Summary: Novel hyperbranched polyphenylenes based on both an A2 + B3 and an AB2 + AB approach were synthesised and characterised. Different monomers were prepared and polymerised using a Diels‐Alder reaction with subsequent decarbonylation. The polymer backbones consist of hexaphenylbenzene units which are linked in different positions and functionalised by cyclopentadienone (A) and/or alkyne groups (B) depending on the monomer ratio. The structure and properties of the resulting polymers were compared to those of hyperbranched polyphenylenes based solely on an AB2 monomer. All branched products showed high thermal stability and good solubility in common organic solvents such as chloroform or toluene. However, due to steric hindrance, the polyphenylenes produced using the A2 + B3 approach exhibited a high percentage of linear units within the polymer structure.
Schematic structure of hyperbranched polyphenylenes from A2 and B3 monomers. 相似文献
Taking into account the dependency on molar mass of the viscometric interaction parameter B, the modified Stockmayer-Fixman-Burchard equation ([η]/M1/2) = KΘ + C″ · A2 · M1/2 is obtained. It relates the intrinsic viscosity, [η], to the second virial coefficient, A2, and to the unperturbed dimensions parameter, KΘ, with C″ being a constant. Hereupon, KΘ can be determined from [η] and A2 data of any binary (solvent/polymer) and/or ternary (solvent 1/solvent 2/polymer) system, BPS and/or TPS. Because of the scarcity of reliable sets of [η] and A2 values mostly for TPS, the application of the above equation to obtain KΘ coefficients rests limited. This limitation can be surmounted by an A2 evaluation from [η] data and trial KΘ values through two-parameter theories taking into account the interpenetrating factor between chains, ψ, as evaluated from the Flory-Krigbaum-Orofino (FKO) theory, from a modified FKO theory, or from the Kurata-Yamakawa theory. An interative process is followed until coincidence between assumed and evaluated KΘ values is reached. The method has been applied to the KΘ evaluation from [η] with literature data for diverse BPS and TPS of polystyrene, poly(methyl methacrylate), poly(dimethylsiloxane), poly(2-vinylpyridine) and poly(1-vinyl-2-pyrrolidone), with the respective KΘ values 7,5 · 10?2, 5,8 · 10?2, 8,2 · 10?2 and 6,4 · 10?2, 7.2·10?2 and · 6,4 · 10?2 mL · mol1/2 · g?3/2 being obtained. Moreover, a single C″ value, mainly C″ = 0,52, holds for all five polymers. 相似文献
Between January 1975 and January 1982, 157 patients with a diagnosis of adenocarcinoma of the rectosigmoid colon underwent curative surgical resection. The median follow-up was three years (range, 2.5 to 9 years). Two patients were excluded from the study for staging purposes because they received preoperative radiation. The remaining patients were categorized in the following stages: carcinoma in situ—3; A—14; B1—14; B2—41; B3—8; C1—1; C2—70; and C3—4. The overall local recurrence rate was 41 percent. The local recurrence according to stage was as follows: stage A—1/14 (7 percent); B1—2/14 (14 percent); B2—15/38 (39 percent); B3—3/8 (38 percent); C1—0/1; C2—31/56 (55 percent); and C3—4/4 (100 percent). Seventeen patients in stages B2 and C2 received postoperative irradiation. Only two patients (2/17, or 12 percent) recurred locally. In this study the local recurrence rate for patients undergoing curative surgical resection only was very high, especially in patients with advanced stage of disease (B2 to C3). There is evidence that postoperative radiotherapy could minimize the local failure rate. 相似文献
This study aimed to investigate the role of endogenous angiotensin II (ANGII) in the upregulation of ANG-II AT1 receptors in adrenal glands during a low-salt intake. To this end male Sprague-Dawley rats were fed a low-salt diet (0.2
mg/g) for 10 days and were treated with the ANGII-AT1 receptor antagonist losartan (40 mg/kg per day) for 2 days, and adrenal mRNA levels for ANGII AT1A and AT1B receptors were determined by RNase protection. The low-salt diet increased AT1A and AT1B receptor mRNA levels by 90% and 220%, respectively. Losartan treatment did not change the basal AT1A mRNA level, but decreased AT1B mRNA by 50%. Treatment of rats on a low-salt diet with losartan did not change the increase of AT1A mRNA but significantly attenuated the increase of AT1B mRNA to 90% of the control value. Stimulation of endogenous ANGII levels by unilateral renal artery clipping for 2 days lowered
AT1A mRNA by 25% and increased AT1B mRNA by 30%. Additional treatment with losartan did not affect the decreased AT1A mRNA levels in rats with a unilateral renal artery clip, but significantly attenuated the increase of AT1B mRNA. These findings suggest that sodium deficiency stimulates adrenal AT1A and AT1B receptor mRNA levels primarily via an ANGII-AT1-independent mechanism. The preferential increase of adrenal AT1B mRNA during a low-salt intake could be explained by the elevation of endogenous ANGII levels during sodium deficiency, suggesting
that endogenous ANGII acts as an enhancer for adrenal AT1B but not for AT1A receptor gene expression via ANGII-AT1 receptors.
