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K Takeda

Publications and source records attributed to K Takeda.

At least 145 records · Page 8Linked to original sources
PubMed2001

Transluminal placement of endovascular stent-grafts for the treatment of type A aortic dissection with an entry tear in the descending thoracic aorta.

PURPOSE: The current therapy for type A aortic dissection is ascending aortic replacement. Operative mortality and morbidity rates have been markedly improved because of recent advances in surgical techniques and anesthesiology. However, type A aortic dissection with an entry tear in the descending thoracic aorta is still a surgical challenge because of the need for extensive aortic replacement. METHODS: Ten patients with type A aortic dissection were treated with endovascular stent-grafts. The false lumen of the ascending aorta was patent in five patients, and it was thrombosed in the other five patients. The entry tears were located in the descending thoracic aorta in all cases. Seven patients had acute dissection, and three patients had subacute dissection. Four patients had pericardial effusion. Stent-grafts were fabricated from expanded polytetrafluoroethylene and Z-stents. RESULTS: Entry closure was achieved in all patients. Complete thrombosis of the false lumen of the ascending aorta was observed after stent-grafting in all patients. A second stent-graft was required in two patients to obtain complete thrombosis of the false lumen of the descending thoracic aorta. No procedure-related complications were observed, with the exception of a minor stroke in one patient. During a mean follow-up period of 20 months, no aortic rupture or aneurysm formation was noted in either the ascending or descending thoracic aorta, and all patients were alive and doing well. The abdominal aortic aneurysm enlarged after stent-grafting in one patient, and this was treated by closing the fenestrations of the abdominal aorta with stent-grafts. CONCLUSION: Stent-graft repair of aortic dissection with an entry tear in the descending thoracic aorta is a safe and effective method and may be an alternative to surgical graft replacement in highly selected patients.

Adult↗
PubMed2001

Assessment of coronary flow velocity reserve using fast velocity-encoded cine MRI for noninvasive detection of restenosis after coronary stent implantation.

PURPOSE: Serial change of the coronary flow velocity reserve was evaluated with fast velocity-encoded cine magnetic resonance imaging (MRI) for noninvasive detection of restenosis after coronary stent implantation. METHOD: In total, 60 MRI flow studies were performed in 10 patients with coronary artery disease who undersvent elective successful stent implantation to the lesion in the proximal left anterior descending artery. Flow velocities in the segment that was distal to the stent were measured before and after intravenous injection of dipyridamole. MRI measurements of coronary flow velocity reserve were repeated every 4 weeks for 6 months, and follow-up angiography was performed 6 months after the procedure. RESULTS: In patients without restenosis (n = 7, % diameter stenosis: 27.8%+/-7.1) at follow-up angiography, the coronary flow velocity reserve remained normal during the 6-month follow-up time. The flow velocity reserve was 2.31+/-0.30 at 1 month and 2.52+/-0.25 at 6 months after stent implantation (p = NS). In contrast, the coronary flow velocity reserve showed a significant decrease after 4 months in patients with restenosis (n = 3, % diameter stenosis: 66.3%+/-8.1) at follow-up angiography. The flow velocity reserve was 2.26+/-0.49 at 1 month and 1.52+/-0.09 at 6 months after stent implantation (p < 0.05). CONCLUSION: Fast velocity-encoded cine MRI is a technique that shows promise in providing non-invasive detection of restenosis of coronary stent implantation.

Adult↗
PubMed2001

Osmotic stress-mediated activation of RET kinases involves intracellular disulfide-bonded dimer formation.

