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Notes: This paper presents the development process, methodology and findings from the first stage of an ongoing collaborative research project undertaken to determine the performance indicators employed by hotel general managers. The main focus of the study is to gain a greater understanding of the decision-making context in which general managers of national and international hotel chains use performance measures (with properties located in Europe). In particular, interest is directed at assessing the match between the "key indicators" used by general managers, their "interpretation" of the indicators and the use made of the indicators for "decision-making". By drawing upon theoretical concepts and empirical evidence in the literature, the content examines performance measurement in a hotel industry context and presents the analysis and evaluation of quantitative results.

Notes: Presents an evaluation of the theoretical context and practical application of different methods of hotel valuation, with particular emphasis on the methods related to the income-generating capacity of a hotel. The findings reveal a wide range of variation and complexity between methods and that each method has benefits and limitations and requires adjustments and assumptions in different market conditions. However, it is concluded that the more sophisticated "income-based" income capitalisation methods constitute the most effective basis for a framework on which to derive the open market value for a hotel as an ongoing business entity, but that one or more of the other main valuation approaches should be drawn on in order to effect the reconciliation of a hotel's final value.

Notes: Presents an approach to hospitality operations managementcurriculum development in higher education programmes. The methodproposed was developed in the context of the hospitality product and themanagement decision making involved in operations management. Thedetermination of curriculum content is illustrated using the accountingcontribution as an example.

Notes: This article presents the results of a project undertaken to increase the effectiveness of decision makingat the property level in the Europe, Middle East, Africa division of an international hotel chain. The objective of the project was to provide the basis for a more informed approach to routine financialplanning and control decisions of property management teams with the aim of enhancing operational profitability. The techniques used to underpin the framework are evaluated in relation to their practical application in the decision-making process and the rationale and method of implementation of the management development programme is explained.The framework was approved by the company's management board for implementation throughout the division and feedback from property management and assessment of financial results suggest the approach has made a significant contribution to profit improvement.

Notes: 〈list xml:id="l1" style="custom"〉1The effects of angiotensin II (AngII) on water and electrolyte transport are biphasic and dose-dependent, such that low concentrations (10−12 to 10−9 mol/L) stimulate reabsorption and high concentrations (10−7 to 10−6 mol/L) inhibit reabsorption. Similar dose-response relationships have been obtained for luminal and peritubular addition of AngII.2The cellular responses to AngII are mediated via AT1 receptors coupled via G-regulatory proteins to several possible signal transduction pathways. These include the inhibition of adenylyl cyclase, activation of phospholipases A2, C or D and Ca2+ release in response to inositol-1,4,5,-triphosphate or following Ca2+ channel opening induced by the arachidonic acid metabolite 5,6,-epoxy-eicosatrienoic acid. In the brush border membrane, transduction of the AngII signal involves phospholipase A2, but does not require second messengers.3Angiotensin II affects transepithelial sodium transport by modulation of Na+/H+ exchange at the luminal membrane and Na+/HCO3 cotransport, Na+/K+-ATPase activity and K+ conductance at the basolateral membrane.4Atrial natriuretic factor (ANF) does not appear to affect proximal tubular sodium transport directly, but acts via specific receptors on the basolateral and brush border membranes to raise intracellular cGMP levels and inhibit AngII-stimulated transport.5It is concluded that there is a receptor-mediated action of ANF on proximal tubule reabsorption acting via elevation of cGMP to inhibit AngII-stimulated sodium transport. This effect is exerted by peptides delivered at both luminal and peritubular sides of the epithelium and provides a basis for the modulation by ANF of proximal glomerulotubular balance. The evidence reviewed supports the concept that in the proximal tubule, AngII and ANF act antagonistically in their roles as regulators of extracellular fluid volume.

Notes: 1. Disturbances in cardiovascular responsiveness to endogenous endothelin-1 (ET-1) may play a significant role in the pathogenesis of essential hypertension. In this study the inotropic responses of cardiomyocytes derived from normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rat (SHR) strains to ET-1 (10-11-10-8 mol/L) were characterized. Isotonic contraction cycles of ventricular cardiomyocytes isolated from age-matched (11 week) WKY and SHR rats were recorded using a rapid digital imaging technique and evaluated by computation of a range of normalized parameters.2. The maximum effect of ET-1, eliciting a 60–70% increase in myocyte shortening after 3 min, was observed at 10-9 mol/L in both strains, and was associated with elevations in the rate of shortening and lengthening, abbreviated latency, contractile cycle prolongation and delayed time to peak shortening.3. No evidence for a significant strain dependent difference in the relative responsiveness to ET-1 was detected. This finding indicates that altered sensitivity to ET-1 is unlikely to be a major factor underlying the development of hypertension in this model.4. The distinct nature of the alterations in contractile parameters produced by ET-1 compared with angiotensin II (AII) suggests that the prevailing cellular mechanisms of action of these peptides are different and that ET-1 is not a paracrine or autocrine inotropic intermediate for AII

