bluuebunny/crossref_metadata_2025_split huggingface dataset:
Can early dietetic intervention improve outcomes in patients with hip fracture?
Authors: Klemm Haydn J. , Bailey Jacqueline K. , Desneves Katherine J. , Crowe Timothy C. 
Published: January 2016

AbstractAimTo assess whether the introduction of a new approach to nutritional care for hip fracture patients, in both acute and subacute admissions, can improve nutritional status, length of stay and pressure injuries.MethodsMedical records of patients admitted to Austin Health, Melbourne, Australia with a fractured hip between January and June 2014 after implementation of a new nutritional care guideline were compared to a historical control group admitted between January and June 2013 prior to introduction of the guideline. Data were collected for both acute and subacute admissions and included length of stay, date of first contact with a dietitian, subjective global assessment category and occurrence of pressure injuries.ResultsThere was a significantly shorter length of stay overall for patients who received care under the new guideline (21.6 ± 15.1 vs 26.4 ± 20.4 days; P = 0.043) and during the subacute admission (20.1 ± 10.6 vs 28.8 ± 15.8 days; P < 0.001); however, there was no significant difference in the acute hospital length of stay period. The post‐guideline group had a significantly shorter time between admission and first contact with a dietitian (4.8 ± 3.3 vs 7.5 ± 6.2 days; P < 0.001). Post‐guideline patients also had a significantly lower incidence of pressure injuries with 29, compared to 41 in pre‐guideline patients (P = 0.045). There were significantly less malnourished patients in the post‐guideline group compared to the pre‐guideline group across both acute and subacute admissions (29% vs 35%; P = 0.015).ConclusionsA nutritional care guideline for patients with hip fractures is associated with improved patient outcomes with a significant reduction in overall and subacute length of stay and pressure injury incidence and earlier dietetic assessment and intervention.
Downstream Dissipation of Storm Flow Heat Pulses: A Case Study and its Landscape‐Level Implications
Authors: Somers Kayleigh A. , Bernhardt Emily S. , McGlynn Brian L. , Urban Dean L. 
Published: January 2016

AbstractStorms in urban areas route heat and other pollutants from impervious surfaces, via drainage networks, into streams with well‐described negative consequences on physical structure and biological integrity. We used heat pulses associated with urban storms as a tracer for pavement‐derived stormwater inputs, providing a conservative estimate of the frequency with which these pollutants are transported into and through protected stream reaches. Our study was conducted within a 1.5‐km reach in Durham, North Carolina, whose headwaters begin in suburban stormwater pipes before flowing through 1 km of protected, 100‐year‐old forest. We recorded heat‐pulse magnitudes and distances travelled downstream, analyzing how they varied with storm and antecedent flow conditions. We found heat pulses >1°C traveled more than 1 km downstream of urban inputs in 11 storms over one year. This best‐case management scenario of a reach within a protected forest shows that urban impacts can travel far downstream of inputs. Air temperature and flow intensity controlled heat‐pulse magnitude, while heat‐pulse size, mean flow, and total precipitation controlled dissipation distance. As temperatures and sudden storms intensify with climate change, heat‐pulse magnitude and dissipation distance will likely increase. Streams in urbanized landscapes, such as Durham municipality, where 98.9% of streams are within 1 downstream km of stormwater outfalls, will be increasingly impacted by urban stormwaters.
The Role of Decidual Macrophages During Normal and Pathological Pregnancy
Authors: Ning Fen , Liu Huishu , Lash Gendie E. 
Published: January 2016

AbstractMacrophages perform many specific functions including host defense, homeostasis, angiogenesis, and tissue development. Macrophages are the second most abundant leukocyte population in the non‐pregnant endometrium and pregnant decidua and likely play a central role in the establishment and maintenance of normal pregnancy. Importantly, aberrantly activated uterine macrophages can affect trophoblast function and placental development, which may result in various adverse pregnancy outcomes ranging from pre‐eclampsia to fetal growth restriction or demise. Only by fully understanding the roles of macrophage in pregnancy will we be able to develop interventions for the treatment of these various pregnancy complications. This review discusses the general origin and classification of monocytes and macrophages and focuses on the phenotype and functional roles of decidual macrophage at the maternal–fetal interface in normal pregnancy, as well as discussing the potential contribution of the abnormal state of these cells to various aspects of pregnancy pathologies.
Executive functions predict conceptual learning of science
Authors: Rhodes Sinéad M. , Booth Josephine N. , Palmer Lorna Elise , Blythe Richard A. , Delibegovic Mirela , Wheate Nial J. 
Published: January 2016

