Actual electrolyte intake during the first week of life and morbidity in very-low-birthweight infants.

Aim: To describe sodium and potassium intake, their sources and plasma concentrations, and the association between intake and morbidity in very-low-birthweight (VLBW, <1500 g) infants during the first week of life.

Methods: This retrospective cohort study comprised 951 VLBW infants born at <32 weeks. Infants were divided into three groups according to gestational age: 23-26 (n = 275), 27-29 (n = 433) and 30-31 (n = 243) weeks.

Time of Delivery Contributes to Mortality and Morbidity in Preterm Infants.

Introduction: Knowledge about the time of birth and its impact on premature infants is essential when planning perinatal and neonatal care and resource allocation. We studied the time of birth and its contribution to early death and morbidity in preterm infants.

Methods: We explored the time and mode of birth of infants with birthweight of <1,500 g and gestational age of <32+0/7 weeks.

Very low birthweight infants receive less enteral feeding than what is prescribed.

Aim: Feeding a very low birthweight (VLBW, <1500 g) infant is challenging. Our aims were to study how prescribed enteral feeding is implemented in VLBW infants and to identify factors associating with slow enteral feeding progression.

Methods: Our retrospective cohort included 516 VLBW infants born before 32 weeks of gestation during 2005-2013 and admitted to Children's Hospital, Helsinki, Finland, for at least the two first weeks of life.

Blood pressure changes during the first 24 hours of life and the association with the persistence of a patent ductus arteriosus and occurrence of intraventricular haemorrhage.

Very low birthweight (VLBW) infants are at risk of intraventricular haemorrhage (IVH) and delayed closure of ductus arteriosus. We investigated mean arterially recorded blood pressure (MAP) changes during the first day of life in VLBW infants as potential risk factors for a patent ductus arteriosus (PDA) and IVH. This retrospective cohort study exploring MAP changes during adaption and risk factors for a PDA and IVH comprised 844 VLBW infants admitted to the Helsinki University Children's Hospital during 2005-2013.

Length of Nutritional Transition Associates Negatively with Postnatal Growth in Very Low Birthweight Infants.

Very low birthweight (VLBW, <1500 g) infants may be predisposed to undernutrition during the nutritional transition phase from parenteral to enteral nutrition. We studied the associations among the length of the transition phase, postnatal macronutrient intake, and growth from birth to term equivalent age in VLBW infants. This retrospective cohort study included 248 VLBW infants born before 32 weeks of gestation and admitted to the Children's Hospital, Helsinki, Finland during 2005-2013.

Early oxygen levels contribute to brain injury in extremely preterm infants.

Background: Extremely low gestational age newborns (ELGANs) are at risk of neurodevelopmental impairments that may originate in early NICU care. We hypothesized that early oxygen saturations (SpO), arterial pO levels, and supplemental oxygen (FiO) would associate with later neuroanatomic changes.

Methods: SpO, arterial blood gases, and FiO from 73 ELGANs (GA 26.

Glucocorticoids, sodium transport mediators, and respiratory distress syndrome in preterm infants.

Background: Antenatal glucocorticoids (GCs) reduce respiratory distress syndrome (RDS) in preterm infants and are associated with reduced lung liquid content. Our aim was to assess whether airway gene expression of mediators of pulmonary epithelial sodium and liquid absorption, and further, respiratory morbidity, associate with cord blood GC concentrations.

Methods: The study included 64 infants delivered <32 weeks gestation.

A triple-chamber parenteral nutrition solution was associated with improved protein intake in very low birthweight infants.

Aim: We evaluated the nutrient intakes of very low birthweight (VLBW) infants weighing less than 1500 g and tested the hypothesis that using a triple-chamber parenteral nutrition (PN) solution, containing lipids, glucose and amino acids, would improve protein intake.

Methods: This retrospective cohort study comprised 953 VLBW infants born in 2005-2013 at a gestational age of less than 32 + 0/7 weeks and admitted to the neonatal care unit at Helsinki Children's Hospital, Finland. The infants were divided into four groups according their birth year and PN regime.

Hidden sources like saline flushes make a significant contribution to the fluid intake of very low birthweight infants during the first postnatal week.

Aim: We examined actual fluid intake, and routes of administration, in very low birthweight (VLBW) infants during the first week of life in a neonatal intensive care unit.

Methods: This retrospective cohort study comprised 953 infants born at <32 weeks and 1500 g and treated at Helsinki University Children's Hospital from 2005 to 2013. All parenterally and enterally administered fluids, and their sources, were obtained from our patient information system.

