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Masanori Yamada

Publications and source records attributed to Masanori Yamada.

At least 19 recordsLinked to original sources
PubMed2006

[Approximation of collimator scatter factor Sc by a saturation model].

To more easily estimate accurate values of collimator scatter facor, S(c), we suggest a two-component saturation model that accounts for scatter from the primary collimator and flattening filter and from the collimator jaws. This model, which assumes an exponential distribution of scatter intensity, was tested by in-air measurements using a mini-phantom for 4 MV and 10 MV X-rays of a Clinac 2100 C/D linear accelerator. The results showed a good fit of this model to our measured data (R(2)>0.9993). When the measured value was divided into the primary collimator/flattening filter component and the collimator jaw component, as expected, the former component showed a rapid and full saturation curve with increased field size, while the latter showed an almost linearly increasing curve. Therefore, we think that this saturation model is useful for the estimation of S(c) and is applicable to monitor unit calculation for an asymmetric field.

Filtration↗
PubMed2006

Laminin peptide-conjugated chitosan membrane: Application for keratinocyte delivery in wounded skin.

Tissue engineering requires the delivery and survival of cells to organ sites needing repair. Previously, we showed that an active laminin peptide (AG73: RKR-LQVQLSIRT)-conjugated chitosan membrane promoted cell adhesion and spreading in vitro. Here, we seeded human keratinocytes onto AG73-chitosan membranes and found that nearly 80% of the cells were attached to the membranes within 2 h. The membranes carrying the keratinocytes were inverted and placed onto exposed muscle fascia on the backs of nude mice. After 3 days, the keratinocytes had migrated from the membrane and established a stratified epidermis-like structure on the fascia. Cells recognize the AG73 through transmembrane proteoglycan syndecans, which recognition system has not previously been tested in tissue engineering applications. We suggest that the AG73-chitosan membrane is useful as a therapeutic formulation and is applicable as a cell delivery system such as delivering keratinocytes to a wound bed.

Animals↗
PubMed2006

Heteropolyacid-encapsulated self-assembled materials for anhydrous proton-conducting electrolytes.

The composite material of heteropolyacid (12-phosphotungstic acid; PWA) and polystyrene sulfonic acid (PSS) construct the PWA-encapsulated material by the self-assembly of -SO3H onto the PWA surface; as a result, the fast proton transfer occurred at the interface between the PWA and -SO3H, and the encapsulated material indicated the high anhydrous proton conductivity of 1 x 10(-2) S cm(-1) at 180 degrees C. These anhydrous proton-conducting materials without the existence of water molecules are quite different from customary ion-exchange membrane, such as Nafion, and may have advantages as an electrolyte membrane for polymer electrolyte membrane fuel cells operating at intermediate temperatures under anhydrous conditions but also for electrochemical devices including electrochromic displays, chemical sensors, and others.

Journal Article↗
PubMed2006

Biomembranes for fuel cell electrolytes employing anhydrous proton conducting uracil composites.

The controls of proton transfer through membranes involve fundamental properties of chemical energy conversion in industrial devices as well as living systems. In particular, ion-exchange membranes are generally used as superior proton conductors for polymer electrolyte fuel cells (PEFC) due to the fluidic nature of water, although the cell operation above the boiling point (>100 degrees C) has been considered to provide a higher efficiency and an easier humidity management. We show that biomembranes consisting of uracil and chitin phosphate have large anhydrous proton conductivities over a wide temperature range from room temperature to 160 degrees C with sufficient thermal stabilities. Water-free conductivities exceeding 10(-3) S cm(-1) have been obtained in the elastic polymeric material, and the fuel cell employing the biomembrane as an electrolyte exhibited a stable current generation under non-humidified H2/O2 conditions at 160 degrees C.

Bioelectric Energy Sources↗
PubMed2006

Down-regulation of alpha-synuclein expression can rescue dopaminergic cells from cell death in the substantia nigra of Parkinson's disease rat model.

Fibrillization and aggregation of alpha-synuclein may play a critical role in neurodegenerative diseases like Parkinson's diseases. Adeno-associated virus (AAV) vector delivery of an alpha-synuclein ribozyme was tested for its silencing effect on degenerating nigrostriatal neurons in the MPP(+) model of Parkinson's disease. We designed alpha-synuclein ribozyme against human alpha-synuclein gene expression and constructed alpha-synuclein ribozymes-carrying rAAV vector (designated rAAV-SynRz). Co-transfection of rAAV-SynRz and rAAV-alpha-synuclein into HEK293 cells resulted in down-regulation of alpha-synuclein protein expression in vitro. Then, rAAV-SynRz was injected into the substantia nigra (SN) of MPP(+)-treated rats. Cell counts of TH-positive neurons in the SN revealed that rAAV-SynRz significantly protected TH-positive cells against apoptotic death, compared with those of rAAV-EGFP or no rAAV injected rats. Our results indicate that the use of rAAV-SynRz allowed the survival of higher number of TH-positive neurons in SN in the MPP(+) model. Down-regulation of alpha-synuclein expression could be potentially a suitable target for gene therapy of Parkinson's disease.

