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Biomedical subjects

Toshihiko Ogino

Publications and source records attributed to Toshihiko Ogino.

At least 19 recordsLinked to original sources
PubMed2007

Upregulation of matrix metalloproteinase (MMP)-1 and its activator MMP-3 of human osteoblast by uniaxial cyclic stimulation.

Proper mechanical loading is essential for bone remodeling and maintenance of human skeletal system. Matrix metalloproteinases (MMPs) are secreted by mesenchymal stromal lining cells and osteoblasts to prepare the initiation sites for osteoclastic bone resorption at the beginning of the remodeling cycle. However, only a few studies have addressed the effect of mechanical stress on MMPs and their endogenous tissue inhibitors of matrix metalloproteinases (TIMPs) in osteoblasts. In this study, the response of human osteoblasts to uniaxial cyclic stretching was investigated to clarify this more in detail. Stretching affected the orientation of the osteoblasts, and quantitative reverse transcription-polymerase chain reaction revealed coordinated upregulation of MMP-1 and its activator MMP-3 mRNA by cyclic 5% stretching at 3 h (p < 0.01). Upregulation of cyclooxygenase-2 mRNA was also found in response to cyclic 1 and 5% stretchings at 1, 3, and 6 h (p < 0.01). No changes were found in MMP-2, TIMP-1, and -2. The mRNA expression of MMP-9 was low and MMP-13 was not detected. This study suggests that MMP-1 and -3, enhanced by uniaxial cyclic mechanical stimulation of osteoblasts, are candidate key enzymes in the processing of collagen on bone surface, which might be necessary to allow osteoclastic recruitment leading to bone resorption. The strain might also play a role in cleaning of demineralized bone surface during the reversal phase, before bone formation starts.

Base Sequence↗
PubMed2006

Gene expression and localization of diacylglycerol kinase isozymes in the rat spinal cord and dorsal root ganglia.

The dorsal root ganglion (DRG) and dorsal horn of the spinal cord are areas through which primary afferent information passes enroute to the brain. Previous studies have reported that, during normal neuronal activity, the regional distribution of a second messenger, diacylglycerol (DG), which is derived from phosphoinositide turnover, is diverse in these areas. However, the way that DG is regulated in these organs remains unknown. The present study was performed to investigate mRNA expression and protein localization of DG kinase (DGK) isozymes, which play a central role in DG metabolism. Gene expression for DGK isozymes was detected with variable regional distributions and intensities in the spinal cord. Among the isozymes, most intense signals were found for DGKzeta and DGKiota in the DRG. By immunohistochemical analysis, DGKzeta immunoreactivity was detected heterogeneously in the nucleus and cytoplasm of small DRG neurons with variable levels of distribution, whereas it was detected exclusively in the cytoplasm of large neurons. On the other hand, DGKiota immunoreactivity was distributed solely in the cytoplasm of most of the DRG neurons. Double-immunofluorescent imaging of these isozymes showed that they coexisted in a large population of DRG neurons at distinct subcellular sites, i.e., DGKzeta in the nucleus and DGKiota in the cytoplasm. Thus, DGK isozymes may have different functional roles at distinct subcellular sites. Furthermore, the heterogeneous subcellular localization of DGKzeta between the nucleus and cytoplasm implies the possible translocation of this isozyme in small DRG neurons under various conditions.

Animals↗
PubMed2006

Incidence and development of trigger thumb in children.

PURPOSE: Whether trigger thumb is congenital or acquired remains controversial. The purpose of this study was to identify whether trigger thumb is present at birth and to clarify whether trigger thumb represents a developmental condition. METHODS: We examined 1,116 babies born at Yamagata Prefectural Nihonkai Hospital within 14 days after birth. All patients were examined by the author (N.K.), a hand surgeon. Patients were followed up to determine whether trigger thumb would present later even though it was not present at birth. We informed parents about the development of trigger thumb by providing informational sheets for neonatal screenings after hospital discharge. They were asked to check their child for a year or more to see if any flexion deformity of the interphalangeal joint of the thumb occurred. After discharge from the hospital, the family was responsible for noticing trigger thumb in their infant and seeking medical treatment. RESULTS: Trigger thumb was not identified in any patient at birth. Responses were obtained from 601 families. Trigger thumb manifested in 2 thumbs of 2 children in the screening group at 8 and 11 months after birth; however, 3 additional children developed trigger thumb at 15, 21, and 30 months of age. CONCLUSIONS: The incidence of acquired trigger thumb in children 1 year of age was 3.3 per 1,000 live births. It is unlikely that this study identified all cases of trigger thumb in patients older than 1 year in the primary screening group. The results of this follow-up study, however, suggest that trigger thumb is not present at birth but develops with postnatal growth.

