bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of global microRNA expression reveals oncogenic potential of miR-145 in metastatic colorectal cancer
Authors: Arndt Greg M , Dossey Lesley , Cullen Lara M , Lai Angela , Druker Riki , Eisbacher Michael , Zhang Chunyan , Tran Nham , Fan Hongtao , Retzlaff Kathy , Bittner Anton , Raponi Mitch 
Published: October 2009

Abstract

Background
MicroRNAs (MiRNAs) are short non-coding RNAs that control protein expression through various mechanisms. Their altered expression has been shown to be associated with various cancers. The aim of this study was to profile miRNA expression in colorectal cancer (CRC) and to analyze the function of specific miRNAs in CRC cells. MirVana miRNA Bioarrays were used to determine the miRNA expression profile in eight CRC cell line models, 45 human CRC samples of different stages, and four matched normal colon tissue samples. SW620 CRC cells were stably transduced with miR-143 or miR-145 expression vectors and analyzed in vitro for cell proliferation, cell differentiation and anchorage-independent growth. Signalling pathways associated with differentially expressed miRNAs were identified using a gene set enrichment analysis.

Results
The expression analysis of clinical CRC samples identified 37 miRNAs that were differentially expressed between CRC and normal tissue. Furthermore, several of these miRNAs were associated with CRC tumor progression including loss of miR-133a and gain of miR-224. We identified 11 common miRNAs that were differentially expressed between normal colon and CRC in both the cell line models and clinical samples. In vitro functional studies indicated that miR-143 and miR-145 appear to function in opposing manners to either inhibit or augment cell proliferation in a metastatic CRC model. The pathways targeted by miR-143 and miR-145 showed no significant overlap. Furthermore, gene expression analysis of metastatic versus non-metastatic isogenic cell lines indicated that miR-145 targets involved in cell cycle and neuregulin pathways were significantly down-regulated in the metastatic context.

Conclusion
MiRNAs showing altered expression at different stages of CRC could be targets for CRC therapies and be further developed as potential diagnostic and prognostic analytes. The identified biological processes and signalling pathways collectively targeted by co-expressed miRNAs in CRC provide a basis for understanding the functional role of miRNAs in cancer.
Clinical meaning of age-related expression of fecal cytokeratin 19 in colorectal malignancy
Authors: Chang Chun-Chao , Yang Shung-Haur , Chien Chih-Cheng , Chen Shu-Hung , Pan Shiann , Lee Chia-Long , Lin Chih-Ming , Sun Hsiao-Lun , Huang Chi-Cheng , Wu Yih-Yiing , Yang Ruey-Neng , Huang Chi-Jung 
Published: October 2009

AbstractBackgroundColorectal cancer (CRC) is one of the leading causes of malignant death worldwide. Because young age of onset is often considered a poor prognostic factor for CRC, it is important to identify the poor outcomes of CRC in a younger population and to consider an aggressive approach by implementing early treatment. Our aim was to specifically quantify the fecal cytokeratin 19 (CK19) transcript from CRC patients and investigate its correlation with clinical stage, tumor malignancy, and age.MethodsThe quantitation of fecal CK19 transcript was determined by a quantitative real-time reverse transcription polymerase chain in 129 CRC patients (45 younger than 60 years at diagnosis) and 85 healthy controls. The levels of CK19 protein were examined both in colonic cell lines and tissues.ResultsThe analysis of 45 younger CRC patients (age ≤ 60 years) revealed that patients at the M1 stage had significantly higher expression levels of fecal CK19 mRNA when compared with healthy controls (p< 0.001) and patients at the M0 stage (p= 0.004). Additionally, the degree of consistency between the mean level of fecal CK19 mRNA and the distant metastatic rate in each age interval was up to 89% (p= 0.042).ConclusionThese results indicate that high levels of fecal CK19 mRNA represent a potential marker for colorectal malignancy and for aggressive treatment of younger CRC patients.
Loss of prostasin (PRSS8) in human bladder transitional cell carcinoma cell lines is associated with epithelial-mesenchymal transition (EMT)
Authors: Chen Li-Mei , Verity Nicole J , Chai Karl X 
Published: October 2009

Abstract

Background
The glycosylphosphatidylinositol (GPI)-anchored epithelial extracellular membrane serine protease prostasin (PRSS8) is expressed abundantly in normal epithelia and essential for terminal epithelial differentiation, but down-regulated in human prostate, breast, and gastric cancers and invasive cancer cell lines. Prostasin is involved in the extracellular proteolytic modulation of the epidermal growth factor receptor (EGFR) and is an invasion suppressor. The aim of this study was to evaluate prostasin expression states in the transitional cell carcinomas (TCC) of the human bladder and in human TCC cell lines.

