bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effects of perceived predation risk on pre‐ and post‐metamorphic phenotypes in the common frog
Authors: Stamper C. E. , Downie J. R. , Stevens D. J. , Monaghan P. 
Published: December 2008

AbstractWhere organisms undergo radical changes in habitat during ontogeny, dramatic phenotypic reshaping may be required. However, physiological and functional interrelationships may constrain the extent to which an individual's phenotype can be equally well adapted to their habitat throughout the life cycle. The phenotypic response of tadpoles to the presence of a predator has been reported for several species of anuran but the potential post‐metamorphic consequences have rarely been considered. We reared common frog Rana temporaria tadpoles in the presence or absence of a larval odonate predator, Aeshna juncea, and examined the consequences of the resulting phenotypic adjustment in the aquatic larval stage of the life cycle for the terrestrial juvenile phenotype. In early development tadpoles developed deeper tail fins and muscles in response to the predator and, in experimental trials, swam further than those reared in the absence of a predator. While the difference in swimming ability remained significant throughout the larval period, by the onset of metamorphosis we could no longer detect any differences in the morphological parameters measured. The corresponding post‐metamorphic phenotypes also did not initially differ in terms of morphology. At 12 weeks post‐metamorphosis, however, froglets that developed from predator‐exposed tadpoles swam more slowly and less far than those that developed from tadpoles reared in the absence of predators, the opposite trend to that observed in the larval stage of the life cycle, and had narrower femurs. These results suggest that there may be long‐term costs for subsequent life‐history stages of tailoring the larval phenotype to prevailing environmental conditions.
Ambush site selection and ontogenetic shifts in foraging strategy in a semi‐aquatic pit viper, the Eastern cottonmouth
Authors: Eskew E. A. , Willson J. D. , Winne C. T. 
Published: December 2008

AbstractAlthough habitat selection has been studied in a variety of snake taxa, little is known about habitat selection in aquatic snake species. Additionally, due to their small size and secretive nature, juvenile snakes are seldom included in habitat selection studies. The Eastern cottonmouth Agkistrodon piscivorus is a semi‐aquatic pit viper known to use ambush, sit‐and‐wait foraging strategies. Ambush hunters are likely to select habitats that increase opportunity for successful prey capture while minimizing predation risk and maintaining appropriate thermal and hydric conditions. We characterized the foraging strategy and microhabitat use of cottonmouths at Ellenton Bay, an isolated Carolina bay freshwater wetland on the Savannah River Site in SC, USA. We measured habitat characteristics of 55 ambush sites used by 51 individual cottonmouths located during nighttime visual surveys, as well as 225 randomly selected sites within our search area. Cottonmouths exhibited an ontogenetic shift in foraging strategy with juveniles using predominately ambush foraging around the edge of the wetland while adults were most often encountered actively moving within the wetland. Principal components analysis revealed that juveniles selected foraging microhabitats that were different from random and consisted of mud substrate with sparse vegetation, whereas adults occupied a greater variety of microhabitats that did not differ from random. Concomitantly, free‐ranging cottonmouths exhibited ontogenetic shifts in diet: juveniles consumed mostly salamanders, while adults ate a greater variety of prey including other snakes and birds. Our results highlight the importance of understanding how ontogenetic changes in coloration, diet and predation risk influence foraging strategy and microhabitat selection in snakes.
Wnt signalling in mouse mesenchymal stem cells: impact on proliferation, invasion and MMP expression
Authors: Karow Marisa , Popp Tanja , Egea Virginia , Ries Christian , Jochum Marianne , Neth Peter 
Published: December 2008

