42 research outputs found

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

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    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

    Sotagliflozin added to optimized insulin therapy leads to HbA1c reduction without weight gain in adults with type 1 diabetes: A pooled analysis of inTandem1 and inTandem2

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    Aim: To evaluate whether the addition of sotagliflozin to optimized insulin significantly increases the proportion of adults with type 1 diabetes who achieve HbA1c goals without weight gain. Materials and methods: In a patient-level pooled analysis (n = 1575) of data from two phase 3, 52-week clinical trials (inTandem1 and inTandem2), the change from baseline in HbA1c and weight as well as the proportion of participants achieving an HbA1c of less than 7% without weight gain were compared between groups treated with placebo, sotagliflozin 200 mg and sotagliflozin 400 mg. Results: From a mean baseline HbA1c of 7.7%, mean HbA1c changes at week 24 were 120.36% (95% CI 120.44% to 120.29%) and 120.38% ( 120.45% to 120.31%) with sotagliflozin 200 and 400 mg versus placebo (P =.001 for both), respectively, with sustained effects through week 52. Weight significantly decreased at weeks 24 and 52 in both sotagliflozin groups compared with placebo. At week 52, the proportion of patients who achieved an HbA1c of less than 7% without weight gain was 21.8% with sotagliflozin 200 mg, 26.1% with sotagliflozin 400 mg and 9.1% with placebo (P <.001). Other HbA1c, weight and safety composite variables showed similar significant trends. Conclusion: When added to optimized insulin therapy, sotagliflozin improved glycaemic control and body weight and enabled more adults with type 1 diabetes to achieve HbA1c goals without weight gain over 52 weeks, although there was more diabetic ketoacidosis relative to placebo

    A transgenic mouse model that is useful for analyzing cellular and geographic differentiation of the intestine during fetal development.

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    Regional as well as cell-specific differences in gene expression are established and maintained in the perpetually regenerating intestinal epithelium. We have recently linked regions of the 5\u27-nontranscribed domain of the rat liver: fatty acid binding protein (L-FABP) gene which is normally expressed in both liver and intestine, to a reporter, the human growth hormone (hGH) gene, and examined hGH expression in adult transgenic mice (Sweetser, D. A., Birkenmeier, E. H., Hoppe, P. C., McKeel, D. W., and Gordon, J. I. (1988) Genes Dev. 2, 1318-1332). Our results indicated that cis-acting elements, including an orientation-independent suppressor, could produce a pattern of cellular and geographic expression of hGH which mimics that of the intact, endogenous murine Fabpl gene in both organs. We now show that nucleotides -4000 to +21 of the rat L-FABP gene can direct appropriate: cell-specific, regional, and temporal expression of the hGH reporter during a period of remarkable cellular expansion, cytodifferentiation, and morphologic transformation of the fetal gut epithelium. These studies also indicate that the polyclonal stem cell population located in the intervillous regions of the late fetal intestine exhibits a different pattern of transgene regulation than does the monoclonally derived crypt stem cell population in adult transgenic mice. Nucleotides -4000 to +21 are not sufficient to reproduce the normal temporal pattern of L-FABP gene activation in liver. Precocious expression of growth hormone in this pedigree of transgenic mice results in early induction of insulin-like growth factor I mRNA accumulation in liver but has no effect on insulin-like growth factor II mRNA levels. In contrast, local synthesis of growth hormone in the small intestine does not influence its insulin-like growth factor I or II mRNA levels
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