Assessment of Hemodialysis Adequacy by Ionic Dialysance: Comparison to Standard Method of Urea Removal

Background. The hemodialysis adequacy is one of the most important issues influencing the survival of patients on maintenance hemodialysis (HD). Assessment of measuring the delivered dialysis dose using clearance × time/volume (Kt/V) index requires multiple blood sampling. New methods for assessment of dialysis dose based on ionic dialysance (ID) have been suggested. Online conductivity monitoring (using sodium flux as a surrogate for urea) allows the repeated noninvasive measurement of Kt/V on each HD treatment. In this study we have compared this method with the standard method of estimating Kt/V. Methods. We studied 24 established HD patients over a 4 week time period. Patients were dialyzed using Fresenius 4008S dialysis monitors, equipped with modules to measure ID. Data were manually collected and analyzed using the appropriate statistical software. Urea removal (UR) was measured once a week by a two-pool calculation, estimating an eKt/V. Results. The Kt/V measured by ID highly correlated with the one derived from the measurement of the UR (r = 0.8959, p< 0.0001). The ID underestimated UR by the mean of 6%. The ID varied greatly within individual patients with a median of 1.29 ± 0.22. If the eKt/V ≥ 1.2 is considered adequate, 33% of the patients would have been inadequately dialyzed. The mean HD duration to achieve an adequate dialysis was 4 hours and 47 minutes with high interpatient variability. Conclusion. The ID seems to be an easily obtained measure of the delivered dialysis dose, correlating well with standard UR method. Substantial individual variations imply that repeated measures (ideally for all treatments) are necessary to obtain a real answer to the mean treatment dose being delivered to the patients.     

Percutaneous embolization of idiopathic renal arteriovenous fistula using Amplatzer vascular plug II

Renal arteriovenous fistula (AVF) presents a rare but important condition that can be acquired, congenital, or idiopathic. Embolization techniques have recently been considered the first-line therapy in the treatment of these lesions, but they carry a possible high risk of distal migration of embolic agents into the venous and pulmonary circulation. This risk is especially important with large, high-flow fistulas. In this report, we present a case in which a 31-year-old man with a symptomatic idiopathic AVF was treated with embolization using the Amplatzer vascular plug II after unsuccessful superselective embolization using coils. This method allowed for complete occlusion of the high-flow fistula with good preservation of arterial supply to the renal parenchyma.     

Seropositivity for pathogens associated with chronic infections is a risk factor for all-cause mortality in the elderly: findings from the Memory and Morbidity in Augsburg Elderly (MEMO) Study

GeroScience - Immunostimulation by chronic infection has been linked to an increased risk for different non-communicable diseases, which in turn are leading causes of death in high- and...     

Fertility-sparing surgery for patients with malignant ovarian germ cell tumors: 10 years of clinical experience from a tertiary referral center

Archives of Gynecology and Obstetrics - To describe a case series of patients with malignant ovarian germ cell tumors (MOGCT) treated exclusively with fertility-sparing surgery (FSS) with or...     

Robustness of diffuse reflectance spectra analysis by inverse adding doubling algorithm

Analysing diffuse reflectance spectra to extract properties of biological tissue requires modelling of light transport within the tissue, considering its absorption, scattering, and geometrical properties. Due to the layered skin structure, skin tissue models are often divided into multiple layers with their associated optical properties. Typically, in the analysis, some model parameters defining these properties are fixed to values reported in the literature to speed up the fitting process and improve its performance. In the absence of consensus, various studies use different approaches in fixing the model parameters. This study aims to assess the effect of fixing various model parameters in the skin spectra fitting process on the accuracy and robustness of a GPU-accelerated two-layer inverse adding-doubling (IAD) algorithm. Specifically, the performance of the IAD method is determined for noiseless simulated skin spectra, simulated spectra with different levels of noise applied, and in-vivo measured reflectance spectra from hyperspectral images of human hands recorded before, during, and after the arterial occlusion. Our results suggest that fixing multiple parameters to a priori known values generally improves the robustness and accuracy of the IAD algorithm for simulated spectra. However, for in-vivo measured spectra, these values are unknown in advance and fixing optical parameters to incorrect values significantly deteriorates the overall performance. Therefore, we propose a method to improve the fitting performance by pre-estimating model parameters. Our findings could be considered in all future research involving the analysis of diffuse reflectance spectra to extract optical properties of skin tissue.     

