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Biomedical subjects

Y Ohta

Publications and source records attributed to Y Ohta.

At least 235 records · Page 13Linked to original sources

[Peak inspiratory flow during a diskhaler use in subjects unfamiliar with dry powder devices].

Dry power steroid was firstly introduced in Japan in 1998. We measured peak inspiratory flow (PIF) through a Diskhaler in the following groups: well-trained medical representative (EX group, n = 5), respiratory physicians (RP group, n = 19) and non-medical staffs (NM group, n = 31) who were not familiar with Diskhaler, and asthmatic patients who had been briefly trained by a video movie (TP group, n = 93). When PIF was less than 50 l/m dry powders were frequently remained in the brister. The mean PIF in the EX group was 96.1 +/- 12.6 l/m (mean +/- SD). Since the relationship between the PIF and airway pressure (Paw) during Diskhaler use was expressed as PIF = 16.3 square root of Paw-1.19 (r = 0.97), we calculated PIF from Paw measured by a handy barometer made by ourselves. The mean PIF in RP group was 77.0 +/- 30.1 l/m, and 36.8% of the subjects developed inappropriate PIF (i.e., above 100 l/m or below 50 l/m). In NM group the mean PIF was 53.5 +/- 20.4 l/m which was significantly higher than RP group. In this group 54.8% of the subjects yielded inappropriate PIF. The mean PIF in TP group was 64.9 +/- 24.5 l/m which was significantly lower than that in RP group. Those who developed inappropriate PIF occupied 43.2% of the RP subjects. We concluded that a quantitative presentation of PIF in mandatory to achieve an effective use of Diskhaler.

Adult↗

Clinical significance of perfusion imaging of the left atrial wall and structures in its cavity by contrast echocardiography.

This study examined whether myocardial contrast echocardiography (MCE) can visualize left atrial appendage myocardial perfusion using transesophageal echocardiography (TEE) with intracoronary injection of sonicated albumin. We also evaluated blood flow into normal structures (i.e. muscular trabeculae) and abnormal masses (i.e. fresh thrombi and myxomas) within the left atrium by MCE. TEE images were obtained with a biplane or multiplane 5 MHz transducer in 16 patients without significant coronary artery occlusive disease. Left atrial appendage myocardium was divided into 4 segments in both the transverse and longitudinal planes, and contrast opacification of each segment during MCE was visually evaluated by 2 independent observers. Visual assessment of contrast opacification of prominent muscular trabeculae within the left atrial appendage (6 patients), and of left atrial or left atrial appendage thrombi (4 patients), was also performed. The ratio of background-subtracted peak videointensity from muscular trabeculae or thrombi versus left atrial appendage myocardium was determined as corrected peak videointensity. In 3 patients with myxomas, contrast opacification of the tumor was visually assessed. Ninety-six segments of left atrial appendage myocardium were visually analyzed. Contrast opacification of the left atrial appendage myocardium was identified in 92 of 96 segments (96%, 95% confidence interval 0.90-0.98) by Observer 1 and in 91 of 96 segments (95%, 95% confidence interval 0.88-0.98) by Observer 2. MCE also enhanced the imaging of left atrial appendage muscular trabeculae, but not of left atrial or left atrial appendage thrombi. Corrected peak videointensity from thrombi was significantly lower than that from muscular trabeculae (0.15 +/- 0.11 vs 0.95 +/- 0.18, p < 0.05). All myxomas were distinctly opacified by MCE. Transesophageal MCE with intracoronary injection of sonicated albumin can image left atrial appendage myocardial perfusion. MCE allows the evaluation of blood flow into normal structures and abnormal masses within the left atrium.

Adult↗

[Surgical results on N2 lung cancer with special reference to correlation between tumor size and extension of lymph node metastases].

