The role of sex steroids in the programming of the level of serum corticosteroid-binding globulin (CBG) in the rat has been studied at different stages of ontogenesis. The CBG content in the serum of mature female rats was 2.5 times higher than that in male rats. Sexual dimorphism of CBG content was absent in immature animals of 3-4 weeks of age. Castration of mature rats led to a 40-50% increase in CBG content. The CBG concentration in mature females or castrated adult males treated with testosterone propionate (TP; 3 mg/day for 4 days) was decreased by 40-50% compared with vehicle-treated rats. Oestradiol injection (1 microgram/day for 4 days) had no influence on CBG levels in mature male and ovariectomized adult female rats. Immature rats were castrated on days 1, 7, 14, 21, 28 or 35 of age and the CBG level was determined at 10-12 weeks of age. The CBG content of rats castrated up to day 28 of age was 2.5 times higher than that in mature males and did not differ from that in mature females. The CBG content of male rats castrated on day 35 of age was the same as that of adult castrated males. The CBG level in castrated rats treated with TP (1.25 mg for days 1-3 or 300 micrograms/day for 5 days after castration at day 7 up to day 26) did not differ from that in controls (i.e. vehicle-treated rats).(ABSTRACT TRUNCATED AT 250 WORDS)

It has been proposed that circulating HSCs play a role in graft survival after liver transplantation. The aim was to analyze the relationship between the number of HSCs before and after LDLT and liver function, immune biomarkers, and clinical outcomes in pediatric patients. We studied 15 pairs of adult healthy liver donors and pediatric recipients with ESLD. The CD34/CD45+ cell number was measured in the blood via flow cytometry, and plasma levels of immune biomarkers - via ELISA. CD34/CD45+ cell number in the recipients decreased within the first week after LDLT. The cell number before LDLT was negatively correlated with the plasma levels of CRP and the development of graft dysfunction in the early post-transplant period. After LDLT, the CD34/CD45+ cell number was positively correlated with the pretransplant plasma level of sCD40L, a T-cell activation marker. In adult liver donors, the cell number did not change within the first week after liver resection and was lower than in pediatric recipients. The results suggest that in pediatric recipients, the HSC number may be associated with graft function and could be regarded as a potential predictor of the clinical outcome after LDLT.

The transforming growth factor 1 (TGF1), whose level may depend on the polymorphism of the TGFB1 gene, is involved in the formation of myocardial fibrosis. Myocardial fibrosis in a cardiac allograft may lead to a hearts structural and functional remodeling and subsequent dysfunction. The frequency of occurrence of alleles and genotypes of the TGFB1 gene polymorphic regions rs1800469, rs1800470, and rs1800471 in heart transplant recipients and their association with graft myocardial fibrosis were analyzed. Carriers of the CC genotype (p = 0.023, OR = 0.12, 95% CI: 0.0171.0), and more often the G allele of rs1800471 (p = 0.023, OR = 7.76, 95% CI: 1.060.20), were found among heart transplant recipients less frequently than among healthy individuals. In patients with ischemic heart disease (IHD), the GG genotype was less common (p = 0.035, OR = 2.68, 95% CI: 1.0616.793), while the A allele of rs1800469 was found more frequently (p = 0.035, OR = 0.37 95% CI: 0.1480.942) than in patients with dilated cardiomyopathy (DCM). In heart transplant recipients with the AA genotype of rs1800470, myocardial fibrosis, verified by endomyocardial biopsy, was detected more often than in carriers of the G allele (OR = 10.4, 95% CI: 1.15294.538, p = 0.013). The revealed differences suggest a relationship between TGFB1 gene polymorphism and graft myocardial fibrosis. Studies on a larger group of patients would make it possible to characterize the influence of genetic factors on the formation of myocardial fibrosis in heart transplant recipients.

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