Spatial Pattern of Functional Urban Land Conversion and Expansion under Rapid Urbanization: A Case Study of Changchun, China

As populations continue to be concentrated in cities, the world will become entirely urbanized, and urban space is undergoing a drastic evolution. Understanding the spatial pattern of conversion and expansion of functional urban land, in the context of rapid urbanization, helps us to grasp the trajectories of urban spatial evolution in greater depth from a theoretical and practical level. Using the ESRI ArcGIS 9.3 software platform, methods, such as overlay analysis, transition matrix, and kernel density estimation, were used in order to analyze the spatiotemporal characteristics of different types of functional urban land conversion and expansion in the central city of Changchun. The results show that different types of functional urban land were often expanded and replaced, and the urban spatial structure was constantly evolving. The conversion and expansion of functional urban land show similar characteristics to concentric zone and sector modes and show dynamic changes in different concentric circles and directions at different periods. Our method can accurately identify the different types of functional urban land, and also explore the evolutionary trajectory of urban spatial structure. This study will help to coordinate the development of different functional urban spaces and to optimize the urban spatial structure in the future.

Transcriptome-based phylogeny of the semi-aquatic bugs (Hemiptera: Heteroptera: Gerromorpha) reveals patterns of lineage expansion in a series of new adaptive zones

Key innovations enable access to new adaptive zones and are often linked to increased species diversification. As such, they have attracted much attention, yet their concrete consequences on the subsequent evolutionary trajectory and diversification of the bearing lineages remain unclear. The monophyletic group of water striders and relatives (Hemiptera: Heteroptera: Gerromorpha) represent a group of insects that transited to live on the water-air interface and diversified to occupy ponds, puddles, streams, mangroves and even oceans. This lineage offers an excellent model to study the patterns and processes underlying species diversification following the conquest of new adaptive zones. However, such studies require a reliable and comprehensive phylogeny of the infraorder. Based on whole transcriptomic datasets of 97 species and fossil records, we reconstructed a new phylogeny of the Gerromorpha that resolved inconsistencies and uncovered strong support for previously unknown relationships between some important taxa. We then used this phylogeny to reconstruct the ancestral state of a set of adaptations associated with water surface invasion (fluid locomotion, dispersal and transition to saline waters) and sexual dimorphism. Our results uncovered important patterns and dynamics of phenotypic evolution revealing how the initial event of water surface invasion enabled multiple subsequent transitions to new adaptive zones, representing distinct niches of water surfaces, and further diversification of the group. This phylogeny and the associated transcriptomic datasets constitute highly valuable resources, making Gerromorpha an attractive model lineage to study phenotypic evolution.

The transcriptomic signature of physiological trade-offs caused by larval overcrowding in Drosophila melanogaster

Intraspecific competition at the larval stage is an important ecological factor affecting life-history, adaptation and evolutionary trajectory in holometabolous insects. However, the molecular pathways and physiological trade-offs underpinning these ecological processes are poorly characterised. We reared Drosophila melanogaster at three egg densities (5, 60 and 300 eggs/ml) and sequenced the transcriptomes of pooled third-instar larvae. We also examined emergence time, egg-to-adult viability, adult mass and adult sex-ratio at each density. Medium crowding had minor detrimental effects on adult phenotypes compared to low density and yielded 24 differentially expressed genes (DEGs) including several chitinase enzymes. In contrast, high crowding had substantial detrimental effects on adult phenotypes and yielded 2107 DEGs. Among these, upregulated gene sets were enriched in sugar, steroid and amino acid metabolism as well as DNA replication pathways, whereas downregulated gene sets were enriched in ABC transporters, Taurine, Toll/Imd signalling and P450 xenobiotics metabolism pathways. Overall, our findings show that larval overcrowding has a large consistent effect on several molecular pathways (i.e., core responses) with few pathways displaying density-specific regulation (i.e., idiosyncratic responses). This provides important insights into how holometabolous insects respond to intraspecific competition during development.

