Biomedical subjects

T Murakami

Publications and source records attributed to T Murakami.

At least 433 records · Page 24Linked to original sources

PubMed1999

Involvement of gonadal steroid hormone disturbance in altered prolactin receptor gene expression in the liver of diabetic mice.

The levels of mRNA for long and three short forms of prolactin receptor (PRLR) were examined in the livers of normal (db+/db-) and insulin-resistant diabetic (db+/db+) mice to assess the role of gonadal steroid hormones in the regulation of PRLR gene expression in diabetes mellitus. In females, plasma levels of testosterone in diabetic mice were higher, and those of 17beta-estradiol were lower when compared with levels in normal mice. By contrast, diabetic male mice had lower plasma levels of testosterone than normal males and showed no significant difference in the low circulating level of 17beta-estradiol compared with normal males. The short 3 form of PRLR (PRLR3) mRNA was the most abundant in the liver of both normal and diabetic mice. In addition, the level of PRLR3 mRNA in normal females was 8-fold higher than in normal males. The level of PRLR3 mRNA in diabetic females was approximately a quarter lower than in normal females, whereas the level of PRLR3 mRNA in diabetic males was approximately 2-fold higher than in normal males. During postnatal development, the level of PRLR3 mRNA increased during puberty in normal females, while the level in diabetic females decreased to a nadir at 7 weeks of age followed by a progressive rise. On the other hand, the levels of PRLR3 mRNA in both normal and diabetic males decreased gradually during 5 to 14 weeks of age. Testosterone treatment of diabetic males and females resulted in a 49.1 and 49.8% decrease of PRLR3 mRNA respectively. 17beta-Estradiol treatment slightly (18%) increased levels of PRLR3 mRNA in diabetic males. These results suggest that the hepatic level of PRLR mRNA is regulated by the inhibitory effect of testosterone and the stimulatory effect of estrogen in both normal and diabetic mice.

Animals↗

PubMed1999

Perineuronal nets of proteoglycans in the adult mouse brain are digested by collagenase.

As our previous study has indicated, perineuronal proteoglycans in the adult mouse brain are associated with some collagenous molecules which can be stained with Gömöri's ammoniacal silver and are resistant to hyaluronidase digestion. The present study demonstrated that these molecules are thoroughly digested with collagenase, and suggests that they represent a hyaluronic acid-binding domain of the ligand proteoglycans connecting the perineuronal proteoglycans and nerve cell surface glycoproteins.

Animals↗

PubMed1999

The extracellular matrix in the mouse brain: its reactions to endo-alpha-N-acetylgalactosaminidase and certain other enzymes.

As our previous studies have indicated, the cingulate cortex of the adult mouse brain contains many neurons with rich cell surface glycoproteins which are linked by collagenous ligands to perineuronal proteoglycans. The present study demonstrated that exclusive incubation with endo-alpha-N-acetylgalactosaminidase abolished the lectin Vicia villosa or Wisteria floribunda agglutinin (VVA or WFA) labeling of the nerve cell surface glycoproteins, while it neither interfered with the cationic iron colloid or aldehyde fuchsin stainings of the perineuronal proteoglycans nor abolished the Gömöri's ammoniacal silver impregnation of the collagenous ligands. Double incubations with endo-alpha-N-acetylgalactosaminidase and collagenase did not eliminate the lectin VVA or WFA labeling of the nerve cell surface glycoproteins, though they did eliminate the cationic iron colloid and aldehyde fuchsin stainings of the perineuronal proteoglycans as well as the Gömöri's ammoniacal silver impregnation of the collagenous ligands. Triple incubations with endo-alpha-N-acetylgalactosaminidase, collagenase, and endo-alpha-N-acetylgalactosaminidase abolished the lectin VVA or WFA labeling of the nerve cell surface glycoproteins, and also eliminated the cationic iron colloid and aldehyde fuchsin stainings of the perineuronal proteoglycans and the Gömöri's ammoniacal silver impregnation of the collagenous ligands. These findings indicate that: the nerve cell surface glycoproteins or their terminal N-acetylgalactosamines are digested by endo-alpha-N-acetylgalactosaminidase; these galactosamines associated with the collagenous ligands or perineuronal proteoglycans are not digested by endo-alpha-N-acetylgalactosaminidase; and the terminal N-acetylgalactosamines newly exposed by collagenase incubation are digested by this galactosaminidase. It was further demonstrated that hyaluronidase incubation neither digests the collagenous ligands nor revives the lectin VVA or WFA labeling of the nerve cell surface proteoglycans.

