Oxidation of methyl linoleate in O/W emulsions having droplets of median diameters ranging from 17 nm to 8.0 lm was carried out at 40°C. The oxidation process was analyzed on the basis of a kinetic equation of the autocatalytic type. The induction period was found to be shorter and the oxidation rate constant lower for emulsions with smaller oil droplets. The stoichiometry between methyl linoleate and oxygen was observed to be independent of both the size of oil droplet and the type of the surfactant and was found to be unity during the early stage of the oxidation. However, more oxgen was consumed in the oxidation of the methyl linoleate in the later half of the oxidation process.

Endocytosis is an important route for the intracellular delivery of biomacromolecules, wherein their inefficient endosomal escape into the cytosol remains a major barrier. Based on the understanding that endosomal membranes are negatively charged, we focused on the potential of cationic lytic peptides for developing endosomolysis agents to release such entrapped molecules. As such, a venom peptide, Mastoparan X, was employed and redesigned to serve as a delivery tool. Appending a tri-glutamate unit to the N-terminus attenuates the cytotoxicity of Mastoparan X by about 40 fold, while introduction of a Ni -dipicolylamine complex enhances cellular uptake of the peptide by about 17 fold. Using the optimized peptide, various fluorescently labeled macromolecules were successfully delivered to the cytosol, enabling live-cell imaging of acetylated histones.

Labile heme (LH) is a complex of Fe­(II) and protoporphyrin IX, an essential signaling molecule in various biological systems. Most of the subcellular dynamics of LH remain unclear because of the lack of efficient chemical tools for detecting LH in cells. Here, we report an activity-based fluorescence probe that can monitor the fluctuations of LH in biological events. H-FluNox is a selective fluorescent probe that senses LH using biomimetic N-oxide deoxygenation to trigger fluorescence. The selectivity of H-FluNox to LH is >100-fold against Fe­(II), enabling the discrimination of LH from the labile Fe­(II) pool in living cells. The probe can detect the acute release of LH upon NO stimulation and the accumulation of LH by inhibiting the heme exporter. In addition, imaging studies using the probe revealed a partial heme-export activity of the ATP-binding cassette subfamily G member 2 (ABCG2), potential LH pooling ability of G-quadruplex, and involvement of LH in ferroptosis. The successful use of H-FluNox in identifying fluctuations of LH in living cells offers opportunities for studying the physiology and pathophysiology of LH in living systems.

Nasal natural killer (NK)-cell lymphoma was resistant to various antitumor agents. Although high expression of p-glycoprotein has been reported, other molecular mechanism of the chemo-resistance is largely unknown. Activation of STAT3 and expression of major apoptosis-related proteins Bcl-2, Bcl-x, and Mcl-1 were analyzed by immunohistochemistry. Effects of STAT3 inhibitor AG490 on NK-YS cell line were analyzed by Western blotting and flow cytometric apoptosis assay. STAT3 was activated in six of the nine nasal NK-cell lymphomas (67%). In contrast, STAT3 activation was detected in 35% of diffuse large B-cell lymphoma (DLBCL) and in 10% of follicular lymphoma (FL). Frequent activation of STAT3 was significantly correlated with Mcl-1 expression in nasal NK-cell lymphoma, i.e., Mcl-1 was positive in five of six STAT3-active cases and negative in all three STAT3-inactive ones. In DLBCL, not only six out of seven STAT3-active cases (86%) but also eight out of thirteen STAT3-inactive cases (62%) were positive for Mcl-1 expression. Latent membrane protein-1 was positive in four nasal NK-cell lymphomas, among which three cases showed intermediate STAT3 activation. Inhibition of STAT3 activation by JAK inhibitor AG490 decreased Mcl-1 expression and induced apoptosis in STAT3-active NK-YS cells. Serum starvation rather increased the Mcl-1 level in NK-YS cells, and this effect was also canceled by AG490. These results suggest that activation of STAT3-Mcl-1 axis may play a role in the chemotherapy resistance of nasal NK-cell lymphoma. The pathway may be one of the future therapeutic targets of this intractable disease.

Objectives:  Nasal natural killer (NK)/T‐cell lymphoma is characterized by chemo‐resistance, angiodestruction, and aggressive tumor progression. Few studies exist on molecular characteristics of this disease entity. Methods:  Expression levels of major apoptosis‐related proteins Bcl‐2, Bcl‐x, Mcl‐1, Bax, and a proliferative marker Ki‐67 were analyzed in 11 nasal NK/T‐cell lymphoma cases by immunohistochemical methods. Nine cases were of NK‐cell lineage and two cases were of T‐cell lineage. For comparison, 12 follicular lymphoma (FL) cases and 16 diffuse large B‐cell lymphoma (DLBCL) cases were also studied. Results and conclusions:  Bax expression was low in all nasal NK‐cell lymphoma cases, which constitute the major population of nasal NK/T‐cell lymphoma. Bax expression in nasal NK‐cell lymphoma was similar to FL and significantly lower compared with DLBCL. Bcl‐2 expression was significantly lower in nasal NK/T‐cell lymphoma compared with that of FL and DLBCL. Bcl‐x expression was high in all three lymphomas. Two distinct Mcl‐1 expression groups existed for nasal NK/T‐cell lymphoma (6.2 ± 5.2% and 59.1 ± 12.3%, 95% CI). Ki‐67 expression was high in nasal NK/T‐cell lymphoma, and worse prognostic groups tended to express higher levels of Ki‐67. The results suggest a combination of impaired apoptosis and aggressive proliferation in nasal NK/T‐cell lymphoma, and may provide explanations for its poor prognosis.

IL-8 may facilitate the migration of gingival junctional epithelium by enhancing DNA synthesis, migration and preventing apoptosis of gingival epithelial cells.

No abstract

We have already found several catalytic systems for the polymerizations of four-and five-membered cyclic ethers, which consist of organoaluminum compound and some additives such as water, a-chlorodimethyl ether, acetyl chloride, epichlorohydrin and propylene oxidel. 2). The characters of these catalyst systems have been shown to be of cationic polymerization2).In this paper, we report our findings that the AIE~H,O-cocatalyst systems induce also the polymerization of vinyl ether and produce the crystalline polymer of isobutyl vinyl ether (IBVE) under some conditions. Table 1 shows the polymerization of IBVE by AI (C,H,),-H,O-u-chlorodimethyl ether (CH,OCH&l) system. Table 1. Polymerization of isobutyl vinyl ether by AlEt,-H,O-CH,OCH,Cl system (Monomer, 0.025 mole; AlEt,, 5 mole-% for monomer; CH,OCH,CI, 0.5 mole-yo for monomer; CH,CI,, (solvent) 20 ml.; polymerization a t -78°C. for 24 hrs.)