Intercultural New Media Studies: The Next Frontier in intercultural Communication

New media (ICT\u27s) are transforming communication across cultures. Despite this revolution in cross cultural contact, communication researchers have largely ignored the impact of new media on intercultural communication. This groundbreaking article defines the parameters of a new field of inquiry called Intercultural New Media Studies (INMS), which explores the intersection between ICT\u27s and intercultural communication. Composed of two research areas—(1) new media and intercultural communication theory and (2) culture and new media—INMS investigates new digital theories of intercultural contact as well as refines and expands twentieth-century intercultural communication theories, examining their salience in a digital world. INMS promises to increase our understanding of intercultural communication in a new media age and is the next frontier in intercultural communication

Severe cutaneous reactions to drugs in the setting of a general hospital

Abstract: BACKGROUND: Cutaneous drug reactions are frequently found. Assessing the clinical and epidemiological profile of severe forms is extremely relevant for their better recognition and management. Few studies have assessed the severe forms of cutaneous drug reactions in patients hospitalized in our setting. OBJECTIVES: To assess the clinical and epidemiological aspects of severe cutaneous adverse reactions to drugs in a tertiary hospital in Porto Alegre, Brazil. METHODS: All cases of severe cutaneous adverse reactions to drugs in patients hospitalized from January/2005 to December/2010 were retrospectively analyzed for clinical and epidemiological variables. Cases of Stevens- Johnson Syndrome, Toxic Epidermal Necrolysis, drug hypersensitivity syndrome or Drug Reaction with Eosinophilia and Systemic Symptoms and acute generalized exanthematous pustulosis were included. RESULTS: An occurrence rate of 1 serious reaction for every 3,048 inpatients was found (total of 173,767 inpatients admitted in the period). Drug Reaction with Eosinophilia and Systemic Symptoms was the most frequent presentation. The drugs most frequently involved were anticonvulsants (40.4%), antibiotics (26.3%), and analgesics/anti-inflammatory drugs (10.5%). Thirty seven patients (64.9%) were admitted to hospital because of the cutaneous drug reaction. Ten patients (17.5%) died and in most of those (60%), the drug causing the reaction could not be determined. CONCLUSIONS: The frequency of severe cutaneous adverse reactions to drugs in our setting is significant. Drug Reaction with Eosinophilia and Systemic Symptoms seems to be the most frequent presentation of severe cutaneous drug reactions. Most patients developed cutaneous drug reactions outside the hospital. Mortality rates were higher for Toxic Epidermal Necrolysis and this presentation significantly affected older people. Not knowing the drug causing the reaction was related to mortality

Leucine-Rich α-2-Glycoprotein 1 Suppresses Endothelial Cell Activation Through ADAM10-Mediated Shedding of TNF-α Receptor

Elevated serum concentrations of leucine-rich α-2-glycoprotein (LRG1) have been reported in patients with inflammatory, autoimmune, and cardiovascular diseases. This study aims to investigate the role of LRG1 in endothelial activation. LRG1 in endothelial cells (ECs) of arteries and serum of patients with critical limb ischemia (CLI) was assessed by immunohistochemistry and ELISA, respectively. LRG1 expression in sheared and tumor necrosis factor-α (TNF-α)-treated ECs was analyzed. The mechanistic role of LRG1 in endothelial activation was studied in vitro. Plasma of 37-week-old Lrg1–/– mice was used to investigate causality between LRG1 and tumor necrosis factor receptor 1 (TNFR1) shedding. LRG1 was highly expressed in ECs of stenotic but not normal arteries. LRG1 concentrations in serum of patients with CLI were elevated compared to healthy controls. LRG1 expression was shear dependent. It could be induced by TNF-α, and the induction of its expression was mediated by NF-κB activation. LRG1 inhibited TNF-α-induced activation of NF-κB signaling, expression of VCAM-1 and ICAM-1, and monocyte capture, firm adhesion, and transendothelial migration. Mechanistically, LRG1 exerted its function by causing the shedding of TNFR1 via the ALK5-SMAD2 pathway and the subsequent activation of ADAM10. Consistent with this mechanism, LRG1 and sTNFR1 concentrations were correlated in the serum of CLI patients. Causality between LRG1 and TNFR1 shedding was established by showing that Lrg1–/– mice had lower plasma sTNFR1 concentrations than wild type mice. Our results demonstrate a novel role for LRG1 in endothelial activation and its potential therapeutic role in inflammatory diseases should be investigated further

