Objective To analyze the multi-slice computed tomography (MSCT) enhanced findings in the patients with primary small intestinal stromal tumor(SIST),and to probe the relationship between the imaging findings and the pathologic risk in order to improve the diagnostic accuracy.Methods Thirty patients with primary SIST confirmed by surgical pathology were enrolled in this study.Characterization and compassion of the clinical manifestations and MSCT enhanced findings were carried out between the pathologic low-and high-risk groups.Furthermore,the relationship was analyzed between the enhanced findings and the pathologic risk.Results Among all 30 patients with primary SIST,the lesion was located at duodenum in 5 patients (16.7％),at jejunum in 16 (53.3％),and at ileum in 9 (30％).14 patients were classified in the low risk group with the lesion with the average length of (3.8±0.9) cm,and other 16 in the high-risk group with lesion with the average length of (7.0 ± 1.4) cm.There were no statistical differences between the low-and high-risk groups in CT value in plain and venous phase,and in added value in arterial,venous and delayed phases.However,the significantly differences were observed in CT value in arterial and delayed phases between two groups (P＜0.05).Conclusion MSCT may effectively evaluate the pathologic risk of primary SIST.There are significant differences of the enhanced findings between the low and high-risk groups,which can provide important apreoperative classification for the therapy.

Objective To study the effect of bel-2 siRNA on apoptosis of HL-60 cells.Methods bcl-2 siRNA was synthesized in vitro transcription with silencer siRNA construction kit.The synthesized siRNA was transfected into HL-60 cells with Amine siPORT transfection.We used MTT flow cytometer and hoechst 33258 flourescence stainning t0 evaluate cell proliferation and apoptosis. Results.Bcl-2 siRNA could partially inhibit the growth of HL-60 cells.After incubated with bcl-2 siRNAl for 48 hours,HL-60 cells exhibited morphologic characteristic of apoptosis including chromatin condensation,crescents formation and nuclear fragmentation.Conclusion Effective bcl-2 siRNA can induce apoptosis and inhibit cell proliferation.

Aim To study the interference role of Bcl-2 siRNA on HL-60 cells. Methods Bcl-2 siRNA was synthesized in vitro transcription with silencer siRNA construction kit. The synthesized siRNA was transfected into HL-60 cells with lipid siPORT transfection. Forty-eight hours after the transfection, we used MTT and immunofluorescence to detect cell proliferation and apoptosis,and used RT-PCR and immunofluorescence to detect the level of Bcl-2 mRNA and Bcl-2 protein expression. Result Bcl-2 siRNA reduced the level of Bcl-2 mRNA and Bcl-2 protein expression in HL-60 cells and induced cell apoptosis. There was no difference on the effect of other groups compared with the control. Effective Bcl-2 siRNA specifically degraded Bcl-2 expression in the levels of mRNA and protein and induced HL-60 cells apoptosis.Conclusion These results indicate that siRNA is a highly specific tool for targeted gene knockdown. siRNA-mediated gene silencing is a reliable approach for large-scale screening of gene function and drug target validation.

