Glycine modulates membrane potential, cell volume, and phagocytosis in murine microglia.
Komm, B; Beyreis, M; Kittl, M; Jakab, M; Ritter, M; Kerschbaum, HH;
Amino Acids. 2014; 46(8): 1907-1917.
Fetal cardiac interventions have the potential to alter natural disease progression and reduce morbidity and mortality in children. While there are already encouraging data on fetal outcome, information on maternal morbidity and mortality after intervention is scarce. The aim of the present study was to assess maternal aspects, pregnancy-associated risks and adverse events in 53 intrauterine cardiac interventions.
Between October 2000 and December 2012, 53 fetal cardiac interventions have been performed in 47 patients (43 aortic valve dilations in 39 patients, 7 pulmonary valve dilations in 6 patients and three balloon atrioseptostomies in two patients). Median gestational age was 26 + 4 (20 + 3 - 33 + 1). Interventions were done by ultrasound-guided percutaneous approach under general anesthesia. All medical records and patient charts were analyzed retrospectively.
All women were considered to be healthy in the preoperative assessment, 39 patients (83%) continued pregnancy until term, 8 out of 47 patients had an intrauterine fetal demise (IUFD) and were induced. Post-operative nausea was reported in 29.7% and abdominal pain in 36.2% of patients on the day of operation. Preterm contractions were observed in two patients, no preterm premature rupture of membranes occurred. One severe post-partum hemorrhage was observed in a patient with IUFD and consecutive induction, however unrelated to the balloon valvuloplasty. No ICU admission and no major anesthesia-associated complications (aspiration, anaphylactic reaction, cardiovascular collapse, damage to teeth, laryngeal damage, awareness, hypoxic brain damage) were observed. Maternal mortality was zero. A significant learning curve was observed in terms of duration of intervention.
In our experience percutaneous needle-guided fetal cardiac intervention seems to be a safe procedure for the mother. In 53 procedures no major maternal complication directly related to the intervention was observed.
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Phagocytes form engulfment pseudopodia at the contact area with their target particle by a process resembling cell volume (CV) regulatory mechanisms. We evaluated whether the osmoregulatory active neutral amino acid glycine, which contributes to CV regulation via activation of sodium-dependent neutral amino acid transporters (SNATs) improves phagocytosis in isotonic and hypertonic conditions in the murine microglial cell line BV-2 and primary microglial cells (pMG). In BV-2 cells and pMG, RT-PCR analysis revealed expression of SNATs (Slc38a1, Slc38a2), but not of GlyRs (Glra1-4). In BV-2 cells, glycine (5 mM) led to a rapid Na(+)-dependent depolarization of membrane potential (V mem). Furthermore, glycine increased CV by about 9 %. Visualizing of phagocytosis of polystyrene microspheres by scanning electron microscopy revealed that glycine (1 mM) increased the number of BV-2 cells containing at least one microsphere by about 13 %. Glycine-dependent increase in phagocytosis was suppressed by the SNAT inhibitor α-(methylamino)isobutyric acid (MeAIB), by replacing extracellular Na(+) with choline, and under hypertonic conditions, but not by the GlyR antagonist strychnine or the GlyR agonist taurine. Interestingly, hypertonicity-induced suppression of phagocytosis was rescued by glycine. These findings demonstrate that glycine increases phagocytosis in iso- and hypertonic conditions by activation of SNATs.
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