S3C: Semi-Supervised VQA Natural Language Explanation via Self-Critical Learning

VQA Natural Language Explanation (VQA-NLE) task aims to explain the decision-making process of VQA models in natural language. Unlike traditional attention or gradient analysis, free-text rationales can be easier to understand and gain users' trust. Existing methods mostly use post-hoc or self-rationalization models to obtain a plausible explanation. However, these frameworks are bottlenecked by the following challenges: 1) the reasoning process cannot be faithfully responded to and suffer from the problem of logical inconsistency. 2) Human-annotated explanations are expensive and time-consuming to collect. In this paper, we propose a new Semi-Supervised VQA-NLE via Self-Critical Learning (S3C), which evaluates the candidate explanations by answering rewards to improve the logical consistency between answers and rationales. With a semi-supervised learning framework, the S3C can benefit from a tremendous amount of samples without human-annotated explanations. A large number of automatic measures and human evaluations all show the effectiveness of our method. Meanwhile, the framework achieves a new state-of-the-art performance on the two VQA-NLE datasets.Comment: CVPR202

One-pot synthesis of 2-alkyl cycloketones on bifunctional Pd/ZrO₂ catalyst

2-Alkyl cycloketones are essential chemicals and intermediates for synthetic perfumes and pesticides, which are conventionally produced by multistep process including aldol condensation, separation and hydrogenation. In present work, a batch one-pot cascade approach using aldehydes and cycloketones as the raw materials, and a bifunctional Pd/ZrO2 catalyst was developed for the synthesis of 2-alkyl cycloketones, e.g., cyclohexanone and cycloheptanone. Very high aldehydes (except for paraldehyde with large steric hindrance) conversion and high yields for 2-alkyl cycloketones (e.g., 99 % of conversion for n-butanal and 76 wt.% of yield for 2-butyl cyclohexanone) were obtained at mild temperature of 140 °C. After 10 cycles of reuse, Pd/ZrO2 catalyst showed slight deactivation (ca. 5 % conversion and 10 % yield losses), due to the coke on the catalyst. However, the performance of the catalyst was completely recovered after an oxidative regeneration

Associations between perioperative sleep patterns and clinical outcomes in patients with intracranial tumors: a correlation study

ObjectiveAlthough the quality of perioperative sleep is gaining increasing attention in clinical recovery, its impact role remains unknown and may deserve further exploration. This study aimed to investigate the associations between perioperative sleep patterns and clinical outcomes among patients with intracranial tumors.MethodsA correlation study was conducted in patients with intracranial tumors. Perioperative sleep patterns were assessed using a dedicated sleep monitor for 6 consecutive days. Clinical outcomes were gained through medical records and follow-up. Spearman's correlation coefficient and multiple linear regression analysis were applied to evaluate the associations between perioperative sleep patterns and clinical outcomes.ResultsOf 110 patients, 48 (43.6%) were men, with a median age of 57 years. A total of 618 days of data on perioperative sleep patterns were collected and analyzed. Multiple linear regression models revealed that the preoperative blood glucose was positively related to the preoperative frequency of awakenings (β = 0.125; 95% CI = 0.029–0.221; P = 0.011). The level of post-operative nausea and vomiting was negatively related to perioperative deep sleep time (β = −0.015; 95% CI = −0.027–−0.003; P = 0.015). The level of anxiety and depression was negatively related to perioperative deep sleep time, respectively (β = −0.048; 95% CI = −0.089–0.008; P = 0.020, β = −0.041; 95% CI = −0.076–0.006; P = 0.021). The comprehensive complication index was positively related to the perioperative frequency of awakenings (β = 3.075; 95% CI = 1.080–5.070; P = 0.003). The post-operative length of stay was negatively related to perioperative deep sleep time (β = −0.067; 95% CI = −0.113–0.021; P = 0.005). The Pittsburgh Sleep Quality Index was positively related to perioperative sleep onset latency (β = 0.097; 95% CI = 0.044–0.150; P < 0.001) and negatively related to perioperative deep sleep time (β = −0.079; 95% CI = −0.122–0.035; P < 0.001).ConclusionPerioperative sleep patterns are associated with different clinical outcomes. Poor perioperative sleep quality, especially reduced deep sleep time, has a negative impact on clinical outcomes. Clinicians should, therefore, pay more attention to sleep quality and improve it during the perioperative period.Clinical trial registrationhttp://www.chictr.org.cn, identifier: ChiCTR2200059425