Activated mast cells induce endothelial cell apoptosis by a combined action of chymase and tumor necrosis factor-alpha.

Objective: Activated mast cells (MCs) induce endothelial cell (EC) apoptosis in vitro and are present at sites of plaque erosions in vivo. To further elucidate the role of MCs in endothelial apoptosis and consequently in plaque erosion, we have studied the molecular mechanisms involved in MC-induced EC apoptosis.

Methods And Results: Primary cultures of rat cardiac microvascular ECs (RCMECs) and human coronary artery ECs (HCAECs) were treated either with rat MC releasate (ie, mediators released on MC activation), rat chymase and tumor necrosis factor-alpha (TNF-alpha), or with human chymase and TNF-alpha, respectively.

Inhibition of smooth muscle cell proliferation by a chemically modified tetracycline.

Introduction: Chemically modified tetracyclines (CMTs) are a group of nonantimicrobial derivatives of tetracycline, which exert antiproliferative and anticollagenolytic properties. The molecular mechanisms, however, are poorly understood.

Materials And Methods: The effect of CMT-3 on cultured, subconfluent rat aortic smooth muscle cells (SMCs) was analyzed by [(3)H]-thymidine incorporation, counting cell numbers, and flow cytometry analysis.

Mast cell chymase induces smooth muscle cell apoptosis by disrupting NF-kappaB-mediated survival signaling.

Chymase released from activated mast cells induces apoptosis of vascular smooth muscle cells (SMCs) in vitro by degrading the pericellular matrix component fibronectin, so causing disruption of focal adhesion complexes and Akt dephosphorylation, which are necessary for cell adhesion and survival. However, the molecular mechanisms of chymase-mediated apoptosis downstream of Akt have remained elusive. Here, we show by means of RT-PCR, Western blotting, EMSA, immunocytochemistry and confocal microscopy, that chymase induces SMC apoptosis by disrupting NF-kappaB-mediated survival signaling.

Proteolysis of the pericellular matrix: a novel element determining cell survival and death in the pathogenesis of plaque erosion and rupture.

The 2 major general concepts about the cell biology of atherogenesis, growth of smooth muscle cells, and lipid accumulation in macrophages, ie, foam cell formation, have not been able to satisfactorily explain the genesis of acute coronary syndromes. Rather, the basic pathology behind the acute atherothrombotic events relates to erosion and rupture of unstable coronary plaques. At the cellular level, we now understand that a switch from cellular growth to cellular death, notably apoptosis, could be involved in turning at least some types of atherosclerotic plaques unstable.

Regulation of smooth muscle cell growth, function and death in vitro by activated mast cells--a potential mechanism for the weakening and rupture of atherosclerotic plaques.

The fibrous cap of a lipid-containing atherosclerotic plaque consists of collagen produced by arterial smooth muscle cells (SMCs) of synthetic phenotype. A thick cap protects the lipid-rich core, whereas a thin cap predisposes it to rupture, with ensuing acute clinical complications, such as myocardial infarction. Among the pathological mechanisms leading to plaque weakening and rupture, one possibility is loss of the matrix-synthesizing SMCs.

Mast cell-mediated apoptosis of endothelial cells in vitro: a paracrine mechanism involving TNF-alpha-mediated down-regulation of bcl-2 expression.

Degranulated mast cells are present in the subendothelial space of eroded (de-endothelialized) coronary atheromas. Upon degranulation, mast cells secrete into the surrounding tissue an array of preformed and newly synthesized mediators, including proapoptotic molecules, such as chymase and TNF-alpha. In a co-culture system involving rat serosal mast cells and rat cardiac (microvascular) endothelial cells, we could show, by means of competitive RT-PCR, immunoblotting, immunocytochemistry, annexin staining, flow cytometry, and DNA-laddering, that stimulation of mast cells with ensuing degranulation rapidly (within 30 min) down-regulated the expression of both bcl-2 mRNA and protein, with subsequent induction of apoptosis in the endothelial cells.

Mast cell chymase induces smooth muscle cell apoptosis by a mechanism involving fibronectin degradation and disruption of focal adhesions.

Objective: Chymase released from activated mast cells has been shown to induce apoptosis of vascular smooth muscle cells (SMCs) in vitro. The proteolytic activity of chymase is essential for the proapoptotic effect, but the mechanism of chymase-induced apoptosis has remained unknown.

Methods And Results: Here we show by means of FACS analysis, immunohistochemistry, and Western blotting that mast cell-derived chymase induces SMC apoptosis by a mechanism involving degradation of an extracellular matrix component, fibronectin (FN), with subsequent disruption of focal adhesions.