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Articles by K Ohashi
Total Records ( 7 ) for K Ohashi
  P Li , R Shibata , S Maruyama , M Kondo , K Ohashi , N Ouchi and T. Murohara
 

Recent clinical trials demonstrated that PPAR agonist fenofibrate reduces cardiovascular events, including limb amputation in people with type 2 diabetes. Here, we investigated whether fenofibrate modulates the revascularization process in a mouse model of hindlimb ischemia. Treatment with fenofibrate led to acceleration of revascularization of ischemic hindlimb relative to the contralatereal limb in wild-type (WT) mice, as measured by laser Doppler blood flow and capillary density analyses. Treatment of WT mice with fenofibrate increased the serum levels of adiponectin, which has protective actions on the vasculature. Of importance, fenofibrate had no effects on the revascularization in ischemic limbs of adiponectin-deficient (APN-KO) mice. Fenofibrate stimulated the phosphorylation of AMPK and eNOS in the ischemic muscles in WT mice but not in APN-KO mice. AMPK inhibitor compound C suppressed fenofibrate-induced increase in limb perfusion and AMPK phosphorylation in ischemic muscle in WT mice without affecting adiponectin levels. NOS inhibitor l-NAME also blocked the increased blood flow of ischemic limbs in fenofibrate-treated WT mice. Our observations suggest that fenofibrate could promote revascularization in response to ischemia through adiponectin-dependent AMPK signaling.

  K Ohashi and J. D. Thomson
  Background

Trapline foraging (repeated sequential visits to a series of feeding locations) has been often observed in pollinators collecting nectar or pollen from flowers. Although field studies on bumble-bees and hummingbirds have clarified fundamental aspects of this behaviour, trapline foraging still poses several difficult questions from the perspectives of both animals and plants. These questions include whether and how traplining improves foraging performance, how animals develop traplines with accumulating foraging experience, and how traplining affects pollen flow or plant reproduction.

Scope

First, we review our previous work performed by using computer simulations and indoor flight-cage experiments with bumble-bees foraging from arrays of automated feeders. Our findings include the following: (1) traplining benefits foragers that are competing for resources that replenish in a decelerating way, (2) traplining is a learned behaviour that develops over a period of hours and (3) the establishment of traplines could be hampered by spatial configuration of plants such as zigzags. Second, using a simulation model linking pollinator movement and pollen transfer, we consider how service by pollinators with different foraging patterns (searchers or trapliners) would affect pollen flow. Traplining increases mating distance and mate diversity, and reduces ‘iterogamy’ (self-pollination caused by return visits) at the population level. Furthermore, increased visitation rates can have opposite effects on the reproductive success of a plant, depending on whether the visitors are traplining or searching. Finally, we discuss possible consequences of traplining for plants in the light of new experimental work and modelling.

Conclusions

We suggest that trapline foraging by pollinators increases variation among plant populations in genetic diversity, inbreeding depression and contributions of floral traits to plant fitness, which should in turn affect the rates and directions of floral evolution. More theoretical and empirical studies are needed to clarify possible outcomes of such a neglected side of pollination.

  K Kuromoto , M Watanabe , K Adachi , K Ohashi and Y. Iwatani
  Background

It is important to predict the development of pre-eclampsia (PE) during early pregnancy to prevent its occurrence later on. In this study, we studied urinary biochemical parameters and blood pressure (BP) during and after pregnancy to find useful parameters for predicting PE.

Methods

A case-control study was performed in 25 PE patients and 172 normotensive pregnant women. Twelve biochemical parameters were measured in spot urine, and the systolic and diastolic BPs were measured using an automated device during pregnancy and six to eight weeks after birth.

