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This study examines the spatiotemporal characteristics of diurnal precipitation over Luzon and the nearby oceans in boreal spring. The study focuses on exploring the impact of the interaction between large- and local-scale circulation changes on the modulation of diurnal precipitation. We analyze the satellite precipitation data obtained from the Tropical Rainfall Measuring Mission and Global Precipitation Measurement Mission during the spring (March-May) of 2001-2019. The results show that the spring diurnal precipitation over Luzon and the nearby oceans consists of a clear eastward propagation signal. The direction of this propagation is opposite to that of the prevailing low-level easterly wind in spring and differs from the well-known westward propagation direction of diurnal precipitation over Luzon in summer. Diagnoses of the possible maintenance mechanisms suggest that the eastward propagation diurnal precipitation can be attributed to the interaction between the topography and multiple-scale circulation changes, including the mountain-valley breeze, island-scale land-sea breeze (LSB), large-scale LSB-like circulation, and mid-to-upper-level prevailing wind fields. This finding highlights the importance of considering multiple-scale circulation changes in the modulation of spring diurnal precipitation over the East Asia-western North Pacific region.

This study examines the interannual variation of the Convective Afternoon Rainfall (CAR) activity (including frequency and intensity) in Taiwan during the summers (JJA) of 1961-2012 with a focus on identifying its relationship with the changes in sea surface temperature anomalies over the Niño3.4 region [SSTA(Niño3.4)] and the underlying physical mechanisms. Our analyses show that during the colder (warmer) phase of SSTA(Niño3.4), the subtropical high system over the region east of Taiwan is enhanced (weakened), the local surface wind convergence is enhanced (weakened), and the local thermal instability is enhanced (weakened), which facilitates (suppresses) the formation of CAR in Taiwan. This consistent negative relationship between the interannual variation of CAR frequency in Taiwan and SSTA(Niño3.4) occurs throughout 1961-2012. In contrast, the relationship between the interannual variation of CAR intensity in Taiwan and SSTA(Niño3.4) changed from positively correlated to negatively correlated in the late 1980s. This change is attributed to the change in the moisture supply for maintaining the CAR intensity in Taiwan from an increase (decrease) in the warmer (colder) phase of SSTA(Niño3.4) before the mid-1980s to the opposite after the late 1980s. These findings highlight how the rainfall characteristics in East Asia may change in response to changes in SSTA(Niño3.4).

Although we have shown that avian reovirus (ARV) p17-mediated inhibition of Akt leads to induction of autophagy, the precise mechanisms remain largely unknown. This study has identified a specific mechanism by which ARV coordinately regulates the degradation of ribosomal proteins by p17-mediated activation of E3 ligase MDM2 that targets ribosomal proteins and by σA-mediated upregulation of proteasome PSMB6. In addition to downregulating ribosomal proteins, p17 reduces mTORC2 assembly and disrupts mTORC2-robosome association, both of which inactivate mTORC2 leading to inhibition of Akt phosphorylation at S473. Furthermore, we discovered that p17 binds to and inhibits the CDK2/cyclin A2 complex, further inhibiting phosphorylation of Akt S473. The negative effect of p17 on mTORC2 assembly and Akt phosphorylation at S473 is reversed in cells treated with insulin or overexpression of CDK2. The carboxyl terminus of p17 is necessary for interaction with CDK2 and for induction of autophagy. Furthermore, p17-mediated upregulation of LC3-II could be partially reversed by overexpression of CDK2. The present study provides mechanistic insights into cooperation between p17 and σA proteins of ARV to negatively regulate Akt by downregulating complexes of mTORC2 and CDK2/cyclin A2 and upregulating PSMB6, which together induces autophagy and cell cycle arrest and benefits virus replication.

The accumulation of myeloid-derived suppressor cells (MDSCs) has been observed in solid tumors and is correlated with tumor progression; however, the underlying mechanism is still poorly understood. In this study, we identified a mechanism by which tumor cells induce MDSC accumulation and expansion in the bladder cancer (BC) microenvironment via CXCL2/MIF-CXCR2 signaling. Elevated expression of CXCL2 and MIF and an increased number of CD33 + MDSCs were detected in BC tissues, and these increases were significantly associated with advanced disease stage and poor patient prognosis (P<0.01). A positive association was observed between CXCL2 or MIF expression and the number of tumor-infiltrating CD33 + MDSCs (P<0.01). Subsequently, we demonstrated that CD45 + CD33 + CD11b + HLA-DR - MDSCs from fresh BC tissues displayed high levels of suppressive molecules, including Arg1, iNOS, ROS, PDL-1 and P-STAT3, and stronger suppression of T-cell proliferation. Interestingly, these CD45 + CD33 + CD11b + HLA-DR - MDSCs exhibited increased CXCR2 expression compared with that in peripheral blood from BC patients or healthy controls (P<0.05). Chemotaxis assay revealed that bladder cancer cell line J82 induced MDSC migration via CXCL2/MIF-CXCR2 signaling in vitro. Mechanistic studies demonstrated that J82-induced MDSC trafficking and CXCR2 expression were associated with increased phosphorylation of p38, ERK and p65. Conversely, inhibition of the phosphorylation of p38, ERK or p65 decreased J82-induced MDSC trafficking and CXCR2 expression. CXCL2/MIF-stimulated activation of the mitogen-activated protein kinase and nuclear factor kappa B pathways in MDSCs was MyD88 dependent. Overall, our results identify the CXCL2/MIF-CXCR2 axis as an important mediator in MDSC recruitment and as predictors and potential therapeutic targets in BC patients.

