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Volume 234 (2014)
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Volume 234, Issue 4
December
Displaying 1-10 of 10 articles from this issue
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Regular Contribution
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Saulo J.A. Felizola, Yasuhiro Nakamura, Yohei Ozawa, Yoshikiyo Ono, Ry ...Article type: Regular Contribution
2014 Volume 234 Issue 4 Pages 249-254
Published: 2014
Released on J-STAGE: November 14, 2014
JOURNAL FREE ACCESS FULL-TEXT HTMLThe activating transcription factor 3 (ATF3) is a member of the cAMP-responsive element-binding (CREB) protein family of transcription factors. ATF3 is expressed in H295R human adrenocortical carcinoma cells and considered a rapid-responder gene to angiotensin-II stimulation. However, the functions of ATF3 in human adrenocortical tissues have remained unknown. In this study, we analyzed the localization and possible regulatory mechanisms of ATF3 in human adrenocortical cells and tissues. The expression levels of ATF3 mRNA were analyzed in 66 aldosterone-producing adenomas (APA) and 14 cortisol-producing adenomas (CPA) using real-time RT-PCR. To localize the ATF3 protein, we performed immunohistochemical analysis in 20 non-pathological adrenal glands, 9 adrenal glands with idiopathic hyperaldosteronism (IHA), 20 APA, and 5 CPA using a mouse monoclonal antibody against human ATF3. We showed that ATF3 mRNA levels were higher in APA compared to CPA (P = 0.0053). ATF3 was immunolocalized to the zona glomerulosa of non-pathological adrenal glands and adrenal glands with IHA, and diffusely detected in the tumor cells of APA and CPA. Subsequently, H295R cells were treated for 6 h with each inhibitor of Src kinase (SRC), PKC, JAK2, and calcium-dependent calmodulin kinase-II (CaMKII) in the presence or absence of angiotensin-II. The expression levels of ATF3 mRNA were increased by angiotensin-II (about 3.5-fold induction), but the magnitude of the induction was significantly decreased in the presence of an inhibitor for SRC (PP2) or CaMKII (KN93). These results suggest that ATF3 is a downstream target of SRC and CaMKII signaling, and may be involved in adrenocortical aldosterone synthesis.View full abstractDownload PDF (1352K) Full view HTML -
Yongqiang Sun, Ji-Yuan Zhang, Sa Lv, Huan Wang, Man Gong, Ning Du, Hon ...Article type: Regular Contribution
2014 Volume 234 Issue 4 Pages 255-261
Published: 2014
Released on J-STAGE: November 14, 2014
JOURNAL FREE ACCESS FULL-TEXT HTMLPrimary biliary cirrhosis (PBC) is a progressive autoimmune liver disease that can cause a series of complications, including cirrhosis, liver failure and hepatocellular carcinoma. Interleukin-33 (IL-33) is expressed in various non-hematopoietic cells and a certain population of immune cells, and exerts its biological effects by binding to the specific receptor, suppression of tumorigenicity 2 (ST2). A soluble form of ST2 (sST2) has been postulated to act as a decoy receptor for IL-33. In this study, we aimed to investigate the role of IL-33 in the pathogenesis of PBC. The study included 20 healthy controls and 68 patients with PBC. We thus found the increased serum IL-33 levels in PBC patients. Its elevated levels were positively correlated with serum alkaline phosphatase levels (a key parameter for the definition of PBC) and with Child-Pugh scores, which were used to determine the prognosis of liver cirrhosis. Moreover, the serum concentrations of sST2 were significantly higher in PBC patients compared with healthy subjects, irrespective of the disease severity. Importantly, the cells that express IL-33 and/or myeloperoxidase (a marker for neutrophils) were accumulated in the livers of PBC patients, and their number increased with the severity of liver lesions. Lastly, in vitro chemotaxis assays revealed that IL-33 enhanced the migration of neutrophils. These data suggest that IL-33 may affect the progress of PBC by recruiting neutrophils to the liver. This expanded knowledge of IL-33 in PBC patients is important for developing therapeutic strategies (e.g., neutralization of IL-33), selecting optimal clinical management, and predicting prognosis.View full abstractDownload PDF (1354K) Full view HTML -
Kuang-Ming Liao, Wei-Chieh Lin, Tzu-Chieh Lin, Chung-Yi Li, Yea-Huei K ...Article type: Regular Contribution
2014 Volume 234 Issue 4 Pages 263-269
Published: 2014
Released on J-STAGE: November 28, 2014
