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Biomedical subjects

Naoki Matsuo

Publications and source records attributed to Naoki Matsuo.

18 recordsLinked to original sources
PubMed2007

[Characteristics of and strategy for cancer pain].

75% of cancer patients have pain, which can greatly affect their quality of life. In cancer patients, not only physical pain but also total pain must be treated. Cancer pain can be classified as nociceptive pain or neuropathic pain according to neural mechanism. It is important to consider the underlying cause and mechanism. In 80% to 90% of patients, pain can be alleviated by the WHO (World Health Organization) guidelines, which have been established as standard treatment for cancer pain. Therefore, all physicians involved in cancer care should become skilled in this analgesic therapy. This article mainly explains the characteristics of cancer pain and the WHO guidelines.

Humans↗
PubMed2006

MR imaging and 1H-MR spectroscopy of a case of van der Knaap disease.

Van der Knaap disease, characterized by megalencephalic leukoencephalopathy and subcortical cysts, is a rare and recently defined condition. We discuss here the MR image (MRI) and MR spectroscopy (MRS) features in a 30-year-old man with S93L homozygous mutation in the MLC1 gene. MRI demonstrated high intensity diffuse white matter with T2-weighted image and subcortical cysts in the parietal and temporal lobes and MRS showed mildly reduced N-acetylaspartate (NAA) in areas of severe T2 elongation with a long TE sequence. A peak of lactate/lipid was indicated at a chemical shift of 1.3 ppm with a short TE sequence. The peak for myo-inositol was normal in areas of severe and mild T2 elongation with short TE MRS. These findings suggest that demyelination progresses slowly in van der Knaap disease and that MRS with long and short TE is useful for the evaluation of neural metabolization associated with van der Knaap disease.

Adult↗
PubMed2005

The rice mutant dwarf bamboo shoot 1: a leaky mutant of the NACK-type kinesin-like gene can initiate organ primordia but not organ development.

That plant dwarfism is caused by hormonal defects related to gibberellin and brassinosteroid has been well documented. Other contributing elements, however, have not been elucidated. Here, we report on one of the most severe dwarf mutants of rice, dwarf bamboo shoot 1 (dbs1). Most mutant plants died within 1 month after sowing, but a few (5.2%) survived and grew. Vacuolation enlarged cells in the leaf primordia and seminal root before abortion, which disrupted the organized cell files in these organs. Relative to the severe defects in shoot and root growth, the overall structure of the dbs1 embryo was almost normal. Similarly, initiation and organogenesis of the leaf primordia at the shoot apical meristem and those of the lateral root primordia at the root elongation zone occurred normally. These observations suggest that DBS1 is involved in the growth and development of organs but not in organ initiation or organogenesis. Positional cloning of DBS1 revealed that it encoded a NACK-type kinesin-like protein (OsNACK), homologous to the essential components of a mitogen-activated protein kinase cascade during plant cytokinesis. A BLAST search indicated that DBS1 was the only gene encoding the OsNACK-type protein in the rice genome, and the dbs1 mutant produced only small amounts of the translatable DBS1 mRNA. Thus, we conclude that the dbs1 mutation causes a severe defect in DBS1 function but does not completely shut it down. We discuss the leaky phenotype of dbs1 under the restricted functioning of OsNACK.

Cell Division↗
PubMed2005

Plasmacytoid DCs help lymph node DCs to induce anti-HSV CTLs.

Antiviral cell-mediated immunity is initiated by the dendritic cell (DC) network in lymph nodes (LNs). Plasmacytoid DCs (pDCs) are known to migrate to inflamed LNs and produce interferon (IFN)-alpha, but their other roles in antiviral T cell immunity are unclear. We report that LN-recruited pDCs are activated to create local immune fields that generate antiviral cytotoxic T lymphocytes (CTLs) in association with LNDCs, in a model of cutaneous herpes simplex virus (HSV) infection. Although pDCs alone failed to induce CTLs, in vivo depletion of pDCs impaired CTL-mediated virus eradication. LNDCs from pDC-depleted mice showed impaired cluster formation with T cells and antigen presentation to prime CTLs. Transferring circulating pDC precursors from wild-type, but not CXCR3-deficient, mice to pDC-depleted mice restored CTL induction by impaired LNDCs. In vitro co-culture experiments revealed that pDCs provided help signals that recovered impaired LNDCs in a CD2- and CD40L-dependent manner. pDC-derived IFN-alpha further stimulated the recovered LNDCs to induce CTLs. Therefore, the help provided by pDCs for LNDCs in primary immune responses seems to be pivotal to optimally inducing anti-HSV CTLs.

