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Y Hatano

Publications and source records attributed to Y Hatano.

At least 19 recordsLinked to original sources

A clinical analysis of 52 adult patients with hemophagocytic syndrome: the prognostic significance of the underlying diseases.

We retrospectively analyzed 52 adult patients with hemophagocytic syndrome (HPS). The underlying diseases were heterogeneous, including malignant lymphoma (lymphoma-associated hemophagocytic syndrome [LAHS]) in 26 patients, systemic lupus erythematosus in 3 patients, viral infections in 7 patients, and bacteria] or fungal infections in 6 patients. More than 83% of patients received prednisolone as an initial treatment. Multiple-agent chemotherapies (cyclophosphamide, doxorubicin, and vincristine) were administered to 96% of LAHS patients after a histopathological diagnosis of lymphoma. HPSs were controllable and remissions were achieved except for those patients with LAHS, fulminant Epstein-Barr virus-associated HPS, and an immunosuppressive state. Twenty-one (81%) of the LAHS patients had uncontrollable HPS and died of multiple organ failure and disseminated intravascular coagulation. The median survival time of LAHS patients was 83 days. In contrast, 3 (12%) of the other HPS patients died of multiple organ failure within 44 days.The clinical manifestations and the laboratory findings of LAHS and the other HPSs were too variable to establish the prognosis based only on the findings at the onset of HPS. The prognostic factors of adult HPS were found to be the underlying diseases, notably malignant lymphoma and infections, accompanied by the immunosuppressive state.

Adult↗

Budding of fowlpox and pigeonpox viruses at the surface of infected cells.

Chick embryo fibroblasts and chorioallantoic membranes infected with fowlpox virus (FWPV) or pigeonpox virus (PPV) were examined by transmission and scanning electron microscopy. Immature virus particles were observed in finely granular areas, i.e. virus factories, of the cytoplasm. These particles had various forms depending on their stages of development. Many tubular structures were also seen in these regions. Mature virus particles with ellipsoidal or brick-shaped forms enclosing electron-dense cores were detected throughout the cytoplasm. Notably, there was a high frequency of virus budding at the cell surface, but only occasional virus wrapping in the cytoplasm. Another remarkable feature of the infected cells was accumulation of many virions just beneath the plasma membrane, indicating that this phenomenon is closely related to virus budding. Based on the observed frequency of budding, this mechanism seems to be the predominant way for FWPV and PPV to exit the cell.

Animals↗

Cibenzoline has an inhibitory effect on vasorelaxation mediated by adenosine triphosphate-sensitive K(+) channels in the rat carotid artery.

UNLABELLED: Studies in cardiac myocytes have shown that cibenzoline reduces adenosine triphosphate (ATP)-sensitive K(+) currents, suggesting that this class Ia antiarrhythmic drug may modify the activity of ATP-sensitive K(+) channels in these preparations. The effects of class Ia antiarrhythmic drugs on vasodilation mediated by ion channels have not been studied. Therefore, we designed this study to examine whether cibenzoline may produce changes in vasorelaxation in response to a selective ATP-sensitive K(+) channel opener, levcromakalim, in the isolated rat carotid artery. Rings of rat carotid arteries without endothelium were suspended for isometric force recording. Concentration-response curves were obtained in a cumulative fashion. During submaximal contraction to phenylephrine (3 x 10(-7) M), vasorelaxation in response to levcromakalim (10(-8) to 10(-5) M) or 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene (NOC-7; 10(-10) to 10(-5) M) was obtained. During contraction to phenylephrine, levcromakalim induced concentration-dependent vasorelaxation. A selective ATP-sensitive K(+) channel antagonist, glibenclamide (5 x 10(-6) M), completely abolished vasorelaxation in response to levcromakalim, whereas a selective Ca(2+)-dependent K(+) channel antagonist, iberiotoxin (5 x 10(-8) M), did not affect the relaxation. Cibenzoline (10(-6) to 10(-5) M) significantly reduced vasorelaxation to levcromakalim in a concentration-dependent fashion. In contrast, cibenzoline (10(-5) M) did not alter vasorelaxation to a nitric oxide donor, NOC-7. These results suggest that from the clinically relevant concentrations, a novel class Ia antiarrhythmic drug, cibenzoline, impairs carotid vasodilation mediated by ATP-sensitive K(+) channels. IMPLICATIONS: In isolated rat carotid artery, cibenzoline (10(-6) to 10(-5) M) reduced vasorelaxation to levcromakalim in a concentration-dependent fashion. These results suggest that from the clinically relevant concentrations, a novel class Ia antiarrhythmic drug, cibenzoline, impairs carotid vasodilation mediated by adenosine triphosphate-sensitive K(+) channels.

