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Biomedical subjects

Y Nakata

Publications and source records attributed to Y Nakata.

At least 127 records · Page 7Linked to original sources
PubMed1999

Improvement of the physical properties of pepsin-solubilized elastin-collagen film by crosslinking.

Pepsin-solubilized elastin (PSE)-conjugated collagen film was prepared from a collagen matrix with PSE by drying it and crosslinking the constituents with water-soluble carbodiimide or microbial transglutaminase to improve the physical properties of the collagen film. The crosslinking reduced the solubility and improved the thermal stability, the thermal transition properties, and the elasticity of the control film in water. In particular, water-soluble carbodiimide strongly influenced these properties. The PSE-conjugated collagen film showed good permeation by water-soluble tasting substances such as oligosaccharides and amino acids, but poor permeation by polysaccharide, protein, and hydrophobic substances such as retinol and cholesterol.

Calorimetry, Differential Scanning↗
PubMed1999

Poor reproducibility of false-positive tilt testing results in healthy volunteers.

Positive responses to head-up tilt testing occur in healthy subjects. However, the reproducibility of "false-positive" tilt testing results has not been clarified. To study the reproducibility of "false-positive" responses, we prospectively performed 2 tilt tests separated by 1 to 10 (mean 3.2) weeks in 20 healthy males aged 23 to 40 years (mean 30 years). The baseline tilt test (80 degrees for 30 minutes) ended positive in 4 (20%) subjects on the initial test and 2 (10%) on the second test with only 1 (5%) who had consecutive positive responses. No additional positive responses were noted during the isoproterenol (0.01 microgram/kg/min)-tilt test for 10 minutes. We demonstrated that a false-positive response occurred in 5 (25%) of 20 young males who underwent 2 tilt tests, however, only 1 (5%) subject had consecutive positive responses. Poor reproducibility may be characteristic of false-positive responses in head-up tilt testing.

Adult↗
PubMed1999

[Evaluation of 99mTc-MAG3 (mercaptoacetyltriglycine) renography for pediatric patients].

It is difficult to evaluate renal function with 99mTc-MAG3 renography in both adult and pediatric patients. We examined 109 pediatric patients with various renal diseases using 99mTc-MAG3 renography. Tenal diseases were classified as follows: 9 vesicoureteral reflux, 4 ureteropelvic junctional stenosis, 3 double pelvis, 23 hydronephrosis, 4 glomerulonephritis, 4 nephrotic syndrome, 24 hemolytic uremic syndrome, 10 others; and 24 patients without abnormal findings on other examinations. After hydration and sedation, 100-200 MBq of 99mTe-MAG3 was injected intravenously. All patients were placed in the supine position, and dynamic data acquisition at 12 sec/frame x 100 frames was performed from the back. The renograms were prepared with the ROIs (regions of interest) set to include the entire kidney. Tmax and T1/2 of renograms were measured for 26 kidneys with no abnormal findings. The correlations between Tmax or T1/2 and age (days after birth) were determined by a linear or logarithmic function. The logarithmic function (Y = 7.49 - 0.56 logeX, r2 = 0.134) yielded a higher correlation than did the linear function (Y = 5.16 - 0.00194X, r2 = 0.089) between Tmax and age. For T1/2 and age (days after birth), the linear function (Y = 8.07 - 0.00451X, r2 = 0.222) yielded a higher correlation than the logarithmic function (Y = 11.9 - 0.986 logeX, r2 = 0.192). Our findings suggest that prolonged Tmax is normalized more rapidly than T1/2 after birth in infants. A delayed excretion phase is not suggestive of renal dysfunction, but is characteristic of renograms in pediatric patients. Abnormality was detected in all patients with hydronephrosis using 99mTc-MAG3 renography. On the other hand, a quantitative study was required because renography detected no abnormality for some of patients with disorders of renal parenchyma.

Adolescent↗
PubMed1999

[Quantitative assessment of 201Tl-SPECT in tumors of bone and soft tissue].

