Enhancement of OVA-induced murine lung eosinophilia by co-exposure to contamination levels of LPS in Asian sand dust and heated dust.

BackgroundA previous study has shown that the aggravation of Asian sand dust (ASD) on ovalbumin (OVA)-induced lung eosinphilia was more severe in lipopolysaccharide (LPS)-rich ASD than in SiO2-rich ASD. Therefore, the effects of different LPS contamination levels in ASD on the aggravation of OVA-induced lung eosinophilia were investigated in the present study.MethodsBefore beginning the in vivo experiment, we investigated whether the ultra-pure LPS would act only on TLR4 or not using bone marrow-derived macrophages (BMDMs) of wild-type, TLR2-/-, TLR4-/- and MyD88-/- BALB/c mice. ASD collected from the desert was heated to remove toxic organic substances (H-ASD). BALB/c mice were instilled intratracheally with 12 different testing samples prepared with LPS (1 ng and 10 ng), H-ASD, and OVA in a normal saline solution. The lung pathology, cytological profiles in the bronchoalveolar lavage fluid (BALF), the levels of inflammatory cytokines/chemokines in BALF and OVA-specific immunoglobulin in serum were investigated.ResultsThe LPS exhibited no response to the production of TNF-α and IL-6 in BMDMs from TLR4-/-, but did from TLR2-/-. H-ASD aggravated the LPS-induced neutrophilic lung inflammation. In the presence of OVA, LPS increased the level of eosinophils slightly and induced trace levels of Th2 cytokines IL-5 and IL-13 at the levels of 1 ng and 10 ng. In the presence of OVA and H-ASD, LPS induced severe eosinophil infiltration and proliferation of goblet cells in the airways as well as remarkable increases in Th2 cytokines IL-5 and IL-13 in BALF. The mixture containing LPS (1 ng) showed adjuvant activity on OVA-specific IgE and IgG1 production.ConclusionsThe results suggest that H-ASD with naturally-occurring levels of LPS enhances OVA-induced lung eosinophilia via increases in Th2-mediated cytokines and antigen-specific immunoglobulin. These results indicate that LPS is a strong candidate for being a major aggravating substance in ASD

Interfacial Fe segregation and its influence on magnetic properties of CoFeB/MgFeO multilayers

We investigated the effect of Fe segregated from partially Fe-substituted MgO (MgFeO) on the magnetic properties of CoFeB/MgFeO multilayers. X-ray photoelectron spectroscopy (XPS) as well as magnetic measurements revealed that the segregated Fe was reduced to metal and exhibited ferromagnetism at the CoFeB/MgFeO interface. The CoFeB/MgFeO multilayer showed more than 2-fold enhancement in perpendicular magnetic anisotropy (PMA) energy density compared with a standard CoFeB/MgO multilayer. The PMA energy density was further enhanced by inserting an ultrathin MgO layer in between CoFeB and MgFeO layers. Ferromagnetic resonance measurement also revealed a remarkable reduction of magnetic damping in the CoFeB/MgFeO multilayers.Comment: 15 pages, 5 figure

Lung inflammation by fungus, Bjerkandera adusta isolated from Asian sand dust (ASD) aerosol and enhancement of ovalbumin-induced lung eosinophilia by ASD and the fungus in mice.

BackgroundBjerkandera adusta (B. adusta) is one of the most important etiological fungi associated with chronic cough. However, precise details of the inflammatory response to exposure are not well understood yet. B. adusta was recently identified in Asian sand dust (ASD) aerosol. Therefore, in the present study the exacerbating effects of ASD on B. adusta-induced lung inflammation and B. adusta + ASD on ovalbumin (OVA)-induced murine lung eosinophilia were investigated using experimental mice.MethodsIn order to prepare testing samples, B. adusta obtained from ASD aerosol was inactivated by formalin and ASD collected from the atmosphere was heated to remove toxic organic substances (H-ASD). CD-1 mice were instilled intratracheally with 12 different samples prepared with various combinations of B. adusta, H-ASD, and OVA in a normal saline solution. The lung pathology, cytological profiles in bronchoalveolar lavage fluid (BALF), and the levels of inflammatory cytokines/chemokines in BALF were investigated.ResultsH-ASD aggravated the lung eosinophilia induced by B. adusta alone, which also aggravated the lung eosinophilia induced by OVA. The mixture of OVA, H-ASD, and B. adusta caused serious fibrous thickening of the subepithelial layer, eosinophil infiltration, and proliferation of goblet cells in the airways along with remarkable increases of IL-13, eotaxin, IL-5, and MCP-3 in BALF.ConclusionsThe results of the present study demonstrated that B. adusta isolated from ASD aerosol induces allergic lung diseases. H-ASD enhanced allergic reactions caused by OVA or B. adusta. A mixture of B. adusta, H-ASD, and OVA caused the most remarkable exacerbation to the allergic airway inflammation via remarkable increases of pro-inflammatory mediators