Search for rare quark-annihilation decays, B --> Ds(*) Phi

We report on searches for B- --> Ds- Phi and B- --> Ds*- Phi. In the context of the Standard Model, these decays are expected to be highly suppressed since they proceed through annihilation of the b and u-bar quarks in the B- meson. Our results are based on 234 million Upsilon(4S) --> B Bbar decays collected with the BABAR detector at SLAC. We find no evidence for these decays, and we set Bayesian 90% confidence level upper limits on the branching fractions BF(B- --> Ds- Phi) Ds*- Phi)<1.2x10^(-5). These results are consistent with Standard Model expectations.Comment: 8 pages, 3 postscript figues, submitted to Phys. Rev. D (Rapid Communications

Glyoxalase-I Is a Novel Prognosis Factor Associated with Gastric Cancer Progression

Glyoxalase I (GLO1), a methylglyoxal detoxification enzyme, is implicated in the progression of human malignancies. The role of GLO1 in gastric cancer development or progression is currently unclear. The expression of GLO1 was determined in primary gastric cancer specimens using quantitative polymerase chain reaction, immunohistochemistry (IHC), and western blotting analyses. GLO1 expression was higher in gastric cancer tissues, compared with that in adjacent noncancerous tissues. Elevated expression of GLO1 was significantly associated with gastric wall invasion, lymph node metastasis, and pathological stage, suggesting a novel role of GLO1 in gastric cancer development and progression. The 5-year survival rate of the lower GLO1 expression groups was significantly greater than that of the higher expression groups (log rank P = 0.0373) in IHC experiments. Over-expression of GLO1 in gastric cancer cell lines increases cell proliferation, migration and invasiveness. Conversely, down-regulation of GLO1 with shRNA led to a marked reduction in the migration and invasion abilities. Our data strongly suggest that high expression of GLO1 in gastric cancer enhances the metastasis ability of tumor cells in vitro and in vivo, and support its efficacy as a potential marker for the detection and prognosis of gastric cancer

Palladium nanoparticles supported on fluorine-doped tin oxide as an efficient heterogeneous catalyst for Suzuki coupling and 4-nitrophenol reduction

Immobilization of palladium nanoparticles onto the fluorine-doped tin oxide (FTO) as support Pd/FTO, resulted in a highly active heterogeneous catalyst for Suzuki-Miyaura cross-coupling reactions and 4-nitrophenol reduction. The Pd/FTO catalyst has been synthesized by immobilization of palladium nanoparticles onto FTO via a simple impregnation method. ICP-MS analysis confirmed that there is 0.11 mmol/g of palladium was loaded successfully on FTO support. The crystallinity, morphologies, compositions and surface properties of Pd/FTO were fully characterized by various techniques. It was further examined for its catalytic activity and robustness in Suzuki coupling reaction with different aryl halides and solvents. The yields obtained from Suzuki coupling reactions were basically over 80%. The prepared catalyst was also tested on mild reaction such as reduction of 4-nitrophenol (4-NP) to 4-aminophenol (4-AP). Pd/FTO catalyst exhibited high catalytic activity towards 4-NP reduction with a rate constant of 1.776 min(-1) and turnover frequency (TOF) value of 29.1 hr(-1). The findings revealed that Pd/FTO also maintained its high stability for five consecutive runs in Suzuki reactions and 4-NP reductions. The catalyst showed excellent catalytic activities by using a small amount of Pd/FTO for the Suzuki coupling reaction and 4-NP reduction

