Miracle-dz/UniFAR-FTUs huggingface dataset:
Social Power Increases Interoceptive Accuracy

Building on recent psychological research showing that power increases self-focused attention, we propose that having power increases accuracy in perception of bodily signals, a phenomenon known as interoceptive accuracy. Consistent with our proposition, participants in a high-power experimental condition outperformed those in the control and low-power conditions in the Schandry heartbeat-detection task. We demonstrate that the effect of power on interoceptive accuracy is not explained by participants’ physiological arousal, affective state, or general intention for accuracy. Rather, consistent with our reasoning that experiencing power shifts attentional resources inward, we show that the effect of power on interoceptive accuracy is dependent on individuals’ chronic tendency to focus on their internal sensations. Moreover, we demonstrate that individuals’ chronic sense of power also predicts interoceptive accuracy similar to, and independent of, how their situationally induced feeling of power does. We therefore provide further support on the relation between power and enhanced perception of bodily signals. Our findings offer a novel perspective–a psychophysiological account–on how power might affect judgments and behavior. We highlight and discuss some of these intriguing possibilities for future research.
Classically or alternatively activated bovine monocyte-derived macrophages in vitro do not resemble CD163/Calprotectin biased macrophage populations in the teat

The functional phenotype of resident macrophages significantly determines the character of an inflammatory response. In this study we identified two phenotypes of tissue macrophages in bovine teat tissue based on expression of Calprotectin and CD163. To investigate a possible link between the dichotomy in phenotype and functional properties of cells in association with different host mediators we set up an in vitro model with bovine monocyte-derived macrophages (MdM). In vitro differentiated MdM invariably and uniformly expressed both antigens. Classically activated MdM (IFN-γ priming and LPS stimulation) showed a decreased CD163 expression while alternative activation (IL-4/IL-13 priming) did not change expression of CD163 and Calprotectin. Differently activated MdM showed a clearly distinct expression of genes related to classical (IL-12, inducible NO synthase) or alternative activation (IL-10, arginase I). The presence of the inflammatory host mediator prostaglandin E2 (PGE2) neither influenced expression of Calprotectin and CD163 nor gene expression profiles in MdM generated in the presence of PGE2 (PGE2-MdM). Supernatants of PGE2-MdM, however, significantly dampened the migration of neutrophilic granulocytes. The results of this study highlight the discrepancy between in vivo and in vitro obtained macrophages and point to the necessity to analyze the functional capacities of bovine tissue macrophages in situ.
Transient Liquid Phase Die Attach for High-Temperature Silicon Carbide Power Devices

Recently, silicon carbide power devices have been receiving attention for applications above 300 °C. For high-temperature applications, the die attached for these devices has to withstand the maximum operating temperature. In this paper, a transient liquid phase (TLP) die attach technique was demonstrated for two binary alloy systems, Ag-In and Au-In, on Si3N4 substrates. A nearly void-free joint was developed using the Ag-In alloy. Two inter-metallic phases of Agln2 and Ag2ln, along with pure Ag were identified. After annealing at 400 °C, the silver appears to be more evenly spread to form a silver-rich Ag-In alloy with a Ag composition of 70-75 wt. %, even though a nearly pure silver phase is still found in the region where the silver was initially deposited on the Si3N4 substrate. For the Au-In system, there was no indication of bonding degradation at the interface after annealing at 400 °C for 100 h in air. Two inter-metallic phases, Auln and Auln2, along with pure gold, were identified in the Au-In TLP joint. After annealing, the bonding interface became a more Au-rich Au-In alloy. The die attach pull strength, after thermal annealing, increased to approximately twice the minimum strength. The uniformity of the bonds improves and they become more homogeneous because the formation of intermetallic phases continues during thermal annealing.
Host Defenses Against Cryptococcosis