Adenoviridae↗
PubMed2006

Hepatic ischemia/reperfusion upregulates the susceptibility of hepatocytes to confer the induction of inducible nitric oxide synthase gene expression.

During hepatic ischemia/reperfusion (I/R), proinflammatory cytokines such as tumor necrosis factor alpha and interleukin (IL) 1beta stimulate the induction of inducible nitric oxide synthase (iNOS) in hepatocytes, followed by massive production of nitric oxide. We hypothesized that I/R upregulated the susceptibility of hepatocytes to confer the induction of iNOS gene expression. This study was designed to investigate whether cell susceptibility occurs in response to I/R and to delineate the mechanisms underlying the susceptibility. Hepatocytes were isolated from rats with hepatic I/R or sham, cultured, and treated with IL-1beta. The iNOS induction and its signal including inhibitor kappaB (IkappaB) kinase/nuclear factor kappaB (NF-kappaB) and Akt/type 1 interleukin 1 receptor (IL-1R1) were analyzed. Hepatocytes isolated from rats with I/R markedly increased the production of nitric oxide when stimulated by IL-1beta as compared with sham control. Ischemia/R also increased the levels of iNOS protein and its messenger RNA. Furthermore, I/R enhanced the activation of transcription factor NF-kappaB and the transactivation of iNOS promoter. However, I/R had no effects on the degradation of IkappaB and the nuclear translocation of p65 subunit of NF-kappaB. In contrast, I/R increased the phosphorylation of Akt and the upregulation of IL-1R1 induction, which is essential signal for the transcriptional activation of iNOS in addition to IkappaB kinase/NF-kappaB. These results demonstrate that I/R may augment hepatocyte susceptibility for the induction of iNOS gene expression through the enhancement of IL-1R1.

Animals↗
PubMed2006

[Three cases of drug-induced akathisia due to antiemetics during cancer palliative care].

Three cases of drug-induced akathisia during palliative care in terminal cancer patients were reported. Antiemetics (metoclopramide and prochlorperazine) possessing a central antidopaminergic effect were suspected to have caused the akathisia. Akathisia, as well as extrapyramidal symptoms, is a common and unpleasant complex neurobehavioral adverse effect of conventional antipsychotic drugs. But it is not widely recognized by general clinicians. This syndrome consists of subjective (feeling of inner restlessness, mental unease, or dysphoria and the urge to move) and objective components (restless movement, including rocking on one's feet, walking in position shuffling and tramping the legs,and crossing and uncrossing one's legs while sitting). In severe cases, patients constantly pace up and down in an attempt to relieve the sense of unrest. While the pathophysiology of drug-induced akathisia remains unknown, antagonism of the mesocortical and mesolimbic dopaminergic pathways is a plausible if not completely satisfactory hypothesis. The notion that dopaminergic blockade underlies the emergence of akathisia is supported by the PET studies. Since akathisia is a drug-induced adverse effect, optimal management involves its prevention rather than treatment. Drugs which have been found to have some efficacy in the treatment of akathisia are anticholinergics, beta-blockers, benzodiazepines and clonidine. Though a number of other treatments have been proposed, no trial-based evidences for treatment of akathisia have been available. It is important that akathisia is recognized and treated appropriately as an adverse reaction to drugs and a further increase in antipsychotic medication dosage may further exacerbate the condition.

Adult↗
PubMed2005

A self-ordered, crystalline glass, mesoporous nanocomposite with high proton conductivity of 2 x 10(-2) S cm-1 at intermediate temperature.

We prepared a TiO2-P2O5 self-ordered, crystalline glass, mesoporous nanocomposite (CGMN) with water-holding capacity at an intermediate temperature region (130-200 degrees C). This TiO2-P2O5 CGMN showed the high proton conductivity of 2 x 10-2 S cm-1 at 160 degrees C under fully saturated humidification conditions (100% RH). Additionally, these conductivities were stable at intermediate temperature conditions. The TiO2-P2O5 CGMN may have a potential not only for the fuel cell electrolytes operated at intermediate temperature conditions but also for electrochemical devices, including electrochromic displays, chemical sensors, lithium rechargeable batteries, and others.

Crystallization↗
PubMed2005

Possibility for neurogenesis in substantia nigra of parkinsonian brain.

