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Smart beta strategy is an increasingly frequent approach to investment analysis for portfolio selection and optimization and it can be combined with environmental, social, and governance (ESG) considerations. In order to verify the impact of the integration between ESG and smart beta analysis, first we apply a portfolio rebalancing based on ESG scores on securities selected according to different smart beta strategies (ex-post ESG rebalancing approach). Secondly, we apply different smart beta approaches to sustainable portfolios, screened according to the issuers’ ESG scores (ex-ante ESG screening approach). We find that ESG rebalancing and screening are able to impact both on return and risk statistics, but with a different level of efficiency for each smart beta strategy. ESG rebalancing proves to be particularly efficient when it is applied to a “Value” portfolio. On the other hand, when smart beta is applied to ESG-screened portfolios, “Growth” is the strategy which shows the highest increase in risk-adjusted performance, particularly in the US. Minimum volatility proves to be the most efficient smart beta strategy for sustainable portfolios. In general, the increase in the level of sustainability does not deteriorate the risk-adjusted performances of most smart beta strategies.

The study makes a comparison between the performance of equity portfolios characterized by high ESG score stocks and portfolios with low ESG score stocks. In particular, we analyze three ESG scores: MSCI ESG Rating, Sustainalytics scores and S&P DJI/Robeco ESG Scores, by examining the European stock market in two periods: medium/long term (five years) and short-term (one year). First of all, we associate each component of the index in relation to its MSCI ESG Rating, Sustainalytics score and S&P DJI/Robeco ESG Scores. We build two portfolios: · First quartile portfolio 1Q (according to MSCI; Sustainalytics; and S&P DJI/Robeco ESG Scores), including securities of companies with the highest ESG score, based on ESG best-in-class screening strategy. · Fourth quartile portfolio 4Q (according to MSCI; Sustainalytics; and S&P DJI/Robeco ESG Scores), including securities of companies with the lowest ESG scores. We aim to answer the following questions: a) do portfolios with higher ESG scores stocks lead to better performances than those including stocks with low ESG scores? b), Are there some sectors that drive the performance within the sector breakdown? Results show a divergence between the composition of the first quartile, whereas there is more homogeneity in the fourth quartile.

In this study, the recently launched Sentinel-2 (S2) optical satellite and the active radar Sentinel-1 (S1) satellite supported by active fire data from the MODIS sensor were used to detect and monitor forest fires in the Congo Basin. In the context of a very strong El Niño event, an unprecedented outbreak of fires was observed during the first months of 2016 in open forests formations in the north of the Republic of Congo. The anomalies of the recent fires and meteorological situation compared to historical data show the severity of the drought. Burnt areas mapped by the S1 SAR and S2 Multi Spectral Instrument (MSI) sensors highlight that the fires occurred mainly in Marantaceae forests, characterized by open tree canopy cover and an extensive tall herbaceous layer. The maps show that the origin of the fires correlates with accessibility to the forest, suggesting an anthropogenic origin. The combined use of the two independent and fundamentally different satellite systems of S2 and S1 captured an extent of 36,000 ha of burnt areas, with each sensor compensating for the weakness (cloud perturbations for S2, and sensitivity to ground moisture for S1) of the other.

The fate, properties and determination of microplastics (MPs) and nanoplastics (NPs) in soil are poorly known. In fact, most of the 300 million tons of plastics produced each year ends up in the environment and the soil acts as a log-term sink for these plastic debris. Therefore, the aim of this review is to discuss MP and NP pollution in soil as well as highlighting the knowledge gaps that are mainly related to the complexity of the soil ecosystem. The fate of MPs and NPs in soil is strongly determined by physical properties of plastics, whereas negligible effect is exerted by their chemical structures. The degradative processes of plastic, termed ageing, besides generating micro-and nano-size debris, can induce marked changes in their chemical and physical properties with relevant effects on their reactivity. Further, these processes could cause the release of toxic oligomeric and monomeric constituents from plastics, as well as toxic additives, which may enter in the food chain, representing a possible hazard to human health and potentially affecting the fauna and flora in the environment. In relation to their persistence in soil, the list of soil-inhabiting, plastic-eating bacteria, fungi and insect is increasing daily. One of the main ecological functions attributable to MPs is related to their function as vectors for microorganisms through the soil. However, the main ecological effect of NPs (limited to the fraction size < than 50 nm) is their capacity to pass through the membrane of both prokaryotic and eukaryotic cells. Soil biota, particularly earthworms and collembola, can be both MPs and NPs carriers through soil profile. The use of molecular techniques, especially omics approaches, can gain insights into the effects of MPs and NPs on composition and activity of microbial communities inhabiting the soil and into those living on MPs surface and in the gut of the soil plastic-ingesting fauna.

