White LED Lighting Increases the Root Productivity of Panax ginseng C. A. Meyer in a Hydroponic Cultivation System of a Plant Factory.

To identify effective light spectra for increasing the productivity of Panax ginseng, we conducted experiments in a controlled environment using a hydroponic cultivation system in a plant factory. We investigated the effect of single LEDs (red, blue, and yellow) and mixed LEDs (red + blue and red + blue + white). The relationships between four light spectra (red, blue, yellow, and white) and physiological responses (net photosynthetic rate, stomata conductance, transpiration rate, and intercellular CO2 partial pressure), as well as growth responses (shoot and root biomass), were analyzed using multivariate statistical analysis. Among the four physiological response variables, shoot biomass was not increased by any pathway, and root biomass was increased only by the intercellular CO2 partial pressure. Red and yellow light increased shoot biomass, whereas white light promoted an increase in the net photosynthetic rate and enhanced root biomass. In contrast, blue light was less effective than the other light spectra in increasing both shoot and root biomass. Therefore, red and yellow light are the most effective light spectra for increasing shoot biomass and white light is effective for increasing root biomass in a plant factory that uses artificial LED lighting. Furthermore, the intercellular CO2 partial pressure is an important physiological variable for increasing the root biomass of P. ginseng.

Approaches for 3D Integration Using Plasma-Enhanced Atomic-Layer-Deposited Atomically-Ordered InGaZnO Transistors with Ultra-High Mobility.

As the scale-down and power-saving of silicon-based channel materials approach the limit, oxide semiconductors are being actively researched for applications in 3D back-end-of-line integration. For these applications, it is necessary to develop stable oxide semiconductors with electrical properties similar to those of Si. Herein, a single-crystal-like indium-gallium-zinc-oxide (IGZO) layer (referred to as a pseudo-single-crystal) is synthesized using plasma-enhanced atomic layer deposition and fabricated stable IGZO transistors with an ultra-high mobility of over 100 cm2  Vs-1 . To acquire high-quality atomic layer deposition-processed IGZO layers, the plasma power of the reactant is controlled as an effective processing parameter by evaluating and understanding the effect of the chemical reaction of the precursors on the behavior of the residual hydrogen, carbon, and oxygen in the as-deposited films. Based on these insights, this study found that there is a critical relationship between the optimal plasma reaction energy, superior electrical performance, and device stability.

Selectively Nitrogen Doped ALD-IGZO TFTs with Extremely High Mobility and Reliability.

Achieving high mobility and reliability in atomic layer deposition (ALD)-based IGZO thin-film transistors (TFTs) with an amorphous phase is vital for practical applications in relevant fields. Here, we suggest a method to effectively increase stability while maintaining high mobility by employing the selective application of nitrous oxide plasma reactant during plasma-enhanced ALD (PEALD) at 200 °C process temperature. The nitrogen-doping mechanism is highly dependent on the intrinsic carbon impurities or nature of each cation, as demonstrated by a combination of theoretical and experimental research. The Ga2O3 subgap states are especially dependent on plasma reactants. Based on these insights, we can obtain high-performance indium-rich PEALD-IGZO TFTs (threshold voltage: -0.47 V; field-effect mobility: 106.5 cm2/(V s); subthreshold swing: 113.5 mV/decade; hysteresis: 0.05 V). In addition, the device shows minimal threshold voltage shifts of +0.45 and -0.10 V under harsh positive/negative bias temperature stress environments (field stress: ±2 MV/cm; temperature stress: 95 °C) after 10000 s.

Early Exotic Vegetation Development Is Affected by Vine Plants and Bird Activity at Rapidly Exposed Floodplains in South Korea.

For the study on the relationships between the seed dispersal of exotic plants and bird population, flora, avifauna, vegetation patches, and the dynamics of seed banks were investigated in and around the exposed floodplains of the large rivers, and the causes of exotic vegetation development were determined with respect to plant life form, bird population characteristics, and landscape using multivariate analysis. The number of dominant exotic plant species observed in exposed areas was higher than that observed in an abandoned field and paddy field undergoing secondary succession. Additionally, the area occupied by exotic vegetation in exposed areas increased with the increase in number of vine plants and small terrestrial birds, whereas the relationship between vine and runner plants was inversely proportional. Therefore, to control exotic plants in exposed floodplains surrounding large rivers, it is necessary to remove vines and shrubs along the waterfront where small resident birds carrying plant seeds live and to maintain and manage runner plant populations. Furthermore, implementing an ecological landscape management strategy, such as afforestation through the planting of trees, may also be effective.

