Miracle-dz/UniFAR-FTUs huggingface dataset:
Co-channel interference avoidance in two-tier LTE femtocell systems using control information

Macrocell Base stations, called the Enhanced NodeB (eNB) are mainly aiming to serve outdoor users. However, due to insufficient signal strength this solution has difficulty in serving indoor users. To address this problem, the Femtocell, called the Home eNB(HeNB), system has been deployed in the LTE system. Since the HeNBs and the eNB use the same frequency band and the same frame structure, co-channel interference between HeNBs and eNB is unavoidable. To solve this problem, we propose a co-channel interference (CCI) avoidance scheme using the control information in the downlink subframe. Simulation results show the proposed scheme outperforms the conventional two-tier LTE femtocell systems in terms of the outage probability and the system throughput.
Integrating Splitting Transformations into an ILP Instruction Scheduler

Instruction scheduling is an essential technique in a compiler that generates high quality code. This paper, presents an integer linear programming (ILP) based approach to local instruction scheduling for multiple-issue processors with arbitrary latencies and non-identical functional units. Then the ILP model is extended to use splitting transformations. Such transformations replace single operations with equivalent multiple instruction sequences, when use of the sequence would improve overall performance. The target architecture of our instruction scheduler is a graphics accelerator. This approach is compared to the heuristic approach used in a production compiler. The contributions of this paper are: (1) We study performance of the heuristic algorithms for instruction scheduling; (2) We introduce a novel integer linear programming approach for optimum instruction scheduling of multiple-issue processors that can split operations ; and (3) We provide experimental results of running different graphics applications with our optimal scheduler. The results show that an optimum instruction scheduler can improve measured performance by up to 8% in 12% of the programs (shaders) in our benchmarks.
Mutations That Disrupt the Carboxyl-Terminus of γ-Sarcoglycan Cause Muscular Dystrophy

Recently, mutations in the genes encoding several of the dystrophin-associated proteins have been identified that produce phenotypes ranging from severe Duchenne-like autosomal recessive muscular dystrophy to the milder limb-girdle muscular dystrophies (LGMDs). LGMD type 2C is generally associated with a more severe clinical course and is prevalent in northern Africa. A previous study identified a single base pair deletion in the gene encoding the dystrophin-associated protein gamma-sarcoglycan in a number of Tunisian muscular dystrophy patients. To investigate whether gamma-sarcoglycan gene mutations cause autosomal recessive muscular dystrophy in other populations, we studied 50 muscular dystrophy patients from the United States and Italy. The muscle biopsies from these 50 patients showed no abnormality of dystrophin but did show diminished immunostaining for the dystrophin-associated protein alpha-sarcoglycan. Four patients with a severe muscular dystrophy phenotype were identified with homozygous, frameshifting mutations in gamma-sarcoglycan. Two of the four have microdeletions that disrupt the distal carboxyl-terminus of gamma-sarcoglycan yet result in a complete absence of gamma-and beta-sarcoglycan suggesting the importance of this region for stability of the sarcoglycan complex. This region of gamma-sarcoglycan, like beta-sarcoglycan, has a number of cysteine residues similar to those in epidermal growth factor cysteine-rich regions.
Pharyngeal Patency in Response to Advancement of the Mandible in Obese Anesthetized Persons

Background: During anesthesia in humans, anterior displacement of the mandible is often helpful to relieve airway obstruction. However, it appears to be less useful in obese patients. The authors tested the possibility that obesity limits the effectiveness of the maneuver. Methods: Total muscle paralysis was induced under general anesthesia in a group of obese persons (n = 9; body mass index, 32 +/‐ 3 kg sup ‐2) and in a group of nonobese persons (n = 9; body mas index, 21 +/‐ 2 kg sup ‐2). Nocturnal oximetry confirmed that none of them had sleep‐disordered breathing. The cross‐sectional area of the pharynx was measured endoscopically at different static airway pressures. A static pressure‐area plot allowed assessment of the mechanical properties of the pharynx. The influence of mandibular advancement on airway patency was assessed by comparing the static pressure‐area relation with and without the maneuver in obese and nonobese persons. Results: Mandibular advancement increased the retroglossal area at a given pharyngeal pressure, and mandibular advancement increased the retropalatal area in nonobese but not in obese persons at a given pharyngeal pressure. Conclusion: Mandibular advancement did not improve the retropalatal airway in obese persons.
The RNA-binding protein Vg1 RBP is required for cell migration during early neural development