Methods
Normal human bladder tissues and TCC on a bladder cancer tissue microarray (TMA) were evaluated for prostasin expression by means of immunohistochemistry. A panel of 16 urothelial and TCC cell lines were evaluated for prostasin and E-cadherin expression by western blot and quantitative PCR, and for prostasin gene promoter region CpG methylation by methylation-specific PCR (MSP).

Results
Prostasin is expressed in the normal human urothelium and in a normal human urothelial cell line, but is significantly down-regulated in high-grade TCC and lost in 9 (of 15) TCC cell lines. Loss of prostasin expression in the TCC cell lines correlated with loss of or reduced E-cadherin expression, loss of epithelial morphology, and promoter DNA hypermethylation. Prostasin expression could be reactivated by demethylation or inhibition of histone deacetylase. Re-expression of prostasin or a serine protease-inactive variant resulted in transcriptional up-regulation of E-cadherin.

Conclusion
Loss of prostasin expression in bladder transitional cell carcinomas is associated with epithelial-mesenchymal transition (EMT), and may have functional implications in tumor invasion and resistance to chemotherapy.
Habitat stability and occurrences of malaria vector larvae in western Kenya highlands
Authors: Himeidan Yousif E , Zhou Guofa , Yakob Laith , Afrane Yaw , Munga Stephen , Atieli Harrysone , El-Rayah El-Amin , Githeko Andrew K , Yan Guiyun 
Published: October 2009

Abstract

Background
Although the occurrence of malaria vector larvae in the valleys of western Kenya highlands is well documented, knowledge of larval habitats in the uphill sites is lacking. Given that most inhabitants of the highlands actually dwell in the uphill regions, it is important to develop understanding of mosquito breeding habitat stability in these sites in order to determine their potential for larval control.

Methods
A total of 128 potential larval habitats were identified in hilltops and along the seasonal streams in the Sigalagala area of Kakamega district, western Kenya. Water availability in the habitats was followed up daily from August 3, 2006 to February 23, 2007. A habitat is defined as stable when it remains aquatic continuously for at least 12 d. Mosquito larvae were observed weekly. Frequencies of aquatic, stable and larvae positive habitats were compared between the hilltop and seasonal stream area using χ2-test. Factors affecting the presence/absence of Anopheles gambiae larvae in the highlands were determined using multiple logistic regression analysis.

Results
Topography significantly affected habitat availability and stability. The occurrence of aquatic habitats in the hilltop was more sporadic than in the stream area. The percentage of habitat occurrences that were classified as stable during the rainy season is 48.76% and 80.79% respectively for the hilltop and stream area. Corresponding frequencies of larvae positive habitats were 0% in the hilltop and 5.91% in the stream area. After the rainy season, only 23.42% of habitat occurrences were stable and 0.01% larvae positive habitats were found in the hilltops, whereas 89.75% of occurrences remained stable in the stream area resulting in a frequency of 12.21% larvae positive habitats. The logistic regression analysis confirmed the association between habitat stability and larval occurrence and indicated that habitat surface area was negatively affecting the occurrence of An. gambiae larvae. While An. gambiae and An. funestus larvae occurred throughout the study period along the streams, a total of only 15 An. gambiae larvae were counted in the hilltops, and no An. funestus were found. Moreover, no larvae managed to develop into adults in the hilltops, and the density of adult An. gambiae was consistently low, averaging at 0.06 females per house per survey.

Conclusion
The occurrence of malaria vector larvae in the hilltop area was uncommon as a result of the low availability and high instability of habitats. To optimize the cost-effectiveness of malaria interventions in the western Kenya highlands, larval control should be focused primarily along the streams, as these are likely the only productive habitats at high altitude.
Amyloid-β colocalizes with apolipoprotein B in absorptive cells of the small intestine
Authors: Galloway Susan , Takechi Ryusuke , Pallebage-Gamarallage Menuka MS , Dhaliwal Satvinder S , Mamo John CL 
Published: October 2009

Abstract

Background
Amyloid-β is recognized as the major constituent of senile plaque found in subjects with Alzheimer's disease. However, there is increasing evidence that in a physiological context amyloid-β may serve as regulating apolipoprotein, primarily of the triglyceride enriched lipoproteins. To consider this hypothesis further, this study utilized an in vivo immunological approach to explore in lipogenic tissue whether amyloid-β colocalizes with nascent triglyceride-rich lipoproteins.

