bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cardiac responses of rats submitted to postnatal protein restriction
Authors: Murça Tatiane Moisés , Magno Tatiana Soares dos Reis , De Maria Marilda Luz de Andrade , Capuruço Carolina Andrade Bragança , Chianca Deoclécio Alves , Ferreira Anderson José 
Published: May 2012

Undernutrition during critical stages of development and childhood has important effects on cardiovascular homeostasis. The present study was undertaken to evaluate the in vivo and ex vivo cardiac function of rats submitted to postnatal protein restriction. Male Wistar rats (28 days old) were fed a regular (20%) or low-protein (6%) diet over 5 weeks. After this period, cardiac function was analyzed by echocardiography and isolated heart preparation. Furthermore, the density of cardiac noradrenergic fibers and hematological profile were evaluated. We found that malnourished rats exhibited elevated arterial blood pressure, increased fractional shortening (echocardiography), increased systolic tension, increased ±dT/dt (isolated heart technique), impaired diastolic function characterized by a slight increase in the left ventricular end-diastolic diameter (echocardiography) and decreased diastolic tension (isolated heart technique), and cardiac hypertrophy evidenced by augmentation of the posterior left ventricular wall and discrete hematological changes. In addition, malnourished rats exhibited increased noradrenergic fiber density in their hearts (0.08% ± 0.02% area in control rats vs. 0.17% ± 0.03% area in malnourished rats). Our current data demonstrate that postnatal protein restriction causes cardiac adaptation characterized by an early overworking heart. This is at least in part mediated by an increase in the efferent sympathetic fibers to the heart. These findings provide important information for efforts to prevent and manage the consequences of undernutrition in the human population.
Neuromuscular fatigue recovery following rapid and slow stretch–shortening cycle movements
Authors: Wadden Katie P. , Button Duane C. , Kibele Armin , Behm David G. 
Published: May 2012

The purpose of this study was to investigate underlying mechanisms and neuromuscular recovery patterns following rapid and slow stretch–shortening cycle (SSC) movements performed to fatigue. Fourteen (10 moderately trained (MT) and four highly trained (HT)) subjects completed rapid and slow SSC movements to fatigue. The rapid SSC movement consisted of continuous drop jumps from a 30 cm platform until a predetermined jump height was no longer maintained, and the slow SSC movement consisted of continuous squats to 90° of knee flexion at a load of 65% of subject’s one-repetition maximum until no further repetitions could be completed. Although blood lactate measures were significantly (p < 0.002) higher after the rapid SSC condition versus after the slow SSC condition, the recovery of neuromuscular properties (maximum voluntary contractions, twitch force, muscle compound action potential) following the two conditions to fatigue did not differ. The duration of the rapid SSC movement was dependent on the training status of the subject; HT subjects performed the rapid SSC longer (68.2%) than the MT subjects until fatigued. Thus, the neuromuscular fatigue recovery patterns were independent of the type of SSC movement, condition duration, and subject training status. Because rapid and slow SSC exercises induce similar fatigue patterns, training programs incorporating rapid SSC exercises can be developed similar to that prescribed in traditional slow SSC resistance training programs.
Trends in aerobic fitness among Canadians, 1981 to 2007–2009
Authors: Craig Cora L. , Shields Margot , Leblanc Allana G. , Tremblay Mark S. 
Published: May 2012

Public health surveillance systems often monitor physical activity trends, but fitness assessment is relatively rare. This study investigated secular changes in aerobic fitness among Canadian adults and children. Participants aged 8–69 years were from 2 nationally representative surveys, conducted in-home in 1981 and in mobile examination centers in 2007–2009. In both surveys, submaximal step tests using progressive age- and sex-specific exercise stages were completed after initial screening (Physical Activity Readiness Questionnaire, heart rate, blood pressure). Between surveys, the step-test protocol had been modified to reduce underestimation of fitness among fitter and older individuals. Maximal oxygen uptake was estimated for adults using validated historical and updated prediction equations, adjusted to reflect protocol differences. Because these equations are not validated for young people, maximal aerobic power was predicted at a heart rate of 200 beats·min–1by regressing observed heart rates on the oxygen costs of stepping for children and youth who completed at least 2 exercise stages. Overall, despite protocol differences, we found that the aerobic fitness levels of Canadians were lower in 2007–2009 than in 1981, with declines apparent in all age and both sex groups, thereby increasing the number of those at risk of adverse health outcomes. Future work is required to validate prediction equations of aerobic fitness for young people to make it possible to compare fitness levels over the lifespan and across time.
Agreement between anthropometric and dual-energy X-ray absorptiometry assessments of lower-limb volumes and composition estimates in youth-club rugby athletes
Authors: Carvalho Humberto M. , Coelho-e-Silva Manuel J. , Franco Sérgio , Figueiredo António J. , Tavares Óscar M. , Ferry Béatrice , Hidalgo-Hermanni Ilsabeth , Courteix Daniel , Malina Robert M. 
Published: May 2012

