Delirium prevalence in a Colombian hospital,association with geriatric syndromes and complications during hospitalization

BackgroundThe aim of this paper is to describe the prevalence of Delirium and the factors associated with its presentation and complications identified in a geriatric unit in Colombia.Material and methodsThis is a retrospective observational study that included all patients admitted consecutively for two years in a geriatric unit of a hospital in Bogotá, Colombia. We assessed delirium prevalence with the Confusion Assessment Method (CAM). The independent variables were age, sex, functional impairment (Barthel < 90), malnutrition (MNA < 12), pressure ulcers at admission, state of the social support network, number of comorbidities, polypharmacy (5 or more drugs), complications such as ICU requirement, hospital stay, in-hospital functional impairment and mortality were also evaluated. As an exclusion criterion: not having CAM registered in the medical record, all the patients had this information.ResultsWe studied 1599 subjects with a mean age of 86 years (IQR 9). Delirium prevalence was 51.03%. Delirium was associated with a higher rate of: pressure ulcers on admission [OR 3.76 (CI 2.60–5.43 p < 0.001)], functional impairment [OR 2.38 (CI 1.79–3.16 p < 0.001)], malnutrition [OR 2.06 (CI 1.56–2.73 p < 0.001)], and infection [OR 1.46 (CI 1.17–1.82 p < 0.001)]. Moreover delirium has a higher association with mortality [OR 2.80 (1.03–7.54 p = 0.042)], in-hospital functional decline [OR 1.82 (1.41–2.36 p < 0.001)], and longer hospital stay [OR 1.04 (1.04–1.09 p = 0.006)]; independently of age, sex, pressure ulcers on admission, functional impairment, malnutrition, dementia, infection and limited social network.ConclusionOur study suggests that infectious diseases and geriatric syndromes such as, functional dependence, pressure ulcers, malnutrition or major cognitive impairment are independently associated with the presence of delirium on admission. Additionally, the presence of delirium is independently associated during hospitalization with complications, longer hospital stay, functional impairment and mortality.     

Postoperative plasma copeptin levels independently predict delirium and cognitive dysfunction after coronary artery bypass graft surgery

Copeptin can reflect individual's stress state and are correlated with poor outcome of critical illness. The occurrence of postoperative delirium (POD) and cognitive dysfunction (POCD) is associated with worse outcome after coronary artery bypass graft (CABG) surgery. The present study aimed to investigate the ability of postoperative plasma copeptin level to predict POD and POCD in patients undergoing CABG surgery. Postoperative plasma copeptin levels of 108 patients were measured by an enzyme-linked immunosorbent assay. It was demonstrated that plasma copeptin levels were substantially higher in patients with POD than without POD (1.8 ± 0.6 ng/mL vs. 1.1 ± 0.3 ng/mL; P < 0.001) and in patients with POCD than without POCD (1.9 ± 0.6 ng/mL vs. 1.1 ± 0.4 ng/mL; P < 0.001). Plasma copeptin level and age were identified as independent predictors for POD [odds ratio (OR), 67.386; 95% confidence interval (CI), 12.031–377.426; P < 0.001 and OR, 1.202; 95% CI, 1.075–1.345; P = 0.001] and POCD (OR, 28.814; 95% CI, 7.131–116.425; P < 0.001 and OR, 1.151; 95% CI, 1.030–1.285; P = 0.003) using a multivariate analysis. For prediction of POD, the area under receiver operating characteristic curve (AUC) of the copeptin concentration (AUC, 0.883; 95% CI, 0.807–0.937) was markedly higher than that of age (AUC, 0.746; 95% CI, 0.653–0.825; P = 0.020). For prediction of POCD, the AUC of the copeptin concentration (AUC, 0.870; 95% CI, 0.792–0.927) was markedly higher than that of age (AUC, 0.735; 95% CI, 0.641–0.815; P = 0.043). Thus, postoperative plasma copeptin level may be a useful, complementary tool to predict POD and POCD in patients undergoing CABG surgery.     