UHRF1 is required for basal stem cell proliferation in response to airway injury

Cellular senescence is a cell fate characterized by an irreversible cell cycle arrest, but the molecular mechanism underlying this senescence hallmark remains poorly understood. Through an unbiased search for novel senescence regulators in airway basal cells, we discovered that the epigenetic regulator ubiquitin-like with PHD and ring finger domain-containing protein 1 (UHRF1) is critical for regulating cell cycle progression. Upon injury, basal cells in the mouse airway rapidly induce the expression of UHRF1 in order to stimulate stem cell proliferation and tissue repair. Targeted depletion of Uhrf1 specifically in airway basal cells causes a profound defect in cell cycle progression. Consistently, cultured primary human basal cells lacking UHRF1 do not exhibit cell death or differentiation phenotypes but undergo a spontaneous program of senescence. Mechanistically, UHRF1 loss induces G1 cell cycle arrest by abrogating DNA replication factory formation as evidenced by loss of proliferating cell nuclear antigen (PCNA) puncta and an inability to enter the first cell cycle. This proliferation defect is partially mediated by the p15 pathway. Overall, our study provides the first evidence of an indispensable role of UHRF1 in somatic stem cells proliferation during the process of airway regeneration

Cardiolipin externalization mediates prion protein (PrP) peptide 106–126-associated mitophagy and mitochondrial dysfunction

Proper mitochondrial performance is imperative for the maintenance of normal neuronal function to prevent the development of neurodegenerative diseases. Persistent accumulation of damaged mitochondria plays a role in prion disease pathogenesis, which involves a chain of events that culminate in the generation of reactive oxygen species and neuronal death. Our previous studies have demonstrated that PINK1/Parkin-mediated mitophagy induced by PrP106−126 is defective and leads to an accumulation of damaged mitochondria after PrP106−126 treatment. Externalized cardiolipin (CL), a mitochondria-specific phospholipid, has been reported to play a role in mitophagy by directly interacting with LC3II at the outer mitochondrial membrane. The involvement of CL externalization in PrP106−126-induced mitophagy and its significance in other physiological processes of N2a cells treated with PrP106−126 remain unknown. We demonstrate that the PrP106−126 peptide caused a temporal course of mitophagy in N2a cells, which gradually increased and subsequently decreased. A similar trend in CL externalization to the mitochondrial surface was seen, resulting in a gradual decrease in CL content at the cellular level. Inhibition of CL externalization by knockdown of CL synthase, responsible for de novo synthesis of CL, or phospholipid scramblase-3 and NDPK-D, responsible for CL translocation to the mitochondrial surface, significantly decreased PrP106−126-induced mitophagy in N2a cells. Meanwhile, the inhibition of CL redistribution significantly decreased PINK1 and DRP1 recruitment in PrP106−126 treatment but had no significant decrease in Parkin recruitment. Furthermore, the inhibition of CL externalization resulted in impaired oxidative phosphorylation and severe oxidative stress, which led to mitochondrial dysfunction. Our results indicate that CL externalization induced by PrP106−126 on N2a cells plays a positive role in the initiation of mitophagy, leading to the stabilization of mitochondrial function

The enormous repetitive Antarctic krill genome reveals environmental adaptations and population insights

Antarctic krill (Euphausia superba) is Earth’smost abundant wild animal, and its enormous biomass is vital to the Southern Ocean ecosystem. Here, we report a 48.01-Gb chromosome-level Antarctic krill genome, whose large genome size appears to have resulted from inter-genic transposable element expansions. Our assembly reveals the molecular architecture of the Antarctic krill circadian clock and uncovers expanded gene families associated with molting and energy metabolism, providing insights into adaptations to the cold and highly seasonal Antarctic environment. Population-level genome re-sequencing from four geographical sites around the Antarctic continent reveals no clear population structure but highlights natural selection associated with environmental variables. An apparent drastic reduction in krill population size 10 mya and a subsequent rebound 100 thousand years ago coincides with climate change events. Our findings uncover the genomic basis of Antarctic krill adaptations to the Southern Ocean and provide valuable resources for future Antarctic research

Catalytic Function of PLA2G6 Is Impaired by Mutations Associated with Infantile Neuroaxonal Dystrophy but Not Dystonia-Parkinsonism

Mutations in the PLA2G6 gene have been identified in autosomal recessive neurodegenerative diseases classified as infantile neuroaxonal dystrophy (INAD), neurodegeneration with brain iron accumulation (NBIA), and dystonia-parkinsonism. These clinical syndromes display two significantly different disease phenotypes. NBIA and INAD are very similar, involving widespread neurodegeneration that begins within the first 1-2 years of life. In contrast, patients with dystonia-parkinsonism present with a parkinsonian movement disorder beginning at 15 to 30 years of age. The PLA2G6 gene encodes the PLA2G6 enzyme, also known as group VIA calcium-independent phospholipase A(2), which has previously been shown to hydrolyze the sn-2 acyl chain of phospholipids, generating free fatty acids and lysophospholipids.We produced purified recombinant wildtype (WT) and mutant human PLA2G6 proteins and examined their catalytic function using in vitro assays with radiolabeled lipid substrates. We find that human PLA2G6 enzyme hydrolyzes both phospholipids and lysophospholipids, releasing free fatty acids. Mutations associated with different disease phenotypes have different effects on catalytic activity. Mutations associated with INAD/NBIA cause loss of enzyme activity, with mutant proteins exhibiting less than 20% of the specific activity of WT protein in both lysophospholipase and phospholipase assays. In contrast, mutations associated with dystonia-parkinsonism do not impair catalytic activity, and two mutations produce a significant increase in specific activity for phospholipid but not lysophospholipid substrates.These results indicate that different alterations in PLA2G6 function produce the different disease phenotypes of NBIA/INAD and dystonia-parkinsonism. INAD/NBIA is caused by loss of the ability of PLA2G6 to catalyze fatty acid release from phospholipids, which predicts accumulation of PLA2G6 phospholipid substrates and provides a mechanistic explanation for the accumulation of membranes in neuroaxonal spheroids previously observed in histopathological studies of INAD/NBIA. In contrast, dystonia-parkinsonism mutations do not appear to directly impair catalytic function, but may modify substrate preferences or regulatory mechanisms for PLA2G6

