Sexual dimorphic distribution of G protein-coupled receptor 30 in pain-related regions of the mouse brain.

Sex differences in pain sensitivity have contributed to the fact that medications for curing chronic pain are unsatisfactory. However, the underlying mechanism remains to be elucidated. Brain-derived estrogen participates in modulation of sex differences in pain and related emotion. G protein-coupled receptor 30 (GPR30), identified as a novel estrogen receptor with a different distribution than traditional receptors, has been proved to play a vital role in regulating pain affected by estrogen. However, the contribution of its distribution to sexually dimorphic pain-related behaviors has not been fully explored. In the current study, immunofluorescence assays were applied to mark the neurons expressing GPR30 in male and female mice (in metestrus and proestrus phase) in pain-related brain regions. The neurons that express CaMKIIα or VGAT were also labeled to observe overlap with GPR30. We found that females had more GPR30-positive (GPR30+ ) neurons in the primary somatosensory (S1) and insular cortex (IC) than males. In the lateral habenula (LHb) and the nucleus tractus solitarius (NTS), males had more GPR30+ neurons than females. Moreover, within the LHb, the expression of GPR30 varied with estrous cycle phase; females in metestrus had fewer GPR30+ neurons than those in proestrus. In addition, females had more GPR30+ neurons, which co-expressed CaMKIIα in the medial preoptic nucleus (mPOA) than males, while males had more than females in the basolateral complex of the amygdala (BLA). These findings may partly explain the different modulatory effects of GPR30 in pain and related emotional phenotypes between sexes and provide a basis for comprehension of sexual dimorphism in pain related to estrogen and GPR30, and finally provide new targets for exploiting new treatments of sex-specific pain.

Acceleration of nitrogen removal performance in a biofilm reactor augmented with Pseudomonas sp. using polycaprolactone as carbon source for treating low carbon to nitrogen wastewater.

Heterotrophic nitrification-aerobic denitrification (HN-AD) process was achieved in a moving bed biofilm reactor after 180-days acclimation using PCL as carbon source for low C/N wastewater treatment. A novel HN-AD strain, JQ-H3, with ability of PCL degradation was augmented to improve nitrogen removal. TN removal efficiencies of 82.31%, 90.05%, and 93.16% were achieved in the augmented reactor (R2), at different HRTs of 24 h, 20 h, and 16 h, while in the control reactor (R1), the TN removal efficiencies were 59.24%, 74.61%, and 76.68%. The effluent COD in R2 was 10.17 mg/L, much lower than that of 42.45 mg/L in R1. Microbial community analysis revealed that JQ-H3 has successfully proliferated with a relative abundance of 4.79%. Relative abundances of functional enzymes of nitrogen cycling remarkably increased due to bioaugmentation based on the analysis of PICRUSt2. This study provides a new approach for enhancing nitrogen removal in low C/N sewage treatment via the HN-AD process.