Identifying and correcting invalid citations due to DOI errors in Crossref data

This work aims to identify classes of DOI mistakes by analysing the open bibliographic metadata available in Crossref, highlighting which publishers were responsible for such mistakes and how many of these incorrect DOIs could be corrected through automatic processes. By using a list of invalid cited DOIs gathered by OpenCitations while processing the OpenCitations Index of Crossref open DOI-to-DOI citations (COCI) in the past two years, we retrieved the citations in the January 2021 Crossref dump to such invalid DOIs. We processed these citations by keeping track of their validity and the publishers responsible for uploading the related citation data in Crossref. Finally, we identified patterns of factual errors in the invalid DOIs and the regular expressions needed to catch and correct them. The outcomes of this research show that only a few publishers were responsible for and/or affected by the majority of invalid citations. We extended the taxonomy of DOI name errors proposed in past studies and defined more elaborated regular expressions that can clean a higher number of mistakes in invalid DOIs than prior approaches. The data gathered in our study can enable investigating possible reasons for DOI mistakes from a qualitative point of view, helping publishers identify the problems underlying their production of invalid citation data. Also, the DOI cleaning mechanism we present could be integrated into the existing process (e.g. in COCI) to add citations by automatically correcting a wrong DOI. This study was run strictly following Open Science principles, and, as such, our research outcomes are fully reproducible

Identifying and correcting invalid citations due to DOI errors in Crossref data

This work aims to identify classes of DOI mistakes by analysing the open bibliographic metadata available in Crossref, highlighting which publishers were responsible for such mistakes and how many of these incorrect DOIs could be corrected through automatic processes. By using a list of invalid cited DOIs gathered by OpenCitations while processing the OpenCitations Index of Crossref open DOI-to-DOI citations (COCI) in the past two years, we retrieved the citations in the January 2021 Crossref dump to such invalid DOIs. We processed these citations by keeping track of their validity and the publishers responsible for uploading the related citation data in Crossref. Finally, we identified patterns of factual errors in the invalid DOIs and the regular expressions needed to catch and correct them. The outcomes of this research show that only a few publishers were responsible for and/or affected by the majority of invalid citations. We extended the taxonomy of DOI name errors proposed in past studies and defined more elaborated regular expressions that can clean a higher number of mistakes in invalid DOIs than prior approaches. The data gathered in our study can enable investigating possible reasons for DOI mistakes from a qualitative point of view, helping publishers identify the problems underlying their production of invalid citation data. Also, the DOI cleaning mechanism we present could be integrated into the existing process (e.g. in COCI) to add citations by automatically correcting a wrong DOI. This study was run strictly following Open Science principles, and, as such, our research outcomes are fully reproducible

Identifying and correcting invalid citations due to DOI errors in Crossref data

This work aims to identify classes of DOI mistakes by analysing the open bibliographic metadata available in Crossref, highlighting which publishers were responsible for such mistakes and how many of these incorrect DOIs could be corrected through automatic processes. By using a list of invalid cited DOIs gathered by OpenCitations while processing the OpenCitations Index of Crossref open DOI-to-DOI citations (COCI) in the past two years, we retrieved the citations in the January 2021 Crossref dump to such invalid DOIs. We processed these citations by keeping track of their validity and the publishers responsible for uploading the related citation data in Crossref. Finally, we identified patterns of factual errors in the invalid DOIs and the regular expressions needed to catch and correct them. The outcomes of this research show that only a few publishers were responsible for and/or affected by the majority of invalid citations. We extended the taxonomy of DOI name errors proposed in past studies and defined more elaborated regular expressions that can clean a higher number of mistakes in invalid DOIs than prior approaches. The data gathered in our study can enable investigating possible reasons for DOI mistakes from a qualitative point of view, helping publishers identify the problems underlying their production of invalid citation data. Also, the DOI cleaning mechanism we present could be integrated into the existing process (e.g. in COCI) to add citations by automatically correcting a wrong DOI. This study was run strictly following Open Science principles, and, as such, our research outcomes are fully reproducible

