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T Maeda

Publications and source records attributed to T Maeda.

At least 451 records · Page 25Linked to original sources
PubMed1997

An ultrastructural study of calcitonin gene-related peptide-immunoreactive nerve fibers innervating the rat posterior longitudinal ligament. A morphologic basis for their possible efferent actions.

STUDY DESIGN: The present study investigated ultrastructural characteristics of calcitonin gene-related peptide-immunoreactive nerve fibers in the posterior longitudinal ligament of the rat lumbar spine. OBJECTIVES: To provide a morphologic basis for assessment of the afferent and, in particular, efferent functions of calcitonin gene-related peptide immunoreactive nerves in the posterior longitudinal ligament and their eventual role in degenerative spondylarthropathies and low back pain. SUMMARY OF BACKGROUND DATA: Previous studies using light-microscopic localization of sensory neuronal markers such as calcitonin gene-related peptide have reported the presence of sensory fibers in the supporting structures of the vertebral column. Meanwhile, accumulating research data have suggested efferent properties for calcitonin gene-related peptide, i.e., a trophic action that alters the intrinsic properties of target cells not through transient action of synaptic transmission, but through long-lasting signal transmission by the secreted neuropeptides. To verify such trophic, paracrine actions of the calcitonin gene-related peptide-containing fibers in the posterior longitudinal ligament, however, ultrastructural details of the terminals and their spatial relationship to their eventual target structures have to be elucidated. METHODS: Rat posterior longitudinal ligaments were stained immunohistochemically for calcitonin gene-related peptide. Light-microscopic analysis of the semithin sections facilitated subsequent electron microscopy of specific sites of the posterior longitudinal ligament to determine ultrastructural details and nerve fiber-target relationships. RESULTS: The rat lumbar posterior longitudinal ligament was found to be innervated by two distinctive calcitonin gene-related peptide immunoreactive nerve networks. In immunoelectronmicroscopy, the fibers of the deep network had numerous free nerve endings, whereas those of the superficial network showed spatial associations with other non-calcitonin gene-related peptide immunoreactive components of the network. In both systems, naked axons not covered by the Schwann cells made close spatial contact with smooth muscle cells: of blood vessels and resident posterior longitudinal ligament fibroblasts. CONCLUSIONS: The ultrastructural characteristics of the innervation of the rat posterior longitudinal ligament would be compatible not only with a nociceptive function, but also with neuromodulatory, vasoregulatory, and trophic functions, as has already been established in some visceral organs.

Animals↗
PubMed1997

DNA cleavage reaction and linoleic acid peroxidation induced by tea catechins in the presence of cupric ion.

Tea catechins with cupric ion promoted extensive DNA cleavage and fatty acid peroxidation in vitro under aerobic conditions. Neither cupric ions nor polyphenolic compounds including catechins alone induced DNA cleavage. While catalase significantly inhibited the DNA cleavage induced by catechins-Cu2+, superoxide dismutase (SOD) did not, indicating that H2O2 is probably involved in the DNA cleavage. These results suggest that the pro-oxidant property of catechins, which are generally considered to be anti-oxidants and anticarcinogens, is responsible for the O2 reducing ability of catechins catalyzed by cupric ion.

Aerobiosis↗
PubMed1997

Morphological investigation of the neuroprotective effects of graded hypothermia after diverse periods of global cerebral ischemia in gerbils.

