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Biomedical subjects

M Hori

Publications and source records attributed to M Hori.

At least 217 records · Page 12Linked to original sources
PubMed2000

Single breath-hold T2-weighted MR imaging of the liver: value of single-shot fast spin-echo and multishot spin-echo echoplanar imaging.

OBJECTIVE: The objective of our study was to evaluate the efficacy of single breath-hold T2-weighted MR imaging for detection of focal hepatic lesions. MATERIALS AND METHODS: T2-weighted MR images were retrospectively reviewed from 51 patients with 85 solid and 59 nonsolid lesions using the following four sequences: conventional spin-echo, respiratory-triggered fast spin-echo, single-shot fast spin-echo, and multishot spin-echo echoplanar imaging. Images were reviewed on a hepatic segment-by-segment basis; T2-weighted images of a total of 408 hepatic segments were reviewed separately and independently for solid and nonsolid lesions by four radiologists. Quantitative, qualitative, and receiver operating characteristic analyses were performed. RESULTS: For solid lesions, no significant differences were seen among the lesion-to-liver contrast-to-noise ratios with the four sequences. In terms of solid lesion detection, no significant difference was seen between the diagnostic accuracy of multishot spin-echo echoplanar (Az = 0.90) and respiratory-triggered fast spin-echo (Az = 0.91) imaging, which showed the best performance of the four sequences. For nonsolid lesion detection, respiratory-triggered fast spin-echo and single-shot fast spin-echo imaging were judged the best (Az = 0.94). CONCLUSION: Breath-hold single-shot fast spin-echo and multishot spin-echo echoplanar sequences can be substituted for conventional spin-echo and respiratory-triggered fast spin-echo T2-weighted sequences.

Adult↗
PubMed2000

Carotid intima-media thickness in Japanese type 2 diabetic subjects: predictors of progression and relationship with incident coronary heart disease.

OBJECTIVE: To examine carotid intima-media thickness (IMT), predictors of its progression, and its relationship with incident coronary heart disease (CHD) in type 2 diabetic Japanese patients. RESEARCH DESIGN AND METHODS: Carotid IMT of 287 subjects with type 2 diabetes (mean age 61.6 years) without CHD or cerebrovascular disease was examined at baseline and after a mean follow-up of 3.1 years. RESULTS: The annual progression of IMT (means +/- SEM) was 0.04+/-0.004 mm/year. Stepwise multivariate analysis demonstrated that independent risk factors for progress of IMT were the initial IMT (P<0.001), the average HbA1c level (P<0.001), and age (P = 0.001). Both the initial IMT (odds ratio [OR] 4.9, 95% CI 1.7-14.1) and a low average HDL cholesterol (OR 0.2, 0.1-0.8) were identified as predictors of incident nonfatal CHD (angina pectoris or nonfatal myocardial infarction; 3-year incidence 10.1%) after adjusting for age, sex, average HbA1c, and other risk factors. CONCLUSIONS: The predictors of the progression of carotid IMT in Japanese type 2 diabetic subjects were its baseline thickness and the average HbA1c during the follow-up. Baseline carotid IMT and low HDL cholesterol predicted the incidence of nonfatal CHD.

Asian People↗
PubMed2000

Chronic myelomonocytic leukemia derived from a possible common progenitor of monocytes and natural killer cells.

The neural cell adhesion molecule, CD56, is expressed on acute myelogenous leukemia (AML) cells in 17-20% of the patients. However, the clinical and biological significance of its expression in AML has not been well analyzed from the standpoint of CD56 expression and its association with differentiation to a natural killer (NK) cell lineage. Here we present a 78-year-old patient with chronic myelomonocytic leukemia (CMML) whose leukemic cells had features of both monocytes and NK cells. We demonstrated that the leukemic cells were positive for CD4, CD56 and interleukin-2 (IL-2) receptor beta chain (CD112) in addition to myelomonocytic markers such as CD33, CD11b and CD11c. These leukemic cells proliferated well in vitro in response to 10-100 U/ml of IL-2, and functionally showed significant cytotoxicity against K562 target cells in a 4-hour (51) Cr release assay. All the above data indicate that these cells possessed at least some of the biological features of NK cells. Accordingly, we speculate that the leukemic cells in this patient may have been derived from a possible common progenitor of monocytes and NK cells.