Methods: From September 3, 2018, to March 23, 2024, participants with essential hypertension (receiving antihypertensive medication treatment, hypertension group) and normal blood pressure (control group) were recruited from the Cardiology Department of Shanghai Hospital of Traditional Chinese Medicine, the Coronary Care Unit of Shanghai Tenth People's Hospital, the Physical Examination Center of Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, and the Gaohang Community Health Service Center. This study employed the propensity score matching (PSM) method to reduce study participants selection bias. Spectral information in the facial visible light spectrum of the subjects was collected using a flame spectrometer, and the spectral chromaticity values were calculated using the equal-interval wavelength method. The study analyzed the differences in spectral reflectance across various facial regions, including the entire face, forehead, glabella, nose, jaw, left and right zygomatic regions, left and right cheek regions as well as differences in parameters within the Lab color space between the two subject groups. Feature selection was conducted using least absolute shrinkage and selection operator (LASSO) regression, followed by the application of various machine learning algorithms, including logistic regression (LR), support vector machine (SVM), random forest (RF), Naïve Bayes (NB), and eXtreme Gradient Boosting (XGB). The reduced-dimensional dataset was split in a 7 : 3 ratio to establish a classification and assessment model for facial coloration related to primary hypertension. Additionally, model fusion techniques were applied to enhance the predictive power. The performance of the models was evaluated using metrics including the area under the curve (AUC) and accuracy. Shapley Additive exPlanations (SHAP) was used to interpret the outcomes of the models. Results: A total of 114 participants were included in both hypertension and control groups. Reflectance analysis across the entire face and eight predefined areas revealed that the hypertensive group exhibited significantly higher reflectance of corresponding color light in the blue-violet region (P < 0.05) and a lower reflectance in the red region (P < 0.05) compared with control group. Analysis of Lab color space parameters across the entire face and eight predefined areas showed that hypertensive group had significantly lower a and b values than control group (P < 0.05). LASSO regression analysis identified a total of 18 facial color features that were highly correlated with hypertension, including the a values of the chin and the right cheek, the reflectance at 380 nm and at 780 nm of the forehead. The results of the multi-model classification showed that the RF classification model was the most effective, with an AUC of 0.74 and an accuracy of 0.77. The combined model of RF + LR + SVM outperformed a single model in their classification performance, achieving an AUC of 0.80 and an accuracy of 0.76. SHAP model visualization results indicated that the top three contributors to ideal prediction results based on the characteristics from the facial spectrum were the reflectance at 380 nm across the entire face and of the nose as well as the a value of the chin. Conclusion Within the same age group, patients with essential hypertension exhibited significant and regular changes in facial color and facial spectral reflectance parameters after the administration of antihypertensive drugs. Furthermore, facial reflectance indicators, such as the overall reflectance at 380 nm and the a value of the chin, could offer valuable references for clinically assessing the drug efficacy and health status of patients with essential hypertension.

AIM: In order to investigate the change of CD36 expression in atherosclerosis. METHODS: Chinese minipigs were fed a normal control diet (CD) or a high fat/high cholesterol diet (HFHC) for 12 months after common carotid artery injury induced by balloon denudation. Plasma total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) were determined by commercially enzymatic methods. CD36 mRNA and protein levels were determined by reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting and immunohistochemistry, respectively. RESULTS: After HFHC for 12 months, plasma total cholesterol, HDL cholesterol and triglyceride in HFHC minipigs were increased compared with the control. CD36 expression and aorta PPAR? in HFHC minipigs were upregulated. CONCLUSION: HFHC may induce hyper cholesterolemia, hypertriglyceridemia and upregulation of CD36 and aortic PPAR? expression.