Enhanced performance and stability in InGaZnO NIR phototransistors with alumina-infilled quantum dot solid.

The optimized ALD infilling process for depositing Al2O3 in the vertical direction of PbS QDs enhances the photoresponsivity, relaxation rate and the air stability of PbS QDs hybrid IGZO NIR phototransistors. Infilled Al2O3, which is gradually deposited from the top of PbS QDs to the PbS/IGZO interface (1) passivates the trap sites up to the interface of PbS/IGZO without disturbing charge transfer and (2) prevents QDs deterioration caused by outside air. Therefore, an Al2O3 infilled PbS QD/IGZO hybrid phototransistor (AI-PTs) exhibited enhanced photoresponsivity from 96.4 A/W to 1.65 × 102 A/W and a relaxation time decrease from 0.52 to 0.03 s under NIR light (880 nm) compared to hybrid phototransistors without Al2O3 (RF-PTs). In addition, AI-PTs also showed improved shelf stability over 4 months compared to RF-PTs. Finally, all devices we manufactured have the potential to be manufactured in an array, and this ALD technique is a means of fabricating robust QDs/metal oxide hybrids for optoelectronic devices.

Reduction of Persistent Photoconduction with IGZO/ZnON-Tandem-Structure Visible-Near-Infrared Phototransistors.

Indium-gallium-zinc oxide- and zinc oxynitride-based heterojunction phototransistors were successfully demonstrated to control the persistent photoconduction (PPC) effect and be also responded sensitively at the range from visible to near-infrared. ZnON plays a key role in extending the spectral response at various frequencies of operation. The devices show significantly different photoresponse and photorecovery characteristics depending on the number of stacked layers of IGZO and ZnON. After negative bias and illumination stress was applied to the devices for 1 h, tandem-structure-based phototransistors recovered remarkably better than single-component IGZO devices. We suggest that the improvements to photoresponse and photorecovery result from the presence of potential wells between two IGZO layers and the energy band alignment of the tandem structure.

Association between GDF15, poverty and mortality in urban middle-aged African American and white adults.

Mortality disparities are influenced by race and poverty. There is limited information about whether poverty influences biologic markers of mortality risk. Emerging data suggests that growth differentiation factor 15 (GDF15) is associated with mortality; however, the interplay between GDF15, sociodemographic factors and mortality is not known. We sought to evaluate the interactions between GDF15 and sex, race and poverty status on mortality. Serum GDF15 was measured in 1036 African American and white middle-aged men and women above and below 125% of the Federal poverty status from the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) study. Multivariable adjusted Cox regression models were used to assess the association between log-transformed GDF15 (logGDF15) and 12-year mortality outcomes (all-cause, cardiovascular- and cancer-specific outcomes) and interactions with sex, race and poverty status. Likelihood ratio tests were used to assess significance of the interaction terms. Median GDF15 was 655.2 pg/mL (IQR = 575.1). During 12.2 years of follow-up, 331 died of which 94 cardiovascular- and 87 were cancer-specific deaths. One unit of increase in logGDF15 was associated with a hazard ratio for all-cause mortality, cardiovascular- and cancer-specific mortality of 2.26 (95% confidence interval [CI], 1.94-2.64), 2.74 (95%CI, 2.06-3.63) and 1.41 (95%CI, 1.00-2.00), respectively. There was an interaction between logGDF15 and poverty status on all-cause mortality (p<0.05). The GDF15×poverty status interaction term improved model calibration for all-cause mortality. Our study provides the first evidence that the effect of elevated GDF15 on all-cause mortality is modified by poverty status.

CRP Stimulates GDF15 Expression in Endothelial Cells through p53.