Notes: 1. Independent of its effects on renal haemodynamics and glomerular filtration, angiotensin II (All) has direct actions on the proximal tubule involving transepithelial Na+, H+, HCO3-, and water reabsorption, ammoniagenesis, gluconeogenesis and renal growth.2. The effects of AH on water and electrolyte transport are biphasic and dose-dependent, such that low concentrations (10-12–10-9 mol/L) stimulate reabsorption whereas high concentrations (10-7-10-6 mol/L) inhibit reabsorption. Similar dose-response relations have been obtained for luminal and peritubular addition of AIL3. The cellular responses to All are mediated via an AT-1 receptor coupled via G-regulatory proteins to several parallel signal transduction pathways. Low doses inhibit the basolateral adenylate cyclase, lower intracellular cAMP and withdraw the inhibitory effect of protein kinase A on the luminal Na/H exchanger. Stimulation of this exchanger may also occur due to All-receptor activation of phospholipase C to release diacyl glycerol, or by local transduction in the brush-border membrane involving phospholipase A2.4. Inhibition of proximal fluid reabsorption is associated with increased intracellular Ca2+ released from intracellular stores, or entering via voltage-sensitive channels in response to the release of inositol-l,4,5,-trisphosphate, or following Ca2+ channel opening induced by the arachidonic acid metabolite 5,6,-epoxy-eicosatrienoic acid.5. The stimulatory actions of peritubular All on proximal transport are inhibited by physiological concentrations of atrial natriuretic factor (ANF) and by parathyroid hormone (PTH).6. It is concluded that intrarenal All acts to maintain optimal matching of fluid reabsorption and filtered load in response to changes in sodium balance, as well as to promote acidification of the urine during acidosis and perhaps to potentiate tubular growth following renal injury.

Notes: 1. The antihypertensive agent rilmenidine has threefold higher affinity for I1 imidazoline receptors compared with α2-adrenoceptors and acts on the central nervous system by reducing sympathetic activity and in the kidney by inhibiting Na+/H+ exchange activity.2. In the present study, we examined: (i) the effects of luminal and peritubular administration of rilmenidine on fluid absorption in superficial proximal tubules; and (ii) the nature of the receptors involved in mediating the action of this drug in the presence of specific antagonists (efaroxan, idazoxan and 2-methoxy-idazoxan). Studies were performed in anaesthetized Sprague-Dawley rats using shrinking split-drop micropuncture.3. Luminal administration of rilmenidine (10−5 and 10−13 mol/L) inhibited proximal tubular fluid absorption. Peritubular rilmenidine at 10−12 and 10−13 mol/L also inhibited fluid uptake, whereas rilmenidine at 10−11 mol/L had a significant stimulatory action.4. In the presence of the I2 〉 I1/α2-adrenoceptor antagonist idazoxan (10−5 mol/L), luminal rilmenidine (10−5 mol/L) stimulated fluid absorption. Stimulation of fluid uptake was also observed when rilmenidine (10−5 mol/L) and the I1 imidazoline receptor antagonist efaroxan (10−5 mol/L) were added together in the luminal fluid. Luminal administration of the selective α2-adrenoceptor antagonist 2-methoxy-idazoxan (10−5 mol/L) resulted in significant attenuation of the inhibitory action of luminal rilmenidine (10−5 mol/L). This indicates that both I1 imidazoline receptors and α2-adrenoceptors are involved in the luminal actions of rilmenidine.5. The effects of luminal and peritubular administration of α-methylnoradrenaline (an α2-adrenoceptor agonist) were compared with those of rilmenidine. Luminal α-methylnoradrenaline, at higher concentrations (10−7 and 10−5 mol/L), inhibited fluid absorption, as was seen with peritubular rilmenidine, but, in contrast with rilmenidine, no stimulatory action was observed. Peritubular α-methylnoradrenaline inhibited fluid uptake at higher concentrations (10−5 and 10−7 mol/L), whereas rilmenidine at these concentrations had no effect. The differences in the concentration-dependent responses for rilmenidine and α-methylnoradrenaline indicate that both imidazoline receptors and α2-adrenoceptors are involved in the actions of these compounds on proximal fluid uptake.

Notes: 1. Cultured renomedullary interstitial cells (RMIC) isolated from 4-week-old Sprague-Dawley rat kidneys possess ETA receptors, as identified by reverse transcription–polymerase chain reaction (RT-PCR).2. Treatment with endothelin (ET)-1 (10−6 mol/L) increases the intracellular inositol 1,4,5-trisphosphate concentrations within 10 s and intracellular calcium concentrations after 7 s.3. Endothelin-1 (10−7 and 10−10 mol/L) induced increases in intracellular cAMP concentrations, but only in the presence of Nω-nitro-L-arginine, a nitric oxide synthase (NOS) inhibitor. Addition of ET-1 (10−10 mol/L) to the RMIC culture led to increases in intracellular cGMP concentrations through activation of NOS.4. In the presence of ET-1 (10−7 and 10−10 mol/L) and during NOS inhibition, RMIC responded with increased cell proliferation and extracellular matrix (ECM) synthesis. These responses were abolished by BQ-123 (10−6 mol/L), suggesting mediation via the ETA receptor subtype. The proliferative effect of ET-1 was also abolished by atrial natriuretic peptide (10−6 mol/L).5. The present study provides evidence that binding of ET-1 to ETA receptors on RMIC activates several intracellular second messenger systems that mediate cell proliferation and ECM synthesis.6. These results also highlight an important interaction between ET-1 and nitric oxide in the control of RMIC function.