Miracle-dz/UniFAR-FTUs huggingface dataset:
Transactions on Dependable and Secure Computing Privacy Leakage of Location Sharing in Mobile Social Networks: Attacks and Defense

—Along with the popularity of mobile social networks (MSNs) is the increasing danger of privacy breaches due to user location exposures. In this work, we take an initial step towards quantifying location privacy leakage from MSNs by matching the users' shared locations with their real mobility traces. We conduct a three-week real-world experiment with 30 participants and discover that both direct location sharing (e.g., Weibo or Renren) and indirect location sharing (e.g., Wechat or Skout) can reveal a small percentage of users' real points of interests (POIs). We further propose a novel attack to allow an external adversary to infer the demographics (e.g., age, gender, education) after observing users' exposed location profiles. We implement such attack in a large real-world dataset involving 22,843 mobile users. The experimental results show that the attacker can effectively predict demographic attributes about users with some shared locations. To resist such attacks, we propose SmartMask, a context-based system-level privacy protection solution, designed to automatically learn users' privacy preferences under different contexts and provide a transparent privacy control for MSN users. The effectiveness and efficiency of SmartMask have been well validated by extensive experiments.
Limb Muscle Strength is Impaired Bilaterally after Stroke

University of North Carolina Hospitals, Chapel Hill, North Carolina, USA.Abstract. The purpose of this study was to describe the nature and implications of strength deficits onthe sides ipsilateral and contralateral to stroke. Subjects consisted of 16 patients who experienced a firststroke (2–40 days before testing) with hemiparesis (7 left, 9 right). The strengths of proximal (shoulderabduction, hip flexion), middle (elbow flexion and knee extension), and distal (wrist extension, ankledorsiflexion) muscle actions were measured by hand-held dynamometry. Muscle strength deficits werecalculated by subtracting measured forces from predicted forces determined from regression equations.The Functional Independence Measure was used to grade independence in transfers and gait. Analysis ofvariance (ANOVA) showed that the patients’ strength was impaired bilaterally. Further ANOVAsdemonstrated that impairments did not differ significantly from proximal to distal on the side contralateralto the lesion but that impairments were significantly greater proximally than distally on the side ipsilateralto the lesion. Muscle strength impairments tended to correlate significantly with one another (within andbetween sides) and with functional independence. The results challenge some traditional views of themuscle strength deficits that accompany stroke.Key words: Measurement, Stroke, Motor performance, Dynamometry. (This article was submitted Mar. 25, 1995, and was accepted Apr. 10, 1995)
Versatile hardware and software tools for educating students in power electronics

A new power electronics laboratory has been constructed at the University of Missouri-Rolla. Key components of the laboratory are a set of custom-designed hardware and software tools. The novel hardware tools include five mobile power electronics testbeds that each contain the semiconductor devices, gate-drive boards, voltage and current sensors, and computer interface connections required to study a wide range of circuit topologies and control techniques. Novel software tools include a set of virtual instruments used for control, data capture, and data analysis. A description of these tools, along with their use in power electronics courses, laboratory exercises, and student research projects, is presented.
Sequential Conformational Rearrangements Dictate the Dynamics of Class C GPCR Activation

Fluorescent probes reveal the roles of domain rearrangement and dimerization in GPCR activation. Heterotrimeric GTP-binding protein (G protein)–coupled receptors (GPCRs) are the largest family of cell surface receptors; they allow cells to respond to a wide range of endogenous and environmental signals. Class C GPCRs represent a discrete group within the GPCR family, with distinct structural characteristics. Receptors belonging to this class—such as γ-aminobutyric acid type B (GABAB) receptors or metabotropic glutamate receptors (mGluRs)—form constitutive dimers. However, the conformational changes within such a dimeric receptor that are associated with agonist activation are still not well understood. A study by Hlavackova et al. investigates the role of dimer formation in mGluR1 activation. Using fluorescence resonance energy transfer approaches to assess inter- and intrasubunit conformational changes, the authors present an elegant study that sheds light on the kinetics of domain rearrangements in a class C GPCR upon ligand binding
Officer Perceptions of Risk of Contracting HIV/AIDS in Prison: A Two-State Comparison

