Histogram analysis of diffusion kurtosis imaging derived maps may distinguish between low and high grade gliomas before surgery.

OBJECTIVE: To investigate the value of histogram analysis of diffusion kurtosis imaging (DKI) maps in the evaluation of glioma grading. METHODS: A total of 39 glioma patients who underwent preoperative magnetic resonance imaging (MRI) were classified into low-grade (13 cases) and high-grade (26 cases) glioma groups. Parametric DKI maps were derived, and histogram metrics between low- and high-grade gliomas were analysed. The optimum diagnostic thresholds of the parameters, area under the receiver operating characteristic curve (AUC), sensitivity, and specificity were achieved using a receiver operating characteristic (ROC). RESULT: Significant differences were observed not only in 12 metrics of histogram DKI parameters (P<0.05), but also in mean diffusivity (MD) and mean kurtosis (MK) values, including age as a covariate (F=19.127, P<0.001 and F=20.894, P<0.001, respectively), between low- and high-grade gliomas. Mean MK was the best independent predictor of differentiating glioma grades (B=18.934, 22.237 adjusted for age, P<0.05). The partial correlation coefficient between fractional anisotropy (FA) and kurtosis fractional anisotropy (KFA) was 0.675 (P<0.001). The AUC of the mean MK, sensitivity, and specificity were 0.925, 88.5% and 84.6%, respectively. CONCLUSIONS: DKI parameters can effectively distinguish between low- and high-grade gliomas. Mean MK is the best independent predictor of differentiating glioma grades. KEY POINTS: • DKI is a new and important method. • DKI can provide additional information on microstructural architecture. • Histogram analysis of DKI may be more effective in glioma grading.

[Wuling capsule played an assistant role in primary prevention of post-stroke depression: a clinical research].

OBJECTIVE: To observe the primary prevention role of Wuling Capsule (WC) on poststroke depression (PSD) patients. METHODS: Acute stroke patients were recruited and randomized into 2 groups by stratification, 55 in each group. All patients received same routine treatment of cardiovascular diseases. Patients in the experimental group additionally took WC (0.33 g each pill), 3 pills per day, three times per day; while those in the control group additionally took placebos, 3 pills per day, three times per day. Two weeks consisted of one therapeutic course. The diagnosis of PSD was performed once every other week. Those in accordance with PSD diagnosis discontinued any drug therapy. Those not in accordance with PSD diagnosis continued the drug therapy for 1-12 therapeutic course(s) (in total of 6 months). If they were still not in accordance with PSD diagnosis, then they discontinued the drug therapy. The morbidity of PSD, the average time of depression occurrence, Hamilton depression rating scale (HAMD) score, and adverse reactions were observed. RESULTS: The 1-, 3-, and 6-month morbidity of PSD was 8%, 16%, and 34% in the experimental group, while they were 19.6%, 29.4%, and 54.9% in the control group. The occurrence rate was lower in the experimental group than in the control group. Besides, there was statistical difference in the 6-month occurrence rate between the two groups (chi2 = 4.465, P < 0.05). The average time of PSD occurrence was longer in the experimental group than in the control group (14.96 +/- 8.31 weeks vs. 9.36 +/- 6.06 weeks; t=6.762, P < 0.05). The HAMD score at the PSD occurrence was 11.96 +/- 2.14 in the experimental group, lower than that of the control group (14.57 +/- 4.24), showing statistical difference (t=5.641, P < 0.05). CONCLUSION: WC was superior to the placebos in lowering the incidence of PSD, delaying the occurrence time of PSD, attenuating the depression degree of PSD, and had certain preventive effect on the incidence of PSD.

THBS1/CD47 Modulates the Interaction of γ-Catenin With E-Cadherin and Participates in Epithelial-Mesenchymal Transformation in Lipid Nephrotoxicity.

Hyperlipidemia, an important risk factor for cardiovascular and end-stage renal diseases, often aggravates renal injury and compromises kidney function. Here, histological analysis of human kidney samples revealed that high lipid levels induced the development of renal fibrosis. To elucidate the mechanism underlying lipid nephrotoxicity, we used two types of mouse models (Apoe-/- and C57BL/6 mice fed a 45 and 60% high-fat diet, respectively). Histological analysis of kidney tissues revealed high-lipid-induced renal fibrosis and inflammation; this was confirmed by examining fibrotic and inflammatory marker expression using Western blotting and real-time polymerase chain reaction. Oxidized low-density lipoprotein (OX-LDL) significantly induced the fibrotic response in HK-2 tubular epithelial cells. RNA-sequencing and Gene Ontology analysis of differentially expressed mRNAs in OX-LDL-treated HK-2 tubular epithelial cells and real-time PCR validation in Apoe-/- mice showed that the expression of thrombospondin-1 (THBS1) in the high-fat group was significantly higher than that of the other top known genes, along with significant overexpression of its receptor CD47. THBS1 knockdown cells verified its relation to OX-LDL-induced fibrosis and inflammation. Liquid chromatography tandem mass spectrometry and STRING functional protein association network analyses predicted that THBS1/CD47 modulated the interaction between γ-catenin and E-cadherin and was involved in epithelial-mesenchymal transition, which was supported by immunoprecipitation and immunohistochemistry. CD47 downregulation following transfection with small-hairpin RNA in OX-LDL-treated tubular epithelial cells and treatment with anti-CD47 antibody restored the expression of E-cadherin and attenuated renal injury, fibrosis, and inflammatory response in OX-LDL-treated cells and in type 2 diabetes mellitus. These findings indicate that CD47 may serve as a potential therapeutic target in long-term lipid-induced kidney injury.