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Biomedical subjects

Akira Yamaguchi

Publications and source records attributed to Akira Yamaguchi.

At least 37 records · Page 2Linked to original sources
PubMed2005

Morphological analysis of the relation between immunoglobulin A production in the small intestine and the enteric nervous system.

To investigate the relation between the enteric nervous system and immunocytes, fecal immunoglobulin (Ig) A and the distribution of IgA-positive cells close to nerve fibers in the lamina propria around the crypts of the small intestine were examined after intraperitoneal injection of lipopolysaccharides (LPS). In mice, IgA in the feces 1 h (LPS1) and 6 h (LPS6) after LPS injection increased compared to that in the control group. In the ileum lamina propria of the LPS1 group, the number of IgA-positive cells close to the epithelial basement membrane was increased. In the LPS6 group, on the other hand, there was a significant increase in the number of IgA-positive cells close to both the basement membrane and the nerve fibers. Our data suggest that LPS induced an increase in the number of IgA-positive cells migrating to the nerve fibers, and that migration to the nerve fibers is as important as migration to the basement membrane for IgA production.

Animals↗
PubMed2005

Expression profile of Xenopus banded hedgehog, a homolog of mouse Indian hedgehog, is related to the late development of endochondral ossification in Xenopus laevis.

Late development of endochondral ossification occurs at the boundary between the growth cartilage and bone marrow during the formation of long bones in Xenopus laevis. Since the Indian hedgehog (Ihh) is involved in endochondral ossification in mouse, we investigated the expression of Xenopus banded hedgehog (X-bhh), which is a homolog of mouse Ihh. RT-PCR analysis demonstrated that the X-bhh mRNA was detected from an early stage of limb formation to formation of femurs in mature frogs, and it was associated with the expression of Xenopus-ptc1 (X-ptc1), Xenopus-gli1 (X-gli1), Xenopus-type II collagen (X-col II), Xenopus-runx2 (X-runx2), and Xenopus-osteocalcin (X-ocn) mRNAs. In situ hybridization revealed that chondrogenic cells observed at early limb development expressed X-bhh and X-gli1. At later stages of limb development, chondrocytes, located slightly away from the boundary between the cartilage and bone marrow, expressed the X-bhh, X-ptc1, and X-gli1 mRNAs; however, the mesenchymal cells at the boundary failed to express these mRNAs. The X-bhh, X-ptc1, and X-gli1 mRNAs as well as those of X-runx2 and X-ocn were expressed by the mesenchymal cells in the periosteal region at the tip of the cortical bone, indicating an intimate relationship between X-bhh expression and bone formation in this region. Considered collectively, the present study suggests that X-bhh evolutionally acquired the function to induce osteogenesis; however, the expression profile of X-bhh in epiphysis is closely related to the late development of endochondral ossification in X. laevis.

Animals↗
PubMed2005

Possible one-dimensional 3He quantum fluid formed in nanopores.

Heat capacity measurements have been made down to 5 mK for 3He fluid films adsorbed in one-dimensional (1D) nanometer-scale pores, 28 A in diameter, preplated with 4He of 1.47 atomic layers. At low 3He density, the heat capacity shows a density-dependent, Schottky-like peak near 150 mK asymptoting to the value corresponding to a 2D Boltzmann gas at high temperatures. The peak behavior is attributed to the crossover from a 2D gas to a 1D state at low temperatures. The degenerate state of the 1D 3He fluid is indicated by a predominantly linear temperature dependence below about 30 mK.

Journal Article↗
PubMed2005

Critical regulation of bone morphogenetic protein-induced osteoblastic differentiation by Delta1/Jagged1-activated Notch1 signaling.

