Preoperative hyperglycemia predicts infected total knee replacement

BackgroundDiabetes increases the risk of surgical site infections. In many patients undergoing total knee replacement, however, diabetes has not been diagnosed. The purpose of this study was to analyze the applicability of preoperative screening for hyperglycemia in identifying patients predisposed to infected knee replacement.MethodsA recent series of 1565 primary total knee replacements performed due to osteoarthritis in a specialized, publicly funded hospital for joint replacement was reviewed.ResultsPreoperative hyperglycemia was significantly associated with infected knee replacement: during the 1-year follow-up infection occurred in 0.44%, 0.93% and 2.42% of patients with preoperative plasma glucose < 6.1 mmol/l (< 110 mg/dl), 6.1–6.9 mmol/l (110–125 mg/dl) and ≥ 7.0 mmol/l (≥ 126 mg/dl). In age- and gender-adjusted analysis the patients with the highest glucose levels had a 4-fold risk for infected knee replacement compared to the patients with the lowest glucose. Obesity increased the risk of infected knee replacement, but the effect of hyperglycemia on the infection rates remained significant also after adjustment for body mass index. None of the patients with normal but 2.8% of patients with increased glycosylated hemoglobin (> 6.5%) experienced infected knee replacement.ConclusionObesity and hyperglycemia associate with a higher risk of infected knee replacement. Preoperative screening of plasma glucose is an efficient way to identify patients in increased risk of infection following primary total knee replacement.     

Determinants of left ventricular diastolic function—The Cardiovascular Risk in Young Finns Study

Decreased left ventricular (LV) diastolic function is associated with increased all‐cause mortality and risk for a heart failure. The determinants of LV diastolic function have been mainly studied in elderly populations; however, the origin of LV heart failure may relate to the lifestyle factors acquired during the life course. Therefore, we examined biochemical, physiological, and lifestyle determinants of LV diastolic function in 34–49‐year‐old participants of the Cardiovascular Risk in Young Finns Study (Young Finns Study). In 2011, clinical examination and echocardiography were performed for 1928 participants (880 men and 1048 women; aged 34–49 years). LV diastolic function was primarily defined using E/é‐ratio (population mean 4.8, range 2.1–9.0). In a multivariate model, systolic blood pressure (P < 0.005), female sex (P < 0.005), age (P < 0.005), waist circumference (P = 0.024), smoking (P = 0.028), serum alanine aminotransferase (P = 0.032) were directly associated with E/é‐ratio, while an inverse association was found for height (P < 0.005). Additionally, a higher E/é‐ratio was found in participants with concentric hypertrophy compared to normal cardiac geometry (P < 0.005). Other indicators of the LV diastolic function including E/A‐ratio and left atrial volume index showed similarly strong associations with systolic blood pressure and age. In conclusion, we identified systolic blood pressure, waist circumference and smoking as modifiable determinants of the LV diastolic function in the 34–49‐year‐old participants of the Young Finns Study.     

Serum sialic acid as a marker of alcohol consumption: effect of liver disease and heavy drinking

BACKGROUND: Serum sialic acid (SA) has been suggested as a new marker of alcohol consumption. There are, however, only a few studies on the clinical value of such measurements. The relationship between serum SA and liver disease is also unknown. METHODS: We determined serum SA concentrations in a sample of 51 alcoholics and 20 healthy controls by using high-performance liquid chromatography with an anion-exchange column and pulsed amperometric detection. The alcoholic sample included 32 patients with liver disease, the severity of which was assessed by previously established combined clinical, laboratory, and morphological indices. In addition, there were 19 heavy drinkers without significant liver disease despite a well documented history of excessive alcohol consumption. RESULTS: The (mean +/- SD) SA concentrations (1.449 +/- 0.3019 mmol/liter) were significantly higher in the alcoholics than in the healthy controls (1.154 +/- 0.1702 mmol/liter). With the optimal cutoff limit for serum SA (1.425 mmol/liter), a specificity of 1.00 and sensitivity of 0.51 were obtained. The diagnostic accuracy of serum SA according to receiver operating characteristic analysis was good, with the area under the curve being 0.805 (0.052). Unlike the traditional serum markers of alcohol consumption (gamma-glutamyl transferase, carbohydrate-deficient transferrin, and aspartate amino transferase), serum SA was not found to be different between the alcoholics with or without liver disease. CONCLUSIONS: Our study suggests that serum SA is a sensitive marker of excessive alcohol consumption. Such measurements may also prove to be of value in conditions in which the results of the traditional markers reflect the severity of liver disease rather than alcohol consumption.     

