Search PubMed⌕ Search

Biomedical subjects

Kenichi Kato

Publications and source records attributed to Kenichi Kato.

33 records · Page 2Linked to original sources

1-D cobalt(II) spin transition compound with strong interchain interaction: [Co(pyterpy)Cl(2)].X.

Cobalt(II) compounds [Co(pyterpy)Cl(2)].MeOH (1.(MeOH)) and [Co(pyterpy)Cl(2)].2H(2)O (1.(2H(2)O)) were synthesized. The compound 1.(MeOH) forms the quasi 3-D networks by making pi-pi stacking between the 1-D chains. The methanol molecules from 1.(MeOH) can be removed by heating, and substituted by absorption of water molecules. The MeOH molecules in 1.(MeOH) are removed by heating at 410 K, and they are substituted by water molecules to form 1.(2H(2)O). 1.(2H(2)O) exhibits a S = (3)/(2) (HS) left arrow over right arrow S = (1)/(2) (LS) spin transition with a thermal hysteresis. We have succeeded in constructing a guest dependent 1-D spin-crossover cobalt(II) compound.

Journal Article↗

Rapid involution of proliferative fasciitis.

A process of evolution and involution is a characteristic feature of reactive fibrous lesions, but has not been emphasized in either the radiology or pathology literature. We report a case of proliferative fasciitis, pseudotumorous fibrous proliferation similar to nodular fasciitis, showing evolution and involution during a 1-month period. A 35-year-old Japanese woman presented with a tender soft tissue mass in the forearm that had grown over a 2-week period. MR imaging revealed a soft tissue mass of nonspecific signal intensity on the muscle fascia. Needle biopsy revealed diffuse proliferation of fibroblastic spindle cells representing proliferative fasciitis. Two weeks after biopsy the mass had rapidly decreased in size, and the pain subsided. MR imaging obtained 1 month later demonstrated only minimal residual reactive change along the fascia. Conservative treatment may be a reasonable treatment option for this condition.

Adult↗

Peliosis hepatis during postpartum period: successful embolization of hepatic artery.

Peliosis hepatis is a rare disorder characterized by the presence of blood-filled spaces in the liver, and it usually has a chronic presentation pattern. It has been reported mainly in adult patients in association with various pharmacological agents and infections. The present report concerns a postpartum patient in whom peliosis hepatis initially presented as active intraperitoneal hemorrhage from peliotic liver lesions, with no obvious etiology. We report here a 31-year-old woman who developed symptomatic peliosis hepatis and underwent superselective hepatic artery embolization, with control of the bleeding. We also present the sonographic, computed tomographic, and magnetic resonance images and laparoscopic findings. The patient recovered well and was discharged without any complaints. The pathogenesis in this patient remains unclear, but it is suggested that in her case estrogens and progesterone could not have been responsible for the development of peliosis hepatis.

Adult↗

Differences in the contribution of HLA-DR and -DQ haplotypes to susceptibility to adult- and childhood-onset type 1 diabetes in Japanese patients.

To clarify heterogeneity in Japanese adult-onset type 1 diabetes, we analyzed the HLA-DR and -DQ haplotypes, depending on the clinical phenotype, and compared them with those in childhood-onset type 1 diabetes (CO). The patients in a previously reported Ehime Study were divided into subgroups by the mode of onset of diabetes: 68 acute-onset type 1 diabetic patients (AO) and 28 slowly progressive type 1 diabetic patients (SO). HLA haplotypes were compared with those of 80 CO patients and 190 control subjects. Two major susceptible HLA haplotypes in the Japanese, DRB1*0405-DQB1*0401 (DR4) and DRB1*0901-DQB1*0303 (DR9), were significantly increased in the AO and CO groups, but only DR9 was increased in the SO group. AO subjects had a higher frequency of DR9 than CO subjects. Accordingly, the DR9:DR4 frequency increased with increasing age of onset. Another susceptible haplotype, DRB1*0802-DQB1*0302 (DR8), was involved only in the CO group. Analysis of haplotype combinations revealed that DR4 and DR9 had significant dosage effects on the AO and CO groups (P < 0.0001), but only DR9 had such an effect in the SO group (P < 0.03). These results suggest differences in the contribution of HLA class II haplotypes to susceptibility of type 1 diabetes depending on the clinical phenotype and also indicate that HLA class II haplotypes may be associated with the onset age of type 1 diabetes.

