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A Seto

Publications and source records attributed to A Seto.

At least 19 recordsLinked to original sources
PubMed2003

Effective extracellular trehalose production by Cellulosimicrobium cellulans.

A bacterium isolated from a petal of Casa Blanca Lily (ST26 strain) produced a marked amount of extracellular trehalose (alpha- d-glucopyranosyl-[1,1]-alpha- d-glucopyranose) in culture medium containing glucose. 16S rDNA-based phylogeny showed that ST26 belongs to, or is related to, Cellulosimicrobium cellulans, a close relative of Cellulomonas spp. Various Cellulomonas strains obtained from culture collections also showed extracellular trehalose productivity, suggesting that trehalose production is a common property of this bacterial genus. ST26 accumulated trehalose in medium supplied with glucose but not with sucrose, glycerol or maltose. Effective extracellular trehalose production by ST26 was achieved by supplying 0.5-1% ammonium sulfate and 0.5-1% CaCO(3). The addition of CaCO(3) adjusted the pH of the culture to around 5.0. The optimized culture conditions yielded trehalose from glucose at a conversion rate of 61%. The addition of ammonium sulfate greatly reduced the dry cell weight of ST26 and intracellular content of trehalose, which suggests that the addition of ammonium sulfate makes ST26 cells leak trehalose into the medium. ST26 effectively propagated in minimal medium containing trehalose as a sole carbon source, which suggests that trehalose serves as a carbohydrate reserve of this organism.

Ammonium Sulfate↗
PubMed2001

Crystallization and preliminary crystallographic studies of RhoGDI in complex with the radixin FERM domain.

The Rho guanine nucleotide-dissociation inhibitor (RhoGDI) is a general regulator that forms a complex with the GDP-bound form of Rho-family GTPases and suppresses their activation. The FERM domains of ERM (ezrin/radixin/moesin) proteins bind to RhoGDI and dissociate Rho from RhoGDI. The formation of a complex between RhoGDI and the FERM domain is an important step in the regulatory cycle of Rho activation. In this study, crystals of RhoGDI complexed with the FERM domain of radixin were obtained. The crystals of the binary complex belong to the space group P2(1)2(1)2, with unit-cell parameters a = 130.9 (2), b = 151.2 (2), c = 71.2 (1) A, and contain two protein complexes in the crystallographic asymmetric unit. A 2.9 A resolution data set was collected using synchrotron radiation at SPring-8.

Animals↗
PubMed2001

Involvement of MAPK activation in bacterial endotoxin-inducible tissue factor upregulation in human monocytic THP-1 cells.

BACKGROUND: Monocytic tissue factor (mTF) hypercoagulation leading to thrombotic complications is commonly observed following sepsis. OBJECTIVE: We herein study the intracellular mechanism of mTF upregulation in human model monocytic THP-1 cells in response to bacterial endotoxin (lipopolysaccharide, LPS; Escherichia coli O111:B04), determining if mitogen-activated protein kinase (MAPK) activation is involved in the signaling. METHODS: We assessed mTF upregulation by its cell surface expression, protein synthesis, and functional activity based on flow cytometry, Western blotting analysis, and a single-stage clotting assay, respectively. RESULTS: A 3-h challenge with LPS (100 ng/ml) drastically induced mTF functional activity, accompanied by elevated surface mTF expression and synthesis. The suppression by genistein (G) of LPS-inducible mTF upregulation implied the involvement of protein tyrosine kinase activation in mTF upregulation. LPS activated MAPK, which was significantly depressed by G, SB 203580 (SB), and PD 98058 (PD). Interestingly, inclusion of SB and PD also markedly diminished LPS-inducible mTF upregulation. The parallelism between MAPK and mTF activities revealed the involvement of MAPK activation in such mTF upregulation. Based on the ability of SB and PD to respectively block LPS-inducible tyrosine phosphorylation of p38 MAPK and Erk1/2, it was evident that tyrosine phosphorylation of MAPKs is required for mediating LPS-inducible mTF synthesis and upregulation. Contrasting with the established prevention of mTF upregulation by these inhibitors, failure to offset the already LPS-induced mTF activity seemed to be consistent with the view that LPS readily activated MAPK responsible for mTF synthesis. CONCLUSION: Our data suggest that the tyrosine phosphorylation of MAPKs (p38 and Erk1/2) leading to their activation could be a prerequisite for LPS induction of mTF synthesis contributing to the upregulation of mTF-initiated extrinsic coagulation.

