Biomedical subjects

M Noda

Publications and source records attributed to M Noda.

At least 271 records · Page 15Linked to original sources

PubMed1997

Use of interimplant displacement to measure mandibular distortion during jaw movements in humans.

It has been reported that the mandibular body and the dental arch distort during jaw movements because of contraction of the jaw muscles. In the present study the relative position between two biointegrated implants approx. 10 mm apart was measured during maximum opening and protrusive movements of the jaw using a magnetic sensor system. Mandibular distortion was evaluated as the change in the sensor signal. In all participants the distal implant deviated to the lingual side relative to the mesial implant and the deviation with jaw protrusion was larger than that with opening movement. The linear displacement of the two implants ranged from 8 to 25 microns during maximum opening and from 10 to 37 microns during jaw protrusion. Further investigation is required to establish the mechanism of this mandibular distortion, which may be of relevance to implant therapy.

Adult↗

PubMed1997

Sulfhydryl modification inhibits K+ (M) current with kinetics close to acetylcholine in rodent NG108-15 cells.

The effects of sulfhydryl reagents on M-type voltage-dependent potassium currents (IK(M)) were examined in NG108-15 cells transformed to express ml muscarinic acetylcholine receptors (mAChRs), a NGPM1-27 clone. Focal application of glutathione at millimolar concentrations dissolved in acidic solutions caused a transient inward current in NGPM1-27 cells at holding potentials of -30mV, associated with an inhibition of IK(M). The glutathione-induced response was mimicked by cysteine. These effects were also reproduced by superfusion with micromolar concentrations of HgCl2, AgNO3, N-methylmaleimide and p-chloromercuribenzoic acid (pCMB), agents which target protein thiols. Glutathione, HgCl2, AgNO3 and pCMB inhibited the peak conductance of IK(M) without shifting the half activating voltage (V1/2), which was comparable to the acetylcholine (ACh)-induced response. The voltage dependence of time constants for IK(M) deactivation in sulfhydryl reagent-, ACh- and non-treated cells resembled, but differed from that in Ba(2+)-treated cells. These results reveal that there is an accessible cysteine moiety, but not a disulfide bond, either on the M channel protein itself or on a protein directly involved in agonist-M channel coupling.

Acetylcholine↗

PubMed1997

Helix-loop-helix-type transcription factor (HES-1) is expressed in osteoblastic cells, suppressed by 1,25(OH)2 vitamin D3, and modulates 1,25(OH)2 vitamin D3 enhancement of osteopontin gene expression.

The active form of vitamin D, 1,25(OH)2 vitamin D3 (D3), is a potent modulator of osteoblastic function. In this study, we examined, the expression of a negative-type basic helix-loop-helix transcription factor, HES-1, in osteoblastic cells and the regulation of its expression by D3. We found that HES-1 is expressed as a 1.7 kb mRNA in rat osteoblastic osteosarcoma ROS17/2.8 cells. Treatment with D3 suppressed HES-1 mRNA levels by about 50%. This suppression was observed within 24 h and lasted for at least 48 h. The suppressive effect was dose-dependent starting at 10(-9) mol/L and saturated at 10(-8) mol/L. The vitamin D3 suppression of HES-1 mRNA level was blocked by actinomycin D as well as cycloheximide, suggesting the involvement of transcriptional control, which requires new protein synthesis. Proteins in the crude nuclear extracts prepared from ROS17/2.8 cells bound to the N-box sequence (CACNAG). To examine the function of HES-1 in osteoblasts, HES-1 was overexpressed in ROS17/2.8 cells. Overexpression of HES-1 suppressed the vitamin D-dependent upregulation of osteopontin gene expression in these cells. Vitamin D suppression of HES-1 gene expression was also observed in normal rat calvaria-derived osteoblast-enriched cells. These results indicate that HES-1 is expressed in osteoblastic cells and is involved in vitamin D3 regulation of osteoblastic gene expression.

Animals↗

PubMed1997

Tyrosine kinase dependent expression of TGF-beta induced by stretch in mesangial cells.

