128 research outputs found
Compressed zero-divisor graphs of noncommutative rings
We extend the notion of the compressed zero-divisor graph to
noncommutative rings in a way that still induces a product preserving functor
from the category of finite unital rings to the category of
directed graphs. For a finite field , we investigate the properties of
, the graph of the matrix ring over , and give a purely
graph-theoretic characterization of this graph when . For
we prove that every graph automorphism of is induced by a
ring automorphism of . We also show that for finite unital rings
and , where is semisimple and has no homomorphic image isomorphic to a
field, if , then . In particular,
this holds if with .Comment: 30 page
Categorial properties of compressed zero-divisor graphs of finite commutative rings
We define a compressed zero-divisor graph of a finite
commutative unital ring , where the compression is performed by means of the
associatedness relation. We prove that this is the best possible compression
which induces a functor , and that this functor preserves categorial
products (in both directions). We use the structure of to
characterize important classes of finite commutative unital rings, such as
local rings and principal ideal rings.Comment: 14 page
The total zero-divisor graph of commutative rings
In this paper we initiate the study of the total zero-divisor graphs over
commutative rings with unity. These graphs are constructed by both relations
that arise from the zero-divisor graph and from the total graph of a ring. We
characterize Artinian rings with the connected total zero-divisor graphs and
give their diameters. Moreover, we compute major characteristics of the total
zero-divisor graphs of the ring of integers modulo and
prove that the total zero-divisor graphs of and
are isomorphic if and only if
Novel selenium and/or copper substituted hydroxyapatite-gelatin-chitosan-eggshell membrane nanocomposite scaffolds for bone tissue engineering applications
Limitations with the majority of bone therapeutic treatments include low availability, ethical constraints and low biological compatibility. Although a number of choice materials have been exploited successfully, there has always been scope for improvement as well as development of the next-generation of materials. Herein, scaffolds - developed from gelatin, chitosan and eggshell membranes - were crosslinked using tannic acid, and further infused with selenium and/or copper substituted hydroxyapatite nanoparticles to generate a novel nanocomposite substrate. FESEM images of the nanocomposite scaffolds revealed the presence of interconnected pores, mostly spread over the whole surface of the scaffold, alongside XRD and FTIR profiling that detailed the formation of hydroxyapatite as a sole phase. Moreover, physical characterisation of the nanocomposite confirmed that the hydroxyapatite particulates and the eggshell membrane fibres were uniformly distributed and contributed to the surface roughness of the scaffold. Biocompatibility and cytotoxicity of the novel constructs were assessed using the mouse-derived osteoblastic cell line, MC3T3-E1, and standard cell culture assays. Metabolic activity assessment (i.e. MTS assay), LDH-release profiles and Live/Dead staining demonstrated good cell adhesion, viability, and proliferation rates. Accordingly, this work summarises the successful development of a novel construct which may be exploited as a clinical/therapeutic treatment for bone repair as well as a possible translational application as a novel biomaterial for the drug development pipeline
A method for improving the efficiency of DNA extraction from clotted blood samples
Funding information: This study was supported by a grant from the Research Council of the Mashhad University of Medical Sciences (Grant No: 931680). The authors would like to thank Dr. Hossein Eshghi at Department of Chemistry, Faculty of Science, the Ferdowsi University of Mashhad for his assistance in the experiment and Mohammad Sadegh Khorami who contributed to this study. We are also particularly grateful to the Research Council of the Mashhad University of Medical Sciences (MUMS) for the financial support of this studyPeer reviewedPublisher PD
A National PointâofâCare Ultrasound Competition for Medical Students
Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146850/1/jum14670_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146850/2/jum14670.pd
Antimicrobial resistance among migrants in Europe: a systematic review and meta-analysis
BACKGROUND: Rates of antimicrobial resistance (AMR) are rising globally and there is concern that increased migration is contributing to the burden of antibiotic resistance in Europe. However, the effect of migration on the burden of AMR in Europe has not yet been comprehensively examined. Therefore, we did a systematic review and meta-analysis to identify and synthesise data for AMR carriage or infection in migrants to Europe to examine differences in patterns of AMR across migrant groups and in different settings. METHODS: For this systematic review and meta-analysis, we searched MEDLINE, Embase, PubMed, and Scopus with no language restrictions from Jan 1, 2000, to Jan 18, 2017, for primary data from observational studies reporting antibacterial resistance in common bacterial pathogens among migrants to 21 European Union-15 and European Economic Area countries. To be eligible for inclusion, studies had to report data on carriage or infection with laboratory-confirmed antibiotic-resistant organisms in migrant populations. We extracted data from eligible studies and assessed quality using piloted, standardised forms. We did not examine drug resistance in tuberculosis and excluded articles solely reporting on this parameter. We also excluded articles in which migrant status was determined by ethnicity, country of birth of participants' parents, or was not defined, and articles in which data were not disaggregated by migrant status. Outcomes were carriage of or infection with antibiotic-resistant organisms. We used random-effects models to calculate the pooled prevalence of each outcome. The study protocol is registered with PROSPERO, number CRD42016043681. FINDINGS: We identified 2274 articles, of which 23 observational studies reporting on antibiotic resistance in 2319 migrants were included. The pooled prevalence of any AMR carriage or AMR infection in migrants was 25·4% (95% CI 19·1-31·8; I2 =98%), including meticillin-resistant