Growth differentiation factor 15 (GDF15) is a multifunctional, secreted protein that is a direct target gene of p53. GDF15 is a prospective biomarker of cardiovascular disease (CVD). C-reactive protein (CRP), like GDF15, is implicated in inflammation and an independent biomarker of CVD. However, the molecular interactions between GDF15 and CRP remain unexplored. In women, we found a significant relationship between hsCRP and GDF15 serum and mRNA levels. In vitro treatment of cultured human aortic endothelial cells (HAECs) with purified CRP or transfection of a CRP plasmid into HAECs induced GDF15 expression. Dual-luciferase reporter assays confirmed that CRP significantly increased the levels of GDF15 promoter luciferase activity, indicating that CRP induces GDF15 transcription. Chromatin immunoprecipitation (ChIP) assays confirmed that p53 was recruited to both p53 binding sites 1 and 2 in the GDF15 promoter in response to CRP. We have uncovered a linkage between CRP and GDF15, a new clue that could be important in the pathogenesis of endothelial inflammation.

Longitudinal associations of nursing staff turnover with patient outcomes in long-term care hospitals in Korea.

AIMS: To describe the characteristics of long-term care hospitals in 2010-2013 and to examine the longitudinal associations of nursing staff turnover with patient outcomes. BACKGROUND: The number of long-term care hospitals has exploded in Korea since the national long-term care insurance was launched in 2008. The care quality deviation across long-term care hospitals is large. METHODS: This was a longitudinal secondary data analysis using the Health Insurance Review and Assessment Service's data. RESULTS: From 2010 to 2013, the nursing staff turnover rate decreased. The number of patients per registered nurse increased while that per total nursing staff and skill mix decreased. All adverse patient outcomes decreased. Higher nursing staff turnover and lower RN proportions were associated with adverse patient outcomes. CONCLUSIONS: Since the launch of the long-term care insurance, total nursing staffing, turnover rate and patient outcomes have improved, while the skill mix has decreased. Systematic efforts to decrease nursing staff turnover should be implemented for better long-term care patient outcomes. IMPLICATIONS FOR NURSING MANAGEMENT: In addition to maintaining high levels of nurse staffing and skill mix, supportive work environments and competitive wages and benefits could reduce turnover, and ultimately adverse patient outcomes. Health care policy should separate nursing staffing levels for registered nurses and certified nursing assistants.

MicroRNAs Modulate Oxidative Stress in Hypertension through PARP-1 Regulation.

Oxidative stress is thought to contribute to aging and age-related diseases, such as cardiovascular and neurodegenerative diseases, and is a risk factor for systemic arterial hypertension. Previously, we reported differential mRNA and microRNA (miRNA) expression between African American (AA) and white women with hypertension. Here, we found that the poly-(ADP-ribose) polymerase 1 (PARP-1), a DNA damage sensor protein involved in DNA repair and other cellular processes, is upregulated in AA women with hypertension. To explore this mechanism, we identified two miRNAs, miR-103a-2-5p and miR-585-5p, that are differentially expressed with hypertension and were predicted to target PARP1. Through overexpression of each miRNA-downregulated PARP-1 mRNA and protein levels and using heterologous luciferase reporter assays, we demonstrate that miR-103a-2-5p and miR-585-5p regulate PARP1 through binding within the coding region. Given the important role of PARP-1 in DNA repair, we assessed whether overexpression of miR-103a-2-5p or miR-585-5p affected DNA damage and cell survival. Overexpression of these miRNAs enhanced DNA damage and decreased both cell survival and colony formation. These findings highlight the role for PARP-1 in regulating oxidative DNA damage in hypertension and identify important new miRNA regulators of PARP-1 expression. These insights may provide additional avenues to understand hypertension health disparities.

Enhancing undergraduate nursing students' global health competencies in South Korea.

OBJECTIVES: As the need for greater global health competency increases for health care professionals in South Korea, educational efforts for nursing students have begun. This study examined the effectiveness of two educational courses for freshmen and sophomores that were designed to improve students' global health competencies. DESIGN AND SAMPLE: A trend study was conducted for all undergraduate nursing students enrolled in a 4-year undergraduate nursing program in 2013 and 2014. MEASURES: We assessed students' global health competencies (1-knowledge and interests in global health and health equity, 2-global health skills, and 3-learning needs) in 2013 and 2014 and analyzed variance between mean scores by year and by course exposure, using 95% confidence intervals. RESULTS: Students who took both global health courses (sophomores in both years) reported higher global health-related knowledge and interests than did freshmen (p < .01); these scores were not sustained a year later. CONCLUSIONS: The two courses may have improved students' global health competencies. Reinforcement of knowledge in later courses may be needed to build on the global competencies.

