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Background Endemic presence of Klebsiella pneumoniae resistant to carbapenem in Italy has been due principally to the clonal expansion of CC258 isolates; however, recent studies suggest an ongoing epidemiological change in this geographical area. Methods 50  K. pneumoniae strains, 25 carbapenem-resistant (CR-Kp) and 25 susceptible (CS-Kp), collected from march 2014 to march 2016 at the Laboratory of Bacteriology of the Paolo Giaccone Polyclinic University hospital of Palermo, Italy, were characterized for antibiotic susceptibility and fully sequenced by next generation sequencing (NGS) for the in silico analysis of resistome, virulome, multi-locus sequence typing (MLST) and core single nucleotide polymorphism (SNP) genotypes Results MLST in silico analysis of CR-Kp showed that 52% of isolates belonged to CC258, followed by ST395 (12%), ST307 (12%), ST392 (8%), ST348 (8%), ST405 (4%) and ST101 (4%). In the CS-Kp group, the most represented isolate was ST405 (20%), followed by ST392 and ST15 (12%), ST395, ST307 and ST1727 (8%). The in silico β-lactamase analysis of the CR-Kp group showed that the most detected gene was bla SHV (100%), followed by bla TEM (92%), bla KPC (88%), bla OXA (88%) and bla CTX-M (32%). The virulome analysis detected mrk operon in all studied isolates, and wzi-2 was found in three CR-Kp isolates (12%). Furthermore, the distribution of virulence genes encoding for the yersiniabactin system, its receptor fyu A and the aerobactin system did not show significant distribution differences between CR-Kp and CS-Kp, whereas the Klebsiella ferrous iron uptake system ( kfu A, kfu B and kfu C genes), the two-component system kvg AS and the microcin E495 were significantly ( p  < 0.05) prevalent in the CS-Kp group compared to the CR-Kp group. Core SNP genotyping, correlating with the MLST data, allowed greater strain tracking and discrimination than MLST analysis. Conclusions Our data support the idea that an epidemiological change is ongoing in the Palermo area (Sicily, Italy). In addition, our analysis revealed the co-existence of antibiotic resistance and virulence factors in CR-Kp isolates; this characteristic should be considered for future genomic surveillance studies.

Chronic neuropathic pain profoundly impairs quality of life and often remains refractory to pharmacological or surgical management. Spinal cord stimulation (SCS) is considered a second-line therapy when conventional treatments fail. In this context, high-frequency spinal cord stimulation (HFSCS) targeting the cervicomedullary junction (CMJ) has emerged as a promising option for drug-refractory facial pain syndromes, including trigeminal neuropathy, though clinical evidence remains limited. We report the case of a 67-year-old woman who developed severe right-sided trigeminal neuropathic pain following petroclival meningioma surgery. After multiple unsuccessful interventions, she underwent implantation of a 10 kHz HFSCS system targeting the CMJ. An epidural lead was placed at the C1-C2 level and connected to an implantable pulse generator, delivering continuous stimulation. The procedure produced complete relief of paroxysmal electric shock-like pain and neurophysiological evidence of reduced trigeminal nociceptive activity. Analgesia was sustained for 6 years, with a transient relapse due to battery depletion, which resolved completely after generator replacement. These findings confirm the long-term efficacy and durability of CMJ-targeted HFSCS and highlight the importance of structured follow-up and device maintenance. HFSCS at the CMJ may represent a safe and durable therapeutic option for refractory trigeminal neuropathy, warranting validation through larger prospective studies.

Since the emergence of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the need for an effective vaccine has appeared crucial for stimulating immune system responses to produce humoral/cellular immunity and activate immunological memory. It has been demonstrated that SARS-CoV-2 variants escape neutralizing immunity elicited by previous infection and/or vaccination, leading to new infection waves and cases of reinfection. The study aims to gain into cases of reinfections, particularly infections and/or vaccination-induced protection. We conducted a retrospective descriptive study using data collected during the SARS-CoV-2 pandemic. This analysis involved Reverse Transcriptase Quantitative Polymerase Chain Reaction (RT-qPCR) and Next Generation Sequencing (NGS). RT-qPCR was performed on 416,466 naso-oropharyngeal swabs, with 10,380 samples further analyzed using NGS technology. RT-qPCR identified 350 cases of reinfection, of which 228 were subjected to detailed analysis via NGS. Our findings revealed two interesting cases involving pediatric patients who were not vaccinated. Positive results were observed in these cases within a short interval (< 60 days) and the “nature” of the infection, whether attributable to Reinfection or Viral Persistence, was investigated. Specifically, we discuss a case involving an unvaccinated 18-month-old child, which may represent one of the earliest instances of BA.5/BA.5 reinfection identified worldwide.

