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Avian infectious bronchitis (IB) is a highly contagious infectious disease caused by infectious bronchitis virus (IBV), which is prevalent in many countries worldwide and causes serious harm to the poultry industry. At present, many commercial IBV vaccines have been used for the prevention and control of IB; however, IB outbreaks occur frequently. In this study, two new strains of IBV, SX/2106 and SX/2204, were isolated from two flocks which were immunized with IBV H120 vaccine in central China. Phylogenetic and recombination analysis indicated that SX/2106, which was clustered into the GI-19 lineage, may be derived from recombination events of the GI-19 and GI-7 strains and the LDT3-A vaccine. Genetic analysis showed that SX/2204 belongs to the GVI-1 lineage, which may have originated from the recombination of the GI-13 and GVI-1 strains and the H120 vaccine. The virus cross-neutralization test showed that the antigenicity of SX/2106 and SX/2204 was different from H120. Animal experiments found that both SX/2106 and SX/2204 could replicate effectively in the lungs and kidneys of chickens and cause disease and death, and H120 immunization could not provide effective protection against the two IBV isolates. It is noteworthy that the pathogenicity of SX/2204 has significantly increased compared to the GVI-1 strains isolated previously, with a mortality rate up to 60%. Considering the continuous mutation and recombination of the IBV genome to produce new variant strains, it is important to continuously monitor epidemic strains and develop new vaccines for the prevention and control of IBV epidemics.

Objective: To investigate the effects of a heavy-load eccentric exercise on rat skeletal muscle cell apoptosis and endoplasmic reticulum stress (ERS), and the expression of inositol requiring enzyme 1 (IRE1)-c-Jun N-terminal kinase (JNK) pathway proteins, and to explore the effects of IRE1-JNK on skeletal muscle cell apoptosis induced by ERS via in vivo inhibition experiments. Methods: One hundred and twenty healthy male SD rats were randomly divided into a non-exercise control group (C), an exercise group (e), an inhibition only group (Z), and an exercise plus inhibition group (EZ), with 30 in each group. Soleus muscle samples were obtained from each of the above-mentioned groups immediately on 12 h, 24 h, 48 h and 72 h after the exercise. Rats in E and EZ groups underwent a continuous downhill run of a speed of 16 m /min for 90 min and at an incline of 16°. each rat in Z and EZ groups got an intraperitoneal injection of 2 mg/mL STF-083010 dissolved by physiological saline, with a dose of 15 mL/kg body weight. The apoptosis was observed by detecting Caspase3 activity; and the expression of GRP78, JNK, IRe1, TRAF2 and ASK1 was detected by Western blot. Two-way ANOVA with Post-hoc Bonferroni correction was performed for analyzing the main effect and interaction of the treatment and duration, and for comparing the difference between groups. Results: 1) The activity of Caspase 3 in group E was significantly increased after one-time heavy-load eccentric exercise (P < 0.05), peaked at 12 h, and returned to the baseline level at 72h. except at 72 h, the activity of Caspase 3 in EZ group was significantly higher than that in C group (P < 0.05), and was significantly lower than that in E group (P < 0.05). 2) Compared with group C and group Z, the expression of GRP78 protein in group E was significantly increased (P < 0.05). Compared with group E, the expression of GRP78 protein in EZ group was decreased, but not significantly (P > 0.05). 3) The expressions of IRE1, TRAF2, ASK1 and JN K in group E were significantly higher than those of group Z (P < 0.05); except at 0h, they were significantly higher in group E than in group C (P < 0. 0 5). The expressions of IRe1, TRAF2, ASK1 and JNK protein were significantly higher than those in group C and Z (P < 0. 0 5), and w ere significantly lower than those in group E (P < 0. 0 5). Conclusion: A continous heavy-load eccentric exercise caused ERS and apoptosis. IRE1 inhibitor can reduce the expression of the proteins in IRE1-JNK pathway and improve the apoptosis induced by the exercise. It is speculated that the apoptosis induced by the heavy load exercise may be related to the activation of IRE1-JN K after ERS. [ABSTRACT FROM AUTHOR]

Gelsolin is an actin-binding protein and acts as an important regulator of cell survival. This study aimed to determine the function of gelsolin in the radioresistance of non–small cell lung cancer cells. We examined the expression of gelsolin in radioresistant A549 and H460 cells and their parental cells. The effects of gelsolin overexpression and knockdown on the clonogenic survival and apoptosis of non–small cell lung cancer cells after irradiation were studied. The involvement of phosphoinositide 3-kinase/Akt signaling in the action of gelsolin was checked. We found that gelsolin was significantly upregulated in radioresistant A549 and H460 cells. Overexpression of gelsolin significantly (P< .05) increased the number of colonies from irradiated A549 and H460 cells compared to transfection of empty vector. In contrast, knockdown of gelsolin significantly (P< .05) suppressed colony formation after irradiation. Gelsolin-overexpressing cells displayed reduced apoptosis in response to irradiation, which was coupled with decreased levels of cleaved caspase-3 and poly adenosine diphosphate-ribose polymerase. Ectopic expression of gelsolin significantly (P< .05) enhanced the phosphorylation of Akt compared to nontransfected cells. Pretreatment with the phosphoinositide 3-kinase inhibitor LY294002 (20 μmol/L) significantly decreased clonogenic survival and enhanced apoptosis in gelsolin-overexpressing A549 and H460 cells after irradiation. Taken together, gelsolin upregulation promotes radioresistance in non–small cell lung cancer cells, at least partially, through activation of phosphoinositide 3-kinase/Akt signaling.