bluuebunny/crossref_metadata_2025_split huggingface dataset:
Composite versus single transportable carbohydrate solution enhances race and laboratory cycling performance
Authors: Rowlands David S. , Swift Marilla , Ros Marjolein , Green Jackson G. 
Published: May 2012

When ingested at high rates (1.8–2.4 g·min–1) in concentrated solutions, carbohydrates absorbed by multiple (e.g., fructose and glucose) vs. single intestinal transporters can increase exogenous carbohydrate oxidation and endurance performance, but their effect when ingested at lower, more realistic, rates during intermittent high-intensity endurance competition and trials is unknown. Trained cyclists participated in two independent randomized crossover investigations comprising mountain-bike races (average 141 min; n = 10) and laboratory trials (94-min high-intensity intervals followed by 10 maximal sprints; n = 16). Solutions ingested during exercise contained electrolytes and fructose + maltodextrin or glucose + maltodextrin in 1:2 ratio ingested, on average, at 1.2 g carbohydrate·kg–1·h–1. Exertion, muscle fatigue, and gastrointestinal discomfort were recorded. Data were analysed using mixed models with gastrointestinal discomfort as a mechanism covariate; inferences were made against substantiveness thresholds (1.2% for performance) and standardized difference. The fructose–maltodextrin solution substantially reduced race time (–1.8%; 90% confidence interval = ±1.8%) and abdominal cramps (–8.1 on a 0–100 scale; ±6.6). After accounting for gastrointestinal discomfort, the effect of the fructose–maltodextrin solution on lap time was reduced (–1.1%; ±2.4%), suggesting that gastrointestinal discomfort explained part of the effect of fructose–maltodextrin on performance. In the laboratory, mean sprint power was enhanced (1.4%; ±0.8%) with fructose–maltodextrin, but the effect on peak power was unclear (0.7%; ±1.5%). Adjusting out gastrointestinal discomfort augmented the fructose–maltodextrin effect on mean (2.6%; ±1.9%) and peak (2.5%; ±3.0%) power. Ingestion of multiple transportable vs. single transportable carbohydrates enhanced mountain-bike race and high-intensity laboratory cycling performance, with inconsistent but not irreconcilable effects of gut discomfort as a possible mediating mechanism.
Should postactivation potentiation be the goal of your warm-up?
Authors: MacIntosh Brian R. , Robillard Marie-Eve , Tomaras Elias K. 
Published: May 2012

Athletes expect improved high-intensity performance following warm-up, and postactivation potentiation (PAP) is assumed to contribute to this improvement. However, the scientific evidence supporting this assumption is incomplete. PAP is known to result from prior muscle activation, and should enhance maximal effort contractions of very short duration. However, PAP dissipates over 4–6 min after the PAP-inducing contraction, so PAP should not contribute to enhanced performance more than 5 min after the warm-up.
Beneficial effects of cod protein on skeletal muscle repair following injury
Authors: Dort Junio , Sirois Amélie , Leblanc Nadine , Côté Claude H. , Jacques Hélène 
Published: May 2012

This study examined the effect of peanut and cod proteins on post-damage skeletal muscle repair, compared with casein. We hypothesized that because of their high arginine content, these proteins would improve the resolution of inflammation and muscle mass recovery following injury. One hundred and twenty-eight male Wistar rats were assigned to isoenergetic diets composed of casein and peanut (experiment 1) or cod protein (experiment 2). After 21 days of feeding, one tibialis anterior muscle (TA) was injured with bupivacaine, while the contralateral TA was injected with saline (sham muscle). Measurements were taken at days 0, 3, 14, and 24 post-injury. Compared with casein, peanut protein reduced muscle mass at days 0 (–12%, p = 0.005) and 14 post-injury in the injured muscle (–13%, p = 0.04), and lowered myofiber cross-sectional area in both the sham (–21%, p = 0.008) and injured muscles (–26%, p = 0.05) at day 24 post-injury, showing that peanut protein has a weak potential to support muscle growth. At day 14 post-injury, muscle mass in the sham (13%, p = 0.02) and injured muscles (12%, p = 0.01) was higher in cod-protein-fed rats, indicating better muscle mass recovery, than in casein-fed rats. Cod protein tended (p = 0.06) to decrease the density of neutrophils (–24%) at day 14 post-injury in the injured muscle, and to decrease the density of ED1+macrophages at day 24 post-injury in both sham (–29%, p = 0.03) and injured (–40%, p = 0.01) muscles. No effects were observed for peanut protein. These data indicate that cod protein is better for promoting growth and regeneration of skeletal muscle after trauma, partly because of the improved resolution of inflammation.
Moderate-intensity, premeal cycling blunts postprandial increases in monocyte cell surface CD18 and CD11a and endothelial microparticles following a high-fat meal in young adults
Authors: Strohacker Kelley , Breslin Whitney L. , Carpenter Katie C. , Davidson Tiffany R. , Agha Nadia H. , McFarlin Brian K. 
Published: May 2012