A theme of the late modernity perspective as applied to prisons is maximizing safety and minimizing risk in the face of an uncertain work environment. Correctional officers in two states were surveyed about how their knowledge of HIV relates to their perceptions of risk. Officers who knew less about HIV, had less formal education, feared contact with prisoners known to be HIV positive, and who viewed prisoner tattooing, intravenous drug use, and sex as common at the unit in which they worked were more likely to perceive a higher risk of contracting HIV on the job.
Celebrating 30 Years of Wnt Signaling

Researchers gathered to share the latest findings on Wnt signaling in development and disease. Wnt signal transduction is crucial for embryonic development and tissue homeostasis in multicellular animals. Hyperactivation of the Wnt pathway drives tumor formation, yet activation of the Wnt pathway in stem cells holds great promise for injury repair and regeneration. Between 27 June and 1 July 2012, scientists from all over the globe gathered in the beachfront town of Egmond aan Zee in the Netherlands to celebrate the 30th anniversary of this blossoming and exciting field. The latest advances and breakthroughs were discussed at the aptly named European Molecular Biology Organization conference 30 Years of Wnt Signalling. Many presenters discussed unpublished data, a hallmark of past and hopefully future Wnt meetings. This Meeting Report summarizes some of the highlights of this conference, including the presentation of the long-awaited crystal structure of a Wnt protein bound to its receptor and the identification of exciting new possibilities for targeting the pathway in treating disease.
A Plant Homolog of Animal Glutamate Receptors Is an Ion Channel Gated by Multiple Hydrophobic Amino Acids

Hydrophobic amino acids, rather than glutamate, activate the Arabidopsis glutamate receptor homolog AtGLR1.4. Ionotropic Amino Acid Sensor Sequence similarity suggests that there are plant homologs of animal ionotropic glutamate receptors, which are ligand-gated, glutamate-activated ion channels. Tapken et al. showed that the Arabidopsis homolog AtGLR1.4 behaved as anything but a glutamate-activated channel. Of the 20 amino acids tested on AtGLR1.4 expressed in Xenopus oocytes, methionine was the most effective and potent of the seven amino acids that activated the channel, arginine was the most effective competitive antagonist of methionine-activated current, and glutamate did not affect channel activity. Electrophysiological analysis showed that AtGLR1.4 was a nonselective cation channel. Analysis of leaves from knockout plants indicated that AtGLR1.4 mediated membrane depolarization in response to methionine but not glutamate. Thus, to call these glutamate receptors in plants is a misnomer. Ionotropic glutamate receptors (iGluRs) are ligand-gated cation channels that mediate neurotransmission in animal nervous systems. Homologous proteins in plants have been implicated in root development, ion transport, and several metabolic and signaling pathways. AtGLR3.4, a plant iGluR homolog from Arabidopsis thaliana, has ion channel activity and is gated by asparagine, serine, and glycine. Using heterologous expression in Xenopus oocytes, we found that another Arabidopsis iGluR homolog, AtGLR1.4, functioned as a ligand-gated, nonselective, Ca2+-permeable cation channel that responded to an even broader range of amino acids, none of which are agonists of animal iGluRs. Seven of the 20 standard amino acids—mainly hydrophobic ones—acted as agonists, with methionine being most effective and most potent. Nine amino acids were antagonists, and four, including glutamate and glycine, had no effect on channel activity. We constructed a model of this previously uncharacterized ligand specificity and used knockout mutants to show that AtGLR1.4 accounts for methionine-induced membrane depolarization in Arabidopsis leaves.
Anti-Tobacco Education in Vacation Bible School in Mississippi: The Morality of Tobacco Prevention

Knowledge, attitudes, and behavior regarding the morality of tobacco use of 355 mostly African-American youth in Mississippi, were measured before and after tobacco prevention lessons in summer vacation Bible school. Knowledge and behavioral intentions were strong initially and did not change. Two attitudes improved: youth favored anti-tobacco policy and activism even more after the lessons compared to before. One attitude deteriorated: youth favored banning young people from tobacco less strongly after the lessons compared to before. Educational implications for introducing tobacco prevention, which may seem to be a secular topic, into a religious setting such as summertime Bible school, include covering important topics such as the perniciousness of tobacco companies, the negative influence of tobacco advertisements, the benefits of anti-tobacco policies, and ways to increase young people's personal comfort with anti-tobacco activism.
mTORC1 Status Dictates Tumor Response to Targeted Therapeutics

