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Makoto Kanda

Publications and source records attributed to Makoto Kanda.

10 recordsLinked to original sources
PubMed2006

Dispersion and separation of small-diameter single-walled carbon nanotubes.

The dispersion of small-diameter single-walled carbon nanotubes (SWNTs) produced by the CoMoCAT method in tetrahydrofuran (THF) with the use of amine was studied. The absorption, photoluminescence, and Raman spectroscopies showed that the dispersion and centrifugation process leads to an effective separation of metallic SWNTs from semiconducting SWNTs. Since this method is simple and convenient, it is highly applicable to an industrial utilization for widespread applications of SWNTs.

Journal Article↗
PubMed2005

Large-scale separation of metallic and semiconducting single-walled carbon nanotubes.

In the applications of single-walled carbon nanotubes (SWNTs), it is extremely important to separate semiconducting and metallic SWNTs. Although several methods have been reported for the separation, only low yields have been achieved at great expense. We show a separation method involving a dispersion-centrifugation process in a tetrahydrofuran solution of amine, which makes metallic SWNTs highly concentrated to 87% in a simple way.

Journal Article↗
PubMed2005

Hypokalemic rhabdomyolysis due to WDHA syndrome caused by VIP-producing composite pheochromocytoma: a case in neurofibromatosis type 1.

A 47-year-old woman with neurofibromatosis type 1 suffered from general muscle weakness and watery diarrhea. Laboratory findings showed elevated muscular enzymes, severe hypokalemia and excessive production of catecholamines and vasoactive intestinal polypeptide (VIP). A computed tomography scan showed a 10 cm left adrenal mass, in which [(131)I]-metaiodobenzylguanidine scintigraphy showed high uptake. After she underwent surgical removal of the tumor, all the symptoms and signs subsided. A histological study revealed that the mass consisted of pheochromocytoma and ganglioneuroma, respectively producing catecholamines and VIP. In immunohistochemical staining of neurofibromin, pheochromocytoma and ganglion cells showed positive staining, whereas the staining was negative for nerve bundles and Schwann cells. We concluded that the patient had hypokalemic rhabdomyolysis due to watery diarrhea, hypokalemia and achlorhydria (WDHA) syndrome, which was induced by a VIP-producing composite pheochromocytoma. Composite pheochromocytoma is a neuroendocrine tumor that is composed of pheochromocytoma and ganglioneuroma, both derived from the neural crest. Deficiency of neurofibromin in Schwann cells might have played an important role in the development and the growth of the composite pheochromocytoma in this patient.

3-Iodobenzylguanidine↗
PubMed2005

HMG-CoA reductase inhibitors do not improve glucose intolerance in spontaneously diabetic Goto-Kakizaki rats.

We examined whether 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) improve glucose intolerance in spontaneously diabetic Goto-Kakizaki (GK) rats or not. The fasting blood glucose, plasma insulin, and serum cholesterol levels were significantly higher in GK rats than those in age-matched Wistar rats. All rats were given orally once a day 0.5% carboxymethylcellulose, pravastatin 8 mg/kg, simvastatin 8 mg/kg, or atorvastatin 8 mg/kg. An oral glucose tolerance test (OGTT) was performed before and 3, 6 and 12 weeks after statin treatments. The hyperglycemic response to OGTT in GK rats significantly exceeded that in Wistar rats. The plasma insulin level in GK rats increased with age until 14-week-old (treated for 6 weeks), and then decreased. Glucose intake significantly increased the plasma insulin in almost all rats. The increment of plasma insulin due to OGTT in GK rats appeared to be less than that in Wistar rats, because the basal level was already high in GK rats. Pravastatin, simvastatin, and atorvastatin did not modify changes in blood glucose and plasma insulin induced by glucose intake. In conclusion, long-term treatments of GK rats with statins did not improve glucose intolerance observed during OGTT.

Animals↗
PubMed2005

[In vitro susceptibilites to levofloxacin and various antibacterial agents of 11,475 clinical isolates obtained from 52 centers in 2002].

The susceptibilities of bacteria to fluoroquinolones (FQs), especially levofloxacin, and other antimicrobial agents were investigated using 11,475 clinical isolates collected in Japan during 2002. Methicillin susceptible staphylococci, Streptococcus pyogenes, Streptococcus pneumoniae, Moraxella catarrhalis, the family of Enterobactericeae, Haemophilus influenzae and Acinetobacter spp. exhibited stable and high susceptibilities to FQs. The rate of FQs-resistant MRSA was 80 approximately 90%, being markedly higher than that of FQs-resistant MSSA. The FQs-resistance rate of MRCNS was also higher than that of MSCNS, however, it was lower than that of MRSA. No FQs-resistant clinical isolates of Salmonella spp. were detected in any of the surveys. Thirteen of Escherichai coli 696 isolates, 8 of Klebsiella pneumoniae 630 isolates and 33 of Proteus mirabilis 373 isolates produced extended-spectrum beta-lactamase (ESBL), furthermore 6 of 13 in E. coli, 1 of 8 in K. pneumoniae and 14 of 31 ESBL-producing isolates, and in P. mirabilis were FQs resistant. Attention should be focused in the future on the emergence of ESBL in relation to FQs resistance. The rate of FQs-resistant P. aeruginosa isolated from urinary tract infection (UTI) was 40 approximately 60%, while 15 approximately 25% of isolates from respiratory tract infection (RTI) were resistant. IMP-1 type metallo beta-lactamase producing organisms were found in 49 of P. aeruginosa 1,095 isolates, 7 of S. marcescens 586 isolates and 4 of Acinetobacter spp. 474 isolates, respectively. Glycopeptide-resistant enterococci or S. aureus was not found.