High-fat meals promote transient increases in proatherogenic factors, implicating the postprandial state in cardiovascular disease (CVD) progression. Although low-grade inflammation is associated with CVD, little research has assessed postprandial inflammation. Because of its anti-inflammatory properties, premeal exercise may counteract postprandial inflammation. The purpose of this study was to determine postprandial alterations in monocytes and circulating markers of endothelial stress and inflammation following a high-fat meal in young adults with or without premeal cycle exercise. Each subject completed two trials and was randomized to rest or cycle at a moderate intensity prior to eating a high-fat meal. Flow cytometry was used to assess monocyte cell surface receptor expression and concentration of endothelial microparticles (EMP). Plasma cytokines were assessed using Luminex MagPix. Statistical analysis was completed using separate linear mixed models analyses with first-order autoregressive (AR(1)) heterogeneous covariance structure. Significance was set at P ≤ 0.05. Percentage increases in classic monocyte CD11a and CD18 were greater overall in the postprandial period in the meal-only condition compared with the meal + exercise condition (P < 0.05). EMP concentration was 47% greater 3 h after the meal compared with premeal values in the meal-only condition (P < 0.05); no significant increase was observed in the meal + exercise condition. Premeal cycling blunted postprandial increases in EMP and CD11a and CD18. Acute, moderate-intensity exercise may help counteract possibly deleterious postprandial monocyte and endothelial cell activation.
Overweight and obese boys reduce food intake in response to a glucose drink but fail to increase intake in response to exercise of short duration
Authors: Tamam Shlomi , Bellissimo Nick , Patel Barkha P. , Thomas Scott G. , Anderson G. Harvey 
Published: May 2012

The effect of short duration exercise (EXR) on food intake (FI) and energy balance (EB) is not well understood in either normal weight (NW) or overweight (OW) and obese (OB) 9–14 years old children. Our purpose was to describe the effects of activity and a glucose drink on short term FI, appetite, and EB in NW, OW, and OB boys. Each boy received in random order either a noncaloric Sucralose sweetened control or glucose (1.0 g·kg–1 body weight) drink 5 min after either exercise (EXR) or sedentary (SED) activity. Boys exercised for 15 min at their ventilation threshold (VT) in experiment 1 or at 25% above their VT in experiment 2. FI was measured at an ad libitum pizza meal 30 min after drink consumption. FI was lower after the glucose drink (p < 0.001) but not affected by activity, even though EXR increased appetite (p < 0.001). OW/OB boys ate more total food than NW boys (p = 0.020). EB over the duration of the experiments was reduced by EXR in OW/OB boys (p = 0.013) but not in NW boys in either experiment (p > 0.05). We conclude that intake regulation in OW/OB boys in response to a glucose drink is similar to NW boys, but it may be less responsive to activity.
Denaturing gradient gel electrophoresis for nonlethal detection of Aeromonas salmonicida in salmonid mucus and its potential for other bacterial fish pathogens
Authors: Quinn Robert A. , Stevenson Roselynn M.W. 
Published: May 2012

Denaturing gradient gel electrophoresis (DGGE) of 16S rDNA was used to nonlethally detect Aeromonas salmonicida and other bacteria in salmonid skin mucus. Mucus samples from wild spawning coho salmon ( Oncorhynchus kisutch ) with endemic A. salmonicida and from cultured lake trout ( Salvelinus namaycush ) were tested by PCR–DGGE and were compared with mucus culture on Coomassie brilliant blue agar and internal organ culture. PCR–DGGE gave a highly reproducible 4-band pattern for 9 strains of typical A. salmonicida, which was different from other Aeromonas spp. Aeromonas salmonicida presence in mucus was evident as a band that comigrated with the bottom band of the A. salmonicida 4-band pattern and was verified by sequencing. PCR–DGGE found 36 of 52 coho salmon positive for A. salmonicida, compared with 31 positive by mucus culture and 16 by organ culture. Numerous other bacteria were detected in salmonid mucus, including Pseudomonas spp., Shewanella putrefaciens , Aeromonas hydrophila and other aeromonads. However, Yersinia ruckeri was not detected in mucus from 27 lake trout, but 1 fish had a sorbitol-positive Y. ruckeri isolated from organ culture. Yersinia ruckeri seeded into a mucus sample suggested that PCR–DGGE detection of this bacterium from mucus was possible. PCR–DGGE allows nonlethal detection of A. salmonicida in mucus and differentiation of some Aeromonas spp. and has the potential to allow simultaneous detection of other pathogens present in fish mucus.
Nitrogen source and growth stage of Candida albicans influence expression level of vacuolar aspartic protease Apr1p and carboxypeptidase Cpy1p
Authors: Bauerová Václava , Pichová Iva , Hrušková-Heidingsfeldová Olga 
Published: May 2012

