bluuebunny/crossref_metadata_2025_split huggingface dataset:
Power to the patient: care tracks and empowerment a recipe for improving rehabilitation for hip fracture patients
Authors: Löfgren Susanne , Hedström Margareta , Ekström Wilhelmina , Lindberg Lene , Flodin Lena , Ryd Leif 
Published: June 2014

Background/AimNew surgical procedures, early operation and medical optimisation in patients with hip fracture have shown positive results on length of hospital stay. Our aims were to investigate whether patient empowerment along with an individually designed, postoperative rehabilitation programme could reduce length of hospital stay and whether the patients would have better chances to return to their previous living.Design/MethodPatients were recruited during a 12‐month period 2009–2010, with an intervention group treated with an individually designed, postoperative rehabilitation programme and a control group treated in a traditional way according to the hospitals routines. Final assessment was performed 4 month after surgery. The postoperative programme for the intervention group consisted of four standardised care tracks adapted individually for the patients. Assessments of Activity of Daily Living, American Society of Anesthesiologists classification of medical disease status and Short Portable Mental Status Questionnaire and living conditions were used to determine which care track was most appropriate. The patients were cared for with focus of empowerment in their rehabilitation.ResultsThe study involved 503 hip fracture patients, 285 patients in the intervention group and 218 patients in the control group. The mean length of stay was 4 days shorter in the intervention group than in the control group (p = 0.04). Varied only to a small extent between the age groups in the intervention group and was greater between the age groups in the control. Patients in the intervention group returned to their previous living in 90% compared with 80% in the control group (p < 0.05). There were no significant differences between the age groups.ConclusionPatient empowerment administrated by specially trained nursing staff and with specialised, tailor‐made rehabilitation programme may be of benefit in helping patients to a shorter hospital stay and to return to their previous living.
Women's experiences of Takotsubo cardiomyopathy in a short‐term perspective – a qualitative content analysis
Authors: Dahlviken Rønnaug M. , Fridlund Bengt , Mathisen Lars 
Published: June 2014

BackgroundTakotsubo cardiomyopathy is a reversible condition mimicking acute myocardial infarction. The phenomenon is associated with emotional and physical stressful trigger events. Evidence‐based patient counselling should be based on disease‐specific knowledge of patient experiences.AimThe aim of the study was to describe women's experiences of Takotsubo cardiomyopathy in a short‐term perspective.DesignThe study design was explorative and descriptive.MethodSemi‐structured interviews were conducted with 14 women diagnosed with Takotsubo cardiomyopathy, 1 day to 9 months after hospitalisation. The transcriptions underwent qualitative content analysis.FindingsThe main theme that emerged was Takotsubo cardiomyopathy as a continuous process of making sense and adapting. To begin with, understanding and coping with signs and symptoms were described as having a diversity of signs and symptoms, taking actions towards signs and symptoms, receiving treatment for suspected ST/non ST‐elevation myocardial infarction diagnosis and finally being diagnosed with Takotsubo cardiomyopathy. Understanding the context of illness was expressed as getting treated for Takotsubo cardiomyopathy diagnosis and having previous stressful conditions of life. The changing perspective that emanated was a combination of having prospects and expectations and experiencing limitations. Finally, managing to live with Takotsubo cardiomyopathy was manifested as returning home with the illness and receiving follow‐up health care.ConclusionInformation on regaining prior health status and capacity within a short‐term perspective may not be accurate. These women struggle and require education and counselling from healthcare professionals to comprehend and manage having a Takotsubo cardiomyopathy diagnosis. Women experiencing Takotsubo cardiomyopathy may be a target group for holistic and individual health care with a longer duration of follow‐up.
Export Performance, Invoice Currency and Heterogeneous Exchange Rate Pass‐through
Authors: Fabling Richard , Sanderson Lynda 
Published: June 2014

