Explaining cooperative groups via social niche construction

Cooperative behaviours can be defined as those that benefit others at an apparent cost to self. How these kinds of behaviours evolve has been a topic of great interest in evolutionary biology, as the Darwinian paradigm seems to suggest that nature will be “red in tooth and claw” and that we would not expect one organism to evolve to help another. The evolution-of-cooperation literature has therefore generally been about showing how the altruism involved in these cases is only apparent (see Bergstrom 2002 for an excellent review). Consider kin selection, in which interactions are more likely to occur between related individuals. The cost of altruism to the individual is real but, having identified the correct score-keeping level as the genetic one, it turns out that the cooperative act is not costly but profitable. More generally, successful explanations for cooperation rely on the presence of a population structure that clusters cooperators together, such that they enjoy the benefits of each others' actions. However, the question that has been left largely unaddressed is how does this structure itself evolve? If we want to really explain why organisms cooperate, then we need to explain not just their adaptation to their social environment, but how they came to live in that environment. Recent work by Powers (2010) and Powers et al. (in press) has addressed this question. They show that social behaviour can exert indirect selection pressure on population structure-modifying traits, causing individuals to adaptively modify their population structure to support greater cooperation. Moreover, they argue that any component of selection on structure-modifying traits that is due to social behaviour must be in the direction of increased cooperation; that component of selection cannot be in favour of the conditions for greater selfishness. Powers et al. then examine the conditions under which this component of selection on population structure exists. They argue that not only can population structure drive the evolution of cooperation, as in classical models, but that the benefits of greater cooperation can in turn drive the evolution of population structure: a positive feedback process that they refer to as social niche construction (after Odling-Smee et al. 2003). Maynard Smith and Szathmary (1995) note that most of the big unanswered questions in biology are not about how a particular behaviour is selected for at one level of organization but about the emergence of whole new levels of organization, e.g., the transition from single- to multi-celled organisms, or from solitary insects to eusocial colonies. Any satisfactory account of these transitions must explain how the individuals came to live in a population structure that supported high degrees of cooperation, as well as showing that cooperation is individually advantageous given that structure. The social niche construction process identified by Powers et al. can explain some of the major transitions, by showing how a new selective level can begin through evolution of individual characters, such as group size preference or dispersal tendency. The potential emergence of reliable cooperation via the co-evolution of individual cooperative and population-structuring behaviours demonstrates that groups of cooperating agents can create an environment in which they become so “locked in” to their group identity that the group warrants redescription as an individual in its own right. Consider the move from independent protozoans, to an intermediate cooperative stage as in slime moulds, to fully multi-cellular animals. Such creation of population structures that support cooperation parallels negotiation of a social contract. What are the philosophical implications of this perspective for understanding and explaining human social behaviour? On the one hand, it gives respectability and unique explanatory value to group-selectionist accounts. Explaining the origin of within-group cooperation and the origin of the groups themselves become part of the same project, which in turn means that we cannot understand social and cooperative behaviour in humans without understanding human population-structuring traits, e.g., living in family groups, group fission-fusion behaviours, migratory behaviours, etc. What will the explanations we seek look like? de Pinedo and Noble (2008) have argued that the description of evolved behaviour cannot be exclusively in mechanistic terms: we need both explanations that focus on an agent’s interaction with its environment, and explanations that focus on the physical or computational enabling conditions of such an interaction. In a context in which what counts as an agent is taken for granted, de Pinedo and Noble argue that both agent and sub-agent level explanations will be required. The perspective being outlined here forces an expansion of that position and reminds us that agency is not to be taken for granted; that it emerges from a lower level of organization after a history of selection brings simpler entities together in a coherent cooperative whole. The implication is that truly multi-level explanations will be necessary in the area of social behaviour. We explain the origin of the multi-cellular organism as the result of a cooperative merger of single-celled organisms, and we explain the origin of a super-organism such as an ant colony in a similar way. At each transition, the autonomous agents of the previous level become component mechanisms in the next, but no explanatory level can be entirely done away with. A human being is an example of a multi-cellular organism with a highly developed social aspect, occupying an intermediate point between radical individual independence and total group cohesion. To fully explain human behaviour, we need to know about the cellular machinery that enables personal-level agency. But we also need to know how human machinery fits together into families, communities and nations that will, at least partially, have their own emergent goals and purposes: “partially” because we are not yet a super-organism, of course. In conclusion, the perspective we outline suggests a view of the social contract as not at all unique to Hobbesian rational agents who have become tired of an insecure and violent lifestyle. Instead the ongoing negotiation of the social contract amongst ourselves can be seen as echoing earlier, now-successfully-concluded negotiations between the entities that became our genes and then our cells