JOURNAL FREE ACCESS FULL-TEXT HTMLPatients with chronic obstructive pulmonary disease (COPD) are predisposed to respiratory failure with ventilator dependency. This study aims to determine the risk of prolonged mechanical ventilation (PMV), defined as 22 days or more of mechanical ventilation dependency after the first day of hospital admission (index date) in patients diagnosed with COPD. A retrospective cohort was conducted using medical claim data of Taiwan’s National Health Insurance Research Database. Eligible study subjects were those who had a diagnosis of COPD made between January 1, 2005 and December 31, 2009. Patients were then followed until being registered as a PMV case, death, or the end of the study. The comorbidities were measured from January 1, 1997 to the index date by the ICD-9 code. The study sample consisted of 6,341 patients with COPD with a mean age of 73.89 (± 12.01) years. Over a maximum of 6 years of follow-up, 654 patients developed PMV dependency, with an incidence density of 41.56 per 1,000 person-years. Patients aged 70 years and older were at significantly increased risk for PMV dependency, compared to those aged 40-49 years after adjusting for confounders. Expenses per visit and hospital visits per year, representing the severity of the COPD, were also associated with an elevated risk of PMV. Most patients developed PMV dependency within the first two years after the index date. Physicians should be aware that elderly patients with COPD have a high risk of PMV after first hospitalization, and these patients need to be closely monitored.View full abstractDownload PDF (820K) Full view HTML -
Xiaosong Qin, Guang Chen, Yonghui Feng, Xiaotong Zhu, Yunting Du, Wei ...Article type: Regular Contribution
2014 Volume 234 Issue 4 Pages 271-280
Published: 2014
Released on J-STAGE: December 04, 2014
JOURNAL FREE ACCESS FULL-TEXT HTMLChloroquine (CQ), a well-known anti-malarial drug, has long been used for the treatment of autoimmune diseases because of its profound immunomodulatory effects. However, whether this drug modifies anti-malaria immune response is still not clear. Here we studied the immunomodulatory role of CQ in a mouse model of malaria. DBA/2 mice were infected with Plasmodium yoelii (Py) parasite (intraperitoneal injection of parasitized erythrocytes) and divided into three groups. Two groups received single dose of CQ (gavage administration) at 6 hours after Py infection (post-6h) and 3 days after Py infection (post-3d), respectively. The third group received saline as control. The course of disease was monitored and the changes of immune response were investigated. It is shown that mice from the post-6h group took longer time to clear the parasites compared with those of the post-3d group. The activation of T helper cells, macrophages, and B cells was significantly suppressed in mice with post-6h CQ treatment as compared with control mice on day 3 and day 5 after infection. In contrast, no such changes were found in mice from the post-3d group. Dendritic cells (DCs) from the post-6h CQ treated mice were less mature as compared with those from control mice as well as those from the post-3d group. Taken together, our data suggest that treatment with CQ early in infection inhibits protective immune response against Py infection possibly via mechanisms involving the modulation of DC’s function. Our finding provided important information for reasonable use of CQ in malaria chemotherapy.View full abstractDownload PDF (1542K) Full view HTML -
MinKyu Kim, KiHun Cho, WanHee LeeArticle type: Regular Contribution
2014 Volume 234 Issue 4 Pages 281-286
Published: 2014
Released on J-STAGE: December 05, 2014
JOURNAL FREE ACCESS FULL-TEXT HTMLStroke patients live with balance and walking dysfunction. Walking is the most important factor for independent community activities. The purpose of this study was to investigate the effect of a community walking training program (CWTP) within the real environment on walking function and social participation in chronic stroke patients. Twenty-two stroke patients (13 male, 50.45 years old, post stroke duration 231.64 days) were randomly assigned to either the CWTP group or the control group. All subjects participated in the same standard rehabilitation program consisting of physical and occupational therapy for 60 min per day, five times a week, for four weeks. In addition, the CWTP group participated in CWTP for 30 min per day, five times a week, for four weeks. Walking function was assessed using the 10-m walk test (measurement for 10-meter walking speed), 6-min walk assessment (measurement of gait length for 6-minutes), and community gait assessment. Social participation was assessed using a social participation domain of stroke impact scale. In walking function, greater improvement was observed in the CWTP group compared with the control group (P < 0.05). In addition, social participation improved more in the CWTP group compared with the control group (P < 0.05). These findings demonstrate the efficacy of CWTP on walking function and social participation in chronic stroke patients. Therefore, we suggest that CWTP within the real environment may be an effective method for improving walking function and social participation of chronic stroke patients when added to standard rehabilitation.View full abstractDownload PDF (1304K) Full view HTML -
Dragana P. Srebro, Sonja M. Vucković, Katarina R. Savic Vujovic, Milic ...Article type: Regular Contribution
2014 Volume 234 Issue 4 Pages 287-293
Published: 2014
