Miracle-dz/UniFAR-FTUs huggingface dataset:
Energy Efficient Optimization of Wireless-Powered 5G Full Duplex Cellular Networks: A Mean Field Game Approach

This paper studies the power allocation of an ultra-dense cellular network consisting of multiple full-duplex (FD) base stations (BSs) serving a large number of half-duplex (HD) user equipments (UEs) located in a wide geographical area. Each BS consists of a baseband unit (BBU) that is responsible for signal processing and BS control, and a radio remote unit (RRU) that corresponds to a radio transceiver remotely built closer to the UEs. We consider a wireless-powered cellular network in which the BBU can periodically charge the RRU. We model the energy efficiency and coverage optimization problem for this network as a mean field game. We consider the weighted energy efficiency of the BS as the main performance metrics and evaluate the optimal strategy that can be adopted by the FD BSs in an ultra-dense network setting. Based on the interference and network energy efficiency models of the mean field game theory, Nash equilibrium of our proposed game is derived. Utilizing solutions of Hamilton–Jacobi–Bellman (HJB) and Fokker–Planck–Kolmogorov (FPK) equations, a new power transmission strategy is developed for the BSs to optimize the energy efficiency of 5G cellular networks with full duplex transmissions. Simulation results indicate that the proposed strategy not only improves the energy efficiency but also ensures the average network coverage probability converges to a stable level.
Mean-field Analysis of Batch Normalization

Batch Normalization (BatchNorm) is an extremely useful component of modern neural network architectures, enabling optimization using higher learning rates and achieving faster convergence. In this paper, we use mean-field theory to analytically quantify the impact of BatchNorm on the geometry of the loss landscape for multi-layer networks consisting of fully-connected and convolutional layers. We show that it has a flattening effect on the loss landscape, as quantified by the maximum eigenvalue of the Fisher Information Matrix. These findings are then used to justify the use of larger learning rates for networks that use BatchNorm, and we provide quantitative characterization of the maximal allowable learning rate to ensure convergence. Experiments support our theoretically predicted maximum learning rate, and furthermore suggest that networks with smaller values of the BatchNorm parameter achieve lower loss after the same number of epochs of training.
Comparing parentage inference software: reanalysis of a red deer pedigree

Knowledge of the parentage of individuals is required to address a variety of questions concerning the evolutionary dynamics of wild populations. A major advance in parentage inference in natural populations has been the use of molecular markers and the development of statistical methods to analyse these data. Cervus, one of the most widely used parentage inference programs, uses molecular data to determine parent–offspring relationships. However, Cervus does not make use of all available information: additional phenotypic information may exist predicting parent–offspring relationships, and additional genetic information may be exploited by simultaneously considering multiple types of relationships rather than just pairwise or just parent–offspring relationships. Here we reanalyse data from a wild red deer population using two programs capable of using this additional information, MasterBayes and COLONY2, and quantify the impact of these alternative approaches by comparison with a ‘known pedigree’ estimated using a larger suite of microsatellite makers for a subset of the population. The use of phenotypic information and multiple relationships increased the number of correct assignments. We highlight the differences between programs, particularly the use of population‐ rather than individual‐level statistical confidence in Cervus. We conclude that the use of additional information allows MasterBayes and COLONY2 to assign more correct paternities, whereas their use of individual‐ rather than population‐level confidence generates fewer erroneous assignments. We suggest that maximal information may be gained by combining outputs from different programs. Higher accuracy and completeness of pedigree information will improve parameters estimated from pedigree information in studies of natural populations.
AMP-activated Kinase (AMPK) Promotes Innate Immunity and Antiviral Defense through Modulation of Stimulator of Interferon Genes (STING) Signaling*