Obesity dependent metabolic signatures associated with nonalcoholic fatty liver disease progression

Our understanding of the mechanisms by which nonalcoholic fatty liver disease (NAFLD) progresses from simple steatosis to steatohepatitis (NASH) is still very limited. Despite the growing number of studies linking the disease with altered serum metabolite levels, an obstacle to the development of metabolome-based NAFLD predictors has been the lack of large cohort data from biopsy-proven patients matched for key metabolic features such as obesity. We studied 467 biopsied individuals with normal liver histology (n=90) or diagnosed with NAFLD (steatosis, n=246; NASH, n=131), randomly divided into estimation (80% of all patients) and validation (20% of all patients) groups. Qualitative determinations of 540 serum metabolite variables were performed using ultra-performance liquid chromatography coupled to mass spectrometry (UPLCMS). The metabolic profile was dependent on patient body-mass index (BMI), suggesting that the NAFLD pathogenesis mechanism may be quite different depending on an individual’s level of obesity. A BMI-stratified multivariate model based on the NAFLD serum metabolic profile was used to separate patients with and without NASH. The area under the receiver operating characteristic curve was 0.87 in the estimation and 0.85 in the validation group. The cutoff (0.54) corresponding to maximum average diagnostic accuracy (0.82) predicted NASH with a sensitivity of 0.71 and a specificity of 0.92 (negative/positive predictive values = 0.82/0.84). The present data, indicating that a BMI-dependent serum metabolic profile may be able to reliably distinguish NASH from steatosis patients, have significant implications for the development of NASH biomarkers and potential novel targets for therapeutic intervention

Engineering Pseudomonas putida for isoprenoid production by manipulating endogenous and shunt pathways supplying precursors

Background: The soil bacterium Pseudomonas putida is a promising platform for the production of industrially valuable natural compounds. In the case of isoprenoids, the availability of biosynthetic precursors is a major limiting factor. In P. putida and most other bacteria, these precursors are produced from pyruvate and glyceraldehyde 3-phosphate by the methylerythritol 4-phosphate (MEP) pathway, whereas other bacteria synthesize the same precursors from acetyl-CoA using the unrelated mevalonate (MVA) pathway. Results: Here we explored different strategies to increase the supply of isoprenoid precursors in P. putida cells using lycopene as a read-out. Because we were not aiming at producing high isoprenoid titers but were primarily interested in finding ways to enhance the metabolic flux to isoprenoids, we engineered the well-characterized P. putida strain KT2440 to produce low but detectable levels of lycopene under conditions in which MEP pathway steps were not saturated. Then, we compared lycopene production in cells expressing the Myxococcus xanthus MVA pathway genes or endogenous MEP pathway genes (dxs, dxr, idi) under the control of IPTG-induced and stress-regulated promoters. We also tested a shunt pathway producing isoprenoid precursors from ribulose 5-phosphate using a mutant version of the Escherichia coli ribB gene. Conclusions: The most successful combination led to a 50-fold increase in lycopene levels, indicating that P. putida can be successfully engineered to substantially increase the supply of metabolic substrates for the production of industrially valuable isoprenoids

Deep Sclerectomy With a New Nonabsorbable Uveoscleral Implant (Esnoper-Clip) : 1-Year Outcomes

Altres ajuts: AJL Ophthalmics supports the Health Sciences Research Institute "Germans Trias i Pujol" Foundation.520 _

Effectiveness of a Step Counter Smartband and Midwife Counseling Intervention on Gestational Weight Gain and Physical Activity in Pregnant Women With Obesity (Pas and Pes Study): Randomized Controlled Trial

