PubMed Health⌕ Search

Biomedical subjects

I Ogawa

Publications and source records attributed to I Ogawa.

At least 19 recordsLinked to original sources
PubMed2006

Periostin is frequently overexpressed and enhances invasion and angiogenesis in oral cancer.

Oral squamous-cell carcinoma (OSCC) is one of the most common types of human cancer. Typically OSCC cells show persistent invasion that frequently leads to local recurrence and distant lymphatic metastasis. We previously identified Periostin as the gene demonstrating the highest fold change expression in the invasive clone by comparing the transcriptional profile of parent OSCC cell line and a highly invasive clone. Here, we demonstrated that Periostin overexpression enhanced invasiveness in oral cancer cell lines. To know the role of Periostin in invasion, angiogenesis and metastasis in OSCC cases, we first examined the expression of Periostin mRNA in 31 OSCC cases by RT-PCR and Periostin protein in 74 OSCC cases by immunohistochemistry. Then, we compared the Periostin expression with invasion pattern, metastasis and blood vessel density. Periostin mRNA and protein overexpression were frequently found in OSCC cases and Periostin expression was well correlated with the invasion pattern and metastasis. Moreover, blood vessel density of Periostin-positive cases was higher than those of Periostin-negative cases. Interestingly, recombinant Periostin enhanced capillary formation in vitro in a concentration-dependant manner. In summary, these findings suggest that Periostin may promote invasion and angiogenesis in OSCC, and that Periostin can be a strong marker for prediction of metastasis in oral cancer patients.

Biomarkers, Tumor↗
PubMed2005

Optical circuit design based on a wavefront-matching method.

We propose an optical circuit design method for coherent waves as a boundary value problem. The method produces a very compact circuit in which the refractive index pattern is automatically synthesized for given input and output fields with a numerical calculation. We employ the method to design a 1.3/1.55 microm wavelength demultiplexer and also describe the features of a circuit generated by use of the method.

Journal Article↗
PubMed2005

Metastatic retinoblastoma of the maxilla and mandible.

Metastatic retinoblastoma of the jaws is very rare. We present a 4-year-old boy with metastatic retinoblastoma that involved both the maxilla and mandible simultaneously. Enhanced CT indicated bone-destructive masses with partially non-enhanced area and enhanced margin in the right maxilla and left mandible. MRI showed well-delineated masses that were isointense on T(1) weighted images and hyperintense on T(2) weighted images. Four weeks after chemotherapy and bone marrow transplantation, the size of lesions remarkably decreased. The patient died 19 months later with extensive tumour metastases despite additional chemotherapy. In this case, the dental crypt of a permanent tooth was considered the potential target through which retinoblastoma metastasized to the jaws.

Child, Preschool↗
PubMed2004

Immuno-localization of COX-1 and COX-2 in the rat molar periodontal tissue after topical application of lipopolysaccharide.

Up-regulation of prostaglandin E2 (PGE2) production in the periodontal tissue is considered to be important for periodontal tissue destruction. The purpose of the study was to demonstrate the dynamic changes of immuno-localization of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in rat periodontal tissue after topical application of lipopolysaccharide (LPS: 5 mg/ml in physiological saline) from Escherichia coli into the rat molar gingival sulcus. In the normal periodontal tissue, small numbers of junctional epithelium (JE) cells and numerous osteocytes embedded in alveolar bone constitutively expressed COX-1. The COX-1 expression was not effected by LPS application. JE cells, especially in the coronal portion of JE also expressed COX-2. LPS application induced the JE cells with consequent transient expression of COX-2 with a peak at day 1. These findings suggest that JE cells may play a critical role in first defense line against LPS challenge and PGE2 from JE cells may be responsible for the initiation of periodontal inflammation. In the deep periodontal tissue, cementoblasts and osteoblasts showed constitutive expression of COX-2, which may be induced by continuous cyclic tension force due to occlusal pressure. LPS application caused a transient up-regulation of COX-2 expression in periodontal ligament fibroblasts, cementoblasts and osteoblasts. It is suggested that the inducible production of PGE2 via COX-2 by these cells may be associated with connective tissue destruction and alveolar bone resorption.

Administration, Topical↗
PubMed2004

The inflammatory paradental cyst: a critical review of 342 cases from a literature survey, including 17 new cases from the author's files.

