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Biomedical subjects

M Ito

Publications and source records attributed to M Ito.

At least 55 records · Page 3Linked to original sources
PubMed2005

Eradication of Helicobacter pylori increases the incidence of hyperlipidaemia and obesity in peptic ulcer patients.

BACKGROUND: Eradication of Helicobacter pylori improves clinical symptoms and quality of life in patients with peptic ulcer. AIM: To investigate the effect of eradication of H. pylori on body mass index and incidence of hyperlipidaemia in patients with peptic ulcer. PATIENTS AND METHODS: The study population comprised 50 patients (42 men, 8 women; mean age, 51 years; 28 gastric ulcer, 22 duodenal ulcer) who underwent physical and blood examination before and 1 year after undergoing eradication therapy and 100 sex- and age-matched control subjects. Body mass index, total cholesterol and triglyceride were measured before and 1 year after therapy. RESULTS: The eradication therapy group showed a significant increase in body mass index (22.7+/-2.5 kg/m2 before eradication versus 23.6+/-2.6 kg/m2 after eradication, p < 0.01), serum total cholesterol (204.1+/-33.2 mg/dL versus 221.2+/-38.8 mg/dL, p < 0.01), and triglyceride. Additionally, the eradication therapy group showed a significant increase in the incidence of hypercholesterolemia (30% versus 58%, p<0.01), hypertriglyceridaemia (28% versus 44%, p < 0.01) and obesity (12% versus 22%, p <0.05) 12 months after therapy. CONCLUSION: Our findings show that eradication of H. pylori significantly increases the incidence of hyperlipidaemia and obesity in patients with peptic ulcer.

Adult↗
PubMed2005

Characterization of SSU and LSU rRNA genes of three Trypanosoma (Herpetosoma) grosi isolates maintained in Mongolian jirds.

Trypanosoma (Herpetosoma) grosi, which naturally parasitizes Apodemus spp., can experimentally infect Mongolian jirds (Meriones unguiculatus). Three isolates from A. agrarius, A. peninsulae, and A. speciosus (named SESUJI, HANTO, and AKHA isolates, respectively) of different geographical origin (AKHA from Japan, and the others from Vladivostok), exhibited different durations of parasitaemia in laboratory jirds (2 weeks for HANTO, and 3 weeks for the others). To assess the genetic background of these T. grosi isolates, their small (SSU) and large subunit (LSU) ribosomal RNA genes (rDNA) were sequenced along with those of 2 other Herpetosoma species from squirrels. The SSU rDNA sequences of these 3 species along with available sequences of 3 other Herpetosoma trypanosomes (T. lewisi, T. musculi and T. microti) seemed to reflect well the phylogenetic relationship of their hosts. Three isolates of T. grosi exhibited base changes at 2-6 positions of 2019-base 18S rDNA, at 5-29 positions of 1817/1818-base 28Salpha rDNA, or 1-5 positions of 1557-1559-base 28Sbeta rDNA, and none was separated from the other 2 isolates by rDNA nucleotide sequences. Since base changes of Herpetosoma trypanosomes at the level of inter- and intra-species might occur frequently in specified rDNA regions, the molecular analysis on these regions of rodent trypanosomes could help species/strain differentiation and systematic revision of Herpetosoma trypanosome species, which must be more abundant than presently known.

Animals↗
PubMed2005

Multiple myeloma oncogene 1 (MUM1)/interferon regulatory factor 4 (IRF4) upregulates monokine induced by interferon-gamma (MIG) gene expression in B-cell malignancy.

