Wrongful Improvers as a Guiding Principle for Application of the FTC’s IP Deletion Requirement

The 2021 Federal Trade Commission (FTC) investigation into cloud storage app developer Everalbum resulted in a consent decree that required Everalbum to delete not only unlawfully collected data, but also algorithms created using that data. The FTC had imposed this kind of penalty only once before. Questions remain about how the FTC will apply this so-called intellectual property (IP) deletion requirement in the future. This Comment argues that situations where companies develop intellectual property from misappropriated consumer data are analogous to cases where courts seek to apply the property law rule of the wrongful improver, i.e., where one party knowingly improves another’s property. The rule requires that courts grant title to the owner of the original property regardless of how much the value of the property has increased. Applying the wrongful improver rule can guide the FTC’s future application of the IP deletion requirement in two ways. First, application of the rule suggests that the IP deletion requirement should apply regardless of what type of data (biometric or non-biometric) has been misappropriated. Second, the rule indicates that a company must forfeit not only rights to their particular copy of their IP, but also all the IP rights that attach to it. Application of this rule will thereby strengthen the FTC’s power to punish offenders and more significantly deter companies from unlawfully collecting consumer data

Human Cytomegalovirus Upregulates Expression of HCLS1 Resulting in Increased Cell Motility and Transendothelial Migration during Latency.

Human cytomegalovirus establishes a lifelong, latent infection in the human host and can cause significant morbidity and mortality, particularly, in immunocompromised individuals. One established site of HCMV latency and reactivation is in cells of the myeloid lineage. In undifferentiated myeloid cells, such as CD14+ monocytes, virus is maintained latently. We have recently reported an analysis of the total proteome of latently infected CD14+ monocytes, which identified an increase in hematopoietic lineage cell-specific protein (HCLS1). Here we show that this latency-associated upregulation of HCLS1 occurs in a US28-dependent manner and stabilizes actin structure in latently infected cells. This results in their increased motility and ability to transit endothelial cell layers. Thus, latency-associated increases in monocyte motility could aid dissemination of the latently infected reservoir, and targeting this increased motility could have an impact on the ability of latently infected monocytes to distribute to tissue sites of reactivation.This work was funded by the British Medical Research Council, Grant from the British Medical Research Council (Grant G0701279) and the Cambridge NIHR BRC Cell Phenotyping Hub

Interferon-Responsive Genes Are Targeted during the Establishment of Human Cytomegalovirus Latency.

Human cytomegalovirus (HCMV) latency is an active process which remodels the latently infected cell to optimize latent carriage and reactivation. This is achieved, in part, through the expression of viral genes, including the G-protein-coupled receptor US28. Here, we use an unbiased proteomic screen to assess changes in host proteins induced by US28, revealing that interferon-inducible genes are downregulated by US28. We validate that major histocompatibility complex (MHC) class II and two pyrin and HIN domain (PYHIN) proteins, myeloid cell nuclear differentiation antigen (MNDA) and IFI16, are downregulated during experimental latency in primary human CD14+ monocytes. We find that IFI16 is targeted rapidly during the establishment of latency in a US28-dependent manner but only in undifferentiated myeloid cells, a natural site of latent carriage. Finally, by overexpressing IFI16, we show that IFI16 can activate the viral major immediate early promoter and immediate early gene expression during latency via NF-κB, a function which explains why downregulation of IFI16 during latency is advantageous for the virus.IMPORTANCE Human cytomegalovirus (HCMV) is a ubiquitous herpesvirus which infects 50 to 100% of humans worldwide. HCMV causes a lifelong subclinical infection in immunocompetent individuals but is a serious cause of mortality and morbidity in the immunocompromised and neonates. In particular, reactivation of HCMV in the transplant setting is a major cause of transplant failure and related disease. Therefore, a molecular understanding of HCMV latency and reactivation could provide insights into potential ways to target the latent viral reservoir in at-risk patient populations

The Solidarity Economy in the Families of Cascas (La Libertad) and San Agustín (Arequipa): A Comparative Study

The present study was carried out with the objective of knowing, making visible and articulating how family enterprises are presented in two communities of Peru, one from the north: Cascas (La Libertad) and another from the South: San Agustín (Arequipa), allowing the construction of synergies with a territoriality criterion. The solidarity economy achieves the support of people, promotes the development of initiatives, becomes a generator of economic income, a source of skills development, creation of more community economies and extension of the middle class. The methods used are inductive - deductive and analytical - synthetic, which allowed an analysis of the content of family economies, using the techniques questionnaire of closed questions and in-depth interviews, with 100 families from each of the selected communities as the object of study. and autonomy of the family members, allows the equitable distribution and management of resources, bringing as a goal the well-being of these families

Implications of tactile enrichment on the behaviour and whisker movements of four species of carnivorans