Hypothermia is known to be the most effective method to protect the neuronal damage induced by ischemia. In the present study, we investigated the histopathological consequences of hippocampal CA1 pyramidal neurons as well as the glial reactions in the hippocampus, after diverse periods of ischemic insult at graded intra-ischemic hypothermia ranging from 32 to 20 degrees C. Gerbils were exposed to forebrain ischemia by clamping the bilateral common carotid arteries for 5-120 min depending upon the temperatures. The morphological study was performed 7 days after ischemia or sham-operation. Histopathological evaluation of delayed neuronal death (DND) was performed by Cresyl violet (CV) staining and MAP2 immunoreactivity. Glial reactions were examined by GFAP immunostaining and isolectin B4 histochemistry, corresponding to astrocytes and microglia, respectively. The forebrain ischemia at 32 degrees C for 10 min and at 28 degrees C for 20 min did not induce DND in the CA1 region. However, the ischemia at 32 degrees C for 20 min and at 28 degrees C for 30 min caused extensive degeneration of CA1 pyramidal neurons as observed in normothermic ischemic animals. Under the condition of deep hypothermia, the ischemia for 60 min at 24 degrees C and for 120 min at 20 degrees C which were the longest durations of each temperature within the limitation of the animal survival following 7 days, induced no DND in CA1 pyramidal neurons. The reactive changes of astrocytes were observed not only in ischemic animals with DND, but also in ischemic animals without DND. Computer image analysis showed that the area fraction of GFAP-positive structures in the CA1 region was significantly increased in both ischemic cases with and without DND compared with each sham group. In contrast, the distribution of activated microglia was much more restricted to the CA1 region and they were always accompanied by DND at 7 days postischemia. The present results demonstrate the remarkable neuroprotective effect of deep hypothermia that has been widely used in cardiovascular surgeries as the cerebroprotective strategy during total circulatory cessation. The findings also suggest that even under the condition of hypothermia, glial reactions may play an important role in neuronal survival and death after ischemia.

Animals↗
PubMed1997

Nicotine protects cultured cortical neurons against glutamate-induced cytotoxicity via alpha7-neuronal receptors and neuronal CNS receptors.

We examined the effects of nicotine on glutamate-induced cytotoxicity using primary cultures of rat cortical neurons. The cell viability decreased significantly when cultures were exposed to glutamate for 10 min and then incubated with glutamate-free medium for 1 h. The exposure of cultures to nicotine (10 microM) for 8-24 h prior to glutamate application ameliorated the glutamate-induced cytotoxicity, with no significant effect of nicotine alone on the cell viability. Neuroprotection by nicotine was dependent on the incubation period. alpha-bungarotoxin (alpha-BTX) and methyllycaconitine (MLA), both of which are alpha7-neuronal receptor antagonists, and dihydro-beta-erythroidine (DHbetaE), a neuronal central nervous system (CNS) receptor antagonist, each significantly antagonized the protection by nicotine against glutamate-induced cytotoxicity. Ionomycin, a calcium ionophore, and S-nitrosocysteine (SNOC), a nitric oxide (NO) donor, also induced cytotoxicity in a manner similar to glutamate. Nicotine protected cultures against ionomycin-induced cytotoxicity, but not against SNOC-induced cytotoxicity. These results suggest that nicotine protects cultured cortical neurons against glutamate-induced cytotoxicity via alpha7-neuronal receptors and neuronal CNS receptors by reducing NO-formation triggered by Ca2+ influx.

Aconitine↗
PubMed1997

Adenosquamous carcinoma of the liver: clinicopathologic characteristics and cytokeratin profile.

BACKGROUND: The clinicopathologic characteristics, biologic behavior, and histogenesis of primary adenosquamous carcinoma (ASC) of the liver have yet to be fully clarified. METHODS: Eight cases of ASC of the liver were analyzed both clinicopathologically and immunohistochemically using antibodies of cytokeratin (CK) 7, CK 8, CK 18, CK 19, and CK 903 (CK 5, CK 10, CK 11, and CK 14). The survival curve of the 6 patients with surgically resected ASC was compared with that of the 32 patients with common cholangiocarcinoma (CC). RESULTS: Most ASCs had invasive pathologic features, including venous invasion, lymphatic permeation, and intrahepatic metastases. There were lymph node metastases from 7 tumors (88%), and most of the metastases were adenocarcinoma. All adenocarcinoma (AC) components were positive for both CK 7 and CK 19. The squamous cell carcinoma (SCC) components were positive for CK 7 in all cases but were positive for CK 19 in only 5 cases (62.5%). The ACs were positive for CK 903 in only 3 cases (37.5%), whereas all SCCs were positive for CK 903. Almost all ACs were positive for both CK 8 and CK 18, whereas the SCCs were positive for CK 8 in only 3 cases (37.5%) and for CK 18 in no cases. All 6 patients with surgically resected ASC died of the disease within 1 year postoperatively. Their survival curve was significantly worse than that of the 32 patients with common CC (P < 0.001). The two patients on whom autopsy was performed also died within 1 year after diagnosis. CONCLUSIONS: ASC tended to have more aggressive biologic behavior and a poorer prognosis than common CC. The authors' immunohistochemical analysis of CK expression indicated that most of the ASCs of the liver that were studied developed from a squamous transformation of the preexisting CC.

