Biomedical subjects

Atsushi Takeda

Publications and source records attributed to Atsushi Takeda.

At least 19 recordsLinked to original sources

PubMed2026

Fusarium oxysporum f. sp. crypti, a novel forma specialis causing Fusarium wilt of mitsuba, Cryptotaenia japonica.

Fusarium oxysporum isolates causing Fusarium wilt in mitsuba (Cryptotaenia japonica Hassk.; also referred to as Japanese honeywort, Japanese honewort, or Japanese parsley) have traditionally been classified as f. sp. apii. However, some reports have indicated that the host-pathogenic F. oxysporum isolates derived from mitsuba are nonpathogenic to celery, the principal host of f. sp. apii. In this study, we aimed to elucidate the differences among isolates from mitsuba, coriander, and celery in terms of host range, phylogenetic relationships, genomic synteny, and effector profiles. Inoculation assays revealed a clear distinction in host range between the mitsuba, coriander, and celery isolates. Phylogenetic analyses based on the rDNA intergenic spacer and translation elongation factor sequences indicated a distant relationship between mitsuba isolates and those from coriander and celery. Whole-genome analysis based on high-quality de novo-assembled genomes, including telomere-to-telomere-level assemblies of isolates from mitsuba, coriander, and celery, showed that the mitsuba isolates possess conserved accessory chromosomal regions absent in celery and coriander isolates. Moreover, effector profiling identified a specific pattern of effector repertoires shared by the mitsuba isolates. These findings suggest that the host-pathogenic F. oxysporum isolates derived from mitsuba represent a forma specialis distinct from f. sp. apii. Thus, we propose designating the F. oxysporum isolates from mitsuba that cause Fusarium wilt as Fusarium oxysporum f. sp. crypti forma specialis nova.

Cryptotaenia japonica↗

PubMed2006

Inhibition of presynaptic activity by zinc released from mossy fiber terminals during tetanic stimulation.

Zinc exists in high densities in the giant boutons of hippocampal mossy fibers. On the basis of the evidence that zinc decreases extracellular glutamate concentration in the hippocampus, the presynaptic action of zinc released from mossy fibers during high-frequency (tetanic) stimulation was examined using hippocampal slices. The increase in zinc-specific fluorescent signals was observed in both extracellular and intracellular compartments in the mossy fiber terminals during the delivery of tetanic stimuli (100 Hz, 1 sec) to the dentate granule cell layer, suggesting that zinc released from mossy fibers is immediately retaken up by mossy fibers. When mossy fiber terminals were preferentially double-stained with zinc and calcium indicators and tetanic stimuli (100 Hz, 1 sec) were delivered to the dentate granule cell layer, the increase in calcium orange signal during the stimulation was enhanced in mossy fiber terminals by addition of CaEDTA, a membrane-impermeable zinc chelator, and was suppressed by addition of zinc. The decrease in FM4-64 signal (vesicular exocytosis) during tetanic stimulation (10 Hz, 180 sec), which induced mossy fiber long-term potentiation, was also enhanced in mossy fiber terminals by addition of CaEDTA and was suppressed by addition of zinc. The present study demonstrates that zinc released from mossy fibers may be a negative-feedback factor against presynaptic activity during tetanic stimulation.

Animals↗

PubMed2005

Roles of MMP-2/-9 in cardiac dysfunction during early multiple organ failure in an ovine animal model.

Biventricular dilation and severe cardiac dysfunction are observed during septic shock. However, when endotoxemia and vasoconstrictor-masked hypovolemia work in concert in the pathogenesis of shock, the clinical scenario is more adverse compared to one of the insults acting alone. Matrix metalloproteinases (MMPs) are involved in chronic and acute heart failure by degrading the mechanical scaffold of the heart and several intracellular proteins. Therefore, the roles of MMP-2, MMP-9, MT1-MMP, focal adhesion kinase (FAK), and Paxillin in hearts of early multiple organ failure induced by norfenefrine-masked hypovolemia and endotoxemia were investigated in an ovine model. Experimental groups included (1) norfenefrine-masked hypovolemia plus endotoxemia (NMH+ENDO) (n=6), (2) norfenefrine-masked hypovolemia without endotoxemia (NMH) (n=6), (3) recurrent endotoxemia during normovolemia (ENDO) (n=6), and (4) healthy untreated controls (CON) (n=3). Apoptosis was determined by TUNEL-staining. Gel zymography revealed significantly increased MMP-2 activity in NMH+ENDO compared to ENDO and controls. MMP-9 activity was significantly elevated in all experimental groups. MMP-2 was significantly increased at the protein level, while MMP-9 was unaltered. MT1-MMP was not significantly changed in any group. Increased MMP activities were associated with cardiac deterioration. MMP-2/-9 activity and phosphorylated Paxillin (p-Paxillin) expression correlated positively with cardiomyocyte apoptosis. This study underscores the pivotal roles of MMP in acute cardiac dysfunction during early multiple organ failure in combined vasoconstrictor-masked hypovolemic and endotoxemia shock.

