Sinteza bioulja s fenolformaldehidnim smolama u alkalnim uvjetima: fizička, kemijska i toplinska svojstva smola i svojstvo lijepljenog spoja

In the present study, bio-oil produced from vacuum pyrolysis of woody biomass has been investigated as a source of chemical feedstock. Bio-based resins were produced using the bio- oil with phenol substitutions ranging from 10 to 30 wt%. The conventional GC/MS analysis was carried out for the evaluation of the chemical composition of bio-oil. TGA, DSC and FT-IR analyses were used in order to characterize the bio-oil-phenol-formaldehyde (BPF) resins. The bonding quality of wood samples bonded with the BPF resins was investigated under different pre-treatment conditions. The highest shear strength was observed for the control samples bonded with the laboratory PF resin. As the amount of bio-oil was increased up to 30 wt%, the shear strength of the samples decreased from 12.08 to 11.76 N/mm2. The bonding performance was not negatively affected by the combination of bio-oil under dry conditions. According to TS EN 12765 standard, the relevant performance requirements for bonded samples under dry conditions must be at least 10 N/mm2. Relating to the standard, all samples bonded with BPF resins obtained the requirements for durability class C1. Under wet conditions, the bonding performance was negatively affected by the addition of bio-oil. However, the BPF resins fulfilled the durability requirements for C1, C2, and C3 specified in EN 12765 (2002).U radu je predstavljeno istraživanje mogućnosti upotrebe bioulja dobivenoga vakuumskom pirolizom drvne biomase kao izvora kemijske sirovine. Biosmole su dobivene zamjenom 10 – 30 % mase (ili težinskog udjela) fenola biouljima. Analiza kemijskog sastava bioulja provedena je GC/MS metodom. Za karakterizaciju biouljnih fenolformaldehidnih smola (BPF) primijenjene su TGA, DSC i FT-IR analiza. Kvaliteta spoja uzoraka drva slijepljenih BPF smolama ispitivana je pri različitim uvjetima predobrade. Najveća čvrstoća na smicanje postignuta je na kontrolnim uzorcima lijepljenim laboratorijskim PF smolama. S povećanjem udjela bioulja do 30 % mase (ili težinskog udjela), čvrstoća na smicanje smanjila se s 12,08 na 11,76 N/mm2. Prema normi TS EN 12765, čvrstoća na smicanje u suhim uvjetima treba biti najmanje 10 N/mm2. Kombinacija bioulja s fenolformaldehidnim smolama nije negativno utjecala na svojstva slijepljenog spoja u suhim uvjetima i svi uzorci lijepljeni BPF smolama zadovoljili su zahtjeve klase trajnosti C1. U vlažnim uvjetima dodatak bioulja negativno je utjecao na svojstva slijepljenog spoja. Međutim, BPF smole ispunile su zahtjeve trajnosti za klase C1, C2 i C3 propisane normom EN 12765 (2002)

Extracellular adenosine regulates naive T cell development and peripheral maintenance

Adenosine produced as a byproduct of metabolic activity is present in all tissues and produces dose-dependent suppression of TCR signaling. Naive T cell maintenance depends on inhibition of TCR signals by environmental sensors, which are yet to be fully defined. We produced mice with a floxed adenosine A(2A) receptor (A(2A)R) gene, Adora2a, and show that either global A(2A)R deletion or cre-mediated T cell deletion elicits a decline in the number of naive but not memory T cells. A(2A)R signaling maintains naive T cells in a quiescent state by inhibiting TCR-induced activation of the phosphatidylinositide 3-kinase (PI3K)-AKT pathway, thereby reducing IL-7R alpha down-regulation and naive T cell apoptosis. Patterns of IL-7R alpha expression on T cells in chimeric mice reconstituted with Adora2a(+/+) and Adora2a(-/-) bone marrow cells suggest that decreased IL-7R alpha in naive T cells is a cell-intrinsic consequence of Adora2a deletion. In addition, A(2A)R expression increases in early thymic T cell development and contributes to progression of double-negative thymic precursors to single-positive thymocytes with increased IL-7R alpha expression. Therefore, A(2A)R signaling regulates T cell development and maintenance to sustain normal numbers of naive T cells in the periphery