The purpose of this study was to assess the agreement of lower-limb volume estimates based on anthropometry and dual-energy X-ray absorptiometry (DXA) as a reference method in male rugby athletes. Predictive models using body mass and skinfolds were tested to improve the relative agreement between protocols (anthropometry, DXA). Rugby players (n = 41; 19.9 ± 2.2 years) volunteered for the study. Lower-limb total and fat-free volumes were estimated by anthropometry and also derived using DXA. Cross-validation between the anthropometry technique and DXA was then performed. Lower-limb volume estimates by anthropometry overestimated reference values and tended to be further from the reference values with the increase of scale. For the total sample, standard errors of measurement for volume estimates by anthropometry were 1.99 L and 1.34 L for total and fat-free volumes, respectively. Correlations with reference values were 0.81 for lower-limb volume and 0.90 for lower-limb fat-free volume. Correlations between estimated prediction equations and reference values showed higher correlations (r = 0.96 for lower-limb volume and r = 0.93 for lower-limb fat-free volume) compared with anthropometric estimates. Overall, the agreement of anthropometry method to quantify lower-limb volumes with DXA as a reference in young adult rugby players is acceptable and is a practical method when more expensive and complex techniques are not available. The consideration of body mass and lower-limb skinfolds increases the precision of lower-limb volume estimates using anthropometry in the young adult rugby players.
Characterizing the binding of nucleotide ATP on serum albumin by 31P NMR diffusion
Authors: Song Zhiyan , Zhao Hua , Olubajo Olarongbe , Hall Lewis B. , Orr Chauncey N. , Askew Courtney B. 
Published: May 2012

The pulsed-field-gradient (PFG) 31P NMR diffusion spectra were measured under varied sample conditions to characterize the low-affinity binding of adenosine 5′-triphosphate (ATP) on human serum albumin (HSA) or bovine serum albumin (BSA). The NMR diffusion constants of ATP, ATP–HSA, or ATP–BSA were illustrated as function of ATP concentrations. The binding curves of ATP–HSA and ATP–BSA were identical but strikingly different from the ATP curve. Using a “Scatchard plot”, the apparent binding constant (K) and number of ATP binding sites (n) on serum albumin were evaluated as K = 75.25 (mol/L)–1 and n = 10, respectively. At a pH < 5.0 and a pH > 9.0 or a temperature > 45 °C, the diffusion data of ATP–HSA were found to increase remarkably, suggesting that the dissociation of ATP from HSA was largely enhanced, probably because of pH- or heat-induced protein structural change, degradation, or aggregation. In addition, our data indicated that ADP was strongly competitive with ATP for the low-affinity binding to HSA, but heptanone and Cl– were essentially noncompetitive. These results are important for further elucidating the interaction of ATP with serum albumin and its possible effect on related bioprocesses. The method can be well applied to study the binding of other nucleotides/nucleosides on proteins.
Synthesis of new γ-lactones from preactivated monosubstituted pyrazines and TMS–ketene acetals
Authors: Garduño-Alva Azucena , Ortega-Alfaro M. Carmen , López-Cortés José G. , Chávez Isabel , Barroso-Flores Joaquin , Toscano Rubén A. , Rudler Henri , Álvarez-Toledano Cecilio 
Published: May 2012

The double addition of bis(trimethylsilyl) ketene acetals (1a–1b, R1 = CH3, –(CH2)5–) to 2-substituted pyrazines promoted by triflic anhydride leads to γ-lactones in a single step. A systematic study involving electron-withdrawing and electron-donating groups (R2 = CN, COOMe, PhCH=CH, Cl, Me, OMe) in the pyrazine ring reveals a strong dependence of electronic effects on the regiochemistry of nucleophilic addition.
Antimicrobial characterization and safety aspects of the bacteriocinogenicEnterococcus hiraeF420 isolated from Moroccan raw goat milk
Authors: Achemchem F. , Cebrián R. , Abrini J. , Martínez-Bueno M. , Valdivia E. , Maqueda M. 
Published: May 2012