BACKGROUND: A total of 325 cases of inflammatory paradental cysts (IPCs) and 17 own cases were reviewed. Although known since 1930, the IPC is still unrecognized by many clinicians. The IPCs show a relative frequency of 0.9-4.7%. The majority of cysts occur distally or distobuccally to vital, permanent mandibular molars with a history of pericoronitis (IPC/3rd mandibular molar alone accounts for 64.9%). Radiologically, the cyst appears as a well-defined, semilunar unilocular radiolucency. MATERIALS AND METHODS: Cases of inflammatory paradental cysts and related lesions were retrieved from a worldwide literature survey. In addition, 17 new cases from the files of the authors have been added. RESULTS: The mean ages for patients with IPC/1st, 2nd and 3rd mandibular molars are 8.7, 17.4 and 27.6 years, respectively. The male:female ratio was 1 : 0.9 for IPC/1st and 2nd mandibular molars, and 1 : 0.4 for 3rd mandibular molar. CONCLUSION: Reduced enamel epithelium, cell rests of Malassez and remnants of the dental lamina stimulated by inflammation are thought to play a role in the pathogenesis of IPC. Histological features are indistinguishable from those of the inflammatory, periapical (radicular) cyst.

Adolescent↗
PubMed2004

Tumour necrosis factor-alpha but not interferon-gamma is the main inducer of inducible protein-10 in skin fibroblasts from patients with atopic dermatitis.

BACKGROUND: Inducible protein (IP)-10 belongs to the CXC chemokine subfamily and acts through the CXCR3 receptors that attract T lymphocytes. Keratinocytes are thought to be the main cell source of this chemokine in the skin, but other sources need to be elucidated. OBJECTIVES: To determine whether skin fibroblasts, besides keratinocytes, are able to produce IP-10 and the possible involvement of these cells in pathogenesis of atopic dermatitis (AD). METHODS: We studied the production pattern of IP-10 in dermal fibroblasts obtained from healthy donors, AD patients and in the HaCaT cell line (normal human keratinocytes) used as control. We stimulated fibroblasts after the sixth and seventh passage with tumour necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-4, and by means of reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assay analysis detected the production pattern of IP-10. To determine whether a different pattern of production of IP-10 by fibroblasts corresponds to the level of this chemokine in the plasma of patients with AD, we also checked the plasma IP-10 levels in 33 AD patients and 10 healthy donors. RESULTS: The pattern of chemokine production between dermal fibroblasts and HaCaT cells was different. The main inducer of IP-10 in fibroblasts was TNF-alpha, whereas IFN-gamma was the main inducer of IP-10 in HaCaT cells. We demonstrate that fibroblasts from AD patients have higher IP-10 expression and are more sensitive to TNF-alpha stimulation compared with healthy controls. Consequently, IP-10 levels in plasma of AD patients were higher than in healthy donors. CONCLUSIONS: Skin fibroblasts could be an important source of IP-10. TNF-alpha is the main inducer of IP-10 by skin fibroblasts, but not IFN-gamma or IL-4. The increased level of IP-10 in the plasma of patients with AD could be connected with increased activity of skin fibroblasts.

Adult↗
PubMed2003

Inhibition of CD44v9 upregulates the invasion ability of oral squamous cell carcinoma cells.

The aim of the present study has been to determine the role of CD44v9 in the metastatic process of oral squamous cell carcinoma (OSCC). We have examined the expression intensity of CD44v9 in four OSCC cell lines, and using cell culture insert investigated the invasion ability of the cells expressing CD44v9 at higher levels (HSC-2, HSC-3), and the cells expressing this protein at lower levels (HSC-4, KB) with or without the treatment with an anti-CD44v9 antibody. In the highly expressing cells, the addition of anti-CD44v9 antibody enhanced their invasion ability, whereas it showed no effect on the invasion ability of the weakly expressing cells. These results suggest that the reduction of CD44v9 expression may weaken cell-to-cell adhesion in OSCC and make the tumor cells detach easily from their nests, resulting in the enhancement of their invasion ability. It may ultimately promote the establishment of a metastatic lesion.

Antigens, Neoplasm↗
PubMed2003

Verruciform xanthoma--biological profile of 282 oral lesions based on a literature survey with nine new cases from Japan.

