OBJECTIVE: To analyze the correlation between acne and Northwest dryness syndrome in the Xinjiang region to provide an epidemiological foundation for the prevention and treatment of acne in the region. METHODS: The correlations among acne, clinical syndromes of Northwest dryness syndrome, and Northwest dryness syndrome were evaluated using the syndrome fitness index and canonical correlation analysis. RESULTS: The acne group had a Northwest dryness syndrome rate of 24.13%, and the control group 10.34%(χ2=7.733, P<0.01). There was no significant difference in the fitness index for acne and for the sub-syndromes of Northwest dryness syndrome(P> 0.05). The first canonical correlation coefficient was 0.5656(P<0.01). The acne-dependent variable group had the largest damp-heat syndrome load(0.8709), and the independent variable had the largest lung-heart-spleen pyretic dryness load(0.6766). CONCLUSION: Northwest dryness syndrome is a risk factor for acne in the Xinjiang region. Exogenous dryness and endogenous damp are frequently seen as subsyndromes in Northwest dryness syndrome in acne patients in the region. Acne was correlated with the damp-heat and lung-heart-spleen pyretic dryness sub-syndromes of Northwest dryness syndrome.
Yan WangXiaozhong WangHaiyan YuanJing JingHuaike ChenXiaohong RenLili ZhangHuitian ZhangMingxin Zhou
The Notch signaling pathway plays a key role in angiogenesis and endothelial cell formation, but it remains unclear whether it is involved in vascular repair by endothelial progenitor cells after traumatic brain injury. Therefore, in the present study, we controlled the Notch signaling pathway using overexpression and knockdown constructs. Activation of the Notch signaling pathway by Notch1 or Jagged1 overexpression enhanced the migration, invasiveness and angiogenic ability of endothelial progenitor cells. Suppression of the Notch signaling pathway with Notch1 or Jagged1 si RNAs reduced the migratory capacity, invasiveness and angiogenic ability of endothelial progenitor cells. Activation of the Notch signaling pathway in vivo in a rat model of mild traumatic brain injury promoted neurovascular repair. These findings suggest that the activation of the Notch signaling pathway promotes blood vessel formation and tissue repair after brain trauma.