AbstractUsing comprehensive, shipment‐level merchandise trade data for a small, open economy, we examine heterogeneity in exporters' exchange rate pass‐through (ERPT) behaviour. We draw together two recent studies of ERPT, linking invoice currency decisions and firm performance to heterogeneity in ERPT. Like these studies, we find that the short‐run reaction of export unit values to exchange rate fluctuations is significantly related to both invoice currency choice and exporter characteristics when these are analysed separately. However, we then show that when the two factors are jointly accounted for, the role of exporter characteristics largely disappears. That is, some firm types are more inclined to invoice in the producer currency, while others use either the local or a vehicle currency. In the short run, this translates into differences in exchange rate pass‐through because of price rigidity in the invoice currency. Firm characteristics do not have an independent impact on pass‐through beyond their effect on currency composition. Differences across invoice currencies diminish over time, but do not disappear, as prices adjust to reflect bilateral exchange rate movements.
Endoplasmic reticulum stress‐mediated autophagy protects against lipopolysaccharide‐induced apoptosis in HL‐1 cardiomyocytes
Authors: Zou Xiaojing , Xu Jianjun , Yao Shanglong , Li Jian , Yang Yan , Yang Le 
Published: June 2014

New Findings
What is the central question of this study?
Cardiac dysfunction in sepsis is associated with apoptosis of cardiomyocytes. Is endoplasmic reticulum (ER) stress induced in lipopolysaccharide (LPS)‐treated cardiomyocytes? Does ER stress‐induced autophagy protect against LPS‐induced apoptosis of cardiomyocytes? What is the mechanism in detail?
What is the main finding and its importance?
Our results indicate that ER stress is activated and mediates autophagy in LPS‐treated murine atrium‐derived cardiac HL‐1 cells. Protein kinase regulated by RNA‐like ER‐associated kinase (PERK), one arm of ER stress, is involved in protecting against LPS‐induced apoptosis of HL‐1 cells by promotion of autophagy.
Apoptosis of cardiomyocytes limits the contractile efficiency of the heart during sepsis. Prosurvival autophagy has been proposed as a novel mechanism to maintain normal heart function. Here, we demonstrated that autophagy was activated in lipopolysaccharide (LPS)‐treated HL‐1 cells, and it counteracted the LPS‐induced apoptosis. We investigated further the mechanism by which LPS triggered autophagy in HL‐1 cells. We discovered that endoplasmic reticulum (ER) stress played an important role in LPS‐triggered autophagy. The ER activated a survival pathway through the ER‐localized transmembrane protein PERK, which was essential for LPS‐induced autophagy. Lipopolysaccharide increased expression of GRP78, phosphorylated PERK and phosphorylated eukaryotic initiation factor 2α. Similar results were observed after administration of tunicamycin, a well‐known ER stressor. Most importantly, we found that 4‐phenylbutyrate, an inhibitor of ER stress, suppressed LPS‐activated autophagy in the presence of LPS in HL‐1 cells. The same results were observed after small interfering RNA‐mediated silencing of PERK protein. We also noticed that LPS‐induced apoptosis appeared early, at 4 h. Our findings revealed that PERK, one arm of ER stress, facilitated survival of LPS‐treated HL‐1 cells by promoting autophagy, and could serve as a potential therapeutic strategy to alleviate septic myocardial dysfunction.
Mechanomyogram amplitude correlates with human gastrocnemius medialis muscle and tendon stiffness both before and after acute passive stretching
Authors: Longo Stefano , Cè Emiliano , Rampichini Susanna , Devoto Michela , Limonta Eloisa , Esposito Fabio 
Published: June 2014