Adenosine Triphosphate↗

Mild alkalinization and acidification differentially modify the effects of lidocaine or mexiletine on vasorelaxation mediated by ATP-sensitive K+ channels.

BACKGROUND: The previous study by the authors showed that the class Ib antiarrhythmic drug lidocaine impairs but mexiletine augments vasorelaxation mediated by adenosine triphosphate-sensitive K+ channels. Lidocaine and mexiletine have different values of the negative logarithm of the drug-proton dissociation constant, indicating that the ion channel-blocking effects of these drugs under different pH levels may vary. However, the role of pH in the effects of lidocaine and mexiletine on vasodilation mediated by K+ channels has not been studied. Therefore, the current study was designed to examine whether the inhibition and augmentation of vasorelaxation in response to an adenosine triphosphate-sensitive K+ channel opener, levcromakalim, by the clinically relevant concentrations of lidocaine or mexiletine are modified by mild alkalinization or acidification in the isolated rat aorta. METHODS: Rings of the rat aorta without endothelium were suspended for isometric force recording. Three types of modified Krebs-Ringer solutions (pH 7.2, 7.4, and 7.6) were prepared by changing the composition of NaCl and NaHCO3. During contractions in response to phenylephrine (3 x 10(-7) M), relaxations in response to levcromakalim (10(-8) to 10(-5) M) were obtained. Lidocaine (10(-5) to 10(-4) M), mexiletine (10(-5) to 10(-4) M), or glibenclamide (10(-5) M) was applied 15 min before addition of phenylephrine. RESULTS: Relaxations in response to levcromakalim, which are abolished by the selective adenosine triphosphate-sensitive K+ channel antagonist glibenclamide (10(-5) M), were not different among the three pH groups. In the normal Krebs-Ringer solution of pH 7.4, lidocaine significantly reduced these relaxations in a concentration-dependent fashion. Alkalinization of pH 7.6 augmented the inhibitory effect of lidocaine on these relaxations, whereas acidification of pH 7.2 substantially abolished this effect. In contrast, mexiletine pH independently augmented relaxations in response to levcromakalim. Glibenclamide (10(-5) M) abolished these relaxations in arteries treated with mexiletine (10(-4) M) in any pH group. CONCLUSIONS: These results suggest that even under conditions of such mild alkalosis or acidosis, vasorelaxation via adenosine triphosphate-sensitive K+ channels is dependent on pH in the presence of clinically relevant concentrations of lidocaine but not mexiletine.

ATP-Binding Cassette Transporters↗

Halothane but not isoflurane attenuates interleukin 1beta-induced nitric oxide synthase in vascular smooth muscle.

BACKGROUND: Inducible nitric oxide synthase (iNOS) is induced by endotoxin or cytokines, such as interleukin (IL)-1, through a protein synthesis pathway. Halothane reportedly inhibits protein synthesis in various tissues. The aim of the current study was to examine the effect of halothane on the IL-1beta-evoked induction of NOS in vascular smooth muscle. METHODS: After removal of the endothelium, arterial rings of rat aorta were mounted in an isometric force recording system. The effects of halothane (1.0-3.0%) or isoflurane (3.0%) on IL-1beta (20 ng/ml)-induced inhibition of the contractile responses to KCl (30 mM) and phenylephrine (10(-9)-10(-5) M) were studied. The cyclic guanosine monophosphate and cyclic adenosine monophosphate contents were determined by radioimmunoassay. Expression of iNOS and iNOS mRNA were measured by Western or Northern blot analysis, respectively. RESULTS: Halothane (1.0-3.0%) but not isoflurane (3%) significantly reduced the ML-1beta-induced inhibition of contraction in a concentration-dependent manner. The cyclic guanosine monophosphate content of the vascular smooth muscle increased significantly after a 5-h exposure to IL-1beta. Halothane at 3.0% significantly inhibited the increase in cyclic guanosine monophosphate content induced by IL-1beta. Halothane had no effect on cyclic adenosine monophosphate content. IL-1beta-induced expression of iNOS and iNOS mRNA in the rat aorta were inhibited significantly by halothane. CONCLUSION: The current study demonstrated that halothane but not isoflurane inhibits IL-1beta-stimulated hyporesponsiveness to vasoconstrictive agents in vascular smooth muscle and that this inhibitory effect of halothane involves the inhibition of iNOS mRNA expression. Thus, these findings suggest that halothane may have some sites to affect nitric oxide-signaling pathway.

