Publications by authors named "Kazuki Tsukamoto"

7 Publications

  • Page 1 of 1

Characterization of plant immunity-activating mechanism by a pyrazole derivative.

Biosci Biotechnol Biochem 2020 Jul 11;84(7):1427-1435. Epub 2020 Apr 11.

Department of Bioscience and Biotechnology, Fukui Prefectural University , Fukui, Japan.

A newly identified chemical, 4-{3-[(3,5-dichloro-2-hydroxybenzylidene)amino]propyl}-4,5-dihydro-1-pyrazol-5-one (BAPP) was characterized as a plant immunity activator. BAPP enhanced disease resistance in rice against rice blast disease and expression of a defense-related gene without growth inhibition. Moreover, BAPP was able to enhance disease resistance in dicotyledonous tomato and plants against bacterial pathogen without growth inhibition, suggesting that BAPP could be a candidate as an effective plant activator. Analysis using and  mutants suggested that BAPP induced systemic acquired resistance (SAR) by stimulating between salicylic acid biosynthesis and NPR1, the SA receptor protein, in the SAR signaling pathway.
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http://dx.doi.org/10.1080/09168451.2020.1750341DOI Listing
July 2020

Comprehensive analysis of coding variants highlights genetic complexity in developmental and epileptic encephalopathy.

Nat Commun 2019 06 7;10(1):2506. Epub 2019 Jun 7.

Department of Human Genetics, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004, Japan.

Although there are many known Mendelian genes linked to epileptic or developmental and epileptic encephalopathy (EE/DEE), its genetic architecture is not fully explained. Here, we address this incompleteness by analyzing exomes of 743 EE/DEE cases and 2366 controls. We observe that damaging ultra-rare variants (dURVs) unique to an individual are significantly overrepresented in EE/DEE, both in known EE/DEE genes and the other non-EE/DEE genes. Importantly, enrichment of dURVs in non-EE/DEE genes is significant, even in the subset of cases with diagnostic dURVs (P = 0.000215), suggesting oligogenic contribution of non-EE/DEE gene dURVs. Gene-based analysis identifies exome-wide significant (P = 2.04 × 10) enrichment of damaging de novo mutations in NF1, a gene primarily linked to neurofibromatosis, in infantile spasm. Together with accumulating evidence for roles of oligogenic or modifier variants in severe neurodevelopmental disorders, our results highlight genetic complexity in EE/DEE, and indicate that EE/DEE is not an aggregate of simple Mendelian disorders.
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http://dx.doi.org/10.1038/s41467-019-10482-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6555845PMC
June 2019

Antibodies against peptides of NMDA-type GluR in cerebrospinal fluid of patients with epileptic spasms.

Eur J Paediatr Neurol 2016 Nov 13;20(6):865-873. Epub 2016 Jul 13.

National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, NHO, 886 Urushiyama, Aoi-ku, Shizuoka 420-8688, Japan.

Objective: We investigated the contribution of antibodies against N-methyl-d-aspartate (NMDA)-type glutamate receptor (GluR) in cerebrospinal fluid (CSF) to the clinical features of patients with epileptic spasms (ES).

Methods: CSF samples were collected from 33 patients with ES with median (range) age 1.8 (0.2-8.5) years. Thirty patients without ES with 3.5 (0.5-7.0) years were also studied as disease controls. The CSF levels of antibodies against peptides of NMDA-type GluR subunits (GluN2B & GluN1) were measured by enzyme-linked immunosorbent assay.

Results: The levels of antibodies against the n-terminal of GluN2B (GluN2B-NT2), c-terminal of GluN2B (GluN2B-CT) and n-terminal of GluN1 (GluN1-NT), were significantly higher in patients with ES than in disease controls (p < 0.01, p < 0.01 & p = 0.03). Levels of antibodies to GluN2B-NT2 & CT were not related with ACTH therapy nor conventional CSF factors (cell counts, protein level, etc). Levels of antibodies to GluN2B-NT2 & CT showed evidence of correlation within a linear regression model with intervals from the onset to the examination of CSF until 25 months (p = 0.01 & p = 0.01). The correlation was significant in patients with unknown cause (p = 0.01). Five of 33 patients (four unknown cause & one chromosomal anomaly) had higher level of antibodies to GluN2B-NT2 exceeding mean + 1 SD of all ES patients, and they had poor motor (score 0) and cognitive outcomes (score 0 or 1).