Recent studies indicate that sustained mTORC1 signaling can cause resistance to pathway-specific kinase inhibitors in cancer. Genomics has revolutionized and personalized our approach to cancer therapy, with clinical trials now frequently involving patient stratification based on tumor genotype. Rational drug design specifically targeting the most common genetic events and aberrantly regulated pathways in human cancers makes this approach possible. However, our understanding of the wiring of oncogenic signaling networks and the key downstream effectors driving human cancers is incomplete, limiting our ability to predict clinical responses or identify mechanisms of resistance to targeted therapeutics. Recent studies in independent cancer lineages driven by distinct oncogenic signaling events point to a common downstream target, the mammalian (or mechanistic) target of rapamycin complex 1 (mTORC1), which dictates the cellular and clinical response to pathway-specific inhibitors. mTORC1 is a highly integrated signaling node that promotes anabolic cell growth and proliferation and lies downstream of multiple oncogenes and tumor suppressors, including those influencing the PI3K-Akt and RAS-RAF-MEK-ERK pathways. Studies are now suggesting that to effectively target the major oncogenic signaling pathway in a given tumor, mTORC1 must be inhibited, and that its sustained activation is a major mechanism of resistance to such targeted therapies.
Ecological Salivary Cortisol Analysis— Part 2

BACKGROUND: Although bio-psycho-social health research is an ideal, samples adequate for complex modeling require biomarker specimens from hundreds of participants. Ecological sampling departs from laboratory study norms, with implications for analysis. OBJECTIVE: To inform ecological study designs, this article compares salivary cortisol levels and effect sizes of “focal” psychiatric factors, such as trauma history, posttraumatic stress diagnosis, comorbidity, and chronic stress, and “nuisance” factors, including endocrine disorders and medications and physiological factors such as gestational age and smoking. STUDY DESIGN: This is a descriptive analysis of ecologically collected cortisol specimens, assayed in an ongoing perinatal psychobiological study, addressing methodological considerations. RESULTS: Focal and nuisance factors are often interdependent with similar effect sizes. Careful specimen deletion decisions and model specification are needed to achieve the hoped-for external validity while maintaining internal validity. CONCLUSIONS: Results of multivariate models lend support to the validity and usefulness of an ecological approach to incorporating biomarkers in health research. J Am Psychiatr Nurses Assoc, 2008; 14(4), 285-296. DOI: 10.1177/1078390308321939
Dynamic Reprogramming of Signaling Upon Met Inhibition Reveals a Mechanism of Drug Resistance in Gastric Cancer

Understanding how inhibitors rewire the Met receptor pathway points to a strategy for more effective gastric cancer treatment. Met with Resistance in Gastric Cancer The hepatocyte growth factor receptor Met is associated with poor prognosis in various cancers, but the efficacy of Met inhibitors is often impeded by resistance. By comparing transcriptional changes at multiple time points after stimulation or inhibition of Met, Lai et al. identified critical mediators of Met-induced proliferation and Met inhibitor resistance in gastric cancer cell lines. Cancer cells or tumors exposed to Met inhibitors had decreased abundance of phosphatases, and this correlated with reactivation of the pro-proliferative MEK-ERK pathway and the emergence of drug resistance. Combining Met and MEK inhibitors was more cytotoxic to gastric cancer cells in culture than was either inhibitor alone, suggesting that this combination strategy may be effective in gastric cancer. The Met receptor tyrosine kinase is activated or genetically amplified in some gastric cancers, but resistance to small-molecule inhibitors of Met often emerges in patients. We found that Met abundance correlated with a proliferation marker in patient gastric tumor sections, and gastric cancer cell lines that have MET amplifications depended on Met for proliferation and anchorage-independent growth in culture. Inhibition of Met induced temporal changes in gene expression in the cell lines, initiated by a rapid decrease in the expression of genes encoding transcription factors, followed by those encoding proteins involved in epithelial-mesenchymal transition, and finally those encoding cell cycle–related proteins. In the gastric cancer cell lines, microarray and chromatin immunoprecipitation analysis revealed considerable overlap between genes regulated in response to Met stimulation and those regulated by signal transducer and activator of transcription 3 (STAT3). The activity of STAT3, extracellular signal–regulated kinase (ERK), and the kinase Akt was decreased by Met inhibition, but only inhibitors of STAT3 were as effective as the Met inhibitor in decreasing tumor cell proliferation in culture and in xenografts, suggesting that STAT3 mediates the pro-proliferative program induced by Met. However, the phosphorylation of ERK increased after prolonged Met inhibition in culture, correlating with decreased abundance of the phosphatases DUSP4 and DUSP6, which inhibit ERK. Combined inhibition of Met and the mitogen-activated protein kinase kinase (MEK)–ERK pathway induced greater cell death in cultured gastric cancer cells than did either inhibitor alone. These findings indicate combination therapies that may counteract resistance to Met inhibitors.
Specificity of the CheR2 Methyltransferase in Pseudomonas aeruginosa Is Directed by a C-Terminal Pentapeptide in the McpB Chemoreceptor