We showed that osmotic stress induces activation of c-RET and second-set activation of constitutively activated RET-MEN2B. A few percentage of RET proteins normally formed disulfide-bonded dimers in the cell, and osmotic stress promoted formation of these dimers. The disulfide-bonded dimers displayed higher levels of autophosphorylation and catalytic activity per molecule than did monomers. Osmotic stress also promoted activation and disulfide-bonded dimerization of the extracellular domain-depleted mutant RET (RET-PTC-1), suggesting that the target amino acid(s) for dimerization is located intracellularly rather than in the cysteine-rich region of the extracellular domain. In the mutant c-RET and RET-PTC-1 in which Cys987 of c-RET or Cys376 of RET-PTC-1 was replaced with Ala, the levels of intrinsic kinase activity were greatly reduced and barely increased in response to osmotic stress. Correspondingly, the Cys376-defective RET-PTC-1 did not form any demonstrable levels of dimers even after exposure to osmotic stress. In contrast, another RET-PTC-1 mutant that had a replacement of Cys365 with Ala mostly behaved like parental RET-PTC-1. These results suggest that Cys987 of c-RET or Cys376 of RET-PTC-1 plays a crucial role in maintenance and promotion of dimerization and activation of the RET kinases.

3T3 Cells↗
PubMed2001

ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis.

Apoptosis signal-regulating kinase (ASK) 1 is activated in response to various cytotoxic stresses including TNF, Fas and reactive oxygen species (ROS) such as H(2)O(2), and activates c-Jun NH(2)-terminal kinase (JNK) and p38. However, the roles of JNK and p38 signaling pathways during apoptosis have been controversial. Here we show that by deleting ASK1 in mice, TNF- and H(2)O(2)-induced sustained activations of JNK and p38 are lost in ASK1(-/-) embryonic fibroblasts, and that ASK1(-/-) cells are resistant to TNF- and H(2)O(2)-induced apoptosis. TNF- but not Fas-induced apoptosis requires ROS-dependent activation of ASK1-JNK/p38 pathways. Thus, ASK1 is selectively required for TNF- and oxidative stress-induced sustained activations of JNK/p38 and apoptosis.

Animals↗
PubMed2001

Discrimination of bacterial lipoproteins by Toll-like receptor 6.

Bacterial lipoproteins (BLP) trigger immune responses via Toll-like receptor 2 (TLR2) and their immunostimulatory properties are attributed to the presence of a lipoylated N-terminus. Most BLP are triacylated at the N-terminus cysteine residue, but mycoplasmal macrophage-activating lipopeptide-2 kD (MALP-2) is only diacylated. Here we show that TLR6-deficient (TLR6(-/-)) cells are unresponsive to MALP-2 but retain their normal responses to lipopeptides of other bacterial origins. Reconstitution experiments in TLR2(-/-) TLR6(-/-) embryonic fibroblasts reveal that co-expression of TLR2 and TLR6 is absolutely required for MALP-2 responsiveness. Taken together, these results show that TLR6 recognizes MALP-2 cooperatively with TLR2, and appears to discriminate between the N-terminal lipoylated structures of MALP-2 and lipopeptides derived from other bacteria.

Animals↗
PubMed2001

Gramine increase associated with rapid and transient systemic resistance in barley seedlings induced by mechanical and biological stresses.

Systemic acquired resistance (SAR) is one of the intriguing issues for studying the mechanism in signal transduction system in a whole plant. We found that SAR and increase of an antifungal compound were induced rapidly and transiently in barley (Hordeum vulgare L. cv. Goseshikoku) by mechanical and biological stresses. One of the major antifungal compounds was identified as an indole alkaloid, gramine (N,N-dimethyl-3-aminomethylindole), by mass spectrum and NMR analyses. Gramine is well known as a constitutive compound of barley, but it increased significantly in the primary and secondary leaves of barley seedlings within 12 h after pruning or inoculating with the powdery mildew fungi of barley (Blumeria graminis f.sp. hordei) and wheat (B. graminis f.sp. tritici). However, in the leaf detached from unwounded seedlings or in the leaf inoculated with the barley powdery mildew fungus, gramine did not increase at all. In the water droplets contacted with barley leaves, the amount of leaked gramine increased dependently upon the time after the seedling was injured mechanically. We also found a tight correlation between gramine increase and enhancement of resistance to the barley powdery mildew fungus in barley leaves treated with an endogenous elicitor. Furthermore, such a systemic resistance was not observed in a barley cultivar Morex that lacks the biosynthetic pathway of gramine. From these results, we conclude that gramine is the excellent marker in rapid and transient systemic acquired resistance in barley.