Testing Genetic Susceptibility Loci for Alcoholic Heart Muscle Disease

BACKGROUND: Although many heavy alcohol users have subclinical alcoholic heart muscle disease, only a very few develop severe dilated cardiomyopathy. Therefore, and because cardiac abnormalities correlate only weakly with the duration or quantity of drinking, individual susceptibility differences may exist. In this work we examined whether common gene variants previously associated with cardiac hypertrophy or altered alcohol metabolism could modify the effects of alcohol on the heart. METHODS: We studied 700 middle-aged male victims of sudden death who underwent a medicolegal autopsy. In addition to routine postmortem examination, the weights and the cavity and wall dimensions of the left and right ventricle were measured. Coronary artery stenoses were determined from a silicone rubber cast of the arteries. Alcohol consumption and cardiovascular risk factors were assessed by a structured interview of the spouse. The following gene polymorphisms were determined by using polymerase chain reaction restriction fragment length polymorphism and solid-phase minisequencing techniques: angiotensin converting enzyme I/D, angiotensin II type 1 receptor 1166A/C, aldosterone synthase -344C/T, alcohol dehydrogenases 2 and 3, acetaldehyde dehydrogenase 2, and cytochrome P-450 2E1 DraI, PstI, RsaI, and MspI. RESULTS: The most consistent effects of alcohol (p < 0.05) were a higher total heart weight and a larger right ventricle size with increasing daily drinking. However, these and other effects of alcohol were statistically fully independent of the studied genotypes. CONCLUSIONS: The gene polymorphisms selected for and analyzed in our study are unlikely to modify the effects of alcohol on the heart. Other unknown factors determine the individual susceptibility to alcoholic heart muscle disease.     

Automated reference region extraction and population-based input function for brain [11C]TMSX PET image analyses

[¹¹C]TMSX ([7-N-methyl-¹¹C]-(E)-8-(3,4,5-trimethoxystyryl)-1,3,7-trimethylxanthine) is a selective adenosine A2A receptor (A_2AR) radioligand. In the central nervous system (CNS), A_2AR are linked to dopamine D₂ receptor function in striatum, but they are also important modulators of inflammation. The golden standard for kinetic modeling of brain [¹¹C]TMSX positron emission tomography (PET) is to obtain arterial input function via arterial blood sampling. However, this method is laborious, prone to errors and unpleasant for study subjects. The aim of this work was to evaluate alternative input function acquisition methods for brain [¹¹C]TMSX PET imaging. First, a noninvasive, automated method for the extraction of gray matter reference region using supervised clustering (SCgm) was developed. Second, a method for obtaining a population-based arterial input function (PBIF) was implemented. These methods were created using data from 28 study subjects (7 healthy controls, 12 multiple sclerosis patients, and 9 patients with Parkinson''s disease). The results with PBIF correlated well with original plasma input, and the SCgm yielded similar results compared with cerebellum as a reference region. The clustering method for extracting reference region and the population-based approach for acquiring input for dynamic [¹¹C]TMSX brain PET image analyses appear to be feasible and robust methods, that can be applied in patients with CNS pathology.     

Validation of [11C]ORM‐13070 as a PET tracer for alpha2c‐adrenoceptors in the human brain

