Epileptic seizures (ES) and psychogenic nonepileptic seizures (PNES) can be difficult to differentiate from each other in the emergency department (ED) setting. We have previously shown that the anion gap (AG) can help differentiate between ES and PNES in the ED. In this study, we explored whether additionally considering leukocytosis can help better differentiate between ES and PNES. We screened a total of 1354 subjects seen in the ED of a tertiary care medical center; 27 PNES and 27 ES patients were identified based on clinical description and subsequent electroencephalography (EEG). Multivariable logistic regression analysis was used to model the association between ES, leukocytosis, and AG. Our results indicated that within 9 hours after the index event, serum AG (adjusted odds ratio [aOR] 2.07) and white blood cell (WBC) count (aOR 1.61) were both independently associated with ES. We derived an equation to help differentiate between ES and PNES: 1.5*AG+WBC. A score > 24.8 indicated a > 90% likelihood of ES. A score < 15.5 indicated a < 10% likelihood of ES (ie, the alternate diagnosis of PNES should be considered). This study for the first time provides evidence to help differentiate PNES and ES utilizing acidosis and leukocytosis.

EphrinB3 is important in the regulation of cell proliferation, differentiation and migration via cellcell contact, and can activate the reelin pathway during brain development. However, the effect of ephrinB3 on hippocampal neurogenesis and the reelin pathway in epilepsy remains to be fully elucidated. In the present study, the expression of ephrinB3 in pilocarpineinduced status epilepticus (SE) rats was investigated. SYBR Greenbased reverse transcriptionquantitative polymerase chain reaction analysis, immunohistochemical labeling and western blot analysis were used to detect the gene and protein expression levels of ephrinB3 and reelin pathway proteins. Immunofluorescence staining of doublecortin (DCX) was utilized to analyze hippocampal neurogenesis. The data revealed that the mRNA and protein expression levels of ephrinB3 in the hippocampus decreased during the spontaneous seizure period. Of note, the expression of reelin and its downstream phosphorylation disabled 1 (pDab1) were also notably decreased during the spontaneous seizure period, which showed similar dynamic changes as in the expression of ephrinB3. In addition, it was found that the number of DCXlabeled neuronal progenitor cells was increased in the hippocampus following pilocarpineinduced SE. To further clarify the role of ephrinB3 in neurogenesis and the reelin pathway in epilepsy, an exogenous ephrinB3 clustering stimulator, EphB3Fc, was infused into the bilateral hippocampus of the rats postSE. Following EphB3Fc injection, it was found that the expression levels of reelin and pDab1 were significantly increased in the epileptic rats following EphB3Fc injection. The number of DCXlabeled neuronal progenitor cells was reduced in the hippocampus of the epileptic rats. Furthermore, the intensity and frequency of spontaneous recurrent seizures and electroencephalographic seizures were attenuated in the epileptic rats postinjection. These results demonstrated the critical role of ephrinB3 in regulation of the reelin pathway and hippocampal neurogenesis in epilepsy, providing experimental evidence that ephrinB3 functions as a potential protective factor in epilepsy, at least in animals.

Cell- or network-driven oscillators underlie motor rhythmicity. The identity of C. elegans oscillators remains unknown. Through cell ablation, electrophysiology, and calcium imaging, we show: (1) forward and backward locomotion is driven by different oscillators; (2) the cholinergic and excitatory A-class motor neurons exhibit intrinsic and oscillatory activity that is sufficient to drive backward locomotion in the absence of premotor interneurons; (3) the UNC-2 P/Q/N high-voltage-activated calcium current underlies A motor neuron's oscillation; (4) descending premotor interneurons AVA, via an evolutionarily conserved, mixed gap junction and chemical synapse configuration, exert state-dependent inhibition and potentiation of A motor neuron's intrinsic activity to regulate backward locomotion. Thus, motor neurons themselves derive rhythms, which are dually regulated by the descending interneurons to control the reversal motor state. These and previous findings exemplify compression: essential circuit properties are conserved but executed by fewer numbers and layers of neurons in a small locomotor network.

Central pattern generators are cell- or network-driven oscillators that underlie motor rhythmicity. The existence and identity of C. elegans CPGs remain unknown. Through cell ablation, electrophysiology, and calcium imaging, we identified oscillators for reverse locomotion. We show that the cholinergic and excitatory class A motor neurons exhibit intrinsic and oscillatory activity, and such an activity can drive reverse locomotion without premotor interneurons. Regulation of their oscillatory activity, either through effecting an endogenous constituent of oscillation, the P/Q/N high voltage-activated calcium channel UNC-2, or, via dual regulation, inhibition and activation, by the descending premotor interneurons AVA, determines the propensity, velocity, and sustention of reverse locomotion. Thus, the reversal motor executors themselves serve as oscillators; regulation of their intrinsic activity controls the reversal motor state. These findings exemplify anatomic and functional compression: motor executors integrate the role of rhythm generation in a locomotor network that is constrained by small cell numbers.

Oligosaccharide chains of newly synthesized membrane receptors are trimmed and modified to optimize their trafficking and/or signalling before delivery to the cell surface. For most membrane receptors, the functional significance of oligosaccharide chain modification is unknown. During the maturation of Rh1 rhodopsin, a Drosophila light receptor, the oligosaccharide chain is trimmed extensively. Neither the functional significance of this modification nor the enzymes mediating this process are known. Here, we identify a dmppe (Drosophila metallophosphoesterase) mutant with incomplete deglycosylation of Rh1, and show that the retained oligosaccharide chain does not affect Rh1 localization or signalling. The incomplete deglycosylation, however, renders Rh1 more sensitive to endocytic degradation, and causes morphological and functional defects in photoreceptors of aged dmppe flies. We further demonstrate that the dMPPE protein functions as an Mn(2+)/Zn(2+)-dependent phosphoesterase and mediates in vivo dephosphorylation of alpha-Man-II. Most importantly, the dephosphorylated alpha-Man-II is required for the removal of the Rh1 oligosaccharide chain. These observations suggest that the glycosylation status of membrane proteins is controlled through phosphorylation/dephosphorylation, and that MPPE acts as the phosphoesterase in this regulation.