Systematic lymph node dissection was performed for every patients undergoing surgical intervention. Since 1981, there were 218 stage IIIA-N2 patients who underwent resection with two operative mortality. The five-year survival rate of whole cases was 22.6%, and that of 152 completely resected cases was 30.0%. Favorable factors on long-term survival of pN2 patients were cN0, T1-2 N2M0, single mediastinal node involvement, and tumor less than 20 mm or less. The five-year survival rates of stage IIIA-N2 patients with tumor diameter of < or = 20 mm, 21-30 mm, 31-50 mm, and > or = 51 mm were 48.1%, 27.7%, 31.2%, and 16.7%, respectively. When micrometastases to lymph node in the p-stage I patients (diagnosed by H-E staining) were examined by immunohistochemical staining, 36 patients (27%) out of 132 verified micrometastases in the lymph nodes.

Humans↗

Spinal inputs from lateral columns to reticulospinal neurons in lampreys.

This study characterizes the inputs from the lateral columns of the spinal cord to reticulospinal neurons in the lampreys, using the in vitro isolated brainstem and spinal cord preparation. Synaptic responses to the electrical stimulation of the lateral columns were recorded in reticulospinal neurons of the posterior and middle rhombencephalic reticular nuclei. The responses consisted of a mixture of excitation and inhibition. They were markedly potentiated when using trains of two to five pulses, suggesting that the larger part of these synaptic responses was mediated via an oligosynaptic pathway. An early component, however, persisted when using twin pulses at 10-20 Hz on the ipsilateral side, suggesting the presence of an early mono- or disynaptic component. When increasing the stimulation strength, an early fast rising excitatory component appeared. It most likely resulted from an antidromic activation of vestibulospinal axons in the lateral tracts, which make en passant synaptic contacts with reticulospinal neurons. Responses were practically abolished by adding CNQX and AP5 to the Ringer's solution. The late component of excitatory responses was decreased by AP5, suggesting that NMDA receptors were activated. The NMDA receptor-mediated component was larger when using trains of stimuli or in Mg2+-free Ringer's. The application of NMDA depolarized reticulospinal neurons. The glycinergic inhibitory component was markedly increased in Mg2+-free Ringer's. Moreover, GABAB-receptor activation with (-)-baclofen abolished both excitatory and inhibitory responses. Taken together, the present results indicate that ascending lateral column axons generate large excitatory and inhibitory synaptic potentials in reticulospinal neurons. The possible role of these inputs in modulating the activity of reticulospinal neurons during locomotion is discussed.

2-Amino-5-phosphonovalerate↗

Protective and preventive effects of teprenone on gastric mucosal lesions in rats.

We have reported that neutrophil infiltration into gastric mucosa is closely related to gastric mucosal lesion development in rats with water immersion restraint stress. In this study, we examined the effect of teprenone, which is known to prevent gastric mucosal injury through stimulation of gastric mucus synthesis and secretion, on neutrophil infiltration into the gastric mucosa of rats with water immersion restraint stress. Pre- and post-administration of teprenone (200 mg/kg, p.o.) significantly attenuated the neutrophil infiltration into the gastric mucosa and the lesion development found at 6 h of water immersion restraint stress with preservation of gastric mucosal hexosamine and adherent mucus levels. These results indicate that teprenone exerts protective and preventive actions against water immersion restraint stress-induced gastric mucosal lesions in rats and suggest that these actions could be related to the preservation of gastric mucus synthesis and secretion and inhibition of neutrophil infiltration into the gastric mucosal tissue.

Animals↗

Diagnostic value of plasma thrombin-antithrombin III complex and D-dimer concentration in patients with varicose veins for exclusion of deep-vein thrombosis.

The aim of this study was to evaluate the usefulness of determining plasma D-dimer (DD) and thrombin-antithrombin III complex (TAT) levels in the diagnostic workup for the screening of deep-venous thrombosis (DVT) among varicose vein patients. One hundred forty consecutive patients being treated for DVT or varicose veins underwent color-flow duplex scanning, and 25 patients had DVT and the remaining 115 had primary varicose veins. When DD and TAT were analyzed statistically in combination, it was determined that the combination of either positive DD (cutoff level 1.0 microg/ml) or positive TAT (cutoff level 3.0 microg/l) had a sensitivity of 100% for DVT with a specificity, positive predictive value, and negative predictive value of 79%, 51%, and 100%, respectively. This study demonstrates plasma levels of DD (less than 1.0 microg/ml) and TAT (less than 3.0 microg/l) in combination to be useful for the exclusion of DVT among patients with varicose veins. Patients with negative hematological data may safely undergo surgical treatment for varicose veins without further evaluation such as duplex scanning or contrast venography.