Acetylgalactosamine↗

PubMed1999

Cytoplasmic delayed neuronal death in the myenteric plexus of the rat small intestine after ischemia.

The present study demonstrates light and electron microscopic changes in neurons in the myenteric plexus of the rat ileum following four-hour ischemia. Macroscopically, an intestinal constriction occurred at the damaged portion at three weeks after ischemia; the segment oral to the constriction markedly swelled at four weeks. In light microscopy, at three weeks after ischemia, the myenteric neurons appeared spongy or foamy, containing many vacuoles in their somatic cytoplasm. At four weeks, the neuronal cytoplasm and nerve fiber bundles had disintegrated to form vacant spaces in the myenteric plexus. The neuronal nucleus of the damaged plexus did not show positive nick-end labeling. In electron microscopy, neuronal cytoplasm revealed degenerative signs already at one week after ischemia: a distended endoplasmic reticulum and swollen mitochondria with fragmentary cristae. The nerve fibers also showed destruction of the mitochondria, and degenerative changes in the postsynaptic sites appeared earlier than the presynaptic terminals. The results suggest that intestinal ischemia causes delayed neuronal death, which differs from the apoptotic process previously demonstrated in the ischemia-damaged brain.

Animals↗

PubMed1999

Perineuronal nets of proteoglycans in the adult mouse brain, with special reference to their reactions to Gömöri's ammoniacal silver and Ehrlich's methylene blue.

As our previous studies have indicated, many subsets of neurons in the vertebrate brain possess a sulfated proteoglycan surface coat which reacts to cationic iron colloid and aldehyde fuchsin. The present study demonstrated that this surface coat is supravitally stained with Ehrlich's methylene blue, and doubly with this blue and aldehyde fuchsin, a finding suggesting its being identical to Cajal's superficial reticulum (red superficial) and to Golgi's reticular coating (revetement reticulare). The perineuronal surface coat was further stained with Gömöri's ammoniacal silver, and doubly with this silver and cationic iron colloid. These neurons with such a proteoglycan surface coat usually expressed cell surface glycoproteins which were labeled with lectin Wisteria floribunda agglutinin. Hyaluronidase digestion did not interfere with this lectin labeling of the glycoproteins, methylene blue and Gömöri's ammoniacal silver staining of the surface coat, while it erased the cationic iron colloid and aldehyde fuchsin staining of the surface coat. These findings suggest that the perineuronal proteoglycan surface coat is associated with some additional molecules which are resistant to hyaluronidase digestion and stainable with methylene blue and Gömöri's ammoniacal silver. The possibility is suggested that these molecules might represent "ligand proteoglycans" connecting the perineuronal proteoglycans and cell surface glycoproteins.

Animals↗

PubMed1999

Percutaneous microwave hepatic tumor coagulation with segmental hepatic blood flow occlusion in seven patients.

OBJECTIVE: We assess the usefulness of microwave hepatic tumor coagulation therapy with balloon occlusion of segmental hepatic blood flow for eight recurrent metastatic hepatic tumors in seven patients. CONCLUSION: Limited early experience with microwave hepatic tumor coagulation therapy and segmental hepatic blood flow occlusion has been positive, suggesting that further clinical evaluation is warranted.

