Objective:To apply digital analysis to quantify hyperechogenicity of substantia nigra, and explore its clinical value for diagnosis of Parkinson′s disease (PD).Methods:The cross-sectional study included 652 PD patients (PD group) and 99 healthy controls (healthy control group) from November 2017 to October 2020 in Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology. All subjects underwent transcranial sonography. The diagnostic accuracy of substantia nigra hyperechogenicity using digital analysis was compared with that in a manual measurement in PD. Furthermore, the receiver operating characteristic (ROC) curve analysis was applied to explore its diagnosis value in PD.Results:There were 482 subjects including 400 in the PD group and 82 in the healthy control group, whose quantified results of substantia nigra hyperechogenicity could be used for analysis. The ROC analysis showed that the area under the curve of the quantified larger substantia nigra hyperechoic region detection for diagnosing PD was 0.858 (95% CI 0.805-0.910), the sensitivity was 87.8%, and the specificity was 73.2%, consistent with that of doctors (area under the curve: 0.884). Further more, among these PD patients, there was no correlation between larger substantia nigra hyperechogenicity and age, age of onset, course of disease, non-motor symptoms, and motor symptoms (all P>0.05). Conclusions:Digital analysis was used to quantify the changes in substantia nigra hyperechogenicity in this seudy. The results showed that diagnostic accuracy for PD based on digital analysis was consistent with that of experienced clinicians.

Objective: To investigate the neuroprotective effect of Ghrelin on traumatic brain injury (TBI) in mice. Methods: TBI model of C57BL / 6 mice was established by electronic cortical impact instrument (eCCI). According to the random figure table method, twenty-four mice were randomly divided into sham group(Sham group), TBI group and Ghrelin intervention group(Ghrelin group) with 8 mice in each group. The model of TBI was established in TBI group and Ghrelin group.The mice in Ghrelin group was injected intraperitoneally 0.5 g/kg before and 1 h after injury respectively. And the mice Sham group and TBI group were injected with the same amount of normal saline. The changes of cerebral blood perfusion (CBP) were monitored in real time by laser speckle contrast analysis(LSCI), the changes of neuroelectrophysiology were observed by monitoring motor evoked potential (MEP), and the status of neurological deficit was evaluated by modified neurological deficit score (mNSS). Results: Compared with Sham group, the mice in TBI group had significantly lower cerebral blood perfusion(CBP) (t=-12.36, P<0.01), longer latency and lower amplitude of motor evoked potential (MEP) (t=5.03, -11.55, all P<0.01), and significantly higher mNSS scores (t=9.34, P<0.01). However, compared with the TBI group, the cerebral blood perfusion(CBP) of Ghrelin group increased significantly at 12 h after TBI((196.87±17.36) PU/mm² vs (123.62±8.04)PU/mm², t=10.45, P<0.01), while the latency of MEP decreased((5.30±0.33)ms vs (6.80±0.97)ms, t=-5.01, P<0.01), the amplitude of MEP increased((2.21±0.16)mV vs (1.27±0.27)mV, t=9.65, P<0.01). And compared with the TBI group, the neurological deficit score of Ghrelin group decreased significantly at 24 h after TBI((4.9±1.2) vs (8.4±2.6), t=-3.87, P<0.01). Conclusion Ghrelin exhibits a significant neuroprotective role by increasing cerebral blood flow perfusion, reducing the degree of neurological deficit and promoting motor function recovery in TBI mice.

Objective: To investigate the effects of Casein kinase 2-interacting protein 1 (CKIP-1) gene silencing on the proliferation of glioma cells U87-MG. Methods: The recombinant lentiviral vectors targeting CKIP-1 gene or negative control were constructed and then used to infect glioma U87-MG cell line.The effects of knock-down on the mRNA or protein expression of CKIP-1 were evaluated by real-time qPCR and western blotting.Cell cycle was detected by the flow cytometry assay, and cell proliferation changes were evaluated by cell counting, MTT, and BrdU assay, respectively.Lastly, the colony formation was used to investigate the effect of CKIP-1 knock-down on the clone formation. Results: Compared with the group of Ctrl, CKIP-1 siRNA was observed to significantly inhibit CKIP-1 expression at the mRNA levels (Ctrl (1.01±0.13) vs CKIP-1 siRNA (0.23±0.02), P<0.01) and protein levels in the U87-MG cells.Also, CKIP-1 suppression mediated by RNAi decreased the ratio of G0/G1 phase (Ctrl (69.64±0.79) vs CKIP-1 siRNA(62.64±0.66), P<0.01), increased that of G2/M phase (Ctrl (8.36±0.52) vs CKIP-1 siRNA(13.87±2.90), P<0.05), and significantly inhibited the cell proliferation and clone formation (Colony number: Ctrl (25±2) vs CKIP-1 siRNA(2±1), P<0.05) of transfected U87-MG cells. Conclusion Knocking down the expression of CKIP-1 significantly inhibit cell proliferation in human U87-MG glioma cells, indicating that CKIP-1 is involved in the development of gliomas and could promote the cell proliferation.