Objective This study was to investigate the effect of caloric restriction on the plasticity of visual cortex in adult monocular deprivation (MD) amblyopic mice,as well as to promote the treatment of amblyopia,and to explore the possible molecular mechanism of this benefical effect.Methods Fifty healthy newborn Kunming mice of clean grade were randomly divided into 3 groups using a random number table method:normal control group (n =14),MD+ ad libitum group (n=18) and MD+ caloric restriction group (n=18).A mouse model of adult MD amblyopia was established,and caloric restriction intervention and ad libitum were performed on MD + caloric restriction group and MD+ ad libitum group,respectively.The visual acuity and flash visual evoked potential (F-VEP) of each group were detected.The synaptic structure of visual cortex neurons was observed by transmission electron microscope,and the expression of phosphorylated AMP-activated protein kinase-α(p-AMPKα) and silent information regulator 1 (SIRT1) in visual cortex were detected by Western blot.The animal feeding and use was in accordance with the standards set by the ARVO.Results The weight of mice in MD+ caloric restriction group increased from the beginning of the first week,and was significantly lower than that in the MD + ad libitum group (P＜0.05).Compared with the MD+ ad libitum group,the visual acuity was restored,the latency was shortened,and the amplitude of F-VEP was increased in the deprived eyes of MD+ caloric restriction group (all at P＜0.05).Transmission electron microscope observation showed that the width of synaptic gap of visual cortical neurons was significantly narrower,and the thickness of postsynaptic density was significantly thicker in MD+ caloric restriction group than that in the MD+ ad libitum group (both at P＜0.05);compared with the normal control group,the synaptic gap was widened and the postsynaptic density was significantly thicker than that in the MD+ ad libitum group (both at P＜0.05).Western blot showed that the expression of p-AMPKα in visual cortex in the normal control group,MD+ caloric restriction group and MD+ ad libitum group was 0.89±0.03,0.94±0.02 and 0.74 ±0.02,and the expression of SIRT1 was 0.97±0.11,0.95±0.14 and 0.58±0.13,respectively,showing significant differences among the three groups (F =14.57,P =0.00;F=23.91,P=0.00),the expressions of p-AMPKα and SIRT1 in visual cortex were increased in MD+ caloric restriction group than those in M D+ ad libitum group (both at P＜0.05).Conclusions Caloric restriction can restore the ultrastructure of synapses and improve the visual cortical plasticity in adult MD mice,so that help to improve visual function.Its mechanism may be related to the activation of AMPK-SIRT1 pathway.

Objective To examine role and possible mechanism of enriched environment (EE) on regulating recovery of visual function in adult monocular deprivation amblyopia mice.Methods A total of 72 healthyKunming mice were divided into normal control group,monocular deprivation (MD) group,MD+EE group and M D+ fluoxetine group by random number table.Except for the normal control group,the mice in the other groups were sutured on the right eyelid 21 days after birth to establish MD amblyopia model.the mice were fed in standard environment or EE for 4 weeks according to the group.Visual acuity and flash visual evoked potential (F-VEP) of mice in each group were detected.The distribution of microtubule associated protein 2 (MAP2) in visual cortex of adult amblyopic mice were detected by immunohistochemistry.The expression of MAP2,synaptophysin (SYP) and postsynaptic density protein-95 (PSD-95) protein in visual cortex of adult amblyopic mice were detected by western blot.The experimental protocol was approved by the Animal Care and Use Committee of Hunan Children's Hospital and conformed to the National Institutes of Health Guide for the Care and Use of Laboratory Animals.Results There was a significant difference in the visual acuity of deprived eye among each group (F=114.632,P＜0.001).The visual acuity in MD group is lower than that in normal control group,with a significant difference (t =15.480,P＜0.001).Compared with MD group,visual acuity was restored in MD+ EE group and MD +fluoxetine group,with significant differences (t =15.071,P ＜ 0.001;t =14.841,P ＜ 0.001).There was a significant difference in the P2 latency and amplitude of F-VEP in deprived eye among each group (F=36.510,P=0.000;F=34.140,P=0.000).Compare with normal control group,P2 latency was prolonged and P2 amplitude of F-VEP was decreased in deprived eye in MD group,with significant differences (t =10.220,P =0.000;t =10.09,P =0.000).Western blot assay showed that there was a significant difference in the expression of MAP2 in visual cortex contralateral deprived eye among each group (F=18.142,P=0.000).The expression of MAP2 in MD group was significantly lower than that in normal contral group (t=3.056,P＜0.01);Compared with MD group,MAP2 expression was increased in MD+EE group and MD+fluoxetine group (t =2.541,P =0.031;t =2.157,P =0.017).There were significant differences in the expression of SYP and PSD-95 in visual cortex contralateral to deprived eye among each group (F =12.871,P =0.000;F =25.060,P =0.000).Compared with normal contral group,SYP and PSD-95 expression in visual cortex were down-regulated in MD group,with significant differences (t =6.054,P =0.000;t =8.631,P =0.000).The expression of SYP and PSD-95 protein in MD+EE group and MD+fluoxetine group were significantly higher than those in MD group (all at P＜0.05).Conclusions EE can recover visual function through up-regulating the expression of MAP2,which can modulate the dendritic branch trim and neural plasticity of visual cortex in adult MD mice.

