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We searched for the |$\alpha$| condensed state in |$^{13}$| C by measuring the |$\alpha$| inelastic scattering at |$E_\alpha = 388$| MeV at forward angles including 0 |$^\circ$|⁠. We performed a distorted-wave Born approximation calculation with the single-folding potential and multipole decomposition analysis to determine the isoscalar transition strengths in |$^{13}$| C. We found a bump structure around |$E_x = 12.5$| MeV due to the isoscalar monopole (⁠|$IS0$|⁠) transition. A peak-fit analysis suggested that this bump consisted of several |$1/2^-$| states. We propose that this bump is due to the mirror state of the 13.5 MeV state in |$^{13}$| N, which dominantly decays to the |$\alpha$| condensed state in |$^{12}$| C. It was speculated that the |$1/2^-$| states around |$E_x = 12.5$| MeV were candidates for the |$\alpha$| condensed state, but the |$3\alpha + n$| orthogonality condition model suggests that the |$\alpha$| condensed state is unlikely to emerge as the negative parity states. We also found two |$1/2^+$| or |$3/2^+$| states at |$E_x = 14.5$| and 16.1 MeV excited with the isoscalar dipole (⁠|$IS1$|⁠) strengths. We suggest that the 16.1 MeV state is a possible candidate for the |$\alpha$| condensed state predicted by the cluster model calculations on the basis of the good correspondence between the experimental and calculated level structures. However, the theoretical |$IS1$| transition strength for this state is significantly smaller than the measured value. Further experimental information is strongly desired to establish the |$\alpha$| condensed state in |$^{13}$| C. [ABSTRACT FROM AUTHOR]

Background The Janus kinase ( JAK) inhibitor, tofacitinib, has shown efficacy for the treatment of psoriasis in a phase IIb trial ( A3921047; NCT00678210). Objectives To report haematology data from the phase IIb trial, given the importance of JAK-dependent signalling in haematopoiesis. Methods Patients with moderate-to-severe chronic plaque psoriasis were randomized to receive tofacitinib 2, 5 or 15 mg, or placebo, twice daily over 12 weeks. Blood samples were collected at screening, baseline, weeks 2, 4, 8 and 12 during treatment, and weeks 14 and 16 during off-treatment follow-up. Results Baseline haematology was similar across patients receiving tofacitinib 2 mg ( n = 49), 5 mg ( n = 49) or 15 mg ( n = 49), or placebo ( n = 50). Tofacitinib conferred dose-dependent decreases in haemoglobin, haematocrit and red blood cell counts, while reticulocyte counts initially declined, before recovering by week 8, and exceeding baseline levels after treatment cessation. With regard to white blood cells, tofacitinib had no clear dose-dependent effects on basophils or monocytes, but appeared to be associated with transient or reversible dose-dependent decreases in neutrophil and eosinophil counts and transient increases in lymphocyte counts, which were primarily attributable to increases in B-cell counts. Natural killer cell counts declined with tofacitinib. Conclusions Tofacitinib conferred tolerable, dose-dependent changes in haematological parameters during short-term administration in patients with psoriasis. The effects did not appear to be progressive, and were often transient or reversible. [ABSTRACT FROM AUTHOR]

The mechanism of the susceptibility of splenectomized mice to Streptococcus pneumoniae infection and the therapeutic effect of interleukin (IL)-18 were investigated. We demonstrated that, although S. pneumoniae challenge induced IL-12 production, it did not induce either interferon (IFN)- gamma or IL-18 production in mice with or without a splenectomy. Liver mononuclear cells stimulated with heat-killed S. pneumoniae but not with viable S. pneumoniae produced IFN- gamma in vitro. However, IL-18 pretreatment recovered the low serum immunoglobulin (Ig) M levels in splenectomized mice and completely inhibited mortality after S. pneumoniae infection without any IFN- gamma up-regulation. Injection of IgM from noninfected control mice into splenectomized mice before infection confirmed the essential role that IgM plays against S. pneumoniae infection. Therefore, low serum IgM levels but not a low IFN- gamma response in splenectomized mice cause lethality in S. pneumoniae infection, and IL-18 pretreatment protects them from infection by increasing IgM levels before infection. Copyright © 2006 Infectious Diseases Society of America [ABSTRACT FROM AUTHOR]