Serum and urinary selenium levels in obese children: A cross-sectional study

ObjectiveTo determine serum and urinary selenium (Se) levels in children with and without obesity, and to assess if Se influences the risk of obesity.Subjects and methodsHigh-resolution-continuum source-atomic absorption spectrometry (HR-CS-AAS) was used to determine the content of Se in 80 children (age 6–17; 40 boys, 40 girls). Correlations between variables were tested with the use of Spearman's correlation coefficient. U Mann–Whitney test was applied to assess the difference of Se contents in samples. Measured metabolic risk factors (blood pressure, glucose level, triglycerides (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and total cholesterol), age, gender, and BMI were correlated. Logistic regression models were fitted to identify predictors of obesity interacting with selenium content in serum and urine, separately.ResultsObese children, regardless of gender, had lower Se content. Se level in serum (p = 0.001, OR 0.74, 95%CI 0.62–0.88) and total cholesterol (p = 0.001, OR 1.19, 95%CI 1.08–1.31) were the independent factors significantly influencing the risk of obesity in children. Two separate models were observed for Se in urine: (i) Se level (p < 0. 0001, OR 0.70, 95%CI 0.58–0.84) and glucose level (p < 0.0001, OR 1.22, 95%CI 1.10–1.35), and (ii) Se level (p = 0.002, OR 0.60 95%CI 0.43–0.83) and total cholesterol level (p = 0.003, OR 1.16, 95%CI 1.05–1.28).ConclusionThe current study suggests a possible role of Se in obesity. Further research needs to be performed to check if obese children are an at-risk group for Se deficiency.     

Effect of 593C > T GPx1 SNP alone and in synergy with 47C > T SOD2 SNP on the outcome of critically ill patients

During critical illness and sepsis there is severe antioxidant depletion, and this scenario raises the critical ill patient’s mortality risk. Glutathione peroxidase (GPx) is one of the first endogenous antioxidant defense enzymes, and it works cooperatively with superoxide dismutase (SOD) and catalase (CAT) to detoxify free radicals from the cellular environment. Genetic studies are important to understand the complexity of human oxidative stress and how the organism responds to an extreme situation such as critically care conditions. Previous studies with a GPx1 single nucleotide polymorphism (593C > T SNP; rs1050450; protein variant in GPx1: Pro198Leu) showed 593T carriers and 593TT homozygotes present higher risk to develop different diseases. We assessed the relationship of the genotype distribution of GPx1 SNP in critically ill patients with their conditions (organ dysfunction, sepsis, and septic shock) and their outcome. We monitored 626 critically ill patients daily from the ICU (intensive care unit) admission to their discharge from hospital, or death. Our study revealed a significant association between 593TT GPx1 genotype and mortality; the mortality rate was higher in homozygous 593TT GPx1 (N = 94) when compared with the group of subjects with genotypes 593CT or 593CC GPx1 (N = 532) (52% vs. 38%, P = 0.009; OR = 1.79; 95% CI = 1.13–2.85). Evaluating the subgroup of 293 ICU patients with sepsis, a pooled analysis including two genetic variants GPx1 and SOD2 (47C > T SNP, rs4880; protein variant in MnSOD: Ala–9Val) showed a significant difference in relation to progression to septic shock. The frequency of septic shock among septic patients with 593T GPx1 and 47C SOD2 alleles (N = 122) was higher when compared with septic patients carrying other settings of genotypes (N = 174) (78% vs. 66%; P = 0.028; OR = 1.81; 95% CI = 1.03–3.18). Accepting the previously reported functional effects of these two SNPs on GPx1 and SOD2 gene expressions and, consequently, on GPx1 and MnSOD enzyme activities, we believe our results may be considered as an important contribution for the understanding of oxidative imbalance during the critical ill.     

