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

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

Taloyhtiön pihasaneeraus : Esimerkkikohteena As Oy Kananlaulu

Työn taustana käytettiin lähiöiden suurimman aikakauden, 1960- ja 1970-lukujen kerrostalojen ajankohtaista peruskorjaustarvetta. Peruskorjaustarve koskee niin kiinteistön piha-aluetta kuin kiinteistön muitakin osia. Pihojen suurin korjaustarve perustuu kuluneiden kalusteiden, varusteiden, kasvillisuuden ja muiden osien huonokuntoisuuteen. Lisäksi muuttuneet turvallisuusvaatimukset sekä esteettömyyden haasteet tuovat lisätarvetta pihojen saneerauksille. Työni tavoitteena oli lisätä viihtyisyyttä ja parantaa Asunto Oy Kananlaulun piha-aluetta sen saneerauksella. Saneerauksessa huomioidaan metsälähiön tyypilliset pihasuunnittelun erityispiirteet. Piha-alueen analyysin avulla arvioitiin sen nykytilaa paikan päällä kohteessa. Samalla tutustuttiin myös suunnitelma- ja urakka-asiakirjoihin. Työn pohjana tutkittiin kerrostalorakentamisen ja niiden piha-aluerakentamisen kehitystä Suomessa. Tietopohjaksi haettiin tietoa myös kerrostalopihojen kunnostuksesta ja kunnostusprosessista. Tuloksena oli kirjallinen selostus piharakentamisen vaiheista. Työni toimeksiantajana oli VRJ Pohjois-Suomi Oy. Työn tulokset ovat hyödynnettävissä kerrostalopihojen peruskorjaushankkeissa. Asunto Oy Kananlaulun piha-analyysi ja pihasaneeraus voidaan liittää osaksi Kaukovainion kehittämistä. Työn tulokset antavat myös minulle itselleni mahdollisuuden kehittää omaa osaamistani viherrakentamisen työnjohdossa.As a background for the work was used the topical need of renovation in the block of flats in the suburbs built in the 1960- and 1970´s. The renovation need applies both to the yard and the other parts of the property. The biggest need of renovation is based on the poor condition of the worn out equipment, vegetation and other parts of the yard. Furthermore the changed requirements of safety and accessibility increase the renovation need. The goal on my work was to add the comfort and attractiveness of the yard of Asunto Oy Kananlaulu. During the renovation the typical characteristics of a wooden suburb were taken into account. The present situation of the yard was estimated on site. At the same time I familiarized myself the documents of planning and subcontracting. For the background of the work the development of the building of the block of flats and their yards was investigated. Also the renovation of yards and the process of renovation was studied. The result of the work is a written report of the stages of the yard construction. The principal of the work was VRJ Pohjois-Suomi Oy. The results of the work can be utilized in high-rise yards’ renovation projects. The analyses and renovation of the yard can be linked to the development of Kaukovainio area. The results of the work gave me the possibility to develop my own skills on supervision of work at green construction

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

Uniaxial strain effects on the superconducting transition in Re-doped Hg-1223 cuprate superconductors

The effects of uniaxial strain and hydrostatic pressure on Hg0.83Re0.18Ba2Ca2.4Cu3.6O14 [Hg0.83(Re0.18)-1223] were investigated by ac magnetic measurements under stress corresponding to a pressure of 20 GPa at maximum. According to a previous thermal study based on the Ehrenfest relation, in-plane contraction should increase the superconducting transition temperature Tc, whereas out-of-plane contraction should decrease Tc. This suggests that the increase in Tc under hydrostatic-pressure contraction must be smaller than that under in-plane contraction. However, the present uniaxial-strain experiments revealed enhancement of Tc under both in-plane and out-of-plane contraction, and the largest enhancement was observed under hydrostatic-pressure contraction. According to a band calculation, all contraction styles induce hole doping from the HgO blocks to the CuO2 blocks, and hydrostatic-pressure contraction yields the largest hole doping among three contractions. This behavior explains well a series of changes in Tc in the stress region of below 8 GPa. More specifically, under hydrostatic-pressure contraction, Tc exhibited an increase, a decrease, and another increase with increasing pressure, and this multistep change is similar to that observed in Bi-2223-type cuprate superconductors, suggesting that it is necessary to distinguish the effect of strain on the middle CuO2 plane in the three-CuO2-plane package from that on the outer planes