Released on J-STAGE: December 06, 2014
JOURNAL FREE ACCESS FULL-TEXT HTMLThe N-methyl-d-aspartate (NMDA) receptor, an ionotropic glutamate receptor, may play a significant role in the development and maintenance of an inflammatory pain. Activation of NMDA receptors may cause nitric oxide (NO) release through activation of NO synthase (NOS). MK-801, a noncompetitive NMDA receptor antagonist is commonly used as a neuropharmacological tool. The interaction between MK-801 and NOS in the inflammatory pain has not been evaluated before. We investigated whether MK-801 affects inflammatory pain and whether NOS modulates the effect of MK-801. Carrageenan-induced hyperalgesia was evaluated by measuring the withdrawal response to mechanical stimuli, using an electronic version of the von Frey anesthesiometer in Wistar rats. MK-801 given subcutaneously (0.5-20 μg/kg) or intraplantarly (0.1 and 0.15 μg/paw) significantly reduced mechanical hyperalgesia. Intraplantarly given MK-801 exerted a local antihyperalgesic effect, because when applied to the contralateral side it did not reduce mechanical sensitivity in the ipsilateral side. N-nitro-L-arginine methyl ester hydrochloride (5 and 10 mg/kg), a non-selective NOS inhibitor, significantly reduced the effects of MK-801. N-ω-Propyl-L-arginine hydrochloride (0.5-2 mg/kg), a selective inhibitor of neuronal NOS, increased the antihyperalgesic effect of MK-801, whereas S-methylisothiourea (5-15 μg/kg), a selective inhibitor of inducible NOS, lowered the antihyperalgesic effect of MK-801. Importantly, each NOS inhibitor given alone did not affect carrageenan-induced hyperalgesia. In conclusion, MK-801 is effective against inflammatory pain and its antihyperalgesic effect is modulated in a different ways by NOS, being enhanced by a neuronal NOS inhibitor but reduced by an inducible NOS inhibitor.View full abstractDownload PDF (953K) Full view HTML -
Gokhan Aydemir, Ferhat Cekmez, Gokhan Kalkan, M.Kursat Fidanci, Guven ...Article type: Regular Contribution
2014 Volume 234 Issue 4 Pages 295-298
Published: 2014
Released on J-STAGE: December 17, 2014
JOURNAL FREE ACCESS FULL-TEXT HTMLDespite major advances in intensive care, sepsis continues to be a major cause of morbidity and mortality. Vitamin D is involved in various physiologic functions, including cellular responses during infection and inflammation. The aim of this study was to evaluate diagnostic value of 25-hydroxyvitamin D in childhood sepsis because it can be fatal if diagnosis delayed. The study included 40 children with sepsis and 20 children without sepsis (control group). We included only the patients with high probable sepsis, judged by clinical and laboratory findings, including positive blood culture. Blood samples were collected from patients with sepsis before treatment (pre-treatment group) and 48-72 hours later (post-treatment group). Treatment varied from ampicillin-sulbactam to cephalosporin. Blood samples were collected from control group once on admission. Serum 25-hydroxyvitamin D levels were significantly higher in sepsis (pre-treatment group) than control group (74 ± 8 ng/ml vs. 28 ± 12 ng/ml, p = 0.01) and the serum 25-hydroxyvitamin D levels were decreased to 44 ± 5 ng/ml (p = 0.01) after treatment. Moreover, we found significant positive correlation between 25-hydroxyvitamin D and each of well-know sepsis markers, C-reactive protein, tumor necrosis factor-α and interleukin-6. A cut-off point of 20 ng/mL for serum 25-hydroxyvitamin D showed 84% sensitivity and 76% specificity for sepsis diagnosis. This is the first study evaluating the diagnostic role of vitamin D in pediatric sepsis, thereby suggesting that serum 25-hydroxyvitamin D level can be used as a diagnostic marker for sepsis with high sensitivity and specificity.View full abstractDownload PDF (392K) Full view HTML -
Ryuta Kitanishi, Tadashi Matsuda, Shinpei Watanabe, Masatoshi Saito, T ...Article type: Regular Contribution
2014 Volume 234 Issue 4 Pages 299-307
Published: 2014
Released on J-STAGE: December 12, 2014
JOURNAL FREE ACCESS FULL-TEXT HTMLWhite matter injury in premature infants is known to be major cause of long-term neurocognitive disability, but the pathogenic mechanism remains unclear, hampering our ability to develop preventions. Periventricular leukomalacia is a severe form of white matter injury. In the present study, we explored the effects of cerebral ischemia and/or intrauterine inflammation on the development of oligodendroglia in the cerebral white matter using chronically instrumented fetal sheep. Each fetus received one of three insults: hemorrhage, inflammation and their combination. In the hemorrhage group, 40% of the fetoplacental blood volume was acutely withdrawn, and 24 hours after removal, the blood was returned to the fetus. The inflammation group received intravenous granulocyte-colony stimulating factor and intra-amniotic endotoxin and thus suffered from necrotizing funisitis and chorioamnionitis. The inflammatory hemorrhage group underwent acute