201Tl-SPECT was performed to diagnose the malignancy of bone and soft tissue tumors by visual and quantitative assessment in 48 patients (17 malignant lesions and 31 benign lesions). SPECT images were obtained in the early phase (15 min after injection) and the delayed phase (240 min). By visual assessment a tumor was considered malignant if high accumulation was found in the tumor in the early phase and the accumulation was confirmed in the delayed phase. Tumors which did not meet these criteria were considered benign. For quantitative assessment, the ROI (region of interest) accumulation ratios of the tumor to the contralateral normal tissue in the early phase (ER) and in the delayed phase (DR), the ROI accumulation ratio of the delayed phase to the early phase of the tumor (Td/Te), and the ROI accumulation ratio of the delayed phase to the early phase of the contralateral normal tissue (Nd/Ne) were obtained. Sixteen patients with malignant tumors each had a high accumulation each but 12 of 31 benign lesions had no high accumulation on visual assessment. Furthermore, the accuracy was 85.4%, sensitivity 94.1%, and specificity 80.6%. Quantitative assessment was performed for 36 cases of high accumulation. The ER of malignant and benign lesions was 5.51 +/- 3.73 and 2.75 +/- 2.17, respectively, and the ER of malignant lesions was significantly higher than that of benign lesions. The DR did not demonstrate a significant difference. If the tumor having an ER greater than 3.9 was assumed to be malignant, the accuracy for differentiating malignant lesions from benign lesions was 85.4%. The Td/Te of benign lesions (0.97 +/- 0.28) was higher than that of malignant lesions (0.77 +/- 0.09). The Nd/Ne of normal tissue which contained muscles in both lesions were higher than 1.4. In conclusion, 201Tl-SPECT was very useful for the differential diagnosis of benign or malignant bone and soft tissue tumors. The ER was important for quantitative assessment, but a delayed image was necessary for visual assessment.

Adolescent↗
PubMed1999

[Pleural malignant mesothelioma complicated by multiple myeloma].

A 79-year-old woman was admitted because of dyspnea. Chest X-ray films and computed tomographic scans disclosed left pleural effusion and diffuse pleural thickening. A diagnosis of multiple myeloma was made on the basis of blood tests and bone marrow aspiration biopsy findings. Multiple myeloma was the suspected cause of the pleural lesions. However, a postmortem diagnosis of malignant mesothelioma of the pleura was made on the basis of histological and immunohistological studies of autopsy specimens.

Aged↗
PubMed1999

Interleukin-1beta induces substance P release from primary afferent neurons through the cyclooxygenase-2 system.

Substance P (SP) is synthesized in the dorsal root ganglion (DRG) and released from primary afferent neurons to convey information regarding noxious stimuli. The effects of the proinflammatory cytokine interleukin-1 (IL-1) beta on the release of SP were investigated using primary cultured rat DRG cells. Recombinant mouse IL-1beta added to the cells at 0.1 ng/ml increased the SP-like immunoreactivity (SPLI) in the culture medium after incubation for 6 h by approximately 50% as compared with that of nontreated DRG cells. The effect of IL-1beta was Ca(2+)-dependent and significantly inhibited by 100 ng/ml IL-1 receptor-specific antagonist (IL-1r antagonist), cyclooxygenase (COX) inhibitors such as 0.1 mM aspirin, 1 microg/ml indomethacin, and 1 microM NS-398 (specific for COX-2), and 1 microM dexamethasone. Furthermore, a 1-h incubation with IL-1beta markedly increased the inducible COX-2 mRNA level, which was inhibited by an IL-1r antagonist and dexamethasone, whereas IL-1beta showed no effect on the level of constitutive COX-1 mRNA. These observations indicated that IL-1beta induced the release of SP from the DRG cells via specific IL-1 receptors, the mechanism of which might involve prostanoid systems produced by COX-2. This could be responsible for the hyperalgesic action with reference to inflammatory pain in the primary afferent neuron to spinal cord pathway.

