NF-kappaB P50/P65 hetero-dimer mediates differential regulation of CD166/ALCAM expression via interaction with micoRNA-9 after serum deprivation, providing evidence for a novel negative auto-regulatory loop

CD166/ALCAM plays an important role in tumor aggression and progression as well as protecting cancer cells against apoptosis and autophagy. However, the mechanism by which pro-cell death signals control CD166 expression remains unclear. Here we show that following serum deprivation (SD), upregulation of CD166 protein is shorter than that of CD166 mRNA. Molecular analysis revealed both CD166 and miR-9-1 as two novel NF-κB target genes in hepatoma cells. In vivo activation and translocation of the NF-κB P50/P65 hetero-dimer into the nucleus following the phosphorylation and accompanied degradation of its inhibitor, IκBα, contributes to efficient transcription of both genes following SD. We show that following serum starvation, delayed up-regulation of miR-9 represses translation of CD166 protein through its target sites in the 3′-UTR of CD166 mRNA. We also propose that miR-9 promotes cell migration largely due to inhibition of CD166. Collectively, the study elucidates a novel negative auto-regulatory loop in which NF-κB mediates differential regulation of CD166 after SD

Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study

Funder: European Society of Intensive Care Medicine; doi: http://dx.doi.org/10.13039/501100013347Funder: Flemish Society for Critical Care NursesAbstract: Purpose: Intensive care unit (ICU) patients are particularly susceptible to developing pressure injuries. Epidemiologic data is however unavailable. We aimed to provide an international picture of the extent of pressure injuries and factors associated with ICU-acquired pressure injuries in adult ICU patients. Methods: International 1-day point-prevalence study; follow-up for outcome assessment until hospital discharge (maximum 12 weeks). Factors associated with ICU-acquired pressure injury and hospital mortality were assessed by generalised linear mixed-effects regression analysis. Results: Data from 13,254 patients in 1117 ICUs (90 countries) revealed 6747 pressure injuries; 3997 (59.2%) were ICU-acquired. Overall prevalence was 26.6% (95% confidence interval [CI] 25.9–27.3). ICU-acquired prevalence was 16.2% (95% CI 15.6–16.8). Sacrum (37%) and heels (19.5%) were most affected. Factors independently associated with ICU-acquired pressure injuries were older age, male sex, being underweight, emergency surgery, higher Simplified Acute Physiology Score II, Braden score 3 days, comorbidities (chronic obstructive pulmonary disease, immunodeficiency), organ support (renal replacement, mechanical ventilation on ICU admission), and being in a low or lower-middle income-economy. Gradually increasing associations with mortality were identified for increasing severity of pressure injury: stage I (odds ratio [OR] 1.5; 95% CI 1.2–1.8), stage II (OR 1.6; 95% CI 1.4–1.9), and stage III or worse (OR 2.8; 95% CI 2.3–3.3). Conclusion: Pressure injuries are common in adult ICU patients. ICU-acquired pressure injuries are associated with mainly intrinsic factors and mortality. Optimal care standards, increased awareness, appropriate resource allocation, and further research into optimal prevention are pivotal to tackle this important patient safety threat

Correction to: Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study

The original version of this article unfortunately contained a mistake

Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study

Funder: European Society of Intensive Care Medicine; doi: http://dx.doi.org/10.13039/501100013347Funder: Flemish Society for Critical Care NursesAbstract: Purpose: Intensive care unit (ICU) patients are particularly susceptible to developing pressure injuries. Epidemiologic data is however unavailable. We aimed to provide an international picture of the extent of pressure injuries and factors associated with ICU-acquired pressure injuries in adult ICU patients. Methods: International 1-day point-prevalence study; follow-up for outcome assessment until hospital discharge (maximum 12 weeks). Factors associated with ICU-acquired pressure injury and hospital mortality were assessed by generalised linear mixed-effects regression analysis. Results: Data from 13,254 patients in 1117 ICUs (90 countries) revealed 6747 pressure injuries; 3997 (59.2%) were ICU-acquired. Overall prevalence was 26.6% (95% confidence interval [CI] 25.9–27.3). ICU-acquired prevalence was 16.2% (95% CI 15.6–16.8). Sacrum (37%) and heels (19.5%) were most affected. Factors independently associated with ICU-acquired pressure injuries were older age, male sex, being underweight, emergency surgery, higher Simplified Acute Physiology Score II, Braden score 3 days, comorbidities (chronic obstructive pulmonary disease, immunodeficiency), organ support (renal replacement, mechanical ventilation on ICU admission), and being in a low or lower-middle income-economy. Gradually increasing associations with mortality were identified for increasing severity of pressure injury: stage I (odds ratio [OR] 1.5; 95% CI 1.2–1.8), stage II (OR 1.6; 95% CI 1.4–1.9), and stage III or worse (OR 2.8; 95% CI 2.3–3.3). Conclusion: Pressure injuries are common in adult ICU patients. ICU-acquired pressure injuries are associated with mainly intrinsic factors and mortality. Optimal care standards, increased awareness, appropriate resource allocation, and further research into optimal prevention are pivotal to tackle this important patient safety threat

Relevance research on carotid atherosclerosis and levels of serum cathepsin K and cystatin C on patients with ischemic cerebral vascular disease