Functional involvement of the Notch pathway in osteoblastic differentiation has been previously investigated using the truncated intracellular domain, which mimics Notch signaling by interacting with the DNA-binding protein CBF-1. However, it is unclear whether Notch ligands Delta1 and Jagged1 also induce an identical cellular response in osteoblastic differentiation. We have shown that both Delta1 and Jagged1 were expressed concomitantly with Notch1 in maturating osteoblastic cells during bone regeneration and that overexpressed and immobilized recombinant Delta1 and Jagged1 alone did not alter the differentiated state of MC3T3-E1 and C2C12 cells. However, they augmented bone morphogenetic protein-2 (BMP2)-induced alkaline phosphatase activity and the expression of several differentiation markers, except for osteocalcin, and ultimately enhanced calcified nodule and in vivo ectopic bone formation of MC3T3-E1. In addition, both ligands transmitted signal through the CBF-1-dependent pathway and stimulated the expression of HES-1, a direct target of Notch pathway. To test the necessity of Notch signaling in BMP2-induced differentiation, Notch signaling was inhibited by the dominant negative extracellular domain of Notch1, specific inhibitor, or small interference RNA. These treatments decreased alkaline phosphatase activity as well as the expression of other differentiation markers and inhibited the promoter activity of Id-1, a target gene of the BMP pathway. These results indicate the functional redundancy between Delta1 and Jagged1 in osteoblastic differentiation whereby Delta1/Jagged1-activated Notch1 enhances BMP2-induced differentiation through the identical signaling pathway. Furthermore, our data also suggest that functional Notch signaling is essential not only for BMP2-induced osteoblast differentiation but also for BMP signaling itself.

Alkaline Phosphatase↗
PubMed2005

A dinuclear MnIII-CuII single-molecule magnet.

The reaction of 1/3 equivalent of CuCl2.2H2O with MnCl2.4H2O and 5-bromo-2-salicylideneamino-1-propanol (H(2)5-Br-sap) in methanol gave dark brown crystals of [MnIIICuIICl(5-Br-sap)2(MeOH)] (1). Complex 1 has an alkoxo-bridged dinuclear core of MnIII and CuII ions, which have elongated octahedral and square-planar coordination geometries, respectively. In dc magnetic susceptibility measurements, chi(m)T values increased as the temperature was lowered, followed by a sudden decrease below 20 K. This behavior is indicative of the occurrence of intramolecular ferromagnetic interactions, and fitting gave an S=5/2 spin ground state with an exchange coupling constant J(MnCu) of +78 cm(-1). Magnetization data collected as a function of temperature and applied magnetic field were analyzed by using a spin Hamiltonian with isotropic Zeeman and axial zero-field splitting (ZFS) terms, and a negative D(5/2) value (-1.86 cm(-1)) was obtained. A high-field EPR (HFEPR) spectrum (342.0 GHz) at 4.2 K was composed of four peaks, and two additional peaks at higher magnetic field appeared as the temperature was increased. The temperature dependences in the HFEPR spectra are indicative of a negative D(5/2) value, and fitting of the data gave D(5/2)=-1.81 cm(-1). In the ac magnetic susceptibility measurements, frequency dependent in-phase (chi(m)') and out-of-phase (chi(m)'') signals with peak maxima at 0.7-1.5 K were observed and small peaks below 0.7 K appeared. The ac susceptibility data supports that 1 is a single-molecule magnet (SMM). Arrhenius plots for the chi(m)'' peaks from 0.7-1.5 K gave the re-orientation energy barrier (DeltaE) of 10.5 K with a pre-exponential factor of 8.2x10(-8) s.

Copper↗
PubMed2005

Distinct roles of EGF repeats for the Notch signaling system.

Notch is a single-pass transmembrane receptor that mediates cell fate choice in various species and developmental contexts. The Notch signal is transduced by its intracellular domain, which acts as a transcriptional activator, and is released from the plasma membrane by proteolytic cleavages. This process is initiated by intercellular association of the epidermal growth factor (EGF) repeats between Notch and the DSL (Delta, Serrate, Lag-2) ligands but the detailed mechanism is yet to be clarified. Here we demonstrate that Notch1 can form homodimers, which is achieved by its EGF motifs. The Notch1 dimer formation increased in response to ligand presentation and HES1 promoter was stimulated, implying that receptor homodimerization is an important initial step in Notch signal transduction. EGF motifs also serve as a protection against proteases, including TNF-alpha converting enzyme, which prevents Notch1 from ligand-independent activation. Multiple functions of the Notch EGF motifs, such as the prevention of constitutive activation, reciprocal interaction with the ligands and lateral interaction for homodimerization, appear to constitute crucial elements of the Notch signaling system.

