[Two surgical cases of pulmonary aspergilloma].
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Aged↗
Biomedical subjects
K Hashimoto
Publications and source records attributed to K Hashimoto.
[A case of bronchioloalveolar carcinoma with multiple cystic shadows on chest CT].
A 68-year-old woman was admitted to our hospital in 1998 with shortness of breath on exertion. On the first admission, chest radiography revealed multiple nodular shadows and areas of ground-glass appearance mainly in the basal lung fields, and chest CT scans showed multiple thin-walled cystic lesions in both lung fields. Bronchioloalveolar carcinoma was diagnosed by transbronchial lung biopsy. The CA 19-9 level in the serum was abnormally high. The disease progressed, and the patient died 7 months after diagnosis. We report this case because CT scans showed multiple cystic lesions, which is very rare. The mechanism of cystic formation in this case of lung cancer may have involved disruption of the alveolar structure and enlargement of disrupted spaces or of the check valve mechanism.
Adenocarcinoma, Bronchiolo-Alveolar↗
Synthesis of oligosaccharide with controlled sequence.
A simple method for the synthesis of alternate heteropolysaccharide was investigated. Two types of modified glucose were combined into a cellobiose-type disaccharide monomer having only acetyl groups except a free hydroxyl group at C-3'. Polycondensation of this monomer, using stannic tetrachloride as catalyst, easily gave a novel copolysaccharide having regularly alternating 1,3-beta and 1,4-beta linkages.
Journal Article↗
[Parainfluenza myopathy].
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Diagnosis, Differential↗
Beneficial effect of balloon-induced pulsatility on brain oxygenation in hypothermic cardiopulmonary bypass.
BACKGROUND: Sufficient O2 delivery to meet the demand is an important factor for protecting the brain during cardiopulmonary bypass (CPB). This study was designed to investigate the influences of temperature, pulsatility of blood flow (intra-aortic balloon pump-induced) and flow rate during CPB on the cerebral oxygenation. METHODS: Patients were divided into five groups. Normothermia (36 degrees C): pulsatile (n=8, 2.5 L/min/m2), nonpulsatile (n=12, 2.5 L), and nonpulsatile perfusion (n=12, 2.8 L); hypothermia (30 degrees C): pulsatile (n=9, 2.5 L) and nonpulsatile perfusion (n=11, 2.5 L). The oxygen saturation (SjVO2), lactate and CPK-BB levels in the jugular venous blood were measured. RESULTS: In all of the normothermic groups, the SjVO2 value decreased during the CPB (p<0.1-0.01). No remarkable change was observed in the hypothermic groups, with the exception during the rewarming period in the nonpulsatile group. A higher SjVO2 and a lower frequency of SjVO2 values <50% were observed in the hypothermic pulsatile group, as compared with those in the normothermic groups (p<0.05). The levels of CPK-BB were nearly the same, however the levels of lactate were higher in the normothermic pulsatile and nonpulsatile (2.5 L) groups (p<0.05). CONCLUSIONS: We concluded that the hypothermic CPB was advantageous over normothermic CPB in regard to the SjVO2 levels and lactate production. The beneficial effect of intra-aortic balloon pump assist was only obtained in the hypothermic CPB.
Aged↗
[Three-dimensional computed tomography angiography of coronary artery bypass graft with electron beam tomography].
OBJECTIVES: Assessment of coronary artery bypass graft patency by three-dimensional reconstructed computed tomography angiography (3D-CTA) derived from electrocardiography-gated contrast-enhanced electron beam tomography (EBT) was evaluated. METHODS: Thirty-nine patients with 99 grafts (45 arterial grafts and 54 venous grafts) underwent 3D-CTA and selective coronary angiography within a 3-week interval. 3D-CTA images of the coronary bypass grafts were compared with the coronary angiography images used as the control. RESULTS: 3D-CTA defined 42 of 44 arterial grafts as patent (sensitivity: 95%), all 47 venous grafts as patent (sensitivity: 100%) and all 7 venous grafts as occlusive (specificity: 100%). The overall sensitivity and specificity were 98% and 88%, respectively. CONCLUSIONS: 3D-CTA is an useful noninvasive technique with adequate sensitivity and specificity to assess coronary artery bypass graft patency.