The interaction of pathogenic Cryptococcus species with their various hosts is somewhat unique compared to other fungal pathogens such as Aspergillus fumigatus and Candida albicans. Cryptococcus shares an intimate association with host immune cells, leading to enhanced intracellular growth. Furthermore, unlike most other fungal pathogens, the signs and symptoms of cryptococcal disease are typically self-inflicted by the host during the host’s attempt to clear this invader from sensitive organ systems such as the central nervous system. In this review, we will summarize the story of host-Cryptococcus interactions to date and explore strategies to exploit the current knowledge for treatment of cryptococcal infections.
The medullary dorsal reticular nucleus enhances the responsiveness of spinal nociceptive neurons to peripheral stimulation in the rat

Single‐unit spinal recordings combined with application of glutamate into the medullary dorsal reticular nucleus were used to assess the action of this nucleus upon deep dorsal horn neurons in rats. Injection of high glutamate concentrations (10 and 100 mm) induced a dramatic and long‐lasting increase of the responses of wide‐dynamic range neurons to electrical stimulation of the sciatic nerve in the noxious range, without affecting ongoing discharges. Post‐stimulus time histograms revealed that this increase concerned the post‐discharge, but not A‐ or C‐fibre‐mediated responses, which remained unchanged independently of the stimulation frequency applied. The onset of the glutamate‐induced response enhancement occurred with a concentration‐dependent time delay and developed slowly until its maximum. These data indicate that the medullary dorsal reticular nucleus exerts a facilitating action upon deep dorsal horn wide‐dynamic range neurons by enhancing their capacity to respond to peripheral stimulation through prolongation of their discharge. This action is accompanied by the strengthening of wind‐up of deep dorsal horn wide‐dynamic range neurons, hence providing a plausible substrate for chronic pain states. These results are in agreement with previous behavioural studies suggesting a pronociceptive role for the dorsal reticular nucleus [Almeida et al. (1996) Brain Res. Bull., 39, 7–15; Almeida et al. (1999) Eur. J. Neurosci. , 11, 110–122], and support the involvement of a reverberating circuit, previously described in morphological studies [Almeida et al. (1993) Neuroscience, 55, 1093–1106; Almeida et al. (2000) Eur. J. Pain, 4, 373–387], which probably operates only at a certain threshold of activation.
Young male daily smokers are nicotine dependent and experience several unsuccessful quit attempts

Abstract Objective. Previous studies on smoking cessation have generally been conducted with adolescents or adults. Very little is known about the cessation attempts, their success, and/or use of pharmacological aids in young adult smokers who want to quit. The present study aimed to investigate quitting attempts in a group of both young male daily and occasional smokers. Design and subjects. 614 male smokers aged 18–26 years completed a standardized questionnaire about their smoking habits, quit attempts, and aids used in smoking cessation. Results. Nearly all daily smokers (95.3%, 95% CI 93.1–96.8) were nicotine addicted to some extend according to the standardized questionnaire, and the more addicted they were, the more often they had tried to quit (p = 0.025). Of the daily smokers, 55.6% (95% CI 51.3–59.9) had made quit attempts and 36.2% (95% CI 32.1–40.4) had used nicotine replacement therapy (NRT). In all, 34.1% (95% CI 25.2–44.3) of all occasional smokers reported having intended to quit but they had seldom made more than one attempt whereas 20.2% of daily smokers had made at least three attempts. The stronger the nicotine dependence in daily smokers was, the more likely the subject was to have attempted to use NRT (quite dependent 23.8% vs. totally dependent 48.9%) (p < 0.001). Conclusions. A high proportion of young male daily smokers were nicotine addicted. Young smokers make many unsuccessful attempts to stop smoking using nicotine replacement therapy (NRT) on their own. A better availability of professional cessation services directed to young adult smokers is needed.
Role and timing of GTP binding and hydrolysis during EF-G-dependent tRNA translocation on the ribosome