Amino Acid Motifs↗
PubMed2005

Laryngeal phonation after tracheoesophageal diversion.

When tracheoesophageal diversion is performed, laryngeal phonation is usually impossible. We, however, experienced the case of a 65 year-old female patient, who was able to do so. Fluoroscopic and videoendoscopic examinations elucidated her mechanism of phonation. This is the first detailed report describing the mechanism of laryngeal phonation after the procedure. Our case is compared with a few other similar cases found in available literature.

Aged↗
PubMed2005

A simple method to dissociate sensory-attentional and motor-intentional biases in unilateral visual neglect.

A variant of a line bisection test was devised. Patients with unilateral visual neglect and control subjects were asked to perform the test, which consisted of two subtasks: a verbal and a manual task. The verbal task was newly designed and did not require manual responses from the subjects. The manual task was similar to conventional line bisection tasks. This paper reports and discusses the results obtained from each task and their correlations. This technique is compatible with bedside examinations, does not require a complex apparatus, and provides useful data for the assessment of unilateral visual neglect.

Aged↗
PubMed2005

Abnormal expression of Rb pathway-related proteins in salivary gland acinic cell carcinoma.

Salivary gland acinic cell carcinoma (ACC) is a relatively rare neoplasm, and limited information is available regarding its molecular pathogenesis. Because the deregulation of Rb pathway is common to most human tumors, we immunohistochemically investigated the expression of Rb pathway-related proteins, including Rb, Rb proteins phosphorylated at serine 780 and 795 (pRb-S780 and pRb-S795, respectively), cyclin D1, and p16INK4a in 18 cases of ACC. The expression of topoisomerase II-alpha and Ki-67 was also examined to evaluate cell proliferation. All the ACCs exhibited substantial numbers of positive cells against Rb antibody that recognizes both unphosphorylated and phosphorylated Rb proteins. The numbers of positive cells for pRb-S795 and cyclin D1 significantly increased in ACCs as compared with normal salivary glands. Double immunofluorescent staining demonstrated that pRb-S795 was colocalized with cyclin D1 in most tumor cells. However, neither significant change of the expression of Rb protein phosphorylated at serine 780 nor its colocalization with cyclin D1 was observed. The loss of p16INK4a is infrequent, but its expression was correlated with phosphorylated Rb proteins. Our results suggest that serine 795 but not serine 780 is the preferred phosphorylation site induced by cyclin D1. This phosphorylation appeared to be critical for inactivation of Rb-mediated growth suppression and may play an important role in the pathogenesis of ACC.

Adolescent↗
PubMed2005

Combined expression of p53, cyclin D1 and epidermal growth factor receptor improves estimation of prognosis in curatively resected oral cancer.

p53, cyclin D1 and epidermal growth factor receptor (EGFR) are molecular markers that regulate the cell cycle or cell growth and play important roles in tumor development and progression. In this study, we examined the impact of immunohistochemical expression of these markers on tumor progression in 140 oral cancers. p53, cyclin D1 and EGFR were expressed in 64 cases (46%), 54 cases (39%) and 54 cases (39%), respectively, but there was no inter-relationship between any two of these markers. In the association of these markers with clinicopathological features, EGFR expression alone was significantly associated with poor differentiation (P=0.0008) and invasive growth pattern (P=0.0003). Any of these markers, including EGFR, had no significant impact on survival. Coexpression of all these markers, however, was significantly associated with invasive growth pattern (P=0.0149) and shortened survival (P=0.0181), and was a significant and independent unfavorable prognostic factor (P=0.0002), along with tumor size (P=0.0040), nodal metastasis (P=0.0137) and growth pattern (P=0.0017) in a multivariate analysis. Simultaneous coexpression of these markers in oral cancers might prove to be a useful indicator for identification of low- or high-risk patients.

Adult↗
PubMed2005

Frequent promoter hypermethylation of RASSF1A and p16INK4a and infrequent allelic loss other than 9p21 in betel-associated oral carcinoma in a Vietnamese non-smoking/non-drinking female population.

