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Interpreting natural language is an increasingly important task in computer algorithms due to the growing availability of unstructured textual data. Natural Language Processing (NLP) applications rely on semantic networks for structured knowledge representation. The fundamental properties of semantic networks must be taken into account when designing NLP algorithms, yet they remain to be structurally investigated. We study the properties of semantic networks from ConceptNet, defined by 7 semantic relations from 11 different languages. We find that semantic networks have universal basic properties: they are sparse, highly clustered, and many exhibit power-law degree distributions. Our findings show that the majority of the considered networks are scale-free. Some networks exhibit language-specific properties determined by grammatical rules, for example networks from highly inflected languages, such as e.g. Latin, German, French and Spanish, show peaks in the degree distribution that deviate from a power law. We find that depending on the semantic relation type and the language, the link formation in semantic networks is guided by different principles. In some networks the connections are similarity-based, while in others the connections are more complementarity-based. Finally, we demonstrate how knowledge of similarity and complementarity in semantic networks can improve NLP algorithms in missing link inference. [ABSTRACT FROM AUTHOR]

Transcutaneous electrical nerve stimulator (TENS) has been demonstrated to be beneficial in glycemic control in animal models, but its application in humans has not been well studied. We randomly assigned 160 patients with type 2 diabetes on oral antidiabetic drugs 1:1 to the TENS study device (n = 81) and placebo (n = 79). 147 (92%) randomized participants (mean [SD] age 59 [10] years, 92 men [58%], mean [SD] baseline HbA1c level 8.1% [0.6%]) completed the trial. At week 20, HbA1c decreased from 8.1% to 7.9% in the TENS group (− 0.2% [95% CI − 0.4% to − 0.1%]) and from 8.1% to 7.8% in the placebo group (− 0.3% [95% CI − 0.5% to − 0.2%]) (P = 0.821). Glycemic variability, measured as mean amplitude of glycemic excursion (MAGE) at week 20 were significantly different in the TENS group vs. the placebo group (66 mg/dL [95% CI 58, 73] vs. 79 mg/dL [95% CI 72, 87]) (P = 0.009). Our study provides the clinical evidence for the first time in humans that TENS does not demonstrate a statistically significant HbA1c reduction. However, it is a safe complementary therapy to improve MAGE in patients with type 2 diabetes. [ABSTRACT FROM AUTHOR]

Cancers are immunologically heterogeneous. A range of immunotherapies target abnormal tumor immunity via different mechanisms of actions (MOAs), particularly various tumor-infiltrate leukocytes (TILs). We modeled loss of function (LOF) in four common anti-PD-1 antibody-responsive syngeneic tumors, MC38, Hepa1-6, CT-26 and EMT-6, by systematical depleting a series of TIL lineages to explore the mechanisms of tumor immunity and treatment. CD8+-T-cells, CD4+-T-cells, Treg, NK cells and macrophages were individually depleted through either direct administration of anti-marker antibodies/reagents or using DTR (diphtheria toxin receptor) knock-in mice, for some syngeneic tumors, where specific subsets were depleted following diphtheria toxin (DT) administration. These LOF experiments revealed distinctive intrinsic tumor immunity and thus different MOAs in their responses to anti-PD-1 antibody among different syngeneic tumors. Specifically, the intrinsic tumor immunity and the associated anti-PD-1 MOA were predominately driven by CD8+ cytotoxic TILs (CTL) in all syngeneic tumors, excluding Hepa1-6 where CD4+ Teff TILs played a key role. TIL-Treg also played a critical role in supporting tumor growth in all four syngeneic models as well as M2-macrophages. Pathway analysis using pharmacodynamic readouts of immuno-genomics and proteomics on MC38 and Hepa1-6 also revealed defined, but distinctive, immune pathways of activation and suppression between the two, closely associated with the efficacy and consistent with TIL-pharmacodynamic readouts. Understanding tumor immune-pathogenesis and treatment MOAs in the different syngeneic animal models, not only assists the selection of the right model for evaluating new immunotherapy of a given MOA, but also can potentially help to understand the potential disease mechanisms and strategize optimal immune-therapies in patients. [ABSTRACT FROM AUTHOR]

