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 Nakajima
Total Records ( 3 ) for K Nakajima
  K Nakajima , J Kobayashi , H Mabuchi , T Nakano , Y Tokita , T Nagamine , S Imamura , M Ai , S Otokozawa and E. F. Schaefer
  Background

The relationship between plasma angiopoietin-like protein 3 (ANGPTL3), and lipoprotein lipase (LPL) activity and hepatic triglyceride lipase (HTGL) activity has not been investigated in the metabolism of remnant lipoproteins (RLPs) and high-density lipoprotein (HDL) in human plasma.

Methods

ANGPTL3, LPL activity, HTGL activity, RLP-C and RLP-TG and small, dense LDL-cholesterol (sd LDL-C) were measured in 20 overweight and obese subjects in the fasting and postprandial states.

Results

Plasma TG, RLP-C, RLP-TG and sd LDL-C were inversely correlated with LPL activity both in the fasting and postprandial states, but not correlated with HTGL activity and ANGPTL3. However, plasma HDL-C was positively correlated with LPL activity both in the fasting and postprandial states, while inversely correlated with HTGL activity. ANGPTL3 was inversely correlated with HTGL activity both in the fasting and postprandial states, but not correlated with LPL activity.

Conclusion

HTGL plays a major role in HDL metabolism, but not RLP metabolism. These findings suggest that ANGPTL3 is strongly associated with the inhibition of HTGL activity and regulates HDL metabolism, but not associated with the inhibition of LPL activity for the metabolism of RLPs in human plasma.

  N Sasaki , T Yamashita , M Takeda , M Shinohara , K Nakajima , H Tawa , T Usui and K. i. Hirata
 

Background— Accumulating evidence suggests that several subsets of regulatory T cells that actively mediate immunologic tolerance play crucial roles in atherogenesis. Recently, orally administered anti-CD3 monoclonal antibody has been shown as an inducer of novel regulatory T cells expressing latency-associated peptide (LAP) on their surface, which potently prevents systemic autoimmunity. In the present study, we hypothesized that oral anti-CD3 antibody treatment may inhibit atherosclerosis in mice.

Methods and Results— Six-week-old apolipoprotein E–deficient mice on a standard diet were orally given anti-CD3 antibody or control immunoglobulin G on 5 consecutive days, and atherosclerosis was assessed at age 16 weeks. Oral administration of anti-CD3 antibody significantly reduced atherosclerotic lesion formation and accumulations of macrophages and CD4+ T cells in the plaques compared with controls. We observed a significant increase in LAP+ cells and CD25+Foxp3+ cells in the CD4+ T-cell population in anti-CD3–treated mice, in association with increased production of the antiinflammatory cytokine transforming growth factor-β and suppressed T-helper type 1 and type 2 immune responses. Neutralization of transforming growth factor-β in vivo abrogated the preventive effect of oral anti-CD3 antibody.

Conclusions— Our findings indicate the atheroprotective role of oral anti-CD3 antibody treatment in mice via induction of a regulatory T-cell response. These findings suggest that oral immune modulation may represent an attractive therapeutic approach to atherosclerosis.

  I Matsunari , H Aoki , Y Nomura , N Takeda , W. P Chen , J Taki , K Nakajima , S. G Nekolla , S Kinuya and K. Kajinami
  Background—

Although both 123I-metaiodobenzylguanidine (123I-MIBG) imaging and 11C-hydroxyephedrine (11C-HED) positron emission tomography (PET) are used for assessing cardiac sympathetic innervation, their relationship remains unknown. The aims were to determine whether 123I-MIBG parameters such as heart-to-mediastinum ratio (H/M) are associated with quantitative measures by 11C-HED PET and to compare image quality, defect size, and location between 123I-MIBG single-photon emission computed tomography (SPECT) and 11C-HED PET.

Methods and Results—

Twenty-one patients (mean left ventricular ejection fraction, 39±15%) underwent 123I-MIBG imaging and 11C-HED PET. Early (15-minute), late (3-hour) H/M, and washout rate (WR) were calculated for 123I-MIBG. Myocardial retention and WR was calculated for 11C-HED. Using a polar map approach, defect was defined as the area with relative activity <60% of the maximum. Both the early (r=0.76) and late (r=0.84) 123I-MIBG H/M were correlated with 11C-HED retention. 123I-MIBG WR was correlated with 11C-HED WR (r=0.57). Defect size could not be measured in 3 patients because of poor quality 123I-MIBG SPECT, whereas 11C-HED defect was measurable in all patients. Although defect size measured by early or late 123I-MIBG SPECT was closely correlated with that by 11C-HED PET (early: r=0.94; late: r=0.88), the late 123I-MIBG overestimated defect size particularly in the inferior and septal regions.

Conclusions—

123I-MIBG H/M gives a reliable estimate of cardiac sympathetic innervation as measured by 11C-HED PET. Furthermore, despite the close correlation in defect size, 11C-HED PET appears to be more suitable for assessing regional abnormalities than does 123I-MIBG SPECT.

 
 
 
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility