Miracle-dz/UniFAR-FTUs huggingface dataset:
Specific Inhibition of Orthopoxvirus Replication by a Small Interfering RNA Targeting the D5R Gene

Background Concerns about the potential use of smallpox in bioterrorism have stimulated interest in the development of novel antiviral treatments. Currently, there are no effective therapies against smallpox and new treatment strategies are greatly needed. Methods In this study, specifically designed small interfering RNAs (siRNAs), targeting five proteins essential for orthopoxvirus replication, were investigated for their ability to inhibit vaccinia virus strain Western Reserve (VACVWR) replication. Results Among these siRNAs, 100 nM siD5R-2, an siRNA targeting the D5 protein, decreased VACVWR replication up to 90% when used either prophylactically or therapeutically in human lung carcinoma A549 cells. This siRNA induced a striking concentration-dependent inhibition of VACVWR replication and a prolonged prophylactic antiviral effect that lasted for 72 h, at a concentration of 100 nM. Confocal microscopy of Alexa–siD5R-2-treated VACVWR-infected cells confirmed a decrease in viral replication. Furthermore, siD5R-2 was shown to specifically reduce the D5R mRNA and protein expression using real-time reverse tran-scriptase-PCR and western blotting analysis, without inducing interferon-β in A549 cells. We also demonstrated the antiviral potency of siD5R-2 against different pathogenic orthopoxviruses, such as cowpox and monkeypox viruses, which were inhibited up to 70% at the lowest concentration (1 nM) tested. Finally, siD5R-2 showed antiviral effects in VACVWR-infected human keratinocyte and fibroblast cell cultures. Conclusions These results suggest that siD5R-2 could be a potential candidate to treat poxvirus infections.
Mapping of a plasmid, coding for colonization, factor antigen I and heat-stable enterotoxin production, isolated from an enterotoxigenic strain of Escherichia coli

The non-autotransferring plasmid NTP113 codes for production of colonization factor antigen I and heat-stable enterotoxin, NTP113, which has a molecular weight of 58 X 10(6), was digested with BamHI, EcoRI, and HindIII and combinations of these restriction endonucleases, and the products of these digestions were analyzed by agarose gel electrophoresis. The results were used to construct a partial restriction map of NTP113. Transposons coding for resistance to ampicillin, kanamycin, and tetracycline were inserted into NTP113, and we obtained a series of deletion mutants, as determined by the loss of tetracycline or kanamycin resistance from strains carrying the insertion mutants. A number of plasmid mutants obtained by insertion or deletion did not code for colonization factor antigen I, but most of these mutants still coded for heat-stable enterotoxin production. The position of the inserted transposons and of the deletions were determined on the restriction map. Two regions of NTP113 were required for the expression of colonization factor antigen I, and the two sites were separated by a length of DNA corresponding to a molecular weight of about 25 X10(6).
Involvement of Cell-Cell Interactions in the Rapid Stimulation of Cas Tyrosine Phosphorylation and Src Kinase Activity by Transforming Growth Factor-β1*

Transforming growth factor-β (TGF-β) regulates a wide range of physiological and pathological cellular processes, including cell migration, mesenchymal transition, extracellular matrix synthesis, and cell death. Cas (Crk-associated substrate, 130 kDa), an adaptor protein localized at focal adhesions and stress fibers, is also known to have important functions in cell migration and the induction of immediate-early gene expression. Here, we report that a rapid and transient tyrosine phosphorylation of Cas is induced by TGF-β1 and that E-cadherin-mediated cell-cell interaction and the Src kinase pathway are involved in this early TGF-β signaling. The addition of TGF-β1 to epithelial cells rapidly induced tyrosine phosphorylation of Cas and promoted the formation of complexes between focal adhesion molecules. Cas phosphorylation required the integrity of the actin cytoskeleton but was not dependent on cell adhesion, implying that Cas-dependent signaling may be distinct from integrin signaling. TGF-β1 also stimulated Src kinase activity, and specific inhibitors of Src completely blocked the induction of Cas phosphorylation by TGF-β1. The Cas phosphorylation and Src kinase activation seen in our results were induced in an epithelial phenotype-specific manner. Stable transfection of E-cadherin to L929 cells and L cells as well as E-cadherin blocking assay revealed that E-cadherin-mediated cell-cell interactions were essential for both Cas phosphorylation and Src kinase activation. Taken together, our data suggest that rapid Cas phosphorylation and Src kinase activation may play a novel role in TGF-β signal transduction.
The Envelope Glycoprotein of Human Endogenous Retrovirus Type W Uses a Divergent Family of Amino Acid Transporters/Cell Surface Receptors