We examined the relationship between executive functions and both factual and conceptual learning of science, specifically chemistry, in early adolescence. Sixty‐three pupils in their second year of secondary school (aged 12–13 years) participated. Pupils completed tasks of working memory (Spatial Working Memory), inhibition (Stop‐Signal), attention set‐shifting (ID/ED), and planning (Stockings of Cambridge), from theCANTAB. They also participated in a chemistry teaching session, practical, and assessment on the topic of acids and alkalis designed specifically for this study. Executive function data were related to (1) the chemistry assessment which included aspects of factual and conceptual learning and (2) a recent school science exam. Correlational analyses between executive functions and both the chemistry assessment and science grades revealed that science achievements were significantly correlated with working memory. Linear regression analysis revealed that visuospatial working memory ability was predictive of chemistry performance. Interestingly, this relationship was observed solely in relation to the conceptual learning condition of the assessment highlighting the role of executive functions in understanding and applying knowledge about what is learned within science teaching.
Anti‐oxidative effect of AST‐120 on kidney injury after myocardial infarction
Authors: Fujii Hideki , Yonekura Yuriko , Yamashita Yusuke , Kono Keiji , Nakai Kentaro , Goto Shunsuke , Sugano Mikio , Goto Sumie , Fujieda Ayako , Ito Yoshiharu , Nishi Shinichi 
Published: January 2016

Background and PurposeChronic kidney disease (CKD) is a crucial risk factor for cardiovascular disease (CVD), and combined CKD and CVD further increases morbidity and mortality. Here, we investigated effects of AST‐120 on oxidative stress and kidney injury using a model of myocardial infarction (MI) in rats.Experimental ApproachAt 10 weeks, male spontaneously hypertensive rats (SHR) were divided into three groups: SHR (n = 6), MI (n = 8) and MI + AST‐120 (n = 8). AST‐120 administration was started at 11 weeks after MI. At 18 weeks, the rats were killed, and blood and urine, mRNA expression and renal histological analyses were performed. Echocardiography was performed before and after MI.Key ResultsAt 18 weeks, the BP was significantly lower in the MI and MI+AST‐120 groups than in the SHR group. Elevated levels of indoxyl sulfate (IS), one of the uremic toxins, in serum and urine were reduced by AST‐120 treatment, compared with the MI group. Markers of oxidative stress in urine and serum biomarkers of kidney injury were decreased in the MI+AST‐120 group compared with the other two groups. Renal expression of mRNAs for kidney injury related‐markers were decreased in the MI+AST‐120 group, compared with the MI group. In vitro data also supported the influence of IS on kidney injury. Immunohistological analysis showed that intrarenal oxidative stress was reduced by AST‐120 administration.Conclusions and ImplicationsSerum IS was increased after MI and treatment with AST‐120 may have protective effects on kidney injury after MI by suppressing oxidative stress.
α1B‐Adrenoceptor signalling regulates bone formation through the up‐regulation of CCAAT/enhancer‐binding protein δ expression in osteoblasts
Authors: Tanaka Kenjiro , Hirai Takao , Kodama Daisuke , Kondo Hisataka , Hamamura Kazunori , Togari Akifumi 
Published: January 2016

Background and PurposeThe sympathetic nervous system regulates bone remodelling, in part, through ß2‐adrenoceptor signalling. However, the physiological role of α1‐adrenoceptor signalling in bone in vivo remains unclear. Therefore, to obtain a deeper understanding of bone remodelling by the sympathetic nervous system, we investigated the role of α1B‐adrenoceptor signalling in bone metabolism.Experimental ApproachPrazosin, a nonspecific α1‐adrenoceptor antagonist, was administered for 2 weeks in C57BL6 mice, and efficacy was evaluated by bone microarchitecture using microcomputed tomography and determination of bone formation by fluorescent labelling of bone. We also compared the bone phenotype of α1B‐adrenoceptor null mice (α1B−/−) with that of wild‐type littermates.Key ResultsWe demonstrated that the systemic administration of prazosin decreased bone formation. In addition, α1B‐adrenoceptor‐deficient mice had a lower bone mass due to decreased bone formation but did not exhibit any changes in bone‐resorbing activity. Furthermore, stimulation with phenylephrine, a non‐specific α1‐adrenoceptor agonist, increased the expression of the transcriptional factor CCAAT/enhancer‐binding protein δ (Cebpd) in MC3T3‐E1 osteoblastic cells. The overexpression of Cebpd induced cellular proliferation in MC3T3‐E1 cells, whereas the silencing of Cebpd suppressed it.Conclusions and ImplicationsTaken together, these results suggested that α1B‐adrenoceptor signalling is required for bone formation and regulated cellular proliferation through a mechanism relevant to the up‐regulation of Cebpd in osteoblasts and, thus, provide new evidence for the physiological importance of α1B‐adrenoceptor signalling in bone homeostasis.
Madecassoside ameliorates bleomycin‐induced pulmonary fibrosis in mice through promoting the generation of hepatocyte growth factor via PPAR‐γ in colon
Authors: Xia Ying , Xia Yu‐Feng , Lv Qi , Yue Meng‐Fan , Qiao Si‐Miao , Yang Yan , Wei Zhi‐Feng , Dai Yue 
Published: January 2016

