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Biomedical subjects

H Yamamoto

Publications and source records attributed to H Yamamoto.

At least 199 records · Page 11Linked to original sources

Effectiveness of endoscopic biliary drainage for unresectable hepatocellular carcinoma associated with obstructive jaundice.

Endoscopic biliary drainage (EBD) for unresectable hepatocellular carcinoma (HCC) associated with obstructive jaundice remains controversial because of the short survival of these patients. To evaluate the effectiveness of this procedure, we retrospectively studied 18 patients who had unresectable HCC with obstructive jaundice and underwent EBD with polyethylene stents, over a 10-year period. Nine patients with tumor thrombus involving the first branches of the portal vein or portal trunk (Vp3) formed group A and the other 9 (Vp0-Vp2) formed group B. The serum albumin level and serum total bililubin level differed significantly between the two groups (P < 0.05 and P < 0.005. Student's t-test), but prothrombin time did not. The obstructive jaundice was mainly caused by direct tumor invasion in 6 patients from group A and 3 from group B, by blood clots and/or tumor fragments in 2 patients from group A and 3 from group B, by the tumor protruding into the common hepatic duct in 2 patients from group B. and by tumor compression of the common bile duct in 1 patient from each group. Drainage was successful in 4 patients (44%) from group A and in all 9 patients (100%) from group B. Among the 5 patients with unsuccessful drainage in group A, 4 had obstruction of both the left and right hepatic ducts and 3 had multiple tumors in both lobes. The mean survival time (mean +/- SD) after EBD was 47 +/- 44 days in group A and 181 +/- 70 days in group B. In group A. the average survival time was only 85 days in the 4 patients with successful drainage. However, an improvement in the quality of life after EBD was observed in one-third of the Vp3 patients and in all of the Vp0-Vp2 patients. In summary, satisfactory palliation is possible with successful EBD, but this is difficult in most patients with Vp3 portal thrombus, direct tumor invasion involving both hepatic ducts, and multiple tumors in both lobes. It is important to determine the site, extent, and nature of the obstruction, as well as liver function and the presence of portal thrombus, before performing EBD.

Aged↗

Mechanical augmentation of the vertebral body by calcium phosphate cement injection.

The effectiveness of transpedicular calcium phosphate cement (CPC) injection as a new treatment for osteoporotic compression fracture of vertebrae was evaluated by measuring the compressive strength and the mode of failure in vertebrae experimentally injected with CPC. Forty-five human cadaver vertebrae were divided into three groups: a control group; group A, in which CPC was injected into the upper half of the vertebral body; and group B, in which CPC was injected into the whole vertebra. The load-displacement curve characteristically had two peaks in group A, and decreased rapidly after failure in group B. The failure site was the cancellous bone immediately below the cranial endplate in the control group, cancellous bone immediately below the CPC injection area in group A, and in the CPC injection area in group B. Although mechanical strength was greatest in those vertebrae in which the entire cancellous bone was replaced with CPC, the compressive strength of the vertebrae was also increased by partial replacement of cancellous bone with CPC injection. In terms of mode of failure and mechanical gradient with adjacent vertebrae, there were several advantages for those vertebrae in which the cranial half of the cancellous bone was replaced with CPC.

Aged↗

Comparison of in-vitro activities of SCH27899 and other antibiotics against Mycoplasma pneumoniae.

We examined the in-vitro activities of various antibiotics against 25 strains of Mycoplasma pneumoniae (22 clinical isolates and 3 standard strains). In the 22 clinical isolates, the 90% minimum inhibitory concentrations (MIC 90) of SCH27899, ofloxacin, levofloxacin, ciprofloxacin, erythromycin, clarithromycin, roxithromycin, clindamycin, and minocycline were 16, 2, 2, 4, 0.0039, 0.0039, 0.016, 2, and 4 microg/ml, respectively. The minimum bactericidal concentrations (MBC 90) of SCH27899, ofloxacin, levofloxacin, ciprofloxacin, erythromycin, clarithromycin, roxithromycin, clindamycin, and minocycline were 64, 4, 2, 8, 0.0625, 0.0625, 0.125, 8, and 64 microg/ml, respectively. The low sensitivity of M. pneumoniae to SCH27899 may be a result of the impermeability of the bacteria to this molecule. The results of this study suggest that SCH27899 would not be a suitable antimicrobial agent to use in the alternative chemotherapy of M. pneumoniae infection.