ABSTRACT The human endogenous retrovirus type W (HERV-W) family includes proviruses with intact protein-coding regions that appear to be under selection pressure, suggesting that some HERV-W proviruses may remain active in higher primates. The envelope glycoprotein (Env) encoded by HERV-W is highly fusogenic, is naturally expressed in human placental syncytiatrophoblasts, and has been reported to function as a superantigen in lymphocyte cultures. Recent evidence suggested that HERV-W Env can mediate syncytium formation by interacting with the human sodium-dependent neutral amino acid transporter type 2 (hASCT2; gene name, SLC1A5) (J.-L. Blond, D. Lavillette, V. Cheynet, O. Bouton, G. Oriol, S. Chapel-Fernandez, B. Mandrand, F. Mallet, and F.-L. Cosset, J. Virol. 74:3321-3329, 2000) and that it can pseudotype human immunodeficiency virus cores (D. S. An, Y. Xie, and I. S. Y. Chen, J. Virol. 75:3488-3489, 2001). By using cell-cell fusion and pseudotype virion infection assays, we found that HERV-W Env efficiently uses both hASCT2 and the related transporter hASCT1 (gene name, SLC1A4) as receptors. In addition, although HERV-W Env mediates only slight syncytium formation or infection of mouse cells, it utilizes the mouse transporters mASCT1 and mASCT2 when their sites for N-linked glycosylation are eliminated by mutagenesis. Consistent with their role as a battlefield in host-virus coevolution, the viral recognition regions in ASCT1 and ASCT2 of humans and mice are highly divergent compared with other regions of these proteins, and their ratios of nonsynonymous to synonymous nucleotide sequence changes are extremely large. The recognition of ASCT1 and ASCT2 despite this divergence of their sequences strongly suggests that the use of both receptors has been highly advantageous for survival and evolution of the HERV-W family of retroviruses.
Pro-socially shareable entertainment television programmes: a programming alternative in developing countries?

Over the period 1975-82, the Mexican television network created and aired seven entertainment soap operas promoting educational-development themes like adult literacy, smaller family size norms, and an higher social status for women. These emissions earned high ratings in Mexico and in other Latin American countries where they were subsequently broadcast. Evidence suggests that many of the social objectives of the soaps were met. In light of such success, the authors investigated the potential of pro-socially shareable entertainment television programs in developing countries. These programs use entertaining media formats to carry pro-social messages to a wide, yet culturally-proximate audience group. Entertainment television genres such as melodramatic soap operas offer certain advantages for carrying pro-socially shareable messages to audiences. The possibility of using other television genres and media channels, however, also needs to be seriously considered. Pro-socially shareable entertainment programs do have their limitations and problems, with a certain degree of message dilution invariably accompanying the quest for shareability. Targeting specific problems in specific audience groups is difficult and the identity of a relatively small homogeneous group can be threatened in a larger culturally proximate group. The value-laden nature of pro-social content can also be problematic.
Ceramide Regulates the Transcription of Cyclooxygenase-2

