[Role of microRNA-155 in Brain Metastasis of Hypoxic Lung Cancer].

Objective: To clarify the relationship between hypoxia stress and the microRNA-155 released from lung cancer cells, to reveal the possible mechanism of brain metastases of lung cancer.

Methods: The hypoxia model of A549 lung cancer cells was established. Lung cancer cells were cultured under the hypoxia condition or normal oxygen condition as control for 0.

[Effect of Hypoxia Inducible Factor-1 Alpha on Brain Metastasis from Lung Cancer and Its Mechanism].

Objective: To study the relationship between hypoxia and the hypoxia inducible factor-1α (HIF-1α) from lung cancer cells, to reveal the possible mechanism of brain metastases of lung cancer.

Methods: The hypoxia model of A549 lung cancer cells was established. After hypoxia culture of A549 cells for 0.

[Effect of Aspirin on Brain Metastasis of Lung Cancer and Its Possible Mechanism].

Objective: To determine the effect of prostaglandin E2 (PGE2) on brain metastasis of lung cancer,and to explore the possible mechanism of aspirin (PGE2 inhibitor) reducing brain metastasis of lung cancer.

Methods: Radioimmunoassay was performed to measure the expression level of PGE2 in cell supernatant collected from cells treated with or without aspirin (8 mmol/L) at different time points. After establishing blood-brain barrier (BBB) model using Transwell, lung cancer cells was added to upper chamber of transwell and was then treated with aspirin (8 mmol/L).

[Effect of Brucea Javanica Oil Emulsion on the Invasiveness of Glioma Cells and Its Possible Mechanism].

Objective: To investigate the effect of brucea javanica oil emulsion on the invasiveness of glioma cells and hosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT) signaling pathway.

Methods: C6 glioma cells were treated by brucea javanica oil emulsion. The inhibition rate of glioma cells was detected by MTT, Western blot was used to detect protein expression levels of PI3K, AKT, and nuclear factor (NF)-κB in glioma cells.

Cyclooxygenase inhibitor induces the upregulation of connexin-43 expression in C6 glioma cells.

The present study was performed to determine whether aspirin, a cyclooxygenase (COX) inhibitor, has an effect on the expression of connexin 43 (Cx43) in C6 glioma cells. Using an glioma invasion model, the expression of Cx43 protein in C6 cells was significantly increased following aspirin treatment at a dose of 8 mmol/l for 30, 60 and 120 min via western blot analysis. The peak value of the Cx43 expression was observed in C6 cells after 120 min of aspirin treatment, which was significantly reduced by prostaglandin E2 (PGE2).

Interleukin-1β induces the upregulation of caveolin-1 expression in a rat brain tumor model.

The aim of the present study was to investigate the expression of caveolin-1 in rat brain glioma tissue, and to determine whether interleukin-1β (IL-1β) has a role in this process. Using glioma cells, a tumor-burdened rat model was established, and the expression of caveolin-1 protein in the tumor sites was significantly increased following intracarotid infusion of IL-1β (3.7 ng/kg/min), as indicated by western blot analysis.

Antitumor Activity of Tenacissoside H on Esophageal Cancer through Arresting Cell Cycle and Regulating PI3K/Akt-NF-κB Transduction Cascade.

Objective. The purpose of the study was to elucidate the molecular mechanism of tenacissoside H (TDH) inhibiting esophageal carcinoma infiltration and proliferation. Methods.

[The Methylation of p16 Gene Promoter in Carcinogenesis and Development of Breast Cancer].

Objective: To investigate the protein expression of the p16 gene and the methylation of its promoter in breast cancer, and to analyze the correlation between the p16 DNA methylation and the clinicopathological features.

Methods: Immuno-histochemistry technique (SP method) and methylation-specific-PCR (MSP) were used to detect p16 protein expression and the methylation of the p16 promoter in 47 breast cancer samples as well as in 20 hyperplasia samples of mammary glands. Results The p16 protein expression in breast cancer samples significantly lower when compared with those of hyperplasia samples (48.

Histone acetylation and expression of mono-aminergic transmitters synthetases involved in CUS-induced depressive rats.

Histone acetylation has been linked to depression, the etiology of which involves many factors such as genetics, environments, and epigenetics. The aim of the present study was to investigate whether it was associated with epigenetic histone modification and gene expression of enzymes responsible for the biosynthesis of norepinephrine and serotonin in rat depression model induced by chronic unpredictable stress (CUS). Eight-week-old male Sprague-Dawley rats were exposed to CUS over 28 days.

Antidepressive effect of paroxetine in a rat model: upregulating expression of serotonin and norepinephrine transporter.

