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H Uehara

Publications and source records attributed to H Uehara.

At least 55 records · Page 3Linked to original sources
PubMed1999

[Light-guided tracheal intubation using a Trachlight: causes of difficulty and skill acquisition].

We studied the reasons why tracheal intubation using a lighted stylet (Trachlight) was sometimes difficult for unexperienced intubators. We also examined light-guided intubation skill acquisition in inexperienced anesthesiologists. Two anesthesiologists, with no prior experience in using a Trachlight, performed orotracheal intubation using a Trachlight in 60 anesthetized patients (30 patients each). During intubation, an assistant observed the advancement of the tracheal tube using a fiberscope passed nasally and recorded the reason for difficulty in intubation. The time to successful intubation was also measured. Data were divided into epochs of 10 cases, and the intubation time and the incidence of difficult cases were compared between the groups. Tracheal intubation was successful using the Trachlight in 59 of 60 patients. The incidence of difficult cases, defined as cases requiring two or more attempts, was 31.7%. Fiberscopy showed that when the tube tip was located in the vallecula or in the esophagus, it was sometimes difficult to determine the position of the tube tip by transillumination of the soft tissues of the neck, and this results in the need for multiple attempts. Both the intubation time and the incidence of difficult cases decreased significantly between the first and last epoch. The present study confirms that light-guided intubation is sometimes difficult when the tube tip is advanced to the vallecula or to the esophagus. An acceptable level of skill in light-guided intubation is achieved within 30 uses.

Adult↗
PubMed1999

[Diagnosis of myocardial viability by exercise echocardiography].

This study determined whether the diagnosis of myocardial viability could be established on the basis of the contractile reserve during low level exercise with an ergometer using echocardiography. The study involved 22 patients with transmural old myocardial infarction who underwent exercise echocardiography, followed by coronary intervention after a mean 4 days. Exercise echocardiography was started from 50 W and stepped up by 25 W every 3 min up to a maximum of 150 W. Low level exercise was administered for 1 to 2 min at 50 W. A 16-segment model was used for the left ventricular wall motion, which was evaluated by five-grade scoring, ranging from normokinesis to dyskinesis. If patients showed improvement by one point or more in the score for segments of dyskinesis, akinesis, or severe hypokinesis on the exercise echocardiography, they were considered to have positive viability. The golden standard for the diagnosis of myocardial viability was that wall motion abnormalities before exercise echocardiography should be improved by one point or more after coronary intervention. Before exercise echocardiography, there were 152 segments showing wall motion abnormalities assessed as severe hypokinesis or more. After coronary intervention, improvement of the wall motion by one grade or more was found in 2 of the 18 segments (11%) for dyskinesis, in 38 of the 96 segments (40%) for akinesis, and in 22 of the 38 segments (58%) for severe hypokinesis; improvement for the segments of severe hypokinesis was significantly better than those for dyskinesis and akinesis. Out of 19 segments with akinesis before exercise echocardiography in which wall motion was improved during low level exercise, 16 segments (84%) showed improvement in wall motion after coronary intervention. Out of 77 segments with akinesis before exercise echocardiography in which no change or worsening was seen during low level exercise, 22 segments (29%) showed improved wall motion after coronary intervention. There were 38 segments with severe hypokinesis before exercise echocardiography; out of 12 segments in which wall motion was improved during low level exercise, 7 segments (58%) showed improved wall motion after coronary intervention. Out of 26 segments with severe hypokinesis before exercise echocardiography in which no change or worsening was seen during low level exercise, 11 segments (42%) showed improved wall motion after coronary intervention. Wall motion was improved after coronary intervention in 20 of 25 segments (80%) that showed the biphasic response, in 4 of 7 segments (57%) that showed improvement, in 14 of 43 segments (33%) that showed worsening, in 24 of 77 segments (31%) for no change; the biphasic response showed a significantly higher improvement compared to worsening or no change. If segments in which wall motion was improved during low level exercise are regarded as positive viability segments, occurrences of the sensitivity, specificity and diagnostic accuracy of myocardial viability were 50%, 84%, and 71%, respectively.

Echocardiography↗
PubMed1999

Late recurrence of acinic cell carcinoma of the parotid gland.

