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Biomedical subjects

Y Hatano

Publications and source records attributed to Y Hatano.

At least 19 recordsLinked to original sources
PubMed1996

Translocation (9;11;22)(p22;q23;q11). A new type of complex variant translocation of t(9;11)(p22;q23) with MLL rearrangement.

We describe a patient with acute monocytic leukemia (M5a, FAB classification) associated with a new type of variant translocation (9;11). Southern blot analysis showed the rearrangement of the MLL (ALL-1/HRX) gene at 11q23. Fluorescence in situ hybridization (FISH) with painting probes of chromosomes 9, 11, and 22 revealed the translocation as t(9;11;22) (p22;q23;q11). This is more evidence that the production of chimeric mRNA following the translocation of the LTG9 (MLLT3/AF9) gene at 9p22 to 11q is a critical event in this leukemia subtype.

Adult↗
PubMed1996

Electron microscopic observations of aberrant capsids of pseudorabies virus.

Interactions between four strains of pseudorabies virus (PrV) and seven kinds of cell lines were examined. Three kinds of cells (SKL, CPK and PK-15) were especially infected with PrV at an MOI of about 10 PFC/cell. At sequential intervals after infection, cells of these types were collected for electron microscopic observations and the infectious doses of culture fluids were assayed. Developmental features of PrV were found to be very similar to those of herpes simplex virus (HSV), with the slight difference that PrV developed a little earlier and more vigorously than did HSV. At the late stage of infection, aberrant capsids of PrV were observed frequently in the nucleus of SKL but rarely in the nuclei of CPK and PK-15. The titer of infectious virus produced by SKL was much larger than that produced by CPK and PK-15. Immuno-electron microscopic examination using a monoclonal antibody against the major capsid protein of PrV clearly demonstrated that the complete and aberrant capsids have a common epitope. The mechanism of the formation of aberrant capsids is discussed.

Animals↗
PubMed1995

Granulocyte colony-stimulating factor downregulates allogeneic immune responses by posttranscriptional inhibition of tumor necrosis factor-alpha production.

We report downregulatory effects of granulocyte colony-stimulating factor (G-CSF) on allogeneic immune responses in vitro. G-CSF did not affect the proliferative response of peripheral blood mononuclear cells (PBMC) against allogeneic Daudi cells but did inhibit tumor necrosis factor (TNF)-alpha secretion. In contrast with G-CSF, granulocyte-macrophage (GM)-CSF and interleukin (IL)-3 enhanced alloactivation-induced TNF-alpha production. G-CSF-mediated suppression of TNF-alpha production was not affected by fixation of stimulators. G-CSF did not inhibit TNF-alpha mRNA expression or accelerate mRNA degradation, whereas pentoxifylline inhibited the expression of TNF-alpha mRNA. These results indicate that G-CSF acts directly on responder cells and modulates TNF-alpha production at posttranscriptional levels. Suppression of TNF-alpha secretion was accompanied by an increase of intracellular cyclic adenosine monophosphate (cAMP) concentration in alloactivated PBMC. The cell-permeable cAMP analogue, dibutyryl cAMP, suppressed TNF-alpha secretion without affecting TNF-alpha mRNA expression. G-CSF showed an inhibitory effect on the development of cytotoxic effector cells against allogeneic Daudi cells. Anti-TNF-alpha monoclonal antibody (MoAb) also inhibited the induction of cytolytic activity, and the inhibitory effects of G-CSF and anti-TNF-alpha MoAb on killer activity generation were overcome by adding exogenous TNF-alpha. Hence, impaired generation of cytolytic effector cells by G-CSF is believed to be the result of reduced TNF-alpha production. Collectively, the results described above suggest that G-CSF downregulates allogeneic immune responses by posttranscriptionally inhibiting TNF-alpha production.

Antibodies, Monoclonal↗
PubMed1995

cDNA cloning of BR gamma, a novel brain-specific isoform of the B regulatory subunit of type-2A protein phosphatase.