The translocation of tRNA and mRNA through the ribosome is promoted by elongation factor G (EF-G), a GTPase that hydrolyzes GTP during the reaction. Recently, it was reported that, in contrast to previous observations, the affinity of EF-G was much weaker for GTP than for GDP and that ribosome-catalyzed GDP–GTP exchange would be required for translocation [Zavialov AV, Hauryliuk VV, Ehrenberg M (2005) J Biol 4:9]. We have reinvestigated GTP/GDP binding and show that EF-G binds GTP and GDP with affinities in the 20 to 40 μM range (37°C), in accordance with earlier reports. Furthermore, GDP exchange, which is extremely rapid on unbound EF-G, is retarded, rather than accelerated, on the ribosome, which, therefore, is not a nucleotide-exchange factor for EF-G. The EF-G·GDPNP complex, which is very labile, is stabilized 30,000-fold by binding to the ribosome. These findings, together with earlier kinetic results, reveal that EF-G enters the pretranslocation ribosome in the GTP-bound form and indicate that, upon ribosome-complex formation, the nucleotide-binding pocket of EF-G is closed, presumably in conjunction with GTPase activation. GTP hydrolysis is required for rapid tRNA–mRNA movement, and Pi release induces further rearrangements of both EF-G and the ribosome that are required for EF-G turnover.
Apolipoprotein E Polymorphism and Atherosclerosis

The relationship between apolipoprotein (apo) E and vascular disease has been the subject of a considerable amount of research. However, this relationship is far from clearly defined. This deficiency appears to be due to a multitude of factors. Among these are differences in ethnicity, age (and possibly gender), diagnostic criteria, and environmental factors (eg, diet and smoking) that have contributed to the contradictory findings. Several diseases and their treatment may also influence this relationship. There are also documented interactions between apo E genotypes and other genes or vascular risk factors. One possible clinically relevant application of identifying the apo E genotype could be to assess the response to a particular drug treatment. It may also be that apo E polymorphism will become a good predictor of vascular death (eg, from myocardial infarction or stroke) rather than an indicator of the risk of developing vascular disease but without an acute ischemic event. More research is required to define the place of apo E genotyping in the management of vascular disease in its various forms. Whatever the future brings, the evaluation of apo E genotypes will need to be rapid, cheap, and technically undemanding before this investigation becomes widely available and clinically relevant.
Effects of Factor VIII Concentrates on the Immune System of Patients with Hemophilia

The introduction of high-purity factor VIII (FVIII) concentrates in the treatment of patients with hemophilia A has raised the issue that the use of these products may change on the immune system of the recipients. There is now clear evidence that high-purity concentrates, particularly those produced by immune-affinity chromatography or recombinant DNA technology, slow the fall in CD4 cells that occurs in HIV seropositive patients. It remains to be demonstrated that this biological effect results in clinical benefits and that the occurrence of AIDS is slowed or delayed by the use of high-purity concentrates. On the other hand, concern has been expressed about the possibility that high-purity products might render patients with hemophilia less immunotolerant, facilitating the onset of FVIII antibodies. Follow-up studies of previously untreated hemophiliacs infused for the first time with recombinant FVIII products have ignited this concern, because approximately one fourth of severe hemophiliacs developed inhibitors. However, most of the inhibitors were transient, so that ultimately they had little influence on the efficacy of replacement therapy. It was subsequently realized that inhibitors develop with high frequency even in hemophiliacs treated with less pure, plasma-derived products, provided testing is prospective and as frequent as for studies of recombinant FVIII. On the whole, these data have provided new insights on the natural history of inhibitor development in previously untreated hemophiliacs, showing that low-titer, short-lasting inhibitors develop more frequently than previously recognized.
IQGAP1 Is a Component of Cdc42 Signaling to the Cytoskeleton*