The host protein Stimulator of Interferon Genes (STING) has been shown to be essential for recognition of both viral and intracellular bacterial pathogens, but its regulation remains unclear. Previously, we reported that mitochondrial membrane potential regulates STING-dependent IFN-β induction independently of ATP synthesis. Because mitochondrial membrane potential controls calcium homeostasis, and AMP-activated protein kinase (AMPK) is regulated, in part, by intracellular calcium, we postulated that AMPK participates in STING activation; however, its role has yet to be been defined. Addition of an intracellular calcium chelator or an AMPK inhibitor to either mouse macrophages or mouse embryonic fibroblasts (MEFs) suppressed IFN-β and TNF-α induction following stimulation with the STING-dependent ligand 5,6-dimethyl xanthnone-4-acetic acid (DMXAA). These pharmacological findings were corroborated by showing that MEFs lacking AMPK activity also failed to up-regulate IFN-β and TNF-α after treatment with DMXAA or the natural STING ligand cyclic GMP-AMP (cGAMP). As a result, AMPK-deficient MEFs exhibit impaired control of vesicular stomatitis virus (VSV), a virus sensed by STING that can cause an influenza-like illness in humans. This impairment could be overcome by pretreatment of AMPK-deficient MEFs with type I IFN, illustrating that de novo production of IFN-β in response to VSV plays a key role in antiviral defense during infection. Loss of AMPK also led to dephosphorylation at Ser-555 of the known STING regulator, UNC-51-like kinase 1 (ULK1). However, ULK1-deficient cells responded normally to DMXAA, indicating that AMPK promotes STING-dependent signaling independent of ULK1 in mouse cells.
Expanded polyalanine tracts function as nuclear export signals and promote protein mislocalization via eEF1A1 factor

Polyalanine (poly(A)) diseases are caused by the expansion of translated GCN triplet nucleotide sequences encoding poly(A) tracts in proteins. To date, nine human disorders have been found to be associated with poly(A) tract expansions, including congenital central hypoventilation syndrome and oculopharyngeal muscular dystrophy. Previous studies have demonstrated that unexpanded wild-type poly(A)-containing proteins localize to the cell nucleus, whereas expanded poly(A)-containing proteins primarily localize to the cytoplasm. Because most of these poly(A) disease proteins are transcription factors, this mislocalization causes cellular transcriptional dysregulation leading to cellular dysfunction. Correcting this faulty localization could potentially point to strategies to treat the aforementioned disorders, so there is a pressing need to identify the mechanisms underlying the mislocalization of expanded poly(A) protein. Here, we performed a glutathione S-transferase pulldown assay followed by mass spectrometry and identified eukaryotic translation elongation factor 1 α1 (eEF1A1) as an interacting partner with expanded poly(A)-containing proteins. Strikingly, knockdown of eEF1A1 expression partially corrected the mislocalization of the expanded poly(A) proteins in the cytoplasm and restored their functions in the nucleus. We further demonstrated that the expanded poly(A) domain itself can serve as a nuclear export signal. Taken together, this study demonstrates that eEF1A1 regulates the subcellular location of expanded poly(A) proteins and is therefore a potential therapeutic target for combating the pathogenesis of poly(A) diseases.
Clinical Investigation : Head and Neck Cancer “ Pharyngocise ” : Randomized Controlled Trial of Preventative Exercises to Maintain Muscle Structure and Swallowing Function During Head-and-Neck Chemoradiotherapy

“Pharyngocise”: Randomized Controlled Trial of Preventative Exercises to Maintain Muscle Structure and Swallowing Function During Head-and-Neck Chemoradiotherapy Giselle Carnaby-Mann, M.P.H. , Ph.D.,* Michael A. Crary, Ph.D.,y Ilona Schmalfuss, M.D.,z and Robert Amdur, M.D.x Departments of *Behavioral Science and Community Health, ySpeech Language and Hearing Sciences, and xRadiation Oncology, University of Florida, Gainesville, FL; zDepartment of Radiology, North Florida/South Georgia Veterans Health System, Gainesville, FL
A Disease-associated Mutant of NLRC4 Shows Enhanced Interaction with SUG1 Leading to Constitutive FADD-dependent Caspase-8 Activation and Cell Death*