A cDNA clone for a novel isoform of the B regulatory subunit of type 2A protein phosphatase (BR) was isolated from a rat brain cDNA library by hybridization under low-stringency conditions with the BR beta cDNA fragment as a probe. The novel cDNA encodes a protein of 447 amino acids. The identities of amino acid sequences of the novel isoform with those of rat BR alpha and BR beta were 80% and 85%, respectively, with a unique sequence at the C-terminal. Since this isoform is thought to be encoded by a third gene for the B regulatory subunit, it was named BR gamma. The mRNA for BR gamma was 4.2 kb. The expression level of BR gamma was high in the brain and spinal cord of rats, and its expression was also detected in mouse and human brains, but in contrast to BR beta, it was not detected in the testes of rats or mice. Thus BR gamma is though to be a brain-specific isoform of the B regulatory subunit.

Amino Acid Sequence↗
PubMed1995

Analysis of molluscum contagiosum virus genomes isolated in Japan.

The genomes of 477 Japanese strains of molluscum contagiosum virus (MCV) were analyzed using an in-gel digestion method with the restriction enzyme BamHI, and classified into four types, including a newly detected type (MCV type 4). All type 1 (MCV-1) genomes examined so far in Japan showed a common difference from the genome of the MCV-1 prototype (MCV-1p), the type reported to be most prevalent in Europe. The common markers of the variants of MCV-1 were 24-kbp fusion fragments generated by the loss of a BamHI site between the D2 and F fragments of MCV-1p. These variants of MCV-1 were classified into three groups (MCV-1va, MCV-1vb, MCV-1vc), with the variability among them being due to additions and losses of BamHI sites located in the right terminus and around the E and I fragments of MCV-1va. The restriction map of MCV-4 was generated and lined up with those of the other types. Cross-hybridization analysis revealed that the organization of all types of MCV genomes were essentially colinear. Considerable numbers of BamHI restriction sites were conserved between MCV-2 and 4, indicating a close analogy between them. The overall prevalence of MCV, as shown by the ratios of MCV-1 (MCV-1p):MCV-2:MCV-3:MCV-4, was 436(0):13:24:4. Thus, the molecular epidemiology of MCV in Japan is characterized by the absence of the European prototype of MCV-1, the exclusive occurrence and abundance of variants of MCV-1, a greater prevalence of MCV-3 over MCV-2, and the presence of MCV-4.

Genetic Variation↗
PubMed1995

Syndrome of inappropriate secretion of antidiuretic hormone in patients with lymphoma-associated hemophagocytic syndrome.

We report three lymphoma patients in whom the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was observed during the course of lymphoma-associated hemophagocytic syndrome (LAHS). The clinical course was devoid of any known mechanism for SIADH which could be attributable to lymphoma or antineoplastic treatment. Alternatively, high serum levels of interleukin-1 beta and tumor necrosis factor-alpha, which stimulate the secretion of antidiuretic hormone, may have contributed to the development of SIADH in our patients, who were receiving glucocorticoids. In conclusion, LAHS patients should be considered to be at high risk for SIADH.

Aged↗
PubMed1995

The effect of inhaled anesthetics on the platelet aggregation and the ligand-binding affinity of the platelet thromboxane A2 receptor.

The mechanism by which anesthetics suppress platelet aggregation has not been elucidated. We determined the effects of halothane, enflurane, and isoflurane on human platelet aggregation induced by adenosine diphosphate (ADP), epinephrine, and a thromboxane A2 (TXA2) analog, and on ligand binding to the platelet TXA2 receptor. Halothane (2.6 mM) strongly suppressed ADP- and epinephrine-induced secondary aggregation of platelets, without significant alteration of primary aggregation. Platelet aggregation induced by a specific TXA2 agonist, (+)-9,11-epithia-11,12-methano-TXA2 (STA2), was suppressed by halothane, enflurane, and isoflurane in a concentration-dependent manner; the concentration of halothane, enflurane, and isoflurane which induced 50% inhibition (IC50) were 3.2, 12.3, and 15.7 mM, respectively (or 4.7, 9.8, and 24 minimum alveolar anesthetic concentration [MAC], respectively). The binding of a specific TXA2 receptor antagonist, 3H-S145, was significantly reduced by halothane (14-28 mM), but not by enflurane (20 mM) and isoflurane (20 mM). Scatchard analysis revealed that halothane (14 mM) increased Kd from 0.53 nM to 14.3 nM but did not alter Bmax significantly. These results indicate that halothane has a stronger suppressive effect on platelet aggregation than enflurane and isoflurane, and that the effect of halothane on platelet aggregation is due to reduction of the ligand-binding affinity of the platelet TXA2 receptor.

