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Summary Background & aims Abnormalities of parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) secretion may cause calcium-phosphate (Ca–P) metabolism disorders in nephrolithiasis. Post-phosphate-load alterations in serum Ca, P and PTH, phosphaturia and calciuria enable monitoring hormonal regulation of Ca–P homeostasis. Our study aimed to determine differences in: 1.selected Ca–P metabolism parameters between healthy and kidney-stone-forming individuals, 2.PTH and FGF23 secretion induced by sodium-phosphate-load(NaP-load) in patients with/without hypercalciuria, 3.secretion of Ca–P related hormones in patients with low and normal/high serum concentrations of 25-hydroxyvitamin D3 (25OHD3). Methods Sodium phosphates NaH2PO4/Na2HPO4-100mmol were administered orally for five days in 19 hypercalciuric [urinary Ca(U–Ca) 6.5 ± 1.7 mmol/d]–HSF, 35 normocalciuric (2.5±1 mmol/d)–NSF stone-forming patients and 19 controls (U–Ca 2.5 ± 1.4 mmol/d)–CG. On days 1 and 5 PTH-,FGF23-,Ca-,P were determined before and after NaP-load. The areas under PTH, FGF23 curves (AUC) were calculated. U–Ca, urinary phosphate (U–P) and sodium (U–Na) were also determined. Results Following NaP-load, patients and controls exhibited expected alterations in Ca–P homeostasis. Despite changes in phosphate and PTH, no differences in FGF23 concentrations were observed. Patients differed from controls in having higher AUCPTH, calciuria and natriuresis, taking longer for PTH and P to normalize and lack of correlation between AUCPTH and phosphaturia. Post-NaP-load hypocalciuric effect of PTH secretion in NSF was less pronounced than in CG. In the HSFs, the hypocalciuric effect was more pronounced than in NSFs, but insufficient to correct hypercalciuria. In all stone-formers with low 25OHD3 concentrations, the AUCFGF23 was significantly increased on first (1215 ± 605vs766 ± 315 p = 0.0457) and fifth days (1211 ± 641vs777 ± 299 p = 0.041) of NaP-load, compared to normal/high 25OHD3-patients. Hypercalciuric patients with low 25OHD3 concentrations had greater AUCPTH5 than those with normal/high 25OHD3 (1005 ± 401vs835 ± 220 p = 0.0341). Conclusions Compared to controls, kidney-stone-forming patients exhibited enhanced PTH secretion after NaP-load. The HSFs showed a more pronounced hypocalciuric effect than NSFs, but insufficient to correct hypercalciuria. In hypercalciuric stone-formers with low 25OHD3, FGF23 engagement in hyperphosphatemia reduction increased.

Wstep: Leptyna reguluje odpowiedź immunologiczną organizmow. Mlodziencze idiopatyczne zapalenie stawow (MIZS) jest przewleklą chorobą stawow u dzieci prowadzącą do przewleklych zmian w narządach ukladu ruchu. Material i metody: U dzieci z MIZS (n = 42) i zdrowych osobnikow (n = 28) analizowano nastepujące parametry: stezenie leptyny (LEP), wskaźnik masy ciala (BMI), hematokryt (HTC), zawartośc hemoglobiny (HB), liczba elementow morfotycznych krwi (WBC, LYMPH), odczyn OB i obecnośc przeciwcial ANA Hep-2. Grupe MIZS podzielono na: dzieci dluzej chorujące (51–148 miesiecy) n = 22 (IA) i krocej chorujące (2–18 miesiecy) n = 20 (IB). Wyniki: Tylko u 58,3% dzieci grupy IA i 50% dzieci grupy IB potwierdzono obecnośc przeciwcial przeciwjądrowych ANA Hep-2. U chorych dzieci wykazano wyzsze poziomy LYMPH i OB oraz wieksze zroznicowanie wynikow, w porownaniu do dzieci zdrowych. Najwyzsze stezenie LEP dla grupy IA wynosilo 37,50 ng/cm3, (Me 5,85) dla IB 40,10 ng/cm3, (Me2,46), w porownaniu z IC, gdzie wynosilo odpowiednio 3,74 ng/cm3 (Me 2,85). Średnia wartośc BMI dla grupy IA wynosila 16,61 kg/m2, dla IC 18,91 kg/m2, a mediana dla IB 15,89 kg/m2 . U dzieci z BMI l 23 kg/m2, grupy IA i IB, stwierdzono nizsze stezenia leptyny w porownaniu z grupą kontrolną (p = 0,04). Stwierdzono wplyw schorzenia na zroznicowanie stezenia leptyny w przeliczeniu na BMI w obu grupach dzieci chorych. U chorych dzieci, z krotszym czasem trwania choroby, wykazano wieksze zroznicowanie wartości stezenia leptyny w przeliczeniu na BMI, niz u zdrowych. Wnioski: Dzieci z mlodzienczym idiopatycznym zapaleniem stawow z BMIl23 kg/m2 mają nizsze stezenie leptyny niz dzieci grupy kontrolnej. Dzieci z MIZS z krotszym czasem trwania choroby, charakteryzują sie wiekszym zroznicowaniem stezenia leptyny w przeliczeniu na jednostke BMI, w porownaniu ze zdrowymi dziecmi. (Endokrynol Pol 2015; 66 (5): 417–421)