Alkaloids↗
PubMed2001

Maternal exposure to a low dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) suppressed the development of reproductive organs of male rats: dose-dependent increase of mRNA levels of 5alpha-reductase type 2 in contrast to decrease of androgen receptor in the pubertal ventral prostate.

To assess the health risks associated with exposure to 2,3,7,8-tetrachlorodebenzo-p-dioxin (TCDD), we studied the effects of a relatively low dose of TCDD on the male reproductive system of rats, using the experimental protocol of T. A. Mably et al. (1992, Toxicol. Appl. Pharmacol. 114, 97-107, 108-117, 118-126), and searched for the most sensitive and reliable among several indices of TCDD toxicity. Pregnant Holtzman rats were given a single oral dose of 0, 12.5, 50, 200, or 800 ng TCDD/kg body weight on gestational day (GD) 15, and male offspring were sacrificed on postnatal day (PND) 49 or 120. GC-MS analysis of the abdominal fat tissue and testis clearly showed increased amounts of TCDD in these offspring. However, there was no TCDD effect on body weight of offspring. There were no changes on testicular or epididymal weights by TCDD administration, even at the 800-ng/kg dose in rats sacrificed on either PND 49 or 120. In addition, TCDD administration resulted in no changes in daily sperm production or sperm reserve at any of the doses used. However, the weight of the urogenital complex, including the ventral prostate, was significantly reduced at doses of 200 and 800 ng TCDD/kg in rats sacrificed on PND 120. Moreover, the anogenital distance (AGD) of male rats sacrificed on PND 120 showed a significant decrease in the groups receiving doses greater than 50 ng TCDD/kg. TCDD administration resulted in no apparent dose-dependent changes in levels of either serum testosterone or luteinizing hormone. Interestingly, reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that, in the ventral prostates of the PND 49 group, TCDD administration resulted in both a dose-dependent increase in 5alpha-reductase type 2 (5alphaR-II) mRNA level and a dose-dependent decrease in androgen receptor (AR) mRNA level. These results suggest that low-dose TCDD administration had a greater effect on the development of the external genital organs and ventral prostate than on development of the testis and other internal genital organs. Moreover, it is highly suggested that the decrease in the size of the ventral prostate by maternal TCDD exposure might be due to decreased responsiveness of the prostate to androgen due to an insufficient expression level of androgen receptor during puberty.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed2001

Recent advances in the pathology of alcoholic myopathy.

This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chairs were Victor R. Preedy and Junko Adachi. The presentations were (1) Alcoholic myopathy: Past, present and future, by Timothy J. Peters and Victor R. Preedy; (2) Protein adducts in the type I and II fiber-predominant muscles of the ethanol-fed rat, by Simon Worrall, Seppo Parkkila, and Onni Niemela; (3) Hydroperoxides and changes in alcoholic myopathy, by Junko Adachi, Migiwa Asamo, and Yasuhino Ueno; and (4) A close association between testicular atrophy, muscle atrophy, and the increase in protein catabolism after chronic ethanol administration, by Kunihiko Takeda, Masayoshi Yamauchi, Kazuhiko Sakamoto, Masaru Takagi, Hisato Nakajima, and Gotaro Toda.

Alcoholism↗
PubMed2001

Association of polymorphism in the alcohol dehydrogenase 2 gene with alcohol-induced testicular atrophy.

BACKGROUND: Alcohol abuse can induce testicular atrophy, but it only occurs in some alcoholics. Alcohol dehydrogenase (ADH) is located principally on the Leydig cells. METHODS: To investigate whether genetic polymorphism of alcohol dehydrogenase (ADH) 2 and aldehyde dehydrogenase (ALDH) 2 was related to alcoholic testicular atrophy, we determined restriction fragment-length polymorphisms of the ADH2 and ALDH2 genes in 43 Japanese male alcoholics and 50 healthy subjects. An orchidometer was used to determine the testicular size. RESULTS: Less than 16 ml in testicular size was defined as testicular atrophy. Testicular atrophy was found in 24 (55.8%) cases out of 43 alcoholics. Digestion with MaeIII and MboII after polymerase chain reaction amplification showed that the ADH21 allele frequency was significantly higher in patients with testicular atrophy than in those without testicular atrophy (chi2 = 4.665, p = 0.031), whereas no significant association was observed between testicular atrophy and the ALDH2 gene. CONCLUSIONS: The ADH21 allele may be associated with alcoholic testicular atrophy.