Child, Preschool↗
PubMed2006

Using sonography for the early detection of elbow injuries among young baseball players.

OBJECTIVE: The aim of this study was to determine the usefulness of sonography for detecting elbow injuries among young baseball players. SUBJECTS AND METHODS: One hundred fifty-three volunteers ranging in age from 9 to 12 years and belonging to youth baseball teams participated. Sonography of the elbow was performed in the field when baseball exercises were being conducted. We analyzed the relationship between elbow pain and sonographic abnormalities and the relationship between pitchers and sonographic abnormalities. RESULTS: Sonography showed that 33 subjects had medial epicondylar fragmentation and two had early-stage osteochondritis dissecans of the capitellum. In 25 subjects who agreed to further examination and treatment, radiography confirmed the sonographic findings. All of the 23 subjects with medial epicondylar fragmentation, who stopped throwing, obtained union of the bone and returned to baseball. The two subjects with osteochondritis dissecans of the capitellum underwent surgery before the osteochondral fragment became loosened. Sonographic abnormalities correlated with episodes of elbow pain. Pitchers statistically significantly had sonographic abnormalities. CONCLUSION: Sonography in the field can provide an opportunity to detect and treat elbow injuries before they become more advanced.

Age Factors↗
PubMed2005

Long-term prevention of skeletal complications by pamidronate in a patient with bone metastasis from endometrial carcinoma: a case report.

INTRODUCTION: Bisphosphonates are an effective treatment for bone metastases from breast cancer. However, it is unclear whether they are effective for bone metastases from endometrial carcinoma. CASE: A 70-year-old woman previously treated for endometrial carcinoma was referred to our hospital due to osteolytic destruction of the left ischial tuberosity. Technetium-99m-HMDP bone scintigraphy revealed abnormal uptake in the ischium. Biopsy revealed a metastatic bone tumor, but computed tomography scans did not show general metastatic spread. The patient received intravenous administration of pamidronate and three cycles of chemotherapy (epirubicin + paclitaxel + carboplatin). Three years later, the bone lesion showed prominent sclerotic changes with no evidence of disease recurrence radiologically. CONCLUSION: Pamidronate may prevent skeletal complications in selected patients with bone metastasis due to endometrial carcinoma.

Aged↗
PubMed2005

Methylation status of EXT1 and EXT2 promoters and two mutations of EXT2 in chondrosarcoma.

Germline mutation and functional loss of EXT1 or EXT2 are commonly found in multiple osteochondromas and predispose to the development of chondrosarcoma. Mutations of EXT1 and EXT2 have rarely been detected in sporadic secondary chondrosarcomas from osteochondroma; these frequently display loss of heterozygosity at the EXT1 and EXT2 loci, but primary chondrosarcomas typically do not. To evaluate promoter methylation (which is an epigenetic gene silencing mechanism) of EXT1 and EXT2, we performed methylation-specific polymerase chain reaction (PCR) for 20 chondrosarcoma cases (12 primary, 3 secondary to osteochondroma, 2 secondary to enchondromatosis, 2 extraskeletal ordinary, and 1 clear cell) and in five cell lines. In addition, mutation analysis of the EXT1 and EXT2 coding regions was performed using PCR-single-strand conformation polymorphism and sequencing analysis for 12 of the 20 chondrosarcoma cases (8 primary, 1 secondary to enchondromatosis, 1 secondary to osteochondroma, and 2 extraskeletal ordinary) and five cell lines. Promoter methylation of EXT1 and EXT2 was not detected in any of the cases, and both EXT1 and EXT2 were expressed in all cell lines. Two missense mutations in EXT2 (D227E and R299H) were detected among the chondrosarcoma cases. When considering tumor development in primary chondrosarcoma, we should include mutations in EXT2, along with the status of other members of the EXT gene family.

5' Untranslated Regions↗
PubMed2005

Developmental abnormalities in rat embryos leading to tibial ray deficiencies induced by busulfan.