Animals↗
PubMed1999

Expression of endothelin-1 in rats developing hypobaric hypoxia-induced pulmonary hypertension.

Experimental pulmonary hypertension induced in a hypobaric hypoxic environment (HHE) is characterized by structural remodeling of the heart and pulmonary arteries. Endothelin-1 (ET-1), a 21-amino acid peptide, is a novel and long-lasting vasoconstrictor that increases pulmonary arterial pressure in both in vivo and in vitro experiments. To study the effects of HHE on ET-1 activity in the lungs, 59 male rats were subjected to the equivalent of an altitude of 5500 m for 1 to 4 weeks. In rats exposed to HHE, the mean pulmonary arterial pressure increased significantly from 15.2+/-0.3 (ground level) to 30.6+/-1.5 mm Hg (5500-m level) at 4 weeks, whereas their mean systemic arterial pressure remained normal. The levels of ET-1 mRNA and protein, measured respectively by Northern blot analysis and enzyme immunoassay, increased rapidly in the lungs on exposure to HHE. By in situ hybridization and immunohistochemistry, respectively, ET-1 mRNA and protein were detected in control rats in nonciliated bronchiolar epithelial cells and alveolar epithelial cells, as well as in the endothelial cells of pulmonary arteries, but minimally in the smooth muscle cells of pulmonary arteries. ET-1 mRNA- and protein-reactive smooth muscle cells in pulmonary arteries and ET-1 mRNA-reactive airway epithelial cells were significantly more abundant in rats exposed to HHE than in ground level controls. These results suggest the possibility that in smooth muscle cells in pulmonary arteries and airway epithelial cells, ET-1 may play an autocrine or paracrine role in the remodeling of blood vessels during the development of the pulmonary hypertension that is induced by HHE.

Altitude↗
PubMed1998

Response to head-up tilt testing in patients with situational syncope.

The results of head-up tilt testing were compared between 24 patients with situational syncope and 44 age-matched patients with typical vasovagal syncope. Patients with situational syncope showed poor positive responses, especially in the passive tilt results (8.3% vs. 39%, p = 0.0078).

Adult↗
PubMed1998

Control of endotoxin shock by the dried preparation of low virulent Streptococcus pyogenes OK-432.

Bacterial endotoxin, lipopolysaccharide (LPS), is a causative agent of Gram-negative septic shock. However, if preadministered at a low dose, LPS makes mice resistant to subsequent endotoxin challenge, the phenomenon known as LPS tolerance. Here we demonstrated that the pharmaceutical preparation of Gram-positive Streptococcus pyogenes, OK-432, also induced a state analogous to LPS tolerance if administered 6-48 h prior to LPS challenge. The preadministration of OK-432 increased the lethal dose of LPS threefold in BDF1 mice, and this was accompanied by reduced gene expression of IL-6, IFN-gamma, inducible nitric oxide synthase, and IL-10 in spleen and peritoneal cells. Serum concentrations of IL-6 and IFN-gamma were also suppressed by the preadministration of OK-432. In contrast to the LPS tolerance, the levels of TNF-alpha mRNA were not suppressed in OK-432-administered mice, and their peritoneal cells produced high levels of TNF-alpha and soluble TNF receptor p75 in response to LPS in vitro. Peritoneal cells from OK-432 but not LPS-administered mice were hyporesponsive to IFN-gamma in terms of nitric oxide synthesis, and this hyporesponsiveness to IFN-gamma was abrogated by anti-IL-10 antibodies. Likewise, peritoneal cells from both OK-432- and LPS-administered mice were hyporesponsive to LPS, serum, TNF-alpha, IFN-gamma, and PMA in terms of IL-6 production. Anti-IL-10 antibodies increased IL-6 production eightfold in cells from OK-432-administered mice, but marginally in cells from LPS-administered mice. Even in peritoneal cells from OK-432-administered mice, anti-IL-10 antibodies failed to fully restore IL-6 production. Thus, the hyporesponsive state of peritoneal cells was mediated by both IL-10-dependent and -independent mechanisms. These results demonstrated that OK-432 controlled endotoxin shock by blocking the cytokine cascade from TNF-alpha.