Results
In murine absorptive epithelial cells of the small intestine, amyloid-β had remarkable colocalization with chylomicrons (Manders overlap coefficient = 0.73 ± 0.03 (SEM)), the latter identified as immunoreactive apolipoprotein B. A diet enriched in saturated fats doubled the abundance of both amyloid-β and apo B and increased the overlap coefficient of the two proteins (0.87 ± 0.02). However, there was no evidence that abundance of the two proteins was interdependent within the enterocytes (Pearson's Coefficient < 0.02 ± 0.03), or in plasma (Pearson's Coefficient < 0.01).

Conclusion
The findings of this study are consistent with the possibility that amyloid-β is secreted by enterocytes as an apolipoprotein component of chylomicrons. However, secretion of amyloid-β appears to be independent of chylomicron biogenesis.
Diagnostic evaluation of food-related allergic diseases
Authors: Eckman John , Saini Sarbjit S , Hamilton Robert G 
Published: October 2009

Abstract
Food allergy is a serious and potentially life-threatening problem for an estimated 6% of children and 3.7% of adults. This review examines the diagnostic process that begins with a patient's history and physical examination. If the suspicion of IgE-mediated food allergy is compelling based on the history, skin and serology tests are routinely performed to provide confirmation for the presence of food-specific IgE antibody. In selected cases, a provocation challenge may be required as a definitive or gold standard reference test for confirmation of IgE mediated reactions to food. Variables that influence the accuracy of each of the diagnostic algorithm phases are discussed. The clinical significance of food allergen-specific IgE antibody cross-reactivity and IgE antibody epitope mapping of food allergens is overviewed. The advantages and limitations of the various diagnostic procedures are examined with an emphasis on future trends in technology and reagents.
CD74 interacts with APP and suppresses the production of Aβ
Authors: Matsuda Shuji , Matsuda Yukiko , D'Adamio Luciano 
Published: October 2009

Abstract

Background
Alzheimer disease (AD) is characterized by senile plaques, which are mainly composed of β amyloid (Aβ) peptides. Aβ is cleaved off from amyloid precursor protein (APP) with consecutive proteolytic processing by β-secretase and γ-secretase.

Results
Here, we show that CD74, the invariant chain of class II major histocompatibility complex, interacts with APP and serves as a negative regulator of Aβ. CD74 resembles other APP interacters such as BRI2 and BRI3, since all of them reduce the level of Aβ. However, unlike BRIs, CD74 does not reduce the secretion of sAPPα or sAPPβ. Interestingly, in HeLa cells, over expression of CD74 steers APP, but not Notch, to large vacuoles created by CD74.

Conclusion
Taken together, we propose that CD74 inhibits Aβ production by interacting with and derailing normal trafficking of APP.
Whole-genome resequencing of Escherichia coli K-12 MG1655 undergoing short-term laboratory evolution in lactate minimal media reveals flexible selection of adaptive mutations
Authors: Conrad Tom M , Joyce Andrew R , Applebee M Kenyon , Barrett Christian L , Xie Bin , Gao Yuan , Palsson Bernhard Ø 
Published: October 2009

Abstract
Background
Short-term laboratory evolution of bacteria followed by genomic sequencing provides insight into the mechanism of adaptive evolution, such as the number of mutations needed for adaptation, genotype-phenotype relationships, and the reproducibility of adaptive outcomes.

Results
In the present study, we describe the genome sequencing of 11 endpoints of Escherichia coli that underwent 60-day laboratory adaptive evolution under growth rate selection pressure in lactate minimal media. Two to eight mutations were identified per endpoint. Generally, each endpoint acquired mutations to different genes. The most notable exception was an 82 base-pair deletion in the rph-pyrE operon that appeared in 7 of the 11 adapted strains. This mutation conferred an approximately 15% increase to the growth rate when experimentally introduced to the wild-type background and resulted in an approximately 30% increase to growth rate when introduced to a background already harboring two adaptive mutations. Additionally, most endpoints had a mutation in a regulatory gene (crp or relA, for example) or the RNA polymerase.