Emerging data demonstrate promising results of related haploidentical allogeneic hematopoietic stem cell transplantation (haplo-HCT) for the treatment of hematologic malignancies. Data about G-CSF primed PBSC as reliable source of graft with myeloablative conditioning are lacking. We updated the outcomes in 130 adult patients with high-risk hematologic malignancies who received haplo-PBSC transplantation consecutively under busulfan-based conditioning. PBSC were freshly isolated and infused without ex vivo T-cell depletion into the recipients. Myeloid recovery was achieved in 99.2% patients with full donor chimerism. The cumulative incidence of acute grade 3-4 GvHD, overall and extensive chronic GvHD was 14.9%, 38.6% and 16.5%, respectively. The 3-year non-relapse mortality rate was 24.1%. Non-remission prior to transplant was associated with higher incidence of relapse (P=0.006), inferior overall survival (P=0.017) and leukemia-free survival (P=0.024). These data suggest that PBSC is a reliable graft source in haploidentical, unmanipulated transplant settings under myeloablative conditioning in patients with high-risk hematologic malignancies.

Femtosecond electron bunches with keV energies and eV energy spread are needed by condensed matter physicists to resolve state transitions in carbon nanotubes, molecular structures, organic salts, and charge density wave materials. These semirelativistic electron sources are not only of interest for ultrafast electron diffraction, but also for electron energy-loss spectroscopy and as a seed for x-ray FELs. Thus far, the output energy spread (hence pulse duration) of ultrafast electron guns has been limited by the achievable electric field at the surface of the emitter, which is 10 MV/m for DC guns and 200 MV/m for RF guns. A single-cycle THz electron gun provides a unique opportunity to not only achieve GV/m surface electric fields but also with relatively low THz pulse energies, since a single-cycle transform-limited waveform is the most efficient way to achieve intense electric fields. Here, electron bunches of 50 fC from a flat copper photocathode are accelerated from rest to tens of eV by a microjoule THz pulse with peak electric field of 72 MV/m at 1 kHz repetition rate. We show that scaling to the readily-available GV/m THz field regime would translate to monoenergetic electron beams of ~100 keV.

Assembly of nanowires into ordered macroscopic structures with new functionalities has been a recent focus. In this Letter, we report a new route for ordering hydrophilic Ag nanowires with high aspect ratio by flowing through a glass capillary. The present glass capillary with well-defined silver nanowire films inside can serve as a portable and reusable substrate for surface-enhanced Raman spectroscopy (SERS), which may provide a versatile and promising platform for detecting mixture pollutions. By controlling the flow parameters of nanowire suspensions, initially random Ag nanowires can be aligned to form nanowire arrays with tunable density, forming cambered nanowire films adhered onto the inner wall of the capillary. Compared with the planar ordered Ag nanowire films by the Langmuir-Blodgett (LB) technique, the cambered nanowire films show better SERS performance.

The signaling mechanisms responsible for BCR/ABL-induced regulation of Mcl-1 expression in chronic myelogenous leukemia (CML) cells remain unclear. In this study, we show that BCR/ABL could upregulate sphingosine kinase-1 (SPK1) expression via multiple signal pathways, including mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K) and Janus kinase 2 (JAK2), leading to increase cellular SPK1 activity in CML cells. Retrovirus-mediated overexpression of bcr-abl gene in NIH-3T3, Ba/F3 and HL-60 cells results in upregulation and increased cellular activity of SPK1, whereas treatment of CML cells with specific inhibitors of the BCR/ABL, PI3K, MAPK and JAK2 pathways decreases BCR/ABL-induced SPK1 expression and cellular activity. BCR/ABL also induces upregulation of Mcl-1 expression in CML cells. Inhibition of SPK1 by adenovirus-mediated transfer of small interfering RNA or N,N-dimethylsphingosine reduced expression of Mcl-1 in CML cells. Our data indicated that BCR/ABL induces SPK1 expression and increases its cellular activity, leading to upregulation of Mcl-1 in CML cells. SPK1 silencing enhances the STI571-induced apoptosis of CML cell lines. It is suggested that SPK1 may be a potential therapeutic target in CML.