Please see the Editorial Comment by Hyeon Yu, discussing this article. Background: Complete pathologic necrosis (CPN) is associated with improved survival in patients who undergo liver transplantat...

Summary The implementation of an in-hospital fracture liaison service facilitated prompt initiation of anti-osteoporosis treatment following a hip fracture (HF), increasing follow-up and treatment rates. This led to a 48% reduction in the risk of subsequent HF and a 29% decrease in mortality rates. Purpose To demonstrate the impact of an institutional fracture liaison service (FLS) which allowed in-hospital anti-osteoporosis treatment following hip fracture (HF) on subsequent HF and mortality rate. Methods We retrospectively evaluated patients aged 65 years and older, admitted with an osteoporotic HF, who were transferred following surgery for rehabilitation in the geriatrics department in two time periods: before and after the implementation of an institutional FLS (“geriatric-pre-FLS” and “geriatric-FLS” cohorts, respectively). Data were captured from electronic records and the two cohorts were compared following an assessment of baseline characteristics, follow-up, and anti-osteoporosis treatment initiation. A multivariable Cox regression model evaluated differences between the cohorts regarding subsequent HF and mortality rates. Results Three hundred and eighteen and 448 patients comprised the geriatric-pre-FLS (07/2008–06/2014) and the geriatric-FLS (03/2016–03/2020) cohorts, respectively. Baseline characteristics were comparable between the cohorts (median age 81 vs. 82, p = 0.08 and female sex 73% vs. 70%, p = 0.48, respectively). Rates of endocrine consultation (3.5% vs. 99%%, p < 0.001), DXA-BMD testing (7.5% vs. 34%, p < 0.001), and parenteral anti-osteoporosis treatment (4% vs. 76.6%, p < 0.001) were all higher in the geriatric-FLS cohort. The implementation of the FLS led to a 48% reduction in subsequent HF risk (HR 0.52; 95% CI 0.37–0.74, p < 0.001) and a 29% decrease in mortality rate (HR 0.71; 95% CI 0.54–0.92, p = 0.011). Conclusions The implementation of an in-hospital FLS facilitated prompt initiation of anti-osteoporosis treatment following a HF, increased follow-up and treatment rates, and resulted in a 48% reduction in subsequent HF risk and a 29% reduction in mortality rates.

The effects of particulate matter (PM) air pollution on adipose tissue have mainly been studied in animal models. The aim of this study was to examine the potential associations between PM exposure and 25 cellular markers in human omental (OM) and subcutaneous (SC) adipose tissue. The PM exposure assessments for both PM_2.5 (PM <2.5 μm in diameter) and PM₁₀ (<10 μm) were based upon a novel hybrid satellite-based spatio-temporally resolved model. We calculated the PM exposure above the background threshold for 1 week (acute phase), 3 and 6 months (intermediate phase), and 1 year (chronic phase) prior to tissue harvesting and tested the associations with adipose cell metabolic effects using multiple linear regressions and heat maps strategy. Chemokine levels were found to increase after acute and intermediate exposure duration to PM₁₀. The levels of stress signaling biomarkers in the SC and OM tissues rose after acute exposure to PM₁₀ and PM_2.5. Macrophage and leucocyte counts were associated with severity of PM exposure in all three duration groups. Adipocyte diameter decreased in all exposure periods. Our results provide evidence for significant contribution of air pollutants exposure to adipose tissue inflammation as well as for pathophysiological mechanisms of metabolic dysregulation that may be involved in the observed responses.

An accurate assessment of pollutants’ exposure and precise evaluation of the clinical outcomes pose two major challenges to the contemporary environmental health research. The common methods for exposure assessment are based on residential addresses and are prone to many biases. Pollution levels are defined based on monitoring stations that are sparsely distributed and frequently distanced far from residential addresses. In addition, the degree of an association between outdoor and indoor air pollution levels is not fully elucidated, making the exposure assessment all the more inaccurate. Clinical outcomes’ assessment, on the other hand, mostly relies on the access to medical records from hospital admissions and outpatients’ visits in clinics. This method differentiates by health care seeking behavior and is therefore, problematic in evaluation of an onset, duration, and severity of an outcome. In the current paper, we review a number of novel solutions aimed to mitigate the aforementioned biases. First, a hybrid satellite-based modeling approach provides daily continuous spatiotemporal estimations with improved spatial resolution of 1 × 1 km² and 200 × 200 m² grid, and thus allows a more accurate exposure assessment. Utilizing low-cost air pollution sensors allowing a direct measurement of indoor air pollution levels can further validate these models. Furthermore, the real temporal-spatial activity can be assessed by GPS tracking devices within the individuals’ smartphones. A widespread use of smart devices can help with obtaining objective measurements of some of the clinical outcomes such as vital signs and glucose levels. Finally, human biomonitoring can be efficiently done at a population level, providing accurate estimates of in-vivo absorbed pollutants and allowing for the evaluation of body responses, by biomarkers examination. We suggest that the adoption of these novel methods will change the research paradigm heavily relying on ecological methodology and support development of the new clinical practices preventing adverse environmental effects on human health.

Hypokalemia is common among critically ill patients. Parenteral correction of hyperkalemia depends on dosages and patient characteristics. Our aims were to assess changes in potassium levels following parenteral administration, and to derive a formula for predicting rises in serum potassium based on patient characteristics. We conducted a population-based retrospective cohort study of adults hospitalized in a general intensive care unit for 24 h or more between December 2006 and December 2017, with hypokalemia. The primary exposures were absolute cumulative intravenous doses of 20, 40, 60 or 80 mEq potassium supplement. Adjusted linear mixed models were used to estimate changes in serum potassium. Of 683 patients, 422 had mild and 261 moderate hypokalemia (serum potassium 3.0–3.5 mEq/L and 2.5–2.99 mEq, respectively). Following doses of 20–80 mEq potassium, serum potassium levels rose by a mean 0.27 (±0.4) mEq/L and 0.45 (±0.54) mEq/L in patients with mild and moderate hypokalemia, respectively. Changes were associated with creatinine level, and the use of mechanical ventilation and vasopressors. Among critically ill patients with mild to moderate hypokalemia, increases in serum potassium after intravenous potassium supplement are influenced by several clinical parameters. We generated a formula to predict the expected rise in serum potassium based on clinical parameters.