Animals↗

PubMed2005

Development of micro-PIC as a time-resolved X-ray area detector.

The application of a two-dimensional micro-pixel gas chamber (micro-PIC) to X-ray diffraction studies, and its performance, are reported. micro-PIC has a 10 cm x 10 cm detection area, and a fast-readout system for real-time X-ray imaging has been developed. Using the timing of each incoming X-ray measured by micro-PIC, continuous rotation photograph measurements were carried out for a 400 microm-diameter spherical organic crystal of Ylid (C(11)H(10)O(2)S), and then diffraction spots were successfully obtained within 2theta of 49 degrees. As a result, good internal agreement factors of 3.7% and 7.0% were confirmed among each of the symmetrically equivalent reflections for exposure times of 3700 s and 98 s, respectively.

Journal Article↗

PubMed2005

Increase in hippocampal cell death after treatment with kainate in zinc deficiency.

Susceptibility to kainate-induced seizures is enhanced by zinc deficiency. To evaluate kainate-induced excitotoxicity in zinc deficiency, the relationship between kainate-induced seizures and hippocampal cell death was examined in control and zinc-deficient mice. Mice were fed a control and zinc-deficient diet for 4 weeks, and then intraperitoneally injected with 12 mg/kg kainate every 60 min three times. The rate of dead mice to the total mice was higher in zinc-deficient group than in control group 3 days after the last injection of kainate. In the survivals, which exhibited tonic convulsions in both control and zinc-deficient groups, kainate-induced hippocampal cell death was also analyzed by cresyl violet staining. Neuronal loss was more observed in the CA1, CA2 and CA3 pyramidal cell layers of zinc-deficient group than those of the control group. TUNEL-positive cells were significantly more detected in the CA1 and CA3 pyramidal cell layers of zinc-deficient group. These results demonstrate that kainate-induced hippocampal cell death occurs more easily in zinc deficiency. Extracellular zinc concentration detected with ZnAF-2 was significantly decreased in the hippocampal CA3 of zinc-deficient mice, in agreement with the previous data measured by in vivo microdialsysis. Synaptically released zinc may be less involved in kainate-induced hippocampal cell death in zinc deficiency.

Animals↗

PubMed2005

A plant RNA virus suppresses RNA silencing through viral RNA replication.

RNA interference (RNAi) is a post-transcriptional gene-regulatory mechanism that operates in many eukaryotes. RNAi is induced by double-stranded RNA (dsRNA) and is mainly involved in defence against transposons and viruses. To counteract RNAi, viruses have RNAi suppressors. Here we show a novel mechanism of RNAi suppression by a plant virus Red clover necrotic mosaic virus (RCNMV). To suppress RNAi, RCNMV needs multiple viral components, which include viral RNAs and putative RNA replicase proteins. A close relationship between the RNA elements required for negative-strand RNA synthesis and RNAi suppression suggests a strong link between the viral RNA replication machinery and the RNAi machinery. In a transient assay, RCNMV interferes with the accumulation of small-interfering RNA (siRNAs) in RNAi induced by a hairpin dsRNA and it also interferes with microRNA (miRNA) biogenesis. An Arabidopsis dcl1 mutant showed reduced susceptibility to RCNMV infection. Based on these results, we propose a model in which, to replicate, RCNMV deprives the RNAi machinery of Dicer-like enzymes that are involved in both siRNA and miRNA biogenesis.

3' Untranslated Regions↗

PubMed2005

Reverse remodeling following insertion of left ventricular assist devices (LVAD): a review of the morphological and molecular changes.

