Optimization of magnetic flux density for fast MREIT conductivity imaging using multi-echo interleaved partial fourier acquisitions

BACKGROUND: Magnetic resonance electrical impedance tomography (MREIT) has been introduced as a non-invasive method for visualizing the internal conductivity and/or current density of an electrically conductive object by externally injected currents. The injected current through a pair of surface electrodes induces a magnetic flux density distribution inside the imaging object, which results in additional magnetic flux density. To measure the magnetic flux density signal in MREIT, the phase difference approach in an interleaved encoding scheme cancels out the systematic artifacts accumulated in phase signals and also reduces the random noise effect by doubling the measured magnetic flux density signal. For practical applications of in vivo MREIT, it is essential to reduce the scan duration maintaining spatial-resolution and sufficient contrast. In this paper, we optimize the magnetic flux density by using a fast gradient multi-echo MR pulse sequence. To recover the one component of magnetic flux density B(z), we use a coupled partial Fourier acquisitions in the interleaved sense. METHODS: To prove the proposed algorithm, we performed numerical simulations using a two-dimensional finite-element model. For a real experiment, we designed a phantom filled with a calibrated saline solution and located a rubber balloon inside the phantom. The rubber balloon was inflated by injecting the same saline solution during the MREIT imaging. We used the multi-echo fast low angle shot (FLASH) MR pulse sequence for MRI scan, which allows the reduction of measuring time without a substantial loss in image quality. RESULTS: Under the assumption of a priori phase artifact map from a reference scan, we rigorously investigated the convergence ratio of the proposed method, which was closely related with the number of measured phase encode set and the frequency range of the background field inhomogeneity. In the phantom experiment with a partial Fourier acquisition, the total scan time was less than 6 seconds to measure the magnetic flux density B(z) data with 128×128 spacial matrix size, where it required 10.24 seconds to fill the complete k-space region. CONCLUSION: Numerical simulation and experimental results demonstrated that the proposed method reduces the scanning time and provides the recovered B(z) data comparable to what we obtained by measuring complete k-space data

The Distribution Strategy Of A Representative Fair Trade Organization In Korea: The Case Of Beautiful Coffee

This case study analyzes the distribution strategy of Beautiful Coffee, a leading fair trade organization in Korea. Because of their focus on matters of public interest, fair trade organizations often face financial difficulties, and such difficulties can limit their growth and force them to pursue differentiated distribution strategies. The results indicate that Beautiful Coffee can serve as a good role model for fair trade organizations and have important practical implications for firms pursuing sustainable growth as a social enterprise

Ca2+ Signaling Triggered by Shear-Autocrine P2X Receptor Pathway in Rat Atrial Myocytes

Background/Aims: The atrium is exposed to high shear stress during heart failure and valvular diseases. We aimed to understand atrial shear-induced Ca2+ signaling and its underlying mechanisms. Methods: Pressurized micro-flow was applied to single rat atrial myocytes, and Ca2+ signal, membrane potential, and ATP release were assessed using confocal imaging, patch clamp technique, and luciferin-luciferase assay, respectively. Results: Shear stress (∼16 dyn/cm2) induced global Ca2+ waves (∼0.1 events/s) from the periphery to the center of cells in a transverse direction (“T-wave”; ∼145 μm/s). Pharmacological interventions and simultaneous recording of membrane potential and Ca2+ demonstrated that shear-induced T-waves resulted from action potential (AP)-triggered Ca2+ release from the sarcoplasmic reticulum. T-waves were not sensitive to inhibitors of known shear signaling mechanisms except connexin hemichannels and ATP release. Shear stress caused ATP release from these myocytes (∼1.1x10-17 moles/unit membrane, µm2); ATP release was increased by enhancement of connexin hemichannels and suppressed by inhibition of the hemichannels, but not affected by inhibitors of other ATP release pathways. Blockade of P2X receptor, but not pannexin or the Na+-Ca2+ exchanger, eliminated shear-induced T-wave initiation. Conclusion: Our data suggest that shear stress triggers APs and concomitant Ca2+ signaling via activation of P2X receptors by connexin hemichannel-mediated ATP release in atrial myocytes

MUC1 expressing tumor growth was retarded after human mucin 1 (MUC1) plasmid DNA immunization