Honeybees (Apis mellifera) are constantly subjected to many biotic stressors including parasites. This study examined honeybees infected with Nosema ceranae (N. ceranae). N. = ceranae infection increases the bees energy requirements and may contribute to their decreased survival. RNA-seq was used to investigate gene expression at days 5, 10 and 15 Post Infection (P. I) with N. ceranae. The expression levels of genes, isoforms, alternative transcription start sites (TSS) and differential promoter usage revealed a complex pattern of transcriptional and post-transcriptional gene regulation suggesting that bees use a range of tactics to cope with the stress of N. ceranae infection. N. ceranae infection may cause reduced immune function in the bees by: (i) disturbing the host amino acids metabolism (ii) down-regulating expression of antimicrobial peptides (iii) down-regulation of cuticle coatings and (iv) down-regulation of odorant binding proteins.

Background and Objectives: Higher level of aggression and antisocial behavior have been found in the period following head trauma. These changes are attributable to specific brain alterations that generally involved frontal lobe, insula and limbic system. A descriptive review was conducted on the specificity of aggressive behavior in relation to traumatic brain injury by evaluating numerous variables, focusing on age at the time of trauma and neuroimaging studies. Materials and Methods: We searched on PubMed and the Web of Science databases to screen references of included studies and review articles for additional citations. From an initial 738 publications, only 27 met the search criteria of describing the relationship between aggression, brain alterations and traumatic brain injury. Results: These findings showed that traumatic brain injury (TBI) is related to changes in behavior, personality and mood. Conclusions: The development of aggressive and criminal behavior is associated with multiple factors, including the etiology of injury, environmental, psychosocial and personality factors and age at the time of trauma.

Background The emergence of carbapenem-resistant Klebsiella pneumoniae strains is threatening antimicrobial treatment. Methods Sixty-eight carbapenemase-producing K. pneumoniae strains isolated at Luigi Sacco University Hospital-ASST Fatebenefratelli Sacco (Milan, Italy) between 2012 and 2014 were characterised microbiologically and molecularly. They were tested for drug susceptibility and carbapenemase phenotypes, investigated by means of repetitive extra-genic palindromic polymerase chain reaction (REP-PCR), and fully sequenced by means of next-generation sequencing for the in silico analysis of multi-locus sequence typing (MLST), their resistome, virulome and plasmid content, and their core single nucleotide polymorphism (SNP) genotypes. Results All of the samples were resistant to carbapenems, other β-lactams and ciprofloxacin; many were resistant to aminoglycosides and tigecycline; and seven were resistant to colistin. Resistome analysis revealed the presence of blaKPC genes and, less frequently blaSHV , blaTEM , blaCTX-M and blaOXA , which are related to resistance to carbapenem and other β-lactams. Other genes conferring resistance to aminoglycoside, fluoroquinolone, phenicol, sulphonamide, tetracycline, trimethoprim and macrolide-lincosamide-streptogramin were also detected. Genes related to AcrAB-TolC efflux pump-dependent and pump-independent tigecycline resistance mechanisms were investigated, but it was not possible to clearly correlate the genomic features with tigecycline resistance because of the presence of a common mutation in susceptible, intermediate and resistant strains. Concerning colistin resistance, the mgrB gene was disrupted by an IS5-like element, and the mobile mcr-1 and mcr-2 genes were not detected in two cases. The virulome profile revealed type-3 fimbriae and iron uptake system genes, which are important during the colonisation stage in the mammalian host environment. The in silico detected plasmid replicons were classified as IncFIB(pQil), IncFIB(K), ColRNAI, IncX1, IncX3, IncFII(K), IncN, IncL/M(pMU407) and IncFIA(HI1). REP-PCR showed five major clusters, and MLST revealed six different sequence types: 512, 258, 307, 1519, 745 and 101. Core SNP genotyping, which led to four clusters, correlated with the MLST data. Isolates of the same sequencing type often had common genetic traits, but the SNP analysis allowed greater strain tracking and discrimination than either the REP-PCR or MLST analysis. Conclusion Our findings support the importance of implementing bacterial genomics in clinical medicine in order to complement traditional methods and overcome their limited resolution.

