3,042 research outputs found
-positivity and Schmidt number under orthogonal group symmetries
In this paper, we study -positivity and Schmidt number under standard
orthogonal group symmetries. The Schmidt number is a widely used measure of
quantum entanglement in quantum information theory. First of all, we exhibit a
complete characterization of all -positive orthogonally covariant maps. This
generalizes the earlier results in [Tom85]. Then, we optimize some averaging
techniques to establish duality relations between orthogonally covariant maps
and orthogonally invariant operators. This new framework enables us to
effectively compute the Schmidt numbers of all orthogonally invariant quantum
states
Malignancies in Korean Patients with Inflammatory Myopathy
The aim of this study was to assess the prevalence and the common type of malignancies in Korean patients with polymyositis (PM) and dermatomyositis (DM) and to evaluate the differences of clinical and laboratory findings between patients with malignancy and those without malignancy. Forty-one Korean patients, who were diagnosed as PM or DM, were enrolled in this study. They fulfilled the Bohan and Peter's criteria for a definite diagnosis of PM and DM. Patients with PM were 25 and those with DM were 16. Eleven out of 41 patients (26.8%) had malignancies. The malignancy was diagnosed simultaneously or later in 81.8% of patients with inflammatory myopathy (IM). The breast cancer was the most common malignancy. In this study, forty three years old as a screening age for malignancy had 88.9% sensitivity and 50.2% specificity. The serum levels of creatine kinase (CK) were significantly lower in patients with malignancy than those without malignancy
Biosynthesis of phenylpropanoids and their protective effect against heavy metals in nitrogen-fixing black locust (Robinia pseudoacacia)
Purpose: To examine the effect of various heavy metals (HMs) on phenylpropanoid pathway compounds in Robinia pseudoacacia.Methods: A series of pot culture experiments were performed to understand how the metabolic profile of phenylpropanoid compounds were affected by various HMs, such as redox-active HMs (AgNO3 and CuCl2), and non-redox-active HMs (HgCl2). Phenylpropanoid compound level was evaluated by high performance liquid chromatography.Results: The total phenylpropanoid level in leaves increased significantly in all the treated groups when compared to that in the untreated group (p < 0.05). However, a significant effect on the total phenylpropanoid levels was only found for redox-active HMs (p < 0.05), whereas non-redox-active HMs showed less accumulation. Chlorogenic acid and rutin were the two major phenylpropanoid compounds found after the plants were subjected to redox and non-redox-active HMs stress. However, when compared to these two compounds, the levels of catechin hydrate, epicatechin, p-coumaric acid, kaempferol, and quercetin were lower. Caffeic acid level was significantly decreased in both redox and non-redox-active HMs when compared to that in the control (p < 0.05). In addition, trans-cinnamic acid accumulation was altered based on the types and concentration of HMs.Conclusion: Phenylpropanoid metabolic pathway participated in the HM tolerance process for the protection of R. pseudoacacia from oxidative damage caused by HMs, thus allowing the species to grow in highly HMs-contaminated areas.
Keywords: Heavy metals, Non-redox-active metals, Phenylpropanoid compounds, Redox-active metals, Robinia pseudoacaci
Effects of a radiation dose reduction strategy for computed tomography in severely injured trauma patients in the emergency department: an observational study
<p>Abstract</p> <p>Background</p> <p>Severely injured trauma patients are exposed to clinically significant radiation doses from computed tomography (CT) imaging in the emergency department. Moreover, this radiation exposure is associated with an increased risk of cancer. The purpose of this study was to determine some effects of a radiation dose reduction strategy for CT in severely injured trauma patients in the emergency department.</p> <p>Methods</p> <p>We implemented the radiation dose reduction strategy in May 2009. A prospective observational study design was used to collect data from patients who met the inclusion criteria during this one year study (intervention group) from May 2009 to April 2010. The prospective data were compared with data collected retrospectively for one year prior to the implementation of the radiation dose reduction strategy (control group). By comparison of the cumulative effective dose and the number of CT examinations in the two groups, we evaluated effects of a radiation dose reduction strategy. All the patients met the institutional adult trauma team activation criteria. The radiation doses calculated by the CT scanner were converted to effective doses by multiplication by a conversion coefficient.</p> <p>Results</p> <p>A total of 118 patients were included in this study. Among them, 33 were admitted before May 2009 (control group), and 85 were admitted after May 2009 (intervention group). There were no significant differences between the two groups regarding baseline characteristics, such as injury severity and mortality. Additionally, there was no difference between the two groups in the mean number of total CT examinations per patient (4.8 vs. 4.5, respectively; p = 0.227). However, the mean effective dose of the total CT examinations per patient significantly decreased from 78.71 mSv to 29.50 mSv (p < 0.001).</p> <p>Conclusions</p> <p>The radiation dose reduction strategy for CT in severely injured trauma patients effectively decreased the cumulative effective dose of the total CT examinations in the emergency department. But not effectively decreased the number of CT examinations.</p
