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Hiroaki Satoh

Publications and source records attributed to Hiroaki Satoh.

At least 19 recordsLinked to original sources
PubMed2007

Sleep stage determines the expression pattern of sleep apneas.

We report on an obese man with sleep stage-dependent apnea. His type of apnea was predominantly central during non-rapid eye movement (NREM) sleep, while it was obstructive during rapid eye movement (REM) sleep. We found significantly more and more severe apneas during REM sleep compared to NREM sleep. His apneas were remarkably reduced by position adjustment, suggesting that upper airway collapse played a key role in the induction of both types of apnea. As his apneic patterns were dependent on the sleep stages, we assumed that the balance between upper airway obstruction and instability of central respiratory control might be important in determining the expression types.

Adult↗
PubMed2007

Thymic and pulmonary mucosa-associated lymphoid tissue lymphomas in a patient with Sjögren's syndrome and literature review.

Mucosa-associated lymphoid tissue lymphoma (MALToma) has been reported in several organs. Among MALTomas, thymic and pulmonary MALTomas are rare. The present report describes a patient with Sjögren's syndrome who presented thymic and pulmonary MALTomas. Although the exact pathogenetic relationship between these two tumours is uncertain, it is likely that the underlying immune dysregulation related to Sjögren's syndrome contributed to the occurrence and the unusual manifestation of MALTomas in this patient.

Adult↗
PubMed2006

Small intestinal metastasis from small cell lung cancer.

A 71-year-old man who had small cell lung cancer was referred to our institution. Before starting chemotherapy, anemia progressed and stool examination was positive for occult blood. An abdominal computed tomography scan with contrast medium enhancement of the gastrointestinal tract disclosed a small intestinal tumor. Histological examination after the surgery confirmed that the tumor was metastasis of lung cancer. The patient survived for 3 years after the resection. Although clinically apparent metastases of lung cancer to the small intestine are rare and are reported to have a poor prognosis, early detection and intervention might enhance the chance of survival.

Aged↗
PubMed2006

Differential effects of apolipoprotein E isoforms on lipolysis of very low-density lipoprotein triglycerides.

Apolipoprotein (apo) E plays a key role in lipoprotein metabolism and has been proposed to modulate triglyceride (TG) lipolysis. However, no systematic investigation on lipolysis using all 3 isoforms of apoE has been performed. To clarify the role of common human apoE isoforms in the lipolysis of very low-density lipoprotein (VLDL) TGs, we overexpressed human apoE isoforms in apoE and low-density lipoprotein receptor-deficient mice using adenoviral-mediated gene transfer and used VLDL particles obtained from these mice for in vitro lipolysis assay. Overexpression of apoE, regardless of its isoforms, increased the TG content of VLDL in mice in vivo. In vitro analysis of the effect of apoE on lipolysis revealed that irrespective of its isoforms, apoE did inhibit TG lipolysis at every concentration of apoE examined, and this inhibitory effect became more pronounced as the apoE content of VLDL increased. No difference was observed in TG lipolysis activity among isoforms at low apoE/TG ratio; however, intermediate ratios of apoE/TG, which reflect physiologic VLDL apoE/TG ratios, demonstrated a significantly greater level of lipolysis inhibition in apoE2, but less so in apoE4 compared with other isoforms. This differential effect by apoE isoforms on lipolysis was attenuated at higher apoE/TG ratios; nevertheless, apoE2 still inhibited lipolysis significantly more than did apoE4. Enrichment of VLDL with apoE decreased both the apoC contents and apoC-II/C-III ratios of VLDL, contributing, at least in part, to the inhibitory function of apoE on lipolysis. The present study clarifies the differential lipolysis-modulating effect of apoE isoforms, which would help explain the difference in pre- and postprandial TG levels among humans carrying different apoE isoforms.

Adenoviridae↗
PubMed2006

Prospective study of fever and pneumonia after flexible fiberoptic bronchoscopy in older people.