Interleukin 18 function in atherosclerosis is mediated by the interleukin 18 receptor and the Na-Cl co-transporter

Interleukin-18 (IL18) participates in atherogenesis through several putative mechanisms1, 2. Interruption of IL18 action reduces atherosclerosis in mice3, 4. Here, we show that absence of the IL18 receptor (IL18r) does not affect atherosclerosis in apolipoprotein E–deficient (Apoe−/−) mice, nor does it affect IL18 cell surface binding to or signaling in endothelial cells. As identified initially by co-immunoprecipitation with IL18, we found that IL18 interacts with the Na-Cl co-transporter (NCC; also known as SLC12A3), a 12-transmembrane-domain ion transporter protein preferentially expressed in the kidney5. NCC is expressed in atherosclerotic lesions, where it colocalizes with IL18r. In Apoe−/− mice, combined deficiency of IL18r and NCC, but not single deficiency of either protein, protects mice from atherosclerosis. Peritoneal macrophages from Apoe−/− mice or from Apoe−/− mice lacking IL18r or NCC show IL18 binding and induction of cell signaling and cytokine and chemokine expression, but macrophages from Apoe−/− mice with combined deficiency of IL18r and NCC have a blunted response. An interaction between NCC and IL18r on macrophages was detected by co-immunoprecipitation. IL18 binds to the cell surface of NCC-transfected COS-7 cells, which do not express IL18r, and induces cell signaling and cytokine expression. This study identifies NCC as an IL18-binding protein that collaborates with IL18r in cell signaling, inflammatory molecule expression, and experimental atherogenesis

Mobility control ability and stability investigation of nitrogen foam under high temperature and high salinity condition

Abstract The mobility disparity between oil and water accounted for the poor water swept efficiency. Previous research has testified that nitrogen foam can increase sweep area and control water and gas mobility. However, the former studies have largely covered the mobility control ability performance in some conventional reservoir rather than that under high temperature and high salinity. This paper presents the results of a laboratory study of nitrogen foam at the experimental condition (113 °C and 21.28 × 104 mg/L) on its mobility control ability investigation, including different gas-to-liquid ratio, injection rate and core permeability; additionally, a novel method on studying the stability of mobility control ability of foam was utilized. Nitrogen foam injection was conducted in core holder to investigate the shape discrepancy of each resistance factor and residual resistance curve. The results showed that the most moderate gas-to-liquid ratio and injection rate were 2:1 and 1 mL/min, respectively; foam performed more significant mobility control ability with the increase in permeability. After 5 days’ aging, nitrogen foam still got enough mobility control ability to block water channeling. The above results demonstrate that, under high temperature and high salinity condition, nitrogen foam still can act as a promising economical method for improving the mobility difference between water and oil by applying appropriate injection parameters

A novel multiple attribute decision making method based on q-rung dual hesitant uncertain linguistic sets and Muirhead mean

This paper aims to propose a new multi-attribute decision making (MADM) method in complicated and fuzzy decision-making environment. To express both decision makers (DMs’) quantitative and qualitative evaluation information comprehensively and consider their high hesitancy in giving their assessment values in MADM process, we combine q-rung dual hesitant fuzzy sets (q-RDHFSs) with uncertain linguistic variables and develop a new tool, called the q-rung dual hesitant uncertain linguistic sets (q-RDHULSs). First, the definition, operations and comparison method of q-RDHULSs are proposed. Second, given the interrelationship among multiple q-rung dual hesitant uncertain linguistic variables (q-RDHULVs) we introduce some aggregation operators (AOs) to fuse q-rung dual hesitant uncertain linguistic (q-RDHUL) information based on the Muirhead mean, i.e. the q-RDHUL Muirhead mean operator, the q-RDHUL weighted Muirhead mean operator, the q-RDHUL dual Muirhead mean operator, and the q-RDHUL weighted dual Muirhead mean operator. To cope with MADM problems with q-RDHUL information, we propose a new method based on the proposed AOs. Afterwards, we apply the proposed method to an enterprise informatization level evaluation problem to verify its effectiveness. In addition, we also explain why our proposed method is more powerful and flexible than others