Slow Adaptive OFDMA Systems Through Chance Constrained Programming

Adaptive OFDMA has recently been recognized as a promising technique for providing high spectral efficiency in future broadband wireless systems. The research over the last decade on adaptive OFDMA systems has focused on adapting the allocation of radio resources, such as subcarriers and power, to the instantaneous channel conditions of all users. However, such "fast" adaptation requires high computational complexity and excessive signaling overhead. This hinders the deployment of adaptive OFDMA systems worldwide. This paper proposes a slow adaptive OFDMA scheme, in which the subcarrier allocation is updated on a much slower timescale than that of the fluctuation of instantaneous channel conditions. Meanwhile, the data rate requirements of individual users are accommodated on the fast timescale with high probability, thereby meeting the requirements except occasional outage. Such an objective has a natural chance constrained programming formulation, which is known to be intractable. To circumvent this difficulty, we formulate safe tractable constraints for the problem based on recent advances in chance constrained programming. We then develop a polynomial-time algorithm for computing an optimal solution to the reformulated problem. Our results show that the proposed slow adaptation scheme drastically reduces both computational cost and control signaling overhead when compared with the conventional fast adaptive OFDMA. Our work can be viewed as an initial attempt to apply the chance constrained programming methodology to wireless system designs. Given that most wireless systems can tolerate an occasional dip in the quality of service, we hope that the proposed methodology will find further applications in wireless communications

25th annual computational neuroscience meeting: CNS-2016

The same neuron may play different functional roles in the neural circuits to which it belongs. For example, neurons in the Tritonia pedal ganglia may participate in variable phases of the swim motor rhythms [1]. While such neuronal functional variability is likely to play a major role the delivery of the functionality of neural systems, it is difficult to study it in most nervous systems. We work on the pyloric rhythm network of the crustacean stomatogastric ganglion (STG) [2]. Typically network models of the STG treat neurons of the same functional type as a single model neuron (e.g. PD neurons), assuming the same conductance parameters for these neurons and implying their synchronous firing [3, 4]. However, simultaneous recording of PD neurons shows differences between the timings of spikes of these neurons. This may indicate functional variability of these neurons. Here we modelled separately the two PD neurons of the STG in a multi-neuron model of the pyloric network. Our neuron models comply with known correlations between conductance parameters of ionic currents. Our results reproduce the experimental finding of increasing spike time distance between spikes originating from the two model PD neurons during their synchronised burst phase. The PD neuron with the larger calcium conductance generates its spikes before the other PD neuron. Larger potassium conductance values in the follower neuron imply longer delays between spikes, see Fig. 17.Neuromodulators change the conductance parameters of neurons and maintain the ratios of these parameters [5]. Our results show that such changes may shift the individual contribution of two PD neurons to the PD-phase of the pyloric rhythm altering their functionality within this rhythm. Our work paves the way towards an accessible experimental and computational framework for the analysis of the mechanisms and impact of functional variability of neurons within the neural circuits to which they belong

26th Annual Computational Neuroscience Meeting (CNS*2017): Part 3 - Meeting Abstracts - Antwerp, Belgium. 15–20 July 2017

This work was produced as part of the activities of FAPESP Research,\ud Disseminations and Innovation Center for Neuromathematics (grant\ud 2013/07699-0, S. Paulo Research Foundation). NLK is supported by a\ud FAPESP postdoctoral fellowship (grant 2016/03855-5). ACR is partially\ud supported by a CNPq fellowship (grant 306251/2014-0)

Suprabasin Is Hypomethylated and Associated with Metastasis in Salivary Adenoid Cystic Carcinoma

<div><h3>Background</h3><p>Salivary gland adenoid cystic carcinoma (ACC) is a rare cancer, accounting for only 1% of all head and neck malignancies. ACC is well known for perineural invasion and distant metastasis, but its underlying molecular mechanisms of carcinogenesis are still unclear.</p> <h3>Principal Findings</h3><p>Here, we show that a novel oncogenic candidate, suprabasin (SBSN), plays important roles in maintaining the anchorage-independent and anchorage-dependent cell proliferation in ACC by using SBSN shRNA stably transfected ACC cell line clones. SBSN is also important in maintaining the invasive/metastatic capability in ACC by Matrigel invasion assay. More interestingly, SBSN transcription is significantly upregulated by DNA demethylation induced by 5-aza-2′-deoxycytidine plus trichostatin A treatment and the DNA methylation levels of the SBSN CpG island located in the second intron were validated to be significantly hypomethylated in primary ACC samples versus normal salivary gland tissues.</p> <h3>Conclusions/Significance</h3><p>Taken together, these results support SBSN as novel oncogene candidate in ACC, and the methylation changes could be a promising biomarker for ACC.</p> </div

<i>SBSN</i> is important in maintaining anchorage-independent and anchorage-dependent growth in SACC83.