Adenylyl Cyclases↗

The role of oxygen-derived free radicals in augmented relaxations to levcromakalim in the aorta from hypertensive rats.

Hydrogen peroxide and peroxynitrite induce relaxations via ATP-sensitive K+ channels, indicating that oxygen-derived free radicals may activate these channels. Levels of free radicals are increased throughout the arterial wall in animal models of atherosclerosis, and therefore, vasorelaxation via ATP-sensitive K+ channels may be augmented in chronic hypertension. The present study was designed to determine whether relaxations to an ATP-sensitive K+ channel opener, levcromakalim, are increased in the aorta from spontaneously hypertensive rats (SHR) and whether free radical scavengers reduce these relaxations. Rings of aortas without endothelium taken from age-matched Wistar-Kyoto rats (WKY) and SHR were suspended for isometric force recording. Relaxations to levcromakalim (10(-8) to 10(-5) M), which are abolished by glibenclamide (10(-5) M), were augmented in the aorta from SHR, compared to those in the aorta from WKY. In the aorta from SHR, catalase (1200 U/ml), but neither superoxide dismutase (150 U/ml) nor deferoxamine (10(-4) M), reduced relaxations to levcromakalim, whereas in the aorta from WKY, the free radical scavengers did not affect these relaxations. These results suggest that in chronic hypertension, vasorelaxation to an ATP-sensitive K+ channel opener is augmented and that hydrogen peroxide produced in smooth muscle cells may partly contribute to these relaxations.

Animals↗

Fish meal vs. corn gluten meal as a protein source for dry cat food.

To compare the effects of two dietary protein sources, fish meal (FM) and corn gluten meal (CGM), fecal moisture content, nitrogen balance and urinary excretion were examined in adult cats. The dietary protein source did not cause a significant difference in daily food intake, water intake, urine volume, dry matter digestibility or urinary nitrogen excretion, but fecal moisture content was lower (P<0.02) in the CGM group. The HCl-insoluble fraction of urinary sediment tended to be higher in the CGM group (P<0.10), although urinary pH was similar in the two groups. These results suggest that CGM is comparable with FM in respect to nutritional value and the urine acidifying effect, but FM may be preferable to CGM for the prevention of constipation and struvite urolithiasis in cats.

Animal Feed↗

Effect of supplementation of dry cat food with D,L-methionine and ammonium chloride on struvite activity product and sediment in urine.

Feeding dry foods supplemented with urine acidifier (D,L-methionine (Met) or ammonium chloride) decreased urinary pH and struvite activity product in clinically normal cats. As a result, the number of struvite crystals in urine was greatly reduced. Supplementation with 3% Met but not 1% Met caused decrease in the urinary concentration of sediment, which resulted from a reduction in the HCl-soluble fraction. The concentration of HCl-insoluble sediment was not affected by supplementation with the urine acidifier.

Ammonium Chloride↗

Thiopental enhances human platelet aggregation by increasing arachidonic acid release.

Conflicting results have been reported regarding the effect of thiopental on aggregation and cytosolic calcium levels in platelets. The present study attempted to clarify these phenomena. Using platelet-rich plasma or washed suspensions, platelet aggregation, thromboxane (TX) B2 formation, arachidonic acid (AA) release, and cytosolic free calcium concentrations ([Ca2+]i) were measured in the presence or absence of thiopental (30-300 microM). Platelet activation was induced by adenosine diphosphate (ADP, 0.5-15 microM), epinephrine (0.1-20 microM) arachidonic acid (0.5-1.5 mM), or (+)-9,11-epithia-11,12-methano-TXA2 (STA2, 30-500 nM). Measurements of primary aggregation were performed in the presence of indomethacin (10 microM). Low concentrations of ADP and epinephrine, which did not induce secondary aggregation in a control study, induced strong secondary aggregation in the presence of thiopental (> or = 100 microM). Thiopental (> or = 100 microM) also increased the TXB2 formation induced by ADP and epinephrine. Thiopental (300 microM) increased ADP- and epinephrine-induced 3H-AA release. Thiopental (300 microM) also augmented the ADP- and epinephrine-induced increases in [Ca2+]i in the presence of indomethacin. Thiopental appears to enhance ADP- and epinephrine-induced secondary platelet aggregation by increasing AA release during primary aggregation, possibly by the activation of phospholipase A2.

Arachidonic Acid↗

Bronchial cuff pressure change caused by left-sided double-lumen endobronchial tube displacement.