Acinic cell carcinoma of the salivary glands is a rare cancer representing a low grade malignancy. The recurrence of a tumor is sometimes encountered, usually within 5 years of initial operation. We describe an unusual recurrence after a long interval following primary surgery. In 1987, a 60-year-old woman underwent excision of a mass in the superficial lobe of the right parotid gland under the preoperative diagnosis of a benign tumor. A histologic diagnosis of acinic cell carcinoma was made by examining sections from the resected mass. The patient noted several small nodules in the right parotid region in 1995, but she did not visit our clinic until 1998 when tenderness developed. A locally recurrent tumor and cervical lymph nodes containing metastases were resected and postoperative radiotherapy was given 11 years after the first operation. At least 10 years of follow-up may be necessary for patients with acinic cell carcinoma because of slow-tumor growth.

Carcinoma, Acinar Cell↗
PubMed1998

Up-regulation of vascular endothelial growth factor induced by hepatocyte growth factor/scatter factor stimulation in human glioma cells.

Recent findings suggest that hepatocyte growth factor/scatter factor (HGF/SF) contributes to the malignant progression of human gliomas. We investigated the effect of HGF/SF on vascular endothelial growth factor (VEGF) expression of c-Met/HGF receptor-positive human glioma cell lines. Treatment of the glioma cells with various concentrations of HGF/SF resulted in an enhanced secretion of VEGF proteins accompanying increased transcription of VEGF mRNA in a dose-dependent fashion. Since malignant gliomas frequently co-express HGF/SF and its receptor, these results suggest that HGF/SF could act as an indirect angiogenic factor through autocrine induction of VEGF expression and secretion in malignant gliomas.

Endothelial Growth Factors↗
PubMed1998

Alpha1-adrenoceptor stimulation enhances experimental gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effect of prolonged administration of the norepinephrine-mimicking agent metaraminol, the alpha1-adrenergic agonist phenylephrine and the alpha2-adrenergic agonist clonidine on the incidence of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), the ornithine decarboxylase activity of the gastric cancer and the labeling index of the gastric mucosa were investigated in Wistar rats. Rats received s.c. injections of metaraminol, phenylephrine or clonidine every other day after 20 weeks of oral treatment with MNNG. At week 52, administration of metaraminol and phenylephrine at the higher dose significantly increased the incidence of gastric cancers, the ornithine decarboxylase activity of the gastric cancers and the labeling index of the antral epithelial cells. Administration of phenylephrine at the lower dose and clonidine at both doses had no significant effect on the incidence of gastric cancers, the ornithine decarboxylase activity of the gastric cancers or the labeling index of the gastric mucosa. Our results suggest that adrenoreceptor stimulation enhances gastric carcinogenesis and that such enhancement is mediated through alpha1-adrenoceptors without alpha2-adrenoceptor involvement.

Adrenergic alpha-Agonists↗
PubMed1998

Attenuation by methionine of monochloramine-enhanced gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

Helicobacter pylori appears to play a major role in the development of gastric cancer in humans. The mechanism behind the carcinogenic or co-carcinogenic effects of H. pylori has not been established. Ammonia, generated by urea from H. pylori, has been studied as a possible cause. However, the ammonia-monochloramine system has been shown to play a more important role in H. pylori-associated mucosal injury. Therefore, the effects of combined administration of monochloramine and methionine, singly or together, on the development of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in inbred Wistar rats. After receiving oral MNNG and regular chow pellet for 25 weeks, rats received regular chow pellets or chow pellets containing 20% ammonium acetate, and normal tap water or water containing 30 mM sodium hypochlorite, with or without a subcutaneous injection of methionine, until the end of the experiment (week 52). Treatment with both ammonium acetate and sodium hypochlorite, which produce monochloramine, significantly increased the incidence of gastric cancers in week 52, whereas the concomitant administration of methionine with ammonium acetate and sodium hypochlorite significantly attenuated such enhanced gastric carcinogenesis. Spectrophotometric examination revealed that methionine scavenged monochloramine. Our findings suggest that H. pylori-associated gastric carcinogenesis may be mediated by monochloramine.

