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Aim: Periodontitis (PD) is the sixth most prevalent disease around the world and is involved in the development and progression of multiple systemic diseases. Previous studies have reported that PD may aggravate liver injuries. The objective of this study was to investigate whether and how PD affects liver fibrosis. Materials and Methods: Ligature‐induced PD (LIP) was induced in male C57/B6J mice, and sub‐gingival plaques (PL) from patients with PD were applied to mouse teeth. Liver fibrosis was induced by carbon tetrachloride (CCl4) injection. The mice were randomly divided into six groups: Oil, Oil+LIP, Oil+LIP+PL, CCl4, CCl4+LIP, and CCl4+LIP+PL. Alveolar bone resorption was evaluated by methylene blue staining. Hepatic function was analysed by serum alanine aminotransferase and hepatic hydroxyproline. Picrosirius red and α‐smooth muscle actin (SMA) staining were used to evaluate the fibrotic area. RNA sequencing and quantitative RT‐PCR were used to measure gene expression. Western blotting was used to measure protein levels. Flow cytometry was used to analyse the accumulation of immune cells. Mouse microbiota were analysed using 16S rRNA gene sequencing. Results: Mice in the CCl4+LIP+PL group displayed higher serum alanine aminotransferase and hepatic hydroxyproline as well as more Picrosirius red‐positive and α‐SMA‐positive areas in liver samples than those of the CCl4 group, suggesting that PD (LIP+PL) aggravated CCl4‐induced hepatic dysfunction and liver fibrosis. Consistently, the expression of fibro‐genic genes and the protein levels of transforming growth factor β were much higher in the CCl4+LIP+PL group than in the CCl4 group. Flow cytometry revealed that PD increased the accumulation of immune cells, including Kupffer cells, B cells, and Th17 cells, in the liver of mice with CCl4 treatment. PD also increased the expression of inflammatory genes and activated pro‐inflammatory nuclear factor‐kappa B pathway in the livers of CCl4‐injected mice. Moreover, PD altered both oral and liver microbiota in CCl4‐injected mice. Conclusions: PD aggravates CCl4‐induced hepatic dysfunction and fibrosis in mice, likely through the increase of inflammation and alteration of microbiota in the liver. [ABSTRACT FROM AUTHOR]

Objectives: Typically, prognostic capability of gene expression profiling (GEP) is studied in the context of clinical trials, for which 50%‐80% of patients are not eligible, possibly limiting the generalizability of findings to routine practice. Here, we evaluate GEP analysis outside clinical trials, aiming to improve clinical risk assessment of multiple myeloma (MM) patients. Methods: A total of 155 bone marrow samples from MM patients were collected from which RNA was analyzed by microarray. Sixteen previously developed GEP‐based markers were evaluated, combined with survival data, and studied using Cox proportional hazard regression. Results: Gene expression profiling‐based markers SKY92 and the PR‐cluster were shown to be independent prognostic factors for survival, with hazard ratios and 95% confidence interval of 3.6 [2.0‐6.8] (P <.001) and 5.8 [2.7‐12.7] (P <.01) for overall survival (OS). A multivariate model proved only SKY92 and the PR‐cluster to be independent prognostic factors compared to cytogenetic high‐risk patients, the International Staging System (ISS), and revised ISS. A substantial number of high‐risk individuals could be further identified when SKY92 was added to the cytogenetic, ISS, or R‐ISS. In the cytogenetic standard‐risk group, ISS I/II, and R‐ISS I/II, 13%, 23%, and 23% of patients with adverse survivals were identified. Conclusions: For the first time, this study confirmed the prognostic value of GEP markers outside clinical trials. Conventional prognostic models to define high‐risk MM are improved by the incorporation of GEP markers. [ABSTRACT FROM AUTHOR]

Background: Pressure ulcers (PUs) are encountered in all types of care settings. The incidence of PUs in the intensive care unit (ICU) is higher for a variety of reasons. The Braden Scale is a widely used tool to assess the risk of PU, but its predictive power is controversial in ICU settings. In this systematic review and meta‐analysis, we aimed to evaluate the predictive accuracy of the Braden Scale for measurement of risk of PU in adult ICU patients. Methods: A comprehensive literature search in English databases (PubMed, Cochrane Library, OVID, and Web of Science), Chinese databases (SinoMed, CNKI, and Wanfang), and gray literature was performed. Studies assessing the predictive value of the Braden Scale for risk of PU in adult ICU patients were searched. Quality of the studies was scored with Quality Assessment of Diagnostic Accuracy Studies‐2. Country, study design, setting, blinding, and characteristics of included studies were extracted. Results: Eleven full‐text articles containing 10 044 patients, comprising 1058 patients with PUs were included. The pooled sensitivity and specificity of the Braden Scale for predicting PU risk in ICU adults were 0.89 (95% CI, 0.87‐0.91; I2 = 94.9%, P =.0000) and 0.28 (95% CI, 0.27‐0.29; I2 = 99.2%, P =.0000), respectively. The pooled DOR was 6.29 (95% CI: 4.09‐9.68). The overall weighted AUC was 0.7812 ± 0.0331 (95% CI: 0.7163‐0.8461) and the Q* value was 0.7196 ± 0.0283 (95% CI: 0.6641‐0.7751). Significant heterogeneity was noted among the included studies. Meta‐regression analysis showed that there was no heterogeneity in blinding (P =.074), study design (P =.679), or cut‐off value (P =.821). Conclusions: This meta‐analysis demonstrated that the Braden Scale had a moderate predictive validity with good sensitivity and low specificity in adult critically ill patients. Further development and modification of this tool or generation of a new tool with higher predictive power is warranted for use in ICU populations. Relevance to clinical practice: The first step in prevention of PU is risk assessment. In this meta‐analysis, we aimed to evaluate the predictive power of the Braden Scale for assessing risk of PU in ICU adult patients, which could potentially guide clinical practice. [ABSTRACT FROM AUTHOR]