Performance of Dual-Hop Relaying Over Shadowed Ricean Fading Channels
In this paper, an analytical approach for evaluating performance of dual-hop cooperative link over shadowed Ricean fading channels is presented. New lower bound expressions for the probability density function (PDF), cumulative distribution function (CDF) and average bit error probability (ABEP) for system with channel state information (CSI) relay are derived. Some numerical results are presented to show behavior of performance gain for the proposed system. Analytical exact and lower bound expression for the outage probability (OP) of CSI assisted relay are obtained and required numerical results are compared.
Immunosuppressive drugs play a crucial role in the inhibition of immune reaction and prevention of graft rejection as well as in the pharmacotherapy of autoimmune disorders. Effective immunosuppression should provide an adequate safety profile and improve treatment outcomes and the patients’ quality of life. High-risk transplant recipients may be identified, but a definitive prediction model has still not been recognized. Therapeutic drug monitoring (TDM) for immunosuppressive drugs is an essential, but at the same time insufficient tool due to low predictability of drug exposition and marked pharmacokinetic variability. Parallel therapeutic, biochemical and clinical monitoring may successfully optimize and individualize therapy for transplanted recipients, providing optimal medical outcomes. Modern pharmacotherapy management should include new biomarkers with better sensitivity and specificity that can identify early cell damage. The aim of this study was to point out the importance of finding new biomarkers that would enable early detection of adverse drug events and cell damage in organ transplant recipients. We wanted to confirm the importance of routine biochemical monitoring in improving the safety of immunosuppressive treatment.
This study sought to compare the biometric values and intraocular lens (IOL) power obtained by standard ultrasound and optical biometry.
We examined 29 eyes in preparation for cataract surgery. None of the patients had refractive surgery or corneal anomaly. In all patients, the horizontal and vertical refractive power of the cornea was determined using a keratometer (Bausch&Lomb). The axial length of the eye was determined via A-scan ultrasound (BVI-compact-V-plus) using Hollady’s formula. The IOL power and complete biometric measurements were obtained via an IOL Master-500-Zeiss using the Hollady-2 formula. All obtained values were compared and analysed using the statistical program SPSS 20.
The average age of treated patients was 71.21±1.68 years. In 16 patients with dense cataracts (55.17%), it was not possible to determine the IOL power by optical biometry. Optical biometry obtained significantly increased axial length values of 24.04±0.29 mm compared with those obtained with ultrasound biometry (23.89±0.28 mm, p=0.003). The mean refractive cornea power values of the horizontal meridian measured using a keratometer (42.50±0.47 D) and an IOL Master (42.69±0.49 D) were not statistically different (p=0.187). The mean values of the refractive cornea power of the vertical meridian obtained using a keratometer (42.62±0.48D) and an IOL Master (43.36±0.51 D) exhibited a statistically significant difference (p=0.000). The keratometer obtained statistically significant lower mean values of corneal refractive power (42.73±0.32 D) compared with those obtained with optical biometry (43.22±0.35 D, p=0.000). Ultrasound biometry obtained significantly increased the mean values of IOL power (20.19±0.48D) compared with those obtained with optical biometry (19.71±0.48 D, p=0.018).
The large number of patients who receive an operation for dense cataracts indicate the need for representation of both biometric methods in our clinical practice.
The Investigation of Cytokines and Oxidative Stress in Patients with Systemic Lupus Erythematosus
Numerous factors can influence the onset of SLE and development of some clinical disease manifestations with various organ involvements and occurrence of characteristic symptoms and disease signs. This paper studies the balance between proinflammatory and antiinflammatory cytokines, investigates the presence of oxidative stress measuring certain prooxidative factors and determines the activation of antioxidative protection pathways aiming to establish possible correlations between the studied parameters. ELISA, enzymatic spectrophotometry and colorimetric methods were used to determine the above-mentioned parameters. The results obtained indicate that disturbed pro/antioxidative status is associated with the change of antioxidative factors, with the fall od SOD activity and increase of GPx and CAT activity in the erythrocytes of all studied groups of patients. At the same time, the cytokine production was altered, not only compared to the healthy control samples, but also in various clinical disease manifestations. Altered relationships of pro and antiinflammatory cytokines and the consequential disorders of other studied systems provide us with useful strategic targets for diagnostic monitoring and possible therapeutic interventions in SLE patients.