Cell Line↗
PubMed2001

Effect of dietary seal and fish oils on lipid metabolism in hamsters.

Eicosapentaenoic and docosahexaenoic acids were distributed mainly in the sn-1 and 3 positions of seal oil triacylglycerols and in the sn-2 position of fish oil triacylglycerols. Seal oil-rich or fish oil-rich fats having constant polyunsaturated (PUFAs)/monounsaturated/saturated fatty acids and n-6/n-3 PUFAs ratios were fed to hamsters for 3 weeks. The control fat contained linoleic acid as the sole PUFA. The concentration of triacylglycerols in the liver was significantly lower in the fish oil group than in the control group. Phospholipid concentration in serum was lower and that in the liver was higher in the seal oil group compared with the fish oil group. The activities of fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH), and the malic enzyme were significantly lower in both the fish and seal oil groups than in the control group. Dietary seal oil more effectively reduced arachidonic acid content in liver phosphatidylcholine and phosphatidylethanolamine and serum phosphatidylcholine than fish oil. These results showed that different intramolecular distribution of n-3 PUFAs influenced glycerolipid metabolism and arachidonic acid content in serum and liver phospholipids of hamsters.

Animals↗
PubMed2000

Establishment and characterization of a prostatic small-cell carcinoma cell line (PSK-1) derived from a patient with Klinefelter syndrome.

BACKGROUND: Prostatic small-cell carcinoma (SMCC) is an extremely aggressive, rarely occurring tumor, and there has been no previous report of prostatic SMCC in association with Klinefelter syndrome. This study reports on the first such case and the establishment of the first cell line of SMCC from this tumor. METHODS: Prostatic SMCC tissue was derived from a 29-year-old man with Klinefelter syndrome. Characteristics of the culture tumor cells were evaluated with cell growth in vitro, neuron-specific enolase (NSE) secretion ability, tumorigenicity in nude mice, chemosensitivity to anticancer drugs, and karyotypic analysis. RESULTS: A culture cell line (PSK-1) was successfully established from prostatic SMCC with Klinefelter syndrome. PSK-1 cells had a polygonal epithelioid morphology and demonstrated loss of contact inhibition. These cells secreted NSE into the culture supernatant. Tumors produced in nude mice were histologically similar to the original SMCC. In a chemosensitivity test, PSK-1 cells were found to be sensitive in vitro to cisplatin, etoposide, and doxorubicin, but resistant to dacarbazine and 5-fluorouracil. Cytogenetic analysis showed that the PSK-1 cells at passage 35 revealed 76-84 chromosomes, with a mode of 82 chromosomes. CONCLUSIONS: PSK-1 cells could represent some properties of the original tumor cells, and could be used in studies on the etiology and treatment of this disease.

Adult↗
PubMed2000

[A case of free rupture of abdominal aortic aneurysm into the peritoneal cavity during posture change after induction of anesthesia].

We report a case in which posture change for radiography after induction of anesthesia caused free rupture of the abdominal aortic aneurysm (AAA) into the peritoneal cavity, resulting in shock, although in the patient an AAA had ruptured into only the retroperitoneal space and hemodynamics had been stable preoperatively. The massive bleeding was controlled with autotransfusion using a washing salvaging autotransfusion device and a roller pump for hemodialysis. In addition, international mild hypothermia was effective for protection of the brain from suspected ischemia during shock. Meticulous attention should be paid for anesthetic management of patients with ruptured AAA even if their hemodynamic status is stable.

Aged↗
PubMed2000

[Anesthetic management of a patient with deep venous thrombosis using temporary inferior vena cava filter].