Aminoglycosides↗

Antimicrobial activity of everninomicin against clinical isolates of Enterococcus spp., Staphylococcus spp., and Streptococcus spp. tested by Etest.

The in-vitro antimicrobial activity of everninomicin, a novel oligosaccharide antibiotic, was tested against clinical isolates of 11 methicillin-susceptible Staphylococcus aureus (MSSA) strains, 11 methicillin-resistant S. aureus (MRSA) strains, 22 Staphylococcus epidermidis strains, 23 Enterococcus faecalis strains, 23 Enterococcus faecium strains, 23 Enterococcus avium strains, 27 Streptococcus pneumoniae strains, 22 Streptococcus pyogenes strains, and 20 Streptococcus agalactiae strains. The minimum inhibitory concentrations (MICs) of everninomicin were determined by Etest and compared with those of vancomycin, teicoplanin, and minocycline. The Etest showed that everninomicin exhibited excellent activity (MIC, <0.016 to 1.5 microg/ml) against the gram-positive cocci tested. The antimicrobial activity of everninomicin against S. aureus and S. epidermidis was stronger than that of vancomycin, teicoplanin, and minocycline, in particular against MRSA, with an MIC50 of 0.38 microg/ml and an MIC90 of 0.5 microg/ml. Against strains of enterococci and streptococci, everninomicin was more active than vancomycin, but as active as teicoplanin.

Aminoglycosides↗

Characterization of MRSA transmission in an emergency medical center by sequence analysis of the 3'-end region of the coagulase gene.

The distribution of methicillin-resistant Staphylococcus aureus (MRSA) isolates at the St. Marianna University affiliated emergency medical center (EMC) was studied by sequence analysis of the 3'-end region of the coagulase gene. We collected a total of 42 MRSA isolates, consisting of 20 strains from the hospital environment, 13 strains from the nostrils or fingers of medical staff, and 9 strains from inpatients in the EMC. We compared our results with those from 27 stock strains of known coagulase serotype and 2 strains reported in the literature. All 69 strains tested have four to six tandem repeats in the 3'-end region of the coagulase gene. Among the 42 MRSA isolates collected, the base sequence of the 3'-end region of the coagulase gene was identical in 28 of them (67%). The number of isolates originating from the hospital environment, medical staff, and patients, respectively, that were identical to this representative strain were 18 (90%), 6 (46%), and 4 (44%). Phylogenetic analysis using the DNA sequences of the tandem repeat region demonstrated that almost all strains from the patients formed a concordant cluster with the representative strain from the hospital ward. We also assessed the value of sequence analysis of the 3'-end region of the coagulase gene as an epidemiological marker. Our results indicate that sequence analysis of the 3'-end region of the coagulase gene of MRSA may be a potent epidemiologic typing system.

Bacterial Typing Techniques↗

Thoracic and thoracoabdominal aneurysm repair under deep hypothermia using subclavian arterial perfusion.