The Ras-GAP related protein IQGAP1 binds several proteins, including actin, calmodulin, E-cadherin and the Rho family GTPase Cdc42. To gain insight into its in vivo function, IQGAP1 was overexpressed in mammalian cells. Transfection of IQGAP1 significantly increased the levels of active, GTP-bound Cdc42, resulting in the formation of peripheral actin microspikes. By contrast, transfection of an IQGAP1 mutant lacking part of theGAP-related domain (IQGAP1ΔGRD) substantially decreased the amount of GTP-bound Cdc42 in cell lysates. Consistent with these findings, IQGAP1ΔGRD blocked Cdc42 function in cells that stably overexpress constitutively active Cdc42 and abrogated the effect of bradykinin on Cdc42. In cells transfected with IQGAP1ΔGRD, bradykinin was unable to activate Cdc42, translocate Cdc42 to the membrane fraction, or induce filopodia production. IQGAP1ΔGRD transfection altered cellular morphology, producing small, round cells that closely resemble Cdc42−/− cells. Some insight into the mechanism was provided by in vitroanalysis, which revealed that IQGAP1ΔGRD increased the intrinsic GTPase activity of Cdc42, thereby increasing the amount of inactive, GDP-bound Cdc42. These data imply that IQGAP1 has a crucial role in transducing Cdc42 signaling to the cytoskeleton.
Breathing sounds spectral and higher order statistics changes from wakefulness to sleep in apneic and non-apneic people

Breathing sounds analysis conveys valuable information in relation to obstructive sleep apnea (OSA) during both sleep and wakefulness. In this study, we investigated whether the breathings sounds spectral and higher order statistics characteristics (HOS) change from wakefulness to sleep, and more importantly whether this change is associated with severity of OSA. Tracheal breathing sounds of 6 individuals with severe OSA and 6 non-OSA individuals during wakefulness and stage 2 of sleep, both in supine position, were used in this study. The sounds were recorded simultaneously with full overnight polysomnography (PSG) assessment. First, the sounds of 5 noise-free breathing cycles were extracted and sequestered into inspiratory and expiratory phase segments manually for each study subject. After normalizing each sound segment to its energy, spectral and HOS features were calculated. Several features including the median bispectral frequency (MBF), spectral bandwidth (BW) and bispectrum Harmonic Mean (HM) were found to change statistically significantly from wakefulness to sleep mostly in severe OSA group but not as much in non-OSA group. The most prominent and consistent change between the two groups of OSA and non-OSA was observed in MBF; it changed from wakefulness to sleep in the two groups in an opposite manner; this observation is congruent with the hypothesis that the upper airway in OSA population has an increased non-homogeneity.
Transcript Initiation and 5′-End Modifications Are Separable Events during Vesicular Stomatitis Virus Transcription

ABSTRACT In this report we describe a novel, bipartite vesicular stomatitis virus (VSV) replication system which was used to study the effect of mutations in the transcription start sequence on transcript initiation and 5′-mRNA modifications. The bipartite replication system consisted of two genomic RNAs, one of which (VSVΔG) was a recombinant VSV genome with the G gene deleted and the other (GFC) contained the G gene and two non-VSV reporter genes (green fluorescent protein [GFP] and chloramphenicol acetyltransferase [CAT]). Coinfection of cells with these two components resulted in high-level virus production and gave titers similar to that from wild-type-VSV-infected cells. Mutations were introduced within the first 3 nucleotides of the transcription start sequence of the third gene (CAT) of GFC. The effects of these changes on the synthesis and accumulation of CAT transcripts during in vivo transcription (e.g., in infected cells), and during in vitro transcription were determined. As we had reported previously (E. A. Stillman and M. A. Whitt, J. Virol. 71:2127–2137, 1997), changing the first and third nucleotides (NT-1 and NT-3) reduced CAT transcript levels in vivo to near undetectable levels. Similarly, changing NT-2 to a purine also resulted in the detection of very small amounts of CAT mRNA from infected cells. In contrast to the results in vivo, the NT-1C mutant and all of the second-position mutants produced near-wild-type amounts of CAT mRNA in the in vitro system, indicating that the mutations did not prevent transcript initiation per se but, rather, generated transcripts that were unstable in vivo. Oligo (dT) selection and Northern blot analysis revealed that the transcripts produced from these mutants did not contain a poly(A)+ tail and were truncated, ranging in size from 40 to 200 nucleotides. Immunoprecipitation analysis of cDNA-RNA hybrids with an antibody that recognizes trimethylguanosine revealed that the truncated mutant transcripts were not properly modified at the 5′ end, indicating the transcripts either were not capped or were not methylated. This is the first demonstration that transcript initiation and capping/methylation are separable events during VSV transcription. A model is proposed in which polymerase processivity is linked to proper 5′-end modification. The model suggests that a proofreading mechanism exists for VSV and possibly other nonsegmented minus-strand RNA viruses, whereby if some transcripts do not become capped during transcription in a normal infection, a signal is transduced such that the polymerase undergoes abortive elongation and the defective transcript is terminated prematurely and subsequently degraded.
Prediction of chemical-protein interactions: multitarget-QSAR versus computational chemogenomic methods.