Vacuoles play an important role in the physiology of pathogenic Candida spp. However, information on Candida albicans vacuolar enzymes, their properties, and regulation is scarce. Expression of the genes APR1 and CPY1 encoding vacuolar aspartic protease and serine carboxypeptidase, respectively, was analyzed using a clinical isolate of C. albicans. The transcription of both APR1 and CPY1 was upregulated in midexponential phase, together with increasing size of the vacuoles, when C. albicans was cultivated in yeast extract–peptone–dextrose agar at 30 °C. However, simultaneous upregulation of protein synthesis occurred only for Cpy1p. Analysis of APR1 and CPY1 expression under nitrogen-limited conditions revealed that the genes were regulated on both the transcriptional and translational levels and detectable amounts of Apr1p were synthesized only when C. albicans was grown in nitrogen-limited media.
Abundance and composition dynamics of soil ammonia-oxidizing archaea in an alpine fir forest on the eastern Tibetan Plateau of China
Authors: Wang Ao , Wu Fu-Zhong , Yang Wan-Qin , Wu Zhi-Chao , Wang Xu-Xi , Tan Bo 
Published: May 2012

Real-time qPCR and clone library sequencing targeting amoA genes were used to investigate the seasonal dynamics of an ammonia-oxidizing archaea (AOA) community in an alpine fir forest in western China. AOA were detected at all sampling dates, and there were significant variations in archaeal amoA gene copy numbers (7.63 × 105to 8.35 × 108per gram of dry soil) throughout the nongrowing season. Compared with ammonia-oxidizing bacteria (AOB), the AOA displayed a higher abundance on the majority of sampling dates during the freeze–thaw period. All of the AOA sequences fell within soil and sediment lineages and were affiliated with 7 clusters. Compared with the other clusters, cluster 1 was more sensitive to low temperature and was the dominant group in August. In contrast, cluster 3 dominated the AOA community in winter and probably represents a group of cold-adapted archaea. Redundancy analysis (RDA) revealed that the seasonality of the AOA community was mainly attributed to changes in soil temperature and nutrient availability (e.g., dissolved organic nitrogen and carbon). Our results indicate that AOA exist in frozen soils in the alpine coniferous forest ecosystem of the eastern Tibetan Plateau. Moreover, soil temperature may directly and (or) indirectly affect AOA abundance and composition and may further influence the soil N cycle during the winter.
Protective immune responses in mice induced by intramuscular and intranasal immunization with aMycoplasma pneumoniaeP1C DNA vaccine
Authors: Zhu Cuiming , Wu Yimou , Chen Sufang , Yu Minjun , Zeng Yanhua , You Xiaoxing , Xiao Jinhong , Wang Shiping 
Published: May 2012

Mycoplasma pneumoniae is an important causative agent of atypical pneumonia. This study was to determine the ability of a DNA expression vector, which encodes the carboxy terminal region of the M. pneumoniae P1 protein (P1C), to induce humoral and cellular immune responses and to protect against M. pneumoniae infection in BALB/c mice. Mice were immunized with pcDNA3.1/P1C by either intramuscular injection (i.m.) or intranasal inoculation (i.n.). Our results showed that p1c DNA immunization generates detectable antibodies specific to M. pneumoniae, and elicits high levels of IgG1, IgG2a, and IgG2b isotypes (P < 0.01). The levels of IFN-γ and IL-4 in spleen cells of the immunized mice were significantly elevated by immunization via both the i.m. and i.n. methods. Moreover, p1c DNA-immunized mice exhibited detectable protection against M. pneumoniae infection. The lung tissue inflammation was relieved and the histopathologic score (HPS) of pcDNA3.1/P1C-immunized mice was significantly decreased than those in phosphate-buffed saline (PBS) or vaccine-vector-immunized mice (P < 0.01), whereas there were no significant differences in HPS between i.m. and i.n. vaccination (P > 0.05). Our results suggest that pcDNA3.1/P1C could be useful for developing a vaccine against M. pneumoniae infection.
Abstract A10: Increased mesenchymal progenitor cells in RB1−/− bone
Authors: Kong Elizabeth , Gutierrez Gabriel , Thomas David , Hinds Philip 
Published: May 2012

