microRNA-181a inhibits ocular neovascularization by interfering with vascular endothelial growth factor expression.

Aim: Excess angiogenesis or neovascularization plays a key role in the pathophysiology of several ocular diseases such as retinopathy of prematurity, diabetic retinopathy, and exudative age-related macular degeneration. microRNA-181a (miR-181a) was found highly expressed in retina and choroidal tissues. This study intends to investigate the role of miR-181a in the regulation of ocular neovascularization in different pathophysiological conditions.

Generation of lymphocytic microparticles and detection of their proapoptotic effect on airway epithelial cells.

Interest in the biological roles of cell membrane-derived vesicles in cell-cell communication has increased in recent years. Microparticles (MPs) are one such type of vesicles, ranging in diameter from 0.1 μm to 1 μm, and typically shed from the plasma membrane of eukaryotic cells undergoing activation or apoptosis.

Lymphocyte-derived microparticles induce bronchial epithelial cells' pro-inflammatory cytokine production and apoptosis.

Objective: The aim of this study was to determine if human CEM (human lymphoblastoma) T cell-derived microparticles (LMPs) could directly induce human bronchial epithelial cells (BECs) apoptosis and cytokine production. We also tested if LMPs phagocytosis by BECs played a role in mediating these effects.

Methods: We generated LMPs from CEM (human lymphoblastoma) T cells to investigate their effects on a human BEC cell line (16HBE) in vitro.

Low density lipoprotein receptor mediates anti-VEGF effect of lymphocyte T-derived microparticles in Lewis lung carcinoma cells.

Nonstop proliferation and vigorous neovascularization are two prominent characteristics of cancer. Antiangiogenic therapy has emerged as an important modality in treatment of solid tumors. Our previous work demonstrated that microparticles derived from apoptotic T-lymphocytes (LMPs) not only reduced the viabilities of high-proliferating cells, but also exhibited potent antiangiogenic effects through inhibition of the vascular endothelial growth factor (VEGF)/VEGF receptor 2 signalling pathway.

The role of lysophosphatidic acid receptor (LPA1) in the oxygen-induced retinal ganglion cell degeneration.

Purpose: Although previous studies have demonstrated that hypoxia induces retinal ganglion cell (RGC) apoptosis and that transient retinal ischemia upregulates the expression of lysophosphatidic acid (LPA) receptors, it remains to be determined whether LPA(1) receptor mediates RGC degeneration during retinopathy of prematurity (ROP). By using an immortalized RGC line (RGC-5), primary neonatal RGC cultures, and oxygen-induced retinopathy (OIR) to model ROP, the authors explored whether LPA(1) receptor induces RGC degeneration and the potential mechanisms thereof.

Methods: OIR was induced by exposing rat pups to alternating cycles of hyperoxia/hypoxia from postnatal day (P) 0 to P14.

Lymphocytic microparticles inhibit angiogenesis by stimulating oxidative stress and negatively regulating VEGF-induced pathways.

Recent studies have demonstrated that lymphocyte-derived microparticles (LMPs) impair endothelial cell function. However, no data currently exist regarding the contribution of LMPs in the regulation of angiogenesis. In the present study, we investigated the effects of LMPs on angiogenesis in vivo and in vitro and demonstrated that LMPs strongly suppressed aortic ring microvessel sprouting and in vivo corneal neovascularization.

The postnatal changes in red blood cell NO levels.

Aim: To determine the levels of RBC HbSNO and HbFe(II)NO using chemiluminescence in very low birth weight infants breathing room air, during the first 2 days of life.

Method: RBC NO values were compared to the levels obtained in cord blood at birth from infants of similar gestational age. Five infants ranging from 25 to 27 weeks of gestation were sampled between 12 and 24 h after birth.

The effect of adult hemoglobin on red blood cell nitric oxide levels during fetal development.

Objective: To compare the levels of S-nitrosohemoglobin (HbSNO) at different gestational ages in newborn infants and correlate the levels of HbSNO with HbA and HbF.

Method: Cord blood samples of 22 newborn infants of different gestational ages (25-41 weeks) were analyzed. The levels of HbF and HbA were determined by HPLC and of HbSNO by chemiluminescence.

Developmental changes in NO bioavailability in fetal erythrocytes.

S-nitrosohemoglobin (HbSNO), where hemoglobin (Hb) is nitrosated at Cysbeta93, presumably controls delivery of the vasorelaxant nitric oxide (NO) to hypoxic tissues in an oxygen-sensitive manner. Little is known about how Hb regulates NO bioavailability during fetal development. A study was planned to determine the levels of HbSNO and HbFe(II)NO (NO bound to FeII of heme) in the cord blood of newborn infants of different gestational ages and establish their relationship with the levels of fetal Hb (HbF).

Fetal hemoglobin synthesis determined by gamma-mRNA/gamma-mRNA + beta-mRNA quantitation in infants at risk for sudden infant death syndrome being monitored at home for apnea.

Objective: Fetal hemoglobin (HbF) levels in the hemolysates obtained from infants who died from sudden infant death syndrome (SIDS) are reported to be markedly increased compared with controls. This finding could have been explained by increased HbF synthesis caused by episodes of hypoxemia in the SIDS infants. A prospective study in a group of infants being monitored at home after an apparent life-threatening event (ALTE) and considered at increased risk for SIDS was conducted with an improved ribonuclease protection assay.

The effect of blood transfusion on the hemoglobin oxygen dissociation curve of very early preterm infants during the first week of life.

A study was conducted during the first week of life to determine the changes in P50 (PO2 required to achieve a saturation of 50% at pH 7.4 and 37 degrees C) and the proportions of fetal hemoglobin (HbF) and adult hemoglobin (HbA) prior to and after transfusion in very early preterm infants. Eleven infants with a gestational age < or = 27 weeks have been included in study.

Photoprotection prevents TPN-induced lung procollagen mRNA in newborn guinea pigs.

Background: Photo-exposed intravenous multivitamin solutions (MVP) carry a peroxide load. Peroxidation induces gene expression of procollagen. We hypothesized that photo exposure of the MVP solution might promote pulmonary fibrosis.