Liability-driven investment and pension fund exposure to emerging markets: A Minskyan analysis

This paper explores the determinants and implications of the growing allocation of insurance companies and pension funds to emerging markets. The key contention put forward is that liabilities are at the core of the portfolio choice of insurance companies and pension funds, and that this has important consequences for the stability of asset demand. The paper supports this contention with a theoretical framework based on Hyman Minsky and the results from 22 semi-structured interviews with European insurance companies and pension funds’ executives, investment consultants, and asset managers. It shows that the rising insurance companies and pension funds’ demand for emerging markets’ assets has to be analysed in the context of the pressures resulting from structural funding deficits and low yields. Emerging markets’ assets are sought as part of the sector’s strategy to increase returns and, given their subordinate integration into a spatially uneven international monetary and financial system, remain not suited to directly meet insurance companies and pension funds’ liabilities. This causes insurance companies and pension funds’ demand for these assets to be volatile and independent of conditions in these countries, reproducing emerging markets’ monetary and financial subordination. By stressing the structural financial (in)stability implications insurance companies and pension funds’ liabilities have for emerging markets’ asset demand, the paper contributes to the literature on insurance companies and pension funds’ investments in emerging markets and bridges the gap between those which have noted the importance of liability conditions for insurance companies and pension funds and the literature pointing to the destabilising impact of insurance companies and pension funds due to behavioural and agency issues. Moreover, by basing itself on a Minskyan theoretical framework, it responds to recent calls for a more systematic incorporation of heterodox economic thought into financial geography

Gut–brain axis and neurodegeneration : State-of-the-art of meta-omics sciences for microbiota characterization

Recent advances in the field of meta-omics sciences and related bioinformatics tools have allowed a comprehensive investigation of human-associated microbiota and its contribution to achieving and maintaining the homeostatic balance. Bioactive compounds from the microbial community harboring the human gut are involved in a finely tuned network of interconnections with the host, orchestrating a wide variety of physiological processes. These includes the bidirectional crosstalk between the central nervous system, the enteric nervous system, and the gastrointestinal tract (i.e., gut\u2013brain axis). The increasing accumulation of evidence suggest a pivotal role of the composition and activity of the gut microbiota in neurodegeneration. In the present review we aim to provide an overview of the state-of-the-art of meta-omics sciences including metagenomics for the study of microbial genomes and taxa strains, metatranscriptomics for gene expression, metaproteomics and metabolomics to identify and/or quantify microbial proteins and metabolites, respectively. The potential and limitations of each discipline were highlighted, as well as the advantages of an integrated approach (multi-omics) to predict microbial functions and molecular mechanisms related to human diseases. Particular emphasis is given to the latest results obtained with these approaches in an attempt to elucidate the link between the gut microbiota and the most common neurodegenerative diseases, such as multiple sclerosis (MS), Alzheimer\u2019s disease (AD), Parkinson\u2019s disease (PD), and amyotrophic lateral sclerosis (ALS)

Undefined Benefit: Fixing the UK Pensions System

The UK's financialised pensions system is marked by inequality, insecurity and instability. We require a radical reimagining to build a system fit for purpose

Comparative computational analysis of SARS-CoV-2 nucleocapsid protein epitopes in taxonomically related coronaviruses

Several research lines are currently ongoing to address the multitude of facets of the pandemic COVID-19. In line with the One-Health concept, extending the target of the studies to the animals which humans are continuously interacting with may favor a better understanding of the SARS-CoV-2 biology and pathogenetic mechanisms; thus, helping to adopt the most suitable containment measures. The last two decades have already faced severe manifestations of the coronavirus infection in both humans and animals, thus, circulating epitopes from previous outbreaks might confer partial protection from SARS-CoV-2 infections. In the present study, we provide an in-silico survey of the major nucleocapsid protein epitopes and compare them with the homologues of taxonomically-related coronaviruses with tropism for animal species that are closely inter-related with the human beings population all over the world. Protein sequence alignment provides evidence of high sequence homology for some of the investigated proteins. Moreover, structural epitope mapping by homology modelling revealed a potential immunogenic value also for specific sequences scoring a lower identity with SARS-CoV-2 nucleocapsid proteins. These evidence provide a molecular structural rationale for a potential role in conferring protection from SARS-CoV-2 infection and identifying potential candidates for the development of diagnostic tools and prophylactic-oriented strategies

Phenotypic and genomic identification of Staphylococcus epidermidis GOI1153754-03-14 isolated from an infected orthopedic prosthesis

Introduction: Staphylococcus epidermidis GOI1153754-03-14 is able to colonize orthopedic implants and to cause septic non-unions, as validated in a recent in vivo study (Lovati, 2016). To pore over the mechanisms leading to the biofilm formation on metallic implants, in the present study, we carried out the phenotypic and genotypic characterization of the clinical isolate S. epidermidis GOI1153754-03-14.Materials and Methods: The antimicrobial susceptibility and minimum inhibitory concentration (MIC) of the strain were evaluated through the Vitek2 System (Biomerieux), as well as its ability to form biofilm in vitro through a spectrophotometric assay (Stepanovich, 2000).The genomic DNA was extracted by Bacterial Genomic DNA Isolation Kit (Norgen Biotek Corp.). Libraries were prepared with the ThruPLEX DNA-seq (Rubicon Genomics) and then sequenced on the Illumina MiSeq platform through the MiSeq Reagent Kit v3 (600-cycles) to produce 300 bp paired-end reads (Illumina Inc.). Reads were quality-trimmed and gene annotated thanks to the RAST software (Aziz, 2008).Results: The antimicrobial susceptibility along with the MIC values are reported in Table 1. The outputs resulted in 51 contigs (Average = 50,720.6 Mb) with 396X fold average coverage. The total genome is 2,586,753 bp long with a GC content of 31.84% and an N50 value of 7 bp. The whole genome is composed by 2,467 protein-encoding genes and 64 RNAs (55 tRNAs and 9 rRNAs). The entire genome sequence has been deposited in the European Nucleotide Archive (ENA) under the accession no. FWCG01000000 (Bottagisio, 2017).Discussion: The genotypic and phenotypic characterization of the S. epidermidis GOI1153754-03-14 will enable a better comprehension of the mechanisms involved in the biofilm formation on orthopedic implants paving the way for innovative preventative and therapeutic strategies. Moreover, the sequence of this clinical strain is mandatory to develop dedicated proteomics analysis in order to highlight functional mechanism of biofilm formation

