Molecular Detection of Babesia spp. (Apicomplexa: Piroplasma) in Free-Ranging Canids and Mustelids From Southern Italy.

Babesiosis is an emerging tick-borne disease caused by apicomplexan parasites with widespread geographical distribution and various wildlife species as reservoir hosts. The aims of this study were to investigate the prevalence and assess the role of free-ranging canids and mustelids in the maintenance of Babesia spp. in southern Italy. PCR analysis of splenic samples targeting the 18S rRNA gene revealed the presence of Babesia spp. in 36 of 82 (43.9%) red foxes (Vulpes vulpes) including 29 (58%) from Campania region and seven (21.8%) from Calabria region, in seven of 13 (53.8%) Eurasian badgers (Meles meles), and in one of 13 (7.7%) gray wolves (Canis lupus). Samples from other host species including 9 Eurasian otters (Lutra lutra), 1 stone marten (Martes foina), 1 least weasel (Mustela nivalis), and 1 European polecat (Mustela putorius) tested Babesia spp. negative. Sequence analysis of the 18S rRNA gene demonstrated the presence of B. vulpes in the red fox and two sequence types of badger-associated Babesia spp. in the Eurasian badger. The Babesia sp. sequence detected in the gray wolf was identical to a badger-associated Babesia sp. This study shows that the number of Babesia spp. infecting free-ranging carnivores in Italy is higher than currently believed, and suggests that these hosts may play an important role in the maintenance of the sylvatic cycle of these parasites. It is the first report of badger-associated Babesia spp. in Italy and in a gray wolf

Parasite Load and STRs Genotyping of Toxoplasma gondii Isolates From Mediterranean Mussels ( Mytilus galloprovincialis) in Southern Italy

oxoplasmosis is a zoonotic food-borne disease caused by Toxoplasma gondii, a land-derived protozoan parasite that infects a broad range of terrestrial and aquatic hosts. T. gondii may reach coastal waters via contaminated freshwater runoff and its oocysts may enter into the marine food web. Marine invertebrates as mussels being filter feeders are exposed and may concentrate T. gondii oocysts representing a potential source of infection for animals and humans. The present works investigated the prevalence, parasite burden and genotypes of T. gondii in the Mediterranean mussels (Mytilus galloprovincialis) from southern Italy. We sampled a total of 382 individual Mediterranean mussels from May to August 2018 from seven production sites in the Gulf of Naples (Campania region). An additional sample including 27 farmed Mediterranean mussels was obtained in February 2018 from a mollusk depuration plant in Corigliano Calabro (Calabria region). T. gondii DNA was detected in 43 out of 409 (10.5%) Mediterranean mussels from seven out of eight sampling sites. The number of T. gondii copies/g in the digestive gland ranged from 0.14 to 1.18. Fragment analysis of Short Tandem Repeats (STRs) at 5 microsatellite loci was performed from 10 T. gondii PCR positive samples revealing the presence of five distinct genotypes including one corresponding to type I and four atypical genotypes. These findings suggest potential implications of epidemiological importance for human and animal health because both type I and atypical genotypes could be highly pathogenic

Human Bocavirus NS1 and NS1-70 Proteins Inhibit TNF-α-Mediated Activation of NF-κB by targeting p65.

Human bocavirus (HBoV), a parvovirus, is a single-stranded DNA etiologic agent causing lower respiratory tract infections in young children worldwide. Nuclear factor kappa B (NF-κB) transcription factors play crucial roles in clearance of invading viruses through activation of many physiological processes. Previous investigation showed that HBoV infection could significantly upregulate the level of TNF-α which is a strong NF-κB stimulator. Here we investigated whether HBoV proteins modulate TNF-α-mediated activation of the NF-κB signaling pathway. We showed that HBoV NS1 and NS1-70 proteins blocked NF-κB activation in response to TNF-α. Overexpression of TNF receptor-associated factor 2 (TRAF2)-, IκB kinase alpha (IKKα)-, IκB kinase beta (IKKβ)-, constitutively active mutant of IKKβ (IKKβ SS/EE)-, or p65-induced NF-κB activation was inhibited by NS1 and NS1-70. Furthermore, NS1 and NS1-70 didn't interfere with TNF-α-mediated IκBα phosphorylation and degradation, nor p65 nuclear translocation. Coimmunoprecipitation assays confirmed the interaction of both NS1 and NS1-70 with p65. Of note, NS1 but not NS1-70 inhibited TNF-α-mediated p65 phosphorylation at ser536. Our findings together indicate that HBoV NS1 and NS1-70 inhibit NF-κB activation. This is the first time that HBoV has been shown to inhibit NF-κB activation, revealing a potential immune-evasion mechanism that is likely important for HBoV pathogenesis