Adult↗

The absence of evidence for major effects of the frequent SNP +299G>A in the resistin gene on susceptibility to insulin resistance syndrome associated with Japanese type 2 diabetes.

Resistin, specifically secreted from adipocytes, antagonizes insulin and represents a promising candidate gene for type 2 diabetes. We reported that a frequent single nucleotide polymorphism (SNP) +299G>A in this gene is not associated with type 2 diabetes. To determine whether this SNP affects insulin resistance syndrome associated with type 2 diabetes, we examined its effects on susceptibility to obesity, hyperlipidemia and hypertension in type 2 diabetic subjects and on susceptibility to type 2 diabetes by interaction with other frequent genes involved in lipid metabolism, namely, beta3-adrenergic receptor (b3AR) Trp64Arg, phosphodiesterase 3B (PDE3B) c.1389G>A or lysosomal acid lipase (LAL) Thr-6Pro. The 99 type 2 diabetic and 99 control subjects were typed by PCR direct sequencing or PCR-RFLP. No differences in frequencies of obesity, hyperlipidemia and hypertension were found between the type 2 diabetic subjects with G/G and those with G/A or A/A genotypes of the resistin SNP. When the combination of the resistin SNP with each of b3AR, PDE3B and LAL SNPs was assessed, no association with type 2 diabetes was evident. Therefore, the frequent SNP +299G>A in the resistin gene is unlikely to have major effects on susceptibility to insulin resistance syndrome associated with type 2 diabetes in Japanese subjects.

3',5'-Cyclic-AMP Phosphodiesterases↗

Systematic search for single nucleotide polymorphisms in the 5' flanking region of the human phosphodiesterase 3B gene: absence of evidence for major effects of identified polymorphisms on susceptibility to Japanese type 2 diabetes.

The activation of phosphodiesterase 3B (PDE3B) reduces free fatty acid output from adipocytes. A reduced PDE3B gene expression could lead to insulin resistance. To determine whether there are polymorphisms associated with type 2 diabetes in PDE3B gene promoter, this 5(') flanking region was isolated. The transcription initiation site was located 206bp upstream from the translation start site. Sequences of 2kb of the 5(') flanking region for 24 type 2 diabetic Japanese subjects were initially analyzed using PCR direct sequencing, and the regions including the identified polymorphisms were then examined. In 98 controls and 98 type 2 diabetic subjects, -1947T>C, -567G>A, -465G>T, -458T>C, and -1727_-1726insTCAATT were found. Only -465G>T and this insertion had more than 5% frequencies. Since a complete linkage disequilibrium existed between them, -465G>T was further analyzed, along with a previously identified +1389G>A in the coding region, in a total of 200 controls and 207 type 2 diabetic subjects. These allele frequencies were not significantly different between these two groups (controls vs. cases; -465G>T, 12.0% vs. 10.1%, P=0.435; +1389G>A, 30.3% vs. 33.3%, P=0.408). These genotype distributions were not significantly different between these two groups. The T/T genotype at -465 was rare although this frequency could be higher in type 2 diabetes (4/207 subjects) than controls (0/200 subjects). The linkage disequilibrium existed between -465G>T and +1389G>A, and the estimated haplotype frequencies defined by these SNPs were not significantly different between the cases and controls. Thus, the identified polymorphisms are unlikely to have major effects on susceptibility to Japanese type 2 diabetes.

3',5'-Cyclic-AMP Phosphodiesterases↗

Systematic search for single nucleotide polymorphisms in the FOXC2 gene: the absence of evidence for the association of three frequent single nucleotide polymorphisms and four common haplotypes with Japanese type 2 diabetes.

