Biomedical subjects

Takashi Kurihara

Publications and source records attributed to Takashi Kurihara.

13 recordsLinked to original sources

PubMed2005

Asynchronous, all-optical signal processing based on the self-frequency shift of a gigahertz Raman soliton.

Ultrafast asynchronous all-optical signal processing is experimentally demonstrated. It is based on the intensity-dependent, self-frequency shift of a gigahertz Raman soliton. We demonstrate error-free, asynchronous, all-optical, bit-by-bit, self-signal recognition and demultiplexing from contended optical packets without use of an optical buffer, control pulse, or bit-phase synchronization. Fourfold, contended, 9.95-Gbit/s optical packets are transmitted through a conventional repeater span of 80 km and simultaneously demultiplexed to multiwavelength 9.95-Gbit/s optical packets with 0.5-dB processing sensitivity. Furthermore, we successfully accomplish demultiplexing from overlapping signals in contended optical packets with better than 3-dB recognition sensitivity. We confirm the capability of realizing a 3x cascade operation from bit-error-rate measurements.

Journal Article↗

PubMed2005

Generation of a superstable Lorentzian pulse train with a high repetition frequency based on a Fabry-Perot resonator integrated with an electro-optic phase modulator.

A simple technique for converting a continuous-wave laser beam into a stable Lorentzian pulse train with a high repetition frequency is demonstrated experimentally. We generated transform-limited pulses of up to 40 GHz, which were composed of higher-order sidebands produced by a Fabry-Perot resonator integrated with an electro-optic phase modulator (EOM). The rf power supplied to the EOM determines the pulse width in the pulse train. This approach enables the pulse width to be continuously tuned from 2.1 to 7.0 ps at the same repetition frequency without any wavelength shift. Furthermore, we experimentally evaluated the stability of the pulse train's amplitude and obtained stable bit-error-free operation at 9.95 GHz.

Journal Article↗

PubMed2004

Programmable select multiwavelength gigahertz Raman soliton pulse generation.

The generation of programmable multiwavelength pulses based on the self-frequency shift of a Raman soliton is demonstrated. The approach produces tunable multiwavelength picosecond pulses. Only select multiwavelength signals with a tuning range of approximately 50 nm are generated with a repetition rate of 9.95 GHz at each wavelength channel. A bit error rate (BER) of better than 1 x 10(-9) was successfully obtained for all the measured multiwavelength Raman soliton pulses. Furthermore, it was found that the signal has an excellent relative intensity noise (RIN) of better than -135.5 dBc/Hz. The BER and RIN measurements show that the frequency-shifted Raman soliton pulses are promising for use in measurement systems, optical gating, signal processing, and wavelength routing optical packet networks with the ability to provide 1:1 communication and 1:N multicasting.

Journal Article↗

PubMed2004

Blocking the R-type (Cav2.3) Ca2+ channel enhanced morphine analgesia and reduced morphine tolerance.

Morphine is the drug of choice to treat intractable pain, although prolonged administration often causes undesirable side-effects including analgesic tolerance. It is speculated that voltage-dependent Ca(2+) channels (VDCCs) play a key role in morphine analgesia and tolerance. To examine the subtype specificity of VDCCs in these processes, we analysed mice lacking N-type (Ca(v)2.2) or R-type (Ca(v)2.3) VDCCs. Systemic morphine administration or exposure to warm water swim-stress, known to induce endogenous opioid release, resulted in greater analgesia in Ca(v)2.3(-/-) mice than in controls. Moreover, Ca(v)2.3(-/-) mice showed resistance to morphine tolerance. In contrast, Ca(v)2.2(-/-) mice showed similar levels of analgesia and tolerance to control mice. Intracerebroventricular (i.c.v.) but not intrathecal (i.t.) administration of morphine reproduced the result of systemic morphine in Ca(v)2.3(-/-) mice. Furthermore, i.c.v. administration of an R-type channel blocker potentiated morphine analgesia in wild-type mice. Thus, the inhibition of R-type Ca(2+) current could lead to high-efficiency opioid therapy without tolerance.

Analgesics, Opioid↗

PubMed2004

Excessive alcohol intake increases the risk of arterial stiffening in men with normal blood pressure.

