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We encountered a case of four cysts of intraductal papillary-mucinous tumor in the pancreas, a 25-mm diameter tumor, a 20-mm tumor, and a 10-mm tumor in the pancreatic body and tail, and a 5-mm diameter tumor in the uncinatus process, and the smallest diameter intraductal papillary-mucinous tumor (5 mm) was regarded as an invasive papillary adenocarcinoma, while the other three intraductal papillary-mucinous tumors were adenomas. A 63-year-old asymptomatic male was indicated of the presence of multiple pancreatic tumors by computed tomography during a physical examination. Endoscopic retrograde cholangiopancreatography revealed three cysts (25 mm, 20 mm, 10 mm diameter tumor) in the pancreatic body and tail, and one cyst 5 mm) in the uncinatus process. Cytologic examination of the pancreatic juice determined them as Class V. Based on a diagnosis of malignant intraductal papillary-mucinous tumors, he underwent distal pancreatectomy with removal of the uncinatus process. Pathologically, three cysts in the body and tail of the pancreas were found to be adenomas, but the 5-mm cyst in the uncinatus process was found to be an invasive intraductal papillary-mucinous tumor. The interstitium had been invaded by cancer, and the uncinatus process was the cancer positive surgical margin, and cystological examination of the pancreatic juice through repeated endoscopic retrograde cholangiopancreatography resulted in a class V, so the patient underwent a total pancreatectomy. When diagnosing intraductal papillary-mucinous tumor(s), there is the possibility of incorrectly differentiating between benignancy and malignancy when the diagnosis is based on cyst diameter, as is conventional.

The effect of Shiga-like toxin II (SLT-II), which was derived from Escherichia coli O157:H7, on doxorubicin transport across the blood–brain barrier (BBB) and P-glycoprotein function, was investigated in ddY mice. Doxorubicin (30 mg kg −1 ) was administered intravenously or fluorescein isothiocyanate labeled dextran (FD-4) was infused (20 μg min −1 ) to the mice, who had received an intravenous injection of SLT-II (0.2 μg/animal) 6 or 24 h earlier. Blood and brain were removed 4 h after injection of doxorubicin or 60 min after infusion of FD-4. SLT-II significantly elevated the brain concentration and brain-to-plasma concentration ratio ( K p ) of doxorubicin and FD-4 24 h after injection, but did not alter 6 h after. Cyclosporin A (200 mg kg −1 ) significantly increased the K p value of doxorubicin in the control mice, but did not alter it in mice treated 24 h earlier with SLT-II. Pentoxifylline (100 mg kg −1 ) a TNF-α production inhibitor, ameliorated SLT-II-induced increases in the brain concentrations of both drugs and the K p value of FD-4, suggesting that TNF-α, at least in part, causes damage to the brain capillaries. Western blot analysis revealed that SLT-II increased the protein level of P-glycoprotein in the brain of mice 6 h after injection and the increased level remained unchanged for 24 h. SLT-II did not change ATP content in the brain of mice. These results suggest that the increased P-glycoprotein level cannot explain SLT-II-induced increase in the doxorubicin accumulation in brain. The present findings indicate that SLT-II impairs the BBB function and doxorubicin transport across the BBB, while it overexpresses P-glycoprotein.

The effect of Shiga-like toxin II (SLT-II) (2 μg/animal), which was derived from Escherichia coli O157:H7, on renal handling of levofloxacin (LVX), a model drug for quinolone antimicrobial agents, was investigated in rats 24 h after intravenous injection. In histopathological examination, acute tubular injury was observed in SLT-II-treated rats, but the glomeruli were not injured. SLT-II significantly increased the steady-state concentration of LVX in plasma to 1.5-fold that of control rats. SLT-II induced significant decreases in the glomerular filtration rate (GFR) and renal clearance (CL R ) of LVX. SLT-II slightly, but significantly, increased the unbound fraction and decreased renal plasma flow with no change in the extraction ratio of p -aminohippurate. SLT-II significantly increased concentrations of tumor necrosis factor alpha (TNF-α) and nitrite and nitrate (NOx) in plasma. The TNF-α inhibitor pentoxifylline partly, but significantly, inhibited SLT-II-induced decreases in the GFR and CL R of LVX; in contrast, S -methylisothiourea, a selective inhibitor of inducible nitric oxide synthase, did not. Western blotting analysis revealed that SLT-II did not alter the levels of multidrug resistance-associated protein 2 (Mrp2) and P-glycoprotein in kidneys 24 h after injection, assuming the lack of involvement of Mrp2 and P-glycoprotein in SLT-II-induced acute renal tubular injury and renal handling of LVX observed 24 h after SLT-II injection. The present study suggests that SLT-II impairs the renal handling of LVX by decreasing GFR and causing decreased renal plasma flow.

