Miracle-dz/UniFAR-FTUs huggingface dataset:
Molecular dissection of Phaseolus vulgaris polygalacturonase-inhibiting protein 2 reveals the presence of hold/release domains affecting protein trafficking toward the cell wall

The plant endomembrane system is massively involved in the synthesis, transport and secretion of cell wall polysaccharides and proteins; however, the molecular mechanisms underlying trafficking toward the apoplast are largely unknown. Besides constitutive, the existence of a regulated secretory pathway has been proposed. A polygalacturonase inhibitor protein (PGIP2), known to move as soluble cargo and reach the cell wall through a mechanism distinguishable from default, was dissected in its main functional domains (A, B, C, D), and C sub-fragments (C1–10), to identify signals essential for its regulated targeting. The secretion patterns of the fluorescent chimeras obtained by fusing different PGIP2 domains to the green fluorescent protein (GFP) were analyzed. PGIP2 N-terminal and leucine-rich repeat domains (B and C, respectively) seem to operate as holding/releasing signals, respectively, during PGIP2 transit through the Golgi. The B domain slows down PGIP2 secretion by transiently interacting with Golgi membranes. Its depletion leads, in fact, to the secretion via default (Sp2-susceptible) of the ACD-GFP chimera faster than PGIP2. Depending on its length (at least the first 5 leucine-rich repeats are required), the C domain modulates B interaction with Golgi membranes allowing the release of chimeras and their extracellular secretion through a Sp2 independent pathway. The addition of the vacuolar sorting determinant Chi to PGIP2 diverts the path of the protein from cell wall to vacuole, suggesting that C domain is a releasing rather than a cell wall sorting signal.
Cloud-MERVS: An IoT Cloud-Based Error Recovery Video Streaming Scheme

Internet of Thing (IoT) cloud system is a field attracting a great deal of recent attention. Vehicular networks is a key area in IoT, as they can offer novel experiences in infotainment, as well as driving assistance such as like real-time traffic forecasting, advertisements and on board entertainment. Most of these applications rely on high quality video sharing, which is still an open research topic in Vehicular networks. We proposed a Cloud-MERVS technique for video streaming in Vehicular networks, which integrates IoT cloud system techniques and the Multi-channel Error Recovery Video Streaming (MERVS), to provide a more satisfying driving and travel experience. There are two types of service providers in cloud computing: Control Service Providers (CSPs) and Video Service Providers (VSPs). CSPs are responsible for collecting advertisement messages from the VSPs. The VSPs are the real video and service providers. Some VSPs are connected to a selected CSP to form a Group Service Provider (GSP), which is organized in a hierarchical structure for to improve efficiency. The design is implemented in Network Simulator-2 (NS-2). In this paper, several verification simulations are conducted, and the simulation results are presented.
The interaction Stability and Transparency for Scaled Teleoperation System

In this paper, a bilateral controller for a microteleoperation system is presented using passivity approaches. We showed that the application of wave variable formalism allows the passivity of the system in spite of the communication delays between the master and the slave and the varying scaling factors. Conditions of the passivity and of the transparency are given for the micro teleoperation system. Finally, experimental results are presented showing the stability-transparency performances of the resulting system with constant and variable time-delay.
Role of Rb during Neurogenesis and Axonal Guidance in the Developing Olfactory System