Plasma visfatin,a possible prognostic marker in aneurysmal subarachnoid hemorrhage

Visfatin is linked to inflammation and associated with clinical outcomes of intracerebral hemorrhage. This study was designed to investigate whether visfatin might serve as a marker of severity and prognosis in aneurysmal subarachnoid hemorrhage. In this study, plasma visfatin levels of 172 consecutive patients and 172 sex and age-matched healthy subjects were determined using enzyme-linked immunosorbent assay. The recorded clinical outcomes included in-hospital mortality and 6-month mortality and unfavorable outcome (Glasgow Outcome Scale score of 1–3). Plasma visfatin level was substantially higher in patients than in healthy controls (92.1 ± 20.5 ng/mL vs. 12.4 ± 3.2 ng/mL; P < 0.001), was significantly associated with the World Federation of Neurological Surgeons (WFNS) score (r = 0.569, P < 0.001) and Fisher score (r = 0.657, P < 0.001), was an independent predictor of in-hospital mortality [odds ratio (OR), 1.378; 95% confidence interval (CI), 1.036–1.866; P = 0.002] and 6-month mortality (OR, 1.261; 95% CI, 1.018–1.745; P = 0.004) and unfavorable outcome (OR, 1.207; 95% CI, 1.012–1.682; P = 0.008) in multivariate logistic regression analysis and had high predictive value for in-hospital mortality [area under curve (AUC), 0.849; 95% CI, 0.787–0.899; P < 0.001] and 6-month mortality (AUC, 0.868; 95% CI, 0.808–0.915; P < 0.001) and unfavorable outcome (AUC, 0.859; 95% CI, 0.797–0.907; P < 0.001) using receiver operating characteristic curves. AUCs of visfatin were similar to those of WFNS score and Fisher score (all P > 0.05), but visfatin did not improve the predictive values of WFNS score and Fisher score (all P > 0.05). Thus, visfatin may be associated with clinical severity of aneurysmal subarachnoid hemorrhage and also have prognostic value for clinical outcomes.     

ADIPOQ gene polymorphisms and cancer risk: A meta-analysis

The results of studies investigating the association between ADIPOQ gene polymorphisms and risk of cancer have been inconsistent and often contradictory. The present meta-analysis was conducted in order to overcome the limitations of any individual study and to provide a more precise overall effect estimate. Relevant studies were identified by searching PubMed and Embase for articles published through May 2012. The strength of the relationship between the ADIPOQ gene and risk of cancer was assessed using odds ratios (ORs). Either a fixed-effects or a random-effects model was used to calculate the overall risk estimates. Fifteen studies were included and five SNPs were considered. A significant association was found between SNP rs2241766 and risk of cancer in the recessive genetic model (OR: 0.768, 95% CI: [0.626, 0.942], P = 0.011); a significant relationship was also found between SNP rs1501299 and risk of cancer in both an allele contrast (OR: 0.141, 95%CI: [0.113, 0.176], P < 0.001) and the dominant genetic model (OR: 0.904, 95%CI: [0.830, 0.985], P = 0.021); no association was found with the rs266729, rs822395, or rs822396 SNPs. Adjusted ORs were also considered, but no statistically significant association was found in homozygote contrasts for any of the five SNPs after adjustment. Our results suggest that two polymorphisms, SNP rs2241766 and SNP rs1501299, of the ADIPOQ gene may be associated with reduced risk of cancer. However, the overall strength of association is mild to moderate, and additional well-designed studies are needed to confirm the present conclusion.     

The impact of chemokine receptor CXCR4 on breast cancer prognosis: A meta-analysis

