PSXVI-10 The effectiveness of using the enzyme-mineral complex in the nutrition of broiler chickens

The aim of the study was to study the effect of a complex of a multienzyme feed additive (Axtra® XAR 102 TPT (Danisco Animal Nutrition) 0.05% of finished feed; I gr) and in combination with ultrafine particles (UFP) of Cu (1.25 mg / kg; II gr) on productivity and morphobiochemical parameters of blood of broiler chickens (BC). BC were divided into 3 groups (n = 15). The results showed that the combined use of the enzyme preparation (EP) and Cu UFPs has a greater effect on the increase in live weight [19.6% (P < 0.05)]. The introduction of only an EP into the diet has a lesser effect on the increase in live weight, which was 18.8% ahead of the control. In the experimental groups, there was an increase in the coefficient of digestibility of nutrients (P < 0.05). The addition of Cu UFPs increased the digestibility of crude fat [3.3% (P < 0.05)]. Analysis of metabolites in blood serum demonstrates the absence of the toxic effect of the introduced additives. There was a decrease in aspartate aminotransferase: in group I by 8.3%, in group II by 4.6% (P < 0.05). The composition of the lipid profile changed, stimulation of erythropoiesis and an increase in the amount of hemoglobin were registered both with joint and separate feeding of the EP and Cu UFPs. Thus, the introduction of just an EP reduced cholesterol levels by 10%, and in combination with Cu UFPs by 2.15%, triglycerides by 33.1% (P < 0.05). Thus, it was found that the combination of a multi-enzyme preparation and Cu UFPs has the potential to be used as a biologically active feed additive and causes an increase in the digestibility, and therefore, the productivity of BC. The research was carried out with financial support from RSF (20-16-00078).

Renal Medicine

The kidney causes problems for medical students and junior doctors alike— the convoluted journey from plasma to urine, the conundrum of what is reabsorbed and excreted where, and the tangled web of the glomerulonephritides are traditionally learnt, rather than actually understood. As in all clinical medicine, a good place to start is with the fundamen­tals of the organ in question. Passage from plasma to urine follows the pathway: ● Blood ● Glomerulus ● Tubules ● Collecting duct ● Ureter ● Bladder ● Urethra. The primary functions of the kidney are: ● Removal of toxins ● Electrolyte homeostasis ● Maintenance of acid– base balance ● Activation of vitamin D ● Stimulation of erythropoiesis ● Maintenance of blood volume. The challenge then is to implement these basics by being sensitive to deviations from normal physiology: recognizing the accumulation of any potential toxins (hyperkalaemia, uraemia, and acidosis) or the lack of any synthetic products (hypocalcaemia and anaemia), suggesting triggers for such deviations, and pinpointing the specific parts of the anatomy that may be malfunctioning in some way so as to cause impairment. Despite its bad reputation, the kidney reveals more about itself than any other organ and, in theory, should be the easiest to monitor. It achieves this through its raison d’être: urine. Its presence, absence, con­tents, smell, and colour offer a running commentary on the activity of the renal tract at any given point in time— it is the internal, intangible work­ings of specialized cells made physical, measurable, and dippable. So, far from being those much- feared Objective Structured Clinical Examination (OSCE) stations, the dipstick and the catheter are our friends. Or they should be, for it is our ability to harness the information that they pro­vide, allied to the series of numbers on the oft- requested ‘U&Es’ (urea and electrolytes), against a background of wide- ranging symptoms that will make us sensitive to the running of the kidney. This— not just our ability to regurgitate the three types of renal tubular acidosis— is what is at stake in this chapter.

TOXIC EFFECTS ASSESSMENT OF NICKEL OXIDE NANOPARTICLES BY INHALATION

The article presents in an experiment obtained principal results based on repeated low-level inhalation exposures of laboratory animals (white rats, outbred) to nickel oxide nanoparticles with a diameter of (23 ± 5) nm, 4 hours a day, 5 times a week for up to 10 months in a «nose only» installation. It was shown that non-specific body reactions to the action of NiO NPs include: diverse manifestations of systemic toxicity with a particularly pronounced influence on liver and kidney function, redox balance, damage to some areas of brain tissue, associated with proven movement of the nanoparticles themselves from the nasal mucosa along the olfactory tract; some cytological signs of probable development for allergic syndrome; paradoxically low severity of pulmonary pathology by pneumoconiotic type explained by a small chronic delay of nanoparticles in the lungs; the genotoxic effect of the organismal level, even at those low levels of chronic exposure, at which systemic toxicity is rather poorly. Along with that, NiO NPs also induce phase-stimulation of erythropoiesis, which is relatively specific for the toxic nickel effects.