BACKGROUND: Hypothermic circulatory arrest is a valuable adjunct for thoracic and thoracoabdominal aortic aneurysm repair. Retrograde aortic perfusion through the femoral artery, however, carries a risk of cerebral embolism or malperfusion. To avoid these complications we adopted antegrade aortic perfusion through a prosthetic graft attached to the left subclavian artery through a left thoracotomy. METHODS: Ten patients had repair of descending thoracic and thoracoabdominal aortic aneurysm under deep hypothermia with antegrade aortic perfusion through the left subclavian artery. Hypothermic circulatory arrest was used because proximal aortic control was hazardous due to rupture or intraluminal disease, or for spinal cord protection. RESULTS: There was no brain injury and one hospital death. The cause of death was massive bleeding from the gastrointestinal tract not related to deep hypothermia or the perfusion method. All 9 survivors were alive and well after a mean follow-up period of 9 months. CONCLUSIONS: Using the left subclavian artery as a site of aortic perfusion can avoid retrograde aortic perfusion, hence reducing the potential for brain injury due to embolic stroke or malperfusion through a dissected thoracoabdominal aorta.

Aged↗

Synthesis of active high mannose-type lipoprotein lipase in human adipose tissues.

Lipoprotein lipase (LPL) activity in the retroperitoneal adipose tissue of a patient with Cushing's syndrome and in the subcutaneous adipose tissue of a patient with aseptic necrosis of the femoral head was higher than that in the corresponding tissues of the control subjects. The amount of [35S]methionine incorporated into LPL was also higher in these patients than in control subjects. However, the ratio of activity and amount of radioactivity in the LPL of patients was identical to that of control subjects, indicating that LPL synthesized in the adipose tissues of patients had a normal specific activity. LPL with Mr = 57000 was composed of two types of subunits: one type was partially endo H-sensitive, yielding a product with Mr = 55000, and the other was totally endo H-sensitive, yielding a product with Mr = 52000. Both retroperitoneal and subcutaneous adipose tissues of control subjects contained nearly equal amounts of partially and totally endo H-sensitive subunits. In the retroperitoneal adipose tissue of a patient with Cushing's syndrome, 8% of subunits were partially endo H-sensitive and 92% were totally endo H-sensitive. In the subcutaneous adipose tissue of a patient with aseptic necrosis of the femoral head, 21% of subunits were partially endo H-sensitive and 79% were totally endo H-sensitive. The 24-h treatment of subcutaneous adipose tissue of a control subject with 1 mM 1-deoxymannojirimycin (dMM) caused the synthesis of active, but totally endo H-sensitive, LPL. Thus, in human adipose tissue, the processing of one oligosaccharide chain of an LPL subunit to a complex type chain in the trans Golgi was not necessary for the expression of activity.

Adipose Tissue↗

7-Deoxyloganin 7-hydroxylase in Lonicera japonica cell cultures.

The activity of 7-deoxyloganin 7-hydroxylase, an enzyme catalyzing the conversion of 7-deoxyloganin into loganin, was detected in a microsomal preparation from the cell suspension cultures of Lonicera japonica. It was dependent on NADPH and molecular oxygen. The enzymatic reaction was inhibited by carbon monoxide as well as by several cytochrome P450 inhibitors, especially ketoconazole, indicating that the reaction was mediated by cytochrome P450. The enzyme showed substrate specificity for 7-deoxyloganin. The K(m) values for 7-deoxyloganin and NADPH were estimated as 170 and 18 microM, respectively, from Lineweaver-Burk plots.

Carbon Monoxide↗

8-dimethylallylnaringenin 2'-hydroxylase, the crucial cytochrome P450 mono-oxygenase for lavandulylated flavanone formation in Sophora flavescens cultured cells.

8-dimethylallylnaringenin (8-DMAN) 2'-hydroxylase, which is indispensable for the formation of a lavandulylated flavanone, sophoraflavanone G, was detected in cell suspension cultures of Sophora flavescens. The enzyme catalyzes the 2'-hydroxylation of 8-DMAN to leachianone G, and is tightly bound to the membrane. It required NADPH and molecular oxygen as cofactors, and was inhibited by several cytochrome P450 inhibitors such as carbon monoxide and cytochrome c, indicating that the reaction is mediated by a cytochrome P450 monooxygenase. The optimum pH of 8-DMAN 2'-hydroxylase was 8.5, and the enzyme hydroxylated only 8-DMAN. Apparent Km values for 8-DMAN and NADPH of the enzyme were 55 and 34 microM, respectively.

