Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
 
Articles by K Aoki
Total Records ( 3 ) for K Aoki
  J Kato , Y Ogawa , W Kojima , K Aoki , S Ogawa and K. Iwasaki
  Background

The low and moderate doses of dexmedetomidine reduce arterial pressure and heart rate (HR), suggesting attenuation of sympathetic activity and dominance of cardiac-vagal activity. These autonomic responses under dexmedetomidine sedation may attenuate cardiovascular reflex responses to temporal reduction in arterial pressure, inducing a severe hypotension. We therefore investigated the effects of dexmedetomidine on cardiovascular reflex responses to temporal reduction in arterial pressure induced by the thigh cuff method.

Methods

Twelve healthy men received placebo, low-dose (loading 3 µg kg–1 h–1 for 10 min; maintenance 0.2 µg kg–1 h–1 for 60 min), and moderate-dose (loading 6 µg kg–1 h–1 for 10 min; maintenance 0.4 µg kg–1 h–1 for 60 min) dexmedetomidine infusions in a randomized, double-blind, crossover study. After 70 min of drug infusion, systolic arterial pressure (SAP) and HR responses after thigh cuff deflation were evaluated as indices of cardiovascular reflex.

Results

Reduction in SAP (SAP) [placebo 8 (4), low 12 (4), moderate 19 (5) mm Hg] after thigh cuff deflation was significantly greater in dexmedetomidine than placebo infusions, in a dose-dependent manner. The change in HR (HR), HR/SAP, and the percentage restoration of SAP were lower with dexmedetomidine compared with placebo.

Conclusions

The present results indicated that dexmedetomidine weakens arterial pressure preservation and HR responses after thigh cuff deflation, suggesting attenuated cardiovascular reflexes. Therefore, it must be cautioned that dexmedetomidine can lead to further and sustained reduction in arterial pressure during transient hypotension induced by postural changes, haemorrhage, and/or other stresses.

  D Rendic , M Sharrow , T Katoh , B Overcarsh , K Nguyen , J Kapurch , K Aoki , I. B. H Wilson and M. Tiemeyer
 

Addition of fucose (Fuc) to glycoprotein N-linked glycans or in O-linkage directly to Ser/Thr residues modulates specific cell–cell interactions and cell signaling events. Vertebrates and invertebrates add Fuc in 6-linkage to the reducing terminal N-acetylglucosamine residue of N-glycans. In Drosophila and other invertebrates, Fuc can also be added in 3-linkage to the same residue. These difucosylated N-glycans are recognized by anti-horseradish peroxidase (anti-HRP) antisera, providing a well-established marker for insect neural tissue. To understand the mechanisms and consequences of tissue-specific glycan expression, we identified a single 3-fucosyltransferase (FucTA) that produces the anti-HRP epitope in Drosophila embryos. FucTA transcripts are temporally and spatially restricted to cells that express the anti-HRP epitope and are missing in a mutant that lacks neural 3-fucosylation. Transgenic expression of FucTA, but not of any other candidate 3-fucosyltransferase, rescues the anti-HRP epitope in the embryonic nervous system of this mutant. Mass spectrometric characterization of the N-glycans of Drosophila embryos overexpressing FucTA confirms that this enzyme is indeed responsible for the biosynthesis of difucosylated glycans in vivo. Whereas ectopic expression of FucTA in the larval wing disc produces mild wing notching, the heterochronic, pan-neural expression of FucTA in early differentiating neurons generates neurogenic and cell migration phenotypes; this latter effect is associated with reduced GDP-Fuc levels in the embryo and indicates that the diversion of fucosylation resources towards fucosylation of N-glycans has an impact on developmental signaling associated with O-fucosylation.

  M Kodama , K Tsukamoto , K Yoshida , K Aoki , S Kanegasaki and G. Quinn
 

Pancreatic β cell regeneration remains poorly understood, yet stimulation of adult β cell neogenesis could lead to therapies for type 1 and type 2 diabetes. We studied the effect of embryonic stem (ES) cell transplantation on pancreas regeneration following β cell injury. Female Balb/c nude mice were treated with streptozotocin to induce hyperglycemia and received an ES cell transplant 24 hr later beneath the renal capsule. Transplantation of ES cells prevented hyperglycemia in a subset of mice, maintaining euglycemia and mild glucose tolerance up to 5 weeks. Pancreata of euglycemic mice showed histological evidence of β cell regeneration and expression of pancreas and duodenum transcription factor-1 (PDX-1) and neurogenin 3 (Ngn3) in ductal epithelium. Cell tracing analysis indicated that significant β cell neogenesis from progenitor cells occurred between 2 to 3 weeks following injury in ES cell–transplanted mice but not in sham-transplanted animals. Significantly, whereas pancreas-localized ES cells or their derivatives were adjacent to sites of regeneration, neogenic pancreatic epithelia, including Ngn3+ cells, were endogenous. In conclusion, transplanted ES cells can migrate to the injured pancreas. Transplantation is associated with enhanced endogenous regeneration characterized by expression of Ngn3 and increased β cell differentiation from endogenous progenitor cells. This manuscript contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials. (J Histochem Cytochem 57:1149–1158, 2009)

 
 
 
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility