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Biomedical subjects

T Taniguchi

Publications and source records attributed to T Taniguchi.

At least 505 records · Page 28Linked to original sources
PubMed1993

A multidie technique for the fabrication of porcelain laminate veneers.

Porcelain veneers are a challenge for the dentist and dental technician when they are an integral part of complex restorative treatment plans. A multidie technique is described that allows construction of laminate veneers on removable refractory dies in a stone master cast. This system provides flexibility and accuracy with less chair time when used in combination with epoxy resin dies. Multiple restorative techniques can be used simultaneously with one master cast, and emphasis is directed to harmonious working relationships between the dentist, dental technician, and patient.

Dental Casting Investment↗
PubMed1993

Alteration of human platelet protein kinase C with normal aging.

Using a two-site enzyme immunoassay, we determined the content of type II protein kinase C (PKC) in human platelets from 24 donors of various ages without any neurological, hematological or malignant disorders. The content of type II PKC in the membranous fraction was positively correlated with aging. The content of PKC in the cytosolic fraction tended to decline with aging, but the correlation was not significant. The total amount of PKC also had no significant correlation with aging. Age-related changes in platelet protein content were not observed. These results suggested that the subcellular distribution of type II PKC in human platelets is altered with normal aging.

Adolescent↗
PubMed1993

Fetal mononuclear cells show a comparable capacity with maternal mononuclear cells to produce IL-8 in response to lipopolysaccharide in chorioamnionitis.

IL-8 is a chemotactic and activating cytokine for neutrophils which eliminate invading bacteria by releasing bactericidal metabolites. Cord blood mononuclear cells (CBMCs) obtained from neonates born to mothers with chorioamnionitis actively produced a significantly higher amount of IL-8 than those of neonates without chorioamnionitis, suggesting that the mononuclear cells of fetuses with chorioamnionitis had been activated in utero. As lipopolysaccharide (LPS) can often be detected in the uteroplacental space in chorioamnionitis, the LPS-mediated activation mechanism of neonatal mononuclear cells was analyzed in vitro to produce IL-8. Neonatal mononuclear cells stimulated with LPS increased IL-8 production in a time- and dose-dependent manner. The ability of term or preterm neonatal mononuclear cells to produce IL-8 was comparable with that of adult (maternal) mononuclear cells, suggesting functional maturity of the neonatal or fetal mononuclear cells to produce IL-8. However, IL-8 production by neonatal CBMCs was down-regulated by dexamethasone, a glucocorticoid which is clinically administered to mothers to promote fetal lung maturity in preterm delivery. Our present study revealed a regulatory mechanism of fetal IL-8 production, suggesting that functionally mature fetal mononuclear cells produce IL-8 in response to LPS in chorioamnionitis and activate the fetal defense mechanism against infection.

Cells, Cultured↗
PubMed1993

Placental interleukin-6 production is enhanced in intrauterine infection but not in labor.

OBJECTIVE: Because interleukin-6 is an important mediator in the host defense mechanism against infection and tissue damage, we studied the capacity of placentas with or without either labor or chorioamnionitis in the third trimester to produce interleukin-6. STUDY DESIGN: The placental blocks were cultured, and their interleukin-6 titers were measured by a bioassay. RESULTS: Placentas with labor produced a similar amount of interleukin-6 to placentas without labor. In contrast, placentas with chorioamnionitis produced much more interleukin-6 than the placentas with or without labor (p < 0.0001). CONCLUSION: Placental interleukin-6 is thus surmised to participate in potentiation of the placental and fetomaternal defense mechanisms together with placental interleukin-1 during chorioamnionitis.

Chorioamnionitis↗
PubMed1993

Neuronal damage in the rat hippocampus induced by in vivo hypoxia.

Rats were subjected to hypoxia for 30 min in a chamber containing 5% O2 and 95% N2. The distribution of damaged neurons in the hippocampus was then examined at various predetermined times, ranging from 3 hours to 21 days after hypoxia. Hematoxylin-eosin stained sections showed shrunken and eosinophilic neurons in the CA3 and CA4 regions. Similar, but less severe, changes were also observed in the granule cell layer of the dentate gyrus. In contrast, neurons in the CA1 region were relatively resistant to hypoxia. These results showed the susceptibility of the hippocampus to hypoxia, although the affected neurons are not the same as those vulnerable to ischemia.

