Defect characterization of InAs/InGaAs quantum dot p-i-n photodetector grown on GaAs-on-V-grooved-Si substrate

The performance of semiconductor devices on silicon can be severely degraded by the presence of dislocations incurred during heteroepitaxial growth. Here, the physics of the defect mechanisms, characterization of epitaxial structures, and device properties of waveguide photodetectors (PDs) epitaxially grown on (001) Si are presented. A special GaAs-on-V-grooved-Si template was prepared by combining the aspect ratio trapping effects, superlattice cyclic, and strain-balancing layer stacks. A high quality of buffer structure was characterized by atomic force microscopy (AFM) and electron channeling contrast imaging (ECCI) results. An ultralow dark current density of 3.5 × 10–7A/cm2 at 300 K was measured under −1 V. That is 40× smaller than the best reported value of epitaxially grown InAs/GaAs quantum dot photodetector structure on GaP/Si substrate. Low frequency noise spectroscopy was used to characterize the generation and recombination related deep levels. A trap with an activation energy of 0.4 eV was identified, which is near the middle bandgap. With low frequency noise spectroscopy along with the current–voltage and capacitance–voltage characterizations, the recombination lifetime of 27 μs and trap density of 5.4 × 1012 cm–3 were estimated

VHZ is a novel centrosomal phosphatase associated with cell growth and human primary cancers

<p>Abstract</p> <p>Background</p> <p>VHZ is a VH1-like (member Z) dual specific protein phosphatase encoded by DUSP23 gene. Some of the dual specific protein phosphatases (DSPs) play an important role in cell cycle control and have shown to be associated with carcinogenesis. Here, the expression of VHZ associated with cell growth and human cancers was investigated.</p> <p>Results</p> <p>We generated a mouse monoclonal antibody (mAb clone#209) and rabbit polyclonal antibodies (rAb) against VHZ. We performed cell proliferation assay to learn how VHZ is associated with cell cycle by retroviral transduction to express VHZ, VHZ(C95S), and control vector in MCF-7 cells. Overexpression of VHZ [but not VHZ(C95S)] in MCF-7 cells promoted cell proliferation compared to control cells. shRNA-mediated knockdown of VHZ in MCF-7 cells showed that reduction of VHZ resulted in increased G1 but decreased S phase cell populations. Using indirect immunofluorescence, we showed that both exogenous and endogenous VHZ protein was localized at the centrosome in addition to its cytoplasmic distribution. Furthermore, using immunohistochemistry, we revealed that VHZ protein was overexpressed either in enlarged centrosomes (VHZ-centrosomal-stain) of some invasive ductal carcinomas (IDC) Stage I (8/65 cases) or in entire cytoplasm (VHZ-cytosol-stain) of invasive epithelia of some IDC Stage II/III (11/47 cases) of breast cancers examined. More importantly, upregulation of VHZ protein is also associated with numerous types of human cancer, in particular breast cancer. VHZ mAb may be useful as a reagent in clinical diagnosis for assessing VHZ positive tumors.</p> <p>Conclusions</p> <p>We generated a VHZ-specific mAb to reveal that VHZ has a novel subcellular localization, namely the centrosome. VHZ is able to facilitate G1/S cell cycle transition in a PTP activity-dependent manner. The upregulation of its protein levels in primary human cancers supports the clinical relevance of the protein in cancers.</p

Across-Platform Imputation of DNA Methylation Levels Incorporating Nonlocal Information Using Penalized Functional Regression: Cross-Platform Imputation of Methylation Profile

DNA methylation is a key epigenetic mark involved in both normal development and disease progression. Recent advances in high-throughput technologies have enabled genome-wide profiling of DNA methylation. However, DNA methylation profiling often employs different designs and platforms with varying resolution, which hinders joint analysis of methylation data from multiple platforms. In this study, we propose a penalized functional regression model to impute missing methylation data. By incorporating functional predictors, our model utilizes information from nonlocal probes to improve imputation quality. Here, we compared the performance of our functional model to linear regression and the best single probe surrogate in real data and via simulations. Specifically, we applied different imputation approaches to an acute myeloid leukemia dataset consisting of 194 samples and our method showed higher imputation accuracy, manifested, for example, by a 94% relative increase in information content and up to 86% more CpG sites passing post-imputation filtering. Our simulated association study further demonstrated that our method substantially improves the statistical power to identify trait-associated methylation loci. These findings indicate that the penalized functional regression model is a convenient and valuable imputation tool for methylation data, and it can boost statistical power in downstream epigenome-wide association study (EWAS)