Carbon Monoxide↗

Stretch induces a growth factor in alveolar cells via protein kinase.

Positive-pressure mechanical ventilation can injure the lung, causing edema and alveolar inflammation in a complication termed ventilator-induced lung injury (VILI). Cytokines such as interleukin-8 (IL-8) reportedly are important in this inflammatory response. On the other hand, hepatocyte growth factor (HGF) promotes regeneration of the lung, and delays pulmonary fibrosis. We postulated that cyclic stretch upregulates production and release of both of mediators. Human alveolar epithelial cells (A549) cultured on a silicoelastic membrane were tested for mRNA expression and release of IL-8 and HGF after cyclic stretch in vitro. Stretch induced mRNA expression and release of these mediators. The signaling pathway from cyclic stretch to release of IL-8 and HGF appeared to involve protein kinase C in the signal transduction pathway.

Cells, Cultured↗

Depth profiles of volatile halogenated hydrocarbons in seawater in the Bay of Bengal.

Measurements were made of bromocarbons (CHBr3 and CH2Br2), iodocarbons (CH2I2 and CH2ClI), and dimethylsulfide (DMS, CH3SCH3) in seawater collected from the Bay of Bengal under tropical stratified conditions. These compounds showed different depth profiles, characteristic of each group. CH2I2 and CH2ClI showed very similar depth profiles to chlorophyll-a, suggesting their production by phytoplankton followed by rapid decay in seawater. The CH2I2 maximum at a depth a little below the CH2ClI maximum was consistent with its more significant photolytic decay. The bromocarbons were less localized in their distributions than were the iodocarbons, suggesting their longer residence time in seawater after their release from phytoplankton. Both of these profiles were different from the pattern of DMS, which had its maxima above the chlorophyll-a maximum layer near the surface.

Environmental Monitoring↗

UV-irradiation-induced DNA immobilization and functional utilization of DNA on nonwoven cellulose fabric.

Immobilization of double-stranded DNA onto nonwoven cellulose fabric by UV irradiation and utilization of DNA-immobilized cloth were examined. The immobilized DNA was found to be stable in water, with the maximum amount of fabric-immobilized DNA being approximately 20 mg/g of nonwoven fabric. The DNA-immobilized cloth could effectively accumulate endocrine disruptors and harmful DNA intercalating pollutants, such as dibenzo-p-dioxin, dibenzofuran, biphenyl, benzo[a]pyrene and ethidium bromide. Additionally, DNA-immobilized cloth was found to bind metal ions, such as Ag+, Cu2+, and Zn2+. The maximum amounts of bound Ag+, Cu2+, and Zn2+ onto DNA-immobilized cloth (1 g) were approximately 5, 2, and 1 mg, respectively. DNA-immobilized cloth containing Ag+ showed antibacterial activity against Escherichia coli and Staphylococcus aureus. DNA-immobilized cloth without metal ion and with Cu2+ or Zn2+ did not show antibacterial activity. These results suggest that immobilized DNA imparts useful functionality to cloth. DNA-immobilized cloth prepared by UV irradiation has potential to serve as a useful biomaterial for medical, engineering, and environmental application.

Cellulose↗

Quantitative determination of gelatinase activity among enterococci.