Aged↗
PubMed2000

QT dispersion is increased in diabetic patients with foot ulcer.

QT dispersion, a measure of inhomogenous ventricular repolarization, was measured in diabetic patients with foot ulcer. We recruited 75 patients with non insulin-dependent diabetes mellitus: patients with neuropathic ulcer (n=15, NU group), with ischemic ulcer (n=20, IU group), with previous myocardial infarction (n=20, MI group) and without any diabetic microangiopathies (n=20, DC group). We also studied normal control subjects (n=15, NC group). The interlead variability of rate corrected QT interval (QTc dispersion) was calculated. QTc interval in the MI group was significantly higher than that in the NC or DC but showed no difference in the NU and IU groups. QTc dispersion in the IU (54+/-15 msec) as well as MI (60+/-21 msec) group were significantly higher than the NC (36+/-18 msec) or DC group (39+/-14 msec). This may be due to complicated coronary artery disease in the IU group. Furthermore, QTc dispersion was also increased (49+/-14 msec) in the NU group in which cardiac autonomic nervous dysfunction was suggested. Patients with both types of diabetic ulcer demonstrated increased QT dispersion due to atherosclerosis or neurological disorder.

Aged↗
PubMed2000

ABC transporter genes, kasKLM, responsible for self-resistance of a kasugamycin producer strain.

We previously reported that a 7.6-kb DNA fragment from Streptomyces kasugaensis M338-M1, a kasugamycin (KSM) producer, included KSM acetyltransferase gene (kac338) and some other genes possibly involved in KSM biosynthesis. As an extension of that study, a 10-kb SacI-KpnI DNA fragment, located approximately 5-15-kb upstream of kac33, was cloned and a 4.2-kb SacI-EcoRI fragment therefrom was sequenced, revealing one incomplete (designated ORF J) and three complete open reading frames (designated kasK, kasL and kasM). The coding frames of kasK, L and M overlap one another with terminator/initiator ATGA sequence. RT-PCR analysis of a DNA region including kasKLM indicated the presence of one transcript that is long enough to span the three genes. The kasK gene potentially encodes an ATP-binding protein of the ATP-binding cassette (ABC) transporter superfamily. Homology search for the deduced KasK protein shows similarity to other ABC transporters involved in self-resistance of a mithramycin and possibly doxorubicin producer strain. The kasL and kasM genes encode different integral membrane proteins, both having six putative transmembrane helices. An expression plasmid for kasKLM (pTV-KLM) was constructed and these genes were expressed in E. coli JM 109, which had been sensitive to KSM. The transformant acquired resistance to KSM, suggesting that KasK, L and M proteins as a set in S. kasugaensis M338-M1 pump out KSM to protect the producer from its toxic metabolite.

ATP-Binding Cassette Transporters↗
PubMed2000

New triene-ansamycins, thiazinotrienomycins F and G and a diene-ansamycin, benzoxazomycin.

New triene-ansamycins designated thiazinotrienomycins F (TT-F) and G (TT-G) and a new diene-ansamycin, benzoxazomycin, were isolated from a culture broth of Streptomyces sp. MJ672-m3 and their structures were elucidated by spectroscopic analyses. The Mean Graphs of TT-G suggests that the tumor growth inhibitory activities are almost as strong as TT-B, in respect of GI50 and TGI against several human cancer cell lines.

Alanine↗
PubMed2000

[Intravenous contrast echocardiography].

Intravenous contrast echocardiography has become possible in Japan because of the release of the commercially available contrast agent, Levovist. Intravenous administration of Levovist satisfactorily stains the left ventricular cavity, which makes it possible to clearly delineate the endocardial border. Clear delineation of the endocardial border provides easy and accurate measurement of left ventricular dimension and wall thickness, and wall motion abnormalities can be easily and accurately judged, too. Another benefit of intravenous contrast echocardiography is the assessment of myocardial perfusion. Our preliminary experimental and clinical experiences showed the possibility of myocardial staining with intravenous contrast echocardiography. Impressive myocardial staining is obtainable with the combined use of intermittent and contrast harmonic power Doppler imaging. In order to obtain reproducible and clear myocardial contrast images, we have to pay attention to how to inject contrast and settings of ultrasound equipment, i.e., mechanical index, gain setting, depth of focus point, and pulse repetition frequency, artifacts. In the near future, a lot of issues should be standardized to make it possible to compare myocardial contrast echo studies.