The Retinoblastoma protein, Rb, was shown to regulate distinct aspects of neurogenesis in the embryonic and adult brain besides its primary role in cell cycle control. It is still unknown, however, whether Rb is required for tissue morphogenesis and the establishment of synaptic connections between adjacent tissues during development. We have investigated here the role of Rb during development of the olfactory system (OS), which heavily relies on reciprocal interactions between the olfactory epithelium (OE) and the olfactory bulb (OB). We show that mice carrying a telencephalic-specific deletion of Rb display several neurogenic defects in the OS during late development. In the OE, loss of Rb leads to ectopic proliferation of late-born progenitors (Tuj-1+), abnormal radial migration and terminal maturation of olfactory sensory neurons (OSNs). In the OB, deletion of Rb causes severe lamination defects with loss of clear boundaries between distinct layers. Importantly, starting around E15.5 when OB glomerulogenesis is initiated, many OSNs axons that project along the olfactory nerve layer (ONL) fail to properly innervate the nascent bulb, thus resulting in partial loss of connectivity between OE-OB and gradual neuronal degeneration in both tissues peaking at birth. This deficiency correlates with deregulated expressions of two key chemo-repellant molecules, Robo2/Slit1 and Nrp2/Sema3F that control the formation of dorsal-ventral topographic map of OSNs connections with OB glomeruli. This study highlights a critical requirement for Rb during neurogenesis and the establishment of proper synaptic connections inside the OS during development.
Increased expression and processing of caspase‐12 after traumatic brain injury in rats

Traumatic brain injury (TBI) disrupts tissue homeostasis resulting in pathological apoptotic activation. Recently, caspase‐12 was reported to be induced and activated by the unfolded protein response following excess endoplasmic reticulum (ER) stress. This study examined rat caspase‐12 expression using the controlled cortical impact TBI model. Immunoblots of fractionalized cell lysates found elevated caspase‐12 proform (∼60 kDa) and processed form (∼12 kDa), with peak induction observed within 24 h post‐injury in the cortex (418% and 503%, respectively). Hippocampus caspase‐12 proform induction peaked at 24 h post‐injury (641%), while processed form induction peaked at 6 h (620%). Semi‐quantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR) analysis confirmed elevated caspase‐12 mRNA levels after TBI. Injury severity (1.0, 1.2 or 1.6 mm compression) was associated with increased caspase‐12 mRNA expression, peaking at 5 days in the cortex (657%, 651% and 1259%, respectively) and 6 h in the hippocampus (435%, 451% and 460%, respectively). Immunohistochemical analysis revealed caspase‐12 induction in neurons in both the cortex and hippocampus as well as in astrocytes at the contusion site. This is the first report of increased expression of caspase‐12 following TBI. Our results suggest that the caspase‐12‐mediated ER apoptotic pathway may play a role in rat TBI pathology independent of the receptor‐ or mitochondria‐mediated apoptotic pathways.
Docking of Yeast Vacuoles Is Catalyzed by the Ras-like GTPase Ypt7p after Symmetric Priming by Sec18p (NSF)

Vacuole inheritance in yeast involves the formation of tubular and vesicular “segregation structures” which migrate into the bud and fuse there to establish the daughter cell vacuole. Vacuole fusion has been reconstituted in vitro and may be used as a model for an NSF-dependent reaction of priming, docking, and fusion. We have developed biochemical and microscopic assays for the docking step of in vitro vacuole fusion and characterized its requirements. The vacuoles must be primed for docking by the action of Sec17p (α-SNAP) and Sec18p (NSF). Priming is necessary for both fusion partners. It produces a labile state which requires rapid docking in order to lead productively to fusion. In addition to Sec17p/Sec18p, docking requires the activity of the Ras-like GTPase Ypt7p. Unlike Sec17p/Sec18p, which must act before docking, Ypt7p is directly involved in the docking process itself.
Analysis of CSMA/CA Mechanism of IEEE 802.15.6 under Non-Saturation Regime

We have developed an analytical model for a non-saturated IEEE 802.15. 6 wireless body area network (WBAN) operating under an error-prone channel. The most suitable vehicle for improving network performance was found to be the choice of access phase lengths based on traffic loads for different user priorities (UPs). It was also found that the deployment of exclusive access phase (EAP) is not necessary in a typical WBAN; in fact, short exclusive and random access phases (EAP and RAP, respectively) lead to inefficient use of available bandwidth. We have also found that four user priorities (out of the eight available) typically suffice to achieve even the most stringent requirements for WBAN performance.
Inhibition of Macrophage Functions by the C-Terminus of Murine S100A9 Is Dependent on B-1 Cells

