Miracle-dz/UniFAR-FTUs huggingface dataset:
Hexanoic acid protects tomato plants against Botrytis cinerea by priming defence responses and reducing oxidative stress.

Treatment with the resistance priming inducer hexanoic acid (Hx) protects tomato plants from Botrytis cinerea by activating defence responses. To investigate the molecular mechanisms underlying hexanoic acid-induced resistance (Hx-IR), we compared the expression profiles of three different conditions: Botrytis-infected plants (Inf), Hx-treated plants (Hx) and Hx-treated + infected plants (Hx+Inf). The microarray analysis at 24 h post-inoculation showed that Hx and Hx+Inf plants exhibited the differential expression and priming of many Botrytis-induced genes. Interestingly, we found that the activation by Hx of other genes was not altered by the fungus at this time point. These genes may be considered to be specific targets of the Hx priming effect and may help to elucidate its mechanisms of action. It is noteworthy that, in Hx and Hx+Inf plants, there was up-regulation of proteinase inhibitor genes, DNA-binding factors, enzymes involved in plant hormone signalling and synthesis, and, remarkably, the genes involved in oxidative stress. Given the relevance of the oxidative burst occurring in plant-pathogen interactions, the effect of Hx on this process was studied in depth. We showed by specific staining that reactive oxygen species (ROS) accumulation in Hx+Inf plants was reduced and more restricted around infection sites. In addition, these plants showed higher ratios of reduced to oxidized glutathione and ascorbate, and normal levels of antioxidant activities. The results obtained indicate that Hx protects tomato plants from B. cinerea by regulating and priming Botrytis-specific and non-specific genes, preventing the harmful effects of oxidative stress produced by infection.
Maintaining Database Consistency in Peer to Peer Networks

We present an algorithm for persistent consistent distributed commit (distributed database commit) in a dynamic, asynchronous, peer to peer network. The algorithm has constant overhead in time and space and almost constant communication complexity, allowing it to scale to very large size networks. Previous solutions required linear overhead in communication and space, making them unscalable. We introduce a modular solution based on several well dened blocks with clear formal specications. These blocks can be implemented in a variety of ways and we give examples of possible implementations. Most of the existing solutions require acknowledgments from every participant for each action. Our algorithm is highly ecien t by aggregating these acknowledgments. Also, in contrast with existing solutions, our algorithm does not require any membership knowledge. Components are detected based on local information and the information is disseminated on an overlay spanning tree. The algorithm may prove to be more suited for practical implementation than the existing ones, because of its simplicity.
The quality of home spirometry in school children with asthma.

BACKGROUND Handheld electronic spirometers provide the opportunity for more comprehensive monitoring of lung function at home than has hitherto been available. The aim of this study was to assess the quality of spirometric data collected at home by 90 asthmatic schoolchildren aged 7-14 years. METHODS After training, children carried out twice daily recordings at home for four consecutive periods of 4 weeks using a data storage spirometer (Vitalograph), encouraged by 4-weekly visits from a research nurse. Compliance (proportion of blows recorded at correct time of day), technical quality (by machine criteria), and valid data recorded (the multiple of compliance and technical ability) were assessed. RESULTS Mean compliance declined from 81.4% to 70.4% (p<0.001) between the first and last month, although the technical quality of the manoeuvres (81.9% and 80.1%, respectively) did not change significantly (p=0.48). CONCLUSIONS There was a steady reduction of valid data over the four periods (from 73.6% to 64.3%, 59.7%, and 57.6%) with wide individual differences. Even under ideal conditions, home spirometry provides an incomplete (and therefore potentially biased) picture of long term changes in pulmonary function.
Role of Acid-Sensing Ion Channel 1a in the Secondary Damage of Traumatic Spinal Cord Injury