Increased glomerular hydraulic pressure has been suggested as a major causative factor in the development of glomerular sclerosis. The elevation of glomerular pressure increases the magnitude of stretch to mesangial cells. The study was, therefore, designed to investigate the effect of mechanical stretch on expression of TGF-beta and extracellular matrix components in cultured rat mesangial cells. The results showed that mechanical stretch stimulated mRNA expression for TGF-beta1 and TGF-beta3 in a time dependent manner, and that mesangial cells secreted substantial amounts of TGF-beta proteins in response to stretch. Stretch was also shown to stimulate mRNA expression for collagen types I and IV, and fibronectin, major components of mesangial extracellular matrix. The stretch-induced mRNA expression for extracellular matrix components was inhibited by neutralizing antibody to TGF-beta. Moreover, stretch-induced mRNA expression of TGF-beta was inhibited by tyrosine kinase inhibitors, genistein or herbimycin A, whereas Ca channel blockers nitrendipine or Gd3+, and inhibitors for protein kinase A or C had no effect. These findings indicate that stretch induced TGF-beta mRNA primarily through tyrosine kinase-dependent mechanisms in cultured rat mesangial cells, and the secreted TGF-beta may play a significant role for the stretch-induced expression of extracellular matrix proteins. Our results suggest that stretch-induced TGF-beta of mesangial cells might be a mediator in the progression of glomerular sclerosis as an autocrine/paracrine factor.

Angiotensin II↗

PubMed1997

Overexpression of adhesion molecule L1 in NG108-15 neuroblastoma X glioma hybrid cells enhances dibutyryl cyclic AMP-induced neurite outgrowth and functional synapse formation with myotubes.

The role of adhesion molecule L1 in synapse formation was examined by transient transfection of L1 cDNA in neuroblastoma x glioma hybrid NG108-15 cells. L1 overexpression was found in approximately 50% of the transfected NG108-15 cell population. Neurite outgrowth induced by 0.25 mM dibutyryl cyclic AMP (cAMP) was much greater in L1-transfected NG108-15 cells than that in nontransfected and mock-transfected cells. The proportion of cells with neurites and the number of neurites per cells were increased in L1-transfected cells after 2 days of dibutyryl cAMP treatment. The proportion of cells with branched neurites and the average length of neurites were higher at day 4. A significantly higher rate of synapse formation with myotubes was apparent in the late phase of coculture (days 4-7) in L1-transfected cells than in control cells. The miniature end-plate potential frequency in myotubes was the same for the three types of NG108-15 cells. These results show that overexpression of L1 in NG108-15 cells facilitates synaptic connections by enhancing branching and elongation of neurites induced with dibutyryl cAMP, rather than by increasing probability of acetylcholine release.

Animals↗

PubMed1997

Possibilities and limitations of endoscopic resection for early gastric cancer.

BACKGROUND AND STUDY AIMS: To date, the accepted criteria for endoscopic resection of early gastric cancer have been: a) elevated-type mucosal cancer less than 2 cm in size, and b) depressed-type mucosal cancer without ulceration less than 1 cm in size. In this study, we attempted to expand these indications. PATIENTS AND METHODS: Sixty patients with early gastric cancer who did not meet the above criteria underwent endoscopic treatment, and were divided into four groups: those with elevated tumours larger than 2 cm with submucosal invasion (group 1 a); those without submucosal invasion (group 1 b); those with depressed tumours larger than 1 cm (group 2); and those with ulcerated tumours (group 3). The patients were treated with endoscopic resection using a two-channel scope, followed by additional laser irradiation or heater-probe coagulation (combination therapy) if residual cells were found. Follow-up was by endoscopy and biopsy for more than two years. RESULTS: Endoscopic treatment was effective in 87% of the patients (52 of 60), half of whom required combination therapy. In submucosal cancers, endoscopic treatment was effective in 76% of patients (13 of 17). However, tumours with deep invasion into the submucosa could not be cured. Mucosal cancers larger than 20 mm could be completely resected in 44% of patients (eight of 18) using endoscopic resection, but all five patients with tumours larger than 30 mm had incomplete resections. CONCLUSIONS: These results indicate that complete resection using endoscopic resection alone is possible in early gastric cancers measuring up to 30 mm in diameter. Tumours larger than 30 mm, and those with deep submucosal invasion, cannot be curatively treated by the current endoscopic modalities.