Objective: Chemoradiotherapy (CRT) is the standard treatment for limited-stage small cell lung cancer (LS-SCLC), which can exert anti-tumor effects by regulating immune cells. Different immune cell subsets are associated with a specific sensitivity to CRT. The purpose of this study was to characterize the proportion or composition of peripheral lymphocytes in patients with LS-SCLC before and after CRT, and evaluate their prognostic value. Methods: A total of 98 patients with LS-SCLC were enrolled. The expression of CD3, CD4, CD8, CD45RA, CD45RO, CD38, CD56, and CD19 on the surface of peripheral blood cells was detected by flow cytometry and retrospectively analyzed. The relationship between the proportion of lymphocyte subsets, progression-free survival (PFS), and overall survival (OS) was evaluated using a log-rank test and Cox regression model. Results: The median PFS was 12.3 months and the median OS was 21.7 months. Compared with the pre-treatment specimens, post-treatment lymphocytes had increased proportions of CD3+, CD3+CD8+, CD8+CD38+ T cells, and NKT cells, and a decreased proportion of CD3+CD4+ T cells, CD4+CD45RA+ T cells, B cells, NK cells, and CD4/CD8 ratio. Univariate and multivariate analyses showed that prophylactic cranial irradiation, high percentages of CD4+CD45RA+, CD8+CD38+ T cells after CRT independently predicted superior PFS. Male patients with a high baseline CD4+CD45RO+ T cell ratio predicted a poor OS. Conclusions: CRT induced changes in the proportion of circulating lymphocyte subsets in LS-SCLC, which is helpful for designing a regimen of immune drugs to be combined with CRT. The prognostic value of the proportion of lymphocytes aids in understanding the role of peripheral immune profiles in LS-SCLC. [ABSTRACT FROM AUTHOR]

A correction to this paper has been published: https://doi.org/10.1007/s00262-021-02929-0 [ABSTRACT FROM AUTHOR]

Dissolved gas analysis (DGA) is an effective technique to evaluate the operation status of the power transformer, and to guarantee the safe operation of the power system. Using density functional theory (DFT), we proposed the application of Pd-doped SnS2 (Pd-SnS2) monolayer as a sensing material to detect H2 and C2H2 in transformer oil. The electronic and geometric structures of Pd-doping behavior on SnS2 were also analyzed to give insight into the physicochemical property of the active surface. The adsorption configuration, density of state (DOS), frontier molecular orbital theory as well as recovery property of the adsorption systems were comprehensively studied to estimate the suitability of our proposed material for sensing application. Our calculations showed that Pd-doping exerts some deformations on the SnS2 monolayer and leads to the narrowed bandgap of such surface. Meanwhile, Pd-SnS2 monolayer has stronger adsorption performance upon C2H2 compared to H2. And the desirable interaction with C2H2 makes it possible for application of a resistance-type sensor given the good electrical response and recovery property. Our calculations are meaningful to suggest novel sensing material for application in the field of electrical engineering. [ABSTRACT FROM AUTHOR]

From the perspective of probability, the stability of a modified Cooper-Frieze model is studied in the present paper. Based on the concept and technique of the first-passage probability in the Markov theory, we provide a rigorous proof for the existence of the steady-state degree distribution, and derive the explicit formula analytically. Moreover, we perform extensive numerical simulations of the model, including the degree distribution and the clustering. [ABSTRACT FROM AUTHOR]

