4,710 research outputs found
Yeast metabolism in fresh and frozen dough : a thesis presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Food Technology at Massey University, Palmerston North, New Zealand
No full textAuthor also known as SM LovedayFresh bakery products have a very short shelf life, which limits the extent to which manufacturing can be centralised. Frozen doughs are relatively stable and can be manufactured in large volumes, distributed and baked on-demand at the point of sale or consumption. With appropriate formulation and processing a shelf life of several months can be achieved.Shelf life is limited by a decline in proofing rate after thawing, which is attributed to a) the dough losing its ability to retain gas and b) insufficient gas production, i.e. yeast activity. The loss of shelf life is accelerated by delays between mixing and freezing, which allow yeast cells the chance to ferment carbohydrates.This work examined the reasons for insufficient gas production after thawing frozen dough and the effect of pre-freezing fermentation on shelf life. Literature data on yeast metabolite dynamics in fermenting dough were incomplete. In particular there were few data on the accumulation of ethanol, a major fermentation end product which can be injurious to yeast.Doughs were prepared in a domestic breadmaker using compressed yeast from a local manufacturer and analysed for glucose, fructose, sucrose, maltose and ethanol. Gas production after thawing declined within 48 hours of frozen storage. This was accelerated by 30 or 90 minutes of fermentation at 30;C prior to freezing.Sucrose was rapidly hydrolysed and yeast consumed glucose in preference to fructose. Maltose was not consumed while other sugars remained. Ethanol, accumulated from consumption of glucose and fructose, was produced in approximately equal amounts to CO2, indicating that yeast cells metabolised reductively.Glucose uptake in fermenting dough followed simple hyperbolic kinetics and fructose uptake was competitively inhibited by glucose. Mathematical modelling indicated that diffusion of sugars and ethanol in dough occurred quickly enough to eliminate solute gradients brought about by yeast metabolism
Sorafenib inhibits imatinib-resistant KIT and platelet-derived growth factor receptor beta gatekeeper mutants.
No full textPurpose: Targeting of KIT and platelet-derived growth factor receptor (PDGFR) tyrosine kinases by imatinib is an effective anticancer strategy. However, mutations of the gatekeeper residue (T670 in KIT and T681 in PDGFRh) render the two kinases resistant to imatinib. The aim of this study was to evaluate whether sorafenib (BAY 43-9006), a multitargeted ATP-competitive inhibitor of KIT and PDGFR, was active against imatinib-resistant KIT and PDGFRh kinases. Experimental Design: We used in vitro kinase assays and immunoblot with phosphospecific antibodies to determine the activity of sorafenib on KIT and PDGFRh kinases. We also exploited reporter luciferase assays to measure the effects of sorafenib on KIT and DGFRh downstream signaling events. The activity of sorafenib on interleukin-3 ^ independent proliferation of Ba/F3 cells expressing oncogenic KIT or its imatinib-resistant T670I mutant was also tested.
Results: Sorafenib efficiently inhibited gatekeeper mutants of KIT and PDGFRh (IC50 for KIT T670I, 60 nmol/L ; IC50 for PDGFRh T681I, 110 nmol/L). Instead, it was less active against activation loop mutants of the two receptors (IC50 for KIT D816V, 3.8 Amol/L ; IC50 for PDGFRh D850V, 1.17 Amol/L) that are also imatinib-resistant. Sorafenib blocked receptor autophosphorylation and signaling of KIT and PDGFRh gatekeeper mutants in intact cells as well as activation of AP1-responsive and cyclin D1 gene promoters, respectively. Finally, the compound inhibited KIT-dependent proliferation of Ba/F3 cells expressing the oncogenic KIT mutant carrying the T670I mutation.
Conclusions: Sorafenib might be a promising anticancer agent for patients carrying KIT and PDGFRh gatekeeper mutations
Converting SrI <sub>2</sub> :Eu <sup>2+</sup> into a near infrared scintillator by Sm <sup>2+</sup> co-doping
No full text The luminescence and scintillation properties of SrI 2 single crystals doped with 5% Eu 2+ and 0.05%, 0.2% and 0.5% Sm 2+ are evaluated. X-ray excited and photoluminescence measurements show energy transfer from excited Eu 2+ ions to Sm 2+ ions. At a concentration of 0.5% Sm 2+ , the luminescence consists almost entirely of 740 nm emission from Sm 2+ 5d-4f transitions. Co-doping SrI 2 :5% Eu 2+ with Sm 2+ provides a novel method to bypass the self-absorption problem encountered in large SrI 2 :Eu 2+ crystals and, at the same time, provides a unique near-infrared emitting scintillator with a light yield of approximately 40,000 photons/MeV. Accepted Author ManuscriptRST/Fundamental Aspects of Materials and EnergyRST/Luminescence Material
'Laws 'Needefull in Later to be Abrogated': Intersex and the Sources of Christian Theology
No full textThis is the author accepted manuscript. The final version is available from Palgrave Macmillan via the DOI in this record
Introduction: Troubling Bodies?
No full textThis is the author accepted manuscript. The final version is available from Palgrave Macmillan via the DOI in this record
BAY 43-9006 inhibition of oncogenic RET mutants.