MUM1 (multiple myeloma oncogene 1)/IRF4 (interferon regulatory factor 4) is a transcription factor that is activated as a result of t(6;14)(p25;q32) in multiple myeloma. MUM1 expression is seen in various B-cell lymphomas and predicts an unfavorable outcome in some lymphoma subtypes. To elucidate its role in B-cell malignancies, we prepared MUM1-expressing Ba/F3 cells, which proliferated until higher cellular density than the parental cells, and performed cDNA microarray analysis to identify genes whose expression is regulated by MUM1. We found that the expression of four genes including FK506-binding protein 3 (FKBP3), the monokine induced by interferon-gamma(MIG), Fas apoptotic inhibitory molecule (Faim) and Zinc-finger protein 94 was altered in the MUM1-expressing cells. We then focused on MIG since its expression was immediately upregulated by MUM1. In reporter assays, MUM1 activated the MIG promoter in cooperation with PU.1, and the interaction between MUM1 and the MIG promoter sequence was confirmed. The expression of MIG was correlated with that of MUM1 in B-CLL cell lines, and treatment with neutralizing antibodies against MIG and its receptor, CXCR3, slightly inhibited the proliferation of two MUM1-expressing lines. These results suggest that MUM1 plays roles in the progression of B-cell lymphoma/leukemia by regulating the expression of various genes including MIG. Leukemia (2005) 19, 1471-1478. doi:10.1038/sj.leu.2403833; published online 16 June 2005.

Animals↗
PubMed2005

Burkholderia pickettii spondylitis.

STUDY DESIGN: Case report describing Burkholderia pickettii spondylitis in a healthy adult. OBJECTIVES: To describe this very rare form of spondylitis and to discuss some of the difficulties in the diagnosis of B. pickettii spondylitis. SETTING: Department of Orthopaedic Surgery, Nayoro City General Hospital, Japan. METHODS: A 48-year-old woman presented with a complaint of severe back pain radiating from the right side of her chest. Plain radiographs of the spine showed osteolytic destruction of the right side of the T10 vertebral body at T10 level, with an involvement of the pedicle. Magnetic resonance image of the spine showed a low signal intensity from the T10 vertebral body on a Tl-weighted image and an increased signal intensity on T2-weighted sequence image. These lesions were enhanced when a contrast medium was used. The patient underwent open biopsy and specimens were collected through the right pedicle. RESULTS: Diagnosis was established on the basis of direct identification of the microorganism. Histological findings were consistent with examination of B. pickettii spondylitis. Chemotherapy (intravenous cefepime and per os minocycline) resulted in complete cure. CONCLUSION: B. pickettii is widely distributed in aqueous sources in nature and has not previously been considered to be an aggressive pathogen towards humans. This case report will help to improve our understanding of the ecology and virulent pathogenicity of this organism. A biopsy is an essential and reliable method for the early etiologic diagnosis, which will lead to prevent the development of more severe complications such as spinal cord compression.

Burkholderia Infections↗
PubMed2005

Changes in placental dipeptidyl peptidase IV in preeclampsia with intrauterine growth restriction.

The purpose of this study was to examine alterations in placental expression of dipeptidyl peptidase IV (DPPIV). The localization of DPPIV was compared in control and preeclamptic placentas. Enzyme activity, mRNA, and protein expression were also measured. In term placentas, DPPIV was expressed preferentially in the fetal vascular endothelial cells within stem villi and only weakly in the villous stromal cells. DPPIV activity in control placentas showed no remarkable changes throughout gestation. Levels of activity in samples from normotensive control cases and women having preeclampsia with or without intrauterine growth restriction were 11.8 +/- 2.1, 13.4 +/- 1.1, and 15.3 +/- 0.62 pmol pNA/min/mg protein, respectively. The preeclamptic placentas with intrauterine growth restriction thus showed significantly higher levels of activity than the controls (p < 0.05). We propose that placental DPPIV influences fetal metabolism via the degradation of fetoplacental circulating bioactive peptides, including incretins, resulting in the regulation of fetal growth.

Adult↗
PubMed2005

Effect of long-term half-dose famotidine therapy on corpus gastritis in peptic ulcer disease.

BACKGROUND: Recent studies showed that acid-suppressive therapy aggravates corpus gastritis in patients with Helicobacter pylori infection. AIM: The aim of this study was to evaluate the effect of famotidine, a histamine receptor antagonist on corpus gastritis in patients with peptic ulcer disease. METHODS: We enrolled 287 patients, 173 with duodenal ulcer and 114 with gastric ulcer and 100 patients with H. pylori-positive gastritis as control subjects. Patients with peptic ulcer were classified according to whether or not they received famotidine-maintenance therapy (20 mg/day) after primary treatment. At the time of endoscopy, biopsy specimens were obtained from the antrum and the corpus. The degrees of neutrophil and lymphocyte infiltration, atrophy and intestinal metaplasia were scored according to the updated Sydney System. RESULTS: The degrees of neutrophil infiltration and atrophy in the corpus were significantly less in patients with gastric ulcer or duodenal ulcer than in patients with H. pylori-positive gastritis (P < 0.01). Differences in the degrees of neutrophil infiltration and atrophy in the corpus between the non-maintenance group and the maintenance group were not significant. CONCLUSION: Long-term therapy with famotidine does not appear to lead to an increase in the incidence of corpus gastritis or corpus atrophy in patients with peptic ulcer disease.

