Background. Current studies claim that peptides such as leptin, adiponectin, ghrelin, and nesfatin-1 found in breast milk may be responsible for the growth of infants. Therefore, we aimed to determine the association between breast milk total ghrelin and nesfatin-1 levels and anthropometric measurements of infants who were small for gestational age (SGA). Methods. 20 SGA and 20 appropriate for gestational age (AGA) infants were enrolled in the study. Anthropometric measurements of infants were carried out at birth, 1st, and 4th months. In addition, total ghrelin and nesfatin-1 levels in the breast milk were concomitantly measured. Results. Total ghrelin at the 4th month in breast milk waslower-level in the SGA group (p=0.015). In both groups, nesfatin-1 levels at the 4th month were lower than the values at the 1st month. Additionally, nesfatin-1 levels of SGA infants at the 4th month were higher (p=0.035). Conclusions. Breast milk total ghrelin and nesfatin-1 levels differed in both groups, and it is probably referred to the growth discrepancy of these infants during the first months of life. Furthermore, we consider that higher breast milk nesfatin-1 levels at the 4th month may be a preventive against obesity in SGA infants who have potential risk for obesity in childhood and adulthood.

OBJECTIVES: This study was aimed to explore the effects of follistatin on cisplatin-induced renal dysfunction, histopathological changes, apoptosis, infl ammation and oxidative damage in rats. BACKGROUND: Follistatin plays an important role in the developmental and regeneration processes of kidney by blocking the actions of activin, which is a member of transforming growth factor-β superfamily. METHODS: Twenty seven rats were separated into 4 equal groups: Control, Cp (cisplatin, 6 mg/kg, intrapertoneally (ip)), F1 (cisplatin + 1 μg/day follistatin ip for 4 consecutive days) and F4 (cisplatin + 4 μg/day follistatin ip single dose) groups. Renal health was monitored by blood urea nitrogen, serum creatinine and histological analysis. Apoptosis, infl ammation and oxidative stress was investigated in kidney tissue. Activin A levels in serum and kidney were evaluated as well. RESULTS: Follistatin administration showed a considerable nephroprotective effect against cisplatin-induced nephrotoxicity by preventing renal functional and structural abnormalities, apoptosis and infl ammation. The activin A levels in both serum and kidney were also suppressed by follistatin administration. CONCLUSION: Exogenous follistatin ameliorates acute kidney injury, by blocking activin A. The renoprotective effect of follistatin against cisplatin-induced nephrotoxicity appears to be associated with its anti-infl ammatory, antiapoptotic and direct nephroprotective actions (Tab. 1, Fig. 7, Ref. 23).

Our aim was to evaluate the acute cardiac toxicity of adjuvant trastuzumab treatment and its possible relation to changes in oxidative stress. Electrocardiographic and echocardiographic tissue Doppler imaging (TDI) parameters, activity of antioxidant enzymes (superoxide dismutase; SOD), and products of oxidative stress (malondialdehyde; MDA) were analyzed in 30 patients with early-stage breast cancer who had adjuvant trastuzumab treatment. There was a significant prolongation of QT interval after trastuzumab treatment. There was also a significant decrease in left ventricular ejection fraction (LVEF), TDI-derived S' parameters, and SOD enzyme activity and increase in MDA levels after trastuzumab infusion. There was a positive correlation between changes in SOD activity and LVEF and a negative correlation between changes in MDA levels and LVEF. This study demonstrated a correlation between decreases in LVEF and increases in products of the oxidative stress in patients who had adjuvant trastuzumab treatment.

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