During metastases, cancer cells are temporarily exposed to the condition in which interactions with extracellular environment can be restricted (anchorage-independence). We demonstrate that the sensitivity of prostate cancer cell lines, DU145 and PC-3, to genotoxic treatment (cisplatin and?-irradiation) increased several folds when cells were forced to grow in anchorage-independence. This enhanced drug sensitivity was associated with a severe impairment of homologous recombination-directed DNA repair (HRR). The mechanism involves Rad51, which is the major enzymatic component of HRR. The protein level of Rad51 and its recruitment to DNA double-strand breaks (DSBs) were both attenuated. Rad51 deficiency in anchorage-independence was not associated with Rad51 promoter activity, and was not compensated by a constitutive overexpression of Rad51 cDNA. Instead, Rad51 protein level and its ability to colocalize with DSBs were restored in the presence of proteosome inhibitors, or when cells from the suspension cultures were allowed reattachment. Presented results indicate that anchorage-independence sensitizes prostate cancer cells to genotoxic agents; however, it also attenuates faithful component of DNA repair by targeting stability of Rad51. This temporal attenuation of HRR may contribute to the accumulation mutations after DNA damage, and possibly the selection of new adaptations in cells, which survived genotoxic treatment.Oncogene (2005) 24, 3748-3758. doi:10.1038/sj.onc.1208537 Published online 14 March 2005 [ABSTRACT FROM AUTHOR]

Medulloblastomas represent about 25% of all pediatric intracranial neoplasms. These highly malignant tumors arise from the cerebellum, affecting mainly children between ages 5 and 15. Although the etiology of medulloblastomas has not yet been elucidated, several reports suggest that both the cellular protein insulin-like growth factor I (IGF-I) and the early protein of the human polyomavirus JC (JCV T antigen) may contribute to the development of these tumors. The results of this study show a potential functional cooperation between these two proteins in the process of malignant transformation. Both medulloblastoma cell lines and medulloblastoma biopsies are characterized by the abundant presence of the IGF-I receptor (IGF-IR) and its major signaling molecule, insulin receptor substrate 1 (IRS-1). Importantly, IRS-1 is translocated to the nucleus in the presence of the JCV T antigen. Nuclear IRS-1 was detected in T antigen–positive cell lines and in T antigen–positive biopsies from patients diagnosed with medulloblastoma. The IRS-1 domain responsible for a direct JCV T antigen binding was localized within the N-terminal portion of IRS-1 molecule and the competition for IRS-1 T antigen binding by a dominant-negative mutant of IRS-1 inhibited growth and survival of JCV T antigen-transformed cells in anchorage-independent culture condition. [ABSTRACT FROM AUTHOR]

Insulin-like growth factor I receptor (IGF-IR) has been implicated in the normal and malignant growth of many cell types including cells from the central nervous system. In the cerebellar cortex IGF-IR mRNA is found in granular cells and IGF-I stimulation is mitogenic and protects cells from low-potassium-induced apoptosis. Since primitive neuroectodermal tumors/medulloblastomas (PNETs/medulloblastomas) are suspected to originate from the external cerebellar granular layer, it is reasonable to postulate that IGF-IR and/or its signaling molecules may contribute to the transformation of these poorly differentiated cells. To study activation of the IGF-IR system in medulloblastomas, we have utilized an antibody (anti-pY1316) that specifically recognizes the phosphorylated (active) form of the IGF-IR. Medulloblastoma biopsy specimens were positive when examined immunohistochemically with anti-Y1316 antibody. Further analysis of the IGF-IR system was performed in three human (Daoy, TE-671, D283 Med) and four mouse (BsB8, BsB13, Bs-1b, Bs-1c) medulloblastoma cell lines. All the murine cell lines examined express IGF-IR and PI3-kinase at relatively normal levels, and grossly overexpress IRS-1, when compared with normal mouse cerebellum. Within 15 min following IGF-I stimulation both mouse and human cell lines phosphorylate the β subunit of the IGF-IR, IRS-1, Akt, and MAP kinases. They respond with cell proliferation when stimulated solely with IGF-I and are strongly inhibited when challenged with a dominant negative mutant of the IGF-IR (486/STOP), or with antisense oligonucleotides against the IGF-IR mRNA. Oncogene (2001) 20, 3857–3868. [ABSTRACT FROM AUTHOR]

