ViP-Mixer: A Convolutional Mixer for Video Prediction

Video prediction aims to predict future frames from a video's previous content. Existing methods mainly process video data where the time dimension mingles with the space and channel dimensions from three distinct angles: as a sequence of individual frames, as a 3D volume in spatiotemporal coordinates, or as a stacked image where frames are treated as separate channels. Most of them generally focus on one of these perspectives and may fail to fully exploit the relationships across different dimensions. To address this issue, this paper introduces a convolutional mixer for video prediction, termed ViP-Mixer, to model the spatiotemporal evolution in the latent space of an autoencoder. The ViP-Mixers are stacked sequentially and interleave feature mixing at three levels: frames, channels, and locations. Extensive experiments demonstrate that our proposed method achieves new state-of-the-art prediction performance on three benchmark video datasets covering both synthetic and real-world scenarios.Comment: Under revie

Inter-industrial embodied carbon transfers in a developed subnational region: a case study of Guangdong Province, China

The close production and consumption relationship between industries leads to the embodied CO2 transfer among industrial sectors along with the exchange of products. Thus, grasping the situation of embodied carbon transfers from the demand side is of great significance for better reducing a country or region’s CO2 emissions. This study investigates the embodied carbon transfers in Guangdong Province from 2002 to 2017 from the industrial dimension by applying a hypothetical extraction method. An enhanced generalized RAS method was utilized to predict the intersectoral carbon transfers in 2025 and 2030. The results show that, from 2002 to 2017, the average proportion of carbon emission output of 72.11% made the production and supply of electricity and heat sector the main CO2 emission transfer exporter, while the other service and construction sectors were the leading importers. Moreover, the embodied carbon transfers between these three sectors are the main carbon transfer paths. By 2025, the other service sectors will become the largest embodied carbon importers, surpassing the construction sector. Therefore, it is necessary to control the consumption demand of other service and construction sectors on the demand side to reduce carbon emissions driven by demand

Morphological Characterization of a New and Easily Recognizable Nuclear Male Sterile Mutant of Sorghum (\u3ci\u3eSorghum bicolor\u3c/i\u3e)

Sorghum (Sorghum bicolor L. Moench) is one of the most important grain crops in the world. The nuclear male sterility (NMS) trait, which is caused by mutations on the nuclear gene, is valuable for hybrid breeding and genetic studies. Several NMS mutants have been reported previously, but none of them were well characterized. Here, we present our detailed morphological characterization of a new and easily recognizable NMS sorghum mutant male sterile 8 (ms8) isolated from an elite inbred BTx623 mutagenized by ethyl methane sulfonate (EMS). Our results show that the ms8 mutant phenotype was caused by a mutation on a single recessive nuclear gene that is different from all available NMS loci reported in sorghum. In fertile sorghum plants, yellow anthers appeared first during anthesis, while in the ms8 mutant, white hairy stigma emerged first and only small white anthers were observed, making ms8 plants easily recognizable when flowering. The ovary development and seed production after manual pollination are normal in the ms8 mutant, indicating it is female fertile and male sterile only. We found that ms8 anthers did not produce pollen grains. Further analysis revealed that ms8 anthers were defective in tapetum development, which led to the arrest of pollen formation. As a stable male sterile mutant across different environments, greenhouses, and fields in different locations, the ms8 mutant could be a useful breeding tool. Moreover, ms8 might be an important for elucidating male gametophyte development in sorghum and other plants

SOD1G93A transgenic mouse CD4+ T cells mediate neuroprotection after facial nerve axotomy when removed from a suppressive peripheral microenvironment

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease involving motoneuron (MN) axonal withdrawal and cell death. Previously, we established that facial MN (FMN) survival levels in the SOD1G93A transgenic mouse model of ALS are reduced and nerve regeneration is delayed, similar to immunodeficient RAG2-/- mice, after facial nerve axotomy. The objective of this study was to examine the functionality of SOD1G93A splenic microenvironment, focusing on CD4+ T cells, with regard to defects in immune-mediated neuroprotection of injured MN. We utilized the RAG2-/- and SOD1G93A mouse models, along with the facial nerve axotomy paradigm and a variety of cellular adoptive transfers, to assess immune-mediated neuroprotection of FMN survival levels. We determined that adoptively transferred SOD1G93A unfractionated splenocytes into RAG2-/- mice were unable to support FMN survival after axotomy, but that adoptive transfer of isolated SOD1G93A CD4+ T cells could. Although WT unfractionated splenocytes adoptively transferred into SOD1G93A mice were able to maintain FMN survival levels, WT CD4+ T cells alone could not. Importantly, these results suggest that SOD1G93A CD4+ T cells retain neuroprotective functionality when removed from a dysfunctional SOD1G93A peripheral splenic microenvironment. These results also indicate that the SOD1G93A central nervous system microenvironment is able to re-activate CD4+ T cells for immune-mediated neuroprotection when a permissive peripheral microenvironment exists. We hypothesize that dysfunctional SOD1G93A peripheral splenic microenvironment may compromise neuroprotective CD4+ T cell activation and/or differentiation, which, in turn, results in impaired immune-mediated neuroprotection for MN survival after peripheral axotomy in SOD1G93A mice