Racial differences in microRNA and gene expression in hypertensive women.

Systemic arterial hypertension is an important cause of cardiovascular disease morbidity and mortality. African Americans are disproportionately affected by hypertension, in fact the incidence, prevalence, and severity of hypertension is highest among African American (AA) women. Previous data suggests that differential gene expression influences individual susceptibility to selected diseases and we hypothesized that this phenomena may affect health disparities in hypertension. Transcriptional profiling of peripheral blood mononuclear cells from AA or white, normotensive or hypertensive females identified thousands of mRNAs differentially-expressed by race and/or hypertension. Predominant gene expression differences were observed in AA hypertensive females compared to AA normotensives or white hypertensives. Since microRNAs play important roles in regulating gene expression, we profiled global microRNA expression and observed differentially-expressed microRNAs by race and/or hypertension. We identified novel mRNA-microRNA pairs potentially involved in hypertension-related pathways and differently-expressed, including MCL1/miR-20a-5p, APOL3/miR-4763-5p, PLD1/miR-4717-3p, and PLD1/miR-4709-3p. We validated gene expression levels via RT-qPCR and microRNA target validation was performed in primary endothelial cells. Altogether, we identified significant gene expression differences between AA and white female hypertensives and pinpointed novel mRNA-microRNA pairs differentially-expressed by hypertension and race. These differences may contribute to the known disparities in hypertension and may be potential targets for intervention.

Posttranscriptional Regulation of the Inflammatory Marker C-Reactive Protein by the RNA-Binding Protein HuR and MicroRNA 637.

C-reactive protein (CRP), an acute-phase plasma protein, is a major component of inflammatory reactions functioning as a mediator of innate immunity. It has been widely used as a validated clinical biomarker of the inflammatory state in trauma, infection, and age-associated chronic diseases, including cancer and cardiovascular disease (CVD). Despite this, the molecular mechanisms that regulate CRP expression are not well understood. Given that the CRP 3' untranslated region (UTR) is long and AU rich, we hypothesized that CRP may be regulated posttranscriptionally by RNA-binding proteins (RBPs) and by microRNAs. Here, we found that the RBP HuR bound directly to the CRP 3' UTR and affected CRP mRNA levels. Through this interaction, HuR selectively increased CRP mRNA stability and promoted CRP translation. Interestingly, treatment with the age-associated inflammatory cytokine interleukin-6 (IL-6) increased binding of HuR to CRP mRNA, and conversely, HuR was required for IL-6-mediated upregulation of CRP expression. In addition, we identified microRNA 637 (miR-637) as a microRNA that potently inhibited CRP expression in competition with HuR. Taken together, we have uncovered an important posttranscriptional mechanism that modulates the expression of the inflammatory marker CRP, which may be utilized in the development of treatments for inflammatory processes that cause CVD and age-related diseases.

N-acetyl cysteine suppresses the foam cell formation that is induced by oxidized low density lipoprotein via regulation of gene expression.

Foam cells derived from macrophages have been implicated as markers of early stage atherosclerosis development. In this study, we found that N-acetyl cysteine (NAC), a well-known inhibitor of reactive oxygen species (ROS), decreased the generation of ROS and suppressed foam cell formation in the presence of oxidized low density lipoprotein through down-regulation of cluster of differentiation 36 expression. We investigated gene expression profiles in order to determine the effects of NAC on foam cell formation using a microarray analysis. The level of apolipoprotein E, which is involved in lipid efflux, was increased and the levels of the antioxidant genes glutathione peroxidase 1 and 3 were also increased. The expression levels of the oxidative stress response and the DNA repair genes were decreased. These results were confirmed using quantitative real-time PCR. Our results indicate that oxidative stress plays an important role in foam cell formation, and that regulation of oxidation using antioxidants is a potential therapeutic method for blocking atherosclerosis development.

Inhibitory effect of Trolox on the migration and invasion of human lung and cervical cancer cells.