Interactive documentary and the reinvention of digital journalism, 2015–2020

Interactive documentary (i-docs), an innovative hybrid form at the intersection of film, journalism, and digital games, has matured beyond its first wave of experimentation, gaining distinction among the most highly evolved immersive media of the twenty-first century. The latest generation of i-docs is currently winning accolades at both major film festivals and game design summits. This study charts the evolutionary trajectory of North America’s most recent and influential wave of i-docs in works mostly appearing since 2015. It culturally situates i-docs as immersive media that extend experimentation with narrative journalism into the realm of fine art and social activism. Building on the foundation of activist, highly empathic news experiences established in the early 2010s, the most recent advances in i-docs range from live action VR to animated digital games. Such works include the Canadian National Film Board’s 2018 AR (augmented reality) experience East of the Rockies, Occupied’s 2019 Cannes entry The Holy City VR, Roger Ross Williams’ 2019 Tribeca debut Traveling While Black, and iNK Stories Verité VR Series’ 2017 Blindfold and Hero, winner of the prestigious Storyscapes Award at Tribeca in 2018. The vanguard of i-docs has expanded collaboration between film, news, and digital game industries to provide new forms of citizen engagement through advocacy journalism aimed at social and political change. Through the use of John Pavlik’s (2019) critical framework for understanding immersive journalism, this article examines the texts, producers, and industrial contexts of the most recent and influential North American i-docs, as one branch of the form defined by Gaudenzi, Aston, and Rose. Principles of transparency, social responsibility, and a commitment to veracity in i-docs epitomize the esthetic and political potential of digital journalism as an empathic alternative to traditional news coverage.

Attenuated replication and pathogenesis of SARS-CoV-2 B.1.1.529 Omicron

SARS-CoV-2 Omicron emerged in November 2021 and is rapidly spreading among the human populations. The variant contains 34 changes in its spike protein including 15 substitutions at the receptor-binding domain (RBD). While recent reports reveal that the Omicron variant can robustly escape from vaccine and therapeutic neutralization antibodies, the pathogenicity of the virus remains unknown. Here, we investigate the virological features and pathogenesis of the Omicron variant using in vitro and in vivo models. Our results demonstrate that the replication of the Omicron variant is dramatically attenuated in Calu3 and Caco2 but not in VeroE6 cells. Further mechanistic investigations reveal that the Omicron variant is deficient in transmembrane serine protease 2 (TMPRSS2) usage in comparison to that of WT, Alpha, Beta, and Delta variant, which explained its inefficient replication in Calu3 and Caco2 cells. Importantly, the replication of the Omicron variant is markedly attenuated in both the upper and lower respiratory tract of infected K18-hACE2 mice in comparison to that of WT and Delta variant, which results in its dramatically ameliorated lung pathology. When compared with SARS-CoV-2 WT, Alpha, Beta, and Delta variant, infection by the Omicron variant causes the least body weight loss and mortality rate. Overall, our study demonstrates that the Omicron variant is significantly attenuated in virus replication and pathogenicity in comparison with WT and previous variants. Our data suggest the current global vaccination strategy has forced SARS-CoV-2 into a new evolutionary trajectory towards reduced replication fitness in exchange of better immune escape. These findings are critical for setting policy in the pandemic control and disease management of COVID-19.

Examination of Antiviral Resistance in Venezuelan Equine Encephalitis Virus

Venezuelan equine encephalitis virus (VEEV) is a New World Alphavirus that causes Venezuelan equine encephalitis (VEE), which is characterized by a febrile illness that can progress to neurological disease and death. While no major outbreaks of VEE have occurred since 1995, VEEV is a virus of concern as, in addition to its spread through mosquitos, it can be aerosolized and used as a bioweapon. Unfortunately, there are currently no FDA-approved vaccines or antivirals against VEEV. Efforts have been made to discover small molecules with an inhibitory effect on VEEV, but the potential for emergence of antiviral resistance to these compounds will remain a concern because VEEV is an RNA virus with a high mutation rate and grows to high titers. To examine the evolutionary trajectory of antiviral resistance in VEEV, we developed a next-generation sequencing pipeline to examine single-nucleotide polymorphisms that emerged after repeated passaging of the virus with increasing concentrations of antiviral compounds. In addition, we examined the effect of the microenvironment on the evolution of antiviral resistance, both in cell culture and mouse models. We found that VEEV evolves resistance to the compound ML336 and its derivatives through mutations in the nsP2 and nsP4 genes, but the number, timing of emergence, and the extent of penetrance of these SNPs depend on the compound. These mutations emerged more slowly when infecting an astrocyte cell line. We also found that neurons in the mouse brain did not impose a selective pressure on VEEV during an infection. These results demonstrate how the population dynamics of RNA viruses can be tracked over time and the extent to which they are affected by selective pressures, as well as opening questions about how viruses can mutate and adapt at the molecular level.