The relationship between carotid atherosclerosis (AS) and levels of serum cathepsin K (CatK) and cystatin C (CysC) on patients with ischemic cerebral vascular disease (ICVD) was explored. In total, 266 patients with ICVD who were admitted in our hospital were enrolled. According to the results of carotid ultrasound, they were randomly divided into plaque group (n = 133) and control group (n = 133). According to atherosclerotic plaque type distribution, the plaque group was divided into stable plaque group and unstable group. The relationship between levels of serum CatK and CysC of two groups and carotid AS indicator (such as intima-media thickness (IMT)) were analyzed with Spearman’s correlation. Spearman’s correlation analysis showed that IMT level was positively correlated with stability of carotid atherosclerotic plaque ( P  < 0.05). The level of serum CatK in plaque group was significantly higher than control group, and the level of serum CysC in plaque group was significantly lower than control group ( P  < 0.05); the level of serum CatK in unstable plaque group was significantly higher than stable plaque group, and the level of serum CysC in unstable plaque group was significantly lower than stable plaque group ( P  < 0.05). Serum CatK and IMT levels were positively correlated, and serum CysC and CatK levels were negatively correlated ( P  < 0.05). CatK and CysC levels may be used as serum markers for predicting carotid AS plaque instability, providing a new observational index for prevention and treatment of ICVD caused by carotid AS plaque

Comparison the effects of carotid endarterectomy with carotid artery stenting for contralateral carotid occlusion.

BackgroundThere have been inconsistent results regarding the use of carotid artery endarterectomy (CEA) versus carotid artery stenting (CAS) for contralateral carotid occlusion (CCO). This study aimed to determine the optimal revascularization technique for patients with CCO.MethodsWe systematically searched the PubMed, Embase, and Cochrane Library databases to identify eligible studies published from inception to January 2, 2021. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to calculate pooled effect estimates using a random-effects model. Sensitivity, subgroup, and publication bias analyses were also performed.ResultsSix studies involving 6,953 patients were selected for inclusion in this meta-analysis. Our results showed that while CEA was not associated with an increased risk of stroke compared to CAS (OR: 1.07; 95% CI: 0.75-1.51; P = 0.713), CEA was associated with a reduced risk of death compared to CAS (OR: 0.45; 95% CI: 0.29-0.70; P ConclusionThis study found that CEA and CAS resulted in similar outcomes for patients with CCO, while the risk of death was reduced in patients treated with CEA. Further high-level evidence should be collected to verify the results of this study

Organic pollutant removal from marine diesel engine off-gases under electron beam and hybrid electron beam and wet scrubbing process

The removal of organic pollutants from ship emission was studied using two processes namely electron beam (EB) and hybrid EB with wet scrubbing process. A mobile accelerator unit was used to treat 4915 Nm3 /h of flue gas emitted from a tugboat in Riga Shipyard. A volume of 3 m3 seawater containing 36.8 mM of NaClO2 oxidant was used as a wet scrubber solution. Organic pollutants, mainly volatile organic pollutants (VOCs), were collected at three different sampling points, before and after irradiation vessels, and after wet-scrubber unit, respectively. They were collected with glass sampling bottles, tedlar bags, Coconut Shell Charcoal (CSC) sorbents and XAD-2 sorbents. CH3OH and CH3OH/CH2Cl2 (1:1) were used to extract VOCs from CSC and XAD-2 sorbents, respectively. Syringe filters were used to obtain the solid-free extraction solutions. They were concentrated using a micro-extractor under continuously blowing high-purity Ar. A gas chromatography–mass spectrometry (GC-MS) was used for analysis. The identified organic compounds were: aliphatic hydrocarbons (dodecane C12H26 to eicosane C20H42), aromatic hydrocarbon (toluene), esters (C3H7COOCH3, (C4H9OCO)2C6H4), nitro compounds (C3H5NO3, C4H7NO2) and acid (C7H15COOH). After 4.2 kGy EB irradiation, around 50–100% aliphatic hydrocarbons, 83% toluene and 7.5% (C4H9OCO)2C6H4 were removed from the off-gases, and after EB hybrid wet-scrubber process, most organic compounds including nitro compounds were removed. Only trace amount of toluene, hexadecane, octadecane and dibutyl phthalate were found to be present in the gas phase

Downregulation of IL6 Targeted MiR-376b May Contribute to a Positive IL6 Feedback Loop During Early Liver Regeneration in Mice

Background/Aims: MicroRNAs (miRNAs) are a group of endogenous, small, noncoding RNAs implicated in a variety of biological processes, including cell proliferation, apoptosis, differentiation and metabolism. The present study aims to explore the potential role and molecular mechanism of miR-376b during the early phase of liver regeneration. Methods: MiRNA profiling microarrays were used to assess the changes in miRNA expression. For functional analysis, cell proliferation, apoptosis assays, real time quantitative PCR and westernblot analysis were performed. Results: The comprehensive miRNA expression profiling assays on regenerating liver tissues 4 h after partial hepatectomy (PH) showed that three miRNAs (miR-127, miR-376b and miR-494) located in the Dlk1-Gtl2 miRNA cluster were significantly downregulated. In vitro functional studies demonstrated that high-level interleukin 6 (IL6) inhibited the expression of miR-376b, and miR-376b mimics treatment decreased cell proliferation and increased apoptosis. Further target analysis showed that miR-376b reduced the mRNA and protein expression levels of NF-kappa-B inhibitor zeta (NFKBIZ) and signal transducers and transcription activators 3 (STAT3). Additionally, IL6-induced miR-376b downregulation would, in turn, increase the expression of IL-6 possibly via a feedback loop involving NFKBIZ or/and STAT3. Conclusion: During the early phase of liver regeneration, miR-376b expression was significantly decreased. Our findings reveal that a regulatory circuitry between miR-376b and IL-6 may exist, which trigger the initiation of liver regeneration