Diarrhea Is a Hallmark of Inflammation in Pediatric COVID-19

: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a pathogen with enteric tropism. We compared the clinical, biochemical and radiological features of children hospitalized for acute SARS-CoV-2 infection, classified in two groups based on the presence of diarrhea. Logistic regression analyses were used to investigate the variables associated with diarrhea. Overall, 407 children were included in the study (226 males, 55.5%, mean age 3.9 ± 5.0 years), of whom 77 (18.9%) presented with diarrhea, which was mild in most cases. Diarrhea prevalence was higher during the Alpha (23.6%) and Delta waves (21.9%), and in children aged 5-11 y (23.8%). Other gastrointestinal symptoms were most commonly reported in children with diarrhea (p < 0.05). Children with diarrhea showed an increased systemic inflammatory state (higher C-reactive protein, procalcitonin and ferritin levels, p < 0.005), higher local inflammation as judged by mesenteric fat hyperechogenicity (adjusted Odds Ratio 3.31, 95%CI 1.13-9.70) and a lower chance of previous immunosuppressive state (adjusted Odds Ratio 0.19, 95%CI 0.05-0.70). Diarrhea is a frequent feature of pediatric COVID-19 and is associated with increased systemic inflammation, which is related to the local mesenteric fat inflammatory response, confirming the implication of the gut not only in multisystem inflammatory syndrome but also in the acute phase of the infection

PRNP P39L variant is a rare cause of frontotemporal dementia in Iialian population

The missense P39L variant in the prion protein gene (PRNP) has recently been associated with frontotemporal dementia (FTD). Here, we analyzed the presence of the P39L variant in 761 patients with FTD and 719 controls and found a single carrier among patients. The patient was a 67-year-old male, with a positive family history for dementia, who developed apathy, short term memory deficit, and postural instability at 66. Clinical and instrumental workup excluded prion disease. At MRI, bilateral frontal lobe atrophy was present. A diagnosis of FTD was made, with a mainly apathetic phenotype. The PRNP P39L mutation may be an extremely rare cause of FTD (0.13%)

Staphylococcus aureus nosocomial infections: The role of a rapid and low-cost characterization for the establishment of a surveillance system

Continuous surveillance on resistance patterns and characterization of Staphylococcus aureus represent simple and low-cost techniques to understand and evaluate the effectiveness of infection control and antimicrobial prescribing measures. In this study we analyzed the antibiotic susceptibility and trends for S. aureus strains collected from bacteraemia cases in a five year period. Between 2004 and 2008 we noted a progressive decrease in the number of S. aureus isolates compared to all pathogens from clinical specimens and S. aureus bloodstream infections (BSI) reflected a similar trend. In particular we analyzed 185 isolates from blood cultures: 89 isolates were MSSA and 96 isolates were MRSA. Molecular SCCmec typing of these strains showed an absolute prevalence of types I and II, whereas five spa types from 96 isolates were obtained. Resistance pattern analysis allowed us to place MRSA strains into 12 antibiotypes and the major antibiotype was resistant to penicillin, gentamicin, erythromycin, clindamycin and ciprofloxacin. The predominant antibiotype among the MSSA isolates was resistant only to penicillin. In addition, 19.1% of MSSA are susceptible to all antibiotics tested. We also found a close association between antibiotyping 1 and genotyping t002/SCCmecI of MRSA strains, suggesting a nosocomial scenario dominated by a few particular clones

The miR-17-92 cluster counteracts quiescence and chemoresistance in a distinct subpopulation of pancreatic cancer stem cells