Animals↗
PubMed1998

Inhibition by galanin of experimental carcinogenesis induced by azaserine in rat pancreas.

The effects of galanin on pancreatic carcinogenesis induced by azaserine and on the norepinephrine concentration in the pancreas were investigated in male Wistar rats. Rats were given weekly injections of 10 mg/kg body weight of azaserine for 25 weeks and 8 microg/kg body weight of galanin in depot form every other day for 62 weeks. Azaserine-induced pancreatic lesions were examined with hematoxylin and eosin and histochemical techniques. In week 62, quantitative histological examination showed that prolonged administration of galanin significantly reduced the number and size (as percent of parenchyma) of adenosine triphosphatase-positive pancreatic lesions, which are correlated closely with the ultimate development of pancreatic cancer. The number of pancreatic adenocarcinomas in rats treated with galanin was significantly less than in controls. Galanin also significantly decreased the bromodeoxyuridine-labeling index of azaserine-induced pancreatic lesions and the norepinephrine concentration in the pancreas. Our findings indicate that galanin inhibits pancreatic carcinogenesis and that such inhibition may be related to the suppression of sympathetic nervous system activity and subsequently to the inhibition of cell proliferation in neoplastic lesions of the pancreas.

Animals↗
PubMed1998

Promotion by the alpha-adrenoceptor agonist phenylephrine, but not by the beta-adrenoceptor agonist isoproterenol, of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of prolonged administration of the alpha-adrenoceptor agonist phenylephrine and the beta-adrenoceptor agonist isoproterenol on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine and on the labeling index of gastric mucosa were compared in Wistar rats. Rats received subcutaneous injections of 3 or 6 mg/kg body weight of phenylephrine or 0.1 or 0.2 mg/kg body weight of isoproterenol every other day after 25 weeks of oral treatment with the carcinogen. Long-term administration of phenylephrine at a high dose, but not at a low dose, significantly increased the incidence of gastric cancers and the labeling index of antral epithelial cells at the end of the experiment in week 52. However, administration of isoproterenol at either dosage had no significant effect on the incidence of gastric cancers and the labeling index of antral epithelial cells. These findings indicate that increased activity of the sympathetic nervous system enhances gastric carcinogenesis through alpha-adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1998

Contribution of the Breakdown of the Born-Oppenheimer Approximation to Higher Order Dunham Coefficients

By means of a Deltaomega and DeltaB formalism for correction parameters, expressions were derived for higher-order Dunham coefficients, Y*vJ04, Y*vJ12, and Y*vJ21, in which contributions of the breakdown of the Born-Oppenheimer approximation were taken into account. Including Y*vJ04, Y*vJ12, and Y*vJ21, and Dunham's Y09, Y17, and Y25 coefficients in addition to the lower-order Y*vJij and Yk1 in the analysis, an extensive data set of the vibrational-rotational and the rotational transitions for four isotopomers of lithium hydride was fitted simultaneously to a single set of molecular constants within experimental errors. Since lithium hydride is a very light molecule, expressions shown in the present article should provide a means applicable to most cases of the spectral analysis of diatomic molecules in the 1Sigma state. Copyright 1998 Academic Press.

Journal Article↗
PubMed1998

Dunham Treatment Including Effects of the Born-Oppenheimer Breakdown for Open-Shell Diatomic Molecules in 2Sigma States.

A Dunham treatment of an effective Hamiltonian for diatomic molecules in 2Sigma states that includes contributions of the Born-Oppenheimer breakdown has yielded an expression for vibrational-rotational energy by an expansion in powers of (v + (1/2))i[N(N + 1)]j-k(N'/2)k, where N' is N for the J = N + (1/2) spin-doublet state and -(N + 1) for the J = N - (1/2) state and k = 0, 1, ellipsis, j. Analytic expressions for the expansion coefficients Y*vJijk provide a potential model appropriate for the spectral fits for molecules in 2Sigma states. The expansion coefficients Y*vJij0 for the k = 0 terms are exactly the same as the Y*vNij coefficients given for 1Sigma states, the Dunham coefficients Yij modified by the contributions of the Born-Oppenheimer breakdown, provided that a spin contribution originating from off-diagonal electronic corrections of the electronic part of the spin-orbit interaction can be ignored. Spin-rotation energy is given by the terms with coefficients Y*vJijk (k >/= 1). There are no Y*vJijk (k >/= 2) terms in the previously known methods of analysis for 2Sigma molecules. The present potential model is applied to the reported vibrational-rotational spectra of CaH and all spectral lines of 40CaH and 40CaD isotopomers are fitted to a single set of molecular constants simultaneously with significantly smaller standard deviations. Copyright 1998 Academic Press.