Formation of Supermassive Black Holes

Evidence shows that massive black holes reside in most local galaxies. Studies have also established a number of relations between the MBH mass and properties of the host galaxy such as bulge mass and velocity dispersion. These results suggest that central MBHs, while much less massive than the host (~ 0.1%), are linked to the evolution of galactic structure. In hierarchical cosmologies, a single big galaxy today can be traced back to the stage when it was split up in hundreds of smaller components. Did MBH seeds form with the same efficiency in small proto-galaxies, or did their formation had to await the buildup of substantial galaxies with deeper potential wells? I briefly review here some of the physical processes that are conducive to the evolution of the massive black hole population. I will discuss black hole formation processes for `seed' black holes that are likely to place at early cosmic epochs, and possible observational tests of these scenarios.Comment: To appear in The Astronomy and Astrophysics Review. The final publication is available at http://www.springerlink.co

Upregulation of miR-29a and genomic DNA hypermethylation in normal karyotype AML showing DNMT3A mutation

Acute Myeloid Leukaemia (AML) is frequently associated to normal karyotype and DNMT3A mutations (R882). Since we previously demonstrated distinctive miRNA expression in some AML groups, we study 384 miRNA in 9 selected DNMT3A-mutated NK-AML patients. Comparing these data with our previous results obtained in 31 DNMT3A-unmutated AML, we focused on a significant up-regulation of miR-155, miR-29a, miR-196b and miR-25. We investigated expression of these miRNAs in additional 24 DNMT3A-mutated AML patients and we confirm the up-regulation of miR-155, miR-29a and miR-196b; in particular, we judged very interesting the over expression of miR-29a since is known to directly target DNMT3A, TET1 and TDG mRNAs. Evaluating the expression levels of these targets in 17 AML DNMT3A-mutated patients, we revealed a no significant differences in expression of DNMT3A and TDG but a significant down-regulation of TET1. These data suggest that miR-29a acts as DNA methylation-regulator: in presence of DNMT3A activating mutations and TET1 down-regulation it may probably cause a perturbation of DNA methylation. In fact, analyzing the methylation of the bone marrow genomic DNA from 3 DNMT3A-mutated and 3 DNMT3A-unmutated cases by Methylation Sensitive Arbitrarily Primed-PCR, we found a genomic hypermethylation of DNMT3A-mutated cells compared to the unmutated ones. How DNMT3A mutations contribute to leukemogenesis is not yet well characterized. Uncovering how DNMT3A mutations affect DNA methylation and epigenetic regulation of gene expression may have important implications in treatment selection because DNA hypomethylating agents are increasingly used in AML therapies, and response to these drugs may be affected by DNMT3A changed function

Analysis of epidermal growth factor receptor expression as a predictive factor for response to gefitinib (‘Iressa’, ZD1839) in non-small-cell lung cancer

Gefitinib ('Iressa', ZD1839) is an orally active epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that has demonstrated antitumour activity and favourable tolerability in Phase II studies. We investigated whether EGFR expression levels could predict for response to gefitinib in patients with advanced non-small-cell lung cancer (NSCLC), who received gefitinib (250 mg day(-1)) as part of a worldwide compassionate-use programme. Tissue samples were analysed by immunohistochemistry to assess membrane EGFR immunoreactivity. Of 147 patients enrolled in our institution, 50 patients were evaluable for assessment of both clinical response and EGFR expression. The objective tumour response rate was 10% and disease control was achieved in 50% of patients. Although high EGFR expression was more common in squamous-cell carcinomas than adenocarcinomas, all objective responses were observed in patients with adenocarcinoma. Response and disease control with gefitinib were not associated with high EGFR expression. Overall, median survival was 4 months, and the 1-year survival rate was 18%. Strong EGFR staining correlated with shorter survival time for all patients. Gefitinib demonstrated promising clinical activity in this group of patients with NSCLC. These results have also shown that EGFR expression is not a significant predictive factor for response to gefitinib

Small but crucial : the novel small heat shock protein Hsp21 mediates stress adaptation and virulence in Candida albicans

Peer reviewedPublisher PD