Immunoinformatic analysis of the SARS-CoV-2 envelope protein as a strategy to assess cross-protection against COVID-19

Envelope protein of coronaviruses is a structural protein existing in both monomeric and homo-pentameric form. It has been related to a multitude of roles including virus infection, replication, dissemination and immune response stimulation. In the present study, we employed an immunoinformatic approach to investigate the major immunogenic domains of the SARS-CoV-2 envelope protein and map them among the homologue proteins of coronaviruses with tropism for animal species that are closely inter-related with the human beings population all over the world. Also, when not available, we predicted the envelope protein structural folding and mapped SARS-CoV-2 epitopes. Envelope sequences alignment provides evidence of high sequence homology for some of the investigated virus specimens; while the structural mapping of epitopes resulted in the interesting maintenance of the structural folding and epitope sequence localization also in the envelope proteins scoring a lower alignment score. In line with the One-Health approach, our evidences provide a molecular structural rationale for a potential role of taxonomically related coronaviruses in conferring protection from SARS-CoV-2 infection and identifying potential candidates for the development of diagnostic tools and prophylactic-oriented strategies

Inducible nitric oxide synthase increases secretion from inflamed salivary glands

Objective. Salivary gland secretion is dependent on cholinergic stimulation via autonomic nerves and calcium signalling in acinar cells. Secretory dysfunction associated with SS may be partly caused by the damaging effects of increased glandular concentrations of nitric oxide (NO) derived from up-regulation of inducible NO synthase (iNOS) that accompanies glandular inflammation. The present study examines the effects of increased iNOS expression on salivary gland secretory function

Co-administration of H-ferritin-doxorubicin and Trastuzumab in neoadjuvant setting improves efficacy and prevents cardiotoxicity in HER2 + murine breast cancer model

Neoadjuvant chemotherapy has been established as the standard of care for HER2-positive breast cancer since it allows cancer down-staging, up to pathological complete response. The standard of care in the neoadjuvant setting for HER2-positive breast cancer is a combination of highly cytotoxic drugs such as anthracyclines and the anti-HER2 monoclonal antibody. Despite this cocktail allows a pathological complete response in up to 50%, their co-administration is strongly limited by intrinsic cardiotoxicity. Therefore, only a sequential administration of anthracyclines and the anti-HER2 treatment is allowed. Here, we propose the anthracycline formulation in H-Ferritin nanocages as promising candidate to solve this unmet clinical need, thanks to its capability to increase anthracyclines efficacy while reducing their cardiotoxicity. Treating a murine model of HER2-positive breast cancer with co-administration of Trastuzumab and H-Ferritin anthracycline nanoformulation, we demonstrate an improved tumor penetration of drugs, leading to increased anticancer efficacy and reduced of cardiotoxicity

Environmental Factors in the Relapse and Recurrence of Inflammatory Bowel Disease:A Review of the Literature

The causes of relapse in patients with Crohn's disease (CD) and ulcerative colitis (UC) are largely unknown. This paper reviews the epidemiological and clinical data on how medications (non-steroidal anti-inflammatory drugs, estrogens and antibiotics), lifestyle factors (smoking, psychological stress, diet and air pollution) may precipitate clinical relapses and recurrence. Potential biological mechanisms include: increasing thrombotic tendency, imbalances in prostaglandin synthesis, alterations in the composition of gut microbiota, and mucosal damage causing increased permeability

Regulation of the polymeric immunoglobulin receptor by the classical and alternative NF-κB pathways in intestinal epithelial cells

The polymeric immunoglobulin receptor (pIgR) transports IgA antibodies across intestinal epithelial cells (IECs). Expression of pIgR is upregulated by proinflammatory signaling pathways via activation of nuclear factor-κB (NF-κB). Here, we examined the contributions of the RelA-dependent classical and RelB-dependent alternative pathways of NF-κB to pIgR regulation in the HT-29 human IEC line following stimulation with tumor necrosis factor (TNF), lipopolysaccharide (LPS; Toll-like receptor 4 (TLR4) ligand), and polyinosinic: polycytidylic acid (pIC; TLR3 ligand). Whereas induction of proinflammatory genes such as interleukin-8 (IL-8) required only RelA, pIgR expression was regulated by complex mechanisms that involved both RelA and RelB. Upregulation of pIgR expression by ligation of the lymphotoxin-β receptor suggested a direct role for the alternative NF-κB pathway. Inhibition of mitogen-activated protein kinases reduced the induction of IL-8, but enhanced the induction of pIgR by TNF and TLR signaling. Regulation of pIgR through unique signaling pathways could allow IECs to sustain high levels of IgA transport while limiting the proinflammatory responses