Staphylococcus aureus (7·8%, 4·8-10·7; I2 =92%) and antibiotic-resistant Gram-negative bacteria (27·2%, 17·6-36·8; I2 =94%). The pooled prevalence of any AMR carriage or infection was higher in refugees and asylum seekers (33·0%, 18·3-47·6; I2 =98%) than in other migrant groups (6·6%, 1·8-11·3; I2 =92%). The pooled prevalence of antibiotic-resistant organisms was slightly higher in high-migrant community settings (33·1%, 11·1-55·1; I2 =96%) than in migrants in hospitals (24·3%, 16·1-32·6; I2 =98%). We did not find evidence of high rates of transmission of AMR from migrant to host populations. INTERPRETATION: Migrants are exposed to conditions favouring the emergence of drug resistance during transit and in host countries in Europe. Increased antibiotic resistance among refugees and asylum seekers and in high-migrant community settings (such as refugee camps and detention facilities) highlights the need for improved living conditions, access to health care, and initiatives to facilitate detection of and appropriate high-quality treatment for antibiotic-resistant infections during transit and in host countries. Protocols for the prevention and control of infection and for antibiotic surveillance need to be integrated in all aspects of health care, which should be accessible for all migrant groups, and should target determinants of AMR before, during, and after migration. FUNDING: UK National Institute for Health Research Imperial Biomedical Research Centre, Imperial College Healthcare Charity, the Wellcome Trust, and UK National Institute for Health Research Health Protection Research Unit in Healthcare-associated Infections and Antimictobial Resistance at Imperial College London
Nanoanalytical analysis of bisphosphonate-driven alterations of microcalcifications using a 3D hydrogel system and in vivo mouse model
Vascular calcification predicts atherosclerotic plaque rupture and cardiovascular events. Retrospective studies of women taking bisphosphonates (BiPs), a proposed therapy for vascular calcification, showed that BiPs paradoxically increased morbidity in patients with prior acute cardiovascular events but decreased mortality in event-free patients. Calcifying extracellular vesicles (EVs), released by cells within atherosclerotic plaques, aggregate and nucleate calcification. We hypothesized that BiPs block EV aggregation and modify existing mineral growth, potentially altering microcalcification morphology and the risk of plaque rupture. Three-dimensional (3D) collagen hydrogels incubated with calcifying EVs were used to mimic fibrous cap calcification in vitro, while an ApoEâ/â mouse was used as a model of atherosclerosis in vivo. EV aggregation and formation of stress-inducing microcalcifications was imaged via scanning electron microscopy (SEM) and atomic force microscopy (AFM). In both models, BiP (ibandronate) treatment resulted in time-dependent changes in microcalcification size and mineral morphology, dependent on whether BiP treatment was initiated before or after the expected onset of microcalcification formation. Following BiP treatment at any time, microcalcifications formed in vitro were predicted to have an associated threefold decrease in fibrous cap tensile stress compared to untreated controls, estimated using finite element analysis (FEA). These findings support our hypothesis that BiPs alter EV-driven calcification. The study also confirmed that our 3D hydrogel is a viable platform to study EVmediated mineral nucleation and evaluate potential therapies for cardiovascular calcification
The ASIASAFE road safety handbook: the best practices in traffic safety between Europe â Indonesia, Malaysia, and Vietnam
This handbook on Road Traffic Safety, titled "The ASIASAFE Road Safety Handbook: The Best Practices in Traffic Safety between Europe â Indonesia, Malaysia, and Vietnam," is a collaborative effort involving nine universities across Asia and Europe. It represents over three years of intensive research, discussions, and consultations with relevant agencies in participating countries.
The six Asian universities involved are the Malaysia University of Science and Technology, Universiti Malaya (Malaysia), Universitas Gadjah Mada, Universitas Muhammadiyah (Indonesia), and Nguyen Tat Thanh University, University of Transport and Communications (Vietnam). The three European universities are Linkoping University (Sweden), University of Porto (Portugal), and University of Rome "Tor Vergata" (Italy).
While every effort has been made to ensure the accuracy and relevance of the information provided in this handbook, it is essential to acknowledge that each country has its own unique conditions and circumstances concerning road traffic safety. Therefore, the content of this handbook should be adopted and adapted according to the specific situations and needs of individual countries.
Readers are advised to exercise caution and discretion in implementing the recommendations and strategies outlined in this handbook, considering the local context and consulting with relevant authorities and experts as needed. The authors and contributing institutions do not accept any responsibility for the consequences of actions taken based on the information provided in this handbook
Hypoxia shapes the immune landscape in lung injury and promotes the persistence of inflammation
Hypoxemia is a defining feature of acute respiratory distress syndrome (ARDS), an often-fatal complication of pulmonary or systemic inflammation, yet the resulting tissue hypoxia, and its impact on immune responses, is often neglected. In the present study, we have shown that ARDS patients were hypoxemic and monocytopenic within the first 48âh of ventilation. Monocytopenia was also observed in mouse models of hypoxic acute lung injury, in which hypoxemia drove the suppression of type I interferon signaling in the bone marrow. This impaired monopoiesis resulted in reduced accumulation of monocyte-derived macrophages and enhanced neutrophil-mediated inflammation in the lung. Administration of colony-stimulating factor 1 in mice with hypoxic lung injury rescued the monocytopenia, altered the phenotype of circulating monocytes, increased monocyte-derived macrophages in the lung and limited injury. Thus, tissue hypoxia altered the dynamics of the immune response to the detriment of the host and interventions to address the aberrant response offer new therapeutic strategies for ARDS
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