Improving mobility of silicon metal-oxide-semiconductor devices for quantum dots by high vacuum activation annealing

To improve mobility of fabricated silicon metal-oxide-semiconductor (MOS) quantum devices, forming gas annealing is a common method used to mitigate the effects of disorder at the Si/SiO2 interface. However, the importance of activation annealing is usually ignored. Here, we show that a high vacuum environment for implantation activation is beneficial for improving mobility compared to nitrogen atmosphere. Low-temperature transport measurements of Hall bars show that peak mobility can be improved by a factor of two, reaching 1.5 m^2/(Vs) using high vacuum annealing during implantation activation. Moreover, the charge stability diagram of a single quantum dot is mapped, with no visible disturbance caused by disorder, suggesting possibility of fabricating high-quality quantum dots on commercial wafers. Our results may provide valuable insights into device optimization in silicon-based quantum computing.Comment: 13 pages, 4 figure

Effect of Bushen yixue decoction on follicular development in experimental androgen-sterilized anovulatory rats and its possible mechanism of action

Purpose: To explore the activities of Bushen yixue decoction (BSY) against follicular development in anovulatory rats.Methods: Rats were divided into normal, normal control, clomifene citrate (positive control, orally, 5 mg/kg), and BSY (orally, 50, 100, 200 mg/kg) groups. Anovulatory rats were prepared by testosterone propionate injection (1.5 mg/rat). After 70 days, daily vaginal smears were performed for 10 days until no obvious sexual cycle was observed, indicating that androgen-sterilized anovulatory rats were successfully established. High performance liquid chromatography (HPLC) was used to analyse BSY chemical composition. Levels of follicular stimulating hormone (FSH), luteinizing hormone (LH), oestradiol (E2), progesterone (P), prolactin (PRL), inhibin (INH), activin (ACT) and follistatin (FS) were determined by radioimmunoassay or enzyme linked immunosorbent assay (ELISA). Western blotting was used to determine Bcl-2, cleaved-caspase-3, Bax, MMP-9 and VEGF in ovarian tissues.Results: BSY increased (p < 0.05) the levels of FSH, LH, E2 (p < 0.05) and ACT, but decreased (p < 0.05) the levels of PRL, INH and FS, relative to control rats. Expressions of VEGF (p < 0.01), MMP-9 (p < 0.05) and Bcl-2 (p < 0.01) were up-regulated by BSY, whereas Bax (p < 0.01) and C-caspase-3 (p < 0.01) were down-regulated.Conclusion: BSY promotes follicular development of anovulatory rats via regulating INH-ACT-FS hormones, VEGF, MMP-9, Caspase-3, Bax, and Bcl-2. Thus, BSY may have the potential to be developed for clinical management of infertility.Keywords: Bushen yixue decoction, Follicular development, Inhibin-Activin-Follistatin (INH-ACT-FS) system, Androgen-sterilized anovulatory rat

Sulfated tyrosines 27 and 29 in the N-terminus of human CXCR3 participate in binding native IP-10

Aim: Human CXCR3, a seven-transmembrane segment (7TMS), is predominantly expressed in Th1-mediated responses. Interferon-γ-inducible protein 10 (IP-10) is an important ligand for CXCR3. Their interaction is pivotal for leukocyte migration and activation. Tyrosine sulfation in 7TMS is a posttranslational modification that contributes substantially to ligand binding. We aimed to study the role of tyrosine sulfation of CXCR3 in the protein's binding to IP-10. Methods: Plasmids encoding CXCR3 and its mutants were prepared by PCR and site-directed mutagenesis. HEK 293T cells were transfected with plasmids encoding CXCR3 or its variants using calcium phosphate. Transfected cells were labeled with [35S]-cysteine and methionine or [35S]-Na2SO3 and then analyzed by immunoprecipitation to measure sulfation. Experiments with 125I-labeled IP-10 were carried out to evaluate the affinity of CXCR3 for its ligand. Calcium influx assays were used to measure intercellular signal transduction. Results: Our data show that sulfate moieties are added to tyrosines 27 and 29 of CXCR3. Mutation of these two tyrosines to phenylalanines substantially decreases binding of CXCR3 to IP-10 and appears to eliminate the associated signal transduction. Tyrosine sulfation of CXCR3 is enhanced by tyrosyl protein sulfotransferases (TPSTs), and it is weakened by shRNA constructs. The binding ability of CXCR3 to IP-10 is increased by TPSTs and decreased by shRNAs. Conclusions: This study identifies two sulfated tyrosines in the N-terminus of CXCR3 as part of the binding site for IP-10, and it underscores the fact that tyrosine sulfation in the N-termini of 7TMS receptors is functionally important for ligand interactions. Our study suggests a molecular target for inhibiting this ligand-receptor interaction