Excessive alcohol intake is a known atherosclerotic cardiovascular risk factor. However, the relation between excessive alcohol intake and atherosclerotic cardiovascular risk in subjects with normal blood pressure has not been fully elucidated. This cross-sectional study investigated the relationship between alcohol intake and arterial stiffness, as assessed using brachial-ankle pulse wave velocity, in men with normal blood pressure. Middle-aged male workers who were found to have a normal blood pressure during an annual health check-up performed in May-July 2000 (n=1,682) were enrolled in the study. The subjects' laboratory data were analyzed, and information on drinking and smoking habits was obtained by a self-administered questionnaire. The brachial-ankle pulse wave velocity was measured using volume plethysmography. The mean brachial-ankle pulse wave velocities of men with an alcohol intake of 40-59 g/day and > or =60 g/day were larger than those of non-drinkers and men with an alcohol intake of <20 g/day. A multivariate general linear model was used to identify the association between alcohol intake and brachial-ankle pulse wave velocity after controlling for other risk factors using a multivariate analysis. An alcohol intake of more than 60 g of ethanol/day was significantly associated with an elevated brachial-ankle pulse wave velocity, after controlling for conventional atherosclerotic cardiovascular risk factors. In conclusion, the present results suggest that excessive alcohol intake increases the atherosclerotic cardiovascular risk associated with arterial stiffening in men with normal blood pressure.

Adult↗

PubMed2003

Orthogonal aperture multiplexing for multilayered waveguide holographic read-only memories.

A multilayered waveguide holographic read-only memory is a promising candidate for the next generation of optical data storage systems. We improved the data density of the memory by using a multiplexing method with a set of orthogonal optical masks. We multiplexed as many as nine images into one waveguide hologram, and all the observed images had negligible cross talk. This made it possible to achieve a ninefold increase in data density. We provide experimental results for both metallic and liquid-crystal masks.

Journal Article↗

PubMed2003

Acetic acid conditioning stimulus induces long-lasting antinociception of somatic inflammatory pain.

A wide variety of noxious stimuli are known to induce a powerful inhibition of pain sensation evoked at a remote region of the body. Here we show that an intraperitoneal acetic acid (AA) conditioning stimulus produces long-lasting inhibition of formalin-evoked somatic inflammatory pain behavior in mice. This novel long-lasting antinociception was completely blocked by the 5-hydroxytryptamine type 2A/2C (5-HT(2A/2C)) receptor antagonists, ketanserin and ritanserin, but not by the opioid receptor antagonist, naloxone, and alpha-adrenergic receptor antagonists, phentolamine and yohimbine. In contrast, the 5-HT(3/4) receptor antagonist, tropisetron, significantly potentiated this long-lasting antinociception. The conditioning stimulus significantly upregulated the levels of both tryptophan hydroxylase immunoreactivity in the medulla oblongata and the 5-HT(2A/2C) receptor mRNA level in the spinal cord. These results suggested that the visceral noxious stimulus caused a long-lasting augmentation of the serotonergic inhibitory system and downregulated the somatic inflammatory nociceptive transmission.

Acetic Acid↗

PubMed2003

Sensitivity to human serum of gammaretroviruses produced from pig endothelial cells transduced with glycosyltransferase genes.

Reduction of pig cell-surface alpha-galactosyl (Gal) epitope, Galalpha1, 3Galbeta1, 4GlcNAc-R, by the introduction of glycosyltransferase genes is effective in suppressing hyperacute rejection (HAR) in pig-to-human xenotransplantation. The transmission of porcine endogenous retroviruses (PERVs) has been recognized as a potential risk factor associated with xenotransplantation. In this study, effects of the introduction of glycosyltransferase genes to pig cells on the sensitivity of gammaretroviruses to human serum were investigated. Pig endothelial cells (PEC), PEC transduced with alpha1,2 fucosyltransferase (FT), alpha2,3 sialyltransferase (ST), or N-acetylglucosaminyltransferase III (GnT-III), and human embryonic kidney (HEK) 293 cells were transduced with the LacZ gene with the packaging signal of murine leukemia virus (MuLV) under the control of the long terminal repeat of MuLV by a pseudotype infection. Then, the cells were further infected with PERV subtype B (PERV-B) or feline leukemia virus subgroup B (FeLV-B). Culture supernatants of the infected cells were mixed with human serum (HS) and then inoculated to HEK293 cells. The inoculated cells were histochemically stained and lacZ-positive blue foci were counted. Glycosyltransferase activity, xenoantigenicity, and alpha-Gal epitope density in the cells were measured at the time of the infection experiments. PERV-B or FeLV-B particles from the parental PEC were efficiently neutralized by HS, while those from PEC transduced with alpha1,2FT, alpha2,3ST or GnT-III were less sensitive to HS. The transduced PEC exhibited high levels of activity of the introduced glycotransferases, and expressed fewer xenoantigens and cell-surface alpha-Gal epitopes. Our results suggest that gammaretroviruses including PERVs produced by transgenic pigs, that are generally modified to reduce the cell-surface alpha-Gal epitope to overcome the HAR in xenotransplantation, are less sensitive to HS.