Adolescent↗
PubMed2005

Aberrantly differentiated cells in benign pilomatrixoma reflect the normal hair follicle: immunohistochemical analysis of Ca-binding S100A2, S100A3 and S100A6 proteins.

BACKGROUND: Pilomatrixoma is a common benign cutaneous tumour containing differentiated hair matrix cells. This tumour is mainly composed of basophilic, transitional, shadow and squamoid cells. Although some S100 proteins are expressed in a tissue-specific manner in the hair follicle (e.g. S100A2 in the outer root sheath, S100A3 in the cortex and cuticle, and S100A6 in the inner root sheath), little information is available concerning their distribution in the aberrantly differentiated tissues of pilomatrixoma. OBJECTIVES: To characterize the disordered epithelial elements of pilomatrixoma by localizing S100A2, S100A3 and S100A6 proteins. METHODS: Immunohistochemistry and dual-immunofluorescence microscopy were performed on 22 pilomatrixoma specimens using antibodies specific to the three proteins. RESULTS: Tissue-specific distribution of the S100 proteins investigated was preserved in the morphologically disordered tumour tissues. Anti-S100A2 antibody stained squamoid cells and putative outer root sheath cells; basophilic and potential hair matrix cells were occasionally stained. S100A3 staining was found in transitional cells and putative cortical cells, and was strong in both dispersed cells and hair-like structures surrounding cells which were presumably cuticular cells. Anti-S100A6 antibody labelled some S100A3-negative transitional cell strands, potentially inner root sheath cells. CONCLUSIONS: The epithelial elements of pilomatrixoma can be characterized using S100 proteins as biochemical markers. Our results show that pilomatrixomas retain a certain degree of differentiation indicative of distinct hair-forming cells.

Basophils↗
PubMed2005

A successfully treated case of mycetoma due to Nocardia veterana.

We report a successfully treated case of mycetoma from which an unusual Nocardia species was isolated. The isolate was identified as N. veterana by biochemical characterization and 16S ribosomal RNA gene sequencing, and it has not been previously reported as a causative agent of human mycetomas. Treatment with various antibiotics over 6 years and surgical resection failed to cure the disease. However, the combination of intravenous imipenem/cilastatin and amikacin along with oral clarithromycin and minocycline proved very effective in this case. This is the first case report of mycetoma due to N. veterana in a clinical setting.

Adult↗
PubMed2005

Netherton syndrome in two Japanese siblings with a novel mutation in the SPINK5 gene: immunohistochemical studies of LEKTI and other epidermal molecules.

BACKGROUND: Netherton syndrome (NS) is a severe autosomal recessive disorder characterized by ichthyosiform erythroderma, bamboo hair and atopy. The disease is caused by mutations in the SPINK5 gene, which encodes a putative serine protease inhibitor, LEKTI (lymphoepithelial Kazal-type-related inhibitor). Previous studies have clearly shown a crucial role for LEKTI in skin barrier formation. OBJECTIVES: To identify pathogenic mutations in two Japanese siblings with NS, and further to investigate the consequences of the mutations at the protein level. METHODS: To screen for mutations in the SPINK5 gene, all of its exons and splice junctions were amplified by polymerase chain reaction and directly sequenced. In addition, immunohistochemical staining of LEKTI, desmoglein (Dsg) 1 and elafin was performed with their specific antibodies. RESULTS: Mutation analysis resulted in the identification of compound heterozygous mutations, Q713X and R790X, in the SPINK5 gene of both patients. The former one is a novel mutation. Immunohistochemical studies in one patient demonstrated a complete absence of LEKTI and a strong expression of elafin in the patient's skin. Dsg1 was normally expressed in our patient. CONCLUSIONS: In this report, we describe compound heterozygous mutations in the SPINK5 gene in two Japanese siblings with NS. The result of immunohistochemistry shows LEKTI deficiency and upregulation of elafin in the skin of one patient. Furthermore, our data indicate that degradation of Dsg1 does not always occur in NS.

