Search

A circuit for balancing Li-ion battery cells is proposed. This circuit requires one small transformer and N + 3 bilateral switches to equalize the charging states of N serially connected battery cells. The transformer works as an energy carrier, and the switches select two unbalanced cells that require an energy transfer from one to the other cell. The circuit was tested for a 12-cell Li-ion battery under static, cyclic, and dynamic charging/discharging conditions. Under static condition, the power-transfer efficiency was measured as 80.4% at a balancing power of 0.78 W; two 4400-mA·h battery cells at a state of charge $(\text{SOC}) = 70$ and 80% were equalized after 78 min. The results of cyclic and dynamic charging/discharging conditions show that the circuit is appropriate for balancing the Li-ion battery cells for vehicles and energy storage systems.

Aim cAMP signal transduction cascade activation is important in regulating neurogenesis in adult rodents by increasing the proliferation of newborn cells. Although the ventricular-subventricular zone (V-SVZ) and subgranular zone (SGZ) both contain large populations of neural stem/precursor cells; it remains unclear whether an alternative target of cAMP, the exchange protein directly activated by cAMP (Epac2), is involved in adult neurogenesis in the V-SVZ and SGZ. Here, we investigated the cell-specific expression of Epac2 protein in the V-SVZ and SGZ of the adult mouse brain. Methods Immunohistochemical analyses were performed using antibodies against Epac2, glial fibrillary acidic protein (GFAP), doublecortin (DCX), and beta-catenin, to examine the co-localization of Epac2 protein and neural stem/precursor cells in the V-SVZ and SGZ in three 8-week-old male mice. Results In the V-SVZ of the lateral ventricle, most GFAP-positive adult neural stem cells (NSC, defined as type B cells) and 75% of DCX-positive migrating neuroblasts (type A cells) expressed Epac2 proteins. Ninety-three percent of beta-catenin-positive ependymal cells (type E cells), which are in direct contact with NSCs and the ventricles, also expressed Epac2 protein. Similarly, in the SGZ of the hippocampus, Epac2-immunopositive signals were shown by 83% of GFAP-positive radial-glia-like NSCs (type 1 cells), 86% of DCX-positive transiently amplifying cells (type 2 and type 3 cells), and 71% of DCX-positive immature neurons. The present data suggest that a PKA-independent cAMP signaling pathway via Epac2 may be party to adult neurogenesis in the V-SVZ and the SGZ.

This study aimed to validate a deep learning model’s diagnostic performance in using computed tomography (CT) to diagnose cervical lymph node metastasis (LNM) from thyroid cancer in a large clinical cohort and to evaluate the model’s clinical utility for resident training. The performance of eight deep learning models was validated using 3838 axial CT images from 698 consecutive patients with thyroid cancer who underwent preoperative CT imaging between January and August 2018 (3606 and 232 images from benign and malignant lymph nodes, respectively). Six trainees viewed the same patient images (n = 242), and their diagnostic performance and confidence level (5-point scale) were assessed before and after computer-aided diagnosis (CAD) was included. The overall area under the receiver operating characteristics (AUROC) of the eight deep learning algorithms was 0.846 (range 0.784–0.884). The best performing model was Xception, with an AUROC of 0.884. The diagnostic accuracy, sensitivity, specificity, positive predictive value, and negative predictive value of Xception were 82.8%, 80.2%, 83.0%, 83.0%, and 80.2%, respectively. After introducing the CAD system, underperforming trainees received more help from artificial intelligence than the higher performing trainees (p = 0.046), and overall confidence levels significantly increased from 3.90 to 4.30 (p

This study aimed to assess the efficacy of a new povidone-iodine (PVP-I) foam dressing (Betafoam) vs foam dressing (Medifoam) for the management of diabetic foot ulcers. This study was conducted between March 2016 and September 2017 at 10 sites in Korea. A total of 71 patients (aged ≥19 years) with type 1/2 diabetes and early-phase diabetic foot ulcers (Wagener classification grade 1/2) were randomised to treatment with PVP-I foam dressing or foam dressing for 8 weeks. Wound healing, wound infection, patient satisfaction, and adverse events (AEs) were assessed. The PVP-I foam and foam dressing groups were comparable in the proportion of patients with complete wound healing within 8 weeks (44.4% vs 42.3%, P = .9191), mean (±SD) number of days to complete healing (31.00 ± 15.07 vs 33.27 ± 12.60 days; P = .6541), and infection rates (11.1% vs 11.4%; P = 1.0000). Median satisfaction score (scored from 0 to 10) at the final visit was also comparable between groups (10 vs 9, P = .2889). There was no significant difference in AE incidence (27.8% vs 17.1%, P = .2836), and none of the reported AEs had a causal relationship with the dressings. The results of this study suggest that PVP-I foam dressing has wound-healing efficacy comparable with foam dressing, with no notable safety concerns. This study was funded by Mundipharma Korea Ltd and registered at ClinicalTrials.gov (identifier NCT02732886).

As smartphones have evolved into more sophisticated devices that can be used anytime and anywhere and most of the smartphone users save and use all their information on their smartphones, they have become major attack targets by hackers. Hackers can steal personal information through malicious code installed on smartphones and gain financial benefits through micropayment systems and advertising services. The number of mobile malware has been exponentially increasing, along with the benefits that can be gained from smartphones infected with malware. In particular, the openness of the Android market and the high market share of Android devices allow malicious code to easily spread, therefore most of the mobile malicious code is targeting Android devices for attacks. In this paper, we investigate the characteristics of adware that is the fast-growing Android-based mobile malicious code, propose a learning algorithm for detecting malicious adware attacks, and present attack detection rates.

We predict two topological superconducting phases in microscopic models arising from the Berry phase associated with the valley degree of freedom in gapped Dirac honeycomb systems. The first one is a topological helical spin-triplet superconductor with a nonzero center-of-mass momentum that does not break time-reversal symmetry. We also find a topological chiral-triplet superconductor with Chern number $\ifmmode\pm\else\textpm\fi{}1$ with equal-spin pairing in one valley and opposite-spin-triplet pairing in the other valley. Our results are obtained for the Kane-Mele model in which we have explored the effect of three different interactions, onsite attraction $U$, nearest-neighbor density-density attraction $V$, and nearest-neighbor antiferromagnetic exchange $J$, within self-consistent Bogoliubov--de Gennes theory. Transition metal dichalcogenides and cold atom experiments are promising platforms to explore these phases.