The F420 strain, isolated from raw goat milk and identified as Enterococcus hirae , was selected because of its strong activity against Gram-positive bacteria, including Listeria monocytogenes . Interestingly, the F420 strain lacks the virulence genes and decarboxylase activity of histidine, lysine, and ornithine, and it is susceptible to 11 of 14 tested antibiotics, including vancomycin. The antimicrobial compounds produced by E. hirae F420 strain showed high resistance to heat treatment and to acidic and basic pHs. The MALDI-TOF mass spectrometry analysis coupled with the sequence of peptide and structural gene analysis of one of the purified enterocins showed 100% identity with enterocin P (EntP), previously described in E. faecium strains. The structural gene for EntP is located on a plasmid of 65 kb. Other enterocins with molecular mass higher than 7 kDa were also detected. This is the first report of the production of EntP by E. hirae species naturally occurring in foods. The biotechnological characteristics of the F420 strain and its enterocins indicate their potential for application in the control of L. monocytogenes and other undesirable bacteria in food systems.
Distribution of class 1 integrons among enteropathogenicEscherichia coli
Authors: Najibi S. , Bakhshi B. , Fallahzad S. , Pourshafie M.R. , Katouli M. , Sattari M. , Alebouyeh M. , Tajbakhsh M. 
Published: May 2012

The aim of this study was to investigate the incidence of and resistance gene content of class 1 integrons among enteropathogenic Escherichia coli (EPEC) and non-EPEC and to investigate intraspecies genetic diversity of EPEC strains isolated from children with diarrhea in Iran. Twenty-eight EPEC and 16 non-EPEC strains isolated from children with diarrhea were tested for the presence of a class 1 integron associated integrase gene (int1). Sequence analysis was performed to identify the resistance gene content of integrons. Genetic diversity and cluster analysis of EPEC isolates were also investigated using enterobacterial repetitive intergenic concensus – polymerase chain reaction (ERIC–PCR) fingerprinting. Twenty-three (82%) EPEC isolates and 11 (68.7%) non-EPEC isolates harbored the int1 gene specific to the conserved integrase region of class 1 integrons. Sequence analysis revealed the dominance of dfrA and aadA gene cassettes among the isolates of both groups. ERIC–PCR fingerprinting of EPEC isolates revealed a high diversity among these isolates. The widespread distribution of 2 resistance gene families (dfrA and aadA) among both groups of EPEC and non-EPEC isolates indicates the significance of integrons in antibiotic resistance transfer among these bacteria. Furthermore, clonal diversity of EPEC isolates harbouring a class 1 integron also suggests the circulation of these mobile elements among a diverse population of EPEC in this country.
Abstract A13: Decitabine treatment of c-Myc transformed cancer cells is augmented by the removal of the checkpoint kinase Chk1
Authors: Höglund Andreas , Nilsson Jonas A. 
Published: May 2012

Abstract
Decitabine, or DacogenTM (also known as 5-Aza-2′-deoxycytidine), is a FDA approved drug currently in clinical use against myelodysplastic syndrome, a pre-stage of acute myeloid leukemia (AML). Decitabine is a DNA methyltransferase inhibitor which causes rapid genome-wide demethylation, reactivating genes silenced during tumorigenesis. We have recently shown that Decitabine is a valid therapeutic agent in treatment of c-Myc transformed tumor cells and that overexpression of c-Myc sensitized mouse embryonic fibroblasts to Decitabine treatment. In vivo modeling using cells overexpressing c-Myc showed a delayed tumor development in animals treated with a single dose of Decitabine. Futhermore, Decitabine treatment was shown to cause DNA damage that was further relayed in a p53-independent manner through the checkpoint kinase Chk1. In the light of this, we decided to combine Decitabine treatment with a commercially available Chk1 inhibitor (SB218078). In this study we show that combinatorial treatment with Chk1 inhibitor and Decitabine augments the separate treatment regimes. Furthermore, we also show that RNAi against Chk1 sensitizes tumor cells from the λ-Myc transgenic mice to Decitabine treatment. This demonstrates the therapeutic possibilities of using Chk1 inhibitors in combination with DNA damage agents in treatment of c-Myc transformed cells.
Citation Information: Cancer Res 2009;69(23 Suppl):A13.
Abstract A16: Requirement of functionally active BRCA2 protein for the expression of IRF9-regulated genes in human breast cells
Authors: Mittal Mukul K. , Chaudhuri Gautam 
Published: May 2012

