Physicians are not always comfortable deferring treatment of a stenosis in the left anterior descending (LAD) artery because of the perception that there is a high risk of major adverse cardiac events (MACE). The authors describe, using the DEFINE-FLAIR (Functional Lesion Assessment of Intermediate Stenosis to Guide Revascularisation) trial, MACE rates when LAD lesions are deferred, guided by physiological assessment using fractional flow reserve (FFR) or the instantaneous wave-free ratio (iFR).
No abstract is provided for this article.
Hydration models can aid in the prediction, understanding and description of hydration behaviour over time as the move towards more sustainable cements continues.\nHYDCEM is a new model to predict the phase assemblage, degree of hydration and heat release over time for cements undergoing hydration for any w/c ratio and curing temperatures up to 450C. HYDCEM, written in MATLAB, complements more sophisticated thermodynamic models by predicting these properties over time using user-friendly inputs within one code. A number of functions and methods based on up to date cement hydration behaviour from the literature are hard-wired into the code along with user-changeable inputs including w/c ratio, curing temperature, chemical compositions, densities and enthalpies. Predictions of hydration product volumes from the silicate, aluminate and ferrite phases can be determined, including C-S-H, calcium hydroxide, hydrogarnet (if applicable) ettringite and monosulfate. A number of comparisons have been made with published phase assemblages using thermodynamic models and HYDCEM predictions to assess its accuracy and usefulness.\nThis paper presents simulations of cement hydration and microstructure development with and without the additional of ground limestone using the HYDCEM model, both in terms of monocarbonate growth at the expense of monosulfate and ettringite. Comparisons with published phase assemblages show good agreement in terms of volumetric growth and behaviour.
1 Exogenous tachykinins modulate cholinergic neurotransmission in rabbit and guinea-pig airways. We have investigated the effect of selective tachykinin receptor agonists and antagonists on cholinergic neurotransmission evoked by electrical field stimulation (EFS) of bronchial rings in rabbit, guinea-pig and human airways in vitro to assess which type of tachykinin receptor is mediating this facilitatory effect. 2 Bronchial rings were set up for isometric tension recording. Contractile responses to EFS (60 V, 0.4 ms, 2 Hz for 10 s every min) and exogenous acetylcholine (ACh) were obtained and the effects of selective tachykinin agonists and antagonists were investigated. 3 In rabbit bronchi the endogenous tachykinins, substance P (SP) and neurokinin A (NKA) (10 nM) potentiated cholinergic responses to EFS (by 287.6 ± 121%, P < 0.01 and 181.4 ± 56.5%, P < 0.001 respectively). 4 The NK1 receptor selective agonist, [Sar9]SP sulphone (10 nM) evoked a maximal facilitatory action on cholinergic responses of 334.9 ± 63% (P < 0.01) (pD2 = 8.5 ± 0.06) an effect which was blocked by the selective NK1-receptor antagonist, CP 96,345 (100 nM) (P < 0.05) but not by the NK2 receptor antagonist, MEN 10,376 (100 nM). The NK2 receptor selective agonist, [βAla8]NKA(4–10) (10 nM), produced a maximum enhancement of 278 ± 83.5% (P < 0.01) (pD2 = 8.7 ± 0.1) an effect which was blocked by MEN 10,376 (100 nM) (P < 0.05) and not by CP 96,345. [MePhe7]NKB, an NK3 receptor selective agonist was without effect. 5 The rank order of potency of NK2 receptor antagonists against enhancement of cholinergic responses by [βAla8]NKA(4–10) was MEN 10,376 > L 659,877 > R 396. This pattern together with the observation of the full agonist activity of MDL 28,564 indicates that the NK2 receptors in the rabbit bronchus are similar to those which are present in the rabbit pulmonary artery. 6 Neither [Sar9]SP sulphone (5 nM) nor [βAla8]NKA(4–10) (1 nM) had any effect on contractile responses to ACh (10 μm) suggesting a pre-junctional mechanism of action. 7 By contrast, in guinea-pig bronchi only the NK1-receptor agonist [Sar9]SP sulphone (3 nM) was effective in enhancing cholinergic neurotransmission but the effect was relatively small (maximal enhancement 25.7 ± 5.5%, P < 0.01). In human bronchial rings all the selective neurokinin agonists were without effect on cholinergic neurotransmission. 8 These results suggest that tachykinins may play an important role in modulating cholinergic neurotransmission in rabbit (via NK1 and NK2 receptors) and guinea-pig airways (via NK1 receptor) but have no demonstrable effect on human airways.