Background: C-X-C chemokine receptor type 4 (CXCR4) has been implicated in the invasiveness and metastasis of diverse cancers. However, the published data remain controversial on the correlation between CXCR4 expression level, as well as its subcellular distribution in tumor cells, and the clinical outcome of patients with breast cancer. Methods: To identify the precise role of CXCR4 in the clinical outcome of breast cancer, we performed a meta-analysis including 15 published studies. Original data included the hazard ratios (HRs) of overall survival (OS) and disease-free survival (DFS) in breast cancer with high CXCR4 expression versus low expression. We pooled hazard ratios (HRs) with 95% confidence intervals (CIs) to estimate the hazard. Results: A total of 15 published studies (including 3104 patients) were eligible. Overall survival (OS) and disease-free survival (DFS) of breast cancer were found to be significantly related to CXCR4 expression level, with the HR being 1.65 (95%CI: 1.34–2.03; P < 0.00001) and 1.94 (95%CI: 1.42–2.65; P < 0.00001) respectively. Stratified analysis according to subcellular distribution of CXCR4 showed that high expression in whole cells, cytoplasm and nucleus could predict unfavorable OS, with the HR of 2.02 (95%CI: 1.43–2.85; P < 0.0001), 1.57 (95%CI: 1.13–2.18; P = 0.007), and 1.47 (95%CI: 1.19–1.81; P = 0.0004) respectively. As for DFS, elevated expression level of CXCR4 both in whole cells and cytoplasm predicted a poor outcome, with the HR being 2.23 (95%CI: 1.48–3.37; P = 0.0001) and 1.76 (95%CI: 1.11–2.80; P = 0.02), while high expression in the nucleus had no statistical significance, with HR 1.15 (95%CI: 0.52–2.55; P = 0.73). Conclusions: Increased CXCR4 expression, especially in whole cells and cytoplasm, may serve as a poor prognostic indicator in patients with breast cancer. Future studies are warranted to investigate the relationship between CXCR4 expression and survival of patients with breast carcinoma, which could help predict the clinical outcome and guide clinical decision-making for therapy.     

Plasma copeptin concentration and outcome after pediatric traumatic brain injury

Higher plasma copeptin level has been associated with poor outcomes of critical illness. The present study was undertaken to investigate the plasma copeptin concentrations in children with traumatic brain injury (TBI) and to analyze the correlation of copeptin with disease outcome. Plasma copeptin concentrations of 126 healthy children and 126 children with acute severe TBI were measured by enzyme-linked immunosorbent assay. Twenty-one patients (16.7%) died and 38 patients (30.2%) had an unfavorable outcome (Glasgow Outcome Scale score of 1–3) at 6 months. Plasma copeptin level was obviously higher in patients than in healthy children (46.2 ± 20.8 pmol/L vs. 9.6 ± 3.0 pmol/L, P < 0.001). Plasma copeptin level was identified as an independent predictor for 6-month mortality [odds ratio (OR) 1.261, 95% confidence interval (CI) 1.112–1.538, P = 0.005] and unfavorable outcome (OR 1.313, 95% CI 1.146–1.659, P = 0.003). The predictive value of copeptin was similar to that of Glasgow Coma Scale (GCS) score for 6-month mortality [area under curve (AUC) 0.832, 95% CI 0.755–0.892 vs. AUC 0.873, 95% CI 0.802–0.926, P = 0.412] and unfavorable outcome (AUC 0.863, 95% CI 0.790–0.918 vs. AUC 0.885, 95% CI 0.816–0.935, P = 0.596). Copeptin improved the AUC of GCS score for 6-month unfavorable outcome (AUC 0.929, 95% CI 0.869–0.967, P = 0.013), but not for 6-month mortality (AUC 0.887, 95% CI 0.818–0.936, P = 0.600). Thus, plasma copeptin level represents a novel biomarker for predicting 6-month clinical outcome in children with TBI.     