Anti-Bacterial Agents↗
PubMed2003

All hydrophobic HMG-CoA reductase inhibitors induce apoptotic death in rat pulmonary vein endothelial cells.

3-Hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitors (statins) are effective in patients with hypercholesterolemia to reduce risk of cardiovascular diseases, because of not only their lowering cholesterol effects but also their pleiotropic effects, such as improvement of endothelial cell dysfunction. On the other hand, statins prevent cell proliferation of various cells, including endothelial cells. We examined effects of all statins available at present on the viability of cultured rat pulmonary vein endothelial cells. Lovastatin, simvastatin, atorvastatin, fluvastatin and cerivastatin, which are hydrophobic statins, markedly reduced cell viability associated with DNA fragmentation, DNA laddering and activation of caspase-3, suggesting apoptotic cell death. Pravastatin, which is a hydrophilic statin, however, did not induce cell apoptosis. Apoptosis induced by hydrophobic statins was associated with activation of apoptosis-related intracellular signal transduction systems; attenuation of localization of RhoA to the membrane, induction of Rac1, and increase in phosphorylation of c-Jun N-terminal kinase and c-Jun. Endothelial cell apoptosis is underlying the improvement of the endothelial dysfunction with hydrophobic statins.

Animals↗
PubMed2003

Insertion (21;8)(q22;q22q22): a masked t(8;21) in a patient with acute myelocytic leukemia.

A 43-year-old man was diagnosed with acute myelocytic leukemia with cellular maturation (AML-M2, according to the French-American-British classification criteria). A cytogenetic study with a G-banding method initially reported the karyotype as 45,X,-Y; however, dual-color, dual-fusion fluorescence in situ hybridization (FISH) with probes for the AML1 and the ETO genes showed an unusual pattern of signals, presenting one fusion signal on chromosome 21. Molecular study by reverse transcriptase polymerase chain reaction revealed the presence of a typical AML1/ETO chimeric gene. FISH with whole-chromosome painting probes targeting chromosomes 8 and 21 revealed insertion of part of 8 chromosome into the long arm of chromosome 21. We concluded that complicated translocations involving chromosomes 8 and 21 in this patient resulted in the development of the chimeric gene, AML1/ETO, on the long arm of chromosome 21. This aberrant location of AML1/ETO gene and the final karyotype of 45,X,-Y,ins(21;8)(q22;q22q22) could not be determined without molecular analysis. This abnormality is considered a masked t(8;21).

Adult↗
PubMed2003

Effects of atorvastatin and pravastatin on glucose tolerance in diabetic rats mildly induced by streptozotocin.

Effects of atorvastatin and pravastatin on glucose tolerance in mildly induced diabetic rats by streptozotocin at 24 mg/kg, i.v. were studied. Non-diabetic and diabetic rats were given orally 0.5% carboxymethylcellulose (control), 8 mg/kg atorvastatin or 8 mg/kg pravastatin once a day for 6 weeks. An oral glucose tolerance test (OGTT) was carried out 1, 2, 3, and 6 weeks after the administration. The blood glucose and plasma insulin levels measured before OGTT in the diabetic rats were not different from those in the non-diabetic rats. However, the hyperglycemic response to OGTT in the diabetic rats significantly exceeded that in the non-diabetic rats. The plasma insulin increased by OGTT in the diabetic rats appeared to be lower than that in the non-diabetic rats. Statin treatments for 1 week did not modify the OGTT-induced hyperglycemia appreciably, although there were some significant differences. More than 2 weeks after administration, the blood glucose levels at several time points after a glucose intake in the atorvastatin-treated diabetic rats were significantly higher than the respective levels in the control diabetic rats. Neither atorvastatin nor pravastatin modified the OGTT-induced insulin secretion. Statins, especially atorvastatin, may influence the glucose tolerance in mildly induced diabetic rats without alterations of insulin secretion.

Administration, Oral↗
PubMed2003

[Activities of antimicrobial agents against 8,474 clinical isolates obtained from 37 medical institutions during 2000 in Japan].

A survey was conducted to determine the antimicrobial activity of fluoroquinolones and other antimicrobial agents against 8,474 clinical isolates obtained from 37 Japanese medical institutions in 2000. A total of 25 antimicrobial agents were used, comprising 4 fluoroquinolones, 13 beta-lactams, minocycline, chloramphenicol, clarithromycin, azithromycin, gentamicin, amikacin, sulfamethoxazole-trimethoprim, and vancomycin. A high resistance rate of over 85% against fluoroquinolones was exhibited by methicillin-resistant Staphylococcus aureus (MRSA) and Enterococcus faecium. Isolates showing resistance to fluoroquinolones among methicillin-resistant coagulase-negative Staphylococci, Enterococcus faecalis, and Pseudomonas aeruginosa from UTI accounted for 30-60%. However, many of the common pathogens were still susceptible to fluoroquinolones, such as Streptococcus pneumoniae (including penicillin-resistant isolates), Streptococcus pyogenes, methicillin-susceptible S. aureus (MSSA), methicillin-susceptible coagulase-negative Staphylococci, Moraxella catarrhalis, the Enterobacteriaceae family, and Haemophilus influenzae (including ampicillin-resistant isolates). About 85% of P. aeruginosa isolated from RTI were susceptible to fluoroquinolones. In conclusion, this survey of sensitivity to antimicrobial agents clearly indicated trend for increasing resistance to fluoroquinolones among MRSA, Enterococci, and P. aeruginosa isolated from UTI, although fluoroquinolones are still effective against other organisms and P. aeruginosa from RTI as has been demonstrated in previous studies.

Anti-Bacterial Agents↗