Recent studies of enhanced hippocampal neurogenesis by antidepressants suggest enhancement of neurogenesis is a potentially effective therapy in neurodegenerative diseases. In this study, we evaluated nigral neurogenesis in animals and autopsy brains including patients with Parkinson's disease (PD). First, proliferating cells in substantia nigra were labeled with retroviral transduction of green fluorescent protein, which is an efficient method to label neuronal stem cells. Subsequent differentiation of labeled cells was followed; many transduced cells became microglia, but no differentiation into tyrosine hydroxylase-positive neurons was detected at 4 weeks after injection, in both intact rodents and those treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Second, polysialic acid (PSA)-like immunoreactivity, indicative of newly differentiated neurons, was detected in the substantia nigra of rodent, primate, and human midbrains. A large number of PSA-positive cells were detected in the substantia nigra pars reticulata of some patients with PD. In rats and a macaque monkey, the dopamine-depleted hemispheres showed more PSA staining than the intact side. A small number of tyrosine hydroxylase-positive cells were PSA-positive. Our results suggest enhanced neural reconstruction in PD, which may be important in the design of new therapies against the progression of PD.

Aged↗
PubMed2005

Prognostic factors in breast cancer: the value of the Nottingham Prognostic Index for patients treated in a single institution.

PURPOSE: The Nottingham Prognostic Index (NPI) is used to predict survival in patients with breast cancer. This index is based on tumor size, lymph node stage, and histological grade and allows the stratification of patients into three different prognostic groups. Our aim was to verify the effect of some prognostic variables on survival and to establish the independent influence of each of these variables by a survival regression analysis. We applied the NPI to the same group of patients to assess its predictive power and reproducibility. METHODS: We evaluated 311 women with breast cancer treated between January 1993 and December 1998. RESULTS: In a multivariate analysis (Cox proportional hazard model), only size, lymph node involvement, and histological grade were independent prognostic factors. The survival curves obtained after applying the NPI were similar to those for the factors with independent prognostic significance derived from our multivariate analysis. CONCLUSION: The NPI allows us to accurately predict prognosis, and we advocate its standardized use.

Adult↗
PubMed2005

Parkin gene therapy for alpha-synucleinopathy: a rat model of Parkinson's disease.

Parkin is known to mitigate alpha-synuclein-induced neuronal cell death in vitro, which suggests that the parkin gene therapy is a candidate for therapeutic strategies for Parkinson's disease (PD). In the present study, the parkin gene therapy was investigated for its ameliorative effects on alpha-synucleinopathy in substantia nigra (SN) of rats. A recombinant adeno-associated viral (rAAV) vector system has frequently been used for the gene transfer to rat SN, and we have previously demonstrated that this technique induced the alpha-synucleinopathy, which closely resembles pathogenetic changes in PD. Therefore, in the present study, the effect of parkin was examined by co-infection of rAAV-parkin with rAAV-alpha-synuclein into dopaminergic neurons in SN. At 13 weeks post-rAAV infection, alpha-synuclein overexpression induced dopaminergic neuron loss, while co-expression of parkin mitigated the alpha-synuclein toxicity. Moreover, alpha-synuclein-induced dopaminergic neuron loss consequently resulted in motor dysfunction, which was also mitigated by parkin. Taken together, our results indicate that the parkin gene therapy is effective against alpha-synucleinopathy, suggesting its potential suitability for patients with PD.

Animals↗
PubMed2004

Predicting invasion in mammographically detected microcalcifcation: a preliminary report.

BACKGROUND: With the increased use of mammography for breast cancer screening, the diagnosis of ductal carcinoma in situ (DCIS) too has increased. This study was carried out to identify clinical and radiological factors that may predict the presence of invasive disease within mammographically detected microcalcifcation. MATERIALS AND METHODS: A retrospective analysis of 13 vacuum-assisted breast biopsies (Mammotome) of mammographic calcification, which were reported to be either DCIS or invasive disease on final histopathology, was carried out. Final surgical pathology was correlated with pre-operative features (clinical, radiological and core histology) to predict the presence of an invasive component. RESULTS: The overall sensitivity of Mammotome was 81.8%, while for invasion it was 50%. Small size, granular morphology, increased number and area of calcification cluster may help in predicting invasion on mammography. CONCLUSIONS: Mammotome biopsy fails to detect invasion correctly in half the cases despite ascertaining correctness of biopsy with post biopsy x-ray.

Journal Article↗
PubMed2004

Caspase-11 mediates inflammatory dopaminergic cell death in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease.

