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Search Results: 1 - 10 of 2298 matches for " Makoto Tominaga "
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Brain Activity Stimulated by Prism Adaptation Tasks Utilized for the Treatment of Unilateral Spatial Neglect: A Study with fNIRS
Hiroshi Taniguchi,Makoto Hiyamizu,Takanori Tominaga,Shu Morioka
Rehabilitation Research and Practice , 2012, DOI: 10.1155/2012/312781
Abstract: We investigated the neurological basis for efficacy of prism adaptation therapy, which is used for the treatment of poststroke unilateral spatial neglect (USN). Study subjects were 6 USN-positive (+), 6 USN-negative patients, and 6 healthy volunteer control subjects. USN was identified by the Behavioural Inattention Test (BIT). During the tasks, brain activity was assessed with fNIRS via changes in oxyHb concentration per unit length. There was no significant difference in the number of errors in the task between the 3 groups. However, in the USN(+) group there was a significantly greater reduction in oxyHb levels in the right parietal association cortex during the prism adaptation task than in the other 2 groups ( ). There was an immediate improvement in USN symptoms as well as a significant increase in oxyHb levels during the prism adaptation in the channels covering the right frontal and parietal lobes in 2 patients in the USN(+) group ( ). This result suggested that decreased activity in the right parietal association cortex, which is related to spatial perception, during the prism adaptation task and task-induced reorganization of the right frontal and parietal areas were involved in improvement in USN symptoms. 1. Introduction Recently, it was shown that prism adaptation therapy not only instantly improved unilateral spatial neglect (USN) symptoms but also enhanced balancing ability in patients with USN after stroke [1, 2]. Also reported has been the use of prism adaptation therapy for the treatment of USN to achieve improvement in USN symptoms as well as in movements [1–3]. This therapy is aimed at inducing the USN patient to pay attention to the neglect space by reaching out with an upper limb toward an object using deviated visual information caused by a prism [1]. The prism deviates the visual information so soon after the start of the task that the patient cannot precisely reach an object. However, repeated attempts enable the patient to successfully reach the object through adaptive learning [4]. When the patient attempts such reaching movements under normal visual conditions without prism-mounted eyeglasses after prism adaptation therapy, the patient’s motion deviates to the opposite side of the object as an aftereffect. Hence, the prism adaptation task has a physical exercise component as well as an adaptive process of feedback control of deviated movements so that the brain is forced to correct or reorganize spatial perception. Neural mechanisms of action for these prism adaptation effects have been reported exclusively in healthy
Evolution of Vertebrate Transient Receptor Potential Vanilloid 3 Channels: Opposite Temperature Sensitivity between Mammals and Western Clawed Frogs
Shigeru Saito ,Naomi Fukuta,Ryuzo Shingai,Makoto Tominaga
PLOS Genetics , 2011, DOI: 10.1371/journal.pgen.1002041
Abstract: Transient Receptor Potential (TRP) channels serve as temperature receptors in a wide variety of animals and must have played crucial roles in thermal adaptation. The TRP vanilloid (TRPV) subfamily contains several temperature receptors with different temperature sensitivities. The TRPV3 channel is known to be highly expressed in skin, where it is activated by warm temperatures and serves as a sensor to detect ambient temperatures near the body temperature of homeothermic animals such as mammals. Here we performed comprehensive comparative analyses of the TRPV subfamily in order to understand the evolutionary process; we identified novel TRPV genes and also characterized the evolutionary flexibility of TRPV3 during vertebrate evolution. We cloned the TRPV3 channel from the western clawed frog Xenopus tropicalis to understand the functional evolution of the TRPV3 channel. The amino acid sequences of the N- and C-terminal regions of the TRPV3 channel were highly diversified from those of other terrestrial vertebrate TRPV3 channels, although central portions were well conserved. In a heterologous expression system, several mammalian TRPV3 agonists did not activate the TRPV3 channel of the western clawed frog. Moreover, the frog TRPV3 channel did not respond to heat stimuli, instead it was activated by cold temperatures. Temperature thresholds for activation were about 16 °C, slightly below the lower temperature limit for the western clawed frog. Given that the TRPV3 channel is expressed in skin, its likely role is to detect noxious cold temperatures. Thus, the western clawed frog and mammals acquired opposite temperature sensitivity of the TRPV3 channel in order to detect environmental temperatures suitable for their respective species, indicating that temperature receptors can dynamically change properties to adapt to different thermal environments during evolution.
