Cross-sector, sessional employment of pharmacists in rural hospitals in Australia and New Zealand: a qualitative study exploring pharmacists’ perceptions and experiences

Background: Many rural hospitals in Australia and New Zealand do not have an on-site pharmacist. Sessional employment of a local pharmacist offers a potential solution to address the clinical service needs of non-pharmacist rural hospitals. This study explored sessional service models involving pharmacists and factors (enablers and challenges) impacting on these models, with a view to informing future sessional employment. Methods: A series of semi-structured one-on-one interviews was conducted with rural pharmacists with experience, or intention to practise, in a sessional employment role in Australia and New Zealand. Participants were identified via relevant newsletters, discussion forums and referrals from contacts. Interviews were conducted during August 2012-January 2013 via telephone or Skype™, for approximately 40–55 minutes each, and recorded.Results: Seventeen pharmacists were interviewed: eight with ongoing sessional roles, five with sessional experience, and four working towards sessional employment. Most participants provided sessional hospital services on a weekly basis, mainly focusing on inpatient medication review and consultation. Recognition of the value of pharmacists’ involvement and engagement with other healthcare providers facilitated establishment and continuity of sessional services. Funds pooled from various sources supplemented some pharmacists’ remuneration in the absence of designated government funding. Enhanced employment opportunities, district support and flexibility in services facilitated the continuous operation of the sessional service. Conclusions: There is potential to address clinical pharmacy service needs in rural hospitals by cross-sector employment of pharmacists. The reported sessional model arrangements, factors impacting on sessional employment of pharmacists and learnings shared by the participants should assist development of similar models in other rural communities

Metabolic Factors Limiting Performance in Marathon Runners

Each year in the past three decades has seen hundreds of thousands of runners register to run a major marathon. Of those who attempt to race over the marathon distance of 26 miles and 385 yards (42.195 kilometers), more than two-fifths experience severe and performance-limiting depletion of physiologic carbohydrate reserves (a phenomenon known as ‘hitting the wall’), and thousands drop out before reaching the finish lines (approximately 1–2% of those who start). Analyses of endurance physiology have often either used coarse approximations to suggest that human glycogen reserves are insufficient to fuel a marathon (making ‘hitting the wall’ seem inevitable), or implied that maximal glycogen loading is required in order to complete a marathon without ‘hitting the wall.’ The present computational study demonstrates that the energetic constraints on endurance runners are more subtle, and depend on several physiologic variables including the muscle mass distribution, liver and muscle glycogen densities, and running speed (exercise intensity as a fraction of aerobic capacity) of individual runners, in personalized but nevertheless quantifiable and predictable ways. The analytic approach presented here is used to estimate the distance at which runners will exhaust their glycogen stores as a function of running intensity. In so doing it also provides a basis for guidelines ensuring the safety and optimizing the performance of endurance runners, both by setting personally appropriate paces and by prescribing midrace fueling requirements for avoiding ‘the wall.’ The present analysis also sheds physiologically principled light on important standards in marathon running that until now have remained empirically defined: The qualifying times for the Boston Marathon

Increasing Dietary Fat Elicits Similar Changes in Fat Oxidation and Markers of Muscle Oxidative Capacity in Lean and Obese Humans

In lean humans, increasing dietary fat intake causes an increase in whole-body fat oxidation and changes in genes that regulate fat oxidation in skeletal muscle, but whether this occurs in obese humans is not known. We compared changes in whole-body fat oxidation and markers of muscle oxidative capacity differ in lean (LN) and obese (OB) adults exposed to a 2-day high-fat (HF) diet. Ten LN (BMI = 22.5±2.5 kg/m2, age = 30±8 yrs) and nine OB (BMI = 35.9±4.93 kg/m2, 38±5 yrs, Mean±SD) were studied in a room calorimeter for 24hr while consuming isocaloric low-fat (LF, 20% of energy) and HF (50% of energy) diets. A muscle biopsy was obtained the next morning following an overnight fast. 24h respiratory quotient (RQ) did not significantly differ between groups (LN: 0.91±0.01; OB: 0.92±0.01) during LF, and similarly decreased during HF in LN (0.86±0.01) and OB (0.85±0.01). The expression of pyruvate dehydrogenase kinase 4 (PDK4) and the fatty acid transporter CD36 increased in both LN and OB during HF. No other changes in mRNA or protein were observed. However, in both LN and OB, the amounts of acetylated peroxisome proliferator-activated receptor γ coactivator-1-α (PGC1-α) significantly decreased and phosphorylated 5-AMP-activated protein kinase (AMPK) significantly increased. In response to an isoenergetic increase in dietary fat, whole-body fat oxidation similarly increases in LN and OB, in association with a shift towards oxidative metabolism in skeletal muscle, suggesting that the ability to adapt to an acute increase in dietary fat is not impaired in obesity

Carbohydrate Dependence During Prolonged, Intense Endurance Exercise

A major goal of training to improve the performance of prolonged, continuous, endurance events lasting up to 3 h is to promote a range of physiological and metabolic adaptations that permit an athlete to work at both higher absolute and relative power outputs/speeds and delay the onset of fatigue (i.e., a decline in exercise intensity). To meet these goals, competitive endurance athletes undertake a prodigious volume of training, with a large proportion performed at intensities that are close to or faster than race pace and highly dependent on carbohydrate (CHO)-based fuels to sustain rates of muscle energy production [i.e., match rates of adenosine triphosphate (ATP) hydrolysis with rates of resynthesis]. Consequently, to sustain muscle energy reserves and meet the daily demands of training sessions, competitive athletes freely select CHO-rich diets. Despite renewed interest in high-fat, low-CHO diets for endurance sport, fat-rich diets do not improve training capacity or performance, but directly impair rates of muscle glycogenolysis and energy flux, limiting high-intensity ATP production. When highly trained athletes compete in endurance events lasting up to 3 h, CHO-, not fat-based fuels are the predominant fuel for the working muscles and CHO, not fat, availability becomes rate limiting for performance

Specificity of MAPK signaling towards FLO11 expression is established by crosstalk from cAMP pathway

In budding yeast, elements of a single MAP Kinase cascade are shared to regulate a wide range of functions such as mating, differentiation and osmotic stress. However, cells have programmed to execute correct event in response to a given input signal without cross activating other responses. Studies have observed that magnitude and duration of MAPK activation encodes specificity. Similarly, the differential regulation of Tec1p, a transcriptional activator of invasive growth gene, FLO11 by MAP kinases has been observed to bring specificity in mating and invasive growth signaling. However, the understanding of interactions between the shared components and other signaling pathways related to the phenotypic response in contributing towards specificity remains unclear. We specifically address the crosstalk of cAMP pathway with MAPK pathway in haploid invasive growth and show the contribution and importance of cAMP pathway towards invasive growth irrespective of the activation status of MAPK pathway. Our analysis shows that crosstalk from cAMP pathway in haploids might offer an advantage in terms of amplifying the observed weak signaling through MAPK pathway. Further, we show that such a crosstalk in haploids leads to higher FLO11 expression than diploids. We also demonstrate the positive and negative role of Tpk1 and Tpk3 in haploid invasive growth. Finally, we observe that a cross-inhibition at gene level brought about by cAMP pathway controlled inhibitor, Sfl1, perhaps help in deamplifying the MAPK signal and also in preventing FLO11 expression in the absence of cAMP pathway activation