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A new surfactant, Pluronic F127 (P123), is studied as a component of the poloxamer micellar systems. A common finding in the solubilizing behavior of Pluronics is the existence of three regimes: in solution with low concentrations of the surfactant, P123, the micelles are known to be rodlike (rodlike micelles, LMs). At higher concentrations, a second size distribution of micelle forms is present in addition to rodlike micelles: wormlike micelles (WMs) have been extensively studied by differential scanning calorimetry (DSC), rheology, and X-ray diffraction (XRD). In this work, the behavior of wormlike micelles (WMs) in the solutions of P123 in water-alcohol systems is investigated. A rich set of phenomena associated with the transfer of surfactant from the organic phase into an aqueous phase at different hydrophobic fractions, compositions, temperatures, and aqueous dielectric constants is observed. The conventional Langmuir isotherm for the composition spread in the mixture of P123 and alcohol is replaced by a two-stage modified Langmuir isotherm that is dependent on the dielectric constant of the aqueous phase. The DSC, rheology, and XRD studies confirm that micelles and “alcoholysis” can take place in water-alcohol solutions of P123. The proposed mechanism shows that in WMs, the alcohol can penetrate into the inner core of micelles and block some, but not all, water channels. In contrast to the traditional assumption that all water channels are formed by PPO blocks, the current model includes only PPB blocks (for PPO), but not blocks of PPO.(ABSTRACT TRUNCATED AT 250 WORDS)Screenshot: Kontiki
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Methotrexate (MTX) is an antineoplastic agent that exerts its cytotoxic action by inhibiting thymidylate synthase (TS), which is an essential enzyme of the de novo thymidylate (dTMP) biosynthetic pathway. In addition to cytotoxicity, MTX inhibits cell proliferation by inducing autophagy. Here, we examined whether MTX-induced autophagy is a response to TS inhibition in human acute myelogenous leukemia (AML) cells. MTX treatment induced degradation of TS, resulting in depletion of dTMP and autophagy induction in HL-60 and NB4 cells. In a TS-overexpressing NB4 cell line, MTX-induced autophagy was enhanced. MTX-induced autophagy was suppressed by the TS inhibitor UMP, but not by other nucleotide analogues with activity against TS. Furthermore, depletion of TS protein induced autophagy in HL-60 cells, whereas overexpression of TS blocked MTX-induced autophagy. In contrast, MTX did not induce autophagy in TS-deficient TK6 cells. Interestingly, Bcl-2 overexpression blocked MTX-induced autophagy. We also examined the effect of MTX on autophagy in mice bearing HL-60 xenografts. Systemic MTX treatment inhibited tumor growth in vivo in a TS-dependent manner. Thus, our findings suggest that MTX-induced autophagy in AML cells is a response to TS inhibition. The molecular basis for this phenomenon is thymidylate depletion, which leads to inhibition of Pol γ-dependent DNA synthesis and subsequently to impairment of repair of damaged DNA.Kaepernick in FSU: The saga that makes sense
William Wooldridge | The Daily Times
Show Caption Hide Caption Tim Tebow is going back to college, but it will not be at Florida. We explain