Effect of different carbon sources on sulfate reduction and microbial community structure in bioelectrochemical systems.

Microbial electrolysis cells (MECs) have rapidly developed into a promising technology to treat sulfate-rich wastewater that lacks electron donors. Hence, a better understanding of the effect on the microbial community structure caused by different sources in bioelectrochemical systems is required. This study sought to investigate the effect of different carbon sources (NaHCO3, ethanol, and acetate were employed as sole carbon source respectively) on the performance of sulfate-reducing biocathodes. The sulfate reduction efficiency enhanced by the bioelectrochemical systems was 8.09 - 11.57% higher than that of open-circuit reference experiments. Furthermore, the optimum carbon source was ethanol with a maximum sulfate reduction rate of 170 mg L-1 d-1 in the bioelectrochemical systems. The different carbon sources induced significant differences in sulfate reduction efficiency as demonstrated by the application of a micro-electrical field. Microbial community structure and network analysis revealed that all three kinds of carbon source systems enriched large proportions of sulfate-reducing bacteria and electroactive bacteria but were significantly distinct in composition. The dominant sulfate-reducing bacteria that use NaHCO3 and acetate as carbon sources were Desulfobacter and Desulfobulbus, whereas those that use ethanol as carbon source were Desulfomicrobium and Desulfovibrio. Our results suggest that ethanol is a more suitable carbon source for sulfate reduction in bioelectrochemical systems.

Functions of Wnt signaling pathway in hair cell differentiation and regeneration.

Wnt signaling pathway plays important roles in the development and homeostasis of multicellular organisms. Through their bindings with the Frizzled receptors, the Wnt ligands regulate a wide range of developmental processes, such as axis patterning, cell division, and cell fate specification. Wnt signaling plays vital roles in the development of inner ear of the mouse. In the early stages of inner ear development, Wnt signaling specifies the size of the placode and the formation of the otic vesicle. In later stages, Wnt signaling mediates hair cell specification and orients the stereociliary bundles in a uniform direction. In this review, we summarize the current knowledge on the roles of Wnt signaling in hair cell differentiation and regeneration, which may provide references and insights for investigators in the field.

Activation of α2 adrenoceptors inhibited NMDA receptor-mediated nociceptive transmission in spinal dorsal horn of mice with inflammatory pain.

The α2 adrenoceptor is highly enriched in spinal dorsal horn and involved in descending noradrenergic pain modification. Following peripheral tissue injury, intrathecal application of α2 adrenoceptor agonists effectively alleviates the pathological pain hypersensitivity, although the precise mechanisms are not fully understood. The present study induced inflammatory pain by intraplantar injection of Complete Freund's Adjuvant (CFA), and prepared the spinal cord slices to assay the possible influence of α2 adrenoceptor agonist clonidine on the synaptic transmission mediated by NMDA receptor (NMDAR), a critical player in spinal sensitization. Whole-cell patch clamp recordings in lamina II neurons illustrated that clonidine significantly decreased the amplitudes of NMDAR-mediated monosynaptic responses in inflamed mice through activation of α2A-subtype adrenoceptor. No significant alteration in the paired-pulse ratio before and after clonidine application indicated the postsynaptic origin. Intracellular loading of nonhydrolyzable GDP analog GDP-ß-S blocked, whereas direct inhibition of cAMP-dependent protein kinase (PKA) mimicked, the inhibitory effect of clonidine on NMDAR currents, implicating that Gαi protein/PKA signaling was involved in clonidine action. Biochemical analysis in vivo revealed that intrathecal clonidine administration specifically decreased the content of GluN2B subunit-containing NMDAR at synaptosomal membrane fraction, a result associated closely with the alleviation of inflammatory pain. Electrophysiological recordings in vitro further demonstrated that GluN2B receptor-selective inhibitor ifenprodil dramatically reduced NMDAR synaptic responses in inflamed mice and more importantly, occluded the synaptic inhibition produced by clonidine. These data suggested that the noradrenergic suppression of inflammatory pain might involve the blockade of GluN2B receptor-mediated nociceptive transmission in spinal dorsal horn.

Ca2+ /calmodulin-dependent protein kinase II in spinal dorsal horn contributes to the pain hypersensitivity induced by γ-aminobutyric acid type a receptor inhibition.

The fast inhibitory synaptic transmission mediated by the γ-aminobutyric acid type A receptor (GABAA R) within spinal dorsal horn exerts a gating control over the synaptic conveyance of nociceptive information from the periphery to higher brain regions. Although a large body of evidence has demonstrated that the impairment of GABAergic inhibition alone is sufficient to elicit pain hypersensitivity in intact animals, the underlying mechanisms remain to be characterized. The present study shows that Ca(2+) /calmodulin-dependent protein kinase II (CaMKII) is an important signaling protein downstream of reduced GABAergic inhibition. We found that pharmacological removal of inhibition by intrathecal application of the GABAA R antagonist bicuculline significantly enhanced the autophosphorylation of CaMKII at Thr286 in spinal dorsal horn of mice. In addition to increased CaMKII activity, bicuculline also promoted CaMKII interaction with N-methyl-D-aspartate (NMDA)-subtype glutamate receptors and induced the translocation of CaMKII from cytosolic compartments to the synaptosomal membrane fraction. Immunoblotting analysis revealed that the phosphorylation levels of NMDA receptor NR2B subunit at Ser1303 and of AMPA-subtype glutamate receptor GluR1 subunit at Ser831, two important CaMKII phosphorylation sites, were substantially enhanced after bicuculline application. Behavioral tests illustrated that intrathecal administration of the CaMKII inhibitor KN-93, NMDA receptor antagonist D-APV, or AMPA receptor antagonist GYKI 52466 effectively ameliorated the mechanical allodynia evoked by bicuculline. These data thus indicate that CaMKII signaling is critical for the reduced inhibition to evoke spinal sensitization.