The biological profile of oral verruciform xanthoma (VX) is presented based on a world-wide literature survey of 282 cases. From 1979 onwards, extraoral cases have also been reported. This rare, harmless lesion with a sessile or pedunculated base is a red/pink, papillary/granular/verrucous mucosal growth, occurring in females (mean age, 54.9 yrs) and males (mean age, 44.2 yrs) in a female:male ratio of 1:1.1. The most common location is by far the gingival margin and other areas of the masticatory oral mucosa. Comparison between 173 non-Japanese and 109 Japanese patients with oral VX showed few discrepancies in epidemiological data, indicating only few significant ethnic differences between the two cohorts. Histomorphologically, the epithelium covering the lesion can be divided into three groups: (A) a verrucous, (B) a papillary and (C) a flat pattern. The hallmark of all VX, irrespective of the lesion being intra- or extraoral is, however, the presence of vacuolated, foam or xanthoma cells which ultimately replace the connective tissue between the epithelial ridges. The xanthoma cells have been shown to be cells of the monocyte/macrophage lineage. The present concept of the etiology and pathogenesis of VX, including the possible viral (HPV) association is revised, based on both intra- and some extraoral cases, and it is concluded that it is still far from being clarified.

Adolescent↗
PubMed2001

High expression of S-phase kinase-interacting protein 2, human F-box protein, correlates with poor prognosis in oral squamous cell carcinomas.

Reduced expression of p27(Kip1), a cyclin-dependent kinase (Cdk) inhibitor, is frequently found in various cancers, including oral squamous cell carcinoma (OSCC), and is attributable to an enhancement of its degradation. Skp2, an F-box protein necessary for DNA replication, is required for the ubiquitinylation and subsequent degradation of p27(Kip1). In the present study, we examined the expression of Skp2 and its correlation with the expression of p27(Kip1) protein or p27(Kip1) degradation in OSCC. Using immunohistochemistry, we found that high expression of Skp2 was present in 49% of OSCCs and only 20% of epithelial dysplasias. Significantly, high expression of Skp2 was correlated with poor prognosis of OSCC patients. We also found an inverse correlation between the expression of Skp2 and p27 by immunohistochemical analysis. A similar correlation was observed in OSCC cell lines and OSCC tissues by Western blot analysis. Interestingly, OSCC tissues with Skp2 expression had high p27(Kip1) degradation activity. These findings indicate that (a) Skp2 may play an important role for the development of OSCC, (b) Skp2 can be a novel target for OSCC treatment as well as a strong prognostic marker, and (c) the reduction in p27(Kip1) protein may be brought about by enhancement of its degradation mediated by increased levels of Skp2 protein.

Adult↗
PubMed2001

Cytokine expression in rat molar gingival periodontal tissues after topical application of lipopolysaccharide.

It is well known that proinflammatory cytokines produced by host cells play an important role in periodontal tissue destruction. However, the localization of the cytokines in in vivo periodontal tissues during development of periodontal disease has not been determined. Immunohistochemical expression of proinflammatory cytokines including IL-1alpha, IL-1beta, and TNF-alpha was examined at 1 and 3 h, and 1, 2, 3, and 7 days after topical application of lipopolysaccharide (LPS; 5 mg/ml in physiological saline) from E. coli into the rat molar gingival sulcus. In the normal periodontal tissues, a small number of cytokine-positive epithelial cells were seen in the junctional epithelium (JE), oral sulcular and oral gingival epithelium, in addition to macrophages infiltrating in the subjunctional epithelial area and osteoblasts lining the alveolar bone surface. Epithelial remnants of Malassez existing throughout periodontal ligament were intensely positive for IL-1beta but negative for the other two cytokines. At 3 h after the LPS treatment, almost all cells in the JE were strongly positive for the cytokines examined. In addition, several cytokine-positive cells, including neutrophils, macrophages, and fibroblasts, were seen in the subjunctional epithelial connective tissue. At day 2, expression of the cytokines in the JE gradually decreased, while cytokine-positive cells in the connective tissue increased in number. Positive staining of the cytokines was seen in osteoclasts and preosteoclasts which appeared along the alveolar bone margin in this period. The number of cytokine-positive cells decreased by day 7. These findings indicate that, in addition to macrophages, neutrophils, and fibroblasts, the JE cells are a potent source of TNF-alpha, IL-1alpha, and IL-1beta reacting to LPS application, and suggest that JE cells may play an important role in the first line of defense against LPS challenge, and the proinflammatory cytokines transiently produced by various host cells may be involved in the initiation of inflammation and subsequent periodontal tissue destruction.

Animals↗
PubMed2001

Magnetic resonance imaging in hemifacial hyperplasia.

