Implementation of a miniaturized planar tri-band microstrip patch antenna for wireless sensors in mobile applications

This article belongs to the Special Issue Applications of Antenna Technology in Sensors.Antennas in wireless sensor networks (WSNs) are characterized by the enhanced capacity of the network, longer range of transmission, better spatial reuse, and lower interference. In this paper, we propose a planar patch antenna for mobile communication applications operating at 1.8, 3.5, and 5.4 GHz. A planar microstrip patch antenna (MPA) consists of two F-shaped resonators that enable operations at 1.8 and 3.5 GHz while operation at 5.4 GHz is achieved when the patch is truncated from the middle. The proposed planar patch is printed on a low-cost FR-4 substrate that is 1.6 mm in thickness. The equivalent circuit model is also designed to validate the reflection coefficient of the proposed antenna with the S11 obtained from the circuit model. It contains three RLC (resistor–inductor–capacitor) circuits for generating three frequency bands for the proposed antenna. Thereby, we obtained a good agreement between simulation and measurement results. The proposed antenna has an elliptically shaped radiation pattern at 1.8 and 3.5 GHz, while the broadside directional pattern is obtained at the 5.4 GHz frequency band. At 1.8, 3.5, and 5.4 GHz, the simulated peak realized gains of 2.34, 5.2, and 1.42 dB are obtained and compared to the experimental peak realized gains of 2.22, 5.18, and 1.38 dB at same frequencies. The results indicate that the proposed planar patch antenna can be utilized for mobile applications such as digital communication systems (DCS), worldwide interoperability for microwave access (WiMAX), and wireless local area networks (WLAN).The authors appreciate the financial support from Universidad Carlos III de Madridand and the European Union's Horizon 2020 research and innovation program under Marie Sklodowska-Curie Grant 801538

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

Surgical site infection after gastrointestinal surgery in high-income, middle-income, and low-income countries: a prospective, international, multicentre cohort study

Background: Surgical site infection (SSI) is one of the most common infections associated with health care, but its importance as a global health priority is not fully understood. We quantified the burden of SSI after gastrointestinal surgery in countries in all parts of the world. Methods: This international, prospective, multicentre cohort study included consecutive patients undergoing elective or emergency gastrointestinal resection within 2-week time periods at any health-care facility in any country. Countries with participating centres were stratified into high-income, middle-income, and low-income groups according to the UN's Human Development Index (HDI). Data variables from the GlobalSurg 1 study and other studies that have been found to affect the likelihood of SSI were entered into risk adjustment models. The primary outcome measure was the 30-day SSI incidence (defined by US Centers for Disease Control and Prevention criteria for superficial and deep incisional SSI). Relationships with explanatory variables were examined using Bayesian multilevel logistic regression models. This trial is registered with ClinicalTrials.gov, number NCT02662231. Findings: Between Jan 4, 2016, and July 31, 2016, 13 265 records were submitted for analysis. 12 539 patients from 343 hospitals in 66 countries were included. 7339 (58·5%) patient were from high-HDI countries (193 hospitals in 30 countries), 3918 (31·2%) patients were from middle-HDI countries (82 hospitals in 18 countries), and 1282 (10·2%) patients were from low-HDI countries (68 hospitals in 18 countries). In total, 1538 (12·3%) patients had SSI within 30 days of surgery. The incidence of SSI varied between countries with high (691 [9·4%] of 7339 patients), middle (549 [14·0%] of 3918 patients), and low (298 [23·2%] of 1282) HDI (p < 0·001). The highest SSI incidence in each HDI group was after dirty surgery (102 [17·8%] of 574 patients in high-HDI countries; 74 [31·4%] of 236 patients in middle-HDI countries; 72 [39·8%] of 181 patients in low-HDI countries). Following risk factor adjustment, patients in low-HDI countries were at greatest risk of SSI (adjusted odds ratio 1·60, 95% credible interval 1·05–2·37; p=0·030). 132 (21·6%) of 610 patients with an SSI and a microbiology culture result had an infection that was resistant to the prophylactic antibiotic used. Resistant infections were detected in 49 (16·6%) of 295 patients in high-HDI countries, in 37 (19·8%) of 187 patients in middle-HDI countries, and in 46 (35·9%) of 128 patients in low-HDI countries (p < 0·001). Interpretation: Countries with a low HDI carry a disproportionately greater burden of SSI than countries with a middle or high HDI and might have higher rates of antibiotic resistance. In view of WHO recommendations on SSI prevention that highlight the absence of high-quality interventional research, urgent, pragmatic, randomised trials based in LMICs are needed to assess measures aiming to reduce this preventable complication

In vitro studies on human first trimester forebrain cells : differentiation and interactions with immunoregulating molecules

