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( Masamichi Kimura ),( Yoshihisa Tsuji ),( Masako Iwai ),( Masahiro Inagaki ),( Ali Madian ),( Takuya Yoshino ),( Minoru Matsuura ),( Hiroshi Nakase ) 대한장연구학회 2015 Intestinal Research Vol.13 No.2
Behcet`s disease (BD) is a systemic vasculitis, while myelodysplastic syndrome (MDS) is a heterogeneous group of clonal hematologic disorders characterized by ineffective hematopoiesis. Some studies suggest a relationship between MDS and BD, especially intestinal BD, and trisomy 8 seems to play an important role in both diseases. There are several reports on patients with BD comorbid with MDS involving trisomy 8 that frequently have intestinal lesions refractory to conventional medical therapies. Tumor necrosis factor (TNF)-αis strongly involved in the pathophysiology of several autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease, and BD. In addition, TNF-α plays an important role in the pathophysiology of MDS by inhibiting normal hematopoiesis and inducing the programmed cell death of normal total bone marrow cells and normal CD34+ cells. Recent clinical reports demonstrate the favorable effect of TNF-α antagonists in patients with refractory intestinal BD and in those with MDS. We present the case of a patient with intestinal BD and MDS involving trisomy 8 who was successfully treated with adalimumab. (Intest Res 2015;13:166-169)
Effect of ammonia treatment on white birch wood
Yamashita, Daichi,Kimura, Satoshi,Wada, Masahisa,Samejima, Masahiro,Takabe, Keiji Walter de Gruyter und Co 2018 Holzforschung Vol. No.
<P><B>Abstract</B></P><P>Transverse sections of white birch (<I>Betula platyphylla</I>) were treated with anhydrous ammonia at 60-140°C (ammonia treatment, AT). As a result, the crystal structure of cellulose in the AT samples changed to cellulose III<SUB>I</SUB>, and acetamide was produced. The surface area of the AT samples, the amount of sugar released upon acid hydrolysis and the lignin content were not changed. However, a small amount of lignin became acid soluble. Mäule color reaction, indicative of the presence of syringyl lignin, showed decreasing color intensities with increasing temperature of AT. The results can be easily interpreted that AT affects ester linkages and side chains of hemicelluloses and syringyl lignin. In addition, AT was carried out on 1-μm thick transverse sections and block specimens. Xylanase treatment and immunolabeling revealed that AT enhances xylan degradation, but ray cells are resistant to xylanase even after AT. On the block sample, a deposited xylan layer appeared on the inner surface of fiber cell walls. Apparently, xylan moved to the surface in contact with the fluid ammonia during AT. The vessel cell wall did not show a similar migration effect, indicating a cell wall-specific interaction with ammonia.</P>
Presynaptic Mechanism Underlying Regulation of Transmitter Release by G Protein Coupled Receptors
Takahashi, Tomoyuki,Kajikawa, Yoshinao,Kimura, Masahiro,Saitoh, Naoto,Tsujimoto, Tetsuhiro The Korean Society of Pharmacology 2004 The Korean Journal of Physiology & Pharmacology Vol.8 No.2
A variety of G protein coupled receptors (GPCRs) are expressed in the presynaptic terminals of central and peripheral synapses and play regulatory roles in transmitter release. The patch-clamp whole-cell recording technique, applied to the calyx of Held presynaptic terminal in brainstem slices of rodents, has made it possible to directly examine intracellular mechanisms underlying the GPCR-mediated presynaptic inhibition. At the calyx of Held, bath-application of agonists for GPCRs such as $GABA_B$ receptors, group III metabotropic glutamate receptors (mGluRs), adenosine $A_1$ receptors, or adrenaline ${\alpha}2$ receptors, attenuate evoked transmitter release via inhibiting voltage-activated $Ca^{2+}$ currents without affecting voltage-activated $K^+$ currents or inwardly rectifying $K^+$ currents. Furthermore, inhibition of voltage-activated $Ca^{2+}$ currents fully explains the magnitude of GPCR-mediated presynaptic inhibition, indicating no essential involvement of exocytotic mechanisms in the downstream of $Ca^{2+}$ influx. Direct loadings of G protein ${\beta}{\gamma}$ subunit $(G{\beta}{\gamma})$ into the calyceal terminal mimic and occlude the inhibitory effect of a GPCR agonist on presynaptic $Ca^{2+}$ currents $(Ip_{Ca})$, suggesting that $G{\beta}{\gamma}$ mediates presynaptic inhibition by GPCRs. Among presynaptic GPCRs glutamate and adenosine autoreceptors play regulatory roles in transmitter release during early postnatal period when the release probability (p) is high, but these functions are lost concomitantly with a decrease in p during postnatal development.