Carrier Proteins↗
PubMed2005

In vivo tumouricidal effects of LAD-1 monoclonal antibody on murine RL-male-1 lymphoma mediated by enhanced phagocytosis.

We have reported previously that the LAD-4 monoclonal antibody (mAb) directed against a fibronectin receptor (FNR) on RL-male-1 T lymphoma cells in BALB/c mice partially inhibited their migration to the liver. In the present study, we examined the mechanism by which another anti-FNR mAb, LAD-1, exerts its antitumourigenic effects. Administration of LAD-1 significantly prolonged survival of BALB/c mice challenged previously with RL-male-1 cells. LAD-1 enhanced phagocytosis of RL-male-1 cells by hepatic macrophages and clodronate-mediated macrophage depletion abrogated the antitumour activity of LAD-1. In vitro experiments revealed that a pan-caspase inhibitor, zVAD-fmk, did not affect the ability of LAD-1 to inhibit the proliferation of RL-male-1 cells. These data suggest that the antitumour effects of LAD-1 may be dependent on stimulation of tumour cell phagocytosis and are apoptosis-independent. Thus, LAD-1-induced phagocytosis of lymphoma cells by hepatic macrophages in mice may, at least in part, be responsible for the prolonged survival of the mice.

Animals↗
PubMed2005

Overexpression of Ets-1 proto-oncogene in latent and clinical prostatic carcinomas.

AIMS: The high incidence of clinically diagnosed prostatic cancer is exceeded by the frequency of tumours detected at autopsy. The Ets-1 proto-oncogene is expressed by a variety of malignant and normal tissues. Therefore, in this study, expression of Ets-1 protein was investigated in 'latent' prostatic cancer detected at autopsy, compared with benign prostatic hyperplasia, normal prostatic tissues and clinical prostatic cancer. METHODS AND RESULTS: Using immunohistochemistry, we analysed Ets-1 expression in 95 prostatic specimens including 19 cases of latent prostatic carcinoma (LPC) and 55 cases of clinical prostatic carcinoma (CPC), 11 cases of benign prostatic hyperplasia (BPH) and 10 cases of normal prostate (NP). Differences in the incidence of LPC and CPC suggest different courses for the biological progression of prostatic cancer. There was a significant difference in the degree of Ets-1 expression in CPC and LPC (P < 0.05). Ets-1 was not expressed in BPH and NP, but in malignant cases (57 of 74; 77.0%) commonly demonstrated immunoreactivity in the tumour cells. In our study the expression of Ets-1 between benign and malignant, and well, moderately and poorly differentiated adenocarcinomas of prostatic cancer showed significant differences. The presence of Ets-1 mRNA was confirmed by in-situ hybridization in human prostatic tissues. CONCLUSION: Our results suggest that Ets-1 might play an important role in carcinogenesis and/or the progression of human prostatic carcinomas.

Humans↗
PubMed2005

Cyclin D1 overexpression in thyroid papillary microcarcinoma: its association with tumour size and aberrant beta-catenin expression.

AIMS: Cyclin D1 is a target molecule transcriptionally activated by aberrant beta-catenin in Wnt signalling. Thyroid papillary microcarcinoma (PMC) may be considered a precursor of papillary thyroid cancer (PTC). Ki67 is widely used as a proliferation marker. The aim of this study was to determine whether cyclin D1 overexpression is involved in early thyroid carcinogenesis. METHODS AND RESULTS: Thirty-five cases of PMC were examined immunohistochemically, including 11 cases less than 5 mm (PMC < 5) and 24 cases more than 5 mm (PMC > 5), and 18 PTC cases (size 11-15 mm). Cyclin D1 expression was significantly lower in PMC < 5 than in PMC > 5, while there was no significant difference between PMC > 5 and PTC. Statistical analysis revealed significant correlations between cyclin D1 labelling index (LI) and Ki67 LI (P = 0.0272)/cytoplasmic beta-catenin expression (P < 0.001) in PMC and PTC. Four of five PMC > 5 cases with lymph node (LN) metastases displayed a high cyclin D1 LI and strong cytoplasmic beta-catenin expression. CONCLUSIONS: Cyclin D1 overexpression and correlation with aberrant beta-catenin expression were demonstrated in PMC. Cyclin D1 expression was significantly associated with tumour size and LN metastases in PMC. Cyclin D1 may be up-regulated at an early stage of thyroid carcinogenesis and promote tumour growth and metastatic potency in PMC through activation of the Wnt/beta-catenin pathway.

