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Articles by T Kudo
Total Records ( 2 ) for T Kudo
  T Kushikata , H Yoshida , M Kudo , T Kudo and K. Hirota
  Background

Central orexinergic and noradrenergic neurones are involved in the control of sleep and wakefulness. In addition, previous reports suggest that both neurones may have an important role to play in general anaesthesia. In the present study, we have determined whether general anaesthesia would affect plasma orexin A (OXA) and norepinephrine concentrations.

Methods

Twenty-two patients undergoing elective ophthalmic surgery under general anaesthesia with propofol, fentanyl, and vecuronium were studied. Arterial blood was collected before and 1 and 2 h after induction of anaesthesia and at emergence to measure plasma OXA, propofol, norepinephrine, and epinephrine concentrations. During anaesthesia, the propofol infusion rate was changed to maintain the bispectral index between 40 and 50.

Results

Plasma OXA and norepinephrine did not change during anaesthesia but significantly increased after emergence compared with pre-anaesthesia [from 19.9 (sd 3.2) to 28.3 (4.3) pM, P<0.01, and from 1351 (146) to 1798 (251) pM, P<0.05, respectively]. Plasma epinephrine did not change. There was a significant correlation between plasma OXA and norepinephrine (P<0.05) and also between plasma propofol and OXA (P<0.05) and norepinephrine (P<0.01).

Conclusions

We found that plasma OXA and norepinephrine significantly increased during emergence from propofol–fentanyl anaesthesia.

  H Suzuki , E Yamamoto , M Nojima , M Kai , H. o Yamano , K Yoshikawa , T Kimura , T Kudo , E Harada , T Sugai , H Takamaru , T Niinuma , R Maruyama , H Yamamoto , T Tokino , K Imai , M Toyota and Y. Shinomura
 

Altered expression of microRNA (miRNA) is strongly implicated in cancer, and recent studies have shown that the silencing of some miRNAs is associated with CpG island hypermethylation. To identify epigenetically silenced miRNAs in gastric cancer (GC), we screened for miRNAs induced by treatment with 5-aza-2’-deoxycytidine and 4-phenylbutyrate. We found that miR-34b and miR-34c are epigenetically silenced in GC and that their downregulation is associated with hypermethylation of the neighboring CpG island. Methylation of the miR-34b/c CpG island was frequently observed in GC cell lines (13/13, 100%) but not in normal gastric mucosa from Helicobacter pylori-negative healthy individuals. Transfection of a precursor of miR-34b and miR-34c into GC cells induced growth suppression and dramatically changed the gene expression profile. Methylation of miR-34b/c was found in a majority of primary GC specimens (83/118, 70%). Notably, analysis of non-cancerous gastric mucosae from GC patients (n = 109) and healthy individuals (n = 85) revealed that methylation levels are higher in gastric mucosae from patients with multiple GC than in mucosae from patients with single GC (27.3 versus 20.8%; P < 0.001) or mucosae from H. pylori-positive healthy individuals (27.3 versus 20.7%; P < 0.001). These results suggest that miR-34b and miR-34c are novel tumor suppressors frequently silenced by DNA methylation in GC, that methylation of miR-34b/c is involved in an epigenetic field defect and that the methylation might be a predictive marker of GC risk.

 
 
 
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