Pentapeptide sequences in a bacterial chemoreceptor mediate adaptation by recruiting a methyltransferase. Guided by a Pentapeptide Sensory adaptation is critical to chemotaxis and survival in bacteria. The chemosensory response is modified by reversible methylation of the cytoplasmic domain of the chemoreceptor. Some chemoreceptors have a pentapeptide sequence at the C terminus, which can bind the methyltransferases or methylesterases, increasing their local concentration. García-Fontana et al. investigated the selectivity of the interactions between the methyltransferases of the CheR family and chemoreceptors in Pseudomonas aeruginosa. Of the four methyltransferases and 26 chemoreceptors, a functional interaction (binding and methylation) was only detected between CheR2 and the chemoreceptor McpB (methyl-accepting chemotaxis protein B), which has the pentapeptide GWEEF at its C terminus. Both the physical and functional interactions between CheR2 and McpB were abolished by deletion of either GWEEF in McpB or a tripeptide motif in CheR2, which was partially conserved in pentapeptide-binding CheRs in other bacteria species. The findings identify a specificity mechanism in the functional modification of bacterial chemoreceptors. Methyltransferases of the CheR family and methylesterases of the CheB family control chemoreceptor methylation, and this dynamic posttranslational modification is necessary for proper chemotaxis of bacteria. Studies with enterobacteria that contain a single CheR or CheB show that, in addition to binding at the methylation site, some chemoreceptors bind CheR or CheB through additional high-affinity sites at distinct pentapeptide sequences in the chemoreceptors. We investigated the recognition of chemoreceptors by CheR proteins in the human pathogen Pseudomonas aeruginosa PAO1. Of the four methyltransferases in PAO1, we detected an interaction only between CheR2 and the chemoreceptor methyl-accepting chemotaxis protein B (McpB), which contains the pentapeptide GWEEF at its carboxyl terminus. Furthermore, CheR2 was also the only paralog that methylated McpB in vitro, and deletion of the pentapeptide sequence abolished both the CheR2-McpB interaction and the methylation of McpB. When clustered according to protein sequence, bacterial CheR proteins form two distinct families—those that bind pentapeptide-containing chemoreceptors and those that do not. These two families are distinguished by an insertion of three amino acids in the β-subdomain of CheR. Deletion of this insertion in CheR2 prevented its interaction with and methylation of McpB. Pentapeptide-containing chemoreceptors are common to many bacteria species; thus, these short, distinct motifs may enable the specific assembly of signaling complexes that mediate different responses.
Huwe1-Mediated Ubiquitylation of Dishevelled Defines a Negative Feedback Loop in the Wnt Signaling Pathway