Adenosine Diphosphate↗
PubMed1995

Combined dorsal forearm and lateral arm flap.

The free latissimus dorsi musculocutaneous flap and the free groin flap have been used for the coverage of medium- to large-sized soft-tissue defects in the hand. However, these are often too bulky for the hand, requiring secondary operation for thinning. We have used the dorsal forearm flap combined with the lateral arm flap for the coverage of large soft-tissue defects in the hand. This flap is based on the reversed vascular pedicle of the posterior interosseous artery. The posterior radial collateral branch of the profunda brachii artery is then anastomosed to the recipient vessel to augment the vascular supply to the lateral arm flap. We have used this combination flap in two clinical cases and achieved one-stage soft-tissue reconstruction of the hand.

Adult↗
PubMed1995

Endothelium-dependent and -independent vasodilation of isolated rat aorta induced by caffeine.

Caffeine (10(-4)-10(-3) M) induced concentration-dependent relaxations of phenylephrine-precontracted rat aortic rings with endothelium. Endothelial denudation significantly, but only partially, attenuated caffeine-induced relaxation. Pretreatment with NG-nitro-L-arginine, oxyhemoglobin, and methylene blue attenuated the relaxations to an extent similar to endothelial denudation. Guanosine 3',5'-cyclic monophosphate (cGMP) and adenosine 3',5'-cyclic monophosphate (cAMP) contents of aortic strips with endothelium increased significantly after exposure to caffeine (10(-3) M). Endothelial denudation attenuated caffeine-induced cGMP increase. Pretreatment with ryanodine (2 x 10(-5) M), which has been shown to combine with receptors on endoplasmic reticulum (ER) of endothelium, attenuated caffeine-induced relaxation and cGMP content increase of rings with endothelium. Pretreatment with caffeine potentiated sodium nitroprusside-induced relaxations and cGMP increase of rings without endothelium. These results demonstrated that caffeine-induced relaxation comprises two components. In the endothelium-dependent mechanism, caffeine promotes nitric oxide synthesis in endothelium by release of Ca2+ from ER through a ryanodine-sensitive Ca2+ channel, and the suppression of cGMP degradation also contributes to the relaxation. In the endothelium-independent mechanism, caffeine acts as a 3',5'-cyclic-nucleotide phosphodiesterase inhibitor.

Animals↗
PubMed1995

Vasodilative effect of adrenomedullin in isolated arteries of the dog.

Adrenomedullin is known to induce profound hypotension in vivo, but the direct effect of this peptide on isolated arteries has not been demonstrated. This study estimated the vasodilative effects of adrenomedullin in comparison with those of calcitonin gene-related peptide (CGRP) in basilar, mesenteric, coronary, renal and femoral arteries isolated from the dog. Adrenomedullin (3 to 100 nM) and CGRP (1 to 30 nM) induced concentration-dependent relaxation of these arteries with and without endothelium, and the relaxing effects were slightly greater in endothelium-intact arteries than in denuded ones. The vasodilative potency of adrenomedullin relative to CGRP was smaller in the femoral artery than in basilar, mesenteric, coronary and renal arteries.

Adrenomedullin↗
PubMed1995

Laparoscopic nephrectomy using a retroperitoneal approach: comparison with a transabdominal approach.

To evaluate the efficacy of the retroperitoneal approach in laparoscopic nephrectomy, our procedures involving laparoscopic nephrectomy using a retroperitoneal approach are described and the clinical results of six patients treated in this way are compared with those of 32 transabdominally nephrectomized patients. Of the six retroperitoneally nephrectomized patients, six kidneys were successfully removed without severe complication, and 28 kidneys were successfully removed in the 32 intraabdominally approached group. Three of the 28 patients had complications requiring open laparotomy. The operating time was 2.7 hours in the 6 retroperitoneal patients and 4.4 hours in the 28 transabdominal patients. Estimated blood loss was 92 ml in the retroperitoneal group and 450 ml in the transabdominal group. The mean postoperative hospital stay was 8 days and 9 days, respectively. These results indicate that the retroperitoneal approach might be preferable in laparoscopic nephrectomy.