Objective: To determine the cellular and molecular mechanisms by which acid-sensing ion channel 1a (ASIC1a) plays its role in the secondary injury after traumatic spinal cord injury (SCI), and validate the neuroprotective effect of ASIC1a suppression in SCI model in vivo. Background: Secondary damage after traumatic SCI contributes to the exacerbation of cellular insult and thereby contributes to spinal cord dysfunction. However, the underlying mechanisms remain largely unknown. Acidosis is commonly involved in the secondary injury process after the injury of central nervous system, but whether ASIC1a is involved in secondary injury after SCI is unclear. Methods: Male Sprague–Dawley rats were subjected to spinal contusion using a weight-drop injury approach. Western blotting and immunofluorescence assays were used to observe the change of ASIC1a expression after SCI. The TUNEL staining in vivo as well as the cell viability and death assays in spinal neuronal culture were employed to assess the role of ASIC1a in the secondary spinal neuronal injury. The electrophysiological recording and Ca2+ imaging were performed to reveal the possible underlying mechanism. The antagonists and antisense oligonucleotide for ASIC1a, lesion volume assessment assay and behavior test were used to estimate the therapeutic effect of ASIC1a on SCI. Results: We show that ASIC1a expression is markedly increased in the peri-injury zone after traumatic SCI. Consistent with the change of ASIC1a expression in injured spinal neurons, both ASIC1a-mediated whole-cell currents and ASIC1a-mediated Ca2+ entry are significantly enhanced after injury. We also show that increased activity of ASIC1a contributes to SCI-induced neuronal death. Importantly, our results indicate that down-regulation of ASIC1a by antagonists or antisense oligonucleotide reduces tissue damage and promotes the recovery of neurological function after SCI. Conclusion: This study reveals a cellular and molecular mechanism by which ASIC1a is involved in the secondary damage process after traumatic SCI. Our results suggest that blockade of Ca2+-permeable ASIC1a may be a potential neuroprotection strategy for the treatment of SCI patients.
Adaptive Subcarrier PSK Intensity Modulation in Free Space Optical Systems

We propose an adaptive transmission technique for free space optical (FSO) systems, operating in atmospheric turbulence and employing subcarrier phase shift keying (S-PSK) intensity modulation. Exploiting the constant envelope characteristics of S-PSK, the proposed technique offers efficient utilization of the FSO channel capacity by adapting the modulation order of S-PSK, according to the instantaneous state of turbulence induced fading and a pre-defined bit error rate (BER) requirement. Novel expressions for the spectral efficiency and average BER of the proposed adaptive FSO system are presented and performance investigations under various turbulence conditions, turbulence models, and target BER requirements are carried out. Numerical results indicate that significant spectral efficiency gains are offered without increasing the transmitted average optical power or sacrificing BER requirements, especially in moderate-to-strong turbulence conditions. Furthermore, the proposed variable rate transmission technique is applied to multiple input multiple output (MIMO) FSO systems, providing additional improvement in the achieved spectral efficiency as the number of the transmit and/or receive apertures increases.
Frequency Response of the Renal Vasculature in Congestive Heart Failure

Background—The renal vasoconstrictor response to renal nerve stimulation is greater in congestive heart failure (CHF) rats than in control rats. This study tested the hypothesis that the enhanced renal vasoconstrictor response to renal nerve stimulation in CHF is a result of an impairment in the low-pass filter function of the renal vasculature. Methods and Results—In response to conventional graded-frequency renal nerve stimulation, the reductions in renal blood flow at each stimulation frequency were greater in CHF rats than control rats. A pseudorandom binary sequence pattern of renal nerve stimulation was used to examine the frequency response of the renal vasculature. Although this did not affect the renal blood flow power spectrum in control rats, there was a 10-fold increase in renal blood flow power over the frequency range of 0.01 to 1.0 Hz in CHF rats. On analysis of transfer function gain, attenuation of the renal nerve stimulation input signal was similar in control and CHF rats over the frequency range of 0.001 to 0.1 Hz. However, over the frequency range of 0.1 to 1.0 Hz, although there was progressive attenuation of the input signal (−30 to −70 dB) in control rats, CHF rats exhibited a flat gain response (−20 dB) without progressive attenuation. Conclusions—The enhanced renal vasoconstrictor response to renal nerve stimulation in CHF rats is caused by an alteration in the low-pass filter function of the renal vasculature, resulting in a greater transfer of input signals into renal blood flow in the 0.1 to 1.0 Hz range.
Spectrogram dimensionality reductionwith independence constraints