Presynaptic Mechanism Underlying Regulation of Transmitter Release by G Protein Coupled Receptors
Tomoyuki Takahashi,Yoshinao Kajikawa,Masahiro Kimura,Naoto Saitoh,Tetsuhiro Tsujimoto 대한생리학회-대한약리학회 2004 The Korean Journal of Physiology & Pharmacology Vol.8 No.2
A variety of G protein coupled receptors (GPCRs) are expressed in the presynaptic terminals of central and peripheral synapses and play regulatory roles in transmitter release. The patch-clamp whole-cell recording technique, applied to the calyx of Held presynaptic terminal in brainstem slices of rodents, has made it possible to directly examine intracellular mechanisms underlying the GPCR-mediated presynaptic inhibition. At the calyx of Held, bath-application of agonists for GPCRs such as GABA<SUB>B</SUB> receptors, group III metabotropic glutamate receptors (mGluRs), adenosine A<SUB>1</SUB> receptors, or adrenaline α2 receptors, attenuate evoked transmitter release via inhibiting voltage-activated Ca<SUP>2</SUP> currents without affecting voltage-activated K<SUP></SUP> currents or inwardly rectifying K<SUP></SUP> currents. Furthermore, inhibition of voltage-activated Ca<SUP>2</SUP> currents fully explains the magnitude of GPCR-mediated presynaptic inhibition, indicating no essential involvement of exocytotic mechanisms in the downstream of Ca<SUP>2</SUP> influx. Direct loadings of G protein βγ subunit (Gβγ) into the calyceal terminal mimic and occlude the inhibitory effect of a GPCR agonist on presynaptic Ca<SUP>2</SUP> currents (Ip<SUB>Ca</SUB>), suggesting that Gβγmediates presynaptic inhibition by GPCRs. Among presynaptic GPCRs glutamate and adenosine autoreceptors play regulatory roles in transmitter release during early postnatal period when the release probability (p) is high, but these functions are lost concomitantly with a decrease in p during postnatal development.
Kana Tozaki,Junpei KIMURA,Nobuyuki Ryu,Testuo Nasu,Anton Pernthaner,Wayne R. Hein,Masahiro Yasuda 대한수의학회 2013 Journal of Veterinary Science Vol.14 No.1
The follicle-associated epithelium (FAE) of Peyer’s patches (PPs) contains M cells that are important for reducing mucosal immune responses by transporting antigens into the underlying lymphoid tissue. We generated a monoclonal antibody (C6) that reacted with the FAE of calf ileal PPs, and analyzed the characteristics of C6 using immunohistochemistry and Western blotting. FAE of the ileal PP was stained with C6 during both late fetal developmental and postnatal stages. Neither the villous epithelial cell nor intestinal crypt basal cells were stained at any developmental stage. During the prenatal stages, FAE of the jejunal PP was C6-negative. However, a few C6-positive cells were distributed diffusely in some FAE of the jejunal PPs during the postnatal stages. The protein molecular weight of the antigen recognized by C6 was approximately 45 kDa. These data show that C6 is useful for identifying the FAE in ileal PPs and further suggest that differentiation of the FAE in these areas is independent of external antigens.
Rimmed Vacuoles in Myositis Associated with Antimitochondrial Antibody
Rui Shimazaki,Akinori Uruha,Hideki Kimura,Utako Nagaoka,Tomoya Kawazoe,Satoshi Yamashita,Takashi Komori,Kazuhito Miyamoto,Shiro Matsubara,Keizo Sugaya,Masahiro Nagao,Eiji Isozaki 대한신경과학회 2020 Journal of Clinical Neurology Vol.16 No.3