Sharp magnetization switching and large magnetoresistance (MR) were previously discovered in single crystals of 2H-${\mathrm{Fe}}_{x}{\mathrm{TaS}}_{2}$ and attributed to the Fe superstructure and its defects. We report similar sharp switching and large MR in 1T-${\mathrm{Fe}}_{x}{\mathrm{TiS}}_{2}$ ($0.086\phantom{\rule{0.28em}{0ex}}\ensuremath{\le}\phantom{\rule{0.28em}{0ex}}x\phantom{\rule{0.28em}{0ex}}\ensuremath{\le}0.703$) while providing a side-by-side comparison of the only two such ferromagnetic transition-metal dichalcogenides. The switching field ${H}_{s}$ and MR values are similar in both 1T-${\mathrm{Fe}}_{x}{\mathrm{TiS}}_{2}$ and 2H-${\mathrm{Fe}}_{x}{\mathrm{TaS}}_{2}$, with a larger than expected bowtie $\ensuremath{\rho}(H)$ and a sharper hysteresis loop for $H\ensuremath{\parallel}c$ in the former. The Curie and Weiss temperatures remain roughly constant below $x\phantom{\rule{0.16em}{0ex}}\ensuremath{\sim}\phantom{\rule{0.16em}{0ex}}1/3$ in the $T=\text{Ti}$ single crystals before increasing monotonically for higher $x$, while ${H}_{s}$ and MR reach maxima where defects in the superstructure exist, or a minimum near superstructure compositions, and they remain constant above $x\ensuremath{\sim}0.4$. Despite previous reports, electron diffraction shows only the $\sqrt{3}\ifmmode\times\else\texttimes\fi{}\sqrt{3}$ superstructure in 1T-${\mathrm{Fe}}_{x}{\mathrm{TiS}}_{2}$. Glassy behavior is shown to coexist within the ferromagnetic state in 1T-${\mathrm{Fe}}_{x}{\mathrm{TiS}}_{2}$ for compositions between 0.1 and 0.703. A simple theoretical model considering first-, second- and third-neighbor interactions yields a phase diagram that accounts for both spin glass behavior and different superstructures.

Acquired resistance to CDK4/6 small molecule inhibitors in breast cancer arises through mechanisms that are yet uncharacterized. In this study, we used a kinome-wide siRNA screen to identify kinases which when downregulated yields sensitivity to the CDK4/6 inhibitor ribociclib. In this manner, we identified PDK1 as a key modifier of ribociclib sensitivity in estrogen receptor-positive MCF-7 breast cancer cells. Pharmacological inhibition of PDK1 with GSK2334470 in combination with ribociclib or palbociclib, another CDK4/6 inhibitor, synergistically inhibited proliferation and increased apoptosis in a panel of ER+ breast cancer cell lines. Ribociclib-resistant breast cancer cells selected by chronic drug exposure displayed a relative increase levels of PDK1 and activation of the AKT pathway. Analysis of these cells revealed that CDK4/6 inhibition failed to induce cell cycle arrest or senescence. Mechanistic investigations showed that resistant cells coordinately upregulated expression of cyclins A, E and D1, activated phospho-CDK2 and phospho-S477/T479 AKT. Treatment with GSK2334470 or the CDK2 inhibitor dinaciclib was sufficient to reverse these events and restore the sensitivity of ribociclib-resistant cells to CDK4/6 inhibitors. Ribociclib in combination with GSK2334470 or the PI3Kα inhibitor alpelisib decreased xenograft tumor growth more potently than each drug alone. Taken together, our results highlight a role for the PI3K-PDK1 signaling pathway in mediating acquired resistance to CDK4/6 inhibitors.

Additional file 1. Materials and Methods.

The HER2 tyrosine kinase inhibitor (TKI) neratinib is clinically active in patients with HER2-mutant cancers. However, responses are heterogeneous across tumor types and generally short lived, suggesting mechanisms of de novo and acquired resistance. We developed neratinib-resistant HER2-mutant 5637 bladder and OVCAR8 ovarian cancer cells by gradual dose escalation. RNA sequencing identified TORC1 signaling as an actionable mechanism of drug resistance. Treatment with the TORC1 inhibitor everolimus or genetic inactivation of RAPTOR or RHEB ablated p-S6 levels and restored sensitivity to the TKI. The combination of everolimus and neratinib potently arrested growth of neratinib-resistant xenografts. RNA-seq and RAS activity assays revealed significant enrichment of the RAS pathway in neratinib-resistant cells. siRNA mediated knockdown of RAS isoforms also abrogated p-S6 and neratinib resistance. Finally, DNA sequencing of HER2-mutant tumors from patients clinically refractory to neratinib showed enrichment of somatic alterations associated with aberrant activation of the mTOR pathway.

β-Lapachone has been reported to have anticancer and various other therapeutic effects, but is limited in clinical applications by its low bioavailability. pH-Dependent isomerization can be suggested as one plausible factor influencing its low bioavailability. Since it is known that β-lapachone is converted to its isomer, α-lapachone in hydrochloric acid (HCl) solution, isomerization in the human body may be driven by HCl in the gastric fluid. The purpose of this study was to evaluate the possibility of isomerization of β-lapachone in the human body. Chemical reactions were conducted using simulated gastric fluid (SGF, pH 1.2) and simulated intestinal fluid (SIF, pH 7.5) at 37°C. β-Lapachone was observed in SGF at 37°C for 1 hour and SIF for 3 hours. In addition, biofluid analysis was performed on plasma samples 1 hour and 4 hours, and on urine sample 12 hours after oral administration of 100 mg MB12066, a synthetic β-lapachone, in healthy adult male. All samples were analyzed using liquid chromatography-tandem mass spectrometry. Only β-lapachone peaks existed in the spectra obtained from SGF and SIF. No isomerization of β-lapachone was observed in the analysis of any of the human samples. In the current study, the possibility of pH-dependent isomerization of β-lapachone in the human body was not confirmed.

This paper compares artificial intelligence (AI) methods to predict mechanical properties of sheet metal in stamping processes. The deviation of the mechanical properties of each blank leads to unpredicted failures in stamping processes, such as fracture and spring back. The research team of this paper has been building a real time control system for stamping process in a smart factory. In order to facilitate that, it is necessary to predict the mechanical properties of each blank with non-destructive testing. The regression models based on the linear algebraic scheme have traditionally brought reliable results in terms of matching the measured non-destructive testing values to the mechanical properties. With a parallel to algebraic regression models, in recent studies on various domains, AI models have been adopted to improve the accuracy of the end-results and effectiveness of the models. This paper discusses the applicability of AI models for predicting the mechanical properties based on the eddy-current non-destructive testing method. For the study, 6 input features are collected through the eddy-current non-destructive testing to map eddy-current input data to mechanical properties of the blank. Yield stress and uniform elongation were predicted by using five AI methods, i.e., regularized linear regression, support vector regularized linear regression, support vector regression, multi-layer neural network, random forest regression, and gradient boosting regression were compared. The model performance, validated with 20% of test data that are intact during the training phase, is the main discussion point of this paper. Future works to improve the predictive accuracy of AI models is also discussed.