Objective To assess possible changes in leptin and ghrelin secretion due to etanercept in juvenile idiopathic arthritis (JIA). Methods 50 patients with JIA and 16 age-matched controls were enrolled into this prospective, cross-sectional study. Serum leptin, total and acyl ghrelin were measured in addition to white blood cell (WBC) and lymphocyte counts. Results 25 patients received etanercept and 25 conventional therapies (including methotrexate) for JIA. There was no difference between treatment and control groups in leptin or ghrelin levels and no evidence of a relationship between leptin and ghrelin in patients with JIA. In all children with JIA there was a correlation between leptin and body mass index (BMI). However, compared with children in the conventional treatment group, children in the etanercept group showed a positive correlation between total ghrelin and BMI and those with a low BMI showed a negative correlation between acyl ghrelin and BMI. Conclusion No differences in leptin and ghrelin concentrations were found when patients with JIA and controls were compared or when patients who received etanercept were compared with those who received conventional treatment for JIA.

The study aimed to evaluate the impact of adenosine receptors (ARs) on human colon tumor cells (HCT 116, HT-29) growth and sensitivity to 5-Fluorouracil (5-FU) an anticancer chemotherapeutic drug. The exposure of cancer cells to a selective A(3)-AR agonist (IB-MECA) resulted in an increase in HT-29 cells number, whereas the number of HCT 116 cells decreased significantly. In the presence of IB-MECA (1 μM) the percentage of apoptotic HT-29 cells significantly decreased, whereas the number of apoptotic and necrotic HCT 116 cells increased by 3- and 2,5-fold, respectively. The application of a selective A(2A)-AR agonist resulted in the increased survival of HCT 116 cells, but not HT-29 cells. The blockade of A(2A)-AR with ZM 241385 (0.1 μM) significantly increased the cytotoxicity of 5-FU (1 μM) in HCT 116 cells but not in HT-29 cells. The suppression of A(3)-AR with MRS 1523 (1 μM) increased the sensitivity of HT-29 cells to 5-FU while response of HCT 116 cells to 5-FU decreased. The growth promoting effect of IB-MECA in HT-29 cells was associated with the decreased intracellular cAMP level, whereas IB-MECA growth inhibitory effect in HCT 116 cells was abolished by okadaic acid (2 nM) indicating the involvement of protein phosphatase PP2A.