Background and PurposeMadecassoside has potent anti‐pulmonary fibrosis (PF) effects when administered p.o., despite having extremely low oral bioavailability. Herein, we explored the mechanism of this anti‐PF effect with regard to gut hormones.Experimental ApproachA PF model was established in mice by intratracheal instillation of bleomycin. Haematoxylin and eosin stain and Masson's trichrome stain were used to assess histological changes in the lung. Quantitative‐PCR and Western blot detected mRNA and protein levels, respectively, and cytokines were measured by ELISA. Small interfering RNA was used for gene‐silencing. EMSA was applied to detect DNA‐binding activity.Key ResultsAdministration of madecassoside, p.o., but not its main metabolite madecassic acid, exhibited a direct anti‐PF effect in mice. However, i.p. madecassoside had no anti‐PF effect. Madecassoside increased the expression of hepatocyte growth factor (HGF) in colon tissues, and HGF receptor antagonists attenuated its anti‐PF effect. Madecassoside facilitated the secretion of HGF from colonic epithelial cells by activating the PPAR‐γ pathway, as shown by an up‐regulation of PPAR‐γ mRNA expression, nuclear translocation and DNA‐binding activity both in vitro and in vivo. Also GW9662, a selective PPAR‐γ antagonist, almost completely prevented the madecassoside‐induced increased expression of HGF and amelioration of PF.Conclusions and ImplicationsThe potent anti‐PF effects induced by p.o. madecassoside in mice are not mediated by its metabolites or itself after absorption into blood. Instead, madecassoside increases the activity of PPAR‐γ, which subsequently increases HGF expression in colonic epithelial cells. HGF then enters into the circulation and lung tissue to exert an anti‐PF effect.
Tectono‐sedimentary evolution of the northern Iranian Plateau: insights from middle–late Miocene foreland‐basin deposits
Authors: Ballato Paolo , Cifelli Francesca , Heidarzadeh Ghasem , Ghassemi Mohammad R. , Wickert Andrew D. , Hassanzadeh Jamshid , Dupont‐Nivet Guillaume , Balling Philipp , Sudo Masafumi , Zeilinger Gerold , Schmitt Axel K. , Mattei Massimo , Strecker Manfred R. 
Published: January 2016

AbstractSedimentary basins in the interior of orogenic plateaus can provide unique insights into the early history of plateau evolution and related geodynamic processes. The northern sectors of the Iranian Plateau of the Arabia–Eurasia collision zone offer the unique possibility to study middle–late Miocene terrestrial clastic and volcaniclastic sediments that allow assessing the nascent stages of collisional plateau formation. In particular, these sedimentary archives allow investigating several debated and poorly understood issues associated with the long‐term evolution of the Iranian Plateau, including the regional spatio‐temporal characteristics of sedimentation and deformation and the mechanisms of plateau growth. We document that middle–late Miocene crustal shortening and thickening processes led to the growth of a basement‐cored range (Takab Range Complex) in the interior of the plateau. This triggered the development of a foreland‐basin (Great Pari Basin) to the east between 16.5 and 10.7 Ma. By 10.7 Ma, a fast progradation of conglomerates over the foreland strata occurred, most likely during a decrease in flexural subsidence triggered by rock uplift along an intraforeland basement‐cored range (Mahneshan Range Complex). This was in turn followed by the final incorporation of the foreland deposits into the orogenic system and ensuing compartmentalization of the formerly contiguous foreland into several intermontane basins. Overall, our data suggest that shortening and thickening processes led to the outward and vertical growth of the northern sectors of the Iranian Plateau starting from the middle Miocene. This implies that mantle‐flow processes may have had a limited contribution toward building the Iranian Plateau in NW Iran.
De novo loss‐of‐function mutations in X‐linked SMC1A cause severe ID and therapy‐resistant epilepsy in females: expanding the phenotypic spectrum
Authors: Jansen S. , Kleefstra T. , Willemsen M.H. , de Vries P. , Pfundt R. , Hehir‐Kwa J.Y. , Gilissen C. , Veltman J.A. , de Vries B.B.A. , Vissers L.E.L.M. 
Published: January 2016