We present an algorithm to find a low-dimensional decomposition of a spectrogram by formulating this as a regularized non-negative matrix factorization (NMF) problem with a regularization term chosen to encourage independence. This algorithm provides a better decomposition than standard NMF when the underlying sources are independent. It is directly applicable to non-square matrices, and it makes better use of additional observation streams than previous nonnegative ICA algorithms.
Mechanistic Models Predict Efficacy of CCR5‐Deficient Stem Cell Transplants in HIV Patient Populations

Combination antiretroviral therapy (cART) effectively suppresses viral load in HIV‐infected individuals, but it is not a cure. Bone marrow transplants using HIV‐resistant stem cells have renewed hope that cure is achievable but key questions remain e.g., what percentage of stem cells must be HIV‐resistant to achieve cure? As few patients have undergone transplants, we built a mechanistic model of HIV/AIDS to approach this problem. The model includes major players of infection, reproduces the complete course of the disease, and simulates crucial components of clinical treatments, such as cART, irradiation, host recovery, gene augmentation, and donor chimerism. Using clinical data from 172 cART‐naïve HIV‐infected individuals, we created virtual populations to predict performance of CCR5‐deficient stem‐cell therapies and explore interpatient variability. We validated our model against a published clinical study of CCR5‐modified T‐cell therapy. Our model predicted that donor chimerism must exceed 75% to achieve 90% probability of cure across patient populations.
A revisit of Generative Model for Automatic Image Annotation using Markov Random Fields

Much research effort on automatic image annotation (AIA) has been focused on generative model, due to its well formed theory and competitive performance as compared with many well designed and sophisticated methods. However, when considering semantic context for annotation, the model suffers from the weak learning ability. This is mainly due to the lack of parameter setting and appropriate learning strategy for characterizing the semantic context in the traditional generative model. In this paper, we present a new approach based on multiple Markov random fields (MRF) for semantic context modeling and learning. Differing from previous MRF related AIA approach; we explore the optimal parameter estimation and model inference systematically to leverage the learning power of traditional generative model. Specifically, we propose new potential function for site modeling based on generative model and build local graphs for each annotation keyword. The parameter estimation and model inference is performed in local optimal sense. We conduct experiments on commonly used benchmarks. On Corel 5000 images, we achieved 0.36 and 0.31 in recall and precision respectively on 263 keywords. This is a very significant improvement over the best reported result of the current state-of-the-art approaches.
Smartphone-based Pedestrian Dead Reckoning as an indoor positioning system

Nowadays, personal positioning systems are more necessary to build many location-based services. Pedestrian Dead Reckoning (PDR), which is a pedestrian positioning technique using the accelerometer sensor to recognize pattern of steps, is an alternative method that has advantages in terms of infrastructure-independent. However, the variation of walking pattern on each individual will make some difficulties for the system to detect displacement. This is really interested authors to develop a sensor-based positioning system that applied generally to all individuals. In the test, 15 test subjects was taken with the distance of each 10m, 20m and 30m. Experiment begins with the feasibility test of accelerometer sensor. In this work, a smartphone with average sampling rate 63.79 Hz and standard deviation of 1.293 is used to records the acceleration. Then, the acceleration data are analyzed to detect step and to estimate the travelled distance using several methods. Detection of steps are able to make an average error of 2.925%, while the most nearly correct displacement estimation is using Scarlet experimental method which is make a distance average error of 1.39metres at all the traveled distance.
Pharmacologic Inhibition of Nedd8 Activation Enzyme Exposes CD4-Induced Epitopes within Env on Cells Expressing HIV-1

