Time filter

Source Type

Guo Y.,Anhui Medical University | Wan S.Y.,82nd Hospital of the Peoples Liberation Army | Zhong X.,Anhui Medical University | Zhong M.K.,Anhui Medical University | Pan T.R.,Anhui Medical University
Neuroendocrinology Letters

OBJECTIVE: To examine the effect of levothyroxine (L-T4), vitamin E or both on oxidative stress status and hippocampal apoptosis in a propylthiouracil (PTU)-induced hypothyroid rat model. METHODS: Sprague-Dawley rats were randomly divided into five groups: Control, PTU+PTU+L-T4+PTU+Vit E, PTU+Vit E+L-T4. In each group we assessed levels of serum triiodothyronine (T3), tetraiodothyronine (T4), thyroid stimulating hormone (TSH), hippocampus cellular apoptosis index (AI), hippocampus nicotinamide adenine denucleotide hydrogen (NADPH) oxidase and superoxide dismutase (SOD). RESULTS: 1) Compared with the control group, NADPH oxidase levels were significantly increased, and SOD levels were significantly reduced in the PTU groups (p<0.05). 2) Compared to the PTU group, SOD levels were significantly increased in the PTU+Vit E and PTU+L-T4+Vit E group (p<0.05). NADPH oxidase levels were significantly decreased in the PTU+L-T4, PTU+Vit E and PTU+ L-T4+Vit E group (p<0.05). 3) Compared with the control group, hippocampus AI increased significantly in the PTU group (p<0.05). Compared with the PTU group, hippocampus AI was significantly reduced in the PTU+L-T4 group and PTU+L-T4+Vit E group (p<0.05). 4) Hippocampus AI was positively correlated with NADPH oxidase expression levels in hippocampus tissue (r=0.644, p<0.01). CONCLUSION: Levothyroxine replacement therapy combined with vitamin E reduces hippocampus AI by improving oxidative stress. This study suggested that the mechanisms of hippocampus tissue injury in a hypothyroid rat model is related to hippocampus apoptosis from increased oxidative stress. © 2014 Neuroendocrinology Letters. Source

Jiang S.,82nd Hospital of the Peoples Liberation Army
Journal of Medical Case Reports

Introduction. Malignant fibrous histiocytoma is a very common subtype of soft-tissue sarcoma in middle and late adulthood. However, malignant fibrous histiocytoma of the testis is very rare in adolescents. Case presentation. We report here the case of a 14-year-old Han Chinese boy, who presented with left scrotal mass lasting for 20 days along with distending pain for 5 days. A physical examination revealed a chicken egg-sized, firm, well-defined mass and unclear epididymis. A B-scan ultrasonography of the left scrotum displayed a 9.0×5.2×4.5cm medium- or low-echoic lobulated mass, which suggested a left testicular neoplasm. A fine needle aspiration cytology examination revealed that the cells obtained from the patient's testicular neoplasm were composed of myxoid spindle, and ovoid cells with nuclear atypia and mitotic activity, and arranged in a whirlpool or storiform pattern. Under histological examination, the tumor cells were arranged in a storiform pattern, which displayed mucoid matrix degeneration, and grew invasively. Consequently, a histopathological diagnosis suggested myxofibrosarcoma (or myxoid malignant fibrous histiocytoma). Conclusions: An ultrasonic examination combined with fine needle aspiration cytology should be helpful for the initial differential diagnosis of testicular malignant fibrous histiocytoma. However, the final confirmation relies on histopathological examination. To the best of our knowledge, this is the first reported case of malignant fibrous histiocytoma of the testis in an adolescent. © 2013 Wang et al.; licensee BioMed Central Ltd. Source

Jiang S.,82nd Hospital of the Peoples Liberation Army | Jiang S.,Bengbu Medical College | Zhao C.,82nd Hospital of the Peoples Liberation Army | Zhao C.,Bengbu Medical College | And 15 more authors.
International Journal of Molecular Medicine

Several aberrant microRNAs (miRNAs or miRs) have been implicated in esophageal cancer (EC), which is widely prevalent in China. However, their role in EC tumorigenesis has not yet been fully elucidated. In the present study, we determined that miR1 was downregulated in esophageal squamous cell carcinoma (ESCC) tissues compared with adjacent non-neoplastic tissues using RT-qPCR, and confirmed this using an ESCC cell line. Using a nude mouse xenograft model, we confirmed that the re-expression of miR1 significantly inhibited ESCC tumor growth. A tetrazolium assay and a trypan blue exclusion assay revealed that miR1 suppressed ESCC cell proliferation and increased apoptosis, whereas the silencing of miR1 promoted cell proliferation and decreased apoptosis, suggesting that miR1 is a novel tumor suppressor. To elucidate the molecular mechanisms of action of miR1 in ESCC, we investigated putative targets using bioinformatics tools. MET, cyclin D1 and cyclin-dependent kinase 4 (CDK4), which are involved in the hepatocyte growth factor (HGF)/MET signaling pathway, were found to be targets of miR1. miR1 expression inversely correlated with MET, cyclin D1 and CDK4 expression in ESCC cells. miR1 directly targeted MET, cyclin D1 and CDK4, suppressing ESCC cell growth. The newly identified miR1/MET/cyclin D1/CDK4 axis provides new insight into the molecular mechanisms of ESCC pathogenesis and indicates a novel strategy for the diagnosis and treatment of ESCC. Source

Zhang N.,Bengbu Medical College | Fu H.,Jiangsu University | Ding Y.,82nd Hospital of the Peoples Liberation Army | Wang X.,Bengbu Medical College | And 2 more authors.
Oncology Reports

Esophageal squamous cell carcinoma (ESCC) is the predominant histologic subtype of esophageal cancer and is characterized by a high mortality rate and geographic differences in incidence. microRNAs (miRNAs) are small, non-coding RNAs that play important roles in the regulation of genes associated with cancer development and progression. In the present study, we demonstrated that microRNA-100 (miR-100) demonstrated markedly lower expression in the ESCC tissues as validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Furthermore, we found that the downregulation of miR-100 was significantly correlated with the status of lymph node metastasis in the 34 ESCC patients. Next, we investigated the role and mechanism of miR-100 in ESCC cells and found that miR-100 modulated the migration and invasion but not the apoptosis and proliferation of ESCC cells in vitro. We further demonstrated that miR-100 directly targeted the mTOR 3'UTR and repressed the expression of mTOR, a tumor-related gene. Similarly, miR-100 has been reported as a tumor suppressor by controlling cell migration and invasion, as it can target mTOR genes. These results provide insight into the potential mechanisms of miR-100 in the pathogenesis of ESCC. Source

Discover hidden collaborations