Miracle-dz/UniFAR-FTUs huggingface dataset:
Can the theory of planned behaviour predict the physical activity behaviour of individuals?

The Theory of Planned Behaviour (TPB) can identify cognitions that predict differences in behaviour between individuals. However, it is not clear whether the TPB can predict the behaviour of an individual person. This study employs a series of n-of-1 studies and time series analyses to examine the ability of the TPB to predict physical activity (PA) behaviours of six individuals. Six n-of-1 studies were conducted, in which TPB cognitions and up to three PA behaviours (walking, gym workout and a personally defined PA) were measured twice daily for six weeks. Walking was measured by pedometer step count, gym attendance by self-report with objective validation of gym entry and the personally defined PA behaviour by self-report. Intra-individual variability in TPB cognitions and PA behaviour was observed in all participants. The TPB showed variable predictive utility within individuals and across behaviours. The TPB predicted at least one PA behaviour for five participants but had no predictive utility for one participant. Thus, n-of-1 designs and time series analyses can be used to test theory in an individual.
Expression of Epidermal Growth Factor in Transgenic Mice Causes Growth Retardation*

The epidermal growth factor (EGF) family of peptides signals through the erbB family of receptor tyrosine kinases and plays important roles in development and tumorigenesis. Both EGF and transforming growth factor (TGF)-α only bind to erbB1 and activate it. The precursor of EGF is distinct from that of TGF-α in having eight additional EGF-like repeats. We have recently shown that the EGF precursor without these repeats is biologically active and leads to hypospermatogenesis in transgenic mice. Here we present evidence that the growth of transgenic mice widely expressing this engineered EGF precursor is also stunted. These mice were consistently born at half the normal weight and reached almost 80% of normal weight at adulthood. The mechanism involved a reduction of serum insulin-like growth factor-binding protein-3. Chondrocyte development in the growth plate was affected, and osteoblasts accumulated in the endosteum and periosteum. Besides these novel findings on the in vivoeffects of EGF on bone development, we observed no sign of tumor formation in our transgenic animals. In contrast to previous reports on TGF-α transgenic mice, we show that the biological functions of EGF and TGF-α are clearly distinct.
Enhancer deletions of the SHOX gene as a frequent cause of short stature: the essential role of a 250 kb downstream regulatory domain

Background: Mutations and deletions of the homeobox transcription factor gene SHOX are known to cause short stature. The authors have analysed SHOX enhancer regions in a large cohort of short stature patients to study the importance of regulatory regions in developmentally relevant genes like SHOX. Methods: The authors tested for the presence of copy number variations in the pseudoautosomal region of the sex chromosomes in 735 individuals with idiopathic short stature and compared the results to 58 cases with Leri–Weill syndrome and 100 normal height controls, using fluorescence in situ hybridisation (FISH), single nucleotide polymorphism (SNP), microsatellites, and multiplex ligand dependent probe amplification (MLPA) analysis. Results: A total of 31/735 (4.2%) microdeletions were identified in the pseudoautosomal region in patients with idiopathic short stature; eight of these microdeletions (8/31; 26%) involved only enhancer sequences residing a considerable distance away from the gene. In 58 Leri–Weill syndrome patients, a total of 29 microdeletions were identified; almost half of these (13/29; 45%) involve enhancer sequences and leave the SHOX gene intact. These deletions were absent in 100 control persons. Conclusion: The authors conclude that enhancer deletions in the SHOX gene region are a relatively frequent cause of growth failure in patients with idiopathic short stature and Leri–Weill syndrome. The data highlights the growing recognition that regulatory sequences are of crucial importance in the genome when diagnosing and understanding the aetiology of disease.
Minimally Invasive Monitoring of Chronic Central Venous Catheter Patency in Mice Using Digital Subtraction Angiography (DSA)