Evolutionary conservation and changes in insect TRP channels
Hironori Matsuura, Takaaki Sokabe, Keigo Kohno, Makoto Tominaga, Tatsuhiko Kadowaki
BMC Evolutionary Biology , 2009, DOI: 10.1186/1471-2148-9-228
Abstract: All the insects examined have 2 TRPV, 1 TRPN, 1 TRPM, 3 TRPC, and 1 TRPML subfamily members, demonstrating that these channels have the ancient origins in insects. The common pattern also suggests that the mechanisms for detecting mechanical and visual stimuli and maintaining lysosomal functions may be evolutionarily well conserved in insects. However, a TRPP channel, the most ancient TRP channel, is missing in B. mori, A. mellifera, and N. vitripennis. Although P. humanus and D. melanogaster contain 4 TRPA subfamily members, the other insects have 5 TRPA subfamily members. T. castaneum, A. mellifera, and N. vitripennis contain TRPA5 channels, which have been specifically retained or gained in Coleoptera and Hymenoptera. Furthermore, TRPA1, which functions for thermotaxis in Drosophila, is missing in A. mellifera and N. vitripennis; however, they have other Hymenoptera-specific TRPA channels (AmHsTRPA and NvHsTRPA). NvHsTRPA expressed in HEK293 cells is activated by temperature increase, demonstrating that HsTRPAs function as novel thermal sensors in Hymenoptera.The total number of insect TRP family members is 13-14, approximately half that of mammalian TRP family members. As shown for mammalian TRP channels, this may suggest that single TRP channels are responsible for integrating diverse sensory inputs to maintain the insect sensory systems. The above results demonstrate that there are both evolutionary conservation and changes in insect TRP channels. In particular, the evolutionary processes have been accelerated in the TRPA subfamily, indicating divergence in the mechanisms that insects use to detect environmental temperatures.Transient receptor potential (TRP) superfamily members of cation channels share six common transmembrane domains and permeability to cations. Despite these similarities, TRP channels are highly unusual among the known families of ion channels in displaying an impressive diversity of cation selectivities and specific activation mechanisms.
Sensitization of TRPV1 by EP1 and IP reveals peripheral nociceptive mechanism of prostaglandins
Tomoko Moriyama, Tomohiro Higashi, Kazuya Togashi, Tohko Iida, Eri Segi, Yukihiko Sugimoto, Tomoko Tominaga, Shuh Narumiya, Makoto Tominaga
Molecular Pain , 2005, DOI: 10.1186/1744-8069-1-3
Abstract: Tissue damage and inflammation produce an array of chemical mediators such as ATP, bradykinin, prostanoids, protons, cytokines and peptides including substance P that can excite or sensitize nociceptors to elicit pain at the site of injury. Among them prostanoids were shown to influence inflammation, and their administration was found to reproduce the major signs of inflammation including augmented pain [1]. Prostaglandin E2 (PGE2) and prostaglandin I2 (PGI2) are the products of arachidonic acid metabolism through the cyclooxygenase pathway. In addition to numerous other physiological actions in vivo, previous studies have indicated important roles for PGE2 in nociception and inflammation [2,3]. PGE2 is generated in most cells in response to mechanical, thermal or chemical injury and inflammatory insult, resulting in sensitization or direct activation of nearby sensory nerve endings. Analgesic effects of non-steroidal anti-inflammatory drugs (NSAIDs) are attributed predominantly to inhibition of prostaglandin synthesis. Prostaglandins act upon a family of pharmacologically distinct prostanoid receptors including EP1, EP2, EP3, EP4 and IP that activate several different G protein-coupled signaling pathways [2,4,5]. Primary sensory neurons in dorsal root ganglion (DRG) are known to express mRNAs encoding several prostanoid receptor subtypes, IP, EP1, EP3 and EP4 [6,7]. The role of IP in inflammation has been clearly shown by the analysis of IP-deficient mice, although the underlying cellular mechanisms still remain to be elucidated [8]. In contrast, the potential involvement of EP receptors other than IP in inflammation and pain generation has not been well studied, although some earlier studies have suggested that prostanoids contribute to the development of pain through EP receptors [9,10].The capsaicin receptor TRPV1 is a non-selective cation channel expressed predominantly in unmyelinated C-fibers [11]. TRPV1 is activated not only by capsaicin, but also by protons
