A permeability model for the hydraulic fracture filled with proppant packs under combined effect of compaction and embedment

The authors acknowledge the financial support from Science Foundation of China University of Petroleum, Beijing (No. 2462014YJRC060 and No.2462014YJRC059)Peer reviewedPostprin

Shocks, Jets, and Emerging Nebulae: Direct Detection and Characterization of Extragalactic Radio Transients in the VLA Sky Survey

For most of their lives, massive stars and supermassive black holes evolve steadily, changing only gradually on human timescales. But on occasion, these cosmic engines erupt, lighting up their surroundings like flashes in the dark. Under the right conditions, the eruptions can manifest as slow radio transients, rising and fading on timescales of weeks to decades. By finding these transients and observing their evolution, we can study otherwise inaccessible aspects of the engines' lives, and piece together their influence on their surroundings. Until recently, most of our knowledge of slow radio transients came from follow-up observations of explosions first discovered as optical and high-energy transients. This avenue of discovery, while illuminating, provides an indelibly incomplete picture of the radio transient landscape. Moreover, each successful follow-up detection typically comes at the cost of many unsuccessful attempts (measured in both telescope and human time). My thesis helps address these issues by finding and characterizing transients directly in radio surveys. By applying novel transient detection techniques to data from the Very Large Array Sky Survey (VLASS), I produced the first uniformly selected sample of radio transients associated with local universe galaxies. The 64 transients in my sample have roughly doubled the total number of directly detected slow radio transients in the literature. This sample has enabled the first volume-limited characterization of the demographics of extragalactic slow radio transients. It has also facilitated the discovery of two previously unseen transient types: the merger of a compact object with a massive star and a decades-old emerging pulsar wind nebula. These early results used only ~15% of the currently available data from VLASS and focused only on extragalactic transients at low redshift. By applying the same techniques to the full survey, I have found ~2000 new transients, increasing the number of known slow radio transients (detected by any means) by a further order of magnitude. With this new sample, my collaborators and I are beginning to shift the study of slow radio transients from the domain of single-object deep-dives to the domain of statistical samples.</p

Mitochondrial DNA Instability in Cells Lacking Aconitase Correlates with Iron Citrate Toxicity

Aconitase, the second enzyme of the tricarboxylic acid cycle encoded by ACO1 in the budding yeast Saccharomyces cerevisiae, catalyzes the conversion of citrate to isocitrate. aco1Δ results in mitochondrial DNA (mtDNA) instability. It has been proposed that Aco1 binds to mtDNA and mediates its maintenance. Here we propose an alternative mechanism to account for mtDNA loss in aco1Δ mutant cells. We found that aco1Δ activated the RTG pathway, resulting in increased expression of genes encoding citrate synthase. By deleting RTG1, RTG3, or genes encoding citrate synthase, mtDNA instability was prevented in aco1Δ mutant cells. Increased activity of citrate synthase leads to iron accumulation in the mitochondria. Mutations in MRS3 and MRS4, encoding two mitochondrial iron transporters, also prevented mtDNA loss due to aco1Δ. Mitochondria are the main source of superoxide radicals, which are converted to H2O2 through two superoxide dismutases, Sod1 and Sod2. H2O2 in turn reacts with Fe2+ to generate very active hydroxyl radicals. We found that loss of Sod1, but not Sod2, prevents mtDNA loss in aco1Δ mutant cells. We propose that mtDNA loss in aco1Δ mutant cells is caused by the activation of the RTG pathway and subsequent iron citrate accumulation and toxicity

Mitochondrial DNA Instability in Cells Lacking Aconitase Correlates with Iron Citrate Toxicity

Aconitase, the second enzyme of the tricarboxylic acid cycle encoded by ACO1 in the budding yeast Saccharomyces cerevisiae, catalyzes the conversion of citrate to isocitrate. aco1 Delta results in mitochondrial DNA (mtDNA) instability. It has been proposed that Aco1 binds to mtDNA and mediates its maintenance. Here we propose an alternative mechanism to account for mtDNA loss in aco1 Delta mutant cells. We found that aco1 Delta activated the RTG pathway, resulting in increased expression of genes encoding citrate synthase. By deleting RTG1, RTG3, or genes encoding citrate synthase, mtDNA instability was prevented in aco1 Delta mutant cells. Increased activity of citrate synthase leads to iron accumulation in the mitochondria. Mutations in MRS3 and MRS4, encoding two mitochondrial iron transporters, also prevented mtDNA loss due to aco1 Delta. Mitochondria are the main source of superoxide radicals, which are converted to H2O2 through two superoxide dismutases, Sod1 and Sod2. H2O2 in turn reacts with Fe2+ to generate very active hydroxyl radicals. We found that loss of Sod1, but not Sod2, prevents mtDNA loss in aco1 Delta mutant cells. We propose that mtDNA loss in aco1 Delta mutant cells is caused by the activation of the RTG pathway and subsequent iron citrate accumulation and toxicity

Mitochondrial DNA Instability in Cells Lacking Aconitase Correlates with Iron Citrate Toxicity

Aconitase, the second enzyme of the tricarboxylic acid cycle encoded by ACO1 in the budding yeast Saccharomyces cerevisiae, catalyzes the conversion of citrate to isocitrate. aco1 Delta results in mitochondrial DNA (mtDNA) instability. It has been proposed that Aco1 binds to mtDNA and mediates its maintenance. Here we propose an alternative mechanism to account for mtDNA loss in aco1 Delta mutant cells. We found that aco1 Delta activated the RTG pathway, resulting in increased expression of genes encoding citrate synthase. By deleting RTG1, RTG3, or genes encoding citrate synthase, mtDNA instability was prevented in aco1 Delta mutant cells. Increased activity of citrate synthase leads to iron accumulation in the mitochondria. Mutations in MRS3 and MRS4, encoding two mitochondrial iron transporters, also prevented mtDNA loss due to aco1 Delta. Mitochondria are the main source of superoxide radicals, which are converted to H2O2 through two superoxide dismutases, Sod1 and Sod2. H2O2 in turn reacts with Fe2+ to generate very active hydroxyl radicals. We found that loss of Sod1, but not Sod2, prevents mtDNA loss in aco1 Delta mutant cells. We propose that mtDNA loss in aco1 Delta mutant cells is caused by the activation of the RTG pathway and subsequent iron citrate accumulation and toxicity

