and ChTX (10(-7) M) significantly inhibited glucose-free/NaCN (10(-3) M)-induced vasodilation by 47%, 62%, and 24%, respectively. No significant inhibitory effect was observed with indomethacin (10(-5) M). Simultaneous application of Glib and ChTX reduced vasodilation by 77%. When Glib and ChTX were added together to nitroarginine, dilation was reduced by 86%. With high K(+) ([K]o = 47.2 mM) Krebs solution, ischemia caused a slight vasodilation (11%), which was significantly inhibited by nitroarginine. CONCLUSIONS: In guinea-pig choroidal arterioles, glucose-free/ NaCN-induced ischemic vasodilation was mainly mediated by NO and K(ATP) channels. A part of NO-mediated vasodilation was induced independent of the opening of K(+) channels.

Animals↗
PubMed1999

Panclavicular ankylosis in pustulotic arthroosteitis. A case report.

A 54-year-old man who had palmoplantar pustulosis showed bilateral, complete osseous fusion of the sternoclavicular and acromioclavicular joints. No significant abnormality was seen in the glenohumeral joint. The left clavicle had a nonunion develop, whereas the right did not. The elevation of the right shoulder was limited to 100 degrees in active and passive measurements. The total external rotation and internal rotation at the side was 135 degrees. This decreased to 90 degrees at 60 degrees elevation and to 10 degrees at maximum (100 degrees) elevation. Based on the kinematic data on normal shoulders, it was thought that the ankylosis of both ends of the clavicle held the scapula unrotated during the arm movement so that, at the arm to trunk angle of 100 degrees, the position of the humerus relative to the scapula was equivalent to that of a normal shoulder in complete elevation. The current case provided an extremely rare clinical setting where shoulder mobility depended only on glenohumeral motion as a result of the complete loss of scapulothoracic motion.

Acromioclavicular Joint↗
PubMed1999

Diagnostic dilemma of "sporadic" cases of dystrophic epidermolysis bullosa: a new dominant or mitis recessive mutation?

Dystrophic forms of epidermolysis bullosa (DEB), characterized by mutations in the type VII collagen gene (COL7A1), are inherited either in an autosomal dominant or autosomal recessive fashion, and sporadic, de novo cases have also been reported. Clinically, the dominant forms (DDEB) can be indistinguishable from the mild, mitis forms of recessively inherited DEB (M-RDEB). This situation poses a dilemma in case of families with 1 mildly affected individual and clinically normal parents: Is it a new dominant or mitis recessive DEB? In this study we review 2 cases with mild DEB, the parents being clinically normal. One of the cases was shown to be a compound heterozygote for 2 silent missense mutations (R2063W/G2366S), thus being diagnosed as M-RDEB. The second case had a single glycine substitution mutation (G2079E) in COL7A1 and had therefore DDEB. These findings have implications for the genetic counseling of these families concerning the risk of recurrence of the disease in subsequent pregnancies in the present and future generations.

Amino Acid Substitution↗
PubMed1999

Requirement of ATM in phosphorylation of the human p53 protein at serine 15 following DNA double-strand breaks.

Microinjection of the restriction endonuclease HaeIII, which causes DNA double-strand breaks with blunt ends, induces nuclear accumulation of p53 protein in normal and xeroderma pigmentosum (XP) primary fibroblasts. In contrast, this induction of p53 accumulation is not observed in ataxia telangiectasia (AT) fibroblasts. HaeIII-induced p53 protein in normal fibroblasts is phosphorylated at serine 15, as determined by immunostaining with an antibody specific for phosphorylated serine 15 of p53. This phosphorylation correlates well with p53 accumulation. Treatment with lactacystin (an inhibitor of the proteasome) or heat shock leads to similar levels of p53 accumulation in normal and AT fibroblasts, but the p53 protein lacks a phosphorylated serine 15. Following microinjection of HaeIII into lactacystin-treated normal fibroblasts, lactacystin-induced p53 protein is phosphorylated at serine 15 and stabilized even in the presence of cycloheximide. However, neither stabilization nor phosphorylation at serine 15 is observed in AT fibroblasts under the same conditions. These results indicate the significance of serine 15 phosphorylation for p53 stabilization after DNA double-strand breaks and an absolute requirement for ATM in this phosphorylation process.

Acetylcysteine↗
PubMed1999

Relationship between morphology of iliolumbar ligament and lower lumbar disc degeneration.

Previous imaging studies have shown little difference in the degree of disc degeneration between L4-L5 and L5-S1. We hypothesized that because the morphology of the iliolumbar ligament affects the stability of the lumbosacral junction, then it could determine the lower lumbar disc degeneration. Fifty-three male and 47 female patients were classified into three groups according to their disc degeneration grade-those in whom the L5-S1 disc was less degenerated (group A), more degenerated (group B), and equally degenerated (group C) compared to the L4-L5 disc on T2-weighted magnetic resonance images. The length and direction of the anterior and posterior iliolumbar ligaments were measured on T1-weighted axial images. The iliolumbar ligament was shorter in group A than in group B or C, and was oriented significantly more posteriorly in group A than in groups B or C. The morphology of the iliolumbar ligament, especially its length and direction, can be a factor influencing the development of disc degeneration at L4-L5 and L5-S1.

Adult↗
PubMed1998

Induction of keratinocyte proliferation and lymphocytic infiltration by in vivo introduction of the IL-6 gene into keratinocytes and possibility of keratinocyte gene therapy for inflammatory skin diseases using IL-6 mutant genes.

To understand biological function of IL-6 in the skin in vivo, we constructed a vector that strongly expressed human IL-6 in keratinocytes and introduced it into rat keratinocytes in vivo by the naked DNA method. The overexpression of IL-6 induced macroscopic erythema and histologically evident keratinocyte proliferation and lymphocytic infiltration in the treated area of rat skin. Since previous studies using IL-6 transgenic mice have not shown skin inflammation of these mice, our result provides the first evidence that IL-6 is related to the pathogenesis of inflammatory skin diseases. ELISA suggested that a certain degree of transgenic IL-6 expression in keratinocytes was required for inducing skin inflammation. Cytokine profile in rat keratinocytes after the gene introduction was examined by reverse transcriptase-PCR assay and revealed that gene expression of rat IL-1alpha and TNF-alpha showed no marked change until 24 h, whereas that of rat IL-6 and TGF-alpha increased with time. We then introduced and expressed the IL-6 mutant genes, which were designed to behave as IL-6Ralpha antagonists, and found that their ability to induce erythema was lower than that of the wild-type gene. Furthermore, preintroduction of some mutant genes delayed the erythema induced by postintroduction of the wild-type IL-6 gene, suggesting that the mutant forms of IL-6 prevent wild-type IL-6 from binding to IL-6Ralpha. This result indicates that keratinocyte gene therapy may be possible for inflammatory skin diseases using IL-6 mutant genes.

Animals↗