On the motivating impact of price and online recommendations at the point of online purchase

This is the post-print version of the Article. The official published version can be accessed from the link below - Copyright @ 2011 ElsevierDo online recommendations have the same motivating impact as price at the point of online purchase? The results (n = 268) of an conjoint study show that: (1) when the price is low or high relatively to market price, it has the strongest impact (positive and negative) on the likelihood of an online purchase of an mp3 player, (2) when the price is average to market price, online recommendation and price are equal in their impact at the point of online purchase, and, (3) the relative impact from price increases when online shopping frequencies increases. The implications these results give are that online retailers should be aware that online recommendations are not as influential as a good offer when consumers purchase electronics online. However, other customer recommendations have a stronger impact on novice online shoppers than towards those consumers that shop more frequently online

Prevention and Intervention Studies with Telmisartan, Ramipril and Their Combination in Different Rat Stroke Models

The effects of AT1 receptor blocker, telmisartan, and the ACE inhibitor, ramipril, were tested head-to head and in combination on stroke prevention in hypertensive rats and on potential neuroprotection in acute cerebral ischemia in normotensive rats. Normotensive Wistar rats were treated s.c. 5 days prior to middle cerebral artery occlusion (MCAO) for 90 min with reperfusion. Groups (n = 10 each): (1) sham, (2) vehicle (V; 0,9% NaCl), (3) T (0,5 mg/kg once daily), (4) R (0,01 mg/kg twice daily), (5) R (0,1 mg/kg twice daily) or (6) T (0,5 mg/kg once daily) plus R (0,01 mg/kg twice daily). Twenty-four and 48 h after MCAO, neurological outcome (NO) was determined. Forty-eight h after MCAO, infarct volume by MRI, neuronal survival, inflammation factors and neurotrophin receptor (TrkB) were analysed.Stroke incidence was reduced, survival was prolonged and neurological outcome was improved in all treated SHR-SP with no differences between treated groups. In the acute intervention study, T and T+R, but not R alone, improved NO, reduced infarct volume, inflammation (TNFα), and induced TrkB receptor and neuronal survival in comparison to V.T, R or T+R had similar beneficial effects on stroke incidence and NO in hypertensive rats, confirming BP reduction as determinant factor in stroke prevention. In contrast, T and T+R provided superior neuroprotection in comparison to R alone in normotensive rats with induced cerebral ischemia

Inhibition of left ventricular fibrosis by tranilast in rats with renovascular hypertension

BACKGROUND: Growth factors such as transforming growth factor-beta (TGF beta) are believed to have an essential role in cardiac fibrosis. Tranilast (N(3,4-dimethoxycinnamoyl) anthranilic acid) attenuates the increased expression of TGF beta mRNA in vitro. OBJECTIVE: To investigate whether tranilast reduces cardiac fibrosis in rats with two-kidney, one-clip (2K1C) renovascular hypertension. In addition, we tested the in-vitro effects of tranilast on cardiac myocytes and non-myocyte cells. METHODS: We analysed hearts from four groups of rats: sham-operated controls; rats with 2K1C renovascular hypertension; rats with 2K1C renovascular hypertension treated for 12 weeks with the angiotensin converting enzyme (ACE) inhibitor, quinapril (6 mg/kg per day); rats with 2K1C renovascular hypertension treated for 12 weeks with tranilast (400 mg/kg per day). RESULTS: Systolic blood pressure was reduced after quinapril treatment. Tranilast did not alter blood pressure (2K1C: 223 +/- 19 mmHg; 2K1C + quinapril: 149 +/- 15 mmHg (P <0.01 compared with 2K1C); 2K1C + tranilast: 204 +/- 32 mmHg). Left ventricular weight was likewise reduced significantly by quinapril, but not significantly by tranilast (2K1C: 1.52 +/- 0.2 g; 2K1C + quinapril: 1.26 +/- 0.18 g (P <0.05 compared with 2K1C); 2K1C + tranilast: 1.37 +/- 0.27 g). Using a computer-aided image analysis system, we demonstrated that tranilast prevented cardiac fibrosis in a blood-pressure-independent manner (P <0.01 compared with 2K1C). Determination of the cardiac hydroxyproline content similarly revealed a significant reduction in cardiac fibrosis by tranilast (2K1C: 4.92 +/- 0.48 mg/mg; 2K1C + tranilast: 3.97 +/- 0.46 mg/mg; P <0.05). The effect of tranilast on cardiac fibrosis was comparable to the effects of a blood-pressure-decreasing dose of the ACE inhibitor, quinapril. Cell culture experiments revealed that tranilast significantly decreased the proliferation of cardiac non-myocyte cells. Proliferation of cardiac myocytes was not altered. CONCLUSION: This study revealed that long-term treatment with tranilast markedly attenuated left ventricular fibrosis in rats with renovascular hypertension. This was most probably the result of an antiproliferative effect of tranilast on cardiac non-myocyte cells. Tranilast thus offers a unique new therapeutic approach to the reduction of TGF beta-mediated cardiac fibrosis in viv