Acute aortic dissection is a rare, life-threatening condition. Clinical manifestations generally include the acute onset of severe chest or back pain. Aortic dissection presenting with signs and symptoms of acute spinal cord damage is the most severe complication and is particularly rare. This paper reports a case of aortic dissection in a 50-year-old man with a 10-year history of hypertension manifesting as acute spinal cord damage (bilateral lower extremity weakness and loss of all types of sensation), acute skeletal muscle ischaemic necrosis with increased levels of creatine kinase, and acute kidney failure with increased levels of serum creatinine and decreased glomerular filtration rate. The patient refused surgical treatment. His clinical condition progressively worsened and he died 3 days later. This case indicates the importance of considering aortic dissection in patients presenting with acute spinal cord damage, acute skeletal muscle necrosis or acute kidney failure, which may allow early diagnosis and reduce the mortality rate.

1. The objective of this study was to verify the functional effects of the c.234G>A substitution in the myostatin (MSTN) gene and ascertain the mechanism by which the variant affects growth traits in the Bian chicken. 2. The c.234G>A substitution was detected by PCR-RFLP analysis in the 7th-generation Bian chickens and three genotypes (AA, AG and GG) were identified. Results showed that the substitution was significantly associated with all studied growth traits, except first-d-weight, in female Bian chickens. 3. Based on these results, the substitution was used in gene-assisted selection for growth traits and thus fast-growth (AA genotype) and slow-growth (GG genotype) lines were successfully established. Significant differences in growth traits were detected between the fast-growth and slow-growth lines from 6 to 16 weeks of age. Furthermore, all slaughter traits, except leg muscle rate, were significantly different between the fast-growth and slow-growth lines. 4. Expression analysis showed that the relative expression level of MSTN in chickens with GG and AG genotypes were significantly higher than that in chickens with an AA genotype, both in breast and leg muscle. Chickens in the slow-growth line had significantly higher relative expression level of MSTN compared to chickens in the fast-growth line, both in breast and leg muscle. 5. The results suggest that the c.234G>A substitution in the myostatin (MSTN) gene negatively regulates the expression of MSTN in the Bian chicken and that it may be used in marker-assisted selection to accelerate the chicken breeding process.

Our previous studies have shown that Magnolol (Mag) improves the symptoms and decreases the levels of cytokines during infection induced by Streptococcus suis (S. suis) in mice. Although some reports show that Mag inhibits lipopolysaccharide-induced inflammatory responses via downregulating mitogen-activated protein kinases (MAPK) and nuclear factor-κB (NF-κB) signaling pathways, the molecular mechanisms underlying Mag-mediated inhibition of S. suis-induced inflammatory responses are poorly understood. Here, RAW264.7 cells were stimulated with S. suis in the presence or absence of Mag. Cell viability and bactericidal effects were examined, and the concentrations of tumor necrosis factor-a (TNF-α), IL-1β (interleukin-1β), IL-6 (interleukin-6), and IL-8 (interleukin-8) were determined by ELISA. The change in ROS (reactive oxygen species) was determined by fluorescence microscopy and ELISA. The levels of Toll-like receptor 2 (TLR2) and MAPK family proteins and NF-κB signaling were determined by Western blot analysis. S. suis induced massive RAW264.7 cell death, a decline in bactericidal activity, the release of inflammatory cytokines, increased oxidative stress, and activation of TLR2/MAPK/NF-κB signaling pathways. Mag treatment significantly suppressed macrophage cell death and caused a decline in bactericidal activity. Furthermore, Mag decreased inflammatory cytokines production and ROS generation. It also prevented p38, extracellular regulated protein kinases (ERK), c-Jun N-terminal kinase (JNK), inhibitor of NF-κB (IκB), and NF-κB phosphorylation induced by S. suis in a dose-dependent manner. Our results indicate that Mag exerts anti-inflammatory and cell-protective effects and mediates the activation of MAPK and NF-κB signaling by downregulating the expression of TLR2 upregulated by S. suis.