BACKGROUND: Little is known about the developmental changes associated with tibial ray deficiencies. The aim of this study was to detect cell death, proliferation, and gene expression that result in tibial ray deficiencies. METHODS: We induced tibial ray deficiencies in rat embryos using a teratogenic agent (busulfan) and observed the developmental changes in 1126 hindlimbs. We performed Nile blue staining, whole mount in situ hybridization for fibroblast growth factor 8 (Fgf8), bone morphogenetic protein 4 (Bmp4) and Sonic hedgehog (Shh), terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) and assessment of cell proliferation by 5-bromo-2'-deoxy-uridine (BrdU)/anti-BrdU immunohistochemistry. RESULTS: In situ hybridization showed reductions in Fgf8 and Bmp4 expression. Histological examination showed a delay of mesenchymal condensation, increased mesenchymal cell death, decreased mesenchymal cell proliferation, and a reduction in the number of mesenchymal cells. These abnormalities may cause hypoplasia of the limb. Bmp4 expression was markedly reduced in the anterior mesenchyme. Shh was expressed in the posterior mesenchyme. We suggest that the posterior skeletal elements may be fully formed owing to Shh expression, but the anterior skeletal elements may be underdeveloped owing to an intense reduction of Bmp4 expression in the anterior mesenchyme, causing hypoplasia of the tibial ray. CONCLUSIONS: The combined effects of increased cell death, decreased cell proliferation, reduction of Fgf8 expression, and intense reduction of Bmp4 expression in the anterior mesenchyme may play an important role in the development of tibial ray deficiency induced by busulfan.

Animals↗
PubMed2005

The short-term reliability of grip strength measurement and the effects of posture and grip span.

PURPOSE: Because of the difficulty in verifying the reliability and validity of grip strength there is still no consensus regarding its measurement, particularly short-term reliability. The present study was conducted to investigate the short-term reliability of grip strength measurement and the effects of posture and grip span. METHODS: One hundred healthy subjects (50 men, 50 women; mean age, 38.2 y; range, 22-58 y) were evaluated. Grip strength was measured twice as a single set by using a dynamometer and the mean value for each hand was recorded. First 3 sets of measurements were performed using 2 different approaches: (1) continuous measurement without rest and (2) interval measurement with a 1-minute rest after each set. Next 1 set of measurements was performed with 3 types of grip span: standard grip span (which was measured as one half the distance between the index finger tip and the metacarpophalangeal joint flexion crease at the base of the thumb), +10% of the standard grip span, and -10% of the standard grip span. Finally 1 set of measurements was performed in 3 postures: standing, sitting, and supine. RESULTS: During continuous measurement the grip strength decreased gradually as the number of sets increased. During interval measurement, however, there was no change among sets for both genders and each hand. On the basis of this result subsequent studies were performed using interval measurement. There was no significant difference in maximum grip strength between the standard and +10% of standard grip span measurements; however, the -10% of standard model gave the minimum grip strength in both genders. With regard to posture the minimum grip strength in both genders was obtained when the subject was supine, with no difference between standing and sitting. CONCLUSIONS: Our study showed that interval measurement with a 1-minute rest after each set yielded a constant value; therefore, we advocate this approach for rapid evaluation of grip strength under different conditions. In addition the influence of grip span and posture should be considered to maximize data accuracy.

Adult↗
PubMed2004

Deep venous thrombosis during neoadjuvant chemotherapy in a patient with osteosarcoma: a case report.

A 29-year-old man with an osteosarcoma of the left distal femur developed asymptomatic deep venous thrombosis (DVT) during neoadjuvant chemotherapy. The thrombotic event occurred in the left common iliac vein and was revealed by pelvic computed tomography (CT). We successfully performed a limb salvage operation with placement of a permanent inferior vena cava filter. The thrombus spontaneously regressed without thrombolytic therapy after surgery. We should consider DVT in patients with musculoskeletal sarcomas who are under long-term hospitalization and immobilization associated with not only surgery but also chemotherapy. To screen for both metastasis and DVT, we recommend contrast-enhanced whole-body CT, including scans of the pelvis.

Adult↗
PubMed2004

Contrast-enhanced magnetic resonance imaging of malignant granular cell tumor with pathological correlation: a case report.

This report presents a case of malignant granular cell tumor in the deltoid muscle and emphasizes the correlation between magnetic resonance (MR) images and pathological findings. A 71-year-old woman developed an elastic hard mass at the left shoulder. MR images revealed a soft tissue tumor with a maximum diameter of 5 cm and low signal intensity on both T1- and T2-weighted images. The lesion with decreased signal intensity on all the images correlated with marked fibrosis mimicking desmoid tumor. Contrast-enhanced MR images provided useful information regarding the choice of biopsy site.

Aged↗
PubMed2004

Developmental failure of phalanges in the absence of growth/differentiation factor 5.