Background Repetitive administration of medication or contrast agents is frequently performed in mice. The introduction of vascular access mini-ports (VAMP) for mice allows long-term vascular catheterization, hereby eliminating the need for repeated vessel puncture. With catheter occlusion being the most commonly reported complication of chronic jugular vein catheterization, we tested whether digital subtraction angiography (DSA) can be utilized to evaluate VAMP patency in mice. Methods Twenty-three mice underwent catheterization of the jugular vein and subcutaneous implantation of a VAMP. The VAMP was flushed every second day with 50 μL of heparinized saline solution (25 IU/ml). DSA was performed during injection of 100 μL of an iodine based contrast agent using an industrial X-ray inspection system intraoperatively, as well as 7±2 and 14±2 days post implantation. Results DSA allowed localization of catheter tip position, to rule out dislocation, kinking or occlusion of a microcatheter, and to evaluate parent vessel patency. In addition, we observed different ante- and retrograde collateral flow patterns in case of jugular vein occlusion. More exactly, 30% of animals showed parent vessel occlusion after 7±2 days in our setting. At this time point, nevertheless, all VAMPs verified intravascular contrast administration. After 14±2 days, intravascular contrast injection was verified in 70% of the implanted VAMPs, whereas at this point of time 5 animals had died or were sacrificed and in 2 mice parent vessel occlusion hampered intravascular contrast injection. Notably, no occlusion of the catheter itself was observed. Conclusion From our observations we conclude DSA to be a fast and valuable minimally invasive tool for investigation of catheter and parent vessel patency and for anatomical studies of collateral blood flow in animals as small as mice.
Signal Peptide-Dependent Inhibition of MHC Class I Heavy Chain Translation by Rhesus Cytomegalovirus

The US2-11 region of human and rhesus cytomegalovirus encodes a conserved family of glycoproteins that inhibit MHC-I assembly with viral peptides, thus preventing cytotoxic T cell recognition. Since HCMV lacking US2-11 is no longer able to block assembly and transport of MHC-I, we examined whether this is also observed for RhCMV lacking the corresponding region. Unexpectedly, recombinant RhCMV lacking US2-11 was still able to inhibit MHC-I expression in infected fibroblasts, suggesting the presence of an additional MHC-I evasion mechanism. Progressive deletion analysis of RhCMV-specific genomic regions revealed that MHC-I expression is fully restored upon additional deletion of rh178. The protein encoded by this RhCMV-specific open reading frame is anchored in the endoplasmic reticulum membrane. In the presence of rh178, RhCMV prevented MHC-I heavy chain (HC) expression, but did not inhibit mRNA transcription or association of HC mRNA with translating ribosomes. Proteasome inhibitors stabilized a HC degradation intermediate in the absence of rh178, but not in its presence, suggesting that rh178 prevents completion of HC translation. This interference was signal sequence-dependent since replacing the signal peptide with that of CD4 or murine HC rendered human HCs resistant to rh178. We have identified an inhibitor of antigen presentation encoded by rhesus cytomegalovirus unique in both its lack of homology to any other known protein and in its mechanism of action. By preventing signal sequence-dependent HC translocation, rh178 acts prior to US2, US3 and US11 which attack MHC-I proteins after protein synthesis is completed. Rh178 is the first viral protein known to interfere at this step of the MHC-I pathway, thus taking advantage of the conserved nature of HC leader peptides, and represents a new mechanism of translational interference.
Factors Associated with Active Smoking, Quitting, and Secondhand Smoke Exposure among Pregnant Women in Greece