Received: 23 May 1997 / Received after revision: 23 February 1998 / Accepted: 11 March 1998 相似文献
Intestinal epithelial barrier function is compromised in inflammatory bowel disease and barrier dysfunction contributes to disease progression. Extracellular nucleotides/nucleosides generated in gut inflammation may regulate barrier function through actions on diverse cell types. Enteric glia modulate extracellular purinergic signaling and exert pathophysiological effects on mucosal permeability. These glia may regulate inflammation with paracrine responses, theoretically mediated via adenosine 2B receptor (A2BR) signaling. As the cell-specific roles of A2BRs in models of colitis and barrier dysfunction are unclear, we studied glial A2BRs in acute dextran sodium sulfate (DSS) colitis. We performed and validated conditional ablation of glial A2BRs in Sox10CreERT2+/?;Adora2bf/f mice. Overt intestinal disease activity indices in DSS-colitis were comparable between Sox10CreERT2+/–;Adora2bf/f mice and littermate controls. However, ablating glial A2BRs protected against barrier dysfunction following acute DSS-colitis. These benefits were associated with the normalization of tight junction protein expression and localization including claudin-1, claudin-8, and occludin. Glial A2BR signaling increased levels of proinflammatory mediators in the colon and cell-intrinsic regulation of genes including Csf3, Cxcl1, Cxcl10, and Il6. Our studies show that glial A2BR signaling exacerbates immune responses during DSS-colitis and that this adenosinergic cell-specific mechanism contributes to persistent gut epithelial barrier dysfunction. 相似文献
Pregnant rats were treated daily with 1 g/L of l-glutamate in their drinking water during pregnancy and/or lactation. The effect on adenosine A1 receptor (A1R) and A2A receptor (A2AR) in brains from both mothers and 15-day-old neonates was assayed using radioligand binding and real time PCR assays. Mothers receiving l-glutamate during gestation, lactation, and throughout gestation and lactation showed a significant decrease in total A1R number (water+water, 302±49 fmol/mg; l-glutamate+water, 109±11 fmol/mg, P<0.01; water+l-glutamate, 52±13 fmol/mg, P<0.01; l-glutamate+l-glutamate, 128±33 fmol/mg, P<0.05). No variations were detected in the Kd parameter. Concerning adenosine A2AR, radioligand binding assays revealed that Bmax parameter remains unaltered in maternal brain in response to glutamate exposure. However, Kd parameter was significantly decreased in all l-glutamate-treated groups (water+water, 5.3±1.3 nM; l-glutamate±water, 0.5±0.1 nM; water+l-glutamate, 0.9±0.1 nM; l-glutamate±l-glutamate, 0.7±0.1 nM, P<0.01 in all cases). In both male and female neonates, A1R was also decreased after long-term glutamate exposure during gestation, lactation, and gestation plus lactation (male neonates: water+water, 564±68 fmol/mg; l-glutamate+water, 61±8 fmol/mg; water+l-glutamate, 95±20 fmol/mg; l-glutamate+l-glutamate, 111±15 fmol/mg; P<0.01 in all cases; female neonates: water+water, 216±35 fmol/mg; l-glutamate+water, 59±9 fmol/mg; water+l-glutamate, 139±16 fmol/mg; l-glutamate+l-glutamate, 97±14 fmol/mg; P<0.01 in all cases). No variations were found in mRNA level coding adenosine A1R in maternal or neonatal brain. Concerning adenosine A2AR, radioligand binding assays revealed that Bmax parameter was significantly increased in male and female neonates exposed to l-glutamate during lactation (male neonates: water+water, 214±23 fmol/mg; water+l-glutamate, 581±49 fmol/mg; P<0.01; female neonates: water+water, 51±10 fmol/mg; water+l-glutamate, 282±52 fmol/mg; P<0.05). No variations were found in mRNA level coding adenosine A2AR in maternal or neonatal brain. In summary, long-term l-glutamate treatment during gestation and lactation promotes a significant down-regulation of A1R in whole brain from both mother and neonates and a significant up-regulation of A2AR in neonates exposed to l-glutamate during lactation. 相似文献