The ceramide signaling pathway is activated by the sphingomyelinase (SMase)-mediated hydrolysis of cell membrane sphingomyelin to ceramide. We determined whether ceramide, a lipid second messenger, induced cyclooxygenase-2 (COX-2) in human mammary epithelial cells. Treatment of cells with neutral SMase or C2- or C6-ceramide enhanced prostaglandin E2 synthesis and increased levels of COX-2 protein and mRNA. Nuclear runoff assays revealed increased rates ofCOX-2 transcription after treatment with SMase and C2- and C6-ceramide. Transient transfections utilizing COX-2 promoter deletion constructs andCOX-2 promoter constructs in which specific enhancer elements were mutagenized indicated that the effects of ceramide were mediated via a cAMP response element. The induction of COX-2 by ceramide was inhibited by calphostin C, an inhibitor of protein kinase C. Induction of COX-2 promoter activity by SMase was blocked by overexpressing kinase-deficient Raf-1. Triggering of the ceramide pathway also led to increases in extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) activities; pharmacological inhibitors of MAPK kinase (MEK) and p38 MAPK blocked the induction of COX-2 by SMase. Overexpressing ERK1, JNK, or p38 led to severalfold increases in COX-2 promoter activity. By comparison, overexpression of dominant negatives for ERK1/2, JNK, or p38 blocked the activation of COX-2 promoter activity by SMase. A dominant negative for c-Jun inhibited the activation ofCOX-2 promoter activity by ceramide. Thus, in response to ceramide, increased MAPK signaling activates c-Jun, which, in turn, induces COX-2 gene expression via the cAMP response element in the COX-2 promoter.
A Survey: Authentication Protocols for Wireless Sensor Network in the Internet of Things; Keys and Attacks

Internet of things (IoT) is a new technology that enables things in a specific environment to communicate with each other over the internet. Objects need to communicate wirelessly with each other, so IoT includes wireless sensor networks (WSN), radio frequency identification (RFID), near field communication (NFC), and many to facilitate the communication process. WSN is a network of connected nodes use sensors to collect and share data between each other. In order to build heterogeneity IoT environments, Wireless Sensor Networks should be established to monitor and record activities of connected things. Standard security protocols are used to provide a seamless and secure connection in Wireless Sensor Networks, especially authentication and access control of nodes. In this paper, the importance of security issues within IoT-WSN environment highlighted, by providing a description of some existing authentication protocols used in wireless sensor network. Additionally, classifies the chosen protocols according to types of the secret key used to achieve their goals and types of attack that each protocol can prohibit in the network. The result presents common attacks in WSN resisted by some chosen protocols. This research considered a base for other researchers in Wireless Sensor Network and Internet of Things field.
Protection from Anthrax Toxin-Mediated Killing of Macrophages by the Combined Effects of Furin Inhibitors and Chloroquine

ABSTRACT Cell surface proteolytic processing of anthrax protective antigen by furin or other furin-related proteases is required for its oligomerization, endocytosis, and function as a translocon for anthrax lethal and edema factors. Countering toxin lethality is essential to developing effective chemotherapies for anthrax infections that have proceeded beyond the stage at which antibiotics are effective. The primary target for toxin is the macrophage, which can be killed by lethal factor via both necrotic and apoptotic pathways. Here we show that three high-affinity inhibitors of furin efficiently blocked killing of murine J774A.1 macrophages by recombinant protective antigen plus lethal factor: RRD-eglin and RRDG-eglin, developed by engineering the protein protease inhibitor eglin c, and the peptide boronic acid inhibitor acetyl-Arg-Glu-Lys-boroArg pinanediol. Inhibition of killing was dose dependent and correlated with prevention of protective antigen processing. Previous studies have shown that weak bases, such as chloroquine, which neutralize acidic compartments, also interfere with toxin-dependent killing. Here we show that combining furin inhibitors and chloroquine strongly augments the inhibition of toxin-dependent killing, suggesting that combined use of antifurin drugs and chloroquine might provide enhanced therapeutic benefits. Reversible furin inhibitors protected against anthrax toxin killing for at least 5 h, but by 8 h, toxin-dependent killing resumed even though furin inhibitors were still active. An irreversible chloromethylketone inhibitor did not exhibit this loss of protection.
Dress accessories, culture and identity in the late roman period