Astrocytes play a critical role in normal brain functions and maintaining the brain microenvironment, and defects in astrocytogenesis during neurodevelopment could give rise to severe mental illness and psychiatric disorders. During neuro-embryogenesis, astrocytogenesis involves astrocytic differentiation of neural precursor cells (NPCs) induced by signals from ciliary neurotrophic factor (CNTF) or pituitary adenylate cyclase-activating peptide (PACAP). However, in contrast to the CNTF signaling pathway, the exact mechanism underlying astrocytic differentiation induced by PACAP is unknown. In the present study, we aimed to verify a signaling pathway specific to PACAP-induced astrocytogenesis, using exchange protein directly activated by cAMP2 (Epac2)-knockout mice. We found that PACAP could trigger astrocytic differentiation of NPCs via Epac2 activation and an increase in the intracellular calcium concentration via a calcium ion influx. Taken together, we concluded that astrocytogenesis stimulated by PACAP occurs through a novel signaling pathway independent from CNTF-JAK/STAT signaling, that is the well-known pathway of astrocytogenesis. [BMB Reports 2016; 49(2): 128-133].

Gaming on phones, tablets and laptops is very popular. Cloud gaming - where remote servers perform game execution and rendering on behalf of thin clients that simply send input and display output frames - promises any device the ability to play any game any time. Unfortunately, the reality is that wide-area network latencies are often prohibitive; cellular, Wi-Fi and even wired residential end host round trip times (RTTs) can exceed 100ms, a threshold above which many gamers tend to deem responsiveness unacceptable. In this paper, we present Outatime, a speculative execution system for mobile cloud gaming that is able to mask up to 120ms of network latency. Outatime renders speculative frames of future possible outcomes, delivering them to the client one entire RTT ahead of time, and recovers quickly from mis-speculations when they occur. Clients perceive little latency. To achieve this, Outatime combines: 1) future state prediction; 2) state approximation with image-based rendering and event time-shifting; 3) fast state checkpoint and rollback; and 4) state compression for bandwidth savings. To evaluate the Outatime speculation system, we use two high quality, commercially-released games: a twitch-based first person shooter, Doom 3, and an action role playing game, Fable 3. Through user studies and performance bench- marks, we find that players strongly prefer Outatime to traditional thin-client gaming where the network RTT is fully visible, and that Outatime successfully mimics playing across a low-latency network.

The existing series hybrid electric bus (SHEB) uses an ultra-capacitor (UC) to extend battery life, mitigate vehicle weight, and reduce cost. However, previous studies did not clearly identify the operation timing and load of the UC for efficiency improvement in an SHEB. This paper proposes novel efficiency improvement factors, with their application criteria for the ideal operation timing and load of the UC in an SHEB. The factors are the threshold of the required power of the motor (TRPM), slope of the power split ratio (SPSR), and y-axis intercept of the power split ratio (YPSR). The TRPM determines the duration of using just the battery. The SPSR or YPSR determine the most efficient load ratio between the battery and UC. The criteria for using them are set using particle swarm optimization. Manhattan, Braunschweig, and Orange County driving cycles were used to reflect various road load conditions. The results showed that the proposed factors and their setting criteria guarantee a significant reduction in the fuel consumption and more energy-efficient SHEBs.

Background: Activating mutations in ERBB2 (HER2) are found in ~2% of solid tumors, including ~5% of metastatic breast cancers. The spectrum of HER2 mutations varies according to tumor type, with kinase domain (KD) missense mutations being most common in breast cancer, while exon 20 insertions are most common in non-small cell lung cancer (NSCLC). Breast cancer cells engineered with activating HER2 mutations show elevated HER2 phosphorylation and enhanced oncogenic growth. Activating mutations of other receptor tyrosine kinases such as EGFR affect receptor internalization, but whether HER2 mutations alter receptor internalization is not yet known. In addition, clinical responses to HER2 antibody-drug conjugates (ADCs) like T-DM1 have been noted in HER2-mutant NSCLC, raising the possibility that HER2 mutations alter receptor internalization, thus enhancing ADC sensitivity. Therefore, we aimed to 1) determine whether mutant HER2 receptor internalization is altered, and 2) determine whether altered internalization contributes to HER2 ADC sensitivity in HER2-mutant breast cancer. Methods: HER2 subcellular localization was investigated by immunofluorescence (IF) in MCF7 cells where HER2L755S, HER2V777L, or HER2L869R (or HER2WT) have been ‘knocked-in' using AAV-mediated recombination. We used ELISA-based endocytosis assays to quantify the internalization efficiency of trastuzumab-labeled HER2 in cell lines with WT and mutant HER2. Cell viability upon treatment with T-DM1 was tested using conventional 2D and 3D growth assays. Results: Partial colocalization of HER2 with clathrin, measured by IF, was observed in MCF7 cells, which was not affected by HER2 mutations. In the endocytosis assay, trastuzumab was inefficiently internalized over a period of 4 hours. In MCF7 or MCF10A breast epithelial cells, introduction of HER2L755S, HER2V777L, or HER2L869R did not significantly affect internalization following trastuzumab labeling, or after stimulation with EGF or neuregulin. In line with these results, MCF7 cells expressing HER2L755S, HER2V777L, or HER2L869R were not sensitive to T-DM1 in 2D cell viability assays or 3D Matrigel assays. In contrast, HER2 internalization was significantly more efficient in BT474 cells with wild-type HER2 amplification, which was accompanied by exquisite sensitivity of BT474 cells to T-DM1 both in vitro and in vivo. HER2 endocytic efficiency was significantly increased in MCF10A cells ectopically expressing HER2S310F, a mutation in the extracellular domain, or HER2A775>YVMA, a common insertion mutation in NSCLC. Conclusion: Breast cancer cells expressing HER2 KD missense mutations do not exhibit enhanced HER2 internalization and are not sensitive to T-DM1. However, cells with the HER2S310F mutation and the HER2A775>YVMA insertion showed enhanced HER2 endocytosis, consistent with clinical responses to T-DM1 in NSCLC patients with these mutations. Citation Format: Hiroaki Akamatsu, Rosa Mino, Marcel Mettlen, Dan Ye, Dhivya R. Sudhan, Albert Lin, Arnaldo Marin, Alberto Servetto, Kyung-min Lee, Sumanta Chatterjee, Sandra L. Schmid, Carlos L. Arteaga, Ariella B. Hanker. HER2 missense mutations in breast cancer cells do not alter HER2 internalization or sensitivity to T-DM1 [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 3675.

