1-[Bicyclo[4.2.0]octa-1(6),2,4-trien-3-yl]-3-[bicyclo[4.2.0]octa-1(6),2,4-trien-3-yl­methyl]imidazolium hexa­fluoro­phos­phate

In the title compound, C20H19N2 +·PF6 −, the two benzocyclo­butene units are essentially planar and they form dihedral angles of 38.0 (2) and 72.7 (2)°, with the central imidazolium ring. In the crystal structure, weak C—H⋯π and π-–π stacking inter­actions [centroid–centroid distance = 3.742 (2) Å] contribute to the stability of the crystal structure. The PF6 − ion is disordered over two positions with site occupancies of 0.869 (9) and 0.131 (9)

Innate immunity and remodelling

A wide variety of cardiac disease states can induce remodelling and lead to the functional consequence of heart failure. These complex disease states involve a plethora of parallel signal transduction events, which may be associated with tissue injury or tissue repair. Innate immunity is activated in hearts injured in different ways, evident as cytokine release from the heart, activation of toll-like receptors involved in recognizing danger, and activation of the transcription factor nuclear factor kappa B. Nuclear factor kappa B regulates gene programmes involved in inflammation as well as the resolution of inflammation. The impact of this is an enigma; while cytokines, toll-like receptors, and nuclear factor kappa B appear to elicit myocardial protection in studies of preconditioning, the literature strongly indicates a detrimental role for activation of innate immunity in studies of acute ischaemia–reperfusion injury. The impact of activation of cardiac innate immunity on the long-term outcome in in vivo models of hypertrophy and remodelling is less clear, with conflicting results as to whether it is beneficial or detrimental. More research using genetically engineered mice as tools, different models of evoking remodelling, and long-term follow-up is required for us to conclude whether activation of the innate immune system is good, bad, or unimportant in chronic injury models

MAFFUCCI'S SYNDROME ASSOCIATED WITH HYPERPARATHYROIDISM

Maffucci's syndrome is a rare, congenital, nonhereditary, mesodermal dysplastic disease characterized by venous malformations and benign cartilaginous tumors. The occurrence of endocrine tumors in Maffucci's syndrome is very rare. We report a case of Maffucci's syndrome associated with hyperparathyroidism and multinodular goiter

Inhibition of chemotaxis in A7r5 rat smooth muscle cells by a novel panel of inhibitors

1. Arginine-specific ADP-ribosyltransferase (ART) activity has been implicated in white cell chemotaxis. In this study, we examined the capacity of a panel of structurally unrelated inhibitors and pseudo-substrates of ART to inhibit chemotaxis of A7r5 rat vascular smooth muscle cells in response to PDGF-BB. 2. The IC(50) values for nicotinamide (12 mM) and novobiocin (165 μM) were similar to those observed for inhibition of chemotaxis by human polymorphonuclear neutrophil leucocytes (PMN), whereas vitamins K(3) (IC(50)=22 μM) and K(1) (IC(50)=95 μM) were less potent than previously described in PMNs. The pseudo-substrates for the enzyme (DEA-BAG, agmatine and arginine-methylester) also inhibited A7r5 chemotaxis, and in addition inhibited cell adhesion at similar concentrations. Vitamin K(3) was unique among the inhibitors of ART, in that it also inhibited cell adhesion. 3. A rat ART1 transcript was amplified by rtPCR from rat skeletal muscle, and was noted to share 94% homology with the mouse ART1 cDNA sequence. No such transcript could be detected in A7r5 cells by Northern blot analysis or rtPCR. 4. Evidence for ART activity on the surface of A7r5 cells was investigated using (32)P-NAD(+) as substrate, and labelled membrane proteins were observed with MWt values of 116, 100, 90 and 70 kDa. Exposure of the labelled proteins to phosphodiesterase yielded (32)P-AMP, and hydrolysis with NaOH yielded (32)P-NAD(+). These results indicated that the labelled proteins were adducts with NAD(+), and not the products of ART activity. The absence of ART catalytic activity in A7r5 cells was confirmed in protocols designed to show ADP-ribosylation of agmatine. 5. We conclude that the chemotactic activity of A7r5 cells is independent of ART activity, and the mechanism whereby the novel panel of inhibitors reduced cell migration remains undefined