I. Maciejewska-Paszek, E. Grochowska-Niedworok, M. Wardas, M. Skiba:Iron, Zinc and Copper in Selected Tissues of Rabbits under Increasing Exposure to Iron. Acta Vet. Brno 2005, 74: 551-555. The aim of this study was to demonstrate the disturbance of zinc/copper balance in tissues as the possible accelerating factor of liver damage after short- and long-term exposure to high doses of iron in case of its accidental overdosing or experimental haemochromatosis. Thirty chinchilla rabbits were administered Jectofer /iron (III) - sorbitol iron complex/ Short-term administration was given to groups A and B, respectively. Long term administration was given to groups C, D and E, respectively. The contents of metals in the fur, muscles, skin and liver were determined by atomic absorption spectrometry (AAS). After short-term administration the highest concentrations of iron in comparison to the control group were observed in liver (about 42-46%) at each collection (p < 0.05), copper concentration in liver slightly decreased (≈23%), but increased in other tissues (by a maximum of 55%). Accumulation of zinc in fur was stable, but a decrease in other tissues like liver, muscles and skin was observed (4 - 35%). After long-term administrations changes in zinc concentration were found (higher in the fur of groups C and D and in the liver in group E; lower in the skin of groups: C and E). On the other hand, the long-term administration of Jectofer caused a decrease in copper concentration in fur (23-70%) but caused a 3-to-5 fold increase in the skin of experimental rabbits. Short-term as well as long-term administration of iron affect changes of copper/zinc equilibrium concentrations in different tissues and in livers of rabbits.

Background: Ghrelin is a stomach-produced polypeptide hormone that stimulates hunger and secretion of growth hormone. Abnormalities in ghrelin secretion are well documented in obese patients, but explored little in patients with various forms of hypertension. Notably, ghrelin is indirectly involved in blood pressure regulation in pregnancy induced hypertension. Material and methods: The present study aimed to assess ghrelin concentration in venous blood of 19 nonpregnant (NP), 20 healthy pregnant (HP) and 20 hypertensive pregnant (PIH). It also included assessing blood ghrelin concentration of 21 obese hypertensive pregnant (OPIH) women before and one hour after eating. Ghrelin secretion was estimated 1-3 days before delivery. Results: All experimental groups of pregnant women (HP, PIH, and OPIH) showed significantly reduced ghrelin plasma level as compared with NP (812 ± 83, 716 ± 66, and 717 ± 52 vs 1057 ± 74, respectively). We found no significant ghrelin reduction after eating in obese hypertensive pregnant women. The blood ghrelin concentration in pregnant women negatively correlated with mean arterial pressure. In spite of the differences in ghrelin concentration in women, whom a decrease in ghrelin concentration after a standard meal was observed compared to women, who didn’t reduce of ghrelin secretion no differences were found in mean arterial pressure. Conclusion: The relationship between arterial hypertension and ghrelin secretion disorders during hypertensive pregnancy is uncertain and requires further examination.

Paracetamol has properties that make it useful in many kinds of drugs that are readily available to users. These drugs are often used for extensive periods of time without a doctor's supervision, which might lead to unexpected overdose. The aim of this work was to assess the extent of liver damage in rabbits after administering them with paracetamol for approximately 2 months. The results we obtained suggest that paracetamol administered for a long time causes liver function impairment. It was, however, not possible to determine the impairment by measuring the activity of aspartate aminotransferase (AST), alanine aminotransferase (ALT) or gamma-glutamylotranspeptidase (GGTP). It was determined by measuring the concentration of ketone bodies and arterial ketone body ratio (AKBR) value. Even when taken in small doses, paracetamol causes changes in liver metabolism when taken for an extended period of time.

The research was carried out on 56 Chinchilla rabbits. The rabbits were divided into 8 groups with one control group. By means of stomach tube the rabbits were administered respectively: carbon tetrachloride (CCl4), synthetic analogue of prostaglandin misoprostol, CCl4 with misoprostol, indomethacin, misoprostol with indomethacin and CCl4 with misoprostol and indomethacin simultaneously. In order to confirm cytoprotective activity of prostaglandin E1 synthetic analogue in experimental acute hepatocellular damage, we measured in arterial blood the concentration of acetoacetate and beta-hydroxybutyrate and calculated molar ratio of their concentrations. The molar ratio of acetoacetate to beta-hydroxybutyrate which had been calculated for individual groups, regardless of the observed changes in ketone bodies' concentrations, in the case of rabbits which were administered CCl4 with misoprostol, had values similar to the ones obtained for the control group. The smallest value of the ketone body concentration ratio was stated at rabbits which were given only CCl4. The results of the research carried out unambiguously indicate hepatoprotective action of the synthetic analogue PGE1 which was administered to the rabbits.