We describe a case of hemifacial hyperplasia due to a combination of lipoma and lipomatosis. The contribution of MRI to the diagnosis of hemifacial hyperplasia and to monitoring growth and development in this condition is demonstrated.

Anatomy, Cross-Sectional↗
PubMed2000

Reduced expression of p27(Kip1) correlates with an early stage of cancer invasion in oral squamous cell carcinoma.

Down-regulation of p27(Kip1) has been reported to correlate with poor survival of various carcinoma patients including oral squamous cell carcinomas (OSCCs). It is still unclear, however, at what stage of oral carcinogenesis the down-regulation of this protein occurs. In this study, therefore, we evaluated immunoexpression of p27(Kip1) protein in 17 cases of oral epithelial dysplasia and succeeding invasive OSCC in the same patient. We reported here that 88% cases showed high p27(Kip1) expression in dysplastic lesions, whereas 82% cases of succeeding invasive OSCC exhibited reduced expression. The reduction of p27(Kip1) expression was also observed in 16 of 19 (84%) early invasive lesions and well correlated with Ki-67 expression which is good indicator of cell proliferation. We also investigated immunoexpression of p53 protein of which abnormality has been known to occur during the early stage of OSCC development. Overexpression of p53 protein was demonstrated in 29% of dysplastic lesions, 42% of early invasive and 71% of invasive OSCCs. These findings suggest that abnormalities of both p53 and p27(Kip1) are involved in the carcinogenesis of OSCC, but they seem to play their role at different stages of oral cancer development, respectively. Reduced expression of p27(Kip1) may concern the cancer invasion directly or indirectly as well as abnormal proliferation.

Carcinoma, Squamous Cell↗
PubMed2000

Immunoexpression of transforming growth factor beta in desmoplastic ameloblastoma.

Desmoplastic ameloblastoma (DA) is an unusual subtype of ameloblastoma histologically characterized by the pronounced collagenized stroma. In the present study, the immunolocalization of transforming growth factor beta (TGF-beta), one of the most potent local factors for modulating extracellular matrix formation, was observed in DA in order to study its participation in the stromal desmoplasia. Seven cases of DA, including a "hybrid" lesion, were studied together with ten cases of ordinary follicular and plexiform ameloblastomas as the control. In contrast to ordinary ameloblastomas, marked immunoexpression was observed in all DAs but one. In the "hybrid" lesion, TGF-beta was not expressed in the area of follicular ameloblastoma but in that of DA. These results show that TGF-beta produced by tumor cells of DA plays a part in the desmoplastic matrix formation.

Adolescent↗
PubMed2000

Reduced expression of CD44 variant 9 is related to lymph node metastasis and poor survival in squamous cell carcinoma of tongue.

Expression of CD44v9 was immunohistochemically studied in 120 biopsy specimens from primary squamous cell carcinoma (SCC) of the tongue and correlated with clinicopathological findings of the SCCs. The tumors were classified into three groups according to immunostaining pattern of CD44v9; 53 cases with distinct positivity in all cancer cells except for those in the central part of nests (Group 1, non-reduced group), 42 cases with reduced expression in peripheral cells of nests (Group 2, reduced group), and 25 cases with complete disappearance of the expression in one or more nests (Group 3, negative group). Nineteen of 25 (76%) tumors in Group 3 and 14 of 42 (33%) in Group 2 exhibited lymph node metastasis, compared with only 8 of 53 (15%) in Group 1. The average survival time in Groups 1, 2 and 3 was 4496+/-204, 3866+/-379 and 2719+/-359 days, respectively and became shorter with the reduction of CD44v9 expression. These results suggest that the down-regulation of CD44v9 in SCC of the tongue may relate to the detachment of tumor cells from primary lesions, establishment of lymph node metastasis and consequently the death of patients.

Adult↗
PubMed2000

Prevention of left ventricular remodeling by percutaneous transluminal coronary angioplasty performed 24 hours after the onset of acute myocardial infarction.