PURPOSE: The bronchial cuff pressures (BCPs) of left-sided double-lumen endobronchial tubes (DLTs) manufactured by Rüsch and Mallinckrodt were measured in 80 patients when the tubes were withdrawn to compare the effect of tube design on BCP change. METHODS: During general anesthesia with muscle relaxation, the cephalad surface of the endobronchial cuff was positioned either 2.5 cm distal to the carina (Rüsch Group R-I; n = 20 and Mallinckrodt Group B-I; n = 20) or just below the carina (Rüsch Group R- II; n = 20 and Mallinckrodt Group B- II; n = 20) and the cuff was inflated to 35 cm H2O. The tube was then withdrawn in 0.5-cm steps until the cuff was 2.0 cm proximal to the carina, the position just before the capnogram or pressure-volume loop of tracheal lumen changed. The BCP at each step was measured. The rate of decrease in BCP was defined as the decrease of BCP divided by the length of displacement of DLT. RESULTS: The rates of decrease from the +2.5 cm position to the end point in Group B-I (7.7+/-0.8 cm H2O x cm(-1) and those from the most proximal acceptable position to the end point in Group B-II (19.5+/-4.8 cm H2O x cm(-1) were greater than those in Group R-I (6.9+/-0.9 cm H2O x cm(-1) (P<0.01) and in Group R-II (12.4+/-3.1 cm H2O x cm(-1)) (P<0.01), respectively. CONCLUSION: The BCP decreased in both of the Mallinckrodt and Rüsch DLTs, and the rates of decrease of the former were greater than those of the latter.

Adult↗

Translocation (1;11)(q23;p15), a novel simple variant of translocation (7;11)(p15;p15), in a patient with AML (M2) accompanied by non-Hodgkin lymphoma and gastric cancer.

We describe a case of an acute myelogenous leukemia (AML) associated with t(1;11) (q23;p15), which is a novel simple variant translocation of t(7;11)(p15;p15). The patient was a Japanese man who had a history of non-Hodgkin lymphoma (NHL) and received MACOP-B combination chemotherapy. Fifteen months after the completion of the treatment, the patient developed AML (M2), which was regarded as a therapy-related leukemia. Cytogenetic study of bone marrow cells showed t(1;11). Although he achieved complete remission by combination chemotherapy, a relapse of NHL and gastric cancer were revealed in the course of the consolidation chemotherapy for AML. The NHL was considered a histological conversion from follicular lymphoma because lymphoma cells carried t(14;18) (q32;q21) and were strongly positive for BCL2 protein. Translocation (1;11), together with AML having t(7;11) or inv(11) involving 11p15, shows that 11p15 is a common acceptor site of these chromosome aberrations and suggests the significance of the NUP98 gene located in 11p15 in therapy-related leukemia.

Antineoplastic Combined Chemotherapy Protocols↗

Role of K+ channels in augmented relaxations to sodium nitroprusside induced by mexiletine in rat aortas.

BACKGROUND: A class Ib antiarrhythmic drug, mexiletine, augments relaxations produced by adenosine triphosphate (ATP) sensitive K+ channel openers in isolated rat aortas, suggesting that it produces changes in the vasodilation mediated by ATP-sensitive K+ channels. Nitric oxide can induce its vasodilator effect via K+ channels, including ATP-sensitive K+ channels, in smooth muscle cells. Effects of mexiletine on arterial relaxations to nitric oxide donors, have not been studied. Therefore, the current study in isolated rat aortas was designed to (1) evaluate whether mexiletine augments relaxation in response to nitric oxide donors, including sodium nitroprusside, and (2) determine the role of K+ channels in mediating effects of mexiletine on such nitric oxide-mediated relaxation. METHODS: Rings of rat aortas without endothelia were suspended for isometric force recording. Concentration-response curves of sodium nitroprusside (10(-10) to 10(-5) M) and 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene (NOC-7; 10(-9) to 10(-5) M) were obtained in the absence and in the presence of mexiletine, in combination with a soluble guanylate cyclase inhibitor, 1H-[1,2,4]oxadiazolo [4,3,-a]quinoxaline-1-one (ODQ), or inhibitors for ATP-sensitive K+ channels (glibenclamide), inward rectifier K+ channels (BaCl2), delayed rectifier K+ channels (4-aminopyridine), large conductance Ca2+-dependent K+ channels (iberiotoxin), or small conductance Ca2+-dependent K+ channels (apamin). RESULTS: Mexiletine (10(-5) or 3 x 10(-5) M) augmented relaxations to sodium nitroprusside and NOC-7. In arteries treated with glibenclamide (10(-5) M), mexiletine (3 x 10(-5) M) did not affect relaxations to nitric oxide donors, whereas mexiletine augmented relaxations to sodium nitroprusside despite the presence of BaCl2 (10(-5) M), 4-aminopyridine (10(-3) M), iberiotoxin (5 x 10(-8) M) and apamin (5 x 10(-8) M). Relaxations to sodium nitroprusside were abolished by ODQ (5 x 10(-6) M), whereas these relaxations were augmented by mexiletine (3 x 10(-5) M) in arteries treated with ODQ (5 x 10(-6) M). CONCLUSIONS: These results suggest that ATP-sensitive K+ channels in vascular smooth muscle, contribute to the augmented vasodilator effect of a nitric oxide donor, sodium nitroprusside induced by mexiletine, and that the vasodilator effect is produced, at least in part, via the guanylate cyclase-independent mechanism.