Summary: Branched poly(arylene ether)s were prepared in an oligomeric A2 + B3 polymerization of phenol endcapped telechelic poly(arylene ether sulfone) oligomers as A2 and TFPPO as trifunctional monomer B3. The molar mass of the A2 oligomer significantly influenced the onset of gelation and the DB. A high level of cyclization during polymerization of low molar mass A2 oligomers (U3 = 660 and U6 = 1 200 g · mol?1) led to a high conversion of functional groups in the absence of gelation, and the level of cyclization reactions in the polymerization decreased as the molar mass of the A2 oligomer was increased. The pronounced steric effect in the polymerization of higher molar mass A2 oligomers (U8 = 1 800 and U16 = 3 400 g · mol?1) resulted in low reactivity of the third aryl fluoride in the B3 monomer. As a result, only slightly branched (U8 = 1 800 g · mol?1) or nearly linear (U16 = 3 400 g · mol?1) high molar mass products were obtained with higher molar mass A2 oligomers. The branched polymers exhibited lower Mark‐Houwink exponents and [η] relative to linear analogs, and differences between the branched polymers and linear analogs were less significant as the molar mass of the A2 oligomers was increased due to a decrease in the overall DB.
Objective: The effects of adenosine (Ado) and subtype-specific activators of adenosine receptors (A1, A2A, A2B and A3) were studied on the release of arachidonic acid (AA) and its metabolites (AAM) from human peripheral mononuclear cells (monocytes).
Materials and method: Adenosine and the selective agonists and antagonists of adenosine receptors were used. 3H-AA and its metabolites released into the medium were determined by measurement of the total 3H radioactivity released without separating the AAM.
Results: In the cells activated by protein kinase C specific phorbol ester (phorbol 12-myristate 13–acetate) and Ca2+ ionophore (A23187), adenosine and two subtype-specific receptor agonists, CPA(A1) and CGS 21680 (A2A) induced concentration-dependent inhibition of the release of AAM, whereas stimulation of A2B or A3 receptors was ineffective. The rank order of potency for the inhibition of AAM release was as follows: CGS 21680 = CPA >
adenosine > NECA (in the presence of ZM 24185 and DPCPX as A2A and A1 adenosine receptor antagonists, respectively) = IB-MECA. Adenosine inhibited the release of AAM only at and above the concentration
of 100 μM, whereas the inhibitory effect of A1 and A2A receptor specific agonists appeared at a concentration of 10-7 M.
Conclusions: It can be concluded that adenosine physiologically may not have a significant effect on the AAM release of circulating monocytes,
but in pathological conditions, where the local Ado concentrations increases, this nucleoside, through activation of A2A and A1 receptors can exert, at least in part, an antiinflammatory action by decreasing proinflammatory AAM production.
Received 15 May 2007; accepted without revision by G. Wallace 26 June 2007 相似文献