BACKGROUND: Betel-chewing, a risk factor for oral carcinoma, is a common habit of elderly Vietnamese females, but concomitant habits of tobacco and alcohol are uncommon. METHODS: In the present study, 36 paraffin-embedded betel-associated oral carcinoma samples including 27 squamous cell carcinoma (SCC) and nine verrucous carcinomas (VC) were analyzed for the hypermethylation of tumor suppressor genes (TSGs) and loss of heterozygosity (LOH) of important TSG loci. Methylation-specific polymerase chain reaction (MSP) was used to identify promoter hypermethylation of p16INK4a and RASSF1A. For LOH analysis, 39 microsatellite markers at 12 chromosomal arms were examined by p olymerase chain reaction (PCR)-based microsatellite assay. RESULTS: Hypermethylation of p16IKN4a was detected in 63% of SCC and 67% of VC. In addition, LOH at 9p21 (locus for p16INK4a) was 58% for SCC and 22% for VC, and hypermethylation of RASSF1A was 93% for SCC and 100% for VC. LOH at 3p21.3-3p22.1 (where RASSF1A is located) was detected in only 12% of SCC and 0% of VC. LOH of other chromosomal arms were infrequent. CONCLUSION: As LOH for chromosomes other than 9p was uncommon, epigenetic silencing of RASSF1A and p16INK4a gene expression by promoter hypermethylation may play a critical role in betel-associated oral carcinogenesis.

Aged↗
PubMed2005

A CCAAT/enhancer binding protein beta isoform, liver-enriched inhibitory protein, regulates commitment of osteoblasts and adipocytes.

Although both osteoblasts and adipocytes have a common origin, i.e., mesenchymal cells, the molecular mechanisms that define the direction of two different lineages are presently unknown. In this study, we investigated the role of a transcription factor, CCAAT/enhancer binding protein beta (C/EBPbeta), and its isoform in the regulation of balance between osteoblast and adipocyte differentiation. We found that C/EBPbeta, which is induced along with osteoblast differentiation, promotes the differentiation of mesenchymal cells into an osteoblast lineage in cooperation with Runx2, an essential transcription factor for osteogenesis. Surprisingly, an isoform of C/EBPbeta, liver-enriched inhibitory protein (LIP), which lacks the transcriptional activation domain, stimulates transcriptional activity and the osteogenic action of Runx2, although LIP inhibits adipogenesis in a dominant-negative fashion. Furthermore, LIP physically associates with Runx2 and binds to the C/EBP binding element present in the osteocalcin gene promoter. These data indicate that LIP functions as a coactivator for Runx2 and preferentially promotes the osteoblast differentiation of mesenchymal cells. Thus, identification of a novel role of the C/EBPbeta isoform provides insight into the molecular basis of the regulation of osteoblast and adipocyte commitment.

Adipocytes↗
PubMed2004

Role of a new member of IGFBP superfamily, IGFBP-rP10, in proliferation and differentiation of osteoblastic cells.

Bone regeneration is critically regulated by various molecules. To identify the new genes involved in bone regeneration, we performed microarray-based gene expression analysis using a mouse bone regeneration model. We identified a new member of the IGFBP superfamily, designated IGFBP-rP10, whose expression is up-regulated at the early phase of bone regeneration. IGFBP-rP10 consists of an IGFBP homologous domain followed by a Kazal-type protein inhibitor domain and an immunoglobulin G-like domain. A real-time-based RT-PCR analysis demonstrated that various tissues including bone expressed IGFBP-rP10 mRNA in various degrees, and confirmed an up-regulation at the early phase of bone regeneration. In situ hybridization revealed that osteoblastic cells expressed IGFPB-rP10 mRNA during bone regeneration. Bone morphogenetic protein-2 increased the expression level of IGFBP-rP10 mRNA in various cells including C3H10T1/2, MC3T3-E1, C2C12, and primary murine osteoblastic cells. The addition of recombinant mouse IGFBP-rP10 promoted the proliferation of these cells but failed to stimulate alkaline phosphatase activity. These results suggest that IGFBP-rP10 is involved in the proliferation of osteoblasts during bone formation and bone regeneration.