The protein S100A9 plays a key role in the control of inflammatory response. The C-terminus of the murine S100A9 protein (mS100A9p) downregulates the spreading and phagocytic activity of adherent peritoneal cells. Murine peritoneal cells are constituted by macrophages and B-1 cells, and the latter exert an inhibitory effect on macrophage functions by secreting interleukin- (IL-) 10. Here, we investigated the influence of B-1 cells on the inhibitory effect evoked by mS100A9p on macrophages. mS100A9p did not alter spreading and phagocytosis either by peritoneal macrophages obtained from mice deprived of B-1 cells or by bone marrow-derived macrophages (BMDMϕ). Nevertheless, when BMDMϕ were cocultivated by direct or indirect contact with B-1 cells treated with mS100A9p, the phagocytosis by BMDMϕ was decreased, showing that the effect of mS100A9p on macrophages was modulated by B-1 cells and/or their secretory compounds. Furthermore, the inhibitory action of mS100A9p on phagocytosis by adherent peritoneal cells was abolished in cells obtained from IL-10 knockout mice. Taken together, the results show that mS100A9p has no direct inhibitory effect on macrophages; however, mS100A9p modulates B-1 cells, which in turn downregulates macrophages, at least in part, via IL-10. These data contribute to the characterization of S100A9 functions involving B-1 cells in the regulation of the inflammatory process.
Oral mucositis and saliva IgA, IgG and IgM concentration during anti-tumor treatment in children suffering from acute lymphoblastic leukemia.

BACKGROUND Oral mucositis is a problem occurring within the oral cavity, which is the most difficult to deal with during anti-tumor treatment. The first symptom reported by the patient is discomfort. Salivary immunoglobulins play an important role in pathological processes occurring in the oral cavity. OBJECTIVES The study objective was to assess the occurrence of oral mucositis and to assess changes in the saliva IgA, IgG, and IgM concentration in children with acute lymphoblastic leukemia during antitumor treatment. MATERIAL AND METHODS The study included 78 children with acute lymphoblastic leukemia (ALL) and a control group of healthy children. All the participants underwent 3 examinations. RESULTS Mucosal opacity followed by redness usually occurred within 2-4 days after the methotrexate infusion. The most severe lesions of the oral mucosa were observed after the 1st month of chemotherapy. Correlations were found between hard-to-heal wounds and ulcers and blood morphology parameters. The mean saliva IgA concentration in children with ALL during chemotherapy was significantly lower than in children in the control group. A comparison of the mean saliva IgG in a given patient in subsequent examinations revealed a significant saliva IgG decrease occurring between the 1st and 3rd examinations. CONCLUSIONS Wounds and ulcers that were difficult to heal were related to blood morphology parameters. A low salivary IgA concentration in children with ALL may result in the development and potentiation of oral lesions typical of mucositis during anti-tumor treatment. A significant decrease in salivary IgG and IgM concentrations in children with ALL during chemotherapy may cause potentiation of pathological lesions in the oral mucosa.
The effect of roll-forming onto fatigue life of railway axles

In the last years, roll-forming has been adopted as a technique to improve the strength against crack propagation in railway axles, but very few scientific analyses and studies of the phenomenon are available in the literature. For this reason, the Maraxil Project was started in order to give the opportunity of experimentally and theoretically investigating some aspects related to this technological process in the case of railway axles made of EA4T, a typical steel for manufacture of high speed axles. Firstly, an experimental campaign on small-scale SE(B) specimens was carried out for determining the crack propagation behavior at stress ratios below -1, which correspond to the ones in presence of the high compressive residual stresses due to the roll-forming procedure. At the same time, the compressive residual stress field along the radial direction and due to the rollforming process was evaluated from axles coming from the production using both hole-drilling and x-ray diffractometry methods. The results obtained from crack propagation tests and residual stress field measurements were used together to build up a predictive crack growth model in presence of very high compressive stresses. This model was, then, validated through dedicated experimental crack propagation tests carried out on full-scale roll-formed axles made of EA4T; good agreement was found between the model and the experiments.
Stress Produces Aversion and Potentiates Cocaine Reward by Releasing Endogenous Dynorphins in the Ventral Striatum to Locally Stimulate Serotonin Reuptake

