Internal market orientation and market-oriented behaviours

Purpose: The purpose of this empirical paper is to investigate internal marketing from a behavioural perspective. The impact of internal marketing behaviours, operationalised as an internal market orientation (IMO), on employees’ marketing and other in-role behaviours (IRB) were examined. ---------- Design/methodology/approach: Survey data measuring IMO, market orientation and a range of constructs relevant to the nomological network in which they are embedded were collected from the UK retail managers. These were tested to establish their psychometric properties and the conceptual model was analysed using structural equations modelling, employing a partial least squares methodology. ---------- Findings: IMO has positive consequences for employees’ market-oriented and other IRB. These, in turn, influence marketing success. Research limitations/implications – The paper provides empirical support for the long-held assumption that internal and external marketing are related and that organisations should balance their external focus with some attention to employees. Future research could measure the attitudes and behaviours of managers, employees and customers directly and explore the relationships between them. ---------- Practical implications: Firm must ensure that they do not put the needs of their employees second to those of managers and shareholders; managers must develop their listening skills and organisations must become more responsive to the needs of their employees. ---------- Originality/value: The paper contributes to the scarce body of empirical support for the role of internal marketing in services organisations. For researchers, this paper legitimises the study of internal marketing as a route to external market success; for managers, the study provides quantifiable evidence that focusing on employees’ wants and needs impacts their behaviours towards the market.

Age, muscle fatigue, and walking endurance in pre-menopausal women

Aging is associated with loss of endurance; however, aging is also associated with decreased fatigue during maximal isometric contractions. The aims of this study were to examine the relationship between age and walking endurance (WE) and maximal isometric fatigue (MIF) and to determine which metabolic/fitness components explain the expected age effects on WE and MIF. Subjects were 96 pre-menopausal women. Oxygen uptake (walking economy) was assessed during a 3-mph walk; aerobic capacity and WE by progressive treadmill test; knee extension strength by isometric contractions, MIF during a 90-s isometric plantar flexion (muscle metabolism measured by 31P MRS). Age was related to increased walking economy (low VO2, r = −0.19, P < 0.03) and muscle metabolic economy (force/ATP, 0.34, P = 0.01), and reduced MIF (−0.26, P < 0.03). However, age was associated with reduced WE (−0.28, P < 0.01). Multiple regression showed that muscle metabolic economy explained the age-related decrease in MIF (partial r for MIF and age −0.13, P = 0.35) whereas walking economy did not explain the age-related decrease in WE (partial r for WE and age −0.25, P < 0.02). Inclusion of VO2max and knee endurance strength accounted for the age-related decreased WE (partial r for WE and age = 0.03, P > 0.80). In premenopausal women, age is related to WE and MIF. In addition, these results support the hypothesis that age-related increases in metabolic economy may decrease MIF. However, decreased muscle strength and oxidative capacity are related to WE.

