Urinary neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, uromodulin, and cystatin C concentrations in an experimental rat model of ascending acute kidney injury induced by pyelonephritis.

Recent evidence suggests that neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), cystatin C (CysC), uromodulin (UMOD), and some interleukins (IL-6 and IL-18) can be considered as diagnostic markers of acute kidney injury (AKI). The aim of this study was to verify the applicability of four urinary (u) markers, namely uNGAL, uKIM-1, uCysC, and uUMOD, for the diagnosis of ascending AKI induced by bacterial pyelonephritis. The study included 30 female rats that were divided into three groups (n = 10 each) and were inoculated transurethrally with various doses of Escherichia coli to induce isolated pyelonephritis (group 1, 105 CFU/ml), pyelonephritis-induced AKI (group 2, 107 CFU/ml), or AKI and urosepsis (group 3, 109 CFU/ml). The inoculate contained a highly virulent E. coli strain isolated from a patient with pyelonephritis. Urine samples were obtained prior to the inoculation and 7, 14, and 21 days thereafter. The concentrations of all assessed proteins were determined in the urine samples by ELISA. All the study groups showed elevated concentrations of uNGAL and uCysC at all study time points. The concentrations of uKIM-1 in group 1 were the same as that at the baseline, whereas it was elevated in groups 2 and 3 at all study time points. The concentrations of uUMOD in groups 1 and 2 tended to decrease with the time from inoculation, whereas it rapidly increased in group 3 at 21 days postinfection. uKIM-1 seems to be the only marker of ascending AKI associated with urinary tract infection. Elevated concentrations of uNGAL, uCysC, and uUMOD were found in both AKI and isolated pyelonephritis. Thus, it can be concluded that none of these markers can be used as a single diagnostic marker of ascending AKI, as it may produce false-negative results, leading to incorrect diagnosis, lack of adequate treatment, and increased mortality risk.

Changes in viability of rat adipose-derived stem cells isolated from abdominal/perinuclear adipose tissue stimulated with pulsed electromagnetic field.

Previous experiments demonstrated that low-frequency electromagnetic field (LF-EMF) may activate cellular death pathways in proliferating cells. Therefore, we hypothesized that LF-EMF may also influence viability of highly proliferating undifferentiated adipose-derived stem cells. Obesity is classified as a civilization disease; its etiopathogenesis is presumed to include both genetic predisposition and influence of modified environmental factors, such as unbalanced diet with excess calories and/or too low physical activity. Obesity may lead to a number of metabolic disorders, including type 2 diabetes mellitus, cardiovascular diseases (associated with atherosclerosis) related to primary hypertension and ischemic heart disease, myocardial infarction and other complications. The aim of this study was to verify if LF-EMF alters viability parameters of adipose-derived stem cells (ADSCs) isolated from rats, cultured in vitro and exposed to pulsed electromagnetic field (PEMF; 7 Hz, 30 mT). ADSCs were obtained from healthy rats and animals with experimentally-induced obesity, both males and females, pups and adults. The animals were fed with chow with either low (LF diet) or high fat content (HF diet) for 21 days. Then, ADSCs were isolated from extracted adipose tissue and used to establish cell cultures. ADSCs from the first passage were exposed to PEMF three times, 4 hours per exposure, at 24-h intervals (experimentally developed protocol of PEMF stimulation). 24 hours after the last exposure to PEMF, viability parameters of ADSCs were analyzed by flow cytometry (FCM). The study demonstrated that LF diet exerted a protective effect on PEMF-exposed ADSCs, especially in the case of male and female pups. In turn, the proportion of early apoptotic cells in PEMF-treated ADSC cultures from adult female rats maintained on HF diet turned out to be significantly higher than in other experimental groups.

Prostaglandin-targeting agents and spectral heart rate variability in experimental partial bladder outlet obstruction in rats.

The purpose of this study was to determine the activity of the autonomic nervous system (ANS), using spectral analysis of the heart rate variability (HRV) in the model of partial bladder outlet obstruction (PBOO) in rats treated with selected non-steroidal anti-inflammatory drugs (NSAID): piroxicam (PRX) or meloxicam (MLX), and following administration of PGF2a prostaglandin analogue (Enzaprost F5). Neither the use of PGF2a analogue nor of MLX, caused significant changes in the HRV spectrum (except for HRV spectrum total power reduction with MLX). The use of PRX caused reduction of the total power and powers of all components of the HRV spectrum (except for VLF). Moreover, increased nLF and reduced nHF were observed. The obtained results suggest that the total prostaglandin synthesis block with a non-selective cyclooxygenase inhibitor (PRX) results in reduced ANS total activity, with decreased parasympathetic activity and a relative sympathetic predominance. The preferential cyclooxygenase-2 block (MLX) caused reduction of the total ANS activity as well, however with no clear disproportion of any part of the ANS. Therefore, prostaglandin synthesis inhibition and associated decrease of parasympathetic activity may constitute an additional and favourable feature of NSAID pharmacodynamics in the treatment of BPH.