Effects of N-substituents on the Polymerization Properties of Maleimide

The effect of the amide function and the carbethoxy function on the polymerization properties of maleimide are reported. The effects of these functions on homopolymerization and copolymerization (with styrene) were examined. These electron-withdrawing groups appeared to decrease the rate of homopolymerization and increase the rate of copolymerization. N-carbamylmaleimide and N-carbethoxymaleimide were copolymerized with styrene in 1,4 -dioxane at 60.0° C at different feed ratios to high conversion. Copolymer composition, determined by elemental analysis and 1H NMR, indicated that while 1:1 copolymers were obtained with an equimolar feed ratio, the two systems were not alternating. It is of note that the copolymerizations were carried out at a very low total monomer concentration of 0.2 mol/L due to the limited solubility of N-carbamylmaleimide in the reaction solvent. If higher concentrations had been possible, 1:1 copolymer formation would have been enhanced. Investigation of the complexation of maleic anhydride, maleimide, N-carbethoxymaleimide, N-carbamylmaleimide, N-phenylmaleimide and N-ethylmaleimide with the electron-donors styrene, furan, and 2-chloroethyl vinyl-ether was accomplished by use of ultraviolet (UV) spectroscopy and 1H NMR spectroscopy. It appeared generally that the electron-withdrawing groups increased the complexation of maleimide with the electron-donating comonomers. There was no evidence of complex formation with 2-chloroethyl vinyl ether for any of the compounds studied. A continuous variation method using UV spectroscopy indicated that all observed charge-transfer complexes (maleic anhydride-styrene; N-carbethoxymaleimide-styrene; N-phenylmaleimide-styrene; maleic anhydride-furan; N-carbamylmaleimide-furan) had 1:1 stoichiometry. The formation constant of complexation between maleimide and styrene was increased towards the value of the complex formation constant for maleic anhydride-styrene when the electron-withdrawing groups -CONH2 and -C02Et were substituted on the maleimide N. The same effect was not observed for complexation with furan. IR spectroscopy and 13c NMR spectroscopy indicate that the electron-withdrawing groups increase the double bond character of the maleimide carbonyl groups. The results of the complexation studies suggest that the carbonyl groups of maleimide may play a significant role in complex formation with styrene. The mechanism of complex formation with furan appears to be different from that of styrene. It was also shown that when N-phenylmaleimide and maleic anhydride (both electron-accepting monomers) are copolymerized, a random copolymer results. When reaction with styrene is considered, the results of this investigation indicate that electron-withdrawing N-substituents influence the polymerization properties of maleimide to be more like those of maleic anhydride

Rupture of the profunda femoris artery in a patient with alcoholic liver disease: a case report

Introduction: Profunda femoris artery aneurysms are rare and often present with rupture. However, to the best of our knowledge, rupture of a non-aneurismal profunda femoris artery has never been reported before. Case presentation: We report the case of a 31-year-old Caucasian man with alcoholic liver disease who presented with rupture of the profunda femoris artery following blunt trauma which was treated by endovascular embolization. Conclusion: Coagulopathy secondary to alcoholic liver disease is a major contributory factor and a high index of suspicion of vascular injury must be attached to such patients following blunt trauma. Although there have no previous documented cases, treatment by endovascular embolization appears to be effective and safe

PTGER1 and PTGER2 receptors mediate regulation of progesterone synthesis and type 1 11β-hydroxysteroid dehydrogenase activity by prostaglandin E2 in human granulosa–lutein cells