Abstract
Interferons are cytokines that induces antiviral, immunomodulatory and antiproliferative effects to cells by inducing the expressions of many effector proteins. Type I interferons are often used to treat advanced stages of breast cancer. Unfortunately, in many cases interferon treatment does not produce any significant effect. We found that transient ablation of the breast cancer susceptibility gene BRCA2 in the human breast cells impairs the expressions of many type I interferon regulated genes. Thus, it appears that type I interferons need functional BRCA2 for their actions. We tested the promoter activity of several of the interferon target genes, such as GBP1, GBP2, ISG15, MX1, MX2, PKR etc. in the BRCA2 knocked-down human breast cells with or without added INF-alpha2a. The interferon-stimulated activity of the promoter decreased significantly in the BRCA2 knocked-down cells, further suggesting a possible role of BRCA2 in the interferon signal transduction pathway. Over expression of BRCA2 in the BRCA2-deficient pancreatic cancer cell Capan1 significantly increased the interferon-stimulated activity of the IFN-alpha-regulated gene promoters in these cells. We tested whether BRCA2 helps mediating the interferon pathway by interacting with the components of this pathway. The classical signal transduction pathway for the type I interferons involve the formation of the ternary complex ISGF3 among phosphorylated STAT1 and STAT2 with IRF9. Immuno-pull-down experiments revealed the binding of STAT1, STAT2 and IRF9 with BRCA2 in the human breast cells. Our study thus proposes a not-known-before role of the breast cancer susceptibility protein BRCA2 in the type I interferon pathway. Supported by the generous funding from US Department of Defense IDEA grant #W81XWH-08-1-0446 to GC.
Citation Information: Cancer Res 2009;69(23 Suppl):A16.
Abstract A17: Transforming growth factor beta stimulates STAT3 tyrosine phosphorylation and cellular invasion through interleukin-6 in human breast cancer cell lines
Authors: Parker Nicole NT , Law Mary E. , Müller-Newen Gerhard , Corsino Pat , Davis Brad , Jahn Stephen , Law Brian K. 
Published: May 2012

Abstract
The signaling mechanisms involving Transforming Growth Factor β (TGFβ) and Signal Transducer and Activator of Transcription 3 (STAT3) are characterized in breast cancer, but the mechanism of crosstalk between these two pathways is poorly understood. In this study we addressed the question of TGFβ-STAT3 cross-signaling in nontransformed epithelial cells and in human breast cancer cell lines.
Breast cancer continues to be a serious disease in the United States. A large component of novel chemotherapeutics specifically target overexpressed or overactivated proteins in cancers. Two examples of these oncogenic molecules are the cytokine TGFβ and the transcription factor STAT3. Although these proteins have each been implicated in early and late stages of cancer and invasion, the mechanism of cross-talk between the TGFβ and STAT3 pathways has not been well characterized.
We have observed that TGFβ treatment is sufficient to induce phosphorylation of STAT3 on its activating Tyr (705) site in nontransformed mouse mammary NMuMG epithelial cells. The time dependence of this relationship implies de novo expression of an intermediate factor that data suggest is Interleukin-6 (IL-6). TGFβ treatment induces gene upregulation of IL-in a time-dependent manner similar to that of TGFβ stimulated STAT3 tyrosine phosphorylation. Inhibition of IL-6 with the mIL-6 Receptor Fusion Protein Inhibitor (mIL-6.RFPI) abrogated TGFβ stimulation of STAT3 tyrosine phosphorylation. Further, TGFβ treatment is sufficient to induce cellular invasion in NMuMG cells. This effect was recapitulated by IL-6 treatment, while IL-6 inhibition markedly reduced TGFβ stimulated invasion.
The human breast cancer cell lines MDA-MB-231 and MDA-MB-361, which are basal-like and luminal breast cancer models, respectively, display varying levels of constitutive STAT3 tyrosine phosphorylation. The MDA-MB-361 cell line exhibits no endogenous STAT3 phosphorylation but responds to TGFβ treatment in the same manner as nontransformed NMuMG mammary epithelial cells. Conversely, the MDA-MB-231 cell line displays high levels of constitutive STAT3 tyrosine phosphorylation, which data suggest is dependent in part on TGFβ signaling and is completely dependent on IL-6 signaling. Taken together, interruption of the TGFβ-IL-6-STAT3 signaling loop in MDA-MB-231 cells is sufficient to abrogate this signaling and dramatically reduce endogenous cellular invasiveness, while induction of the TGFβ-IL-6-STAT3 pathway in MDA-MB-361 cells confers an invasive phenotype on this otherwise noninvasive cell line.
Citation Information: Cancer Res 2009;69(23 Suppl):A17.
Abstract A2: Oncogenic and drug-sensitive ERBB2 mutations in glioblastoma
Authors: Greulich Heidi , Chheda Milan , Chen Tzu-Hsiu , Tanaka Kumiko , Dutt Amit , Wong Kwok-Kin , Hahn William , Meyerson Matthew 
Published: May 2012