ObjectivesTo analyse the prevalence of CECR1 mutations in patients diagnosed with early onset livedo reticularis and/or haemorrhagic/ischaemic strokes in the context of inflammation or polyarteritis nodosa (PAN). Forty-eight patients from 43 families were included in the study.MethodsDirect sequencing of CECR1 was performed by Sanger analysis. Adenosine deaminase 2 (ADA2) enzymatic activity was analysed in monocyte isolated from patients and healthy controls incubated with adenosine and with or without an ADA1 inhibitor.ResultsBiallelic homozygous or compound heterozygous CECR1 mutations were detected in 15/48 patients. A heterozygous disease-associated mutation (p.G47V) was observed in two affected brothers. The mean age of onset of the genetically positive patients was 24 months (6 months to 7 years). Ten patients displayed one or more cerebral strokes during their disease course. Low immunoglobulin levels were detected in six patients. Thalidomide and anti-TNF (tumour necrosis factor) blockers were the most effective drugs. Patients without CECR1 mutations had a later age at disease onset, a lower prevalence of neurological and skin manifestations; one of these patients displayed all the clinical features of adenosine deaminase 2deficiency (DADA2) and a defective enzymatic activity suggesting the presence of a missed mutation or a synthesis defect.ConclusionsDADA2 accounts for paediatric patients diagnosed with PAN-like disease and strokes and might explain an unrecognised condition in patients followed by adult rheumatologist. Timely diagnosis and treatment with anti-TNF agents are crucial for the prevention of severe complications of the disease. Functional assay to measure ADA2 activity should complement genetic testing in patients with non-confirming genotypes.

Several studies have investigated the adsorption of pure DNA on soil particles and its transformation ability. However, the presence of not purified (dirty) rather than pure DNA is more common in the extracellular soil environment. For this reason, we have investigated the adsorption and binding of dirty DNA on montmorillonite (M) and kaolinite (K) and their transforming ability in comparison to pure DNA. After lysis of Bacillus subtilis cells, induced by KCl, dirty DNA was characterized by the presence of cellular wall debris (cwd) and other constitutional organic components (coc). The dirty DNA was then divided into two fractions, one with cellular wall debris (DNA +cwd) and the other without cellular wall debris (DNA -cwd). B. subtilis BD 1512 (Cmr) and BD 170 (Cms) were selected as donor and recipient bacteria, respectively, for adsorption and transformation studies. Both cwd and coc seem to facilitate the adsorption of DNA to clay minerals, whereas only cwd promote the DNA binding on clays, protecting also the DNA fragments below 400 bp against nucleases. Both dirty DNA fractions adsorbed and bound on clay minerals were able to transform competent cells.

BackgroundCongenital anomalies of the kidney and urinary tract (CAKUT) have been underestimated in Hirschsprung disease (HSCR). This paper aims at reporting results of patients with HSCR who underwent kidney and urinary tract assessment.MethodsPatients seen between December 2005 and November 2020 underwent a complete kidney and urinary tract diagnostic workup. Data regarding CAKUT, gender, length of aganglionosis, familial history, HSCR-associated enterocolitis (HAEC), RET genotype, and outcome were collected.ResultsOut of 472 patients, 280 completed the workup and represented the focus. Male to female ratio was 3.24:1. Familial cases accounted for 9.8% of patients. RET mutations were detected in 19.8%. We encountered a total of 61 patients with 70 nephrological issues (21.8%), including 28 hypoplasia/dysplasia, 12 hydronephrosis, 11 vesicoureteric reflux, 7 duplex collecting system, 2 kidney agenesis, 2 horseshoe kidney, and 8 miscellanea, involving 91 kidneys without side preponderance (50 right, 41 left). Of these 61 patients, 20 (7.1% of the whole series) required medical or surgical treatment. When comparing patients with and without CAKUT, familial history proved to occur with a significantly lower frequency in the former as did better patient perspectives of outcome.ConclusionsWe confirmed that all diagnostic workups in HSCR should include a complete kidney and urinary tract diagnostic workup. Our study suggests that genes other than RET could play a role in determining CAKUT. Given worse patient perspectives of outcome, CAKUT seems to significantly interfere with quality of life thus confirming the need for early diagnosis and tailored prevention strategies.