It is well known that bronchial asthma is defined as chronic eosinophilic inflammation of the respiratory tract and that as one of the various types of inflammatory cells, eosinophils induce the airway inflammation of chronic asthma. Granulocyte-macrophage colony-stimulating factor (GM-CSF) has been shown to play an important role in the prolongation of the survival of eosinophils. We investigated the inhibitory effect of the selective phosphodiesterase (PDE) 4 inhibitors, 3,4-dipropyl-4,5,7,8-tetrahydro-3H-imidazo[1,2-i]purin-5-one (XT-611) and rolipram, and the nonselective PDE inhibitor theophylline, against GM-CSF-induced prolongation of the survival of eosinophils isolated from patients with bronchial asthma. Eosinophils (10(6) cells/ml) were incubated in the presence of GM-CSF together with or without theophylline, rolipram or XT-611 at 37 degrees C, and the viable cells were assessed up to 4d using Trypan blue dye exclusion. The presence of theophylline (10(-4) M), rolipram (10(-4)-10(-5) M) or XT-611 (10(-4)-10(-5) M) significantly reduced the GM-CSF (10 pg/ml)-induced prolongation of viability of eosinophils. These findings suggest that selective PDE 4 inhibitors, including XT-611, may effectively reduce the activities of inflammatory cells in the airway of bronchial asthma patients.

OBJECTIVES: We investigated the clinical usefulness of soluble dietary fiber (SDF) for the treatment of diarrhea during enteral nutrition in elderly patients. METHODS: This study included 10 men and 10 women (mean age ± standard deviation: 79.3 ± 5.1 y) who had diarrhea during long-term nutrition management. When administering SDF, the initial dose was 7 g and thereafter gradually increased at 1-wk intervals. After 4 wk, the administration was discontinued for 2 wk to confirm the effects of SDF. RESULTS: After the administration of SDF, serum diamine oxidase activity significantly increased (P < 0.001): The water content of the feces decreased significantly after the administration of fiber (P < 0.01). The frequency of daily bowel movements also decreased significantly (P < 0.05). Simultaneously, the fecal features improved. Concerning intestinal flora, there were no significant changes in the total number of bacteria or the number of anaerobic bacteria. The fecal pH decreased significantly 4 wk after the administration of fiber (P < 0.05). The total level of short-chain fatty acids increased significantly 4 wk after the administration of fiber (P < 0.05). There were no significant changes in the various nutritional indices. CONCLUSIONS: The administration of SDF is useful for controlling spontaneous, favorable bowel movement by improving symptoms of small intestinal mucosal atrophy and normalizing the intestinal flora.

The effect of endotoxin on glucuronidation and hepatobiliary transport of quinolone antimicrobial agents was investigated in rats using sparfloxacin and p-nitrophenyl glucuronide as model drugs. The biliary clearance experiments were performed 24 h after a single intraperitoneal injection of endotoxin (1 mg/kg). Endotoxin significantly delayed the disappearance of sparfloxacin from plasma and increased plasma concentration of its glucuronide after intravenous injection of sparfloxacin (10 mg/kg). Significant decreases in the systemic clearance of sparfloxacin and the biliary clearance of sparfloxacin and the glucuronide were observed. Endotoxin had no effect on in vitro glucuronidation activity using p-nitrophenol as a substrate. When p-nitrophenyl glucuronide (8 mg/kg) was administered in endotoxin-pretreated rats, significant decreases in the systemic clearance, biliary clearance and renal clearance of p-nitrophenyl glucuronide were observed. These findings suggest that endotoxin decreases the biliary excretion of sparfloxacin and its glucuronide probably due to impairment of their hepatobiliary transport systems and renal handling.