Journal Article↗
PubMed1998

Application of SPET using technetium-99m sestamibi in brain tumours and comparison with expression of the MDR-1 gene: is it possible to predict the response to chemotherapy in patients with gliomas by means of 99mTc-sestamibi SPET?

Technetium-99m sestamibi (MIBI) is thought to be passively taken up by metabolically active tumour cells and effluxed from them by P-glycoprotein (Pgp). This 170-kDa membrane-bound protein, encoded by the MDR-1 gene, acts as an energy-dependent efflux pump for several antineoplastic agents, resulting in multidrug resistance. For this reason, it is of interest whether the tumour's response to chemotherapy can be predicted by MIBI single-photon emission tomography (SPET). In this study, MIBI SPET was compared with thallium-201 (Tl) SPET using magnetic resonance imaging as a guide in 16 patients with untreated brain tumours [ten glioblastomas (GBs), two anaplastic astrocytomas (AAs), two low-grade gliomas (LGASs) and two metastatic brain tumours) and in four patients who had received treatment for with brain tumours (two GBs, two AAs). In addition, we investigated the expression of the MDR-1 gene and its product Pgp in the same patients, and compared the results with MIBI SPET findings. MIBI, as well as Tl, was highly accumulated and retained in the enhanced region of malignant gliomas. In addition, MIBI SPET yielded sharp and well-contrasted images, and the margin of the tumour was more clearly defined than with Tl SPET due to a good signal-to-noise ratio. Follow-up MIBI SPET in patients who had received therapy showed marked uptake in a patient with malignant transformation, who deteriorated clinically. Patients with no uptake on MIBI SPET showed no sign of recurrence. Semiquantitative analysis of untreated patients showed a relationship between the early uptake index (UI, ratio of average count/pixel in the lesion to that in the contralateral area on early images) and the degree of malignancy (early UI = 1.08+/-0.06 in LGASs, 4.10+/-0.84 in AAs, 5.71+/-3.47 in GBs, and 7.52+/-1.52 in metastatic brain tumours). The retention index (RI, ratio of delayed to early UI) of MIBI was significantly lower than that of Tl in metastatic brain tumours (P<0.05), but not in malignant gliomas. Histological and biological investigation of gliomas showed that the MDR-1 gene and its product Pgp were expressed only in normal endothelial cells and not in tumour cells or proliferating endothelial cells; Pgp tended to decrease as the degree of malignancy rose. Hence, the presence of Pgp and the grade of malignancy were inversely related in gliomas. By contrast, immunohistochemical study showed strong accumulation of Pgp in metastatic brain tumour cells. These histopathological findings and MIBI SPET findings are compatible with experimental data; MIBI was washed out by Pgp. The main cause of chemoresistance is probably not an increasing drug efflux by Pgp in gliomas. Thus, MIBI SPET is useful for detecting the active lesions, but may not be useful for predicting the response to chemotherapy in gliomas.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1998

Non-carcinogenicity of capsaicinoids in B6C3F1 mice.

The carcinogenicity of a mixture of capsaicinoids (64.5% capsaicin and 32.6% dihydrocapsaicin) was examined in B6C3F1 mice. In a 13-week toxicity study, renal toxicity was observed in 1% capsaicinoid-treated males. Next, groups of 50 mice of each sex were given 0, 0.025, 0.083 or 0.25% capsaicinoids in powdered diet for 79 weeks and killed in week 83. Food intake was reduced in mice of all capsaicinoid-treated groups, especially females, because of the pungency of capsaicinoids, and inhibition of body weight gain was apparent in females. The numbers of tumour-bearing females in the high-dose groups were significantly lower than that in the controls, and the incidences of hepatocellular neoplasms in both sexes were negatively correlated with the dose of capsaicinoids (Cochran-Armitage trend test). Renal cell adenomas developed in one mouse each of 0.025 and 0.25% capsaicinoid-treated males. The incidences of other tumours were similar in the treated and control groups. Thus, the present study indicated that a mixture of capsaicinoids is not carcinogenic in B6C3F1 mice.