Adult↗
PubMed2005

Novel protein kinase C-beta isoform selective inhibitor JTT-010 ameliorates both hyper- and hypoalgesia in streptozotocin- induced diabetic rats.

AIM: Activation of protein kinase C (PKC) is thought to play an important role in the pathogenesis of diabetic microvascular complications. PKC-beta is elevated in hyperglycaemic conditions, both in vivo and in vitro. In this study, pharmacological effects of a novel PKC-beta isoform selective inhibitor, JTT-010 ((2R)-3-(2-aminomethyl-2,3-dihydro-1H-3a-azacyclopenta(a)inden-8-yl)-4-phenylaminopyrrole-2,5-dione monomethanesulphonate), on diabetic neuropathy were examined. METHODS: PKC inhibitory activity of JTT-010 was evaluated with an enzyme assay. For the in vivo study, streptozotocin (STZ)-induced diabetic rats were treated with JTT-010 for 12 weeks and tail/sciatic nerve conduction velocity (NCV) evaluated. Hyper/hypoalgesia was evaluated using tail-flick and formalin tests. RESULTS: JTT-010 inhibited PKC-betaI and -betaII with IC50 values of 4.0 and 2.3 nm respectively. For other PKC isoforms, IC50 values were 54 nm or greater. In STZ-induced diabetic rats showing a reduction in tail/sciatic nerve conduction velocities, JTT-010 (0.3-3 mg/kg) ameliorated the reduction of these velocities. In a formalin test, STZ-induced diabetic rats had hyperalgesia in the first phase. JTT-010 reduced nociceptive response at doses of 0.1 mg/kg or higher. Furthermore, STZ-induced diabetic rats showed hypoalgesia in the second phase of the formalin test and tail-flick test. JTT-010 also ameliorates these symptoms at doses of 0.1 mg/kg or higher. CONCLUSIONS: These observations suggest that PKC-beta contributes not only to diabetic hyperalgesia, but also to hypoalgesia and also contributes to defects in NCV. PKC-beta inhibitor, JTT-010, may be beneficial in suppressing the development of diabetic nerve dysfunction, including hyperalgesia and hypoalgesia.

Animals↗
PubMed2005

Characterization of an immortalized oviduct cell line from the cynomolgus monkey (Macaca fascicularis).

To establish reproductive biological techniques in mammals, it is important to understand the growth environment of the embryo. Oviduct epithelial cells are in close proximity to the embryo during pre-implantation development. We, therefore, established an immortalized oviduct epithelial cell line from the cynomolgus monkey, evaluated the usefulness of these cells as feeder cells for embryo culture, and investigated the gene expression of several growth factors and cytokines in the cells. The immortalized cells were positive for the anti-cytokeratin antibody, as determined by immunocytochemistry, indicating that they are epithelial. They also expressed oviductin, which is specific to oviduct epithelial cells, glyceraldehyde-3-phosphate dehydrogenase (control), leukemia inhibitory factor, vascular endothelial growth factor, epidermal growth factor, insulin-like growth factor 1, transforming growth factor beta-2, and interleukin 4. Mouse embryo development was improved when the immortalized cells were used as feeder cells. This cell line is also useful for studying the factors secreted by oviduct epithelial cells.

Animals↗
PubMed2005

The docking protein FRS2alpha is an essential component of multiple fibroblast growth factor responses during early mouse development.

