Spatial and observational homogeneities of the galaxy distribution in standard cosmologies

This work discusses the possible empirical verification of the geometrical concept of homogeneity of the standard relativistic cosmology considering its various definitions of distance. We study the physical consequences of the distinction between the usual concept of spatial homogeneity (SH), as defined by the Cosmological Principle, and the concept of observational homogeneity (OH), arguing that OH is in principle falsifiable by means of astronomical observations, whereas verifying SH is only possible indirectly. Simulated counts of cosmological sources are produced by means of a generalized number-distance expression that can be specialized to produce either the counts of the Einstein-de Sitter (EdS) cosmology, which has SH by construction, or other types of counts, which do, or do not, have OH by construction. Expressions for observational volumes and differential densities are derived with the various cosmological distance definitions in the EdS model. Simulated counts that have OH by construction do not always exhibit SH features. The reverse situation is also true. Besides, simulated counts with no OH features at low redshift start showing OH characteristics at high redshift. The comoving distance seems to be the only distance definition where both SH and OH appear simultaneously. The results show that observations indicating possible lack of OH do not necessarily falsify the standard Friedmannian cosmology, meaning that this cosmology will not necessarily always produce observable homogeneous densities. The general conclusion is that the use of different cosmological distances in the characterization of the galaxy distribution lead to significant ambiguities in reaching conclusions about the behavior of the large-scale galaxy distribution in the Universe.Comment: 12 pages, 12 figures, LaTeX. Matches the final version sent to the journal. Accepted for publication in "Astronomy and Astrophysics

Heat shock protein 60 reactive T cells in juvenile idiopathic arthritis: what is new?

Juvenile idiopathic arthritis (JIA) is a disease characterized by chronic joint inflammation, caused by a deregulated immune response. In patients with JIA, heat shock proteins (HSPs) are highly expressed in the synovial lining tissues of inflamed joints. HSPs are endogenous proteins that are expressed upon cellular stress and are able to modulate immune responses. In this review, we concentrate on the role of HSPs, especially HSP60, in modulating immune responses in both experimental and human arthritis, with a focus on JIA. We will mainly discuss the tolerogenic immune responses induced by HSPs, which could have a beneficial effect in JIA. Overall, we will discuss the immune modulatory capacity of HSPs, and the underlying mechanisms of HSP60-mediated immune regulation in JIA, and how this can be translated into therapy

Systematic Analysis and Biomarker Study for Alzheimer's Disease.

Revealing the relationship between dysfunctional genes in blood and brain tissues from patients with Alzheimer's Disease (AD) will help us to understand the pathology of this disease. In this study, we conducted the first such large systematic analysis to identify differentially expressed genes (DEGs) in blood samples from 245 AD cases, 143 mild cognitive impairment (MCI) cases, and 182 healthy control subjects, and then compare these with DEGs in brain samples. We evaluated our findings using two independent AD blood datasets and performed a gene-based genome-wide association study to identify potential novel risk genes. We identified 789 and 998 DEGs common to both blood and brain of AD and MCI subjects respectively, over 77% of which had the same regulation directions across tissues and disease status, including the known ABCA7, and the novel TYK2 and TCIRG1. A machine learning classification model containing NDUFA1, MRPL51, and RPL36AL, implicating mitochondrial and ribosomal function, was discovered which discriminated between AD patients and controls with 85.9% of area under the curve and 78.1% accuracy (sensitivity = 77.6%, specificity = 78.9%). Moreover, our findings strongly suggest that mitochondrial dysfunction, NF-κB signalling and iNOS signalling are important dysregulated pathways in AD pathogenesis

Biomarkers as Proxies to Analyse Land-Use History in Northern Jordan

In the semi-arid 'Decapolis region' in northern Jordan, due severe land degradation in the past, 'barren' and 'impoverished' landscapes can be found today. It is widely believed that land degradation in these regions was caused by ancient land use, e.g. overgrazing due to ‘Arab mismanagement'. However, the connection of degradation with land use is far from certain. The 'Decapolis region' is located in an approximately 100 km wide transition zone from Mediterranean to steppe and desert climate. Therefore, the landscape in this region is highly sensitive to climate variations. A major sedimentation phase in the late 6th century AD appears to represent a significant climate change towards more aridity, and might be connected with a cluster of heavy rainfall events in northern Jordan. In fact, more recent studies have found that periods of predominantly pastoral land use in northern Jordan were connected with natural reforestation. Since a dating of sedimentation alone does not deliver clues about the precise reason of deposition, a multidisciplinary team is analyzing the land-use history in the ‘Decapolis’ region. This presentation focusses on ongoing biomarker analyses. Samples were selected considering geoarchaeological data, including phosphorus concentrations, archaeological data, including distribution of potsherds and other fragments on ancient fields and data of further disciplines. Vegetation changes are investigated by analyses of n-alkanes and terpenoids. Manuring with faeces is analysed by specific steroids that are indicative for faeces deposition. Preliminary results showed a high input of omnivorous (pigs, humans) faeces in some areas. Manuring with faeces of herbivores seemed to be less important

Potentially bioavailable iron delivery by iceberg-hosted sediments and atmospheric dust to the polar oceans