Antithrombin III↗

Contribution of brainstem hypoperfusion to the tracheal and phrenic nerve responses to high-pressure lung inflation in the dog.

Lung inflation to high airway pressure is known to produce tracheal constriction following an initial dilation. This is attributed to stimulation of various pulmonary receptors. In an attempt to find cause of this response, we investigated in 20 decerebrated, tracheostomized and paralyzed dogs changes in the tracheal smooth muscle tension, arterial pressure and the phrenic nerve activity to high-pressure lung inflation. A high-pressure lung inflation evoked a contraction of tracheal smooth muscle following its short-lasting relaxation, and a persistent hypotension. After hilar denervation which eliminated all pulmonary afferents, a high-pressure lung inflation still evoked contraction of tracheal smooth muscle (an increase of 3.7 times) and augmented amplitude and frequency of phrenic bursts. Bilateral transections of sympathetic fibers to the lung, or blockade of arterial perfusion to the carotid sinus and denervation of the carotid sinus bilaterally did not alter the tracheal muscle and phrenic responses to a high-pressure lung inflation. We further found that severe hypotension alone caused similar responses of the tracheal smooth muscle contraction and augmented phrenic activity. Finally, when blood supply to the brainstem was transiently obstructed by clamping both the vertebral and internal carotid arteries bilaterally, the same responses were observed. In contrast, when blood hypoperfusion to the brainstem was prevented by means of extracorporeal circulation, a high-pressure lung inflation failed to evoke such contraction of tracheal smooth muscle and or increased phrenic activity. After transection of the vagus nerves bilaterally at the cervical level the tracheal muscle response to lung inflation was abolished but that of phrenic nerve was preserved. We concluded that the tracheal smooth muscle contraction and phrenic responses induced by high-pressure lung inflation may be in part attributed to brainstem hypoperfusion.

Animals↗

Sequential progression of the differentiation program by bone morphogenetic protein-2 in chondrogenic cell line ATDC5.

During embryonic development of long bones, chondroprogenitor cells exhibit the transitions of phenotype, i.e., from type I collagen-expressing cells to type II collagen-expressing chondrocytes through cellular condensation (early-phase differentiation) and then to type X collagen-expressing mineralizing chondrocytes (late-phase differentiation). The chondrogenic cell line ATDC5 displays the sequential transitions of phenotype in a synchronous manner in vitro. Taking advantage of the sequential differentiation, the effects of growth factors were evaluated at each differentiation step of ATDC5 cells. Among the factors examined, bone morphogenetic protein-2 (BMP-2) specifically stimulated a progression of the early-phase differentiation. Rounded chondrocytic cells were formed all over the culture plates by skipping out a cellular condensation stage. Fibroblast growth factor-2 stimulated growth of undifferentiated ATDC5 cells, but failed to stimulate overt chondrogenesis. The proliferation of differentiated cells ceased as cartilage nodules became maturated. At this stage, BMP-2 markedly up-regulated expression of type X collagen mRNA (a 9.1-fold increase) and alkaline phosphatase mRNA (a 7.5-fold increase) within 48 h. On the other hand, it down-regulated expression of type II collagen and parathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor mRNAs, markers of the early differentiation. BMP-2 stimulated the formation of calcified matrix, an end product of terminally differentiated chondrocytes. These results indicated that BMP stimulated the sequential progression of early- and late-phase differentiation of ATDC5 cells.

Alkaline Phosphatase↗

Improved fluorometric enzymatic sorbitol assay in human blood.

