Objective To study the effect of hypothemah on the early inflammatory reaction in acute lung injury induced by intestinal ischemia-repeffusion(IlR)in rabbits.Method Seventy-two healthy rabbits provided by Peking Union Medical Colege Hospital Anhnal center were randomly divided into four groups(n=18 pergroup):(1)normothermia control group (rectal temperature 37-38 C;sham group);(2)normothermia IlR group(rectal temperature 37-38 C);(3)mild hypothermia HR group(rectal temperature 32-35℃);and (4)moderate hypothermia IIR group(rectal temperature 28-31.9C).Acute lung injury was induced by claIllp.ithe superiornteric artery(SMA)for 1 hour and declamping the SMA for 6 hours.Hypothermia WaS induced by surface cooling.Before and 2.4 and 6 hours after IIR,the Olasmlevels o,IL-,IL-6 and IL10 were measured.All rabbits were killed 6 hours after IIR and water content in lung tissue Wttk'assessed.Iaght mieropic examination was performed tbr morphological assessment of the hmg.The data were analyzed by AN()VA.Statistical significance wag dned as a P of<0.05.Results In the IIR groups,the plasma levels ofTHE-a.IL-l,IL-6 and IL-10 and lung water were increased.There Was evidence of acute lung injury from morphologi-cal assessment of the lung.The acute lung injury induced by IIR was improved by hypethennia.Mild hypothermia Was similar to moderate hypothermia for the treatment of acute lung injury induced by IIR.ConclusiotMild hy-pothermia and moderate hypothermia Can significantly improve acute lung injury induced by IIR in rabbits.Mild hypothea had similar efficacy to moderate hypothermia for the treatment of acute lung injury induced by IIR.

Objective:To analyze the expression and relationship of miR-379 and human kinesin family member 4A (KIF4A) in triple-negative breast cancer (TNBC).Methods:A total of 52 patients diagnosed with TNBC in breast department at Puji Branch of Dongguan People′s Hospital between January 2016 and November 2019 were retrospectively selected as the study group. Meanwhile, 70 patients with non-triple-negative breast cancer (NTNBC) diagnosed in the same period were selected as the control group. The expression levels of miR-379 and KIF4A in both groups were detected. The receiver operating characteristic (ROC) curve was drawn, and the area under the curve (AUC) of miR-379 and KIF4A predicting TNBC was calculated; The relationship between the expression levels of miR-379 and KIF4A and clinicopathological parameters, and the correlation between the expression level of miR-379 and KIF4A were analyzed.Results:The expression level of KIF4A in study group was higher than that in control group [(6.93±0.43) vs (3.75±0.25), P<0.05], and the expression level of miR-379 in study group was lower than that in control group [(0.54±0.17) vs (0.87±0.32), P<0.05]. MiR-379 combined with KIF4A expression had the greatest diagnostic value for TNBC: AUC 0.823 (95% CI: 0.730- 0.917), specificity 0.785, sensitivity 0.950; Univariate analysis showed that there were significant difference in the expression of miR-379 in TNBC patients with different clinical stages, tumor diameter, and lymph node metastasis (all P<0.05); There were significant difference in the expression of KIF4A in TNBC patients with different clinical stages and tumor diameter (all P<0.05). Pearson correlation analysis showed that miR-379 expression was negatively correlated with KIF4A expression in TNBC ( r=-0.349, P<0.05). Conclusions:The expression of miR-379 is down-regulated, while the expression of KIF4A is up-regulated in patients with TNBC. The two are related to poor clinicopathological characteristics, which indicates that they can be used for condition evaluation of the patients.

The thalamocortical (TC) circuit is closely associated with pain processing. The hyperpolarization-activated cyclic nucleotide-gated (HCN) 2 channel is predominantly expressed in the ventral posterolateral thalamus (VPL) that has been shown to mediate neuropathic pain. However, the role of VPL HCN2 in modulating TC circuit activity is largely unknown. Here, by using optogenetics, neuronal tracing, electrophysiological recordings, and virus knockdown strategies, we showed that the activation of VPL TC neurons potentiates excitatory synaptic transmission to the hindlimb region of the primary somatosensory cortex (S1HL) as well as mechanical hypersensitivity following spared nerve injury (SNI)-induced neuropathic pain in mice. Either pharmacological blockade or virus knockdown of HCN2 (shRNA-Hcn2) in the VPL was sufficient to alleviate SNI-induced hyperalgesia. Moreover, shRNA-Hcn2 decreased the excitability of TC neurons and synaptic transmission of the VPL-S1HL circuit. Together, our studies provide a novel mechanism by which HCN2 enhances the excitability of the TC circuit to facilitate neuropathic pain.
Animals ; Mice ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels/genetics* ; Neuralgia ; RNA, Small Interfering ; Thalamus/metabolism* ; Up-Regulation