Animals↗
PubMed1993

Alterations of a 200 kDa neurofilament in the rat hippocampus after forebrain ischemia.

Alteration in the concentration of a 200 kDa neurofilament (NF200) in the rat hippocampus after forebrain ischemia and its relationship to hippocampal neuronal death were studied with an anti-200 kDa neurofilament antibody, using immunohistochemical and immunoblotting techniques. In rats subjected to 8 min of transient forebrain ischemia, hematoxylin-eosin staining showed survival of most of the neurons in the hippocampal CA1 region at 1 day and loss of more than 75% of the neurons at 7 days after ischemia. Immunoblotting showed that the concentration of NF200 in the hippocampal homogenate tended to decrease after ischemia, to 69% of that of control at 1 day and to 60% of the control value at 7 days after 8 min of forebrain ischemia. Following 5 min of ischemia as well, the decrease in the concentration of neurofilaments in the hippocampal region preceded histological confirmation of neuronal cell death. These results suggest that degradation of neurofilament triplet proteins occurred even after ischemia of minimal duration and preceded neuronal death. Degradation of cytoskeletal proteins may play an important role in the mechanism of delayed neuronal death after cerebral ischemia.

Animals↗
PubMed1993

Characterization of the DNA binding domain of the mouse IRF-2 protein.

The DNA binding domain of the interferon regulatory factor-2 protein (IRF-2) has been produced and characterized. alpha-chymotrypsin digestion of the purified IRF-2 protein bound to a synthetic binding site yields a peptide fragment of 14 K in molecular weight. N-terminal analysis of this peptide fragment showed that its sequence is the same as that of the intact IRF-2. A peptide fragment of approximately 14 K, IRF-2(113), which corresponds to the N-terminal 113 amino acids of the intact IRF-2 protein, has been expressed in a functional form in Escherichia coli. The first methionine was processed during the expression and the purified IRF-2(113) thus contains 112 amino acids. DNase I footprinting and gel retardation assaying showed that IRF-2(113) binds to a synthetic DNA having the consensus binding site and to the upstream regulatory sequence of the IFN-beta gene as intact IRF-2 does. These results showed that this peptide fragment, IRF-2(113), may be a good material for investigation of the DNA binding domain of IRF-2 and of the DNA-protein interaction.

Amino Acid Sequence↗
PubMed1993

Site dependence of methamphetamine concentrations in blood samples collected from cadavers of people who had been methamphetamine abusers.

Various blood samples were collected from heart cavities and blood vessels in eight autopsy cases of people who had been methamphetamine abusers. Methamphetamine and its metabolite, amphetamine, were determined by gas chromatography-mass spectrometry-selected ion monitoring. In four cases where left and right heart blood samples were collected, methamphetamine concentrations in the left heart blood samples were 1.9-2.6 times higher than those in the right heart blood samples. In three cases where pulmonary vein blood samples were collected, methamphetamine concentrations in the pulmonary vein blood samples were higher than those in other blood samples sites. To interpret the blood methamphetamine concentrations, site dependence should be taken into consideration.

Adult↗
PubMed1993

Cloning of the genes that control formation of the fimbrial colonization factor antigen III (CFA/III) from an enterotoxigenic Escherichia coli.

Enterotoxigenic Escherichia coli strain 260-1 produces colonization factor antigen III and heat-labile enterotoxin. A 55-kb plasmid controlling the expression of the colonization factor antigen was isolated from this strain after it was labeled with ampicillin resistance transposon, Tn3. When this plasmid was introduced into E. coli K-12 strains, it induced the formation of pili that were morphologically and immunologically identical to those on the surface of 260-1 cells, as examined by electron microscopic observation and with the specific antiserum. The physical map of the plasmid was constructed, and the 17.4-kb region was found to be responsible for the expression of the pili.

Agglutination Tests↗
PubMed1993

Recognition DNA sequences of interferon regulatory factor 1 (IRF-1) and IRF-2, regulators of cell growth and the interferon system.