ABSTRACT HIV-1 Vpu decreases the exposure of epitopes within the viral envelope glycoprotein (Env) on the surface of infected cells by downregulating both BST2 and CD4. To test the hypothesis that inhibiting Vpu activity would increase the exposure of these epitopes and sensitize infected cells to antibody-dependent cellular cytotoxicity (ADCC), we treated cells with the Nedd8 activation enzyme (NAE) inhibitor MLN4924, which inhibits the cullin1-based ubiquitin ligase complex coopted by Vpu to degrade cellular targets. Treatment of HeLa cells with MLN4924 or expression of a dominant negative mutant of cullin1 inhibited the Vpu-mediated downregulation of CD4 but not the downregulation of BST2. NAE inhibition also increased the surface exposure of CD4-induced epitopes within Env on HEK293 cells containing an inducible HIV genome, on infected CEM T cells, and on infected primary T cells. In contrast, the Vpu-mediated downregulation of BST2 was substantially inhibited by MLN4924 only when T cells were treated with alpha interferon (IFN-α) to induce high levels of BST2 expression. As reported previously, the absence of vpu or nef and even more so the combined absence of these two genes sensitized infected cells to ADCC. However, NAE inhibition affected ADCC minimally. Paradoxically, even in infected, IFN-treated cells in which NAE inhibition substantially rescued the surface level of BST2, the surface level of Env detected with an antibody recognizing a CD4-independent epitope (2G12) was minimally increased. Mutation of the C-terminal Vpu residue W76, which supports the ability of Vpu to stimulate virion release by displacing BST2 from assembly sites on the plasma membrane by a cullin1-independent mechanism, increased the exposure of Env detected by 2G12 on infected T cells. Thus, inhibiting the displacement function of Vpu together with its ability to degrade CD4 and BST2 may be required to sensitize infected cells to ADCC. IMPORTANCE Pathogenic viruses encode gene products that enable evasion of host immune surveillance mechanisms. One such mechanism is antibody-dependent cellular cytotoxicity (ADCC), whereby host antibodies bind envelope glycoproteins of the virus that are inserted into the cellular membrane and direct the destruction of infected cells. Targeting pharmacologically the activity of HIV-1 Vpu, which contributes to evasion of ADCC, could potentially sensitize infected cells to this immune surveillance mechanism, an outcome that would have therapeutic implications with respect to the goal of curing HIV-1 infection. The Nedd8 activation enzyme inhibitor MLN4924 blocks the activity of the host ubiquitin ligase that Vpu coopts to direct the degradation of CD4 and BST2. We observed that while MLN4924 partially reverses the activity of Vpu and could become part of a therapeutic approach by virtue of CD4-induced epitope exposure, sufficient Vpu activity as an antagonist of BST2 persists despite this drug to allow escape from ADCC.
Epidermal growth factor receptor inhibitors in oncology

Purpose of review Inhibition of the epidermal growth factor receptor (EGFR) by small molecules or antibodies has been pursued as a paradigm to treat human cancers for over two decades. It is now clear that these agents can induce tumor regressions in a variety of human cancers, proving the critical role of EGFR signals for tumor maintenance in subsets of patients with these cancers. Clinically meaningful responses, however, are only transient and further refinement of EGFR-targeted therapies is urgently needed. Recent findings Several studies provide new insights into the molecular basis of EGFR kinase inhibitor resistance, including co-activation of the MET growth factor receptor, loss of the phosphatase and tensin homolog (PTEN) tumor suppressor, and KRAS mutation. Potential strategies are emerging to overcome acquired EGFR kinase inhibitor resistance associated with the T790 M EGFR mutation, including a new compound identified in a chemical library screen and a combination regimen of an anti-EGFR antibody plus a small molecule EGFR kinase inhibitor. Lastly, pulsatile dosing schedules are being pursued to accomplish more complete target inhibition. Summary Current data point toward a strong association between EGFR genotype and EGFR kinase inhibitor response, similar to the findings with other oncogenic kinases (BCR-ABL, HER2, KIT, PDGFRA, BRAF). This relationship is less obvious for antibodies targeting EGFR. More complete inhibition of EGFR in tumor cells and more focused clinical drug development remain important goals toward further success with this class of anticancer agents.
Pharmacotherapy of heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia (HIT) is a life-and-limb threatening condition that is associated with the development of antibodies that activate platelets and the coagulation system in the presence of unfractionated heparin or low molecular weight heparin. The binding of antibody to heparin-PF-4 complexes can activate platelets, leading to an acute, often catastropic, thrombotic diathesis. The most common laboratory finding is the development of thrombocytopenia 5 or more days after beginning heparin treatment, which occur in up to 1 – 5% of patients exposed to heparin, depending on type of heparin and indication for anticoagulation. The onset of thrombocytopenia can be immediate or delayed for several weeks after the exposure to heparin. Approximately 50 – 60% of patients who develop HIT manifest acute venous or arterial thrombosis and a significant percentage of these patients die or develop vascular gangrene of a limb that requires amputation. Given the severe sequelae associated with HIT, recognition and immediate medical management is essential. Treatment of a patient with HIT is complex, as there are several different anticoagulants now available which have been shown to be useful. Optimal management depends on each patient’s individual clinical manifestations, as well as the need for ongoing anticoagulation therapy. No single agent or treatment approach can be considered to be ‘standard practice’ as very few clinical trials have been completed, compare different treatment options. The use of warfarin alone in a patient with HIT, must be avoided in order to avoid the possibility of further activating coagulation, which may hasten the development of venous limb gangrene. There are several different tests available that detect HIT antibodies and each has different sensitivity and specificity for HIT. In this review we discuss the epidemiology and natural history of HIT, risk factors associated with the development of HIT and the clinical and laboratory tests that aid in the diagnosis and treatment. Special emphasis is given to addressing the management of HIT in special populations, particularly patients with renal or liver disease, acute coronary syndromes, pregnancy, paediatrics and patients who require cardiopulmonary bypass surgery.
A delay variation and floorplan aware high-level synthesis algorithm with body biasing

