Activation of autophagy promotes the inhibitory effect of curcumin analog EF-24 against MDA-MB-231 cancer cells.

Breast cancer is the leading cause of cancer deaths in women worldwide. EF-24, an analog of curcumin, has been shown to possess promising anticancer effects. However, the underlying mechanism remains elusive.

Transcriptome-derived stromal and immune scores infer clinical outcomes of patients with cancer.

The stromal and immune cells that form the tumor microenvironment serve a key role in the aggressiveness of tumors. Current tumor-centric interpretations of cancer transcriptome data ignore the roles of stromal and immune cells. The aim of the present study was to investigate the clinical utility of stromal and immune cells in tissue-based transcriptome data.

Changes in fibrinopeptide A peptides in the sera of rats chronically exposed to low doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a ubiquitously distributed endocrine disruptors. To investigate peptide changes in the sera of rats chronically exposed to TCDD and to explore the association of these changes with liver morphology, TCDD was administrated to male rats at doses of 140, 350, and 875 ng/kg/week for 29 weeks. Serum was collected and proteomic analysis was performed using automated Bruker Daltonics ClinProt with matrix-assisted laser desorption/ionization time-of-flight mass spectrometer.

Proteomic analysis of the rat ovary following chronic low-dose exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a ubiquitously distributed endocrine-disrupting chemical and reproductive toxicant. In order to elucidate low-dose TCDD-mediated effects on reproductive or endocrine functions, female Sprague-Dawley rats were orally administered various concentrations (20, 50, or 125 ng/kg once weekly) TCDD for 29 wk. A proteomic analysis of the ovaries by two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization (MALDI) tandem mass spectrometry showed distinct changes in the levels of several proteins that are relevant markers of TCDD toxicity.

[Role of mitogen-activated protein kinase pathway in chloracne].

Objective: To investigate the role of mitogen-activated protein kinase (MAPK) signal transduction pathway in chloracne.

Methods: Immunohistochemical technique was used to detect the expression of phosphorylated epidermal growth factor receptor (p-EGFR) and p-MAPK proteins in the epithelium of chloracne group and control group.

Results: p-EGFR and p-MAPK was found in all chloracne tissues, whereas no expression of p-EGFR and p-MAPK protein was found in control group.

Randomized double-blind multicentre placebo-controlled clinical trial of the clonidine adhesive patch for the treatment of tic disorders.

Objective: The aim of the present study was to evaluate the therapeutic effectiveness and safety of the clonidine adhesive patch in treating tic disorders.

Method: A total of 437 patients, who met Chinese Classification of Mental Disorders-third edition diagnostic criteria for transient tic disorder (5%), chronic motor or vocal tic disorder (40%) or Tourette disorder (55%), aged 6-18 years, were divided randomly into an active treatment group and a clinical control group. Participants in the active treatment group were treated with a clonidine adhesive patch and participants in the clinical control group with a placebo adhesive patch for 4 weeks.

[Effect of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin on the expression of AhR and TGF-alpha].

Objective: To study HaCaT-keratinocyte cell lines, a chosen model of human epidermis in an attempt to analyze the mRNA expression of AhR and TGF-alpha induced by TCDD METHODS: Semi-quantitative reverse transcription PCR-technique was used for assaying the relative levels of AhR and TGF-alpha mRNA of HaCaT-cells during the proliferation period when the cells were cultured for 24 hours.

Results: Relative level of the AhR-transcripts (corrected with beta-actin) decreased with the elevated concentration of TCDD and the relevant coefficient between the proliferation rate and concentration was -0.548, and the differences among all groups were significant (F =4.

Expression of AhR, CYP1A1, GSTA1, c-fos and TGF-alpha in skin lesions from dioxin-exposed humans with chloracne.

Occupational exposure to certain polychlorinated aromatic hydrocarbons such as dioxins has been suggested to cause chloracne which is a kind of skin disease. The molecular mechanisms of dioxin-mediated chloracne have not been clarified. It is possible that dioxins contribute to the pathogenesis through activation of aryl-hydrocarbon receptor (AhR)-mediated transcription and downstream genes such as CYP1A1, GSTA1 and TGF-alpha.