PubMed Health⌕ Search

Biomedical subjects

Junichi Iwamoto

Publications and source records attributed to Junichi Iwamoto.

7 recordsLinked to original sources
PubMed2006

Involvement of cyclooxygenase-2--prostaglandin E2 pathway in interleukin-8 production in gastric cancer cells.

Prostaglandin E(2) (PGE(2)) is thought to play an important role in both inflammatory and anti-inflammatory effects. The effect of PGE(2) on the proinflammatory chemokine interleukin-8 (IL-8) in the gastric epithelial cells has not been defined yet. A gastric cancer cell line (MKN45) and primary gastric fibroblasts were cocultured with Helicobacter pylori standard strain (NCTC11637). The expressions of IL-8 and cyclooxygenase 2 (COX-2) mRNA were examined by reverse transcription polymerase chain reaction (RT-PCR) amplification. The amount of IL-8 antigen secreted by the MKN45 cells and gastric fibroblasts was measured by enzyme-linked immunosorbent assay (ELISA). We examined the effects of H pylori stimulation on IL-8 and COX-2 expression levels and the effects of COX-2 inhibitor on H pylori-induced IL-8 production in the MKN45 cells and gastric fibroblasts. Furthermore, we examined the expressions of subtypes of PGE(2) receptors, the effects of arachidonic acid and PGE(2) on IL-8 production, and the effects of PGE(2) on the total cellular cyclic adenosine monophosphate (cAMP) in MKN45 cells. MKN45 cells and gastric fibroblasts expressed IL-8 and COX-2 mRNA under stimulation with H pylori. The MKN45 cells produced IL-8 and PGE(2) antigen into the culture medium with H pylori stimulation, and the production level of IL-8 and PGE(2) antigen decreased significantly with COX-2 inhibitor pretreatment (concentration: 50 muM). On the other hand, the gastric fibroblasts strongly produced IL-8 antigen even in the unstimulated condition, and the amount of IL-8 antigen was not affected by H pylori stimulation and/or COX-2 inhibitor pretreatment. The MKN45 cells expressed IL-8 mRNA and released IL-8 antigen slightly, and the expression level of IL-8 mRNA and the amount of IL-8 antigen increased significantly with PGE(2) treatment in a dose-dependent manner. PGE(2)-induced IL-8 production was inhibited by pretreatment with EP2 and EP4 antagonists. The MKN45 cells expressed EP2 and EP4 subtypes of PGE(2) receptors, and these expression levels were not affected by H pylori stimulation or PGE(2) treatment. The amount of IL-8 antigen increased slightly, but not significantly, with arachidonic acid treatment. PGE(2) treatment for 15 minutes increased the total cellular cAMP in the MKN45 cells. These results suggest that the COX-2-PGE(2) pathway may be involved in IL-8 production in gastric epithelial cells.

Adenocarcinoma↗
PubMed2006

A mobile phone-based ECG monitoring system.

We have developed a telemedicine system for monitoring a patient's electrocardiogram during daily activities. The recording system consists of three ECG chest electrodes, a variable gain instrumentation amplifier, a low power 8-bit single-chip microcomputer, a 256 KB EEPROM and a 2.4 GHz low transmitting power mobile phone (PHS). The complete system is mounted on a single, lightweight, chest electrode array. When a heart discomfort is felt, the patient pushes the data transmission switch on the recording system. The system sends the recorded ECG waveforms of the two prior minutes and ECG waveforms of the two minutes after the switch is pressed, directly in the hospital server computer via the PHS. The server computer sends the data to the physician on call. The data is displayed on the doctor's Java mobile phone LCD (Liquid Crystal Display), so he or she can monitor the ECG regardless of their location. The developed ECG monitoring system is not only applicable to at-home patients, but should also be useful for monitoring hospital patients.

Amplifiers, Electronic↗
PubMed2005

Expressions of urokinase-type plasminogen activator, its receptor and plasminogen activator inhibitor-1 in gastric cancer cells and effects of Helicobacter pylori.

OBJECTIVE: Destruction of the extracellular matrix is essential for tumor invasion and metastasis. The relationship between Helicobacter pylori (H. pylori) infection and destruction of the extracellular matrix is not yet clear. Urokinase-type plasminogen activator (uPA) plays an important role in the destruction of the extracellular matrix and basement membrane. Urokinase-type plasminogen activator receptor (uPAR) and plasminogen activator inhibitor-1(PAI-1) appear to be associated with these processes. To clarify the role of H. pylori infection in the processes of destruction of the extracellular matrix and basement membrane in cancerous tissue, the effect of H. pylori on the expressions of uPA, uPAR and PAI-1 in cancer cells was investigated. MATERIALS AND METHODS: Gastric cancer cell lines (MKN45, KATO-III) were co-cultured with H. pylori standard strain (NCTC11637), cagA-negative strain and clinical isolated strain. The specific inductions of uPA, uPAR and PAI-1 mRNA were examined by reverse transcription-polymerase chain reaction (RT-PCR) amplification. The secreted uPA antigen was measured by enzyme-linked immunosorbent assay (ELISA). To evaluate the role of transcription factor NF-kappaB in uPA and uPAR gene transcription with H. pylori stimulation, the effect of NF-kappaB inhibitor MG132 on H. pylori-induced uPA and uPAR mRNA expression was examined. RESULTS: The expressions of both uPA and uPAR mRNAs in the gastric cancer cell lines (MKN45 and KATO- III) were increased markedly (uPA mRNA; MKN45: 12-fold, KATO-III: 5-fold) (uPAR mRNA; MKN45: 3-fold, KATO-III: 3-fold) with H. pylori NCTC11637 strain stimulation, whereas the expression levels of uPA and uPAR mRNA did not increase with cagA-negative strain stimulation. These cancer cell lines slightly secreted uPA antigen into the culture medium, and the amount of uPA antigen increased dramatically by stimulation with H. pylori NCTC11637 and cagA-positive clinical isolated strains. These gastric cancer cell lines also slightly secreted PAI-1 antigen into the culture medium, and the amount of PAI-1 antigen was not affected by H. pylori NCTC11637 stimulation. H. pylori-induced uPA and uPAR mRNA expressions were strongly down-regulated by pretreatment with MG132 in both cell lines. CONCLUSIONS: The results of this study indicated the possibility that cagA-positive H. pylori may play an important role not only in tissue remodeling, angiogenesis and wound healing but also in the process of degradation of the extracellular matrix breakdown, tumor invasion and metastasis by inducing uPA and uPAR complex in the gastric cancer cells.

