To discuss the clinical situation and treatment of cervical intramedullary spinal teratoma, two cases of it in our department were presented, and the related literatures were reviewed. A concomitant anomaly of the cervical vertebral canal was found to be accompanied by cervical intramedullary spinal teratoma. MRI showed the tumors with mixed signal intensity. During operation the tumor was found to have both cysts and hard bony nodules. It was very difficult to remove the total tumor. It is concluded that the plain film of cervical vertebra and cervical spine MRI are sensitive to differentiate teratomas from other tumors. Surgery should be the first choice for treatment.

AIM: To detect the signal pathway of apoptosis induced by 4-hydroxyphenyl-retinamide(4-HPR) and the biological effect of parthenolide-induced apoptosis.METHODS: TUNEL staining,FCM analysis,electrophoretic mobile shift assay(EMSA) were used to determine the actual effects and its mechanism of parthenolide on the 4-HPR-induced apoptosis in human hepatoma Hep-3B and SK-Hep-1 cells.RESULTS: The results of TUNEL and PI staining showed that parthenolide selectively enhanced 4-HPR-induced apoptosis in Hep-3B and SK-Hep-1 cells.Subsequent observations using EMSA assay indicated that parthenolide effectively inhibited NF-?B activation during fenretinide-induced apoptosis.CONCLUSION: These findings indicate that parthenolide suppresses 4-HPR-induced apoptosis via inhibition of NF-?B activation and that NF-?B activation during fenretinide-induced apoptosis might have an anti-apoptotic effect.

BACKGROUND: With age and blood pressure increasing, the damaged elastic membrane induced by degenerative vascular matrix results in calcium and collagen deposition, and finally expanded large arteries and aortas are easy to cause arteriosclerosis. OBJECTIVE: To compare the rheological properties of the common carotid artery in the youth and elderly, thus providing a basis for the study on the pathogenesis of atherosclerosis of the common carotid artery. METHODS: Common carotid arteries were respectively removed from the young and elderly cadavers. Ten samples from each group were randomly selected, and subjected to stress relaxation and creep tests. Meanwhile, one sample from each group was selected for histological observation. RESULTS AND CONCLUSION: The stress at 7200 s in the young group was significantly decreased compared with the elderly group (P < 0.05). The strain at 7200 s in the young group was significantly increased compared with the elderly group (P < 0.05). Scanning electron microscope observed that in the elderly group, there were lipid plaques and foam cell accumulation; the internal elastic lamina and middle elastic plate presented with degeneration, rupture and disintegration; and there were abundant plaques and inflammatory cells in the intimal and media, which characterized as atherosclerosis. While no lipid plaques were found in the young group. These results indicate that the elastic fibers and collagen fibers in the common carotid artery arrange in disorder as age increases, and the rheological properties are also changed.

Hypoxia inducible factor-1αis a kind of hypoxia response factor. Acute cerebral ischemia and anoxia can induce up-regula-tion of hypoxia inducible factor-1α, and the downstream genes, which plays a role in both the energy metabolism and collateral circulation after cerebral ischemia. Neural stem and progenitor cells regeneration also benefit the functional outcome after ischemic stroke. Hypoxia in-ducible factor-1αmay induce proliferation and differentiation of neural stem and progenitor cells through Notch, Wnt/β-catenin pathways, etc., in the ischemic stroke model.

Sesamin, a lipid-soluble lignin originally isolated from sesame seeds, which induces cancer cell apoptosis and autophagy. In the present study, has been reported that sesamin induces apoptosis via several pathways in human lung cancer cells. However, whether mitophagy is involved in sesamin induced lung cancer cell apotosis remains unclear. This study, the anticancer activity of sesamin in lung cancer was studied by reactive oxygen species (ROS) and mitophagy. A549 cells were treated with sesamin, and cell viability, migration ability, and cell cycle were assessed using the CCK8 assay, scratch-wound test, and flow cytometry, respectively. ROS levels, mitochondrial membrane potential, and apoptosis were examined by flow cytometric detection of DCFH-DA fluorescence and by using JC-1 and TUNEL assays. The results indicated that sesamin treatment inhibited the cell viability and migration ability of A549 cells and induced G0/G1 phase arrest. Furthermore, sesamin induced an increase in ROS levels, a reduction in mitochondrial membrane potential, and apoptosis accompanied by an increase in cleaved caspase-3 and cleaved caspase-9. Additionally, sesamin triggered mitophagy and increased the expression of PINK1 and translocation of Parkin from the cytoplasm to the mitochondria. However, the antioxidant N-acetyl-L-cysteine clearly reduced the oxidative stress and mitophagy induced by sesamin. Furthermore, we found that cyclosporine A (an inhibitor of mitophagy) decreased the inhibitory effect of sesamin on A549 cell viability. Collectively, our data indicate that sesamin exerts lethal effects on lung cancer cells through the induction of ROS-mediated mitophagy and mitochondrial apoptosis.