After mid-blastula transition, populations of cells within the Xenopus embryo become motile. Using antisense morpholino oligonucleotides, we find that Vg1 RBP, an RNA-binding protein implicated in RNA localization in oocytes, is required for the migration of cells forming the roof plate of the neural tube and, subsequently, for neural crest migration. These cells are properly determined but remain at their site of origin. Consistent with a possible role in cell movement, Vg1 RBP asymmetrically localizes to extended processes in migrating neural crest cells. Given that Vg1 RBP is a member of the conserved VICKZ family of proteins, expressed in embryonic and neoplastic cells, these data shed light on the likely role of these RNA-binding proteins in regulating cell movements during both development and metastasis.
The role of glial activation in descending facilitation from the rostroventromedial medulla (RVM) in models of persistent pain

Substantial evidence shows that activation of glial cells in the spinal cord may promote central sensitization and enhancement of pain. Descending facilitation from the rostroventromedial medulla (RVM) is also recognized as a critical component in the maintenance of chronic pain states, although the precise mechanisms driving this activity are unclear. Here, we investigated the possibility that glial activation in the RVM could promote descending facilitation from the RVM in states of enhanced pain. Peripheral inflammation was induced with carrageenan injected into the plantar aspect of the hindpaw of male Sprague-Dawley rats and behavioral responses to noxious thermal and light tactile stimuli were determined. Microinjection of the glial inhibitors minocycline or fluorocitrate, or of SB 203580, a p38 MAPK inhibitor, produced a significant and time-related reversal of behavioral hypersensitivity resulting from hindpaw inflammation. Moreover, carrageenan-induced inflammation appeared to produce an increase in immunolabeling for activated microglia and astrocytes in the RVM, as well as for phosphorylated p38 MAPK; the latter was localized to both microglia and neurons of the RVM. Microinjection of the glial inhibitors into the RVM appeared to diminish immunofluorescent labeling for activated RVM microglia and astrocytes. Carrageenan-induced inflammation also increased RVM protein levels of Iba1 and GFAP and administration of minocycline or fluorocitrate into the RVM attenuated this effect. To examine a possible mechanism of glial activation, α,β-methylene-ATP was microinjected into the
Retaliation against protocol attacks

Security protocols intend to give their parties reasonable assurance that certain security properties will protect their commu- nication session. However, the literature confirms that the protocols may suffer subtle and hidden attacks. Flawed protocols are custom- arily sent back to the design process, but the costs of reengineer- ing a deployed protocol may be prohibitive. This paper outlines the concept of retaliation: who would steal a sum of money today, should this pose significant risks of having twice as much stolen back tomorrow? When ethics is left behind, attacks are always bal- anced decisions: if an attack can be retaliated, the economics of security may convince the attacker to refrain from attacking, and us to live with a flawed protocol. This new perspective requires a new threat model where any party may decide to subvert the pro- tocol for his own sake, depending on the risks of retaliation. This threat model, which for example is also suitable to studying non- repudiation protocols, seems more appropriate than the Dolev-Yao model to the present technological/social setting. It is demonstrated that machine-assisted protocol verification can can effectively be adapted to the new threat model.
Pneumococcal Cell Wall-Induced Meningitis Impairs Adult Hippocampal Neurogenesis

ABSTRACT Bacterial meningitis is a major infectious cause of neuronal degeneration in the hippocampus. Neurogenesis, a continuous process in the adult hippocampus, could ameliorate such loss. Yet the high rate of sequelae from meningitis suggests that this repair mechanism is inefficient. Here we used a mouse model of nonreplicative bacterial meningitis to determine the impact of transient intracranial inflammation on adult neurogenesis. Experimental meningitis resulted in a net loss of neurons, diminished volume, and impaired neurogenesis in the dentate gyrus for weeks following recovery from the insult. Inducible nitric oxide synthase (iNOS) immunoreactivity was prominent in microglia in nonproliferating areas of the dentate gyrus and hilus region after meningitis induction. Treatment with the specific iNOS inhibitor N6-(1-iminoethyl)-l-lysine restored neurogenesis in experimental meningitis. These data suggest that local central nervous system inflammation in and of itself suppresses adult neurogenesis by affecting both proliferation and neuronal differentiation. Repair of cognitive dysfunction following meningitis could be improved by intervention to interrupt these actively suppressive effects.
The huntingtin N17 domain is a multifunctional CRM1 and Ran-dependent nuclear and cilial export signal