Aged↗
PubMed1997

Soluble and membrane isoforms of Fas/CD95 in fresh adult T-cell leukemia (ATL) cells and ATL-cell lines.

Fas, also designated as Apo-1 and CD95, is a cell membrane receptor (mFas) involved in apoptotic cell death. A soluble form (sFas) lacking the transmembrane domain due to alternative splicing has been isolated. Abnormal expression of sFas and mFas is likely to be involved in lymphoproliferative disorders and auto-immune diseases. Adult T-cell leukemia (ATL) caused by human T-cell-leukemia virus type-1 (HTLV-1) is well known to be a T-cell neoplasm with strong mFas expression, suggesting a role of Fas in the pathology of the disease. We examined protein and mRNA expression of the 2 isoforms of Fas in fresh ATL cells and ATL cell lines. In general, mFas was strongly expressed in ATL cells, and sFas levels in sera were high, especially in malignant ATL. However, expression of the isoforms in some cases of ATL varied; there was no mFas expression on the cell surface and sFas levels were high in serum. In contrast, all ATL cell lines examined showed strong mFas expression and scarce production of sFas in the supernatant, corresponding to strong expression of full-length Fas mRNA and weak to negative expression of alternatively spliced mRNA lacking the transmembrane domain. Our findings indicate that the mode of expression of Fas isoforms in ATL cells is not always homogenous and that Fas may play a role in the malignant behavior and oncogenesis of ATL.

Flow Cytometry↗
PubMed1997

Immunohistochemical localization of calbindin D28k in the periodontal Ruffini endings of rat incisors.

It was examined whether calbindin D28k (CB) might be located in the rat incisor periodontal Ruffini ending, an essential mechanoreceptor in periodontal ligament, by light- and electron-microscopic immunohistochemistry. Some thick nerve fibers showing CB-like immunoreactivity (LI) entered the lingual half of the periodontal ligament of the incisor and showed the dendritic terminal arborization. Electron-dense immunoreaction products indicating CB-LI were distributed diffusely in axoplasm of the axon terminals, no mitochondria, however, were not labeled. Neither cell bodies nor cytoplasmic extensions of the terminal Schwann cells exhibited CB-LI. CB was presumed to be involved in the maintenance of Ca2+ homeostasis in the mechano-electric transduction in mechanoreceptors in the periodontal ligament.

Animals↗
PubMed1997

BDNF prevents NO mediated glutamate cytotoxicity in cultured cortical neurons.

The effects of brain-derived neurotrophic factor (BDNF) on glutamate-induced cytotoxicity were examined using primary cultures of rat cortical neurons. BDNF induced TrkB tyrosine phosphorylation in rat cultured cortical neurons. The cell viability was significantly reduced when cultures were briefly exposed to glutamate and incubated with normal medium for 24 h. Glutamate cytotoxicity was prevented by MK-801, which is a non-competitive blocker of N-methyl-D-aspartate and N(omega)-nitro-L-arginine, which is a blocker of nitric oxide synthetase. Delayed neurotoxicity was also induced by ionomycin, a calcium ionophore, and nitric oxide (NO) donors such as S-nitrosocysteine (SNOC) and 3-morpholinosydnonimine (SIN-1). Incubating cultures with BDNF for 10 min to 24 h protected cortical neurons against glutamate neurotoxicity. The protective effects of BDNF against glutamate cytotoxicity were dependent on both its concentrations and incubation time. BDNF also prevented the ionomycin-, SNOC-, and SIN-1 induced cytotoxicity. These results indicate that BDNF protects cultured cortical neurons from NMDA receptor-mediated glutamate neurotoxicity by reducing cytotoxic action of NO.