Results

A multiple logistic regression analysis showed that the combinations of urinary creatinine (Cr) and systolic BP (SBP) in the first trimester of pregnancy (8.9 ± 2.6 weeks), and of urinary inorganic phosphorus (IP)/Cr and SBP in the second trimester of pregnancy (19.0 ± 1.6 weeks) were useful for predicting PE. The area under the curve in the receiver operator characteristic curve of the combination of urinary Cr and SBP in the first trimester was 0.85 (95% confidence interval [CI] 0.74–0.96), and that of the combination of urinary IP/Cr and SBP in the second trimester was 0.91 (95% CI: 0.86–0.97). When used 249 mg/dL in urinary Cr and 128 mmHg in SBP as their cut-off points, the combination in the first trimester increased the accuracy (sensitivity 75% and specificity 95%) in predicting PE, as compared with that of urinary Cr (29%, 99%) or SBP (50%, 98%).

Conclusions

Combination of urinary Cr and SBP in early pregnancy and that of urinary IP/Cr and SBP in mid-pregnancy are useful for the prediction of PE.

  H Ihara , T Watanabe , N Hashizume , M Totani , K Kamioka , K Onda , S Sunahara , T Suzuki , M Itabashi , Y Aoki , M Ishibashi , S Ito , K Ohashi , T Enomoto , K Saito , K Saeki , Y Nagamura , T Nobori , K Hirota , K Fujishiro , M Maekawa , M Miura and Y. Ohta
  Background

The aim of the present study was to evaluate standard reference material (SRM) 1955 commutability as a reference material for serum folate using automated methods. We also designed so as to reduce the intermethod variability present in different automated methods.

Methods

Using a microbiological assay related to the ‘information value’ of SRM 1955 as a comparison method, we investigated the possibility of standardization for the assay values of serum folate as measured by the automated methods (Access, Centaur and Elecsys). In the assay of 50 patient sera by these automated methods, we corrected observed values by the SRM 1955 and compared with comparison values.

Results

The observed values of SRM 1955 Levels I, II and III were within or outside (but near) a 95% prediction interval obtained from patient sera by the automated methods. The normalized residuals obtained from SRM 1955 were within ±3.0 (in SD units), which enabled us to conclude that the SRM 1955 had a physicochemical characterization similar to native serum. Twelve patients were assessed as hypofolataemia (<6.0 ng/mL) and 38 patients as normal (≥6.0 ng/mL). Before correction, folate levels in six of 12 patients were lower than 6.0 ng/mL, and those in seven of 38 patients were higher than 6.0 ng/mL with the automated methods. After correction, low levels were found in four of 12 patients, and normal levels were found in 33 of 38 patients.

Conclusions

The use of SRM 1955 would help to reduce the intermethod variability present in different automated methods for serum folate measurement.

  K Ohashi , G Vitaliano , A Polcari and M. H. Teicher
 

Context  Seated hyperactivity is a defining feature of the combined and predominantly hyperactive-impulsive subtypes of attention-deficit/hyperactivity disorder (ADHD), but its underlying nature is unknown.

Objective  To determine whether hyperactivity is a consequence of an impaired ability to inhibit activity to low levels or to maintain positional stability.

Design  Case-control study.

Setting  Academic research center and school.

Participants  Sixty-two boys 9 to 12 years of age (of 73 screened), recruited from the community by advertisement, who met DSM-IV criteria for ADHD combined subtype on structured interview. Sixty-two controls were selected by matching for age and sex from a community sample of 1168 subjects in 3 participating school districts. Pupils with Conners' Teacher Rating Scores Revised within ±1 SD of the mean for age were eligible for randomized matching.

Intervention  Infrared motion analysis of head-marker movements (50 Hz) during performance of a 15-minute cognitive control task. Subjects with ADHD were tested at least 18 hours following their last dose of methylphenidate and again 120 minutes after a 0.4-mg/kg probe dose.

Main Outcome Measures  Inhibitory control (spike and basal amplitude) and head-marker stability (approximate entropy, Lyapunov, and spectral exponents).

Results  Inhibitory control measures were 2-fold higher in subjects with ADHD (d' = 0.63-0.95). Group differences in head-marker stability were even greater (d' = 2.20-4.71; receiver operating characteristic area = 0.956-1.0). Methylphenidate restored inhibitory ability to control levels but only partially corrected stability deficits, which still distinguished subjects with ADHD from controls (receiver operating characteristic area = 0.722-0.995).