Background: Women who are pregnant and have obesity and excessive gestational weight gain (GWG) present a higher risk of maternal and perinatal complications. The use of mobile apps and a wristband during pregnancy may contribute to promoting healthy lifestyles and, thus, improving maternal and neonatal health. Objective: This study aims to evaluate the effectiveness of a complex digital health intervention, using a smartband and app with midwife counseling, on GWG and physical activity (PA) in women who are pregnant and have obesity and analyze its impact on maternal and perinatal outcomes. In addition, we aim to study the frequency of use, usability, and satisfaction with the mobile apps used by the women in the intervention group. Methods: A parallel, 2-arm, randomized controlled trial was conducted. A total of 150 women who were pregnant and had obesity were included. The intervention group received a complex combined digital intervention. The intervention was delivered with a smartband (Mi Band 2) linked to the app Mi Fit to measure PA and the Hangouts app with the midwife to provide personal health information. The control group received usual care. The validated Spanish versions of the International Physical Activity Questionnaire-Short Form and the System Usability Scale were used. Satisfaction was measured on a 1- to 5-point Likert scale. Results: We analyzed 120 women, of whom 30 (25%) were withdrawn because of the COVID-19 pandemic. The median GWG in the intervention group was 7.0 (IQR 4-11) kg versus 9.3 (IQR 5.9-13.3) kg in the control group (P=.04). The adjusted mean GWG per week was 0.5 (95% CI 0.4-0.6) kg per week in the control group and 0.3 (95% CI 0.3-0.4) kg per week in the intervention group (df=0.1, 95% CI −0.2 to 0.03; P=.008). During the 35 and 37 gestational weeks, women in the intervention group had higher mean PA than women in the control group (1980 metabolic equivalents of tasks-minutes per week vs 1386 metabolic equivalents of tasks-minutes per week, respectively; P=.01). No differences were observed between the study groups in the incidence of maternal and perinatal outcomes. In the intervention group, 61% (36/59) of the women who were pregnant used the smartband daily, and 75% (44/59) evaluated the usability of the Mi Fit app as excellent. All women in the intervention group used the Hangouts app at least once a week. The mean of the satisfaction scale with the health counseling app and midwife support was 4.8/5 (SD 0.6) points. Conclusions: The use of a complex mobile health intervention was associated with adequate GWG, which was lower in the intervention group than in the control group. In addition, we observed that the intervention group had increases in PA. No differences were observed in maternal perinatal complications. Trial Registration: ClinicalTrials.gov NCT03706872; https://www.clinicaltrials.gov/ct2/show/NCT03706872 JMIR Mhealth Uhealth 2022;10(2):e2888

High seroprevalence of Strongyloides stercoralis among individuals from endemic areas considered for solid organ transplant donation: A retrospective serum-bank based study

BACKGROUND: Strongyloides stercoralis is a worldwide disseminated parasitic disease that can be transmitted from solid organ transplant (SOT) donors to recipients. We determined the serological prevalence of S. stercoralis among deceased individuals from endemic areas considered for SOT donation, using our institution's serum bank. METHODOLOGY: Retrospective study including all deceased potential donors from endemic areas of strongyloidiasis considered for SOT between January 2004 and December 2014 in a tertiary care hospital. The commercial serological test IVD-Elisa was used to determine the serological prevalence of S. stercoralis. PRINCIPAL FINDINGS: Among 1025 deceased individuals during the study period, 90 were from endemic areas of strongyloidiasis. There were available serum samples for 65 patients and 6 of them tested positive for S. stercoralis (9.23%). Only one of the deceased candidates was finally a donor, without transmitting the infection. CONCLUSIONS: Among deceased individuals from endemic areas considered for SOT donation, seroprevalence of strongyloidiasis was high. This highlights the importance of adhering to current recommendations on screening for S. stercoralis among potential SOT donors at high risk of the infection, together with the need of developing a rapid diagnostic test to fully implement these screening strategies

Lack of Helios during neural development induces adult schizophrenia-like behaviors associated with aberrant levels of the TRIF-recruiter protein WDFY1