Cu and Zn isotope ratio variations in plasma for survival prediction in hematological malignancy cases

We have examined potential changes in the isotopic compositions of Fe, Cu and Zn (using multi-collector inductively coupled plasma-mass spectrometry) and the corresponding concentrations (using inductively coupled plasma-atomic emission spectrometry) in plasma from hematological malignancy (HM) patients and assessed their prognostic capability. Together with clinical laboratory test values, data were examined in view of a 5-years survival prediction. Plasma Cu and Zn isotope ratios and their concentrations were significantly different in HM patients compared to matched controls (P<0.05). Both delta Cu-65 and delta Zn-66 values showed significant mortality hazard ratios (HRs) in HM. The group of patients with decreased delta Cu-65 and increased delta Zn-66 values showed significantly poorer survival from the early phase (HR 3.9; P=0.001), forming a unique cohort not identified based on laboratory test values. Well-known prognostic factors for HM, such as the creatinine level, and anemia-related values were highly correlated with the delta Zn-66 value (P<0.05). Time-dependent ROC curves based on the delta Cu-65 or delta Zn-66 value were similar to that based on the creatinine concentration (a well-known prognostic factor in HM), indicating that delta Cu-65 or delta Zn-66 values are useful for prognosis of HM. Variations in stable isotope ratios of essential mineral elements have thus been shown to reflect alterations in their homeostasis due to physiological changes in malignancies with higher sensitivity than concentrations do

The nucleotide and deduced amino acid sequences of porcine liver proline-β-naphthylamidase swEvidence for the identity with carboxylesterase

AbstractA cDNA clone for porcine liver proline-β-naphthylamidase was isolated and sequenced. The deduced amino acid sequence of 567 residues was highly homologous with those of carboxylesterases (EC 3.1.1.1) previously reported for other species. In addition, proline-β-naphthylamidase purified from porcine liver was shown to have strong activity towards p-nitrophenylacetate, a representative substrate for carboxylesterases. These results suggest that proline-β-naphthylamidase is identical with carboxylesterase

Induction of immune tolerance and reduction of aggravated lung eosinophilia by co-exposure to Asian sand dust and ovalbumin for 14 weeks in mice

BACKGROUND: Atmospheric contamination caused by Asian sand-dust (ASD) storms aggravates asthma in both human adults and children. This study aims to investigate a series of manifestations in allergic airway disease caused by co-exposure to allergens and ASD for 6 weeks and 14 weeks. METHODS: CD-1 Mice were instilled intratracheally with 0.1 mg of ASD/mouse four times (6 weeks) or eight times (14 weeks) at 2-week intervals (total dose of 0.4 mg or 0.8 mg/mouse) with or without ovalbumin (OVA). The pathologic changes in the airway, cytological alteration in bronchoalveolar lavage fluid (BALF), and levels of inflammatory cytokines/chemokines in BALF, and OVA-specific IgE and IgG1 antibodies in serum were measured in the treated CD-1 mice. RESULTS: Four-time co-exposure to OVA and ASD aggravates allergic airway inflammation along with Th2-cytokine IL-13 and eosinophil-relevant cytokine/chemokines IL-5, Eotaxin and MCP-3 in BALF, and fibrous thickening of the subepithelial layer in the airway. On the other hand, eight-time co-exposure attenuates these changes along with a significant increase of TGF-β1 in BALF. Adjuvant effects of ASD toward IgG1 and IgE production in sera were, however, still seen in the eight-time co-exposure. CONCLUSIONS: These results indicate that the immune responses in airways are exacerbated by four-time co-exposure to ASD with OVA, but that there is a shift to suppressive responses in eight-time co-exposure, suggesting that the responses are caused by TGF-β1-related immune tolerance

Social dilemma in the excess use of antimicrobials incurring antimicrobial resistance

The emergence of antimicrobial resistance (AMR) caused by the excess use of antimicrobials has come to be recognized as a global threat to public health. There is a ‘tragedy of the commons’ type social dilemma behind this excess use of antimicrobials, which should be recognized by all stakeholders. To address this global threat, we thus surveyed eight countries/areas to determine whether people recognize this dilemma and showed that although more than half of the population pays little, if any, attention to it, almost 20% recognize this social dilemma, and 15–30% of those have a positive attitude toward solving that dilemma. We suspect that increasing individual awareness of this social dilemma contributes to decreasing the frequency of AMR emergencies