Base Sequence↗
PubMed2005

A motion control function evaluation system employing a pen tablet.

We have developed a new pen tablet based system for evaluation of hand motion control function as influenced by brain disease. The system consists of a laptop computer and a pen tablet data entry device. The pen tablet is placed in front of the subject who is instructed to tap the pen at a constant location. When the subject taps the pen, the tablet transfers the pen position to the laptop computer. The computer then saves the tap position, along with the time elapsed between each tap. The subject is instructed to tap 50 times with each hand with the eyes closed. The absolute distance moved between each two successive tap positions is detected. Tapping period, total tapping time and total distance moved are also calculated. Measurements were performed on ten normal subjects and three subjects with cerebral infarction. The results indicate that cerebral infarction subjects' average total tap point distance moved and absolute distance moved are greater than in the normal subjects. Conversely, all subjects in both groups produced only normal variations in tapping period and total tapping time. Our system can therefore quantitatively evaluate hand motion control function by the total and absolute distance moved.

Adult↗
PubMed2003

Expression of urokinase-type plasminogen activator and its receptor in gastric fibroblasts and effects of nonsteroidal antiinflammatory drugs and prostaglandin.

In acute inflammatory condition, little is known about the expression of the urokinase-type plasminogen activator (uPA) and its receptor (uPAR) in the gastric fibroblasts. To clarify the role of human gastric fibroblasts in acute inflammatory conditions such as gastric ulcer, the effects of interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha on the expression of uPA and uPAR, which were suggested to be associated with tissue remodeling, in gastric fibroblasts were investigated. The expression level of uPA mRNA and the amount of uPA antigen increased significantly on treatment with each concentration of IL-1beta (1 and 10 ng/ml) and 10 ng/ml TNF-alpha. On the other hand, the amounts of uPA antigen on cell surfaces were not affected significantly by IL-1beta and TNF-alpha stimulation. The expression level of uPAR mRNA increased in a dose-dependent manner on IL-1beta stimulation. The effect of indomethacin on uPA and uPAR expression in these cells was also examined. When gastric fibroblasts were treated with 50 microM indomethacin, the expression level of uPA mRNA decreased significantly, and the amount of uPA antigen in the culture medium and on cell surfaces decreased significantly with indomethacin in a dose-dependent manner. The increased uPAR mRNA expression caused by IL-1beta was reduced to the basal level by treatment with 50 microM indomethacin. Furthermore, we investigated the role of prostaglandin E2 (PGE2), which is suggested to play major roles in acute inflammation of the stomatch, on uPA and uPAR expression in gastric fibroblasts. The expression level of uPAR mRNA and the amount of uPA antigen on cell surfaces increased in a dose-dependent manner on treatment with PGE2 (10 and 50 ng/ml). These results suggest that uPA and uPAR expression in gastric fibroblasts is involved in the regulating system of PGE2 and that NSAIDs may delay healing of gastric mucosal injury in part through suppressing uPA production via inhibition of endogenous PG production.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2002

Mannose-binding lectin and the prognosis of fulminant hepatic failure caused by HBV infection.

BACKGROUND/AIMS: The mannose-binding lectin (MBL) gene was reported to play an important role in determining the clinical outcome of persistent hepatitis B virus (HBV) infection. We investigated serum MBL concentrations and MBL gene mutations to determine whether they were related to the prognosis of patients with fulminant hepatic failure (FHF) caused by HBV infection. METHODS: We investigated serum MBL concentrations and MBL gene mutations in 43 HBV-infected Japanese patients with FHF and 260 HBsAg-negative healthy controls. Serum MBL concentrations were measured by an enzyme-linked immunosorbent assay, and mutations in the MBL gene were analysed by nested PCR and direct DNA sequencing. RESULTS: Only a mutation in codon 54 of the MBL gene was found. The frequency of this mutation in nonsurvivors (40%, 8/20) was higher than in survivors (13%, 3/23), and the difference was slightly significant (p = 0.043). The H allele frequency in survivors (70.5%, 31/44) was higher than in nonsurvivors (39.5%, 15/38) (p = 0.0048). Because of these factors the mean serum MBL concentration in survivors, 1.61 ,micro/ml (range 0.3-3.86), was significantly higher than in nonsurvivors, 0.79 microg/ml (range 0.04-1.51) (p < 0.0001). The likelihood ratio for nonsurvival was 0 for over 2.0 microg/ml, 0.67 for 1.0-2.0 microg/ml, and 2.24 for 0-1.0 microg/ml. CONCLUSIONS: The mutation in codon 54 of the MBL gene tended to be higher in nonsurvivors than in survivors. The H allele frequency (high producing allele in H/Y) in survivors was higher than that in nonsurvivors. High levels of serum MBL correlated with the survival of patients with FHF due to HBV infection. Serum MBL may be useful as a predictive factor for the survival of patients with FHF caused by HBV.

Adult↗