Animals↗
PubMed1998

Early gastric cancer associated with synchronous liver metastasis and portal tumorous embolism: report of a case.

We report herein the first known case of early gastric cancer with synchronous liver metastasis forming a portal tumorous embolism. A 62-year-old man was found to have multiple liver tumors and a portal tumorous embolism by ultrasonography. A gastroscopy subsequently showed Borrmann type III-like gastric cancer in the antrum. His carbohydrate antigen (CA) 19-9 level was elevated to 8280 U/ml, but the alpha-fetoprotein level was within normal limits. A laparotomy revealed multiple liver metastasis and subpyrolic lymph-node enlargement; a distal partial gastrectomy with group 1 lymph-node dissection for the gastric cancer in the antrum, and cannulation of the proper hepatic artery for postoperative chemotherapy were performed. Histopathologically, the cancer was found to be a medullary type well-differentiated adenocarcinoma. Subpyrolic lymph node metastasis was noted, but cancer invasion was localized to only the mucosal and submucosal layers of the stomach. Thus, the patient was diagnosed as having early gastric cancer. Adjuvant chemotherapy given through the cannula suppressed further elevation of CA19-9 levels, and a total of 26 Gy irradiation to a liver tumor, which had caused ascites by pressing on the inferior vena cava, diminished the ascites. The patient was able to remain at home with treatment for 7 months after radiation therapy, but finally died of cancer with jaundice 13 months after his operation. Therefore, although adjuvant chemotherapy and radiation therapy contributed to improving his quality of life, it could not prolong survival.

Adenocarcinoma↗
PubMed1998

Tissue factor is associated with the nonbacterial thrombotic endocarditis induced by a hypobaric hypoxic environment in rats.

High-altitude hypoxia causes a hypercoagulable state. In our previous study on the blood coagulation system in rats, nonbacterial thrombotic endocarditis (NBTE) developed after 4-12 weeks' exposure to the equivalent of 5500 m in altitude. We hypothesized that TF (tissue factor)-producing cells in the cardiac valves might be induced by the hypobaric hypoxic environment (HHE) and then trigger NBTE. A total of 170 male Wistar rats were housed in a chamber at the equivalent of 5500 m altitude for 1-12 weeks. We measured TF activity in the plasma and studied morphological changes in the mitral valves using immunohistochemical and immunoelectrical methods for TF protein and in situ hybridization for TF mRNA. After 4 weeks or more of exposure to HHE, 28 of the 56 surviving rats had developed NBTE. After 4-8 weeks' exposure to HHE, the plasma TF activity level was significantly higher than in control rats. There was a significant correlation between plasma TF activity and the incidence of NBTE. After 1 weeks' exposure to HHE, immunoreactivity for TF protein was detected in foamy macrophages and stromal cells in the cardiac valves. In rats with NBTE, TF protein was present in foamy macrophages and spindle stromal cells and focally present in the extracellular matrix. TF mRNA was detected in some foamy macrophages within the thrombus, TF protein was localized to the rough endoplasmic reticulum and plasma membrane of many macrophages, some fibroblasts, and a few endocardial cells. TF is associated with the pathogenesis of the NBTE induced by exposure to HHE. The accumulation of TF-producing macrophages during exposure to HHE may be responsible for initiating thrombus formation.

Animals↗
PubMed1998

New remote-controlled growing-rod spinal instrumentation possibly applicable for scoliosis in young children.