Aged↗
[Hypersensitivity syndrome and HHV-6].
Hypersensitivity syndrome (HS) has been recognized as one of severe adverse drug eruptions. HS has several characteristic features as follows. First, the clinical symptoms are high fever, multiple lymphadenopathy, severe skin rash, mononucleosis and multiple visceral involvement. Secondly, those symptoms appear two to six weeks after the initiation of drug administration. Thirdly, HS is induced by the specific drugs, carbamazepine, phenytoin, salazosulfapyridine, allopurinol, diaphenylsulphone, and mexiletine. Recently, we reported the association of HS with reactivation of HHV-6, the causative virus for exanthem subitum. We propose the new disease entity of HHV-6-associated drug eruption (HADE) because HS is composed of two clinical phases, drug allergic reaction in the early phase and HHV-6 reactivation in the late phase.
Adult↗
[Dihydropyrimidine dehydrogenase activity in urothelial cancer--influence of UFT administration on DPD activity].
We measured the dihydropyrimidine dehydrogenase (DPD) activity considered to regulate the sensitivity of pyrimidine fluoride anti-cancer drugs in 50 cases of urothelial cancer (preoperative therapy group 10 cases, non-therapy group 40 cases). The association of DPD activity with pathological factors and TS activity as well as the influence of UFT oral administration on the DPD activity in tumors and blood were studied. The DPD activity in cancer tissue tended to be higher than that in the mucous membranes of the non-tumor region, but the difference was not significant. The DPD activity was high in infiltrative cancer (p < 0.05) but was not associated with atypia. The TS activity and DPD activity were manifested independently. The DPD activity in cancer tissue was significantly higher after UFT administration, with levels of 76.7 +/- 71.0 pmol/mg/min before administration and 220.6 +/- 129.1 pmol/mg/min after (p < 0.05). The DPD activity in peripheral blood was elevated after administration, but no significant difference was found. Since DPD activity is found in urothelial cancer tissue, 5-FU stable to DPD should preferably be used. It is also suggested that using a more potent DPD inhibitor in combination will produce higher anti-tumor effects.
Aged↗
[A case of rheumatoid arthritis associated with minimal change nephrotic syndrome].
A 55-year-old Japanese woman has been treated with various kinds of anti-rheumatic drugs under a diagnosis of rheumatoid arthritis(RA) for 18 years of disease duration. She persistently had right elbow joint pain and swelling and X-ray showed bone erosion on humerus. Thus, the synovectomy was performed with typical histopathology of RA on April 1999. On the end of February 2000, she had suddenly fatigue and anasarca with profound proteinuria of nephrotic syndrome. The renal biopsy showed minimal change glomerulopathy and no cellular infiltration in interstitial tissue by light microscopy and partial fusion of foot process by electron microscopy. Renal function was sustained normally. All of anti-rheumatic drugs including D-penicillamine(D-Pc) except NSAID were stopped and she was treated with bed rest, diet therapy, diuretics and albumin infusion without steroid therapy. Edema and proteinuria gradually disappeared. Membranous and amyloid nephropathy in RA patients associated with nephrotic syndrome are found in high incidence in literature. In low incidence, MCNS is associated with NSAID or D-Pc induced nephropathy in RA. In our case, nephrotic syndrome disappeared in 6 weeks without discontinuation of NSAID and application of steroid therapy. Thus, MCNS might be co-incidentally associated with RA.
Anti-Inflammatory Agents, Non-Steroidal↗
[Change of myosin heavy chain isoform expression and histocytochemical findings in skeletal muscular atrophy due to simulated weightlessness by hindlimb tenotomy].
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Animals↗
[Calcium dependent forms of synaptic plasticity in cerebellar Purkinje cells].
