Evaluating the potential of marginal lands available for sustainable cellulosic biofuel production in Italy

The European Union aims to provide as much as one quarter of its transportation fuels via biofuels derived from renewable sources by 2030. To put this into perspective, the Italian government has recently established an ambitious goal to support the wider uptake of advanced second-generation biofuels, including cellulosic biofuels for the transportation sector. A sustainable way forward is to grow perennial biomass crops on marginal lands, however the nationwide availability of those lands for lignocellulosic feedstock production remains uncertain. We identify and evaluate the potential of marginal lands in Italy to produce sizeable amounts of biomass for sustainable cellulosic biofuel production while limiting land use conflicts and negative ecological impacts. We applied spatial multi-criteria decision analysis techniques in geographic information systems to ultimately generate spatially-explicit national land suitability and availability maps at a fine resolution (250-m). We selected a broad range of leading cellulosic biomass crops that includes poplar (Populus × canadensis Moench), willow (Salix alba Linnaeus), black locust (Robinia pseudoacacia Linnaeus), giant reed (Arundo donax Linnaeus), and vetiver grass (Chrysopogon zizanioides Linnaeus). Based on marginality criteria, our results suggest that such biomass plantations of perennial grasses and short rotation trees may produce 3.1–27.4 billion liters of cellulosic ethanol per year from 462,265 to 2,811,064 million hectares of available marginal lands. This estimated production may fulfill 7.8–69.1% of Italy's current liquid transportation fuel consumption, constrained by the requirement that each modelled location be within 70 km of a potential cellulosic biorefinery. Collectively, this study provides the cornerstone of efforts to rationally meet Italy's need for renewable fuels in a sustainable low-carbon economy future

Case report: Fulminant pneumococcal sepsis in an unvaccinated asplenic patient in Italy

We report a fatal case of overwhelming pneumococcal infection in an asplenic young adult not vaccinated against Streptococcus pneumoniae (S. pneumoniae). Post-mortem microbiological investigations revealed the presence of S. pneumoniae in blood samples and lungs. Serotyping by molecular methods identified the presence of a 6C serotype not comprised in the current 23-valent pneumococcal vaccine, highlighting that a risk of fatal infections may persist even in vaccinated splenectomised individuals

Why stem/progenitor cells lose their regenerative potential

Nowadays, it is clear that adult stem cells, also called as tissue stem cells, play a central role to repair and maintain the tissue in which they reside by their selfrenewal ability and capacity of differentiating into distinct and specialized cells. As stem cells age, their renewal ability declines and their capacity to maintain organ homeostasis and regeneration is impaired. From a molecular perspective, these changes in stem cells properties can be due to several types of cell intrinsic injury and DNA aberrant alteration (i.e epigenomic profile) as well as changes in the tissue microenviroment, both into the niche and by systemic circulating factors. Strikingly, it has been suggested that aging-induced deterioration of stem cell functions may play a key role in the pathophysiology of the various agingassociated disorders. Therefore, understanding how resident stem cell age and affects near and distant tissues is fundamental. Here, we examine the current knowledge about aging mechanisms in several kinds of adult stem cells under physiological and pathological conditions and the principal aging-related changes in number, function and phenotype that determine the loss of tissue renewal properties. Furthermore, we examine the possible cell rejuvenation strategies. Stem cell rejuvenation may reverse the aging phenotype and the discovery of effective methods for inducing and differentiating pluripotent stem cells for cell replacement therapies could open up new possibilities for treating age-related diseases

Role of toll-like receptors in actuating stem/progenitor cell repair mechanisms: Different functions in different cells

Toll-like receptors (TLRs) represent one of the bridges that regulate the cross-talk between the innate and adaptive immune systems. TLRs interact with molecules shared and preserved by the pathogens of origin but also with endogenous molecules (damage/danger-associated molecular patterns (DAMPs)) that derive from injured tissues. This is probably why TLRs have been found to be expressed on several kinds of stem/progenitor cells (SCs). In these cells, the role of TLRs in the regulation of the basal motility, proliferation, differentiation processes, self-renewal, and immunomodulation has been demonstrated. In this review, we analyze the many different functions that the TLRs assume in SCs, pointing out that they can have different effects, depending on the background and on the kind of ligands that they recognize. Moreover, we discuss the TLR involvement in the response of SC to specific tissue damage and in the reparative processes, as well as how the identification of molecules mediating the differential function of TLR signaling could be decisive for the development of new therapeutic strategies. Considering the available studies on TLRs in SCs, here we address the importance of TLRs in sensing an injury by stem/progenitor cells and in determining their behavior and reparative activity, which is dependent on the conditions. Therefore, it could be conceivable that SCs employed in therapy could be potentially exposed to TLR ligands, which might modulate their therapeutic potential in vivo. In this context, to modulate SC proliferation, survival, migration, and differentiation in the pathological environment, we need to better understand the mechanisms of action of TLRs on SCs and learn how to control these receptors and their downstream pathways in a precise way. In this manner, in the future, cell therapy could be improved and made safer