Growth/differentiation factor 5 (GDF5) is a member of the bone morphogenetic protein (BMP) family, which has been implicated in several skeletogenic events including cartilage and bone formation. To study the role of GDF5, we analyzed digit development in brachypodism (bp) mice, which carry functional null mutations of the Gdf5 gene and exhibit a reduction in the length of digit bones and loss of the middle phalanges. In situ detection of apoptosis and whole-mount detection of cell death showed abnormal apoptosis in the developing phalanges of bp mice. In situ hybridization in bp mice showed overexpression of Gdf5 mRNA in the developing phalanges where apoptotic cells were increased. In addition, bp mice exhibited excessive apoptosis in the interdigital regions. The condensed mesenchymal cells were progressively decreased in the developing phalanges and failed to form cartilage models of the middle phalanges. These findings show that excessive apoptosis in the absence of GDF5 results in developmental failure of the phalanges. We conclude that GDF5 is essential for maintenance and growth of the developing phalanges.

Animals↗
PubMed2004

Matrix metalloproteinase-9 expression, tartrate-resistant acid phosphatase activity, and DNA fragmentation in vascular and cellular invasion into cartilage preceding primary endochondral ossification in long bones.

Vascular and cellular invasion into cartilage are essential for endochondral ossification. Recently it has been shown that matrix metalloproteinase-9 (MMP-9)/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes. To study vascular and cellular invasion into cartilage preceding primary endochondral ossification in long bones, precursor femurs from 13- to 16-day-old murine embryos were sectioned. Tartrate-resistant acid phosphatase (TRAP) activity, in situ hybridization for matrix metalloproteinase-9 (MMP-9), immunostaining for CD31, and in situ detection of apoptosis (TUNEL) were studied. TRAP activity, MMP-9 mRNA, and CD31 expression were initially detected in the intertrabecular spaces of the perichondral collar, and then in cells migrating into the cartilage. The first cells involved in the primary invasion into cartilage were CD31-positive vascular endothelial cells and MMP-9-positive cells, followed by TRAP-positive cells. At the cartilage-marrow interface, CD31-positive vascular endothelial cells and MMP-9-positive cells were predominant. These results suggest that MMP-9-positive cells cooperate with vascular endothelial cells in cartilage angiogenesis. TUNEL-positive staining was detected on chondrocytes attached to the inner surface of the perichondral collar, and also detected in the area where cartilage was removed. These results suggest that chondrocytes separated from the cartilage matrix may undergo apoptosis.

Acid Phosphatase↗
PubMed2004

Hyaluronate inhibits the interleukin-1beta-induced expression of matrix metalloproteinase (MMP)-1 and MMP-3 in human synovial cells.

Intra-articular administration of hyaluronate (HA) is an effective treatment for arthritis. HA injections can decrease not only joint pain but also synovial effusion, although little is known concerning the mechanism of HA action. The aim of this study was to investigate the role of HA on the expression and production of matrix metalloproteinase (MMP) in synovial cells activated by interleukin (IL)-1beta in order to achieve a better understanding of exogenous HA function in the extracellular matrix degradation in arthritic joints. Human synovial cells were incubated with HA (0.1-1000 microg/ml) and/or IL-1beta (1 ng/ml). The expression of MMP-1 and MMP-3 mRNAs was analyzed by quantitative real-time polymerase chain reaction. The protein levels of MMP-1 and MMP-3 in cultured media were measured by immunoblotting. Expression of MMP-1 and MMP-3 mRNAs was induced by IL-1beta. The IL-1beta-mediated induction of MMP-1 mRNA expression was attenuated by 10 microg/ml HA (p=0.026) and that of MMP-3 mRNA was strongly down-regulated in the presence of 10 or 1000 microg/ml HA (p<0.001). The increased protein levels of MMP-1 and MMP-3 were also reduced by 1000 microg/ml HA. These data suggest that HA inhibits the expression and production of MMP-1 and MMP-3 in IL-1beta-stimulated human synovial cells. We therefore prepose that intra-articular HA may rescue inflamed joints from bone and cartilage destruction by reducing the production of MMP-1 and MMP-3.

Cells, Cultured↗
PubMed2003

Dendritic cell and effector cell infiltration in soft tissue sarcomas with reactive lymphoid hyperplasia.