Human salivary histatins (Hsts), which belong to a salivary polypeptide family, have potent antifungal activity against Candida albicans and Cryptococcus neoformans, and are expected to be useful as therapeutic reagents against Candida species. However, little is known about the effect of Hsts on host immune systems. Thus we conducted a series of in vitro experiments with rat mast cells to determine whether histatin 5 (Hst 5) or histatin 8 (Hst 8) has a histamine-releasing effect on mast cells. Both Hst 5 and Hst 8 induced histamine release from rat peritoneal mast cells in a dose-dependent manner (10(-9) to 10(-5) M). Hst 5 had a stronger releasing effect than Hst 8. The histamine release induced by Hst 5 (10(-6) M) was increased by the presence of 0.5 mM Ca2+, but decreased by 2mM Ca2+. Alternatively, the histamine release induced by Hst 8 (10(-6) M) was inhibited by the presence of Ca2+ (0.5 to 2 mM). These results suggest that Hsts have limited usefulness as therapeutic agents due to induction of histamine release from mast cells.

Interferon sensitivity-determining region (ISDR) in nonstructural region 5A of hepatitis C virus (HCV) genotype-1b has been reported to be associated with viral load. Viral load is usually small in the patients with mutant type (four or more amino acid substitutions, compared with HCV-J) and large in those with wild (identical to HCV-J) or intermediate type (from one to three amino acid substitutions). A possible correlation was investigated between mutations in ISDR and alterations of viral load during the course of disease.The sequences of ISDR were determined in eight patients with significant changes of viral load and in 11 patients without changes.In two of the eight patients with significant alterations of viral load, ISDR sequences changed significantly. In one patient whose viral load increased after a course of interferon therapy, the number of substitutions, compared with HCV-J, decreased from five to zero or one; the type of ISDR converted from mutant type to wild or intermediate type. In one patient whose viral load decreased significantly after two courses of interferon therapy, the number of substitutions increased from one to six; ISDR changed from intermediate type to mutant type. In the remaining six patients with changes of viral load and in the other 11 patients without changes, the sequences of ISDR did not change significantly.The mutations in ISDR are one of the viral factors involved in the changes in viral load during the course of disease, although the majority of other factors involved are still unknown.

We hypothesized that the relationship between resting levels of sympathetic vasoconstrictor nerve traffic and dilator substance nitric oxide (NO) release is altered after exposure to microgravity, resulting in abnormal peripheral resistance. To examine the hypothesis, we assessed muscle sympathetic nerve activity (MSNA) (microneurography), an indicator of NO release (plasma nitrite/nitrate concentrations) and leg vascular resistance (venous occlusion plethysmography) in 20 healthy male volunteers before and after 14 days of 6 degrees head-down bed rest (HDBR), the ground-based analogue of microgravity. MSNA increased, while plasma nitrite/nitrate concentrations decreased after HDBR. A significant positive correlation observed between MSNA and plasma nitrite/nitrate concentrations before HDBR disappeared after HDBR. Leg vascular resistance increased after HDBR. In conclusion, an imbalance between sympathetic vasoconstrictor traffic and NO release might contribute to elevated peripheral vascular resistance following HDBR.

Recently, TT virus (TTV), associated with posttransfusion hepatitis, was discovered. Prevalence of TTV infection in maintenance hemodialysis (HD) units and its pathogenicity to liver was investigated.A total of 115 patients on HD were assessed for presence of serum TTV. DNA was purified from sera, and nested polymerase chain reaction was done for the detection of TTV DNA.TTV was detected in 59 patients on HD (51.3%), as compared with healthy blood donors (15 of 91 [16.5%], p0.0001). Serum HCV RNA and HBs antigen were positive in 16 and three patients, respectively. The prevalence rate of TTV was already 58.3% in the patients on HD for only 1 yr, and did not change according to the duration of HD until 15 yr on HD. TTV was positive in 51.2% (43 of 84) of the patients with history of blood transfusion, and in 51.6% (16 of 31) of those without it. In HCV-negative patients, alanine aminotransferase (ALT) levels of TTV-positive patients were similar to those of TTV-negative patients. Contrarily, in HCV-positive patients, ALT levels were more frequentlyor =15 IU/L in TTV-positive patients (14 of 18) than in TTV-negative patients (five of 15) (p0.05).TTV infection is remarkably prevalent in patients on HD and in healthy blood donors. It is suggested that TTV generally does not cause liver disease by itself, but there remains the possibility that TTV may aggravate liver disease caused by HCV.