Uridine and pyruvate protect T cells’ proliferative capacity from mitochondrial toxic antibiotics: a clinical pilot study

Antibiotics that inhibit bacterial protein or nucleic acid synthesis and function can exert an off-target action on mitochondria (mitotoxic antibiotics), making actively dividing mammalian cells dependent on uridine and pyruvate supplementation. Based on this rationale, we carried out, for the first time, a randomized pilot study in 55 patients with asymptomatic bacteriuria or positive sperm culture, each treated with a single mitotoxic antibiotic with or without oral supplementation of uridine + pyruvate (Uripyr, Mitobiotix, Italy). The in vivo and ex vivo data show a a 3.4-fold higher value in the differential (before and after the antibiotic treatment) lymphocytes count and a 3.7-fold increase in the percentage of dividing T cells, respectively, in the Uripyr vs the control group. Our findings lay the groundwork to enhance the synergy between antibiotics and the immune system in order to optimize the administration protocols and widen the application potentials of antibiotic therapies as well as to re-evaluate old “forgotten” molecules to fight bacterial infections in the antibiotics resistance era

Frequency of human papillomavirus infection and genotype distribution among women with known cytological diagnosis in a Southern Italian region

Introduction. In the Puglia region (South Italy) about 200 new hospitalizations for cervical cancer are registered every year. The study investigated the frequency of Human Papillomavirus (HPV) infection and the genotype distribution of HPV in a sample of women with known cytology attending the outpatient clinics of four Gynecological Departments of the University of Bari over a four-year period (2005-2008). Methods. Cervical samples from 1,168 women were analyzed for the presence of HPV-DNA through Polymerase Chain Reaction (PCR) in L1 region and reverse hybridization. The cytological results were associated with HPV positivity and type-specific prevalence. Results. Overall, HPV infection was found in 355 (30.4%) women. HPV-DNA was found in 34.4% of women with a cytological diagnosis of ASCUS, in 46.8% of women with Low-grade Squamous Intraepithelial Lesion (LSIL) and in 87.0% of women with High-grade Squamous Intraepithelial Lesion (HSIL)/carcinoma. Also 16.0% of women with normal Pap smear were found to be HPV-DNA positive. The most common HPV genotype was type 16 found in 27.3% of positives, followed by type 53 (11.5%), type 66 (9.2%) and type 31 (9.0%). HPV genotype 18 was found in 6.4% of positives. Types 16 or 18 were detected in about 34% (120/355) of all infected women, in about 33% of LSIL and in 60% of HSIL/ carcinoma HPV-positive women. Among low risk (LR) genotypes, type 61 was found in 10.7% of HPV positive women, type 62 in 8.4%, type 42 in 8.1% and type CP6108 in 7.8%. Discussion and conclusions. The findings of the study give evidence that HPV infection is frequent in the studied cohort of women. The most widespread genotypes found were 16 and 53. These data may represent a benchmark for future evaluation after the recent introduction of vaccination against HPV in 12-year-old girls

Severe acute respiratory syndrome coronavirus 2 may exploit human transcription factors involved in retinoic acid and interferon-mediated response: a hypothesis supported by an in silico analysis

The pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causing coronavirus disease 2019 (COVID-19), resulting in acute respiratory disease, is a worldwide emergency. Because recently it has been found that SARS-CoV is dependent on host transcription factors (TF) to express the viral genes, efforts are required to understand the molecular interplay between virus and host response. By bioinformatic analysis, we investigated human TF that can bind the SARS-CoV-2 sequence and can be involved in viral transcription. In particular, we analysed the key role of TF involved in interferon (IFN) response. We found that several TF could be induced by the IFN antiviral response, specifically some induced by IFN-stimulated gene factor 3 (ISGF3) and by unphosphorylated ISGF3, which were found to promote the transcription of several viral open reading frame. Moreover, we found 22 TF binding sites present only in the sequence of virus infecting humans but not bat coronavirus RaTG13. The 22 TF are involved in IFN, retinoic acid signalling and regulation of transcription by RNA polymerase II, thus facilitating its own replication cycle. This mechanism, by competition, may steal the human TF involved in these processes, explaining SARS-CoV-2's disruption of IFN-I signalling in host cells and the mechanism of the SARS retinoic acid depletion syndrome leading to the cytokine storm. We identified three TF binding sites present exclusively in the Brazilian SARS-CoV-2 P.1 variant that may explain the higher severity of the respiratory syndrome. These data shed light on SARS-CoV-2 dependence from the host transcription machinery associated with IFN response and strengthen our knowledge of the virus's transcription and replicative activity, thus paving the way for new targets for drug design and therapeutic approaches