Studies of haematological parameters of Oreochromis niloticus exposed to Cadmium Chloride (CdCl2, 2H2O)

The effects of Cadmium Chloride on the specimen Nile tilapia (Oreochromis niloticus) were examined for evaluation as acute toxicity for 96 hours. From the recorded information using Probit Analysis-Finney Method [Log-normal Distribution] the results revealed the mean 96 hour LC50 value to be 3.5095 mg/L indicating very high potential toxicity. Also derived value for mean NOEC=0.9062 mg/L defined safe limits of cadmium. In order to assess the effect of prolonged exposure of low concentration of cadmium haematological assessment was made after 24 hour, 7 days and 15 days of exposure. The study of haematological parameters demonstrated significant reduction in Red Blood Cell count, Haemoglobin, Haematocrit and Mean Corpuscular Haemoglobin Concentration (MCHC) and Mean Corpuscular Haemoglobin (MCH); while elevation was reported in Mean Corpuscular Volume (MCV). Leading to conclusion that mature RBCs are destructed and the erythrocyte production is inhibited due to reduction of haemesynthesis. Stimulation of erythropoiesis is considered as one of the reasons for decrement in values of Haemoglobin, Haematocrit and RBC count. DOI: http://dx.doi.org/10.3126/ije.v4i2.12631 International Journal of Environment Vol.4(2) 2015: 116-127

Glucose-lowering therapies in patients with diabetes mellitus and chronic kidney disease

Expansion of diabetic population (predominantly due to type 2 diabetes mellitus) with chronic kidney disease (CKD) comorbidityconstitutes one of the major challenges in modern medicine.Throughout the course of diabetes nephropathy development, from its debut to the terminal stage, survival rate and quality of life arelower than those of other categories of patients. This indicates crucial role of hyperglycemia in accelerated metabolic degradation typicalof CKD.Renal disease severely narrows the spectrum of available glucose-lowering agents. Concurrent treatment for hypertension and dyslipidemia,as well as anti-platelet therapy and stimulation of erythropoiesis becomes a complex issue. A creative and patient-orientedapproach with clear metabolic and cardiovascular goals should be instrumental in its solution.

Pharmacologic inhibition of hepcidin expression reverses anemia of chronic inflammation in rats

Anemia of chronic inflammation (ACI) is the most frequent anemia in hospitalized patients and is associated with significant morbidity. A major underlying mechanism of ACI is the retention of iron within cells of the reticuloendothelial system (RES), thus making the metal unavailable for efficient erythropoiesis. This reticuloendothelial iron sequestration is primarily mediated by excess levels of the iron regulatory peptide hepcidin down-regulating the functional expression of the only known cellular iron export protein ferroportin resulting in blockade of iron egress from these cells. Using a well-established rat model of ACI, we herein provide novel evidence for effective treatment of ACI by blocking endogenous hepcidin production using the small molecule dorsomorphin derivative LDN-193189 or the protein soluble hemojuvelin-Fc (HJV.Fc) to inhibit bone morphogenetic protein-Smad mediated signaling required for effective hepcidin transcription. Pharmacologic inhibition of hepcidin expression results in mobilization of iron from the RES, stimulation of erythropoiesis and correction of anemia. Thus, hepcidin lowering agents are a promising new class of pharmacologic drugs to effectively combat ACI.

A rapid and simple assay to determine pegylated erythropoietin in human serum

Stimulation of erythropoiesis by the third-generation erythropoietin drug, continuous erythropoietin receptor activator (CERA), a pegylated derivative of epoetin-β, has provided valuable therapeutic benefits to patients suffering from renal anemia, but has also rapidly found application as an illicit performance-enhancing strategy in endurance sports. We present here a novel method for selective determination of CERA in serum, based on polyethylene glycol precipitation, followed by a commercial homogeneous immunoassay. The developed method was highly discriminating between serum samples from CERA-treated patients and control subjects, as the covalently linked polyethylene glycol chain in CERA strongly enhanced the solubility of the protein in a polyethylene glycol-containing medium. Intravenous administration of CERA could be detected for several weeks in the majority of subjects tested. This assay outperforms the currently available CERA detection methods in terms of simplicity, convenience, cost, and throughput, making it ideal as a screening tool for doping control.