AbstractBased on the capacity of mesenchymal stem cells (MSC) to differentiate into multiple cell types in vitro and in vivo, MCS may be a suitable source for cell therapy and regeneration strategies. A prerequisite for effective clinical applications of human MSC (hMSC) is a profound knowledge of signal transduction cascades that mediate processes like proliferation, targeted migration and differentiation. Recently, we identified the canonical Wnt signal transduction pathway as a key player in hMSC proliferation and invasion. To evaluate whether those findings are transferable to the equivalent counterparts in mice, we studied important steps in the wingless/int‐1 (Wnt) signal transduction pathway in mouse MSC (mMSC) and mMSC carrying a T cell specific transcription factor (TCF)/lymphoid enhancer binding factor (LEF)‐reporter transgene. We found that the induction of the canonical Wnt pathway resulted in the up‐regulation of the known Wnt target gene cyclin D1, closely associated with an enhanced proliferation capacity of mMSC. Interestingly, the expression of the Wnt target gene membrane type 1‐matrix metalloproteinase (MT1‐MMP) was diminished in mMSC upon Wnt3a stimulation, which came along with an impaired invasion. In line with these findings, MMP‐2 and MMP‐9 expression levels in mMSC were also decreased after Wnt3a treatment. In contrast, inhibition of Wnt signalling by the knockdown of the transcriptional activator β‐catenin resulted in an up‐regulation of MT1‐MMP and mMSC invasion. By comparing these findings with the settings in hMSC, major differences in Wnt‐regulated MMP expression were observed in mMSC. Thus, our data advice caution when mouse model systems represent the pre‐clinical validation of MSC‐mediated therapeutical approaches.
Crocetin protects against cardiac hypertrophy by blocking MEK‐ERK1/2 signalling pathway
Authors: Cai Jun , Yi Fang‐Fang , Bian Zhou‐Yan , Shen Di‐Fei , Yang Long , Yan Ling , Tang Qi‐Zhu , Yang Xin‐Chun , Li Hongliang 
Published: December 2008

AbstractOxidative stress plays a critical role in the progression of pathological cardiac hypertrophy and heart failure. Because crocetin represses oxidative stress in vitro and in vivo, we have suggested that crocetin would repress cardiac hypertrophy by targeting oxidative stress‐dependent signalling. We tested this hypothesis using primary cultured cardiac myocytes and fibroblasts and one well‐established animal model of cardiac hypertrophy. The results showed that crocetin (1–10 μM) dose‐dependently blocked cardiac hypertrophy induced by angiogensin II (Ang II; 1 μM) in vitro. Our data further revealed that crocetin (50 mg/kg/day) both prevented and reversed cardiac hypertrophy induced by aortic banding (AB), as assessed by heart weight/body weight and lung weight/body weight ratios, echocardio‐graphic parameters and gene expression of hypertrophic markers. The inhibitory effect of crocetin on cardiac hypertrophy is mediated by blocking the reactive oxygen species (ROS)‐dependent mitogen‐activated protein kinase (MAPK)/extracellular signal‐regulated kinase‐1/2 (MEK/ERK1/2) pathway and GATA binding protein 4 (GATA‐4) activation. Further investigation demonstrated that crocetin inhibited inflammation by blocking nuclear factor kappa B (NF‐κB) signalling and attenuated fibrosis and collagen synthesis by abrogating MEK‐ERK1/2 signalling. Overall, our results indicate that crocetin, which is a potentially safe and inexpensive therapy for clinical use, has protective potential in targeting cardiac hypertrophy and fibrosis by suppression of ROS‐dependent signalling pathways.
A complex intronic enhancer regulates expression of the CFTR gene by direct interaction with the promoter
Authors: Ott Christopher J. , Suszko Magdalena , Blackledge Neil P. , Wright Jane E. , Crawford Gregory E. , Harris Ann 
Published: December 2008

AbstractGenes can maintain spatiotemporal expression patterns by long‐range interactions between cis‐acting elements. The cystic fibrosis transmembrane conductance regulator gene (CFTR) is expressed primarily in epithelial cells. An element located within a DNase I‐hyper‐sensitive site (DHS) 10 kb into the first intron was previously shown to augment CFTR promoter activity in a tissue‐specific manner. Here, we reveal the mechanism by which this element influences CFTR transcription. We employed a high‐resolution method of mapping DHS using tiled microarrays to accurately locate the intron 1 DHS. Transfection of promoter‐reporter constructs demonstrated that the element displays classical tissue‐specific enhancer properties and can independently recruit factors necessary for transcription initiation. In vitro DNase I footprinting analysis identified a protected region that corresponds to a conserved, predicted binding site for hepatocyte nuclear factor 1 (HNF1). We demonstrate by electromobility shift assays (EMSA) and chromatin immunoprecipitation (ChIP) that HNF1 binds to this element both in vitro and in vivo. Moreover, using chromosome conformation capture (3C) analysis, we show that this element interacts with the CFTR promoter in CFTR‐expressing cells. These data provide the first insight into the three‐ dimensional (3D) structure of the CFTR locus and confirm the contribution of intronic cis‐acting elements to the regulation of CFTR gene expression.
Localized SDF‐1alpha gene release mediated by collagen substrate induces CD117+ stem cells homing
Authors: Wang Weiwei , Li Wenzhong , Ong Lee‐Lee , Furlani Dario , Kaminski Alexander , Liebold Andreas , Lützow Karola , Lendlein Andreas , Wang Jun , Li Ren‐Ke , Steinhoff Gustav , Ma Nan 
Published: December 2008