A patient with deep venous thrombosis caused by a huge uterine leiomyoma underwent abdominal hysterectomy. To prevent pulmonary thromboembolism, the patient received anticoagulant therapy until 6 hr before surgery and temporary inferior vena cava filter was placed. A combination of preoperative anticoagulant therapy and the filter placement during perioperative period enabled this patient to be successfully-managed.

Anesthesia, General↗
PubMed2000

[Anesthetic management for an adult patient with secundum atrial septal defect associated with a large left-to-right shunt].

We describe the case of a 68-year-old woman with secundum atrial septal defect associated with a large left-to-right shunt and congestive heart failure. The patient with a pancreatic tumor was scheduled for hepatic cholangiojejunostomy and cholecystectomy. To determine the ratio of pulmonary to systemic flow (Qp/Qs) as an indicator for the magnitude of left-to-right shunt, oxymetric catheters were placed in the superior vena cava and pulmonary artery. In addition, oxygen delivery was assessed using superior vena cava oxygen saturation (SsvcO2). Although the patient was anesthetized with high-dose fentanyl to supplement nitrousoxide and sevoflurane, the Qp/Qs markedly increased after skin incision. Epidural local anesthetic was then administered. The Qp/Qs decreased to the preoperative value and the hemodynamic condition was improved thereafter. The operative course was uneventful. This case illustrates the potential usefulness of continuous measurement of the Qp/Qs and SsvcO2 for anesthetic management of adult patients with secundum atrial septal defect.

Aged↗
PubMed1999

I. Suppression by compound 48/80 of bacterial endotoxin-inducible monocytic tissue factor activity: direct blockade of factor VII binding to THP-1 monocytes.

Hypercoagulation with upregulated monocytic tissue factor (TF) activity often occurs under a variety of inflammatory conditions including endotoxemia. The antagonism to bacterial endotoxin (LPS) signaling often results in the depression in TF upregulation. We herein report that compound 48/80 (48/80) significantly depressed LPS-induced TF activity in human and cebus monkey peripheral blood monocytes. Employing a model monocyte-like cell line (THP-1), we explored the regulatory mechanism to identify the inhibitory site(s) of 48/80. We determine whether the inhibition results from the blockade of LPS signaling. 48/80 dose-dependently inhibited LPS-induced TF activity. Chase of LPS-challenged cells with 48/80 also significantly offset TF upregulation. In immunofluorescent approaches, FACScan analysis revealed that 48/80 had no effect on either LPS recognition or the expression of its receptors (CD14 and CD11b). Moreover, LPS-induced TF expression as well as synthesis remained unaffected in the presence of 48/80. Consistent with the independence of LPS action, 48/80 was also able to inhibit TF activity induced by A23187, ionomycin, or Quin-2 AM. Interestingly, 48/80 significantly decreased the FVII binding to either resting or LPS-challenged cells. In conclusion, our results elucidate that the inhibitory action of 48/80 was independent of LPS signaling including recognition, receptor expression, and the induced TF expression/ synthesis. However, 48/80 was able to directly block FVII binding to monocytic TF, thereby resulting in such antagonism to LPS-induced TF-initiated extrinsic coagulation.

Animals↗
PubMed1999

Blockade by polyunsaturated n-3 fatty acids of endotoxin-induced monocytic tissue factor activation is mediated by the depressed receptor expression in THP-1 cells.