Impact of residual and intrafractional errors on strategy of correction for image-guided accelerated partial breast irradiation

<p>Abstract</p> <p>Background</p> <p>The cone beam CT (CBCT) guided radiation can reduce the systematic and random setup errors as compared to the skin-mark setup. However, the residual and intrafractional (RAIF) errors are still unknown. The purpose of this paper is to investigate the magnitude of RAIF errors and correction action levels needed in cone beam computed tomography (CBCT) guided accelerated partial breast irradiation (APBI).</p> <p>Methods</p> <p>Ten patients were enrolled in the prospective study of CBCT guided APBI. The postoperative tumor bed was irradiated with 38.5 Gy in 10 fractions over 5 days. Two cone-beam CT data sets were obtained with one before and one after the treatment delivery. The CBCT images were registered online to the planning CT images using the automatic algorithm followed by a fine manual adjustment. An action level of 3 mm, meaning that corrections were performed for translations exceeding 3 mm, was implemented in clinical treatments. Based on the acquired data, different correction action levels were simulated, and random RAIF errors, systematic RAIF errors and related margins before and after the treatments were determined for varying correction action levels.</p> <p>Results</p> <p>A total of 75 pairs of CBCT data sets were analyzed. The systematic and random setup errors based on skin-mark setup prior to treatment delivery were 2.1 mm and 1.8 mm in the lateral (LR), 3.1 mm and 2.3 mm in the superior-inferior (SI), and 2.3 mm and 2.0 mm in the anterior-posterior (AP) directions. With the 3 mm correction action level, the systematic and random RAIF errors were 2.5 mm and 2.3 mm in the LR direction, 2.3 mm and 2.3 mm in the SI direction, and 2.3 mm and 2.2 mm in the AP direction after treatments delivery. Accordingly, the margins for correction action levels of 3 mm, 4 mm, 5 mm, 6 mm and no correction were 7.9 mm, 8.0 mm, 8.0 mm, 7.9 mm and 8.0 mm in the LR direction; 6.4 mm, 7.1 mm, 7.9 mm, 9.2 mm and 10.5 mm in the SI direction; 7.6 mm, 7.9 mm, 9.4 mm, 10.1 mm and 12.7 mm in the AP direction, respectively.</p> <p>Conclusions</p> <p>Residual and intrafractional errors can significantly affect the accuracy of image-guided APBI with nonplanar 3DCRT techniques. If a 10-mm CTV-PTV margin is applied, a correction action level of 5 mm or less is necessary so as to maintain the RAIF errors within 10 mm for more than 95% of fractions. Pre-treatment CBCT guidance is not a guarantee for safe delivery of the treatment despite its known benefits of reducing the initial setup errors. A patient position verification and correction during the treatment may be a method for the safe delivery.</p

MicroRNA-1 acts as a tumor suppressor microRNA by inhibiting angiogenesis-related growth factors in human gastric cancer

Background We recently reported that miR-1 was one of the most significantly downregulated microRNAs in gastric cancer (GC) patients from The Cancer Genome Atlas microRNA sequencing data. Here we aim to elucidate the role of miR-1 in gastric carcinogenesis. Methods We measured miR-1 expression in human GC cell lines and 90 paired primary GC samples, and analyzed the association of its status with clinicopathological features. The effect of miR-1 on GC cells was evaluated by proliferation and migration assay. To identify the target genes of miR-1, bioinformatic analysis and protein array analysis were performed. Moreover, the regulation mechanism of miR-1 with regard to these predicted targets was investigated by quantitative PCR (qPCR), Western blot, ELISA, and endothelial cell tube formation. The putative binding site of miR-1 on target genes was assessed by a reporter assay. Results Expression of miR-1 was obviously decreased in GC cell lines and primary tissues. Patients with low miR-1 expression had significantly shorter overall survival compared with those with high miR-1 expression (P = 0.0027). Overexpression of miR-1 in GC cells inhibited proliferation, migration, and tube formation of endothelial cells by suppressing expression of vascular endothelial growth factor A (VEGF-A) and endothelin 1 (EDN1). Conversely, inhibition of miR-1 with use of antago-miR-1 caused an increase in expression of VEGF-A and EDN1 in nonmalignant GC cells or low-malignancy GC cells. Conclusions MiR-1 acts as a tumor suppressor by inhibiting angiogenesis-related growth factors in human gastric cancer. Downregulated miR-1 not only promotes cellular proliferation and migration of GC cells, but may activates proangiogenesis signaling and stimulates the proliferation and migration of endothelial cells, indicating the possibility of new strategies for GC therapy