<p>Scramble, shRNA 1, shRNA 2, and shRNA 3 indicate the control and three types of <i>SBSN</i> shRNAs used to establish stable clones in SACC83. A, Representative photographs of anchorage-independent growth by soft agar assay. The size of colonies indicates the focus formation ability of each type of stable clone. B, The number of colonies counted in each type of stable clone. C, Anchorage-dependent cell proliferation assay. CCK-8 absorbance indicates the amount of cells at time-points 0, 24, and 48 hours. Scramble clones grew faster than <i>SBSN</i> shRNA stable clones at 24 and 48 hours, p<0.01. Statistical comparisons were performed with Student’s t-test. Error bars indicate the standard deviation of triplicate assays. D. <i>SBSN</i> mRNA levels in different stable clones were determined by qRT-PCR. This confirmed that <i>SBSN</i> was silenced by ∼50% in shRNAs clones compared to scramble clones.</p

<i>SBSN</i> is hypomethylated in primary ACC samples, and its expression is induced by CpG island demethylation in SACC83.

<p>A. We first confirmed 5-aza-dC/TSA-induced expression of <i>SBSN</i> in SACC83 mRNA levels by qRT-PCR. B. Graph of actual data using TaqMan qRT-PCR analysis. X-axis, amplification cycle numbers; y-axis, ΔRn values used to plot signal attributable to the 5′ nuclease reaction, which reflects the quantity of amplicon. <i>SBSN</i> was amplified between 25–30 cycles in 5-aza-dC/TSA treatment, whereas it was amplified between 30–35 cycles in mock treatment. 5-aza-dC/TSA- or mock-treated samples were loaded in the same amount as indicated by <i>GAPDH</i>. C. qMSP was conducted in a paraffin-embedded ACC cohort, which consisted of 62 ACC samples and 25 normal salivary gland tissues. Significant hypomethylation in <i>SBSN</i> was shown in ACC versus normal salivary gland tissue (p<0.0001, Student’s t-test). <i>SBSN</i> methylation scores were normalized by β-actin. Error bars indicate the standard deviation.</p

Clinical and pathologic characteristics of patient populations.

*<p>Time to distant metastasis ranged from 9.1–225.7 months, with a median of 48.1 months.</p

<i>SBSN</i> is important in maintaining invasion and metastatic capability in SACC83.

<p>Matrigel invasion assay was performed with scramble control and three types of <i>SBSN</i> shRNA stable clones made from SACC83, as indicated by scramble, shRNA 1, shRNA 2, and shRNA 3. Representative photos of whole transwell membranes are pictured at 4× magnification; the inset pictures were taken at 20× magnification at randomly selected central locations. This metastasis analysis was performed in triplicate.</p

Genome-wide interaction studies reveal sex-specific asthma risk alleles

Asthma is a complex disease with sex-specific differences in prevalence. Candidate gene studies have suggested that genotype-by-sex interaction effects on asthma risk exist, but this has not yet been explored at a genome-wide level. We aimed to identify sex-specific asthma risk alleles by performing a genome-wide scan for genotype-by-sex interactions in the ethnically diverse participants in the EVE Asthma Genetics Consortium. We performed male- and female-specific genome-wide association studies in 2653 male asthma cases, 2566 female asthma cases and 3830 non-asthma controls from European American, African American, African Caribbean and Latino populations. Association tests were conducted in each study sample, and the results were combined in ancestry-specific and cross-ancestry meta-analyses. Six sex-specific asthma risk loci had P-values &lt; 1 × 10(-6), of which two were male specific and four were female specific; all were ancestry specific. The most significant sex-specific association in European Americans was at the interferon regulatory factor 1 (IRF1) locus on 5q31.1. We also identify a Latino female-specific association in RAP1GAP2. Both of these loci included single-nucleotide polymorphisms that are known expression quantitative trait loci and have been associated with asthma in independent studies. The IRF1 locus is a strong candidate region for male-specific asthma susceptibility due to the association and validation we demonstrate here, the known role of IRF1 in asthma-relevant immune pathways and prior reports of sex-specific differences in interferon responses