Academic literature on the topic 'Position-position auto-correlation function'

ABSTRACT Several phenomena in astrophysics generate light curves with time delays. Among these are reverberation mapping and lensed quasars. In these systems, the measurement of the time delay is complicated by the fact that the delayed components are unresolved and that the light curves are generated from a stochastic process. We derive the likelihood function of the observations given a model of either a combination of time-delayed light curves or a single light curve. This likelihood function is different from the auto-correlation-function-based investigated by previous studies. We demonstrate that given a single-band light curve that is a linear combination of two (or more) time-shifted copies of an original light curve, generated from a probability distribution with some roughly known power spectrum, it is possible to test if the total-flux light curve is a composition of time-delayed copies or, alternatively, is consistent with being a single copy of the original light curve. Furthermore, it is possible to measure the time delays between these components even when the flux ratio is about 1/10. In the era of synoptic sky surveys, this method is useful for identifying lensed quasars and simultaneously measuring their time delays, and also for estimating the reverberation time scales of active galactic nuclei. In a companion paper, we derive another method that uses the centre-of-light astrometric position (e.g. of a lensed quasar) along with the combined flux. We also present the proper likelihood function for fitting a power-law model to a power spectrum. We test the new method on simulations and provide python and matlab implementations.

Abstract Motivation Mitochondria are an essential organelle in most eukaryotes. They not only play an important role in energy metabolism but also take part in many critical cytopathological processes. Abnormal mitochondria can trigger a series of human diseases, such as Parkinson's disease, multifactor disorder and Type-II diabetes. Protein submitochondrial localization enables the understanding of protein function in studying disease pathogenesis and drug design. Results We proposed a new method, SubMito-XGBoost, for protein submitochondrial localization prediction. Three steps are included: (i) the g-gap dipeptide composition (g-gap DC), pseudo-amino acid composition (PseAAC), auto-correlation function (ACF) and Bi-gram position-specific scoring matrix (Bi-gram PSSM) are employed to extract protein sequence features, (ii) Synthetic Minority Oversampling Technique (SMOTE) is used to balance samples, and the ReliefF algorithm is applied for feature selection and (iii) the obtained feature vectors are fed into XGBoost to predict protein submitochondrial locations. SubMito-XGBoost has obtained satisfactory prediction results by the leave-one-out-cross-validation (LOOCV) compared with existing methods. The prediction accuracies of the SubMito-XGBoost method on the two training datasets M317 and M983 were 97.7% and 98.9%, which are 2.8–12.5% and 3.8–9.9% higher than other methods, respectively. The prediction accuracy of the independent test set M495 was 94.8%, which is significantly better than the existing studies. The proposed method also achieves satisfactory predictive performance on plant and non-plant protein submitochondrial datasets. SubMito-XGBoost also plays an important role in new drug design for the treatment of related diseases. Availability and implementation The source codes and data are publicly available at https://github.com/QUST-AIBBDRC/SubMito-XGBoost/. Supplementary information Supplementary data are available at Bioinformatics online.

This paper presents the development of an active vibration control for vibration suppression of the horizontal flexible plate structure using proportional–integral–derivative controller tuned by a conventional method via Ziegler–Nichols and an intelligent method known as particle swarm optimization algorithm. Initially, the experimental rig was designed and fabricated with all edges clamped at the horizontal position of the flexible plate. Data acquisition and instrumentation systems were designed and integrated into the experimental rig to collect input–output vibration data of the flexible plate. The vibration data obtained through experimental study was used to model the system using system identification technique based on auto-regressive with exogenous input structure. The plate system was modeled using particle swarm optimization algorithm and validated using mean squared error, one-step ahead prediction, and correlation tests. The stability of the model was assessed using pole zero diagram stability. The fitness function of particle swarm optimization algorithm is defined as the mean squared error between the measured and estimated output of the horizontal flexible plate system. Next, the developed model was used in the development of an active vibration control for vibration suppression on the horizontal flexible plate system using a proportional–integral–derivative controller. The proportional–integral–derivative gains are optimally determined using two different ways, the conventional method tuned by Ziegler–Nichols tuning rules and the intelligent method tuned by particle swarm optimization algorithm. The performances of developed controllers were assessed and validated. Proportional–integral–derivative-particle swarm optimization controller achieved the highest attenuation value for first mode of vibration by achieving 47.28 dB attenuation as compared to proportional–integral–derivative-Ziegler–Nichols controller which only achieved 34.21 dB attenuation.

Abstract The dominant gain-of-function mutation in the tyrosine kinase JAK2 (1849 G to T) has been detected in over 80% PV patients and in approximately half of ET or PMF patients. The mutation results in a non-synonymous amino acid substitution at position 617 (valine to phenylalanine) in the JH2 pseudo-kinase auto-inhibitory domain. Current models predict that expression of mutant JAK2V617F in patient hematopoietic stem cells leads to activation of signaling pathways important for proliferation and survival. Furthermore, experimental evidence using murine models, in which JAK2V617F is retrovirally over-expressed, display a phenotype that closely resembles PV, including progression to myelofibrosis. Previous reports have indicated that “in vitro” expansion of PV progenitors favors erythroid precursors with decreased JAK2V617F mutational burden (Exp. Hematol. (2007) 35(4): 587–95). Investigators in these studies, however, did not report changes in JAK2V617F frequency in sorted live erythroid progenitors after “in vitro” expansion. Furthermore, CD34+cells from PV patients cultured in the presence of 20% serum indicated an inverse relationship between JAK2V617F frequency and Epo dose (Blood (2006) 108(9):3128–34). However, these reports failed to correlate Epo dose, and JAK2V617F frequency, with live “in vitro” expanded purified erythroid progenitor cells. Using our published procedure (Exp. Hematol. (2007) 35(4): 587–95), we expanded erythroid progenitors from healthy volunteers and JAK2V617F positive PV patients (mutational burden ranging from 20–90%) in serum-free media supplemented with SCF, Tpo, and Flt3L (100 ng/mL each - week 1) followed by SCF (50 ng/mL), IGF1 (50 ng/mL), and Epo (0, 0.003, 0.03, 0.3, and 3 Units/mL - week 2). Progression of progenitor expansion, erythroid lineage commitment, live/dead cells, and JAK2 mutation frequency was followed by flow cytometry and real-time PCR. At the end of week 2, cells were harvested, stained with anti-CD71 (transferrin receptor), anti-CD235A (glycophorin A), and the Aqua Live/Dead cell reagent. Stained cells were fixed in 2% paraformaldehyde, analyzed, and sorted on a FACSAria flow cytometer. Live, expanded progenitor cells were sorted into CD235A positive and negative populations, and subsequently used for estimation of JAK2 frequency by quantitative real-time PCR (Exp. Hematol. (2007) 35(1): 32–38). Our results indicate expansion and erythroid commitment of PV progenitor cells in the absence of Epo correlates with the patients’ intrinsic JAK2V617F burden. Furthermore, irrespective of JAK2V617F frequency in purified peripheral blood granulocytes, an inverse correlation between Epo dose and mutation frequency in “in vitro” expanded purified erythroid progenitors was not observed in all patients examined.