132℃化学指示卡变色不均消除法

１３２℃化学指示卡变色不均消除法ＥｌｉｍｉｎａｔｉｏｎｏｆＣｏｌｏｒ－ｃｈａｎｇｉｎｇＮｏｎｕｎｉｆｏｒｍｏｆｔｈｅ１３２℃ＣｈｅｍｉｃａｌＩｎｄｉｃａｔｉｎｇＣａｒｄ果海青梁安珍ＧｕｏＨａｉｑｉｎｇ，ＬｉａｎｇＡｎｚｈｅｎ（Ｎｏ．２５２Ｈｏｓｐｉ...     

Leptin receptor deficiency confers resistance to behavioral effects of fluoxetine and desipramine via separable substrates

Depression is a complex, heterogeneous mental disorder. Currently available antidepressants are only effective in about one-third to one-half of all patients. The mechanisms underlying antidepressant response and treatment resistance are poorly understood. Recent clinical evidence implicates the involvement of leptin in treatment response to antidepressants. In this study, we determined the functional role of the leptin receptor (LepRb) in behavioral responses to the selective serotonergic antidepressant fluoxetine and the noradrenergic antidepressant desipramine. While acute and chronic treatment with fluoxetine or desipramine in wild-type mice elicited antidepressant-like effects in the forced swim test, mice null for LepRb (db/db) displayed resistance to treatment with either fluoxetine or desipramine. Fluoxetine stimulated phosphorylation of Akt(Thr308) and GSK-3β(Ser9) in the hippocampus and prefrontal cortex (PFC) of wild-type mice but not in db/db mice. Desipramine failed to induce measurable changes in Akt, GSK-3β or ERK1/2 phosphorylation in the hippocampus and PFC, as well as hypothalamus of either genotype of mice. Deletion of LepRb specifically from hippocampal and cortical neurons resulted in fluoxetine insensitivity in the forced swim test and tail suspension test while leaving the response to desipramine intact. These results suggest that functional LepRb is critically involved in regulating the antidepressant-like behavioral effects of both fluoxetine and desipramine. The antidepressant effects of fluoxetine but not desipramine are dependent on the presence of functional LepRb in the hippocampus and cortex.     

The expression and significance of dishevelled in human glioma

Background

The proto-oncogene dishevelled (Dvl) is a critical component of the Wnt/β-catenin signaling pathway, and its elevated expression in various tumor types is associated with malignancy. However, a role for Dvl in glioma has not been explored.

Materials and methods

To determine whether Dvl expression is elevated in human glioma, we examined the protein levels in 67 human glioma samples and 3 normal brain specimens by Western blotting and immunohistochemistry. To investigate a possible association of Dvl with the malignant phenotype in glioma, the correlation of the Dvl immunoreactivity score (IRS) with β-catenin IRS, the tumor proliferation index (PI), and tumor invasion index (II) were determined for each sample.

Results

The Dvl IRS, β-catenin IRS, PI, and II increased significantly with the pathologic grade of glioma (P <0.001) with average scores of 3.46 ± 3.45, 3.92 ± 3.28, 30.93 ± 17.92, and 20.43 ± 11.79, respectively. Furthermore, the PI and II were significantly higher for the Dvl-positive group than the Dvl-negative group (P <0.001). Correlation analysis demonstrated that β-catenin IRS, PI, and II were positively correlated with Dvl IRS.

Conclusions

Dvl overexpression may contribute to the malignant proliferation and invasion of human glioma.     

Green tea polyphenols protect spinal cord neurons against hydrogen peroxide-induced oxidative stress

Green tea polyphenols are strong antioxidants and can reduce free radical damage. To investigate their neuroprotective potential, we induced oxidative damage in spinal cord neurons using hydrogen peroxide, and applied different concentrations(50–200 μg/mL) of green tea polyphenol to the cell medium for 24 hours. Measurements of superoxide dismutase activity, malondialdehyde content, and expression of apoptosis-related genes and proteins revealed that green tea polyphenol effectively alleviated oxidative stress. Our results indicate that green tea polyphenols play a protective role in spinal cord neurons under oxidative stress.