In luteinizing granulosa cells, prostaglandin E2 (PGE2) can exert luteotrophic actions, apparently via the cAMP signalling pathway. In addition to stimulating progesterone synthesis, PGE2 can also stimulate oxidation of the physiological glucocorticoid, cortisol, to its inactive metabolite, cortisone, by the type 1 11β-hydroxysteroid dehydrogenase (11βHSD1) enzyme in human granulosa–lutein cells. Having previously shown these human ovarian cells to express functional G-protein coupled, E-series prostaglandin (PTGER)1, PTGER2 and PTGER4 receptors, the aim of this study was to delineate the roles of PTGER1 and PTGER2 receptors in mediating the effects of PGE2 on steroidogenesis and cortisol metabolism in human granulosa–lutein cells. PGE2-stimulated concentration-dependent increases in both progesterone production and cAMP accumulation (by 1·9±0·1- and 18·7±6·8-fold respectively at 3000 nM PGE2). While a selective PTGER1 antagonist, SC19220, could partially inhibit the steroidogenic response to PGE2 (by 55·9±4·1% at 1000 nM PGE2), co-treatment with AH6809, a mixed PTGER1/PTGER2 receptor antagonist, completely abolished the stimulation of progesterone synthesis at all tested concentrations of PGE2 and suppressed the stimulation of cAMP accumulation. Both PGE2 and butaprost (a preferential PTGER2 receptor agonist) stimulated concentration-dependent increases in cortisol oxidation by 11βHSD1 (by 42·5±3·1 and 40·0±3·0% respectively, at PGE2 and butaprost concentrations of 1000 nM). Co-treatment with SC19220 enhanced the ability of both PGE2 and butaprost to stimulate 11βHSD1 activity (by 30·2±0·2 and 30·5±0·6% respectively), whereas co-treatment with AH6809 completely abolished the 11βHSD1 responses to PGE2 and butaprost. These findings implicate the PTGER2 receptor–cAMP signalling pathway in the stimulation of progesterone production and 11βHSD1 activity by PGE2 in human granulosa–lutein cells

Macrophage Sub-Populations and the Lipoxin A4 Receptor Implicate Active Inflammation during Equine Tendon Repair

Macrophages (Mϕ) orchestrate inflammatory and reparatory processes in injured connective tissues but their role during different phases of tendon healing is not known. We investigated the contribution of different Mϕ subsets in an equine model of naturally occurring tendon injury. Post mortem tissues were harvested from normal (uninjured), sub-acute (3–6 weeks post injury) and chronically injured (>3 months post injury) superficial digital flexor tendons. To determine if inflammation was present in injured tendons, Mϕ sub-populations were quantified based on surface antigen expression of CD172a (pan Mϕ), CD14highCD206low (pro-inflammatory M1Mϕ), and CD206high (anti-inflammatory M2Mϕ) to assess potential polarised phenotypes. In addition, the Lipoxin A4 receptor (FPR2/ALX) was used as marker for resolving inflammation. Normal tendons were negative for both Mϕ and FPR2/ALX. In contrast, M1Mϕ predominated in sub-acute injury, whereas a potential phenotype-switch to M2Mϕ polarity was seen in chronic injury. Furthermore, FPR2/ALX expression by tenocytes was significantly upregulated in sub-acute but not chronic injury. Expression of the FPR2/ALX ligand Annexin A1 was also significantly increased in sub-acute and chronic injuries in contrast to low level expression in normal tendons. The combination of reduced FPR2/ALX expression and persistence of the M2Mϕ phenotype in chronic injury suggests a potential mechanism for incomplete resolution of inflammation after tendon injury. To investigate the effect of pro-inflammatory mediators on lipoxin A4 (LXA4) production and FPR2/ALX expression in vitro, normal tendon explants were stimulated with interleukin-1 beta and prostaglandin E2. Stimulation with either mediator induced LXA4 release and maximal upregulation of FPR2/ALX expression after 72 hours. Taken together, our data suggests that although tenocytes are capable of mounting a protective mechanism to counteract inflammatory stimuli, this appears to be of insufficient duration and magnitude in natural tendon injury, which may potentiate chronic inflammation and fibrotic repair, as indicated by the presence of M2Mϕ

Effect of oleic acid supplementation on prostaglandin production in maternal endometrial and fetal allantochorion cells isolated from late gestation ewes

Elevated circulating non-esterified fatty acids including oleic acid (OA) are associated with many pregnancy related complications. Prostaglandins (PGs) play crucial roles during parturition. We investigated the effect of OA supplementation on PG production using an in vitro model of ovine placenta

