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Volume 235 (2015)
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Volume 235, Issue 3
March
Displaying 1-10 of 10 articles from this issue
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Regular Contribution
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Xiuling Zhang, Ping Li, Minhua Rong, Rongquan He, Xinxi Hou, You Xie, ...Article type: Regular Contribution
2015 Volume 235 Issue 3 Pages 161-169
Published: 2015
Released on J-STAGE: February 28, 2015
JOURNAL FREE ACCESS FULL-TEXT HTMLLung cancer is the most common malignant tumor worldwide. MicroRNA has become an ideal biomarker for cancer diagnosis, prognosis and therapy. The relationship between microRNA-141 and non-small cell lung cancer (NSCLC) is contradictory. Thus, in current study, we aimed to investigate the level of microRNA-141 in NSCLC tissues and to evaluate its potential clinical value. This study enrolled 125 NSCLC patients (75 males and 50 females) with a median age of 61 years (range, 23-90 years). NSCLC patients included 23 squamous cell carcinomas (SCCs), 101 adenocarcinomas (ADCs) and 1 large cell carcinoma. The expression level of microRNA-141 was significantly higher in NSCLC tissues than in adjacent lung tissues (P < 0.001), detected by real time RT-PCR. Receiver operating characteristic (ROC) exhibited a moderate diagnostic value of microRNA-141 for NSCLC with the area under curve of 0.707. The microRNA-141 expression increased with the larger tumor size (P = 0.002), lymph node metastasis (P = 0.018) and advanced stage (P = 0.022) in NSCLC patients. For subgroup analysis, microRNA-141 expression in SCC was correlated with tumor size (r = 0.490, P = 0.018), and in ADC, microRNA-141 level was positively associated with tumor size (r = 0.222, P = 0.026), lymph node metastasis (r = 0.242, P = 0.015) and TNM stage (r = 0.210, P = 0.035). Furthermore, univariate analysis revealed that the expression of microRNA-141 was an independent prognostic indicator of ADC. In conclusion, microRNA-141 is a potential biomarker for the molecular diagnosis and risk stratification of NSCLC.View full abstractDownload PDF (898K) Full view HTML -
Kazuki Noda, Shigeo Godo, Hiroki Saito, Masato Tsutsui, Hiroaki Shimok ...Article type: Regular Contribution
2015 Volume 235 Issue 3 Pages 171-183
Published: 2015
Released on J-STAGE: March 03, 2015
JOURNAL FREE ACCESS FULL-TEXT HTMLDyslipidemia is a life-style disorder and is one of the important risk factors of cardiovascular diseases. Nitric oxide (NO) exerts beneficial effects on lipid metabolism through activation of hepatic sterol regulatory element-binding protein (SREBP)-2, a transcriptional factor for cholesterol metabolism and expression of LDL receptor, while Rho-kinase, an effecter protein of small G protein, RhoA, contributes to the pathogenesis of metabolic syndrome through suppressing the whole body energy consumption. However, the crosstalk between NO and Rho-kinase in regulation of lipid metabolism remains to be elucidated. In the present study, we used male wild-type (WT) mice and mice lacking three isoforms of NO synthase (NOSs−/−). WT mice were fed either normal diet (ND) or high-fat diet (HFD), while NOSs−/− mice were fed ND with or without a selective Rho-kinase inhibitor, fasudil (100 mg/kg/day), for 6 weeks. At 6 weeks, plasma NOx concentration was significantly decreased and Rho-kinase activity and lipid levels were significantly elevated in HFD-fed WT mice and NOSs−/− mice compared with ND-fed WT mice. In the liver, SREBP-2 activity was reduced in NOSs−/− mice. Fasudil ameliorated lipid levels in HFD-fed WT mice and NOSs−/− mice without affecting SREBP-2 activity or LDL receptor expression, whereas it significantly enhanced phosphorylation of AMP-activated kinase (AMPK) in the liver and skeletal muscle. Importantly, the beneficial metabolic effects of fasudil were absent in HFD-fed AMPK−/− mice. These results provide the first evidence that NO and Rho-kinase play opposing roles for the lipid metabolism, suggesting that Rho-kinase inhibitors could be novel therapeutic agents of dyslipidemia.View full abstractDownload PDF (3022K) Full view HTML -
Yohei Ozawa, Yasuhiro Nakamura, Fumiyoshi Fujishima, Saulo J.A. Felizo ...Article type: Regular Contribution
2015 Volume 235 Issue 3 Pages 185-191
Published: 2015
Released on J-STAGE: March 06, 2015