AbstractStromal cell‐derived factor‐1α (SDF‐1α) mediated mobilization and homing of stem cells showed promising potential in stem cell based tissue engineering and regenerative medicine. However local and sustained release of SDF‐1α is indispensable for stem cell mediated regenerative process due to its short half‐life under inflammatory conditions. In this study, a gene activated collagen substrate (GAC) was formed via assembly of plasmid encoding SDF‐1α into a collagen substrate to create a microenvironment favoring stem cell homing. Local release of SDF‐1α from the transfected cells on GAC and its effect on CD117+ stem cell homing were investigated. Non‐viral poly‐ethyleneimine (25kDa PEI)/DNA complexes were mixed with rat tail collagen solution to form the GAC. Optimization of GAC was carried out based on collagen effects on the PEI/DNA complexes, viability and luciferase expression of COS7 cells on GAC. CD117+ stem cells homing in response to SDF‐1α local expression from transfected cells on GAC were investigated in a flow chamber in vitro and in a mouse hind limb model in vivo. The gene expression, migration of CD117+ stem cells and the induced inflammation were investigated with immunostaining, reverse transcription polymerase chain reaction (RT‐PCR) and H&E staining. The optimized parameters for GAC were DNA dosage 10 μg/cm2, molar ratio of PEI nitrogen in primary amine to DNA phosphate (N/P ratio) 4 and mass ratio of collagen to DNA (C/D ratio) 1.0. It kept cell viability above 75% and transfection efficiency around 5.8 × 105 RLU/mg protein. GAC allowed the sustained gene release up to 60 days. GAC mediated SDF‐1α gene release induced migration and homing of CD117+ stem cells in vitro and in vivo significantly, and the inflammation of GAC reduced significantly two weeks after transplantation. GAC is a promising stem cell based therapeutic strategy for regenerative medicine.
Expression of microRNAs in diffuse large B cell lymphoma is associated with immunophenotype, survival and transformation from follicular lymphoma
Authors: Lawrie Charles H. , Chi Jianxiang , Taylor Stephen , Tramonti Daniela , Ballabio Erica , Palazzo Stefano , Saunders Nigel J. , Pezzella Francesco , Boultwood Jacqueline , Wainscoat James S. , Hatton Christian S. R. 
Published: December 2008

AbstractMicroRNAs are naturally occurring small RNA species that regulate gene expression and are frequently abnormally expressed in cancers. However, the role of microRNAs in lymphoma is poorly understood. Therefore, we undertook a comprehensive study of microRNA expression in two of the most common lymphomas: diffuse large B‐cell lymphoma (DLBCL) (n= 80) and follicular lymphoma (FCL) (n= 18) using microarrays containing probes for 464 human microRNAs. Unsupervised cluster analysis revealed distinct expression patterns between these two lymphomas and specific microRNA signatures (including members of the miR‐17–92 cluster) were derived that correctly predicted lymphoma type in >95% of cases. Furthermore, we identified microRNAs in de novo DLBCL (n= 64) associated with germinal centre‐like and non‐germinal centre‐like immunophenotypes, international prognostic index status and event‐free survival in CHOP and rituximab (R)‐CHOP treated patients. Despite the indolent nature of FCL a significant proportion of cases undergo high‐grade transformation to more aggressive DLBCL. In order to see if transformation is associated with changes in microRNA expression we compared transformed DLBCL cases (n= 16) with de novo DLBCL, as well as FCL cases that underwent subsequent transformation (n= 7) with FCL cases that had not transformed at a median follow‐up of 60 months (n= 11). Differential expression of 12 microRNAs correctly predicted >85% of transformed versus de novo DLBCL cases; six microRNAs (miR‐223, 217, 222, 221 and let‐7i and 7b) were found which could similarly predict or transformation in FCL (P< 0.05). These data suggest that microRNAs have potential as diagnostic and prognostic markers in these lymphomas and may be used to identify FCL patients at risk of high‐grade transformation.
Isolation and in vitro chondrogenic potential of human foetal spine cells
Authors: Quintin Aurelie , Schizas Constantin , Scaletta Corinne , Jaccoud Sandra , Gerber Stefan , Osterheld Maria‐Chiara , Juillerat Lucienne , Applegate Lee Ann , Pioletti Dominique P. 
Published: December 2008