The lymph node is the site of antigen presentation, and dendritic cells are sentinels for anti-tumor immunity. However, little is known about the histological features of lymph nodes and dendritic cells in soft tissue sarcomas. The reactive lymph node and infiltration of dendritic cells or effector cells were studied histologically in 10 soft tissue sarcomas with reactive lymphoid hyperplasia. The cases included four malignant fibrous histiocytomas, two malignant peripheral nerve sheath tumors, one synovial sarcoma, one epithelioid sarcoma, one malignant granular cell tumor, and one liposarcoma. The proportions of the T zone, lymphoid follicle, and lymphoid sinus (which was occupied by cells immunopositive for antibodies against CD3, CD20, or CD68) were 33.4% +/- 11.0%, 6.1% +/- 4.9%, and 13.5% +/- 6.5%, respectively. T zone hyperplasia was observed in all cases, and sinus histiocytosis was found in four. The proportion of the T zone in regional lymph nodes of soft tissue sarcoma patients was significantly higher than that in adult autopsy cases without a cancer history. CD8-, TIA-1-, or granzyme B-positive effector cells were found in each sarcoma tissue. Whereas CD1a-positive dendritic cells were not detected, S-100 protein-positive or CD83-positive dendritic cells were observed in five sarcoma tissues. The coefficient correlation between the numbers of effector cells and dendritic cells positive for CD83 or S-100 protein were demonstrated. Although this is a preliminary report, the present study demonstrated that some soft tissue sarcoma patients showed reactive lymphoid hyperplasia. Furthermore, the association between the infiltration of dendritic cells and that of effector cells was observed in patients with soft tissue sarcomas.

Adolescent↗
PubMed2003

FGFR2 mutation in a patient with Apert syndrome associated with humeroradial synostosis.

Most cases of Apert syndrome are due to S252W or P253R mutations in the fibroblast growth factor receptor 2 (FGFR2) gene. Differences in the effects of S252W and P253R mutations on the clinical features of Apert syndrome have been studied, but little is known about the type of FGFR2 mutation in Apert syndrome with humeroradial synostosis. To study a correlation between the FGFR2 mutations and the clinical complications, we examined the FGFR2 gene in a patient with Apert syndrome associated with humeroradial synostosis, and found that the mutation was S252W. This report suggested that S252W mutation in FGFR2 may cause humeroradial synostosis in Apert syndrome.

Acrocephalosyndactylia↗
PubMed2003

Intercalary non-vascularised toe phalanx transplantation for short finger-type symbrachydactyly.

A two-year-old boy with short finger-type symbrachydactyly involving the index, middle, and ring fingers was treated with intercalary nonvascularised toe phalanx transplantation into the middle finger to obtain stability of the middle finger before syndactyly release. He underwent syndactyly release one year after the transplantation. Two years after the transplantation, the clinical result was satisfactory, although X-ray showed fibrous union between the transplanted phalanx and the host phalanx. Intercalary nonvascularised toe phalanx transplantation is one of the way of stabilising a finger after syndactyly release.

Fingers↗
PubMed2002

A novel gene is disrupted at a 14q13 breakpoint of t(2;14) in a patient with mirror-image polydactyly of hands and feet.

Mirror-image polydactyly of hands and feet (MIP) is a very rare congenital anomaly characterized by mirror-image duplication of digits. To isolate the gene responsible for MIP, we performed translocation breakpoint cloning from an MIP patient with t(2;14)(p23.3;q13). We isolated a good candidate gene for MIP that was disrupted by the translocation of the patient. We had previously con structed a 1.2-megabase bacterial artificial chromosome (BAC)/P1-derived artificial chromosome (PAC) contig covering the 14q13 breakpoint of t(2;14)(p23.3;q13). From a 500-kb segment consisting of seven BAC/PAC clones in the contig, we isolated a novel gene (the mirror-image polydactyly 1 gene, designated as MIPOL1, GenBank Accession No. AY059470), in addition to the hepatocyte nuclear factor 3 alpha gene (HNF3A, GenBank Accession No. XM 007360). MIPOL1 spans about 350kb, comprises 15 exons, and encodes 442 amino acids. Northern blot analysis revealed that MIPOL1 expression is definite but very weak in adult heart, liver, skeletal muscle, kidney, and pancreas, and in fetal kidney. In view of the genome sequence and the contig map constructed, the 14q13 breakpoint of the patient was identified as located in intron 11 of MIPOL1, indicating that the gene was disrupted by the translocation, and that the breakage resulted in MIPOL1 protein truncation. Whole-mount in situ hybridization in mouse resulted in mouse Mipol1 signals all over E10.5-E13.5 mouse embryos. Two other unrelated patients with limb anomalies similar to MIP were subjected to mutation analysis of MIPOL1, but none had any mutations. We then isolated BAC clones from the other breakpoint, 2p23.3. A search for genes and expressed sequence tags in a more than 300-kb region around the 2p23.3 breakpoint found only the neuroblastoma-amplified protein gene (NAG, GenBank Accession No. NM 015909), which is located at least 50kb centromeric to the breakpoint and is not likely to be related to MIP. MIPOL1 is a good candidate gene for the MIP type of anomaly.

Chromosomes, Human, Pair 14↗