This study explored the use of the α_2C‐adrenoceptor PET tracer [¹¹C]ORM‐13070 to monitor α_2C‐AR occupancy in the human brain. The subtype‐nonselective α₂‐AR antagonist atipamezole was administered to eight healthy volunteer subjects to determine its efficacy and potency (E_max and EC₅₀) at inhibiting tracer uptake. We also explored whether the tracer could reveal changes in the synaptic concentrations of endogenous noradrenaline in the brain, in response to several pharmacological and sensory challenge conditions. We assessed occupancy from the bound‐to‐free ratio measured during 5–30 min post injection. Based on extrapolation of one‐site binding, the maximal extent of inhibition of striatal [¹¹C]ORM‐13070 uptake (E_max) achievable by atipamezole was 78% (95% CI 69–87%) in the caudate nucleus and 65% (53–77%) in the putamen. The EC₅₀ estimates of atipamezole (1.6 and 2.5 ng/ml, respectively) were in agreement with the drug's affinity to α_2C‐ARs. These findings represent clear support for the use of [¹¹C]ORM‐13070 for monitoring drug occupancy of α_2C‐ARs in the living human brain. Three of the employed noradrenaline challenges were associated with small, approximately 10–16% average reductions in tracer uptake in the dorsal striatum (atomoxetine, ketamine, and the cold pressor test; P < 0.05 for all), but insulin‐induced hypoglycemia did not affect tracer uptake. The tracer is suitable for studying central nervous system receptor occupancy by α_2C‐AR ligands in human subjects. [¹¹C]ORM‐13070 also holds potential as a tool for in vivo monitoring of synaptic concentrations of noradrenaline, but this remains to be further evaluated in future studies. Synapse 69:172–181, 2015. © 2014 Wiley Periodicals, Inc.     

Characterization and electrochemical properties of iron-doped tetrahedral amorphous carbon (ta-C) thin films

Iron-doped tetrahedral amorphous carbon thin films (Fe/ta-C) were deposited with varying iron content using a pulsed filtered cathodic vacuum arc system (p-FCVA). The aim of this study was to understand effects of iron on both the physical and electrochemical properties of the otherwise inert sp³-rich ta-C matrix. As indicated by X-ray photoelectron spectroscopy (XPS), even ∼0.4 at% surface iron had a profound electrochemical impact on both the potential window of ta-C in H₂SO₄ and KOH, as well as pseudocapacitance. It also substantially enhanced the electron transport and re-enabled facile outer sphere redox reaction kinetics in comparison to un-doped ta-C, as measured with electrochemical impedance spectroscopy (EIS) and cyclic voltammetry (CV) using outer-sphere probes Ru(NH₃)₆, IrCl₆, and FcMeOH. These increases in surface iron loading were linked to increased surface oxygen content and iron oxides. Unlike few other metals, an iron content even up to 10 at% was not found to result in the formation of sp²-rich amorphous carbon films as investigated by Raman spectroscopy. Atomic force microscopy (AFM) and transmission electron microscopy (TEM) investigations found all films to be amorphous and ultrasmooth with R_q values always in the range of 0.1–0.2 nm. As even very small amounts of Fe were shown to dominate the electrochemistry of ta-C, implications of this study are very useful e.g. in carbon nanostructure synthesis, where irregular traces of iron can be readily incorporated into the final structures.

Surface iron levels as low as 0.4 at% (XPS) can considerably change the electrochemical properties of initially inert carbon surfaces.     

Apolipoprotein E polymorphism affects carotid artery atherosclerosis in smoking hypertensive men

OBJECTIVE: Smoking is a risk factor for increased carotid artery intima-media thickness (IMT). The apolipoprotein E (apoE) 4 allele has been associated with cardiovascular diseases, but the role of apoE in regard to intima-media thickness (IMT) has remained controversial. The objective was to investigate whether there is some gene-environment interaction between smoking and apoE polymorphism.DESIGN Cross-sectional case-control study. METHODS: IMTs of 511 hypertensive and control men were measured ultrasonographically and the apoE genotypes were determined. Genotypes with the 4 allele were pooled into one group and the genotypes without it into another. RESULTS: A significant interaction between the 4 allele and smoking affecting IMT was observed among the hypertensive smokers, as assessed by analysis of covariance. The mean carotid IMT was significantly greater (1.01 versus 0.90 mm, P = 0.003) in the 4 carriers than in the subjects without 4 among the hypertensive smokers. The number of plaques was also significantly higher. No differences were found in the other subjects (hypertensive non-smokers or controls). Linear regression analysis indicated that the 4 allele was an independent determinant of IMT in the hypertensive smokers but not in the other subjects. The estimated average effect of the 4 allele on the mean IMT in the hypertensive smokers was 0.088 mm (P < 0.001). In the oldest age group, the interaction of smoking and 4 was also seen in the control subjects.CONCLUSION: The findings suggest that the 4 carriers are particularly susceptible to the atherogenic effects of smoking. This interaction is particularly clear in hypertensive subjects.