Non-remitting neutropenia in children and chronic idiopathic neutropenia (CIN) in adults have been described previously as peculiar subgroups of neutropenic patients carrying similar clinical and immunological features. The present collection comprising 25 subjects (16 adults and 9 children) mostly affected with mild (84%) and moderate (16%) neutropenia aimed to identify the underlying (possibly common) genetic background. The phenotype of these patients resemble the one described previously: no severe infections, presence of rheumathological signs, leukopenia in almost all patients and lymphocytopenia in one-third of the cohort. The pediatric patients did not share common genes with the adults, based on the results of the multisample test, while some singular variants in neutropenia potentially associated with immune dysregulation likely consistent with the phenotype were found. SPINK5, RELA and CARD11 were retrieved and seem to be consistent with the clinical picture characterized by neutropenia associated to immune dysregulation. The enrichment and burden tests performed in comparison with a control group underline that the products of expression by the variants involved belong to the autoimmunity and immune regulation pathways (i.e., SPINK5, PTPN22 and PSMB9). Even with the limitation of this study’s low number of patients, these results may suggest that non-remitting neutropenia and CIN in adults deserve deep genetic study and enlarged consideration in comparison with classical neutropenia.

The advent of Whole Genome Sequencing (WGS) broadened the genetic variation detection range, revealing the presence of variants even in non-coding regions of the genome, which would have been missed using targeted approaches. One of the most challenging issues in WGS analysis regards the interpretation of annotated variants. This review focuses on tools suitable for the functional annotation of variants falling into non-coding regions. It couples the description of non-coding genomic areas with the results and performance of existing tools for a functional interpretation of the effect of variants in these regions. Tools were tested in a controlled genomic scenario, representing the ground-truth and allowing us to determine software performance.

Primary immunodeficiencies with selective susceptibility to EBV infection are rare conditions associated with severe lymphoproliferation. We followed a patient, son of consanguineous parents, referred to our center for recurrent periodic episodes of fever associated with tonsillitis and adenitis started after an infectious mononucleosis and responsive to oral steroid. An initial diagnosis of periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis syndrome was done. In the following months, recurrent respiratory infections and episodes of keratitis were also observed, together with a progressive reduction of immunoglobulin levels and an increase of CD20 cells. Cell sorting and EBV PCR showed 25,000 copies for 100,000 leukocytes with predominant infection of B lymphocytes. Lymph node's biopsy revealed reactive lymphadenopathy with paracortical involvement consistent with a chronic EBV infection. Molecular analysis of , and genes did not detect any pathogenic mutation. The patients underwent repeated courses of anti-CD20 therapy with only a partial control of the disease, followed by stem cell transplantation with a complete normalization of clinical and immunological features. Whole exome sequencing of the trio was performed. Among the variants identified, a novel loss of function homozygous c.163-2A>G mutation of the gene, affecting the exon 2 AG-acceptor splice site, fit the expected recessive model of inheritance. Indeed, deficiency of both CD27, and, more recently, of its ligand CD70, has been reported as a cause of EBV-driven lymphoproliferation and hypogammaglobulinemia. Cell surface analysis of patient-derived PHA-T cell blasts and EBV-transformed lymphoblastoid cell lines confirmed absence of CD70 expression. In conclusion, we describe a case of severe chronic EBV infection caused by a novel mutation of CD70 presenting with recurrent periodic fever.