Animals↗
PubMed2005

Ptf1a, a bHLH transcriptional gene, defines GABAergic neuronal fates in cerebellum.

The molecular machinery governing glutamatergic-GABAergic neuronal subtype specification is unclear. Here we describe a cerebellar mutant, cerebelless, which lacks the entire cerebellar cortex in adults. The primary defect of the mutant brains was a specific inhibition of GABAergic neuron production from the cerebellar ventricular zone (VZ), resulting in secondary and complete loss of external germinal layer, pontine, and olivary nuclei during development. We identified the responsible gene, Ptf1a, whose expression was lost in the cerebellar VZ but was maintained in the pancreas in cerebelless. Lineage tracing revealed that two types of neural precursors exist in the cerebellar VZ: Ptf1a-expressing and -nonexpressing precursors, which generate GABAergic and glutamatergic neurons, respectively. Introduction of Ptf1a into glutamatergic neuron precursors in the dorsal telencephalon generated GABAergic neurons with representative morphological and migratory features. Our results suggest that Ptf1a is involved in driving neural precursors to differentiate into GABAergic neurons in the cerebellum.

Age Factors↗
PubMed2005

Serial MR imaging and 1H-MR spectroscopy of unidentified bright objects in a case of neurofibromatosis type 1.

Serial study using MR imaging and 1H-MR spectroscopy (1H-MRS) of unidentified bright objects (UBO) in a 9-year-old boy with neurofibromatosis type 1 (NF1) is described. UBO was indicated in the left globus pallidum at 3 years old, then appeared in the right globus pallidum at 5 years old along with left hemiconvulsion. These UBO gradually disappeared over several years. On 1H-MRS, the ratios of N-acetylaspartate (NAA)/creatine and that of choline/creatine were each mildly reduced in the UBO. These ratios improved in parallel with disappearance of the UBO. In addition, elevation of the lactate/lipid peak was shown in UBO during the early stage, however, it disappeared in the latter. The longitudinal follow-up using MR image and 1H-MRS was useful for metabolic evaluation of UBO in patients with NF1.

Brain↗
PubMed2005

Subarachnoid pressure-dependent change in syrinx size in a patient with syringomyelia associated with adhesive arachnoiditis. Case report.

The pathophysiology of syringomyelia is still not well understood. Current prevailing theories involve the assumption that cerebrospinal fluid (CSF) flows into the syrinx from the subarachnoid space through the perivascular space of Virchow-Robin. Reported here is the case of a patient with syringomyelia in which this course is clearly contradicted. This patient with a holocord syrinx associated with adhesive arachnoiditis was treated 3 years previously with insertion of a subarachnoid-peritoneal shunt and had recently experienced worsening myelopathy. On surgical exploration, the shunt system was functioning normally. The medium-pressure shunt valve was replaced with an adjustable valve with a higher closing pressure setting, thus increasing the CSF pressure in the subarachnoid space. Contrary to prevailing theories, this procedure markedly reduced the size of the syrinx. This case provides direct evidence that the syrinx size is inversely related to subarachnoid CSF pressure and supports the hypothesis that the pressure gradient across the spinal cord parenchyma is the force that generates syringes in syringomyelia.

Arachnoiditis↗
PubMed2005

Dural ossification associated with cervical ossification of the posterior longitudinal ligament: frequency of dural ossification and comparison of neuroimaging modalities in ability to identify the disease.

