A Low Complexity Partial Transmit Sequence for Peak to Average Power Ratio Reduction in OFDM Systems

Partial transmit sequence (PTS) is one of the most important techniques for reducing the peak to average power ratio (PAPR) in OFDM systems. This paper presents a low complexity PTS scheme by applying a new phase sequence. Unlike the conventional PTS which needs several inverse fast Fourier transform (IFFT) operations, the proposed technique requires half IFFT operations only at the expense of slight PAPR degradation. Simulation and results are examined with QPSK modulation and OFDM signal and power amplifier with memory effects

What Immunological Defects Predispose to Non-tuberculosis Mycobacterial Infections?

Nontuberculous mycobacteria (NTM) are categorized as one of the large and diverse groups of environmental organisms which are abundant in water and soil.  NTM cause a variety of diseases in humans that mainly affect the lung. A predisposition to pulmonary NTM is evident in patients with parenchymal structural diseases including bronchiectasis, emphysema, tuberculosis (TB), cystic fibrosis (CF), rheumatologic lung diseases and other chronic diseases with pulmonary manifestations. Lung infections are not the only consequences of being infected by NTM as they can also infect skin and soft tissue and may also cause lymphadenitis (predominantly in young children) and disseminated disease in human immunodeficiency virus (HIV)-infected patients or those with severely compromised immune system. NTM are also found in many subjects without any known risk factors.  Although the recent advances in imaging and microbiologic techniques including gene sequencing have provided a better view of the problems caused by NTM and has enhanced our understanding of the disease, many uncertainties regarding the immunologic response to NTM still exist. There is also limited data on the immunogenetics of NTM infection. Here, the authors reviewed the main immunogenetic defects as well as other immunological conditions which are associated with an increased the risk of NTM infections

The miR-196a SNP Rs11614913 but not the miR-499 rs37464444 SNP is a risk factor for non-small cell lung cancer in an Iranian population

BACKGROUND: Globally, lung cancer represents a major cause of cancer-related deaths. The regulation of gene expression is modulated by small noncoding RNAs called miRNAs that can act as both tumor suppressors and oncogenes. The maturation, expression and binding to target mRNAs is affected by single nucleotide polymorphisms (SNPs) in miRNA genomic regions thereby contributing to cancer susceptibility. SNPs Rs11614913 in miR196a and Rs3746444 in miR-499 are implicated in the development of cancers such as non-small cell lung cancer (NSCLC) in non-Arabic subjects. MATERIALS AND METHODS: A small cohort of 204 participants including 104 lung cancer patients and 100 non-cancer controls subjects were enrolled into the study. The allele frequencies were determined by Polymerase Chain Reaction- Restriction Fragment Length Polymorphism (PCR-RFLP) and their correlation with lung cancer risk was determined. RESULTS: The miR-196a rs11614913 polymorphism increased the risk of NSCLC (CC vs. TT+TC: OR= 2.26, 95%CI= 1.28 - 3.98, P= 0.0046) in a dominant genetic model. No statistically significant association was found between the miR-499 rs37464444 polymorphism and NSCLC. CONCLUSION: The rs11614913 polymorphism in miR-196a, but not the miR-499 rs37464444 polymorphism, increased the risk of NSCLC. Further studies with larger sample sizes in correlation with functional outcomes at the cellular level should be undertaken

Anti-Inflammatory Effects of Lactobacillus Rahmnosus and Bifidobacterium Breve on Cigarette Smoke Activated Human Macrophages

Chronic obstructive pulmonary disease (COPD) is a major global health problem with cigarette smoke (CS) as the main risk factor for its development. Airway inflammation in COPD involves the increased expression of inflammatory mediators such as CXCL-8 and IL-1β which are important mediators for neutrophil recruitment. Macrophages are an important source of these mediators in COPD. Lactobacillus rhamnosus (L. rhamnosus) and Befidobacterium breve (B. breve) attenuate the development of 'allergic asthma' in animals but their effects in COPD are unknown.To determine the anti-inflammatory effects of L. rhamnosus and B. breve on CS and Toll-like receptor (TLR) activation.We stimulated the human macrophage cell line THP-1 with CS extract in the presence and absence of L. rhamnosus and B. breve and measured the expression and release of inflammatory mediators by RT-qPCR and ELISA respectively. An activity assay and Western blotting were used to examine NF-κB activation.Both L. rhamnosus and B. breve were efficiently phagocytized by human macrophages. L. rhamnosus and B. breve significantly suppressed the ability of CS to induce the expression of IL-1β, IL-6, IL-10, IL-23, TNFα, CXCL-8 and HMGB1 release (all p<0.05) in human THP-1 macrophages. Similar suppression of TLR4- and TLR9-induced CXCL8 expression was also observed (p<0.05). The effect of L. rhamnosus and B. breve on inflammatory mediator release was associated with the suppression of CS-induced NF-κB activation (p<0.05).This data indicate that these probiotics may be useful anti-inflammatory agents in CS-associated disease such as COPD

Self-Decision Route Selection for Energy Balancing in wireless sensor betworks.

