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The presence of either microbial-associated or sterile IAI was associated with increased amniotic fluid cathepsin-G concentrations in pregnancies complicated by PPROM. Amniotic fluid cathepsin-G appears to be a potential marker of IAI.

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The obtained results may indicate immaturity of thrombopoiesis in newborns born late preterm. Decrease in platelet count, platelet hematocrit and large platelets can cause disturbances in the hemostatic system and lead to bleeding complications and can increase the risk of infections. Morphological parameters of blood platelets in infants born late preterm differ from those of term neonates as in other preterm infants. This reflects the immaturity of this newborn and shows the need to pay special diagnostic and therapeutic care to them.

Premature ovarian insufficiency (POI) is defined as a loss of ovarian function before the age of 40 years, with a prevalence rate estimated at approximately 1%. It causes infertility and is related to serious long-term health consequences, including reduced life expectancy, increased cardiovascular risk, decreased bone mineral density and neurological disorders. There is currently no effective therapy for POI that is widely available in clinical practice; therefore, the treatment of patients with POI is based on hormone replacement therapy. One of the recent advances in the understanding of the pathophysiology of POI has been the role of microRNAs (miRNAs) and other noncoding RNAs (ncRNAs) in the disease. Moreover, intensive research on human folliculogenesis and reproductive biology has led to the development of novel promising therapeutic strategies with the use of exosomal miRNAs derived from mesenchymal stem cells to restore ovarian function in POI patients. This narrative review focuses on the new studies concerning the role of ncRNAs in the pathogenesis of POI, together with their potential as biomarkers of the disease and targets for therapy.

A substantial number of patients with preterm labor and delivery do not show clinical signs of infection, however, it is the subclinical form which is the main causative factor and often results in premature delivery. The hitherto commonly applied methods of inflammation detection are based either on potentially hazardous amniocentesis or still insufficient inflammation-related protein measurement in the serum or other biological fluids.The advent of new "omics" technologies has led to a paradigm-shift in experimental approach which tends to primarily generate rather than form hypotheses. This has resulted in a surge of wealth of data composed of sets of individual or clusters of new genes and proteins that can be of potential importance as new markers of inflammation leading to preterm labor. It is hoped that as a result of those new methodologies the overall perception of medical research and practice would gradually change from reductionist to systems approach. Despite several successes of reductionism in the diagnosis and treatment of preterm labor it seems that system-based methodology would contribute to a more favorable personalized rather than one-for-all patient assistance. In this review we present the current knowledge on this new attractive field of medical studies with emphasis on early detection of infection related with preterm labor.

Current treatment of painful periods and other symptoms related to primary dysmenorrhea (PD) is usually commenced with non-steroidal anti-inflammatory drugs or oral contraceptives, which fails in about 10% of affected patients. Tamoxifen, a selective estrogen-receptor modulator (SERM), has been demonstrated to directly inhibit uterine contractions, causing improvement in uterine blood flow. It could be considered for application in selected groups of dysmenorrheic patients, for instance carriers of breast cancer-associated antigen (BRCA) genes, breast cancer survivors or women with advanced endometriosis. Thus the aim of the present study was to investigate the effect of short-term treatment with tamoxifen on PD and PD-related symptoms, as well as its direct effect on parameters of intrauterine pressure during the painful menstruation, in a group of dysmenorrheic patients. After two cycles of administration of tamoxifen we noted a significant decrease in bleeding together with reductions in the severity of menstrual cramps, diarrhea, headache, fatigue and anxiety. In intrauterine pressure assessments, tamoxifen significantly decreased propagation of uterine contractions. In conclusion, SERMs such as tamoxifen may constitute a therapeutic option in selected groups of patients, improving dysmenorrheic symptoms. Additionally to its receptor-mediated effects, tamoxifen was shown to exert a direct influence on uterine contractile activity that may explain the decrease of menstrual pain and cramps noted in the studied group.

Background: The exact role of individual inflammatory factor in heart failure with reduced ejection fraction (HFrEF) remains elusive. The study aimed to evaluate three monocyte subsets (classical-CD14++CD16−, intermediate-CD14++CD16+, and nonclassical-CD14+CD16++) in HFrEF patients and to assess the effect of the cardiac resynchronization therapy (CRT) on the changes in monocyte compartment. Methods: The study included 85 patients with stable HFrEF. Twenty-five of them underwent CRT device implantation with subsequent 6-month assessment. The control group consisted of 23 volunteers without HFrEF. Results: The analysis revealed that frequencies of non-classical-CD14+CD16++ monocytes were lower in HFrEF patients compared to the control group (6.98 IQR: 4.95–8.65 vs. 8.37 IQR: 6.47–9.94; p = 0.021), while CD14++CD16+ and CD14++CD16− did not differ. The analysis effect of CRT on the frequency of analysed monocyte subsets 6 months after CRT device implantation showed a significant increase in CD14+CD16++ (from 7 IQR: 4.5–8.4 to 7.9 IQR: 6.5–9.5; p = 0.042) and CD14++CD16+ (from 5.1 IQR: 3.7–6.5 to 6.8 IQR: 5.4–7.4; p = 0.017) monocytes, while the frequency of steady-state CD14++CD16− monocytes was decreased (from 81.4 IQR: 78–86.2 to 78.2 IQR: 76.1–81.7; p = 0.003). Conclusions: HFrEF patients present altered monocyte composition. CRT-related changes in the monocyte compartment achieve levels observed in controls without HFrEF.