Search

This study aimed to determine the prevalence of adverse events in mechanically ventilated adults with COVID-19 who have undergone prone positioning. A total of 100 patients were included retrospectively; 60% were males, the mean age was 64.8 ± 9.1 years, and hospital mortality was 47%. In all, we recorded 118 removals of catheters and tubes in 66 patients; 29.6% were removals of a nasogastric tube, 18.6% of an arterial line, 14.4% of a urinary catheter, and 12.7% of a central venous catheter. Reintubation or repositioning of a tracheotomy tube was required in 19 patients (16.1%), and cardiopulmonary resuscitation in 2 patients (1.7%). We recorded a total of 184 pressure ulcers in 79 patients (on anterior face in 38.5%, anterior thorax in 23.3% and any extremity anteriorly in 15.2%). We observed that body weight (p = 0.021; β = 0.09 (CI95: 0.01–0.17)) and the cumulative duration of prone positioning (p = 0.005; β = 0.06 (CI95: 0.02–0.11)) were independently associated with the occurrence of any adverse event. The use of prone positioning in our setting was associated with a greater number of adverse events than previously reported. Body weight and cumulative duration of prone positioning were associated with the occurrence of adverse events; however, other factors during a COVID-19 surge, such as working conditions, staffing, and staff education, could also have contributed to a high prevalence of adverse events.

Curated online interaction databases and gene ontology tools have streamlined the analysis of highly complex gene/protein networks. However, understanding of disease pathogenesis has gradually shifted from a protein-based core to complex interactive networks where non-coding RNA (ncRNA) is thought to play an essential role. As current gene ontology is based predominantly on protein-level information, there is a growing need to analyze networks with ncRNA. In this study, we propose a gene ontology workflow integrating ncRNA using the NPInter V5.0 database. To validate the proposed workflow, we analyzed our previously published curated biomarker datasets for hidden disease susceptibility processes and pharmacogenomics. Our results show a novel involvement of melanogenesis in psoriasis response to biological drugs in general. Hyperpigmentation has been previously observed in psoriasis following treatment with currently indicated biological drugs, thus calling attention to melanogenesis research as a response biomarker in psoriasis. Moreover, our proposed workflow highlights the need to critically evaluate computed ncRNA interactions within databases and a demand for gene ontology analysis of large miRNA blocks.

Background: The lack of reliable biomarkers in response to anti-TNFα biologicals hinders personalized therapy for Crohn’s disease (CD) patients. The motivation behind our study is to shift the paradigm of anti-TNFα biomarker discovery toward specific immune cell sub-populations using single-cell RNA sequencing and an innovative approach designed to uncover PBMCs gene expression signals, which may be masked due to the treatment or ongoing inflammation; Methods: The single-cell RNA sequencing was performed on PBMC samples from CD patients either naïve to biological therapy, in remission while on adalimumab, or while on ustekinumab but previously non-responsive to adalimumab. Sieves for stringent downstream gene selection consisted of gene ontology and independent cohort genomic profiling. Replication and meta-analyses were performed using publicly available raw RNA sequencing files of sorted immune cells and an association analysis summary. Machine learning, Mendelian randomization, and oligogenic risk score methods were deployed to validate DEGs highly relevant to anti-TNFα therapy response; Results: This study found PLCB1 in CD4+ T cells and CRTAM in double-negative T cells, which met the stringent statistical thresholds throughout the analyses. An additional assessment proved causal inference of both genes in response to anti-TNFα therapy; Conclusions: This study, jointly with an innovative design, uncovered novel candidate genes in the anti-TNFα response landscape of CD, potentially obscured by therapy or inflammation.