Samples for use in the fluorometric enzymatic assay of sorbitol in erythrocytes are normally prepared using HClO4 and K2CO3. We have replaced these reagents with NaOH and ZnSO4. Human whole blood, erythrocyte and plasma samples prepared with NaOH and ZnSO4 are colorless and clear, while erythrocyte samples prepared with HClO4 and K2CO3 are a pale yellow-brown color. The sorbitol dehydrogenase reaction in the supernatant of the mixture of NaOH and ZnSO4 is inhibited, but ethylenediaminetetraacetate completely eliminates this effect. The sorbitol assay in erythrocytes prepared with NaOH and ZnSO4 shows higher sensitivity and reproducibility than did that with HClO4 and K2CO3. Recovery of sorbitol added to erythrocytes is similar in both assay methods. Concentrations of whole blood and erythrocyte sorbitol assayed by the present method are significantly higher in diabetics than in normals. Poorly controlled diabetics had higher whole blood and erythrocyte sorbitol than well-controlled diabetics. Whole blood sorbitol concentrations differed more between diabetic and normal subjects than did erythrocyte sorbitol concentrations.

Adult↗

Direct antigen presentation through binding of donor intercellular adhesion molecule-1 to recipient lymphocyte function-associated antigen-1 molecules in xenograft rejection.

Cellular interactions that lead to graft rejection were examined in a rat-to-mouse xenogeneic combination using species-specific monoclonal antibodies (mAbs) against donor and recipient intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) molecules, respectively. Although both mAbs displayed moderate blocking activity in an in vitro mixed lymphocyte response assay, strong suppression was observed when anti-donor (rat) ICAM-1 mAb was combined with anti-recipient (mouse) LFA-1 mAb. Likewise, significant prolongation of islet xenograft survival was observed with these mAbs. Thus, 0.05 mg of anti-mouse LFA-1 mAb and anti-rat ICAM-1 mAb given on days 0 and 1 produced significant prolongation of graft survival over the control (51+/-20 days vs. 10+/-3 days, P<0.0001), but not when anti-mouse ICAM-1 mAb was combined with anti-mouse LFA-1 mAb (13+/-3 days). In this species combination, mouse T cells were able to proliferate in the presence of rat antigen-presenting cells (APCs) in a cell number-dependent manner, but not in the presence of mouse APCs. The binding assay showed that LFA-1 molecules on mouse T cells can bind immobilized rat ICAM-1 molecules. These results suggest that rat ICAM-1 molecules on APCs can interact with mouse LFA-1 molecules on T cells across a species barrier and that this binding generates the consequent immune responses leading to rejection. mAb treatment against these adhesion molecules of recipient as well as donor is crucial for preventing rejection in a xenogeneic transplantation model.

Animals↗

Increased cellular resistance to oxidative stress by expression of cyanobacterium catalase-peroxidase in animal cells.

To exploit prokaryotic antioxidant enzymes for protection of animal cells from oxidative damage, we expressed catalase-peroxidase of cyanobacterium Synechococcus PCC 7942 in 104C1 cells. The gene for this enzyme was inserted into the mammalian expression vector pRc/CMV. The stable transfectants obtained had higher specific activities of catalase and as a result became more resistant to H2O2 or paraquat than the parental cells. Subcellular fractionation and immunoblot analysis revealed that the expressed catalase-peroxidase was confined to the cytosol; this localization may be the basis for the effective protection of the transfectants from the oxidative cell damage.

Animals↗

Preventive effect of gamma-glutamylcysteinylethyl ester on carbon tetrachloride-induced hepatic triglyceride accumulation in mice.

The effect of gamma-glutamylcysteinylethyl ester (gamma-GCE), which is a precursor of reduced glutathione (GSH), on carbon tetrachloride (CCl4)-induced hepatic triglyceride (TG) accumulation in mice was investigated in comparison with that of GSH. Administration of gamma-GCE (160 micromol/kg), but not GSH (160 micromol/kg), to mice at 3 h after CCl4 injection (1 ml/kg, i.p.) significantly attenuated an increase in hepatic TG concentration at 6, 12, and 24 h after the CCl4 injection. A decrease in hepatic GSH concentration after the CCl4 injection was significantly diminished by the gamma-GCE administration, but not by the GSH administration. The correlation coefficient between hepatic TG concentration and hepatic GSH concentration was -0.627 (P < 0.001) when the results of all mice were grouped together. These results indicate that gamma-GCE can attenuate CCl4-induced hepatic TG accumulation in mice through the maintenance of hepatic GSH level.