Background: The aim of the study was to evaluate parameters of oxidative and nitrosative stress as well as antioxidative parameters in a group of renal transplant recipients with stable graft function and no clinical signs of cardiovascular disease. We also aimed to determine the correlations among these parameters and to evaluate potential differences in all the biomarkers with regard to the immunosuppression protocol.
Methods: We enrolled 57 renal transplant recipients and 31 controls who were age and sex matched with the renal transplant recipients. All of the patients included in this study had post-renal transplant surgery at least 12 months earlier and were on standard immunosuppressive therapy. In this study, we determined thiobarbituric acid-reactive substances in plasma and red blood cells and advanced oxidation protein products, nitrosative stress parameters (asymmetric and symmetric dimethylarginine - ADMA and SDMA), and antioxidative parameters (total SH groups and catalase activity).
Results: The results of our study demonstrated that the levels of oxidative and nitrosative stress were significantly increased compared to the healthy population (p<0.01 except for plasma catalase activity p<0.05). Correlation analysis showed significant positive correlations between: ADMA and SDMA (p<0.01); ADMA and nitrates (p<0.05); SDMA and nitrates (p<0.05); between OS parameters in the experimental group; AOPP and SH groups (p<0.05) and TBARS in plasma and SH groups (p<0.01), SDMA and AOPP (p< 0.05); SDMA and TBARS in plasma (p<0.05); SDMA and SH groups (p<0.01); nitrates and SH groups (p<0.05).
Conclusion: There was no significant difference in oxidative and nitrosative stress parameters with respect to the immunosuppressive protocol.
Decreased nitric oxide (NO) production and/or impaired NO bioavailability may occur in patients with the chronic kidney disease (CKD), and could contribute to elevation of blood pressure, cardiovascular disease (CVD) and progression of renal injury in these patients. Free guanidinomethylated arginine residues occur endogenously as a result of proteolysis of post-translational methylated tissue proteins. The asymmetric dimethyl arginine (ADMA) is a competitive inhibitor of the nitric oxide synthase (NOS) enzymes. The kidney has a predominant role in ADMA elimination by combining two mechanisms; urinary excretion and metabolization of ADMA The degradation of ADMA is accomplished intracellularly by the enzyme dimethylarginine dimethylaminohydrolase (DDAH). ADMA is not only a uremic toxin, but also a strong marker of the endothelial dysfunction and atherosclerosis and a stronger independent predictor of all-cause mortality and cardiovascular outcome in patients with the chronic renal failure. There are at least four mechanisms that may explain the accumulation of ADMA in CKD: increased methylation of proteins, increased protein turnover, decreased metabolism by DDAH and impaired renal excretion. A strong positive correlation between symmetric dimethyl arginine (SDMA) and creatinine suggests that SDMA might be of value as a marker of the renal function. Reduced NO elaboration secondary to accumulation of ADMA and elevated inflammation may be important pathogenic factors for endothelial dysfunction in patients with the renal disease. Elevation of ADMA may be a missing link between CVD and CKD.
Molecular genetic testing is part of modern medical practice. DNA tests are an essential part of diagnostics and genetic counseling in single gene diseases, while their application in polygenic disorders is still limited. Pharmacogenetics studies DNA variants associated with variations in drug efficacy and toxicity, and tests in this field are being developed rapidly. The main method for molecular genetic testing is the polymerase chain reaction, with a number of modifications. New methods, such as next generation sequencing and DNA microarray, should allow simultaneous analysis of a number of genes, even whole genome sequencing. Ethical concerns in molecular genetic testing are very important, along with legislation. After molecular genetic testing, interpretation of results and genetic counseling should be done by professionals. With the example of thrombophilia, we discuss questions about genetic testing, its possibilities and promises.