Gelatinase, hemolysin and aggregation substance have all been reported to be virulence factors of enterococci. In this study, gelatinase production was investigated in isolates of Enterococcus faecalis (n=93), E. faecium (n=49) and E. avium (n=36) recovered from hospitalized patients. Gelatinase was detected in 45% of E. faecalis isolates, but could not be detected in E. faecium and E. avium. Gelatinase activity was then measured by radial diffusion for the 42 gelatinase-positive E. faecalis isolates. To convert gelatinase activity into proteinase K activity, a standard curve was produced by placing different concentrations of proteinase K into wells in the gelatine plate. Gelatinase activity per E. faecalis colony ranged from 2.6 x 10(-7) to 2.2 x 10(-5) microg/ml, proportionate to the activity of proteinase K. An approximately 84-fold difference in gelatinase concentration was observed between the colony producing the highest amount and that producing the lowest amount. This method may be useful for determining the virulence of given isolates in relation to gelatinase production as it is quick, easy and inexpensive to perform.

Adult↗

Suppression of tumor necrosis factor-alpha production and neutrophil infiltration during ischemia-reperfusion injury of the liver after heat shock preconditioning.

BACKGROUND/AIMS: Heat shock preconditioning provides the liver with ischemic tolerance. In this study we examined the effects of heat shock preconditioning on hepatic nonparenchymal cells in light of tumor necrosis factor-alpha (TNF-alpha) production and neutrophil infiltration. METHODS: Rats were exposed to heat shock pretreatment at 42 degrees C in the heat shock group (group HS) and at 37 degrees C in the control group (group C). After a 48-h recovery, the left hepatic lobes were given a 90-min ischemia and reperfused. Plasma concentrations of TNF-alpha, cytokine-induced neutrophil chemoattractant (CINC) and alanine aminotransferase (ALT) were measured. Liver tissues were checked for the presence of TNF-alpha mRNA. Histological staining for CINC and polymorphonuclear leukocyte (PMN) was also evaluated. RESULTS: In group HS, plasma TNF-alpha levels were significantly more suppressed than in group C (P<0.0001). Expressions of TNF-alpha mRNA in the liver was suppressed in group HS. Production of CINC 2 h after reperfusion was reduced in group HS (P<0.05). PMN infiltration was significantly reduced in group HS (P<0.01). In group HS, liver histology revealed less cellular damage and the plasma level of ALT was significantly reduced (P<0.0001). CONCLUSIONS: Heat shock preconditioning suppressed the production of TNF-alpha and CINC in the liver during reperfusion and consequently reduced neutrophil infiltration.

Alanine Transaminase↗

Effects of VIP and NO on the motor activity of vascularly perfused rat proximal colon.

The effects of vasoactive intestinal polypeptide (VIP) and nitric oxide (NO) on the motor activity of the rat proximal colon were examined in an ex vivo model of vascularly perfused rat proximal colon. VIP reduced motor activity and this inhibitory effect was not altered by either atropine, hexamethonium, tetrodotoxin (TTX) nor TTX plus acetylcholine (ACh), but was completely antagonized by NO synthase inhibitor N(G)-nitro-L-arginine (L-NA) and by VIP receptor antagonist, VIP(10-28). These results suggest that VIP may exert a direct inhibitory effect on the motor activity of the rat proximal colon via a VIP receptor located on the smooth muscle and this effect is mediated by NO but not by cholinergic pathways. Atropine and hexamethonium reduced but ACh stimulated motor activity and the effect of ACh was not changed by TTX, suggesting that the cholinergic pathway may exert a direct stimulatory effect on motor activity. Single injection of TTX, VIP(10-28) or L-NA induced a marked increase in motor activity, suggesting that the motor activity of rat proximal colon is tonically suppressed by VIP and NO generating pathways, and elimination of inhibitory neurotransmission by TTX may induce an abnormal increase of the motor activity. The interaction between VIP and NO in regulation of motor activity was further examined by a measurement of NO release from vascularly perfused rat proximal colon. Results showed that NO release was significantly increased during infusion of VIP and this response was reversed by L-NA. These results suggest that VIP generating neurons may inhibit colonic motility by stimulating endogenous NO production in either smooth muscle cells or nerve terminals.

Animals↗

Amyloid beta protein activates PKC-delta and induces translocation of myristoylated alanine-rich C kinase substrate (MARCKS) in microglia.