Amino Acid Sequence↗
PubMed2004

Runx-2 is not essential for the vitamin D-regulated expression of RANKL and osteoprotegerin in osteoblastic cells.

The differentiation and activity of osteoclasts are positively and negatively controlled by receptor activator of nuclear factor-kappaB ligand (RANKL), which is expressed on the surface of osteoblasts and stromal cells, and its decoy receptor osteoprotegerin (OPG), which is secreted by osteoblasts and stromal cells, respectively. The expression of the genes for RANKL and OPG is regulated by 1alpha,25-dihydroxyvitamin D(3) [1alpha,25(OH)(2)D(3)]. Runt-related gene-2 (Runx-2) is essential for osteoblast differentiation and there are several reports that Runx-2 is involved in osteoclast formation. Therefore, to clarify the role of Runx-2 in osteoclastogenesis, we designed a series of experiments using C2 cells and C6 cells, which are derived from calvariae of runx2-deficient mice. Treatment of C2 cells and C6 cells with 1alpha,25(OH)(2)D(3) for 2-4 days increased and decreased the levels of expression of the mRNAs for RANKL and OPG, respectively, and the effects were dose-dependent. However, by day 8, the level of RANKL mRNA had fallen and that of OPG mRNA had risen. Furthermore, C6 cells induced the differentiation of mouse spleen cells into tartrate-resistant acid phosphatase-positive (TRAP-positive) multinucleated cells (osteoclast-like cells) in the presence of 10(-7)M 1alpha,25(OH)(2)D(3). Such formation of osteoclast-like cells was inhibited by exogenous OPG in a dose-dependent manner. Thus, our findings indicate that Runx-2 is not essential for the expression of RANKL and OPG, and the formation of osteoclast-like cells.

3T3 Cells↗
PubMed2004

Growth of a third ferromagnetic solid 3He layer on graphite.

We have measured the nuclear susceptibility of 3He in Grafoil filled with pure liquid 3He over the pressure region between 0.6 and 31.38 bars and at temperatures down to 0.5 mK with a cw NMR method. The nuclear magnetization corresponding to the adsorbed 3He layers on the Grafoil surface shows a strong ferromagnetic tendency with a periodic behavior as a function of liquid pressure. This observation is attributable to the growth of third and fourth solid 3He layers with the liquid pressure increase. The pressure dependence of the Weiss temperature indicates the third layer is completed at 19 bars and the fourth probably at 28 bars. The number of localized spins estimated from the solid magnetization is almost doubled from 0 to 28 bars, being consistent with this scenario.

Journal Article↗
PubMed2004

Reciprocal roles of MSX2 in regulation of osteoblast and adipocyte differentiation.

Mice deficient in the Msx2 gene manifest defects in skull ossification and a marked reduction in bone formation associated with decreases in osteoblast numbers, thus suggesting that Msx2 is involved in bone formation. However, the precise role of Msx2 during osteoblast differentiation is not fully understood. In the present study, we investigated the role of Msx2 in the regulation of osteoblast differentiation in the multipotent mesenchymal cell lines C3H10T1/2 and C2C12 and in murine primary osteoblasts. Introduction of Msx2 induced alkaline phosphatase activity in C3H10T1/2 and C2C12 cells and promoted the calcification of murine primary osteoblasts. This effect of Msx2 was also observed in mesenchymal cells isolated from Runx2-deficient mice. Interestingly the expression of Msx2 was induced by bone morphogenetic protein 2 treatment in Runx2-deficient mesenchymal cells. In contrast, Msx2 diminished peroxisome proliferator-activated receptor gamma (PPARgamma) expression and adipogenesis of the preadipocytic cell line 3T3-F442A. Moreover Msx2 inhibited the transcriptional activity of PPARgamma, CCAAT/enhancer-binding protein beta (C/EBPbeta), and C/EBPdelta and blocked adipocyte differentiation of mesenchymal cells induced by overexpression of PPARgamma, C/EBPalpha, C/EBPbeta, or C/EBPdelta. These data indicate that Msx2 promotes osteoblast differentiation independently of Runx2 and negatively regulates adipocyte differentiation through inhibition of PPARgamma and the C/EBP family.

Adipocytes↗