hemorrhage under the inflammatory state. The sham group received no insults. Importantly, periventricular leukomalacia was not detected in the sham and the inflammation groups. Differentiating oligodendroglia at various developmental stages were identified by immunohistochemical analysis with specific antibodies. No difference in the density of oligodendroglial progenitors was detected among the four groups, whereas oligodendroglial precursors were significantly reduced in the three insult groups, compared to sham control. Moreover, the density of immature oligodendroglia was higher in the inflammation group and the inflammatory hemorrhage group, while the density of mature oligodendroglia was highest in the hemorrhage group. We propose that cerebral ischemia or intrauterine inflammation induces the differentiation of oligodendroglial precursors in preterm fetuses, eventually resulting in their exhaustion.View full abstractDownload PDF (1101K) Full view HTML
Case
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Yuichi Kuroyanagi, Hirohide Kawasaki, Yukihiro Noda, Taichi Ohmachi, S ...Article type: Case
2014 Volume 234 Issue 4 Pages 309-312
Published: 2014
Released on J-STAGE: December 12, 2014
JOURNAL FREE ACCESS FULL-TEXT HTMLInfantile malignant osteopetrosis (IMO) is a rare and fatal autosomal recessive condition characterized by a generalized increased in bone density. Hematopoietic stem cell transplantation (HSCT) is the only effective and rational therapy with achieving long-term disease-free survival. However, complications with HSCT for IMO remain unclear. Here we describe a male infant with IMO, carrying two novel mutations in the T-cell immune regulator 1 (TCIRG1) gene. The TCIRG1 gene encodes the a3 subunit of vacuolar H+-ATPase that plays an essential role in the resorptive function of osteoclasts. Direct sequencing of all 20 exons of the TCIRG1 gene revealed a single nucleotide change in exon 11 (c1305 G > T), which causes the substitution of Asp (GAT) for Glu (GAG) at position 435, and a two-nucleotide deletion in exon 16 (c1952-1953 del CA), causing a frame-shift mutation. However, the functional consequence of each mutation remains to be determined. Allogeneic HSCT was performed in the patient at the age of nine months. Donor engraftment was achieved, and abnormal bone metabolism and extramedullary hematopoiesis were corrected. Graft-versus-host disease was mild (grade I). However, the patient died of complication of pulmonary arterial hypertension at seven months after the HSCT. Postmortem examination revealed prominent vascular wall thickening of the pulmonary artery and macrophage infiltration to alveoli. It should be noted that a patient with IMO has a risk for pulmonary arterial hypertension, and the evaluation of pulmonary arterial flow should be included in the assessment of each patient with IMO even after HSCT.View full abstractDownload PDF (1184K) Full view HTML
Regular Contribution
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Paulus S Rommer, Joachim Greilberger, Sabine Salhofer-Polanyi, Eduard ...Article type: Regular Contribution
2014 Volume 234 Issue 4 Pages 313-317
Published: 2014
Released on J-STAGE: December 18, 2014
JOURNAL FREE ACCESS FULL-TEXT HTMLThe importance of oxidative stress in the pathogenesis of neuroimmunological and neurodegenerative diseases, such as multiple sclerosis (MS), has been discussed for a long time. However, markers for oxidative stress in cerebrospinal fluid are hardly detected. The aim of the present study is to assess whether carbonyl proteins as end products of metabolic processes may serve as a marker for oxidative stress in the cerebrospinal fluid (CSF) of patients with neuroimmunological and neurodegenerative diseases. Levels of carbonyl proteins in the CSF were assessed in 15 patients suffering from MS, four patients with neurodegenerative diseases, including one patient with dementia complicated by carcinomatous meningitis due to breast cancer, and four control subjects with no established neurological disease. Levels of carbonyl proteins were measured with a commercially available KIT. A significant difference (P = 0.025) was shown for mean values of various subgroups with highest levels for patients with neurodegenerative diseases (756.1 pmol/mg), followed by the MS (630.8 pmol/mg) and the control group (356.5 pmol/mg). Post-hoc pair wise comparisons showed significant differences between the MS group and healthy controls (P = 0.016) as well as for patients with neurodegenerative diseases and healthy controls (P = 0.02). This pilot trial showed that carbonyl proteins might serve as measure for oxidative stress in the CSF of relapsing as well as progressive MS patients and in patients with neurodegenerative diseases. Larger trials have to show whether they may serve as biomarkers and be helpful in monitoring patients with MS or neurodegenerative diseases.View full abstractDownload PDF (780K) Full view HTML
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