Although the 17q23 amplicon has been associated with luminal B breast cancer (BC) and high risk of recurrence, a specific gene or genes in this region that would be causal to endocrine resistance have not yet been uncovered. We performed whole transcriptome analysis on RNA extracted from 58 estrogen receptor (ER)+ BCs treated with neoadjuvant letrozole for median 7.2 months. PRR11 (Proline rich 11), located in 17q23, was upregulated in non-responding tumors as defined by relapse after a median follow up of 5 years and/or a preoperative endocrine prognostic index (PEPI) ≥4. Differential gene expression analysis between tumors expressing low vs high PRR11 mRNA showed that BC signatures associated with proliferation, IGF-1 and PI3K signaling were enriched in tumors with high PRR11 expression. Rate of PRR11 amplification is 15.2% in the Metastatic Breast Cancer project, but 9.5% and 9.4% in METABRIC and The Cancer Genome Atlas (TCGA), respectively. Gene Set Enrichment Analysis revealed an enrichment of hallmark gene sets associated with proliferation in PRR11-amplified ER+ BCs in METABRIC and TCGA. Integrated analysis of gene expression with on-treatment Ki67 levels from three independent studies with operable ER+ BCs treated with neoadjuvant aromatase inhibitor (ACOSOG-Z1031, NCT00651976, Llombart-Cussac et al.) showed that PRR11 was the only gene in 17q23 with a significant correlation with a high Ki67 levels across all studies. PRR11 knockdown inhibited E2-independent growth of HCC1428 LTED (long-term estrogen deprived) and MCF7 LTED cells in culture and MCF7 xenografts. PRR11 siRNA also inhibited growth of fulvestrant-resistant and tamoxifen-resistant MCF7 cells. Conversely, PRR11 transduction induced MDA-MB-134VI cell growth under estrogen-depleted conditions. Using a PCR array with 84-cell cycle genes, we identified SKP2, CDKN1A, CCNB2, CCNA2, CKS2 and CCNB1 as genes downregulated by PRR11 knockdown. Except for SKP2 and CDKN1A, expression of all those genes was elevated in PRR11-amplifiedER+ BCs in TCGA and METABRIC. Suggesting a link to activation of PI3K signaling, we found the proline-rich motif of PRR11 associates with the SH3 domain of the p85 regulatory subunit of PI3K. We hypothesized that this association suppresses p85 homodimer formation, thus facilitating binding of PI3Kα (p110α)-p85 dimers to IRS1, retention of p110α at the plasma membrane and, hence, activation of PI3K/AKT. To test this, we co-transfected HEK293T cells with HA-p85 and FLAG-p85. Forced expression of PRR11 reduced HA-p85 and FLAG-p85 homodimers as shown by HA and FLAG pulldowns followed by FLAG and HA immunoblots, respectively. PRR11 overexpression enhanced insulin-stimulated association of IRS1 to p110α and activation of AKT. PRR11 knockdown reduced insulin/IGF-1/2-stimulated p-AKT. In METABRIC and TCGA, PRR11 amplification and PIK3CA mutations are exclusive of each other, suggesting these alterations would be functionally linked with the same pathway. Connectivity map analysis with the list of genes significantly overexpressed in ER+/PRR11-amplified BCs predicted PI3K inhibitors as perturbations that suppress such gene list. In the MGH/Sanger dataset, PRR11-amplified BC cell lines displayed significantly higher sensitivity to the pan-PI3K inhibitor pictilisib compared to cell lines without PRR11 amplification. Finally, inhibition of PI3Kα by siRNA or alpelisib abrogated E2-independent growth and insulin-stimulated growth of PRR11-transduced MDA-MB-134VI and MCF10A cells, respectively, suggesting p110α is required for the growth promoting effects of PRR11. These data suggest that 1) PRR11 is a mediator of resistance to antiestrogens via amplification of PI3K/AKT signaling, and 2) PI3Kα is a potential therapeutic target in ER+ BCs harboring PRR11 amplification. Citation Format: Kyung-min Lee, Angel Guerrero-Zotano, Ariella Hanker, Alberto Servetto, Dhivya Sudhan, Luigi Formisano, Valerie Jansen, Paula González-Ericsson, Melinda Sanders, Thomas Stricker, Lewis Cantley, Carlos Arteaga. A neoadjuvant trial with letrozole identifies PRR11 in the 17q23 amplicon as a mechanism of resistance to endocrine therapy in ER-positive breast cancer [abstract]. In: Proceedings of the 2019 San Antonio Breast Cancer Symposium; 2019 Dec 10-14; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2020;80(4 Suppl):Abstract nr GS6-06.

Background: FGFR1 amplification occurs in about 15% of estrogen receptor-positive (ER+) breast cancers and is associated with resistance to endocrine therapy. In these tumors, nuclear FGFR1 has been shown to interact with ERα and alter gene expression through binding to chromatin. However, the mechanisms underpinning nuclear FGFR1-mediated gene transcription remain unclear. Thus, we sought to elucidate mechanisms to explain the genomic role of FGFR1 in ER+/FGFR1-amplified breast cancer.Results: FGFR1 ChIP-Seq detected 4408 DNA binding sites in CAMA1 ER+/FGFR1-amplified breast cancer cells cultured in estrogen-free conditions; 67% of these sites were enriched at promoter regions, suggesting a role of FGFR1 in gene transcription regulation. ChIP-qPCR assay confirmed FGFR1 binding to promoter regions of genes such as CCND1, MYC, VEGFA, JUNB and SMAD5 in both CAMA1 and MDA-MB-134 ER+/FGFR1-amplified cells and also in an ER+/FGFR1-amplified patient derived xenograft (HCI-011). RNA-Seq of CAMA1 cells revealed that expression of FGFR1-bound genes was substantially higher than non FGFR1-bound genes (p0.25), representing those whose expression is likely regulated by FGFR1. This high signature score was associated with worse disease free survival (DFS; 263.7 months vs not reached; HR=1.72, CI 1.39-2.12; p Citation Format: Alberto Servetto, Rahul Kollipara, Luigi Formisano, Kyung-min Lee, Dhivya R Sudhan, Ariella B Hanker, Sumanta Chatterjee, Albert Lin, Saurabh Mendiratta, Nicholas James, Ralf Kittler, Carlos L Arteaga. Fibroblast growth factor receptor 1 associates with promoters genome-wide and regulates gene transcription in ER+/FGFR1-amplified breast cancer: Implications for endocrine resistance [abstract]. In: Proceedings of the 2019 San Antonio Breast Cancer Symposium; 2019 Dec 10-14; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2020;80(4 Suppl):Abstract nr PD7-04.