Listeria monocytogenes(Listeria) are known to grow and proliferate in the liver while a splenectomy induces host resistance against aListeriainfection despite the fact that a splenectomy inhibits the Th1 response. Therefore, the mechanism by which a splenectomy helps to prevent the growth ofListeriastill remains to be elucidated. After an i.v. challenge ofListeria(1 × 106 CFU) in C57BL/6 mice,Listeriarapidly increased in the spleen but not in the liver until 48 h. However, after this initial phase,Listeriaremarkably grew in the liver. In contrast, when the mice received a splenectomy beforehand, no remarkable growth ofListeriain the liver was observed afterListeriachallenge despite the fact that serum IFN-γ and IL-12 levels at 24 h afterListeriachallenge were significantly lower than those in the sham mice. However, the liver leucocytes from mice by 6 h after infection produced a substantial amount of IFN-γ while spleen MNC did not, whereas spleen leucocytes at 24 h afterListeriachallenge did. Consistently, the IFN-γ and IL-12 levels in the tissue homogenates of the spleen were significantly lower than in those of the liver until 6 h after infection. This defective spleen Th1 response in the early phase ofListeriainfection was corrected by an IL-18 i.p. injection just after theListeriachallenge. Our findings suggest thatListeriaexploit the defective Th1 environment of the spleen in the initial phase and afterwards overcome the host defense mechanism of the liver. [ABSTRACT FROM AUTHOR]

ABSTRACT We present the results of optical photometry of the recurrent nova CI Aql in a later phase of the outburst which occurred in 2000. Our observation revealed that the object reached the quiescent level between 2001 December and 2002 April, and therefore that CI Aql is a unique recurrent nova characterized by an extremely long (1.4–1.7 yr) plateau phase. The light curve obtained in the outburst suggests that the object is the first example of an intermediate between classical and recurrent novae. In comparison with the estimation given in published theoretical calculations, the long duration of the plateau phase supports a higher hydrogen content of the white dwarf envelope, whereas such an abundance of hydrogen requires a later cessation of the wind, which is in disagreement with the sudden fading observed in late November of 2000. The light curve obtained in the later phase of the outburst indicates that the object was fainter and the gradual decline was steeper than predicted. These discrepancies between the observation and the theoretical prediction demand a drastic modification of the present model of CI Aql. [ABSTRACT FROM AUTHOR]

Iron-induced free radical injuries in male and female ddY mice, especially the sex difference and its mechanisms, were studied after an i.p. injection of a renal carcinogen, ferric nitrilotriacetate. Male mice were much more susceptible to iron-induced free radical injuries than female mice. Oxidative modification of proteins and DNA occurred more strongly in males than in females, as measured by protein carbonyl content and 8-hydroxydeoxy-guanosine, respectively. Histochemical detection of 4-hydroxy-2-nonenal-modified proteins using an antibody and DNA fragmentation as detected by the TUNEL method also showed that males are more severely damaged than females, especially in the proximal convoluted tubules. These results could not be explained by the difference in iron status between male and female mice. In fact, the toxic so-called 'free' iron in serum and kidney were not different between male and female mice and storage iron, such as ferritin and hemosiderin, was also comparable in both kidneys. In previous studies we proposed the glutathione cycling hypothesis to explain the sex differences. The half-life of glutathione in the kidney was significantly shorter in males (29 min) than in females (57 min), as determined by the glutathione decrease after buthionine sulfoximine treatment, a specific inhibitor of glutathione synthesis. The specific activity of γ-glutamyltranspeptidase (EC 2.3.2.2) in female mice was 73% of that in male mice. These results suggest that the faster glutathione turnover in males could account for the higher susceptibility to oxidative injury by supplying the reducing equivalent that reduces Fe(III) to Fe(II), thereby facilitating iron-catalyzed free radical reactions. [ABSTRACT FROM PUBLISHER]

The article reports on a case study related to the prediction of smoking behavior in Japanese young adults. Development of effective smoking prevention programs requires determination of factors related to smoking behavior. Some studies have attempted to identify correlates of smoking behavior of Japanese high school students. Eighty-eight second grade students of a senior high school in Saitama prefecture in Japan participated in a prospective study to predict cigarette smoking behavior. This study determined several important factors associated with the smoking behavior.