EEG-based brain-computer interfaces are vulnerable to backdoor attacks

Research and development of electroencephalogram (EEG) based brain-computer interfaces (BCIs) have advanced rapidly, partly due to deeper understanding of the brain and wide adoption of sophisticated machine learning approaches for decoding the EEG signals. However, recent studies have shown that machine learning algorithms are vulnerable to adversarial attacks. This paper proposes to use narrow period pulse for poisoning attack of EEG-based BCIs, which makes adversarial attacks much easier to implement. One can create dangerous backdoors in the machine learning model by injecting poisoning samples into the training set. Test samples with the backdoor key will then be classified into the target class specified by the attacker. What most distinguishes our approach from previous ones is that the backdoor key does not need to be synchronized with the EEG trials, making it very easy to implement. The effectiveness and robustness of the backdoor attack approach is demonstrated, highlighting a critical security concern for EEG-based BCIs and calling for urgent attention to address it

Advances in automated tongue diagnosis techniques

This paper reviews the recent advances in a significant constituent of traditional oriental medicinal technology, called tongue diagnosis. Tongue diagnosis can be an effective, noninvasive method to perform an auxiliary diagnosis any time anywhere, which can support the global need in the primary healthcare system. This work explores the literature to evaluate the works done on the various aspects of computerized tongue diagnosis, namely preprocessing, tongue detection, segmentation, feature extraction, tongue analysis, especially in traditional Chinese medicine (TCM). In spite of huge volume of work done on automatic tongue diagnosis (ATD), there is a lack of adequate survey, especially to combine it with the current diagnosis trends. This paper studies the merits, capabilities, and associated research gaps in current works on ATD systems. After exploring the algorithms used in tongue diagnosis, the current trend and global requirements in health domain motivates us to propose a conceptual framework for the automated tongue diagnostic system on mobile enabled platform. This framework will be able to connect tongue diagnosis with the future point-of-care health system

Aberrant Regulation of HDAC2 Mediates Proliferation of Hepatocellular Carcinoma Cells by Deregulating Expression of G1/S Cell Cycle Proteins

Histone deacetylase 2 (HDAC2) is crucial for embryonic development, affects cytokine signaling relevant for immune responses and is often significantly overexpressed in solid tumors; but little is known about its role in human hepatocellular carcinoma (HCC). In this study, we showed that targeted-disruption of HDAC2 resulted in reduction of both tumor cell growth and de novo DNA synthesis in Hep3B cells. We then demonstrated that HDAC2 regulated cell cycle and that disruption of HDAC2 caused G1/S arrest in cell cycle. In G1/S transition, targeted-disruption of HDAC2 selectively induced the expression of p16INK4A and p21WAF1/Cip1, and simultaneously suppressed the expression of cyclin D1, CDK4 and CDK2. Consequently, HDAC2 inhibition led to the down-regulation of E2F/DP1 target genes through a reduction in phosphorylation status of pRb protein. In addition, sustained suppression of HDAC2 attenuated in vitro colony formation and in vivo tumor growth in a mouse xenograft model. Further, we found that HDAC2 suppresses p21WAF1/Cip1 transcriptional activity via Sp1-binding site enriched proximal region of p21WAF1/Cip1 promoter. In conclusion, we suggest that the aberrant regulation of HDAC2 may play a pivotal role in the development of HCC through its regulation of cell cycle components at the transcription level providing HDAC2 as a relevant target in liver cancer therapy

HDAC1 Inactivation Induces Mitotic Defect and Caspase-Independent Autophagic Cell Death in Liver Cancer

Histone deacetylases (HDACs) are known to play a central role in the regulation of several cellular properties interlinked with the development and progression of cancer. Recently, HDAC1 has been reported to be overexpressed in hepatocellular carcinoma (HCC), but its biological roles in hepatocarcinogenesis remain to be elucidated. In this study, we demonstrated overexpression of HDAC1 in a subset of human HCCs and liver cancer cell lines. HDAC1 inactivation resulted in regression of tumor cell growth and activation of caspase-independent autophagic cell death, via LC3B-II activation pathway in Hep3B cells. In cell cycle regulation, HDAC1 inactivation selectively induced both p21WAF1/Cip1 and p27Kip1 expressions, and simultaneously suppressed the expression of cyclin D1 and CDK2. Consequently, HDAC1 inactivation led to the hypophosphorylation of pRb in G1/S transition, and thereby inactivated E2F/DP1 transcription activity. In addition, we demonstrated that HDAC1 suppresses p21WAF1/Cip1 transcriptional activity through Sp1-binding sites in the p21WAF1/Cip1 promoter. Furthermore, sustained suppression of HDAC1 attenuated in vitro colony formation and in vivo tumor growth in a mouse xenograft model. Taken together, we suggest the aberrant regulation of HDAC1 in HCC and its epigenetic regulation of gene transcription of autophagy and cell cycle components. Overexpression of HDAC1 may play a pivotal role through the systemic regulation of mitotic effectors in the development of HCC, providing a particularly relevant potential target in cancer therapy