Pseudomonas phragmitis sp. nov., isolated from petroleum polluted river sediment.

A Gram-stain-negative, rod-shaped bacterium, motile by means of a single polar flagellum, designated S-6-2T, was isolated from petroleum polluted river sediment in Huangdao, Shandong Province, PR China. The 16S rRNA gene sequence analysis revealed that S-6-2T represented a member of the genus Pseudomonas, sharing the highest sequence similarities with Pseudomonas parafulva (97.5 %) and Pseudomonas fulva (97.5 %). Phylogenetic analysis based on 16S rRNA gene, concatenated 16S rRNA, gyrB, rpoB and rpoD genes and genome core-genes indicated that S-6-2T was affiliated with the members of the Pseudomonas pertucinogena group. The average nucleotide identity (ANI) and genome-to-genome distance between the whole genome sequences of S-6-2T and closely related species of the genus Pseudomonas within the P. pertucinogena group were less than 77.94 % and 20.5 %, respectively. Differences in phenotypic characteristics were also found between S-6-2T and the closely related species. The major cellular fatty acids (>10 %) were summed feature 8 (C18 : 1ω7c/ C18  : 1ω6c), C16 : 0, C17 : 0cyclo and C12 : 0. The predominant respiratory quinone was ubiquinone 9. The major polar lipids were diphosphatidylglycerol (DPG), phosphatidylglycerol (PG), phosphatidylethanolamine (PE), one unidentified lipid (L1), two unidentified phospholipids (PL1 and PL2) and an aminophospholipid (APL). The DNA G+C content of the genome of S-6-2T was 60.1 mol%. On the basis of the evidence from the polyphasic taxonomic study, strain S-6-2T can be classified as representative of a novel species of the genus Pseudomonas, for which the name Pseudomonas phragmitis sp. nov. is proposed. The type strain is S-6-2T (=CGMCC 1.15798T=KCTC 52539T).

Electrical stimulation promotes motor nerve regeneration selectivity regardless of end-organ connection.

Previous studies have demonstrated that end-organ deprivation after peripheral nerve injury results in targeting of regenerating nerve fibers into inappropriate pathways, which leads to poor functional recovery. Here we studied the effect of electrical stimulation on the regeneration selectivity of motor nerves after peripheral nerve injury and end-organ deprivation. We found that end-organ deprivation reduced regenerating selectivity of motor nerves, total number of regenerating motoneurons, and level of neural trophic factors in the regenerating pathways after nerve injury (p < 0.05). Electrical stimulation successfully promoted motor nerve regeneration selectivity regardless of end-organ connections (p < 0.05). This increased selectivity was accompanied by an increase in the protein level of neural trophic factors in the distal nerve stumps by 3 weeks after nerve injury (p < 0.05). There was a similar increase in the protein level of these neural trophic factors in denervated muscle. However, the RNA level of these factors decreased both in the distal nerves and in the muscle. Despite the promising effect of promoting motor nerve regeneration selectivity, electrical stimulation did not prevent motoneuron loss caused by end-organ deprivation. The present study suggests that end organs contribute to the development of selective motor nerve regeneration by increasing the neurotrophic factors in the regeneration pathways. Electrical stimulation is an efficient strategy to ameliorate the deteriorated regeneration microenvironment caused by end-organ deprivation and to promote motor nerve regeneration selectivity when end-organ connections are deprived.