Adult↗

PubMed1997

Up-regulation of the Nedd2 gene encoding an ICE/Ced-3-like cysteine protease in the gerbil brain after transient global ischemia.

We assessed the expression of several genes encoding pro-apoptotic cysteine proteases similar to interleukin-1 beta converting enzyme (ICE) and nematode Ced-3 in association with delayed neuronal death (DND) after transient forebrain ischemia in Mongolian gerbil. The levels of the two species of Nedd2 mRNA concomitantly increased about two-fold in the whole forebrain at 3-6 h after 10-min ischemia and declined to the basal level by 24 h. In situ hybridization revealed that the Nedd2 gene was up-regulated in some neuronal populations in CA1 and CA3 regions of the hippocampus. In contrast, expression of ICE, CPP32/Yama/Apopain, and TX/ICErelll did not change within 48 h. These observations raise the possibility that up-regulation of Nedd2 in the vulnerable neurons may contribute to the proteolytic processes preceding the manifestation of apoptosis and/or necrosis after ischemic insult.

Animals↗

PubMed1997

Characteristics of IgA anti-HIV antibodies in plasma from patients with HIV infection.

The concentration of total IgA and the specificity and molecular size of IgA anti-human immunodeficiency virus (HIV) type-1 antibodies in plasma obtained from individuals at different stages of HIV infection were analyzed. The concentration of total IgA in the plasma was not decreased even in the late stage of HIV infection, in contrast with those of total IgG and IgM. The IgA anti-HIV antibodies differed to the IgG anti-HIV antibodies in their specificity as determined by Western blotting. The IgA antibodies mainly bind to Env glycoproteins. The IgA anti-HIV antibodies in plasma were detected between IgG and IgM by gel filtration, suggesting the presence of polymeric IgA anti-HIV antibodies. These results indicate that the production of non-specific IgA in plasma is enhanced by unknown mechanisms in every stages of HIV infection, and suggest that IgA anti-HIV antibodies in plasma which are possibly polymeric and have unique specificity may play an important role in HIV infection.

Antibody Specificity↗

PubMed1997

New mild acid-labile protecting groups for the guanidino function of N alpha-fluorenylmethoxycarbonyl-L-arginine in solid-phase peptide synthesis: 10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5-yl, 2-methoxy-10,11-dihydoro-5H-dibenzo[a,d]cyclohepten-5-yl and 5H-dibenzo[a,d]cyclohepten-5-yl groups.

10,11-Dihydro-5H-dibenzo[a,d]cyclohepten-5-yl [5-dibenzosuberyl] and 5H-dibenzo[a,d]-cyclohepten-5-yl [5-dibenzosuberenyl] groups have been found to be useful protecting groups for the guanidino function of arginine in solid-phase peptide synthesis on Fmoc chemistry. The arginine derivatives (4a,b,c) derivatized with these groups were easily deprotected with mild acid (less than 30 min with 25% trifluoroacetic acid). Tryptophan-containing peptide sequences, two hexapeptides (6) and (8), were synthesized in good yield by mild acid treatment (50% trifluoroacetic acid in 1 h) of the peptide resins (5a,c-f and 7a,c,d) assembled via 4a,b,c using benzotriazol-1-yl-oxy-tris-(pyrrolidino)-phosphonium hexafluorophosphate-1-hydroxybenzotriazole mediated coupling.

Acids↗

PubMed1997

Spatially and temporally regulated modification of the receptor-like protein tyrosine phosphatase zeta/beta isoforms with keratan sulphate in the developing chick brain.