This thesis has focused on understanding, at the molecular level, growth regulation and differentiation of human first trimester forebrain cells, and the immune signals mediating these processes. Primary cultures were established from human forebrain tissue derived from elective first trimester abortions. Tissues were carefully triturated and plated in serum-containing culture medium without addition of antibiotics or pre-conditioned medium. Human first trimester forebrain cultures were heterogeneous populations of cells and could survive well for at least 6 weeks. The majority was glial cells. The interactions between these cells and immunoregulating molecules were studied. The capacity of these cells at different gestational ages to produce IFN-[gamma] and IL-4 and the effect of IFN-[gamma] on their survival, proliferation and expression of MHC antigens was examined. IFN-[gamma] mRNA expression was recorded at high levels during week 7.5 and 10.5 of gestation. First trimester forebrain cells cultured for 24 h spontaneously produced high amounts of IFN-[gamma], but no measurable levels of IL-4 were detected. In kinetic studies, cultures with and without IFN-[gamma] stimulation did not show MHC antigen induction until day 7 in vitro where incubation with IFN-[gamma] showed expression of MHC class II molecules. Furthermore, natural induction of IL-1ß, IL-4, IL-6, IL-10, TNF-[alpha], IFN-[gamma] and TGF-ß in human first trimester forebrain cells was evaluated. Constitutive cytokine gene expression were detected already at week 5 of gestational age. Expression increased with age and IFN-[gamma] was mainly expressed in the GFAP-positive cells. To investigate the factors that regulate astrocyte chemokine expression, the ability of human first trimester astrocytes to induce ß-family chemokine mRNA, MIP-1[alpha], MIP-1ß, RANTES, and MCP-1 was examined. Human first trimester astrocytes were induced to express the P-family chemokines in a stimulus-dependent fashion. Astrocyte-derived MCP-1, RANTES MIP-1[alpha] and MIP-1ß mRNA were easily induced by LPS, IFN-[gamma] and TNF-[alpha]. UV-inactivated MV, but not CMV, strongly induced expression of these chemokines, especially MCP-1 and MIP-1ß. Moreover, the signalling pathway used by IFN-[gamma] during the process of growth regulation of human astrocytes obtained from the first trimester was investigated. IFN-[gamma] induced significantly higher cell survival compared to that of unexposed cultures. This effect was suppressed by incubation with A47. STAT-1 was translocated into the nucleus upon IFN-[gamma] stimulation, which was also blocked by incubation with A47. The results of these studies provide evidence for communications between immunoregulatory molecules and human first trimester forebrain cells, suggesting momentous roles for cytokines in neuronal and glial cell survival, proliferation and differentiation during brain development

Role of Cytokine Signaling during Nervous System Development

Cytokines are signaling proteins that were first characterized as components of the immune response, but have been found to have pleiotropic effects in diverse aspects of body function in health and disease. They are secreted by numerous cells and are used extensively in intercellular communications to produce different activities, including intricate processes engaged in the ontogenetic development of the brain. This review discusses factors involved in brain growth regulation and recent findings exploring cytokine signaling pathways during development of the central nervous system. In view of existing data suggesting roles for neurotropic cytokines in promoting brain growth and repair, these molecules and their signaling pathways might become targets for therapeutic intervention in neurodegenerative processes due to diseases, toxicity, or trauma

A role for the immune system-released activating agent (ISRAA) in the ontogenetic development of brain astrocytes.

The Immune System-Released Activating Agent (ISRAA) was discovered as a novel molecule that functions as a mediator between the nervous and immune systems in response to a nervous stimulus following an immune challenge. This research investigated the role of ISRAA) in promoting the ontogeny of the mouse brain astrocytes. Astrocyte cultures were prepared from two-month-old BALB/c mice. Recombinant ISRAA protein was used to stimulate astrocyte cultures. Immunohistochemistry and ELISA were utilized to measure ISRAA and IFN-γ levels, IFN-γR expression and STAT1 nuclear translocation. MTT-assay was used to evaluate cellular survival and proliferation. To assess astrocyte cell lysates and tyrosine-phosphorylated proteins, SDS-PAGE and western blot were used. ISRAA was highly expressed in mouse embryonic astrocytes, depending on cell age. Astrocytes aged seven days (E7) showed increased proliferation and diminished differentiation, while 21-day-old (E21) astrocytes depicted reversed effects. IFN-γ was involved in the ISRAA action as ISRAA induced IFN-γ in both age groups, but only E21 astrocytes expressed IFN-γR. ISRAA stimulation of E21 resulted in tyrosine phosphorylation of numerous cellular proteins and the nuclear translocation of STAT1, a signalling pathway utilized by IFN-γ. The results suggest that ISRAA is involved in mouse brain development through the cytokine network involving IFN-γ