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Articles by Y Kawakami
Total Records ( 6 ) for Y Kawakami
  R Akagi , Y Takai , M Ohta , H Kanehisa , Y Kawakami and T. Fukunaga
 

Objective: the present study examined which of muscle volume (MV) and cross-sectional area (CSA) is appropriate for evaluating the relation with elbow flexor muscle strength in young and elderly individuals.

Methods: the subjects were 52 young (20–34 year; 30 men and 22 women) and 51 elderly individuals (60–77 year, 19 men and 32 women). The MV and maximal anatomical CSA (ACSA) of elbow flexors were determined by magnetic resonance imaging. The torque developed during maximal voluntary contraction of isometric elbow joint flexion was converted to force by dividing it by the forearm length of each subject.

Results: torque was significantly correlated with MV in young and elderly individuals (r = 0.564–0.926). Similarly, force was also significantly correlated with ACSA in each of them (r = 0.637–0.906). However, the y-intercepts of the regression lines for the ACSA-force relationship in young men and women were significantly higher than zero. There was no age effect on torque per MV, whereas force per ACSA was significantly higher in young adults than in elderly individuals.

Conclusion: for elbow flexors, MV compared to ACSA is appropriate for evaluating the size–strength relationship and the existence of age-related difference in muscle strength per size.

  S. A Boehme , K Franz Bacon , E. P Chen , T. W Ly , Y Kawakami and K. B. Bacon
 

Mast cells are bone marrow-derived effector cells that can initiate inflammatory responses to infectious organisms or allergens by releasing a multitude of pro-inflammatory factors including prostaglandin (PG) D2. We demonstrate that primary murine bone marrow-derived mast cells (BMMCs) express the PGD2 receptor; chemoattractant receptor-homologous molecule expressed on Th class 2 cells (CRTh2). Activation of CRTh2 on BMMC by PGD2 or the CRTh2-specific agonist, 13,14-dihydro-15-keto-prostaglandin D2 (DK-PGD2), resulted in signaling response including Ca2+ mobilization and phosphorylation of the p42/p44 extracellular signal-regulated kinases (ERKs) kinases. Phosphorylation of the ERKs could be blocked by pertussis toxin, as well as a small molecule antagonist of CRTh2, Compound A. Activation of CRTh2 on BMMC also resulted in the up-regulation of CD23 and CD30 on the cell surface, as well as CD62L shedding. Finally, PGD2 and DK-PGD2 induced the migration of BMMC in vitro and in vivo in response to an intra-dermal DK-PGD2 injection. Both these processes were inhibited by the CRTh2 antagonist. These results raise the possibility that the functional consequences of the PGD2–CRTh2 interaction on mast cells may be relevant in allergic inflammation.

  Y Kawakami , H Numata , K Ito and S. G. Goto
 

In this study, we investigated the diapause incidence in 3 geographic strains of the two-spotted spider mite Tetranychus urticae (Acari: Tetranychidae). Under diapause-inducing conditions of 12:12 light:dark at 15 °C, the diapause incidence was nearly 100% in a strain from northern Japan (Sapporo), whereas it was nearly 0% in 2 strains from southern Japan (Itoman and Takanabe). Reciprocal crosses clearly showed that the nondiapause phenotype is inherited in a completely dominant manner, and no maternal effect was detected. Backcrosses to the Itoman and Takanabe strains suggested that dominant nondiapause alleles control the nondiapause phenotype. To clarify the genetic basis of nondiapause in the northern population, we also established a nondiapausing variant ("selected nondiapause" abbreviated as snd) from the Sapporo strain. Crossing experiments revealed that a single recessive allele is responsible for the nondiapause phenotype. Thus, both dominant and recessive inheritance patterns of diapause were detected in the T. urticae populations studied here.

  M. J Isaacs , Y Kawakami , G. P Allendorph , B. H Yoon , J. C. I Belmonte and S. Choe
 

TGF-β superfamily ligands are homo- or heterodimeric and recruit two type I and two type II Ser/Thr kinase receptors to initiate a transmembrane signaling cascade. Even with the known structure of the homodimer ligands in complex with extracellular domains of both receptor types, the sequential assembly of the signaling complex with its cognate receptors in the cell membrane remains elusive. We generated a bone morphogenetic protein-2/-6 heterodimer carrying two asymmetric interfaces for each receptor type. We demonstrate that the heterodimer possesses high affinity to both receptor types and increased Smad1-dependent signaling activity by both cell-based and chondrogenesis assays. Furthermore, we find that the minimal signaling complex consists of two type II receptors and one type I receptor per dimer. Our study reveals how the engineered heterodimers may use their independent binding interfaces to differentially recruit the different receptors for each receptor type to create new biological properties.

  Y Kawakami , Y Tomimori , K Yumoto , S Hasegawa , T Ando , Y Tagaya , S Crotty and T. Kawakami
 

Threats of bioterrorism have renewed efforts to better understand poxvirus pathogenesis and to develop a safer vaccine against smallpox. Individuals with atopic dermatitis are excluded from smallpox vaccination because of their propensity to develop eczema vaccinatum, a disseminated vaccinia virus (VACV) infection. To study the underlying mechanism of the vulnerability of atopic dermatitis patients to VACV infection, we developed a mouse model of eczema vaccinatum. Virus infection of eczematous skin induced severe primary erosive skin lesions, but not in the skin of healthy mice. Eczematous mice exhibited lower natural killer (NK) cell activity but similar cytotoxic T lymphocyte activity and humoral immune responses. The role of NK cells in controlling VACV-induced skin lesions was demonstrated by experiments depleting or transferring NK cells. The proinflammatory cytokine interleukin (IL)-17 reduced NK cell activity in mice with preexisting dermatitis. Given low NK cell activities and increased IL-17 expression in atopic dermatitis patients, these results can explain the increased susceptibility of atopic dermatitis patients to eczema vaccinatum.

  T Matsumoto , M Ii , H Nishimura , T Shoji , Y Mifune , A Kawamoto , R Kuroda , T Fukui , Y Kawakami , T Kuroda , S. M Kwon , H Iwasaki , M Horii , A Yokoyama , A Oyamada , S. Y Lee , S Hayashi , M Kurosaka , S Takaki and T. Asahara
 

The therapeutic potential of hematopoietic stem cells/endothelial progenitor cells (HSCs/EPCs) for fracture healing has been demonstrated with evidence for enhanced vasculogenesis/angiogenesis and osteogenesis at the site of fracture. The adaptor protein Lnk has recently been identified as an essential inhibitor of stem cell factor (SCF)–cKit signaling during stem cell self-renewal, and Lnk-deficient mice demonstrate enhanced hematopoietic reconstitution. In this study, we investigated whether the loss of Lnk signaling enhances the regenerative response during fracture healing. Radiological and histological examination showed accelerated fracture healing and remodeling in Lnk-deficient mice compared with wild-type mice. Molecular, physiological, and morphological approaches showed that vasculogenesis/angiogenesis and osteogenesis were promoted in Lnk-deficient mice by the mobilization and recruitment of HSCs/EPCs via activation of the SCF–cKit signaling pathway in the perifracture zone, which established a favorable environment for bone healing and remodeling. In addition, osteoblasts (OBs) from Lnk-deficient mice had a greater potential for terminal differentiation in response to SCF–cKit signaling in vitro. These findings suggest that inhibition of Lnk may have therapeutic potential by promoting an environment conducive to vasculogenesis/angiogenesis and osteogenesis and by facilitating OB terminal differentiation, leading to enhanced fracture healing.

 
 
 
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