Porcine reproductive and respiratory syndrome virus (PRRSV) mainly infects porcine alveolar macrophages (PAMs), resulting in porcine reproductive and respiratory syndrome (PRRS) in pigs. Most of the transcriptomic studies on PAMs infected with PRRSV conducted thus far have made use of microarray technology. Here, we investigated the transcriptome of PAMs in vitro at 12 h post-infection with two European PRRSV strains characterized by low (Lelystad, LV) and high (Lena) virulence through RNA-Seq. The expression levels of genes, isoforms, alternative transcription start sites (TSS) and differential promoter usage revealed a complex pattern of transcriptional and post-transcriptional gene regulation upon infection with the two strains. Gene ontology analysis confirmed that infection of PAMs with both the Lena and LV strains affected signaling pathways directly linked to the innate immune response, including interferon regulatory factors (IRF), RIG1-like receptors, TLRs and PKR pathways. The results confirmed that interferon signaling is crucial for transcriptional regulation during PAM infection. IFN-β1 and IFN-αω, but not IFN-α, were up-regulated following infection with either the LV or Lena strain. The down-regulation of canonical pathways, such as the interplay between the innate and adaptive immune responses, cell death and TLR3/TLR7 signaling, was observed for both strains, but Lena triggered a stronger down-regulation than LV. This analysis contributes to a better understanding of the interactions between PRRSV and PAMs and outlines the differences in the responses of PAMs to strains with different levels of virulence, which may lead to the development of new PRRSV control strategies.

Background and Objectives: The connection between cognitive decline and autonomy represents a complex and multifactorial area of research. Cognitive decline manifests as a progressive impairment of higher mental functions and is typical of neurodegenerative conditions such as dementia. Autonomy, on the other hand, is defined as an individual’s ability to independently manage activities of daily living and make informed decisions. The objective of this study was to investigate whether certain daily living skills can persist despite the advancement of dementia, and what factors contribute to their preservation in maintaining autonomy. Materials and Methods: A literature review was conducted using the databases PubMed, Web of Science, Scopus, Cochrane Library, Embase, and PsycInfo. Out of an initial pool of 12,113 studies, only 19 met the inclusion criteria and were selected for analysis. Results: The findings indicate that, in non-institutionalized settings, some daily living abilities may remain preserved despite cognitive deterioration. In contrast, within institutionalized environments, a significant correlation emerged between cognitive decline and the progressive loss of personal autonomy. Conclusions: This study highlights the importance of assessing residual abilities in individuals with dementia. Recognizing and supporting these remaining skills can play a crucial role in enhancing quality of life, delaying institutionalization, and promoting autonomy even in the presence of advanced cognitive decline.

Background: Whipple’s disease (WD) is a rare infection caused by Tropheryma whipplei. Diagnosis is challenging and requires a combination of several data sets, such as patient history, clinical and laboratory investigations, and endoscopy with histology analyses. While persistent diarrhea is a common symptom, WD can affect multiple organs. Case description: We present the case of a 66-year-old immunocompetent patient with WD and a history of Helicobacter pylori infection who developed chronic diarrhea. Colonoscopy and histopathological analysis revealed the presence of foamy macrophages with periodic acid-Schiff-positive particles. Subsequently, molecular methods confirmed the clinical WD diagnosis and metagenomic analyses further identified a co-infection with Giardia intestinalis. The patient fully recovered after 14 months of antibiotic therapy. During pharmacological treatment, clinical and laboratory follow-ups were conducted at 6 and 12 months, and microbiome profiles were also analyzed to identify the most abundant species in the samples. Conclusion: The metagenomic analyses showed the eradication of the two pathogens and a progressive restoration to a healthy/balanced status after antibiotic therapy.

Background: Rapid Eye Movement (REM) sleep behavior disorder (RBD) is a parasomnia resulting from degeneration of pontine and medullary circuits responsible for muscle atonia during REM sleep, leading to dream-enactment behaviors and vocalizations. It is strongly linked to α-synucleinopathies, particularly Parkinson’s disease. Current biomarkers such as neurophysiological measures and imaging support diagnosis and monitoring, but remain invasive or costly. Aim: This study aims to evaluate vocal and speech alterations as exploratory, non-validated candidate biomarkers of REM sleep behavior disorder. Methods: A systematic review was conducted according to PRISMA 2020 guidelines. PubMed, IEEE Digital Library Web of Science, Embase and the Cochrane Library were systematically searched for studies published from database inception to November 2025, as preregistered on the Open Science Framework. Studies were selected through a multi-step screening process and underwent qualitative quality assessment. Results: Twelve studies met inclusion criteria. Individuals with RBD exhibited abnormal nocturnal vocalizations and early lexical, syntactic, and narrative disruptions despite preserved perceptual speech. Quantitative analyses identified consistent deficits in prosody, phonation stability, timing, and articulation, with significant group differences and diagnostic accuracy up to 96% sensitivity. Multilingual cohorts demonstrated progression over time, while digital phenotyping detected emerging Parkinsonian signs with AUC > 0.70. Conclusions: Speech and vocal abnormalities in iRBD reflect early neurodegenerative changes and show promising but still exploratory diagnostic and prognostic potential. Integrating vocal markers with established biomarkers may enhance early detection; however, further research is required to validate a reliable and reproducible vocal signature of prodromal synucleinopathies.