Response of Foraminifera to Anthropogenic Nicotine Pollution of Cigarette Butts: An Experimental Approach

The most often dispersed environmental pollutants that are released both directly and indirectly into the environment that may eventually reach aquatic ecosystems and contaminate aquatic biomes are cigarette butts (CBs). Toxicants such as nicotine, dangerous metals, total particulate matter, and recognized carcinogens can be introduced and transported via CBs into aquatic ecosystems. The examination of the effects of synthetic nicotine on three different species of cultured benthic foraminifera was the focus of this study. Three foraminiferal species from three distinct biomineralization pathways were specifically examined for viability and cellular ultrastructure, including the calcareous perforate Rosalina globularis, the calcareous imperforate Quinqueloculina spp., and the agglutinated Textularia agglutinans. The survival rate, cellular stress, and decalcification were used to assess the toxicological effects of synthetic nicotine. We were able to analyze the reaction of major macromolecules and calcium carbonate to this pollutant using FTIR (Fourier Transform Infrared) spectroscopy. High Performance Liquid Chromatography (HPLC) study was performed to increase our understanding of nicotine bioavailability in the medium culture. Different acute experiments were performed at different dates, and all indicated that synthetic nicotine is acutely hazardous to all three cultured foraminiferal taxa at lethal and sublethal concentrations. Each species responded differently depending on the type of shell biomineralization. Synthetic nicotine enhances shell decalcification and affects the composition of cytoplasmic macromolecules such as lipids and proteins, according to the FTIR spectroscopy investigations. The lipid content rose at lethal concentrations, possibly due to the creation of vesicles. The proteins signal evidences general cellular dyshomeostasis. The integration among the acute toxicity assay, synchrotron, and chemical HPLC analyses provided a valuable approach for the assessment of nicotine as a biomarker of exposure to the toxicants associated with smoking and the impact of this emerging and hazardous material on calcifying marine species

Biomarkers in post-reperfusion syndrome after acute lower limb ischaemia

Ischaemia reperfusion (I/R) injury refers to tissue damage caused when blood supply returns to the tissue after a period of ischaemia. Matrix metalloproteinases (MMPs), neutrophil gelatinase-associated lipocalin (NGAL) and cytokines are biomarkers involved in several vascular complications. The aim of this study was to evaluate the role of MMPs, NGAL and inflammatory cytokines in I/R syndrome. We conducted an open label, multicentric, parallel group study, between January 2010 and December 2013. Patients with acute limb ischaemia were enrolled in this study and were divided into two groups: (i) those subjected to fasciotomy and (ii) those not subjected to fasciotomy, according to the onset of compartment syndrome. Plasma and tissue values of MMPs and NGAL as well as plasma cytokines were evaluated. MMPs, NGAL and cytokine levels were higher in patients with compartment syndrome. Biomarkers evaluated in this study may be used in the future as predictors of I/R injury severity and its possible evolution towards post-reperfusion syndrome

Urinary secretion and extracellular aggregation of mutant uromodulin isoforms

Uromodulin is exclusively expressed in the thick ascending limb and is the most abundant protein secreted in urine where it is found in high-molecular-weight polymers. Its biological functions are still elusive, but it is thought to play a protective role against urinary tract infection, calcium oxalate crystal formation, and regulation of water and salt balance in the thick ascending limb. Mutations in uromodulin are responsible for autosomal-dominant kidney diseases characterized by defective urine concentrating ability, hyperuricemia, gout, tubulointerstitial fibrosis, renal cysts, and chronic kidney disease. Previous in vitro studies found retention in the endoplasmic reticulum as a common feature of all uromodulin mutant isoforms. Both in vitro and in vivo we found that mutant isoforms partially escaped retention in the endoplasmic reticulum and reached the plasma membrane where they formed large extracellular aggregates that have a dominant-negative effect on coexpressed wild-type protein. Notably, mutant uromodulin excretion was detected in patients carrying uromodulin mutations. Thus, our results suggest that mutant uromodulin exerts a gain-of-function effect that can be exerted by both intra- and extracellular forms of the protein

Urinary secretion and extracellular aggregation of mutant uromodulin isoforms.

Uromodulin is exclusively expressed in the thick ascending limb and is the most abundant protein secreted in urine where it is found in high-molecular-weight polymers. Its biological functions are still elusive, but it is thought to play a protective role against urinary tract infection, calcium oxalate crystal formation, and regulation of water and salt balance in the thick ascending limb. Mutations in uromodulin are responsible for autosomal-dominant kidney diseases characterized by defective urine concentrating ability, hyperuricemia, gout, tubulointerstitial fibrosis, renal cysts, and chronic kidney disease. Previous in vitro studies found retention in the endoplasmic reticulum as a common feature of all uromodulin mutant isoforms. Both in vitro and in vivo we found that mutant isoforms partially escaped retention in the endoplasmic reticulum and reached the plasma membrane where they formed large extracellular aggregates that have a dominant-negative effect on coexpressed wild-type protein. Notably, mutant uromodulin excretion was detected in patients carrying uromodulin mutations. Thus, our results suggest that mutant uromodulin exerts a gain-of-function effect that can be exerted by both intra- and extracellular forms of the protein