Protein tyrosine phosphatase zeta (PTPzeta/RPTPbeta) is a proteoglycan-type receptor-like protein tyrosine phosphatase specifically expressed in the brain. In addition to the transmembrane form (PTPzeta-A), the extracellular splice variant (PTPzeta-S) occurs as a major soluble chondroitin sulphate proteoglycan in the brain. We prepared antibodies which specifically recognize PTPzeta-A and -S, and analysed the carbohydrate structures on the two PTPzeta isoforms in the developing chick brain. Immunoprecipitation experiments using these antibodies revealed that almost all of the keratan sulphate recognized by a monoclonal antibody (5D4) was exclusively bound to PTPzeta-A and PTPzeta-S. Addition of keratan sulphate to these proteoglycans markedly increased from embryonic day (E) 11, in contrast to the addition of Le(x) and HNK-1 carbohydrates, which gradually increased during development in accordance with expression of the core proteins, suggesting that keratan sulphate modification plays some specific roles. Moreover, at the early embryonic stage keratan sulphate was observed only in several restricted regions, especially at boundary regions such as the roof plate of the tectum, the zona limitans intrathalamica in the diencephalon, and the mesencephalon-metencephalon boundary. At the mesencephalon-metencephalon boundary, keratan sulphate modification of PTPzeta isoforms was specifically observed from E3 to E6 on a ring of cells encircling the neural tube and their radially oriented processes, which were identified as radial glial fibres. This expression pattern of keratan sulphate spatiotemporally corresponded well to the formation of the fovea isthmi, a groove separating the mesencephalon from the metencephalon. These results suggest that carbohydrates including keratan sulphate on PTPzeta isoforms play important roles in brain development by modulating the cell-cell and/or cell-substrate interactions mediated by these molecules.

Animals↗

PubMed1997

Increased expression of parathyroid hormone-related peptide gene in blood vessels of spontaneously hypertensive rats.

We have shown recently that mechanical stretch of cultured rat aortic smooth muscle cells induces a marked increase in gene expression of the vasorelaxant parathyroid hormone-related peptide. In the present study, we investigated whether mechanical force affected the in vivo parathyroid hormone-related peptide gene expression in blood vessels. Northern blot analysis revealed that stretch of isolated rat aortic strips increased the expression level of parathyroid hormone-related peptide mRNA. The parathyroid hormone-related peptide transcript level in aorta and mesenteric vessels from 18-week-old spontaneously hypertensive rats (SHR) was 2.5- and 2.2-fold higher, respectively, compared with age-matched Wistar-Kyoto (WKY) controls, whereas the parathyroid hormone-related peptide mRNA level in aorta from normotensive 4-week-old SHR was similar to that of age-matched WKY controls. The aortic parathyroid hormone-related peptide content was higher in 18-week-old SHR than in age-matched WKY controls. Moreover, treatment of mature SHR with an angiotensin II type 1 receptor antagonist or hydralazine caused a concomitant decrease in the parathyroid hormone-related peptide transcript level in aorta with lowering of blood pressure. These results suggest that the in vivo parathyroid hormone-related peptide gene expression in blood vessels is under the control of mechanical force, pointing to a role of parathyroid hormone-related peptide in the regulation of vascular tone.

Animals↗

PubMed1997

Clinical manifestations of Takayasu arteritis in India and Japan--new classification of angiographic findings.

In this retrospective review 102 Indian and 80 Japanese patients with Takayasu arteritis were compared in regard to their clinical manifestations and angiographic findings. Regardless of nationality, most patients were initially affected in their teens or twenties. Japanese patients were female in a larger ratio compared with the ratio in India. Clinically, the two groups exhibited several different features. More Japanese patients were found to be pulseless (P < 0.01) whereas many Indian patients were hypertensive (P < 0.01). Inflammatory conditions in Japanese patients were more severe (P < 0.01) and tended to be more prolonged than those in the Indians. More Japanese patients suffered from aortic regurgitation (P < 0.01), but Indians suffered from hypertension (P < 0.01). Angiographic findings revealed that the aortic arch and its branches were mainly involved in Japanese patients (type I, IIa) whereas the abdominal aorta and its branches were mainly involved in Indian patients (type IV). However, the diffusely involved type (type V) was the one most commonly found in both countries. From the analyses of vascular lesions in both Indian and Japanese patients, 510 and 396, respectively, different progressions of vasculitis are speculated. In Japanese patients, vasculitis generally occurs in the ascending aorta, the aortic arch, and/or its branches and extends into the thoracic and abdominal aorta, subsequently forming various complicated lesions with prolonged inflammatory activity. On the other hand, in Indian patients, vasculitis generally occurs in the abdominal aorta involving renal arteries, subsequently extending into the thoracic aorta within one or two decades, simple vascular lesions being formed. Data analysis suggests that this morbid condition progresses differently in India and Japan, in spite of some common etiologic factor(s).

Adult↗

PubMed1997

Expression of Indian hedgehog in osteoblasts and its posttranscriptional regulation by transforming growth factor-beta.