Catheterization↗

PubMed1999

Diffusion-weighted single-shot echoplanar MR imaging for liver disease.

OBJECTIVE: The aims of this study were to determine apparent diffusion coefficients (ADCs) of the abdominal organs and liver lesions, to determine the effect of the magnitude of b values on the ADCs, and to determine whether measured ADCs of liver tumors help differentiate benign from malignant lesions. SUBJECTS AND METHODS: Six healthy volunteers and 126 patients were examined with diffusion-weighted single-shot echo-planar imaging using multiple b values (maximum, 846 sec/mm2). The ADCs of the liver, spleen, kidney, 49 malignant liver lesions (33 hepatocellular carcinomas, 15 metastatic liver tumors, and one cholangiocellular carcinoma), and 30 benign lesions (17 cysts, 12 hemangiomas, and one angiomyolipoma) were calculated. RESULTS: The ADCs of the abdominal organs and liver lesions showed smaller values when calculated with the greater maximum b values. The ADCs of the benign lesions calculated with all the b values of less than 850 sec/mm2 (2.49+/-1.39 x 10(-3) mm2/sec) were significantly (p = .0024) greater than those of the malignant lesions (1.01+/-0.38 x 10(-3) mm2/sec). When the maximum b value is 846 sec/mm2, use of a threshold ADC of 1.6 x 10(-3) mm2/sec would result in a sensitivity of 98% and a specificity of 80% for differentiation of malignant liver lesions from benign lesions. CONCLUSION: Measurement of ADC has good potential for characterizing liver lesions, but the calculated ADCs could be affected by the magnitude of the maximum b value.

Adult↗

PubMed1999

Detection of hepatocellular carcinoma: comparison of low- and high-spatial-resolution dynamic MR images.

OBJECTIVE: The purpose of our study was to compare the diagnostic performance of low- and high-spatial-resolution gadolinium chelate-enhanced triphasic dynamic gradient-recalled echo (GRE) MR images in the detection of hepatocellular carcinoma. MATERIALS AND METHODS: Triphasic dynamic MR images obtained with low (256 x 128) and high (512 x 224) image matrices in 28 patients with 65 hepatocellular carcinomas (HCCs) were retrospectively analyzed. Image review was conducted on a segment-by-segment basis; a total of 215 liver segments, including 56 segments with tumor burden, were reviewed for the presence of HCC by three independent radiologists. Detectability was evaluated with relative sensitivity, specificity, and receiver operating characteristic (ROC) analysis. Image quality was evaluated with rank order analysis. RESULTS: Relative sensitivity was statistically significantly better with high-spatial-resolution images than with low-spatial-resolution images (p < .005). Relative specificity was statistically significantly better with low-spatial-resolution images than with high-spatial-resolution images (p < .001). Diagnostic accuracy determined by ROC curve analysis was marginally higher with high-spatial-resolution (area under ROC curve [Az] = .97) than with low-spatial-resolution (Az = .94, p < .09) images. Image quality was statistically significantly better with high-spatial-resolution images (p < .005). CONCLUSION: High-spatial-resolution dynamic GRE images were superior to low-spatial-resolution images in sensitivity of detecting HCC and in image quality. Triphasic dynamic GRE imaging in the screening and follow-up programs of patients with suspected HCC should be performed using high image matrices.

Adult↗

PubMed1999

Enhancement of topical delivery of a lipophilic drug from charged multilamellar liposomes.

