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Rheology and gel point of the enzymatic hydrolysis of urea in the presence of urease
R. Serrato-Millán,L. Medina-Torres,F. Calderas,B.L. España-Sánchez,M. Estevez,A.R. Hernandez-Martínez,M. Cruz-Soto,I.C. Sánchez,R. Gómez-García,I. Sánchez-Betancourt,M.C. Velasquillo-Martínez,G. Luna- 한국유변학회 2017 Korea-Australia rheology journal Vol.29 No.1
This study reports on the rheology of the gelation kinetics of raw chitosan (CTS) solutions (2% w/v) produced by enzymatic hydrolysis of urea at different urea concentrations (40, 50, 60, 80, and 100 mM) in the presence of urease at 1 U/mL. Viscoelastic parameters and pH values were evaluated during gelation process and the rheological properties of CTS hydrogels produced were monitored after 24 h at 37°C to simulate human body temperatures. pH measurements suggest that above some critical urea concentration (50 mM) the time required (tgel) to reach the critical pH gelation shows no dependence on urea concentration (tgel was ca. 70 minutes). Above 50 mM of urea concentration, CTS hydrogels exhibit an elastic modulus G' higher than the viscous modulus G'' with no frequency dependence characteristic of a gel behavior. Gelation kinetics analyzed by rheology suggest that the G' (i.e., structure) development depends on urea concentration during solution neutralization.
Jeong, K.J.,Cho, K.H.,Panupinthu, N.,Kim, H.,Kang, J.,Park, C.G.,Mills, G.B.,Lee, H.Y. Elsevier BV 2013 Molecular Oncology Vol.7 No.1
Lysophosphatidic acid (LPA) augments proliferation and metastasis of various cancer cells. We recently identified a critical role of the Rho/ROCK pathway for LPA-induced proteolytic enzyme expression and cancer cell progression. In the present study, we elucidate the underlying mechanisms by which LPA induces Rho activation and subsequent cellular invasion, and the reversal of these effects by resveratrol. We observed that both Gi and G13 contribute to LPA-induced EGFR activation. The activated EGFR in turn initiates a Ras/Rho/ROCK signaling cascade, leading to proteolytic enzyme secretion. Further we provide evidence that resveratrol inhibits EGFR phosphorylation and subsequent activation of a Ras/Rho/ROCK signaling. Therefore, we demonstrate a mechanistic cascade of LPA activating EGFR through Gi and G13 thus inducing a Ras/Rho/ROCK signaling for proteolytic enzyme expression and ovarian cancer cell invasion, as well as interference of the cascade by resveratrol through blocking EGFR phosphorylation.
Mills, R.W.,Slingsby, B.M.,Coleman, J.,Collins, R.,Holt, G.,Metelko, C.,Schnellbach, Y. Korean Nuclear Society 2020 Nuclear Engineering and Technology Vol.52 No.9
The standard method for calculating anti-neutrino emissions from a reactor involves knowing the fractional fission rates for the most important fissioning nuclides in the reactor. To calculate these rates requires detailed reactor physics calculations based upon the reactor design, fuel design, burnup dependent fuel composition, location of specific fuel assemblies in the core and detailed operational data from the reactor. This has only been published for a few reactors during specific time periods, whereas to be of practical use for anti-neutrino reactor monitoring it is necessary to be able to predict these on the publicly available information from any reactor, especially if using these data to subtract the anti-neutrino signal from other reactors to identify an undeclared reactor and monitor its operation. This paper proposes a method to estimate the fission fractions for a specific reactor based upon publicly available information and provides a database based upon a series of spent fuel inventory calculations using the FISPIN10 code and its associated data libraries.
