Introduction. Nowadays it is thought that the main cause of premature birth is subclinical infection. However, none of the currently used methods provide effective prevention to preterm labor. The aim of the study was to determine the concentration of selected chemokines in sera of patients with premature birth without clinical signs of infection (n = 62), threatened preterm labor (n = 47), and term births (n = 28). Method. To assess the concentration of chemokines in the blood serum, we used a multiplex method, which allows the simultaneous determination of 40 chemokines per sample. The sets consist of the following chemokines: 6Ckine/CCL21, Axl, BTC, CCL28, CTACK/CCL27, CXCL16, ENA-78/CXCL5, Eotaxin-3/CCL26, GCP-2/CXC, GRO (GROα/CXCL1, GROβ/CXCL2 and GROγ/CXCL3), HCC-1/CCL14, HCC-4/CCL16, IL-9, IL-17F, IL18-BPa, IL-28A, IL-29, IL-31, IP-10/CXCL10, I-TAC/CXCL11, LIF, LIGHT/TNFSF14, Lymphotactin/XCL1, MCP-2/CCL8, MCP-3/CCL7, MCP-4/CCL13, MDC/CCL22, MIF, MIP-3α/CCL20, MIP-3-β/CCL19, MPIF-1/CCL23, NAP-2/CXCL7, MSPα, OPN, PARC/CCL18, PF4, SDF-1/CXCL12, TARC/CCL17, TECK/CCL25, and TSLP. Results. We showed possible implication of 4 chemokines, that is, HCC-4, I-TAC, MIP-3α, and TARC in women with symptoms of preterm delivery. Conclusion. On the basis of our findings, it seems that the chemokines may play role in the pathogenesis of preterm labor. Defining their potential as biochemical markers of preterm birth requires further investigation on larger group of patients.

Introduction. Pregnancy-induced hypertension (PIH) is one of the main clinical problems of unexplained etiopathogenesis. New factors involved in the pathogenesis of this disease are still being searched. The available literature lacks data regarding the differences in tryptophan concentrations in physiological and PIH-complicated pregnancy. Previous studies have shown that L-tryptophan treatment reduces blood pressure in hypertensive rats. The direct vascular effects of tryptophan have not been fully explored. In this study, the stimulating effect of tryptophan on the development of PIH was revealed. The aim of the present study was to assess the differences in plasma tryptophan concentrations in physiological pregnancies and pregnancies complicated with hypertension in the third trimester. Material and methods. The study was carried on 105 complicated by PIH and 105 pregnant women with blood pressure within normal limits between 25 and 41 weeks of gestation. Tryptophan concentration was determined by the automated ion-exchange chromatography using an Amino Acid Analyser (AAA 400) by Ingos, Czech Republic. Tryptophan concentration was expressed in μmol/cm 3 plasma. Results. The mean concentration of tryptophan in the third trimester of physiological pregnancy was found to be 0.035 ± 0.009 μmol/cm

Background. Pregnancy-induced hypertension (PIH) is a significant health issue in pregnancy, complicating 7-10% of pregnancies. L-arginine is an important mediator of vasodilation with a potential preventative role in pregnancy-related hypertensive diseases. Aim of the study. The aim of the present study was to assess the differences in plasma L-arginine concentrations in physiological pregnancies and pregnancies complicated with hypertension in the third trimester. Material and methods. Plasma concentration of L-arginine was determined by ion-exchange chromatography in 210 pregnant women (25-41 weeks of gestation). Plasma L-arginine concentration was expressed in μmol/cm 3. Results. The mean L-arginine concentration was significantly higher in physiological pregnancy (0.102) than in the PIH group (0.034). The analysis of plasma L-arginine concentration in the subgroups of third trimester showed that L-arginine concentration in the PIH group decreased with increasing stage of pregnancy (25-34 hbd-0.051; 35-38 hbd-0.03; 39-41 hbd-0.02). L-arginine concentration in physiological pregnancies was the same in all subgroups (0.1). Conclusions. L-arginine may have a role in the prevention and treatment of pregnancy-induced hypertension. Further well-designed and adequately powered research is warranted.

Objectives: The aim of the study is to determine the impact of the experimental diabetes and the chronic hypoxia on pregnancy development and rat fetal body weight. Material and methods:The experiment was performed on female Wistar rats. Animals were divided into the experimental groups. I -Controls, II -Untreated diabetes, III -Insulin-treated diabetes, IV -No diabetes with chronic hypoxia, V -Untreated diabetes and chronic hypoxia, VI -Insulin-treated diabetes and chronic hypoxia. Diabetes was induced in groups II, III, V and VI with intraperitoneal injection of streptozocin (STZ) at a dose of 40 mg/kg. Chronic hypoxia was induced by placing dams (groups IV, V and VI) in conditions of 10.5% oxygen and 89.5%. Insulin was administered subcutaneously at the dose of 9 IU/kg. Starting from the 6 th day after STZ injection and chronic hypoxia conditions animals were caged together for 12 hours for 3 consecutive days to ensure fertilization. On day 21 of gestation the animals were decapitated, the fetuses were removed and weighted.Results: Mean fetal body weight in separate groups were: I -5.38 g, II -6.04g, III -5.32g, IV-5.56 g, V -3.45 g, VI -6.23 g. Conclusions:Pre-existing type 1 diabetes does not affect fetal body weight compared to healthy newborn control rats. Prolonged hypoxia does not impact on fetal body weight. Chronic hypoxia during pregnancy complicated with untreated type 1 diabetes mellitus leads to significant reduction of fetal body weight. Insulin treatment reversed the detrimental effect of chronic hypoxia on fetal development.

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