FOXC2, a forkhead/winged helix transcription factor, represents a promising candidate gene for type 2 diabetes since transgenic mice that specifically overexpress this gene in adipocytes are lean and insulin sensitive. To determine whether there are single nucleotide polymorphisms (SNPs) in this gene that are associated with type 2 diabetes, sequences of the coding and approximately 1 kb of 5' flanking regions in 24 Japanese type 2 diabetic subjects were initially analyzed using PCR direct sequencing, and the regions containing the identified polymorphisms were then examined. In 200 control subjects, three frequent SNPs were found (g. -512C>T [32.3%] and -350G>T [13.0%] in the 5' flanking region and +1548C>T [10.0%] in the 3' flanking region). Linkage disequilibria were found between all three pairs of these SNPs. Of the eight possible haplotypes defined by these SNPs, only four were found. When the frequencies of these SNPs and the four common haplotypes between 195 type 2 diabetic and 200 control subjects were compared, no association was evident. The +898C>T (Pro300Ser), +907C>A (Leu303Met), 1167_1169delCCA (389delHis), and +1251C>A (Ala417Ala) identified in the coding region were rare, although +907C>A could be higher in type 2 diabetic subjects (1.5%) than in control subjects (0.3%). Thus, the SNPs identified in the FOXC2 gene are unlikely to have major effects on susceptibility to Japanese type 2 diabetes.

Age of Onset↗

Inhibitory effects of cilnidipine on peripheral and brain N-type Ca2+ channels expressed in BHK cells.

We investigated differences in electrophysiological characteristics between peripheral and central N-type Ca(2+) channels, containing alpha(1B-a) and a(1B-c), respectively. In addition, we examined the inhibitory effects of cilnidipine, a dihydropyridine (DHP) derivative, on both channels. Both alpha(1B) subunits were transiently expressed in BHK cells, and then analyzed using the whole-cell patch-clamp technique. The current-voltage relationship showed that alpha(1B-c) currents were activated at more negative potentials than alpha(1B-a) currents. The voltage-dependent steady-state inactivation and activation showed that the V(1/2) values for inactivation and activation of alpha(1B-c) (-88.5+/-1.3 and -33.2+/-1.3 mV) were both significantly more negative than those for alpha(1B-a) (-83.3+/-1.3 and -27.9+/-2.3 mV). Despite the different electrophysiological characteristics of these two N-type channels, cilnidipine blocked both with similar potency within the range 0.1 to 10 microM. Furthermore, cilnidipine had no effect on the I-V relationships or the steady-state inactivation curves. Our data indicate that the spliced positions of alpha(1B-a) and a(1B-c) may affect not only their voltage-sensing abilities but also the kinetics of channel activation and inactivation. The data also suggest that cilnidipine binds to sites independent of those controlling voltage-sensing and channel kinetics in these alpha(1B) subunits.

Animals↗

Systematic search for single nucleotide polymorphisms in the resistin gene: the absence of evidence for the association of three identified single nucleotide polymorphisms with Japanese type 2 diabetes.

Resistin is a novel polypeptide specifically secreted from adipocytes, and its serum levels are increased in obese diabetic mice. Resistin antagonizes insulin and could account for insulin resistance. To determine whether there are single nucleotide polymorphisms (SNPs) in the resistin gene associated with type 2 diabetes, sequences for 24 Japanese type 2 diabetic patients were initially analyzed using PCR direct sequencing. Three SNPs were found in the introns, but none were present in the coding regions. The allele frequencies of genomic -167C>T, +157C>T, and +299G>A in 99 Japanese control subjects were determined to be 3.5, 6.6, and 39.4%, respectively. In each pair of these SNPs, linkage disequilibria were found between either -167C>T and +299G>A or +157C>T and +299G>A. A linkage disequilibrium was also detected among -167C>T, +157C>T, and +299G>A, and only four of the eight possible haplotypes defined by these SNPs were found. A comparison of the frequencies of these SNPs and haplotypes between 99 type 2 diabetes and 99 control subjects revealed no evidence for any association. These identified SNPs, which were in linkage disequilibrium, represent potentially useful tools for searching for their association with specific phenotypes of diabetes.

Adult↗

Clinical, autoimmune, and genetic characteristics of adult-onset diabetic patients with GAD autoantibodies in Japan (Ehime Study).