Background Silica nanoparticles (SiNPs) are widely used for biosensing and diagnostics, and for the targeted delivery of therapeutic agents. Safety concerns about the biomedical and clinical applications of SiNPs have been raised, necessitating analysis of the effects of their intrinsic properties, such as sizes, shapes, and surface physicochemical characteristics, on human health to minimize risk in biomedical applications. In particular, SiNP size-associated toxicological effects, and the underlying molecular mechanisms in the vascular endothelium remain unclear. This study aimed to elucidate the detailed mechanisms underlying the cellular response to exposure to trace amounts of SiNPs and to determine applicable size criteria for biomedical application. Methods To clarify whether these SiNP-mediated cytotoxicity due to induction of apoptosis or necrosis, human ECs were treated with SiNPs of four different non-overlapping sizes under low serum-containing condition, stained with annexin V and propidium iodide (PI), and subjected to flow cytometric analysis (FACS). Two types of cell death mechanisms were assessed in terms of production of reactive oxygen species (ROS), endoplasmic reticulum (ER) stress induction, and autophagy activity. Results Spherical SiNPs had a diameter of 21.8 nm; this was further increased to 31.4, 42.9, and 56.7 nm. Hence, we investigated these effects in human endothelial cells (ECs) treated with these nanoparticles under overlap- or agglomerate-free conditions. The 20-nm SiNPs, but not SiNPs of other sizes, significantly induced apoptosis and necrosis. Surprisingly, the two types of cell death occurred independently and through different mechanisms. Apoptotic cell death resulted from ROS-mediated ER stress. Furthermore, autophagy-mediated necrotic cell death was induced through the PI3K/AKT/eNOS signaling axis. Together, the present results indicate that SiNPs within a diameter of

Protein kinase M ζ is well known for its role in maintaining memory and pain. Previously, we revealed that the activation of protein kinase M ζ in the anterior cingulate cortex plays a role in sustaining neuropathic pain. However, the mechanism by which protein kinase M ζ is expressed in the anterior cingulate cortex by peripheral nerve injury, and whether blocking of protein kinase M ζ using its inhibitor, zeta inhibitory peptide, produces analgesic effects in neuropathic pain maintained chronically after injury, have not previously been resolved. In this study, we show that protein kinase M ζ expression in the anterior cingulate cortex is enhanced by peripheral nerve injury in a transcription-independent manner. We also reveal that the inhibition of protein kinase M ζ through zeta inhibitory peptide treatment is enough to reduce mechanical allodynia responses in mice with one-month-old nerve injuries. However, the zeta inhibitory peptide treatment was only effective for a limited time.

This paper presents methods to accelerate recurrent neural network based language models (RNNLMs) for online speech recognition systems. Firstly, a lossy compression of the past hidden layer outputs (history vector) with caching is introduced in order to reduce the number of LM queries. Next, RNNLM computations are deployed in a CPU-GPU hybrid manner, which computes each layer of the model on a more advantageous platform. The added overhead by data exchanges between CPU and GPU is compensated through a frame-wise batching strategy. The performance of the proposed methods evaluated on LibriSpeech test sets indicates that the reduction in history vector precision improves the average recognition speed by 1.23 times with minimum degradation in accuracy. On the other hand, the CPU-GPU hybrid parallelization enables RNNLM based real-time recognition with a four times improvement in speed., 4 pages, 4 figures, 3 tables, ICASSP2018(Accepted)

Purpose: This study aimed to identify biomarkers of resistance to endocrine therapy in estrogen receptor–positive (ER+) breast cancers treated with prolonged neoadjuvant letrozole.Experimental Design: We performed targeted DNA and RNA sequencing in 68 ER+ breast cancers from patients treated with preoperative letrozole (median, 7 months).Results: Twenty-four tumors (35%) exhibited a PEPI score ≥4 and/or recurred after a median of 58 months and were considered endocrine resistant. Integration of the 47 most upregulated genes (log FC > 1, FDR < 0.03) in letrozole-resistant tumors with transcription-binding data showed significant overlap with 20 E2F4-regulated genes (P = 2.56E−15). In patients treated with the CDK4/6 inhibitor palbociclib before surgery, treatment significantly decreased expression of 24 of the 47 most upregulated genes in letrozole-resistant tumors, including 18 of the 20 E2F4 target genes. In long-term estrogen-deprived ER+ breast cancer cells, palbociclib also downregulated all 20 E2F4 target genes and P-RB levels, whereas the ER downregulator fulvestrant or paclitaxel only partially suppressed expression of this set of genes and had no effect on P-RB. Finally, an E2F4 activation signature was strongly associated with resistance to aromatase inhibitors in the ACOSOG Z1031B neoadjuvant trial and with an increased risk of relapse in adjuvant-treated ER+ tumors in METABRIC.Conclusions: In tumors resistant to prolonged neoadjuvant letrozole, we identified a gene expression signature of E2F4 target activation. CDK4/6 inhibition suppressed E2F4 target gene expression in estrogen-deprived ER+ breast cancer cells and in patients' ER+ tumors, suggesting a potential benefit of adjuvant CDK4/6 inhibitors in patients with ER+ breast cancer who fail to respond to preoperative estrogen deprivation. Clin Cancer Res; 24(11); 2517–29. ©2018 AACR.

The molecular mechanism of long-term memory has been extensively studied in the context of the hippocampus-dependent recent memory examined within several days. However, months-old remote memory maintained in the cortex for long-term has not been investigated much at the molecular level yet. Various epigenetic mechanisms are known to be important for long-term memory, but how the 3D chromatin architecture and its regulator molecules contribute to neuronal plasticity and systems consolidation is still largely unknown. CCCTC-binding factor (CTCF) is an 11-zinc finger protein well known for its role as a genome architecture molecule. Male conditional knock-out mice in which CTCF is lost in excitatory neurons during adulthood showed normal recent memory in the contextual fear conditioning and spatial water maze tasks. However, they showed remarkable impairments in remote memory in both tasks. Underlying the remote memory-specific phenotypes, we observed that female CTCF conditional knock-out mice exhibit disrupted cortical LTP, but not hippocampal LTP. Similarly, we observed that CTCF deletion in inhibitory neurons caused partial impairment of remote memory. Through RNA sequencing, we observed that CTCF knockdown in cortical neuron culture caused altered expression of genes that are highly involved in cell adhesion, synaptic plasticity, and memory. These results suggest that remote memory storage in the cortex requires CTCF-mediated gene regulation in neurons, whereas recent memory formation in the hippocampus does not.SIGNIFICANCE STATEMENTCCCTC-binding factor (CTCF) is a well-known 3D genome architectural protein that regulates gene expression. Here, we use two different CTCF conditional knock-out mouse lines and reveal, for the first time, that CTCF is critically involved in the regulation of remote memory. We also show that CTCF is necessary for appropriate expression of genes, many of which we found to be involved in the learning- and memory-related processes. Our study provides behavioral and physiological evidence for the involvement of CTCF-mediated gene regulation in the remote long-term memory and elucidates our understanding of systems consolidation mechanisms.