Progressive scoliosis in young children has been treated with "spinal instrumentation without fusion" to avoid interference with spinal growth. Patients have to undergo a series of operations to have instruments exchanged for maintaining the correction. We have developed a newly designed remote-controlled growing-rod spinal instrumentation system proposed for the treatment of progressive scoliosis in young children. It can be used to stretch and correct the spinal deformities repeatedly and non-surgically, by means of a remote controller, after the first instrumentation operation. The purpose of this study is to describe the possible clinical application of this system for the treatment of progressive scoliosis in young children. To this end, we used the system in five beagle dogs with induced scoliotic deformities. The maximum distraction force of the instrument was 194 N. Correction of 1 cm was performed non-surgically in awake animals 3 weeks after the instrumentation operation, and then correction of 1 cm was carried out again 6, 9, and 12 weeks after the operation. The average initial Cobb's angle of the induced scoliotic deformities was 25 degrees; this was corrected to 20 degrees, 15 degrees, 8 degrees, and 3 degrees, after the distractions at 3, 6, 9, and 12 weeks, respectively, postoperatively. All corrections were performed non-surgically without apparent complications. By repetitive distractions with the use of our new system, we may be able to reduce the number of operations required in young scoliotic children.

Animals↗
PubMed1998

Novel missense mutation resulting in the substitution of tyrosine by cysteine at codon 597 of the type X collagen gene associated with Schmid metaphyseal chondrodysplasia.

Schmid metaphyseal chondrodysplasia (SMCD) is one of the most common forms of the osteochondrodysplasias. Mutations or deletions in the COL10A1 gene that encodes type X collagen have been shown to cause this disorder. Most of the gene mutations and deletions are located in the non-collagenous carboxy (C)-terminal (NC1) domain. We describe a novel missense mutation in a patient with SMCD that leads to the substitution of Tyr at codon 597 by Cys in the NC1 domain. Sequence analysis indicated that the proband was heterozygous for the mutation. Her parents were homozygous for the normal sequence, indicating the de-novo occurrence of this mutation.

Adult↗
PubMed1998

Calcium signaling and protein kinase C for TNF-alpha secretion in a rat mast cell line.

In mast cells, like other nonexcitable cells, receptor activation produces Ca2+-mobilizing second messengers such as inositol 1,4,5-triphosphate or sphingosine-1-phosphate, which induce Ca2+ release from internal stores. The resulting depletion of Ca2+ stores activates Ca2+ channels in plasma membranes designated as Ca2+ release-activated Ca2+ (CRAC) channels. Ionomycin appears to cause activation of CRAC channels by depleting intracellular Ca2+ stores rather than by acting as an ionophore. We compared the effects of azelastine, an anti-allergic drug, on TNF-alpha secretion, on Ca2+ signal, and on degranulation in an antigen- or ionomycin-stimulated rat mast RBL-2H3 cell line. Azelastine inhibited TNF-alpha release at concentrations lower than those needed for the inhibition of degranulation. In antigen-stimulated cells, azelastine also inhibited equipotently TNF-alpha mRNA expression/protein synthesis, TNF-alpha release and Ca2+ influx. In ionomycin-stimulated cells, however, azelastine inhibited TNF-alpha release to a greater extent than TNF-alpha mRNA expression/protein synthesis and Ca2+ influx, indicating that azelastine inhibits the release process more potently than transcription or production of TNF-alpha by interfering with a signal other than Ca2+. Pretreatment with 1 microM azelastine inhibited ionomycin-induced, but not antigen-induced, protein kinase C translocation to the membranes. These results suggest that TNF-alpha transcription/production is mainly regulated by Ca2+ influx, but the release process of TNF-alpha is regulated by additional mechanism(s) possibly involving activation of protein kinase C.

Animals↗
PubMed1998

Differential effects on D2 dopamine receptor and prolactin gene expression by haloperidol and aripiprazole in the rat pituitary.