AbstractCell therapy for nucleus pulposus (NP) regeneration is an attractive treatment for early disc degeneration as shown by studies using autologous NP cells or stem cells. Another potential source of cells is foetal cells. We investigated the feasibility of isolating foetal cells from human foetal spine tissues and assessed their chondrogenic potential in alginate bead cultures. Histology and immunohistochemistry of foetal tissues showed that the structure and the matrix composition (aggrecan, type I and II collagen) of foetal intervertebral disc (IVD) were similar to adult IVD. Isolated foetal cells were cultured in monolayer in basic media supplemented with 10% Fetal Bovine Serum (FBS) and from each foetal tissue donation, a cell bank of foetal spine cells at passage 2 was established and was composed of around 2000 vials of 5 million cells. Gene expression and immunohistochemistry of foetal spine cells cultured in alginate beads during 28 days showed that cells were able to produce aggrecan and type II collagen and very low level of type I and type X collagen, indicating chondrogenic differentiation. However variability in matrix synthesis was observed between donors. In conclusion, foetal cells could be isolated from human foetal spine tissues and since these cells showed chondrogenic potential, they could be a potential cell source for IVD regeneration.
Cellular repressor of E1A‐stimulated genes attenuates cardiac hypertrophy and fibrosis
Authors: Bian Zhouyan , Cai Jun , Shen Di‐fei , Chen Li , Yan Ling , Tang Qizhu , Li Hongliang 
Published: December 2008

AbstractCellular repressor of E1A‐stimulated genes (CREG) is a secreted glycoprotein of 220 amino acids. It has been proposed that CREG acts as a ligand that enhances differentiation and/or reduces cell proliferation. CREG has been shown previously to attenuate cardiac hypertrophy in vitro. However, such a role has not been determined in vivo. In the present study, we tested the hypothesis that overexpression of CREG in the murine heart would protect against cardiac hypertrophy and fibrosis in vivo. The effects of constitutive human CREG expression on cardiac hypertrophy were investigated using both in vitro and in vivo models. Cardiac hypertrophy was produced by aortic banding and infusion of angiotensin II in CREG transgenic mice and control animals. The extent of cardiac hypertrophy was quantitated by two‐dimensional and M‐mode echocardiography as well as by molecular and pathological analyses of heart samples. Constitutive over‐expression of human CREG in the murine heart attenuated the hypertrophic response, markedly reduced inflammation. Cardiac function was also preserved in hearts with increased CREG levels in response to hypertrophic stimuli. These beneficial effects were associated with attenuation of the mitogen‐activated protein kinase (MAPK)‐extracellular signal‐regulated kinase 1 (MEK‐ERK1)/2‐dependent signalling cascade. In addition, CREG expression blocked fibrosis and collagen synthesis through blocking MEK‐ERK1/2‐dependent Smad 2/3 activation in vitro and in vivo. Therefore, the expression of CREG improves cardiac functions and inhibits cardiac hypertrophy, inflammation and fibrosis through blocking MEK‐ERK1/2‐dependent signalling.
Slow and steady is the key to β‐cell replication
Authors: Brennand Kristen , Melton Doug 
Published: December 2008

Diabetes is a chronic disease of failed glucose homeostasis
Structure and function of the adult pancreas
Diabetes is an attractive target for cellular replacement therapy
In vitro differentiation of β‐cells from embryonic stem cells
β‐cell maintenance and expansion
Strong evidence that new β‐cells come from old β‐cells
All β‐cells contribute equally to islet growth and maintenance
Putative pancreatic stem cells
Reported evidence for bone marrow stem cells giving rise to β‐cells
Reported evidence for spleen stem cells giving rise to β‐cells
Reported evidence for ductal stem cells giving rise to β‐cells
Reported evidence for acini stem cells giving rise to β‐cells
Reported evidence for islet and/or pancreatic stem cells giving rise to β‐cells
β‐cell turnover
β‐cell mass is dynamic
β‐cell replication changes with age
β‐cell replication increases during pregnancy
β‐cell replication increases in cases of increased blood glucose and/or insulin resistance
β‐cell replication is regulated by cell cycle genes
The elusive circulating β‐cell growth factor
Increasing β‐cell replication in vivo
In vitro culture of β‐cells
Summary