Nod-like receptor family card containing 4 (NLRC4)/Ipaf is involved in recognition of pathogen-associated molecular patterns leading to caspase-1 activation and cytokine release, which mediate protective innate immune response. Point mutations in NLRC4 cause autoinflammatory syndromes. Although all the mutations result in constitutive caspase-1 activation, their phenotypic presentations are different, implying that these mutations cause different alterations in properties of NLRC4. NLRC4 interacts with SUG1 and induces caspase-8-mediated cell death. Here, we show that one of the autoinflammatory syndrome-causing mutants of NLRC4, H443P, but not T337A and V341A, constitutively activates caspase-8 and induces apoptotic cell death in human lung epithelial cells. Compared with wild type NLRC4, the H443P mutant shows stronger interaction with SUG1 and with ubiquitinated cellular proteins. Phosphorylation of NLRC4 at Ser533 plays a crucial role in caspase-8 activation and cell death. However, H443P mutant does not require Ser533 phosphorylation for caspase-8 activation and cell death. Caspase-8 activation by NLRC4 and its H443P mutant are dependent on the adaptor protein FADD. A phosphomimicking mutant of NLRC4, S533D does not require SUG1 activity for inducing cell death. Ubiquitin-tagged NLRC4 could induce cell death and activate caspase-8 independent of Ser533 phosphorylation. Our work suggests that SUG1-mediated signaling results in enhanced ubiquitination and regulates FADD-dependent caspase-8 activation by NLRC4. We show that the autoinflammation-associated H443P mutant is altered in interaction with SUG1 and ubiquitinated proteins, triggering constitutive caspase-8-mediated cell death dependent on FADD but independent of Ser533 phosphorylation.
Molecular evolution of shattering loci in U.S. weedy rice

Cultivated rice fields worldwide are plagued with weedy rice, a conspecific weed of cultivated rice (Oryza sativa L.). The persistence of weedy rice has been attributed, in part, to its ability to shatter (disperse) seed prior to crop harvesting. In the United States, separately evolved weedy rice groups have been shown to share genomic identity with exotic domesticated cultivars. Here, we investigate the shattering phenotype in a collection of U.S. weedy rice accessions, as well as wild and cultivated relatives. We find that all U.S. weedy rice groups shatter seeds easily, despite multiple origins, and in contrast to a decrease in shattering ability seen in cultivated groups. We assessed allelic identity and diversity at the major shattering locus, sh4, in weedy rice; we find that all cultivated and weedy rice, regardless of population, share similar haplotypes at sh4, and all contain a single derived mutation associated with decreased seed shattering. Our data constitute the strongest evidence to date of an evolution of weeds from domesticated backgrounds. The combination of a shared cultivar sh4 allele and a highly shattering phenotype, suggests that U.S. weedy rice have re‐acquired the shattering trait after divergence from their progenitors through alternative genetic mechanisms.
Downregulation of miR-199a-5p Disrupts the Developmental Potential of In Vitro-Fertilized Mouse Blastocysts1

ABSTRACT Although in vitro fertilization (IVF), one of the most effective and successful assisted reproductive technologies, is widely used for treating infertility and in animal breeding, increasing evidence indicates that IVF offspring are linked to various short- or long-term consequences. Erroneous epigenetic modifications induced by IVF are suspected of contributing to these consequences. Among these epigenetic modifications, microRNAs may affect embryo implantation and early postimplantation development. Here, we performed comparative microRNA profiling between in vivo-fertilized (IVO group) and in vitro-fertilized (IVF group) mouse embryos at Embryonic Day 3.5 (E3.5) and E7.5. Our dynamic analyses showed that the dysregulated microRNAs were mainly associated with the regulation of genes involved in carcinogenesis, genetic information processing, glucose metabolism, cytoskeleton organization, and neurogenesis. Further analysis showed that miR-199a-5p was consistently downregulated in IVF embryos compared with their IVO counterparts. Through gain- and loss-of-function experiments, we demonstrated that IVF-induced downregulation of miR-199a-5p results in a higher glycolytic rate and lower developmental potential of IVF blastocysts, including cell lineage misallocation and lower fetal survival post implantation. Therefore, preventing downregulation of miR-199a-5p may become an effective strategy for improving the development of IVF peri-implantation embryos in the future.
An Experimental Study of Forbidden Patterns in Geometric Permutations by Combinatorial Lifting

