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Biomedical subjects

S Kawano

Publications and source records attributed to S Kawano.

At least 127 records · Page 7Linked to original sources

Detection of varicella-zoster virus DNA in peripheral mononuclear cells from patients with Ramsay Hunt syndrome or zoster sine herpete.

On the basis of alterations in varicella-zoster virus (VZV) antibody titers, it appears that Bell's palsy in some patients could be associated with VZV reactivation, that is, zoster sine herpete. To obtain stronger evidence of this association, polymerase chain reaction (PCR) was used to detect VZV DNA in auricular lesions or peripheral blood mononuclear cells (PBMCs) from Bell's palsy or Ramsay Hunt syndrome patients. VZV DNA was detected in the auricular lesions of Ramsay Hunt syndrome, in PBMCs from 2 Ramsay Hunt syndrome patients, and in 4 of 17 samples from 16 Bell's palsy patients. Three of these four positive patients were thought to have zoster sine herpete because of hearing difficulty, vertigo, and pain. VZV IgM antibodies were positive in 1 of the 2 patients with Ramsay Hunt syndrome, and in 2 of the 17 samples from the Bell's palsy patients. VZV IgG antibody titers during the acute phase were significantly higher in the patients positive for the PCR or VZV IgM antibody than in those negative for them. These findings provide evidence that Bell's palsy in some patients could be associated with VZV reactivation.

Adolescent↗

Increase of mast cells in the liver and lung may be associated with but not a cause of fibrosis: demonstration using mast cell-deficient Ws/Ws rats.

Tissue fibrosis is frequently associated with an increase of mast cells, and mast cells are regarded as playing a role in the induction of tissue fibrosis. We attempted to examine whether mast cells influenced the induction of fibrosis using Ws/Ws mast cell-deficient rats. The mast cell deficiency of Ws/Ws rats is due to a 12-base pair deletion of the c-kit gene. The activity of c-kit receptor tyrosine kinase is remarkably reduced in Ws/Ws rats. Liver fibrosis was induced by the repeated injections of pig serum, and lung fibrosis was induced by the instillation of bleomycin. Marked fibrosis in the liver and lung did occur in the Ws/Ws rats, and the magnitude of fibrosis was more severe in Ws/Ws rats than in control normal (+/+) rats. The mast cell increase was observed in the liver of +/+ and Ws/Ws rats and in the lung of +/+ rats. However, the number of mast cells in the liver of treated Ws/Ws rats with marked fibrosis was comparable to that observed in the liver of nontreated +/+ rats without fibrosis. Histamine content increased in the liver and lung of +/+ rats after the treatment, but it remained in low levels even after the treatment in Ws/Ws rats. Mast cells and histamine did not appear to play important roles in the induction of fibrosis. Thus, an increase in mast cell number and histamine content may be associated with but not a cause of fibrosis.

Animals↗

[Simultaneous cholecystectomy and CABG for acute cholecystitis and post-infarction angina].

A 71-year-old man was admitted to our hospital with massive GI bleeding and followed by acute myocardial infarction. Severe three vessel coronary artery disease with poor left ventricular performance (EF: 40%) was demonstrated by coronary angiography. He was referred for CABG. He had also cholecystitis, which needed surgical treatment simultaneously. Combined CABG and cholecystectomy were performed without using gastroepiploic artery as a bypass graft, and through separate median sternotomy and through right upper transrectal laparotomy. Postoperative course was uneventful. This combined procedure is beneficial for the patients with acute cholecystitis and unstable angina.

Acute Disease↗

Cyclooxygenase-2 expression in human colon cancer cells increases metastatic potential.

Recent epidemiologic studies have shown a 40-50% reduction in mortality from colorectal cancer in individuals who take nonsteroidal antiinflammatory drugs on a regular basis compared with those not taking these agents. One property shared by all of these drugs is their ability to inhibit cyclooxygenase (COX), a key enzyme in the conversion of arachidonic acid to prostaglandins. Two isoforms of COX have been characterized, COX-1 and COX-2. COX-2 is expressed at high levels in intestinal tumors in humans and rodents. Human colon cancer cells (Caco-2) were permanently transfected with a COX-2 expression vector or the identical vector lacking the COX-2 insert. The Caco-2 cells, which constitutively expressed COX-2, acquired increased invasiveness compared with the parental Caco-2 cells or the vector transfected control cells. Biochemical changes associated with this phenotypic change included activation of metalloproteinase-2 and increased RNA levels for the membrane-type metalloproteinase. Increased invasiveness and prostaglandin production were reversed by treatment with sulindac sulfide, a known COX inhibitor. These studies demonstrate that constitutive expression of COX-2 can lead to phenotypic changes that alter the metastatic potential of colorectal cancer cells.

