[Effect of Clean Heating on Carbonaceous Aerosols in PM2.5 During the Heating Period in Baoding].

In order to study the effects of clean heating measures on the concentration and source of carbonaceous aerosols in PM2.5 in Baoding, we collected PM2.5 samples in Baoding during the winter heating periods of 2014 and 2019. The concentrations of OC and EC in the samples were determined by using a DRI Model 2001A thermo-optical carbon analyzer.The results showed that the average values of ρ(OC) and ρ(EC) in the heating period in 2014 were 60.92 µg·m-3 and 18.15 µg·m-3, and the average values of ρ(OC) and ρ(EC) in the heating period in 2019 were 36.63 µg·m-3 and 6.07 µg·m-3. Compared with those in 2014, the concentrations of OC and EC decreased by 39.87% and 66.56%, respectively, in 2019; the decrease in EC was larger than that in OC, and the meteorological conditions in 2019 were more severe than those in 2014, which was not conducive to the spread of pollutants.The correlation analysis and SOC estimation of OC and EC indicated that the correlation R2 of OC and EC in Baoding in 2014 and 2019 were 0.874 and 0.811, respectively, indicating that OC and EC in Baoding had relatively consistent sources. The average values of ρ(SOC) in 2014 and 2019 were 16.59 µg·m-3 and 11.31 µg·m-3, respectively, and the contribution rates to OC were 27.23% and 30.87%, respectively. This showed that in 2019, compared with that in 2014, the primary pollution decreased, but the secondary pollution increased, and the atmospheric oxidation increased.The analysis of the pollution sources of carbonaceous aerosols revealed that in 2014 and 2019 before and after the implementation of clean heating, the carbonaceous aerosols in the atmosphere were mainly from biomass combustion, coal combustion, and vehicle exhaust emissions. However, the contribution from biomass burning and coal burning decreased in 2019 compared to that in 2014. The decrease in OC and EC concentrations was attributed to the control of coal-fired and biomass-fired sources by clean heating. At the same time, the implementation of clean heating measures reduced the contribution of primary emissions to carbonaceous aerosols in PM2.5 in Baoding City.

Spinal cord stimulation reduces cardiac pain through microglial deactivation in rats with chronic myocardial ischemia.

Angina pectoris is cardiac pain that is a common clinical symptom often resulting from myocardial ischemia. Spinal cord stimulation (SCS) is effective in treating refractory angina pectoris, but its underlying mechanisms have not been fully elucidated. The spinal dorsal horn is the first region of the central nervous system that receives nociceptive information; it is also the target of SCS. In the spinal cord, glial (astrocytes and microglia) activation is involved in the initiation and persistence of chronic pain. Thus, the present study investigated the possible cardiac pain­relieving effects of SCS on spinal dorsal horn glia in chronic myocardial ischemia (CMI). CMI was established by left anterior descending artery ligation surgery, which induced significant spontaneous/ongoing cardiac pain behaviors, as measured using the open field test in rats. SCS effectively improved such behaviors as shown by open field and conditioned place preference tests in CMI model rats. SCS suppressed CMI­induced spinal dorsal horn microglial activation, with downregulation of ionized calcium­binding adaptor protein­1 expression. Moreover, SCS inhibited CMI­induced spinal expression of phosphorylated­p38 MAPK, which was specifically colocalized with the spinal dorsal horn microglia rather than astrocytes and neurons. Furthermore, SCS could depress spinal neuroinflammation by suppressing CMI­induced IL­1ß and TNF­α release. Intrathecal administration of minocycline, a microglial inhibitor, alleviated the cardiac pain behaviors in CMI model rats. In addition, the injection of fractalkine (microglia­activating factor) partially reversed the SCS­produced analgesic effects on CMI­induced cardiac pain. These results indicated that the therapeutic mechanism of SCS on CMI may occur partially through the inhibition of spinal microglial p38 MAPK pathway activation. The present study identified a novel mechanism underlying the SCS­produced analgesic effects on chronic cardiac pain.

Projections from the lateral parabrachial nucleus to the lateral and ventral lateral periaqueductal gray subregions mediate the itching sensation.