Nematicity in quantum Hall systems has been experimentally well established at excited Landau levels. The mechanism of the symmetry breaking, however, is still unknown. Pomeranchuk instability of Fermi liquid parameter $F_{\ell} \le -1$ in the angular momentum $\ell=2$ channel has been argued to be the relevant mechanism, yet there are no definitive theoretical proofs. Here we calculate, using the variational Monte Carlo technique, Fermi liquid parameters $F_\ell$ of the composite fermion Fermi liquid with a finite layer width. We consider $F_{\ell}$ in different Landau levels $n=0,1,2$ as a function of layer width parameter $\eta$. We find that unlike the lowest Landau level, which shows no sign of Pomeranchuk instability, higher Landau levels show nematic instability below critical values of $\eta$. Furthermore, the critical value $\eta_c$ is higher for the $n=2$ Landau level, which is consistent with observation of nematic order in ambient conditions only in the $n=2$ Landau levels. The picture emerging from our work is that approaching the true 2D limit brings half-filled higher Landau-level systems to the brink of nematic Pomeranchuk instability.

Supplementary notes, supplementary figures, and supplementary tables. (DOCX 19232 kb)

This research identifies two types of review patterns, authentic and fake, based on configurations among reviewers and review content elements. We also explain what fake review is with IMT as theoretic background. The results, which are based on the fsQCA method, identify the combinations of configurations for authentic and fake reviews. Each pattern has unique characteristics. Authentic reviews’ patterns are explained by personality theory (i.e., five factor model). Authentic reviews represent personalities that are different, similar to individuals, while fake reviews are composed of three kinds of promotional reviews and are characterized by a reviewer’s low credibility. The fake review pattern is explained by HSM and ELM. This research confirms that different patterns seem to exist for authentic and fake reviews, although authentic reviews may be cited in reverse fake reviews via algorithms. Another finding is that the review business has expanded to the business of social networking.

Persistent organic pollutants (POPs), despite their considerably low levels in humans, are an increasing concern for the general populations given their various adverse health problems, including metabolic and carcinogenic effects. DNA methylation deregulation is thought to be a key mechanism in the development of human chronic diseases including cancer.In an attempt to identify biomarkers monitoring low-dose exposure and hazard, we explored whether organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) may influence the methylation of tumour suppressor gene E-cadherin (CDH1) using peripheral blood cells from 364 healthy Korean subjects.CDH1 methylation was observed in 78.3% of study subjects. Serum concentrations of OCPs or PCBs compounds were higher in CDH1 methylation-positive subjects than in methylation-negative ones. After adjusting for various covariates, the odds ratio of CDH1 methylation of the summary measure of PCBs were 1.0, 2.5 (95% confidence interval: 1.2-5.3), 3.6 (1.6-8.1), 3.6 (1.4-8.6), and 2.5 (1.1-5.7) across quintiles of PCBs (PIn this exploratory study with a small sample, CDH1 methylation might be served as the epigenetic biomarker associated with POPs exposure and adverse health effect.

This paper proposes a drive circuit for ac-direct LED lamps. The proposed circuit consists only of a line filter, an LED bridge, a load inductor, a bidirectional switch, and a switch-control circuit. The switch connects the LED bridge to the power line directly. Each leg of the LED bridge consists of LEDs and a protection diode, all connected in series. The load inductor limits the bridge current. The switch operates at a zero current switching condition, so the circuit has high power efficiency. The circuit can operate at a free-volt input condition ( $85 ). For all input voltage conditions the circuit had PE > 89%, luminous efficiency ∼90 lm/W, power factor >0.9, and 120-Hz flicker index ∼0.3. The circuit satisfies the IEC 61000-3-2 Class C and the EN 55015 regulations. The proposed LED driver is well suited for use in household LED lamps.

This paper proposes a new active cell-balancing method for Li-ion batteries. It uses an $LC$ series resonant circuit as an energy carrier, which transfers the balancing energy directly from the highest charged cell to the lowest charged cell. The method requires $N+5$ bilateral switches and one $LC$ resonant circuit, where $N$ is the number of cells in the string of batteries. The balancing speed is improved by allowing energy transfer between any two cells in the battery string, and power consumption for balancing is reduced by operating all switches in the circuit at a zero-current switching condition. An experimental cell-balancing circuit for a 12-cell Li-ion battery string shows that fast and transformerless balancing is possible using the proposed method. Measured power transfer efficiencies were 93.2% and 78.9% at balancing powers of 0.56 and 1.94 W, respectively.

In this paper, we introduce an SDN-based intrusion prevention system for more secure Science DMZ with no performance limits. The proposed system is structured with intrusion-prevention, intrusion-detection, and prevention-decision subsystems which are physically distributed but informationally connected by an SDN interface. The functional distribution and the application of SDN technology increase the flexibility and extensibility of the proposed system and prevent performance degradation possibly caused by network security equipments on Science DMZ. We verified the feasibility and performance of the proposed system over a testbed set up at KREONET.

Members of the EGFR family are potent mediators of normal cell growth and development. HER2 possesses an active tyrosine kinase domain, but no direct ligand has been identified. To investigate the differential effect of HER2 in breast cell lines, HER2 was overexpressed in MCF-10A, MCF7 and MDA-MB-231 cells. HER2 overexpression promoted proliferation, survival and migration in MCF-10A and MCF-7 cells. No significant differences were seen in proliferation, survival or migration between MDA-MB-231 vec and HER2 cells. The activity of downstream HER2 proteins increased in MCF-10A HER2 and MCF-7 HER2 cells but not in MDA-MB-231 HER2 cells. Exogenously expressed HER2 failed to associate with EGFR or HER3 in MDA-MB-231 cells, while overexpression of HER2 enhanced HER family dimerization in MCF-10A and MCF-7 cells.