To enhance the topical delivery of rhodamine B base (Rho), a model lipophilic compound, the electrostatic interaction between the positive and negative components incorporated in the liposomal bilayer was utilized. The higher in vitro permeability to Rho in rat skin was observed with positive and neutral multilamellar liposomal preparations, the former was prepared with phosphatidylcholine (PC) and stearylamine (SA) and the latter with PC alone, than that given as a solution. Negative liposome composed of PC and dicetyl phosphate (DCP) showed lower skin permeability to Rho. To enhance the Rho retention in the skin, the electrostatic interaction between SA and DCP, which was confirmed by in vitro partition study, was utilized. By pretreating the skin surface with SA solution or empty SA liposome, the skin distribution of Rho given as DCP liposome was substantially enhanced, with increase in the PC distribution into the skin. The pretreatment effect of empty SA liposome was also observed in rats in vivo. In conclusion, it was found that negative DCP liposome provides better drug retention in the skin with lower skin permeability, and the topical drug delivery from DCP liposome was further enhanced by the pretreatment of the skin surface with empty SA liposome.

Administration, Topical↗

PubMed1999

Formation of 8,11,14-octadecatrienoic acid (18:3 n-4) from naturally occurring unique fatty acid, 9,12-hexadecadienoic acid (16:2 n-4), in animal cell cultures.

9,12-Hexadecadienoic acid (16:2 n-4), present in small amounts in fish oils as a naturally occurring unique fatty acid, was incorporated into the phospholipids in rat liver BRL-3A cells to a similar extent as linoleic acid (18:2 n-6). 11,14-Octadecadienoic acid (18:2 n-4) and 8,11,14-octadecatrienoic acid (18:3 n-4) were detected in the cellular lipids of BRL-3A cells when incubated in a medium supplemented with 16:2 n-4 methyl ester. The cellular levels of these acids increased in parallel with 16:2 n-4 methyl ester added to the medium. These compounds were probably formed through conversion from 16:2 n-4 to 16:3 n-4 by delta 6 desaturation, and then 18:3 n-4 was produced by elongation, and part of the surplus 16:2 n-4, not desaturated to 16:3 n-4, elongated to 18:2 n-4. These results suggested that 16:2 n-4 was desaturated by delta 6 desaturase in vitro. It was also shown that 16:2 n-4 inhibited arachidonic acid synthesis from exogenous linoleic acid in BRL-3A cells as efficiently as alpha-linolenic acid (18:3 n-3).

Animals↗

PubMed1999

Hepatic branched-chain alpha-keto acid dehydrogenase complex in female rats: activation by exercise and starvation.

The effects of acute exercise and starvation on hepatic branched-chain alpha-keto acid dehydrogenase (BCKDH) complex activity were examined in female rats fed high (30%)- or low (8%)-protein diets. The total activity of the complex was significantly higher in the high protein-fed rats than in the low protein-fed rats but was not affected by acute exercise and starvation in either diet group. The proportion of the active form of BCKDH complex was less than 10% in both diet groups. Acute exercise and starvation markedly increased the active form of the complex in both diet groups. The activity of BCKDH kinase, which is responsible for inactivation of the BCKDH complex by phosphorylation, tended to be decreased by acute exercise and starvation in both diet groups. These results suggest that the activity of the BCKDH kinase is an important factor determining the proportion of the active form of BCKDH complex in exercise and starvation, and that the female rat is a useful model for studying the regulation of hepatic BCKDH complex activity.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗

PubMed1999

Effects of angiotensin I-converting enzyme inhibitor from Ashitaba (Angelica keiskei) on blood pressure of spontaneously hypertensive rats.

The inhibitory activity of angiotensin I-converting enzyme (ACE) was extracted with 80% ethanol from the leaves of Ashitaba (Angelica keiskei). The present ACE inhibitor was fractionated and separated with various chromatographies. The antihypertensive effects of the sample (G fraction) from Ashitaba on spontaneously hypertensive rats (SHR) were observed by long-term administration for 10 wk. Another sample (S fraction) from Ashitaba also had antihypertensive effects after a single intravenous administration to SHR. The sample was further purified by using several chromatographies. The ACE inhibitor fraction was characterized as follows: no significant absorbance, a zwitterion, a water-soluble substance and a positive ninhydrin reaction. According to a mass spectrum analysis, the molecular weight of the ACE inhibitor was determined to be 303 and Na-salt ions of carboxyl groups were detected. The ACE inhibitor from Ashitaba contained in the anti-hypertensive fraction was speculated to be very similar to authentic nicotianamine based on a comparative study of inhibitory activity, mass spectrum analysis and thin-layer chromatographies.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1999

Transport of rhodamine 123, a P-glycoprotein substrate, across rat intestine and Caco-2 cell monolayers in the presence of cytochrome P-450 3A-related compounds.

