ABSTRACT
OBJECTIVE: Lymph node metastasis is an important trait of breast cancer, and tumors with different lymph node statuses require various clinical treatments. This study was designed to evaluate the lymph node metastasis of breast cancer through pharmacokinetic and histogram analysis via dynamic contrast-enhanced (DCE) MRI. METHODS AND MATERIALS: A retrospective analysis was conducted to quantitatively evaluate the lymph node statuses of patients with breast cancer. A total of 75 patients, i.e. 34 patients with lymph node metastasis and 41 patients without lymph node metastasis, were involved in this research. Of the patients with lymph node metastases, 19 had sentinel lymph node metastasis, and 15 had axillary lymph node metastasis. MRI was conducted using a 3.0 T imaging device. Segmentation was carried out on the regions of interest (ROIs) in breast tumors under DCE-MRI, and pharmacokinetic and histogram parameters were calculated from the same ROIs. Mann-Whitney U test was performed, and receiver operating characteristic curves for the parameters of the two groups were constructed to determine their diagnostic values. RESULTS: Pharmacokinetic parameters, including Ktrans, Kep, area under the curve of time-concentration, and time to peak, which were derived from the extended Tofts linear model for DCE-MRI, could highlight the tumor areas in the breast and reveal the increased perfusion. Conversely, the pharmacokinetic parameters showed no significant difference between the patients with and without lymph node metastases. By contrast, the parameters from the histogram analysis yielded promising results. The entropy of the ROIs exhibited the best diagnostic ability between patients with and without lymph node metastases (p < 0.01, area under the curve of receiver operating characteristic = 0.765, specificity = 0.706, sensitivity = 0.780). CONCLUSION: In comparison with the pharmacokinetic parameters, the histogram analysis of the MR images could reveal the differences between patients with and without lymph node metastases. The entropy from the histogram indicated that the diagnostic ability was highly sensitive and specific. ADVANCES IN KNOWLEDGE: This research gave out a promising result on the differentiating lymph node metastases through histogram analysis on tumors in DCE-MR images. Histogram could reveal the tumors heterogenicity between patients with different lymph node status.
ABSTRACT
Objective:To investigate the protective effect of schisandrin B (SchB)on the cerebral ischemia reperfusion injury of the rats and the influence in HSPA12B/PI3K/Akt signaling pathway,and to explore the mechanisms.Methods:130 SD rats were divided into sham group,cerebral ischemia reperfusion injury model group (model group),low dose of SchB group (SchB 3 mg· kg-1 ,SchB1 group),middle dose of SchB group (SchB 10 mg·kg-1 ,SchB2 group)and high dose of SchB group (SchB 30 mg·kg-1 ,SchB3 group)(n=26).The rats in sham group didn’t plug lines;the rats in model were used to establish ischemia reperfusion models;the rats in SchB1 ,SchB2 and SchB3 groups were firstly pretreated with different doses of SchB for 7 d,and then they were used to build cerebral ischemia reperfusion injury models.The nerve dysfunction of rats was evaluated by neurologic deficit score.The cerebral edema was detected by measuring the content of water in brain tissue.The morphological changes of brain tissue were observed by toluidine blue staining.The levels of nuclear factor kappa B (NF-κB), tumor necrosis factor-α(TNF-α),interleukin-1 (IL-1)and interleukin-6 (IL-6)in the brain tissue were detected by ELISA.Western blotting method was used to detect the protein expression levels of heat shock protein A12B (HSPA12B ), serine-threonine kinase (Akt ) and phosphorylation serine-threonine kinase (p-AKT ). Results:Compared with sham group,the neurologic deficit score of rats in model group was significantly increased (P <0.01),and the content of water in brain tissue was increased (P < 0.01 );the brain tissue structure was loosened,and the mesenchyme appeared edema;the NF-κB,TNF-α,IL-1,and IL-6 levels were increased (P <0.01),and the expression levels of HSPA12B and p-Akt proteins were decreased (P <0.01).Compared with model group,the neurologic deficit scores of the rats in SchB1 ,SchB2 ,and SchB3 groups were decreased (P <0.01),and the contents of water in brain tissue of the rats in SchB2 and SchB3 groups were decreased (P <0.05);the edema of nerve cells was alleviated,and the cavities were reduced;the NF-κB,TNF-α,IL-1,and IL-6 levels were decreased (P <0.05 or P <0.01),the expression levels of the HSPA12B protein in SchB2 ,and SchB3 groups were increased (P <0.05),and the p-Akt protein expression levels of the rats in SchB1 ,SchB2 ,and SchB3 groups were increased (P <0.01).Conclusion:SchB could protect the cerebral ischemia reperfusion injury of rats,its mechanism may be related to regulating the HSPA12B/PI3K/Akt signaling pathway and inhibiting the inflammatory reaction damage to the nerve cells of reperfusion.
ABSTRACT
Objective To copy the mouse aging model with D-galactose,and to investigate the role of Schisandra total lignin (SCL)in the mouse brain tissue aging and its mechanism.Methods 50 mice were radomly divided into control group,model group (100 mg·kg-1 ·d-1),low dose (35 mg·kg-1 ·d-1)of SCL group (SCL-L), middle dose (70 mg· kg-1 · d-1 )of SCL group (SCL-M)and high dose (140 mg· kg-1 · d-1 )of SCL group (SCL-H)(n=10).D-galactose (100 mg·kg-1 ·d-1 )was injected into the mice hypodermically for 10 weeks to induce aging models in all the groups except control group,and 35,70,and 140 mg· kg-1 · d-1 SCL were administered for 10 weeks in SCL groups.The learning and memory abilities were measured by the Water Maze test.The expression levels of Bax,Bcl-2,ubiquitin (Ub),microtubule-associated protein light chain 3 (LC3)in the brain tissue of the mice in various groups were observed by Western blotting method. The LC3 protein expressions in mouse brain cortex and hippocampus were observed by immunohistochemistry.Results In learning and memory test,compared with control group,the swimming time of the mice in model group was increased (P<0.05),and the number of errors was increased (P<0.05);compared with model group,the swimming time in SCL-L,SCL-M and SCL-H groups was decreased (P<0.05)and the number of errors was also decreased (P<0.05). Compared with control group,the expression level of Bax was increased (P<0.05),the expression level of Bcl-2 was decreased (P<0.05),the expression levels of Ub and LC3-Ⅱ/LC3-Ⅰ proteins were increased (P<0.05)in model group;compared with model group,the expression level of Bax was decreased (P<0.05),the expression level of Bcl-2 was incerased (P<0.05),and the expression levels of Ub and LC3-Ⅱ/LC3-Ⅰ proteins were decreased (P<0.05)in SCL-L,SCL-M and SCL-H groups.In control group,the neuronal morphology was normal,and none of brown granules were visible in the cytoplasm of mouse brain cortex and hippocampus and the expression of LC3 protein was negative.In model group,the neurons were degeneration,and the number of LC3 protein positive cells in the cerebral cortex and hippocamptal tissue was increased (P<0.05).In SCL-L,SCL-M and SCL-H groups,the number of degenerative neurons was decreased,and the number of LC3 protein positive cells was decreased (P<0.05).Conclusion SCL can inhibit the D-galactose-induced brain tissue aging in the mice, and the mechanism is related to regulating autophagy and inhibiting apoptosis.