Animals↗
PubMed1997

Effects of B vitamins on glutamate-induced neurotoxicity in retinal cultures.

The effects of B vitamins on glutamate-induced neurotoxicity were examined using primary cultures obtained from the rat retina. Cell viability was markedly reduced by a brief exposure to glutamate followed by incubation with glutamate-free media for 1 h. Glutamate cytotoxicity was reduced in the cultures that had been maintained in thiamine-, pyridoxine- or nicotinamide-containing medium before the exposure to glutamate. Glutamate cytotoxicity was also reduced by chronic application of thiamine pyrophosphate and pyridoxal phosphate, which are active coenzyme forms of thiamine and pyridoxine, respectively. By contrast, chronic application of riboflavin, pantothenate, biotin, folic acid and inositol did not affect glutamate cytotoxicity. None of the B vitamins tested had any effect on glutamate cytotoxicity when added only during the exposure to glutamate. These findings suggest that chronically applied thiamine, pyridoxine and nicotinamide protect retinal neurons against glutamate cytotoxicity.

Animals↗
PubMed1997

Tyrosine hydroxylase-immunoreactive nerve fibres in rat posterior longitudinal ligament.

The nerve supply to the posterior longitudinal ligament (PLL) of the lumbar vertebrae has been the focus of considerable interest to gain insight into the pathogenesis of low back pain. The present study aimed to characterize the sympathetic fibres in the PLL by immuno-electronmicroscopy for tyrosine hydroxylase (TH), the rate limiting enzyme in catecholamine synthesis. The posterior central branches of the segmental lumbar arteries received numerous communicating fibres from the sinuvertebral nerve (SVN), but only shortly after their entrance to the spinal canal. The non-vessel-associated branches of the SVN formed transverse bundles, which met fibres from the opposite side in a plexus-like mid-sagittal network. As these fibres approached the midline, they gradually lost their Schwann cell cover. The free and naked fibres contained numerous terminal-like varicosities. The TH-ir and 6-hydroxydopamine (6-OH-DA) sensitive fibres were intermingled with non-TH-ir fibres. The TH-ir sympathetic fibres had no obvious target structures except for the numerous, intermingled, closely related and communicating terminal-like axons in the mid-sagittal network in contact with non-TH-ir fibres. This may represent a neuroanatomical equivalent reflecting modulatory functions, which could participate in the pathogenesis of low back pain.

Animals↗
PubMed1997

Interaction of Nck-associated protein 1 with activated GTP-binding protein Rac.

Bacterially expressed glutathione S-transferase fusion proteins containing Rac1 were used to identify binding proteins of this Rho family GTPase present in a bovine brain extract. Five proteins of 85, 110, 125, 140 and 170 kDa were detected, all of which were associated exclusively with guanosine 5'-[gamma-thio]triphosphate-bound Rac1, not with GDP-bound Rac1. The 85 and 110 kDa proteins were identified as the regulatory and catalytic subunits respectively of phosphatidylinositol 3-kinase. Several lines of evidence suggested that the 125 kDa protein is identical with Nck-associated protein 1 (Nap1). The mobilities of the 125 kDa protein and Nap1 on SDS/PAGE were indistinguishable, and the 125 kDa protein was depleted from brain extract by preincubation with the Src homology 3 domain of Nck to which Nap1 binds. Furthermore, antibodies to Nap1 reacted with the 125 kDa protein. Nap1 was co-immunoprecipitated with a constitutively active form of Rac expressed in Chinese hamster ovary cells. The observation that complex formation between activated Rac and PAK, but not that between Rac and Nap1, could be reproduced in vitro with recombinant proteins indicates that the interaction of Nap1 with Rac is indirect. The 140 kDa Rac-binding protein is a potential candidate for a link that connects Nap1 to Rac. The multimolecular complex comprising Rac, Nap1 and probably the 140 kDa protein might mediate some of the biological effects transmitted by the multipotent GTPase.

Animals↗
PubMed1997

Direct evidence for increase in excitatory amino acids release during mossy fiber LTP in rat hippocampal slices as revealed by the patch sensor methods.