Effects of cytochrome P-450 3A- and P-glycoprotein (P-gp)-related compounds, erythromycin, midazolam, ketoconazole, verapamil, and quinidine, on transport of rhodamine 123 (Rho-123), a P-gp substrate, were studied in rat intestine and in Caco-2 cells. Ileum was mainly used in rat studies because this segment showed greater P-gp-mediated Rho-123 transport. In an in vitro everted rat ileum, all the compounds examined significantly inhibited the transport of Rho-123 from serosal to mucosal surfaces across the intestine, with different inhibitory potencies among these compounds. In an in vivo rat study, the exsorption of Rho-123 from blood to the intestinal lumen, which was evaluated as exsorption clearance of Rho-123 under a steady-state plasma concentration of Rho-123, was also inhibited when these compounds were added to the intestinal lumen. Similarly, transepithelial transport of Rho-123 from the basolateral to apical side across Caco-2 cell monolayers was inhibited by these compounds. A linear relationship was observed in their inhibitory potencies on Rho-123 transport between in vitro and in vivo studies using rat ileum and between studies with rat ileum and Caco-2 cells. P-gp-mediated transport across the intestine was found to be inhibited not only by P-gp-related but also by all the cytochrome P-450 3A-related compounds examined. Within experimental error, the relative inhibitory potencies were the same between the studies with rat ileum (in vivo, in vitro) and those with Caco-2 cells. Thus, it is suggested that the function of P-gp and its sensitivity to these drugs may be similar in rat intestine and Caco-2 cells.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1999

Measurement of serum leptin in patients with chronic renal failure on hemodialysis.

BACKGROUND: Leptin, the product of the obese gene, is produced exclusively in fat cells. SUBJECTS, MATERIALS AND METHODS: To evaluate the clinical significance of measuring serum leptin in 56 patients with chronic renal failure on hemodialysis (HD), we measured leptin levels using radioimmunoassay in 34 normal volunteers and in 56 patients on HD. RESULTS: Normal serum leptin averaged 5.7 +/- 0.7 (mean +/- SEM) ng/ml, which correlated significantly (p < 0.001) with the body fat percentage as measured by bioelectrical impedance analysis. Serum leptin in HD patients ranged from 1.3 to 142 ng/ml. The mean serum leptin analyzed after the logarithmic conversion was 5.6 ng/ml, which was not significantly different from the normal control value, although the body fat percentage was significantly lower than normal volunteers. There was a significant (p < 0.01) positive correlation between body fat percentage and serum leptin in both normal controls and HD patients. The slope of the regression curve was steeper in HD patients than in normal controls. CONCLUSION: (1) serum leptin levels to body fat mass are significantly higher in HD patients than controls; (2) the variability is much wider in HD patients; and (3) a significant relation exists between percent body fat and log serum leptin, the relation being steeper in HD patients than in controls.

Adipose Tissue↗

PubMed1999

Structural and functional analysis of the control region of the human DNA topoisomerase II alpha gene in drug-resistant cells.

