The transesterification of sunflower seed oil was carried out in supercritical ethanol without using any catalyst.
Ethyl esters of vegetable oils have several outstanding advantages because ethanol is derived from agricultural
products and is renewable and biologically less objectionable in the environment. On the other hand, because
of lower volatility, ignition delay and combustion problems could occur when ethyl esters are used. In the
present work, ethanol is added to enhance the vapor pressure of biodiesel. The bubble-point pressures of
mixtures of biodiesel and ethanol as a function of temperature were measured by comparative ebulliometry
with inclined ebulliometers. Experimental data of vapor pressures and equilibrium temperatures were correlated
by the Antoine equation. The bubble-point lines of pressure versus the composition at different temperatures
and the temperature versus the composition at different pressures were obtained. It is found that the mixtures
of biodiesel and ethanol have visible positive deviations from Raoult's law. The addition of ethanol has a
critical effect on the vapor pressure of fuels.
The current study was to examine the underlying mechanisms responsible for the role of mammalian target of rapamycin (mTOR) in regulating bone cancer-evoked pain and the tolerance of systemic morphine. Breast sarcocarcinoma Walker 256 cells were implanted into the tibia bone cavity of rats and this evoked significant mechanical and thermal hyperalgesia. Our results showed that the protein expression of p-mTOR, mTOR-mediated phosphorylation of 4E-binding protein 4 (4E-BP1), p70 ribosomal S6 protein kinase 1 (S6K1) as well as phosphatidylinositide 3-kinase (p-PI3K) pathways were amplified in the superficial dorsal horn of the spinal cord of bone cancer rats compared with control rats. Blocking spinal mTOR by using rapamycin significantly attenuated activities of PI3K signaling pathways as well as mechanical and thermal hyperalgesia. Additionally, rapamycin enhanced attenuations of protein kinase CE (PKCE)/protein kinase A (PKA) induced by morphine and further extended analgesia of morphine via m-opioid receptor (MOR). Our data for the first time revealed specific signaling pathways leading to bone cancer pain, including the activation of mTOR and PI3K and downstream PKCE/PKA, and resultant sensitization of MOR. Targeting one or more of these signaling molecules may present new opportunities for treatment and management of bone cancer pain often observed in clinics.
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