Background: Reducing hospital-acquired pressure ulcers (PUs) in intensive care units (ICUs) has emerged as an important quality metric for health systems internationally. Limited work has been done to characterize the profile of PUs in the ICU using observational data from the electronic health record (EHR). Consequently, there are limited EHR-based prognostic tools for determining a patient’s risk of PU development, with most institutions relying on nurse-calculated risk scores such as the Braden score to identify high-risk patients. Methods and Results: Using EHR data from 50,851 admissions in a tertiary ICU (MIMIC-III), we show that the prevalence of PUs at stage 2 or above is 7.8 percent. For the 1,690 admissions where a PU was recorded on day 2 or beyond, we evaluated the prognostic value of the Braden score measured within the first 24 hours. A high-risk Braden score (<=12) had precision 0.09 and recall 0.50 for the future development of a PU. We trained a range of machine learning algorithms using demographic parameters, diagnosis codes, laboratory values and vitals available from the EHR within the first 24 hours. A weighted linear regression model showed precision 0.09 and recall 0.71 for future PU development. Classifier performance was not improved by integrating Braden score elements into the model. Conclusion: We demonstrate that an EHR-based model can outperform the Braden score as a screening tool for PUs. This may be a useful tool for automatic risk stratification early in an admission, helping to guide quality protocols in the ICU, including the allocation and timing of prophylactic interventions.
The burden of comorbidity in Autism Spectrum Disorder (ASD) is substantial. The symptoms of autism overlap with many other human conditions, reflecting common molecular pathologies suggesting that cross-disorder analysis will help prioritize autism gene candidates. Genes in the intersection between autism and related conditions may represent nonspecific indicators of dysregulation while genes unique to autism may play a more causal role. Thorough literature review allowed us to extract 125 ICD-9 codes comorbid to ASD that we mapped to 30 specific human disorders. In the present work, we performed an automated extraction of genes associated with ASD and its comorbid disorders, and found 1031 genes involved in ASD, among which 262 are involved in ASD only, with the remaining 779 involved in ASD and at least one comorbid disorder. A pathway analysis revealed 13 pathways not involved in any other comorbid disorders and therefore unique to ASD, all associated with basal cellular functions. These pathways differ from the pathways associated with both ASD and its comorbid conditions, with the latter being more specific to neural function. To determine whether the sequence of these genes have been subjected to differential evolutionary constraints, we studied long term constraints by looking into Genomic Evolutionary Rate Profiling, and showed that genes involved in several comorbid disorders seem to have undergone more purifying selection than the genes involved in ASD only. This result was corroborated by a higher dN/dS ratio for genes unique to ASD as compare to those that are shared between ASD and its comorbid disorders. Short-term evolutionary constraints showed the same trend as the pN/pS ratio indicates that genes unique to ASD were under significantly less evolutionary constraint than the genes associated with all other disorders.
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