Objective Cancer stem cells (CSCs) represent the root of many solid cancers including pancreatic ductal adenocarcinoma, are highly chemoresistant and represent the cellular source for disease relapse. However the mechanisms involved in these processes still need to be fully elucidated. Understanding the mechanisms implicated in chemoresistance and metastasis of pancreatic cancer is critical to improving patient outcomes. Design Micro-RNA (miRNA) expression analyses were performed to identify functionally defining epigenetic signatures in pancreatic CSC-enriched sphere-derived cells and gemcitabine-resistant pancreatic CSCs. Results We found the miR-17-92 cluster to be downregulated in chemoresistant CSCs versus non-CSCs and demonstrate its crucial relevance for CSC biology. In particular, overexpression of miR-17-92 reduced CSC self-renewal capacity, in vivo tumourigenicity and chemoresistance by targeting multiple NODAL/ACTIVIN/TGF-beta 1 signalling cascade members as well as directly inhibiting the downstream targets p21, p57 and TBX3. Overexpression of miR-17-92 translated into increased CSC proliferation and their eventual exhaustion via downregulation of p21 and p57. Finally, the translational impact of our findings could be confirmed in preclinical models for pancreatic cancer. Conclusions Our findings therefore identify the miR-17-92 cluster as a functionally determining family of miRNAs in CSCs, and highlight the putative potential of developing modulators of this cluster to overcome drug resistance in pancreatic CSCs.CH: ERC Advanced Investigator Grant (Pa-CSC 233460), European Community's Seventh Framework Programme (FP7/2007-2013) under grant agreement No 256974 (EPC-TM-NET) and No 602783 (CAM-PaC), the Subdireccion General de Evaluacion y Fomento de la Investigacion, Fondo de Investigacion Sanitaria (PS09/02129 \& PI12/02643), and the Programa Nacional de Internacionalizacion de la I+D, Subprogramma: FCCI 2009 (PLE2009-0105; Ministerio de Economia y Competitividad, Spain). MC: La Caixa Predoctoral Fellowship.S

CSF β-amyloid predicts prognosis in patients with multiple sclerosis

Background: The importance of predicting disease progression in multiple sclerosis (MS) has increasingly been recognised, hence reliable biomarkers are needed. Objectives: To investigate the prognostic role of cerebrospinal fluid (CSF) Amyloid beta1-42 (A) levels by the determination of a cut-off value to classify patients in slow and fast progressors. To evaluate possible association with white (WM) and grey matter (GM) damage at early disease stages. Methods: Sixty patients were recruited and followed-up for three to five years. Patients underwent clinical assessment, CSF analysis to determine Aβ levels, and brain MRI (at baseline and after 1 year). T1-weighted volumes were calculated. T2-weighted scans were used to quantify WM lesion loads. Results: Lower CSF Aβ levels were observed in patients with a worse follow-up EDSS (r=−0.65, p0.05). Conclusions: Low CSF Aβ levels may represent a predictive biomarker of disease progression in MS

Progranulin plasma levels predict the presence of GRN mutations in asymptomatic subjects and do not correlate with brain atrophy: results from the GENFI study.

We investigated whether progranulin plasma levels are predictors of the presence of progranulin gene (GRN) null mutations or of the development of symptoms in asymptomatic at risk members participating in the Genetic Frontotemporal Dementia Initiative, including 19 patients, 64 asymptomatic carriers, and 77 noncarriers. In addition, we evaluated a possible role of TMEM106B rs1990622 as a genetic modifier and correlated progranulin plasma levels and gray-matter atrophy. Plasma progranulin mean ± SD plasma levels in patients and asymptomatic carriers were significantly decreased compared with noncarriers (30.5 ± 13.0 and 27.7 ± 7.5 versus 99.6 ± 24.8 ng/mL, p 61.55 ng/mL, the test had a sensitivity of 98.8% and a specificity of 97.5% in predicting the presence of a mutation, independent of symptoms. No correlations were found between progranulin plasma levels and age, years from average age at onset in each family, or TMEM106B rs1990622 genotype (p > 0.05). Plasma progranulin levels did not correlate with brain atrophy. Plasma progranulin levels predict the presence of GRN null mutations independent of proximity to symptoms and brain atrophy

Tbx1 regulates Vegfr3 and is required for lymphatic vessel development

Defects in lymphangiogenesis are added to the broad clinical manifestations of DiGeorge syndrome, caused by deletion of the T box transcription factor Tbx1