Conclusion: The CSF level of antibodies against GluN2B in ES patients with unknown cause was estimated to increase after onset. We hypothesize that some ES patients may have immune process after the onset of ES.
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http://dx.doi.org/10.1016/j.ejpn.2016.07.006DOI Listing
November 2016

Acute Myositis Associated with Concurrent Infection of Rotavirus and Norovirus in a 2-Year-Old Girl.

Pediatr Rep 2015 Sep 28;7(3):5873. Epub 2015 Sep 28.

Department of Pediatrics, Shimane University School of Medicine , Japan.

Rotavirus and norovirus are common pathogens associated with gastroenteritis in children. Although rotavirus occasionally induces central nervous system disease, only 3 cases with rotavirus-induced acute myositis have been reported in the English literature. We recently treated a female patient with acute myositis associated with gastroenteritis induced by concurrent infection with rotavirus and norovirus. Having suffered from gastroenteritis for 3 days, she suddenly developed myositis affecting her lower extremities with concomitant creatine kinase elevation. Herein, we present our patient and review the previous cases including those reported in the Japanese literature.
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http://dx.doi.org/10.4081/pr.2015.5873DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4594443PMC
September 2015

[Adverse effects of antiepileptic drugs].

Nihon Rinsho 2014 May;72(5):908-19

Adverse effects of antiepileptic drugs are classified into idiosyncratic adverse effects, pharmacology-related adverse effects and biological effect after modification of seizure frequencies. Pharmacology-related adverse effects include those by administered AED and those by mutual interactions. Stevens-Johnson syndrome, one of the idiosyncratic adverse effects, may be predicted by the intrinsic HLA type (e.g., A*31:01 for CBZ). In epileptic patients after acute encephalitis, cutaneous adverse reactions usually occur in a month after encephalitis, but some patients will tolerate the causative AED by the extremely slow re-introduction. Prevention of pharmacology-related adverse effects needs therapeutic drug monitoring, and slow introduction considering dose-response curves for AEDs. Genotype examination of CYP2C9 and 2C19 can contribute to the safe introduction of PHT.
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May 2014

Novel vitamin D3 analogs, 1alpha, 25(OH)2D(3)-26, 23-lactam (DLAMs), antagonize bone resorption via suppressing RANKL expression in osteoblasts.

Biochem Biophys Res Commun 2008 Aug 19;372(3):434-9. Epub 2008 May 19.

Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakamachi, Koganei, Tokyo 184-8588, Japan.

Novel vitamin D analogs, 1alpha, 25-dihydroxyvitamin D(3)-26, 23-lactam (DLAMs) with a lactam moiety in the side chain, were synthesized and examined for their function in bone. In computer docking simulation, DLAM-1P binds to vitamin D receptor (VDR), and its lactam moiety may interfere with VDR helix-12 folding. In co-cultures of mouse bone marrow cells and osteoblasts, (23S,25S)-DLAM-1P dose-dependently suppressed osteoclast differentiation induced by 1alpha, 25-dihydroxyvitamin D(3) [1alpha, 25(OH)(2)D(3)]. Its stereoisomer (23R,25R)-DLAM-1P did not affect the osteoclast differentiation. In osteoblasts, (23S,25S)-DLAM-1P suppressed 1alpha, 25(OH)(2)D(3)-induced mRNA expression of the receptor activator of NF-kappaB ligand (RANKL). In an organ culture using mouse calvaria, bone-resorbing activity induced by 1alpha, 25(OH)(2)D(3) was clearly suppressed by (23S,25S)-DLAM-1P. The other analog, (23S,25S)-DLAM-2P, showed a similar activity to (23S,25S)-DLAM-1P. Therefore, DLAMs act on osteoblasts as an antagonist of 1alpha, 25(OH)(2)D(3) to suppress RANKL-dependent osteoclast formation, suggesting them as a novel candidate for the treatment of pathological bone loss.
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http://dx.doi.org/10.1016/j.bbrc.2008.05.041DOI Listing
August 2008