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Biomedical subjects

M Kanno

Publications and source records attributed to M Kanno.

At least 19 recordsLinked to original sources
PubMed2003

Late recurrence of resistant Trichomonas vaginalis vaginitis: relapse or re-infection?

Distinguishing between re-infection and relapse of trichomonas infections is often a difficult task in the clinical setting. The chronicity of trichomonas infections and the ongoing sexual activity are two confounding factors. We present a patient with recurrent resistant vaginal trichomoniasis shortly following a sexual contact with an untreated partner after a complete response to treatment with tinidazole for nine months. We hypothesise that re-infection occurred from the asymptomatic partner who was an untreated chronic carrier of resistant trichomonas in the urogenital tract.

Adult↗
PubMed2002

Biocompatibility of fluorinated polyimide.

Contact between blood and biomaterial triggers a complex series of events including protein adsorption, leukocyte adhesion and activation, and complement activation. In this article, a series of fluorinated polyimides cured at a different temperatures was prepared, and the biocompatibility of the membranes was evaluated using in vitro protein adsorption, neutrophil adhesion, and complement activation experiments under static conditions. We found that protein adsorption, neutrophil adhesion, and complement activation for the polyimides significantly depends on the curing temperature and decreases with an increase in the temperature and that the polyimide has a good biocompatibility compared with poly(styrene) and polydimethylsiloxane. We concluded that the rearrangement of molecules such as CF(3), sulfone, and ketone at the outermost surface occurs because of curing, which induces an increase in the hydrophobicity and that the cured polyimide suppresses protein adsorption, neutrophil adhesion, and complement activation because of its high hydrophobicity and low surface free energy.

Adsorption↗
PubMed2002

[Recurrent pulmonary embolism with prolonged right heart failure and hypoxia after cerebral bleeding; report of a case].

A 56-year-old woman with right hemiplegia for recent cerebral bleeding suddenly complained of dyspnea and chest pain with hypoxia during rehabilitation. Eight days after this first attack, she suffered prolonged right heart failure and hypoxia due to recurrent pulmonary embolism. Arterial blood gas analysis of room air showed 34.5 mmHg of PaO2 and 29.2 mmHg of PaCO2. Echocardiography showed enlargement of the right atrium and ventricle with pulmonary hypertension. Enhanced chest computed tomography revealed pulmonary emboli from the main pulmonary artery to the periphery. Despite intensive treatment, heart failure and hypoxia did not improve. We conducted pulmonary embolectomy under cardiopulmonary bypass requiring percutaneous cardiopulmonary bypass support for 2 days due to right heart failure. She is currently doing well in the 9 months following surgery.

Cerebral Hemorrhage↗
PubMed2002

Complete response of Sister Mary Joseph Nodule from gastric adenocarcinoma treated with combination chemotherapy of low-dose S-1 and cisplatin.

A case of an unresected, advanced gastric cancer with Sister Mary Joseph nodule was presented. It was treated with new combination chemotherapy of low-dose S-1 and cisplatin producing complete response of periumbilical metastasis. Few treatments are efficacious for umbilical invasion of peritoneal dissemination. A complete response for Sister Mary Joseph nodule from gastric adenocarcinoma has not been ever reported.

Adenocarcinoma↗
PubMed2001

Extrathymic development of V alpha 11 T cells in placenta during pregnancy and their possible physiological role.

The molecular and cellular mechanisms of the feto-maternal immune responses in the placenta in connection with natural abortion remain unclear. In this report we provide evidence that V(alpha11) T cells developed in the placenta may be responsible for the induction of natural abortion. The majority of V(alpha11) TCRs detected during pregnancy showed a consensus motif in the CDR3 region, similar to that of anti-GM3 TCR clones, and were of maternal origin. V(alpha11) TCRs were found in the middle to late stages of gestation due to de novo generation in the placenta, not to migration from the maternal side, as evidenced by the significant increases in the out-of-frame V(alpha11) TCR mRNA and the copy number of circular DNA generated by V(alpha11) gene rearrangements. Furthermore, administration of anti-V(alpha11) Ab to pregnant mice resulted in a significant decrease in the incidence of fetal demise, suggesting that V(alpha11) T cells detected in the placenta develop extrathymically and are involved in natural abortion.

Animals↗
PubMed2001

Destabilization of neutrophil NADPH oxidase by ATP and other trinucleotides and its prevention by Mg(2+).