We had previously established a patch sensor system for detecting overflow of excitatory amino acids (EAA) from hippocampal slices induced by a single electric stimulus. We performed simultaneous recordings of patch sensor current and whole-cell current in rat hippocampal slices. Tetanus of mossy fibers produced long-term potentiation (LTP) of excitatory postsynaptic current (EPSC) recorded from a CA3 pyramidal cell with an increase in single electric stimulus-evoked patch current amplitude recorded with a patch sensor positioned in the stratum lucidum. In Schaffer collateral-CA1 synapses, however, LTP of EPSC was accompanied by an increase in AMPA-evoked whole-cell current, but not with change in patch current in the stratum radiatum. These results indicate that EAA release is increased during mossy fiber LTP but not CA1 LTP.

Animals↗
PubMed1997

Integration patterns of HTLV-I provirus in relation to the clinical course of ATL: frequent clonal change at crisis from indolent disease.

We examined human T-lymphotropic virus type I (HTLV-I) DNA integration in 68 patients with adult T-cell leukemia/ lymphoma (ATL) by Southern blotting using EcoRI, which does not cut within the 9 kb of the genome and probes for pX and gag-pol region of HTLV-I. We detected defective proviral integration as a monoclonal band of various sizes with the pX but not with the gag-pol probe, or a monoclonal band of less than 9 kb with the pX probe, in 20 patients (29.4%). These were designated defective (D) type. With both probes, a single band greater than 9 kb was detected in 34 (50.0%), designated complete (C) type, and two or more bands greater than 9 kb, were designated multiple (M) type, in 14 (20.6%). Advanced age, a high LDH value, and hypercalcemia were more frequent in D type patients. The median survival time (MST) was 6.8, 24.4, and 33.3 months, for D, C, and M types, respectively (log rank P = .006). Among 52 sequentially examined patients, the HTLV-I integration patterns changed in 4 (7.5%). In three of these four, the rearrangements of the T-cell receptor (TCR)b gene concomitantly changed, suggesting the appearance of a new ATL clone. Another patient had the same rearrangement of the TCRb gene, indicating clonal evolution. The HTLV-I integration pattern changed at crisis from indolent to aggressive ATL in three patients. These findings suggested that the HTLV-I integration patterns have clinical implications in ATL pathophysiology. In contrast to the clonal evolution characteristic of the multistep carcinogenesis of most human malignancies, the frequent clonal change of ATL at crisis is a peculiar phenomenon, probably reflecting the emergence of multiple premalignant clones in viral leukemogenesis as suggested in Epstein-Barr virus associated lymphomagenesis in the immunocompromised host.

Aged↗
PubMed1997

Preferential localization of monoamine oxidase type A activity in neurons of the locus coeruleus and type B activity in neurons of the dorsal raphe nucleus of the rat: a detailed enzyme histochemical study.

Using enzyme histochemistry for monoamine oxidase (MAO) activity, we have examined whether MAO type A or type B or both are localized in neurons of the locus coeruleus (LC) and dorsal raphe nucleus (DR) of the rat. After pretreatment with various concentrations of the MAO type A inhibitor clorgyline or the type B inhibitor deprenyl, non-fixed frozen sections of the brain were histochemically stained for MAO activity with tyramine as a common substrate for the two types. MAO activity of the stained neuron was determined by measuring optical density of the staining. Percentage inhibition of the control MAO activity was plotted against increasing concentrations of the inhibitors. MAO activity of LC neurons was inhibited by low concentrations of clorgyline with a monophasic dose-response curve but not with a biphasic curve. Higher concentrations of deprenyl were needed to inhibit of LC neurons. MAO activity of DR neurons was inhibited by low concentrations of deprenyl with a monophasic dose-response curve. Clorgyline inhibited the MAO activity of DR neurons at only higher concentrations. When the sections without inhibitor pretreatment were incubated with the type A preferential substrate serotonin, the MAO activity was strongly stained in LC neurons but very weakly in DR neurons. With the type B preferential substrate beta-phenylethylamine, the staining was intense in DR neurons while very faint in LC neurons. These findings suggest that (i) almost all the MAO activity in LC neurons is of type A, and (ii) the MAO activity in DR neurons is predominantly of type B.