Abstract
The retinoblastoma pathway is deregulated in 90% of human cancers owing to the mutation of one or more pathway members. Yet, the molecular pathogenesis of tumors with a loss of the retinoblastoma gene, RB1, (retinoblastoma and osteosarcoma) are poorly understood. To understand the role of pRb in tumor formation we have focused on a tissue in which malignancies commonly have RB1 deletions, bone. Human osteosarcoma cells, in general, exhibit no signs of terminal differentiation, and are defined by the ability to form bone. We hypothesize that osteosarcoma is caused by molecular/genetic disruptions of the osteogenic differentiation pathway. Homozygous null RB1 mice die during early embryonic day, E11.5-13.5, before any significant skeletal development or mineralization occurs. Therefore, we utilized the cre/lox system to create a bone targeted RB1 knockout animal. RB1−/− mice display defects in bone formation. Furthermore, isolation and characterization of primary calvarial cells (dorsal skull cells) from these animals show that pRb abates progression of pre-osteoblasts to mature osteoblasts. As osteoblasts are known progeny of primitive mesenchymal stem cells (MSC), we next asked if diminished differentiation resulted in an increase in MSCs. MSCs are pluripotent cells that can differentiate into a variety of cell types. I have shown in the absence of RB1, calvarial cells can differentiate into multiple lineages including bone and fat, where as cells fromWT littermates are restricted to the osteoblast lineage. Colony formation assays, a functional in vitro assay, suggest RB1−/− cells have increased progenitor cell number, and through sphere formation assays we have shown an increased self-renewal capacity. There is also a significantly larger population of Sca-1 (a stem cell marker) positive cells in RB1−/− cultures compared toWT littermates. In addition, utilization of microarray technology suggests a unique RB1 dependent gene expression pattern in osteogenesis. This is consistent with our previous work showing the necessity of the pRb/Runx2 (a master regulator in bone development) interaction to turn on osteocalcin transcription, a late marker in differentiation. We have begun to identify a possible mechanism for pRb regulation early in osteogenesis through the Hedgehog signaling pathway that explains the increased pluripotency of mesenchymal cells in the absence of RB1. Therefore, we have identified an increased number of bone progenitor cells that are pluripotent from RB1−/− mice, and a possible mechanism for pRb regulation early in osteogenesis and malignant tumor formation.
Citation Information: Cancer Res 2009;69(23 Suppl):A10.
Abstract A12: YAP-dependent induction of amphiregulin identifies a non-cell-autonomous component of the Hippo pathway
Authors: Zhang Jianmin , Ji Jun-Yuan , Yu Min , Overholtzer Michael , Smolen Gromoslaw A. , Brugge Joan S. , Dyson Nicholas J. , Haber Daniel A. 
Published: May 2012

Abstract
The Hippo signaling pathway was initially identified in Drosophila and components in this pathway are highly conserved in mammals. We and others have recently shown that the Hippo pathway regulates cellular proliferation and survival, thus exerting profound effects on normal cell fate and tumorigenesis. The pivotal effector of this pathway is YAP, a transcriptional co-activator amplified in mouse and human cancers, where it promotes epithelial to mesenchymal transition (EMT) and malignant transformation. To date, studies of YAP target genes have focused on cellautonomous mediators. Here, we show that YAP-expressing MCF10A breast epithelial cells secrete growth factors that enhance the proliferation of neighboring untransfected cells, implicating a non-cell autonomous mechanism. Using cytokine and growth factor array analysis, we identified the epidermal growth factor receptor (EGFR) ligand, amphiregulin (AREG), as a transcriptional target of YAP, whose induction contributes to YAP-mediated cell proliferation and migration. Knockdown of AREG or addition of an EGFR kinase inhibitor abrogates the proliferative effects of YAP expression. Suppression of the negative YAP regulators LATS1/2 is sufficient to induce AREG expression, consistent with a physiological regulation of AREG by the Hippo pathway. Furthermore, genetic interactions between the Drosophila YAP orthologue Yki and Egfr signaling components support the link between these two highly conserved signaling pathways. In conclusion, YAP-dependent secretion of AREG implicates activation of EGFR signaling as an important non-cell autonomous effector of the Hippo pathway, with relevance for the regulation of both physiological and malignant cell proliferation.
Citation Information: Cancer Res 2009;69(23 Suppl):A12.
Abstract A19: Enhanced leptin receptor expression identifies an aggressive subset of Middle Eastern papillary thyroid cancer
Authors: Al-Kuraya Khawla S. , Bavi Prashant , Siraj Abdul K. , Uddin Shahab 
Published: May 2012