Objective:To explore the related factors of poor prognostis in children with Henoch-Sch?nlein purpura nephritis (HSPN), and provide reference for predicting and improving the prognosis of children with HSPN.Methods:The clinical and pathological data of children with HSPN hospitalized in the Department of Nephrology, Children's Hospital Affiliated to Capital Institute of Pediatrics from May 2007 to June 2019 were retrospectively reviewed. According to the prognosis, the patients were divided into complete remission group and persistent abnormal group.Results:(1) Among 108 cases, there were 73 males and 35 females, with the onset age ranging from 5 to 16 years and average age of (9.5±2.8) years. The interval time from the first clinic in our hospital to the last follow-up was 2-131 months, with average of 24.8 months. Renal involvement occurred in the course of Henoch-Sch?nlein purpura from 1 day to 51 months, and the renal biopsy time was 5 days to 60 months after renal involvement. (2) Hematuria with proteinuria type and nephrotic syndrome type were predominant, and there was no significant difference between the two groups. The proportion of gross hematuria in the persistent abnormal group were significantly higher than that in the complete remission group (52.6% vs 31.4%, χ2=4.659, P=0.031). There were significant differences in serum creatinine and urea between the two groups (both P<0.05). The proportion of hyperuricemia in the persistent abnormal group was higher than that in the complete remission group (39.5% vs 21.4%, χ2=3.998, P=0.046). After clinical treatment, though there was no significant difference in proteinuria between the two groups at the beginning of the disease, the negative transformation rate of proteinuria in the complete remission group was higher than that in the persistent abnormal group after 3 months (55.7% vs 34.2%, χ2=4.562, P=0.033). (3) According to International study of Kidney Disease in Children (ISKDC) pathology classification, 14 cases (36.8%), 21 cases (55.3%), 3 cases (7.9%) withⅡ, Ⅲ, Ⅳ level in the persistent abnormal group and 21 cases (30.0%), 49 cases (70.0%), 0 case with Ⅱ, Ⅲ, Ⅳ level (70.0%) in the complete remission group after (20.16±24.86) months of follow-up, and the difference between the two groups was not statisticcally significant ( Z=-0.135, P=0.892). According to the Oxford Classification of IgA nephropathy, 36(33.3%) children had tubule-interstitial lesions (T1, 26%-50% tubular atrophy or interstitial fibrosis), and the proportion in the persistent abnormal group was significantly higher than that in the complete remission group (50.0% vs 24.3%, Z=-2.695, P=0.007). (4) Compared with T0 (0-25% tubular atrophy or interstitial fibrosis), the incidence of gross hematuria and hyperuricemia in the T1 tubule-interstitial lesion were both higher than that (respectively 63.9% vs 27.8%, χ2=13.061, P<0.001; 38.9% vs 22.2%, χ2=3.983, P=0.046). (5) Multivariate logistic regression analysis showed that renal tubule-interstitial lesion was a risk factor for poor prognosis of HSPN ( OR=2.580, 95% CI 1.055-6.310, P=0.038). Conclusions:Renal tubule-interstitial lesion is a risk factor for the persistent abnormal of HSPN. Gross hematuria and hyperuricemia are related to tubule-interstitial lesions.