Elucidation of chemical-protein interactions (CPI) is the basis of target identification and drug discovery. It is time-consuming and costly to determine CPI experimentally, and computational methods will facilitate the determination of CPI. In this study, two methods, multitarget quantitative structure-activity relationship (mt-QSAR) and computational chemogenomics, were developed for CPI prediction. Two comprehensive data sets were collected from the ChEMBL database for method assessment. One data set consisted of 81 689 CPI pairs among 50 924 compounds and 136 G-protein coupled receptors (GPCRs), while the other one contained 43 965 CPI pairs among 23 376 compounds and 176 kinases. The range of the area under the receiver operating characteristic curve (AUC) for the test sets was 0.95 to 1.0 and 0.82 to 1.0 for 100 GPCR mt-QSAR models and 100 kinase mt-QSAR models, respectively. The AUC of 5-fold cross validation were about 0.92 for both 176 kinases and 136 GPCRs using the chemogenomic method. However, the performance of the chemogenomic method was worse than that of mt-QSAR for the external validation set. Further analysis revealed that there was a high false positive rate for the external validation set when using the chemogenomic method. In addition, we developed a web server named CPI-Predictor, , which is available for free. The methods and tool have potential applications in network pharmacology and drug repositioning.
Short telomeres in an oral precancerous lesion: Q-FISH analysis of leukoplakia.

OBJECTIVES A precancerous condition is a lesion that, if left untreated, leads to cancer or can be induced to become malignant. In the oral region, leukoplakia is a lesion that has been regarded as precancerous. In cases of oral carcinoma, we have frequently noticed that a type of leukoplakia histologically demonstrating hyper-orthokeratosis and mild atypia (ortho-keratotic dysplasia; OKD) is often associated with carcinoma, either synchronously or metachronously. Therefore, we consider OKD-type leukoplakia to be a true precancerous lesion. MATERIALS AND METHODS In an attempt to clarify the relationship between OKD as a precancerous condition in the oral mucosa and telomere length, we estimated telomere lengths in this type of leukoplakia using quantitative fluorescence in situ hybridization, and also quantified the frequency of anaphase-telophase bridges (ATBs) in comparison with squamous cell carcinoma in situ (CIS) and the background tissues of CIS and OKD. RESULTS Ortho-keratotic dysplasia was frequently associated with squamous cell carcinoma (45.0%) and showed significantly shorter telomeres than normal control epithelium, CIS, or the background of CIS or OKD. The frequency of ATBs was much higher in OKD than in control epithelium or CIS. CONCLUSION Ortho-keratotic dysplasia appears to be frequently associated with carcinoma, chromosomal instability, and excessively shortened telomeres, not only in the lesion itself but also in the surrounding background. Therefore, when this type of leukoplakia is recognized in the oral region, strict follow-up for oral squamous cell carcinoma is necessary, focusing not only on the areas of leukoplakia, but also the surrounding background.
Why Does Neurorehabilitation Fail?

Following neurorehabilitation, many patients show limited benefit, generalization, or maintenance of gains over time. Some of the reasons that account for modest outcomes are discussed with particular reference to the differences between patients' needs and aspirations, the nature of patient-clinician interactions, and patients' rehabilitation readiness. The role of a more client-centered approach is reviewed, as well as the importance of facilitating patients' capacity to identify problems, develop goals, consider options, and make choices. It is proposed that effective outcomes depend on the clinicians' success in harnessing patients' intrinsic motivation to change.