Elevation of intracellular calcium concentration ([Ca(2+)](i)) induces several forms of long-term synaptic plasticity in cerebellar Purkinje cells (PCs). These include (1) long-term depression (LTD) at parallel fiber (PF) to PC synapses, (2) LTD at climbing fiber (CF) to PC synapses, (3) long-term potentiation (LTP) at synapses from inhibitory interneurons (rebound potentiation). The current knowledge about calcium dependency for these forms of synaptic plasticity is described in this chapter. (1) Induction of PF-LTD is dependent on elevation of [Ca(2+)](i), that derives from two distinct sources. One is through voltage-dependent calcium channel (VDCC). A CF stimulation leads to elevation of [Ca(2+)](i) due to activation of VDCCs. The other is from the internal calcium store. PFs stimulation activates metabotropic glutamate receptor subtype 1 (mGluR1). It leads to production of inositol-1,4,5-triphosphate (IP(3)) and diacylglycerol (DG) which cause calcium release from internal stores and activation of protein kinase C, respectively. The conjunctive activation of PF and CF inputs is necessary for PF-LTD. (2) LTD at CF to PC synapses (CF-LTD) is induced by the mechanisms similar to those involved in PF-LTD. CF-LTD requires elevation of [Ca(2+)](i) and activation of the mGluR1 to PKC cascade. (3) Rebound potentiation is induced by transient elevation of [Ca(2+)](i) due to activation of VDCCs or IP3-mediated calcium release from internal stores. Elevation of [Ca(2+)](i) activates calcium/ calmodulin-dependent protein kinase II and leads to persistent up-regulation of postsynaptic GABAA receptor function. At the three types of synapses described above, elevation of [Ca(2+)](i) also causes short-term depression of neurotransmitter release from presynaptic terminals. Recent studies demonstrate that transient elevation of [Ca(2+)](i) produces endocannabinoids in PCs that act retrogradely onto presynaptic terminals and suppress neurotransmitter release.
English Abstract↗
Proarrhythmic effects of fluoroquinolone antibacterial agents: in vivo effects as physiologic substrate for torsades.
Drug-induced prolongation of the QT interval is often associated with the onset of Torsades de Pointes (TdP) resulting in a life-threatening ventricular arrhythmia. The potential of the proarrhythmic effects of the new fluoroquinolone antibacterial agents, levofloxacin and sparfloxacin, was examined in the chronic complete atrioventricular block dogs with stable idioventricular automaticity using Holter ECG monitoring in conscious state (Experiment 1). Next, to better analyze the mechanisms of the proarrhythmic property, the cardiovascular effects of these two drugs were compared in the halothane-anesthetized dogs under the monitoring of ECG, His bundle electrogram, systemic and left ventricular pressure, monophasic action potential, cardiac output, and effective refractory period (Experiment 2). In Experiment 1, oral administration of 6 mg/kg (n = 4) as well as 60 mg/kg (n = 4) of levofloxacin did not induce any ventricular premature depolarization. On the other hand, oral administration of 60 mg/kg of sparfloxacin (n = 4) induced TdP leading to ventricular fibrillation in all animals within 24 h, while 6 mg/kg of sparfloxacin (n = 4) did not induce any ventricular premature depolarization. In Experiment 2, intravenous administration of 0.3 mg/kg as well as 3.0 mg/kg of levofloxacin slightly increased cardiac output, but no significant changes were detected in the other parameters (n = 6). On the other hand, intravenous administration of 0.3 mg/kg of sparfloxacin prolonged the effective refractory period. Additional administration of 3.0 mg/kg of sparfloxacin decreased the heart rate and prolonged the effective refractory period and ventricular repolarization phase in a similar extent, but no significant changes were detected in the other parameters (n = 6). These results suggest that backward shift of the relative repolarization period in a cardiac cycle may be the mechanism responsible for the torsadegenic effect of sparfloxacin.
Action Potentials↗
Beneficial effect of FR167653 on cold ischemia/reperfusion injury in rat liver transplantation.