In this paper, we propose a delay variation and floorplan aware high-level synthesis algorithm with body biasing, which minimizes the average leakage energy of manufactured chips. To realize a floorplan-oriented high-level synthesis, we utilize a huddle-based distributed register architecture (HDR architecture), one of the DR architectures. HDR architecture divides the chip area into small partitions called a huddle and we can control a body bias voltage for every huddle. During high-level synthesis, we iteratively obtain expected leakage energy for every huddle when applying a body bias voltage. A huddle with smaller expected leakage energy contributes to reducing expected leakage energy of the entire circuit but can increase the latency. We assign CDFG nodes in critical paths to the huddles with larger expected leakage energy and those in non-critical paths to the huddles with smaller expected leakage energy. We expect to minimize the entire leakage energy in a manufactured chip without increasing its latency. Experimental results show that our algorithm reduces the average leakage energy by up to 38.9% without latency and yield degradation compared with typical-case design with body biasing.
Prepulse inhibition of the startle blink reflex is modulated by the short-term consolidation of memory

Prepulse inhibition (PPI) of the startle blink reflex in humans can be modulated by selective attention to the prepulse. The present experiment used a task that isolated the short-term consolidation of memory to determine whether this process modulates PPI. Participants were briefly presented with a display of one or three letters followed by a pattern mask and asked to make a delayed report of the letter(s) shown. Memory recall was better in the 1-letter condition than in the 3-letter condition. Prepulse inhibition was greater in the 3-letter condition than in the 1-letter condition at lead intervals of 120 and 240 ms following the onset of the letter display. Blink modulation did not differ between the letter conditions at lead intervals of 120, 240, 360, and 2600 ms following the mask, ruling out other explanations (e.g., rehearsal) for the earlier difference in PPI. The results suggest that the short-term consolidation of memory, and possibly any cognitive process that requires access to a theoretical limited capacity central processing mechanism, modulated PPI.
The Role of Media Slant in Elections and Economics

We formalize the concept of media slant as a relative emphasis on di¤erent issues of political interest by the media, and we illustrate the e¤ects of the media choice of slant on political outcomes and economic decisions in a rational expectations model. In a two-candidate elec- tion, if the media is biased in favor of the underdog, then it will put more emphasis on issues with a large electoral impact, hoping that the news will deliver an upset victory. Whether citizens are better o¤ with media biased in favor of the underdog or the frontrunner de- pends on the importance of choosing the . right.candidate for citizens versus the impact of political news on the private economic decisions of voters. Balanced media, giving each issue equal coverage, may be worse for voters than partisan media.