The first 17 amino acids of Huntington’s disease (HD) protein, huntingtin, comprise an amphipathic alpha-helical domain that can target huntingtin to the endoplasmic reticulum (ER). N17 is phosphorylated at two serines, shown to be important for disease development in genetic mouse models, and shown to be modified by agents that reverse the disease phenotype in an HD mouse model. Here, we show that the hydrophobic face of N17 comprises a consensus CRM1/exportin-dependent nuclear export signal, and that this nuclear export activity can be affected by serine phospho-mimetic mutants. We define the precise residues that comprise this nuclear export sequence (NES) as well as the interaction of the NES, but not phospho-mimetic mutants, with the CRM1 nuclear export factor. We show that the nuclear localization of huntingtin depends upon the RanGTP/GDP gradient, and that N17 phosphorylation can also distinguish localization of endogenous huntingtin between the basal body and stalk of the primary cilium. We present a mechanism and multifunctional role for N17 in which phosphorylation of N17 not only releases huntingtin from the ER to allow nuclear entry, but also prevents nuclear export during a transient stress response event to increase the levels of nuclear huntingtin and to regulate huntingtin access to the primary cilium. Thus, N17 is a master localization signal of huntingtin that can mediate huntingtin localization between the cytoplasm, nucleus and primary cilium. This localization can be regulated by signaling, and is misregulated in HD.
Application of robust control to a cryogenic current comparator

We describe the design and implementation of an H∞ controller for PTB's 14-bit cryogenic current comparator (CCC). Measurement results obtained using either the newly implemented digital H∞ controller or the conventional analog integrator are consistent. In a wide frequency range, the system's noise figure is improved when using the new controller.
Robust visual tracking with a freely-moving event camera

Event cameras are a new technology that can enable low-latency, fast visual sensing in dynamic environments towards faster robotic vision as they respond only to changes in the scene and have a very high temporal resolution (< 1μs). Moving targets produce dense spatio-temporal streams of events that do not suffer from information loss “between frames”, which can occur when traditional cameras are used to track fast-moving targets. Event-based tracking algorithms need to be able to follow the target position within the spatio-temporal data, while rejecting clutter events that occur as a robot moves in a typical office setting. We introduce a particle filter with the aim to be robust to temporal variation that occurs as the camera and the target move with different relative velocities, which can lead to a loss in visual information and missed detections. The proposed system provides a more persistent tracking compared to prior state-of-the-art, especially when the robot is actively following a target with its gaze. Experiments are performed on the iCub humanoid robot performing ball tracking and gaze following.
Ozone’s Impact on Public Health: Contributions from Indoor Exposures to Ozone and Products of Ozone-Initiated Chemistry

Objective The associations between ozone concentrations measured outdoors and both morbidity and mortality may be partially due to indoor exposures to ozone and ozone-initiated oxidation products. In this article I examine the contributions of such indoor exposures to overall ozone-related health effects by extensive review of the literature as well as further analyses of published data. Findings Daily inhalation intakes of indoor ozone (micrograms per day) are estimated to be between 25 and 60% of total daily ozone intake. This is especially noteworthy in light of recent work indicating little, if any, threshold for ozone’s impact on mortality. Additionally, the present study estimates that average daily indoor intakes of ozone oxidation products are roughly one-third to twice the indoor inhalation intake of ozone alone. Some of these oxidation products are known or suspected to adversely affect human health (e.g., formaldehyde, acrolein, hydroperoxides, fine and ultrafine particles). Indirect evidence supports connections between morbidity/mortality and exposures to indoor ozone and its oxidation products. For example, cities with stronger associations between outdoor ozone and mortality tend to have residences that are older and less likely to have central air conditioning, which implies greater transport of ozone from outdoors to indoors. Conclusions Indoor exposures to ozone and its oxidation products can be reduced by filtering ozone from ventilation air and limiting the indoor use of products and materials whose emissions react with ozone. Such steps might be especially valuable in schools, hospitals, and childcare centers in regions that routinely experience elevated outdoor ozone concentrations.
Strength and timing of motor responses mediated by rebound firing in the cerebellar nuclei after Purkinje cell activation

The cerebellum refines the accuracy and timing of motor performance. How it encodes information to perform these functions is a major topic of interest. We performed whole cell and extracellular recordings of Purkinje cells (PCs) and cerebellar nuclei neurons (CNs) in vivo, while activating PCs with light in transgenic mice. We show for the first time that graded activation of PCs translates into proportional CN inhibition and induces rebound activity in CNs, which is followed by graded motor contractions timed to the cessation of the stimulus. Moreover, activation of PC ensembles led to disinhibition of climbing fiber activity, which coincided with rebound activity in CNs. Our data indicate that cessation of concerted activity in ensembles of PCs can regulate both timing and strength of movements via control of rebound activity in CNs.
Temporal dynamics of the consistency effect in reading Chinese: an event-related potentials study