Abstract
The Cancer Genome Atlas (TCGA) Consortium recently completed a multidimensional analysis of glioblastoma, characterizing somatic alterations across a large sample set, and identifying genetic lesions that likely contribute to tumor fitness (TCGA Network, Nature, 2008). However, functional experiments are required to determine whether significantly altered genes are in fact oncogenes or tumor suppressor genes in glioblastoma. We experimentally analyzed mutations in one of the significantly mutated genes, ERBB2. Unlike ERBB2 mutations in lung adenocarcinoma, ERBB2 mutations in glioblastoma are primarily located in the extracellular region, clustering around the domain that mediates receptor dimerization. We have determined that a subset of the reported mutations are gain-of-function and oncogenic, require kinase activity for oncogenic transformation, and are sensitive to specific small molecule kinase inhibitors. This discovery has therapeutic implications for glioblastoma patients who harbor somatic ERBB2 mutations.
Citation Information: Cancer Res 2009;69(23 Suppl):A2.
Abstract A38: Human kinase screen for breast cancer oncogenes
Authors: Shrestha Yashaswi , Schafer Eric J. , Weir Barbara , Boehm Jesse , Thomas Sapana , Hahn William C. 
Published: May 2012

Abstract
The heterogeneity of breast cancer requires identification of novel genes that promote breast tumor development. Targeting such oncogenes therapeutically promises to improve clinical outcomes. We conducted an in vitro screen to identify human kinases that promote anchorage-independent growth of immortalized human mammary epithelial cells. The screen is based on a transformation model that requires cooperative activation of the PI3K/AKT and MEK/ERK pathways. The pooled screen identified three transforming kinases - PTK6, PAK1 and CAMK4. The functions of these candidates in the PI3K/AKT and/or MEK/ERK pathways are being currently studied to determine their role in breast tumorigenesis.
Citation Information: Cancer Res 2009;69(23 Suppl):A38.
Abstract A4: Guanylate binding protein-1 promotes glioma cell invasion through induction of MMP1 expression
Authors: Li Ming , Furnari Frank B. , Cavenee Webster K. 
Published: May 2012

Abstract
Glioma is the most common and deadly human brain tumor. Epidermal growth factor receptor (EGFR) amplification or constitutively active mutation (EGFRVIII) is one of the most frequent genetic lesions in gliomas. To identify target genes regulated by EGFR signaling, we performed expression array analysis and found that human guanylate binding protein-1 (GBP-1), a large GTPase that is induced by inflammatory cytokines, is one of the predominant genes induced by EGFR/EGF or EGFR VIII kinase activity. Our results demonstrate that EGF/EGFR signaling could dramatically induce Gbp-1 expression at both the mRNA and protein level through the p38 kinase signaling cascade that is distinct from Stat1 signaling used by interferon gamma. Interestingly, we show that Gbp-1 is required for EGFR-mediated matrix metallopeptidase-1 (MMP1) expression, and plays a role in glioma cell invasion in vitro. Overexpression of Gbp-1 induced MMP1 expression in glioma cells, which was independent of Gbp-1 GTPase activity. In contrast, siRNA-mediated knockdown of Gbp-1 inhibited MMP1 expression and in turn blocked cell invasion as well. Consistently, we found that GBP-1 is overexpressed and positively correlated with EGFR/EGFRVIII and MMP1 expression in human glioma clinical samples and glioma cell lines. Therefore, this study suggests that Gbp-1 may be a novel therapeutic target in glioma.
Citation Information: Cancer Res 2009;69(23 Suppl):A4.