Are ChatGPT and Other Similar Systems the Modern Lernaean Hydras of AI?

The rise of Generative Artificial Intelligence systems (“AI systems”) has created unprecedented social engagement. AI code generation systems provide responses (output) to questions or requests by accessing the vast library of open-source code created by developers over the past few decades. However, they do so by allegedly stealing the open-source code stored in virtual libraries, known as repositories. This Article focuses on how this happens and whether there is a solution that protects innovation and avoids years of litigation. We also touch upon the array of issues raised by the relationship between AI and copyright. Looking ahead, we propose the following: (a) immediate changes to the licenses for open-source code created by developers that will limit access and/or use of any open-source code to humans only; (b) we suggest revisions to the Massachusetts Institute of Technology (“MIT”) license so that AI systems are required to procure appropriate licenses from open-source code developers, which we believe will harmonize standards and build social consensus for the benefit of all of humanity, rather than promote profit-driven centers of innovation; (c) we call for urgent legislative action to protect the future of AI systems while also promoting innovation; and (d) we propose a shift in the burden of proof to AI systems in obfuscation cases

Ectopic A-lattice seams destabilize microtubules

Natural microtubules typically include one A-lattice seam within an otherwise helically symmetric B-lattice tube. It is currently unclear how A-lattice seams influence microtubule dynamic instability. Here we find that including extra A-lattice seams in GMPCPP microtubules, structural analogues of the GTP caps of dynamic microtubules, destabilizes them, enhancing their median shrinkage rate by >20-fold. Dynamic microtubules nucleated by seeds containing extra A-lattice seams have growth rates similar to microtubules nucleated by B-lattice seeds, yet have increased catastrophe frequencies at both ends. Furthermore, binding B-lattice GDP microtubules to a rigor kinesin surface stabilizes them against shrinkage, whereas microtubules with extra A-lattice seams are stabilized only slightly. Our data suggest that introducing extra A-lattice seams into dynamic microtubules destabilizes them by destabilizing their GTP caps. On this basis, we propose that the single A-lattice seam of natural B-lattice MTs may act as a trigger point, and potentially a regulation point, for catastrophe

Soil surface temperatures reveal moderation of the urban heat island effect by trees and shrubs

Urban areas are major contributors to air pollution and climate change, causing impacts on human health that are amplified by the microclimatological effects of buildings and grey infrastructure through the urban heat island (UHI) effect. Urban greenspaces may be important in reducing surface temperature extremes, but their effects have not been investigated at a city-wide scale. Across a midsized UK city we buried temperature loggers at the surface of greenspace soils at 100 sites, stratified by proximity to city centre, vegetation cover and land-use. Mean daily soil surface temperature over 11 months increased by 0.6 °C over the 5 km from the city outskirts to the centre. Trees and shrubs in non-domestic greenspace reduced mean maximum daily soil surface temperatures in the summer by 5.7 °C compared to herbaceous vegetation, but tended to maintain slightly higher temperatures in winter. Trees in domestic gardens, which tend to be smaller, were less effective at reducing summer soil surface temperatures. Our findings reveal that the UHI effects soil temperatures at a city-wide scale, and that in their moderating urban soil surface temperature extremes, trees and shrubs may help to reduce the adverse impacts of urbanization on microclimate, soil processes and human health

Are ChatGPT and Other Similar Systems the Modern Lernaean Hydras of AI?

The rise of Generative Artificial Intelligence systems (“AI systems”) has created unprecedented social engagement. AI code generation systems provide responses (output) to questions or requests by accessing the vast library of open-source code created by developers over the past few decades. However, they do so by allegedly stealing the open-source code stored in virtual libraries, known as repositories. This Article focuses on how this happens and whether there is a solution that protects innovation and avoids years of litigation. We also touch upon the array of issues raised by the relationship between AI and copyright. Looking ahead, we propose the following: (a) immediate changes to the licenses for open-source code created by developers that will limit access and/or use of any open-source code to humans only; (b) we suggest revisions to the Massachusetts Institute of Technology (“MIT”) license so that AI systems are required to procure appropriate licenses from open-source code developers, which we believe will harmonize standards and build social consensus for the benefit of all of humanity, rather than promote profit-driven centers of innovation; (c) we call for urgent legislative action to protect the future of AI systems while also promoting innovation; and (d) we propose a shift in the burden of proof to AI systems in obfuscation cases

Are hedgerows effective corridors between fragments of woodland habitat? An evidence-based approach