New Findings
What is the central question of this study?
The aim of this study was to determine the possible correlations between the mechanomyogram signal amplitude and the stiffness at the muscle–tendon unit, muscle and tendon levels, which were only hypothesised in previous investigations.
What is the main finding and its importance?
The main findings of this study are that the amplitude of the mechanomyogram was correlated inversely, albeit with small r2 values, with muscle–tendon unit, muscle and tendon stiffness both before and after application of stretching.
The study aimed to assess the level of correlation between muscle–tendon unit (MTU) stiffness and mechanomyogram (MMG) signal amplitude of the human gastrocnemius medialis muscle, both before and after acute passive stretching. The passive torque (Tpass), electrically evoked peak torque (pT) and myotendinous junction displacement were determined at different angles of dorsiflexion (0, 10 and 20 deg), while maximum voluntary isometric torque (Tmax) was assessed only at 0 deg. Measurements were repeated after a bout of passive stretching. From the MMG signal, the root mean square (RMS) and peak to peak (p‐p) were calculated. The MTU, muscle and tendon stiffness were determined by ultrasound and Tpass measurements. Before stretching, correlations between MMG RMS and MTU, muscle and tendon stiffness were found (R2 = 0.22–0.46). After stretching, Tpass, Tmax, pT and MTU, muscle and tendon stiffness decreased by 25 ± 7, 16 ± 2, 9 ± 2, 22 ± 7, 23 ± 8 and 28 ± 5%, respectively (P < 0.05). During voluntary and electrically evoked contractions, MMG p‐p decreased by 9 ± 2 and 5 ± 1%, while MMG RMS increased by 48 ± 7 and 50 ± 8%, respectively (P < 0.05). Correlations between MMG RMS and MTU, muscle and tendon stiffness were still present after stretching (R2 = 0.44–0.60). In conclusion, correlations between MMG RMS and stiffness exist both before and after stretching, suggesting that a slacker MTU leads to larger muscle fibre oscillations. However, care must be taken in using MMG amplitude as an indirect index to estimate stiffness owing to the relatively small R2 values of the investigated correlations.
Rapidly alternating photoperiods disrupt central and peripheral rhythmicity and decrease plasma glucose, but do not affect glucose tolerance or insulin secretion in sheep
Authors: Varcoe Tamara J. , Gatford Kathryn L. , Voultsios Athena , Salkeld Mark D. , Boden Michael J. , Rattanatray Leewen , Kennaway David J. 
Published: June 2014

New Findings
What is the central question of this study?
Disrupting circadian rhythms in rodents perturbs glucose metabolism and increases adiposity. In this study, we asked whether circadian rhythm disruption, induced by exposure of sheep to rapidly alternating photoperiods (RAPs), also disrupts metabolic homeostasis in a large diurnal animal model.
What is the main finding and its importance?
Exposure to RAPs disrupted central (melatonin and core body temperature) and peripheral rhythmicity (skeletal muscle clock gene expression). This led to reduced nocturnal plasma glucose concentrations, but did not affect glucose tolerance and glucose‐stimulated insulin secretion. These results suggest that RAP‐induced circadian rhythm disruption has minimal effect on glucose homeostasis in the sheep.
Disrupting circadian rhythms in rodents perturbs glucose metabolism and increases adiposity. To determine whether these effects occur in a large diurnal animal, we assessed the impact of circadian rhythm disruption upon metabolic function in sheep. Adult ewes (n = 7) underwent 3 weeks of a control 12 h light–12 h dark photoperiod, followed by 4 weeks of rapidly alternating photoperiods (RAPs) whereby the time of light exposure was reversed twice each week. Measures of central (melatonin secretion and core body temperature) and peripheral rhythmicity (clock and metabolic gene expression in skeletal muscle) were obtained over 24 h in both conditions. Metabolic homeostasis was assessed by glucose tolerance tests and 24 h glucose and insulin profiles. Melatonin and core body temperature rhythms resynchronized within 2 days of the last photoperiod shift. High‐amplitude Bmal1, Clock, Nr1d1, Cry2 and Per3 mRNA rhythms were apparent in skeletal muscle, which were phase advanced by up to 3.5 h at 2 days after the last phase shift, whereas Per1 expression was downregulated at this time. Pparα, Pgc1α and Nampt mRNA were constitutively expressed in both conditions. Nocturnal glucose concentrations were reduced following chronic phase shifts (zeitgeber time 0, −5.5%; zeitgeber time 12, −2.9%; and zeitgeber time 16, −5.7%), whereas plasma insulin, glucose tolerance and glucose‐stimulated insulin secretion were not altered. These results demonstrate that clock gene expression within ovine skeletal muscle oscillates over 24 h and responds to changing photoperiods. However, metabolic genes which link circadian and metabolic clocks in rodents were arrhythmic in sheep. Differences may be due to the ruminant versus monogastric digestive organization in each species. Together, these results demonstrate that despite disruptions to central and peripheral rhythmicity following exposure to rapidly alternating photoperiods, there was minimal impact on glucose homeostasis in the sheep.
Effects of detraining on the temporal expression of positive and negative angioregulatory proteins in skeletal muscle of mice
Authors: Olenich Sara A. , Audet Gerald N. , Roberts Kathleen A. , Olfert I. Mark 
Published: June 2014