Ryanodine receptor phosphorylation in human heart failure

Heart failure is a complex disorder, characterized by activation of the sympathetic nervous system, leading to dysregulated Ca2+ homeostasis in cardiac myocytes and tissue remodeling. In a variety of diseases, cardiac malfunction is associated with aberrant fluxes of Ca2+ across both the surface membrane and the internal Ca2+ store, the sarcoplasmic reticulum (SR). One prominent hypothesis residues is that in heart failure, the activity of the ryanodine receptor (RyR2) Ca2+ release channel in the SR is increased due to excess phosphorylation and that this contributes to excess SR Ca2+ leak in diastole, reduced SR Ca2+ load and decreased contractility (Huke & Bers, 2008). There is controversy over which serine residues in RyR2 are hyperphosphorylated in animal models of heart failure and whether this is via the CaMKII or the PKA-linked signaling pathway. S2808, S2814 and S2030 in RyR2 have been variously claimed to be hyperphosphorylated. Our aim was to examine the degree of phosphorylation of these residues in RyR2 from failing human hearts. The use of human tissue was approved by the Human Research Ethics Committee, The Prince Charles Hospital, EC28114. Left ventricular tissue samples were obtained from an explanted heart of a patient with endstage heart failure (Emery Dreifuss Muscular Dystrophy with cardiomyopathy) and non-failing tissue was from a patient with cystic fibrosis undergoing heart-lung transplantation with no history of heart disease. SR vesicles were prepared as described by Laver et al. (1995) and examined with SDS-Page and Western Blot. Transferred proteins were probed with antibodies to detect total protein phosphorylation, phosphorylation of RyR2 serine residues S2808, S2814, S2030 and for the key proteins calsequestrin, triadin, junctin and FKBP12.6. To avoid membrane stripping artifact, each membrane was exposed to one phosphorylation-specific antibody and signal densities quantified using Bio-Rad Quantity One software. We found no distinguishable difference between failing and healthy hearts in the protein expression levels of RyR2, triadin, junctin or calsequestrin. We found an expected upregulation of total RyR2 phosphorylation in the failing heart sample, compared to a matched amount of RyR2 (quantified using densiometry) in healthy heart. Probing with antibodies detecting only the phosphorylated form of the specific RyR2 residues showed that the increase in total RyR2 phosphorylation in the failing heart was due to hyperphosphorylation of S2808 and S2814. We found that S2030 phosphorylation levels were unchanged in human heart failure. Interestingly, we found that S2030 has a basal level of phosphorylation in the healthy human heart, different from the absence of basal phosphorylation recently reported in rodent heart (Huke & Bers, 2008). Finally, preliminary results indicate that less FKBP 12.6 is associated with RyR2 in the failing heart, possibly as a consequence of PKA activation. In conclusion, residues S2808 and S2814 are hyperphosphorylated in human heart failure, presumably due to upregulation of the CaMKII and/or PKA signaling pathway as a result of chronic activation of the sympathetic nervous system. Such changes in RyR2 phosphorylation are believed to contribute to the leaky RyR2 phenotype associated with heart failure, which increases the incidence of arrhythmia and contributes to the severely impaired contractile performance of the failing heart. Huke S & Bers DM. (2008). Ryanodine receptor phosphorylation at serine 2030, 2808 and 2814 in rat cardiomyocytes. Biochemical and Biophysical Research Communications 376, 80-85. Laver DR, Roden LD, Ahern GP, Eager KR, Junankar PR & Dulhunty AF. (1995). Cytoplasmic Ca2+ inhibits the ryanodine receptor from cardiac muscle. Journal of Membrane Biology 147, 7-22. Proceedings

Comparison between maximal lengthening and shortening contractions for biceps brachii muscle oxygenation and hemodynamics

Eccentric contractions (ECC) require lower systemic oxygen (O2) and induce greater symptoms of muscle damage than concentric contractions (CON); however, it is not known if local muscle oxygenation is lower in ECC than CON during and following exercise. This study compared between ECC and CON for changes in biceps brachii muscle oxygenation [tissue oxygenation index (TOI)] and hemodynamics [total hemoglobin volume (tHb) = oxygenated-Hb + deoxygenated-Hb], determined by near-infrared spectroscopy over 10 sets of 6 maximal contractions of the elbow flexors of 10 healthy subjects. This study also compared between ECC and CON for changes in TOI and tHb during a 10-s sustained and 30-repeated maximal isometric contraction (MVC) task measured immediately before and after and 1–3 days following exercise. The torque integral during ECC was greater (P < 0.05) than that during CON by ∼30%, and the decrease in TOI was smaller (P < 0.05) by ∼50% during ECC than CON. Increases in tHb during the relaxation phases were smaller (P < 0.05) by ∼100% for ECC than CON; however, the decreases in tHb during the contraction phases were not significantly different between sessions. These results suggest that ECC utilizes a lower muscle O2 relative to O2 supply compared with CON. Following exercise, greater (P < 0.05) decreases in MVC strength and increases in plasma creatine kinase activity and muscle soreness were evident 1–3 days after ECC than CON. Torque integral, TOI, and tHb during the sustained and repeated MVC tasks decreased (P < 0.01) only after ECC, suggesting that muscle O2 demand relative to O2 supply during the isometric tasks was decreased after ECC. This could mainly be due to a lower maximal muscle mass activated as a consequence of muscle damage; however, an increase in O2 supply due to microcirculation dysfunction and/or inflammatory vasodilatory responses after ECC is recognized.