Redox-active iron was demonstrated in mouse kidney by Timm's sulphide-silver staining after an injection of a renal carcinogen, iron-nitrilotriacetate (Fe-NTA). The iron was on the apical site of tubular epithelia of the renal proximal convoluted portion and in the tubules of the straight portion 30 min after the Fe-NTA injection. As the epithelial cells of the proximal tubules died, the iron disappeared in the dead cells and was stored in the cytoplasm of the more distal tubular epithelia. Biochemically, redox-active iron in the kidney rapidly increased to four times higher than the control 30 min after the Fe-NTA injection, then decreased to a plateau which was still higher than the control. Iron tightly stored in iron-storage proteins increased gradually by 3 h after the injection and then decreased at 5 h. The iron-induced free radical injuries, such as lipid peroxidation and protein oxidation, were demonstrated in the renal proximal tubules by histochemistry. The nuclei of the proximal tubular epithelia shrank and fragmented with the free radical injuries, and were positive for terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling. DNA ladder was demonstrated in the mice renal cortexes by agarose gel electrophoresis. It was elucidated that redox-active iron caused free radical injuries in the proximal tubules of mice kidneys after the injection of a renal carcinogenic iron (Fe-NTA) and induced the apoptosis of the proximal tubular epithelial cells. [ABSTRACT FROM PUBLISHER]

Assessment of the allergenic potency of enzymes involves the use of a guinea pig model in which specific IgG1 antibody titers are used as the endpoint. The passive cutaneous anaphylaxis (PCA) assay is used to measure specific IgG1 antibody. This report describes the development and validation of an enzyme-linked immunosorbent assay (ELISA) to measure guinea pig specific IgGl antibody as an alternative to the PCA assay. Cross reactivity of various rabbit and mouse (monoclonal) anti-guinea pig IgG1 preparations were evaluated using purified IgGl and IgG2 from serum of guinea pigs immunized with ovalbumin. The two subclasses ofguinea pig IgG were purified by first using Protein A affinity chromatography, followed by anion exchange chromatography and fluid phase isoelectric focusing. Affinity-purified rabbit anti-guinea pig IgG1 was shown to have minimal cross reactivity toward IgG2, while providing a strong signal with IgG1. The ELISA was designed as an antigen capture system in which the following are added in sequence: (1) enzyme antigen (passively adsorbed to the plate), (2) diluted serum samples from guinea pigs immunized with enzyme, (3) affinity-purified rabbit anti-guinea pig IgG1, (4) alkaline phosphatase-conjugated donkey anti-rabbit IgG, and (5) nitrophenyl phosphate substrate. Three replicate ELISA and PCA analyses were conducted on sera samples of varying titers from guinea pigs immunized with either Alcalase (protease), BPN' (protease), and Termamyl (amylase) enzyme. The correlation coefficients ( between the ELISA and PCA assay for Alcalase, BPN', and Termamyl were 0.826, 0.945, and 0.755, respectively. These findings demonstrate that the specific antibody ELISA developed in this study is a valid alternative to the PCA assay to measure anti-enzyme guinea pig IgG1. [ABSTRACT FROM PUBLISHER]