Increased interleukin-17 production via a phosphoinositide 3-kinase/Akt and nuclear factor κB-dependent pathway in patients with rheumatoid arthritis
Inflammatory mediators have been recognized as being important in the pathogenesis of rheumatoid arthritis (RA). Interleukin (IL)-17 is an important regulator of immune and inflammatory responses, including the induction of proinflammatory cytokines and osteoclastic bone resorption. Evidence for the expression and proinflammatory activity of IL-17 has been demonstrated in RA synovium and in animal models of RA. Although some cytokines (IL-15 and IL-23) have been reported to regulate IL-17 production, the intracellular signaling pathways that regulate IL-17 production remain unknown. In the present study, we investigated the role of the phosphoinositide 3-kinase (PI3K)/Akt pathway in the regulation of IL-17 production in RA. Peripheral blood mononuclear cells (PBMC) from patients with RA (n = 24) were separated, then stimulated with various agents including anti-CD3, anti-CD28, phytohemagglutinin (PHA) and several inflammatory cytokines and chemokines. IL-17 levels were determined by sandwich enzyme-linked immunosorbent assay and reverse transcription–polymerase chain reaction. The production of IL-17 was significantly increased in cells treated with anti-CD3 antibody with or without anti-CD28 and PHA (P < 0.05). Among tested cytokines and chemokines, IL-15, monocyte chemoattractant protein-1 and IL-6 upregulated IL-17 production (P < 0.05), whereas tumor necrosis factor-α, IL-1β, IL-18 or transforming growth factor-β did not. IL-17 was also detected in the PBMC of patients with osteoarthritis, but their expression levels were much lower than those of RA PBMC. Anti-CD3 antibody activated the PI3K/Akt pathway; activation of this pathway resulted in a pronounced augmentation of nuclear factor κB (NF-κB) DNA-binding activity. IL-17 production by activated RA PBMC is completely or partly blocked in the presence of the NF-κB inhibitor pyrrolidine dithiocarbamate and the PI3K/Akt inhibitor wortmannin and LY294002, respectively. However, inhibition of activator protein-1 and extracellular signal-regulated kinase 1/2 did not affect IL-17 production. These results suggest that signal transduction pathways dependent on PI3K/Akt and NF-κB are involved in the overproduction of the key inflammatory cytokine IL-17 in RA
Development of a Conjunctivitis Outpatient Rate Prediction Model Incorporating Ambient Ozone and Meteorological Factors in South Korea
Ozone (O3) is a commonly known air pollutant that causes adverse health effects. This study developed a multi-level prediction model for conjunctivitis in outpatients due to exposure to O3 by using 3 years of ambient O3 data, meteorological data, and hospital data in Seoul, South Korea. We confirmed that the rate of conjunctivitis in outpatients (conjunctivitis outpatient rate) was highly correlated with O3 (R2 = 0.49), temperature (R2 = 0.72), and relative humidity (R2 = 0.29). A multi-level regression model for the conjunctivitis outpatient rate was well-developed, on the basis of sex and age, by adding statistical factors. This model will contribute to the prediction of conjunctivitis outpatient rate for each sex and age, using O3 and meteorological data
Signal Transduction Mechanisms Underlying Group I mGluR-mediated Increase in Frequency and Amplitude of Spontaneous EPSCs in the Spinal Trigeminal Subnucleus Oralis of the Rat
Group I mGluRs (mGluR1 and 5) pre- and/or postsynaptically regulate synaptic transmission at glutamatergic synapses. By recording spontaneous EPSCs (sEPSCs) in the spinal trigeminal subnucleus oralis (Vo), we here investigated the regulation of glutamatergic transmission through the activation of group I mGluRs. Bath-applied DHPG (10 μM/5 min), activating the group I mGluRs, increased sEPSCs both in frequency and amplitude; particularly, the increased amplitude was long-lasting. The DHPG-induced increases of sEPSC frequency and amplitude were not NMDA receptor-dependent. The DHPG-induced increase in the frequency of sEPSCs, the presynaptic effect being further confirmed by the DHPG effect on paired-pulse ratio of trigeminal tract-evoked EPSCs, an index of presynaptic modulation, was significantly but partially reduced by blockades of voltage-dependent sodium channel, mGluR1 or mGluR5. Interestingly, PKC inhibition markedly enhanced the DHPG-induced increase of sEPSC frequency, which was mainly accomplished through mGluR1, indicating an inhibitory role of PKC. In contrast, the DHPG-induced increase of sEPSC amplitude was not affected by mGluR1 or mGluR5 antagonists although the long-lasting property of the increase was disappeared; however, the increase was completely inhibited by blocking both mGluR1 and mGluR5. Further study of signal transduction mechanisms revealed that PLC and CaMKII mediated the increases of sEPSC in both frequency and amplitude by DHPG, while IP3 receptor, NO and ERK only that of amplitude during DHPG application. Altogether, these results indicate that the activation of group I mGluRs and their signal transduction pathways differentially regulate glutamate release and synaptic responses in Vo, thereby contributing to the processing of somatosensory signals from orofacial region
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