Hypervariable region 1 (HVR1) proteins of hepatitis C virus (HCV) have been reported to react broadly with sera of patients with HCV infection. However, the variability of the broad reactivity of individual HVR1 proteins has not been elucidated. We assessed the reactivity of 25 different HVR1 proteins (genotype 1b) with sera of 81 patients with HCV infection (genotype 1b) by Western blot. HVR1 proteins reacted with 2–60 sera. The number of sera reactive with each HVR1 protein significantly correlated with the number of amino acid residues identical to the consensus sequence defined by Puntoriero et al. (G. Puntoriero, A. Lahm, S. Zucchelli, B. B. Ercole, R. Tafi, M. Penzzanera, M. U. Mondelli, R. Cortese, A. Tramontano, G. Galfre', and A. Nicosia. 1998. EMBO J. 17, 3521–3533.) (r = 0.561, P < 0.005). The most widely reactive HVR1 protein, 12-22, had a sequence similar to the consensus sequence. The peptide with C-terminal 13-amino-acids sequence of HVR1 protein 12-22 (NH2-CSFTSLFTPGPSQK) was injected into rabbits as an immunogen. The rabbit immune sera reacted with 9 of 25 HVR1 proteins of genotype 1b including HVR1 protein 12-22 and with 3 of 12 proteins of genotype 2a. These results indicate that the HVR1 protein broadly reactive with patients' sera has a sequence similar to the consensus sequence, can induce broadly reactive sera, and could be one of the candidate immunogens in a prophylactic vaccine against HCV.

Klebsiella pneumoniae endotoxin has been found to decrease hepatic P450-mediated drug-metabolizing enzyme activity in a time-dependent manner. In this study, we investigated the role of nitric oxide (NO) in the decrease in hepatic drug-metabolizing enzyme activity caused by endotoxin in vivo. We measured in vivo pharmacokinetic parameters of antipyrine in rats treated with endotoxin and/or a selective inhibitor of inducible NO synthase (iNOS), S -methylisothiourea. Intraperitoneal injection of endotoxin (1 mg/kg of body weight) dramatically decreased the systemic clearance of antipyrine, reflecting reduced hepatic drug-metabolizing enzyme activity, and significantly increased the level of nitrite and nitrate (NOx) in the plasma. S -Methylisothiourea (10 mg/kg) reversed this decreasing antipyrine clearance and reduced the level of NOx in plasma. Repeated injections of an NO donor, (±)-( E )-4-ethyl-2-[( E )-hydroxyimino]-5-nitro-3-hexenamide (FK-409; 10 mg/kg), at a dose which maintained plasma NOx at the same levels as those caused by endotoxin injection, also decreased the systemic clearance of antipyrine. These findings suggest that the overproduction of NO observed in this animal model is at least partially responsible for the significant reduction in the hepatic drug-metabolizing enzyme activity that may happen in a gram-negative bacterial infection.

We studied three patients with dural arteriovenous fistula (DAVF). Major symptoms were progressive dementia and parkinsonism, both of which progressed in step-wise fashion. Two of the three patients showed diffuse cerebral white matter lesions on brain CT and MRI. Progressive dementia and parkinsonism in our patients could be caused by diffuse cerebral parenchymal disturbance: impaired cerebral circulation due to severe venous hypertension. DAVF is important for the differential diagnosis in patients with progressive dementia and parkinsonism.

Anti-cyclic citrullinated peptide (CCP) antibodies are useful for the diagnosis of rheumatoid arthritis (RA) because of their higher specificity.1 First-generation anti-CCP (CCP1) ELISAs were based on synthetic peptides derived from human filaggrin.2 The second-generation anti-CCP (CCP2) test, which contains epitopes selected from libraries of citrullinated peptides, performs better than anti-CCP1.3 4 Recently, a third-generation anti-CCP (CCP3) test was introduced. We compare the performance of the anti-CCP3 test with that of two anti-CCP2 tests, and assess their value in diagnosing RA. A total of 502 participants were studied: 227 patients fulfilling the American College of Rheumatology criteria for RA,5 173 patients with non-RA autoimmune diseases (details are indicated …

