Portable wireless ultrasound has been emerging as a new ultrasound device due to its unique advantages including small size, lightweight, wireless connectivity and affordability. Modern portable ultrasound devices can offer high quality sonogram images and even multiple ultrasound modes such as color Doppler, echocardiography, and endovaginal examination. However, none of them can provide elastography function yet due to the limitations in computational performance and data transfer speed of wireless communication. Also phase-based strain estimator (PSE) that is commonly used for conventional elastography cannot be adopted for portable ultrasound, because ultrasound parameters such as data dumping interval are varied significantly in the practice of portable ultrasound. Therefore, this research aims to propose a new elastography method suitable for portable ultrasound, called the robust phase-based strain estimator (RPSE), which is not only robust to the variation of ultrasound parameters but also computationally effective. Performance and suitability of RPSE were compared with other strain estimators including time-delay, displacement-gradient and phase-based strain estimators (TSE, DSE and PSE, respectively). Three types of raw RF data sets were used for validation tests: two numerical phantom data sets modeled by an open ultrasonic simulation code (Field II) and a commercial FEA (Abaqus), and the one experimentally acquired with a portable ultrasound device from a gelatin phantom. To assess image quality of elastograms, signal-to-noise (SNRe) and contrast-to-noise (CNRe) ratios were measured on the elastograms produced by each strain estimator. The computational efficiency was also estimated and compared. Results from the numerical phantom experiment showed that RPSE could achieve highest values of SNRe and CNRe (around 5.22 and 47.62 dB) among all strain estimators tested, and almost 10 times higher computational efficiency than TSE and DSE (around 0.06 vs. 5.76 s per frame for RPSE and TSE, respectively).
Dataset ; Echocardiography ; Elasticity Imaging Techniques ; Gelatin ; Methods ; Ultrasonics ; Ultrasonography

0.9 between all observers). Receiver operating characteristic curve analysis showed that the predictive power for CAD was improved when max-CIMT and plaque information (plaque≥2) was added [area under the curve (AUC): 0.838] to the traditional clinical CV risk factors (AUC: 0.769). The cutoff values for CAD prediction with the standard device and the WHUS device were 1.05 mm (AUC: 0.807, sensitivity: 0.78, specificity: 0.53) and 1.10 mm (AUC: 0.725, sensitivity: 0.98, specificity: 0.27), respectively.CONCLUSION: max-CIMT measured by a WHUS device showed excellent agreement and repeatability, compared with standard ultrasound. Combined max-CIMT and plaque information added predictive power to the traditional clinical CV risk factors in detecting high-risk CAD patients.]]>
Carotid Artery, Common ; Carotid Intima-Media Thickness ; Coronary Angiography ; Coronary Artery Disease ; Humans ; Mass Screening ; Risk Factors ; ROC Curve ; Sensitivity and Specificity ; Ultrasonography ; Wireless Technology

PURPOSE: Growth inhibitory effects of lipid soluble components of the Korean red ginseng and the antineoplastic mechanism against human melanoma cell lines were investigated. To examine molecular mechanism of growth inhibitory effects of GX-PE, we analyzed the effect of GX-PE on cell cycle progression and expression of cell cycle regulatory factors such as retinoblastoma gene product (Rb), p27 (Kip1), p21 (WAF1), cdk2, cdk4 and cyclin D1 which are known to regulate cell cycle progression. MATERIALS AND METHODS: Petroleum ether extract of the Korean red ginseng (GX-PE) was added to cultures of three human melanoma cell lines, SK-MEL-1, SK-MEL-2, and SK-MEL-5. Proliferation was measured by 3H-thymidine incorporation assay. Cell cycle and expression of cell cycle regulatory factors were analyzed by flow cytometry and Western blotting, respectively. RESULTS: Growth of melanoma cells was inhibited by GX-PE in proportion to the concentration. GX-PE significantly inhibited cell cycle progression at G1 phase. GX-PE increased expression of negative cell cycle regulators, i.e., p27 (Kip1) in SK-MEL-2 and p21 (WAF1) and Rb in SK-MEL-1. CONCLUSION: These results suggest that GX-PE inhibits proliferation of melanoma cells at a G1-S transition point of the cell cycle. The effect of GX-PE is most likely due to induction of negative cell cycle regulatory factors.
Blotting, Western ; Cell Cycle* ; Cell Line* ; Cyclin D1 ; Ether ; Flow Cytometry ; G1 Phase ; Genes, Retinoblastoma ; Humans* ; Melanoma* ; Panax* ; Petroleum

The protein encoded by the Gene Associated with Retinoid-Interferon-Induced Mortality-19 (GRIM-19) is located in the mitochondrial inner membrane and is homologous to the NADH dehydrogenase 1-alpha subcomplex subunit 13 of the electron transport chain.Multiple sclerosis (MS) is a demyelinating disease that damages the brain and spinal cord.Although both the cause and mechanism of MS progression remain unclear, it is accepted that an immune disorder is involved. We explored whether GRIM-19 ameliorated MS by increasing the levels of inflammatory cytokines and immune cells; we used a mouse model of experimental autoimmune encephalomyelitis (EAE) to this end. Six-to-eight-week-old male C57BL/6, IFNγ-knockout (KO), and GRIM-19 transgenic mice were used; EAE was induced in all strains. A GRIM-19 overexpression vector (GRIM19 OVN) was electrophoretically injected intravenously. The levels of Th1 and Th17 cells were measured via flow cytometry, immunofluorescence, and immunohistochemical analysis. IL-17A and IFNγ expression levels were assessed via ELISA and quantitative PCR. IL-17A expression decreased and IFNγ expression increased in EAE mice that received injections of the GRIM19 OVN. GRIM-19 transgenic mice expressed more IFNγ than did wild-type mice; this inhibited EAE development. However, the effect of GRIM-19 overexpression on the EAE of IFNγ-KO mice did not differ from that of the empty vector. GRIM-19 expression was therapeutic for EAE mice, elevating the IFNγ level. GRIM-19 regulated the Th17/Treg cell balance.