Abdomen↗
PubMed1994

Mechanisms of inhibition of endothelium-dependent relaxation by halothane, isoflurane, and sevoflurane.

Volatile anaesthetics inhibit endothelium-dependent relaxation, but the underlying mechanism(s) have not been clarified. In an attempt to elucidate the mechanism(s), we determined the effects of halothane, isoflurane and sevoflurane on relaxation induced by acetylcholine and sodium nitroprusside (SNP) and the cGMP formation elicited by exogenous nitric oxide (NO) and SNP in rat aortas. Acetylcholine (10(-7)-10(-5) M)-induced relaxation was attenuated by halothane (2%), isoflurane (2%) and sevoflurane (4%). SNP (10(-8) M)-induced relaxation was reduced by halothane (2%), but not by isoflurane (2%) or sevoflurane (4%). The cGMP level of NO-stimulated aorta was reduced by halothane (2%) and sevoflurane (4%), but not by isoflurane (2%). The cGMP level of SNP (10(-7) M)-stimulated aorta was reduced by halothane (2%), but not by isoflurane (2%) and sevoflurane (4%). We conclude that the mechanisms responsible for the inhibition of endothelium-dependent relaxation differ among anaesthetics. Isoflurane inhibits the relaxation mainly by inhibiting the formation of NO in the endothelium. In contrast, the effect of halothane on endothelium-dependent relaxation may be largely due to the inhibition of action of NO in the vascular smooth muscle and the effect of sevoflurane may be to inactivate NO or to inhibit the action of NO.

Anesthetics↗
PubMed1994

Halothane and isoflurane preferentially inhibit prostanoid-induced vasoconstriction of rat aorta.

In a previous study, we demonstrated that halothane and isoflurane inhibit binding of thromboxane A2 to its receptors on human platelets and thus inhibit prostanoid-induced aggregation strongly. The aim of this study was to determine whether volatile anaesthetics inhibit prostanoid-induced vasoconstriction preferentially. Rat isolated aortic rings were mounted in organ baths and their isometric tension was measured. They were contracted with STA2 (a stable thromboxane A2 analogue), prostaglandin F2 alpha (PGF2 alpha), phenylephrine, and 20 mM KCl, and then exposed to halothane (0.5-3%), isoflurane (0.5-3%), and sodium nitroprusside (SNP, 10(-9)-3 x 10(-7) M). Halothane (2-3%) and isoflurane (2-3%) induced greater relaxation of aortic rings precontracted with STA2 and PGF2 alpha than of those precontracted with phenylephrine (P < 0.01). Halothane induced greater relaxation of rings precontracted with KCl than phenylephrine only at 3%, whereas isoflurance relaxed rings precontracted with KCl more than those with phenylephrine at 0.5, 2 and 3% (P < 0.05). In contrast, SNP relaxed rings precontracted with PGF2 alpha. KCl and phenylephrine equally, but induced smaller relaxations of those precontracted with STA2 (P < 0.05). We conclude that halothane and isoflurane inhibit prostanoid-induced vasoconstriction preferentially, possibly by interacting with prostanoid receptors.

Acetylcholine↗
PubMed1994

Influence of polychlorinated biphenyls on the growth of chicken embryos.

Incubation of chicken embryos with either 0.01 or 0.03 ppm polychlorinated biphenyls (PCBs) for 12, 15, or 18 d resulted in a significant decrease in liver and body weight associated with enhanced mortality. Teratological examination revealed an increased frequency of malformations including hydrops, eventration, wry neck, and brevicollis. PCB exposure was also found to produce histologic damage to liver and cutaneous tissue. Our data demonstrate that exposure of chicks to PCBs during development results in a retardation of growth, an increased incidence of malformations, and histopathologic damage.

Animals↗
PubMed1994

Halothane and enflurane constrict canine mesenteric arteries by releasing Ca2+ from intracellular Ca2+ stores.