We study the problem of deciding if a given triple of permutations can be realized as geometric permutations of disjoint convex sets in $\mathbb{R}^3$. We show that this question, which is equivalent to deciding the emptiness of certain semi-algebraic sets bounded by cubic polynomials, can be "lifted" to a purely combinatorial problem. We propose an effective algorithm for that problem, and use it to gain new insights into the structure of geometric permutations.
DDX4-EGFP transgenic rat model for the study of germline development and spermatogenesis †

Abstract Spermatogonial stem cells (SSC) are essential for spermatogenesis and male fertility. In addition, these adult tissue stem cells can be used as vehicles for germline modification in animal models and may have application for treating male infertility. To facilitate the investigation of SSCs and germ lineage development in rats, we generated a DEAD-box helicase 4 (DDX4) (VASA) promoter-enhanced green fluorescent protein (EGFP) reporter transgenic rat. Quantitative realtime polymerase chain reaction and immunofluorescence confirmed that EGFP was expressed in the germ cells of the ovaries and testes and was absent in somatic cells and tissues. Germ cell transplantation demonstrated that the EGFP-positive germ cell population from DDX4-EGFP rat testes contained SSCs capable of establishing spermatogenesis in experimentally infertile mouse recipient testes. EGFP-positive germ cells could be easily isolated by fluorescence-activated cells sorting, while simultaneously removing testicular somatic cells from DDX4-EGFP rat pup testes. The EGFP-positive fraction provided an optimal cell suspension to establish rat SSC cultures that maintained long-term expression of zinc finger and BTB domain containing 16 (ZBTB16) and spaltlike transcription factor 4 (SALL4), two markers ofmouse SSCs that are conserved in rats. The novel DDX4-EGFP germ cell reporter rat described here combined with previously described GCS-EGFP rats, rat SSC culture and gene editing tools will improve the utility of the rat model for studying stem cells and germ lineage development. Summary Sentence A DDX4 (VASA)-EGFP transgenic rat was produced to facilitate investigations of stem cells and germ lineage development.
UBE3B Is a Calmodulin-regulated, Mitochondrion-associated E3 Ubiquitin Ligase*

Recent genome-wide studies found that patients with hypotonia, developmental delay, intellectual disability, congenital anomalies, characteristic facial dysmorphic features, and low cholesterol levels suffer from Kaufman oculocerebrofacial syndrome (KOS, also reported as blepharophimosis-ptosis-intellectual disability syndrome). The primary cause of KOS is autosomal recessive mutations in the gene UBE3B. However, to date, there are no studies that have determined the cellular or enzymatic function of UBE3B. Here, we report that UBE3B is a mitochondrion-associated protein with homologous to the E6-AP C terminus (HECT) E3 ubiquitin ligase activity. Mutating the catalytic cysteine (C1036A) or deleting the entire HECT domain (amino acids 758–1068) results in loss of UBE3B's ubiquitylation activity. Knockdown of UBE3B in human cells induces changes in mitochondrial morphology and physiology, a decrease in mitochondrial volume, and a severe suppression of cellular proliferation. We also discovered that UBE3B interacts with calmodulin via its N-terminal isoleucine-glutamine (IQ) motif. Deletion of the IQ motif (amino acids 29–58) results in loss of calmodulin binding and a significant increase in the in vitro ubiquitylation activity of UBE3B. In addition, we found that changes in calcium levels in vitro disrupt the calmodulin-UBE3B interaction. These studies demonstrate that UBE3B is an E3 ubiquitin ligase and reveal that the enzyme is regulated by calmodulin. Furthermore, the modulation of UBE3B via calmodulin and calcium implicates a role for calcium signaling in mitochondrial protein ubiquitylation, protein turnover, and disease.
Option Comparison Network for Multiple-choice Reading Comprehension