Adult↗
PubMed2001

Measures for preventing recurrence after pterygium surgery.

PURPOSE: To introduce an improved technique of pterygium surgery and to compare postoperative results between this technique and previous techniques. METHODS: In a retrospective survey, the records of 216 consecutive eyes with primary pterygium that underwent surgery by three different techniques were reviewed. The new technique (mini-flap technique) involves making a small excision of the pterygium body, removing the pterygium head by scraping with forceps, applying mitomycin C (MMC), and performing a small conjunctival transposition flap. The previous technique (large-flap technique II) involved making a large excision in the pterygium body, removing the pterygium head with a knife, applying MMC, and performing a large transposition flap. Large-flap technique I is the same as large-flap technique II except for the use of intraoperative MMC. The recurrence rate of each technique was estimated by the Kaplan-Meier life table analysis. RESULTS: The recurrence rates estimated at 1 year after surgery were 15.5% in large-flap technique I, 4.2% in large-flap technique II, and 0% in the mini-flap technique. Large-flap technique II or the mini-flap technique had significantly lower recurrence rates compared with large-flap technique I ( p = 0.02 and p < 0.01, respectively). The mini-flap technique had a significantly lower incidence of conjunctival scarring or granuloma compared with large-flap technique I and large-flap technique II ( p = 0.05 and p = 0.03, respectively.) CONCLUSIONS: The mini-flap technique was useful for preventing recurrence and was technically easier and induced fewer postoperative complications than large-flap techniques I and II.

Aged↗
PubMed2001

Enhanced gamma interferon production through activation of Valpha14(+) natural killer T cells by alpha-galactosylceramide in interleukin-18-deficient mice with systemic cryptococcosis.

We showed recently that activation of Valpha14(+) natural killer T cells (NKT cells) by alpha-galactosylceramide (alpha-GalCer) resulted in increased gamma interferon (IFN-gamma) production and host resistance to intravenous infection with Cryptococcus neoformans. In other studies, interleukin-18 (IL-18) activated NKT cells in collaboration with IL-12, suggesting the possible contribution of this cytokine to alpha-GalCer-induced IFN-gamma synthesis. Here we examined the role of IL-18 in alpha-GalCer-induced Th1 response by using IL-18KO mice with this infection. In these mice, levels of IFN-gamma in serum and its synthesis in vitro by spleen cells stimulated with live organisms were not reduced, but rather enhanced, compared to those in wild-type (WT) mice, while such production was completely absent in IL-12KO mice. The enhanced production of IFN-gamma correlated with increased IL-12 synthesis but not with reduced production of IL-4, which was rather increased. IFN-gamma synthesis in IL-18KO mice was abolished by neutralizing anti-IL-12 antibody and significantly inhibited by neutralization of endogenous IL-4 with a specific monoclonal antibody. In addition, administration of recombinant IL-4 significantly enhanced the production of IFN-gamma in WT mice. Finally, the enhanced production of IFN-gamma in IL-18KO mice correlated with increased host defense against cryptococcal infection, as indicated by enhancement in alpha-GalCer-related clearance of microorganisms. Our results indicated that in IL-18KO mice, IFN-gamma synthesis was enhanced through overproduction of IL-12 and IL-4 after intravenous infection with C. neoformans and a ligand-specific activation of Valpha14(+) NKT cells.

Animals↗
PubMed2001

Hydrogen peroxide-forming NADH oxidase belonging to the peroxiredoxin oxidoreductase family: existence and physiological role in bacteria.