Anthropogenic modification of the countryside has resulted in much of the landscape consisting of fragments of once continuous habitat. Increasing habitat connectivity at the landscape-scale has a vital role to play in the conservation of species restricted to such remnant patches, especially as species may attempt to track zones of habitat that satisfy their niche requirements as the climate changes. Conservation policies and management strategies frequently advocate corridor creation as one approach to restore connectivity and to facilitate species movements through the landscape. Here we examine the utility of hedgerows as corridors between woodland habitat patches using rigorous systematic review methodology. Systematic searching yielded 26 studies which satisfied the review inclusion criteria. The empirical evidence currently available is insufficient to evaluate the effectiveness of hedgerow corridors as a conservation tool to promote the population viability of woodland fauna. However, the studies did provide anecdotal evidence of positive local population effects and indicated that some species use hedgerows as movement conduits. More replicated and controlled field investigations or long term monitoring are required in order to allow practitioners and policy makers to make better informed decisions about hedgerow corridor creation and preservation. The benefits of such corridors in regard to increasing habitat connectivity remain equivocal, and the role of corridors in mitigating the effects of climate change at the landscape-scale is even less well understood

Characterization of RP1L1, a highly polymorphic paralog of the retinitis pigmentosa 1 (RP1) gene

Retinitis pigmentosa (RP) is a genetically heterogeneous inherited retinal degeneration which affects approximately 1 of 3,500 people worldwide. Individuals affected with retinitis pigmentosa exhibit night blindness, followed by a progressive reduction of visual field, which usually culminates in legal or complete blindness. Reduced or absent electroretinogram (ERG) and bone spicule-like pigmentary deposits accompany these symptoms Despite the large number of recent disease gene discoveries, much work still remains to completely understand the genetics of retinitis pigmentosa. Mutation analysis of the known disease-associated genes fails to identify mutations in at least 50% of cases and prevelences determined by linkage mapping are often inflated. For instance, despite the relatively large number of families originally mapped to the RP10 locus, mutations in the RP10 gene, IMPDH1, appear to account for less than 5% of adRP cases (unpublished data). The RP11 locus, estimated to be responsible for approximately 20% of adRP cases, also shows less than predicted mutation frequencies One strategy that can be used to find new adRP genes is to identify candidates that have sequence similarity to known adRP genes or that share functional pathways. For instance, three of the recently identified adRP disease-associated genes, HPRP3, PRPF8, and PRPF31, encode pre-mRNA splicing factors that participate in a common pathway. Using this strategy, we decided to characterize the nearest relative of RP1, and to determine if mutations in this newly characterized gene cause adRP. Purpose: To determine the full-length sequence of a gene with similarity to RP1 and to screen for mutations in this newly characterized gene, named retinitis pigmentosa 1-like 1(RP1L1). Since mutations in the RP1 gene cause autosomal dominant retinitis pigmentosa, it is possible that mutations in RP1's most sequence similar relative, RP1L1, may also be a cause of inherited retinal degeneration. Methods: A combination of cDNA clone sequencing, RACE, and database analysis were used to determine the RP1L1 mRNA sequence and its genomic organization. PCR analysis, semi-quantitative RT PCR, and in situ hybridization were used to determine the expression pattern of RP1L1. Single-strand conformational analysis and automated sequencing were used to screen probands from 60 adRP families for potential disease-causing mutations in RP1L1. Results: The human RP1L1 gene is encoded in 4 exons, which span 50 kb on chromosome 8p. The length of the RP1L1 mRNA is large, over 7 kb, but its exact length is variable between individuals due to the presence of several length polymorphisms, including a 48 bp repeat. RP1L1 encodes a protein with a minimal length of 2,400 amino acids and a predicted weight of 252 kDa. Expression of RP1L1 is limited to the retina and appears to be specific to photoreceptors. Mutational analysis of 60 autosomal dominant retinitis pigmentosa probands revealed the presence of 38 sequence substitutions in RP1L1. Over half of these substitutions result in alteration of the RP1L1 protein, but none of these substitutions appear to be pathogenic. Conclusions: The RP1L1 gene encodes a large, highly polymorphic, retinal-specific protein. No RP1L1 disease-causing mutations were identified in any of the samples tested, making it unlikely that mutations in RP1L1 are a frequent cause of autosomal dominant retinitis pigmentosa. Additional experiments will be needed to determine if mutations in RP1L1 cause other forms of inherited retinal degeneration

Tumor-infiltrating DCs suppress nucleic acid-mediated innate immune responses through interactions between the receptor TIM-3 and the alarmin HMGB1

The mechanisms by which tumor microenvironments modulate nucleic acid-mediated innate immunity remain unknown. Here, we identified the receptor TIM-3 as key to circumventing the stimulatory effects of nucleic acids in tumor immunity. TIM-3 is highly expressed on tumor-associated dendritic cells (DC) in murine tumors and cancer patients. DC-derived TIM-3 suppresses innate immune responses through Toll-like receptor and cytosolic sensor recognition of nucleic acids via a galectin-9 independent mechanism. Instead, TIM-3 interacts with the HMGB1 to interfere with recruitment of nucleic acids into DC endosomes and attenuates the therapeutic efficacy of DNA vaccination and chemotherapy by reducing immunogenicity of nucleic acids released from dying tumor cells. Together, these findings define a novel mechanism by which tumor microenvironments suppress antitumor immunity mediated by nucleic acids