Neutrophil NADPH oxidase (O(2)(-) generating enzyme) activated in a cell-free system was deactivated by dilution. When ATP was included in dilution the deactivation was further accelerated. The deactivation by dilution was biphasic, and the half-life of the enzyme was significantly shortened by ATP in each phase. ADP and AMP had little effect on the enzyme longevity while GTP and CTP had a similar effect to ATP. Staurosporine, a wide-range inhibitor of protein kinases, had no effect on ATP-induced deactivation, suggesting that the effect was not due to a protein phosphorylation. Mg(2+) addition largely prevented the deactivation by ATP. Chemical crosslinking of the activated oxidase prevented the deactivation by dilution and ATP, suggesting that the deactivation is caused by dissociation of the oxidase complex. Estimation of actin filament (F-actin) showed that the F-actin level was markedly reduced by addition of ATP. The ATP effect on the deactivation was not prominent in a semi-recombinant system which does not contain cytosol. These results suggest that ATP-induced deactivation is largely due to the chelation of Mg(2+) and are consistent with the concept that Mg(2+) stabilizes the oxidase complex by stabilizing F-actin.

Actins↗
PubMed2001

Identification of leukemia inhibitory factor as a potent mast cell growth-enhancing factor produced by mouse keratinocyte cell line, KCMH-1.

Inoculation of KCMH-1 cells, a keratinocyte-derived cell line established from a chemically induced skin tumor, into the skin of mice results in accumulation of mast cells around the resulting tumors. The conditioned medium of KCMH-1 cells enhances the growth of mast cells in vitro when they are cultured in the presence of NIH/3T3 fibroblasts, suggesting an important role for keratinocytes in mast cell hyperplasia in the skin. The aim of this study was to identify this mast cell growth-enhancing factor (MCGEF) by screening a KCMH-1 cDNA library. We first established a polyclonal antibody raised against the partially purified factor obtained from KCMH-1-conditioned medium which neutralized the MCGEF activity in KCMH-1-conditioned medium. Expression cloning of 1 x 10(6) cDNAs from the KCMH-1 cDNA library led to 16 cDNAs. One of these cloned cDNAs was found to be leukemia inhibitory factor (LIF). Both LIF produced by COS cells and the recombinant protein obtained commercially showed MCGEF activity when added to mast cell/fibroblast cocultures. MCGEF activity in KCMH-1-conditioned medium was completely neutralized by an anti-LIF monoclonal antibody. These results suggest that MCGEF produced by KCMH-1 cells is identical to LIF.

3T3 Cells↗
PubMed2001

Nucleotide sequence analysis of the binding site on the inositol 1,4,5-trisphosphate type-1 receptor in bipolar disorder -- a negative study.

Pharmacological studies of bipolar disorder suggest that dysfunction of calcium mobilization via phosphatidylinositol-mediated transduction may be involved in its pathogenesis. The present study tests the hypothesis that dysfunction of calcium mobilization in bipolar disorder is due to the mutation of the nucleotide sequence in the FKBP12 binding site on the inositol 1,4,5-trisphosphate type-1 receptor (IP(3)R1). Nucleotide sequence analysis of the FKBP12 binding site on IP(3)R1 was performed using reverse transcription-polymerase chain reaction and DNA sequencing. The nucleotide sequence in this region was preserved in all subjects. This finding suggests that IP(3)R1 dysfunction through the FKBP12 binding site is not involved in the pathogenesis of bipolar disorder.

Adult↗
PubMed2001

Dose-dependent augmentation effect of bromocriptine in a case with refractory depression.

1. A 52-year-old female with refractory depression had not responded to various treatments including electroconvulsive therapy and augmentation therapy with lithium or triiodothyronine. 2. Addition of bromocriptine 2.5-5 mg/day to imipramine improved her depressive symptoms. However, when the dose was increased to 15 mg/day to treat residual depressive symptoms, her clinical status deteriorated and returned to the original level. The dose reduction to 5mg/day again improved her depressive symptoms. 3. This report confirms the augmentation effect of bromocriptine for refractory depression. It also suggests that there is dose-dependency in this effect.

Bromocriptine↗
PubMed2001

Comparison of plasma alpha glutathione S-transferase concentrations during and after low-flow sevoflurane or isoflurane anaesthesia.

