Objective To verify the pathol ogical basis of high signal intensity on T 1 weighted image after brain ischemia by using the rat model. Methods Fifty-six male Wistar rats, weighing 250 to 300 g, were used for the model of middle cerebral artery occlusion(MCAO). 46 rats model were counted in the results. They were divided into two groups randomly, experimental group (T 1, n =39) and control group (T 0, n =7). Experimental group was further divided into 4 subgroups: 15 minute's MCAO (T 1-a, n =13), 30 minute's MCAO (T 1-b, n =12), 60 minute's MCAO (T 1-c, n =7), and permanent MCAO (T 1-d, n =7). Intraluminal filament technique was used with the method modified by Zea-Longa. Follow-up MRI was applied to observe the time and the position of short T 1 signal. H & E staining and electronic microscope were applied to observe the pathological changes in the position of short T 1 signal. Results In T 0 group ( n = 7), no short T 1 signal was observed in bilateral cerebral hemispheres. In T 1-a subgroup ( n =13), short T 1 signal was observed in 7 rats at the 14 th day. In T 1-b subgroup ( n =12), short T 1 signal was observed in the ischemic side in 8 rats. All of the rats in T 1-c subgroup ( n =7) and T 1-d subgroup ( n =7) were observed to have short T 1 signal. The histological changes of short T 1 signal were hemorrhage, lipid-laden macrophage, denatured protein, and myelinolysis. Earlier short T 1 signal in cortical region was mainly related with hemorrhage, short T 1 signal in the basal ganglia appeared at a later stage, which was induced by lipid-laden macrophages. The occurrence of short T 1 signal was prominently different in the time of MCAO (? 2=29.328, P

Objective:To investigate the efficacy of double balloon enteroscopy (DBE) in the treatment of bleeding from small intestinal vascular lesion and risk factors of bleeding recurrence .Methods:From April 2013 to May 2020, at Air Force Medical Center, the clinical data of 65 patients with confirmed or suspected bleeding from small intestinal vascular lesion were retrospectively analyzed. The patients were divided into DBE treatment group (patients of Yano classification 1a and 1b received argon plasma coagulation, and patients of Yano classification 2 and 3 accepted combination of titanium clip and submucosal injection of lauromacrogol sclerosing agent) and non-DBE treatment group (traditional treatments such as stopping anticoagulant or antiplatelet drugs, blood transfusion, and iron supplementation). The bleeding recurrence of patients with single small intestinal vascular lesion between DBE treatment group and non-DBE treatment group, and patients with single or mulitiple vascular lesion of DBE treatment group were compared. Univariate analysis was used to analyze the clinical data of patients with or without recurrent bleeding. Multivariate logistic regression model was used to analyze the independent risk factors and protective factors of recurrent bleeding in small intestinal vascular lesion. Independent sample t test, chi-square test and Fisher exact probability method were used for statistical analysis. Results:Forty-four (25 of single vascular lesion and 19 of multiple vascular lesion) patients were diagnosed with small intestinal vascular lesions and received DBE treatment (DBE treatment group). Twenty-one patients with single vascular lesion accepted traditional treatment (non-DBE treatment group). The recurrent rate of bleeding in patients with single vascular lesion of DBE treatment group was lower than that in patients with single vascular lesion of non-DBE treatment group and patients with multiple vascular lesion of DBE treatment group (24.0%, 6/25 vs. 71.4%, 15/21 and 12/19), and the differences were statistically significant ( χ2=10.348 and 6.848, P=0.001 and 0.009). The results of univariate analysis showed that the proportion of blood transfusion, hypertension, complicated with valvular heart disease and DBE treatment in patients with rebleeding or not rebleeding from small intestinal vascular lesion was different with statistically significant (69.7%(23/33) vs. 37.5%(12/32), 51.5%(17/33) vs. 18.8%(6/32), 42.4%(14/33) vs. 12.5%(4/32) and 54.5%(18/33) vs. 81.2%(26/32), χ2=6.777, 7.628, 7.265, and 5.298, all P<0.05). The results of multivariate logistic regression analysis indicated that blood transfusion during the course of disease (odds ratien ( OR)=3.736, 95% confidence interval ( CI) 1.082 to 12.898, P=0.037) and complication with valvular heart disease ( OR=4.916, 95% CI 1.107 to 21.829, P=0.036) were independent risk factors of bleeding recurrence in patients with small intestinal vascular lesions. DBE treatment was the protective factor of bleeding recurrence in patients with small intestinal vascular lesion ( OR=0.214, 95% CI 0.057 to 0.808, P=0.023). Conclusions:DBE is effective in the treatment of small intestinal vascular lesion bleeding, especially for single vascular lesion. Blood transfusion during disease course and complication with valvular heart disease are independent risk factors for bleeding recurrence in patients with small intestinal vascular lesion.

NDFIP1 has been previously reported as a tumor suppressor in multiple solid tumors, but the function of NDFIP1 in NSCLC and the underlying mechanism are still unknown. Besides, the WW domain containing proteins can be recognized by NDFIP1, resulted in the loading of the target proteins into exosomes. However, whether WW domain-containing transcription regulator 1 (WWTR1, also known as TAZ) can be packaged into exosomes by NDFIP1 and if so, whether the release of this oncogenic protein via exosomes has an effect on tumor development has not been investigated to any extent. Here, we first found that NDFIP1 was low expressed in NSCLC samples and cell lines, which is associated with shorter OS. Then, we confirmed the interaction between TAZ and NDFIP1, and the existence of TAZ in exosomes, which requires NDFIP1. Critically, knockout of NDFIP1 led to TAZ accumulation with no change in its mRNA level and degradation rate. And the cellular TAZ level could be altered by exosome secretion. Furthermore, NDFIP1 inhibited proliferation in vitro and in vivo, and silencing TAZ eliminated the increase of proliferation caused by NDFIP1 knockout. Moreover, TAZ was negatively correlated with NDFIP1 in subcutaneous xenograft model and clinical samples, and the serum exosomal TAZ level was lower in NSCLC patients. In summary, our data uncover a new tumor suppressor, NDFIP1 in NSCLC, and a new exosome-related regulatory mechanism of TAZ.
Humans ; Carcinoma, Non-Small-Cell Lung/metabolism* ; Carrier Proteins/metabolism* ; Cell Line ; Cell Proliferation ; Exosomes/metabolism* ; Lung Neoplasms/genetics* ; Membrane Proteins/metabolism* ; Transcriptional Coactivator with PDZ-Binding Motif Proteins/metabolism*