A POS-based preordering approach for English-to-Arabic statistical machine translation

In this work, we present a POS-based preordering approach that tackles both long- and short-distance reordering phenomena. Syntactic unlexicalized reordering rules are automatically extracted from a parallel corpus using only word alignment and a source-side language tagging. The reordering rules are used in a deterministic manner; this prevents the decoding speed from being bottlenecked in the reordering procedure. A new approach for both rule filtering and rule application is used to ensure a fast and efficient reordering. The tests performed on the IWSLT2016 English-to-Arabic evaluation benchmark show a noticeable increase in the overall Blue Score for our system over the baseline PSMT system

Axon growth of SNs toward GDNF-expressing VMs.

<p>GDNF- or mock-transfected VMs were prepared by using adenovirus vectors (AdGDNF-VMs and Mock-VMs) and co-cultured with SNs at a close distance (∼1 mm). <b>A)</b> A bright field image of the triangular co-culture (day 5) (left) and its schematic illustration (right). The axons from SN grow predominantly toward AdGDNF-VMs. Bar indicate 1 mm. Video images (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0065202#pone.0065202.s005" target="_blank">Video S2</a>) are available online. <b>B)</b> Sequential time-lapsed images. The pictures were taken at 0, 20, 40, 80 and 160 hours after removal of the glass-ring separation. Bar indicate 1 mm. <b>C)</b> Representative immunolabeling images of neurofilament-M (NF-M, red), α-actinine (AA, green) and GDNF (blue). Left: AdGDNF-VMs close to SNs, Right: Mock-VMs close to SNs. The NFM-positive axons (red fibrous structure) distribute abundantly on AdGDNF-VMs (green+blue), whereas only scarcely on Mock-VMs (green). Bars indicate 20 µm. <b>D)</b> The fraction of axon (NFM-positive area) distributing on VMs (AA-positive area). Values are means±SD of 5 co-cultures in each group. *significantly different from mock-VMs.</p

Pre- and post-synaptic stimulation by nicotine and noradrenalin on the spontaneous beating of cardiomyocytes.

<p><b>A)</b> Effects of nicotine (1 µM). Left: representative recording of extracellular potentials before and 6 min after application of nicotine to a mono-culture of VMs treated for 5 days with GDNF 10 ng/ml ([VM+GDNF]), co-cultures of VMs/SNs treated with vehicle only ([VM/SN+Vehicle], and co-cultures treated 5 days with GDNF 10 ng/ml ([VM/SN+GDNF]). Right: percent changes of spontaneous beating rate from baseline. Values are means±SD (n = 4), *p<0.05 vs. VM+GDNF. <b>B)</b> Effects of noradrenalin (10 µM). Left: representative extracellular potentials of VMs before and 3 min after application of noradrenalin to a mono-culture of VMs/SNs treated for 5 days with GDNF 10 ng/ml ([VM+GDNF]), co-cultures of VMs/SNs treated with vehicle only ([VM/SN+Vehicle]), co-cultures treated 5 days with GDNF 10 ng/ml ([VM/SN+GDNF]). Right: percent changes of spontaneous beating rate from baseline. [VM+Vehicle] : mono-cultures of VMs treated with vehicle only, [VM+NGF]: mono-cultures of VMs treated 5 days with NGF 50 ng/ml, [VM+GDNF]: mono-cultures of VMs treated 5 days with GDNF 10 ng/ml, respectively. Values are means±SD (n = 4). *Significantly different from baseline in each group (p<0.05, n = 4); †p<0.05 vs the VM/SN group (n = 4); #p<0.05 vs the VM/SN+NGF group (n = 4).</p

Expression of β1-adrenergic receptors in sympathetic neurons adjacent to VMs.

<p>Proximity co-cultures of GFP-knocked-in VMs and SNs (5 days) were immunolabeled for neurofilament-M (NFM, blue) and β1-adrenergic receptors (BAR; red). <b>A)</b> Representative fluorescence images of co-cultures treated with vehicle only were used as controls (CONT, top), treated with GDNF 10 ng/ml (middle) and treated with NGF 50 ng/ml (bottom). Pictures from left to right are labeled for GFP+NFM, NFM+BAR, GFP+BAR, and GFP+NFM+BAR. The immunopositive domains for BAR, which are most abundant with GDNF, are recognized on the surface membrane of VMs in contact with axons from SNs; the overlapping is colored by orange (GFP+BAR) or purple (NFM+BAR). <b>B)</b> Treatment with GDNF in co-cultures also leads to nuclear or perinuclear expression of BAR in VMs (white arrow heads). <b>C)</b> The density of immunopositive BAR distributing on VMs (GFP-positive area). Values are means<u>+</u>SD of 4 co-cultures in each group. *Significantly different from control at p<0.05. #Significantly different from co-cultures treated with NGF at p<0.05. Bars indicate 20 µm.</p

Axon Guidance of Sympathetic Neurons to Cardiomyocytes by Glial Cell Line-Derived Neurotrophic Factor (GDNF)

<div><p>Molecular signaling of cardiac autonomic innervation is an unresolved issue. Here, we show that glial cell line-derived neurotrophic factor (GDNF) promotes cardiac sympathetic innervation in vitro and in vivo. <i>In vitro</i>, ventricular myocytes (VMs) and sympathetic neurons (SNs) isolated from neonatal rat ventricles and superior cervical ganglia were cultured at a close distance. Then, morphological and functional coupling between SNs and VMs was assessed in response to GDNF (10 ng/ml) or nerve growth factor (50 ng/ml). As a result, fractions of neurofilament-M-positive axons and synapsin-I-positive area over the surface of VMs were markedly increased with GDNF by 9-fold and 25-fold, respectively, compared to control without neurotrophic factors. Pre- and post-synaptic stimulation of β₁-adrenergic receptors (BAR) with nicotine and noradrenaline, respectively, resulted in an increase of the spontaneous beating rate of VMs co-cultured with SNs in the presence of GDNF. GDNF overexpressing VMs by adenovirus vector (AdGDNF-VMs) attracted more axons from SNs compared with mock-transfected VMs. <i>In vivo</i>, axon outgrowth toward the denervated myocardium in adult rat hearts after cryoinjury was also enhanced significantly by adenovirus-mediated GDNF overexpression. GDNF acts as a potent chemoattractant for sympathetic innervation of ventricular myocytes, and is a promising molecular target for regulation of cardiac function in diseased hearts.</p></div