BACKGROUND: Recent studies suggest that volatile anesthetics cause not only vasodilation but also vasoconstriction, depending on the experimental conditions. However, the mechanism of the constrictive effect of volatile anesthetics has not been clarified. The aim of this study was to evaluate the vasoconstrictor effects of halothane, enflurane, and isoflurane and to elucidate the underlying mechanism. METHODS: Vascular rings of canine mesenteric arteries were mounted in organ baths, and isometric tension changes were recorded. Changes in intracellular free Ca2+ concentration of vascular smooth muscle were examined by using the fluorescent Ca2+ indicator fura 2 and a dual-wavelength fluorometer. RESULTS: Halothane (0.75-2.3%) and enflurane (1.7-3.4%), but not isoflurane (1.2-3.5%), induced a concentration-dependent transient contraction, followed by a slight, sustained contraction. Halothane (1.5%)- and enflurane (3.4%)-induced contractions were reduced by endothelial denudation and enhanced by indomethacin (10(-5) M) treatment but were not affected by L-NG-nitroarginine (10(-5) M) or nifedipine (2 x 10(-7) M) treatment. Ryanodine (2 x 10(-5) M) treatment completely abolished the transient increases in tension and Ca2+ concentration. Even in ryanodine-treated arteries, however, both anesthetics induced a slowly developing sustained contraction, and the sustained contraction induced by enflurane (3.4%) was not accompanied by a significant increase in Ca2+ concentration. CONCLUSIONS: Halothane and enflurane, but not isoflurane, induce vasoconstriction by releasing Ca2+ from intracellular stores. Release of a vasodilating prostanoid and endothelium-derived constricting factor may also be involved in the vasoconstrictor effect. Furthermore, increased Ca2+ sensitivity of contractile machinery may be involved in the effect of enflurane.

Animals↗
PubMed1994

Barbiturates inhibit endothelium-dependent and independent relaxations mediated by cyclic GMP.

The inhibitory effects of volatile and local, but not intravenous, anesthetics on endothelium-dependent relaxations of blood vessels have been demonstrated in vitro by several investigators. The aim of this study was to determine the effects of barbiturates on endothelium-dependent arterial relaxation and elucidate the mechanism(s) responsible. Canine mesenteric arteries and rat aortae were isolated, and tension changes in helical strips were recorded. Endothelium-dependent relaxations elicited by acetylcholine and bradykinin in canine mesenteric arteries, and those by acetylcholine in rat aortae, were significantly attenuated by thiopental (3 x 10(-4) M) pretreatment. Sodium nitroprusside (SNP)-induced, endothelium-independent relaxations were significantly attenuated by thiopental (10(-4)-3 x 10(-4) M). The effects of pentobarbital were less marked than those of thiopental. Acetylcholine (10(-5) M)-stimulated levels of 3',5'-cyclic guanosine monophosphate (cGMP) in rat aortae were reduced significantly by thiopental and pentobarbital (both 10(-3) M), and SNP (3 x 10(-7) M)-stimulated levels were reduced by thiopental (3 x 10(-4)-10(-3) M) and pentobarbital (10(-3) M). We conclude that barbiturates inhibit cGMP-mediated endothelium-dependent and independent arterial relaxations. Inhibition of endothelium-dependent relaxation by barbiturates may be mediated by their effects on vascular smooth muscle itself and not on endothelium.

Acetylcholine↗
PubMed1994

[A study of prostatic tissue levels of cefodizime (CDZM)].

Twenty-four patients suffering from prostate hyperplasia were given venous injections of CDZM of either 1 or 2 g at specific intervals (30 min, 1, 2 and 4 hr) before surgery. Blood samples from the injected vein and tissue samples from the prostate were subsequently taken. In this study, the concentrations of CDZM in the prostate tissue (P) and in serum (S), as well as the ratio of the tissue to serum concentrations (P/S) were determined. In patients given 1 g injections, P ranged from 5.26-48.10 micrograms/g, while S ranged from 25.40-130.00 micrograms/ml and P/S ranged from 12.6-37.0%. In the patients given 2 g injections, P ranged from 9.40-49.20 micrograms/g, S ranged from 62.30-234.00 micrograms/ml and P/S ranged from 9.3-29.1%. CDZM exhibited excellent transmigration to the prostate tissue. Inflammatory bacteria present in prostatitis and urinary tract infections are generally those of E. coli, Proteus sp., but because the P range was much higher than the ratio of MIC, CDZM is expected to be useful against infections in the field of urology.

Aged↗