Groundwater quality and antibiotic resistance of coliform bacteria in Wilgamuwa, an area of Chronic Kidney Disease of unknown etiology (CKDu) in Sri Lanka

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Resolving an inflammatory concept: the importance of inflammation and resolution in tendinopathy

Injuries to the superficial digital flexor tendon (SDFT) are an important cause of morbidity and mortality in equine athletes, but the healing response is poorly understood. One important drive for the healing of connective tissues is the inflammatory cascade, but the role of inflammation in tendinopathy has been contentious in the literature. This article reviews the processes involved in the healing of tendon injuries in natural disease and experimental models. The importance of inflammatory processes known to be active in tendon disease is discussed with particular focus on recent findings related specifically to the horse. Whilst inflammation is necessary for debridement after injury, persistent inflammation is thought to drive fibrosis, a perceived adverse consequence of tendon healing. Therefore the ability to resolve inflammation by the resident cell populations in tendons at an appropriate time would be crucial for successful outcome. This review summarises new evidence for the importance of resolution of inflammation after tendon injury. Given that many anti-inflammatory drugs suppress both inflammatory and resolving components of the inflammatory response, prolonged use of these drugs may be contraindicated as a therapeutic approach. We propose that these findings have profound implications not only for current treatment strategies but also for the possibility of developing novel therapeutic approaches involving modulation of the inflammatory process

Plasma renin activity and aldosterone concentrations in hypertensive cats with and without azotemia and in response to treatment with amlodipine besylate

BACKGROUND: Role of renin‐angiotensin aldosterone system (RAAS) in feline systemic hypertension is poorly understood. OBJECTIVES: Examine plasma renin activity (PRA) and plasma aldosterone concentrations (PAC) in normotensive and hypertensive cats with variable renal function and in response to antihypertensive therapy. ANIMALS: One hundred and ninety‐six cats >9 years from first opinion practice. METHODS: PRA, PAC, and aldosterone‐to‐renin ratio (ARR) were evaluated in cats recruited prospectively and grouped according to systolic blood pressure (SBP) and renal function (nonazotemic normotensive [Non‐Azo‐NT], nonazotemic hypertensive [Non‐Azo‐HT], azotemic normotensive [Azo‐NT], azotemic hypertensive [Azo‐HT]). Changes in PRA and PAC were evaluated with antihypertensive therapy (amlodipine besylate). RESULTS: Plasma renin activity (ng/mL/h; P = .0013), PAC (pg/mL; P < .001), and ARR (P = 0.0062) differed significantly among groups. PRA (ng/mL/h) was significantly lower in hypertensive (Non‐Azo‐HT; n = 25, median 0.22 [25th percentile 0.09, 75th percentile 0.39], Azo‐HT; n = 44, 0.33 [0.15, 0.48]) compared with Non‐Azo‐NT cats (n = 57, 0.52 [0.28, 1.02]). Azo‐HT cats had significantly higher PAC (n = 22, 149.8 [103.1, 228.7]) than normotensive cats (Non‐Azo‐NT; n = 26, 45.4 [19.6, 65.0], Azo‐NT; n = 18, 84.1 [38.6, 137.8]). ARR was significantly higher in Azo‐HT (n = 20, 503.8 [298.8, 1511]) than Azo‐NT cats (n = 16, 97.8 [77.0, 496.4]). Significant increase in PRA was documented with antihypertensive therapy (pretreatment [n = 20] 0.32 [0.15–0.46], posttreatment 0.54 [0.28, 1.51]), but PAC did not change. CONCLUSIONS AND CLINICAL IMPORTANCE: Hypertensive cats demonstrate significantly increased PAC with decreased PRA. PRA significantly increases with antihypertensive therapy. Additional work is required to determine the role of plasma aldosterone concentration in the pathogenesis of hypertension and whether this relates to autonomous production or activation of RAAS without demonstrable increase in PRA