Amphibacillus xylanus and Sporolactobacillus inulinus NADH oxidases belonging to the peroxiredoxin oxidoreductase family show extremely high peroxide reductase activity for hydrogen peroxide and alkyl hydroperoxides in the presence of the small disulfide redox protein, AhpC (peroxiredoxin). In order to investigate the distribution of this enzyme system in bacteria, 15 bacterial strains were selected from typical aerobic, facultatively anaerobic, and anaerobic bacteria. AhpC-linked alkyl hydroperoxide reductase activities were detected in most of the tested strains, and especially high activities were shown in six bacterial species that grow well under aerobic conditions, including aerobic bacteria (Alcaligenes faecalis and Bacillus licheniformis) and facultatively anaerobic bacteria (Amphibacillus xylanus, Sporolactobacillus inulinus, Escherichia coli, and Salmonella enterica serovar Typhimurium). In the absence of AhpC, the purified enzymes from A. xylanus and S. inulinus catalyze the NADH-linked reduction of oxygen to hydrogen peroxide. Similar activities were observed in the cell extracts from each of these six strains. The cell extract of B. licheniformis revealed the highest AhpC-linked alkyl hydroperoxide reductase activity in the four strains, with V(max) values for hydrogen peroxide and alkyl hydroperoxides being similar to those for the enzymes from A. xylanus and S. inulinus. Southern blot analysis of the three strains probed with the A. xylanus peroxiredoxin reductase gene revealed single strong bands, which are presumably derived from the individual peroxiredoxin reductase genes. Single bands were also revealed in other strains which show high AhpC-linked reductase activities, suggesting that the NADH oxidases belonging to the peroxiredoxin oxidoreductase family are widely distributed and possibly play an important role both in the peroxide-scavenging systems and in an effective regeneration system for NAD in aerobically growing bacteria.

Aerobiosis↗
PubMed2001

Loss of mRor1 enhances the heart and skeletal abnormalities in mRor2-deficient mice: redundant and pleiotropic functions of mRor1 and mRor2 receptor tyrosine kinases.

The mammalian Ror family of receptor tyrosine kinases consists of two structurally related proteins, Ror1 and Ror2. We have shown that mRor2-deficient mice exhibit widespread skeletal abnormalities, ventricular septal defects in the heart, and respiratory dysfunction, leading to neonatal lethality (S. Takeuchi, K. Takeda, I. Oishi, M. Nomi, M. Ikeya, K. Itoh, S. Tamura, T. Ueda, T. Hatta, H. Otani, T. Terashima, S. Takada, H. Yamamura, S. Akira, and Y. Minami, Genes Cells 5:71-78, 2000). Here we show that mRor1-deficient mice have no apparent skeletal or cardiac abnormalities, yet they also die soon after birth due to respiratory dysfunction. Interestingly, mRor1/mRor2 double mutant mice show markedly enhanced skeletal abnormalities compared with mRor2 mutant mice. Furthermore, double mutant mice also exhibit defects not observed in mRor2 mutant mice, including a sternal defect, dysplasia of the symphysis of the pubic bone, and complete transposition of the great arteries. These results indicate that mRor1 and mRor2 interact genetically in skeletal and cardiac development.

Animals↗
PubMed2001

Portal venous stent placement in patients with pancreatic and biliary neoplasms invading portal veins and causing portal hypertension: initial experience.

PURPOSE: To evaluate the clinical usefulness of portal venous stent placement in patients with pancreatic or biliary neoplasms invading portal veins and causing portal hypertension. MATERIALS AND METHODS: Thirteen patients underwent portal venous stent placement because of gastrointestinal bleeding (n = 8), risk of gastroesophageal varix rupture (n = 4), ascites (n = 4), thrombocytopenia (n = 3), and/or portal venous thrombosis (n = 3). The main portal vein or both the intrahepatic and main portal veins were invaded in six patients (group A). The main portal vein and splanchnic veins were involved in seven patients (group B). Stents were placed across the stenotic (n = 8) or occluded (n = 5) lesions after percutaneous transhepatic portography. Changes in portal venous pressure, stent patency, and survival were evaluated. RESULTS: Mean portal venous pressure decreased significantly immediately after stent placement, from 24.9 mm Hg +/- 5.9 (SD) to 15.8 mm Hg +/- 4.6 (P <.001). In group A, blood flow through the stent was maintained and the symptoms had subsided at follow-up (mean, 12.5 months). In group B, symptoms were improved in five patients, but the stents were occluded in all but one patient at a mean follow-up of 1.5 months. There was a significant difference in stent patency between the patients with (14%) and those without (100%) splanchnic venous involvement (P <.01). CONCLUSION: Stent placement helped to relieve portal hypertension symptoms. Splanchnic venous involvement was associated with worse stent patency.