BACKGROUND: We evaluated the effect of low-flow sevoflurane anaesthesia, in which compound A is generated, and isoflurane anaesthesia, in which compound A is not generated (n=13 in each group), on hepatocellular integrity using alpha glutathione S-transferase (GST). Alpha GST is a more sensitive and specific marker of hepatocellular damage than is aminotransferase activity and correlates better with hepatic histology. METHODS: Sevoflurane or isoflurane were delivered without nitrous oxide with a fresh gas flow of 1 l/min. Concentrations of compound A in the circuit were measured hourly, and plasma alpha GST concentrations were measured perioperatively. RESULTS: Mean duration of anaesthesia was 338+/-92 min in the sevoflurane group and 320+/-63 min in the isoflurane group. Mean compound A concentration in the sevoflurane group was 28.6+/-9.0 ppm. There was no significant difference in alpha GST concentrations between the sevoflurane and isoflurane groups during or after anaesthesia. CONCLUSION: These results indicate that low-flow sevoflurane and isoflurane anaesthesia have the same effect on hepatic function, as assessed by plasma alpha GST concentrations.

Adult↗
PubMed2001

Alterations in EDHF-mediated hyperpolarization and relaxation in mesenteric arteries of female rats in long-term deficiency of oestrogen and during oestrus cycle.

This study was undertaken to determine whether endothelium-dependent relaxations are altered in mesenteric arteries from young female rats during oestrus cycle and after castration. The contractile response to phenylephrine (Phe) was significantly enhanced in arteries from rats subjected to ovariectomy than in those from sham-operated (control) rats. Treatment of ovariectomized rats with 17beta-oestradiol returned the Phe response to the control level. Arteries from rats at the diestrus stage also exhibited greater contraction in response to Phe. In the presence of 100 microM N(G)-nitro-L-arginine (L-NOARG), the enhancement of the Phe contractile response associated with oestrogen deficiency was not observed. Endothelium-dependent relaxations elicited by acetylcholine (ACh) in arteries precontracted with Phe were significantly reduced in ovariectomized and diestrus rats regardless of whether endothelium-derived nitric oxide (NO) was blocked with L-NOARG. Treatment with 17beta-oestradiol prevented the reduced vascular relaxant response to ACh in ovariectomized rats. The reduction in the ACh responses observed in ovariectomized and diestrus rats was eliminated when 500 nM apamin and 100 nM charybdotoxin were present. ACh-induced endothelium-dependent hyperpolarizations were depressed in arteries from ovariectomized and diestrus rats. The hyperpolarizing response to ACh was significantly improved when ovariectomized rats were treated with 17beta-oestradiol. The resting membrane potentials and pinacidil-induced hyperpolarizations were unaffected by ovariectomy or the diestrus stage. These results suggest that oestrogen-deficient states of both short and long duration reduce the basal release of NO from the endothelium and specifically attenuate endothelium-dependent hyperpolarization and relaxation transduced by endothelium-derived hyperpolarizing factor.

Acetylcholine↗
PubMed2001

The effects of low-flow sevoflurane and isoflurane anesthesia on renal function in patients with stable moderate renal insufficiency.

UNLABELLED: Sevoflurane degrades to Compound A, which is nephrotoxic in rats. Therefore, the renal effects of Compound A is an area of intense debate. We investigated the effects of low-flow sevoflurane and isoflurane anesthesia on renal function in patients with stable renal insufficiency. Seventeen patients with a serum creatinine level of more than 1.5 mg/dL were anesthetized with sevoflurane or isoflurane at a total flow of 1 L/min. Serum creatinine and blood urea nitrogen were measured before anesthesia and again 1, 2, 3, 5, 7, and 14 days after anesthesia. The 24-h creatinine clearance was measured before anesthesia and 7 days after anesthesia. There were no significant differences in the blood urea nitrogen levels, serum creatinine concentrations, or creatinine clearance before and after anesthesia within each group. These results suggest that sevoflurane and isoflurane have similar effects on renal function in patients with moderately impaired renal function. Further study of the effects of low-flow sevoflurane anesthesia on impaired renal function with a larger sample size than ours is required to resolve the issue of sevoflurane safety in patients with renal insufficiency. IMPLICATIONS: The serum creatinine and blood urea nitrogen data indicate that, for exposures of <130 ppm/h in Compound A inspired area under the curve, renal effects of low-flow sevoflurane are similar to those of isoflurane in patients with stable renal insufficiency.

Aged↗
PubMed2001

The carbon dioxide absorption capacity of Amsorb is half that of soda lime.