The role of the WDFY1 protein has been studied as a TLR3/4 scaffold/recruiting protein in the immune system and in different oncogenic conditions. However, its function in brain remains poorly understood. We have found that in mice devoid of Helios (He−/− mice), a transcription factor specifically expressed during the development of the immune cells and the central nervous system, there is a permanent and sustained increase of Wdfy1 gene expression in the striatum and hippocampus. Interestingly, we observed that WDFY1 protein levels were also increased in the hippocampus and dorsolateral prefrontal cortex of schizophrenic patients, but not in the hippocampus of Alzheimer's disease patients with an associated psychotic disorder. Accordingly, young He−/− mice displayed several schizophrenic-like behaviors related to dysfunctions in the striatum and hippocampus. These changes were associated with an increase in spine density in medium spiny neurons (MSNs) and with a decrease in the number and size of PSD-95-positive clusters in the stratum radiatum of the CA1. Moreover, these alterations in structural synaptic plasticity were associated with a strong reduction of neuronal NF-κB in the pyramidal layer of the CA1 in He−/− mice. Altogether, our data indicate that alterations involving the molecular axis Helios-WDFY1 in neurons during the development of core brain regions could be relevant for the pathophysiology of neuropsychiatric disorders such as schizophrenia

A predictive model and risk factors for case fatality of covid-19

This study aimed to create an individualized analysis model of the risk of intensive care unit (ICU) admission or death for coronavirus disease 2019 (COVID-19) patients as a tool for the rapid clinical management of hospitalized patients in order to achieve a resilience of medical resources. This is an observational, analytical, retrospective cohort study with longitudinal follow-up. Data were collected from the medical records of 3489 patients diagnosed with COVID-19 using RT-qPCR in the period of highest community transmission recorded in Europe to date: February–June 2020. The study was carried out in in two health areas of hospital care in the Madrid region: the central area of the Madrid capital (Hospitales de Madrid del Grupo HM Hospitales (CH-HM), n = 1931) and the metropolitan area of Madrid (Hospital Universitario Príncipe de Asturias (MH-HUPA) n = 1558). By using a regression model, we observed how the different patient variables had unequal importance. Among all the analyzed variables, basal oxygen saturation was found to have the highest relative importance with a value of 20.3%, followed by age (17.7%), lymphocyte/leukocyte ratio (14.4%), CRP value (12.5%), comorbidities (12.5%), and leukocyte count (8.9%). Three levels of risk of ICU/death were established: low-risk level (20%). At the high-risk level, 13% needed ICU admission, 29% died, and 37% had an ICU–death outcome. This predictive model allowed us to individualize the risk for worse outcome for hospitalized patients affected by COVID-19

A Predictive Model and Risk Factors for Case Fatality of COVID-19

This study aimed to create an individualized analysis model of the risk of intensive care unit (ICU) admission or death for coronavirus disease 2019 (COVID-19) patients as a tool for the rapid clinical management of hospitalized patients in order to achieve a resilience of medical resources. This is an observational, analytical, retrospective cohort study with longitudinal follow-up. Data were collected from the medical records of 3489 patients diagnosed with COVID-19 using RT-qPCR in the period of highest community transmission recorded in Europe to date: February-June 2020. The study was carried out in in two health areas of hospital care in the Madrid region: the central area of the Madrid capital (Hospitales de Madrid del Grupo HM Hospitales (CH-HM), n = 1931) and the metropolitan area of Madrid (Hospital Universitario Príncipe de Asturias (MH-HUPA) n = 1558). By using a regression model, we observed how the different patient variables had unequal importance. Among all the analyzed variables, basal oxygen saturation was found to have the highest relative importance with a value of 20.3%, followed by age (17.7%), lymphocyte/leukocyte ratio (14.4%), CRP value (12.5%), comorbidities (12.5%), and leukocyte count (8.9%). Three levels of risk of ICU/death were established: low-risk level (20%). At the high-risk level, 13% needed ICU admission, 29% died, and 37% had an ICU-death outcome. This predictive model allowed us to individualize the risk for worse outcome for hospitalized patients affected by COVID-19