Comparison of ELISA and Plaque-Forming Cell Assays for Measuring the Humoral Immune Response to SRBC in Rats and Mice Treated with Benzo[a]pyrene or Cyclophosphamide. TEMPLE, L., KAWABATA, T. T., MUNSON, A. E., AND WHITE, K. L., JR. (1993). . 21, 412–419. The humoral immune response against sheep red blood cells (SRBC) is one of the most sensitive and frequently used endpoints in evaluating the immunotoxicity of drugs and chemicals in experimental animals. Currently, most immunotoxicology studies measure the SRBC IgM antibody response by quantitating the number of SRBC-specific IgM antibody-forming cells using the hemolytic plaque assay. On the other hand, measurement of serum SRBC-specific IgM could be an easier, more cost effective endpoint in evaluating the SRBC antibody response in rodents. A validated method to measure SRBC-specific IgM, however, has not been developed. Thus, the objectives of the studies presented were to develop and validate an enzyme-linked immunosorbent assay (ELISA) for SRBC-specific IgM. Hemoglobin-free, detergent-solubilized membrane preparations were chosen as antigen for the ELISA. Various sources of SRBC were found to be equally useful, and as little as 0.1 μg of protein per well was optimal. Kinetic studies of the IgM response showed the peak day to be on Day 5 (mice) and Day 6 (rats). To validate the usefulness of the method for immunotoxicologic studies, serum SRBC-specific IgM levels and number of SRBC-specific plaque-forming cells were compared in rats and mice treated with two well-characterized immunosuppressive agents: benzo[]pyrene and cyclophosphamide. Administration of these chemicals was found to produce very similar dose-dependent decreases in serum SRBC IgM and IgM-specific plaque-forming cells. These two endpoints were equally sensitive to the effects of the immunosuppressive drugs. Based on the present findings and the sensitivity, simplicity, and potential for automation of the ELISA for SRBC-specific IgM, the ELISA could potentially replace the plaque assay as the first step in testing for potential immunotoxic chemicals. [ABSTRACT FROM PUBLISHER]

The gut mucosal immune system may be a primary target for many ingested chemicals. Methods have been developed to examine the effects of chemicals on the systemic humoral immune response; however, studies to evaluate various methods of assessing the local gut mucosal immune response in a toxicology assay have been limited. The objectives of this study were to examine the effects of the known immunosuppressive compound, cyclosporine (CYS), on the generation of a cholera toxin (CT)-specific gut mucosal IgA response and evaluate the methods used to measure the gut IgA response. Groups of female B6C3F1 mice were left untreated or were treated daily, p.o., with corn oil (vehicle) or CYS at doses of 10 and 50 mg/kg for 20 days. On Days 3 and 13, mice were sensitized p.o. with CT. On Day 21, mice were terminated, gut washings were collected, and lamina propria lymphocytes were extracted from gut tissue with collagenase treatment. Cholera toxin-specific IgA in the gut washings was measured by an ELISA. The numbers of CT-specific IgA (CT-IgA) and total IgA antibody-forming cells (spot-forming cells, SFC) obtained from the lamina propria were determined by the ELISPOT method. A dose of 50 mg/kg CYS produced a significant decrease in the amount of CT-IgA in gut washings. This dose also decreased the number of cells recovered from the lamina propria by at least 50%. The amount of CT-specific SFC/million lamina propria cells decreased with a dose of 10 mg/kg CYS, whereas 50 mg/kg CYS did not alter the response. When the CT-IgA SFC response was calculated on the basis of lamina propria cells obtained per mouse, both the 10 and 50 mg/kg dose were found to suppress the response by at least 50% of control. The amount of IgA-SFC/total lamina propria cells obtained per mouse was also found to be decreased with a dose of 50 mg/kg. Thus, the results indicate that oral exposure to CYS results in a suppressed CT-specific IgA response. In comparing the two endpoints, measurement of CT-specific SFC was a more sensitive indicator. However, collection of gut washings and measurement of CT-IgA by ELISA is much easier than the labor-intensive methods required to isolate lamina propria lymphocytes. [ABSTRACT FROM PUBLISHER]

Extended abstract of a paper presented at Microscopy and Microanalysis 2012 in Phoenix, Arizona, USA, July 29 – August 2, 2012. [ABSTRACT FROM PUBLISHER]