Modeling wellbore instability in hot dry rock under various temperature conditions

Hot Dry Rock (HDR) is a renewable energy source that has garnered attention due to its abundant reserves, widespread distribution, and consistent energy supply. However, the injection of cold water during the drilling and production process of HDR can alter the temperature of the rock in the HDR reservoir, leading to variations in its physical and mechanical properties near the wellbore. These changes can impact the stability and safety of the HDR wellbore. This study investigated the alterations in the physical and mechanical properties of HDR under different temperature conditions. The results revealed that there were negligible changes in the physical and mechanical properties when the temperature rose from 25 °C to 400 °C. However, noticeable changes occurred as the temperature increased from 400 °C to 800 °C, establishing 400 °C as the threshold for physical and mechanical property variations in the granite. Building upon these experimental findings, a segmented wellbore instability model was developed and validated. The model demonstrated that an increased temperature difference between the drilling fluid and the borehole corresponded to an expanded range of borehole failure. Furthermore, higher wellbore temperatures led to more pronounced disparities between the maximum and minimum principal stress of the borehole, rendering it more susceptible to instability. The research also uncovered that the optimal drilling position was influenced by temperature.These research outcomes hold significant importance for understanding the mechanisms of wellbore instability in HDR with high-temperature

Mitochondrial DNA Instability in Cells Lacking Aconitase Correlates with Iron Citrate Toxicity

Aconitase, the second enzyme of the tricarboxylic acid cycle encoded by ACO1 in the budding yeast Saccharomyces cerevisiae, catalyzes the conversion of citrate to isocitrate. aco1Δ results in mitochondrial DNA (mtDNA) instability. It has been proposed that Aco1 binds to mtDNA and mediates its maintenance. Here we propose an alternative mechanism to account for mtDNA loss in aco1Δ mutant cells. We found that aco1Δ activated the RTG pathway, resulting in increased expression of genes encoding citrate synthase. By deleting RTG1, RTG3, or genes encoding citrate synthase, mtDNA instability was prevented in aco1Δ mutant cells. Increased activity of citrate synthase leads to iron accumulation in the mitochondria. Mutations in MRS3 and MRS4, encoding two mitochondrial iron transporters, also prevented mtDNA loss due to aco1Δ. Mitochondria are the main source of superoxide radicals, which are converted to H2O2 through two superoxide dismutases, Sod1 and Sod2. H2O2 in turn reacts with Fe2+ to generate very active hydroxyl radicals. We found that loss of Sod1, but not Sod2, prevents mtDNA loss in aco1Δ mutant cells. We propose that mtDNA loss in aco1Δ mutant cells is caused by the activation of the RTG pathway and subsequent iron citrate accumulation and toxicity

Multimodal Feature Fusion Method for Unbalanced Sample Data in Social Network Public Opinion

With the wide application of social media, public opinion analysis in social networks has been unable to be met through text alone because the existing public opinion information includes data information of various modalities, such as voice, text, and facial expressions. Therefore multi-modal emotion analysis is the current focus of public opinion analysis. In addition, multi-modal emotion recognition of speech is an important factor restricting the multi-modal emotion analysis. In this paper, the emotion feature retrieval method for speech is firstly explored and the processing method of sample disequilibrium data is then analyzed. By comparing and studying the different feature fusion methods of text and speech, respectively, the multi-modal feature fusion method for sample disequilibrium data is proposed to realize multi-modal emotion recognition. Experiments are performed using two publicly available datasets (IEMOCAP and MELD), which shows that processing multi-modality data through this method can obtain good fine-grained emotion recognition results, laying a foundation for subsequent social public opinion analysis

Development of multi-specific humanized llama antibodies blocking SARS-CoV-2/ACE2 interaction with high affinity and avidity

Coronaviruses cause severe human viral diseases including SARS, MERS and COVID-19. Most recently SARS-CoV-2 virus (causing COVID-19) has led to a pandemic with no successful therapeutics. The SARS-CoV-2 infection relies on trimeric spike (S) proteins to facilitate virus entry into host cells by binding to ACE2 receptor on host cell membranes. Therefore, blocking this interaction with antibodies are promising agents against SARS-CoV-2. Here we describe using humanized llama antibody VHHs against SARS-CoV-2 that would overcome the limitations associated with polyclonal and monoclonal combination therapies. From two llama VHH libraries, unique humanized VHHs that bind to S protein and block the S/ACE2 interaction were identified. Furthermore, pairwise combination of VHHs showed synergistic blocking. Multi-specific antibodies with enhanced affinity and avidity, and improved S/ACE2 blocking are currently being developed using an in-silico approach that also fuses VHHs to Fc domains. Importantly, our current bi-specific antibody shows potent S/ACE2 blocking (KD – 0.25 nM, IC100 ∼ 36.7 nM, IC95 ∼ 12.2 nM, IC50 ∼ 1 nM) which is significantly better than individual monoclonal VHH-Fcs. Overall, this design would equip the VHH-Fcs multiple mechanisms of actions against SARS-CoV-2. Thus, we aim to contribute to the battle against COVID-19 by developing therapeutic antibodies as well as diagnostics