Signature of Spin Collective Mode in Local Tunneling Spectra of a d-wave Superconductor

We consider the influence of magnetic excitations on the local density of states in the d-wave superconductor. The magnetic susceptibility is calculated within the renormalized $t-t'-J$ model and its influence on the quasiparticle self-energy is considered using a minimal model originally proposed by Polkovnikov {\it et al.}[cond-mat/0203176]. We find the local density of states possess periodic components both along $(\pi,0)$ and $(\pi,\pi)$ directions with the associated wavevectors changing in magnitude as the quasiparticle energy is varied. Comparison with the STM experiment reveals that the calculated LDOS modulation is inconsistent with the measured data.Comment: Two figures separately attached as .jpg file

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

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

Induction of Apoptosis by Luteolin Involving Akt Inactivation in Human 786-O Renal Cell Carcinoma Cells

There is a growing interest in the health-promoting effects of natural substances obtained from plants. Although luteolin has been identified as a potential therapeutic and preventive agent for cancer because of its potent cancer cell-killing activity, the molecular mechanisms have not been well elucidated. This study provides evidence of an alternative target for luteolin and sheds light on the mechanism of its physiological benefits. Treatment of 786-O renal cell carcinoma (RCC) cells (as well as A498 and ACHN) with luteolin caused cell apoptosis and death. This cytotoxicity was caused by the downregulation of Akt and resultant upregulation of apoptosis signal-regulating kinase-1 (Ask1), p38, and c-Jun N-terminal kinase (JNK) activities, probably via protein phosphatase 2A (PP2A) activation. In addition to being a concurrent substrate of caspases and event of cell death, heat shock protein-90 (HSP90) cleavage might also play a role in driving further cellular alterations and cell death, at least in part, involving an Akt-related mechanism. Due to the high expression of HSP90 and Akt-related molecules in RCC and other cancer cells, our findings suggest that PP2A activation might work in concert with HSP90 cleavage to inactivate Akt and lead to a vicious caspase-dependent apoptotic cycle in luteolin-treated 786-O cells