Biceps brachii muscle oxygenation in electrical muscle stimulation

The purpose of this study was to compare between electrical muscle stimulation (EMS) and maximal voluntary (VOL) isometric contractions of the elbow flexors for changes in biceps brachii muscle oxygenation (tissue oxygenation index, TOI) and haemodynamics (total haemoglobin volume, tHb = oxygenated-Hb + deoxygenated-Hb) determined by near-infrared spectroscopy (NIRS). The biceps brachii muscle of 10 healthy men (23–39 years) was electrically stimulated at high frequency (75 Hz) via surface electrodes to evoke 50 intermittent (4-s contraction, 15-s relaxation) isometric contractions at maximum tolerated current level (EMS session). The contralateral arm performed 50 intermittent (4-s contraction, 15-s relaxation) maximal voluntary isometric contractions (VOL session) in a counterbalanced order separated by 2–3 weeks. Results indicated that although the torque produced during EMS was approximately 50% of VOL (P<0Æ05), there was no significant difference in the changes in TOI amplitude or TOI slope between EMS and VOL over the 50 contractions. However, the TOI amplitude divided by peak torque was approximately 50% lower for EMS than VOL (P<0Æ05), which indicates EMS was less efficient than VOL. This seems likely because of the difference in the muscles involved in the force production between conditions. Mean decrease in tHb amplitude during the contraction phases was significantly (P<0Æ05) greater for EMS than VOL from the 10th contraction onwards, suggesting that the muscle blood volume was lower in EMS than VOL. It is concluded that local oxygen demand of the biceps brachii sampled by NIRS is similar between VOL and EMS.

Application of an optimisation algorithm to configure an internal fixation device

Fractures of long bones are sometimes treated using various types of fracture fixation devices including internal plate fixators. These are specialised plates which are used to bridge the fracture gap(s) whilst anatomically aligning the bone fragments. The plate is secured in position by screws. The aim of such a device is to support and promote the natural healing of the bone. When using an internal fixation device, it is necessary for the clinician to decide upon many parameters, for example, the type of plate and where to position it; how many and where to position the screws. While there have been a number of experimental and computational studies conducted regarding the configuration of screws in the literature, there is still inadequate information available concerning the influence of screw configuration on fracture healing. Because screw configuration influences the amount of flexibility at the area of fracture, it has a direct influence on the fracture healing process. Therefore, it is important that the chosen screw configuration does not inhibit the healing process. In addition to the impact on the fracture healing process, screw configuration plays an important role in the distribution of stresses in the plate due to the applied loads. A plate that experiences high stresses is prone to early failure. Hence, the screw configuration used should not encourage the occurrence of high stresses. This project develops a computational program in Fortran programming language to perform mathematical optimisation to determine the screw configuration of an internal fixation device within constraints of interfragmentary movement by minimising the corresponding stress in the plate. Thus, the optimal solution suggests the positioning and number of screws which satisfies the predefined constraints of interfragmentary movements. For a set of screw configurations the interfragmentary displacement and the stress occurring in the plate were calculated by the Finite Element Method. The screw configurations were iteratively changed and each time the corresponding interfragmentary displacements were compared with predefined constraints. Additionally, the corresponding stress was compared with the previously calculated stress value to determine if there was a reduction. These processes were continued until an optimal solution was achieved. The optimisation program has been shown to successfully predict the optimal screw configuration in two cases. The first case was a simplified bone construct whereby the screw configuration solution was comparable with those recommended in biomechanical literature. The second case was a femoral construct, of which the resultant screw configuration was shown to be similar to those used in clinical cases. The optimisation method and programming developed in this study has shown that it has potential to be used for further investigations with the improvement of optimisation criteria and the efficiency of the program.