Background Pregnant women are exposed to tobacco smoke through active smoking and contact with secondhand smoke (SHS), and these exposures have a significant impact on public health. We investigated the factors that mediate active smoking, successful quitting, and SHS exposure among pregnant women in Crete, Greece. Methods Using a cotinine-validated questionnaire, data were collected on active smoking and exposure to secondhand smoke from 1291 women who had successfully completed the first contact questionnaire of the prospective mother-child cohort (Rhea) in Crete during the 12th week of pregnancy. Results Active smoking at some time during pregnancy was reported by 36% of respondents, and 17% were current smokers at week 12 of gestation. Those less likely to quit smoking during pregnancy were those married to a smoker (OR, 1.76; P = 0.008), those who were multiparous (1.72; P = 0.011), and those with young husbands. Of the 832 (64%) nonsmokers, almost all (94%, n = 780) were exposed to SHS, with the majority exposed at home (72%) or in a public place (64%). Less educated women and younger women were exposed more often than their better educated and older peers (P < 0.001). Adjusting for potential confounders, parental level of education, age, and ethnicity were the main mediators of exposure to SHS during pregnancy. Conclusions Active smoking and exposure to SHS are very prevalent among pregnant women in Greece. The above findings indicate the need for support of population-based educational interventions aimed at smoking cessation in both parents, as well as of the importance of establishing smoke-free environments in both private and public places.
Effect of Chronic Hypertension and Sympathetic Denervation on Wall/Lumen Ratio of Cerebral Vessels

SUMMARY The purposes of this study were to determine whether 1) cerebral vessels undergo hypertrophy during chronic hypertension and 2) sympathetic nenes contribute to cerebral vascular changes In chronic hypertension. Morphometiic studies were undertaken in stroke-prone spontaneously hypertensive rats (SP-SHR) and normotenslve Wistar-Kyoto (WKY) rats. Unilateral superior cerrical gangUonectomy was performed in the SP-SHR at 8 weeks of age. When the rats were approximately 13 months old, they were killed and the brain was fixed with formalin at a perfusion pressure of 80% of the rat's systolic pressure. Wall/lumen ratio was measured in approximately 1200 arteries and arterioles. In parenchymal, but not pial, cerebral vessels there was pronounced vascular hypertrophy in SP-SHR: wall/lumen ratio was 0.08 in WKY and 0.14 in SP-SHR (p < 0.05). Sympathetic denervation attenuated the development of vascular hypertrophy in SP-SHR: wall/lumen ratio was 0.14 in the innervated parenchymal vessels, and 0.10 in denervated vessels (p < 0.05). We conclude that cerebral vessels undergo hypertrophy in stroke-prone SHR and speculate that vascular hypertrophy may protect cerebral vessels by reducing wall stress in chronic hypertension. Sympathetic nerves appear to exert a trophic effect on cerebral vascular muscle in chronic hypertension.
The Bile Acid Sensor Farnesoid X Receptor Is a Modulator of Liver Immunity in a Rodent Model of Acute Hepatitis1

Immune-mediated liver diseases including autoimmune and viral hepatitis are a major health problem worldwide. In this study, we report that activation of the farnesoid X receptor (FXR), a member of the ligand-activated nuclear receptor superfamily and bile sensor highly expressed in the liver, attenuates liver injury in a model of autoimmune hepatitis induced by Con A. We found that FXR gene ablation results in a time-dependent increase of liver expression (up to 20-fold in a 9-mo-old mouse) of osteopontin, a NKT cell-derived extracellular matrix protein and immunoregulatory cytokine. In comparison to wild-type, FXR−/− mice are more susceptible to Con A-induced hepatitis and react to Con A administration by an unregulated production of osteopontin. Administering wild-type mice with a synthetic FXR agonist attenuated Con A-induced liver damage and liver expression of the osteopontin gene. By in vitro studies, we found that FXR is expressed by primarily isolated NKT cells and its ablation favors ostepontin production in response to Con A. Chromatin immunoprecipitation assay and coimmunoprecipitation experiments demonstrate that the short heterodimer partner (SHP), a nuclear receptor and FXR target, was expressed by NKT cell hybridomas and increased in response to FXR activation. FXR activates SHP that interacts with and inhibits c-Jun binding to the osteopontin promoter. These data indicate that in NKT cells, FXR activation causes a SHP-mediated inhibition of osteopontin production. These data support the notion that the bile acid sensor FXR regulates the activation of liver NKT cells.
Grassmannian beamforming for MIMO amplify-and-forward relaying