LNCaP cells are human prostatic cancer cells that have a frame-shift mutation of the tumor suppressor gene PTEN and do not express the insulin receptor substrate-1 (IRS-1), a major substrate of the type 1 insulin-like growth factor receptor (IGF-IR). Ectopic expression of IRS-1 in LNCaP cells increases cell adhesion and decreases cell motility by an IGF-I-independent mechanism. We show now that these effects of IRS-1 are accompanied by serine phosphorylation of IRS-1 and are inhibited by inhibitors of phosphatidylinositol 3-kinase (PI3K). We have confirmed the requirement for PI3K activity and serine phosphorylation by the use of IRS-1 mutants, expressed in LNCaP cells. Serine phosphorylation inhibits IGF-I-induced tyrosyl phosphorylation of IRS-1, which is restored by the expression of wild-type PTEN or by inhibition of PI3K activity. Finally, IRS-1 in LNCaP cells co-immunoprecipitates with integrin α 5 β 1, and the association is again IGF-I-independent. We conclude that in LNCaP cells, IRS-1 is serine phosphorylated by PI3K, generating effects that are different, and even opposite, from those generated by IGF-I. Oncogene (2001) 20, 490–500. [ABSTRACT FROM AUTHOR]

LNCaP prostatic cancer cells are characterized by having a PTEN mutation, low levels of type 1 insulin-like growth factor receptor (IGF-IR) and no IRS-1, one of the major substrates of the IGF-IR. The absence of IRS-1, an activator of PI3-kinase, is compensated in these cells by the mutation in PTEN, an inhibitor of PI3-kinase. However, IGF-IR signaling in the absence of IRS-1 can cause cell differentiation and growth arrest. We hypothesized that these three characteristics may not be unrelated, specifically that, together, they may favor the metastatic spread of prostatic cancer cells without decreasing their growth potential. In support of this hypothesis, we report here that: (1) IRS-1 expression increases cell adhesion and decreases cell motility; (2) over-expression of the IGF-IR, in the absence of IRS-1, causes growth arrest and (3) a combination of IGF-IR and IRS-1 restores the transformed phenotype of LNCaP cells. These findings suggest a mechanism by which prostatic cancer cells can achieve metastatic potential without interfering with their growth potential. Oncogene (2000) 19, 2687–2694 [ABSTRACT FROM AUTHOR]

With the rapid growth of web services on the Internet, it becomes more difficult for users who want to choose the high-quality web services from a large number of functionally equivalent candidate services. Therefore, the prediction of quality of service (QoS) values according to the history of web services has received extensive attention. In recent years, deep learning has achieved great success in speech recognition, image processing, and natural language understanding. However, it is rarely applied to the service recommendation field. Therefore, a novel approach for QoS prediction named NDL (neighborhood-aware deep learning) is proposed. NDL first gets the Top-k neighbors of the user and the service through the Pearson correlation coefficient according to the service QoS information. Then, it extracts the potential features of the user neighbor and the service neighbor; after that, it inputs the QoS values of the user and the user neighbor as well as the QoS values of the service and service neighbors as a convolutional neural network. The results of experiments conducted on a real-world dataset demonstrate that the NDL significantly outperforms the current QoS prediction method in prediction accuracy. [ABSTRACT FROM AUTHOR]