Adenosine A(2B) Receptor Blockade Slows Growth of Bladder and Breast Tumors

The accumulation of high levels of adenosine in tumors activates A(2A) and A(2B) receptors on immune cells and inhibits their ability to suppress tumor growth. Deletion of adenosine A(2A) receptors (A(2A)ARs) has been reported to activate antitumor T cells, stimulate dendritic cell (DC) function, and inhibit angiogenesis. In this study, we evaluated the effects of intermittent intratumor injection of a nonselective adenosine receptor antagonist, aminophylline (AMO; theophylline ethylenediamine) and, for the first time to our knowledge, a selective A(2B)AR antagonist, ATL801. AMO and ATL801 slowed the growth of MB49 bladder and 4T1 breast tumors in syngeneic mice and reduced by 85% metastasizes of breast cancer cells from mammary fat to lung. Based on experiments with A(2A)AR(-/-) or adenosine A(2B) receptor(-/-) mice, the effect of AMO injection was unexpectedly attributed to A(2B)AR and not to A(2A)AR blockade. AMO and ATL801 significantly increased tumor levels of IFN-gamma and the IFN-inducible chemokine CXCL10, which is a ligand for CXCR3. This was associated with an increase in activated tumor-infiltrating CXCR3(+) T cells and a decrease in endothelial cell precursors within tumors. Tumor growth inhibition by AMO or ATL801 was eliminated in CXCR3(-/-) mice and RAG1(-/-) mice that lack mature T cells. In RAG1(-/-) mice, A(2B)AR deletion enhanced CD86 expression on CD11b(-) DCs. Bone marrow chimera experiments demonstrated that CXCR3 and A(2B)AR expression on bone marrow cells is required for the antitumor effects of AMO. The data suggest that blockade of A(2B)ARs enhances DC activation and CXCR3-dependent antitumor responses. The Journal of Immunology, 2012, 188: 198-205

MyD88-Dependent SHIP1 Regulates Proinflammatory Signaling Pathways in Dendritic Cells after Monophosphoryl Lipid A Stimulation of TLR4

We previously showed that monophosphoryl lipid A (MLA) activates TLR4 in dendritic cells (DCs) in a Toll/IL-1R domain-containing adaptor inducing IFN-beta (TRIF)-biased manner: MLA produced from Salmonella minnesota Re595 induced signaling events and expression of gene products that were primarily TRIF dependent, whereas MyD88-dependent signaling was impaired. Moreover, when tested in TRIF-intact/MyD88-deficient DCs, synthetic MLA of the Escherichia coli chemotype (sMLA) showed the same activity as its diphosphoryl, inflammatory counterpart (synthetic diphosphoryl lipid A), indicating that TRIF-mediated signaling is fully induced by sMLA. Unexpectedly, we found that the transcript level of one proinflammatory cytokine was increased in sMLA-treated cells by MyD88 deficiency to the higher level induced by synthetic diphosphoryl lipid A, which suggested MyD88 may paradoxically help restrain proinflammatory signaling by TRIF-biased sMLA. In this article, we demonstrate that sMLA induces MyD88 recruitment to TLR4 and activates the anti-inflammatory lipid phosphatase SHIP1 in an MyD88-dependent manner. At the same time, MyD88-dependent signaling activity at the level of IL-1R-associated kinase 1 is markedly reduced. Increased SHIP1 activity is associated with reductions in sMLA-induced I kappa B kinase alpha/beta and IFN regulatory factor 3 activation and with restrained expression of their downstream targets, endothelin-1 and IFN-beta, respectively. Results of this study identify a pattern that is desirable in the context of vaccine adjuvant design: TRIF-biased sMLA can stimulate partial MyD88 activity, with MyD88-dependent SHIP1 helping to reduce proinflammatory signaling in DCs. The Journal of Immunology, 2011, 186: 3858-3865

Extracellular adenosine regulates naive T cell development and peripheral maintenance

Adenosine produced as a byproduct of metabolic activity is present in all tissues and produces dose-dependent suppression of TCR signaling. Naive T cell maintenance depends on inhibition of TCR signals by environmental sensors, which are yet to be fully defined. We produced mice with a floxed adenosine A(2A) receptor (A(2A)R) gene, Adora2a, and show that either global A(2A)R deletion or cre-mediated T cell deletion elicits a decline in the number of naive but not memory T cells. A(2A)R signaling maintains naive T cells in a quiescent state by inhibiting TCR-induced activation of the phosphatidylinositide 3-kinase (PI3K)–AKT pathway, thereby reducing IL-7Rα down-regulation and naive T cell apoptosis. Patterns of IL-7Rα expression on T cells in chimeric mice reconstituted with Adora2a(+/+) and Adora2a(−/−) bone marrow cells suggest that decreased IL-7Rα in naive T cells is a cell-intrinsic consequence of Adora2a deletion. In addition, A(2A)R expression increases in early thymic T cell development and contributes to progression of double-negative thymic precursors to single-positive thymocytes with increased IL-7Rα expression. Therefore, A(2A)R signaling regulates T cell development and maintenance to sustain normal numbers of naive T cells in the periphery