Highly Stable Copolyimides for Second-Order Nonlinear Optics

Nonlinear optical (NLO) copolyimides exhibiting high glass transition temperatures (Tg) and high thermal stabilities were synthesized to achieve long-term stability of optical nonlinearity at elevated temperatures. The relationship between the chromophore loading level and the physical properties of the copolymers was studied. It was found that decreasing the chromophore loading level increased the glass transition temperature more than 40 °C. As a result, the stability of the electric field induced dipole orientation of the nonlinear optical chromophores was enhanced. The second harmonic generation (SHG) signal maintained 85% of its initial value after 700 h at 180 °C. Sizable second-order nonlinear optical coefficients and electro-optic coefficients were obtained

Model for dual roles of pUL21a in HCMV infection.

<p>pUL21a independently binds to cyclin A or the anaphase-promoting complex (APC) through the RxL or PR domain, respectively, and targets each for proteasome-dependent degradation. pUL21a-induced degradation of the APC bridge, in concordance with pUL97-induced phosphorylation of Cdh1, leads to an increase in APC substrates, which helps to create a favorable, S-phase like cellular environment for DNA synthesis. However, pUL21a-induced degradation of cyclin A allows HCMV to specifically prevent host DNA synthesis. Together, these two independent activities of pUL21a help to subvert host cells for efficient HCMV growth.</p

Activity to regulate Cyclin A is conserved in pUL21a of primate CMVs.

<p>(A) MRC-5 cells expressing tetracycline-inducible pUL21a from HCMV (Hu-UL21a), ChCMV (Ch-UL21a), or RhCMV (Rh-UL21a) were analyzed as described in 2D. Note that the HCMV pUL21a antibody recognized the slightly larger ChCMV pUL21a but not RhCMV pUL21a, likely due to the lack of cross-reactivity with this more divergent protein. (B) Cells expressing pUL21a variants from (A) were infected with either AD<i>gfp</i> or AD<i>sub</i>UL21a at an MOI of 0.1 TCID₅₀/cell with or without tetracycline. Culture supernatant was collected 6 days post infection (dpi) and titer of cell free virus was determined by TCID₅₀ assay. Dashed line indicates the limit of detection.</p

pUL21a induces proteasome-dependent degradation of cyclin A.

<p>(A) MRC-5 cells were mock infected or infected with AD<i>gfp</i> or AD<i>sub</i>UL21a. Infected cells were treated with or without MG132 or epoxomicin for 9 hours prior to collection. Cell lysates were collected at 24 hpi and analyzed by immunoblotting. (B) MRC-5 cells were infected as described in A. Cells were treated with or without MG132 at 9 hpi, and RNA was extracted at 18 hpi. Cyclin A transcripts were quantified by real-time quantitative PCR (RT-qPCR) and normalized to GAPDH. The normalized levels of cyclin A transcripts in mock infected samples were arbitrarily set to 1. <i>p</i> values were determined using the student's t test. *, <i>p</i> value <0.05; n.s. (not significant), <i>p</i> value >0.05. (C) MRC-5 cells expressing tetracycline-inducible wildtype cyclin A (<i>flag</i>Cyclin A) or D-box mutant cyclin A (<i>flag</i>Cyclin A ΔD) were created by lentiviral transduction. Cells were then infected with indicated viruses, treated with or without tetracycline, and analyzed by immunoblotting at 24 hpi. Arrow indicates FLAG-tagged cyclin A variants detected by cyclin A antibody. Protein bands of FLAG-tagged cyclin A (in anti-FLAG blot) and endogenous cyclin A (in anti-cyclin A blot) were quantitated using Image J software and normalized to AD<i>sub</i>UL21a under each condition.</p

Primers used in this study.

<p>^a Restriction sites are underlined; base pair changes to introduce mutations are underlined and in italics.</p

The pUL21a cyclin-binding domain is essential for HCMV to prevent cellular DNA synthesis.

