372 research outputs found

    Protein digestibility of biorefined juice from fresh and ensiled ley crops in growing pigs

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    The study aimed to evaluate the protein and amino acid digestibility of press juice from biorefined ley crops in the form of fresh (FPJ) and silage (SPJ) when included as an ingredient in liquid diets for pigs. The juice was extruded from ley crops mixture (grass-clover). The juice was stored in 10 L plastic containers and frozen at -20° C until the day of use. Eight female pigs (YH) around 9 weeks of age and an average of 24.15 (+2.76) kg BW were randomly assigned to one of the two dietary treatments containing FPJ (n = 4) or SPJ (n = 4). The diets were formulated to meet the nutritional requirements of the pigs, based on 4% of the average BW with the inclusion of 50 % of press juice in the mixture on a dry matter (DM) basis. The dietary treatments were mixed with a protein-free basal diet with an indigestible marker of titanium dioxide (TiO2) in order to calculate the protein and amino acid digestibility. The experimental period lasted for eleven days with seven days for adaptation to the diet and four days of faecal sampling. At the end of the trial the animals were euthanized, and the ileal content was collected for analyses of crude protein, amino acids, and concentration of TiO2. The differentiation of the indigestible marker obtain in the samples were used to calculate the apparent total tract digestibility (ATTD), apparent ileal digestibility (AID) and standardized ileal digestibility (SID) values of crude protein and amino acids for press juice in both fresh and silage form. A statistical general linear model (PROC GLM) was used to analyze the digestibility values between the two dietary treatments. The results of the trial showed that there was no significant difference (p>0.05) for gaining weight in pigs fed with FPJ or SPJ diets. The ATTD of crude protein (CP) and organic matter (OM) were higher (p0.05). In conclusion, the acceptable levels of protein and amino acid digestibility of both FPJ and SPJ evaluated in growing pigs opens the potential to use the protein content found in these biorefinery fractions as an additional protein source to be considered in the inclusion of liquid diets for pigs

    Unemployment insurance and regional economic development

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    Economic development ; Unemployment insurance

    Triggering social interactions:chimpanzees respond to imitation by a humanoid robot and request responses from it

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    Even the most rudimentary social cues may evoke affiliative responses in humans and promote socialcommunication and cohesion. The present work tested whether such cues of an agent may also promotecommunicative interactions in a nonhuman primate species, by examining interaction-promoting behavioursin chimpanzees. Here, chimpanzees were tested during interactions with an interactive humanoid robot, whichshowed simple bodily movements and sent out calls. The results revealed that chimpanzees exhibited twotypes of interaction-promoting behaviours during relaxed or playful contexts. First, the chimpanzees showedprolonged active interest when they were imitated by the robot. Second, the subjects requested ‘social’responses from the robot, i.e. by showing play invitations and offering toys or other objects. This study thusprovides evidence that even rudimentary cues of a robotic agent may promote social interactions inchimpanzees, like in humans. Such simple and frequent social interactions most likely provided a foundationfor sophisticated forms of affiliative communication to emerge

    Expression of LIM kinase 1 is associated with reversible G1/S phase arrest, chromosomal instability and prostate cancer

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    <p>Abstract</p> <p>Background</p> <p>LIM kinase 1 (LIMK1), a LIM domain containing serine/threonine kinase, modulates actin dynamics through inactivation of the actin depolymerizing protein cofilin. Recent studies have indicated an important role of LIMK1 in growth and invasion of prostate and breast cancer cells; however, the molecular mechanism whereby LIMK1 induces tumor progression is unknown. In this study, we investigated the effects of ectopic expression of LIMK1 on cellular morphology, cell cycle progression and expression profile of LIMK1 in prostate tumors.</p> <p>Results</p> <p>Ectopic expression of LIMK1 in benign prostatic hyperplasia cells (BPH), which naturally express low levels of LIMK1, resulted in appearance of abnormal mitotic spindles, multiple centrosomes and smaller chromosomal masses. Furthermore, a transient G1/S phase arrest and delayed G2/M progression was observed in BPH cells expressing LIMK1. When treated with chemotherapeutic agent Taxol, no metaphase arrest was noted in these cells. We have also noted increased nuclear staining of LIMK1 in tumors with higher Gleason Scores and incidence of metastasis.</p> <p>Conclusion</p> <p>Our results show that increased expression of LIMK1 results in chromosomal abnormalities, aberrant cell cycle progression and alteration of normal cellular response to microtubule stabilizing agent Taxol; and that LIMK1 expression may be associated with cancerous phenotype of the prostate.</p

    Economic evaluation of implementation science outcomes in low- and middle-income countries: A scoping review