JOURNAL FREE ACCESS FULL-TEXT HTMLThe clinical outcome for esophageal squamous cell carcinoma (ESCC) patients is often poor because of the invasive nature of this tumor type. AT-rich interactive domain 1A (ARID1A) functions as a tumor suppressor, and its gene mutation has been reported in various human malignancies. ARID1A is a non-catalytic subunit of the SWItch/Sucrose Non Fermentable (SWI/SNF) chromatin-remodeling complex that regulates gene transcription. Decreased expression of ARID1A protein has been reported to decrease the expression of E-cadherin, an adhesion protein. However, the correlation between ARID1A and E-cadherin expression status in ESCC remains largely unknown. To address this issue, we examined the expression of ARID1A and E-cadherin in tumor specimens excised from 83 ESCC patients using immunohistochemical analysis. The intensity of the ARID1A immunoreactivity was significantly lower in tumors with a growth pattern characterized by ill-defined borders than that in tumors with an expansive growth pattern having a well-demarcated border or tumors with an intermediate growth pattern. Thus, decreased ARID1A immunoreactivity correlated with infiltrative growth of ESCC. In contrast, E-cadherin status did not correlate with the infiltrative growth pattern of ESCC. Moreover, ARID1A expression status did not significantly correlate with any of other clinicopathological factors, E-cadherin expression levels, or the clinical outcome of the patients. On the other hand, the patients with tumors expressing low levels of E-cadherin exhibited significantly lower survival rates than those with high expression. In conclusion, reduced ARID1A expression in tumor tissues contributes to infiltrative growth of ESCC, irrespective of E-cadherin expression levels.View full abstractDownload PDF (1405K) Full view HTML -
Ate Dijkstra, Gülendam Hakverdioğlu, Marta Muszalik, Richtsje Andela, ...Article type: Regular Contribution
2015 Volume 235 Issue 3 Pages 193-200
Published: 2015
Released on J-STAGE: March 05, 2015
JOURNAL FREE ACCESS FULL-TEXT HTMLMany countries in Europe and the world have to cope with an aging population. Although health policy in many countries aims at increasing disability-free life expectancy, elderly patients represent a significant proportion of all patients admitted to different hospital departments. The aim of the research was to investigate the relationship between health-related quality of life (HRQOL) and the care dependency status among elderly hospital patients. In 2012, a descriptive survey was administered to a convenience sample of 325 elderly hospital patients (> 60 years) from The Netherlands (N = 125), from Poland (N = 100), and from Turkey (N = 100). We employed the Functional Assessment of Chronic Illness Therapy (FACIT) Measurement System and the Care Dependency Scale. FACIT is a collection of HRQOL questionnaires that assess multidimensional health status in people with various chronic illnesses. From demographic variables, gender (female) (r = −0.13, p < 0.05), age and informal care given by family members (r = −0.27 to 0.27, p < 0.01) were significantly correlated with the care dependency status for the whole samples. All HRQOL variables, hearing aid and duration of illness correlated with care dependency status (r = −0.20 to 0.50, p < 0.01). Moreover, the FACIT sum score (Poland and Turkey) and functional wellbeing (The Netherlands) are significantly associated with the decrease in care dependency status. Thus, the FACIT variables are the most powerful indicators for care dependency. The study provides healthcare professionals insight into improvement of quality of care in all three countries.View full abstractDownload PDF (812K) Full view HTML -
Qin Liu, Zhenhui Lu, Huayu Wu, Li ZhengArticle type: Regular Contribution
2015 Volume 235 Issue 3 Pages 201-213
Published: 2015
Released on J-STAGE: March 10, 2015
JOURNAL FREE ACCESS FULL-TEXT HTMLArticular cartilage is characterized by the lack of blood vessels and has a poor self-healing potential. Limited cell numbers and dedifferentiation of chondrocytes when expanded in vitro are the major obstacles of autologous chondrocyte implantation. Autologous chondrocyte implantation is a cell-based treatment that can be used as a second-line measure to regenerate chondral or osteochondral defects in younger, active patients. There is an urgent need to find an effective chondrogenic protection agent alleviating or inhibiting chondrocyte dedifferentiation. In this study, we explored the effect of taurine (2-aminoethane sulfonic acid) on proliferation and phenotype maintenance of human articular chondrocytes by analyzing the cell proliferation, morphology, viability, and expression of cartilage specific mRNAs and proteins. Primary chondrocytes were isolated from human articular cartilage tissues. Results showed that taurine effectively promoted chondrocyte growth and enhanced accumulation of glycosaminoglycans and collagens in the conditioned media of chondrocytes. Moreover, taurine exposure caused significant increases in the relative expression levels of mRNAs for cartilage specific markers, including aggrecan, collagen type II and SOX9. Aggrecan is a cartilage-specific proteoglycan, and SOX9 is a chondrogenic transcription factor. In contrast, the mRNA expression of collagen type I, a marker for chondrocyte dedifferentiation, was significantly decreased in cells treated with taurine, indicating that taurine inhibits the chondrocyte dedifferentiation. This study reveals that taurine is effective in proliferation promotion and phenotype maintenance of chondrocytes. Thus, taurine may be a useful pro-chondrogenic agent for autologous chondrocyte implantation in the treatment of cartilage repair.View full abstractDownload PDF (4375K) Full view HTML -
