'It will harm business and increase illicit trade': an evaluation of the relevance, quality and transparency of evidence submitted by transnational tobacco companies to the UK consultation on standardised packaging 2012.

INTRODUCTION: Transnational tobacco companies (TTCs) submitted evidence to the 2012 UK Consultation on standardised packaging (SP) to argue the policy will have detrimental economic impacts and increase illicit tobacco trade. METHODS: A content analysis of the four TTC submissions to the consultation assessed the relevance and quality of evidence TTCs cited to support their arguments. Investigative research was used to determine whether the cited evidence was industry connected. Fisher's exact tests were used to compare the relevance and quality of industry-connected and independent from the industry evidence. The extent to which TTCs disclosed financial conflicts of interest (COI) when citing evidence was examined. RESULTS: We obtained 74 pieces of TTC-cited evidence. The quality of the evidence was poor. TTCs cited no independent, peer-reviewed evidence that supported their arguments. Nearly half of the evidence was industry-connected (47%, 35/74). None of this industry-connected evidence was published in peer-reviewed journals (0/35) and 66% (23/35) of it was opinion only. Industry-connected evidence was of significantly poorer quality than independent evidence (p<0.001). COIs were not disclosed by TTCs in 91% (32/35) of cases. CONCLUSIONS: In the absence of peer-reviewed research to support their arguments, TTCs relied on evidence they commissioned and the opinions of TTC-connected third-parties. Such connections were not disclosed by TTCs when citing this evidence and were time consuming to uncover. In line with Article 5.3 of the Framework Convention on Tobacco Control and broader transparency initiatives, TTCs should be required to disclose their funding of all third-parties and any COIs when citing evidence.

Barefoot running improves economy at high intensities and peak treadmill velocity.

AIM: Barefoot running can improve running economy (RE) compared to shod running at low exercise intensities, but data is lacking for the higher intensities typical during many distance running competitions. The influence of barefoot running on the velocity at maximal oxygen uptake (vVO2max) and peak incremental treadmill test velocity (vmax) is unknown. The present study tested the hypotheses that barefoot running would improve RE, vVO2max and vmax relative to shod running. METHODS: Using a balanced within-subject repeated measures design, eight male runners (aged 23.1±4.5 years, height 1.80±0.06 m, mass 73.8±11.5 kg, VO2max 4.08±0.39 L·min(-1)) completed a familiarization followed by one barefoot and one shod treadmill running trial, 2-14 days apart. Trial sessions consisted of a 5 minute warm-up, 5 minute rest, followed by 4×4 minute stages, at speeds corresponding to ~67, 75, 84 and 91% shod VO2max respectively, separated by a 1 minute rest. After the 4th stage treadmill speed was incremented by 0.1 km·h(-1) every 15 s until participants reached volitional exhaustion. RESULTS: RE was improved by 4.4±7.0% across intensities in the barefoot condition (P=0.040). The improvement in RE was related to removed shoe mass (r2=0.80, P=0.003) with an intercept at 0% improvement for RE at 0.520 kg total shoe mass. Both vVO2max (by 4.5±5.0%, P=0.048) and vmax (by 3.9±4.0%, P=0.030) also improved but VO2max was unchanged (p=0.747). CONCLUSION: Barefoot running improves RE at high exercise intensities and increases vVO2max and vmax, but further research is required to clarify the influence of very light shoe weights on RE.

Postoperative pain management in the non-Hispanic white and Mexican American older adult.

The purpose of this study was to assess use of pain relief measures and satisfaction with postoperative pain management among non-Hispanic white and Mexican American older adults after abdominal surgery. Findings revealed interpatient and intraethnic diversity, endorsing the importance of careful patient assessment and examining patient satisfaction for quality assurance/improvement.

Effects of prostaglandin F2 alpha on intracellular pH, intracellular calcium, cell shortening and L-type calcium currents in rat myocytes.

OBJECTIVE: We have studied the mechanisms underlying the positive inotropic action of prostaglandin F2 alpha (PGF2 alpha) by monitoring intracellular calcium transients, intracellular pH, L-type calcium currents and cell shortening in isolated ventricular myocytes. METHODS: Rat myocytes were loaded with fura-2AM for intracellular calcium measurements, or BCECF-AM for pH measurements. Cell shortening was recorded using an edge detection system, and L-type calcium currents measured using whole cell patch clamping. RESULTS: PGF2 alpha (3 nmol l-1-3 mumol l-1 increased single myocyte shortening and reduced resting cell length in a concentration-dependent manner. While myocyte shortening was increased by PGF2 alpha, this was not associated with any change in the amplitude of intracellular calcium transients, diastolic calcium, or L-type calcium currents. However, the same myocytes were capable of responding to catecholamines with increases in calcium transient amplitude and L-type calcium currents. PGF2 alpha (3 mumol l-1 caused a reversible rise in intracellular pH of 0.08 +/- 0.01 pH units (n = 5, p < 0.05). The Na(+)-H+ exchanger inhibitor, HOE 694 (10 mumol l-1, abolished the PGF2 alpha-induced rise in pH and the increase in cell shortening. PGF2 alpha-induced increases in cell shortening and intracellular pH were also attenuated by the protein kinase C (PKC) inhibitor, chelerythrine (2 mumol l-1. CONCLUSION: The positive inotropic action of PGF2 alpha appears to be mediated via activation of the Na(+)-H+ exchanger with the possible involvement of PKC. This suggests that PGF2 alpha-produces intracellular alkalosis, which then sensitizes cardiac myofilaments to calcium.

Structure-activity relationships of some novel coronary dilator derivatives of palmitoyl carnitine in the rat isolated heart.

The structure-activity relationships of some novel coronary dilator derivatives of palmitoyl carnitine in the rat isolated perfused heart are described. It has been shown previously that esterification of palmitoyl carnitine changes the activity of the compound from a coronary constrictor to a coronary dilator. In this study, it was found that the ester group is not a necessary requirement for coronary dilator activity, but only the absence of the negatively charged carboxylic acid group of palmitoyl carnitine, as compounds containing an ethyl group in place of the ester group were also active coronary dilators. Furthermore, substituting the methyl groups attached to the nitrogen atom of the molecule profoundly altered coronary dilator activity. A quaternary ammonium group was a necessary requirement for potent coronary dilator activity.

Effect of palmitoyl carnitine isopropyl ester on the actions of BAY K 8644 and norepinephrine in the perfused rat heart.

We examined the actions of the isopropyl ester of palmitoyl carnitine (P1Pi), a novel vasodilator compound, on coronary constriction mediated by the calcium channel activator BAY K 8644 and positive inotropic responses mediated by norepinephrine (NE) and low sodium perfusion in perfused rat hearts. Langendorff-perfused hearts were given bolus doses of BAY K 8644 or NE. The effects of P1Pi or atenolol on perfusion pressure, heart rate (HR), and developed tension changes induced by these agents were studied. In other experiments, low-sodium perfusion was used to manipulate sodium-calcium exchange in the presence and absence of P1Pi. P1Pi inhibited the coronary constrictor action of BAY K 8644 and also produced a selective inhibition of the inotropic but not the chronotropic action of NE. These effects of P1Pi were not associated with any depression of basal myocardial contractility. P1Pi did not affect the inotropic or coronary constrictor responses induced by low-sodium perfusion. The effects of P1Pi on the responses induced by BAY K 8644 and NE indicate that P1Pi inhibits activated L-type calcium channels while having no effect on sodium-calcium exchange. These effects may be related to the charged nature of this amphiphilic compound.