3T3 Cells↗

No editing of mitochondrial plasmid transcripts in mitochondria of Physarum that have an RNA-editing system.

Two types of RNA editing have been reported in the mitochondria of Physarum; extensive insertions of nucleotides and single-base substitutions. In the Ng strain of P. polycephalum and its derivatives, mitochondria have a specific plasmid (mF) that promotes fusion of mitochondria. We examined the editing of transcripts derived from the mF plasmid. For analysis, we selected three regions of the plasmid, including a DNA fragment that corresponded to missing conserved domains of the RNA polymerase. In contrast to the mitochondrial DNA (mtDNA), no RNA editing of the transcripts of the mF plasmid was detected. Our results suggest that the mechanism of transcription of the mitochondrial plasmid is independent of that of mtDNA, indicating that the plasmid has a different evolutionary origin from the mtDNA.

Animals↗

Ten-year follow-up study on the relation between the development of non-insulin-dependent diabetes mellitus and occupation.

To investigate the relation between occupation and the development of non-insulin-dependent diabetes mellitus (NIDDM), we undertook a 10-year follow-up survey of male employees of a zipper and aluminum sash factory in Japan. Of 1,218 employees we followed 1,087 subjects. We classified the subjects into five occupations: managers, technical workers, clerical workers, workers in transport, and laborers. NIDDM incidence was 3.1% for 10 years. The age-adjusted incidence of the workers in transport was the highest and that in laborers was the lowest. We used a multiple logistic analysis for adjustment with baseline characteristics such as age, BMI, fasting plasma glucose, and family history of diabetes mellitus. Adjusted relative risk of the workers in transport compared with the laborers was significantly high (3.95). Our work suggests that occupation is related to the development of NIDDM.

Adult↗

Binding cells of 125I-iodoamphetamine in rat liver.

We recently reported that transrectal or intestinal portal scintigraphy with 123I-iodoamphetamine (IMP) could be a useful method for the non-invasive and quantitative evaluation of the portosystemic shunt in portal hypertension, but what cells in the liver trap IMP has not been clarified. This study was aimed at elucidating whether IMP was extracted by parenchymal cells, sinusoidal endothelial cells, Kupffer cells or fat storing cells. Each type of liver cell was isolated from rats and cultured. The cells were incubated with 125I-IMP and the radioactivity of the lysate was determined. Nonspecific binding was assessed in the presence of an excess of unlabeled IMP, and specific binding was determined by subtracting the nonspecific from total binding. Specific binding observed in parenchymal cells, endothelial cells and Kupffer cells was 70.2 +/- 0.4, 4.2 +/- 1.4 and 2.3 +/- 0.8 pmol/well, respectively, but no specific binding was observed in fat storing cells. The binding in parenchymal cells was much higher than that in endothelial cells or Kupffer cells (p < 0.005). In addition, the binding to parenchymal cells reached equilibrium within 20 min and was not saturable over the concentration range tested (0.5-10 microM). These findings indicate that IMP is mostly extracted by parenchymal cells in the liver.

Amphetamines↗

Noninvasive identification of left ventricular involvements in arrhythmogenic right ventricular dysplasia: comparison of 123I-MIBG, 201TlCl, magnetic resonance imaging and ultrafast computed tomography.

We examined the feasibility of myocardial 123I-MIBG, 201TlCl, magnetic resonance imaging (MRI) and ultrafast computed tomography (UFCT) for the early detection of left ventricular involvements in 15 patients with arrhythmogenic right ventricular dysplasia (ARVD). Radionuclide ventriculography (RNV) and myocardial imaging with 123I-MIBG, 201TlCl, MRI and UFCT were performed in all 15 patients and in 10 normal subjects. The patients' scans were visually interpreted by two nuclear medicine physicians taking into consideration the extent score (ES) and severity score (SS) calculated by using the bull's-eye view in relation to normal data derived from the normal subjects. The left ventricular ejection fraction (LVEF) was measured by RNV. Fourteen (93%) patients showed regional 123I-MIBG defects, while 12 (80%) patients showed regional 201TlCl defects. The ES and SS were higher in 123I-MIBG than 201TlCl (ES: 31.5 +/- 18.5 vs. 17.5 +/- 18.2, p < 0.01, SS: 34.8 +/- 42.2 vs. 16.9 +/- 37.5, p < 0.01). Abnormal UFCT and MRI findings suggesting fatty involvements of the LV myocardium were demonstrated in 7 patients (Group B), while 7 patients showed regional 123I-MIBG defects without abnormal UFCT and MRI findings (Group A). 123I-MIBG was significantly more sensitive than UFCT and MRI (p < 0.05), although one patient, an exception, showed abnormal UFCT findings for the apex of the LV myocardium without abnormal 123I-MIBG and MRI findings. The LVEF, as a measure of LV systolic function, was better preserved in Group A than in Group B (59.3 +/- 3.6 vs. 45.8 +/- 5.8, p < 0.01). The present findings indicated that myocardial imaging with 123I-MIBG sensitively detects myocardial damage in patients with ARVD in the early stage when cardiac systolic function is still preserved.