Key points
Skeletal muscle capillary regression is associated with elevated thrombospondin‐1 and vascular endothelial growth factor protein expression with detraining.
Vascular endothelial growth factor and nucleolin responses to acute exercise are blunted in the triceps surae muscles following exercise training. In the plantaris and soleus muscles, this blunted response persists up to 28 days after cessation of training.
Effects of detraining on skeletal muscle microvascular density appears to be similar among skeletal muscle of varying oxidative potential and is poorly associated with expression of matrix metalloproteinases‐2 and ‐9 and endostatin.
AbstractTemporal expression of positive and negative angiogenic factors in response to detraining is poorly understood. We report the protein expression of anti‐angiogenic peptides (thrombospondin‐1, TSP‐1; and endostatin) as well as pro‐angiogenic factors (vascular endothelial growth factor, VEGF; matrix metalloproteinases‐2 and ‐9), and nucleolin (a nuclear protein involved with synthesis and maturation of ribosomes) in response to detraining in triceps surae muscles of C57BL/6 mice. Male mice were allowed to exercise voluntarily for 21 days, and then basal and acute response to exercise were evaluated at 1, 7, 14 and 28 days detraining (D1, D7, D14, D28, respectively, n = 12/group). As seen in the D1 mice, training resulted in the increased muscle capillary‐to‐fibre ratio (C/F), increased maximal running time and elevated basal expression of VEGF and matrix metalloproteinase‐9 (P < 0.05). After 7 days of detraining (D7), C/F levels were similar to control levels, but both basal VEGF and TSP‐1 were elevated (P < 0.05). At D14 and D28, TSP‐1 protein was not different compared to baseline levels; however, VEGF was elevated in gastrocnemius (GA), but not the soleus (SOL) or plantaris (PLT) muscles, of D14 mice. Endostatin tended to decrease in D14 and D28 compared to controls. Timing of nucleolin protein expression differed between muscle groups, with increases at D1, D7 and D14 in the PLT, SOL and GA muscles, respectively. The response of VEGF and nucleolin to acute exercise was blunted with training, and remained blunted in the PLT and SOL even after 28 days of detraining, at a time point long after muscle capillarization was observed to be similar to pre‐training levels. These data suggest that TSP‐1 may be a mediator of capillary regression with detraining, even in the face of elevated VEGF, suggesting that pro‐angiogenic regulators may not be able to prevent the regression of skeletal muscle capillaries under physiological conditions. The responses of matrix metalloproteinases, endostatin and nucleolin poorly correlated with detraining‐induced capillary regression.
Asymmetric temporal interactions of sound‐evoked excitatory and inhibitory inputs in the mouse auditory midbrain
Authors: Ono Munenori , Oliver Douglas L. 
Published: June 2014