We consider the problem of beamforming codebook design for limited feedback half-duplex multiple-input multiple output (MIMO) amplify-and-forward (AF) relay system. In the first part of the paper, the direct link between the source and the destination is ignored. Assuming perfect channel state information (CSI), we show that the source and the relay should map their signals to the dominant right singular vectors of the source-relay and relay-destination channels. For the limited feedback scenario, we prove the appropriateness of Grassmannian codebooks as the source and relay beamforming codebooks based on the distributions of the optimal source and relay beamforming vectors. In the second part of the paper, the direct link is considered in the problem model. Assuming perfect CSI, we derive the optimization problem that identifies the optimal source beamforming vector and show that the solution to this problem is uniformly distributed on the unit sphere for independent and identically distributed (i.i.d) Rayleigh channels. For the limited feedback scenario, we justify the appropriateness of Grassmannian codebooks for quantizing the optimal source beamforming vector based on its distribution. Finally, a modified quantization scheme is presented, which introduces a negligible penalty in the system performance but significantly reduces the required number of feedback bits.
Sum of Us: Truthful Self-Selection

We consider directed graphs over a set of agents, where an edge 〈i, j〉 is taken to mean that agent i trusts or supports agent j. Given such a graph, our goal is to select a subset of agents of fixed size that maximizes the sum of indegrees, that is, a subset of most popular or most trusted agents. On the other hand, each agent is only interested in being selected, and may misreport its outgoing edges to this end. This problem formulation captures realistic scenarios where agents choose among themselves, in the context of, e.g., social networks such as Twitter, reputation systems such as Epinions, and Internet search. We wish to design mechanisms—functions that map graphs to selected subsets (without making payments)—which satisfy two constraints: strategyproofness, i.e., agents cannot benefit from misreporting their outgoing edges; and approximation, that is, the mechanism must always select a subset of agents that is close to optimal in terms of the sum of indegrees. Our first major result is a surprising impossibility: no deterministic strategyproof mechanism can yield a finite approximation ratio for any k ∈ {1, . , n−1}, where k is the size of the selected subset and n is the number of agents. Our second major result is a randomized strategyproof mechanism that yields an approximation ratio of four for any value of k, and provides a ratio that approaches one as k grows. ∗Microsoft Israel R&D Center, 13 Shenkar Street, Herzeliya 46725, Israel, and Schools of Mathematics and Computer Science, Tel Aviv University, Tel Aviv, 69978, Israel, Email: nogaa@tau.ac. il. Research supported in part by a USA Israeli BSF grant, by a grant from the Israel Science Foundation, by an ERC advanced grant and by the Hermann Minkowski Minerva Center for Geometry at Tel Aviv University. †Institut fur Informatik, Ludwig-Maximilians-Universitat Munchen, 80538 Munchen, Germany, email: fischerf@tcs.ifi. lmu.de. Part of the work was done while the author was visiting The Hebrew University of Jerusalem. This visit was supported by a Minerva Short-Term Research Grant. ‡Microsoft Israel R&D Center, 13 Shenkar Street, Herzeliya 46725, Israel. Email: arielpro@gmail.com. §Microsoft Israel R&D Center, 13 Shenkar Street, Herzeliya 46725, Israel, and Technion, IIT, Haifa 32000, Israel. Email: moshet@microsoft.com
Alternate reality games for computer science education

Alternate reality games (ARG) are games that often blur the boundaries of reality and fiction. They use many different types of media to deliver an interactive narrative to the players and include puzzles that are part of a bigger quest that the players are trying to solve. They are not widely used in education and there is limited amount of research done considering their benefits to learning. However, especially some commercial entertainment ARGs have managed to engage people in collaborative problem solving very well. Therefore, benefits and issues of using ARGs in education, and especially in computer science education (CSE), are discussed in this paper. Alternate reality games could potentially be used to teach various computer science concepts, to enable student networking, and to promote computer science programs. A case study was conducted in order to research the potential of using alternate reality games in computer science education. The research of the case study is still in progress, but the preliminary results are promising. Therefore, we want to raise discussion of using alternate reality games in computer science education.
Clinical correlations of brain lesion distribution in multiple sclerosis