DIP/WISH deficiency enhances synaptic function and performance in the Barnes maze
Suhail Asrar, Keiko Kaneko, Keizo Takao, Jaina Negandhi, Makoto Matsui, Koji Shibasaki, Tsuyoshi Miyakawa, Robert V Harrison, Zhengping Jia, Michael W Salter, Makoto Tominaga, Tomoko Fukumi-Tominaga
Molecular Brain , 2011, DOI: 10.1186/1756-6606-4-39
Abstract: We found that DIP/WISH-deficient hippocampal CA1 neurons exhibit enhanced long-term potentiation via modulation of both pre- and post-synaptic events. Consistent with these electrophysiological findings, DIP/WISH-deficient mice, particularly at a relatively young age, found the escape hole more rapidly in the Barnes maze test.We conclude that DIP/WISH deletion improves performance in the Barnes maze test in mice probably through increased hippocampal long-term potentiation.DIP (diaphanous interacting protein), also known as WISH (WASP interacting SH3 protein) is a protein involved in cytoskeletal signaling, which regulates actin cytoskeleton and/or microtubule dynamics mainly through negative regulation of Rho [1]. More specifically, we previously reported that DIP/WISH functions as a negative regulator of Rho and a positive regulator of Rho GEF (guanine nucleotide exchange factor) [2]. We also recently showed that mouse embryonic fibroblast (MEF) cells from DIP/WISH-deficient (DIP/WISH-KO) mice have a narrow and long shape with many stress fibers under normal growth conditions [1]. In addition, the DIP/WISH-KO cells exhibited an activation of the Rho-ROCK pathway (particularly with regard to high ROCK activity), a decrease in de novo actin polymerization (especially polymerization requiring arp2/3 activity), and a decrease in cell motility and adhesion as evidenced by an in vitro analysis [1].Spine-head volumes are known to change dynamically and reflect synapse strength. Moreover, spine-head volume changes accompany long-term functional plasticity of glutamatergic synaptic transmission, including long-term potentiation (LTP) and long-term depression (LTD) [3,4]. Actin reorganization represents a primary mechanism necessary to alter spine structures, and actin fibers are most concentrated in dendritic spines. Thus, actin is a critical regulator of spine and dendritic plasticity not only from a biochemical perspective but also from a physical point of view, both of
TRPV1 and TRPV4 Play Pivotal Roles in Delayed Onset Muscle Soreness
Hiroki Ota, Kimiaki Katanosaka, Shiori Murase, Makiko Kashio, Makoto Tominaga, Kazue Mizumura
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0065751
Abstract: Unaccustomed strenuous exercise that includes lengthening contraction (LC) often causes tenderness and movement related pain after some delay (delayed-onset muscle soreness, DOMS). We previously demonstrated that nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF) are up-regulated in exercised muscle through up-regulation of cyclooxygenase (COX)-2, and they sensitized nociceptors resulting in mechanical hyperalgesia. There is also a study showing that transient receptor potential (TRP) ion channels are involved in DOMS. Here we examined whether and how TRPV1 and/or TRPV4 are involved in DOMS. We firstly evaluated a method to measure the mechanical withdrawal threshold of the deep tissues in wild-type (WT) mice with a modified Randall-Selitto apparatus. WT, TRPV1?/? and TRPV4?/? mice were then subjected to LC. Another group of mice received injection of murine NGF-2.5S or GDNF to the lateral gastrocnemius (LGC) muscle. Before and after these treatments the mechanical withdrawal threshold of LGC was evaluated. The change in expression of NGF, GDNF and COX-2 mRNA in the muscle was examined using real-time RT-PCR. In WT mice, mechanical hyperalgesia was observed 6–24 h after LC and 1–24 h after NGF and GDNF injection. LC induced mechanical hyperalgesia neither in TRPV1?/? nor in TRPV4?/? mice. NGF injection induced mechanical hyperalgesia in WT and TRPV4?/? mice but not in TRPV1?/? mice. GDNF injection induced mechanical hyperalgesia in WT but neither in TRPV1?/? nor in TRPV4?/? mice. Expression of NGF and COX-2 mRNA was significantly increased 3 h after LC in all genotypes. However, GDNF mRNA did not increase in TRPV4?/? mice. These results suggest that TRPV1 contributes to DOMS downstream (possibly at nociceptors) of NGF and GDNF, while TRPV4 is located downstream of GDNF and possibly also in the process of GDNF up-regulation.