Animals↗
PubMed1998

Inhibition of experimental gastric carcinogenesis, induced by N-methyl-N'-nitro-N-nitrosoguanidine in rats, by sodium nitroprusside, a nitric oxide generator.

The effects of prolonged administration of sodium nitroprusside (SNP), a generator of nitric oxide (NO), on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and the labelling index of the gastric mucosa were investigated in male Wistar rats. The rats received intra-peritoneal injections of 2 or 4 mg/kg body weight of SNP every other day after 25 weeks' oral treatment with the carcinogen. Prolonged administration of SNP at 4 mg/kg body weight, but not at 2 mg/kg body weight, significantly decreased the incidence of gastric cancers in experimental week 52. However, it did not affect the histological types or depths of involvement of gastric cancers. SNP at 4 mg/kg body weight, but not at 2 mg/kg body weight, also significantly decreased the bromodeoxyuridine labelling index of the antral epithelial cells. These findings indicate that SNP inhibits gastric carcinogenesis and suggest that this effect may be related to the suppression of proliferation of the antral epithelial cells.

Animals↗
PubMed1998

Inhibition by transforming growth factor (34-43)-alpha, a TGF-alpha antagonist, of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effect of prolonged administration of transforming growth factor (34-43)-alpha, an antagonist of TGF-alpha, on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and on the labelling and apoptotic indices and TGF-alpha immunoreactivity of gastric mucosa and gastric cancers was examined in Wistar rats. The rats received intraperitoneal injections of 10 or 20 microg kg(-1) body weight of TGF(34-43)-alpha every other day after oral treatment with MNNG for 25 weeks. Long-term administration of TGF(34-43)-alpha at both doses significantly reduced the incidence of gastric cancers at the end of the experiment in week 52. However, TGF(34-43)-alpha had no significant effect on the number, histological type or depth of involvement of gastric cancers. Administration of TGF(34-43)-alpha also significantly decreased the bromodeoxyuridine labelling index and TGF-alpha immunoreactivity, and significantly increased the apoptotic index of antral mucosa and gastric cancers. These findings indicate that TGF(34-43)-alpha inhibits gastric carcinogenesis, and that its effects are mediated through decreased cell proliferation and TGF-alpha immunoreactivity and increased apoptosis induction in the gastric cancers.

Adenocarcinoma↗
PubMed1998

Suppression by pravastatin, an inhibitor of p21ras isoprenylation, of hepatocarcinogenesis induced by N-nitrosomorpholine in Sprague-Dawley rats.

The effect of pravastatin, an inhibitor of p21ras isoprenylation, on hepatocarcinogenesis induced by N-nitrosomorpholine and on p21ras isoprenylation were investigated in male Sprague-Dawley rats. Rats received i.p. injections of pravastatin (10 and 20 mg kg(-1) body weight) every other day and, from the beginning of the experiment, were given drinking water containing N-nitrosomorpholine for 8 weeks. Visible white nodules and hepatic lesions staining positively for gamma-glutamyl transpeptidase or glutathione-S-transferase, placental type, were examined macroscopically or histochemically. In week 15, pravastatin at both dosages significantly reduced the incidence, number and volume of visible white nodules. Quantitative histological analysis also showed that prolonged administration of pravastatin at both dosages resulted in significant reductions in the number and percentage area of hepatic lesions positive for gamma-glutamyl transpeptidase and glutathione-S-transferase, placental type. Administration of pravastatin also significantly decreased the amount of membrane-associated p21ras in the tumour and the labelling index of neoplastic nodules and increased the apoptoic indices of neoplastic nodules. These findings indicate that pravastatin suppresses hepatocarcinogenesis and suggest that this effect might be related to pravastatin's inhibition of p21ras isoprenylation and its subsequent inhibition of cell proliferation and induction of apoptosis in neoplastic lesions.

Animals↗