Abstract
The putative role of leptin (Ob) and its receptor (Ob-R) in the pathogenesis of various primary human malignancies has been investigated in recent studies. However, the role of leptin and leptin receptor (Ob-R) in papillary thyroid cancer (PTC) has not yet been evaluated. In this study we investigated role of Ob-R in a large tissue microarray cohort of PTC followed by in vitro studies using a panel of PTC cell lines. Ob-R overexpression was seen in 80% PTCs and was significantly associated with poor disease free survival (p=0.0235). PTCs that overexpressed Ob-R showed a aggressive phenotype characterized by older age, extrathyroid extension, larger tumor size, nodal metastasis, advanced stage and tall cell variant histological subtype (p=0.0005, p=0.0006, p=0.0398, p= 0.0004, p=0.0111 and p=0.0003 respectively). Further PTCs with overexpression of Ob-R showed a significant direct association with overexpression of leptin (p=0.0004), XIAP (p&lt;0.0001) and BCL-XL (p&lt;0.0001). In vitro analysis showed that leptin stimulated cell proliferation and inhibited apoptosis via activation of phosphatidylinisitol 3-kinase (PI3K)/AKT signalling pathway. Inhibition of PI3K activity by LY294002, a specific inhibitor of PI3K kinase abrogated leptin-mediated PI3K/AKT signalling. Gene silencing of Ob-R with Ob-R siRNA in PTC cells resulted in down regulation of phospho-AKT, Bcl-XL and XIAP expression suggesting that leptin mediated pathogenesis of PTC occur via involvement of these downstream targets. Altogether these data suggest that leptin plays a critical role in PTC pathogenesis through PI3K/AKT pathway via Ob-R and is a potential prognostic marker associated with an aggressive phenotype and poor disease free survival.
Citation Information: Cancer Res 2009;69(23 Suppl):A19.
Abstract A20: Protein kinase C beta II is crucial for Ewing sarcoma cell survival
Authors: Surdez Dider , Benetkiewicz Magdalena , Perrin Virginie , Delattre Olivier , Tirode Franck 
Published: May 2012

Abstract
Ewing sarcoma, the second most frequent bone tumor of young adults, is most frequently characterized by a specific translocation t(11;22) leading to the formation of the aberrant transcription factor EWS-FLI1. By analyzing transcriptional profiles of Ewing tumors with other pediatric tumors, we identified genes that were highly and very specifically over-expressed in Ewing sarcomas, as compared to the others. Beside already identified EWS-FLI1 targets like NKX2-2 or NR0B1, we focused our attention on a novel potential EWS-FLI1 target gene: the protein kinase C beta (PRKCB). Firstly, we confirmed at the protein level, that PRKCB is highly expressed in different Ewing cell lines. Secondly, EWS-FLI1 shRNA inhibition experiments in different Ewing cell lines demonstrated that the PRKCB over-expression is dependent on the expression of the fusion protein. Thirdly, using luciferase reporter experiments together with chromatin immunoprecipitation, we could show that EWS-FLI1 can bind directly to the PRKCB promoter and regulate its activity, demonstrating that PRKCB is a new direct target of EWS-FLI1. Finally, we investigated the role of the two different PRKCB isoforms in Ewing cells by inhibiting either both or the second one only by knock-down experiments. Both strategies led to a dramatic decrease of cell proliferation together with a massive cell death, indicating that at least PRKCB isoform 2, which seems to be the most expressed isoform in Ewing cells, is crucial for Ewing cell survival. We obtained the same results while using specific inhibitor compounds of PRKCB. Altogether, these results show that protein kinase C beta is highly expressed in Ewing tumors and that its inhibition could be of major interest for developing new therapeutic strategies.
Citation Information: Cancer Res 2009;69(23 Suppl):A20.