The increased accumulation of activated microglia containing amyloid beta protein (Abeta) around senile plaques is a common pathological feature in subjects with Alzheimer's disease (AD). Much less is known, however, of intracellular signal transduction pathways for microglial activation in response to Abeta. We investigated intracellular signaling in response to Abeta stimulation in primary cultured rat microglia. We found that the kinase activity of PKC-delta but not that of PKC-alpha or -epsilon is increased by stimulation of microglia with Abeta, with a striking tyrosine phosphorylation of PKC-delta. In microglia stimulated with Abeta, tyrosine phosphorylation of PKC-delta was evident at the membrane fraction without an overt translocation of PKC-delta. PKC-delta co-immunoprecipitated with MARCKS from microglia stimulated with Abeta. Abeta induced translocation of MARCKS from the membrane fraction to the cytosolic fraction. Immunocytochemical analysis revealed that phosphorylated MARCKS accumulated in the cytoplasm, particularly at the perinuclear region in microglia treated with Abeta. Taken together with our previous observations that Abeta-induced phosphorylation of MARCKS and chemotaxis of microglia are inhibited by either tyrosine kinase or PKC inhibitors, our results provide evidence that Abeta induces phosphorylation and translocation of MARCKS through the tyrosine kinase-PKC-delta signaling pathway in microglia.

Amyloid beta-Peptides↗

Antineutrophil cytoplasmic autoantibody specific for proteinase 3 in a patient with shunt nephritis induced by Gemella morbillorum.

A 17-year-old girl had been placed with ventriculoperitoneal, then ventriculoatrial shunts for congenital hydrocephalus since birth. The patient originally was diagnosed as having a lupus-like disease, but later turned out to have shunt nephritis, presenting with fever, proteinuria, pancytopenia, and hypocomplementemia. Antineutrophil cytoplasmic autoantibody specific for proteinase 3 (PR3-ANCA) was detected in her serum. The patient received oral prednisolone and repeated methylprednisolone pulses, with essentially no beneficial effects. A gram-positive coccus, Gemella morbillorum, was recovered from her blood as well as cerebrospinal fluid, and the culture of the shunt catheter established the diagnosis of shunt nephritis. Removal of the shunt catheter improved symptoms dramatically and decreased PR3-ANCA in serum to an undetectable level. Because steroids had no effects and the control of bacterial infection lowered PR3-ANCA levels, the antibody would have been induced by continuous infection with G morbillorum.

Adolescent↗

Preeclamptic serum enhances endothelin-converting enzyme expression in cultured endothelial cells.

Increased vascular sensitivity to vasoconstrictors, such as angiotensin II and epinephrine, is observed in preeclampsia (PE). Recently, it was suggested that abnormal endothelial function might contribute to the pathophysiologic changes in PE. We investigated vasoconstrictor (angiotensin II and epinephrine)-induced endothelin-1 (ET-1) release from human umbilical vein endothelial cells incubated with sera from women with PE compared with normotensive pregnant and nonpregnant women. Moreover, inositol 1,4,5-trisphosphate production and endothelin-converting enzyme (ECE) expression in human umbilical vein endothelial cells were also evaluated. There were no significant differences in ET-1 release without vasoconstrictors among the three groups (nonpregnant, normotensive pregnant, and PE). No significant differences in basal inositol 1,4,5-trisphosphate production and ECE expression without vasoconstrictors were detected among the three groups. Vasoconstrictor-induced ET-1 release was significantly increased by PE sera. No significant difference was detected in vasoconstrictor-induced inositol 1,4,5-trisphosphate production among the three groups. However, ECE expression after incubation with vasoconstrictor was significantly increased by PE sera. Our results suggest that ET-1 release from endothelial cells may contribute to the increased vascular sensitivity to vasoconstrictors observed in PE, and that vasoconstrictor-induced ET-1 release may be related to enhanced ECE expression.

Adult↗