Animals↗
PubMed1997

TCR in Fas-sensitive T cells from labial salivary glands of patients with Sjögren's syndrome.

Apoptosis is found in labial salivary glands of patients with Sjogren's syndrome (SS). To analyze the pathogenesis of apoptosis in labial salivary glands of SS patients, we examined the expression of Fas Ag and Fas ligand (FasL) and TCR on T cells susceptible to anti-Fas mAbs (CH-11). Fas Ag is expressed on epithelial cells and mononuclear cells in the salivary glands as observed by an immunohistochemical method. FasL is over-expressed specifically on T cells infiltrating into the labial salivary glands as seen by an reverse transcription-PCR method. These results suggest that apoptosis in SS lips is mediated by a Fas/FasL pathway. PCR single-strand conformation polymorphism (SSCP) clearly demonstrated that more than 40% of the T cells accumulated in labial salivary glands are deleted by incubation with CH-11 for 24 h in vitro, indicating that these expanded cells are Fas sensitive. junctional sequence analysis showed that the same conserved amino acid motifs (LAGG, RLA, SLG, QGPG, PGG, GGE, RGR, KPG, AGD, and MLG) in complementarity determining region 3 (CDR3) are found in Fas-sensitive T cell clones, whereas they are not detected in Fas-resistant clones, suggesting that Fas-sensitive T cells recognize restricted T cell epitopes on autoantigens. In conclusion, the findings suggest that Fas-sensitive T cells in labial salivary glands of SS patients are generated by Ag stimulation and might function as autoreactive T cells.

Amino Acid Sequence↗
PubMed1997

The formation of desethyl-piperacillin from piperacillin by human liver S9 in vitro.

Piperacillin (PIPC) has been used as one of the most useful beta-lactam antibiotics over the past 10 years. The metabolism of PIPC has been thoroughly investigated and it has been recognized that PIPC gives few metabolites in laboratory species or humans. Recently, an active metabolite, desethyl-piperacillin (DEt-PIPC), was detected in human plasma and urine after PIPC administration. In the current study, human tissues were obtained from organ donors (n = 3) and subcellular fractions (S9) were prepared. The time course of metabolism by S9 mix from liver, kidney cortex, and kidney medulla was then determined using 0.5 mM PIPC. For comparative purposes, rat liver S9 were also prepared and incubated with PIPC under the same conditions. DEt-PIPC was formed by human liver S9 mix from all three specimens studied, with the rate varying approximately eightfold. No DEt-PIPC was detected in any of the incubations with rat liver S9 mix (n = 3) and kidney S9 mix (n = 3) prepared from either the cortex or medulla. In summary, these data suggest that the formation of the unique human metabolite, DEt-PIPC, can be predicted by in vitro studies with human tissues and that this metabolite is formed predominantly by the liver.

Adult↗
PubMed1997

Evaluation of metabolic heterogeneity in brain tumors using 1H-chemical shift imaging method.

Seventeen brain tumors were measured by 1H-CSI (chemical shift imaging) in a 1.5 T clinical magnetic resonance scanner. The metabolic peaks obtained were evaluated by two methods. One method was to obtain the percentage of each metabolite relative to the combined choline, creatine and NAA peak areas, and the other method was to obtain a ratio of the tumor to contralateral brain. The percentage of choline (%Cho) and choline ratio increased, and the %NAA and NAA ratio decreased in the gliomas and malignant tumors. In relation to grading, %Cho increased but the choline ratio did not. We believed the reason for this was that there were many foci of microscopic necrosis in the glioma grade IV. Free lipids were observed in most of the high grade gliomas and in a malignant tumor. Lactate increased in higher grade tumors. Meningiomas showed the highest %Cho. Statistical differences between the grades of glioma were not detected because many tumors had heterogeneous tissue. One resolution to this problem was metabolite mapping. Mapping of the percentage of metabolites was suitable because it described the regional metabolic changes and the resulting signal to noise ratio was better than that achieved by other methods of evaluation.

Aspartic Acid↗