Regulating the intrinsic interactions between blood vessels and nerve cells has the potential to enhance repair and regeneration of the central nervous system. Here, we evaluate the efficacy of aligned microvessels to induce and control directional axon growth from neural progenitor cells in vitro and host axons in a rat spinal cord injury model. Interstitial fluid flow aligned microvessels generated from co-cultures of cerebral-derived endothelial cells and pericytes in a three-dimensional scaffold. The endothelial barrier function was evaluated by immunostaining for tight junction proteins and quantifying the permeability coefficient (~10−7 cm/s). Addition of neural progenitor cells to the co-culture resulted in the extension of Tuj-positive axons in the direction of the microvessels. To validate these findings in vivo, scaffolds were transplanted into an acute spinal cord hemisection injury with microvessels aligned with the rostral-caudal direction. At three weeks post-surgery, sagittal sections indicated close alignment between the host axons and the transplanted microvessels. Overall, this work demonstrates the efficacy of exploiting neurovascular interaction to direct axon growth in the injured spinal cord and the potential to use this strategy to facilitate central nervous system regeneration. [ABSTRACT FROM AUTHOR]

The ratios of soil carbon (C) to nitrogen (N) and C to phosphorus (P) are much higher in Chinese temperate forest soils than in other forest soils, implying that N and P might limit microbial growth and activities. The objective of this study was to assess stoichiometric responses of microbial biomass, enzyme activities, and respiration to N and P additions. We conducted a nutrient (N, P, and N + P) addition experiment in two temperate soils under Korean pine ( Pinus koraiensis) plantation and natural broadleaf forest in Northeast China and measured the microbial biomass C, N, P; the activities of β-glucosidase (BG), N-acetyl- β-glucosaminidase (NAG), and acid and alkaline phosphomonoesterase (AP); and the microbial respiration in the two soils. Nitrogen addition increased microbial biomass N and decreased microbial biomass C-to-N ratio and microbial respiration in the two soils. Nitrogen addition decreased NAG activity to microbial biomass N ratio, P addition decreased AP activity to microbial biomass P ratio, and N, P, and N + P additions all increased BG activity to microbial biomass C ratio. These results suggest that microbial stoichiometry is not strictly homeostatic in response to nutrient additions, especially for N addition. The responses of enzyme activities to nutrient additions support the resource allocation theory. The N addition induced a decline in microbial respiration, implying that atmospheric N deposition may reduce microbial respiration, and consequently increase soil C sequestration in the temperate region. [ABSTRACT FROM AUTHOR]

Rhynchaenus maculosus is an emerging insect pest with an increasingly serious tendency. Lack of biology information results in the bottleneck of integrated management of this pest. To facilitate an available design of integrated pest management strategy, biology of R. maculosus, including voltinism, life cycle, distribution, and damage has been investigated. Results reveal that R. maculosus is oligophagous and distributes in Heilongjiang, Jilin, and Liaoning provinces, China. This pest produces one generation per year (univoltinism) and overwinters as adults in leaf litter. From mid-April to late-April, active overwintering adults emerge from overwintering sites. The next generation of adult R. maculosus appears from mid-May to early June until mid-August to early September when the beetles move into the overwintering places. The entire time span of adult occurrence ranges from 315.6 ± 3.6 to 336.4 ± 3.2 days (Mean ± SD). Larvae undergo 3 instars with a total duration of 20 to 23 days. R. maculosus larvae feed on Q. wutaishanica and Q. mongolica without host-specific preference between the two host species, but do not harm Q. acutissim. Three species of larval parasites were collected and identified as Braconidae sp., Eulophidae sp., and Ceraphronidae sp. Biological information of R. maculosus provides essential insights for design and implementation of integrated management of this pest. [ABSTRACT FROM AUTHOR]