The present study was designed to elucidate the inflammatory and apoptotic mechanisms of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity in a model of Parkinson's disease. Our results showed that mutant mice lacking the caspase-11 gene were significantly more resistant to the effects of acute treatment with MPTP than their wild-type mice. Thus, the neurotoxicity of MPTP seems to be mediated by the induction of both mitochondrial dysfunction and free radical generation. Previously, we showed that overexpression of the Apaf-1 dominant-negative inhibitor inhibited the mitochondrial apoptotic cascade in chronic MPTP treatment but not in acute MPTP treatment. The present results indicate that MPTP neurotoxicity may be mediated via activation of the caspase-11 cascade and inflammatory cascade, as well as the mitochondrial apoptotic cascade.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2004

Influence of cellularity in human breast carcinoma.

Ninty-three cases of both invasive ductal and lobular carcinoma were examined to clarify the relationship between the clinicopathological factors and cellularity (cell density) or total cancer cells number in carcinoma tissues. The cellularity showed significant correlation with tumor size and vascular invasion, but not with other clinicopathological factors (menopausal status, operation method, ER status, histological grade or type, lymph node stage) and prognosis. The total cancer cell number revealed a positive relationship with survival (overall survival) and disease-free interval (DFI) by univariate analysis, even though it did not show any positive correlation with other clinicopathological factors in this study. Moreover, it was not found to have any stronger impact than other previously reported prognostic factors such as tumor size, lymph node stage or tumor grade by multivariate analysis. From these evidences, we speculate that the cellularity correlates with expansion or invasion of tumor cells and the total number of cancer cells reflects the prognosis of the tumor-bearing host, although it does not play a major role in prediction.

Adult↗
PubMed2004

Up-regulation of IL-1 receptor through PI3K/Akt is essential for the induction of iNOS gene expression in hepatocytes.

BACKGROUND/AIMS: Nuclear translocation and DNA binding of NF-kappaB is essential, as interleukin-1beta (IL-1beta) stimulates the induction of inducible nitric oxide synthase (iNOS) gene expression in hepatocytes. However, recent evidence indicates that the activation of NF-kappaB is not sufficient to induce the NF-kappaB-dependent transcription, and the existence of a second signaling is postulated. METHODS: Primary cultured hepatocytes were treated with IL-1beta, and the expression of iNOS and type 1 IL-1 receptor (IL-1R1) was analyzed in the presence of antisense of IL-1R1, phosphatidylinositol 3-kinase (PI3K) inhibitor, proteasome inhibitor and hypoxia. Moreover, the activities of Akt and NF-kappaB were recorded and the cotransfection was carried out. RESULTS: Antisense experiment revealed that IL-1R1 was required for iNOS transcription. IL-1beta markedly stimulated the induction of IL-1R1, which preceded the induction of iNOS. The IL-1R1 induction was found to be PI3K/Akt-dependent but NF-kappaB-independent. The up-regulation of IL-1R1 was associated with the second activation of Akt, which accelerated the phosphorylation of NF-kappaB p65 subunit. Cotransfection experiments revealed that Akt increased the transcriptional activity of iNOS gene promoter. CONCLUSIONS: These results indicate that the up-regulation of IL-1R1 in concert with the activation of NF-kappaB is required for the transcriptional activation of iNOS gene.

Animals↗
PubMed2004

Overexpression of alpha-synuclein in rat substantia nigra results in loss of dopaminergic neurons, phosphorylation of alpha-synuclein and activation of caspase-9: resemblance to pathogenetic changes in Parkinson's disease.

To elucidate the role of alpha-synuclein in the pathogenesis of Parkinson's disease, both human alpha-synuclein transgenic mice and targeted overexpression of human alpha-synuclein in rat substantia nigra using viral vector-based methods have been studied, however, little is known about the pathogenetic changes of dopaminergic neuron loss. Therefore, it is necessary to address whether the pathogenetic changes in brains with Parkinson's disease are recapitulated in these models. Here, we used the recombinant adeno-associated viral (rAAV) vector system for human alpha-synuclein gene transfer to rat substantia nigra and observed approximately 50% loss of dopaminergic neurons at 13 weeks after infection, which was comparably slower than the progression of neurodegeneration reported in other studies. In the slower progression of neurodegeneration, we identified several important features in common with the pathogenesis of Parkinson's disease, such as phosphorylation of alpha-synuclein at Ser129 and activation of caspase-9. Both findings were also evident in cortical tissues overexpressing alpha-synuclein via rAAV. Our results indicate that overexpression of alpha-synuclein via rAAV apparently recapitulates several important features of brains with Parkinson's disease and dementia with Lewy bodies, and thus alpha-synucleinopathy described here is likely to be an ideal model for the study of the pathogenesis of Parkinson's disease and dementia with Lewy bodies.

Animals↗