Background Several patients with rheumatoid arthritis (RA) have different comorbidities and have to take other drugs at the same time. It is important to recognize such comorbidities in RA patients and consider them before initiating both pharmacotherapy and surgical therapy. Most of comorbidities in RA patients may affect therapeutic choice. Objectives To evaluate the impact of comorbidities to physical functions and treatment selection of patients with RA, we studied comorbidity index in patients with rheumatoid arthritis in our Japanese cohort. Methods A cohort of 413 Japanese patients with RA, who attended Toho University Ohmori hospital Rheumatology center during the period from 2005 to 2010, was retrospectively analyzed until the end 2010. Clinical data containing comorbidity profile and disease activity obtained from medical records. Comorbidity index used Charson comorbidity index; CCI established by Charlson M. et al. We analyzed relationship between the number of comorbidities, CCI and therapeutic processes of patients with rheumatoid arthritis. Results In this cohort data profiles of RA patients were average age 65±14, female ratio 88%, average disease duration 8.3±8.8years, biologics usage 29%, DAS28-ESR 2.9±1.3 and Health Assessment Questionnaire disability index (HAQ-DI) was 0.6±0.7. Frequency of comorbidity was 53% in patients of this cohort. Comorbidities of RA patients were 27.9% hypertension, 12.3% diabetes mellitus, 12.3% interstitial peumonitis, 6.6% cardiovascular disease, 6.6% malignancy, 5.4% thyroid disease, and 2.7% renal diseases. The Japanese RA patient had low percentage of ischemic heart disease compared with a European and American report. Mean of CCI was 0.5±0.8. CCI was correlated with age and functional class classification. RA patients with low CCI included in RA functional class I group. CCI were also correlated with HAQ-DI and DAS28 ESR. RA patients with high CCI score (2$ p p p =0.39). Conclusions CCI is one of the useful index in patients with RA. Therapeutic process of RA patients have been affected by several comorbidites. It is necessary to do treatment preferences in consideration of comorbidities. The therapy that we can choose without being concerned with a comorbidities is necessary in patients with rheumatoid arthritis. Disclosure of Interest None Declared

Background Since proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6, play major pathophysiological roles in rheumatoid arthritis (RA), their inhibitors have recently been developed as potent biological anti-rheumatic drugs. However, they are not curative and the effects are still partial, with many patients failing to respond. Leptin is the product of the ob gene, and is a peptide hormone synthesized almost exclusively by adipocytes that regulates appetite and energy expenditure. It is also suggested that leptin may contribute to inflammation and autoimmunity. We previously reported that serum leptin level was elevated in patients with RA [[1][1]]. Accordingly, we examined the direct effects of leptin on cultured rheumatoid synovial fibroblasts (RSFs) in the present study. Objectives To determine the effects of leptin on the production of proinflammatory cytokines by RSFs. Methods Synovial tissue was obtained at total knee replacement operation from patients with RA who gave consent. RSFs were harvested from the synovial tissues of these patients. Leptin receptor mRNAs were detected by reverse transcription–polymerase chain reaction. Productions of mRNA by RSFs and protein concentrations of TNF-α, IL-1β, and IL-6 in the culture medium were detected by real-time PCR and ELISA kit, respectively. Small interfering RNA (siRNA) was transfected into RSFs to down-regulate the expression of leptin receptor. Effects of inhibitors of janus kinase 2 (JAK2), phosphatidylinositol 3-kinase (PI3K), and mitogen-activated protein kinase (MAPK) on IL-6 production were evaluated. Phosphorylation of signal transducer and activator of transcription 3 (STAT3) in RSFs were determined by Western blot analysis. This study was approved (No. 19021) by Ethics Committee of Toho University School of Medicine. Results We detected leptin receptor mRNAs in RSFs. Expressions of IL-1β and IL-6 mRNAs were enhanced in a concentration-dependent manner by addition of leptin to RSFs. IL-6 secretion by RSFs showed an increase after leptin stimulation, while IL-1β did not increase in the culture media. Leptin-induced production of IL-6 by RSFs was decreased after exposure to siRNA targeting leptin receptor (Ob-Rb). A JAK2 inhibitor, but not PI3K and MAPK inhibitors, decreased leptin-induced IL-6 production. Enhanced phosphorylation of STAT3 was observed in RSFs after stimulation by leptin. Conclusions Leptin possibly acts as a proinflammatory cytokine that up-regulates IL-6 production in RSFs via activation of JAK2/STAT3 in RSFs. Leptin and JAK/STAT pathway may represent a new alternative therapeutic target in the treatment of RA. References 1. Yoshino T, Kusunoki N, Tanaka N, Kaneko K, Kusunoki Y, Endo H, Hasunuma T, Kawai S. Elevated serum levels of resistin, leptin, and adiponectin are associated with C-reactive protein and also other clinical conditions in rheumatoid arthritis. Intern Med. 2011;50:269. Disclosure of Interest None Declared [1]: #p-6