Effetti dell’inquinamento da plastiche sui foraminiferi bentonici

Le plastiche sono divenuti contaminanti ubiquitari negli ecosistemi marini, d’acqua dolce e terrestri che producono rilevanti impatti sulle specie che in essi vivono. Dal 1950 ad oggi sono stati accumulati nell’ambiente circa 5 miliardi di tonnellate di plastica (Geyer et al., 2017). I meccanismi di interazione tra microplastiche e biosfera nonché gli effetti biochimici delle molecole sintetiche, specialmente sugli organismi eucariotici unicellulari marini, sono scarsamente studiati. In particolare, i foraminiferi bentonici costituiscono una componente fondamentale delle comunità marine e svolgono un ruolo chiave nel funzionamento dell’ecosistema e nei cicli biogeochimici. La loro sensibilità e la rapida risposta allo stress ambientale li rendono efficienti indicatori dei cambiamenti climatici e ambientali attuali e del passato (Schönfeld et al., 2012).Per comprendere meglio l’effetto delle plastiche negli oceani e negli organismi marini, abbiamo valutato l’incorporazione di (bio)polimeri e microplastiche in foraminiferi bentonici utilizzando tecniche di spettromicroscopia ad infrarossi in trasformata di Fourier (μFTIR). In questo studio, abbiamo raccolto ed analizzato spettri ed immagini μFTIR dauna selezione di specie di foraminiferi bentonici: Rosalina globularis cresciuta in colture inquinate con la plastica e Cibicidoides lobatulus, Rosalina bradyi e Textularia bocki raccolti su un frammento di plastica trovato sepolto in un sedimento del fondale del Mar Mediterraneo. In particolare, i foraminiferi provenienti dalle colture sono stati intossicati con molecola di di-2-etilesilftalato (DEHP) allo scopo di valutarne l’incorporazione nel citoplasma. Questo studio ha permesso di documentare: (1) la presenza di microplastiche nel citoplasma e nel guscio agglutinante di T. bocki; (2) segnali di stress ossidativo e di aggregazione proteica nella componente cellulare di C. lobatulus, R. bradyi e T. bocki, ancorati alla busta di plastica; (3) l’incorporazione del DEHP nel citoplasma di R. globularis. Questo studio ha confermato il ruolo chiave svolto dai foraminiferi bentonici come proxy per la valutazione degli effetti dell’inquinamento da microplastiche sia a livello cellulare che di biomineralizzazione confermando l’ingresso delle microplastiche e DEHP nei cicli biogeochimici. Questa indagine ha inoltre dimostrato che la microscopia FTIR è uno strumento efficace per studiare, senza l’utilizzo di marcatori specifici, l’interazione su scala molecolare tra plastica, citoplasma e guscio dei foraminiferi

The Temperley-Lieb algebra and its generalizations in the Potts and XXZ models

We discuss generalizations of the Temperley-Lieb algebra in the Potts and XXZ models. These can be used to describe the addition of different types of integrable boundary terms. We use the Temperley-Lieb algebra and its one-boundary, two-boundary, and periodic extensions to classify different integrable boundary terms in the 2, 3, and 4-state Potts models. The representations always lie at critical points where the algebras becomes non-semisimple and possess indecomposable representations. In the one-boundary case we show how to use representation theory to extract the Potts spectrum from an XXZ model with particular boundary terms and hence obtain the finite size scaling of the Potts models. In the two-boundary case we find that the Potts spectrum can be obtained by combining several XXZ models with different boundary terms. As in the Temperley-Lieb case there is a direct correspondence between representations of the lattice algebra and those in the continuum conformal field theory.Comment: 49 page

Nephronophthisis

Nephronophthisis (NPH) is an autosomal recessive disease characterized by a chronic tubulointerstitial nephritis that progress to terminal renal failure during the second decade (juvenile form) or before the age of 5 years (infantile form). In the juvenile form, a urine concentration defect starts during the first decade, and a progressive deterioration of renal function is observed in the following years. Kidney size may be normal, but loss of corticomedullary differentiation is often observed, and cysts occur usually after patients have progressed to end-stage renal failure. Histologic lesions are characterized by tubular basement membrane anomalies, tubular atrophy, and interstitial fibrosis. The infantile form is characterized by cortical microcysts and progression to end-stage renal failure before 5 years of age. Some children present with extrarenal symptoms: retinitis pigmentosa (Senior-Løken syndrome), mental retardation, cerebellar ataxia, bone anomalies, or liver fibrosis. Positional cloning and candidate gene approaches led to the identification of eight causative genes (NPHP1, 3, 4, 5, 6, 7, 8, and 9) responsible for the juvenile NPH and one gene NPHP2 for the infantile form. NPH and associated disorders are considered as ciliopathies, as all NPHP gene products are expressed in the primary cilia, similarly to the polycystic kidney disease (PKD) proteins