Left ventricular assist devices (LVAD) are used to "bridge" patients with end-stage heart failure until transplantation of a donor heart can be performed ("bridge to transplantation"). However, in a subset of patients, support by LVAD sporadically results in improved cardiac function, with heart transplantation no longer necessary even after removal of the LVAD ("bridge to recovery"). Also, LVAD appears to be an optional treatment alternative to heart transplantation in patients with contraindications for organ replacement ("destination therapy"). The processes resulting in these effects have descriptively been termed "reverse remodeling". Although the molecular mechanisms are incompletely understood at present, there are several aspects of the reverse remodeling process that have been identified in the past. Alterations of many molecular pathways are involved in the development of chronic heart failure. Some of these appear to be reversible and have been shown to be regulated by LVAD treatment. LVAD lead to lowered cardiac pressure and volume overload in the myocardium followed by decreased ventricular wall tension, reduced cardiomyocyte hypertrophy, improved coronary perfusion and decreased chronic ischemia. Improved coronary flow and myocardial perfusion as well as decreased ventricular wall tension may possibly alter the molecular systems involved in the development of chronic cardiac insufficiency. Aside from describing the morphological changes, this review focuses on the roles of signal transduction, transcriptional regulation, apoptosis, stress proteins, matrix remodeling, and neurohormonal signaling in the failing human heart before and after mechanical circulatory support.

Adrenergic beta-Agonists↗

PubMed2005

Alzheimer-specific epitopes of tau represent lipid peroxidation-induced conformations.

Several recent studies support a link between tau protein phosphorylation and adduction of tau by reactive carbonyls. Indeed, the phosphorylation-dependent adduction of tau by carbonyl products resulting from lipid peroxidation creates the neurofibrillary tangle-related antigen, Alz50. To determine whether epitopes of carbonyl-modified tau are major conformational changes associated with neurofibrillary tangle formation, we examined seven distinct antibodies raised against neurofibrillary tangles that recognize unique epitopes of tau in Alzheimer disease. Consistently, all seven antibodies recognize tau more strongly (4- to 34-fold) after treatment of normal tau with the reactive carbonyl, 4-hydroxy-2-nonenal (HNE), but only when tau is in the phosphorylated state. These findings not only support the idea that oxidative stress is involved in neurofibrillary tangle formation occurring in brains of Alzheimer disease patients, but also show, for the first time, that HNE modifications of tau promote and contribute to the generation of the major conformational properties defining neurofibrillary tangles.

Aged↗

PubMed2005

Stage-specific expression of microRNAs during Xenopus development.

MicroRNAs (miRNAs) repress target genes at the post-transcriptional level and play important roles in development and cell lineage decision. However, in vertebrates, both the targets of miRNAs and their expression profile during development are poorly understood. Here, we report the detailed expression profiles of miRNAs from oocyte stage to tadpole stage in Xenopus laevis. As development proceeds, a variety of miRNAs start to be expressed. Most miRNAs emerged at a specific stage and were continuously expressed until the tadpole stage. In addition, we identified a novel miRNA that was expressed only at specific stages of development and that is likely to have roles in midblastula transition.

Animals↗

PubMed2005

Tau modifiers as therapeutic targets for Alzheimer's disease.

Fibrillogenesis is a major feature of Alzheimer's disease (AD) and other neurodegenerative diseases. Fibers are correlated with disease severity and they have been implicated as playing a direct role in disease pathophysiology. In studies of tau, instead of finding causality with tau fibrils, we found that tau is associated with reduction of oxidative stress. Biochemical findings show that tau oxidative modifications are regulated by phosphorylation and that tau found in neurofibrillary tangles is oxidatively modified, suggesting that tau is closely linked to the biology, not toxicity, of AD.

Aldehydes↗

PubMed2005

Enhanced excitability of hippocampal mossy fibers and CA3 neurons under dietary zinc deficiency.

On the basis of the evidence that susceptibility to kainate-induced seizures is enhanced by zinc deficiency and that glutamate concentrations in hippocampal extracellular fluid are excessively increased during seizures, excitability of hippocampal mossy fibers and CA3 neurons was examined using hippocampal slices, which were prepare from mice fed a zinc-deficient diet for 4 weeks. The spatio-temporal dynamics of zinc and calcium was monitored using their indicators, membrane-impermeable ZnAF-2 and membrane-permeable fura-2 AM, respectively. When the molecular layer of dentate gyrus was stimulated with 100mM KCl for 1s, the increased percentages of extracellular zinc in the stratum lucidum and CA3 pyramidal cell layer were higher in zinc-deficient mice than in the control mice, implying that glutamate release from the mossy fibers of the dentate granular cells is enhanced by zinc deficiency. Judging from the increased percentages, however, the amount of zinc released was estimated to be less in zinc-deficient mice. On the other hand, the basal calcium concentrations in the stratum lucidum and CA3 pyramidal cell layer detected with fura-2 were higher in zinc-deficient mice than in the control mice, indicating that hippocampal calcium homeostasis is affected by zinc deficiency. Furthermore, the increased percentage of intracellular calcium in the stratum lucidum by stimulation with high K+ was enhanced by the zinc deficiency. The alteration of hippocampal calcium homeostasis seems to enhance excitability of dentate granular cells in zinc deficiency, following by an enhanced excitability of postsynaptic structures in CA3 neurons.

