1.MRI study of cerebral miliary tuberculosis
Ruchen PENG ; Xiuzhi SHEN ; Huanfeng GAO ; Ruiqiang XIN
Chinese Journal of Radiology 2000;0(12):-
Objective To study and analyze the MRI manifestation of miliary tuberculosis of the brain.Methods Twenty-two cases with cerebral miliary tuberculosis of the brain were retrospectively studied with MRI including plain scan and enhanced study with GD-DTPA MRI features regarding the size,shape and distribution of the lesions were summarized and analyzed.Results Miliary tuberculosis of the brain was found most frequently at the junctional area of white and gray matter.The diameter of the lesion was less than 3 mm,therefore,plain scan often failed to display the lesions,however,markedly enhanced tubercles could be demonstrated on enhanced scan.Conclusion Enhanced MRI scan proved to be very helpful in the early detection of miliary tuberculosis of the brain.
2.Correlation between micro-bleeds and hemorrhagic transformation after ischemic stroke
Ruiqiang XIN ; Shuang ZHANG ; Dianping ZHANG ; Lipeng CAI ; Xu NA ; Ruchen PENG
Clinical Medicine of China 2016;32(7):619-621
Objective To investigate the correlation between micro?bleeds and hemorrhagic transformation( HT ) after ischemic stroke. Methods One hundred and forty?five cases patients with acute ischemic stroke who were admitted to Luhe Hospital of Beijing Affiliated to Capital Medical University from 2009 to 2014 were retrospective analyzed. The MBs T2??weighted gradient?echo MRI was performed within 48 hours after admission to examine if there was a micro?bleeds,and the incidence of HT was assessed using follow?up brain MRI or CT in 2 weeks after admission. There were 125 patients with stroke were in without HT group and 20 patients were in HT group. Results There were no significant differences in terms of MBs ( P=0. 170 ) , gender( P=0. 671 ) , age ( P=0. 528 ) , hypertension ( P=0. 597 ) , diabetes ( P=0. 571 ) , hyperlipidaemia ( P=0. 772),smoking(P=0. 672),history of stroke(P=0. 469),coagulation function(P=0. 527),antiplatelet(P=0. 642),anticoagulation(P=0. 611) in HT group and without HT group. Atrial fibrillation((45%(9/20) vs. 22%( 28/125 ) , P = 0. 034 ) , NIHSS score ( 10. 9 ± 0. 5 ) points vs. ( 7. 8 ± 1. 2 ) points, P<0. 001 ) , thrombolysis(20% (4/20) vs.5% (6/125),P = 0.015) have significant differences in two groups.In multivariate logistic regression analysis,atrial fibrillation( OR=2. 421,95%CI 1. 823-3. 256,P=0. 012) ,NIHSS score( OR=9. 303, 95%CI 3. 094-27. 970, P<0. 001 ) were independent predictors for HT after ischemic stroke. Conclusion There is no relationship between MBs and HT after ischemic stroke. Atrial fibrillation,the severe of stroke are independent predictors for HT after ischemic stroke.
3.Imaging Features of Acinetobacter Baumannii Pneumonia
Ruiqiang XIN ; Yancui LI ; Genshen ZHEN ; Junxia CHANG ; Daqing MA
Chinese Journal of Medical Imaging 2017;25(10):748-750
Purpose The incidence and drug resistance rate ofAcinetobacter baumannii pneumonia are becoming more and more serious.To summarize the computed tomography (CT) appearance ofAcinetobacter baumannii pneumonia and to provide evidence for early clinical diagnosis and treatment.Materials and Methods The imaging findings of 49 patients with sputum culture confirmed Acinetobacter baumannii pneumonia were retrospectively analyzed,and the imaging features were summarized.Results The three most common patterns of chest CT findings in Acinetobacter baumannii pneumonia were ground-glass opacification (69.4%,34/49),consolidation (67.3%,33/49),and pleural effusion (53.1%,26/49).While,the most common patterns of chest X-ray were pulmonary plaque (83.7%,41/49),consolidation (36.7%,18/49),and pleural effusion (36.7%,18/49).Further analysis showed that there was no statistically significant difference in the CT and X-ray findings between combined infection of Acinetobacter baumannii with other pathogens and single Acinetobacter baumanniizxcvbnm,infection (P>0.05).Conclusion The three most common changes of chest imaging of Acinetobacter baumannii pneumonia are ground-glass opacification,pulmonary consolidation and pleural effusion.It is of great significance to summarize its imaging features for early diagnosis,treatment and prognosis-predicting.
