No abstract

To improve the selectivity and yield of multiphase reactions, an attempt to intensify gas–liquid mass-transfer operations was undertaken in which screen/grid static mixers were used to promote interphase mass transfer. A modified technique was used to enhance the reproducibility of the results and to account for the depletion effect which becomes critical at high mass-transfer rates. The volumetric mass transfer coefficient, k L a, was found to increase with increasing liquid superficial velocity and gas volume fraction and reached values as high as 4.08 s–1 at low specific energy consumption rates, particularly for slowly coalescent systems, a situation that is encountered in most industrially relevant systems. The gas–liquid reactor/contactor presently investigated takes advantage of the coalescence retardation characteristics of most industrially relevant streams to achieve k L a values that surpassed those of most conventional reactor/contactors by more than an order of magnitude while maintaining a high energy utilization efficiency (up to 0.63 kg O2/kWh). The ability to reach 98% equilibrium within residence times of less than 800 ms, achieved without significantly increasing the power consumption rates, allows for the use of static mixing reactor volumes that are several orders of magnitude smaller than conventional units such as mechanically agitated tanks and bubble columns.

The constitutive activation of Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) signal transduction is well elucidated in STAT3-mediated oncogenesis related to thyroid cancer and is considered to be a plausible therapeutic target. Hence, we investigated whether curcumin, a natural compound, can target the JAK/STAT3 signaling pathway to induce cytotoxic effects in papillary thyroid cancer (PTC) cell lines (BCPAP and TPC-1) and derived thyroid cancer stem-like cells (thyrospheres). Curcumin suppressed PTC cell survival in a dose-dependent manner via the induction of caspase-mediated apoptosis and caused the attenuation of constitutively active STAT3 (the dephosphorylation of Tyr705–STAT3) without affecting STAT3. Gene silencing with STAT3-specific siRNA showed the modulation of genes associated with cell growth and proliferation. The cotreatment of PTC cell lines with curcumin and cisplatin synergistically potentiated cytotoxic effects via the suppression of JAK/STAT3 activity along with the inhibition of antiapoptotic genes and the induction of proapoptotic genes, and it also suppressed the migration of PTC cells by downregulating matrix metalloproteinases and the inhibition of colony formation. Finally, thyrospheres treated with curcumin and cisplatin showed suppressed STAT3 phosphorylation, a reduced formation of thyrospheres, and the downregulated expression of stemness markers, in addition to apoptosis. The current study’s findings suggest that curcumin synergistically enhances the anticancer activity of cisplatin in PTC cells as well as in cancer stem-like cells by targeting STAT3, which suggests that curcumin combined with chemotherapeutic agents may provide better therapeutic outcomes.

No abstract

Rab2 requires glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and atypical protein kinase C (aPKC) for retrograde vesicle formation from vesicular tubular clusters that sort secretory cargo from recycling proteins returned to the endoplasmic reticulum. However, the precise role of GAPDH and aPKC in the early secretory pathway is unclear. GAPDH was the first glycolytic enzyme reported to co-purify with microtubules (MTs). Similarly, aPKC associates directly with MTs. To learn whether Rab2 also binds directly to MTs, a MT binding assay was performed. Purified Rab2 was found in a MT-enriched pellet only when both GAPDH and aPKC were present, and Rab2-MT binding could be prevented by a recombinant fragment made to the Rab2 amino terminus (residues 2-70), which directly interacts with GAPDH and aPKC. Because GAPDH binds to the carboxyl terminus of ␣-tubulin, we characterized the distribution of tyrosinated/detyrosinated ␣-tubulin that is recruited by Rab2 in a quantitative membrane binding assay. Rab2-treated membranes contained predominantly tyrosinated ␣-tubulin; however, aPKC was the limiting and essential factor. Tyrosination/detyrosination influences MT motor protein binding; therefore, we determined whether Rab2 stimulated kinesin or dynein membrane binding. Although kinesin was not detected on membranes incubated with Rab2, dynein was recruited in a dose-dependent manner, and binding was aPKCdependent. These combined results suggest a mechanism by which Rab2 controls MT and motor recruitment to vesicular tubular clusters.

This article is a comprehensive review of the literature dealing with the transfer of carbon dioxide to water where no chemical reactions are taking place. It reviews the studies related to the absorption and desorption kinetics, mass-transfer rates, effect of the contactor geometry, effect of water salinity, and the effects of temperature and pressure on the process in conventional reactors or the more recently common membrane contactors. The available data show inconsistent trends and an abundance of system-and geometry-specific correlations/models to predict the mass-transfer performance, which may explain the inefficient design of most industrially available contactors. Furthermore, no agreement can be found in the literature on the effect of temperature and pressure of the system, as well as the presence of additives in the water, on the solubility of CO 2 .

No abstract

The Transient Receptor Potential Vanilloid type-2 (TRPV2) channel exhibits oncogenicity in different types of cancers. TRPV2 is implicated in signaling pathways that mediate cell survival, proliferation, and metastasis. In leukemia and bladder cancer, the oncogenic activity of TRPV2 was linked to alteration of its expression profile. In multiple myeloma patients, TRPV2 overexpression correlated with bone tissue damage and poor prognosis. In prostate cancer, TRPV2 overexpression was associated with the castration-resistant phenotype and metastasis. Loss or inactivation of TRPV2 promoted glioblastoma cell proliferation and increased resistance to CD95-induced apoptotic cell death. TRPV2 overexpression was associated with high relapse-free survival in triple-negative breast cancer, whereas the opposite was found in patients with esophageal squamous cell carcinoma or gastric cancer. Another link was found between TRPV2 expression and either drug-induced cytotoxicity or stemness of liver cancer. Overall, these findings validate TRPV2 as a prime candidate for cancer biomarker and future therapeutic target.