Animals↗

PubMed2003

Effect of various forms of the C1 esterase inhibitor (C1-INH) and DAF on complement mediated xenogeneic cell lysis.

The purpose of the present study was to assess the effect of various forms of the surface-bound form of the C1 esterase inhibitor (C1-INH-PI) and decay accelerating factor (DAF) on xenogenic cells. cDNAs of various deletion mutants of the C1-INH-PI, such as delta-1-99 amino acid (AA), delta-108-183AA loop, delta-whole loop, delta-exon5, delta-exon6 + 7, and delta-exon5 + 6 + 7, and that of DAF, the delta-short consensus repeat (SCR) 1-DAF were established. While all deletion mutants of C1-INH-PI except the delta-1-99AA were expressed in the cytoplasm but not on the cell surface, the delta-1-99AA was clearly expressed on the xenogeneic cell surface. Amelioration of complement-mediated xenogeneic cell lysis by delta-1-99AA was next tested, and compared with delta-SCR1 DAF. Both molecules blocked human complement-mediated cell lysis by approximately 57 to 90 and 93 to 98%, respectively, in Chinese hamster ovarian tumor (CHO) cells and pig endothelial cells (PECs). The CHO cell transfectants were incubated with 20% normal human serum, and the amounts of C4 and C3 deposition on the cell surface were analysed by flow cytometry. The DAF transfectant showed a large amount of C4-deposition and much less C3-deposition than the controls (approximately 85% suppression), whereas the delta-1-99AA showed approximately a 40% suppression in both C4- and C3-deposition. Consequently, both the delta-1-99AA C1-INH-PI and delta-SCR1 DAF molecules are quite effective in down-regulating the xenogeneic cell lysis, but accomplished this in different manners.

Animals↗

PubMed2003

Plastic change of N-type Ca channel expression after preconditioning is responsible for prostaglandin E2-induced long-lasting allodynia.

BACKGROUND: Although considerable evidence indicates neuronal Ca channels play significant roles in pain perception, their possible importance in hypersensitization after acute inflammation has not been investigated. METHODS: Using carrageenan for inducing hypersensitization, the authors investigated the analgesic effects of intrathecally administered N- and P/Q-type channel blockers, omega-conotoxin GVIA and omega-agatoxin IVA, respectively, and also examined the level of N-type channel expression. RESULTS: Acute inflammation, produced by carrageenan injection in a rat hind paw, caused mechanical hypersensitivity that resolved within several days. Injection of prostaglandin E2 into the same hind paw after resolution caused a markedly prolonged mechanical allodynia lasting more than 4 h. Similar but less potent prolonged allodynia was also induced in the contralateral hind paws. Intrathecal administration of omega-conotoxin GVIA (0.03-0.3 microg) produced dose-dependent inhibition of the allodynia in both control and carrageenan-preconditioned rats. However, the potency of omega-conotoxin GVIA was significantly lower in carrageenan-preconditioned paws than in those in the contralateral and saline-preconditioned paws. In contrast, omega-agatoxin IVA (0.01-0.1 microg) did not reduce the allodynia. Significant up-regulation of N-type channel expression was observed in both dorsal root ganglia and the spinal cord ipsilateral to the carrageenan-preconditioned hind paw. CONCLUSIONS: The results suggest an aggravating role of the N-type channel in pain sensation and a selective plastic change of this channel expression that could underlie the mechanism of hypersensitization after acute inflammation.

Animals↗

PubMed2003

N-type Ca2+ channel.

