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C39H36N5O11Tb, triclinic, P 1‾ $\overline{1}$ (no. 2), a = 10.3365(12) Å, b = 13.0194(15) Å, c = 15.2064(18) Å, α = 108.769(2)°, β = 94.694(2)°, γ = 100.882(2)°, V = 1880.2(4) Å3, Dc = 1.607 g/cm3, Z = 2, Rgt (F) = 0.0315, wRref (F 2) = 0.0836, T = 296.15 K.

C75H76N10O23Tb2, triclinic, P−1‾ $P-\overline{1}$ (no. 2), a = 10.4524(13) Å, b = 12.9626(16) Å, c = 15.2003(18) Å, α = 108.674(2)∘, β = 94.931(2)∘, γ = 101.617(2)∘, V = 1885.8(4) nm3, Z = 1, R gt(F) = 0.0236, wR ref(F 2) = 0.0584, T = 296 K.

The frost heaving pressure generated by water–ice phase change and volume expansion of saturated fractured rock mass in cold regions promote the initiation and expansion of new fractures, and lead to further damage and deterioration of fractured rock mass. To reveal the frost heaving pressure degradation mechanism of fractured rock mass subjected to multiple freeze–thaw cycles, the repeated frost heaving pressure monitoring test was carried out on saturated fractured granite with different macroscopic fractures under different freezing temperatures. The evolution characteristics of cyclic frost heaving pressure and the effect of crack size, freezing temperature and the number of freeze–thaw cycle on the frost heaving pressure of saturated fractured granite were analyzed. The results show that the evolution characteristics of frost heaving pressure in single freeze–thaw cycle is similar, which can be roughly divided into five stages. As the number of freeze–thaw cycles increases, the peak frost heaving pressure decreases exponentially, and the amplitude of peak frost heaving pressure drop increases. The peak frost heaving pressure increases linearly with the increase of crack length. The smaller the crack width, the earlier the frost heaving pressure appears in the freezing and thawing stages. The lower the freezing temperature, the earlier the frost heaving pressure appears. The peak frost heaving pressure increases linearly with the decrease of temperature, and the effect of freezing temperature on the frost heaving pressure weakens with the increase of freeze-thaw cycles. As the freezing temperature decreases, the effect of crack size on the peak frost heaving pressure becomes more significant. The research results can provide reference for the theoretical calculation and numerical analysis on frost heaving pressure of fractured rock masses in cold regions.

C39H36N5O11Tb, triclinic, P 1 ‾ (no. 2), a = 10.3365(12) Å, b = 13.0194(15) Å, c = 15.2064(18) Å, α = 108.769(2)°, β = 94.694(2)°, γ = 100.882(2)°, V = 1880.2(4) Å3, Dc = 1.607 g/cm3, Z = 2, Rgt(F) = 0.0315, wRref(F2) = 0.0836, T = 296.15 K. [ABSTRACT FROM AUTHOR]

Aims: Adenosine 2A receptor (A2AR) is widely expressed in the brain and plays important roles in neuroinflammation, and the nucleotide‐binding oligomerization domain, leucine‐rich repeat, and pyrin domain‐containing protein 3 (NLRP3) inflammasome is a crucial component of the innate immune system while the regulation of A2AR on it in the central nervous system (CNS) has not been clarified. Methods: The effects of microglial A2AR on NLRP3 inflammasome assembly and activation were investigated in wild‐type, A2AR‐ or NLRP3‐knockout primary microglia with pharmacological treatment. Microglial A2AR or NLRP3 conditional knockout mice were used to interrogate the effects of this regulation on neuroinflammation posttraumatic brain injury (TBI). Results: We found that A2AR directly interacted with NLRP3 and facilitated NLRP3 inflammasome assembly and activation in primary microglia while having no effects on mRNA levels of inflammasome components. Inhibition of the interaction via A2AR agonist or knockout attenuated inflammasome assembly and activation in vitro. In the TBI model, microglial A2AR and NLRP3 were co‐expressed at high levels in microglia next to the peri‐injured cortex, and abrogating of this interaction by microglial NLRP3 or A2AR conditional knockout attenuated the neurological deficits and neuropathology post‐TBI via reducing the NLRP3 inflammasome activation. Conclusion: Our results demonstrated that inhibition of the interaction between A2AR and NLRP3 in microglia could mitigate the NLRP3 inflammasome assembly and activation and ameliorate the neuroinflammation post‐TBI. It provides new insights into the effects of A2AR on neuroinflammation regulation post‐TBI and offers a potential target for the treatment of NLRP3 inflammasome‐related CNS diseases. [ABSTRACT FROM AUTHOR]

C75H76N10O23Tb2, triclinic, P − 1 ‾ (no. 2), a = 10.4524(13) Å, b = 12.9626(16) Å, c = 15.2003(18) Å, α = 108.674(2)∘, β = 94.931(2)∘, γ = 101.617(2)∘, V = 1885.8(4) nm3, Z = 1, Rgt(F) = 0.0236, wRref(F2) = 0.0584, T = 296 K. [ABSTRACT FROM AUTHOR]