OBJECTIVES: To assess the frequency of fever and pneumonia after fiberoptic bronchoscopy (FOB) in older people and to evaluate increased risk for these two adverse events with increasing age. DESIGN: Prospective study. SETTING: University hospital system. PARTICIPANTS: Three hundred fifty-eight patients, with 165 (46.1%) patients aged 70 and older, undergoing bronchoscopy. MEASUREMENTS: Indications, abnormal bronchoscopic findings, sampling procedures, final diagnosis, and fever and pneumonia after bronchoscopy. RESULTS: With regard to the indication for bronchoscopy and abnormal bronchoscopic findings, there was no statistical difference between elderly patients (> or =70) and younger patients (<70). Procedures such as forceps biopsy, brushing, and curetting were not performed more often in elderly patients, although final diagnosis of lung cancer was significantly more common in the elderly group (P=.002). The overall incidence of fever after FOB was 6.7%, and that of pneumonia after FOB was 5.6%. The patients aged 70 and older had an incidence of fever after FOB of 3.6% and an incidence of pneumonia of 4.2%, which were not higher than those in patients younger than 70. CONCLUSION: Increasing age is not associated with increasing fever and pneumonia after FOB, and chronological age should not be considered a limiting factor in the decision of whether to perform FOB when it is clinically indicated.

Adult↗
PubMed2006

Simultaneous measurements of KL-6 and SP-D in patients undergoing thoracic radiotherapy.

PURPOSE: Radiation pneumonitis (RP) is a serious complication in patients undergoing thoracic radiotherapy (TRT). Serum KL-6 and SP-D have been shown to increase in several kinds of interstitial pneumonia. To evaluate their clinical usefulness in detecting RP, we serially measured them in patients receiving TRT. MATERIALS AND METHODS: Thirty-nine patients, who received TRT for lung cancer between July 1999 and April 2004, were prospectively studied. Serum levels of KL-6 and SP-D were measured using enzyme-linked immunosorbent assays. Patients were followed up until August 2004 or their deaths. RESULTS: During the period, RP occurred in 19 patients. In five patients with diffuse RP extended outside the radiation field, serum KL-6 levels increased, reaching more than 1,000 U/mL. Serum KL-6 levels at 40 Gy in patients who developed RP were higher than those without it (p = 0.0363, Mann-Whitney U test). In addition, serum KL-6 levels at 40 Gy in patients who developed RP were higher than those of pretreatment (p = 0.0126, Wilcoxon signed rank test). On the other hand, there were no statistical differences between sp-d at 40 Gy and those before TRT (P = 0.1165). CONCLUSIONS: Increased KL-6 at 40 Gy compared with those before treatment in patients undergoing TRT may be of clinical significance. KL-6 proved to be a useful indicator for estimating RP, while usefulness of SP-D was not confirmed in this study.

Aged↗
PubMed2006

Alternative lengthening of telomeres in the human adrenocortical carcinoma cell line H295R.

Telomere maintenance can occur in the absence of telomerase by a mechanism referred to as alternative lengthening of telomeres (ALT). ALT is considered to be rare in tumors of epithelial origin. The biological significance and molecular mechanism of ALT have not been well studied in human cancers. It has been reported that clinical samples of adrenocortical carcinoma show a low incidence of telomerase positivity. We characterized an adrenocortical carcinoma cell line, H295R, focusing on the telomere maintenance mechanism, and compared it with telomerase-positive 293 cells and HeLa cells. Telomerase activity could not be detected in H295R cells by the TRAP assay. Among the essential components of the telomerase holoenzyme, only hTERT expression was undetectable by RT-PCR, indicating that the lack of telomerase activity is due to suppression of hTERT. H295R cells had long and heterogeneous telomere DNA, and FISH revealed large nuclear bodies in a few interphase nuclei, which presumably represented ALT-associated PML bodies. These results suggest that H295R cells have the ALT phenotype. Several proteins that are possibly associated with the telomere maintenance mechanism were examined. TRF1 and TRF2 were expressed in H295R cells as well as in 293 cells and HeLa cells. The ratio of hnRNP B1 to A2 was higher in H295R cells than in 293 cells and HeLa cells. In conclusion, the H295R adrenocortical carcinoma cell line is negative for telomerase and maintains its telomeres by the ALT mechanism. We anticipate that H295R cells will be a good model for understanding the significance and mechanism of ALT in human cancers.

Adrenal Cortex Neoplasms↗
PubMed2005

JNK and tumor necrosis factor-alpha mediate free fatty acid-induced insulin resistance in 3T3-L1 adipocytes.