Sesamin, a lipid-soluble lignin originally isolated from sesame seeds, which induces cancer cell apoptosis and autophagy. In the present study, has been reported that sesamin induces apoptosis via several pathways in human lung cancer cells. However, whether mitophagy is involved in sesamin induced lung cancer cell apotosis remains unclear. This study, the anticancer activity of sesamin in lung cancer was studied by reactive oxygen species (ROS) and mitophagy. A549 cells were treated with sesamin, and cell viability, migration ability, and cell cycle were assessed using the CCK8 assay, scratch-wound test, and flow cytometry, respectively. ROS levels, mitochondrial membrane potential, and apoptosis were examined by flow cytometric detection of DCFH-DA fluorescence and by using JC-1 and TUNEL assays. The results indicated that sesamin treatment inhibited the cell viability and migration ability of A549 cells and induced G0/G1 phase arrest. Furthermore, sesamin induced an increase in ROS levels, a reduction in mitochondrial membrane potential, and apoptosis accompanied by an increase in cleaved caspase-3 and cleaved caspase-9. Additionally, sesamin triggered mitophagy and increased the expression of PINK1 and translocation of Parkin from the cytoplasm to the mitochondria. However, the antioxidant N-acetyl-L-cysteine clearly reduced the oxidative stress and mitophagy induced by sesamin. Furthermore, we found that cyclosporine A (an inhibitor of mitophagy) decreased the inhibitory effect of sesamin on A549 cell viability. Collectively, our data indicate that sesamin exerts lethal effects on lung cancer cells through the induction of ROS-mediated mitophagy and mitochondrial apoptosis.

Neuropathic pain (NP) that contributes to the comorbidity between pain and depression is a clinical dilemma. Neuroinflammatory responses are known to have potentially important roles in the initiation of NP and depressive mood. In this study, we aimed to investigate the effects of paeoniflorin (PF) on NP-induced depression-like behaviors by targeting the hippocampal neuroinflammation through the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-kB) signaling pathway. We used a murine model of NP caused by unilateral sciatic nerve cuffing (Cuff ). PF was injected intraperitoneally once a day for a total of 14 days. Pain and depression-like behavior changes were evaluated via behavioral tests. Pathological changes in the hippocampus of mice were observed by H&E staining. The levels of proinflammatory cytokines in the hippocampus were detected using ELISA. Activated microglia were measured by immunohistochemical staining. The TLR4/NF-kB signaling pathwayassociated protein expression in the hippocampus was detected by western blotting. We found that the PF could significantly alleviate Cuff-induced hyperalgesia and depressive behaviors, lessen the pathological damage to the hippocampal cell, reduce proinflammatory cytokines levels, and inhibit microglial over-activation. Furthermore, PF downregulated the expression levels of TLR4/NF-kB signaling pathwayrelated proteins in the hippocampus. These results indicate that PF is an effective drug for improving the comorbidity between NP and depression.

Neuropathic pain (NP) that contributes to the comorbidity between pain and depression is a clinical dilemma. Neuroinflammatory responses are known to have potentially important roles in the initiation of NP and depressive mood. In this study, we aimed to investigate the effects of paeoniflorin (PF) on NP-induced depression-like behaviors by targeting the hippocampal neuroinflammation through the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-kB) signaling pathway. We used a murine model of NP caused by unilateral sciatic nerve cuffing (Cuff ). PF was injected intraperitoneally once a day for a total of 14 days. Pain and depression-like behavior changes were evaluated via behavioral tests. Pathological changes in the hippocampus of mice were observed by H&E staining. The levels of proinflammatory cytokines in the hippocampus were detected using ELISA. Activated microglia were measured by immunohistochemical staining. The TLR4/NF-kB signaling pathwayassociated protein expression in the hippocampus was detected by western blotting. We found that the PF could significantly alleviate Cuff-induced hyperalgesia and depressive behaviors, lessen the pathological damage to the hippocampal cell, reduce proinflammatory cytokines levels, and inhibit microglial over-activation. Furthermore, PF downregulated the expression levels of TLR4/NF-kB signaling pathwayrelated proteins in the hippocampus. These results indicate that PF is an effective drug for improving the comorbidity between NP and depression.

Diabetic cardiomyopathy (DCM), a serious complication of diabetes mellitus, is associated with changes in myocardial structure and function. This study sought to explore the ability of insulin-like growth factor-1 (IGF-1) to modulate DCM and its related mechanisms. Twenty-four male Wistar rats were injected with streptozotocin (STZ, 60 mg/kg) to mimic diabetes mellitus. Myocardial fibrosis and apoptosis were evaluated by histopathologic analyses, and relevant proteins were analyzed by Western blotting. Inflammatory factors were assessed by ELISA. Markers of oxidative stress were tested by colorimetric analysis. Rats with DCM displayed decreased body weight, metabolic abnormalities, elevated apoptosis (as assessed by the bcl-2/bax ratio and TUNEL assays), increased fibrosis, increased markers of oxidative stress (MDA and SOD) and inflammatory factors (TNF-α and IL-1β), and decreased phosphorylation of Akt and glycogen synthase kinase (GSK-3β). IGF-1 treatment, however, attenuated the metabolic abnormalities and myocardial apoptosis, interstitial fibrosis, oxidative stress and inflammation seen in diabetic rats, while also increasing the phosphorylation levels of Akt and GSK-3β. These findings suggest that IGF-1 ameliorates the pathophysiological progress of DCM along with an activation of the Akt/GSK-3β signaling pathway. Our findings suggest that IGF-1 could be a potential therapeutic choice for controlling DCM.
Animals ; Apoptosis ; Blotting, Western ; Body Weight ; Diabetes Mellitus ; Diabetic Cardiomyopathies* ; Enzyme-Linked Immunosorbent Assay ; Fibrosis ; Glycogen Synthase Kinases ; Humans ; In Situ Nick-End Labeling ; Inflammation ; Insulin-Like Growth Factor I ; Male ; Oxidative Stress ; Phosphorylation ; Rats* ; Rats, Wistar ; Streptozocin