[3H]Spiperone-binding assay to D2 receptors and quantitative ribonuclease protection assay for both isoforms (D2L and D2S receptor) of the D2 receptor mRNA and the prolactin mRNA were performed on pituitaries from the control rat and from the rat injected orally daily with either haloperidol (2 mg/kg) or aripiprazole (24 mg/kg) for 21 days. Haloperidol treatment increased the [3H]spiperone-binding by 28%, the levels of D2L and D2S receptor mRNA by 41% and 38%, respectively, and the level of prolactin mRNA by 26%. In contrast, the treatment with aripiprazole, a newly developed atypical antipsychotic with reduced side effects, decreased the [3H]spiperone-binding by 24% and the levels of D2L and D2S receptor mRNA by 23% and 23%, respectively, and did not have any effect on the level of prolactin mRNA. The same treatment with sulpiride (100 mg/kg) increased the levels of D2L and D2S receptor mRNA by 59% and 62%, respectively, but treatment with clozapine (25 mg/kg) did not cause any effect. Neither treatment changed the ratio of the level of D2S receptor mRNA to the level of D2L receptor mRNA in the pituitary. These findings indicate that D2 receptor densities in the pituitary are influenced differentially by the treatment with these antipsychotics, which could be induced at least partly by the changes in the levels of mRNA without any effects on the splicing mechanisms and thus affect the plasticity of the prolactin mRNA expression. The inhibitory effects of chronic aripiprazole treatment on D2 receptors in the pituitary might underlie this drug's clinical property of reduced hyperprolactinemia side effect.

Administration, Oral↗
PubMed1998

Angiotensin II type 1 receptor gene polymorphism is associated with increase of left ventricular mass but not with hypertension.

A genetic epidemiologic approach is useful to elucidate the genes responsible for hypertension. Genetic analyses of the components of the renin-angiotensin system have succeeded in showing an association between their polymorphism and hypertension. Recently, two types of angiotensin II receptor were cloned and characterized. To examine the genetic contribution of angiotensin II type 1 receptor (AT1) and type 2 receptor (AT2) genes in human essential hypertension, a case-control study was performed in Japanese subjects. The study comprised 321 subjects with hypertension who satisfied the criteria for essential hypertension, together with 215 age and sex matched controls. The significance of the differences in genotype distribution between hypertensive and normotensive subjects was examined by chi2 analysis. Neither AT1 nor AT2 gene variants were associated with human essential hypertension in the Japanese subjects. However, the AT1 receptor gene polymorphism was associated with left ventricular mass index in normotensive subjects. The study results suggest that gene polymorphisms of both angiotensin II receptors are not directly involved in the increase of genetic risk for hypertension, but that the AT1 receptor gene might contribute genetically to the increase of left ventricular mass.

Aged↗
PubMed1998

No association between alpha-adducin 460 polymorphism and essential hypertension in a Japanese population.

Many unknown genetic factors are involved in the pathogenesis of hypertension. Recently, the reverse genetic approach revealed that some genetic variants, such as angiotensinogen, lipoprotein lipase, and alpha-adducin gene polymorphisms, increase the risk for hypertension. Both in rat and human, the genetic predisposition to hypertension was confirmed only for angiotensinogen and alpha-adducin genes. Adducin is a membrane cytoskeletal protein, which is thought to regulate sodium transport. Abnormalities of membrane sodium transport in the kidney play an important role in hypertension. A recent report by Cusi et al showed that the Trp allele of alpha-adducin polymorphism (Gly 460 Trp) is associated with an increased risk of hypertension in whites, which led us to carry out a case-control study to examine whether the same association is observed in the Japanese population. We recruited 170 hypertensive and 194 normotensive Japanese subjects and compared the genotype distribution of alpha-adducin 460 polymorphism between cases and controls and between whites and Japanese. Trp allele frequency of controls in the Japanese subjects was twice as high as in the whites. However, no association was observed between alpha-adducin polymorphism and hypertension. Furthermore, alpha-adducin 460 polymorphism was not associated with any clinical characteristics. Accordingly, we concluded that alpha-adducin 460 polymorphism is not a major genetic risk for hypertension in Japanese people.

Alleles↗