// Sang-Hyun Lee 1, * , In Cheul Jeung 2, * , Tae Woo Park 3 , Kyungmin Lee 1, 3 , Dong Gwang Lee 1, 3 , Young-Lai Cho 4 , Tae Sup Lee 5 , Hee-Jun Na 6 , Young-Jun Park 1 , Hee Gu Lee 1 , Mun Sik Jeong 7 , Kwang-Hee Bae 1 , Sang Chul Lee 1 , Hyo Jin Lee 8 , Young-Guen Kwon 9 , Hyo Jeong Hong 7 , Jang-Seong Kim 1 , Jeong-Ki Min 1, 3 1 Functional Genomics Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea 2 Department of Obstetrics and Gynecology, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea 3 Department of Biomolecular Science, University of Science & Technology, Daejeon, Republic of Korea 4 Department of Chemistry, Dongguk University, Seoul, Republic of Korea 5 Molecular Imaging Research Center, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea 6 Scripps Korea Antibody Institute, Chuncheon, Republic of Korea 7 Department of Systems Immunology, College of Biomedical Science and Institute of Antibody Research, Kangwon National University, Chuncheon, Republic of Korea 8 Department of Internal Medicine and Cancer Research Institute, Chungnam National University School of Medicine, Daejeon, Republic of Korea 9 Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Republic of Korea * These authors have contributed equally to this work Correspondence to: Jeong-Ki Min, e-mail: jekmin@kribb.re.kr Jang-Seong Kim, e-mail: jangskim@kribb.re.kr Hyo Jeong Hong, e-mail: hjhong@kangwon.ac.kr Keywords: Angiogenesis inhibitors, Colorectal carcinoma, Endostatin, Tumor-associated glycoprotein-72, Vascular Endothelial Growth Factor Received: September 12, 2014 Accepted: January 09, 2015 Published: January 22, 2015 ABSTRACT Endostatin is an endogenous angiogenesis inhibitor that exhibits potential anti-tumor efficacy in various preclinical animal models. However, its relatively short in vivo half-life and the long-term, frequent administration of high doses limit its widespread clinical use. In this study, we evaluated whether a fusion protein of murine endostatin (mEndo) to a humanized antibody against tumor-associated glycoprotein 72 (TAG-72), which is highly expressed in several human tumor tissues including colon cancer, can extend the serum half-life and improve the anti-tumor efficacy of endostatin by targeted delivery to the tumor mass. The fusion protein (3E8-mEndo) and mEndo showed improved anti-angiogenic activity in vitro and in vivo , predominantly by interfering with pro-angiogenic signaling triggered by vascular endothelial growth factor (VEGF). Moreover, in mice treated with 3E8-mEndo, we observed a markedly prolonged serum half-life and significantly inhibited tumor growth. The improved anti-tumor activity of 3E8-mEndo can be partially explained by increased local concentration in the tumor mass due to targeted delivery of 3E8-mEndo to implanted colon tumors. Collectively, our data clearly indicate that tumor-targeting antibody fusions to endostatin are a powerful strategy that improves the poor pharmacokinetic profile and anti-tumor efficacy of endostatin.

In this paper, we proposed an algorithm for the identification of relieving or worsening current traffic congestion using historic traffic congestion patterns. Historical congestion patterns were placed in an adjacency list. The patterns were constructed to represent spatial and temporal length for status of a congested road. Then, we found information about historical traffic congestions that were similar to today's traffic congestion and will use that information to show how to change traffic congestion in the future. The most similar pattern to current traffic status among the historical patterns corresponded to starting section of current traffic congestion. One of our experiment results had average error when we compared identified changes of the congestion for one of the sections in the congestion road by using our proposal and real traffic status. The average error was 15 minutes. Another result was for the long congestion road consisting of several sections. The average error for this result was within 10 minutes.

Vehicular applications must not demand too much of a driver's attention. They often run in the background and initiate interactions with the driver to deliver important information. We argue that the vehicular computing system must schedule interactions by considering their priority, the attention they will demand, and how much attention the driver currently has to spare. Based on these considerations, it should either allow a given interaction or defer it. We describe a prototype called Gremlin that leverages edge computing infrastructure to help schedule interactions initiated by vehicular applications. It continuously performs four tasks: (1) monitoring driving conditions to estimate the driver's available attention, (2) recording interactions for analysis, (3) generating a user-specific quantitative model of the attention required for each distinct interaction, and (4) scheduling new interactions based on the above data. Gremlin performs the third task on edge computing infrastructure. Offload is attractive because the analysis is too computationally demanding to run on vehicular platforms. Since recording size for each interaction can be large, it is preferable to perform the offloaded computation at the edge of the network rather than in the cloud, and thereby conserve wide-area network bandwidth. We evaluate Gremlin by comparing its decisions to those recommended by a vehicular UI expert. Gremlin's decisions agree with the expert's over 90% of the time, much more frequently than the coarse-grained scheduling policies used by current vehicle systems. Further, we find that offloading of analysis to edge platforms reduces use of wide-area networks by an average of 15MB per analyzed interaction.

Treatment of adult, noninfectious uveitis remains a challenge for ophthalmologists around the world. The disease accounts for almost 10% of preventable blindness in the US and can be idiopathic or associated with infectious and systemic disorders. Strong evidence is still emerging to indicate that pharmacologic strategies presently used in rheumatologic or autoimmune disease may be translated to the treatment of intraocular inflammation. Corticosteroid monotherapy is widely regarded as wholly inappropriate, due to the unfavorable risk/benefit profile and poor long-term outcomes. Treatment plans have shifted away from low-dose, chronic corticosteroid therapy for maintenance, towards medium- to high-dose therapy for acute inflammation, followed immediately by initiation of immunomodulatory therapy. These therapies follow the 'stepladder approach', whereby least to more aggressive therapies are trialed to induce remission of inflammation, eventually without corticosteroids of any form (topical, local and systemic).This two-part review gives a comprehensive overview of the existing medical treatment options for patients with adult, noninfectious uveitis, as well as important advances for the treatment of ocular inflammation. Part I covers classic immunomodulation and latest information on corticosteroid therapy.The hazard of chronic corticosteroid use for the treatment of adult, noninfectious uveitis is well-documented. Corticosteroid-sparing therapies, which offer a very favorable risk-benefit profile when administered properly, should be substituted.

We report here that CD24 knockdown resulted in decreased expression of Notch1 in MCF-7 cells. CD24-downstream p38MAPK was shown to regulate Notch1 at the level of mRNA stability. We also found that CD24-mediated cell migration, invasion, mammosphere formation, and drug resistance was regulated by its downstream target Notch1. Together, our results indicate that CD24 may regulate the epithelial to mesenchymal transition and stemness through Notch1 signaling in breast cancer cells.

We present the practical resolution limit of a fine electrical structure based on a fiber-coupled electro-optic probing system. The spatial resolution limit was experimentally evaluated on the sub-millimeter to micrometer scale of planar electrical transmission lines. The electrical lines were fabricated to have various potential differences depending on the dimensions and geometry. The electric field between the lines was measured through an electro-optic probe, which was miniaturized up to the optical bare fiber scale so as to investigate the spatial limit of electrical signals with minimal invasiveness. The experimental results show that the technical resolution limitation of a fiber-coupled probe can reasonably approach a fraction of the mode field diameter (~10 &mu, m) of the fiber in use.

한국의 대표적 연구망인 KREONET은 사용자 가상회선 서비스를 위해 사전 예약 기반의 네트워크 서비스 에이전트인 DynamicKL 시스템을 개발하여 왔다. DynamicKL은 오픈 그리드 포럼 (OGF)에서 네트워크 자원 제어서비스를 위해 정의한 표준인 네트워크 서비스 인터페이스 (NSI) 및 그래픽 유저 인터페이스 (GUI)를 이용하여 예약, 할당, 해제, 종결, 조회 가상 회선 서비스를 제공한다. 또한 사용자에 의해 앞서 생성된 가상 회선과 예약들에게 가상회선 별로 보호 절체 관리 기능을 제공하기 위해 RICE 인터페이스를 갖는다. 본 논문은 DynamicKL 프레임워크 안에 구현된 가상회선 별 보호 절체 관리 기능을 가상 회선 서비스 관리 이슈 중 하나로 소개하고 이는 선진 연구망에서 개발한 다른 사전 예약 프레임워크 들과 비교하여 관리 및 안정성이 확보된 가상 회선 서비스를 제공하는데 기여한다. 관리자는 RICE 인터페이스를 사용하여 주회선 링크 장애시 백업 링크 안에 주 가상회선 들의 성공적인 보호 절체 유무 및 주회선 링크 복구 후 주회선 링크 내부에 주 가상회선 들의 성공적인 재생성 유무를 감지 할 수 있다.