No full textWe examined BAY 43-9006 activity against oncogenic RET in vitro and in cellular RET signaling in oncogenic RET-transfected NIH3T3 fibroblasts by using immunocomplex kinase assays and immunoblotting with phospho-specific antibodies. The effects of BAY 43-9006 on proliferation of human TPC1 and TT thyroid carcinoma cells, which harbor spontaneous oncogenic RET alleles, and on RAT1 fibroblasts transformed with oncogenic RET mutants, including mutants that are resistant to other chemotherapeutic agents, were determined using growth curves and flow cytometry. Growth of TT cell-derived xenograft tumors in athymic mice treated orally with BAY 43-9006 or with vehicle was measured. All statistical tests were two-sided. BAY 43-9006 inhibited oncogenic RET kinase activity at half-maximal inhibitory concentrations (IC50s) of 50 nM or less in NIH3T3 cells. It also arrested the growth of NIH3T3 and RAT1 fibroblasts transformed by oncogenic RET and of thyroid carcinoma cells that harbor spontaneous oncogenic RET alleles. Moreover, BAY 43-9006 inhibited the growth of cells carrying RET V804L (IC50 = 110 nM, 95% confidence interval [CI] = 88 to 133 nM) or RET V804M (IC50 = 147 nM, 95% CI = 123 nM to 170 nM), both mutants that are resistant to anilinoquinazolines and pyrazolopyrimidines. After 3 weeks of oral treatment with BAY 43-9006 (60 mg/kg/day), the volume of TT cell xenografts (n = 7) was reduced from 72.5 to 44 mm3 (difference = 28.5 mm3, 95% CI = 7 mm3 to 50 mm3), whereas in vehicle-treated mice (n = 7), mean tumor volume increased to 408 mm3 (difference = 320 mm3, 95% CI = 180 mm3 to 460 mm3; untreated versus treated, P =.02). This inhibition paralleled a decrease in RET phosphorylation. BAY 43-9006 is a powerful inhibitor of the RET kinase. Its potential as a therapeutic tool for RET-positive thyroid tumors, including those expressing V804 mutations merits study
Intrafullerene electron transfers in Sm-containing metallofullerenes: Sm@C-2n (74 <= 2n <= 84)
No full textThe electronic properties of Sm-containing metallofullerenes, Sm@C-74, Sm@C-76 (I, II), Sm@C-78, Sm@C-80, Sm@C-82 (I, II, III) and Sm@C-84 (I, II, III), are characterized by UV-Vis-NIR absorption spectroscopy and electron energy-loss spectroscopy (EELS). the UV-Vis-NIR absorption spectra of Sm@C-74, Sm@C-80, Sm@C-82 (I, II, III) and Sm@C-84 (I, II) are quite similar to those of the corresponding Ca, Sr, Ba, Eu, Tm, Yb-based metallofullerenes. In contrast, the absorption spectra of Sm@C-76 (I, II), Sm@C-78 and Sm@C-84(III) show a novel feature: the onset for Sm@C-78 is observed similar to 2600 nm, which corresponds to a small band gap (similar to0.5 eV). Furthermore, the oxidation states of Sm atom in the various fullerene cages are investigated by EELS, which reveals that the Sm atom takes +2 oxidation state in the fullerene cages. A probable rationale for the tendency to have the Sm2+ state is presented based on a simple thermochemical cycle model. (C) 2001 by Elsevier Science Inc.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000168906500014&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Biochemical Research MethodsBiochemistry & Molecular BiologyComputer Science, Interdisciplinary ApplicationsCrystallographyMathematical & Computational BiologySCI(E)EI30ARTICLE2244-2511
beta-decay spectroscopy of neutron-rich Sm-160,Sm-161,Sm-162 isotopes
No full textNeutron-rich Sm-160,Sm-161,Sm-162 isotopes have been populated at the RIBF, RIKEN via beta decay for the first time. beta-coincident gamma rays were observed in all three isotopes including gamma rays from the isomeric decay of Sm-160 and Sm-162. The isomers in Sm-160 and Sm-162 have previously been observed but have been populated via beta decay for the first time. The isomeric state in Sm-162 is assigned a 4(-) nu 7/2(+)[633]circle times nu 1/2(-)[521] configuration based on the decay pattern. The level schemes of Sm-160 and Sm-162 are presented. The ground states in the parent nuclei Pm-160 and Pm-162 are both assigned a 6(-) nu 7/2(+)[633]circle times pi 5/2(-)[532] configuration based on the population of states in the daughter nuclei. Blocked BCS calculations were performed to further investigate the spin-parities of the ground states in Pm-160, Pm-161, and Pm-162, and the isomeric state in Sm-162.CPCI-S(ISTP)[email protected]
Evidence That Skeletal Muscles Modulate HDL-Cholesterol in Metabolic Healthy Young Adults
No full text: The aim of this study was to investigate whether skeletal muscle (SM) mass correlates with plasma lipids in metabolic healthy young adults. The study was designed as a retrospective observational monocentric study. Data on plasma lipids and SM mass of subjects attending our institution from 1999 to 2014 were analyzed. Inclusion criteria were being 18-45 years old and in apparently good health. SM mass was evaluated by bioelectrical impedance analysis (BIA) using the equation proposed by Janssen and normalized to height as skeletal muscle index (SMI: SM mass/height2). The association between SMI and plasma lipids levels was examined using a crude and adjusted linear regression model including age, sex, BMI and waist circumference as additional covariates. The study population consisted of 450 subjects (273 females) without metabolic syndrome (12.2% with normal body weight, 33.1% overweight, and 54.7% with obesity). SMI, total-cholesterol, LDL-cholesterol, and Triglycerides were higher, whereas HDL-cholesterol was lower in overweight and obese patients as compared with normal weight subjects. SMI was inversely associated with HDL-cholesterol in female patients with obesity but not in male patients with obesity, in normal- or over-weight subjects (p < 0.05). These results suggest that changes in SM mass occurring in obesity could have a role in worsening lipid profile with special reference to HDL-cholesterol
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