By ubiquitylating a protein interaction domain in Dishevelled, Huwe1 acts as a negative feedback regulator of Wnt signaling. UbiqWNTin Feedback The Wnt/β-catenin pathway directs the migration of the Q neuroblasts in Caenorhabditis elegans. In response to Wnt pathway activation, Dishevelled (Dvl) is activated and the degradation of β-catenin is prevented. Dvl activity is regulated by phosphorylation and ubiquitylation. Using an RNA interference screen targeting ubiquitin ligases and deubiquitylating enzymes, de Groot et al. identified the E3 ubiquitin ligase EEL-1 as a Wnt signaling inhibitor that affected Q neuroblast migration. Knockdown of the EEL-1 homolog Huwe1 in human embryonic kidney 293T cells enhanced the activity of the Wnt/β-catenin transcriptional pathway. Huwe1 interacted and colocalized with Dvl. Huwe1 promoted the ubiquitylation of the DIX domain in Dvl and inhibited Dvl multimerization. Thus, Huwe1 functions as an evolutionarily conserved feedback inhibitor of Wnt signaling. Wnt signaling plays a central role in development, adult tissue homeostasis, and cancer. Several steps in the canonical Wnt/β-catenin signaling cascade are regulated by ubiquitylation, a protein modification that influences the stability, subcellular localization, or interactions of target proteins. To identify regulators of the Wnt/β-catenin pathway, we performed an RNA interference screen in Caenorhabditis elegans and identified the HECT domain–containing ubiquitin ligase EEL-1 as an inhibitor of Wnt signaling. In human embryonic kidney 293T cells, knockdown of the EEL-1 homolog Huwe1 enhanced the activity of a Wnt reporter in cells stimulated with Wnt3a or in cells that overexpressed casein kinase 1 (CK1) or a constitutively active mutant of the Wnt co-receptor low-density lipoprotein receptor–related protein 6 (LRP6). However, knockdown of Huwe1 had no effect on reporter gene expression in cells expressing constitutively active β-catenin, suggesting that Huwe1 inhibited Wnt signaling upstream of β-catenin and downstream of CK1 and LRP6. Huwe1 bound to and ubiquitylated the cytoplasmic Wnt pathway component Dishevelled (Dvl) in a Wnt3a- and CK1ε-dependent manner. Mass spectrometric analysis showed that Huwe1 promoted K63-linked, but not K48-linked, polyubiquitination of Dvl. Instead of targeting Dvl for degradation, ubiquitylation of the DIX domain of Dvl by Huwe1 inhibited Dvl multimerization, which is necessary for its function. Our findings indicate that Huwe1 is part of an evolutionarily conserved negative feedback loop in the Wnt/β-catenin pathway.
Effect of a motivational group intervention on exercise self-efficacy and outcome expectations for exercise in schizophrenia spectrum disorders.

BACKGROUND Persons with schizophrenia spectrum disorders (SSDs) contend with multiple barriers to exercise. Interventions are needed to enhance attitudes theoretically linked to exercise behavior. OBJECTIVE To examine the effect of Walk, Address Sensations, Learn About Exercise, Cue Exercise for SSDs (WALC-S) intervention on exercise self-efficacy (SEE) and outcome expectations (OEES) in 97 outpatients with SSDs. DESIGN Experimental, pre- and posttest. Randomization to experimental (WALC-S) or time-and-attention control (TAC) after baseline SEE and OEES measures. Measures repeated after WALC-S or TAC. RESULTS N = 97, 46% female, 43% African American, average age 46.9 years (SD = 2.0). Mean SEE scores were significantly higher in WALC-S participants after intervention, F(1, 95) = 5.92, p = . 0168, however, mean OEES scores were significantly higher in control participants after intervention, F(1, 95) = 5.76, p = . 0183. CONCLUSION This is the first study to examine SEE and OEES in SSDs. Interventions to enhance exercise attitudes are a critical first step toward the ultimate goal of increasing exercise participation.
Extrahepatic cholestasis downregulates Oatp1 by TNF‐α signalling without affecting Oatp2 and Oatp4 expression and sodium‐independent bile salt uptake in rat liver

Hepatic uptake of bile salts is mediated by sodium‐dependent and sodium‐independent transport systems. During extrahepatic cholestasis, both the function and the expression of the Na+/taurocholate cotransporting polypeptide (Ntcp) are downregulated. To test whether sodium‐independent organic anion‐transporting polypeptides are also affected by extrahepatic cholestasis, the function and expression of all three Oatps have been determined in common bile duct‐ligated (CBDL) rats. Oatp1/Oatp1a1 protein mass remained unchanged after CBDL for 1 day, but then declined by 75±7% and 90±17%, respectively, after 3 and 7 days. In contrast, Oatp2/Oatp1a4 and Oatp4/Oatp1b2 protein expression was not affected by CBDL as compared with controls. After CBDL, Oatp1 mRNA was rapidly downregulated by 68±21% of untreated controls (P<0.05) within 24 h, and remained at similar levels at 3 and 7 days. Cytokine‐inactivation studies with etanercept pretreatment demonstrated that TNF‐α‐dependent signals mediated the down‐regulation of this transporter gene at both protein and mRNA levels during obstructive cholestasis. Sodium‐independent uptake of taurocholate and cholate into freshly isolated hepatocyte suspensions showed neither significant differences in Km nor Vmax values. These results indicate that sodium‐independent transport of bile salts may be mediated by Oatp2 and 4 during biliary obstruction, because its expression remains unaffected and may compensate for loss of Oatp1 expression and function in cholestatic hepatocytes.