Neurodevelopmental disorders include a wide range of diseases such as autism spectrum disorders and mental retardation. Mutations in several genes that regulate neural development and synapse function have been identified in neurodevelopmental disorders. Interestingly, some affected genes and pathways in these diseases are associated with the autophagy pathway. Autophagy is a complex, bulky degradative process that involves the sequestration of cellular proteins, RNA, lipids, and cellular organelles into lysosomes. Despite recent progress in elucidating the genetics and molecular pathogenesis of these disorders, little is known about the pathogenic mechanisms and autophagy-related pathways involved in common neurodevelopmental disorders. Therefore, in this review, we focus on the current understanding of neuronal autophagy as well as recent findings on genetics and the roles of autophagy pathway in common neurodevelopmental disorders.

Purpose: Keratin19 (KRT19) is the smallest known type I intermediate filament and is used as a marker for reverse transcriptase PCR–mediated detection of disseminated tumors. In this study, we investigated the functional analysis of KRT19 in human breast cancer. Experimental Design: Using a short hairpin RNA system, we silenced KRT19 in breast cancer cells. KRT19 silencing was verified by Western blot analysis and immunocytochemistry. We further examined the effect of KRT19 silencing on breast cancer cells by cell proliferation, migration, invasion, colony formation assay, cell-cycle analysis, immunocytochemistry, immunohistochemistry, and mouse xenograft assay. Results: Silencing of KRT19 resulted in increased cell proliferation, migration, invasion, and survival. These effects were mediated by upregulation of Akt signaling as a result of reduced PTEN mRNA expression. Silencing of KRT19 decreased the nuclear import of early growth response-1 (Egr1), a transcriptional factor for PTEN transcription, through reduced association between Egr1 and importin-7. We also confirmed that silencing of KRT19 increased tumor formation in a xenograft model. Conclusions: KRT19 is a potential tumor suppressor that negatively regulates Akt signaling through modulation of Egr1 nuclear localization. Clin Cancer Res; 19(16); 4335–46. ©2013 AACR.

This study examined the effects of incorporated-carbon nanotubes (CNTs) on the photovoltaic response of a mesoporous TiO 2 film on a titanium foil subjected to electrophoretic deposition (EPD) at a high voltage of 350 V for use in dye-sensitized solar cells (DSSCs). Microstructural observations showed that after EPD in an alkaline electrolyte for 40 s, the surface area of the CNT/TiO 2 film was relatively higher than that of its TiO 2 counterpart. This was attributed to the incorporated CNTs triggered, local agglomeration of TiO 2 nanoparticles during EPD. The DSSCs with the CNT/TiO 2 film exhibited a higher short-circuit current density than the cell with the TiO 2 film, whereas the open circuit voltage remained constant for both cases. The power conversion efficiency of the CNT/TiO 2 film approached 2.49% due to the increased surface area of the film, which facilitates increased dye absorption. Electrochemical impedance analysis showed that the charge transport resistance at the interface between the photoelectrode and electrolyte decreased when the CNTs were incorporated. This was attributed mainly to the incorporation of CNTs, which provide interpenetration paths for electrons across the entire photoelectrode.

We report here the synthesis and dielectric properties of polymetalloxane dielectric materials for organic field-effect transistor applications. The gate insulators were obtained from polymetalloxanes by condensation polymerization of metal chelates and silicic acid. The solution shows an appreciable stability to self-condensation and a good coating quality. A high dielectric constant 6.16–8.27 was obtained for the prepared films. Organic thin film transistors with this gate dielectric were found to exhibit high performances, including carrier mobility as large as 1.77 cm2/Vs, on-off current ratios above 1×104, threshold voltages below −0.13 V, and subthreshold swing as low as 0.1 V/decade. In addition, the operating voltage ranges as low as 5 volts was obtained. Open image in new window

The dorsal striatum, with its functional microcircuits galore, serves as the primary gateway of the basal ganglia and is known to play a key role in implicit learning. Initially, excitatory inputs from the cortex and thalamus arrive on the direct and indirect pathways, where the precise flow of information is then regulated by local GABAergic interneurons. The balance of excitatory and inhibitory transmission in the dorsal striatum is modulated by neuromodulators such as dopamine and acetylcholine. Under pathophysiological states in the dorsal striatum, an alteration in excitatory and inhibitory transmission may underlie dysfunctional motor control. Here, we review the cellular connections and modulation of striatal microcircuits and propose that modulating the excitatory and inhibitory balance in synaptic transmission of the dorsal striatum is important for regulating locomotion.

Ultrathin doped layers, known as delta-doped layers, were introduced within the intrinsic amorphous silicon (a-Si) active layer to fabricate hydrogenated amorphous silicon (a-Si:H) thin-film transistors (TFTs) with enhanced field-effect mobility. The performance of the delta-doped a-Si:H TFTs depended on the phosphine (PH3) flow rate and the distance from the n+ a-Si to the deltadoping layer. The delta-doped a-Si:H TFTs fabricated using a commercial manufacturing process exhibited an enhanced field-effect mobility of approximately ∼0.23 cm2/Vs (compared to a conventional a-Si:H TFT with 0.15 cm2/Vs) and a desirable stability under a bias-temperature stress test.

Introduction Traumatic neuroma is a reactive process caused by the regeneration of an injured nerve that usually forms a nodular proliferation of small nerve bundles. Penile traumatic neuroma is rare; only a few cases related to circumcision have been reported. Aim To report on a case of traumatic neuroma in the penis after selective dorsal neurotomy (SDN) to treat premature ejaculation. Methods The penile traumatic neuroma was successfully removed by excision and confirmed by histopathology. Results A 55-year-old man who had had several painless, slow-growing nodules on his penis for 2 years presented to our hospital. He had no history of genital trauma, urinary tract infection, or penile surgery, except SDN to treat premature ejaculation. The nodules were excised and the final diagnosis was traumatic neuroma. No recurrence has been detected during 1 year of follow-up. Conclusion The main complications of SDN are recurrence of premature ejaculation, pain or paresthesia on the glans penis, and erectile dysfunction. However, no traumatic neuroma has been reported as a complication. We report that a traumatic neuroma can occur after SDN.