Animals↗

Contribution of NO synthases to neutrophil infiltration in the gastric mucosal lesions in rats with water immersion restraint stress.

A decrease in constitutive NO synthase (cNOS) activity and an increase in inducible NO synthase (iNOS) activity occurred with an increase in myeloperoxidase (MPO) activity, an index of neutrophil infiltration, in the gastric mucosa of rats with water immersion restraint (WIR) stress. This increase in gastric mucosal MPO activity was enhanced by pretreatment with NG-monomethyl L-arginine, a non-selective NOS inhibitor, but was prevented with maintenance of gastric mucosal cNOS activity by pretreatment with aminoguanidine, a selective iNOS inhibitor. The MPO activity was negatively correlated with the cNOS activity in all WIR-stressed rats used (r=-0.723). These results suggest that a decrease in cNOS activity could contribute to an increase in neutrophil infiltration in the gastric mucosa of WIR-stressed rats.

Animals↗

Gamma-glutamylcysteinylethyl ester attenuates progression of carbon tetrachloride-induced acute liver injury in mice.

We examined the effect of gamma-glutamylcysteinylethyl ester (gamma-GCE), which is readily transported into hepatocytes and increases hepatocellular reduced glutathione (GSH) levels, on the progression of carbon tetrachloride (CCl4)-induced liver injury in mice in comparison with that of GSH. Administration of more than 160 micromol/kg of gamma-GCE, but not GSH, to mice at 3 h after intraperitoneal injection of CCl4 (1 ml/kg) significantly attenuated increases in serum aspartate aminotransferase and alanine aminotransferase activities at 24 h after the CCl4 injection. Increases in hepatic lipid peroxide (LPO) concentrations and decreases in hepatic GSH concentrations after the CCl4 injection were significantly diminished by the gamma-GCE (160 micromol/kg) administration, but not by the same dose of GSH. Gamma-GCE, gamma-glutamylcysteine, and cysteine acted as substrates for glutathione peroxidases much less efficiently than GSH in the post-mitochondrial fraction of normal mouse liver cells. These results indicate that gamma-GCE attenuates the progression of CCl4-induced acute liver injury in mice through the maintenance of hepatic GSH levels, leading to inhibition of hepatic LPO formation, which could be due to an efficient utilization of GSH converted from gamma-GCE in the liver cells.

Animals↗

Mode of cell death in the rat metrial gland during peripartum regression.

In the rodent uterus, the metrial gland develops during midpregnancy and undergoes regression prior to parturation. The involution of the gland is reported to be accompanied by the loss of gland cells due to their death in situ. Cell death has been classified by using morphological criteria into two types: necrosis and apoptosis. To study the mechanism involved in the peripartum regression of the rat metrial gland, we examined the mode of cell death in the gland during the last week of gestation. We identified apoptotic cells in the regressing metrial gland by using DNA fragmentation, in situ DNA 3'-end labeling, and electron microscopy. Expression of progesterone receptor (PR) and estrogen receptor (ER) was also demonstrated by immunohistochemistry in the gland. The mean weight of metrial gland nodes decreased after day 18 of pregnancy. The apoptotic granulated metrial gland (GMG) cells that were detected by using the in situ DNA 3'-end labeling method were observed on day 16 of pregnancy, and they increased in number after day 20 of pregnancy. Intense fragmentation of DNA was also found from day 20 to day 22 of pregnancy. Electron microscopy demonstrated apoptotic GMG cells in the regressing metrial glands, confirming the results of the labeling studies. Immunohistochemical study revealed that expression of PR and ER, which were localized mainly in fibroblast-like stromal cells but not in GMG cells, was almost unchanged during late pregnancy. Apoptotic cell death is the major mode of rat metrial gland cell death in the peripartum loss of metrial gland cells.

Animals↗

Relation of inducible nitric oxide synthase activity to lipid peroxidation and nonprotein sulfhydryl oxidation in the development of stress-induced gastric mucosal lesions in rats.

