Effects of oxygen vacancies and interfacial strain on the metal-insulator transition of VO2 nanobeams.

The role of oxygen vacancies and interfacial strain on the metal-insulator transition (MIT) behavior of high-quality VO2 nanobeams (NBs) synthesized on SiO2/Si substrates employing V2O5 as a precursor has been investigated in this research. Selective oxygen vacancies have been generated by argon plasma irradiation. The MIT is progressively suppressed as the duration of plasma processing increases; in addition, the temperature of MIT (TMIT) drops by up to 95 K relative to the pristine VO2 NBs. Incorporating oxygen vacancies into VO2 may increase its electron concentration, which might shift the Fermi levels upward, strengthen the electronic orbital overlap of the V-V chains, and further stabilize the metallic phase at lower temperatures, based on first-principles calculations. Furthermore, in order to evaluate the influence of substrate-induced strain in our situation, the MIT in two distinct types of VO2 NB samples is examined without metal contacts by using the distinctive light scattering characteristics of the metal (M) and insulator (I) phases (i.e., M/I domains) by optical microscopy. It is found that the domain structures in the "clamped" NBs persisted up to ∼453 K, while the "released" NBs (transferred to a new substrate) did not exhibit any domain structures and turned into an entirely M phase with a dark contrast above ∼348 K. When combined with first-principles calculations, the electronic orbital occupancy in the rutile phase contributes to explaining the interfacial strain-induced modulation of MIT. The current findings shed light on how interfacial strain and oxygen vacancies impact MIT behavior. It also suggests several types of control strategies for MIT in VO2 NBs, which are essential for a broader spectrum of VO2 NB applications.

Dhx33 promotes B-cell growth and proliferation by controlling activation-induced rRNA upregulation.

Upon recognition of foreign antigens, naïve B cells undergo rapid activation, growth, and proliferation. How B-cell growth and proliferation are coupled with activation remains poorly understood. Combining CRISPR/Cas9-mediated functional analysis and mouse genetics approaches, we found that Dhx33, an activation-induced RNA helicase, plays a critical role in coupling B-cell activation with growth and proliferation. Mutant mice with B-cell-specific deletion of Dhx33 exhibited impaired B-cell development, germinal center reactions, plasma cell differentiation, and antibody production. Dhx33-deficient B cells appeared normal in the steady state and early stage of activation but were retarded in growth and proliferation. Mechanistically, Dhx33 played an indispensable role in activation-induced upregulation of ribosomal DNA (rDNA) transcription. In the absence of Dhx33, activated B cells were compromised in their ability to ramp up 47S ribosomal RNA (rRNA) production and ribosome biogenesis, resulting in nucleolar stress, p53 accumulation, and cellular death. Our findings demonstrate an essential role for Dhx33 in coupling B-cell activation with growth and proliferation and suggest that Dhx33 inhibition is a potential therapy for lymphoma and antibody-mediated autoimmune diseases.

The intrafollicular concentration of leptin as a potential biomarker to predict oocyte maturity in in-vitro fertilization.

Oocyte maturity is critical to the development potential of the embryo and pregnancy outcomes in natural and in-vitro fertilization (IVF). In IVF, oocyte maturity is typically evaluated using morphological criteria, although such assessment remains highly subjective. To identify reliable biomarkers of oocyte maturity, this study investigates the relationship between follicular cytokine concentrations and oocyte maturity in IVF patients with different ovarian reserves. In this prospective study, follicular fluid was collected during oocyte retrieval and the concentrations of cytokines involved in ovarian folliculogenesis were determined. Follicular fluid cytokine concentrations were compared between participants in three groups according to serum anti-Mullerian hormone (AMH) concentration, as follows: low AMH, < 2 ng/mL; normal AMH, 2-5 ng/mL; and high AMH, > 5 ng/mL. Pearson's correlation coefficient analysis showed that the number of mature oocytes correlated positively and strongly with serum AMH level (r = 0.719; p < 0.01). The leptin concentration in follicular fluid was significantly higher in women with normal AMH level than in those with low or high levels. ROC curve analysis showed that the follicular fluid levels of leptin (area under ROC curve, 0.829; 95% confidence interval, 0.659-0.998; p < 0.01) and SCF (area under ROC curve, 0.706; 95% confidence interval, 0.491-0.921; p = 0.087) were the best predictors of oocyte maturity. At an optimal cut-off value of 16 ng/mL, leptin had positive predictive value (sensitivity) up to 70% and negative predictive value (specificity) of 91% for indicating oocyte maturity. The concentration of leptin in follicular fluid is closely related to ovarian reserve and may serve as a biomarker to predict oocyte maturity.

Glycogen synthase kinase 3 drives thymocyte egress by suppressing ß-catenin activation of Akt.

Molecular pathways controlling emigration of mature thymocytes from thymus to the periphery remain incompletely understood. Here, we show that T cell­specific ablation of glycogen synthase kinase 3 (GSK3) led to severely impaired thymic egress. In the absence of GSK3, ß-catenin accumulated in the cytoplasm, where it associated with and activated Akt, leading to phosphorylation and degradation of Foxo1 and downregulation of Klf2 and S1P1 expression, thereby preventing emigration of thymocytes. A cytoplasmic membrane-localized ß-catenin excluded from the nucleus promoted Akt activation, suggesting a new function of ß-catenin independent of its role as a transcriptional activator. Furthermore, genetic ablation of ß-catenin, retroviral expression of a dominant negative Akt mutant, and transgenic expression of a constitutively active Foxo1 restored emigration of GSK3-deficient thymocytes. Our findings establish an essential role for GSK3 in thymocyte egress and reveal a previously unidentified signaling function of ß-catenin in the cytoplasm.