It remains controversial whether percutaneous transluminal coronary angioplasty (PTCA) performed 24 hours after the onset of acute myocardial infarction (AMI) in coronary arteries with 99% stenosis is useful in preserving left ventricular function. We investigated the effectiveness of PTCA in preventing left ventricular remodeling when it was performed 24 hours after the onset of AMI in infarct-related coronary arteries (IRCAs) having 99% stenosis and thrombolysis in myocardial infarction (TIMI) grade 3 flow. The subjects were 19 patients with AMI (anterior wall, 9 patients; inferior wall, 7 patients; and non-Q, 3 patients) who, within 24 hours of the onset of AMI, underwent coronary angiography and left ventriculography during the acute and/ or chronic phases. The patients were divided into a PTCA group, comprised of patients in whom PTCA was successfully performed 24 hours after the onset of AMI (n = 10), and a non-PTCA group (n = 9). The non-PCTA group included patients who were successfully reperfused by thrombolysis and did not include patients who had spontaneous reperfusion or reperfusion after PTCA. In the non-PTCA group, the left ventricular end-diastolic volume (mean +/- SD) was significantly increased in the chronic phase (86 +/- 23 mL/m(2)) as compared with the acute phase (67 +/- 13 mL/m(2)), whereas in the PTCA group no significant difference was observed between end-diastolic volumes in the acute and chronic phases (67 +/- 26 and 68 +/- 13 mL/m(2), respectively). Left ventricular remodeling is prevented by PTCA when it is performed 24 hours after the onset of AMI in IRCAs with 99% stenosis and TIMI grade 3 flow.

Aged↗
PubMed2000

Prevention of coronary arterial renarrowing by continuous 3-day infusion of tissue plasminogen activator after successful percutaneous transluminal coronary angioplasty: a randomized, double-blind, placebo-controlled study.

Vascular injury resulting from percutaneous transluminal coronary angioplasty (PTCA) and subsequent thrombus formation are important factors in the pathogenesis of coronary arterial restenosis. The present study was undertaken to determine whether infusions of tissue plasminogen activator (tPA), beginning immediately after PTCA, would decrease the renarrowing of the coronary arterial lumen. Patients were randomized and divided into two groups: one group (15 patients, 16 lesions) received continuous, 3-day, intravenous infusions of tPA (0.25 mg/kg/day in 0.9% saline), beginning immediately after successful PTCA, while the other group (17 patients, 17 lesions) received saline alone. Coronary angiography was performed before, immediately after, 24 hours after, and 3 months after PTCA. Coronary stenosis (%), reference diameters, and minimum luminal diameters were measured by quantitative coronary angiography. The incidence of restenosis tended to be lower in the tPA group than in the placebo group (tPA group, 13%; placebo group, 41%; NS), although diameter stenoses before and immediately after PTCA were not significantly different in the two groups. Three months later, however, diameter stenoses were significantly smaller in the tPA group (35.6 +/- 13.3 vs 47.7 +/- 18.9%; P<0.05). Thus, intravenous tPA infusion beginning immediately after successful PTCA may inhibit renarrowing of the coronary arterial lumen.

Aged↗
PubMed2000

p27Kip1 accumulation by inhibition of proteasome function induces apoptosis in oral squamous cell carcinoma cells.

Ubiquitin-mediated proteolysis controls intracellular levels of various cell cycle regulatory proteins, and its inhibition has been shown to induce apoptosis in proliferating cells. In the present study, we examined induction of apoptosis in oral squamous cell carcinoma (OSCC) cells by treatment with specific proteasome inhibitors, carbobenzoxy-L-leucyl-L-leucyl-L-norvalinal and lactacystin. In all three OSCC cell lines examined, apoptotic changes such as apoptotic body formation and DNA fragmentation were observed at various degrees after 24 h of the carbobenzoxy-L-leucyl-L-leucyl-L-norvalinal or lactacystin treatment. HSC2 cells showed the most prominent apoptotic changes among the cell lines examined and demonstrated the highest level of accumulation of p27Kip1 protein after the treatment with proteasome inhibitor. Reduced expressions of cyclin D1 and phospho pRb were also observed after the treatment with proteasome inhibitor. Moreover, 12 h of treatment with the proteasome inhibitor inhibited cdk2/cyclin E kinase activity and increased the ratio of the cell cycle population at the G1 phase. The proteasome inhibitor led to inhibition of cell cycle progression. In addition, activation of CPP32 and reduced expression of Bcl-2 were observed. Because apoptosis induced by the proteasome inhibitor was inhibited by treatment with antisense p27Kip1 oligonucleotide, accumulation of the p27Kip1 protein might play an important role in the apoptosis induced by proteasome inhibitor. The present results suggest that inhibition of proteasome function may be used as a possible target of novel therapy for OSCC.

Acetylcysteine↗