Ca(2+) entry through voltage-dependent Ca(2+) channels (VDCCs) regulates various aspects of physiological function, including neurotransmitter release, regulation of cell membrane excitability, and control of gene expression. VDCCs are classified into several sub-types (L-, N-, P/Q-, R-, and T-types) based on electrophysiological and pharmacological properties. Each type of channels except the T-type is composed of at least four subunits, designated alpha(1), alpha(2), beta, and delta. During the past decade, a number of genes encoding these subunits have been cloned, and cDNA expression studies using heterologous expression systems have revealed the intricate nature of subunit interaction and many biophysical aspects of channel function. In recent years, an entirely new strategy has been introduced in attempts to clarify the physiological role of each of the VDCCs, and this has proven to be very useful in defining previously unknown in vivo functions of VDCCs. In this article, we briefly review the recent advances in our understanding of VDCCs with special emphasis on the N-type channel, which is mainly expressed in neural tissues and is the essential component of neurotransmitter release. We will mainly discuss the subunit composition, channel regulation by G proteins and exocytotic proteins, and the mouse phenotypes in which N-type channel subunits have been deleted by gene targeting technology.

Animals↗

PubMed2002

Changes in expression of voltage-dependent ion channel subunits in dorsal root ganglia of rats with radicular injury and pain.

STUDY DESIGN: Changes in expression of voltage-dependent ion channel subunits were examined in the radicular pain state. Furthermore, antinociceptive effects of gabapentin on radicular pain were compared with effects on peripheral neuropathic pain. OBJECTIVES: To clarify molecular substrates involved in the development of radicular pain, and to investigate the responsiveness of radicular pain to gabapentin. SUMMARY OF BACKGROUND DATA: Peripheral nerve injuries are known to induce dynamic changes of voltage-dependent Na+ and Ca2+ channel subunits expression in dorsal root ganglion neurons. However, the expression profiles of Na+ and Ca2+ channel subunits in the radicular pain state have not been examined. METHODS: Two radicular pain models and one peripheral neuropathic pain model were prepared. By using semiquantitative reverse transcriptase-polymerase chain reaction, the expression levels of several Na+ and Ca2+ channel subunits in the dorsal root ganglions of these pain model rats were investigated. The antinociceptive effects of gabapentin were examined in a behavioral study using the aforementioned pain models. RESULTS: All three neuropathic pain operations induced comparable mechanical allodynia and thermal hyperalgesia. The upregulation of the Na(v)1.3 Na+ channel and Ca(v)alpha2delta Ca2+ channel subunits was observed only in the peripheral nerve injury model. A downregulation of the Na(v)1.9 channel was observed in all three pain model rats. A lower dose of gabapentin was significantly more effective in alleviating the mechanical allodynia of rats with radicular pain. CONCLUSIONS: The reduction of Na(v)1.9 found in all three models may link to the neuropathic pain state, including radicular pain. The lower sensitivity to gabapentin in rats with peripheral neuropathic pain might be partly explained by the marked upregulation of Ca(v)alpha2delta in the dorsal root ganglions, suggesting that gabapentin may be more effective in radicular pain treatment.

Acetates↗

PubMed2002

Transgenic pigs expressing human decay-accelerating factor regulated by porcine MCP gene promoter.

Porcine membrane cofactor protein (pMCP) is abundantly expressed throughout the body with particularly strong expression on the vascular endothelia. Previous studies demonstrated that the promoter of the pMCP gene induced efficient expression of a human complement regulatory protein, decay-accelerating factor (DAF; CD55), in transgenic mice. In the present study, we tried to produce transgenic pigs with two hybrid genes, 0.9/hDAF and 5.4/hDAF, which were composed of human DAF (hDAF) gene regulated under pMCP promoters of different lengths (0.9 and 5.4 kb). Five live founder transgenic pigs were obtained only with the 0.9/hDAF construct. Although, four founder pigs transmitted the transgene to the second generation, the transmission rates varied among founders. We examined the expression of hDAF in tissues of descendants of two lines (Dm1 and Dm4). Human DAF specific RNAs were confirmed by an RT-PCR analysis in all organs examined. Levels of hDAF protein in the organs from the descendants of Dm1 line were higher than those in the corresponding human organs as determined by enzyme-linked immunosorbent assay. Immunohistochemical studies showed that the tissue distribution of hDAF in the descendants of both lines was similar to that of endogenous pMCP. The expression level of hDAF on the vascular endothelial cells in Dm1 line was twice that on the corresponding human cells. We tested whether proinflammatory cytokines upregulate an efficiency of pMCP promoter on hDAF expression in transgenic pigs. Although the expression of hDAF on the human endothelial cells increased with a combination of cytokines, tumor necrosis factor alpha and interferon-gamma, no cytokine-induced upregulation was seen in the cells of transgenic pigs. The endothelial cells from transgenic pigs exhibited high resistance to the human serum-mediated cytolysis.

Animals↗