This study aimed to explore the temporal dynamics of the consistency effect in reading Chinese phonograms. High-consistency and low-consistency characters were used in the homophone judgment task, and the event-related potentials were recorded. The data showed that low-consistency characters elicited greater N170 amplitude in the temporal–occipital region and greater P200 amplitude in the frontal region than high-consistency characters, whereas high-consistency characters showed greater amplitude of the N400 negativity than low-consistency characters. These findings can be interpreted as indicating that low-consistency characters produce a greater activation for the initial analysis of the orthographical and phonological representations, whereas high-consistency characters involve a greater lexical competition in the later stage.
Species Differences in Somatodendritic Dopamine Transmission Determine D2-Autoreceptor-Mediated Inhibition of Ventral Tegmental Area Neuron Firing

The somatodendritic release of dopamine within the ventral tegmental area (VTA) and substantia nigra pars compacta activates inhibitory postsynaptic D2-receptors on dopaminergic neurons. The proposed mechanisms that regulate this form of transmission differ between electrochemical studies using rats and guinea pigs and electrophysiological studies using mice. This study examines the release and resulting dopamine D2-autoreceptor-mediated IPSCs (D2-IPSCs) in the VTA of mouse, rat, and guinea pig. Robust D2-IPSCs were observed in all recordings from neurons in slices taken from mouse, whereas D2-IPSCs in rat and guinea pig were observed less frequently and were significantly smaller in amplitude. In slices taken from guinea pig, dopamine release was more persistent under conditions of reduced extracellular calcium. The decline in the concentration of dopamine was also prolonged and not as sensitive to inhibition of reuptake by cocaine. This resulted in an increased duration of D2-IPSCs in the guinea pig. Therefore, unlike the mouse or the rat, the time course of dopamine in the extracellular space of the guinea pig determined the duration the D2-IPSC. Functionally, differences in D2-IPSCs resulted in inhibition of dopamine neuron firing only in slices from mouse. The results suggest that the mechanisms and functional consequences of somatodendritic dopamine transmission in the VTA vary among species. This highlights the complexity that underlies dopamine-dependent transmission in one brain area. Differences in somatodendritic transmission would be expected in vivo to affect the downstream activity of the mesocorticolimbic dopamine system and subsequent terminal release.
Antiangiogenic (metronomic) chemotherapy for brain tumors: current and future perspectives

Significant advances in the diagnosis and treatment of brain tumors have been made through better imaging, surgical techniques and advances in radiation therapy. However, the cure rate for most adult and pediatric brain tumor patients has not mirrored this success. Angiogenesis, the development of neovascularization, provides the required nutrients and oxygen to an expanding tumor and is controlled by a complex balance of proangiogenic cytokines and antiangiogenic factors. A series of new inhibitors of angiogenesis are now in clinical trials. Most of these rely on inhibiting tumor cell-mediated cytokines or blocking the activation of their cognate receptors. Cytotoxic chemotherapy, by contrast, targets dividing cells but can be modulated to attack dividing endothelial cells. This review will focus on the use of low-dose antiangiogenic (also called metronomic) chemotherapy to inhibit endothelial cell function and resultant neovascularization in the treatment of adult and pediatric brain tumors. By examining the biology and preclinical findings that led to the development of antiangiogenic/metronomic chemotherapy, clinical studies have been undertaken that support the role of this approach in the clinic, and have led to the introduction of a number of markers being used to better predict active combinations and appropriate patient populations.
First language attrition: Morphological disintegration and reconstruction in first language attrition

Introduction The need for long term longitudinal studies of attrition within individuals has long been recognized in attrition (Obler 1982; Weltens 1987). Such longitudinal studies allow insight into the cumulative effects of attrition on the linguistic features of the language involved. This chapter is devoted to one such study. The developmental attrition of L1 (Hebrew) in a young child placed in an L2 (English) dominant environment has been monitored longitudinally through naturalistic observations and systematic probes to study the effect of attrition on the lexicon, syntax, morphology, and phonology of L1. The present contribution highlights one aspect of this study – the disintegration and reconstruction of the L1 verbal system. The study is based on daily notes and bi-weekly recordings of primarily naturalistic observations as well as on occasional elicitation activities and probes designed to ascertain the child's competence in L1. The data were collected primarily in the home environment where the use of L1 dominated. The study focuses on instances of code mixing , where linguistic units (words, phrases, clauses) of one language are juxtaposed with units of another language within a single sentence (Sridhar & Sridhar 1980), and code blending , where morphemes from one language are combined with morphemes of another language within a single word while the phonological features of the respective source languages are retained (Kaufman & Sridhar 1986). Given that code blended words are necessarily of the child's own creation, it follows that code blending provides a window into the child's morphological competence (Aronoff 1983, 1976).