UNLABELLED: A new CO(2) absorbent, Amsorb (A), which does not contain monovalent bases, is ideal because it does not degrade volatile anesthetics to either Compound A (from sevoflurane) or carbon monoxide (from desflurane, enflurane, or isoflurane). The CO(2) absorption capacity of A, however, has not been investigated under clinical conditions. In this study, we compared the longevity (time to exhaustion) and CO(2) absorption capacity (the volume of CO(2) absorbed before CO(2) rebreathing occurs) of A under low-flow anesthesia (1 L/min) with those of two soda lime absorbents-Medisorb (M) and Sodasorb (S)-by using a 750-mL ADU canister and a 1350-mL Aestiva 3000 canister. In the study with the ADU canister, the longevity of A was 213 +/- 71 min, significantly less than those of M (445 +/- 125; P < 0.01) and S (503 +/- 89; P < 0.001). The CO(2) absorption capacity (L/100 g absorbent) of A was 5.5 +/- 1.2, significantly less than those of M (10.7 +/- 1.7) and S (12.1 +/- 1.8; P < 0.001). In the study with the Aestiva 3000 canister, the longevity of A was 218 +/- 61 min, significantly less than those of M (538 +/- 136) and S (528 +/- 103; P < 0.001). The CO(2) absorption capacity (L/100 g absorbent) of A was 7.6 +/- 1.6, significantly less than those of M (14.4 +/- 1.8) and S (14.8 +/- 2.3; P < 0.001). These results indicate that the CO(2) absorption capacity of A is half that of M or S and that the difference in the CO(2) absorption capacity between A and M or S is almost constant, regardless of the canister design. IMPLICATIONS: The CO(2) absorption capacity of Amsorb is half that of Medisorb and Sodasorb under clinical low-flow (1 L/min) anesthesia with either a 750-mL Ohmeda ADU compact or a 1350-mL Ohmeda Aestiva 3000 canister.

Absorption↗
PubMed2001

Early pregnancy does not reduce the C(50) of propofol for loss of consciousness.

UNLABELLED: Requirements for inhaled anesthetics decrease during pregnancy. There are no published data, however, regarding propofol requirements in these patients. Because propofol is often used for induction of general anesthesia when surgery is necessary in early pregnancy, we investigated whether early pregnancy reduces the requirement of propofol for loss of consciousness using a computer-assisted target-controlled infusion (TCI). Propofol was administered using TCI to provide stable concentrations and to allow equilibration between blood and effect-site (central compartment) concentrations. Randomly selected target concentrations of propofol (1.5-4.5 microg/mL) were administered to both pregnant women (n = 36) who were scheduled for pregnancy termination and nonpregnant women (n = 36) who were scheduled for elective orthopedic or otorhinolaryngologic surgery. The median gestation of the pregnant women was 8 wk (range, 6-12 wk). Venous blood samples for analysis of the serum propofol concentration were taken at 3 min and 8 min after equilibration of the propofol concentration. After a 10-min equilibration period of the predetermined propofol blood concentration, a verbal command to open their eyes was given to the patients twice, accompanied by rubbing of their shoulders. Serum propofol concentrations at which 50% of the patients did not respond to verbal commands (C(50) for loss of consciousness) were determined by logistic regression. There was no significant difference in C(50) +/- SE of propofol for loss of consciousness between the Nonpregnant (2.1 +/- 0.2 microg/mL) and Pregnant (2.0 +/- 0.2 microg/mL) groups. These results indicate that early pregnancy does not decrease the concentration of propofol required for loss of consciousness. IMPLICATIONS: The C(50) of propofol for loss of consciousness in early pregnancy did not differ from that in nonpregnant women, indicating that there is no need to decrease the propofol concentration for loss of consciousness when inducing general anesthesia for termination of pregnancy.

Abortion, Induced↗
PubMed2001

Effects of probenecid on renal function in surgical patients anesthetized with low-flow sevoflurane.