De novo missense mutations and in‐frame coding deletions in the X‐linked gene SMC1A (structural maintenance of chromosomes 1A), encoding part of the cohesin complex, are known to cause Cornelia de Lange syndrome in both males and females. For a long time, loss‐of‐function (LoF) mutations in SMC1A were considered incompatible with life, as such mutations had not been reported in neither male nor female patients. However, recently, the authors and others reported LoF mutations in females with intellectual disability (ID) and epilepsy.Here we present the detailed phenotype of two females with de novo LoF mutations in SMC1A, including a de novo mutation of single base deletion [c.2364del, p.(Asn788Lysfs*10)], predicted to result in a frameshift, and a de novo deletion of exon 16, resulting in an out‐of‐frame mRNA splice product [p.(Leu808Argfs*6)]. By combining our patients with the other recently reported females carrying SMC1A LoF mutations, we ascertained a phenotypic spectrum of (severe) ID, therapy‐resistant epilepsy, absence/delay of speech, hypotonia and small hands and feet. Our data show the existence of a novel phenotypic entity – distinct from CdLS – and caused by de novo SMC1A LoF mutations.
Endoplasmic reticulum stress‐mediated upregulation of miR‐29a enhances sensitivity to neuronal apoptosis
Authors: Nolan Katie , Walter Franziska , Tuffy Liam P. , Poeschel Simone , Gallagher Ross , Haunsberger Stefan , Bray Isabella , Stallings Raymond L. , Concannon Caoimhín G. , Prehn Jochen H. M. 
Published: January 2016

AbstractDisturbance of homeostasis within the endoplasmic reticulum (ER) lumen leads to the accumulation of unfolded and misfolded proteins. This results in the activation of an evolutionary conserved stress response termed ER stress that, if unresolved, induces apoptosis. Previously the Bcl‐2 homology domain 3‐Only Protein Puma was identified as a mediator of ER stress‐induced apoptosis in neurons. In the search of alternative contributors to ER stress‐induced apoptosis, a downregulation of the anti‐apoptotic Bcl‐2 family protein Mcl‐1 was noted during ER stress in both mouse cortical neurons and human SH‐SY5Y neuroblastoma cells. Downregulation of Mcl‐1 was associated with an upregulation of microRNA‐29a (miR‐29a) expression, and subsequent experiments showed that miR‐29a targeted the 3′‐untranslated region of the anti‐apoptotic Bcl‐2 family protein, Mcl‐1. Inhibition of miR‐29a expression using sequence‐specific antagomirs or the overexpression of Mcl‐1 decreased cell death following tunicamycin treatment, while gene silencing of Mcl‐1 increased cell death. miR‐29a did not alter the signalling branches of the ER stress response, rather its expression was controlled by the ER stress‐induced transcription factor activating‐transcription‐factor‐4 (ATF4). The current data demonstrate that the ATF4‐mediated upregulation of miR‐29a enhances the sensitivity of neurons to ER stress‐induced apoptosis.
Activation of medullary dorsal horn γ isoform of protein kinase C interneurons is essential to the development of both static and dynamic facial mechanical allodynia
Authors: Pham‐Dang Nathalie , Descheemaeker Amélie , Dallel Radhouane , Artola Alain 
Published: January 2016