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    BACKGROUND: Historically, the focus of cost-effectiveness analyses has been on the costs to operate and deliver interventions after their initial design and launch. The costs related to design and implementation of interventions have often been omitted. Ignoring these costs leads to an underestimation of the true price of interventions and biases economic analyses toward favoring new interventions. This is especially true in low- and middle-income countries (LMICs), where implementation may require substantial up-front investment. This scoping review was conducted to explore the topics, depth, and availability of scientific literature on integrating implementation science into economic evaluations of health interventions in LMICs. METHODS: We searched Web of Science and PubMed for papers published between January 1, 2010, and December 31, 2021, that included components of both implementation science and economic evaluation. Studies from LMICs were prioritized for review, but papers from high-income countries were included if their methodology/findings were relevant to LMIC settings. RESULTS: Six thousand nine hundred eighty-six studies were screened, of which 55 were included in full-text review and 23 selected for inclusion and data extraction. Most papers were theoretical, though some focused on a single disease or disease subset, including: mental health (n = 5), HIV (n = 3), tuberculosis (n = 3), and diabetes (n = 2). Manuscripts included a mix of methodology papers, empirical studies, and other (e.g., narrative) reviews. Authorship of the included literature was skewed toward high-income settings, with 22 of the 23 papers featuring first and senior authors from high-income countries. Of nine empirical studies included, no consistent implementation cost outcomes were measured, and only four could be mapped to an existing costing or implementation framework. There was also substantial heterogeneity across studies in how implementation costs were defined, and the methods used to collect them. CONCLUSION: A sparse but growing literature explores the intersection of implementation science and economic evaluation. Key needs include more research in LMICs, greater consensus on the definition of implementation costs, standardized methods to collect such costs, and identifying outcomes of greatest relevance. Addressing these gaps will result in stronger links between implementation science and economic evaluation and will create more robust and accurate estimates of intervention costs. TRIAL REGISTRATION: The protocol for this manuscript was published on the Open Science Framework. It is available at: https://osf.io/ms5fa/ (DOI: 10.17605/OSF.IO/32EPJ)

    Down-regulation of Cdc6, a cell cycle regulatory gene, in prostate cancer

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    CDC6 plays a critical role in regulation of the onset of DNA replication in eukaryotic cells. We have found that Cdc6 expression is down-regulated in prostate cancer as detected by semiquantitative reverse transcriptase-PCR of prostate cell lines and laser-captured microdissected prostate tissues. This result was substantiated by immunohistochemical analysis of paraffin-embedded tissue sections and immunoblot analysis of benign (BPH-1) and adenocarcinomatous prostatic cells. Furthermore, a 100-fold reduction in the transcription efficiency of the Cdc6 promoter-luciferase construct was noted in the metastatic PC3 cells compared with that in BPH-1 cells. Concentration of the E2F and Oct1 transcription factors that have putative binding sites in the Cdc6 promoter was substantially low in PC3 cells compared with BPH cells. Mutagenesis of the two E2F binding sites on the Cdc6 promoter resulted in increased promoter activity in PC3 cells owing to elimination of the negative regulation by pRb-E2F complex but not to the level of that obtained in BPH cells. We conclude that an altered interaction of transcription factors may be responsible for the down-regulation of Cdc6 transcription in PC3 cells. Our study suggests a potential use of the lack of CDC6 expression as an index of prostate cancer development

    Down-regulation of Cdc6, a cell cycle regulatory gene, in prostate cancer

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    CDC6 plays a critical role in regulation of the onset of DNA replication in eukaryotic cells. We have found that Cdc6 expression is down-regulated in prostate cancer as detected by semiquantitative reverse transcriptase-PCR of prostate cell lines and laser-captured microdissected prostate tissues. This result was substantiated by immunohistochemical analysis of paraffin-embedded tissue sections and immunoblot analysis of benign (BPH-1) and adenocarcinomatous prostatic cells. Furthermore, a 100-fold reduction in the transcription efficiency of the Cdc6 promoter-luciferase construct was noted in the metastatic PC3 cells compared with that in BPH-1 cells. Concentration of the E2F and Oct1 transcription factors that have putative binding sites in the Cdc6 promoter was substantially low in PC3 cells compared with BPH cells. Mutagenesis of the two E2F binding sites on the Cdc6 promoter resulted in increased promoter activity in PC3 cells owing to elimination of the negative regulation by pRb-E2F complex but not to the level of that obtained in BPH cells. We conclude that an altered interaction of transcription factors may be responsible for the down-regulation of Cdc6 transcription in PC3 cells. Our study suggests a potential use of the lack of CDC6 expression as an index of prostate cancer development

    LIM kinase 1 is essential for the invasive growth of prostate epithelial cells - Implications in prostate cancer

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    Mammalian LIM kinase 1 (LIMK1) is involved in reorganization of actin cytoskeleton through inactivating phosphorylation of the ADF family protein cofilin, which depolymerizes actin filaments. Maintenance of the actin dynamics in an ordered fashion is essential for stabilization of cell shape or promotion of cell motility depending on the cell type. These are the two key phenomena that may become altered during acquisition of the metastatic phenotype by cancer cells. Here we show that LIMK1 is overexpressed in prostate tumors and in prostate cancer cell lines, that the concentration of phosphorylated cofilin is higher in metastatic prostate cancer cells, and that a partial reduction of LIMK1 altered cell proliferation by arresting cells at G(2)/ M, changed cell shape, and abolished the invasiveness of metastatic prostate cancer cells. We also show that the ectopic expression of LIMK1 promotes acquisition of invasive phenotype by the benign prostate epithelial cells. Our data provide evidence of a novel role of LIMK1 in regulating cell division and invasive property of prostate cancer cells and indicate that the effect is not mediated by phosphorylation of cofilin. Our study correlates with the recent observations showing a metastasis-associated chromosomal gain on 7q11.2 in prostate cancer, suggesting a possible gain in LIMK1 DNA (7q11.23)
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