Paroxetine is a selective serotonin reuptake inhibitor used for the treatment of depression; this study investigated its other mechanisms by studying the expression and therefore involvement of norepinephrine transporter (NET) and serotonin transporter (5-HTT). Male Sprague-Dawley rats were divided into a vehicle-treated control group (VC), a paroxetine-treated control group (PC), a vehicle-treated model group (VM), and a paroxetine-treated model group (PM). The depression model was established by chronic unpredicted stress.

ReaxFF molecular dynamics simulations of oxidation of toluene at high temperatures.

Aromatic hydrocarbon fuels, such as toluene, are important components in real jet fuels. In this work, reactive molecular dynamics (MD) simulations employing the ReaxFF reactive force field have been performed to study the high-temperature oxidation mechanisms of toluene at different temperatures and densities with equivalence ratios ranging from 0.5 to 2.

Hyperthermia promotes apoptosis and suppresses invasion in C6 rat glioma cells.

Gliomas are a group of heterogeneous primary central nervous system tumors. Hyperthermia has proven to be a potential therapeutic tool for cancers in the clinic. However, the molecular mechanisms of hyperthermia remain unclear.

Role of ROS/RhoA/PI3K/PKB signaling in NS1619-mediated blood-tumor barrier permeability increase.

The calcium-activated potassium channel (K (Ca) channel) activator, NS1619, has been shown to selectively and time-dependently increase the permeability of the blood-tumor barrier (BTB) by downregulating the expression of tight junction (TJ) protein. However, the role of signaling cascades in this process has not been precisely elucidated. This study was performed to determine the role of signaling cascades involving reactive oxygen species (ROS)/RhoA/PI3K/PKB in increasing the permeability of the BTB induced by NS1619.

Effects of fuel additives on the thermal cracking of n-decane from reactive molecular dynamics.

Thermal cracking of n-decane and n-decane in the presence of several fuel additives are studied in order to improve the rate of thermal cracking by using reactive molecular dynamics (MD) simulations employing the ReaxFF reactive force field. From MD simulations, we find the initiation mechanisms of pyrolysis of n-decane are mainly through two pathways: (1) the cleavage of a C-C bond to form smaller hydrocarbon radicals, and (2) the dehydrogenation reaction to form an H radical and the corresponding decyl radical. Another pathway is the H-abstraction reactions by small radicals including H, CH(3), and C(2)H(5).

Dexamethasone enhances calcium-activated potassium channel expression in blood-brain tumor barrier in a rat brain tumor model.

This study was performed to determine whether dexamethasone (DEX) had an effect on calcium-activated potassium channels (KCa channels) in blood-brain tumor barrier (BTB).Using a rat brain glioma model, we found that the expression of KCa channels protein was significantly increased in brain tumor tissue. And bradykinin-induced increase of KCa channels protein was further enhanced after DEX pretreatment for 3 days.

The molecular mechanism of dexamethasone-mediated effect on the blood-brain tumor barrier permeability in a rat brain tumor model.

This study was performed to determine whether dexamethasone (DEX) had an effect on calcium-activated potassium channels (K(Ca) channels) and Occludin protein in blood-brain tumor barrier (BTB). Using a rat brain glioma model, we found that the expression of K(Ca) channels protein and Occludin protein was significantly increased in brain tumor tissue after DEX treatment for 3 days. Compared with non-DEX-treated animals, Evans Blue levels were greatly attenuated in DEX-treated animals.

Bradykinin-induced blood-tumor barrier opening is mediated by tumor necrosis factor-alpha.

Bradykinin has been shown to increase the permeability of blood-tumor barrier (BTB) selectively. This study was performed to determine whether tumor necrosis factor-alpha (TNF-alpha) was involved in the regulation of this biological process. We found that the levels of TNF-alpha mRNA and heat shock factor-1 (HSF1) protein in C6 cells were markedly up-regulated by bradykinin via real-time RT-PCR and Western blot methods.

Multichannel photoinduced intramolecular electron-transfer excitations in a bis-naphthalimide spermine conjugate by time-dependent density functional theory.

Density functional theory was applied to the investigation of photoinduced electron transfer (ET) and the absorption spectrum for a bis-naphthalimide spermine conjugate. The multichannel feature of ET excitation in this system was focused on because four groups may act as electron donors and acceptors. The segment in this conjugate, N-(N-methylpropyl)-1,8-naphthalimide, which contains one donor and acceptor pair, was studied at first.

[Protective effects of local heat preconditioning on hepatic ischemia/reperfusion injury].

Aim: To study the protective mechanism of HSP70 induced by the heat stress pretreatment on the hepatic ischemia/ reperfusion (I/R) injury.

Methods: To establish the models of the hepatic ischemia/ reperfusion injury using pringle's maneuver with or without heat stress pretreatment. The rats were randomly divided into pretreatment group (HP + I/R) and non-pretreatment group (I/R), in which the expression of HSP70, the MDA contents and SOD activity in liver, the activities of serum AST and ALT, and the pathological changes in liver were detected at 0, 4, 8, 12 and 24 h after I/R.