Masatsugu Orui, Yasuhiro Sato, Kanako Tazaki, Ikuko Kawamura, Shuichir ...Article type: Regular Contribution
2015 Volume 235 Issue 3 Pages 215-222
Published: 2015
Released on J-STAGE: March 11, 2015
JOURNAL FREE ACCESS FULL-TEXT HTMLDevastating natural disasters and their aftermath are known to cause psychological distress. However, little information is available regarding suicide rates following tsunami disasters that destroy regional social services and networks. The aim of the present study was to determine whether the tsunami disaster following the Great East Japan Earthquake in March 2011 has influenced suicide rates. The study period was from March 2009 to February 2014. Tsunami disaster-stricken areas were defined as the 16 municipalities facing the Pacific Ocean in Miyagi Prefecture. Inland areas were defined as other municipalities in Miyagi that were damaged by the earthquake. Suicide rates in the tsunami disaster-stricken areas were compared to national averages, using a time-series analysis and the Poisson distribution test. In tsunami disaster-stricken areas, male suicide rates were significantly lower than the national average during the initial post-disaster period and began to increase after two years. Likewise, male suicide rates in the inland areas decreased for seven months, and then increased to exceed the national average. In contrast, female post-disaster suicide rates did not change in both areas compared to the national average. Importantly, the male suicide rates in the inland areas started to increase earlier compared to the tsunami-stricken areas, which may reflect the relative deficiency of mental healthcare services in the inland areas. Considering the present status that many survivors from the tsunami disaster still live in temporary housing and face various challenges to rebuild their lives, we should continue intensive, long-term mental healthcare services in the tsunami-stricken areas.View full abstractDownload PDF (896K) Full view HTML -
Naoko Tachibana, Michiaki Kinoshita, Fuyuki Kametani, Keiko Tanaka, Yu ...Article type: Regular Contribution
2015 Volume 235 Issue 3 Pages 223-231
Published: 2015
Released on J-STAGE: March 17, 2015
JOURNAL FREE ACCESS FULL-TEXT HTMLAutoimmune synaptic encephalitis is characterized by the presence of autoantibodies against synaptic constituent receptors and manifests as neurological and psychiatric disorders. Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is such an autoimmune disorder that predominantly affects young women. It is associated with antibodies against the extracellular region of the NR1 subunit of postsynaptic NMDAR. Each NMDAR functions as a heterotetrameric complex that is composed of four subunits, including NR1 and NR2A, NR2B, or NR2C. Importantly, ovarian teratoma is a typical complication of anti-NMDAR encephalitis in female patients and may contain antigenic neural tissue; however, antigenic sites remain unknown in female patients without ovarian teratoma. The purpose of this study was to investigate the expression of NMDARs in the ovum. We detected NR1 and NR2B immunoreactivity in protein fractions extracted from the bovine ovary and ova by SDS-polyacrylamide gel electrophoresis and immunoblotting analysis. Immunoprecipitates digested with trypsin were analyzed by reverse phase liquid chromatography coupled to tandem mass spectrometry. We obtained the following five peptides: SPFGRFK and KNLQDR, which are consistent with partial sequences of human NR1, and GVEDALVSLK, QPTVAGAPK, and NEVMSSK, which correspond to those of NR2A, NR2B and NR2C, respectively. Immunocytochemical analysis revealed that the bovine ovum was stained with the immunoglobulin G purified from the serum of a patient with anti-NMDAR encephalitis. Taken together, we propose that the normal ovum expresses NMDARs that have strong affinity for the disease-specific IgG. The presence of NMDARs in ova may help explain why young females without ovarian teratomas are also affected by anti-NMDAR encephalitis.View full abstractDownload PDF (1657K) Full view HTML
Invited Review
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Norio SuzukiArticle type: Invited Review
2015 Volume 235 Issue 3 Pages 233-240
Published: 2015
Released on J-STAGE: March 17, 2015
