Corrigendum to "Behaviour of the Foramen Ovale Flow in Fetuses with Intrauterine Growth Restriction".

[This corrects the article DOI: 10.1155/2018/1496903.].

Fructose-1,6-Bisphosphate Prevents Bleomycin-Induced Pulmonary Fibrosis in Mice and Inhibits the Proliferation of Lung Fibroblasts.

Pulmonary fibrosis is a specific form of interstitial pneumonia. In addition to the idiopathic cause, it may be caused by drugs such as bleomycin (BLM)-used in the treatment of tumors. Fructose-1,6-bisphosphate (FBP) is a high-energy endogenous glycolytic compound that has antifibrotic, anti-inflammatory, and immunomodulatory effects. The aim of this study was to investigate the effects of FBP on both BLM-induced pulmonary fibrosis in mice and in a human embryonic lung fibroblast (MRC-5) culture system. C57BL/6 mice were divided into four groups: control, FBP, BLM, and BLM plus FBP. A single dose of bleomycin (7.5 U/kg) was administered intratracheally, and survival, body weight, Ashcroft score, and histological analysis were evaluated. Pulmonary function and bronchoalveolar lavage fluid (BALF) were also evaluated after a single dose of bleomycin (1.2 U/kg-intratracheally). Treatment with FBP (500 mg/kg) was given on day 0 intraperitoneally. Fibroblasts (MRC-5 cells) were used to access the effect of FBP in vitro. In vivo, FBP increased the survival rate and reduced body weight loss (BLM vs. BLM plus FBP-p < 0.05). FBP also prevented BLM-induced loss of pulmonary function and decreased BALF inflammatory cells, level of fibrosis, and superficial collagen density (p < 0.05). In vitro, FBP (0.62 and 1.25 mM) had inhibitory activity on MRC-5 cells and was able to induce senescence in fibroblasts. These results showed that FBP has the potential of reducing the toxic effects of BLM and may provide supportive therapy for conventional methods used for the treatment of cancer.

Behaviour of the Foramen Ovale Flow in Fetuses with Intrauterine Growth Restriction.

Background: Foramen ovale (FO) flow may be altered in IUGR. This study was designed to test this hypothesis. Methods: Forty pregnant women (24-38 weeks) were divided into 3 groups: group I (IUGR), group II (adequate growth and maternal hypertension), and group III (normal controls). Impedance across the FO was assessed by the FO pulsatility index (FOPI): (systolic velocity - presystolic velocity)/mean velocity. Statistical analysis utilized ANOVA, Tukey test, and ROC curves. Results: Mean FOPI in IUGR fetuses (n = 15) was 3.70 ± 0.99 (3.15-4.26); in the group II (n = 12), it was 2.84 ± 0.69 (2.40-3.28), and in the group III (n = 13), it was 2.77 ± 0.44 (2.50-3.04) (p=0.004). FOPI and UtA RI were correlated (r = 0.375, p=0.017), as well as FOPI and UA RI (r = 0.356, p=0.024) and, inversely, FOPI and MCA RI (r = -0.359, p=0.023). Conclusions: The FO flow pulsatility index is increased in fetuses with IUGR, probably as a result of impaired left ventricular diastolic function.