4.Mechanism of SUMO regulating XBP1 mediated endoplasmic reticulum stress on the progression of liver cancer
Ruiqiang XIN ; Xiaoping SONG ; Fan ZHANG ; Ying SUN ; Tao WANG ; Wei SUN
Journal of International Oncology 2020;47(7):397-403
Objective:To investigate the molecular mechanism of SUMO specific protease 1 (SENP1) regulating endoplasmic reticulum stress transcription regulator X-box binding protein 1 (XBP1) in the proliferation of liver cancer cells.Methods:The pathological samples of 180 patients with primary liver cancer in the Department of Hepatobiliary Surgery of Inner Mongolia People′s Hospital from January 2012 to January 2020 were collected. The expressions of SENP1 and XBP1 in liver cancer, adjacent tissues and different liver cancer cell lines were detected. The correlation between SENP1 positive expression and clinicopathological features of liver cancer patients was analyzed. Immunofluorescence and flow cytometry were used to detect the effect of SENP1 siRNA on XBP1 and apoptosis. SUMO1 expression on XBP1 surface was detected and the effect of SENP1 siRNA on SUMO formation of XBP1 was detected by immunoprecipitation.Results:The expression levels of SENP1 in liver cancer and adjacent tissues were 16.332±4.371 and 6.840±2.238, with a statistically significant difference ( t=-5.073, P=0.017). The expression levels of XBP1 in liver cancer and adjacent tissues were 6.641±2.482 and 16.051±4.452, with a statistically significant difference ( t=3.592, P=0.032). The expression of SENP1 was correlated with stage ( χ2=6.724, P=0.010) and metastasis ( χ2=6.265, P=0.012). Immunofluorescence staining showed that the expressions of XBP1 in L02 (0.509±0.219), MHCC97-L (0.092±0.022) and HCCLM3 (0.086±0.014) cells were significantly different ( F=6.378, P=0.004), while the expression of XBP1 in MHCC97-L and HCCLM3 cells was significantly lower than that in L02 cells ( P=0.023; P=0.021). The expression levels of SENP1 in L02, MHCC97-L and HCCLM3 cells were 0.109±0.079, 0.802±0.392 and 0.921±0.352, with a statistically significant difference ( F=7.783, P=0.004), while the expression level of SENP1 in MHCC97-L and HCCLM3 cells was significantly higher than that in L02 cells ( P=0.039; P=0.016). After transfection of SENP1 siRNA into MHCC97-L and HCCLM3 cells, the expressions of XBP1 increased (0.462±0.192, t=3.664, P=0.022; 0.524±0.203, t=3.383, P=0.028); the expressions of SENP1 decreased (0.153±0.093, t=2.790, P=0.049; 0.165±0.104, t=3.568, P=0.023). The results of flow cytometry showed that the apoptosis rates of L02, MHCC97-L, HCCLM3, MHCC97-L+ SENP1 siRNA and HCCLM3+ SENP1 siRNA cells were (20.80±3.11)%, (2.02±1.20)%, (0.12±0.01)%, (7.01±1.80)%, (6.20±2.01)%, with a statistically significant difference ( F=1.025, P=0.030). The apoptosis rate of MHCC97-L and HCCLM3 cells was significantly lower than that of L02 cells ( P=0.040; P=0.010), the apoptosis rate of MHCC97-L+ SENP1 siRNA and HCCLM3+ SENP1 siRNA cells was significantly higher than that of MHCC97-L and HCCLM3 cells (both P=0.009). Immunoprecipitation results showed that the expression levels of XBP1 in L02, MHCC97-L, HCCLM3, MHCC97-L+ SENP1 siRNA, HCCLM3+ SENP1 siRNA cells were 11.943±5.043, 7.467±1.903, 2.051±0.913, 9.532±3.012, 8.731±3.102, and SUMO1 expression levels were 10.158±4.005, 5.871±3.075, 1.941± 0.907, 8.658±4.878, 7.169±4.677, and the differences were statistically significant ( F=11.730, P=0.010; F=8.548, P=0.001). The expressions of XBP1 and SUMO1 in MHCC97-L ( P=0.028; P=0.038) and HCCLM3 ( P<0.001; P<0.001) cells were lower than those in L02 cells, XBP1 expression in HCCLM3+ SENP1 siRNA cells was higher than that in HCCLM3 cells ( P=0.001), and SUMO1 expression in MHCC97-L+ SENP1 siRNA cells and HCCLM3+ SENP1 siRNA cells respectively was higher than that in MHCC97-L ( P=0.045) and HCCLM3 ( P=0.039) cells. Conclusion:SENP1 siRNA can promote the apoptosis of liver cancer cells by up regulating SUMO modification of XBP1.