Iceberg-hosted sediments and atmospheric dust transport potentially bioavailable iron to the Arctic and Southern oceans as ferrihydrite. Ferrihydrite is nanoparticulate and more soluble, as well as potentially more bioavailable, than other iron (oxyhydr)oxide minerals (lepidocrocite, goethite, and hematite). A suite of more than 50 iceberghosted sediments contain a mean content of 0.076 wt% Fe as ferrihydrite, which produces iceberg-hosted Fe fluxes ranging from 0.7 to 5.5 and 3.2 to 25 Gmoles yr 1 to the Arctic and Southern oceans respectively. Atmospheric dust (with little or no combustion products) contains a mean ferrihydrite Fe content of 0.038 wt% (corresponding to a fractional solubility of 1 %) and delivers much smaller Fe fluxes (0.02–0.07 Gmoles yr 1 to the Arctic Ocean and 0.0– 0.02 Gmoles yr 1 to the Southern Ocean). New dust flux data show that most atmospheric dust is delivered to sea ice where exposure to melting/re-freezing cycles may enhance fractional solubility, and thus fluxes, by a factor of approximately 2.5. Improved estimates for these particulate sources require additional data for the iceberg losses during fjord transit, the sediment content of icebergs, and samples of atmospheric dust delivered to the polar regions

Examining Associations between Body Mass Index in 18⁻25 Year-Olds and Energy Intake from Alcohol:Findings from the Health Survey for England and the Scottish Health Survey

Evidence on the relationship between alcohol consumption and body mass index (BMI) is mixed, particularly for young adults. This study explored the relationship between energy obtained from alcoholic beverages and BMI using data for 18-25 year-olds (n = 7691) from pooled cross-sections of the 2008⁻2014 Health Survey for England and the Scottish Health Survey. Energy obtained from alcoholic beverages (excluding mixers) on the heaviest drinking day in the past week was expressed as percentage of total recommended dietary allowance (RDA) of energy (% RDA Energy). Linear regressions were estimated of BMI on alcohol intake categories controlling for intake frequency, physical activity, longstanding illness and other covariates, with separate analyses for men and women, and by beverage type. Significant associations with BMI were observed with the 'Very High' category of alcohol intake (>75% RDA Energy) for men (p 50% to 75% RDA Energy) (p 0⁻25% RDA Energy) category. Young adults drinking the highest levels of alcohol on a single occasion were more likely to be obese than those with the lowest intake. Interventions to address internationally rising youth obesity rates should also consider reducing alcohol consumption by increasing alcohol prices, and reducing availability and marketing exposure

Social withdrawal as a trans-diagnostic predictor of short-term remission: a meta-analysis of five clinical cohorts

Social withdrawal is an early manifestation of several neuropsychiatric disorders, and it is characterised by a gradual disengagement from social interactions, potentially leading to complete isolation. This study investigated the association between social withdrawal at baseline and short-term symptom remission in five independent cohorts, including patients with major depressive disorder (MDD), bipolar spectrum disorders, and schizophrenia. Measures of social withdrawal were derived in each study, and clinical remission was estimated based on the psychopathological severity assessed after short-term psychopharmacological treatment (12weeks). Logistic regression was performed in each sample, adjusting for age and baseline psychopathological severity residualised for social withdrawal. Results were then meta-analysed across samples within a random-effect framework. A total of 4461 patients were included in the analyses (3195 patients with MDD, 655 with bipolar spectrum disorders and 611 with schizophrenia). The meta-analysis showed that higher baseline levels of social withdrawal were associated with a decreased likelihood of short-term remission (ORadj=0.67, 95% CI, 0.58-0.79, P=5.28×10−7), with the strongest effect in patients with schizophrenia. Overall, our study highlighted the need to address social withdrawal in the early phases of the disease to promote symptom remission in patients with major psychiatric disorders. Understanding the neurobiology underlying social withdrawal may aid the development of medications that can specifically reverse social impairment, thereby fostering clinical remission. Int Clin Psychopharmacol 37: 38-45 Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc

Modulation of T Cell Function by Combination of Epitope Specific and Low Dose Anticytokine Therapy Controls Autoimmune Arthritis

Innate and adaptive immunity contribute to the pathogenesis of autoimmune arthritis by generating and maintaining inflammation, which leads to tissue damage. Current biological therapies target innate immunity, eminently by interfering with single pro-inflammatory cytokine pathways. This approach has shown excellent efficacy in a good proportion of patients with Rheumatoid Arthritis (RA), but is limited by cost and side effects. Adaptive immunity, particularly T cells with a regulatory function, plays a fundamental role in controlling inflammation in physiologic conditions. A growing body of evidence suggests that modulation of T cell function is impaired in autoimmunity. Restoration of such function could be of significant therapeutic value. We have recently demonstrated that epitope-specific therapy can restore modulation of T cell function in RA patients. Here, we tested the hypothesis that a combination of anti-cytokine and epitope-specific immunotherapy may facilitate the control of autoimmune inflammation by generating active T cell regulation. This novel combination of mucosal tolerization to a pathogenic T cell epitope and single low dose anti-TNFα was as therapeutically effective as full dose anti-TNFα treatment. Analysis of the underlying immunological mechanisms showed induction of T cell immune deviation