3-Iodobenzylguanidine↗

Precordial leads QRST time integrals for evaluation of right ventricular overload in children with congenital heart diseases.

It was previously shown that body surface QRST isointegral maps of the anterior chest were abnormal in patients with right ventricular overload and that the abnormalities varied with hemodynamic status. The QRST isointegral maps were first characterized by using a departure index map for normal controls. The study group consisted of 14 patients with pulmonary stenosis (PS), 20 with tetralogy of Fallot, (TOF) and 43 with atrial septal defect (ASD). The QRST isointegral maps of these three groups were compared with the data on 23 to 65 age-matched normal children. In mean departure index maps, the patients with right ventricular pressure overload (PS or TOF) showed an increase in departure index on the anterior midchest, while those of right ventricular volume overload (ASD) showed two maxima on the anterior and left lateral chest, with a trough-like negative area between them. Since the abnormal findings were seen on the anterior chest, we evaluated the diagnostic usefulness of QRST time integral values for precordial leads of the routine electrocardiogram (ECG) in a second part of this study. The precordial QRST time integral values from 9 patients with PS and 11 with TOF (0-2 years of age, mean 1.1 years) and 22 ASD patients (6-15 years, mean 10.1 years) were compared with those of the age-matched control children. The QRST time integral values of the precordial leads in right ventricular pressure overload were significantly increased in the right precordial leads (V1, V2). In right ventricular volume overload, the QRST time integral values of the V1, V2, V4, and V6 leads demonstrated a significant deviation from those of the control group. Therefore, a discrimination formula was constructed by using the values of these leads, and the criteria derived from this formula revealed good (98%) diagnostic accuracy. In detection of right ventricular overload, the QRST time integral values of the precordial lead ECG, if confirmed in a larger data set, may be useful as a simple screening method.

Adolescent↗

Immunocytochemical distribution of Ca(2+)-independent protein kinase C subtypes (delta, epsilon, and zeta) in regenerating axonal growth cones of rat peripheral nerve.

In the peripheral nerve, regenerating axonal sprouts usually emanate at nodes of Ranvier, and extend as growth cones along the inner surface of Schwann cells and/or through Schwann cell columns in the distal nerve segment. In order to elucidate the significance of Ca(2+)-independent protein kinase C in nerve regeneration, localizations of delta, epsilon and zeta subtypes were examined immunocytochemically in sprouts and growth cones of regenerating axons, as well as in normal intact nerves in the rat sciatic nerve. In normal nerves, intense immunoreactivities of delta, epsilon and zeta subtypes were present in axons of both myelinated and unmyelinated fibres. Subcellularly, the distribution of these subtypes in the axoplasm was patchy, and discontinuous in the axolemma and subaxolemmal peripheral zones of myelinated nerves. Some thin myelinated axons showed no immunoreactivity for epsilon subtype. Schwann cells of both myelinated and unmyelinated fibres had moderate immunoreactivities for each subtype. In areas of nerve regeneration, axonal sprouts at nodes of Ranvier, and growth cones extending along Schwann cell basal laminae, had intense immunoreactivities for delta, epsilon and zeta subtypes which are distributed diffusely throughout the axoplasm, and on the entire axolemma. In the sprouts, immunoreactivity for epsilon subtype was strong on the axolemma, but weak or almost absent in the axoplasm. These data, together with those of our previous study, indicate that Ca(2+)-independent protein kinase C subtypes (delta, epsilon and zeta) have basically the same distribution patterns as those of Ca(2+)-dependent subtypes in sprouts and growth cones of regenerating axons, as well as in normal intact axons; albeit epsilon subtype is somewhat different in distribution and intensity from delta and zeta subtypes. It is suggested that Ca(2+)-independent subtypes are involved in maintaining growth cone activities along with the Ca(2+)-dependent subtypes.

Amino Acid Sequence↗

Plasma and gastric mucosal endothelin-1 concentrations in patients with peptic ulcer.