Conclusions  Children with ADHD have a deficient ability to inhibit activity to low levels and unstable control of head-marker position characterized by deterministic chaos (sensitivity to initial conditions). These deficits differed in degree of correctability by methylphenidate, suggesting that they may be mediated by different neural circuits (eg, corticostriatal vs cerebrovestibular).

  E Ichihara , K Ohashi , N Takigawa , M Osawa , A Ogino , M Tanimoto and K. Kiura
 

Vandetanib is a novel multitarget tyrosine kinase inhibitor (TKI) that inhibits vascular endothelial growth factor receptor-2 (VEGFR-2), with additional inhibition of epidermal growth factor receptor (EGFR) and rearranged during transfection receptor signaling, which has shown promising results in clinical trials for advanced non–small cell lung cancer. However, the mechanisms of acquired resistance to vandetanib remain unclear. Therefore, we established in vitro vandetanib-resistant PC-9/VanR cells from PC-9, a vandetanib-sensitive lung adenocarcinoma cell line, by chronic exposure to this agent. PC-9/VanR cells were 50-fold more resistant to vandetanib than PC-9 cells in vitro. Compared with PC-9 cells, PC-9/VanR cells showed emergence of an EGFR T790M mutation, moderately elevated MET amplification, and similar VEGFR-2 inhibition by vandetanib. Note that phospho-MET in PC-9/VanR was suppressed following EGFR inhibition by an irreversible EGFR-TKI, indicating that MET signaling of PC-9/VanR was dependent on EGFR signaling and that MET amplification was not the primary mechanism of resistance to vandetanib. In contrast to the in vitro experiment, vandetanib effectively inhibited the growth of PC-9/VanR tumors in an in vivo xenograft model through the antiangiogenesis effects of VEGFR-2 inhibition. In conclusion, the multitarget TKI vandetanib induced or selected for the EGFR T790M mutation as observed previously with highly selective EGFR-TKIs. However, vandetanib retained significant efficacy in vivo against xenografts harboring the T790M mutation, providing a strong scientific rationale for investigating vandetanib in clinical settings where acquired resistance through emergence of EGFR T790M mutations limits the effectiveness of highly selective EGFR-TKIs. [Cancer Res 2009;69(12):5091–8]

  S. A McCalmon , D. M Desjardins , S Ahmad , K. S Davidoff , C. M Snyder , K Sato , K Ohashi , O. M Kielbasa , M Mathew , E. P Ewen , K Walsh , H Gavras and F. J. Naya
 

Rationale: The vasoactive peptide angiotensin II (Ang II) is a potent cardiotoxic hormone whose actions have been well studied, yet questions remain pertaining to the downstream factors that mediate its effects in cardiomyocytes.

Objective: The in vivo role of the myocyte enhancer factor (MEF)2A target gene Xirp2 in Ang II–mediated cardiac remodeling was investigated.

Methods and Results: Here we demonstrate that the MEF2A target gene Xirp2 (also known as cardiomyopathy associated gene 3 [CMYA3]) is an important effector of the Ang II signaling pathway in the heart. Xirp2 belongs to the evolutionarily conserved, muscle-specific, actin-binding Xin gene family and is significantly induced in the heart in response to systemic administration of Ang II. Initially, we characterized the Xirp2 promoter and demonstrate that Ang II activates Xirp2 expression by stimulating MEF2A transcriptional activity. To further characterize the role of Xirp2 downstream of Ang II signaling we generated mice harboring a hypomorphic allele of the Xirp2 gene that resulted in a marked reduction in its expression in the heart. In the absence of Ang II, adult Xirp2 hypomorphic mice displayed cardiac hypertrophy and increased β myosin heavy chain expression. Strikingly, Xirp2 hypomorphic mice chronically infused with Ang II exhibited altered pathological cardiac remodeling including an attenuated hypertrophic response, as well as diminished fibrosis and apoptosis.

Conclusions: These findings reveal a novel MEF2A-Xirp2 pathway that functions downstream of Ang II signaling to modulate its pathological effects in the heart.

 
 
 
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