Caniformia include a range of aquatic, semi-aquatic and terrestrial species, which reveal diversity in their whisker arrangements and shape. Whisker movements play a crucial role in the perception of tactile information, allowing whiskered mammals to distinguish between shapes, sizes, and textures. Despite the significance of whisker movements in sensory perception, few studies have focussed on measuring whisker movements during tactile sensing. Whisker enrichment tasks have the potential to expand behavioural repertoires of animals in captivity and reduce stereotypical behaviours. However, despite whiskers being essential in guiding foraging and exploration in many mammalian species, tactile whisker enrichment tasks are rare. Here, we utilised a novel tactile enrichment device to investigate the whisker movements in four Caniform species in captivity, including two pinnipeds- South African fur seals (Arctocephalus pussilus) and harbour seals (Phoca vitulina), a mustelid – Eurasian otter (Lutra lutra), and a canid – red fox (Vulpes vulpes) during a texture discrimination task. This study is the first to explore the impact of tactile enrichment on the behavioural repertoire of caniforms in captivity and provides the first insight of whisker movements in South African fur seals. The introduction of the tactile enrichment device did not increase the behavioural repertoire, nor did it lead to an increase in stereotypical behaviours or aggression in any of the species. However, it did successfully encourage natural whisker movements in the pinnipeds and otter. The whisker amplitude measure was especially high in the South African fur seals. We suggest that such a complex, discrimination-based enrichment task might only be feasible for more trainable caniforms, such as pinnipeds, rather than more neophobic species, such as the red fox, which did not interact with the enrichment device throughout the study. Therefore, while our enrichment device increased natural whisker movements, an even simpler foraging task might encourage tactile sensing without the requirement for training, making tactile whisker enrichment available to a wider group of species

Collective Management Organisations, Creativity and Cultural Diversity

Glycogen synthase kinase 3 (GSK3) is a central regulator of cellular metabolism, development and growth. GSK3 activity was thought to oppose tumourigenesis, yet recent studies indicate that it may support tumour growth in some cancer types including in non-small cell lung carcinoma (NSCLC). We examined the undefined role of GSK3 protein kinase activity in tissue from human NSCLC.The expression and protein kinase activity of GSK3 was determined in 29 fresh frozen samples of human NSCLC and patient-matched normal lung tissue by quantitative immunoassay and western blotting for the phosphorylation of three distinct GSK3 substrates in situ (glycogen synthase, RelA and CRMP-2). The proliferation and sensitivity to the small-molecule GSK3 inhibitor; CHIR99021, of NSCLC cell lines (Hcc193, H1975, PC9 and A549) and non-neoplastic type II pneumocytes was further assessed in adherent culture.Expression and protein kinase activity of GSK3 was elevated in 41% of human NSCLC samples when compared to patient-matched control tissue. Phosphorylation of GSK3α/β at the inhibitory S21/9 residue was a poor biomarker for activity in tumour samples. The GSK3 inhibitor, CHIR99021 dose-dependently reduced the proliferation of three NSCLC cell lines yet was ineffective against type II pneumocytes.NSCLC tumours with elevated GSK3 protein kinase activity may have evolved dependence on the kinase for sustained growth. Our results provide further important rationale for exploring the use of GSK3 inhibitors in treating NSCLC

New Frontiers-class Uranus Orbiter: Exploring the feasibility of achieving multidisciplinary science with a mid-scale mission

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Disease consequences of higher adiposity uncoupled from its adverse metabolic effects using Mendelian randomisation

Background: Some individuals living with obesity may be relatively metabolically healthy, whilst others suffer from multiple conditions that may be linked to adverse metabolic effects or other factors. The extent to which the adverse metabolic component of obesity contributes to disease compared to the non-metabolic components is often uncertain. We aimed to use Mendelian randomisation (MR) and specific genetic variants to separately test the causal roles of higher adiposity with and without its adverse metabolic effects on diseases. Methods: We selected 37 chronic diseases associated with obesity and genetic variants associated with different aspects of excess weight. These genetic variants included those associated with metabolically ‘favourable adiposity’ (FA) and ‘unfavourable adiposity’ (UFA) that are both associated with higher adiposity but with opposite effects on metabolic risk. We used these variants and two sample MR to test the effects on the chronic diseases. Results: MR identified two sets of diseases. First, 11 conditions where the metabolic effect of higher adiposity is the likely primary cause of the disease. Here, MR with the FA and UFA genetics showed opposing effects on risk of disease: coronary artery disease, peripheral artery disease, hypertension, stroke, type 2 diabetes, polycystic ovary syndrome, heart failure, atrial fibrillation, chronic kidney disease, renal cancer, and gout. Second, 9 conditions where the non-metabolic effects of excess weight (e.g. mechanical effect) are likely a cause. Here, MR with the FA genetics, despite leading to lower metabolic risk, and MR with the UFA genetics, both indicated higher disease risk: osteoarthritis, rheumatoid arthritis, osteoporosis, gastro-oesophageal reflux disease, gallstones, adult-onset asthma, psoriasis, deep vein thrombosis, and venous thromboembolism. Conclusions: Our results assist in understanding the consequences of higher adiposity uncoupled from its adverse metabolic effects, including the risks to individuals with high body mass index who may be relatively metabolically healthyDiabetes UK (17/0005594); Medical Research Council (MR/T002239/1)l; World Cancer Research Fund (IIG_2019_2009); Medical Research Council (MC_UU_00011/1); Diabetes UK (17/0005587); Cancer Research UK (C18281/A29019)