We have reported that increases in lipid peroxide (LPO) formation, nonprotein sulfhydryl (NP-SH) oxidation, and inducible NO synthase (iNOS) activity and a decrease in constitutive NO synthase (cNOS) activity in the gastric mucosa of rats with water immersion restraint (WIR) stress are closely related to gastric mucosal lesion development. Peroxynitrite, which is produced by the reaction of nitric oxide (NO) with superoxide anion, can initiate intracellular LPO formation and NP-SH oxidation, resulting in producing an extreme cellular membrane damage. In this study, the relation of changes in cNOS and iNOS activities to LPO formation and NP-SH oxidation was examined in the gastric mucosa of rats with WIR stress. An increase in iNOS activity, but not a decrease in cNOS activity, correlated well with an increase in LPO concentration (r = 0.750) and NP-SH concentration (r = -0.808) in the gastric mucosa of rats with WIR stress. In addition, the above-mentioned changes in iNOS activity and LPO and NP-SH concentrations with lesion development in the gastric mucosa of rats with WIR stress were attenuated with both prevention of the lesion development and an increase in the concentration of gastric mucosal nitrite/nitrate, the breakdown products of NO, by pretreatment with aminoguanidine, a selective iNOS inhibitor. These results suggest that in the gastric mucosa of WIR-stressed rats, NO produced by increased iNOS could contribute to enhanced LPO formation and NP-SH oxidation, resulting in lesion development.

Animals↗

Relationship between constitutive nitric oxide synthase activity and mucus level in the gastric mucosa of rats with stress.

A decrease in constitutive nitric oxide synthase (cNOS) activity occurred with decreases in hexosamine (an index of mucus synthesis) and adherent mucus (an index of mucus secretion) concentrations in the gastric mucosa of rats with water immersion restraint (WIR) stress. The decreases in gastric mucosal hexosamine and adherent mucus concentrations were enhanced with a further decrease in gastric mucosal cNOS activity by pretreatment with NG-monomethyl L-arginine, a non-selective NOS inhibitor, but were prevented with maintenance of the gastric mucosal cNOS activity by pretreatment with aminoguanidine, a selective inducible NO synthase inhibitor. In all WIR-stressed rats used in this study, gastric mucosal cNOS activity was well correlated with either gastric mucosal hexosamine or adherent mucus concentration (r=0.717 or 0.739, respectively). These results indicate that in the gastric mucosa of WIR-stressed rats, a decrease in cNOS activity is closely related to a decrease in mucus level due to impairment of its synthesis and secretion. (c) 1998 The Italian Pharmacological Society.

Animals↗

Relations between surface expression of the interleukin-2 receptor and release of the soluble form of the receptor in cultured mononuclear cells from patients with rheumatoid arthritis or systemic lupus erythematosus.

The relationship between surface expression of the interleukin-2 receptor (IL-2R) and release of the soluble form of the receptor (sIL-2Ralpha or sCD25) was investigated with peripheral blood mononuclear cells (PBMCs) from individuals with rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE). The spontaneous release of sCD25 was significantly increased in PBMCs from RA patients and decreased in cells from SLE patients, compared with normal controls. However, the extent of sCD25 release from phytohaemagglutinin (PHA)-stimulated PBMCs did not differ between RA or SLE patients and normal controls. The serum concentration of sCD25 was significantly increased in SLE or RA patients compared with the normal controls. Whereas the surface expression of CD25 by unstimulated PBMCs did not differ among the three groups of subjects, this parameter was significantly reduced for PHA-stimulated PBMCs from RA patients relative to those from normal controls. The surface expression of CD25 showed a positive correlation with sCD25 release for PBMCs from SLE patients under either basal or stimulated conditions. No such relation was apparent for cells from RA patients. The surface expression of IL-2Rbeta (CD 122) under basal or stimulated conditions was significantly reduced in PBMCs from RA or SLE patients, compared with cells from normal controls. Thus, the increased concentration of sCD25 in the serum of individuals with these autoimmune rheumatic diseases may result from two different mechanisms: an increase in the spontaneous release of sCD25 in RA, and reduced clearance of this protein in SLE.

Adult↗