OBJECT: The authors' goal in this study was to understand the frequency and pattern of dural ossification (DO, and to evaluate the effectiveness of neuroimaging modalities used to identify this disease in association with ossification of the posterior longitudinal ligament (OPLL). METHODS: One hundred eleven patients with OPLL underwent anterior procedures. Of these patients, 17 (15.3%) had associated ossification of the dura mater. There were 10 cases of DO in the 94 patients with segmental OPLL and seven in the 17 patients with nonsegmental OPLL (seven continuous and 10 mixed-type OPLL). Retrospective evaluation of DO was performed by examining plain x-ray films, polytomography studies, computerized tomography (CT) scans, and magnetic resonance (MR) images. A positive correlation was found between the type of OPLL and the frequency of DO (p < 0.01). The DO was classified into the following three types according to shape: 1) isolated type, 2) double-layer type, and 3) en bloc type, based on its relationship with OPLL. There were 10 lesions of the double-layer type, four en bloc type, and three isolated type; the double-layer pattern of DO was the most common. All DOs as well as OPLLs (17 cases) were identified using bone-window CT scanning. Polytomography was used successfully to identify all 12 OPLLs, whereas DO was recognized in seven of the 12 cases. Magnetic resonance imaging could not identify DO (none of the 17 cases), although OPLL was identified on MR imaging in 12 of the 17 cases. CONCLUSIONS: Three patterns of DO associated with OPLL, that is, isolated, double-layer, and en bloc types, were confirmed by retrospective analysis of neuroimaging findings. Nonsegmental OPLL was likely to be accompanied by DO. Bone-window CT scanning was most useful for identification of DO as well as OPLL, whereas MR imaging was ineffective in recognizing DO.

Adult↗
PubMed2005

Surgery for dural ossification in association with cervical ossification of the posterior longitudinal ligament via an anterior approach.

STUDY DESIGN: Direct removal of an ossified mass via an anterior approach carries good decompression, to one- or two-level ossification of the posterior longitudinal ligament (OPLL) of the cervical spine. Ossification occasionally involves not only the posterior longitudinal ligament (PLL) but also the underlying dura mater. Defect of the dura mater by resection of the dural ossification (DO) can cause cerebrospinal fluid leakage or neural injury. The technique of resection of OPLL with floating of DO provides satisfactory decompression and avoids dural defect or neural injury in OPLL associated with DO. METHODS: Four patients developed cervical myelopathy. Radiological examination revealed cord compression due to OPLL associated with DO. RESULTS: All patients underwent anterior procedures. After the necessary discectomies and corpectomies, OPLL was resected using a high-speed drill with a 4-mm steel burr and then with a 4-mm diamond burr. When the OPLL became paper-thin, it was separated from the dura mater using a microdissector and a Kerrison rongeur. There was a thin layer of the nonossified degenerated PLL between the residual OPLL and DO. Meticulous dissection of the residual OPLL over the DO was performed without removing the DO at this layer. Fixation was performed with a titanium cylindrical cage. CONCLUSION: This technical note describes the successful decompression of the spinal cord by removing OPLL only, and avoidance of dural defect or neural injury in cases of OPLL associated with DO.

Adult↗
PubMed2004

Mitochondrial acetoacetyl-CoA thiolase (T2) deficiency: T2-deficient patients with "mild" mutation(s) were previously misinterpreted as normal by the coupled assay with tiglyl-CoA.

Mitochondrial acetoacetyl-CoA thiolase (T2) deficiency is an inborn error of metabolism that affects the catabolism of isoleucine and ketone bodies. This disorder is characterized by intermittent ketoacidotic episodes. Recently, we diagnosed T2 deficiency in two patients (GK45 and GK47) by the absence of potassium ion-activated acetoacetyl-CoA thiolase activity, whereas these patients were previously misinterpreted as normal by a coupled assay with tiglyl-CoA as a substrate. This method has been widely used for the enzymatic diagnosis of the T2 deficiency in the United States and Europe. We hypothesized that some residual T2 activity showed normal results in the assay. To prove this hypothesis, we analyzed these two patients together with three typical T2-deficient patients (GK46, GK49, and GK50) at the DNA level. Expression analysis of mutant cDNAs clearly showed that GK45 and GK47 had "mild" mutations (A132G, D339-V340insD) that retained some residual T2 activity, at least one of two mutant alleles, whereas the other three patients had null mutations (c.52-53insC, G152A, H397D, and IVS8+1g>t) in either allele. These results raise the possibility that T2-deficient patients with mild mutations have been misinterpreted as normal by the coupled assay with tiglyl-CoA.