Alcohol consumption and risk of upper-tract urothelial cancer

BackgroundUpper-tract urothelial cancer (UTUC), which includes renal pelvic cancer and ureter cancer, is a rare cancer and its prognosis is poor. Smoking and high-risk occupations (e.g., printing and dyestuff working which involves exposure to aniline dyes) are well-known risk factors for UTUC. However, the risk of alcohol consumption in UTUC remains unclear. This study aimed to determine whether alcohol consumption is an independent risk factor for UTUC.MethodsThe study was a case–control study which used the nationwide clinical inpatient database of the Rosai Hospital group in Japan. We identified 1569 cases and 506,797 controls between 1984 and 2014. We estimated the odds ratio (OR) and 95% confidence interval (95%CI) of alcohol consumption for UTUC – never, up to 15 g/day, >15–30 g/day, or >30 g/day – using unconditional logistic regression. We adjusted for the following covariates: age, sex, study period, hospital, history of smoking, and high-risk occupation.ResultsThe risk of UTUC was significantly higher in ever-drinkers compared with never-drinkers (OR = 1.23, 95%CI, 1.08–1.40; P = 0.001). Compared with never-drinkers, the risk threshold for UTUC was >15 g of alcohol consumption per day (equivalent to 6 ounces of Japanese sake containing 23 g of alcohol). A dose-response was observed (P < 0.001).ConclusionAlcohol consumption may be an independent risk factor for UTUC, with a low-risk threshold of 15 g of alcohol per day.     

IGF-I mediated inhibition of leptin receptor expression in porcine hepatocytes

A study was conducted to elucidate hormonal control of leptin receptor gene expression in primary cultures of porcine hepatocytes. Hepatocytes were isolated from swine and seeded into T-25 flasks. Cultures were established in medium containing fetal bovine serum for one day and switched to serum-free medium (William's E medium and 1 ng/mL insulin) for the remainder of the 3 d culture period. For the final 24 h, medium was supplemented with porcine growth hormone (GH, 100 or 500 ng/mL), insulin-like growth factor 1 (IGF-1, 50 to 250 ng/mL) or triiodothyronine (T3, 100 ng/mL). RNA was extracted and relative quantitative RT-PCR was performed with primers for long form leptin receptor. Receptor expression was calculated relative to 18S rRNA. Insulin had no effect (P > 0.05), while T3 increased leptin receptor mRNA abundance (P < 0.05). Treatment with GH or IGF-I reduced leptin receptor expression (P < 0.05). Phosphorylation of ERK1/2 in response to acute leptin treatment was inhibited by previous exposure to GH or IGF-I. Hepatocytes secreted IGF-I under basal conditions and this was enhanced by GH addition. These data suggest porcine hepatocytes may be less sensitive to leptin stimulation due to the actions of endogenous IGF-I on leptin receptor expression.     

Comparison and relationship of thyroid hormones,IL-6, IL-10 and albumin as mortality predictors in case-mix critically ill patients

ObjectiveTo compare the ability of thyroid hormones, IL-6, IL-10, and albumin to predict mortality, and to assess their relationship in case-mix acute critically ill patients.MethodsAPACHE II scores and serum thyroid hormones (FT3, FT4, and TSH), IL-6, IL-10, and albumin were obtained at EICU admission for 79 cases of mix acute critically ill patients without previous history of thyroid disease. Patients were followed for 28 days with patient’s death as the primary outcome. All mean values were compared, correlations assessed with Pearson’ test, and mortality prediction assessed by multivariate logistic regression and ROC.ResultsNon survivors were older, with higher APACHE II score (p = 0.000), IL-6 (p < 0.05), IL-10 (p = 0.000) levels, and lower albumin (p = 0.000) levels compared to survivors at 28 days. IL-6 and IL-10 had significant negative correlation with albumin (p = 0.001) and FT3 (p ⩽ 0.05) respectively, while low albumin had a direct correlation with FT3 (p < 0.05). In the mortality prediction assessment, IL-10, albumin and APACHE II were independent morality predictors and showed to have a good (0.70–0.79) AUC-ROC (p < 0.05). Despite that the entire cohort showed low FT3 serum levels (p = 0.000), there was not statistical difference between survivors and non-survivors; neither showed any significance as mortality predictor.ConclusionsIL-6 and IL-10 are correlated with Low FT3 and hypoalbuminemia. Thyroid hormones assessed at EICU admission did not have any predictive value in our study. And finally, high levels of IL-6 and IL-10 in conjunction with albumin could improve our ability to evaluate disease’s severity and predict mortality in the critically ill patients. When use in combination with APACHE II scores, our model showed improved mortality prediction.     