Loss of C2orf69 defines a fatal autoinflammatory syndrome in humans and zebrafish that evokes a glycogen-storage-associated mitochondriopathy

Summary Human C2orf69 is an evolutionarily conserved gene whose function is unknown. Here, we report eight unrelated families from which 20 children presented with a fatal syndrome consisting of severe autoinflammation and progredient leukoencephalopathy with recurrent seizures; 12 of these subjects, whose DNA was available, segregated homozygous loss-of-function C2orf69 variants. C2ORF69 bears homology to esterase enzymes, and orthologs can be found in most eukaryotic genomes, including that of unicellular phytoplankton. We found that endogenous C2ORF69 (1) is loosely bound to mitochondria, (2) affects mitochondrial membrane potential and oxidative respiration in cultured neurons, and (3) controls the levels of the glycogen branching enzyme 1 (GBE1) consistent with a glycogen-storage-associated mitochondriopathy. We show that CRISPR-Cas9-mediated inactivation of zebrafish C2orf69 results in lethality by 8 months of age due to spontaneous epileptic seizures, which is preceded by persistent brain inflammation. Collectively, our results delineate an autoinflammatory Mendelian disorder of C2orf69 deficiency that disrupts the development/homeostasis of the immune and central nervous systems

Activation of an NLRP3 Inflammasome Restricts Mycobacterium kansasii Infection

Mycobacterium kansasii has emerged as an important nontuberculous mycobacterium pathogen, whose incidence and prevalence have been increasing in the last decade. M. kansasii can cause pulmonary tuberculosis clinically and radiographically indistinguishable from that caused by Mycobacterium tuberculosis infection. Unlike the widely-studied M. tuberculosis, little is known about the innate immune response against M. kansasii infection. Although inflammasome activation plays an important role in host defense against bacterial infection, its role against atypical mycobacteria remains poorly understood. In this report, the role of inflammasome activity in THP-1 macrophages against M. kansasii infection was studied. Results indicated that viable, but not heat-killed, M. kansasii induced caspase-1-dependent IL-1β secretion in macrophages. The underlying mechanism was found to be through activation of an inflammasome containing the NLR (Nod-like receptor) family member NLRP3 and the adaptor protein ASC (apoptosis-associated speck-like protein containing a CARD). Further, potassium efflux, lysosomal acidification, ROS production and cathepsin B release played a role in M. kansasii-induced inflammasome activation. Finally, the secreted IL-1β derived from caspase-1 activation was shown to restrict intracellular M. kansasii. These findings demonstrate a biological role for the NLRP3 inflammasome in host defense against M. kansasii

A Genome-Wide Characterization of MicroRNA Genes in Maize

MicroRNAs (miRNAs) are small, non-coding RNAs that play essential roles in plant growth, development, and stress response. We conducted a genome-wide survey of maize miRNA genes, characterizing their structure, expression, and evolution. Computational approaches based on homology and secondary structure modeling identified 150 high-confidence genes within 26 miRNA families. For 25 families, expression was verified by deep-sequencing of small RNA libraries that were prepared from an assortment of maize tissues. PCR–RACE amplification of 68 miRNA transcript precursors, representing 18 families conserved across several plant species, showed that splice variation and the use of alternative transcriptional start and stop sites is common within this class of genes. Comparison of sequence variation data from diverse maize inbred lines versus teosinte accessions suggest that the mature miRNAs are under strong purifying selection while the flanking sequences evolve equivalently to other genes. Since maize is derived from an ancient tetraploid, the effect of whole-genome duplication on miRNA evolution was examined. We found that, like protein-coding genes, duplicated miRNA genes underwent extensive gene-loss, with ∼35% of ancestral sites retained as duplicate homoeologous miRNA genes. This number is higher than that observed with protein-coding genes. A search for putative miRNA targets indicated bias towards genes in regulatory and metabolic pathways. As maize is one of the principal models for plant growth and development, this study will serve as a foundation for future research into the functional roles of miRNA genes