Cette communication envisage certaines des facons dont les accessoires du vetement ont pu etre utilises dans l’Antiquite tardive, en tenant compte du fait que les articles de vetement peuvent etre utilises pour construire les identites plutot que pour les refleter et que leur signification peut changer selon le contexte (par exemple, le contexte chronologique). L’utilisation du contexte archeologique quand on examine la facon dont les accessoires du vetement etaient utilises (en ce cas, dans la sepulure) se revele etre essentiel pour toute enquete sur leur signification et leur emploi dans une societe donnee. La frequence d’un article particulier employe d’une maniere specifique, suggere-t-on ici, montre, premierement, que celui-ci avait une fonction ou un emploi symbolique particulier et, deuxiemement, revele l’existence dans une aire donnee d’un decodage culturel permettant d’identifier les personnes originaires d’un meme groupe culturel. Ces principes sont illustres d’abord en examinant le lien etroit .
Predator-Prey Management in the National Park Context : Lessons from a Transboundary Wolf , Elk , Moose and Caribou System

Wolves {Canis lupus) are recolonizing much of their former range within the lower 48 states through active recovery (Bangs and Fritts 1996) and natural dispersal (Boyd and Pletscher 1999). Wolf recovery is being touted as one of the great conservation successes of the 20̂ ̂century (Mech 1995; Smith et al. 2003). In addition to being an important single-species conservation success, wolf recovery may also be one of the most important ecological restoration actions ever taken because of the pervasive ecosystem impacts of wolves (Hebblewhite et al. 2005). Wolf predation is now being restored to ecosystems that have been without the presence of major predators for 70 years or more. Whole generations of wildlife managers and biologists have come up through the ranks, trained in an ungulatemanagement paradigm developed in the absence of the world’s most successful predator of ungulates— t̂he wolf. Many questions are now facing wildlife managers and scientists about the role of wolf recovery in an ecosystemmanagement context. The effects wolves will have on economically important ungulate populations is emerging as a central issue for wildlife managers. But, questions about the important ecosystem effects of wolves are also emerging as a flurry of new studies reveals the dramatic ecosystem impacts of wolves and their implications for the conservation of biodiversity (Smith et al. 2003; Fortin et al. 2005; Hebblewhite et al. 2005; Ripple and Beschta 2006; Hebblewhite and Smith 2007). In this paper, I provide for wildlife managers and scientists in areas in the lower 48 states (where wolves are recolonizing) a window to their future by reviewing the effects of wolves on montane ecosystems in Banff National Park (BNP), Alberta. Wolves were exterminated in much of southern Alberta, similar to the lower 48 states, but they recovered through natural dispersal populations
ClpE, a novel type of HSP100 ATPase, is part of the CtsR heat shock regulon of Bacillus subtilis

Clp ATPases, which include the ubiquitous HSP100 family, are classified according to their structural features and sequence similarities. During the course of the Bacillus subtilis genome sequencing project, we identified a gene encoding a new member of the HSP100 family. We designated this protein ClpE, as it is the prototype of a novel subfamily among the Clp ATPases, and have identified homologues in several bacteria, including Listeria monocytogenes, Enterococcus faecalis, Streptococcus pyogenes, Streptococcus pneumoniae, Lactobacillus sakei and Clostridium acetobutylicum. A unique feature of these Hsp100‐type Clp ATPases is their amino‐terminal zinc finger motif. Unlike the other class III genes of B. subtilis (clpC and clpP ), clpE does not appear to be required for stress tolerance. Transcriptional analysis revealed two σA‐type promoters, expression from which was shown to be inducible by heat shock and puromycin treatment. Investigation of the regulatory mechanism controlling clpE expression indicates that this gene is controlled by CtsR and is thus a member of the class III heat shock genes of B. subtilis. CtsR negatively regulates clpE expression by binding to the promoter region, in which five CtsR binding sites were identified through DNase I footprinting and sequence analysis.
Cortical Changes Following Spinal Cord Injury with Emphasis on the Nogo Signaling System