The NMDA-receptor antagonist MK-801 selectively disrupts reversal learning in rats

We tested the hypothesis that inhibition of NMDA-receptors in rats would lead to a selective impairment of reversal learning in a serial reversal task in the Skinner box. Low doses of MK-801 (0.025 and 0.05 mg/kg) did not affect acquisition of the two-lever discrimination, but impaired performance during the first reversal more than during the third reversal. Similar effects were observed during the series of extinction sessions. The high dose (0.1 mg/kg) completely inhibited reversal and extinction learning, as the rats perseverated in pressing the previously rewarded lever(s). We conclude that NMDA receptor blockade leads to a selective impairment in cognitive flexibility, and shows some similarity to transient inactivation of the medial prefrontal cortex in this respect.     

Maternal pre-eclampsia as a risk factor for necrotizing enterocolitis

Objective: Similar pro-inflammatory responses are present in pre-eclampsia (PE) and necrotizing enterocolitis (NEC). We hypothesized that maternal PE is an independent risk factor for the development of NEC.

Methods: A retrospective database of all live births (2008–2011) at a tertiary center was constructed. Infant and maternal characteristics were gathered. Babies born to mothers with or without PE were compared. Data were analyzed using Mann–Whitney U, Pearson's χ², binary logistic regression and relative risks.

Results: Incidence of NEC was 1.5% in non-PE and 4.6% in the PE group (p?<?0.001), but once controlled for gestational age and birth weight, the difference lost statistical significance. PE babies were more frequently preterm (41.4% versus 14.5%, p?<?0.001) and had intrauterine growth restriction (IUGR) (10.2% versus 6.3%, p?<?0.001). Within preterm babies, 9.0% of non-PE and 10.8% of PE babies developed NEC (p?=?0.25). Effect of PE was significant in sub-group of IUGR babies, with NEC in 1.5% of non-PE and 13.6% in PE babies (p?<?0.001).

Conclusions: Maternal PE is an independent risk factor for the development of NEC in some sub-groups of babies, most notably with IUGR. Fetal hypoxia caused by abnormal placentation in PE leads to restricted growth, and may be the underlying mechanism that predisposes the newborn to NEC.     

Combined expression of tau and the Harlequin mouse mutation leads to increased mitochondrial dysfunction, tau pathology and neurodegeneration

Mitochondrial dysfunction and oxidative stress play an important role in ageing and have been implicated in several age-related neurodegenerative conditions including Alzheimer's disease (AD) and other tauopathies characterized by the presence of intracellular accumulations of the hyperphosphorylated microtubule-associated protein tau. To study the interaction between mitochondrial dysfunction and tau pathology in vivo, we generated a novel mouse model by crossbreeding two existing lines: the Harlequin (Hq) mutant mice which suffer from mitochondrial dysfunction and oxidative stress due to a lack of the mitochondrial apoptosis-inducing factor (AIF), and the P301L tau transgenic mice, a mouse model of human tau pathology.Combined expression of the Hq mouse mutation and the tau transgene in the Tau/Hq double mutant mice led to an increase in tau pathology and apoptotic neurodegeneration when compared to single expression of the two mutations. Neurodegeneration was most prominent in the dentate gyrus and was significantly increased in the cerebellum leading to aggravated motor deficits. Functional activity measurements of the mitochondrial respiratory chain (MRC) in the Tau/Hq mice revealed early decreased activities of multiple MRC complexes and depleted ATP levels which preceded neurodegeneration and elevated oxidative stress markers. These results suggest an age-dependent mutual reinforcement of the tau pathology and mitochondrial dysfunction in vivo, which may contribute to neurodegeneration in patients suffering from AD and other age-related tauopathies.