Development and validation of a dynamic 48-hour in-hospital mortality risk stratification for COVID-19 in a UK teaching hospital: a retrospective cohort study.

Objectives: To develop a disease stratification model for COVID-19 that updates according to changes in a patient's condition while in hospital to facilitate patient management and resource allocation.

Design: In this retrospective cohort study, we adopted a landmarking approach to dynamic prediction of all-cause in-hospital mortality over the next 48 hours. We accounted for informative predictor missingness and selected predictors using penalised regression.

Unquantifiably low aldosterone concentrations are prevalent in hospitalised COVID-19 patients but may not be revealed by chemiluminescent immunoassay.

Objective: Previous studies have reported conflicting findings regarding aldosterone levels in patients hospitalised with COVID-19. We therefore used the gold-standard technique of liquid chromatography-tandem mass spectrometry (LCMSMS) to address this uncertainty.

Design: All patients admitted to Cambridge University Hospitals with COVID-19 between 10 March 2020 and 13 May 2021, and in whom a stored blood sample was available for analysis, were eligible for inclusion.

Recognition and management of sepsis by junior doctors.

There is growing evidence that outcomes in sepsis are improved by early recognition and treatment. In this study, we assessed junior doctors' ability to recognise and manage sepsis. We also explored junior doctors' perceptions regarding barriers to delivering timely sepsis care.

The burden of sepsis in the Emergency Department: an observational snapshot.

The primary aim of our study was to establish what proportion of patients in the Emergency Department (ED) fulfill the criteria for sepsis. All adult patients presenting to ED in two 1-week periods, 6 months apart, were included. Notes were reviewed retrospectively to identify which patients fulfilled the criteria for sepsis and severe sepsis.

Identification and initial functional characterization of a human vascular cell-enriched long noncoding RNA.

Objective: Long noncoding RNAs (lncRNAs) represent a rapidly growing class of RNA genes with functions related primarily to transcriptional and post-transcriptional control of gene expression. There is a paucity of information about lncRNA expression and function in human vascular cells. Thus, we set out to identify novel lncRNA genes in human vascular smooth muscle cells and to gain insight into their role in the control of smooth muscle cell phenotypes.

Mitogen-activated protein kinase 14 is a novel negative regulatory switch for the vascular smooth muscle cell contractile gene program.

Objective: Several studies have shown through chemical inhibitors that p38 mitogen-activated protein kinase (MAPK) promotes vascular smooth muscle cell (VSMC) differentiation. Here, we evaluate the effects of knocking down a dominant p38MAPK isoform on VSMC differentiation.

Methods And Results: Knockdown of p38MAPKα (MAPK14) in human coronary artery SMCs unexpectedly increases VSMC differentiation genes, such as miR145, ACTA2, CNN1, LMOD1, and TAGLN, with little change in the expression of serum response factor (SRF) and 2 SRF cofactors, myocardin (MYOCD) and myocardin-related transcription factor A (MKL1).

Expression and promoter analysis of a highly restricted integrin alpha gene in vascular smooth muscle.

Full genome annotation requires gene expression analysis and elucidation of promoter activity. Here, we analyzed the expression and promoter of a highly restricted integrin gene, Itga8. RNase protection and quantitative RT-PCR showed Itga8 to be expressed most abundantly in vascular smooth muscle cells (SMC).

Smooth muscle calponin: an unconventional CArG-dependent gene that antagonizes neointimal formation.

Objective: Smooth muscle calponin (CNN1) contains multiple conserved intronic CArG elements that bind serum response factor and display enhancer activity in vitro. The objectives here were to evaluate these CArG elements for activity in transgenic mice and determine the effect of human CNN1 on injury-induced vascular remodeling.

Methods And Results: Mice carrying a lacZ reporter under control of intronic CArG elements in the human CNN1 gene failed to show smooth muscle cell (SMC)-restricted activity.