Objective: To observe the activation of microglia and the changing rule of inflammatory cytokine as IL-6, IL-10 and nuclear factor-κB (NF-κB) in experimental rabbits after spinal cord ischemia reperfusion (SCIR) injury in order to provide theoretical basis for post-conditioning time. Methods: Rabbit SCIR injury model was established by thoracic aorta balloon occlusion. 54 New Zealand male adult white rabbits were divided into 9 groups: Sham group (the animals received balloon implantation without occlusion), SCIR-0h group (reperfusion was conducted at 0 hour of spinal cord ischemia), SCIR-1h, -2h, -3h, -8h, -24h,-48h and -72h groups. n=6 in each group. The number of normal and apoptosis neurons, the levels of Iba-1, IL-6, IL-10 and NF-κB in spinal tissue were examined and compared among different groups respectively. Results: The number of normal neuron was decreasing with the extended reperfusion time, TUNEL-positive neuron began to increasing in SCIR-8h group and the peak was reached in SCIR-24h group. The expression of Iba-1 began to elevating in SCIR-2h group and the peak was obtained in SCIR-8h group; NF-κB began to rising in SCIR-3h group and the peak was observed in SCIR-8h group; both IL-6 and IL-10 arrived the peak in SCIR-24h group. The expressions of NF-κB, IL-6 and IL-10 were positively related to Iba-1 level. Conclusion: Microglia activation had dynamic changes in experimental SCIR rabbits and the expression levels of NF-κB, IL-6 and IL-10 were positively to microglia activation; post-conditioning time at front and back to microglia activation may reduce neuron injury.

Objective To observe the evolution of astrocytes,GDNF,BDNF and Jak-STAT signal pathway after spinal cord ischemia-reperfusion injury in rabbits.Methods Spinal cord ischemia was induced by means of balloon occlusion of the infrarenal aorta for 22 minutes in 54 male New Zealand white rabbits.We assigned rabbits to 9 groups (n =6),one sham group,eight operation groups.The operation process in the sham group was the same as the operation group except the ischemia reperfusion of the spinal cord.At 0 h,1 h,2 h,3 h,8 h,24 h,48 h and 72 h after reperfusion,animals were sarcrificed and the spinal cord was removed for histologic,immunohistochemical study and western blotting.Results Normal neurons were decreased with the extension of reperfusion time.Levels of GFAP increased at 3 h and reached a peak at 48 h after reperfusion.GDNF was increased reaching two peaks after injury,the first peak was at 3 h,the second was at 72 h.BDNF level was increased and peaked at 24 h after reperfusion.The expression of p-STAT3 showed a biphasic pattern which peaked at 1h and 48 h.GFAP,GDNF,BDNF were rare and the level of p-STAT3 could be neglected in sham group.Conclusion Spinal cord ischemia-reperfusion injury could induce the activation of astrocytes,the expression of GDNF,BDNF and the activation of JakSTAT signal pathway.They showed different expression rules in this study.

Objective: To investigate the correlation between blood glucose and aneurysm rupture, and analyze the correlation factors of aneurysm rupture. Methods: The clinical data of 128 patients with intracranial aneurysms in the First Affiliated Hospital of Kunming Medical University from January 2017 to August 2018 were retrospectively analyzed. Among them, intracranial aneurysm rupture was in 85 cases (rupture group), and unruptured was in 43 cases (unruptured group). The patient′s clinical features and aneurysm morphological features were recorded. Results: The blood glucose, daughter sac rate and regularity of morphology rate in ruptured group were significantly higher than those in unruptured group: (6.74 ± 2.61) mmol/L vs. (5.77 ± 2.11) mmol/L, 60.00% (51/85) vs. 11.63% (5/43), and 68.24% (58/85) vs. 30.23% (13/43), the aneurysm width was significantly smaller than that in unruptured group: (4.53 ± 2.25) mm vs. (5.67 ± 2.68) mm, and there were statistical differences (P<0.05 or <0.01). There were no statistical difference in gender, age, blood pressure, diabetes, hypertension, smoking history, glycosylated hemoglobin, blood lipids, aneurysm length, aneurysm neck, aneurysm length ratio to neck between 2 groups (P>0.05). Univariate Logistic regression analysis result showed that blood glucose, aneurysm width, daughter ascus and irregular shape were the risk factors of rupture of aneurysm (P<0.05 or <0.01). Multivariate Logistic regression analysis result showed that blood glucose, aneurysm width, daughter sac and irregular shape were the independent risk factors of rupture of aneurysm (OR = 1.364, 0.709, 9.441 and 3.935; 95% CI 1.073 to 1.734, 0.565 to 0.889, 2.879 to 30.963 and 1.330 to 11.646; P = 0.011, 0.003, 0.000 and 0.013). The patients were grouped again according to the aneurysm width, and univariate Logistic regression analysis result showed that aneurysm width ≤ 3 mm was the risk factors of rupture of aneurysm (OR = 0.294, 95% CI 0.094 to 0.916, P = 0.035). Conclusions Irregular shape and daughter sac of aneurysm are the independent risk factors of aneurysm rupture, but aneurysm rupture has nothing to do with recent blood sugar levels.

Tripartite motif (TRIM) family proteins are important effectors of innate immunity against viral infections. Here we identified TRIM35 as a regulator of TRAF3 activation. Deficiency in or inhibition of TRIM35 suppressed the production of type I interferon (IFN) in response to viral infection. Trim35-deficient mice were more susceptible to influenza A virus (IAV) infection than were wild-type mice. TRIM35 promoted the RIG-I-mediated signaling by catalyzing Lys63-linked polyubiquitination of TRAF3 and the subsequent formation of a signaling complex with VISA and TBK1. IAV PB2 polymerase countered the innate antiviral immune response by impeding the Lys63-linked polyubiquitination and activation of TRAF3. TRIM35 mediated Lys48-linked polyubiquitination and proteasomal degradation of IAV PB2, thereby antagonizing its suppression of TRAF3 activation. Our in vitro and in vivo findings thus reveal novel roles of TRIM35, through catalyzing Lys63- or Lys48-linked polyubiquitination, in RIG-I antiviral immunity and mechanism of defense against IAV infection.
A549 Cells ; Animals ; Apoptosis Regulatory Proteins/immunology* ; DEAD Box Protein 58/immunology* ; Dogs ; HEK293 Cells ; Humans ; Influenza A Virus, H1N1 Subtype/immunology* ; Madin Darby Canine Kidney Cells ; Mice ; Mice, Knockout ; Orthomyxoviridae Infections/pathology* ; Proteolysis ; RAW 264.7 Cells ; Signal Transduction/immunology* ; THP-1 Cells ; TNF Receptor-Associated Factor 3/immunology* ; Ubiquitination/immunology* ; Viral Proteins/immunology*

Antibodies, Neutralizing ; Antibodies, Viral/isolation & purification* ; B-Lymphocytes/virology* ; COVID-19/virology* ; Humans ; Immunity/genetics* ; RNA, Viral/immunology* ; SARS-CoV-2/pathogenicity* ; Single-Cell Analysis