Serum zinc is associated with plasma leptin and Cu–Zn SOD in elite male basketball athletes

This paper investigates the relationship between plasma trace element and plasma leptin, as well as percent fat mass, in 16 male basketball athletes. Blood samples were obtained before intensive training and 24 h after intensive training to measure plasma zinc (Zn), copper (Cu), calcium (Ca), magnesium (Mg), iron (Fe), and leptin levels. High-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), triglyceride (TG), total and cholesterol (TC) levels were determined using commercially available kits for humans. Subjects presented similar values in terms of age (21.1 ± 2.2 years old), body mass index (23.9 ± 2.00 kg/m²), percent body fat (14.40 ± 1.52%), plasma hemoglobin (150.1 ± 9.4 g/L), plasma Zn (17.47 ± 1.28 μmol/l), plasma Cu (13.42 ± 1.40 μmol/L), plasma Ca (2.41 ± 0.14 mmol/L), and plasma Mg (0.96 ± 0.02 mmol/L). The correlation analysis between degree of plasma leptin and plasma element contents was performed using the SPSS 16.0 software. Plasma Zn correlated positively with plasma leptin (r = 0.746, P < 0.01), Cu–Zn SOD (r = 0.827, P < 0.01), and negatively with percent fat mass (r = –0.598, P < 0.05) under no-training conditions. Meanwhile, plasma Cu, Ca, Mg, and Fe did not correlate with plasma leptin or percent fat mass (P > 0.05). In conclusion, plasma Zn may be involved in the regulation of plasma leptin and may serve as a lipid-mobilizing factor in Chinese men's basketball athletes.     

Plasma leptin level predicts hematoma growth and early neurological deterioration after acute intracerebral hemorrhage

Higher plasma leptin levels have been associated with poor clinical outcomes after intracerebral hemorrhage. Nevertheless, their links with hematoma growth and early neurological deterioration are unknown. Therefore, we aimed to investigate the relationship between plasma leptin levels, hematoma growth, and early neurological deterioration in patients with acute intracerebral hemorrhage. We prospectively studied 102 consecutive patients with acute spontaneous basal ganglia hemorrhage presenting within 6 h from symptoms onset. Significant hematoma growth was defined as hematoma enlargement >33% at 24 h. Early neurological deterioration was defined as an increase of ≥4 points in National Institute of Health Stroke Scale score at 24 h from symptoms onset. We measured plasma leptin levels on admission using an enzyme-linked immunosorbent assay in a blinded fashion. In multivariate logistic regression analysis, plasma leptin level emerged as the independent predictor of hematoma growth (odds ratio, 1.182; 95% confidence interval, 1.061–2.598; P = 0.008) and early neurological deterioration (odds ratio, 1.193; 95% confidence interval, 1.075–2.873; P = 0.004). Using receiver operating characteristic curves, we calculated areas under the curve for hematoma growth (area under curve, 0.844; 95% confidence interval, 0.759–0.908) and early neurological deterioration (area under curve, 0.857; 95% confidence interval, 0.774–0.918). The predictive performance of leptin was similar to, but did not obviously improve that of hematoma volume. Thus, leptin may help in the prediction of hematoma growth and early neurological deterioration after intracerebral hemorrhage.     