We have previously shown that the DNA topoisomerase II alpha (topo II alpha) gene is down-regulated in VP16/VM26-resistant cells at the transcriptional level. To determine the DNA elements responsible for down-regulation, the transcriptional activities of luciferase reporter constructs containing various lengths of the promoter sequences were investigated by transient transfection of two resistant cell lines, KB/VP2 and KB/VM4. The transcriptional activities of the full-length promoter (-295 to +85) and of three deletion constructs (-197, -154 and -74 to +85) were significantly down-regulated in resistant cells. In contrast, the transcriptional activity of the minimal promoter (-20 to +85) in resistant cells was similar to that in parental KB cells. Furthermore, introduction of a mutation in ICE1 abolished the down-regulation of the topo II alpha promoter activity in drug-resistant cells. In vivo footprinting analysis of topo II alpha gene promoter revealed several specific protein-binding sites, a GC box, ICE1, ICE2 and ICE3. In vivo footprinting analysis also identified a cluster of hypersensitive sites. However, there was no marked difference in protein-binding sites between parental and resistant cells. To confirm our previous results, we have established the VP16-resistant cell lines T12-VP1 and T12-VP2 from T12 cells derived from human bladder cancer T24 cells stably transfected with the chloramphenicol acetyltransferase reporter gene driven by the topo II alpha gene promoter. The expression to topo II alpha was down-regulated in both cell lines. We also found that CAT gene expression was significantly decreased to one-fifth of that in T12 parental cells. These results suggest that the expression of the topo II alpha gene requires the binding of multiple factors to the core promoter and is down-regulated at the transcriptional level, probably through binding of a negative factor to ICE1 in drug-resistant cells.

Antigens, Neoplasm↗

PubMed1999

Use of a retractor designed to harvest an internal thoracic artery graft during cardiac surgery for patients with a unilateral lung.

Adequate exposure of the heart is required for safe cardiac surgery. We performed open heart surgery for 2 patients with a unilateral lung. In one patient, coronary artery bypass grafting was performed 13 years after left pneumonectomy for lung cancer. Mitral valve replacement was performed in the other patient whose left lung was entirely collapsed due to tuberculosis. The heart was markedly deviated to the left in both patients. A retractor designed to harvest the internal thoracic artery was very useful to obtain a good operative view of the heart. The operations were uncomplicated, and postoperative recovery was uneventful in both patients.

Aged↗

PubMed1999

Laparoscopic cornuostomy for interstitial pregnancy. A case report.

BACKGROUND: With recent advances in laparoscopic surgery, many reports have described laparoscopic cornual resection for interstitial pregnancy as a safe alternative to laparotomy. We report a laparoscopic cornuostomy for unruptured interstitial pregnancy with myometrium reconstruction. CASE: A 32-year-old woman presented with complaints of abdominal cramps and vaginal spotting after 6 weeks of amenorrhea. Ultrasonographic examination revealed a gestational sac 7 mm in diameter in the left uterine corner. There was clear separation between the endometrium and gestational sac. A 3-mm periumbilical trocar for the laparoscope and a 3-mm trocar in the lower abdomen were used, and the left interstitial pregnancy was confirmed. An additional, 5-mm trocar was used in the lower abdomen for the laparoscopic surgery. The patient underwent a laparoscopic cornuostomy. Myometrium reconstruction was performed by suturing and tying with a laparoscopic technique. CONCLUSION: In this case, minilaparoscopy was useful in the diagnosis and treatment of interstitial pregnancy.

Abdominal Pain↗

PubMed1999

Phylogenic analysis of echovirus type 30 isolated from a large epidemic of aseptic meningitis in Japan during 1997-1998.

During 1997 to 1998, a nationwide epidemic of aseptic meningitis occurred in Japan. More than 4,500 isolates from patients with aseptic meningitis were identified as echovirus type 30. To investigate the character of these isolates, we examined the nucleotide sequences of thirty-seven geographical representatives and compared them with 50 strains isolated during the past 20 years. The phylogenic analysis used partial sequences from either the VP1 or VP4-VP2 region of the viral capsid. This analysis revealed that the isolates were divided into six genomic groups. All isolates identified during 1997-1998 belonged to only two genomic groups; these two groups are thought to be the causative viral agents involved in the recent epidemic.

Enterovirus B, Human↗