Effect of vitamin D supplementation on muscle strength: a systematic review and meta-analysis

Summary This systematic review demonstrates that vitamin D supplementation does not have a significant effect on muscle strength in vitamin D replete adults. However, a limited number of studies demonstrate an increase in proximal muscle strength in adults with vitamin D deficiency. Introduction The purpose of this study is to systematically review the evidence on the effect of vitamin D supplementation on muscle strength in adults. Methods A comprehensive systematic database search was performed. Inclusion criteria included randomised controlled trials (RCTs) involving adult human participants. All forms and doses of vitamin D supplementation with or without calcium supplementation were included compared with placebo or standard care. Outcome measures included evaluation of strength. Outcomes were compared by calculating standardised mean difference (SMD) and 95% confidence intervals. Results Of 52 identified studies, 17 RCTs involving 5,072 participants met the inclusion criteria. Meta-analysis showed no significant effect of vitamin D supplementation on grip strength (SMD −0.02, 95%CI −0.15,0.11) or proximal lower limb strength (SMD 0.1, 95%CI −0.01,0.22) in adults with 25(OH)D levels >25 nmol/L. Pooled data from two studies in vitamin D deficient participants (25(OH)D <25 nmol/L) demonstrated a large effect of vitamin D supplementation on hip muscle strength (SMD 3.52, 95%CI 2.18, 4.85). Conclusion Based on studies included in this systematic review, vitamin D supplementation does not have a significant effect on muscle strength in adults with baseline 25(OH)D >25 nmol/L. However, a limited number of studies demonstrate an increase in proximal muscle strength in adults with vitamin D deficiency. Keywords Muscle – Muscle fibre – Strength – Vitamin D

Investigating the development of the internal and external service tasks of non-executive directors: the case of the Netherlands (1997-2005)

During the last decade, globalisation and liberalisation of financial markets, changing societal expectations and corporate governance scandals have increased the attention for the fiduciary duties of non-executive directors. In this context, recent corporate governance reform initiatives have emphasised the control task and independence of non-executive directors. However, little attention has been paid to their impact on the external and internal service tasks of non-executive directors. Therefore, this paper investigates how the service tasks of non-executive directors have evolved in the Netherlands. Data on corporate governance at the top-100 listed companies in the Netherlands between 1997 and 2005 show that the emphasis on non-executive directors' external service task has shifted to their internal service task, i.e. from non-executive directors acting as boundary spanners to non-executive directors providing advice and counselling to executive directors. This shift in board responsibilities affects non-executive directors' ability to generate network benefits through board relationships and has implications for non-executive directors' functional requirements.

Influence of preexercise muscle glycogen content on transcriptional activity of metabolic and myogenic genes in well-trained humans

To determine whether pre-exercise muscle glycogen content influences the transcription of several early-response genes involved in the regulation of muscle growth, seven male strength-trained subjects performed one-legged cycling exercise to exhaustion to lower muscle glycogen levels (Low) in one leg compared with the leg with normal muscle glycogen (Norm) and then the following day completed a unilateral bout of resistance training (RT). Muscle biopsies from both legs were taken at rest, immediately after RT, and after 3 h of recovery. Resting glycogen content was higher in the control leg (Norm leg) than in the Low leg (435 ± 87 vs. 193 ± 29 mmol/kg dry wt; P < 0.01). RT decreased glycogen content in both legs (P < 0.05), but postexercise values remained significantly higher in the Norm than the Low leg (312 ± 129 vs. 102 ± 34 mmol/kg dry wt; P < 0.01). GLUT4 (3-fold; P < 0.01) and glycogenin mRNA abundance (2.5-fold; not significant) were elevated at rest in the Norm leg, but such differences were abolished after exercise. Preexercise mRNA abundance of atrogenes was also higher in the Norm compared with the Low leg [atrogin: ?14-fold, P < 0.01; RING (really interesting novel gene) finger: ?3-fold, P < 0.05] but decreased for atrogin in Norm following RT (P < 0.05). There were no differences in the mRNA abundance of myogenic regulatory factors and IGF-I in the Norm compared with the Low leg. Our results demonstrate that 1) low muscle glycogen content has variable effects on the basal transcription of select metabolic and myogenic genes at rest, and 2) any differences in basal transcription are completely abolished after a single bout of heavy resistance training. We conclude that commencing resistance exercise with low muscle glycogen does not enhance the activity of genes implicated in promoting hypertrophy.