Robust Digital Predistortion in Saturation Region of Power Amplifiers

This paper proposes a digital predistortion (DPD) technique to improve linearization performance when the power amplifier (PA) is driven near the saturation region. The PA is a non-linear device in general, and the nonlinear distortion becomes severer as the output power increases. However, the PA’s power efficiency increases as the PA output power increases. The nonlinearity results in spectral regrowth, which leads to adjacent channel interference, and degrades the transmit signal quality. According to our simulation, the linearization performance of DPD is degraded abruptly when the PA operates in its saturation region. To relieve this problem, we propose an improved DPD technique. The proposed technique performs on/off control of the adaptive algorithm based on the magnitude of the transmitted signal. Specifically, the adaptation normally works for small and medium signals while it stops for large signals. Therefore, harmful coefficient updates by saturated signals can be avoided. A computer simulation shows that the proposed method can improve the linearization performance compared with the conventional DPD method in highly driven PAs

A Polynomial Digital Pre-Distortion Technique Based on Iterative Architecture

A digital predistortion (DPD) technique based on an iterative adaptation structure is proposed for linearizing power amplifiers (PAs). To obtain proper DPD parameters, a feedback path that converts the PA’s output to a baseband signal is required, and memory is also needed to store the baseband feedback signals. DPD parameters are usually found by an adaptive algorithm by using the transmitted signals and the corresponding feedback signals. However, for the adaptive algorithm to converge to a reliable solution, long feedback samples are required, which increases hardware complexity and cost. Considering that the convergence time of the adaptive algorithm highly depends on the initial condition, we propose a DPD technique that requires relatively shorter feedback samples. Specifically, the proposed DPD iteratively utilizes the short feedback samples in memory while keeping and using the DPD parameters found at the former iteration as the initial condition at the next iteration. Computer simulation shows that the proposed technique performs better than the conventional technique, as the former requires much shorter feedback memory than the latter

Impact of Cigarette Smoking and Exercise on Arterial Stiffness: A Narrative Literature Review

PURPOSE Smoking often causes acute and chronic cardiovascular disorders. Cigarette smoking increases oxidative stress, reduces nitric oxide bioavailability, and changes the extracellular matrix, impairing arterial stiffness. However, regular physical activity and smoking cessation significantly and rapidly reverse the detrimental effects. This narrative review summarizes the relevant research that describes the impacts of cigarette smoking on the cardiovascular system and demonstrates the therapeutic or preventative roles of exercise and smoking cessation in smoking-associated arterial stiffness. METHODS We used scientific search engines, including PubMed, Web of Science, Google Scholar, and Wiley Online Library, to identify previous studies exploring the effects of smoking, exercise, and smoking cessation on arterial stiffness. RESULTS We discussed the most important therapeutic and/or preventive roles of exercise and smoking cessation in decreasing arterial stiffness. Most studies have demonstrated that acute and chronic smoking increase arterial stiffness. Smoking and physical activity were negatively associated. However, this relationship was often attenuated or reversed during adult exercise interventions. In addition, smoking cessation reversed the effects of smoking on arterial stiffness. CONCLUSIONS Smoking increases the risk of acute and chronic cardiovascular disease. Cigarette smoking deteriorates arterial stiffness by altering the vascular walls. However, regular exercise and smoking cessation can improve or prevent impaired arterial stiffness

Acidic pH shock induces the expressions of a wide range of stress-response genes

<p>Abstract</p> <p>Background</p> <p>Environmental signals usually enhance secondary metabolite production in <it>Streptomycetes </it>by initiating complex signal transduction system. It is known that different sigma factors respond to different types of stresses, respectively in <it>Streptomyces </it>strains, which have a number of unique signal transduction mechanisms depending on the types of environmental shock. In this study, we wanted to know how a pH shock would affect the expression of various sigma factors and shock-related proteins in <it>S. coelicolor </it>A3(2).</p> <p>Results</p> <p>According to the results of transcriptional and proteomic analyses, the major number of sigma factor genes were upregulated by an acidic pH shock. Well-studied sigma factor genes of <it>sigH </it>(heat shock), <it>sigR </it>(oxidative stress), <it>sigB </it>(osmotic shock), and <it>hrdD </it>that play a major role in the secondary metabolism, were all strongly upregulated by the pH shock. A number of heat shock proteins including the DnaK family and chaperones such as GroEL2 were also observed to be upregulated by the pH shock, while their repressor of <it>hspR </it>was strongly downregulated. Oxidative stress-related proteins such as thioredoxin, catalase, superoxide dismutase, peroxidase, and osmotic shock-related protein such as vesicle synthases were also upregulated in overall.</p> <p>Conclusion</p> <p>From these observations, an acidic pH shock was considered to be one of the strongest stresses to influence a wide range of sigma factors and shock-related proteins including general stress response proteins. The upregulation of the sigma factors and shock proteins already found to be related to actinorhodin biosynthesis was considered to have contributed to enhanced actinorhodin productivity by mediating the pH shock signal to regulators or biosynthesis genes for actinorhodin production.</p

Dietary Glucose Consumption Promotes RALDH Activity in Small Intestinal CD103(+)CD11b(+) Dendritic Cells