Sorghum bicolor INDETERMINATE1 is a conserved primary regulator of flowering

IntroductionA fundamental developmental switch for plants is transition from vegetative to floral growth, which integrates external and internal signals. INDETERMINATE1 (Id1) family proteins are zinc finger transcription factors that activate flowering in grasses regardless of photoperiod. Mutations in maize Id1 and rice Id1 (RID1) cause very late flowering. RID1 promotes expression of the flowering activator genes Early Heading Date1 (Ehd1) and Heading date 1 (Hd1), a rice homolog of CONSTANS (CO).Methods and resultsMapping of two recessive late flowering mutants from a pedigreed sorghum EMS mutant library identified two distinct mutations in the Sorghum bicolor Id1 (SbId1) homolog, mutant alleles named sbid1-1 and sbid1-2. The weaker sbid1-1 allele caused a 35 day delay in reaching boot stage in the field, but its effect was limited to 6 days under greenhouse conditions. The strong sbid1-2 allele delayed boot stage by more than 60 days in the field and under greenhouse conditions. When sbid1-1 and sbid1-2 were combined, the delayed flowering phenotype remained and resembled that of sbid1-2, confirming late flowering was due to loss of SbId1 function. Evaluation of major flowering time regulatory gene expression in sbid1-2 showed that SbId1 is needed for expression of floral activators, like SbCO and SbCN8, and repressors, like SbPRR37 and SbGhd7.DiscussionThese results demonstrate a conserved role for SbId1 in promotion of flowering in sorghum, where it appears to be critical to allow expression of most major flowering regulatory genes

Th17 Cell Response in SOD1G93A Mice following Motor Nerve Injury

An increased risk of ALS has been reported for veterans, varsity athletes, and professional football players. The mechanism underlying the increased risk in these populations has not been identified; however, it has been proposed that motor nerve injury may trigger immune responses which, in turn, can accelerate the progression of ALS. Accumulating evidence indicates that abnormal immune reactions and inflammation are involved in the pathogenesis of ALS, but the specific immune cells involved have not been clearly defined. To understand how nerve injury and immune responses may contribute to ALS development, we investigated responses of CD4(+) T cell after facial motor nerve axotomy (FNA) at a presymptomatic stage in a transgenic mouse model of ALS (B6SJL SOD1(G93A)). SOD1(G93A) mice, compared with WT mice, displayed an increase in the basal activation state of CD4(+) T cells and higher frequency of Th17 cells, which were further enhanced by FNA. In conclusion, SOD1(G93A) mice exhibit abnormal CD4(+) T cell activation with increased levels of Th17 cells prior to the onset of neurological symptoms. Motor nerve injury exacerbates Th17 cell responses and may contribute to the development of ALS, especially in those who carry genetic susceptibility to this disease

FAK Mediates a Compensatory Survival Signal Parallel to PI3K-AKT in PTEN-Null T-ALL Cells

SummaryMutations and inactivation of phosphatase and tensin homolog deleted from chromosome 10 (PTEN) are observed in 15%–25% of cases of human T cell acute lymphoblastic leukemia (T-ALL). Pten deletion induces myeloproliferative disorders (MPDs), acute myeloid leukemia (AML), and/or T-ALL in mice. Previous studies attributed Pten-loss-related hematopoietic defects and leukemogenesis to excessive activation of phosphatidylinositol 3-kinase (PI3K)/AKT/mTOR signaling. Although inhibition of this signal dramatically suppresses the growth of PTEN-null T-ALL cells in vitro, treatment with inhibitors of this pathway does not cause a complete remission in vivo. Here, we report that focal adhesion kinase (Fak), a protein substrate of Pten, also contributes to T-ALL development in Pten-null mice. Inactivation of the FAK signaling pathway by either genetic or pharmacologic methods significantly sensitizes both murine and human PTEN-null T-ALL cells to PI3K/AKT/mTOR inhibition when cultured in vitro on feeder layer cells or a matrix and in vivo