AbstractThe γ isoform of protein kinase C (PKCγ), which is concentrated in a specific class of interneurons within inner lamina II (IIi) of the spinal dorsal horn and medullary dorsal horn (MDH), is known to be involved in the development of mechanical allodynia, a widespread and intractable symptom of inflammatory or neuropathic pain. However, although genetic and pharmacological impairment of PKCγ were shown to prevent mechanical allodynia in animal models of pain, after nerve injury or reduced inhibition, the functional consequences of PKCγ activation alone on mechanical sensitivity are still unknown. Using behavioural and anatomical approaches in the rat MDH, we tested whether PKCγ activation in naive animals is sufficient for the establishment of mechanical allodynia. Intracisternal injection of the phorbol ester, 12,13‐dibutyrate concomitantly induced static as well as dynamic facial mechanical allodynia. Monitoring neuronal activity within the MDH with phospho‐extracellular signal‐regulated kinases 1 and 2 immunoreactivity revealed that activation of both lamina I–outer lamina II and IIi–outer lamina III neurons, including lamina IIi PKCγ‐expressing interneurons, was associated with the manifestation of mechanical allodynia. Phorbol ester, 12,13‐dibutyrate‐induced mechanical allodynia and associated neuronal activations were all prevented by inhibiting selectively segmental PKCγ with KIG31‐1. Our findings suggest that PKCγ activation, without any other experimental manipulation, is sufficient for the development of static and dynamic mechanical allodynia. Lamina IIi PKCγ interneurons have been shown to be directly activated by low‐threshold mechanical inputs carried by myelinated afferents. Thus, the level of PKCγ activation within PKCγ interneurons might gate the transmission of innocuous mechanical inputs to lamina I, nociceptive output neurons, thus turning touch into pain.
The persistence of long‐term potentiation in the projection from ventral hippocampus to medial prefrontal cortex in awake rats
Authors: Taylor Chanel J. , Ohline Shane M. , Moss Timothy , Ulrich Katharina , Abraham Wickliffe C. 
Published: January 2016

AbstractA potentially vital pathway in the processing of spatial memory is the pathway from ventral hippocampus to medial prefrontal cortex (vHPC–mPFC). To assess long‐term potentiation (LTP) induction and maintenance across days in this pathway, the effects of several induction paradigms were compared in awake, freely moving rats. Two different high‐frequency stimulation (HFS) protocols generated LTP lasting no longer than 1 week. However, after delivering HFS on three consecutive days, LTP lasted an average of 20 days, due mainly to the greater initial induction. Thus the pathway does not require extensive multi‐day stimulation to induce LTP, as for other intra‐neocortical pathways, but also it does not exhibit the extremely long‐lasting and stable LTP previously observed in area CA1 and the dentate gyrus. By using bilaterally placed stimulating and recording electrodes, we found that HFS in one vHPC generated responses and LTP in the contralateral mPFC, even when the ipsilateral mPFC was inactivated by CNQX. We attribute this crossed response to a polysynaptic pathway from the vHPC to the contralateral mPFC. Finally, we found that repeated overnight exposure to an enriched environment also potentiated the vHPC–mPFC response, but this too was a transient effect lasting < 9 days, declining to baseline even before the enriched environment treatment was completed. Overall, these findings are consistent with the view that potentiation of vHPC–mPFC pathway may play a key role in promoting the hippocampus–mPFC interplay that, over days, leads to long‐term storage in the frontal cortex of memories that are independent of the hippocampus.
Measurement equivalence of the newly developed Quality of Life in Childhood Epilepsy Questionnaire (QOLCE‐55)
Authors: Ferro Mark A. , Goodwin Shane W. , Sabaz Mark , Speechley Kathy N. 
Published: January 2016

SummaryObjectiveThe aim of this study was to examine measurement equivalence of the newly developed Quality of Life in Childhood Epilepsy Questionnaire (QOLCE‐55) across age, sex, and time in a representative sample of children with newly diagnosed epilepsy.MethodsData come from 373 children enrolled in the Health‐related Quality of Life in Children with Epilepsy Study (HERQULES), a multisite prospective cohort study. Measurement equivalence was examined using a multiple‐group confirmatory factor analysis framework, whereby increasingly stringent parameter constraints are imposed on the model. Comparison groups were stratified based on age (4–7 years vs. 8–12 years), sex (male vs. female), and time (measurement of health‐related quality of life at diagnosis vs. 24 months later).ResultsThe QOLCE‐55 demonstrated measurement equivalence at the level of strict invariance for each model tested—age: χ2 (3,123) = 4,097.3, p < 0.001; Comparative Fit Index (CFI) = 0.968; Root Mean Square Error of Approximation (RMSEA) = 0.042 (0.038, 0.045); sex: χ2 (3,124) = 4,188.3, p < 0.001; CFI = 0.964; RMSEA = 0.044 (0.040, 0.047); and time: χ2 (3,121) = 5,185.0, p < 0.001; CFI = 0.965; RMSEA = 0.046 (0.043, 0.048).SignificanceThese findings suggest that items comprising the QOLCE‐55 are perceived similarly among groups stratified by age, sex, and time and provide further evidence supporting the validity of the scale in children with epilepsy. Health professionals and researchers should be confident that group comparisons made using the QOLCE‐55 are unbiased and that any group differences detected are meaningful; that is, not related to differences in the interpretation of items by informants. Future research replicating these findings is encouraged.