Multiple-choice reading comprehension (MCRC) is the task of selecting the correct answer from multiple options given a question and an article. Existing MCRC models typically either read each option independently or compute a fixed-length representation for each option before comparing them. However, humans typically compare the options at multiple-granularity level before reading the article in detail to make reasoning more efficient. Mimicking humans, we propose an option comparison network (OCN) for MCRC which compares options at word-level to better identify their correlations to help reasoning. Specially, each option is encoded into a vector sequence using a skimmer to retain fine-grained information as much as possible. An attention mechanism is leveraged to compare these sequences vector-by-vector to identify more subtle correlations between options, which is potentially valuable for reasoning. Experimental results on the human English exam MCRC dataset RACE show that our model outperforms existing methods significantly. Moreover, it is also the first model that surpasses Amazon Mechanical Turker performance on the whole dataset.
Clinical Investigation : Gastrointestinal Cancer A Specific miRNA Signature Correlates With Complete Pathological Response to Neoadjuvant Chemoradiotherapy in Locally Advanced Rectal Cancer

A Specific miRNA Signature Correlates With Complete Pathological Response to Neoadjuvant Chemoradiotherapy in Locally Advanced Rectal Cancer Giuseppina Della Vittoria Scarpati, M.D., Ph.D.,* Francesca Falcetta, Ph.D.,y,1 Chiara Carlomagno, M.D., Ph.D.,* Paolo Ubezio, Ph.D.,y Sergio Marchini, Ph.D.,y Alfonso De Stefano, M.D.,* Vijay Kumar Singh, Ph.D.,z Maurizio D’Incalci, M.D.,y Sabino De Placido, M.D.,* and Stefano Pepe, M.D., Ph.D.x
Efferent innervation of the rat testis.

Previous assessments of the autonomic nerve supply of the male genital tract concluded that the testis received sympathetic input primarily from paraaortic ganglia, particularly the spermatic ganglion. We challenged this consensus by using retrograde axonal tracing to examine the source and distribution of efferent fibers reaching the testis of adult rats. We also used immunohistochemical methods to assess putative neurotransmitters in testicular neurons of the abdominal and pelvic ganglia. The results indicate the majority of retrogradely labeled cell profiles were localized within the major pelvic (38%) and pelvic accessory ganglia (37%), and only a few labeled cell profiles were present in the paraaortic and spermatic ganglia. Injection of FluoroGold and Fast Blue dyes into the respective right and left testis demonstrated that 17% of the neurons in pelvic ganglia were labeled when tracers were microinjected beneath the capsule of the contralateral testis. About 8% of the neurons were labeled both with FluoroGold and Fast Blue, suggesting that certain neurons can provide simultaneous input to the left and right testicles. Immunohistochemical results showed that tyrosine hydroxylase, a marker for noradrenergic fibers, was present in over 33% of the cell profiles labeled with either FluoroGold or Fast Blue. Some 27% of the fluorescent-labeled cell profiles were positive for neuropeptide Y, while 22% were immunoreactive for vasoactive intestinal polypeptide. No evidence for vasoactive intestinal polypeptide immunoreactivity was detected within the testis, but neuropeptide Y-immunoreactive fibers were present in the tunica albuginea and testicular vasculature. Catecholamine fluorescent fibers were distributed sparsely throughout the periphery of the testis in association with the capsule, vasculature, and interstitium. (ABSTRACT TRUNCATED AT 250 WORDS)
IoT-U: Cellular Internet-of-Things Networks Over Unlicensed Spectrum

In this paper, we consider an uplink cellular Internet-of-Things (IoT) network, where a cellular user (CU) can serve as the mobile data aggregator for a cluster of IoT devices. To be specific, the IoT devices can either transmit the sensory data to the base station (BS) directly by cellular communications, or first aggregate the data to a CU through machine-to-machine (M2M) communications before the CU uploads the aggregated data to the BS. To support massive connections, the IoT devices can leverage the unlicensed spectrum for M2M communications, referred to as IoT unlicensed (IoT-U). Aiming to maximize the number of scheduled IoT devices and meanwhile associate each IoT device with the right CU or BS with the minimum transmit power, we first introduce a single-stage formulation that captures these objectives simultaneously. To tackle the NP-hard problem efficiently, we decouple the problem into two subproblems, which are solved by successive linear programming and convex optimization techniques, respectively. The simulation results show that the proposed IoT-U scheme can support more IoT devices than that only using the licensed spectrum.