The antioxidant 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (Trolox) is implicated in migration and invasion of metastatic tumors. However, the molecular mechanism underlying the effect of Trolox on metastatic cancer cells is not known. We found that a non-cytotoxic dose of Trolox decreased phorbol 12-myristate 13-acetate (PMA)-induced invasion and migration of both A549 and HeLa cancer cells. We also found that Trolox suppressed both the expression and the proteolytic activity of matrix metalloproteinase-9 (MMP-9), and that the promoter activity of PMA-induced MMP-9 was inhibited by Trolox. Our results show that Trolox inhibits the transcriptional activity of MMP-9 by suppression of NF-κB transactivation. These results indicate that Trolox inhibits NF-κB-mediated MMP-9 expression, leading to the suppression of migration and invasion in lung and cervical cancer cells. Trolox is a potential agent for clinical use in preventing the invasion and metastasis of human malignant lung and cervical cancers.

The role of 14-3-3ß in transcriptional activation of estrogen receptor α and its involvement in proliferation of breast cancer cells.

The estrogen receptor (ER) functions as a transcription factor that mediates the effects of estrogen. ERα, which plays a crucial role in the development and progression of breast cancer, is activated by estrogen binding, leading to receptor phosphorylation, dimerization, and recruitment of co-activators and chaperons to the estrogen-bound receptor complex. The 14-3-3 proteins bind to target proteins via phosphorylation and influence many cellular events by altering their subcellular localization or acting as a chaperone. However, regulation of ERα expression and transactivation by the 14-3-3 proteins has not been reported. We demonstrate that 14-3-3ß functions as a positive regulator of ERα through a direct protein-protein interaction in an estrogen-dependent manner. Ectopic expression of 14-3-3ß stimulated ERα-mediated transcriptional activity in MCF-7 breast cancer cells. Enhanced ERα transcriptional activity due to 14-3-3ß increased the expressions of the endogenous ERα target genes, leading to proliferation of breast cancer cells. We suggest that 14-3-3ß has oncogenic potential in breast cancer via binding to ERα and activation of the transcriptional activity of ERα.

Celastrol inhibits breast cancer cell invasion via suppression of NF-ĸB-mediated matrix metalloproteinase-9 expression.

BACKGROUND/AIMS: Metastasis is one of the main causes of death for patients with malignant tumors. Induction of matrix metalloproteinase (MMP)-9 is particularly important for the invasiveness of various cancer cells. Celastrol, a triterpenoid isolated from the traditional Chinese medicine, is known to inhibit the proliferation of a variety of tumor cells, including leukemia, glioma, prostate and breast cancer cells. In this study, we investigated the effect of celastrol on the migration and invasion of human breast carcinoma cells. RESULTS: We observed that celastrol suppressed phorbol 12-myristate 13-acetate (PMA)-induced invasion and migration of MCF-7 cells. We also found that celastrol inhibited PMA-induced MMP-9 expression at both the mRNA and the protein levels, and the proteolytic activity of MMP-9 in MCF-7 cells. Our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppression of the DNA binding activity of NF-κB in the MMP-9 promoter, and inhibited degradation of IκBα and nuclear translocation of NF-κB. CONCLUSION: These results indicate that celastrol inhibits NF-κB-mediated MMP-9 expression, resulting in suppression of breast cancer cell invasion and migration that is induced by PMA. Celastrol is a potential agent for clinical use in preventing the invasion and metastasis of human malignant breast tumors.

The role of calpains in ligand-induced degradation of the glucocorticoid receptor.

The glucocorticoid receptor (GR) is a ligand-activated transcription factor that mediates the effects of glucocorticoids in diverse cellular processes, including homeostasis, stress response, and inflammation. Glucocorticoids induce down-regulation of GR at both the mRNA and protein levels, causing reduced hormone responsiveness in response to long-term treatment with glucocorticoid. However, the mechanism involved in this process is still obscure. In this study, we examined whether calpain, a calcium-activated cysteine protease, is involved in ligand-stimulated degradation of GR. In COS-7 cells expressing the human GR, treatment with a calpain inhibitor abolished glucocorticoid-induced down-regulation of GR in a dose dependent manner. The protein level of endogenous GR was also elevated by inhibition of the calpain activity in HeLa cells treated with glucocorticoid. Furthermore, glucocorticoid-induced transcriptional activation of GR was enhanced in cells treated with a calpain inhibitor. These results indicate that calpain is involved in ligand-dependent degradation of GR, thus causing reduced hormone responsiveness.