BACKGROUND: Dehydrofluorination of sevoflurane by carbon dioxide absorbents in anesthesia machines produces compound A, which is nephrotoxic in rats. Several clinical studies indicate that prolonged low-flow sevoflurane anesthesia is associated with an increased urinary excretion of biochemical markers, such as protein. Probenecid, a competitive inhibitor of organic anion transport, diminishes compound A nephrotoxicity in rats. The purpose of the present study was to examine the effects of low- and high-flow sevoflurane anesthesia on urinary excretion of biochemical markers in humans and to examine the effects of probenecid on urinary excretion of these markers. METHODS: Elective surgical patients (n = 64) were assigned to four groups (n = 16 each): low-flow sevoflurane plus probenecid (LSP), low-flow sevoflurane (LS), high-flow sevoflurane plus probenecid (HSP), and high-flow sevoflurane (HS). Probenecid (2.0 g) was administered orally 2 h before the induction of anesthesia in both the LSP and HSP groups. Nothing was administered orally 2 h before the induction of anesthesia in either the LS or HS groups. All patients underwent prolonged low-flow (1 l/min) or high-flow (6 l/min) sevoflurane anesthesia. Urinary excretion of protein, albumin, beta(2)-microglobulin, glucose, and N-acetyl-beta-d-glucosaminidase was measured for up to 7 days postoperatively. RESULTS: Sevoflurane doses were similar in all four groups. There were no differences in blood urea nitrogen, creatinine, or creatinine clearance among the four groups after anesthesia. Average values for urinary excretion of protein, beta(2)-microglobulin, and N-acetyl-beta-d-glucosaminidase in the LS group were significantly higher than those in the other groups (LSP, HSP, HS; P < 0.05). There was no significant difference between the LS and LSP groups in average values for urinary excretion of albumin and glucose, although there were significant differences between the LS and both high-flow sevoflurane groups (HSP, HS). CONCLUSIONS: Low-flow sevoflurane, which produces a sevenfold higher compound A exposure than high-flow sevoflurane, resulted in significant increases of several biochemical markers in half of the patients. Probenecid appears to provide protection against these renal effects.

Adult↗
PubMed2001

Role of endothelial Ni(2+)-sensitive Ca(2+) entry pathway in regulation of EDHF in porcine coronary artery.

Elevation of intracellular Ca(2+) concentration ([Ca(2+)](i)) in endothelial cells is proposed to be required for generation of vascular actions of endothelium-derived hyperpolarizing factor (EDHF). This study was designed to determine the endothelial Ca(2+) source that is important in development of EDHF-mediated vascular actions. In porcine coronary artery precontracted with U-46619, bradykinin (BK) and cyclopiazonic acid (CPA) caused endothelium-dependent relaxations in the presence of N(G)-nitro-L-arginine (L-NNA). The L-NNA-resistant relaxant responses were inhibited by high K(+), indicating an involvement of EDHF. In the presence of Ni(2+), which inhibits Ca(2+) influx through nonselective cation channels, the BK-induced EDHF relaxant response was greatly diminished and the CPA-induced response was abolished. BK and CPA elicited membrane hyperpolarization of smooth muscle cells of porcine coronary artery. Ni(2+) suppressed the hyperpolarizing responses in a manner analogous to removal of extracellular Ca(2+). EDHF-mediated relaxations and hyperpolarizations evoked by BK and CPA in porcine coronary artery showed a temporal correlation with the increases in [Ca(2+)](i) in porcine aortic endothelial cells. The extracellular Ca(2+)-dependent rises in [Ca(2+)](i) in endothelial cells stimulated with BK and CPA were completely blocked by Ni(2+). These results suggest that Ca(2+) influx into endothelial cells through nonselective cation channels plays a crucial role in the regulation of EDHF.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2001

Gas transfer and blood compatibility of asymmetric polyimide hollow fiber.

We have fabricated an asymmetric polyimide hollow fiber for use as a membrane oxygenator. A dry/wet phase inversion process has been applied to a spinning process to prepare the hollow fiber. The fiber structure consisted of a complete defect-free skin layer and a porous substructure characterized by the presence of an open-cell structure and macrovoids. The outer diameter was 480 microm with a wall thickness of 50 microm. Transfer rates of O2 and CO2 in the asymmetric polyimide fiber were 2.3 x 10(-5) and 1.1 x 10(-4) (cm3 (STP)/(cm2 s cmHg)), respectively, which were four times higher than those measured in the polydimethylsiloxane (PDMS) fiber of the presently-available membrane oxygenator. The (QO2/QN2) selectivity of the polyimide fiber was 4.9, indicating that the surface skin layer is essentially defect-free. The blood compatibility of the polyimide hollow fiber has been evaluated in vitro and in vivo. The polyimide had an excellent blood compatibility when compared with PDMS.

Adsorption↗