Key points
The temporal coding of sound is critical for the auditory system.
Little is known about how sound evokes the timing of synaptic currents at higher levels of the auditory system and how the integration of these currents results in neural firing.
In the inferior colliculus, excitatory and inhibitory synaptic currents evoked by long‐duration sounds have different temporal properties with excitatory currents more variable than inhibitory currents.
Within a neuron, the sequence of synaptic events suggests the fastest sound‐evoked excitatory postsynaptic current (EPSCs) usually followed the inhibitory postsynaptic currents (IPSCs), and the slowest EPSCs preceded by IPSCs.
Knowledge about the timing of neural activity in the midbrain is important for understanding how temporally complex sounds such as speech are processed and communicated to higher centres of the system.
AbstractIn the auditory midbrain, synaptic mechanisms responsible for the precise temporal coding of inputs in the brainstem are absent. Instead, in the inferior colliculus (IC), the diverse temporal firing patterns must be coded by other synaptic mechanisms, about which little is known. Here, we demonstrate the temporal characteristics of sound‐evoked excitatory and inhibitory postsynaptic currents (seEPSCs and seIPSCs, respectively) in vivo in response to long‐duration tones. The seEPSCs and seIPSCs differ in the variability of their temporal properties. The seEPSCs have either early or late current peaks, and the early‐peaked currents may be either transient or sustained varieties. The seIPSCs have only early‐peaked sustained responses but often have offset responses. When measured in a single neuron, the seIPSC peaks usually follow early, transient seEPSCs, but the seIPSCs precede latest‐peaking seEPSCs. A model of the firing produced by the integration of asymmetric seEPSCs and seIPSCs showed that the temporal pattern of the early‐peaked sustained neurons was easily modified by changing the parameters of the seIPSC. These results suggest that the considerable variability in the peak time and duration of the seEPSCs shapes the overall time course of firing and often precedes or follows the less variable seIPSC. Despite this, the inhibitory currents are potent in modifying the firing patterns, and the inhibitory response to sound offset appears to be one area where the integration of excitatory and inhibitory synaptic currents is lacking. Thus, the integration of sound‐evoked activity in the IC often employs the asymmetric temporal interaction of excitatory and inhibitory synaptic currents to shape the firing pattern of the neuron.
Mineralocorticoid and AT1 receptors in the paraventricular nucleus contribute to sympathetic hyperactivity and cardiac dysfunction in rats post myocardial infarct
Authors: Huang Bing S. , Chen Aidong , Ahmad Monir , Wang Hong‐Wei , Leenen Frans H. H. 
Published: June 2014

Key points
Central mineralocorticoid receptor (MR) and angiotensin II type 1 receptor (AT1R) activation play a critical role in sympathetic hyperactivity and progressive left ventricle (LV) remodelling and dysfunction after a myocardial infarction (MI).
Intra‐paraventricular nucleus (PVN) infusion of adeno‐associated virus (AAV) carrying small interfering RNA (siRNA) against MR (AAV‐MR‐siRNA) markedly decreases both MR and AT1R expression in the PVN post MI, whereas AAV‐AT1aR‐siRNA only decreases AT1R expression. Both AAVs largely prevent sympathetic hyperactivity and inhibit part of LV remodelling and dysfunction post MI.
These findings indicate that enhanced MR–AT1R signalling in the PVN is critical for sympathetic hyperactivity post MI, and contributes to part of LV dysfunction post MI.
AbstractIntracerebroventricular infusion of a mineralocorticoid receptor (MR) or angiotensin II type 1 receptor (AT1R) blocker in rats attenuates sympathetic hyperactivity and progressive left ventricular (LV) dysfunction post myocardial infarction (MI). The present study examined whether knockdown of MRs or AT1Rs specifically in the paraventricular nucleus (PVN) contributes to these effects, and compared cardiac effects with those of systemic treatment with the β1‐adrenergic receptor blocker metoprolol. The PVN of rats was infused with adeno‐associated virus carrying small interfering RNA against either MR (AAV‐MR‐siRNA) or AT1R (AAV‐AT1R‐siRNA), or as control scrambled siRNA. At 4 weeks post MI, AT1R but not MR expression was increased in the PVN, excitatory renal sympathetic nerve activity and pressor responses to air stress were enhanced, and arterial baroreflex function was impaired; LV end‐diastolic pressure (LVEDP) was increased and LV peak systolic pressure (LVPSP), ejection fraction (EF) and dP/dtmax decreased. AAV‐MR‐siRNA and AAV‐AT1R‐siRNA both normalized AT1R expression in the PVN, similarly ameliorated sympathetic and pressor responses to air stress, largely prevented baroreflex desensitization, and improved LVEDP, EF and dP/dtmax as well as cardiac interstitial (but not perivascular) fibrosis. In a second set of rats, metoprolol at 70 or 250 mg kg−1 day−1 in the drinking water for 4 weeks post MI did not improve LV function except for a decrease in LVEDP at the lower dose. These results suggest that in rats MR‐dependent upregulation of AT1Rs in the PVN contributes to sympathetic hyperactivity, and LV dysfunction and remodelling post MI. In rats, normalizing MR–AT1R signalling in the PVN is a more effective strategy to improve LV dysfunction post MI than systemic β1 blockade.