Introduction: Naked DNA is one of the attractive tools for vaccination studies. We studied naked DNA vaccination against the human tumor antigen, mucin, which is encoded by the MUC1 gene. Methods: We constructed the pcDNA3.0-MUC1 (pcDNA-MUC1) plasmid expressing an underglycosylated MUC1 protein. BALB/c mice were immunized intradermally thrice at 2-weeks intervals with pcDNA-MUC1. Two weeks after the last immunization, tumor challenge experiments were performed using either the CT26 or TA3HA tumor cell lines, both of which transduce human MUC1. Results: Immune cell population monitoring from pcDNA-MUC1-immunized animals indicated that immune cell activation was induced by MUC1-specific immunization. Using intracellular fluorescence activated cell sorting and enzyme-linked immunosorbent spot assay, we reported that interferon-γ secreting CD8+ T cells were mainly involved in MUC1-specific immunization. In all mice immunized with MUC1 DNA, tumor growth inhibition was observed, whereas control mice developed tumors (p < 0.001). Conclusion: Our results suggest that intradermal immunization with MUC1 DNA induces MUC1-specific CD8+ T cell infiltration into tumors, elicits tumor-specific Th1-type immune response, and inhibits tumor growth

PD-1 deficiency protects experimental colitis via alteration of gut microbiota

Programmed cell death-1 (PD-1) is a coinhibitory molecule and plays a pivotal role in immune regulation. Here, we demonstrate a role for PD-1 in pathogenesis of inflammatory bowel disease (IBD). Wild-type (WT) mice had severe wasting disease during experimentally induced colitis, while mice deficient for PD-1 (PD-1(-/-)) did not develop colon inflammation. Interestingly, PD-1(-/-) mice cohoused with WT mice became susceptible to colitis, suggesting that resistance of PD-1(-/-) mice to colitis is dependent on their gut microbiota. 16S rRNA gene-pyrosequencing analysis showed that PD-1(-/-) mice had altered composition of gut microbiota with significant reduction in Rikenellaceae family. These altered colon bacteria of PD-1(-/-) mice induced less amount of inflammatory mediators from colon epithelial cells, including interleukin (IL)-6, and inflammatory chemokines. Taken together, our study indicates that PD-1 expression is involved in the resistance to experimental colitis through altered bacterial communities of colon.112Ysciescopuskc

Depression and suicide risk prediction models using blood-derived multi-omics data

More than 300 million people worldwide experience depression; annually, ~800,000 people die by suicide. Unfortunately, conventional interview-based diagnosis is insufficient to accurately predict a psychiatric status. We developed machine learning models to predict depression and suicide risk using blood methylome and transcriptome data from 56 suicide attempters (SAs), 39 patients with major depressive disorder (MDD), and 87 healthy controls. Our random forest classifiers showed accuracies of 92.6% in distinguishing SAs from MDD patients, 87.3% in distinguishing MDD patients from controls, and 86.7% in distinguishing SAs from controls. We also developed regression models for predicting psychiatric scales with R2 values of 0.961 and 0.943 for Hamilton Rating Scale for Depression???17 and Scale for Suicide Ideation, respectively. Multi-omics data were used to construct psychiatric status prediction models for improved mental health treatment

Trib2 regulates the pluripotency of embryonic stem cells and enhances reprogramming efficiency

Embryonic stem (ES) cells are pluripotent cells characterized by self-renewability and differentiation potential. Induced pluripotent stem (iPS) cells are ES cell-equivalent cells derived from somatic cells by the introduction of core reprogramming factors. ES and iPS cells are important sources for understanding basic biology and for generating therapeutic cells for clinical applications. Tribbles homolog 2 (Trib2) functions as a scaffold in signaling pathways. However, the relevance of Trib2 to the pluripotency of ES and iPS cells is unknown. In the present study, we elucidated the importance of Trib2 in maintaining pluripotency in mouse ES cells and in generating iPS cells from somatic cells through the reprogramming process. Trib2 expression decreased as ES cells differentiated, and Trib2 knockdown in ES cells changed their colony morphology while reducing the activity of alkaline phosphatase and the expression of the pluripotency marker genes Oct4, Sox2, Nanog and Klf4. Trib2 directly interacted with Oct4 and elevated Oct4 promoter activity. During the generation of iPS cells, Trib2 knockdown decreased the reprogramming efficiency of mouse embryonic fibroblasts, whereas Trib2 overexpression significantly increased their reprogramming efficiency. In summary, our results suggest that Trib2 is important for maintaining self-renewal in ES cells and for pluripotency induction during the reprogramming process