Indian hedgehog (Ihh) was recently reported to be expressed in chondrocytes and to regulate chondrocyte differentiation. This report examined the expression of Ihh in osteoblastic cells and its regulation by calcitropic cytokines. We found that Ihh messenger RNA (mRNA) was expressed as a single 2.5-kilobase band at a modest level in rat osteoblastic osteosarcoma ROS17/2.8 cells. In sharp contrast to the previous observation of dpp regulation of hedgehog expression in Drosophila embryos, bone morphogenetic protein-2 did not affect Ihh expression in these cells. On the other hand, treatment with 2 ng/ml transforming growth factor-beta1 (TGFbeta1) increased the steady state level of Ihh mRNA 2- to 4-fold. Western blot analysis of the cell lysates using antisera also showed enhancement of the Ihh protein level by TGFbeta1 treatment. The effect of TGFbeta1 on Ihh mRNA abundance started within 3 h, peaked at 24 h and lasted at least 48 h after the initiation of the treatment. The effect of TGFbeta1 on the increase in Ihh mRNA was dose dependent, starting at 0.2 ng/ml and saturating at 2 ng/ml. Neither actinomycin D nor cycloheximide blocked this effect. Experiments using 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole showed an enhancement of Ihh mRNA stability by TGFbeta1, indicating the presence of posttranscriptional regulation. We then examined the effects of TGFbeta1 on Ihh mRNA in osteoblast-enriched cells isolated from neonatal rat calvariae. TGFbeta1 also enhanced Ihh mRNA expression in these cells. Our data indicate for the first time that Ihh is one of the members of the cytokines produced by osteoblastic cells and that the expression of Ihh is regulated posttranscriptionally by TGFbeta.

Animals↗

PubMed1997

Perturbation of BMP signaling in somitogenesis resulted in vertebral and rib malformations in the axial skeletal formation.

Axial skeletons such as vertebrae, ribs, and scapulae develop from the embryonic somitic mesoderm through interactions with neural tube/notochord and skin ectoderm. Bone morphogenetic proteins (BMPs) seem to play important roles in these tissue interactions; however, the relationship between BMP signaling and the early development of axial skeletons is poorly understood. In this report, we investigated possible roles of BMP signaling in axial skeletal formation. First, we describe the expression patterns of BMP4 and type I receptors for BMP during somitogenesis in chick embryos based on whole mount in situ hybridization. Next, the effects of BMP on axial skeletal morphogenesis were investigated by implantation of BMP proteins into the dorsal mesoderm at the time of somitogenesis. Transcripts for both BMP4 ligand and its receptors are expressed in the dorsal ectoderm and mesoderm. Implantation of BMP4 and BMP2 into the dorsal regions of embryos result in subsequent anomalies of vertebrae, ribs, and scapulae. The effects of BMP implantation on the skeleton are shown to be dependent upon the somitic stage. Vertebral anomalies are restricted to the dorsolateral elements of the vertebrae and specifically observed after BMP implantation into embryonic day 2 (E2) embryos, but not E3 embryos. These results indicate that implantation of BMP into the dorsal part of embryos where endogenous BMP ligand and BMP receptors are expressed perturbs BMP signaling and causes axial skeletal malformations. The findings presented here suggest that BMP signaling may be involved in the early developmental process of the axial skeleton.

Amino Acid Sequence↗

PubMed1997

Cyclooxygenase metabolites possibly produced by endothelial cells mediate the lung injury caused by mechanically stimulated leukocytes.

To determine whether mechanically stimulated leukocytes increase pulmonary vascular permeability and resistance and, if so, whether cyclooxygenase metabolites mediate the increase, we assessed the effects of stimulated and unstimulated leukocytes, and of a cyclooxygenase inhibitor on pulmonary vascular permeability and resistance in isolated perfused lungs from Sprague-Dawley rats. Leukocytes were stimulated by gentle agitation in a glass container for 10 seconds. After baseline measurements were made, stimulated or unstimulated leukocytes were added to the perfusate. The effects of the cyclooxygenase inhibitor, meclofenamate, on the pulmonary vascular filtration coefficient and pulmonary vascular resistance were measured. In the rats that received stimulated leukocytes, the pulmonary vascular filtration coefficient and the vascular resistance were about 2.5 times and 3.3 times higher, respectively, than those in the rats that received unstimulated leukocytes. These increases were completely and partly blocked by meclofenamate. Histological examination indicated that meclofenamate did not prevent the adhesion of leukocytes to the pulmonary vascular endothelium. These findings suggest that mechanically stimulated leukocytes increase pulmonary vascular permeability and that cyclooxygenase metabolites produced by endothelial cells may injure the cells.

