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Hormones have a harmful impact on the environment and their detection in water bodies is an urgent matter. In this work, we present and analyze a sensor device able to detect traces of the synthetic hormone 17α-ethinylestradiol (EE2) below 10-9 M in media of different complexities, namely, ultrapure, mineral and tap waters. This device consists of solid supports with interdigitated electrodes without and with a polyethylenimine (PEI) and poly (sodium 4-styrenesulfonate) (PSS) layer-by-layer film deposited on it. Device response was evaluated through capacitance, loss tangent and electric modulus spectra and the data were analyzed by principal component analysis method. While the three types of spectra were demonstrated to be able to clearly discriminate the different media, loss tangent spectra allow for the detection of EE2 concentration, with a sensitivity of -0.072 ± 0.009 and -0.44 ± 0.03 per decade of concentration, for mineral and tap water, respectively. Detection limits values were found to be lower than the ones present in the literature and presenting values of 8.6 fM (2.6 pg/L) and of 7.5 fM (22.2 pg/L) for tap and mineral waters, respectively. Moreover, the obtained response values follow the same behavior with EE2 concentration in any medium, meaning that loss tangent spectra allow the quantification of EE2 concentration in aqueous complex matrices.Gut dysbiosis in patients with chronic kidney disease (CKD) may induce chronic inflammation and increase morbidity. Phosphate-binding agents, generally used in patients with CKD, may potentially change the composition of the gut microbiota. This study aimed to compare the microbiota composition in hemodialysis patients treated with ferric citrate or calcium carbonate. read more The stool microbiota was investigated in hemodialysis patients treated with ferric citrate (n = 8) and calcium carbonate (n = 46) using 16S rRNA gene amplicon sequencing profiling using linear discriminant analysis of effect size. Further predictive functional profiling of microbial communities was obtained with Tax4Fun in R. Hemodialysis patients treated with calcium carbonate had a significantly reduced microbial species diversity (Shannon index and Simpson index) and an increased microbial alteration ratio compared with patients treated with ferric citrate. A distinct microbial community structure was found in patients treated with ferric citrate, with an increased abundance of the Bacteroidetes phylum and a decreased abundance of the phylum Firmicutes. Members of the order Lactobacillales were enriched in patients treated with calcium carbonate, whereas taxa of the genera Ruminococcaceae UCG-004, Flavonifractor, and Cronobacter were enriched in patients treated with ferric citrate phosphate binder. In conclusion, Ferric citrate therapy results in a more diverse microbiome community compared to calcium carbonate therapy in hemodialysis patients with phosphate binder treatment. The gut microbiome reflects the phosphate binder choice in hemodialysis patients, further affecting the physiological environment in the gastrointestinal tract.

Restless legs syndrome (RLS) is a common sensory motor neurological disorder that is related to iron-dopamine dysregulation and immune system alteration. We aimed to assess the effects of serum hepcidin, an iron-regulating hormone, in drug-naive RLS patients compared to healthy controls and to evaluate its role in helping to predict clinical improvement after treatment with dopamine agonist.

Nonanemic and drug-naive RLS patients (

= 18) and healthy controls (

= 15) were enrolled. The serum hepcidin and iron-related values in the serum were measured upon the first visit in both groups and 12 weeks later after dopaminergic treatment in 12 patients. Information about sociodemographic characteristics, sleep-related profiles, mood and anxiety was obtained upon the first visit in all participants as well as after treatment in RLS patients.

Serum hepcidin levels exhibited no significant differences between patients with drug-naïve RLS and healthy controls at diagnosis (7.1 ± 2.4 vs. 7.0 ± 3.2 ng/mL,

= 0.357). Decreased hepcidin levels were significantly associated with decreased RLS severity (β = 0.002, 95% CI = 0.00-0.00,

= 0.005) and improved quality of life (β = 0.002, 95% CI = 0.00-7.01,

= 0.044) in a dose-dependent manner after 12 weeks of treatment with a dopamine agonist. This association was independent of age, sex, inflammatory markers, sleep quality, insomnia, daytime sleepiness, depression and anxiety.

This study demonstrates the role of hepcidin in evaluating the positive therapeutic response in RLS.

This study demonstrates the role of hepcidin in evaluating the positive therapeutic response in RLS.Background and objectives The aims of this study were to delineate the contribution of specific fascial layers of the myofascial unit to myofascial pain and introduce the use of ultrasound-guided fascial layer-specific hydromanipulation (FLuSH) as a novel technique in the treatment of myofascial pain. Materials and Methods The clinical data of 20 consecutive adult patients who underwent myofascial injections using FLuSH technique for the treatment of myofascial pain were reviewed. The FLuSH technique involved measuring the pain pressure threshold using an analog algometer initially and after each ultrasound guided injection of normal saline into the specific layers of the myofascial unit (superficial fascia, deep fascia, or muscle) in myofascial points corresponding with Centers of Coordination/Fusion (Fascial Manipulation®). The outcome measured was the change in pain pressure threshold after injection of each specific fascial layer. Results Deep fascia was involved in 73%, superficial fascia in 55%, and muscle in 43% of points. A non-response to treatment of all three layers occurred in 10% of all injected points. The most common combinations of fascial layer involvement were deep fascia alone in 23%, deep fascia and superficial fascia in 22%, and deep fascia and muscle in 18% of injected points. Each individual had on average of 3.0 ± 1.2 different combinations of fascial layers contributing to myofascial pain. Conclusions The data support the hypothesis that multiple fascial layers are responsible for myofascial pain. In particular, for a given patient, pain may develop from discrete combinations of fascial layers unique to each myofascial point. Non-response to treatment of the myofascial unit may represent a centralized pain process. Adequate treatment of myofascial pain may require treatment of each point as a distinct pathologic entity rather than uniformly in a given patient or across patients.

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