OBJECTIVE: To characterize the clinical, autoimmune, and genetic features in Japanese adult-onset diabetic patients with GAD autoantibodies. RESEARCH DESIGN AND METHODS: GAD autoantibodies (GADab) were screened in 4,980 diabetic patients with age of onset >20 years in the hospital-based Ehime Study, and the GADab-positive (GADab(+)) patients were then divided into two groups according to their insulin secretion and compared with nondiabetic subjects. The insulin-deficient state was defined as <0.33 nmol/l serum C-peptide (CPR) at 2 h postprandial or 6 min after a 1-mg glucagon load. RESULTS: GADab was detected in 188 (3.8%) of the 4,980 diabetic patients tested. Of these patients, 72 (38.3%) were classified as insulin deficient, 97 (51.6%) were classified as non-insulin deficient, and 19 (10.1%) were unclassified. The GADab(+) insulin-deficient patients were characterized by young age at onset of diabetes, low BMI, low maximum BMI, and high levels of HbA(1c). The prevalence of IA-2 autoantibodies and thyrogastric autoantibodies in the GADab(+) insulin-deficient patients were significantly higher than those in the GADab(+) non-insulin-deficient patients (P < 0.05). GADab(+) patients with insulin deficiency had increased frequencies of HLA DRB1*0405-DQB1*0401, *0802-*0302, and *0901-*0303 haplotypes, whereas the frequency of only HLA DRB1*0405-DQB1*0401 was increased in the case of GADab(+) non-insulin-deficient patients. Of note is the fact that the GADab(+) non-insulin-deficient group did not differ from healthy control subjects with respect to type 1 diabetes protective haplotype HLA DRB1*1502-DQB1*0601. A total of 13% of the GADab(+) patients with diabetes had genotypes comprising the DRB1*1501-DQB1*0602 or *1502-*0601 and were characterized by old age at onset of diabetes, high BMI, resistance to the insulin-deficient state, low titer of GADab, and low frequency of other organ-specific autoantibodies. CONCLUSIONS: We conclude that GADab(+) non-insulin-deficient patients differ from GADab(+) patients with insulin deficiency with respect to clinical characteristics, humoral autoimmunity to other organ-specific autoantibodies, as well as HLA class II genes.

Adult↗

[A patient with metastatic gastrointestinal stromal tumor who responded to STI571].

We report a case of gastrointestinal stromal tumor (GIST) with multiple hepatic metastases that responded to tyrosine kinase inhibitor STI571. A 30-year-old woman underwent total gastrectomy on July 10, 1998, with a diagnosis of submucosal tumor of the stomach. Pathological analysis of the primary lesion revealed strong expression of c-kit, and it was diagnosed as GIST. The patient underwent tumor excision due to peritoneal recurrence on May 1, 2000 and November 13, 2000. On August 8, 2001, multiple liver metastases were detected by abdominal CAT scan. Treatment with STI571 at a dose of 400 mg/day for 28 days was initiated on September 14, 2000. CAT scan showed rapid tumor shrinkage after 3 weeks of treatment (reduction rate of 56%) and the response continued after 7 weeks of treatment (reduction rate of 71%). Thus, we evaluated the response as PR. Leukocytopenia, edema, diarrhea and nausea were observed; however, all toxicities were mild and tolerable. This case suggests the efficacy of STI571 for metastatic GIST.

Adult↗

Multislice CT angiography through an implantable catheter and port system: early experience in detection of vascular complications during hepatic arterial infusion chemotherapy.

OBJECTIVE: The purpose of this study was to evaluate the use of multislice CT in the evaluation of vascular patency in patients during hepatic arterial infusion chemotherapy of liver tumors. MATERIALS AND METHODS: Thirty-three patients were prospectively examined by CT angiography through the indwelling catheter and port system. Visibility of hepatic arteries and vascular patency were graded 0 to 3 and were compared with digital subtraction angiography (DSA). RESULTS: Average visualization scores of CT angiography and DSA were 1.7 and 2.5, respectively, in common hepatic artery (CHA) and proper hepatic artery (PHA), 2.5 and 2.3 in right hepatic artery (RHA), 2.6 and 2.6 in left hepatic artery (LHA), 2.3 and 2.2 in segmental RHA, and 2.1 and 2.0 in segmental LHA. Stenoses were found in proximal hepatic arteries in 9 on CT angiography and 13 on DSA. Stenoses were found in branches of the hepatic artery in 21 on CT angiography and 16 on DSA. CONCLUSION: The authors' results indicate that multislice CT angiography of the hepatic arteries is equivalent to DSA and may demonstrate vascular complications of hepatic arterial infusion chemotherapy.

Adult↗