Background  Human bocavirus (HBoV) was first discovered in Sweden in 2005 and has now been found worldwide; however its role in clinically relevant diseases has not yet been clearly defined. Objectives  To gain new insight into HBoV infection among children hospitalized with acute respiratory infections in Rome. Methods  Between November 2004 and May 2007, 415 nasal washings were tested for the presence of an extensive range of respiratory viruses using molecular methods. Results  Viral pathogens were detected in 214 children (51·6%), 28·9% being respiratory syncytial virus (RSV) and 9·6% being rhinovirus positive. Of the 34 children (8·2%) who tested positive for HBoV, 21 (61·8%) were co‐infected with another respiratory virus, mainly RSV. Human bocavirus was the only pathogen identified in four pneumonia and six bronchiolitis cases in March 2005 and January 2007, respectively. Human bocavirus was also detected in one child hospitalized with gastroenteritis and in another with erythema. Conclusions  In the examined population, HBoV was the third most common virus detected but with a high rate of co‐infection with other respiratory viruses. Human bocavirus appeared to be the etiological agent in some pneumonia and bronchiolitis cases in which tests for all likely respiratory pathogens were negative.

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High-flow humidified nasal cannula (HFNC) is often\ud used to relieve respiratory distress in children with acute\ud pulmonary disease, although its effects on respiratory mechanics\ud have not been objectively studied. The purpose of this study was\ud to test the feasibility of measuring pharyngeal (PP) and\ud esophageal (Pes) pressures of young children on HFNC oxygen\ud therapy through a specifically designed new monitoring,\ud acquisition, and elaboration system (MAES). Through MAES we\ud recorded and elaborated Pes and PP tracings obtained through\ud esophageal and pharyngeal catheters in a group of young children\ud hospitalized in a Pediatric Intensive Care Unit because of\ud respiratory distress. All traces were recorded during spontaneous\ud breathing and on HFNC 1 and 2 L/kg/min. To determine the\ud onset and the end of inspiration, the Pes and PP signals were\ud synchronized with the inspiratory flow obtained by a flow\ud transducer placed in the HFNC circuit. Direct measurement of\ud inspiratory flow by a face mask pneumotachograph also allowed\ud for inspiratory tidal volume (TV) measurement which was used\ud together with Pes curve to build Campbell’s diagram as well as\ud the static lung and chest wall recoil curves required for pressure\ud time product (PTP) evaluation. Using MAES we were able to\ud obtain: time interval between the beginning of inspiratory effort\ud and inspiration (Tdelay), TV, intrinsic positive end expiratory\ud pressure (PEEPi), total inspiratory Pes variation (ΔPes),\ud transpulmonary pressure at end of inspiration (Ptpei), dynamic\ud lung compliance (CLdyn), total lung resistance (RLtot) along with\ud all the relevant components of the inspiratory work of breathing\ud (WOB) and PTP. We believe that this new system will allow\ud clinicians for a bedside monitoring of respiratory distress in\ud infants treated with HFNC and to modify flow rates accordingly.\ud Index Terms—biological system modeling, biomedica

BackgroundHypereosinophilia-associated syndromes are a heterogeneous group of diseases characterized by sustained and elevated blood eosinophilia with evidence of eosinophil-induced organ damage. Classically, Eosinophilic granulomatosis with polyangiitis (EGPA) and Hypereosinophilic syndrome (HES) present several overlapping clinical and laboratory features, making it challenging to correctly insert patients in restricted and well-defined categories with specific and more effective therapeutic approaches. Therefore, great efforts are ongoing searching for novel biomarkers able to differentiate these two disorders in daily practice.ObjectivesTo detect T cell receptor gamma (TCRG) clonal rearrangements in EGPA and HES, comparing the frequency distribution of V region and J region segment utilization in the study population.MethodsIn this single center study, we included consecutive patients with a diagnosis of EGPA and HES. Inclusion criteria were: documentation of a persistent peripheral eosinophilic count of ≥1.5 x109/L and signs or symptoms of organ involvement. Clinical and laboratory data of the patients were collected. Sequence-based determination of the frequency distribution of TCRG Gene Rearrangements was performed using next-generation sequencing with the Illumina MiSeq (LymphoTrack TRG assay, Invivoscribe).ResultsWe included 21 patients (9 with EGPA and 12 with HES). Four EGPA patients were MPO-ANCA positive. We detected TCRG clonal rearrangements in 44% (4/9) patients with EGPA and in 42% (5/12) patients with HES (p-value = n.s). No association was observed between TCRG clonal rearrangements and ANCA status in EGPA patients. Recurrent TCRG gene rearrangements were observed; in particular, Vg10JgP1 (5 cases) and Vg4Jg1/2 (4 cases) were detected in both EGPA and HES, whereas Vg9Jg1/2 (2 cases) and Vg10Jg1/2 (2 cases) were found only in patients with HES.ConclusionsEven if preliminary, this study reveals a similar T cell receptor gamma repertoire in EGPA and HES, thus suggesting a possible antigen-driven inflammatory response underlying hypereosinophilia in both EGPA and HES. Moreover, our results would suggest that the TCR clonality cannot be used as a tool for the differential diagnosis between EGPA and HES.Disclosure of InterestNone declared