Gene Expression Analysis Reveals Novel Gene Signatures Between Young and Old Adults in Human Prefrontal Cortex

Human neurons function over an entire lifetime, yet the molecular mechanisms which perform their functions and protecting against neurodegenerative disease during aging are still elusive. Here, we conducted a systematic study on the human brain aging by using the weighted gene correlation network analysis (WGCNA) method to identify meaningful modules or representative biomarkers for human brain aging. Significantly, 19 distinct gene modules were detected based on the dataset GSE53890; among them, six modules related to the feature of brain aging were highly preserved in diverse independent datasets. Interestingly, network feature analysis confirmed that the blue modules demonstrated a remarkably correlation with human brain aging progress. Besides, the top hub genes including PPP3CB, CAMSAP1, ACTR3B, and GNG3 were identified and characterized by high connectivity, module membership, or gene significance in the blue module. Furthermore, these genes were validated in mice of different ages. Mechanically, the potential regulators of blue module were investigated. These findings highlight an important role of the blue module and its affiliated genes in the control of normal brain aging, which may lead to potential therapeutic interventions for brain aging by targeting the hub genes

Quantitative analysis of preferential utilization of AAV ITR as the packaging terminal signal

Genetic engineering advances have led to recombinant adeno-associated virus (rAAV) becoming an invaluable tool for the development of effective gene therapies. The production of rAAV is susceptible to off-target heterogeneous packaging, the effects of which are still being understood. Here, rAAV vectors with four-genome lengths were produced using both adherent and suspension HEK293 cells to understand the 5′ITR termination. AAV8 vectors were produced from the human FVIII plasmid for a full-length cargo of 4,707 nucleotides with specific truncations, creating smaller genomes. Conventionally, rAAV is characterized by differentiating empty capsids from full capsids, but for this work, that description is incomplete. The small genomes in this study were characterized by charge detection-mass spectrometry (CD-MS). Using CD-MS, packaged genomes in the range conventionally attributed to partials were resolved and quantified. In addition, alkaline gels and qPCR were used to assess the identity of the packaged genomes. Together, these results showed a propensity for unit-length genomes to be encapsidated. Packaged genomes occurred as replication intermediates emanating from the 5′ITR, indicating that HEK293 cells prefer unit-length genomes as opposed to the 5′ITR termination and heterogeneous DNA packaging observed previously from Sf9 cell systems. As both manufacturing processes are used and continually assessed to produce clinical material, such an understanding will benefit rAAV design for basic research and gene therapy

Exacerbation of facial motoneuron loss after facial nerve axotomy in CCR3-deficient mice

We have previously demonstrated a neuroprotective mechanism of FMN (facial motoneuron) survival after facial nerve axotomy that is dependent on CD4+ Th2 cell interaction with peripheral antigen-presenting cells, as well as CNS (central nervous system)-resident microglia. PACAP (pituitary adenylate cyclase-activating polypeptide) is expressed by injured FMN and increases Th2-associated chemokine expression in cultured murine microglia. Collectively, these results suggest a model involving CD4+ Th2 cell migration to the facial motor nucleus after injury via microglial expression of Th2-associated chemokines. However, to respond to Th2-associated chemokines, Th2 cells must express the appropriate Th2-associated chemokine receptors. In the present study, we tested the hypothesis that Th2-associated chemokine receptors increase in the facial motor nucleus after facial nerve axotomy at timepoints consistent with significant T-cell infiltration. Microarray analysis of Th2-associated chemokine receptors was followed up with real-time PCR for CCR3, which indicated that facial nerve injury increases CCR3 mRNA levels in mouse facial motor nucleus. Unexpectedly, quantitative- and co-immunofluorescence revealed increased CCR3 expression localizing to FMN in the facial motor nucleus after facial nerve axotomy. Compared with WT (wild-type), a significant decrease in FMN survival 4 weeks after axotomy was observed in CCR3−/− mice. Additionally, compared with WT, a significant decrease in FMN survival 4 weeks after axotomy was observed in Rag2−/− (recombination activating gene-2-deficient) mice adoptively transferred CD4+ T-cells isolated from CCR3−/− mice, but not in CCR3−/− mice adoptively transferred CD4+ T-cells derived from WT mice. These results provide a basis for further investigation into the co-operation between CD4+ T-cell- and CCR3-mediated neuroprotection after FMN injury