After spinal cord injury, structural as well as functional modifications occur in the adult CNS. Sites of plastic changes include the injured spinal cord itself as well as cortical and subcortical structures. Previously, cortical reorganization in response to sensory deprivation has mainly been studied using peripheral nerve injury models, and has led to a degree of understanding of mechanisms underlying reorganization and plastic changes. Deprivation or damage-induced CNS plasticity is not always beneficial for patients, and may underlie the development of conditions such as neuropathic pain and phantom sensations. Therefore, efforts not only to enhance, but also to control the capacity of plastic changes in the CNS, are of clinical relevance. Novel methods to stimulate plasticity as well as to monitor it, such as transcranial magnetic stimulation and functional magnetic resonance imaging, respectively, may be useful in diverse clinical situations such as spinal cord injury and stroke. Here, human and animal studies of spinal cord injury are reviewed, with special emphasis on the contribution of the Nogo signaling system to cortical plasticity.
REFERENCE INTERVALS FOR PLASMA BIOCHEMICAL AND HEMATOLOGIC MEASURES IN LOGGERHEAD SEA TURTLES (CARETTA CARETTA) FROM MORETON BAY, AUSTRALIA

Biochemical and hematologic reference intervals have been reported for loggerhead sea turtles (Caretta caretta, Linnaeus 1758), but low sample numbers and simple statistical analyses have constrained their diagnostic usefulness. During June 2007–May 2008, 101 loggerhead sea turtles in Moreton Bay, Queensland, Australia, were captured by hand from boats; clinically assessed to determine health status; blood was sampled; and biochemical and hematologic variables were measured. Of these turtles, 66 were classified as clinically healthy and 23 as unhealthy. Reference intervals were calculated using data from clinically healthy turtles. Of the clinically unhealthy turtles, 82 and 45% had at least one biochemical and hematologic result, respectively, outside of at least one of the calculated intervals. However, only low proportions of unhealthy loggerhead sea turtles had abnormal results for each variable. The highest percentage of unhealthy turtles that were outside at least one estimated reference interval was 35%, for thrombocyte counts. Neither sex nor maturity category (mature versus large immature) influenced the risk of being clinically unhealthy. These are the first plasma biochemical and hematologic reference intervals reported for loggerhead sea turtles from the southwestern Pacific Ocean. We conclude that, for loggerhead sea turtles in Moreton Bay, separate reference intervals are required for mature and immature turtles for thrombocyte counts and for male and female turtles for lymphocyte, heterophil, and total white cell counts; otherwise, a single reference interval can be used regardless of age or sex. When estimating reference intervals in loggerhead sea turtles, it is desirable to use both methods for calculating reference intervals used in this study because intervals can differ substantially between methods for some variables. Joint interpretation using reference intervals from both methods allows the categorization of results as “normal,” “suspect,” or “abnormal. ”
Intrapericardial Adenine Nucleosides Induce Elevation of Endothelin-1 Concentration in the Pericardial Space of the Dog Heart

The adenine nucleosides, adenosine (ADO) and inosine (INO), and the endothelin-1 (ET-1) play an important role in the regulation of coronary and myocardial functions. The pericardial fluid accumulates these regulatory agents and reflects well their levels in the myocardial interstitium. This offers a possibility to examine the local adenine nucleoside-endothelin interactions in heart tissue. We have previously demonstrated that increased levels of intrapericardial (i.p.) ET-1 enhanced significantly the adenine nucleoside concentrations of the pericardial fluid samples. In this study the effects of i.p.-administered ADO and INO were investigated on the pericardial concentrations of ET-1 in the in situ dog heart. The ET-1 concentrations were determined (enzymelinked immunosorbent assay) in the samples obtained from the pericardial fluid and from the arterial plasma before and after i.p. administration of increasing doses of ADO (10, 100 and 1000 μM, n = 8) and INO (1, 10 and 100 mM, n = 8). Standard hemodynamic variables were recorded continuously. We found that i.p. ADO and INO induced dose-dependent increases of pericardial ET-1 levels after a 15-minute incubation period in pericardial (ET-1max,ADO, +121 ± 26%, P < 0.02; and ET-1max,INO, +84 ± 27%, P < 0.05) but not in the plasma samples. The i.p. nucleosides elicited slight but characteristic alterations in the heart rate and ventricular contractility (dP/dt). The results suggest that the pericardial adenine nucleosides interact with the myocardial ET-1 and this effect may be provoked from, and can also be detected in, the pericardium.