Activation of the dynorphin/κ-opioid receptor (KOR) system by repeated stress exposure or agonist treatment produces place aversion, social avoidance, and reinstatement of extinguished cocaine place preference behaviors by stimulation of p38α MAPK, which subsequently causes the translocation of the serotonin transporter (SERT, SLC6A4) to the synaptic terminals of serotonergic neurons. In the present study we extend those findings by showing that stress-induced potentiation of cocaine conditioned place preference occurred by a similar mechanism. In addition, SERT knock-out mice did not show KOR-mediated aversion, and selective reexpression of SERT by lentiviral injection into the dorsal raphe restored the prodepressive effects of KOR activation. Kinetic analysis of several neurotransporters demonstrated that repeated swim stress exposure selectively increased the Vmax but not Km of SERT without affecting dopamine transport or the high-capacity, low-affinity transporters. Although the serotonergic neurons in the dorsal raphe project throughout the forebrain, a significant stress-induced increase in cell-surface SERT expression was only evident in the ventral striatum, and not in the dorsal striatum, hippocampus, prefrontal cortex, amygdala, or dorsal raphe. Stereotaxic microinjections of the long-lasting KOR antagonist norbinaltorphimine demonstrated that local KOR activation in the nucleus accumbens, but not dorsal raphe, mediated this stress-induced increase in ventral striatal surface SERT expression. Together, these results support the hypothesis that stress-induced activation of the dynorphin/KOR system produces a transient increase in serotonin transport locally in the ventral striatum that may underlie some of the adverse consequences of stress exposure, including the potentiation of the rewarding effects of cocaine.
Privilege escalation attack through address space identifier corruption in untrusted modern processors

Privilege escalation attacks are one of the major threats jeopardizing microprocessor operation. Such attacks aim to maliciously increase the privilege level of the executed process, in order to access unauthorized resources. Modern microprocessors include complex memory management modules, with various different privilege levels and numerous ways to change the privilege level. In this paper, we present a malicious modification in the microprocessor process switch mechanism. Contrary to recent work presented in literature, the modification can be deployed during manufacturing process, as it consists of a trivial addition of a gate or wire sizing. The minimal footprint, however, comes at the cost of small window of attack opportunities. Experimental results show that a modification-aware application can gain escalated privileges within a few thousand clock cycles. Moreover, the malicious code has been added to SPEC benchmarks, and we show that the modified benchmarks can get escalated privileges before the end of typical workload, with minimal performance overhead.
Applications of the turbo recognition approach to layout analysis

Turbo recognition (TR) is a statistical model-based approach to the nearly optimal recognition of document layout structure. We exhibit some of the features of TR and show how it can be applied to a variety of physical and logical layout analysis tasks. Applications to documents with mixed content would benefit from integration with local texture analysis methods.
Enhance the stability of MANET by using Mobile Agent

In recent years, people are more rely on wireless network services so that they may obtain latest information at any time anywhere. Of wireless networks, to effectively allow several or more mobile devices to send data with one another has become an important research topic. In our research, the Mobile Agent is adapted to assists Mobile Host within the working area, and takes advantage of Active Route-Maintenance Protocol to ensure the stability of routing path.
Integrated CMOS Analog Neural Network Ability to Linearize the Distorted Characteristic of HPA Embedded in Satellites

New satellites generations have regenerative payload. Received signals are demodulated in order to be processed, before being modulated again and amplified on-board. For correcting non-linearities due to high power amplifier (HPA) operating near saturation, a predistortion system based on neural networks (NNs) was developed. For size, consumption and bandwidth purposes, the multi-layer perceptron (MLP) type NNs were implemented in a 0.6 mum CMOS ASIC. This paper presents the linearization ability of the analog integrated NN to correct the AM/AM distortion due to the HPA for changing simulation conditions (temperature drifts, ageing variations).
The Disruption of ND10 during Herpes Simplex Virus Infection Correlates with the Vmw110- and Proteasome-Dependent Loss of Several PML Isoforms