Interferon (IFN) regulatory factor 1 (IRF-1) and IRF-2 were originally identified as transcription factors involved in the regulation of the IFN system. IRF-1 functions as a transcriptional activator, while IRF-2 represses IRF-1 function. More recently, evidence has been provided that IRF-1 and IRF-2 manifest antioncogenic and oncogenic properties, respectively, and that loss of one or both of the IRF-1 alleles may be critical for the development of human hematopoietic neoplasms. Both factors show a high degree of structural similarity in their N-terminal DNA-binding domains, and previous studies suggested that IRF-1 and IRF-2 bind to similar or identical cis elements within type I IFN (IFN-alpha and -beta) and IFN-inducible genes. However, the exact recognition sequences of these two factors have not yet been determined; hence, the spectrum of the IRF-responsive genes remains unclear. In this study, we determined the DNA sequences recognized by IRF-1 and IRF-2, using a polymerase chain reaction-assisted DNA-binding site selection method. We report that sequences selected by this method and the affinities for each sequence were virtually indistinguishable between IRF-1 and IRF-2. We confirm the presence of two contiguous IRF recognition sequences within the promoter region of the IFN-beta gene and of at least one such sequence in all of the IFN-inducible genes examined. Furthermore, we report the presence of potential IRF sequences in the upstream region of several genes involved in cell growth control.

Base Sequence↗
PubMed1993

The IL-2 receptor complex: its structure, function, and target genes.

Proliferation of T lymphocytes is triggered by the interaction of IL-2 with its specific receptor following T lymphocyte activation. The receptor for IL-2 consists of at least three distinct subunits, the alpha chain (IL-2R alpha), the beta chain (IL-2R beta), and the gamma chain (IL-2R gamma). Although the role of IL-2R gamma in IL-2 signalling remains unclear, IL-2R beta is the subunit critical for receptor-mediated signalling. Because IL-2R beta lacks any apparent catalytic motifs, IL-2R beta may be physically or functionally coupled to other signalling molecules. Structure-function studies of IL-2R beta have revealed that at least two distinct cytoplasmic regions of IL-2R beta are involved in IL-2-induced cellular signalling. The "serine-rich" region of IL-2R beta was identified as a region critical for IL-2-induced mitotic signalling from experiments in which IL-2R beta mutant cDNAs lacking a particular cytoplasmic region or regions were expressed in an IL-3-dependent mouse pro-B cell line (BAF-B03). Meanwhile, another cytoplasmic region of IL-2R beta, the "acidic" region, is responsible for its physical association with an src-family protein tyrosine kinase (PTK), p56lck and is critical for activating the p56lck PTK following IL-2 stimulation. It is now evident that IL-2R beta is linked to at least two intracellular signalling pathways that mediate nuclear proto-oncogene induction. One pathway is linked to tyrosine phosphorylation events, mediated by a src-family protein tyrosine kinase (PTK), and that pathway leads to the induction of the c-fos, c-jun, and other genes of this family. Another pathway leads to c-myc gene induction by an as yet unknown mechanism. We discuss the complex signalling machinery that links the cell surface receptor to the nuclear events.

Animals↗
PubMed1993

Assessment of protein kinase C isozymes by two-site enzyme immunoassay in human brains and changes in Alzheimer's disease.

We assessed the amount of protein kinase C (PKC) in samples from postmortem normal human and Alzheimer's disease (AD) brains by a two-site enzyme immunoassay that quantitatively identified types alpha, beta, and gamma isozymes. In the normal human brain matter, type beta was the main type present, the majority of each isozyme of PKC being present in the membranous fraction of the brain tissues. In AD brains, the amount of type beta PKC was significantly reduced in the membranous fraction of the temporal cortical tissues. The amounts of types alpha and gamma in the membranous fraction and types alpha, beta, and gamma in the cytosolic fraction in AD brains were lower than in the control brains, but the difference was not significant. There was also a significant decrease in the levels of PKC in the membranous fraction of AD brains, as measured by radioactive phorbol ester binding. These results suggest that the type beta PKC isozyme is mainly present in the human temporal cortex and that reduced levels of type beta PKC in the membranous fraction may reflect a biochemical deficit related specifically to the pathogenesis of AD.

