We report on the surface behavior of the asymmetric heteroarm poly(ethylene oxide) (PEO)/polystyrene (PS) star polymer on the air−water interface on a solid substrate. These amphiphilic star polymers with different numbers of hydrophobic arms and a similar hydrophilic block differ by architecture (four and three arm molecules, PEO-b-PS3 and PEO-b-PS2), the length of PS chains (molecular weight from about 10 000 up to 24 000), and the number of PS arms (three and two). Detailed analysis revealed that well-developed circular domain surface morphology was formed at the air−water interface. Similar to linear diblock PEO−PS copolymers, the asymmetric heteroarm star polymers at low surface pressure formed circular nanoscale aggregates composed of PS arms. At higher surface pressure, the packing of circular domains became denser, but no clear transition to cylindrical structures was observed in condensed monolayers, contrary to linear block copolymers of similar composition. Therefore, we suggest that for star architecture the formation of highly curved interfaces is heavily favored, domain structure. This surface morphology remained stable even at very high compression close to the monolayer collapse unlike linear diblock copolymers with their tendency for structural reorganization even at very modest compressions.

Liquid-phase adsorption of benzothiophene over isotypic MOFs such as MIL-47 and MIL-53(Al, Cr) has shown that a metal ion of a MOF-type material has a dominant role in adsorptive desulfurization and MIL-47 has a remarkable performance.

Background: Runt-related transcription factor 2 (Runx2) is a key factor in bone development. Hypoxia-inducible factor-1␣ (HIF-1␣) is the primary regulator of blood vessel formation. Results: Runx2 bound and activated HIF-1␣ by competing with von Hippel-Lindau protein (pVHL), protecting HIF-1␣ from degradation. Conclusion: Runx2 stabilizes HIF-1␣ during endochondral bone formation. Significance: Runx2/HIF-1␣ stimulate the invasion of blood vessels in hypertrophic zones.

LncRNA snaR was found to be up-regulated in breast cancer cells, and the cancer progression of MDA-MB-231 cells was significantly suppressed by down-regulation of snaR. Therefore, snaR knockdown has potential as a treatment modality for triple-negative breast cancer.

No abstract