Conclusions
The 82 base-pair deletion found in the rph-pyrE operon of many endpoints may function to relieve a pyrimidine biosynthesis defect present in MG1655. In contrast, a variety of regulators acquire mutations in the different endpoints, suggesting flexibility in overcoming regulatory challenges in the adaptation.
Effects of Maternal Dexamethasone Treatment in Early Pregnancy on Pituitary-Adrenal Axis in Fetal Sheep
Authors: Braun Thorsten , Li Shaofu , Sloboda Deborah M. , Li Wei , Audette Melanie C. , Moss Timothy J. M. , Matthews Stephen G. , Polglase Graeme , Nitsos Ilias , Newnham John P. , Challis John R. G. 
Published: October 2009

AbstractFetal exposure to elevated levels of bioactive glucocorticoids early in gestation, as in suspected cases of congenital adrenal hyperplasia, may result in adverse neurological events. Fetal hypothalamic-pituitary-adrenal development and function may be involved. We investigated immediate and long-term effects of maternal dexamethasone (DEX) administration early in pregnancy on fetal growth and pituitary-adrenal activity in sheep. Pregnant ewes carrying singleton fetuses (total n = 119) were randomized to control (2 ml saline/ewe) or DEX-treated groups (im injections of 0.14 mg/kg ewe weight · 12 h) at 40–41 d gestation (dG). At 50, 100, 125, and 140 dG, fetal plasma and tissues were collected. DEX-exposed fetuses were lighter than controls at 100 dG (P &lt; 0.05) but not at any other times. Fetal plasma ACTH levels and pituitary POMC and PC-1 mRNA levels were similar between groups. Fetal plasma cortisol levels were significantly reduced after DEX exposure in both male and female fetuses at 50 dG (P &lt; 0.05), were similar at 100 and 125 dG, but were significantly higher than controls at 140 dG. At 140 dG, there was increased adrenal P450C17 and 3β-HSD mRNA in female fetuses and reduced expression of ACTH-R mRNA in males. Fetal hepatic CBG mRNA levels mimicked plasma cortisol patterns. DEX exposure reduced CBG only in males at 50 dG (P &lt; 0.05). Placental mRNA levels of 11β-HSD2 were increased after DEX in males (P &lt; 0.05). Therefore, in sheep, early DEX may alter the developmental trajectory of the fetal hypothalamic-pituitary-adrenal axis, directly increasing fetal adrenal activation but not anterior pituitary function. In females, this effect may be attributed, in part, to increased fetal adrenal steroidogenic activity.
Effects of Endogenous Growth Differentiation Factor 9 on Activin A-Induced Inhibin B Production in Human Granulosa-Lutein Cells
Authors: Shi Feng-Tao , Cheung Anthony P. , Huang He-Feng , Leung Peter C. K. 
Published: October 2009

Background: We recently reported on the effects of exogenous growth differentiation factor 9 (GDF9) in enhancing activin A-induced inhibin βB-subunit mRNA and inhibin B levels in human granulosa-lutein (hGL) cells by modulating key components of the activin signaling pathway. We undertook the following study to characterize the role of endogenous GDF9 in this regard.Methods: We compared inhibin subunit (α, βA, and βB) mRNA and inhibin B levels and activation of activin receptors (ACVRs) and Smad signaling pathway in hGL cells obtained from women undergoing in vitro fertilization and cultured with and without activin A treatment after GDF9-targeting small interfering RNA transfection. GDF9, inhibin subunits, ACVR2B/1B and Smad2/3/4/7 mRNA and/or protein levels, Smad phosphorylation, and inhibin B were assessed with RT-PCR, immunoblotting, and ELISA. Data were analyzed by ANOVA followed by Tukey’s test.Results: GDF9 was detected as mRNA and protein in hGL cells and protein in follicular fluid from all 11 patients tested. Reduced endogenous GDF9 expression after targeting small interfering RNA transfection was associated with decreased ACVR2B/1B and Smad2/3/4 but increased inhibitory Smad7 mRNA and protein levels and, consequently, reduced activin A-induced βB-subunit mRNA and inhibin B levels.Conclusions: We report here for the first time autocrine roles for endogenous GDF9 in hGL cells in enhancing activin A-induced βB-subunit mRNA and inhibin B levels via key components of the activin signaling pathway. However, the relative contributions of GDF9 in granulosa cells vs. oocyte as autocrine/paracrine regulators of βB-subunit and inhibin B production in normal and abnormal human ovarian functions remain to be determined.
Mitochondrial Function and Insulin Resistance in Overweight and Normal-Weight Children
Authors: Fleischman Amy , Kron Matthew , Systrom David M. , Hrovat Mirko , Grinspoon Steven K. 
Published: October 2009