BACKGROUND: Monocytic hypercoagulation often occurs in inflammatory conditions. We have previously reported that polyunsaturated n-3 fatty acids (n-3 FA) including eicosapentaenoic acid (20:5) and docosahexaenoic acid (22:6) prevent the activation of monocytic tissue factor (TF) induced by bacterial endotoxin [lipopolysaccharide (LPS)] in cell cultures and animals. HYPOTHESIS: We herein explore the mode of inhibitory action of n-3 FA to determine if LPS transmembrane signaling is blocked, exerting such antagonism. RESULTS: Exposure of human leukemia monocytic THP-1 cells to bacterial endotoxin (Escherichia coli 0111:B04, 1.5 microg/ml) for 6 h significantly activated TF activity and the production of nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha), and interleukin (IL)-1beta in conditioned medium. Pretreatment with n-3 FA, 20:5 and 22:6 at 10 microM, resulted in time-dependent suppression of not only TF activation but also the elicitation of NO, TNF-alpha, and IL-1beta. These LPS responses were substantially depressed by more than 50% after a 72-h pretreatment. FACScan analysis showed that n-3 FA readily prevented fluorescein isothiocyanate (FITC)-conjugated LPS from binding to THP-1 cells by approximately 70%. The observation that anti-CD14 mAb diminished FITC-LPS binding in a dose-dependent fashion has revealed CD14 dependency in LPS recognition. LPS upregulated CD14 expression, which was significantly arrested by n-3 FA. Similarly, the upregulation of the expression of CD11b, another proposed LPS receptor, was also minimally but significantly depressed by n-3 FA. CONCLUSION: The present study demonstrates that n-3 FA are able to block LPS transmembrane signaling via suppression of the receptor upregulation, mediating a variety of significant antagonisms against LPS action.

CD11 Antigens↗
PubMed1999

Development of rapid atrial fibrillation with a wide QRS complex after neostigmine in a patient with intermittent Wolff-Parkinson-White syndrome.

We report the case of a 67-yr-old man with intermittent Wolff-Parkinson-White (WPW) syndrome in whom neostigmine produced life-threatening tachyarrhythmias. The patient was scheduled for microsurgery for a laryngeal tumour. When he arrived in the operating room, the electrocardiogram showed normal sinus rhythm with a rate of 82 beat min-1 and a narrow QRS complex which remained normal throughout the operative period. On emergence from anaesthesia, the sinus rhythm (87 beat min-1) changed to atrial fibrillation with a rate of 80-120 beat min-1 and a normal QRS complex. We did not treat the atrial fibrillation because the patient was haemodynamically stable. Neostigmine 1 mg without atropine was then administered to antagonize residual neuromuscular block produced by vecuronium. Two minutes later, the narrow QRS complexes changed to a wide QRS complex tachycardia with a rate of 110-180 beat min-1, which was diagnosed as rapid atrial fibrillation. As the patient was hypotensive, two synchronized DC cardioversions of 100 J and 200 J were given, which restored sinus rhythm. No electrophysiological studies of anticholinesterase drugs have been performed in patients with WPW syndrome. We discuss the use of these drugs in this condition.

Aged↗
PubMed1999

Malposition of the epiglottis after tracheal intubation via the intubating laryngeal mask.

The intubating laryngeal mask has been reported to be a successful method of tracheal intubation although advancement of the tracheal tube via the laryngeal inlet into the trachea cannot be seen. Damage to the larynx or other tissues may occur during blind passage of a tracheal tube. We report a case in which the tracheal tube, advanced blindly, tucked the epiglottis into the laryngeal inlet, resulting in oedema of the epiglottis. This case illustrates the potential for airway obstruction after extubation when using the intubating laryngeal mask as a blind intubation guide.

Epiglottis↗
PubMed1999

Overproduction of gamma interferon in B/Jas inbred rabbits with herpes simplex virus encephalitis.

Inbred rabbits of the B/Jas strain are highly susceptible to herpes simplex virus type-1 (HSV-1) encephalitis, developing seizures of encephalitis after intravenous injection of the KOS strain of the virus. Anti-viral interferon activity became detectable in the serum just prior to or at the onset of seizures, its level being lower in the serum than in the cerebrospinal fluid. The activity was of gamma interferon, as suggested by the acid instability and the inability of Mx protein induction. An immunohistochemical analysis of the brain tissues of encephalitic rabbits showed that MHC class I antigen was expressed on the microglia cells of inflamed lesions but not on these cells in uninflamed areas. These findings were discussed in correlation with the pathogenesis of herpetic encephalitis in the inbred rabbits.

Animals↗