<p>MRC-5 cells were infected with indicated viruses in the presence of viral DNA replication inhibitor phosphonoacetic acid (PAA). Cells were collected at 24 and 48 hpi, fixed, and co-stained with propidium iodide (PI) and antibody to viral protein pUL44. Cell cycle profiles were analyzed by flow cytometry. (A) The PI and pUL44 staining profiles of representative mock- and wildtype virus- infected cells at 48 hpi. Also shown is gating used to separate pUL44-positive (infected) and pUL44-negative (uninfected) cells. (B) Both 24 and 48 hpi DNA content profiles of mock-infected cells or pUL44-positive, virus-infected cells. (C) Percentage of pUL44-positive, virus-infected cells in G1, S, or G2/M phase at 48 hpi based on DNA content. <i>p</i> values were based on the numbers of S phase cells and determined using the student's t test. *, <i>p</i> value <0.05; n.s. (not significant), <i>p</i> value >0.05. Shown are data from two independent experiments.</p

Depletion of cyclin A alleviates the requirement of pUL21a for HCMV replication.

<p>(A) MRC-5 cells were infected with indicated viruses at an MOI of 0.01 TCID₅₀/cell and production of cell free virus was determined by TCID₅₀ assay at indicated time points. (B) MRC-5 cells were infected with indicated viruses at an MOI of 3, and cell lysates were collected at 24 and 48 hpi and analyzed by immunoblotting. * indicates nonspecific cross-reacting bands. (C) MRC-5 cells were treated with siRNA against cyclin A (siCyclin A) or luciferase control (siCont), and then infected with indicated virus at an MOI of 3. At 96 hpi, production of cell free virus was determined by TCID₅₀ assay, and (D) cell lysates were analyzed by immunoblotting.</p

Effective dose and volume fraction received more than 50 Gy of the bladder in radiotherapy with different PTV margins.

Effective dose and volume fraction received more than 50 Gy of the bladder in radiotherapy with different PTV margins.</p

Electric Field Dependent Photocurrent Decay Length in Single Lead Sulfide Nanowire Field Effect Transistors

We determined the minority carrier diffusion length to be ∼1 μm in single PbS nanowire field effect transistors by scanning photocurrent microscopy. PbS nanowires grown by the vapor−liquid−solid method were p-type with hole mobilities up to 49 cm2/(V s). We measured a photoresponse time faster than 14 μs with near-unity charge separation efficiency at the contacts. For the first time, we also observed a field-dependent photocurrent decay length, indicating a drift dominant carrier transport at high bias

Long non-coding RNA growth arrest specific transcript 5 acting as a sponge of MicroRNA-188-5p to regulate SMAD family member 2 expression promotes myocardial ischemia-reperfusion injury

The purpose of this work is to probe into the potential role of long non-coding RNA growth arrest specific transcript 5 (lncGAS5)/ microRNA (miR)-188-5p/SMAD2 axis in MIRI. Through ligating the left anterior descending (LAD) coronary artery, MIRI animal model and hypoxia/reoxygenation (H/R) myocardial injury model in vitro were established. Via adenovirus or plasmid transfection, lncGAS5/MiR-188-5p/SMAD2 expression was up-regulated or down-regulated in the study. RT-qPCR was applied to check LncGAS5/MiR-188-5p/SMAD2 mRNA expression, HE staining for histopathological staining, TUNEL staining and flow cytometry to examine cardiomyocyte apoptotic rate, CCK-8 to check cell viability, ELISA to detect inflammatory factor levels, Western blot to examine Bax, Bcl-2, cleaved caspase-3, NF-κB and SMAD2 expression, and dual luciferase reporter experiment to examine the targeting relationship of miR-188-5p with LncGAS5 and SMAD2. The results indicated that LncGAS5 and SMAD2 were highly expressed in MIRI and miR-188-5p was under-expressed. Silencing LncGAS5 and SMAD2 or overexpressing miR-188-5p could reduce MIRI in myocardial tissue, cardiomyocyte apoptosis, inhibit Bax, cleaved caspase-3 and NF-κB expressions and promote Bcl-2 expression, while reducing inflammatory factors TNF -α, IL-1β and IL-6 levels. Overexpressing LncGAS5 promoted MIRI. Additionally, the impact of silencing LncGAS5 on MIRI could be reversed through inhibiting miR-188-5p. LncGAS5 acted as a sponge of miR-188-5p to target SMAD2 expression. In conclusion, Silencing LncGAS5 is available to improve MIRI through regulating miR-188-5p/SMAD2 axis, and may be used as a potential target for treating MIRI in the future.</p