Lipid infusion and high fat feeding are established causes of systemic and adipose tissue insulin resistance. In this study, we treated 3T3-L1 adipocytes with a mixture of free fatty acids (FFAs) to investigate the molecular mechanisms underlying fat-induced insulin resistance. FFA treatment impaired insulin receptor-mediated signal transduction and decreased insulin-stimulated GLUT4 translocation and glucose transport. FFAs activated the stress/inflammatory kinases c-Jun N-terminal kinase (JNK) and IKKbeta, and the suppressor of cytokine signaling protein 3, increased secretion of the inflammatory cytokine tumor necrosis factor (TNF)-alpha, and decreased secretion of adiponectin into the medium. RNA interference-mediated down-regulation of JNK blocked JNK activation and prevented most of the FFA-induced defects in insulin action. Blockade of TNF-alpha signaling with neutralizing antibodies to TNF-alpha or its receptors or with a dominant negative TNF-alpha peptide had a partial effect to inhibit FFA-induced cellular insulin resistance. We found that JNK activation by FFAs was not inhibited by blocking TNF-alpha signaling, whereas the FFA-induced increase in TNF-alpha secretion was inhibited by RNA interference-mediated JNK knockdown. Together, these results indicate that 1) JNK can be activated by FFAs through TNF-alpha-independent mechanisms, 2) activated JNK is a major contributor to FFA-induced cellular insulin resistance, and 3) TNF-alpha is an autocrine/paracrine downstream effector of activated JNK that can also mediate insulin resistance.

3T3-L1 Cells↗
PubMed2005

G protein-coupled receptor kinase 2 mediates endothelin-1-induced insulin resistance via the inhibition of both Galphaq/11 and insulin receptor substrate-1 pathways in 3T3-L1 adipocytes.

G protein-coupled receptor kinases (GRKs) regulate seven-transmembrane receptors (7TMRs) by phosphorylating agonist-activated 7TMRs. Recently, we have reported that GRK2 can function as a negative regulator of insulin action by interfering with G protein-q/11 alpha-subunit (Galphaq/11) signaling, causing decreased glucose transporter 4 (GLUT4) translocation. We have also reported that chronic endothelin-1 (ET-1) treatment leads to heterologous desensitization of insulin signaling with decreased tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and Galphaq/11, and decreased insulin-stimulated glucose transport in 3T3-L1 adipocytes. In the current study, we have investigated the role of GRK2 in chronic ET-1-induced insulin resistance. Insulin-induced GLUT4 translocation was inhibited by pretreatment with ET-1 for 24 h, and we found that this inhibitory effect was rescued by microinjection of anti-GRK2 antibody or GRK2 short interfering RNA. We further found that GRK2 mediates the inhibitory effects of ET-1 by two distinct mechanisms. Firstly, adenovirus-mediated overexpression of either wild-type (WT)- or kinase-deficient (KD)-GRK2 inhibited Galphaq/11 signaling, including tyrosine phosphorylation of Galphaq/11 and cdc42-associated phosphatidylinositol 3-kinase activity. Secondly, ET-1 treatment caused Ser/Thr phosphorylation of IRS-1 and IRS-1 protein degradation. Overexpression of KD-GRK2, but not WT-GRK2, inhibited ET-1-induced serine 612 phosphorylation of IRS-1 and restored activation of this pathway. Taken together, these results suggest that GRK2 mediates ET-1-induced insulin resistance by 1) inhibition of Galphaq/11 activation, and this effect is independent of GRK2 kinase activity, and 2) GRK2 kinase activity-mediated IRS-1 serine phosphorylation and degradation.

3T3-L1 Cells↗
PubMed2005

Increased serum levels of endostatin in patients with idiopathic pulmonary fibrosis.

Endostatin is an angiogenesis inhibitor that is an endogenously produced proteolytic fragment of type XVIII collagen. Serum levels of endostatin have been studied extensively in patients with malignant diseases. Recently, elevated serum endostatin levels were observed in patients with systemic sclerosis accompanying pulmonary fibrosis. To determine whether elevated serum endostatin can be observed in patients with idiopathic pulmonary fibrosis (IPF), we measured serum levels of endostatin in 69 patients with benign respiratory disease using an ELISA kit. The median of the serum endostatin levels in these patients was 50.8 pg/mL. Seven of 11 patients (63.6%) with collagen disease-associated pulmonary fibrosis (CDPF), and 19 of 24 patients (79.2%) with IPF had higher serum endostatin levels than the median level of the 69 patients. There was no statistical difference in serum endostatin levels between the patients with IPF and those with CDPF (P=0.7898). Serum endostatin levels in 24 patients with IPF were significantly higher than those in 34 patients with respiratory diseases other than IPF and CDPF (P=0.0001). Elevated serum levels of endostatin were observed in patients with IPF. Although the mechanisms are unclear, elevated serum levels of endostatin may be related to the fibrosing process in the lung.

Adult↗