Update on Inpatient Glycemic Control in Hospitals in the United States

ObjectiveTo provide data on glucose control in hospitals in the United States, analyzing measurements from the largest number of facilities to date.MethodsPoint-of-care bedside glucose (POC-BG) test results were extracted from 575 hospitals from January 2009 to December 2009 by using a laboratory information management system. Glycemic control for patients in the intensive care unit (ICU) and non-ICU areas was assessed by calculating patient-day-weighted mean POC-BG values and rates of hypoglycemia and hyperglycemia. The relationship between POC-BG levels and hospital characteristics was determined.ResultsA total of 49,191,313 POC-BG measurements (12,176,299 ICU and 37,015,014 non-ICU values) were obtained from 3,484,795 inpatients (653,359 in the ICU and 2,831,436 in non-ICU areas). The mean POC-BG was 167 mg/dL for ICU patients and 166 mg/dL for nonICU patients. The prevalence of hyperglycemia (> 180 mg/ dL) was 32.2% of patient-days for ICU patients and 32.0% of patient-days for non-ICU patients. The prevalence of hypoglycemia (< 70 mg/dL) was 6.3% of patient-days for ICU patients and 5.7% of patient-days for non-ICU patients. Patient-day-weighted mean POC-BG levels varied on the basis of hospital size (P < .01), type (P < .01), and geographic location (P < .01) for ICU and non-ICU patients, with larger hospitals (≥ 400 beds), academic hospitals, and US hospitals in the West having the lowest mean POC-BG values. The percentage of patient-days in the ICU characterized by hypoglycemia was highest among larger and academic hospitals (P < .05) and least among hospitals in the Northeast (P < .001).ConclusionHyperglycemia is common in hospitals in the United States, and glycemic control may vary on the basis of hospital characteristics. Increased hospital participation in data collection may support a national benchmarking process for the development of optimal practices to manage inpatient hyperglycemia. (Endocr Pract. 2011;17:853-861)     

Tri-axial accelerometer analysis techniques for evaluating functional use of the extremities

Activity monitors provide an objective mechanism for evaluating patient function. It is unclear what similarities or unique information may be yielded using different analyses. Fifteen patients scheduled to undergo shoulder arthroplasty and fifteen matched control subjects wore tri-axial accelerometer activity monitors bilaterally at the lower (wrist) and upper (biceps) arm for 3 days. Measures of central tendency, variance, sample entropy, and asymmetry were calculated. A novel technique to evaluate time distribution of activity intensity was also performed. Within both groups there was a difference in central tendency and variance when comparing dominant and non-dominant limbs for both the lower (Controls: Mean Activity, P < 0.001; Max Activity, P < 0.001; Patients: Mean Activity, P = 0.044; Max Activity, P = 0.009) and upper (Controls: Mean Activity, P < 0.001; Max Activity, P = 0.046; Patients: Mean Activity, P = 0.002; Max Activity, P = 0.049) arm. Within group differences were also present for lower arm entropy in both groups (Controls, P < 0.001; Patients P = 0.041), and at the upper arm for patients (P = 0.003). There were differences between groups for the asymmetry index for both the lower (P = 0.033) and upper arm (P = 0.005), and maximum activity level of the lower arm (P = 0.05). Between group differences were present for time distribution of activity intensity, as the involved upper arm of patients was inactive for a greater time than controls (P = 0.013). These results highlight unique information provided by multiple analysis methods, and include a novel approach of evaluating the distribution of time spent across variable intensity activities.     

Mortalidad en pacientes con demencia que cursaron internación en unidades de cuidados críticos

ObjectiveTo determine the mortality and comorbidities associated of patients with dementia admitted to the Intensive Care Unit (ICU) on the hospitalization and at one year of follow-up.Materials and methodsA retrospective observational cohort study was carried out between 2012 and 2017 at the Hospital Italiano de San Justo, of patients who were admitted to the ICU, these were observed up to hospitalary death, out hospital death one year of hospitalization, the disenrollment from the institution's health plan or the end of the follow-up.ResultsA total of 163 patients were included for analysis. We recorded those 79 patients (48.47%) died one year after the hospitalization, of them 25 (15.34%) in ICU and 8 (4.91%) in general room. The most frequent causes of death were respiratory. The factors most associated with mortality were: orotracheal intubation (HR = 2.01; 95% CI: 1.11-3.65; P = .02), history of leukemia (HR = 8.55; 95% CI: 1.82-40.05; P ≤ .05), elevated Charlson (HR = 1.16, 95% CI: 1.04-1.41; P = .05), and elevated APACHE II at admission (HR = 1.07; 95% CI: 1.03-1.11; P ≤ .05).ConclusionsThe present study expresses the prognosis of patients with a diagnosis of dementia admitted to the ICU and that depends not only on their baseline neurological status but also on the severity at admission and comorbidities.     