BACKGROUND: Proinflammatory cytokines such as interleukin 1-beta (IL-1beta) and tumor necrosis factor-a (TNF-alpha) play an important role in the development of hepatic ischemia/reperfusion injury. FR167653 has been characterized as a potent suppressant of IL-1beta and TNF-alpha production. The aim of this study was to evaluate the effect of FR167653 on cold ischemia/ reperfusion injury in rat liver transplantation. METHODS: Donor livers were preserved with cold University of Wisconsin solution for 48 hr and transplanted orthotopically. Immediately after reperfusion, FR167653 (1 mg/kg, FR-treated group) or normal saline solution (control group) was administered i.v.. The severity of liver injury was determined by hepatic enzyme levels as well as by histological findings. The accumulation of IL-1beta and TNF-alpha mRNA in the liver was analyzed by semi-quantitative reverse transcription-polymerase chain reaction. Tissue factor expression was subjected to immunohistochemical analysis. RESULTS: In the FR-treated group, release of aspartate aminotransferase and alanine aminotransferase after reperfusion was significantly lower (P<0.05 and P<0.02, respectively), and histological liver injury was less prominent, than in the control group. Accumulation of IL-1beta and TNF-alpha mRNA was suppressed in the FR-treated liver. Tissue factor expression on Kupffer cells and sinusoidal endothelial cells, marked in the control group, was almost absent in the FR-treated group. Seven-day survival in the FR-treated group (75%) was significantly better than that in the control group (12.5%) (P<0.01). CONCLUSIONS: These results indicate that treatment with FR167653 ameliorates cold ischemia/reperfusion injury in liver transplantation.
Animals↗
Frequent altered expression of fragile histidine triad protein in human colorectal adenomas.
Fragile histidine triad (FHIT) gene is involved in deletions on the short arm of chromosome 3 in various human cancers. We found that 47% of colorectal adenomas, which is a higher frequency than that of K-ras, showed altered expression of the Fhit protein by Western blot analysis. The amount of Fhit protein was inversely correlated with the degree of dysplasia. Importantly, 27% of low-grade dysplastic adenomas showed altered expression of Fhit protein. Additionally, expression of human Fhit protein in human colon carcinoma cell line SW480 exhibited a marked inhibition of growth and rendered SW480 cells highly susceptible to undergo apoptosis compared with control cells. These findings suggest that altered expression of the FHIT gene is a quite early aberration in the development of colorectal tumors and that Fhit protein may act as a tumor suppressor.
Acid Anhydride Hydrolases↗
Crystal structure and magnetic properties of an octacyanometalate-based three-dimensional tungstate(V)-manganese(II) bimetallic assembly.
A single crystal of the title compound [MnII6(H2O)9[W(V)(CN)8]4 x 13H2O]n was synthesized in a hot aqueous solution containing octacyanotungstate, Na3[W(CN)8] x 3H2O, and Mn(ClO4)2 x 6H2O. The compound crystallized in the monoclinic system, space group P2(1)/c with cell constants a = 15.438(2) A, b = 14.691(2) A, c = 33.046(2) A, beta = 94.832(9) degrees, and Z = 4. The crystal consists of a W(V)-CN-MnII linked three-dimensional network [[MnII(H2O)]3[MnII(H2O)2]3[W(V)(CN)8]4]n and H2O molecules as crystal solvates. There are two kinds of W sites: one is close to a dodecahedron geometry with six bridging and two terminal CN ligands; the other is close to a bicapped trigonal prism with seven bridging and one terminal CN ligands. The field-cooled magnetization measurement showed that the compound exhibits a spontaneous magnetization below Tc = 54 K. Further magnetization measurements on the field dependence reveal it to be a ferrimagnet where all of the MnII ions are antiparallel to all the W(V) ions.
Journal Article↗
Identification of hypoxia-inducible factor 1 ancillary sequence and its function in vascular endothelial growth factor gene induction by hypoxia and nitric oxide.
Transcription of hypoxia-inducible genes is regulated by hypoxia response elements (HREs) located in either the promoter or enhancer regions. Analysis of these elements reveals the presence of one or more binding sites for hypoxia-inducible factor 1 (HIF-1). Hypoxia-inducible genes include vascular endothelial growth factor (VEGF), erythropoietin, and glycolytic enzyme genes. Site-directed mutational analysis of the VEGF gene promoter revealed that an HIF-1 binding site (HBS) and its downstream HIF-1 ancillary sequence (HAS) within the HRE are required as cis-elements for the transcriptional activation of VEGF by either hypoxia or nitric oxide (NO). The core sequences of the HBS and the HAS were determined as TACGTG and CAGGT, respectively. These elements form an imperfect inverted repeat, and the spacing between these motifs is crucial for activity of the promoter. Gel shift assays demonstrate that as yet unknown protein complexes constitutively bind to the HAS regardless of the presence of these stimuli in several cell lines, in contrast with hypoxia- or NO-induced activation of HIF-1 binding to the HBS. A common structure of the HRE, which consists of the HBS and the HAS, is seen among several hypoxia-inducible genes, suggesting the presence of a novel mechanism mediated by the HAS for the regulation of these genes.