Adult↗
PubMed2001

Mr flow measurement in the internal mammary artery-to-coronary artery bypass graft: comparison with graft stenosis at radiographic angiography.

PURPOSE: To evaluate the sensitivity and specificity of breath-hold magnetic resonance (MR) flow measurement for detection of significant stenosis in internal mammary artery bypass grafts. MATERIALS AND METHODS: Twenty-six consecutive patients who had undergone coronary artery bypass surgery were examined. Breath-hold velocity-encoded cine MR images were obtained at the midpoint of the internal mammary artery between its origin from the subclavian artery and the distal anastomosis to the left anterior descending artery. RESULTS: MR images were obtained successfully in 24 patients. At conventional angiography, no significant stenosis was observed in 17 patients (group A), and significant stenosis (diameter > 70%) was observed in seven patients (group B). The mean diastolic-to-systolic peak velocity ratio in group B (0.61 +/- 0.44 [SD]) was significantly lower than that in group A (1.88 +/- 0.96; P <.01). Evaluation of graft stenosis with the diastolic-to-systolic peak velocity ratio revealed a sensitivity of 86% and a specificity of 88%. The mean blood flow rate at baseline in group B (16.9 mL/min +/- 5.5) was significantly lower than that in group A (79.8 mL/min +/- 38.2; P <.01). The sensitivity and specificity of MR blood flow measurement in predicting significant stenosis were 86% and 94%, respectively. The mean pharmacologic flow reserve ratios were 2.00 +/- 1.43 in group A and 1.39 +/- 1.46 in group B (P >.05). CONCLUSION: Fast MR blood flow measurement at baseline is highly useful for predicting significant stenosis in internal mammary arterial grafts.

Aged↗
PubMed2001

Strain dependence of airway hyperresponsiveness reflects differences in eosinophil localization in the lung.

Different strains of mice exhibit different degrees of airway hyperresponsiveness after sensitization to and airway challenge with ovalbumin. Antibody responses in BALB/c mice far exceeded those in C57BL/6 mice; in contrast, although responsiveness to methacholine was much higher in the BALB/c mice, the number of eosinophils in the bronchoalveolar lavage fluid was higher in C57BL/6 animals. Sensitized and challenged BALB/c mice developed increases in lung resistance and decreases in dynamic compliance after methacholine or 5-hydroxytryptamine inhalation. C57BL/6 mice only exhibited significant levels of responsiveness when dynamic compliance was monitored in response to inhaled 5-hydroxytryptamine. Eosinophils accumulated in the peribronchial and peripheral lung tissue in BALB/c mice but were distributed diffusely in the peripheral lung tissue of C57BL/6 mice. Thus, in addition to differences in antibody responses and cholinergic agonist reactivity, differences in the responses of large and small airways may reflect the selective distribution of eosinophils in lung tissue.

Animals↗
PubMed2001

gammadelta T cells as regulators of airway hyperresponsiveness.

Airway responsiveness (AR) is determined by complex mechanisms reflecting lung responses to airborne stimuli. Murine studies have identified a number of potential factors modulating AR and thus have contributed to the current understanding of these mechanisms. In allergic inflammation, immune cells, in particular alphabeta T cells, have emerged as important contributors to increased AR. We have found that in contrast to alphabeta T cells, gammadelta T cells can have a negative regulatory effect on AR. Here, we review the current studies on gammadelta T cells in allergic inflammation and discuss their role in modulating AR. We propose that gammadelta T cells exhibit different immune properties depending on the type of stimulus and inflammation. These differential immune properties appear to be associated with specific gammadelta T cell subsets, which control AR to airborne stimuli. In particular, our recent data indicate that the Vgamma4(+) T cell subset acts as an important negative regulator of AR and contributes to maintaining normal lung function in mice.

Animals↗