Retinal dehydrogenase (RALDH) enzymatic activities catalyze the conversion of vitamin A to its metabolite Retinoic acid (RA) in intestinal dendritic cells (DCs) and promote immunological tolerance. However, precise understanding of the exogenous factors that act as initial trigger of RALDH activity in these cells is still evolving. By using germ-free (GF) mice raised on an antigen free (AF) elemental diet, we find that certain components in diet are critically required to establish optimal RALDH expression and activity, most prominently in small intestinal CD103(+)CD11b(+) DCs (siLP-DCs) right from the beginning of their lives. Surprisingly, systematic screens using modified diets devoid of individual dietary components indicate that proteins, starch and minerals are dispensable for this activity. On the other hand, in depth comparison between subtle differences in dietary composition among different dietary regimes reveal that adequate glucose concentration in diet is a critical determinant for establishing RALDH activity specifically in siLP-DCs. Consequently, pre-treatment of siLP-DCs, and not mesenteric lymph node derived MLNDCs with glucose, results in significant enhancement in the in vitro generation of induced Regulatory T (iTreg) cells. Our findings reveal previously underappreciated role of dietary glucose concentration in establishing regulatory properties in intestinal DCs, thereby extending a potential therapeutic module against intestinal inflammation11Ysciescopu

Gut microbiota regulates lacteal integrity by inducing VEGF-C in intestinal villus macrophages

A lacteal is a blunt-ended, long, tube-like lymphatic vessel located in the center of each intestinal villus that provides a unique route for drainage of absorbed lipids from the small intestine. However, key regulators for maintaining lacteal integrity are poorly understood. Here, we explore whether and how the gut microbiota regulates lacteal integrity. Germ depletion by antibiotic treatment triggers lacteal regression during adulthood and delays lacteal maturation during the postnatal period. In accordance with compromised lipid absorption, the button-like junction between lymphatic endothelial cells, which is ultrastructurally open to permit free entry of dietary lipids into lacteals, is significantly reduced in lacteals of germ-depleted mice. Lacteal defects are also found in germ-free mice, but conventionalization of germ-free mice leads to normalization of lacteals. Mechanistically, VEGF-C secreted from villus macrophages upon MyD88-dependent recognition of microbes and their products is a main factor in lacteal integrity. Collectively, we conclude that the gut microbiota is a crucial regulator for lacteal integrity by endowing its unique microenvironment and regulating villus macrophages in small intestine.Peer reviewe

Transcriptional activation of hypoxia-inducible factor-1 (HIF-1) in myeloid cells promotes angiogenesis through VEGF and S100A8

Emerging evidence indicates that myeloid cells are essential for promoting new blood vessel formation by secreting various angiogenic factors. Given that hypoxia-inducible factor (HIF) is a critical regulator for angiogenesis, we questioned whether HIF in myeloid cells also plays a role in promoting angiogenesis. To address this question, we generated a unique strain of myeloid-specific knockout mice targeting HIF pathways using human S100A8 as a myeloid-specific promoter. We observed that mutant mice where HIF-1 is transcriptionally activated in myeloid cells (by deletion of the von Hippel-Lindau gene) resulted in erythema, enhanced neovascularization in matrigel plugs, and increased production of vascular endothelial growth factor (VEGF) in the bone marrow, all of which were completely abrogated by either genetic or pharmacological inactivation of HIF-1. We further found that monocytes were the major effector producing VEGF and S100A8 proteins driving neovascularization in matrigel. Moreover, by using a mouse model of hindlimb ischemia we observed significantly improved blood flow in mice intramuscularly injected with HIF-1-activated monocytes. This study therefore demonstrates that HIF-1 activation in myeloid cells promotes angiogenesis through VEGF and S100A8 and that this may become an attractive therapeutic strategy to treat diseases with vascular defects.X1137Ysciescopu

The integration of InGaP LEDs with CMOS on 200 mm silicon wafers

The integration of photonics and electronics on a converged silicon CMOS platform is a long pursuit goal for both academe and industry. We have been developing technologies that can integrate III-V compound semiconductors and CMOS circuits on 200 mm silicon wafers. As an example we present our work on the integration of InGaP light-emitting diodes (LEDs) with CMOS. The InGaP LEDs were epitaxially grown on high-quality GaAs and Ge buffers on 200 mm (100) silicon wafers in a MOCVD reactor. Strain engineering was applied to control the wafer bow that is induced by the mismatch of coefficients of thermal expansion between III-V films and silicon substrate. Wafer bonding was used to transfer the foundry-made silicon CMOS wafers to the InGaP LED wafers. Process trenches were opened on the CMOS layer to expose the underneath III-V device layers for LED processing. We show the issues encountered in the 200 mm processing and the methods we have been developing to overcome the problems

Spontaneous Proliferation of CD4+ T Cells in RAG-Deficient Hosts Promotes Antigen-Independent but IL-2-Dependent Strong Proliferative Response of Naïve CD8+ T Cells

The fast and intense proliferative responses have been well documented for naïve T cells adoptively transferred into chronic lymphopenic hosts. This response known as spontaneous proliferation (SP), unlike antigen-independent lymphopenia-induced proliferation (LIP), is driven in a manner dependent on antigens derived from commensal microbiota. However, the precise nature of the SP response and its impact on homeostasis and function for T cells rapidly responding under this lymphopenic condition are still unclear. Here we demonstrate that, when naïve T cells were adoptively transferred into specific pathogen-free (SPF) but not germ-free (GF) RAG−/− hosts, the SP response of these cells substantially affects the intensity and tempo of the responding T cells undergoing LIP. Therefore, the resulting response of these cells in SPF RAG−/− hosts was faster and stronger than the typical LIP response observed in irradiated B6 hosts. Although the intensity and tempo of such augmented LIP in SPF RAG−/− hosts were analogous to those of antigen-dependent SP, the former was independent of antigenic stimulation but most importantly, dependent on IL-2. Similar observations were also apparent in other acute lymphopenic settings where antigen-dependent T cell activation can strongly occur and induce sufficient levels of IL-2 production. Consequently, the resulting T cells undergoing IL-2-driven strong proliferative responses showed the ability to differentiate into functional effector and memory cells that can control infectious pathogens. These findings therefore reveal previously unappreciated role of IL-2 in driving the intense form of T cell proliferative responses in chronic lymphopenic hosts