Contrast Media↗
PubMed2000

[Animal models of cardiomyopathy].

Animal models of cardiomyopathy have been used in many studies for our understanding of the pathophysiology of this disease. Syrian hamster, BIO 14.6, one of the most widely used models of cardiomyopathy, was reported to be caused by large deletion in the exon 1 and the promoter region of the delta-sarcoglycan gene. Cardiac hypertrophy or heart failure has been induced in dogs, rabbits, rats and many other animals by various manipulations such as drugs, pressure and/or volume overload and chronic rapid pacing. Recently, transgenic or knockout mice were examined to investigate the pathogenesis and development of the disease. It is important to select appropriate models for the aim of the studies.

Animals↗
PubMed2000

Induction of cyclooxygenase-2 in rat gastric mucosa by rebamipide, a mucoprotective agent.

Recent studies indicate an expression of mitogen-inducible cyclooxygenase (COX-2) in gastric mucosa. Rebamipide, a mucoprotective agent enhances prostaglandin (PG) synthesis. The present study was designed to clarify the mechanism for rebamipide-induced mucosal protection. Male Sprague-Dawley rats were administered 5, 15, or 50 mg/kg/day rebamipide for 14 days. The expression of constitutive cyclooxygenase (COX-1) and COX-2 in gastric mucosa was determined using Western blot analysis. Another series of rats was used to examine 1) the levels of PGE(2) in stomach with and without pretreatment with a COX-2 inhibitor; 2) the protective action of rebamipide against gastric damage caused by 0.6 N HCl; and 3) the effects of a COX-2 inhibitor on rebamipide-induced gastric mucosal protection. COX-2 expression was enhanced, whereas COX-1 expression did not change significantly in the gastric mucosa of rats after treatment with rebamipide. The gastric mucosal PGE(2) was higher in the rebamipide groups than in the vehicle-treated group. Rebamipide also suppressed gastric damage induced by HCl in a dose-dependent manner. A COX-2 inhibitor blocked the rebamipide-induced increase in mucosal PGE(2), and mucosal protection induced by rebamipide. The results indicate that rebamipide induces COX-2 expression, increases PGE(2) levels, and enhances gastric mucosal defense in a COX-2-dependent manner. Thus, COX-2 has an important role in the effects of rebamipide on gastric mucosal protection.

Alanine↗
PubMed1999

Deficiency of intercellular adhesion molecule 1 fails to mitigate selective neuronal death after transient global ischemia.

Recent studies have shown a crucial role of intercellular adhesion molecule 1 (ICAM-1) in expansion of infarction after focal cerebral ischemia. The purpose of the present study was to assess whether ICAM-1 is involved in selective neuronal vulnerability and reactive gliosis after transient forebrain ischemia. ICAM-1 knockout mice and wild-type mice were subjected to transient forebrain ischemia for 5, 10 or 15 min, and the hippocampus and caudoputamen were examined 7 days later with conventional histological and immunohistochemical methods. Bilateral common carotid artery occlusion with less than 10% of baseline cortical microperfusion for 10 or 15 min resulted in ischemic neuronal damage in the hippocampus and caudoputamen. The frequency and the severity of neuronal damage were similar in wild-type and knockout mice. Proliferation of reactive astrocytes in the hippocampus was also similar in both types of mice. Therefore, it is highly unlikely that ICAM-1 plays a key role in delayed neuronal death after transient global ischemia or in astroglial responses after ischemic neuronal injury.

Animals↗
PubMed1999

Identification of oxidative stress-regulated genes in rat aortic smooth muscle cells by suppression subtractive hybridization.