To explore relations between spatial distribution of multiple sclerosis (MS) lesions, and disability. In MS, the presence of asymptomatic brain lesions challenges the prediction of disability based on conventional brain MRI. Hypothesizing that symptomatology may partly be determined by lesion location, this retrospective study explored relations between lesion location and disability using voxelwise analyses in standard space.
Direct Feedback Alignment Provides Learning in Deep Neural Networks

Artificial neural networks are most commonly trained with the back-propagation algorithm, where the gradient for learning is provided by back-propagating the error, layer by layer, from the output layer to the hidden layers. A recently discovered method called feedback-alignment shows that the weights used for propagating the error backward don't have to be symmetric with the weights used for propagation the activation forward. In fact, random feedback weights work evenly well, because the network learns how to make the feedback useful. In this work, the feedback alignment principle is used for training hidden layers more independently from the rest of the network, and from a zero initial condition. The error is propagated through fixed random feedback connections directly from the output layer to each hidden layer. This simple method is able to achieve zero training error even in convolutional networks and very deep networks, completely without error back-propagation. The method is a step towards biologically plausible machine learning because the error signal is almost local, and no symmetric or reciprocal weights are required. Experiments show that the test performance on MNIST and CIFAR is almost as good as those obtained with back-propagation for fully connected networks. If combined with dropout, the method achieves 1.45% error on the permutation invariant MNIST task.
Periodic Structures in the Equatorial Ionosphere (Postprint)

Abstract : The plasma densities detected by the Planar Langmuir Probe (PLP) on board the Communication/Navigation Outage Forecasting System (C/NOFS) satellite have been analyzed for the June 2008 period. This interval, which corresponds to one of the quietest periods in the space era, exhibited broad plasma decreases (BPDs) which we have reported previously. In order to treat the data quantitatively, we have detrended the PLP data by using the International Reference Ionosphere model to remove variations in density due to changes in spacecraft altitude and latitude along the orbit. In this paper we present results of a statistical analysis of C/NOFS detrended plasma densities during June 2008 as well as neutral densities from the Gravity Recovery and Climate Experiment measured during the same period. The results show periodic structures in both charged and neutral species, most evident in limited local times. These structures resemble wave-4 nonmigrating tides. BPDs persist in the detrended data and appear as one of the minima in the periodic signatures, most strikingly on the nightside.
Evolution of Mutational Robustness in an RNA Virus

Mutational (genetic) robustness is phenotypic constancy in the face of mutational changes to the genome. Robustness is critical to the understanding of evolution because phenotypically expressed genetic variation is the fuel of natural selection. Nonetheless, the evidence for adaptive evolution of mutational robustness in biological populations is controversial. Robustness should be selectively favored when mutation rates are high, a common feature of RNA viruses. However, selection for robustness may be relaxed under virus co-infection because complementation between virus genotypes can buffer mutational effects. We therefore hypothesized that selection for genetic robustness in viruses will be weakened with increasing frequency of co-infection. To test this idea, we used populations of RNA phage φ6 that were experimentally evolved at low and high levels of co-infection and subjected lineages of these viruses to mutation accumulation through population bottlenecking. The data demonstrate that viruses evolved under high co-infection show relatively greater mean magnitude and variance in the fitness changes generated by addition of random mutations, confirming our hypothesis that they experience weakened selection for robustness. Our study further suggests that co-infection of host cells may be advantageous to RNA viruses only in the short term. In addition, we observed higher mutation frequencies in the more robust viruses, indicating that evolution of robustness might foster less-accurate genome replication in RNA viruses.