Abstract: To investigate the protective effect and mechanisms of silent information regulator 1(SIRT1) agonist resveratrol on monocrotaline-induced Hepatic sinusoidal obstruction syndrome(HSOS) in rats. Methods: Thirty-two male Sprauge-Dawley(SD) rats were randomly divided into three group, with 8 rats in the control group and 12 rats in each of the monocrotaline group and resveratrol group. The monocrotaline group and resveratrol group were given monocrotaline(160 mg/kg) by single gavage. The resveratrol group was intraperitoneally injected with resveratrol solution [30 mg/(kg·d)] one day before intragastric administration. The experiment was terminated 2 days after the monocrotaline administration. Serum alanine aminotransferase(ALT), aspartate aminotransferase(AST), total bilirubin(TBiL), glutathione(GSH) and malondialdehyde(MDA) in liver homogenate were detected. The pathological change of liver tissue was observed. The protein expression levels of SIRT1, hypoxia-inducible factor-1α(HIF-1α), and vascular endothelial growth factor(VEGF) in liver were detected by Westernblot. Results: Compared with the control group, the serum ALT, AST and TBiL in monocrotaline group increased(allP<0.01), GSH in liver homogenate decreased(P<0.01), MDA increased(P<0.01). Disordered arrangement, degeneration and necrosis of liver cells, congestion and dilation of hepatic sinuses and damage of central vein endothelium were observed. SIRT1 decreased(P<0.01), HIF-1α and VEGF protein expression increased(allP<0.01). After resveratrol treatment, serum ALT, AST and TBiL obviously decreased(P<0.05;P<0.05;P<0.01). GSH in liver homogenate increased(P<0.01), MDA decreased(P<0.01). And resveratrol also could inhibit the liver pathological damage caused by monocrotaline. SIRT1 protein expression increased(P<0.01), HIF-1α and VEGF protein expression also decreased(allP<0.01). Conclusion Resveratrol can improve Hepatic sinusoidal obstruction syndrome caused by monocrotaline in rats, and the mechanism is related to its activation of SIRT1, inhibition of HIF-1α/VEGF signaling pathway and antioxidanion.

Objective : To explore the mechanism of hippocampal corticotropin-releasing hormone ( CRH) receptor type 1 ( CRHR1 ) in chronic stress-induced learning and memory impairment in early aged mice． Methods: C57BL /6J mice aged 12 －14 months were divided into two groups according to gender，and then divided into wild type (WT) group and hippocampal CRHR1 conditional gene knockout (KN) group according to genotype．Mice in each group were randomly divided into control group and stress group，and the stress group was subjected to chronic unpredictable stress ( CUS ) for 30 days． Genotyping of mice was performed using polymerase chain reaction ( PCR) ，agarose gel electrophoresis and real-time fluorescence quantitative PCR (RT-qPCR) ．The new object rec- ognition experiment and Morris Water maze measured learning and memory ability．Golgi-Cox staining was used to observe damage to hippocampal neuronal dendrites． The protein expressions of target protein of rapamycin (mTOR) ，p-mTOR (Ser2448) ，ribosomal protein S6 kinase ( p70S6K) and p-p70S6K ( Thr389 / Thr412 ) were detected by Western blot．Serum levels of corticotropin releasing hormone ( CRH) were measured by ELISA. Results : Compared to mice without chronic stress，the cognitive coefficient of WT stress groups decreased after chron- ic stress，and the difference was statistically significant (P ＜0. 05) ，while there was no significant difference in cognitive coefficient of KN stress groups before and after chronic stress．Compared with the WT stress group，the escape latency of the WT control group was shortened (P＜0. 05) ，and the number of crossing the platform and tar- get quadrant increased (P ＜0. 01) ，and there was no significant difference in the KN groups above． Compared with the WT control group，the WT stress group had a significant reduction in the neuronal complexity in the hipp- ocampal CA1，CA3 and DG regions (P ＜0. 05) and significant reductions in the expression of p-mTOR and p- p70S6K in the hippocampus (P＜0. 05) ．There was no significant difference in the expression of p-mTOR between the KN stress group and the KN control group (P＞0. 05) ，except that the expression of p-mTOR in the hippocam- pus of the female group decreased (P＜0. 05) ．In addition，the serum level of CRH in the stress group was higher than that in the control group (P＜0. 01) ． Conclusion Hippocampal CRHR1 regulates learning and memory im- pairment and neuronal dendrite damage in early aged mice induced by chronic stress．The mechanism may be that high levels of CRH induced by chronic stress cannot bind to CRHR1 receptor，thereby enhancing the expression of down-regulated mTOR / p70S6K signaling pathway.