Animals↗

Inhibitory effects of halothane, isoflurane, sevoflurane, and pentobarbital on the constriction induced by hypocapnia and bicarbonate in isolated canine cerebral arteries.

The effects of halothane, isoflurane, sevoflurane (0.5, 1 and 2 MAC) and pentobarbital (10(-5) M, 10(-4) M and 3 x 10(-4) M) on hypocapnia- and bicarbonate-induced constriction of isolated dog middle cerebral arteries were investigated in vitro. The isometric tension of isolated cerebral arterial rings was measured in an organ bath containing Krebs bicarbonate solution, aerated with 5% CO2 and 95% O2. Hypocapnia, induced by replacing the bathing solution with one that had been equilibrated with 2.5% CO2 and 97.5% O2, produced a sustained vasoconstriction (268 +/- 36 mg, mean +/- SEM). Exposure of arterial rings to a bathing solution that contained double the concentration of NaHCO3 (50 mM) elicited a phasic constriction followed by a gradual decrease in tension (309 +/- 34 mg). Although halothane, isoflurane, and sevoflurane attenuated both hypocapnia- and bicarbonate-induced constrictions in a dose-dependent manner, the inhibition of these constrictions was greater in rings treated with halothane than in those treated with isoflurane or sevoflurane when compared at equipotent concentrations. These alkaline-induced constrictions were attenuated by pentobarbital only at the highest concentration of 3 x 10(-4) M. Halothane (1 and 2 MAC) attenuated the constriction induced by hypocapnia to a greater extent than that induced by 15 mM KCl, whereas pentobarbital (10(-4) M and 3 x 10(-4) M) attenuated hypocapnia-induced constriction less than KCl-induced constriction. These results indicate that alkaline-induced constriction is more vulnerable to halothane than other volatile anesthetics and pentobarbital. The mechanisms of the inhibitory effects of halothane and pentobarbital on alkaline-induced cerebral vasoconstriction seem to differ; the inhibitory effect of pentobarbital, but not of halothane may be, in part, ascribed to its inhibitory effect on the Ca++ influx.

Anesthetics, Inhalation↗

A case of pencil core granuloma with an unusual temporal profile.

The patient is a 47-year-old female with a bluish tumor resembling malignant melanoma at the macroscopic level on the medial aspect of her left big toe. The patient had crushed a pencil with this toe about 30 years previously and, since then, a bluish lesion had been present. About 15 years ago, the lesion had suddenly increased in size over the course of a few months. Subsequently, the size of the lesion had not changed noticeably. Ultrasonography, but not magnetic resonance imaging was a helpful preoperative examination to distinguish the lesion from malignant melanoma. The excised lesion contained a piece of material that resembled pencil lead and bluish mud. X-ray microanalysis of the lead-like material revealed that its composition was similar to that of pencil lead. Histologic examination showed features of foreign-body reaction, except for necrotic change and few histiocytes.

Female↗

Mesonephric adenocarcinoma of the urinary bladder: a case report.

We report a very rare case of mesonephric adenocarcinoma of the urinary bladder, the origin of which is still uncertain. A non-papillary and broad-based tumor was located in the trigone and bladder neck on cystoscopic examination. Pelvic magnetic resonance imaging in T2-weighted images revealed a mass invading into the muscular layer of the bladder wall. Histologic examination of bladder cup-biopsy specimens showed adenocarcinoma. She underwent total cystectomy and pelvic lymph node dissection. Histologically, the tumor was chiefly composed of cells with eosinophilic cytoplasm and partly of cells with clear cytoplasm or hobnail-shaped cells, arranged in tubular or papillary structures, and infiltrated peri-vesical fat tissues. She died of metastatic disease 22 months after surgery. To the best of our knowledge, the present case is the 19th reported in the literature.

Adenocarcinoma, Clear Cell↗