Growth performance and carcass traits of forage-fed hair sheep wethers

The objective of the present study was to compare live animal performance and carcass characteristics of 3/4 or 7/8 Dorper (DO; n = 30), purebred Katahdin (KA; n = 20), purebred St. Croix (SC; n = 17) and purebred Suffolk (SU; n = 10) lambs born in the spring and fall of 2001. After weaning, lambs were supplemented with up to 680 g of a corn-soybean meal supplement while grazing bermudagrass pastures overseeded with ryegrass. Lambs were slaughtered at approximately 210 d of age. From birth to weaning, DO lambs gained faster (P < 0.001) than KA or SC lambs, whereas KA lambs had higher (P < 0.001) ADG than SC lambs. Additionally, DO and SU wethers had greater (P < 0.02) ADG from weaning to slaughter than SC or KA wethers. Suffolk lambs were heavier (P < 0.001) at slaughter and produced heavier (P < 0.001) carcasses than lambs from hair-sheep breeds. Carcasses of KA lambs were fatter (actual fat thickness; P < 0.02) resulting in higher yield grades (P < 0.03) than carcasses of DO, SC, or SU lambs. Carcasses of DO and SU had larger (P < 0.001) longissimus muscle (LM) areas than those of KA or SC carcasses, whereas kidney fat weight and percentage were greater (P < 0.001) in carcasses from KA and SC than DO and SU lambs. Lean maturity was similar (P = 0.32) among breed-types. However, skeletal maturity was greater (P < 0.001) in SU than hair-sheep carcasses. Flank-streaking scores were similar (P = 0.19) among the breed-types, but conformation scores were higher (P < 0.001) for DO and SU carcasses and resulted in higher (P < 0.001) quality grades than SC carcasses. The LM of SU lambs was lighter (higher L^* values; P < 0.05) than that of KA and SC lambs, whereas the LM from DO lambs was redder (higher a^* values; P < 0.001) than SC and SU and more (P < 0.001) yellow than that of the other breed-types. Chops from SU lambs were tougher (higher shear force values; P < 0.007) than chops from the hair-sheep breeds. Results of this study indicate that ADG, carcass muscularity and meat quality were similar between DO and SU lambs, and, although fatter, carcass muscularity of KA was similar to that of DO lambs.     

Metabolic syndrome in relation to Barrett⿿s esophagus and esophageal adenocarcinoma: Results from a large population-based case-control study in the Clinical Practice Research Datalink

Gastroesophageal reflux disease (GERD) causes local chronic inflammation that increases risks of Barrett⿿s esophagus (BE) and esophageal adenocarcinoma (EA), yet symptomatic GERD is absent in approximately half of all such patients. Obesity exacerbates GERD and is also a component of metabolic syndrome (MetS). We evaluated the hypothesis that MetS is a GERD-independent mechanism by which obesity is associated with increased risks of BE and EA using data from the UK Clinical Practice Research Datalink. BE cases (n = 10,215) and EA cases (n = 592) were each individually matched to five population controls based on age, sex, and general practice. MetS was defined as occurrence of at least three of the following: obesity, type 2 diabetes, hypertension, and high cholesterol. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using conditional logistic regression. MetS was marginally associated with BE (OR = 1.12, 95%CI 1.00⿿1.25). Similar effects were found for the individual component factors of obesity, hypertension, and high cholesterol. History of GERD modified the association (P-_{effect modification} <1E⿿5), with the MetS-BE association confined to patients without a history of GERD (OR = 1.33, 95%CI 1.12⿿1.58). No association between MetS and risk of EA was detected in the main or stratified analyses. In this large population-based case-control study, individuals with MetS had a marginally increased risk of BE in the absence of GERD. The systemic inflammatory state (MetS) may represent a reflux-independent inflammatory pathway that increases the risk of BE. MetS did not increase risk of EA in this study population.