Vaccines provide disproportional protection to the increased hospitalisation risk posed by the Delta variant of SARS-CoV2: a meta-analysis

Variants of SARS-CoV2 that achieved global dominance (Alpha and Delta) have been associated with increased hospitalisation risk. A quantification of this risk across studies is currently lacking for Delta. Furthermore, how risk for severe disease changes in both vaccinated and unvaccinated individuals is important as the underlying risks determine public health impact. The surplus risk of Delta versus Alpha on hospitalisation was determined using random-effects meta-analysis. Infection with the Delta compared to the Alpha variant increased hospitalisation risk (unvaccinated: log HR 0.62, CI: 0.41 -- 0.84, P < 0.0001; linear HR 1.87). This finding should inform our response to future variants of concern, currently Omicron. SARS-CoV2 variants that achieve dominance, have achieved this through a higher rate of infection and this evolutionary trajectory has also come with a correlated higher risk of severe disease. The surplus risk posed by Delta was significantly lower however in the vaccinated (model estimate -0.40, CI: -0.73 -- -0.07, P = 0.017). Vaccination thus provided a disproportionate level of protection to hospitalisation with the Delta variant and provides further rationale for vaccination for SARS-CoV2 as a durable public health measure.

Striking Antibody Evasion Manifested by the Omicron Variant of SARS-CoV-2

The Omicron (B.1.1.529) variant of SARS-CoV-2 was only recently detected in southern Africa, but its subsequent spread has been extensive, both regionally and globally1. It is expected to become dominant in the coming weeks2, probably due to enhanced transmissibility. A striking feature of this variant is the large number of spike mutations3 that pose a threat to the efficacy of current COVID-19 vaccines and antibody therapies4. This concern is amplified by the findings from our study. We found B.1.1.529 to be markedly resistant to neutralization by serum not only from convalescent patients, but also from individuals vaccinated with one of the four widely used COVID-19 vaccines. Even serum from persons vaccinated and boosted with mRNA-based vaccines exhibited substantially diminished neutralizing activity against B.1.1.529. By evaluating a panel of monoclonal antibodies to all known epitope clusters on the spike protein, we noted that the activity of 18 of the 19 antibodies tested were either abolished or impaired, including ones currently authorized or approved for use in patients. In addition, we also identified four new spike mutations (S371L, N440K, G446S, and Q493R) that confer greater antibody resistance to B.1.1.529. The Omicron variant presents a serious threat to many existing COVID-19 vaccines and therapies, compelling the development of new interventions that anticipate the evolutionary trajectory of SARS-CoV-2.

Evidence for a mouse origin of the SARS-CoV-2 Omicron variant

The rapid accumulation of mutations in the SARS-CoV-2 Omicron variant that enabled its outbreak raises questions as to whether its proximal origin occurred in humans or another mammalian host. Here, we identified 45 point mutations that Omicron acquired since divergence from the B.1.1 lineage. We found that the Omicron spike protein sequence was subjected to stronger positive selection than that of any reported SARS-CoV-2 variants known to evolve persistently in human hosts, suggesting the possibility of host-jumping. The molecular spectrum (i.e., the relative frequency of the twelve types of base substitutions) of mutations acquired by the progenitor of Omicron was significantly different from the spectrum for viruses that evolved in human patients, but was highly consistent with spectra associated with evolution in a mouse cellular environment. Furthermore, mutations in the Omicron spike protein significantly overlapped with SARS-CoV-2 mutations known to promote adaptation to mouse hosts, particularly through enhanced spike protein binding affinity for the mouse cell entry receptor. Collectively, our results suggest that the progenitor of Omicron jumped from humans to mice, rapidly accumulated mutations conducive to infecting that host, then jumped back into humans, indicating an inter-species evolutionary trajectory for the Omicron outbreak.