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To develop predictive criteria for COVID-19-associated cytokine storm (CS), a severe hyperimmune response that results in organ damage in some patients infected with COVID-19. We hypothesised that criteria for inflammation and cell death would predict this type of CS.

We analysed 513 hospitalised patients who were positive for COVID-19 reverse transcriptase PCR and for ground-glass opacity by chest high-resolution CT. To achieve an early diagnosis, we analysed the laboratory results of the first 7 days of hospitalisation. We implemented logistic regression and principal component analysis to determine the predictive criteria. We used a 'genetic algorithm' to derive the cut-offs for each laboratory result. We validated the criteria with a second cohort of 258 patients.

We found that the criteria for macrophage activation syndrome, haemophagocytic lymphohistiocytosis and the HScore did not identify the COVID-19 cytokine storm (COVID-CS). We developed new predictive criteria, with sensitivity and specificity of 0.85 and 0.80, respectively, comprising three clusters of laboratory results that involve (1) inflammation, (2) cell death and tissue damage, and (3) prerenal electrolyte imbalance. The criteria identified patients with longer hospitalisation and increased mortality. These results highlight the relevance of hyperinflammation and tissue damage in the COVID-CS.

We propose new early predictive criteria to identify the CS occurring in patients with COVID-19. The criteria can be readily used in clinical practice to determine the need for an early therapeutic regimen, block the hyperimmune response and possibly decrease mortality.
We propose new early predictive criteria to identify the CS occurring in patients with COVID-19. The criteria can be readily used in clinical practice to determine the need for an early therapeutic regimen, block the hyperimmune response and possibly decrease mortality.
Currently, use of social networking services (SNSs) for interprofessional collaboration is increasing. However, few studies have reported on virtual interprofessional interactions in community healthcare services. Revealing such structural characteristics of the networks can provide insight into the functions of the interprofessional information-sharing network and lead to smoother collaboration. Thus, we aimed to explore the structure of SNS-based information-sharing clinical networks.

Social network analysis (SNA).

We selected a community in City X in Japan.

We analysed SNS-based information-sharing clinical network data linked to patients receiving home medical care or care services between January and December 2018. A network was created for each patient to allow healthcare professionals to post and view messages on the web platform. In the SNA, healthcare professions registered in a patient group were represented as nodes, and message posting/viewing relationships were represented as links in these with high outdegree centrality (home care workers, physical therapists, and registered dieticians). Visiting nurses and nurses in the clinic played a central role, but visiting nurses tended to have higher indegree and outdegree centrality, while nurses in the clinic had higher closeness and betweenness centrality in networks with heavier care requirement.

The SNS-based information-sharing clinical network structure showed that different professions played some form of a central role. Associations between network structures and patient outcomes, cost effectiveness and other factors warrant further investigation.
The SNS-based information-sharing clinical network structure showed that different professions played some form of a central role. Associations between network structures and patient outcomes, cost effectiveness and other factors warrant further investigation.Diabetes is associated with increased cardiovascular risk and higher occurrence of infections. These complications suggest altered responses of the innate immune system. Recent studies have shown that energy metabolism of monocytes is crucial in determining their functionality. Here we investigate whether monocyte metabolism and function are changed in patients with diabetes and aim to identify diabetes-associated factors driving these alterations. Patients with type 1 diabetes (T1D) (n = 41) and healthy age-, sex-, and BMI-matched control subjects (n = 20) were recruited. Monocytes were isolated from peripheral blood to determine immune functionality, metabolic responses, and transcriptome profiles. Upon ex vivo stimulation with Toll-like receptor (TLR) 4 or TLR-2 agonists, monocytes of patients with T1D secreted lower levels of various cytokines and showed lower glycolytic rates compared with monocytes isolated from matched control subjects. learn more Stratification based on HbA1c levels revealed that lower cytokine secretion was coupled to higher glycolytic rate of monocytes in patients with a higher glycemic burden. Circulating monocytes displayed an enhanced inflammatory gene expression profile associated with high glycemic burden. These results suggest that a high glycemic burden in patients with T1D is related to expression of inflammatory genes of monocytes and is associated with an impaired relationship between metabolism and inflammatory function upon activation.Mutations in TP53-the most commonly mutated gene in cancer-remain poorly understood. Recent work shows that the effects of mutations in this p53-encoding gene are dependent on context, including allelic state and the presence of microbial metabolites.An intact gut microbiome was needed to protect genetically vulnerable mice from developing leukemia.Glucocorticoid signaling promoted a dysfunctional phenotype for tumor-infiltrating CD8+ T cells.Autophagy dampened T cell-mediated immunity to promote growth of tumors with high mutational burden.The MEK inhibitor trametinib caused MEK to engage KSR more efficiently than MEK engaged BRAF.Chromosome copy-number variations are a hallmark of cancer. Among them, the prevalent chromosome 17p deletions are associated with poor prognosis and can promote tumorigenesis more than TP53 loss. Here, we use multiple functional genetic strategies and identify a new 17p tumor suppressor gene (TSG), plant homeodomain finger protein 23 (PHF23). Its deficiency impairs B-cell differentiation and promotes immature B-lymphoblastic malignancy. Mechanistically, we demonstrate that PHF23, an H3K4me3 reader, directly binds the SIN3-HDAC complex through its N-terminus and represses its deacetylation activity on H3K27ac. Thus, the PHF23-SIN3-HDAC (PSH) complex coordinates these two major active histone markers for the activation of downstream TSGs and differentiation-related genes. Furthermore, dysregulation of the PSH complex is essential for the development and maintenance of PHF23-deficient and 17p-deleted tumors. Hence, our study reveals a novel epigenetic regulatory mechanism that contributes to the pathology of 17p-deleted cancers and suggests a susceptibility in this disease.
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