AbstractThe β‐cells of the pancreas are responsible for insulin production and their destruction results in type I diabetes. β‐cell maintenance, growth and regenerative repair is thought to occur predominately, if not exclusively, through the replication of existing β‐cells, not via an adult stem cell. It was recently found that all β‐cells contribute equally to islet growth and maintenance. The fact that all β‐cells replicate homogeneously makes it possible to set up straightforward screens for factors that increase β‐cell replication either In vitro or in vivo. It is possible that a circulating factor may be capable of increasing β‐cell replication or that intrinsic cell cycle regulators may affect β‐cell growth. An improved understanding of the in vivo maintenance and growth of β‐cells will facilitate efforts to expand β‐cells In vitro and may lead to new treatments for diabetes.
Postgenomic Analysis of
Streptococcus thermophilus
Cocultivated in Milk with
Lactobacillus delbrueckii
subsp.
bulgaricus
: Involvement of Nitrogen, Purine, and Iron Metabolism
Authors: Herve-Jimenez Luciana , Guillouard Isabelle , Guedon Eric , Boudebbouze Samira , Hols Pascal , Monnet Véronique , Maguin Emmanuelle , Rul Françoise 
Published: December 2008

ABSTRACT

Streptococcus thermophilus
is one of the most widely used lactic acid bacteria in the dairy industry, in particular in yoghurt manufacture, where it is associated with
Lactobacillus delbrueckii
subsp.
bulgaricus
. This bacterial association, known as a proto-cooperation, is poorly documented at the molecular and regulatory levels. We thus investigate the kinetics of the transcriptomic and proteomic modifications of
S. thermophilus
LMG 18311 in response to the presence of
L. delbrueckii
subsp.
bulgaricus
ATCC 11842 during growth in milk at two growth stages. Seventy-seven different genes or proteins (4.1% of total coding sequences), implicated mainly in the metabolism of nitrogen (24%), nucleotide base (21%), and iron (20%), varied specifically in coculture. One of the most unpredicted results was a significant decrease of most of the transcripts and enzymes involved in purine biosynthesis. Interestingly, the expression of nearly all genes potentially encoding iron transporters of
S. thermophilus
decreased, whereas that of iron-chelating
dpr
as well as that of the
fur
(
perR
) regulator genes increased, suggesting a reduction in the intracellular iron concentration, probably in response to H
2
O
2
production by
L. bulgaricus
. The present study reveals undocumented nutritional exchanges and regulatory relationships between the two yoghurt bacteria, which provide new molecular clues for the understanding of their associative behavior.
Characterization of Two Novel α-Glucosidases fromBifidobacterium breveUCC2003
Authors: Pokusaeva Karina , O'Connell-Motherway Mary , Zomer Aldert , Fitzgerald Gerald F. , van Sinderen Douwe 
Published: December 2008

ABSTRACTTwo α-glucosidase-encoding genes (agl1andagl2) fromBifidobacterium breveUCC2003 were identified and characterized. Based on their similarity to characterized carbohydrate hydrolases, the Agl1 and Agl2 enzymes are both assigned to a subgroup of the glycosyl hydrolase family 13, the α-1,6-glucosidases (EC 3.2.1.10). Recombinant Agl1 and Agl2 into which a His12sequence was incorporated (Agl1Hisand Agl2His, respectively) exhibited hydrolytic activity towards panose, isomaltose, isomaltotriose, and four sucrose isomers—palatinose, trehalulose, turanose, and maltulose—while also degrading trehalose and, to a lesser extent, nigerose. The preferred substrates for both enzymes were panose, isomaltose, and trehalulose. Furthermore, the pH and temperature optima for both enzymes were determined, showing that Agl1Hisexhibits higher thermo and pH optima than Agl2His. The two purified α-1,6-glucosidases were also shown to have transglycosylation activity, synthesizing oligosaccharides from palatinose, trehalulose, trehalose, panose, and isomaltotriose.