JOURNAL FREE ACCESS FULL-TEXT HTMLErythrocytes play an essential role in the delivery of oxygen from the lung to every organ; a decrease in erythrocytes (anemia) causes hypoxic stress and tissue damage. To maintain oxygen homeostasis in adult mammals, when the kidney senses hypoxia, it secretes an erythroid growth factor, erythropoietin (Epo), which stimulates erythropoiesis in the bone marrow. Recently, studies using genetically modified mice have shown that the in vivo expression profile of the Epo gene changes dramatically during development. The first Epo-producing cells emerge in the neural crest and neuroepithelium of mid-stage embryos and support primitive erythropoiesis in the yolk sac. Subsequently, Epo from the hepatocytes stimulates erythropoiesis in the fetal liver of later stage embryos in a paracrine manner. In fact, erythroid lineage cells comprise the largest cell population in the fetal liver, and hepatocytes are distributed among the erythroid cell clusters. Adult erythropoiesis in the bone marrow requires Epo that is secreted by renal Epo-producing cells (REP cells). REP cells are widely distributed in the renal cortex and outer medulla. Hypoxia-inducible Epo production both in hepatocytes and REP cells is controlled at the gene transcription level that is mainly mediated by the hypoxia-inducible transcription factor (HIF) pathway. These mouse studies further provide insights into the molecular mechanisms of the cell-type specific, hypoxia-inducible expression of the Epo gene, which involves multiple sets of cis- and trans-regulatory elements.View full abstractDownload PDF (2078K) Full view HTML
Regular Contribution
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Tomoyuki Shimokaze, Kazuhiro Akaba, Emi SaitoArticle type: Regular Contribution
2015 Volume 235 Issue 3 Pages 241-248
Published: 2015
Released on J-STAGE: March 18, 2015
JOURNAL FREE ACCESS FULL-TEXT HTMLPreterm infants may develop acute systemic hypotension that responds to glucocorticoid therapy, but not to volume loading or vasopressors, during the postnatal period. This condition is termed late-onset circulatory collapse (LCC) that develops a few weeks after birth in relatively stable infants. LCC may cause periventricular leukomalacia, periventricular necrosis in the white matter. The aim of this study was to identify the clinical characteristics of LCC. We retrospectively reviewed the clinical data of infants with LCC. Among 41 infants born at < 29 weeks of gestation between 2010 and 2014, we identified 14 infants (median gestational age 25.6 weeks) with LCC. All infants were stable before the acute onset of circulatory collapse at a median age of 21 days, which is characterized by the decreased physical activity, systolic blood pressure (12 mmHg decrease), urine output (76% decrease), and serum sodium level (4 mEq/L decrease), and the increased resistance index in the cerebral and renal arteries on Doppler ultrasonography. Both left ventricular dimension and contraction were well preserved. Three infants developed hyperkalemia. The median time from the initial hydrocortisone dose to improvements was 4 h (interquartile range 3-5 h). Hydrocortisone therapy was effective, but had to be withdrawn slowly to prevent relapse. The median duration of hydrocortisone therapy was 23 days. There was no evidence of periventricular leukomalacia in any of the infants. None of the infants developed adrenal insufficiency during the follow-up period. During the acute stage of LCC, the main priority is the early initiation of glucocorticoid therapy.View full abstractDownload PDF (545K) Full view HTML -
Ryuhei Maejima, Tomoyuki Koike, Kenichiro Nakagawa, Katsunori Iijima, ...Article type: Regular Contribution
2015 Volume 235 Issue 3 Pages 249-253
Published: 2015
Released on J-STAGE: March 19, 2015
JOURNAL FREE ACCESS FULL-TEXT HTMLGastroesophageal reflux disease (GERD) is a common disease, in which the reflux of gastric acid causes mucosal damage of the esophagus and/or troublesome symptoms. Esomeprazole, a proton pump inhibitor, has been used for treatment of GERD in Japan since 2011; namely, only little is known about its effect on gastric acid secretion in Japanese. We, therefore, assessed the relationship between dose and timing of esomeprazole administration and gastric acid inhibition in 11 healthy male Japanese volunteers by directly examining gastric acid secretion capacity. In this randomized, open-label, three-way crossover study, the subjects were dosed with esomeprazole 10 mg or 20 mg once a day (q.d.), or 20 mg twice a day (b.i.d.) for 14 days, and pentagastrin-stimulated gastric acid secretion was measured by endoscopic gastrin test. At steady states, gastric acid inhibition rates were significantly higher in esomeprazole 20 mg b.i.d. (median 100.0%, interquartile range [IQR] 99.4-100%, P = 0.027) or 20 mg q.d. (100.0%, IQR 99.7-100%, P = 0.016), compared with 10 mg q.d. (98.4%, IQR 84.4-100%). At trough states, esomeprazole 20 mg b.i.d. showed significantly higher gastric acid inhibition (99.6%, IQR 99.0-100%) than did 20 mg q.d. (84.2%, IQR 76.4-88.8%, P = 0.002) or 10 mg q.d. (64.9%, IQR 59.1-76.7%, P = 0.001). Thus, esomeprazole 20 mg b.i.d. was sufficient to inhibit > 99% gastric acid secretion in healthy subjects. We propose that esomeprazole 20 mg b.i.d. is effective for treating Japanese patients with refractory GERD who require long-lasting gastric acid inhibition.View full abstractDownload PDF (893K) Full view HTML
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