Aged↗
PubMed1993

"Transinsular approach" for the treatment of a medial temporal arteriovenous malformation.

A new approach for the treatment of arteriovenous malformations in the medial temporal lobe is proposed. This approach, referred to as the "transinsular approach," comprises incising the superior part of the anterior insula and exploring the plexal point of the anterior choroidal artery through the space between the dissected insula and the frontal lobe. A representative case of a patient with a large medial temporal arteriovenous malformation that was successfully extirpated by this approach is reported. The advantages of this approach and the functional results of partial incision of the insula are discussed.

Adult↗
PubMed1993

Histological observations on the schizonts in cattle infected with Japanese Theileria sergenti.

Histological observations were performed on the schizonts of Japanese Theileria sergenti in three calves necropsied 8 and 10 days after application of nymphal Haemaphysalis longicornis infected with T. sergenti. In all the three calves, schizonts were observed in the cytoplasm of huge cells formed in the drainage lymph nodes, liver and spleen. The huge cells were 50 to 200 microns in diameter. Schizonts had granular appearance and an irregular shape and were 1 to 7 microns in diameter. Ultrastructurally, schizonts had more than one nuclei and were formed in the unit enlarged cell. Schizonts showed a specific reaction against anti-T. sergenti anti serum, therefore, it was concluded that the schizonts were those of T. sergenti histologically.

Animals↗
PubMed1993

Species differences of testosterone 16-hydroxylases in liver microsomes of guinea pig, rat and dog.

1. In hepatic microsomes, remarkable species differences in the activity of testosterone 16-hydroxylase was observed in guinea pig, dog, and rat. The activity of testosterone 16 beta-hydroxylase was higher than that of 16 alpha-hydroxylase in guinea pig, whereas 16 alpha-hydroxylated testosterone was predominant as the metabolite in dog and rat. 2. Since P4502B isoenzyme has been shown to be a catalyst for testosterone 16-hydroxylations, we compared the catalytic properties of the P4502B subfamily (P450GP-1, P450b and P450PBD-2) purified from liver microsomes of guinea pig, dog, and rat, respectively. P450GP-1, P450b and P450PBD-2 showed different stereoselectivities for hydroxylation of testosterone at the 16-position. 3. P450GP-1, P450b and P450PBD-2 together comprised 47, < 0.1 and 23% of total P450 in liver microsomes of untreated guinea pig, rat and dog, respectively, indicating that the amounts of the P4502B isoenzyme in untreated animals were clearly different in these three animal species. Both 16 alpha- and 16 beta-hydroxylations of testosterone in liver microsomes of phenobarbital-treated guinea pig, rat and dog were inhibited by anti-P450GP-1, anti-P450b and anti-P450PBD-2 antibodies, respectively. 4. These and other results indicate that the species difference observed in testosterone 16-hydroxylation may be, in part, due to differences in the amounts of P450 of the P4502B subfamily, and their stereoselectivities for 16-hydroxylation.

Animals↗
PubMed1993

[A case of sudden death of a patient with glycogen storage disease type 1--delayed aftereffect of a traffic accident].

A case of sudden death of a 22-year-old man with glycogen storage disease type 1 is reported. Autopsy revealed striking hepatomegaly with round edges. The liver was yellowish and weighed 2840 g. Histologic findings showed excessive deposition of PAS-positive material in the hepatocytes and in the proximal renal tubular epithelium cells, which means the accumulation of glycogen. A mass surrounding splenic artery was seen in the hilus of the spleen. There was about 2000 ml of fresh blood and clots in the abdominal cavity due to bleeding from a ruptured mass. The mass was composed of a hematoma with connective tissue surrounding it and was a pseudoaneurysm. The mass was considered to have been formed from bleeding due to injury to a branch of a splenic artery. Consideration of these findings led to the conclusion that death was caused by loss of blood from rupture of the mass and that the mass was formed due to injury of the branch of the splenic artery in a traffic accident 2 years earlier but not the pathogenesis of glycogen storage disease.

Accidents, Traffic↗