Background: Obesity has become an epidemic in children, associated with an increase in insulin resistance and metabolic dysfunction. Mitochondrial function is known to be an important determinant of glucose metabolism in adults. However, little is known about the relationship between mitochondrial function and obesity, insulin resistance, energy expenditure, and pubertal development in children.
Methods: Seventy-four participants, 37 overweight (≥85th percentile body mass index for age and sex) and 37 normal-weight (&lt;85th percentile) without personal or family history of diabetes mellitus were enrolled. Subjects were evaluated with an oral glucose tolerance test, metabolic markers, resting energy expenditure, Tanner staging, and 31P magnetic resonance spectroscopy of skeletal muscle for mitochondrial function.
Results: Overweight and normal-weight children showed no difference in muscle ATP synthesis [phosphocreatine (PCr) recovery after exercise] (32.4 ± 2.3 vs. 34.1 ± 2.1, P = 0.58). However, insulin-resistant children had significantly prolonged PCr recovery when compared with insulin-sensitive children, by homeostasis model assessment for insulin resistance quartile (ANOVA, P = 0.04). Similarly, insulin-resistant overweight children had PCr recovery that was prolonged compared with insulin-sensitive overweight children (P = 0.01). PCr recovery was negatively correlated with resting energy expenditure in multivariate modeling (P = 0.03). Mitochondrial function worsened during mid-puberty in association with insulin resistance.
Conclusion: Reduced skeletal muscle mitochondrial oxidative phosphorylation, assessed by PCr recovery, is associated with insulin resistance and an altered metabolic phenotype in children. Normal mitochondrial function may be associated with a healthier metabolic phenotype in overweight children. Further studies are needed to investigate the long-term physiological consequences and potential treatment strategies targeting children with reduced mitochondrial function.
Hydrogen Embrittlement Coverage by U.S. Government Standardization Documents
Authors: Clegg Edward T. 
Published: October 2009

This paper covers the Defense Specifications and Standards Program (DSSP). It describes the Department of Defense (DoD) standardization organization, discusses types of standardization documents, defines standardization terms, and covers requirements and test methods for hydrogen embrittlement in defense standardization documents. The DSSP is administered by the Deputy Under Secretary of Defense for Research and Engineering through the Defense Materials Specification and Standards Office (DMSSO). Authority is delegated by the DMSSO to Army, Navy, Air Force, and Defense Logistics Agency Departmental Standardization Offices (DEPSOs) for portions of the DSSP program. These DEPSOs further delegate responsibility among the forty plus standardization offices located at military installations. The Army Materials Technology Laboratory (AMTL) is one of these standardization offices.
The coverage of hydrogen embrittlement by DoD standardization documents is also discussed. The requirement section of specifications states the required hydrogen embrittlement relief treatment, and the quality assurance section describes the test methods to determine if embrittlement relief treatment has been successful.
Electrochemical Sensor for the Determination of Hydrogen in Metals by Potential Measurements
Authors: Mackor Adri , Wim de Kreuk C. , Schoonman Joop 
Published: October 2009

An electrochemical sensor is described for the nondestructive determination of the activity of mobile elemental hydrogen in a wide range of metals, like steel and palladium. The sensor is based on the principle of a concentration cell. In this cell one of the electrodes is either the sample metal to be investigated or an ultrathin palladium layer in direct contact with the sample, acting as a sensing electrode. The other electrode functions as the reference, for which we have used palladium hydride or molybdenum bronze. The electrolyte is a liquid or preferably solid proton conductor. A version, using molybdenum bronze and thin palladium film (20 nm) electrodes and hydrogen uranyl phosphate tetrahydrate, has been found to be especially valuable because of its selectivity and long-term stability.
Various metal samples from research and industry have been investigated to yield significant potential differences between samples containing (mobile) hydrogen and those which were low in hydrogen content. The qualitative and quantitative information from these hydrogen measurements may be used for many purposes provided that suitable calibration procedures are carried out.