Base Sequence↗
The effect of the antipsychotic drug mosapramine on the expression of Fos protein in the rat brain: comparison with haloperidol, clozapine and risperidone.
In this study, we examined the effect of the acute p.o. administration of the antipsychotic drug mosapramine, as well as the antipsychotic drugs clozapine, haloperidol and risperidone, on the expression of Fos protein in the medial prefrontal cortex, nucleus accumbens and dorsolateral striatum of rat brain. The administration of mosapramine (1 or 3 mg/kg) significantly increased the number of Fos protein positive neurons in the medial prefrontal cortex, but not in the dorsolateral striatum. In addition, mosapramine (1, 3 or 10 mg/kg) produced a dose-dependent increase in the number of Fos protein positive neurons in the nucleus accumbens. The acute administration of 10 mg/kg of mosapramine significantly increased the number of Fos protein positive neurons in all brain regions. The acute administration of clozapine (30 mg/kg), similarly to mosapramine at lower doses (1 or 3 mg/kg), significantly increased the number of Fos protein positive neurons in the medial prefrontal cortex and nucleus accumbens, but not dorsolateral striatum. In contrast, haloperidol (0.3 mg/kg) significantly increased the number of Fos protein positive neurons in the nucleus accumbens and dorsolateral striatum, but not medial prefrontal cortex. The acute administration of risperidone (0.3 or 1 mg/kg) did not affect the number of Fos protein positive neurons in the medial prefrontal cortex, nucleus accumbens or dorsolateral striatum of rat brain, whereas a 3 mg/kg dose of risperidone significantly increased the number of Fos protein positive neurons in all brain regions. These results suggest that the ability of mosapramine to enhance expression of Fos protein in the medial prefrontal cortex may contribute to a clozapine-like profile with respect to actions on negative symptoms in schizophrenia. Furthermore, the lack of effect of low doses of mosapramine on Fos protein expression in the dorsolateral striatum, an area believed to play a role in movement, suggests that it may have a lower tendency to induce neurological side effects.
Animals↗
cAMP response element-binding protein-binding protein mediates thyrotropin-releasing hormone signaling on thyrotropin subunit genes.
Transcription of pituitary alpha-glycoprotein hormone subunit (alpha-GSU) and thyrotropin beta subunit (TSH-beta) genes is stimulated by thyrotropin-releasing hormone (TRH). Since cAMP response element-binding protein (CREB)-binding protein (CBP) integrates a number of cell signaling pathways, we investigated whether CBP is important for TRH stimulation of the TSH subunit genes. Cotransfection of E1A in GH(3) cells completely blocked TRH stimulation of the TSH subunit genes, suggesting that CBP is a key factor for TRH signaling in the pituitary. CBP and Pit-1 acted synergistically in TRH stimulation of the TSH-beta promoter, and amino acids 1-450 of CBP were sufficient for the TRH effect. In contrast, on the human alpha-GSU promoter, CREB and P-Lim mediated TRH signaling. Intriguingly, CREB was phosphorylated upon TRH stimulation, leading to CBP recruitment to the alpha-GSU promoter. CBP also interacted with P-Lim in a TRH-dependent manner, suggesting that P-Lim is an important factor for non-cAMP response element-mediated TRH stimulation of this promoter. Distinct domains of CBP were required for TRH signaling by CREB and P-Lim on the alpha-GSU promoter, amino acids 450-700 and 1-450, respectively. Thus, the amino terminus of CBP plays a critical role in TRH signaling in the anterior pituitary via both Pit-1-dependent and -independent pathways, yielding differential regulation of pituitary gene products.
CREB-Binding Protein↗