Animals↗

PubMed2005

Transethmoidal intranasal meningoencephalocele in an adult with recurrent meningitis.

Intranasal meningoencephalocele is a rarely encountered congenital malformation. We report a case of transethmoidal intranasal meningoencephalocele in a 52-year old man with recurrent purulent meningitis. After treatment of the acute meningitis, frontal craniotomy followed by the removal of the stalk of the meningoencephalocele and repair of the bony defect was successfully performed. He has had no further meningitis or CSF rhinorrhea post-operatively. Detailed neuroradiological examination and appropriate surgical treatment are important to prevent fatal neurological complications of intranasal meningoencephalocele.

Cerebral Angiography↗

PubMed2005

Periodic episodes of aphasia as an unusual manifestation of partial status epilepticus.

Recurrent episodes of aphasia due to partial status epilepticus is an uncommon clinical entity. We report here a 78-year-old-woman with episodic aphasia which occurred periodically. During the ictal period, she was conscious, but had difficulty in speech and could not comprehend verbal commands. The ictal EEG showed continuous spike and sharp waves over the left frontotemporal area. After the administration of antiepileptic drugs, her language activity returned to near the baseline level and the epileptic discharges were significantly reduced. Nonconvulsive partial status epilepticus should be considered in the differential diagnosis of recurrent aphasia, even if the symptoms occur periodically.

Aged↗

PubMed2005

Tau phosphorylation in Alzheimer's disease: pathogen or protector?

During the past decade, hypotheses concerning the pathogenesis of most neurodegenerative diseases have been dominated by the notion that the aggregation of specific proteins and subsequent formation of cytoplasmic and extracellular lesions represent a harbinger of neuronal dysfunction and death. As such, in Alzheimer's disease, phosphorylated tau protein, the major component of neurofibrillary tangles, is considered a central mediator of disease pathogenesis. We challenge this classic notion by proposing that tau phosphorylation represents a compensatory response mounted by neurons against oxidative stress and serves a protective function. This novel concept, which can also be applied to protein aggregates in other neurodegenerative diseases, opens a new window of knowledge with broad implications for both the understanding of mechanisms underlying disease pathophysiology and the design of new therapeutic strategies.

Alzheimer Disease↗

PubMed2005

Discordance of influence of hypertension on mortality and cardiovascular risk in hemodialysis patients.

BACKGROUND: Hemodialysis patients are at significantly increased risk for both morbidity and mortality from cardiovascular disease. However, most recent reports have indicated elevated mortality risk associated with low blood pressure, rather than high blood pressure. We added nonfatal cardiovascular events as an outcome in addition to cardiovascular and all-cause mortality to analyze the risk of hypertension. METHODS: One hundred sixty-four patients receiving regular hemodialysis between January and December 1998 were examined and prospectively followed up until the end of 2003. The primary end point was hospital admission or death from cardiovascular disease. Secondary end points were cardiovascular and all-cause mortality. RESULTS: During the 5-year follow-up period, 52 patients experienced cardiovascular events and 45 patients died (18 patients, from cardiovascular disease). Based on Cox analysis, high systolic blood pressure (relative risk [RR], 1.23; 95% confidence interval [CI], 1.07 to 1.43; P = 0.004) and older age were independently associated with cardiovascular events. Elevated systolic blood pressure (RR, 1.25; 95% CI, 0.99 to 1.59; P = 0.063) was a marginal predictor for cardiovascular mortality. Age, serum albumin level, malignant neoplasm, and diabetes were independent risk factors for all-cause mortality, whereas there was no association between blood pressure and all-cause mortality. The hazard ratio for cardiovascular events after adjustment for age, sex, and diabetes was lowest in patients with systolic blood pressure of 140.1 mm Hg or less and progressively increased with the increase in systolic blood pressure. CONCLUSION: Hypertension is a potent risk factor for cardiovascular disease in hemodialysis patients, as in the general population, whereas there is no association of hypertension with mortality. Active reduction in systolic blood pressure is important to minimize the occurrence of cardiovascular events.

