[Study on the correlation between the thickness of superficial fascia at Dazhui(GV14) and cervical spondylosis].

OBJECTIVE: To observe the correlation between the thickness of superficial fascia at Dazhui (GV14) acupoint and cervical spondylosis, so as to explore the essence of its morphological and structural changes of acupoint sensitivity. METHODS: A retrospective study was conducted. According to the diagnostic criteria of "Guidelines for Diagnosis, Treatment and Rehabilitation of Cervical Spondylosis" (2017), 344 cases of cervical spine magnetic resonance imaging (MRI) examination were included and divided into control group (73 cases) and observation group (271 cases). The control group was healthy population, and the observation group was patients with cervical spondylosis conforming to the diagnostic criteria, including cervical spondylosis of neck type, cervical spondylosis radiculopathy, cervical spondylotic myelopathy, cervical spondylosis of vertebral artery type, and sympathetic cervical spondylosis. According to MRI images of cervical spine, the structure of GV14 acupoint including skin, superficial fascia layer and aponeurosis ligament layer were measured. RESULTS: The acupoint depth and the superficial fascia thickness at GV14 in the observation group were (56.6±8.8) mm and (22.8±7.6) mm, the acupoint depth and the superficial fascia thickness at GV14 were (49.8±7.0) mm and (16.6±6.6)mm in the control group, which were significantly greater in the observation group than in the control group (P<0.01). The superficial fascia thickness at GV14 of cervical spondylotic mye-lopathy, cervical spondylosis of neck type and cervical spondylosis radiculopathy in the observation group was (23.8±8.1)mm, (23.0±7.3)mm and (22.6±6.5)mm, the acupoint depth of GV14 was (58.7±8.8)mm, (56.2±9.1)mm and (55.8±6.4)mm, which were significantly thicker than the superficial fascia thickness and the acupoint depth in the control group (P<0.01). In the observation group，the superficial fascia thickness of GV14 of cervical spondylosis myelopathy was significantly thicker than those of sympathetic cervical spondylosis (17.8±8.1) mm and cervical spondylosis of vertebral artery type (19.9±5.9) mm (P<0.01, P<0.05). In the observation group, the depth of GV14 of cervical spondylosis myelopathy was thicker than that of cervical spondylosis of neck type, cervical spondylosis radiculopathy, sympathetic cervical spondylosis and cervical spondylosis of vertebral artery type(P<0.05，P<0.01)； the depth of GV14 of sympathetic cervical spondylosis was thinner than that of cervical spondylosis of neck type and cervical spondylosis radiculopathy (P<0.01). CONCLUSION: The superficial fascia thickness at GV14 was correlated with cervical spondylosis, and it is also related to cervical spondylotic myelopathy, cervical spondylosis of neck type and cervical spondylosis radiculopathy. The morphological and structural changes of GV14 in the state of cervical spondylosis were mainly the thickness of the superficial fascia.

Crosstalk between PML and p53 in response to TGF-ß1: A new mechanism of cardiac fibroblast activation.

Cardiac fibrosis is a common pathological cardiac remodeling in a variety of heart diseases, characterized by the activation of cardiac fibroblasts. Our previous study uncovered that promyelocytic leukemia protein (PML)-associated SUMO processes is a new regulator of cardiac hypertrophy and heart failure. The present study aimed to explore the role of PML in cardiac fibroblasts activation. Here we found that PML is significantly upregulated in cardiac fibrotic tissue and activated cardiac fibroblasts treated with transforming growth factor-ß1 (TGF-ß1). Gain- and loss-of-function experiments showed that PML impacted cardiac fibroblasts activation after TGF-ß1 treatment. Further study demonstrated that p53 acts as the transcriptional regulator of PML, and participated in TGF-ß1 induced the increase of PML expression and PML nuclear bodies (PML-NBs) formation. Knockdown or pharmacological inhibition of p53 produced inhibitory effects on the activation of cardiac fibroblasts. We further found that PML also may stabilize p53 through inhibiting its ubiquitin-mediated proteasomal degradation in cardiac fibroblasts. Collectively, this study suggests that PML crosstalk with p53 regulates cardiac fibroblasts activation, which provides a novel therapeutic strategy for cardiac fibrosis.