ABSTRACT The small nuclear structures known as ND10 or PML nuclear bodies have been implicated in a variety of cellular processes including response to stress and interferons, oncogenesis, and viral infection, but little is known about their biochemical properties. Recently, a ubiquitin-specific protease enzyme (named HAUSP) and a ubiquitin-homology family protein (PIC1) have been found associated with ND10. HAUSP binds strongly to Vmw110, a herpesvirus regulatory protein which has the ability to disrupt ND10, while PIC1 was identified as a protein which interacts with PML, the prototype ND10 protein. We have investigated the role of ubiquitin-related pathways in the mechanism of ND10 disruption by Vmw110 and the effect of virus infection on PML stability. The results show that the disruption of ND10 during virus infection correlates with the loss of several PML isoforms and this process is dependent on active proteasomes. The PML isoforms that are most sensitive to virus infection correspond closely to those which have recently been identified as being covalently conjugated to PIC1. In addition, a large number of PIC1-protein conjugates can be detected following transfection of a PIC1 expression plasmid, and many of these are also eliminated in a Vmw110-dependent manner during virus infection. These observations provide a biochemical mechanism to explain the observed effects of Vmw110 on ND10 and suggest a simple yet powerful mechanism by which Vmw110 might function during virus infection.
Age-Related Changes in Neuronal Nicotinic Acetylcholine Receptor Subunit α4 Expression Are Modified by Long-Term Nicotine Administration

The distribution of the neuronal nicotinic acetylcholine receptor subunit α4 (nAChRα4) in the brains of young (2–4 months) or aged (24–28 months) CBA/J mice was examined using immunohistochemical staining. Anti-nAChRα4 immunoreactivity corresponded with nAChRα4 RNA expression and high-affinity [3H]nicotine binding. Immunostaining in aged mice relative to that in young animals was diminished in the medial septum and diagonal band but was unchanged in the globus pallidus and substantia nigra. The staining of neurons was almost completely absent in the hippocampus of aged animals. The oral administration of nicotine to aged animals for 6 weeks did not alter nAChRα4 expression relative to that in aged controls. However, the long-term delivery of nicotine (11 months) to 14-month-old animals corresponded with the highly specific preservation of nAChRα4 expression in some neurons of the dentate gyrus region and in neurite processes of remaining neurons of the hippocampal CA1 region. These results support the conclusion that the loss of nAChRα4 expression occurs in key cholinergic regions during normal aging. Furthermore, sustained long-term nicotine delivery may promote highly region-specific retention of nAChR expression, but only if initiated before normal age-related receptor decline.
Large-scale Automated Reading with Reach Discovers New Cancer Driving Mechanisms

PubMed, a repository and search engine for biomedical literature, now indexes more than 1 million articles each year. This exceeds the processing capacity of human domain experts, limiting our ability to truly understand many diseases. We present Reach, a system for automated, large-scale reading of biomedical papers that can extract mechanistic descriptions of biological processes with relatively high precision. We demonstrate that combining the extracted pathway fragments with existing biological data analysis algorithms that rely on curated models helps identify and explain a large number of previously unidentified mutually exclusive altered signaling pathways in seven different cancer types. This work shows that combining curated “big mechanisms” with extracted “big data” can lead to a causal, predictive understanding of cellular processes and unlock downstream applications.
A Runtime System Architecture for Ubiquitous Support of OpenMP

In this work we present the runtime architecture of the OMPi OpenMP compiler. OMPi is a source-to-source C translator featuring a portable, modular and extensible runtime system. It allows for OpenMP threads to map to different execution entities which range from kernel/user-level threads to processes, providing transparent support of OpenMP applications on both SMP machines and clusters of SMPs. When operating within an SMP machine, arbitrary threading libraries can be employed; currently a multitude of such libraries is available, including one which is based on portable user-level threading, for high-performance nested parallelism support. When operating on a cluster, processes are used as the execution entities and different software DSM cores can be utilized under a unified interface; the runtime system uses a hybrid approach whereby its internal bookkeeping is done through explicit message passing, while user-program shared variables are handled by the DSM core.