Graves’ disease (GD) was believed to be a polygenic disease. Several chromosomal regions were linked to GD, and the 5q31 chromosome regions containing several interleukin genes cluster were worth observing. In this study, IL4, IL13, IRF1 and UGRP1 genes were sequenced, and 5, 3, 7 and 7 polymorphisms respectively were discovered. Then an extended association study for the attracting polymorphisms was performed with 146 sporadic Graves’ patients, 142 unrelated controls and the 54 multiplex Graves’ families. However, the genotype and allele frequency distribution of these polymorphisms had similar distribution between the Graves’ patients and unrelated controls, and transmission disequilibrium tests indicated that none of them showed dominant transmission from heterozygous parents to the affected offsprings. Comparison of the clinical variables of the Graves’ patients indicated that the onset ages of the patients carrying TT at IRF1 6477 T/G locus were younger than those having variant allele (TG, GG); the difference was of statistical significance ( P=0.005, Pc=0.020). Our association study revealed that, IL4, IL13, IRF1 and UGRP1 genes in chromosomal 5q31 regions might not confer susceptibility to Chinese GD. But those individuals who were TT homozygous at IRF1 6477 T/G locus seemed to be attacked by GD much earlier than others. [ABSTRACT FROM AUTHOR]

Id1 is a helix-loop-helix transcriptional factor that controls growth and survival of neuronal cells. Downregulation of Id1 expression is required to initiate differentiation and cell-cycle withdrawal in primary neuronal culture as well as in PC12 cells. The HIV-1 transactivating factor, Tat, has been suspected of causing neuronal dysfunction that often leads to the development of HIV-associated dementia in AIDS patients. We found that the expression of Tat in PC12 cells promotes serum-independent growth, formation of large colonies in soft agar, and the acceleration of tumor growth in nude mice. In addition, Tat showed the ability to inhibit the nerve growth factor (NGF)-induced neuronal differentiation of PC12 cells. Our results show that the Tat-mediated signaling events, which lead to serum-independent growth and the inhibition of NGF-induced differentiation, have a common cellular target: the upregulation of Id1 expression. In the absence of NGF, expression of Id1 is required to promote serum-independent proliferation of PC12/Tat cells, as the inhibition of Id1 by antisense DNA restored the serum-dependent growth of PC12/Tat cells. In the presence of NGF, Tat utilizes an additional pathway that involves phosphorylation of Stat5a, to upregulate Id1 expression and block neuronal cell differentiation. Suppression of Stat5a by use of its dominant-negative mutant reversed the transient expression of Id1 and the blockage of NGF-mediated differentiation in PC12/Tat cells. Finally, the treatment of PC12 cells with recombinant Tat also enhanced the NGF-induced Id1 expression, further pointing to Id1 as a target for Tat. Taken together, these studies suggest additional targets for Tat action in neuronal cells and provide new insights into the mechanisms involved in the dysregulation of neuronal functions.Oncogene (2004) 23, 7701-7711. doi:10.1038/sj.onc.1207828 Published online 13 September 2004 [ABSTRACT FROM AUTHOR]

In materials science, performance prediction of materials plays an important role in improving the quality of materials as well as preventing serious damage to the environment and threat to public safety. Traditional regression analysis models in materials science are not yet perfect, limited to capture nonlinearities of data and time-consumption for prediction, and have a poor ability to handle a large amount of data. This leads to a demand for analyses of materials data using novel computer science methods. In recent years, artificial neural networks (ANNs) are increasingly performing as a strong tool to establish the relationships among data and being successfully applied in materials science due to their generalization ability, noise tolerance and fault tolerance. In this paper, some typical ANN applications for predicting various properties (corrosion, structural, tribological and so on) of different materials serving multiple environments (atmosphere, stress, weld and so on) are reviewed. It highlights the significance of ANN in materials-related problems in separate sections arranged by the level of simplicity, ranging from simple ANN models alone to more complicated ANN models along with the hybrid use of other computing and input-ranking methods, and the trend of ANN in the context of materials science with some limitations. [ABSTRACT FROM AUTHOR]

