[Benggang (collapsing hill) erosion hazard zoning based on the minimum cumulative resistance model: A case study of a small watershed in Anxi County, Fujian, China]. / 基于最小累积阻力模型的崩岗侵蚀危险性分区­­ä»¥å®‰æºªåŽ¿å°æµåŸŸä¸ºä¾‹.

In order to understand the possibility and spatial pattern of Benggang (collapsing hill) erosion in risk assessment and distinguish the primary and secondary areas in Benggang prevention, we took a small watershed in Anxi County (Fujian, China) as the study area and Benggang as the source, and constructed the Benggang expansion resistance surface using the minimum cumulative resistance (MCR) model and divided the risk zoning. The results showed that the area around Benggang displayed a low resistance value, while the northwest and southeast areas displayed a high resistance value. The Benggang expansion resistance surface had an island type form. Based on resistance surface, the research region was divided into very high-risk, high-risk, medium risk, low-risk and very low-risk zones. We proposed corresponding Benggang management suggestions for those zones. A total of 21 strategic saddle points were extracted based on the resistance surface morphology. The strategic points in the lower safety zone were considered as the priority areas for Benggang prevention. We compared the hazard results based on the MCR model and the information quantity method. These results were consistent in spatial distribution, indicating the reliability of the results of hazard zoning by the MCR model.

Chemokine receptor CXCR4 activates the RhoA/ROCK2 pathway in spinal neurons that induces bone cancer pain.

BACKGROUND: Chemokine receptor CXCR4 has been found to be associated with spinal neuron and glial cell activation during bone cancer pain. However, the underlying mechanism remains unknown. Furthermore, the RhoA/ROCK2 pathway serves as a downstream pathway activated by CXCR4 during bone cancer pain. We first validated the increase in the expressions of CXCR4, p-RhoA, and p-ROCK2 in the spinal dorsal horn of a well-characterized tumor cell implantation-induced cancer pain rat model and how these expressions contributed to the pain behavior in tumor cell implantation rats. We hypothesized that spinal blockade of the CXCR4-RhoA/ROCK2 pathway is a potential analgesic therapy for cancer pain management. METHODS: Adult female Sprague-Dawley rats (body weight of 180-220 g) and six- to seven-week old female Sprague-Dawley rats (body weight of 80-90 g) were taken. Ascitic cancer cells were extracted from the rats (body weight of 80-90 g) with intraperitoneally implanted Walker 256 mammary gland carcinoma cells. Walker 256 rat mammary gland carcinoma cells were then injected (tumor cell implantation) into the intramedullary space of the tibia to establish a rat model of bone cancer pain. RESULTS: We found increased expressions of CXCR4, p-RhoA, and p-ROCK2 in the neurons in the spinal cord. p-RhoA and p-ROCK2 were co-expressed in the neurons and promoted by overexpressed CXCR4. Intrathecal delivery of CXCR4 inhibitor Plerixafor (AMD3100) or ROCK2 inhibitor Fasudil abrogated tumor cell implantation-induced pain hypersensitivity and tumor cell implantation-induced increase in p-RhoA and p-ROCK2 expressions. Intrathecal injection of stromal-derived factor-1, the principal ligand for CXCR4, accelerated p-RhoA expression in naive rats, which was prevented by postadministration of CXCR4 inhibitor Plerixafor (AMD3100) or ROCK2 inhibitor Fasudil. CONCLUSIONS: Collectively, the spinal RhoA/ROCK2 pathway could be a critical downstream target for CXCR4-mediated neuronal sensitization and pain hypersensitivity in bone cancer pain, and it may serve as a potent therapeutic target for pain treatment.

Local injection to sciatic nerve of dexmedetomidine reduces pain behaviors, SGCs activation, NGF expression and sympathetic sprouting in CCI rats.

Neuropathic pain has become an intractable health threat, with its profound effect on quality of life. Dorsal root ganglia (DRG) is evidenced to play a crucial role in neuropathic pain. The peripheral nociceptive afferents seem to be essential not only to initiate the process of neuropathic pain, but also to maintain and modulate it. Dexmedetomidine (DEX), a highly selective agonist of α2-adrenergic receptor (α2-AR), has provided significant analgesia in neuropathic pain. In the present study, we found that local injection to sciatic nerve of DEX alleviated heat hypersensitivity induced by chronic constriction injury (CCI). Western blotting revealed that DEX inhibited the over-expression of nerve growth factor (NGF) significantly. Immunohistofluorescence results showed that DEX inhibited glia cells activation and sympathetic sprouting simultaneously in DRG. Our study suggests that DEX attenuates neuropathic pain in CCI rats by down-regulation of satellite glial cells (SGCs) activation, NGF expression and sympathetic sprouting.