In many wireless sensor network (WSN) applications, data from the monitored environmental phenomenon only need to be sampled intermittently and transmitted to the base station. Hence, an intelligent protocol that balances the traffic load among the nodes and minimizes their energy usage, especially during routing and idle listening, which is necessary to extend the network lifetime. In this paper, a load balancing model that balances the rate of energy dissipation of the sensor nodes across the network is proposed. The proposed energy balancing scheme distributes the traffic load regularly and slowly over the sensor nodes during routing, such that the overall network life time is optimized, and the sensors die almost all at the same time. The proposed energy balancing protocol reduces the high energy consumption during the transmission and reception states, this is done by introducing multi-hop instead of single-hop communication of each node with the sink. Simulation results show that the proposed energy balancing protocol reduces the transmission energy usage by up to 64%, while the reception energy usage is reduced up to 67%. Moreover, the system throughput as well as the network lifetime increased up to 79% and 66%, respectively

An improved routing mechanism using bio-inspired for energy balancing in wireless sensor networks

Planning of energy-efficient protocols is critical for wireless sensor networks (WSNs) because of the constraints on sensor node's energy. Therefore, the routing protocol should be able to achieve uniform power dissipation during transmission to the sink node. In this paper, we present a self-optimization scheme for WSN which is able to utilize and optimize the sensor nodes' resources, especially the batteries, to achieve balanced energy consumption across all sensors. This method is based on Ant Colony Optimization (ACO) meta heuristic which is adopted to enhance the paths with the best quality function. The assessment of this function depends on multi-criteria metrics such as the minimum residual battery power, hop numbers and average energy of both route and network. This method also distribute the traffic load of sensor nodes throughout the WSN leading to reduced energy usage, extended network life time and reduced packet loss. Simulation results show that our scheme performs much better than Energy Efficient Ant-Based Routing (EEABR) in terms of energy consumption and efficiency

Effect of mesenchymal stem cell-derived exosomes on the induction of mouse tolerogenic dendritic cells

Dendritic cells (DCs) orchestrate innate inflammatory responses and adaptive immunity through T‐cell activation via direct cell–cell interactions and/or cytokine production. Tolerogenic DCs (tolDCs) help maintain immunological tolerance through the induction of T‐cell unresponsiveness or apoptosis, and generation of regulatory T cells. Mesenchymal stromal cells (MSCs) are adult multipotent cells located within the stroma of bone marrow (BM), but they can be isolated from virtually all organs. Extracellular vesicles and exosomes are released from inflammatory cells and act as messengers enabling communication between cells. To investigate the effects of MSC‐derived exosomes on the induction of mouse tolDCs, murine adipose‐derived MSCs were isolated from C57BL/6 mice and exosomes isolated by ExoQuick‐TC kits. BM‐derived DCs (BMDCs) were prepared and cocultured with MSCs‐derived exosomes (100 μg/ml) for 72 hr. Mature BMDCs were derived by adding lipopolysaccharide (LPS; 0.1μg/ml) at Day 8 for 24 hr. The study groups were divided into (a) immature DC (iDC, Ctrl), (b) iDC + exosome (Exo), (c) iDC + LPS (LPS), and (d) iDC + exosome + LPS (EXO + LPS). Expression of CD11c, CD83, CD86, CD40, and MHCII on DCs was analyzed at Day 9. DC proliferation was assessed by coculture with carboxyfluorescein succinimidyl ester‐labeled BALB/C‐derived splenocytes p. Interleukin‐6 (IL‐6), IL‐10, and transforming growth factor‐β (TGF‐β) release were measured by enzyme‐linked immunosorbent assay. MSC‐derived exosomes decrease DC surface marker expression in cells treated with LPS, compared with control cells ( ≤ .05). MSC‐derived exosomes decrease IL‐6 release but augment IL‐10 and TGF‐β release (p ≤ .05). Lymphocyte proliferation was decreased (p ≤ .05) in the presence of DCs treated with MSC‐derived exosomes. CMSC‐derived exosomes suppress the maturation of BMDCs, suggesting that they may be important modulators of DC‐induced immune responses

miR-1224 Expression is Increased in Human Macrophage After Infection With Bacillus Calmette-Guerin (BCG)

Introduction: Tuberculosis remains a major threat to human health. Understanding the strategies mycobacterium takes to overcome immune defense is important to control the infection. miRNAs are master regulators of most pathways in the human body. Infection with mycobacterium impacts upon host metabolic pathways to obtain the nutrition for its intracellular survival. In this study, we aimed to investigate the effect of BCG infection on the expression of three miRNAs (miR-1224, -484 and -425), which have been previously demonstrated to be important in infection and metabolic pathways. Methods: Blood-derived monocyte derived macrophage (MDM) cultures were prepared and infected with BCG at a multiplicity of infection (MOI) =10 or left uninfected as a control. 72h post-infection, the cultured cells were subjected to RNA extraction, cDNA synthesis and real-time PCR. Expression levels miRNAs were normalized to the levels of U6 snRNA (Rnu6) using the 2–ΔΔCt method Results: Infection with BCG resulted in a highly significant increase in miR-1224 expression (24.4±3.8-fold induction) in human MDMs. The induction of miR-484 (1.8±0.3-fold increase) and of miR-425 (1.2±0.2-fold increase) was less increased compared to miR-1224. Discussion: Mycobacterium tolerate an hostile microenvironment by escaping from lysosomal degradation and providing a lipid-rich niche by trigger with and re-pattering host metabolism. These data highlight the potential importance of miR-1224 in the host metabolic response to TB infection and a possible role of miR-484 in the reprogramming of metabolic pathways in infected cells. Further work is required to determine whether these miRNAs may also be useful as biomarkers for the diagnosis or monitoring of treatment in TB patients. Conclusion: This study Highlighted the potential roles of miRNAs in host immunologic responses upon mycobacterium infection. Further work is required to determine whether these miRNAs may also be useful as biomarkers for the diagnosis or monitoring of treatment in TB patients