Background: Small-cell lung cancer (SCLC) remains an aggressive cancer with short-term survival due to limited therapeutic options. Apatinib is a small-molecule tyrosine kinase inhibitor that selectively inhibits vascular endothelial growth factor receptor-2. This study aimed to investigate the efficacy and safety of apatinib in patients with extensive-stage (EC) SCLC who had progressed after two or three previous therapies.Methods: Eligible patients were histologically confirmed ES-SCLC after two or three previous treatments, including a platinum-based regimen. Patients received apatinib at an initial dose of 500 mg once daily. The primary endpoint was the objective response rate.Results: Forty patients were enrolled. At the data cut-off time (November 15, 2018), the median follow-up was 7.4 months; no patients remained on treatment, and five were still in follow-up. An objective response was achieved in 7 of 40 patients (17.5%) in the intention-to-treat population, and 7 of 38 patients (18.4%) in the per-protocol population. The median progression-free survival and overall survival were 3.0 months and 5·8 months, respectively. The most commonly observed grade 3 or greater treatment-related adverse events were hypertension, hand-foot syndrome, increased L-gamma-glutamyltransferase.Conclusions: Apatinib exhibited efficacy and an acceptable safety profile in previously heavily-treated ES-SCLC patients. Further exploration of apatinib in phase III trials is warranted.Trial Registration: NCT02945852. [ABSTRACT FROM AUTHOR]

First identified as histone-modifying proteins, lysine acetyltransferases (KATs) and deacetylases (KDACs) antagonize each other through modification of the side chains of lysine residues in histone proteins. Acetylation of many non-histone proteins involved in chromatin, metabolism or cytoskeleton regulation were further identified in eukaryotic organisms, but the corresponding enzymes and substrate-specific functions of the modifications are unclear. Moreover, mechanisms underlying functional specificity of individual KDACs remain enigmatic, and the substrate spectra of each KDAC lack comprehensive definition. Here we dissect the functional specificity of 12 critical human KDACs using a genome-wide synthetic lethality screen in cultured human cells. The genetic interaction profiles revealed enzyme-substrate relationships between individual KDACs and many important substrates governing a wide array of biological processes including metabolism, development and cell cycle progression. We further confirmed that acetylation and deacetylation of the catalytic subunit of the adenosine monophosphate-activated protein kinase (AMPK), a critical cellular energy-sensing protein kinase complex, is controlled by the opposing catalytic activities of HDAC1 and p300. Deacetylation of AMPK enhances physical interaction with the upstream kinase LKB1, leading to AMPK phosphorylation and activation, and resulting in lipid breakdown in human liver cells. These findings provide new insights into previously underappreciated metabolic regulatory roles of HDAC1 in coordinating nutrient availability and cellular responses upstream of AMPK, and demonstrate the importance of high-throughput genetic interaction profiling to elucidate functional specificity and critical substrates of individual human KDACs potentially valuable for therapeutic applications. [ABSTRACT FROM AUTHOR]

Investigates the T antigen and the pathway from IGF-IR supporting homologous recombination directed DNA repair. Role of the JC virus encoding regulatory protein T antigen in the viral life cycle with transforming properties in vitro; Detection of JC virus in brain tumors; Mechanism on the inducement of malignant transformation in T antigen.

Magnon-tuning non-volatile magnetic dynamics is investigated in a CoZr/PMN-PT structure by measuring ferromagnetic resonance at room temperature. The electric-field control of ferromagnetic resonance shows loop-like behavior, which indicates non-volatile electric-field control of the magnetism. Further, fitting the curves of in-plane rotating angle versus ferromagnetic resonance field under different electric fields shows that the effective magnetic field changes in loop-like manner with the electric field. The resulting change in non-volatile saturation magnetization with electric field is consistent with that of a polarization electric field curve. A 1.04% change of saturation magnetization is obtained, which can be attributed to a magnon-driven magnetoelectric coupling at the CoZr/PMN-PT interface. This magnon-driven magnetoelectric coupling and its dynamic magnetic properties are significant for developing future magnetoelectric devices. [ABSTRACT FROM AUTHOR]

A correction to the article "Retraction: Functional dissection of lysine deacetylases reveals that HDAC1 and p300 regulate AMPK" published in the 2012 issue is presented.