ABSTRACT: Lateral and ventral lateral subregions of the periaqueductal gray (l/vlPAG) have been proved to be pivotal components in descending circuitry of itch processing, and their effects are related to the subclassification of neurons that were meditated. In this study, lateral parabrachial nucleus (LPB), one of the most crucial relay stations in the ascending pathway, was taken as the input nucleus to examine the modulatory effect of l/vlPAG neurons that received LPB projections. Anatomical tracing, chemogenetic, optogenetic, and local pharmacological approaches were used to investigate the participation of the LPB-l/vlPAG pathway in itch and pain sensation in mice. First, morphological evidence for projections from vesicular glutamate transporter-2-containing neurons in the LPB to l/vlPAG involved in itch transmission has been provided. Furthermore, chemogenetic and optogenetic activation of the LPB-l/vlPAG pathway resulted in both antipruritic effect and analgesic effect, whereas pharmacogenetic inhibition strengthened nociceptive perception without affecting spontaneous scratching behavior. Finally, in vivo pharmacology was combined with optogenetics which revealed that AMPA receptor-expressing neurons in l/vlPAG might play a more essential role in pathway modulation. These findings provide a novel insight about the connections between 2 prominent transmit nuclei, LPB and l/vlPAG, in both pruriceptive and nociceptive sensations and deepen the understanding of l/vlPAG modulatory roles in itch sensation by chosen LPB as source of ascending efferent projections.

Projecting neurons in spinal dorsal horn send collateral projections to dorsal midline/intralaminar thalamic complex and parabrachial nucleus.

Itch is an annoying sensation that always triggers scratching behavior, yet little is known about its transmission pathway in the central nervous system. Parabrachial nucleus (PBN), an essential transmission nucleus in the brainstem, has been proved to be the first relay station in itch sensation. Meanwhile, dorsal midline/intralaminar thalamic complex (dMITC) is proved to be activated with nociceptive stimuli. However, whether the PBN-projecting neurons in spinal dorsal horn (SDH) send collateral projections to dMITC, and whether these projections involve in itch remain unknown. In the present study, a double retrograde tracing method was applied when the tetramethylrhodamine-dextran (TMR) was injected into the dMITC and Fluoro-gold (FG) was injected into the PBN, respectively. Immunofluorescent staining for NeuN, substance P receptor (SPR), substance P (SP), or FOS induced by itch or pain stimulations with TMR and FG were conducted to provide morphological evidence. The results revealed that TMR/FG double-labeled neurons could be predominately observed in superficial laminae and lateral spinal nucleus (LSN) of SDH; Meanwhile, most of the collateral projection neurons expressed SPR and some of them expressed FOS in acute itch model induced by histamine. The present results implicated that some of the SPR-expressing neurons in SDH send collateral projections to the dMITC and PBN in itch transmission, which might be involved in itch related complex affective/emotional processing to the higher brain centers.

Collateral Projections from the Medullary Dorsal Horn to the Ventral Posteromedial Thalamic Nucleus and the Parafascicular Thalamic Nucleus in the Rat.

Medullary dorsal horn (MDH), the homolog of spinal dorsal horn, plays essential roles in processing of nociceptive signals from orofacial region toward higher centers, such as the ventral posteromedial thalamic nucleus (VPM) and parafascicular thalamic nucleus (Pf), which belong to the sensory-discriminative and affective aspects of pain transmission systems at the thalamic level, respectively. In the present study, in order to provide morphological evidence for whether neurons in the MDH send collateral projections to the VPM and Pf, a retrograde double tracing method combined with immunofluorescence staining for substance P (SP), SP receptor (SPR) and Fos protein was used. Fluoro-gold (FG) was injected into the VPM and the tetramethylrhodamine-dextran (TMR) was injected into the Pf. The result revealed that both FG- and TMR-labeled projection neurons were observed throughout the entire extent of the MDH, while the FG/TMR double-labeled neurons were mainly located in laminae I and III. It was also found that some of the FG/TMR double-labeled neurons within lamina I expressed SPR and were in close contact with SP-immunoreactive (SP-ir) terminals. After formalin injection into the orofacial region, 41.4% and 34.3% of the FG/TMR double-labeled neurons expressed Fos protein in laminae I and III, respectively. The present results provided morphological evidence for that some SPR-expressing neurons within the MDH send collateral projections to both VPM and Pf and might be involved in sensory-discriminative and affective aspects of acute orofacial nociceptive information transmission.