Stange, Daniel E.,Koo, B.K.,Huch, M.,Sibbel, G.,Basak, O.,Lyubimova, A.,Kujala, P.,Bartfeld, S.,Koster, J.,Geahlen, Jessica H.,Peters, Peter J.,van Es, Johan H.,van de Wetering, M.,Mills, Jason C.,Cle Cell Press ; MIT Press 2013 Cell Vol.155 No.2
Proliferation of the self-renewing epithelium of the gastric corpus occurs almost exclusively in the isthmus of the glands, from where cells migrate bidirectionally toward pit and base. The isthmus is therefore generally viewed as the stem cell zone. We find that the stem cell marker Troy is expressed at the gland base by a small subpopulation of fully differentiated chief cells. By lineage tracing with a Troy-eGFP-ires-CreERT2 allele, single marked chief cells are shown to generate entirely labeled gastric units over periods of months. This phenomenon accelerates upon tissue damage. Troy<SUP>+</SUP> chief cells can be cultured to generate long-lived gastric organoids. Troy marks a specific subset of chief cells that display plasticity in that they are capable of replenishing entire gastric units, essentially serving as quiescent ''reserve'' stem cells. These observations challenge the notion that stem cell hierarchies represent a ''one-way street.''
Musashi RNA-binding protein 2 regulates estrogen receptor 1 function in breast cancer
Kang, M-H,Jeong, K J,Kim, W Y,Lee, H J,Gong, G,Suh, N,Győ,rffy, B,Kim, S,Jeong, S-Y,Mills, G B,Park, Y-Y Macmillan Publishers Limited, part of Springer Nat 2017 Oncogene Vol.36 No.12
<P>Musashi RNA-binding protein 2 (MSI2) has important roles in human cancer. However, the regulatory mechanisms by which MSI2 alters breast cancer pathophysiology have not been clearly identified. Here we demonstrate that MSI2 directly regulates estrogen receptor 1 (ESR1), which is a well-known therapeutic target and has been shown to reflect clinical outcomes in breast cancer. Based on gene expression data analysis, we found that MSI2 expression was highly enriched in estrogen receptor (ER)-positive breast cancer and that MSI2 expression was significantly correlated with ESR1 expression, including expression of ESR1 downstream target genes. In addition, MSI2 levels were associated with clinical outcomes. MSI2 influenced breast cancer cell growth by altering ESR1 function. MSI2 alters ESR1 by binding specific sites in ESR1 RNA and by increasing ESR1 protein stability. Taken together, our findings identified a novel regulatory mechanism of MSI2 as an upstream regulator of ESR1 and revealed the clinical relevance of the RNA-binding protein MSI2 in breast cancer.</P>
hTERT mediates norepinephrine-induced Slug expression and ovarian cancer aggressiveness
Choi, M J,Cho, K H,Lee, S,Bae, Y J,Jeong, K J,Rha, S Y,Choi, E J,Park, J H,Kim, J M,Lee, J-S,Mills, G B,Lee, H Y Macmillan Publishers Limited 2015 Oncogene Vol.34 No.26
Stress hormones have been implicated in both tumor initiation and progression. Human telomerase reverse transcriptase (hTERT) is overexpressed in cancer cells and associated with malignant tumor progression and poor outcome. We thus sought to determine whether the stress hormone norepinephrine (NE) could induce hTERT expression and subsequently ovarian cancer progression. Unexpectedly, NE induced hTERT transcript and protein expression, and subsequently ovarian cancer cell invasion. Pharmacologic inhibition of β2-adrenergic receptor 2 and protein kinase A, as well as silencing of hypoxia-inducible factor-1α and c-Myc expression, profoundly attenuated NE-induced hTERT expression. Strikingly, stimulation of the cells with NE or ectopic expression of hTERT induced expression of Slug, ovarian cancer cell epithelial–mesenchymal transition (EMT) and invasion. Silencing of hTERT expression abrogated NE-induced ovarian cancer cell invasion, EMT and Slug expression. In addition, silencing of Slug expression significantly inhibited NE- and hTERT-induced ovarian cancer cell EMT and invasion. Moreover, continuous exposure to NE was sufficient to enhance in vivo hTERT expression and metastasis of ovarian cancer cells to the lung. Finally, we provide evidence that hTERT links Src to Slug expression in NE-induced ovarian cancer EMT and metastasis. We thus demonstrate a novel role of hTERT in stress hormone-induced ovarian cancer aggressiveness through inducing Slug, providing novel biomarkers and potential therapeutic targets for ovarian cancer.