A suppression subtractive hybridization technique was used to identify reactive oxygen species (ROS)-regulated genes in rat vascular smooth muscle cells. Three genes out of 89 clones, identified as fibronectin, p105 coactivator and ECA39, showed increased expression after treatment with H(2)O(2). The mRNA expressions of these three genes were induced in a time- and dose-dependent manner, independent of protein kinase C activation. Immunohistochemical staining showed that the p105 coactivator expression was markedly induced in the neointima of balloon-injured rat carotid arteries. These results suggest that ROS may play an important role in the development of atherosclerosis by regulating the gene expressions we identified in this study.

Animals↗
PubMed1999

Functional role of c-Src in gap junctions of the cardiomyopathic heart.

Given the essential role played by gap junctions in the coordination of cardiac muscle contraction, it is plausible that down-regulation of gap junctional conduction is in part responsible for the contractile dysfunction observed in hypertrophied and failing hearts. In the present study, we analyzed the expression and function of the gap junction protein, connexin43, in the ventricular myocardium of hereditary cardiomyopathic, Syrian BIO 14.6 hamsters. Immunoprecipitation and immunoblot analyses revealed that levels of tyrosine phosphorylated connexin43 were increased in BIO 14.6 hamsters at the late stage of congestive heart failure. Furthermore, the increased tyrosine phosphorylation was correlated with increased c-Src activity. The functional consequences of tyrosine phosphorylation of connexin43 in gap junction were assessed using transfected cells expressing constitutively active c-Src. It was found that constitutively active c-Src diminished propagation of Ca(2+) waves in HEK293 cells and reduced gap junctional conductance between pairs of cardiac myocytes. We, therefore, conclude that during the progression of cardiac dysfunction in the cardiomyopathic heart, gap junctional communication is reduced via c-Src-mediated tyrosine phosphorylation of connexin43.

Animals↗
PubMed1999

NF-kappaB subunit p65 binds to 53BP2 and inhibits cell death induced by 53BP2.

Nuclear factor kappaB (NF-kappaB) is a transcription factor that controls the expression of many cellular and viral genes. The p65 (RelA) subunit plays a critical role as a transcriptional activator and recent observations have highlighted its role in the control of apoptosis. Here we report that 53BP2, a protein previously identified by interaction with wild type p53 and Bcl-2, also binds to p65 in a yeast two-hybrid system. This specific interaction was confirmed by pull-down assay in vitro and by a mammalian two-hybrid assay in vivo. We observed that full-length 53BP2 fused to GFP had a punctate distribution in cytoplasm, predominantly in perinuclear region whereas the N-terminal 53BP2 localized in cytoplasm and C-terminal 53BP2 localized in the nucleus. Furthermore, we found that overexpression of GFP-53BP2 induced apoptosis in transiently transfected cells. Neither the N-terminal nor the C-terminal of 53BP2 fused to GFP induced cell death. Interestingly, co-transfection with a p65 expression plasmid significantly inhibited 53BP2-induced cell death. The previous findings that 53BP2 bound to p53 and Bcl-2 together with our present observations suggest that 53BP2 may play a central role in the regulation of apoptosis and cell growth.

Animals↗
PubMed1999

Delayed transfection of DNA after riboflavin mediated photosensitization increases G:C to C:G transversions of supF gene in Escherichia coli mutY strain.

We have previously reported that the majority of base substitution mutations of the Escherichia coli supF gene induced by riboflavin mediated photosensitization were G:C to C:G changes, in addition to G:C to T:A changes which were probably caused by 8-hydroxyguanine (oh(8)Gua), in wild type and mutM mutator mutant strains. This implies that lesions other than oh(8)Gua are produced by riboflavin-photosensitization. G:C to C:G base substitutions have been found in the mutations induced by ionizing radiation and reactive oxygen species, as well as spontaneous mutation. To characterize the G:C to C:G mutation, riboflavin- photosensitized plasmid DNA carrying the supF gene was left at room temperature for 5 h in the dark before transfection. The delayed transfection gave a mutational spectrum different from that for immediate transfection. G:C to C:G transversions significantly increased in mutY mutator strain, in which the transversion was not detected in the immediate transfection. Lesions causing G:C to C:G changes increased during 5-h holding after photosensitization and MutY protein presumably takes part in this type of base change mutation.

Base Sequence↗