Background Osteoporosis is a serious complication of systemic glucocorticoid (GC) therapy. Bisphosphonate is recommended, however insufficient result have been reported in some cases. Menatetrenone (vitamin K 2 ;VK) is a stimulator of bone formation in vitro and in vivo . We recently have reported that severity of GC-induced osteoporosis might be determined by serum basal sRANKL levels in patients with systemic autoimmune disease [1]. In the present study, we conducted post-hoc analysis to determine whether VK influenced bone metabolism markers in these patients. Objectives To study the efficacy of VK on serum bone metabolism markers and on bone mineral density (BMD) in patients under GC therapy. Methods This study was approved by the Ethics Committee at Toho University Omori Hospital (No. 21-61). Detailed study design was previously shown elsewhere [1]. Briefly, sixty patients (40 women) with systemic lupus erythematosus (n=21), vasculitis syndrome (n=19), polymyositis/dermatomyositis (n=15), and adult-onset Still’s disease (n=5) who were started to received prednisolone (30-60mg daily) were enrolled. Serum samples were obtained just before and 1 to 4 weeks after the start of GC therapy. All patients received bisphosphonate for our regimen of GC therapy. Twenty patients received VK 45 mg daily from 2 weeks after GC therapy. As bone formation markers, serum levels of osteocalcin (OC), procollagen type I N-terminal peptide (PINP), undercarboxylated OC (ucOC), and bone alkaline phosphatase (BAP) were measured. As bone resorption markers, serum levels of type I collagen cross-linked N-telopeptide (NTx) and tartrate resistant acid phosphatase isoform 5b (TRACP-5b) were measured. The BMD of lumbar spine was measured before and after (at 15 months) GC therapy. Results Serum levels of OC and ucOC were significantly (P Conclusions Additional use of VK partially restored serum OC level from the suppressed level by GC therapy. In addition, the BMD value in the VK group was not changed after GC therapy. These results suggest that VK may possibly provide some effects on bisphosphonate therapy to prevent from GC-induced osteoporosis. References Kaneko K, et al. Changes of serum soluble receptor activator for nuclear factor-κB ligand after glucocorticoid therapy reflect regulation of its expression by osteoblast. J Clin Endocrinol Metab . 2012; 97:E1909-1917. Disclosure of Interest None Declared

In this paper, a self deployable large disk antenna is proposed for power transmission between locations in space. Its mechanism of self deployment is examined through a geometrical study. This antenna is discussed for use in a power transmitting test using an S-520 sounding rocket in a few years time.

Enteric adenoviruses (EAd), adenovirus (Ad) types 40 and 41, have been established as causative agents of gastroenteritis. By electron microscopic (EM) survey of acute gastroenteritis in children in the Matsuyama area, Ad were detected in 275 of 6476 fecal samples obtained from 1980 to 1993. Two-hundred-thirteen Ad-positive samples were tested for serotyping by the enzyme-linked immunosorbent assay (ELISA) using three monoclonal antibodies, Ad group-specific, Ad 40 type-specific and Ad41 type-specific antibody. Of 199 samples serotyped by ELISA, 65 were identified as Ad40, 73 as Ad41, 1 as double infection with Ad40 and Ad41, and 60 as Non-EAd. About 70% of Adenovirus detected by EM were suggested to be EAd. Other epidemiological feature was as follows: EAd were detected throughout the year. The predominant serotype was Ad40 during 1980-1985, while Ad41 were observed after 1986. EAd were detected most frequently from the children aged 0-3 years. The incidence of fever in EAd positive group was lower (30%) than that (67%) in the Non-EAd positive group. The incidence of vomiting, nausea and respiratory symptoms was higher in Ad41 associated infections than Ad40.