Peptic ulcer in the human stomach causes localized destruction of the gastric wall, which may be associated with focal vascular insufficiency. Endothelin-1, an extremely potent vasoconstrictor peptide, modulates regional blood flow in the vasculature of stomach, suggesting a role for endothelin-1 in peptic ulcer. We examined the relationship among endogenous plasma and mucosal endothelin-1 concentrations and the severity and area of ulcer in 19 patients with gastric ulcers and eight healthy adults. Endothelin-1 concentrations were measured by enzyme immunoassay in plasma and gastric mucosal specimens from ulcer margins, corpus, and antrum. The severity and area of ulcer were assessed endoscopically. Plasma endothelin-1 concentrations in active (P < 0.01 compared with normal) and healing (P < 0.05) stages of ulcer were significantly greater than those in normal subjects. Plasma endothelin-1 concentrations, but not mucosal endothelin-1 concentrations in the ulcer margin, were significantly associated with the severity of the ulcer. There was a significant positive correlation between plasma endothelin-1 concentrations and area of ulcer (r = 0.70, P < 0.01). In conclusion, locally increased endothelin-1 may be an important mediator contributing to the pathogenesis of peptic ulcer.

Adult↗

Genetic analysis of 8;21 chromosomal translocation without AML1 gene involvement in MDS-AML.

We have investigated a case of acute myelocytic leukaemia derived from myelodysplastic syndrome (MDS-AML) with an 8;21 translocation. In this case the AML1/MTG8 (ETO) fusion transcript was not detected by reverse transcriptase-polymerase chain reaction (RT-PCR), and the rearrangement of the AML1 gene locus was not detected by Southern blot nor pulse field gel electrophoresis (PFGE) analyses using specific probes for the AML1 gene. Fluorescence in-situ hybridization (FISH) study using cosmid probes for 21q22 revealed that the breakpoint of 21q22 was telomeric to the AML1 gene locus and centromeric from D21S259, 351, 3421 loci. This is the first report concerning the t(8;21)(q22;q22) carrying AMLs (de novo AML, MDS-AML and therapy-related AML) to show that the breakpoint at 21q22 is located outside the AML1 gene locus. It is also noteworthy that the cell-surface antigen expression pattern of the bone marrow (BM) blasts was changed from CD7+ CD2+ CD13+ CD33+ CD19- CD11b+ CD14+ CD36+ to CD7- CD2- CD13+ CD19+ CD11b- CD14- CD33+ CD34+ CD36- CD56+ during leukaemic progression, and the pattern in leukaemic phase was similar to the characteristic phenotype of de novo AML cases with t(8;21), when the AML1/MTG8 fusion transcripts are always detected by RT-PCR.

Blotting, Southern↗

Expression of the cyclooxygenase-2 gene in gastric epithelium.

This study examined the mRNA level of cyclooxygenase-2 (cox-2) in a rat gastric mucosal cell line after growth stimulation in vitro and in rat gastric mucosa before and after acid-induced injury in vivo. RGMI cells were stimulated with fetal calf serum in the in vitro study. Thereafter, the cox-2 mRNA level was examined by Northern analysis. Effects of NS-398, a specific inhibitor of cox-2, and indomethacin on prostaglandin production and cell proliferation were examined in RGM1 cells. In the in vivo study, rats were given 1 ml of 0.6 N hydrochloric acid into the stomach. The level of cox-2 mRNA was examined in rat gastric mucosa after acid administration. Cox-2 mRNA increased 20-60 min after growth stimulation in RGM1 cells. Both NS-398 and indomethacin suppressed prostaglandin production and cell proliferation after growth stimulation. Expression of cox-2 mRNA was observed 40 and 60 min after administration of 0.6 N HCl. Gastric lesions developed within 60 min after HCl administration and healed significantly within 48 h. The present study shows the expression of cox-2 in gastric epithelial cells in vitro and in gastric mucosa after injury in vivo. The results also suggest that cox-2 is involved in de novo synthesis of prostaglandins and cell proliferation in gastric epithelium.

Animals↗

Helicobacter pylori and gastric carcinogenesis.

This article consists of three independent studies regarding Helicobacter pylori-related gastric carcinogenesis. Ammonia, a Helicobacter product, promoted chemically induced gastric carcinogenesis in animals. Moreover, an extract of Helicobacter stimulated inflammatory production of nitric oxide (NO), a potent mutagen that causes G:C-->A:T transition. Meta-analysis of recent studies demonstrated that G:C-->A:T transition is one of the most common mutations in the p53 tumor suppressor gene in early phases of human gastric carcinogenesis. Therefore, bacterial factors such as ammonia and host factors, including inflammatory NO production, might play important roles in H. pylori-induced gastric carcinogenesis.

Ammonia↗