Cardiovascular Diseases↗

PubMed2005

Natural isolates of Brome mosaic virus with the ability to move from cell to cell independently of coat protein.

Brome mosaic virus (BMV) requires encapsidation-competent coat protein (CP) for cell-to-cell movement and the 3a movement protein (MP) is involved in determining the CP requirement for BMV movement. However, these conclusions have been drawn by using BMV strain M1 (BMV-M1) and a related strain. Here, the ability of the MPs of five other natural BMV strains to mediate the movement of BMV-M1 in the absence of CP was tested. The MP of BMV M2 strain (BMV-M2) efficiently mediated the movement of CP-deficient BMV-M1 and the MPs of two other strains functioned similarly to some extent. Furthermore, BMV-M2 itself moved between cells independently of CP, demonstrating that BMV-M1 and -M2 use different movement modes. Reassortment between CP-deficient BMV-M1 and -M2 showed the involvement of RNA3 in determining the CP requirement for cell-to-cell movement and the involvement of RNAs 1 and 2 in movement efficiency and symptom induction in the absence of CP. Spontaneous BMV MP mutants generated in planta that exhibited CP-independent movement were also isolated and analysed. Comparison of the nucleotide differences of the MP genes of BMV-M1, the natural strains and mutants capable of CP-independent movement, together with further mutational analysis of BMV-M1 MP, revealed that single amino acid differences at the C terminus of MP are sufficient to alter the requirement for CP in the movement of BMV-M1. Based on these findings, a possible virus strategy in which a movement mode is selected in plant viruses to optimize viral infectivity in plants is discussed.

Base Sequence↗

PubMed2005

Characterization of Striped jack nervous necrosis virus subgenomic RNA3 and biological activities of its encoded protein B2.

Striped jack nervous necrosis virus (SJNNV), which infects fish, is the type species of the genus Betanodavirus. This virus has a bipartite genome of positive-strand RNAs, designated RNAs 1 and 2. A small RNA (ca. 0.4 kb) has been detected from SJNNV-infected cells, which was newly synthesized and corresponded to the 3'-terminal region of RNA1. Rapid amplification of cDNA ends analysis showed that the 5' end of this small RNA (designated RNA3) initiated at nt 2730 of the corresponding RNA1 sequence and contained a 5' cap structure. Substitution of the first nucleotide of the subgenomic RNA sequence within RNA1 selectively inhibited production of the positive-strand RNA3 but not of the negative-strand RNA3, which suggests that RNA3 may be synthesized via a premature termination model. The single RNA3-encoded protein (designated protein B2) was expressed in Escherichia coli, purified and used to immunize a rabbit to obtain an anti-protein B2 polyclonal antibody. An immunological test showed that the antigen was specifically detected in the central nervous system and retina of infected striped jack larvae (Pseudocaranx dentex), and in the cytoplasm of infected cultured E-11 cells. These results indicate that SJNNV produces subgenomic RNA3 from RNA1 and synthesizes protein B2 during virus multiplication, as reported for alphanodaviruses. In addition, an Agrobacterium co-infiltration assay established in transgenic plants that express green fluorescent protein showed that SJNNV protein B2 has a potent RNA silencing-suppression activity, as discovered for the protein B2 of insect-infecting alphanodaviruses.

Animals↗

PubMed2005

Ferric cycle activity and Alzheimer disease.

Elevated plasma homocysteine is an independent risk factor for the development of Alzheimer disease, however, the precise mechanisms underlying this are unclear. In this article, we expound on a novel hypothesis depicting the involvement of homocysteine in a vicious circle involving iron dysregulation and oxidative stress designated as the ferric cycle (Dwyer et al., 2004). Moreover, we suspect that the development of a critical heme deficiency in vulnerable neurons is an additional consequence of ferric cycle activity. Oxidative stress and heme deficiency are consistent with many pathological changes found in Alzheimer disease including mitochondrial abnormalities and impaired energy metabolism, cell cycle and cell signaling abnormalities, neuritic pathology, and other features of the disease involving alterations in iron homeostasis such as the abnormal expression of heme oxygenase-1 and iron response protein 2. Based on the ferric cycle concept, we have developed a model of Alzheimer disease development and progression, which offers an explanation for why sporadic Alzheimer disease is different than normal aging and why familial Alzheimer disease and sporadic Alzheimer disease could have different etiologies but a common end-stage.

Alzheimer Disease↗