Seroepizootiological study of hantavirus infection among 393 urban rats (Rattus norvegicus) captured in six regions in Japan during the period from 1990 to 1994 was carried out by the indirect fluorescent antibody (IFA) test and Western blot (WB). Fifteen out of 393 (3.8%) rat sera were antibody-positive by IFA, i.e., Tokyo Port (12.8%, 6/47), Shimizu Port (5.7%, 2/35), Otaru Port (1.5%, 1/65) and Nagoya City (3.6%, 6/167). In two other regions, i.e., Kasai Seaside Park and Haneda Airport, rat sera were antibody-negative. One serum with a lower IFA titer, 1:64, from Otaru Port was confirmed to be antibody-positive by WB, while two sera from Shimizu Port (IFA titer, 1:32 and 1:64) were not. In Nagoya City, one out of four sera (IFA titer, 1:32) and one of two sera (IFA titer, 1:64) were also confirmed to be antibody-positive by WB. Continuous hantavirus infection among rats in Tokyo Port, Shimizu Port and Nagoya City and the existence of hantavirus among rats in Otaru Port were demonstrated.

The prevalence of antibodies to hantavirus among Rattus norvegicus in Nagoya city was examined during the period from 1986 to 1993. Eight sera of 675 were antibody positive in an indirect fluorescent antibody test. Antibody positive rats were found in 1988, 1990, 1991 and 1992 and the numbers of rats were 1, 1, 3 and 3, respectively. A hantavirus strain was isolated from a rat captured in 1990 at a residential area adjoining to a pier in Nagoya port. The virus strain, named NR-9, was identified antigenically as the Seoul type of hantavirus in a neutralization test. Suckling rats inoculated with NR-9 strain survived, while those with SR-11 strain succumbed. A difference between the virulence of strains, NR-9 and SR-11 was demonstrated.

A method of explaining the recently observed acceleration of cosmic expansion as well as inflation in the early universe is presented within the same framework. The goal is to construct an inflation model based on supergravity and the slow-roll approximation (SRA) that both satisfactorily predicts observed inflationary parameters and at the same time explains the accelerated expansion of the universe. The model is based on a modification of string-based modular invariant supergravity previously proposed by the present authors. It realizes slow-roll inflation in the Einstein frame and is successful in explaining Wilkinson Microwave Anisotropy Probe (WMAP) observational data, through fine-tuning procedure of free parameters. The parameter dependence of the model is considered in detail in order to determine the range for which the SRA can be applied. Within the allowed range of parameter values, a vacuum energy of ~10-120 can be obtained, which coincides with the cosmological constant, and can play the role of dark energy in the universe. The calculated inflationary parameters fit very well to seven-year WMAP data. The ratio of the scalar and tensor power spectra is predicted to be r ~6.8 ×10-2, and this may soon be verified by observations by the Planck satellite. The non-Gaussianity parameter fNL is also estimated by the slow-roll parameters.

A smooth surface of the poly(3-hexylthiophene) (P3HT)-doped-(6,6)-phenyl-C61-butyric acid methyl ester (PCBM) thin film was achieved by mixing different solvents for the electrospray deposition method. As a result, the high power-conversion efficiency (PCE) of the bulk-heterojunction organic photovoltaic cell (OPV) was comparable to that obtained in the case of the spin-coating method. By optimizing the additional solvent in o-dichlorobenzene, the P3HT/PCBM active layer with the root-means-square roughness of 2.23 nm and the PCE of 2.2% was fabricated employing acetonitrile as the additional solvent., 本著作物の著作権は公益社団法人応用物理学会に帰属します。©（公社）応用物理学会 2012

Some evidence indicates that nitric oxide (NO) contributes to inflammation, while other evidence supports the opposite conclusion. To clarify the role of NO in inflammation, we studied carrageenin-induced pleurisy in rats treated with an NO donor (NOC-18), a substrate for NO formation (L-arginine), and/or an NO synthase inhibitor (S-(2-aminoethyl) isothiourea or -nitro-L-arginine). We assessed inflammatory cell migration, nitrite/nitrate values, lipid peroxidation and pro-inflammatory mediators. NOC-18 and L-arginine reduced the migration of inflammatory cells and edema, lowered oxidative stress, and normalized antioxidant enzyme activities. NO synthase inhibitors increased the exudate formation and inflammatory cell number, contributed to oxidative stress, induced an oxidant/antioxidant imbalance by maintaining high , and enhanced the production of pro-inflammatory mediators. L-arginine and NOC-18 reversed the proinflammatory effects of NO synthase inhibitors, perhaps by reducing the expression of adhesion molecules on endothelial cells. Thus, our results indicate that NO is involved in blunting—not enhancing—the inflammatory response.