Animals↗

PubMed1997

Augmentation of insulin release by glucose in the absence of extracellular Ca2+: new insights into stimulus-secretion coupling.

Glucose stimulates insulin secretion in the pancreatic beta-cell by means of a synergistic interaction between at least two signaling pathways. One, the K(ATP) channel-dependent pathway, increases the entry of Ca2+ through voltage-gated channels by closure of the K(ATP) channels and depolarization of the beta-cell membrane. The resulting increase in [Ca2+]i stimulates insulin exocytosis. The other, a K(ATP) channel-independent pathway, requires that [Ca2+]i be elevated and augments the Ca2+-stimulated release. These mechanisms are in accord with the belief that glucose-stimulated insulin secretion has an essential requirement for extracellular Ca2+ and increased [Ca2+]i. However, when protein kinases A and C are activated simultaneously, a large effect of glucose to augment insulin release can be seen in the absence of extracellular Ca2+, under conditions in which [Ca2+]i is not increased, and even when [Ca2+]i is decreased to low levels by intracellular chelation with BAPTA. In the presence or absence of Ca2+, there are similarities in the characteristics of augmentation of insulin release that suggest that only one augmentation mechanism may be involved. These similarities include time course, glucose dose-responses, augmentation by nutrients other than glucose such as alpha-ketoisocaproate (alpha-KIC), and augmentation by the fatty acids palmitate and myristate. However, augmentation in the presence and absence of Ca2+ is distinctly different in GTP dependency. Therefore, exocytosis under these two conditions appears to be triggered differently-one by Ca2+ and the other by GTP or a GTP-dependent mechanism. The augmentation pathways are likely responsible for time-dependent potentiation of secretion and for the second phase of glucose-stimulated insulin release.

Animals↗

PubMed1997

Expression of fibroblast growth factor 2 mRNA in early and advanced gastric cancer.

We examined the expression of FGF-2 mRNA in 16 early and 14 advanced gastric cancer by in situ hybridisation to elucidate its role in cancer progression. Anti-sense RNA probes were synthesized by transcribing the subcloned vector with T7 RNA polymerase in the presence of digoxigenin-labeled UTP. FGF-2 mRNA was located mainly in the cytoplasm around the nuclei of endothelial cells, fibroblasts and carcinoma cells. The expression was more frequently in the diffuse type carcinomas (4/7, 57%) than in the intestinal type tumours (5/23, 22%). The survival rates of advanced gastric cancers with FGF-2 mRNA expression were significantly lower than those without FGF-2 mRNA expression (p < 0.01). No significant correlation was seen with other clinicopathological factors. These results suggest that FGF-2 may play an important role for the growth of diffuse type gastric cancers, particularly at their advanced stage.

Aged↗

PubMed1997

Hypoglycemic activity of to-kai-san (Chinese medicines) in normal and KK-Ay mice.

The hypoglycemic effect of To-Kai-San (TS) was studied in normal mice, streptozotocin-induced diabetic mice, one of the animal models of insulin-dependent diabetes mellitus (IDDM) with hypoinsulinemia, and KK-Ay mice, one of the animal models of non-insulin-dependent diabetes mellitus (NIDDM) with hyperinsulinemia. TS (1,500 mg/kg) reduced the blood glucose of the KK-Ay mice from 441 +/- 36 to 285 +/- 52 mg/100 ml 7 h after a single oral administration (p < 0.001). However, no changes in blood glucose were observed in the normal and STZ-induced diabetic mice. TS also decreased the blood glucose 20 days after repeated administration to normal and KK-Ay mice. In addition, TS-treated KK-Ay mice showed decreased plasma insulin levels after both single and repeated administration. From these findings, it is believed that TS may require the presence of insulin to display its activity.

Administration, Oral↗