The docking protein FRS2alpha is a major mediator of fibroblast growth factor (FGF) signaling. However, the physiological role of FRS2alpha in vivo remains unknown. In this report, we show that Frs2alpha-null mouse embryos have a defect in anterior-posterior (A-P) axis formation and are developmentally retarded, resulting in embryonic lethality by embryonic day 8. We demonstrate that FRS2alpha is essential for the maintenance of self-renewing trophoblast stem (TS) cells in response to FGF4 in the extraembryonic ectoderm (ExE) that gives rise to tissues of the placenta. By analyzing chimeric embryos, we found that FRS2alpha also plays a role in cell movement through the primitive streak during gastrulation. In addition, experiments are presented demonstrating that Bmp4 expression in TS cells is controlled by mitogen-activated protein kinase-dependent FGF4 stimulation. Moreover, both the expression of Bmp4 in ExE and activation of Smad1/5 in epiblasts are reduced in Frs2alpha-null embryos. These experiments underscore the critical role of FRS2alpha in mediating multiple processes during embryonic development and reveal a potential new link between FGF and Bmp4 signaling pathways in early embryogenesis.

Animals↗
PubMed2005

Loss of heterozygosity on chromosome 10p14-p15 in colorectal carcinoma.

High frequencies of loss of heterozygosity (LOH) on chromosome 10p14-p15 have been reported in various tumors, including gliomas, pulmonary carcinoid tumors and cervical, hepatic, prostatic and esophageal carcinomas. However, LOH on chromosome 10p14-p15 in colorectal tumors has not been reported. Therefore, we examined LOH on chromosome 10p14-p15 in 60 colorectal carcinomas (21 superficial and 39 advanced types) by microsatellite assay. Three microsatellite loci, D10S191 (10p14), D10S558 and D10S249 (10p15) were examined by polymerase chain reaction [early colorectal carcinomas, LOH of markers D10S191 (36%), D10S558 (7%) and D10S249 (11%), and in advanced colorectal carcinomas, LOH of markers D10S191 (20%), D10S558 (13%) and D10S249 (33%)]. There were no significant associations between LOH on chromosome 10p14-p15 and clinicopathologic features, including patient age, sex, tumor location, depth of invasion, histologic type, lymph node metastasis and prognosis. These data suggest that a putative tumor suppressor gene associated with colorectal carcinogenesis may be located on chromosome 10p14-p15 and that alteration of this gene may be involved in the development but not progression of colorectal tumors.

Aged↗
PubMed2005

Ultrasound evaluation of the fibrosis stage in chronic liver disease by the simultaneous use of low and high frequency probes.

A liver biopsy is currently considered the definitive diagnostic modality for establishing the severity of hepatic fibrosis. We analysed the diagnostic sensitivity and accuracy of ultrasound (US) using both low frequency and high frequency probes as a repeatable, inexpensive, and reliable method to determine the fibrosis stage in chronic liver disease and then compared our results with the histological findings. A total of 103 patients with chronic liver disease (60 males and 43 females, average age 51 years old) who had undergone both a liver biopsy and US with 2-5 MHz frequency and 5-12 MHz frequency probes were prospectively evaluated in this study. An US scoring system using both the low frequency and high frequency probes was performed by evaluating the edge, surface and parenchymal texture of the liver. Each score was obtained by evaluating three parameters; the bluntness of the liver edge, the irregularity of the surface and the coarseness of the parenchymal texture were evaluated and then compared with the histological findings. The US scores of the liver edge (rs: 0.6668), liver surface (rs: 0.9007) and liver parenchymal texture (rs: 0.8853) correlated significantly with the fibrosis stage obtained based on the biopsy findings. The accumulated US scores of these three parameters, however, was found to be the most reliable indicator (rs: 0.9524). Patients with an accumulated score of 6.5 or more were all found to have fibrosis stage 4 in which the accuracy of our scoring system for correctly predicting cirrhosis was found to be 100% sensitive. When an accumulated US score of 3 was interpreted to indicate mild fibrosis (a fibrosis score of 0 or 1), all 42 patients with stage 0 or 1 fibrosis were found to have an accumulated US score of 3 or less (a probability of 100%) and 42 of 53 patients with a score of 3 or less were found to have stage 0 or 1 fibrosis (specificity of 79.2%). An ultrasound evaluation of the liver fibrosis stage based on the scoring system using both low and high frequency probes was found to be a reliable and effective alternative to the histological staging in chronic liver diseases.

Biopsy↗