Acetyl-CoA C-Acyltransferase↗
PubMed2004

MR imaging and 1H-MR spectroscopy in a case of cerebral infarction with transient cerebral arteriopathy.

A case of cerebral infarction with transient cerebral arteriopathy in a 12-year-old female is described. The child showed with an acute onset of left hemiplegia, central facial palsy and aphasia. She was diagnosed with right internal carotid artery obstruction with no predisposing factors for cerebral infarction. A serial MR image and MR spectroscopy of the brain was performed. MR angiography revealed reversible vascular changes in the right middle cerebral artery after several months. The ratio of choline/creatine was elevated and that of N-acetylaspartate (NAA)/creatine was depressed in the cerebral lesion, however, they were normalized during the remission phase with long echo time-MR spectroscopy. The elevation of the lactate peak was clarified with short echo time-MR spectroscopy. The longitudinal follow up using MR angiography, and MR spectroscopy with long and short echo time was useful for the evaluation of reversible vascular change with cerebral infarction in children.

Aspartic Acid↗
PubMed2004

Indigenous pulmonary Propionibacterium acnes primes the host in the development of sarcoid-like pulmonary granulomatosis in mice.

Although many cases of sarcoidosis are self-limiting with spontaneous remission, uncontrolled pulmonary granulomatosis with fibrosis produces intolerable long-term respiratory symptoms in a minority of patients. Individuals with chronic pulmonary sarcoidosis require an alternative therapy to corticosteroidal treatment because of its insufficient effectiveness. Although many researchers have considered infection as the triggering factor for this disease, the mechanisms by which the candidate causative organisms induce this disorder remain unclear. We report here that extrapulmonary sensitization to Propionibacterium acnes, which is one of the candidates to date, induced pulmonary Th-1 granulomas mainly in the subpleural and peribronchovascular regions often observed in sarcoidosis. These granulomas appear to be caused by indigenous P. acnes pre-existing in the lower respiratory tract of the normal lung, which is believed to be germ-free, and by an influx of P. acnes-sensitized CD4(+) T cells from the circulation. Importantly, the eradication of indigenous P. acnes with antibiotics alleviated the granulomatous lung disease. This is the first report to present clear evidence of the contribution of an indigenous pulmonary bacterium to the formation of granulomatous lesions in the lung. We propose that treatment targeting indigenous P. acnes in the lung may be a possible remedy for pulmonary sarcoidosis.

Animals↗
PubMed2003

Single base substitutions at the initiator codon in the mitochondrial acetoacetyl-CoA thiolase (ACAT1/T2) gene result in production of varying amounts of wild-type T2 polypeptide.

Initiator codon mutations are relatively uncommon and less well characterized compared to other types of mutations. We identified a novel initiator codon mutation (c.2T>C) heterozygously in a Japanese patient (Patient GK30) with mitochondrial acetoacetyl-CoA thiolase (T2) gene deficiency (ACAT1 deficiency); c.149delC was on the other allele. We examined translation efficiencies of nine mutant T2 cDNAs harboring one-base substitutions at the initiator methionine codon using in vivo transient expression analysis. We found that all the mutants produced wild-type T2 polypeptide, to various degrees (wild type (100%) > c.1A>C (66%) > c.2T>C, c.3G>C, c.3G>T (22%) > c3G>A, c.1A>G (11%) > c.2T>A, c.2T>G, c.1A>T (7.4%)). T2 mRNA expression levels in Patient GK08 (a homozygote of c.2T>A) and Patient GK30 fibroblasts, respectively, were almost the same as in control fibroblasts, when examined using semiquantitative PCR. This means that initiator codon mutations did not affect T2 mRNA levels. We propose that all one-base substitutions at the initiator methionine codon in the T2 gene could be mutations, which retain some residual T2 activity.