TRPM8 mechanism of autonomic nerve response to cold in respiratory airway
Hong Xing, Jennifer X Ling, Meng Chen, Richard D Johnson, Makoto Tominaga, Cong-Yi Wang, Jianguo Gu
Molecular Pain , 2008, DOI: 10.1186/1744-8069-4-22
Abstract: Normally, a breath of cold air is warmed up to near body temperature through heat exchange in the upper airway, mainly the nose, before the air enters the bronchopulmonary system. Temperature exchange, however, is compromised under conditions including flu, allergy, and other respiratory diseases. Exercise in cold weather can also result in the rapid inhalation of cold air into the trachea and bronchi, and the air temperature there can drop as low as about 20°C due to an insufficient temperature exchange [1,2]. Respiratory responses to cold air are reflexive, including cough, airway constriction and mucosal secretion. These responses may have some protective roles for bronchopulmonary tissues when exposed to potentially hazardous cold environment. However, the responses can be harmful in people having certain respiratory diseases. For example, cold is a major environmental factor that exacerbates existing asthma conditions and directly triggers asthma [3]. Inhalation of cold air is a direct cause of airway constriction to trigger exercise asthma in athletes performing winter sports [4,5]. Clinically, the "cold air challenge test", a test of bronchopulmonary reactivity and airway resistance, has been used for asthma diagnosis for over 20 years [6,7] because many asthma patients show bronchopulmonary hyper-reactivity and increased airway resistance to cold air challenge.Respiratory responses to cold may be through a neural reflex mechanism [8,9]. The main afferent nerves that innervate the bronchopulmonary system are derived from the vagus nerve. Factors that stimulate these nerves trigger an autonomic reflex to cause airway constriction and mucosal secretion [10,11]. If respiratory responses to cold are indeed mediated by bronchopulmonary vagal afferents, what is the molecular mechanism by which cold initiates the autonomic responses?Recently, studies have identified a molecular mechanism for sensing cold by the somatic sensory nerve endings of the skin [12-19]. It h
Periodicity Detection Method for Small-Sample Time Series Datasets
Daisuke Tominaga
Bioinformatics and Biology Insights , 2012, DOI: 10.4137/BBI.S5983
Abstract: Time series of gene expression often exhibit periodic behavior under the influence of multiple signal pathways, and are represented by a model that incorporates multiple harmonics and noise. Most of these data, which are observed using DNA microarrays, consist of few sampling points in time, but most periodicity detection methods require a relatively large number of sampling points. We have previously developed a detection algorithm based on the discrete Fourier transform and Akaike’s information criterion. Here we demonstrate the performance of the algorithm for small-sample time series data through a comparison with conventional and newly proposed periodicity detection methods based on a statistical analysis of the power of harmonics. We show that this method has higher sensitivity for data consisting of multiple harmonics, and is more robust against noise than other methods. Although “combinatorial explosion” occurs for large datasets, the computational time is not a problem for small-sample datasets. The MATLAB/GNU Octave script of the algorithm is available on the author’s web site: http://www.cbrc.jp/%7Etominaga/piccolo/.
Rings decomposed into direct sums of J-rings and nil rings
Hisao Tominaga
International Journal of Mathematics and Mathematical Sciences , 1985, DOI: 10.1155/s0161171285000230
Abstract: Let R be a ring (not necessarily with identity) and let E denote the set of idempotents of R. We prove that R is a direct sum of a J-ring (every element is a power of itself) and a nil ring if and only if R is strongly €-regular and E is contained in some J-ideal of R. As a direct consequence of this result, the main theorem of [1] follows.
Periodicity Detection Method for Small-Sample Time Series Datasets
Daisuke Tominaga
Bioinformatics and Biology Insights , 2010,
Abstract:
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