Acetyl-CoA C-Acetyltransferase↗
PubMed2003

Roles of STEF/Tiam1, guanine nucleotide exchange factors for Rac1, in regulation of growth cone morphology.

Rho family GTPases are suggested to be pivotal for growth cone behavior, but regulation of their activities in response to environmental cues remains elusive. Here, we describe roles of STEF and Tiam1, guanine nucleotide exchange factors for Rac1, in neurite growth and growth cone remodeling. We reveal that, in primary hippocampal neurons, STEF/Tiam1 are localized within growth cones and essential for formation of growth cone lamellipodia, eventually contributing to neurite growth. Furthermore, experiments using a dominant-negative form demonstrate that STEF/Tiam1 mediate extracellular laminin signals to activate Rac1, promoting neurite growth in N1E-115 neuroblastoma cells. STEF/Tiam1 are revealed to mediate Cdc42 signal to activate Rac1 during lamellipodial formation. We also show that RhoA inhibits the STEF/Tiam1-Rac1 pathway. These data are used to propose a model that extracellular and intracellular information is integrated by STEF/Tiam1 to modulate the balance of Rho GTPase activities in the growth cone and, consequently, to control growth cone behavior.

Animals↗
PubMed2003

Dynamic and coordinated expression profile of dbl-family guanine nucleotide exchange factors in the developing mouse brain.

Dbl-family guanine nucleotide exchange factors (Dbl-GEFs) act as activators of Rho-like small G proteins such as Rac1, Cdc42 and RhoA. Recently, some GEFs have been suggested to play important roles in the development of the nervous system. Here, we report a comprehensive expression profile analysis of 20 Dbl-GEFs that have yet to be well investigated. Northern analyses of murine mRNAs from brains of E13, E17, P7 and adult mice revealed expression of 18 out of 20 GEFs in some or all stages. In addition, we found that three human GEFs were highly expressed in the brain. Examination of the spatial expression patterns of five GEFs in embryos or neonatal brain by in situ hybridization revealed distinct patterns for each GEF. Our study reveals the dynamic and coordinated expression profiles of the Dbl-GEFs and provides a basic framework for understanding the function of GEFs in neural development.

Amino Acid Sequence↗
PubMed2001

Characterization of STEF, a guanine nucleotide exchange factor for Rac1, required for neurite growth.

Accumulating evidence suggests that Rho family GTPases play critical roles in the organization of the nervous system. We previously identified a guanine nucleotide exchange factor of Rac1, STEF (SIF and Tiam 1-like exchange factor), which can induce ruffling membrane in KB cells and is predominantly expressed in the brain during development. Here, we characterize the molecular nature of STEF and its involvement in neurite growth. Deletion analyses revealed distinct roles for individual domains: PHnTSS for membrane association, DH for enzymatic activity, and PHc for promoting catalytic activity. Ectopic expression of STEF in N1E-115 neuroblastoma cells induced neurite-like processes containing F-actin, betaIII tubulin, MAP2, and GAP43 in a Rac1-dependent manner even under the serum-containing neurite-inhibiting conditions. We further found that a PHnTSS STEF fragment specifically inhibited the function of both STEF and Tiam1, a closely related Rac1 guanine nucleotide exchange factor. Suppression of endogenous STEF and Tiam1 activities in N1E-115 cells by ectopically expressed PHnTSS STEF resulted in inhibition of neurite outgrowth in serum-starved conditions, which usually induce neurite formation. Furthermore, these inhibitory effects were rescued by exogenously expressed STEF or Tiam1, suggesting that STEF and Tiam1 are involved in neurite formation through the activation of Rac1 and successive cytoskeletal reorganization of neuronal cells during development.

Blotting, Western↗