Beta2-adrenergic receptor agonist inhibits keratinocyte proliferation by mechanisms involving nitric oxide.

Introduction: Beta2-adrenoceptors regulate proliferation of keratinocytes. Nitric oxide (NO) produced by keratinocytes through stimulation of nitric oxide synthase (NOS) mediates keratinocyte proliferation. Aim: In this study, the mechanism interaction β-ARs and NO production on keratinocyte will be explored, and the important for proliferation will be studied.

Various UVB doses affect change of raf kinase inhibitor protein, nitric oxide and proliferation in keratinocytes.

UVB is a potent modulator of cell growth and differentiation in the skin. The UVB irradiation has been used in treating hyperproliferative dermatoses. Otherwise, UVB radiation is also the major risk factor for developing skin cancer.

RKIP expression of liver and kidney after arsenic exposure.

Arsenic is associated with cancers of kidney and liver. Raf kinase inhibitor protein (RKIP) has been identified as a member of a novel class of molecules that suppress the metastatic spread of tumors. In order to investigate the effect of arsenic to RKIP of liver and kidney, the expression of RKIP of liver and kidney with As (III) was explored in this study.

The expression of RKIP, RhoGDI, galectin, c-Myc and p53 in gastrointestinal system of Cr(VI)-exposed rats.

Hexavalent chromium (CrVI) is considered to be a risk factor in the formation of human cancer. Raf kinase inhibitor protein (RKIP), Rho-GDIα, galectin, c-Myc and p53 play important roles in cancer formation. The purpose of this study was to determine if Cr(VI) induces the formation of gastrointestinal cancer.

Hexavalent chromium inhibited the expression of RKIP of heart in vivo and in vitro.

Background: Chromium (Cr) is considered to be a risk factor to the cardiovascular effects of fine particulate matter components to PM2.5 from traffic in highway patrol officers. RKIP (raf kinase inhibitor protein) is a physiological inhibitor of GRK-2 (G-protein-coupled receptor kinase 2) and affects β-adrenergic signaling and contractile activity in cardiomyocytes.

Gene expression profiles for predicting the efficacy of the anticancer drug 5-fluorouracil in breast cancer.

Chemotherapy is an important postsurgery adjuvant therapy in the treatment of breast cancer. However, because of the individual genotype differences of patients, the drug efficacy differs from person to person, even when the same chemotherapy drug is administered. The purpose of this research was to probe the gene expression profiles to predict the efficacy of 5-fluorouracil (5-FU), the common drug used in chemotherapy for various type of cancers, in Taiwanese breast cancer patients.

Enhancing detection of circulating tumor cells with activating KRAS oncogene in patients with colorectal cancer by weighted chemiluminescent membrane array method.

Background: In 2008, the National Comprehensive Cancer Network suggested conducting a KRAS mutations test in metastatic colorectal cancer (mCRC) patients prior to administering therapy that uses anti-epidermal growth factor receptor (EGFR) monoclonal antibody. However, tests of KRAS mutations have been limited when traditional molecular techniques, such as polymerase chain reaction (PCR) combined direct sequencing, are used to obtain and analyze patients' cancer tissues. If the primary tumor or metastatic tissues of patients with mCRC is unavailable, then such analysis will not be feasible.

A fast and convenient new technique to detect the therapeutic target, K-ras mutant, from peripheral blood in non-small cell lung cancer patients.

Activating mutation of the K-ras gene was one of the earliest discoveries of genetic alterations in lung cancer. Moreover, K-ras somatic mutations might be suggested for predicting resistance to molecular antibodies targeting the epidermal growth factor receptor (EGFR). However, activated K-ras mutant detection methods are limited to traditional techniques.

Nitric oxide enhances expression of raf kinase inhibitor protein in keratinocytes.

Several reports have focused on the potential of nitric oxide (NO) to influence the proliferation and differentiation cascade in a number of mammalian cells. The purpose of this study was to determine the relationship between expression of raf kinase inhibitor protein (RKIP) and proliferation in keratinocyte with NO treatment. Normal human keratinocytes were treated with SNAP (NO donor) doses of 10(-7), 10(-6), 10(-5), 10(-4) and 0 m (control group) separately.

Monoclonal antibody-based quantitation of poly(ethylene glycol)-derivatized proteins, liposomes, and nanoparticles.

Covalent attachment of poly(ethylene glycol) (PEG) molecules to drugs, proteins, and liposomes is a proven technology for improving their bioavailability, safety, and efficacy. Qualitative and quantitative analysis of PEG-derivatized molecules is important for both drug development and clinical applications. We previously reported the development of a monoclonal IgM antibody (AGP3) to PEG.

Genetic and cellular characterizations of human TCF4 with microsatellite instability in colon cancer and leukemia cell lines.

It has been reported that the mutational inactivation of the adenomatous polyposis coli (APC) and beta-catenin genes play important roles in colorectal carcinogenesis. However, alteration of the components in the Wnt signaling pathway in colorectal cancer (CRC) with microsatellite instability (MSI) has been elucidated. To define the precise role of the Wnt signaling components in CRC and leukemia cell lines with MSI, mutational analyses of the T cell factor 4 (TCF4) genes were performed.

Liriodenine inhibits the proliferation of human hepatoma cell lines by blocking cell cycle progression and nitric oxide-mediated activation of p53 expression.

Liriodenine was isolated from the leaves of Michelia compressa. This study was designed to assess cell cycle arrest, the production of nitric oxide (NO) and p53 expression in liriodenine-treated human hepatoma cell lines, including wild-type p53 (Hep G2 and SK-Hep-1). As evidenced by flowcytometric studies, liriodenine induced cell cycle G(1) arrest and inhibited DNA synthesis in Hep G2 and SK-Hep-1 cell lines.

The change of beta-adrenergic system after cessation of lead exposure.

For understanding a reversible or irreversible harm of beta-adrenergic system in lead induced cardiovascular disease (hypertension), We set up animal model to estimate the change of blood pressure and sympathetic nervous system after lead exposure withdrawn in the study. We address three topics in this study: (a) the relationship between withdrawal time of lead exposure and beta-adrenergic receptor, plasma catecholamine level, blood pressure, and lead level in heart, aorta, and kidney in lead-induced hypertensive rats after lead exposure stopped; (b) the relationship between blood pressure and beta-adrenergic receptor in heart, aorta, and kidney; (c) the estimation of relationship between lead withdrawn and the variation of beta-adrenergic system. Wistar rats were chronically fed with 2% lead acetate (experimental group) and water (control group) for 2 months.

Beta-adrenergic receptor density and adenylate cyclase activity in lead-exposed rat brain after cessation of lead exposure.

To understanding the reversible or irreversible harm to the beta-adrenergic system in the brain of lead-exposed rats, this study sets up an animal model to estimate the change in the sympathetic nervous system of brain after lead exposure was withdrawn. We address the following topics in this study: (a) the relationship between withdrawal time of lead exposure and brain beta-adrenergic receptor, blood lead level, and brain lead level in lead-exposed rats after lead exposure was stopped; and (b) the relationship between lead level and beta-adrenergic receptor and cyclic AMP (c-AMP) in brain. Wistar rats were chronically fed with 2% lead acetate and water for 2 months.

Expression of nitric oxide synthases in keratinocytes after UVB irradiation.

The importance of nitric oxide (NO) in mediating vasodilation, neurotransmission, and immune and inflammatory responses has been demonstrated. Human keratinocyte express inducible nitric oxide synthase (iNOS) and the neuronal constitutive isoform of NOS (ncNOS). We established an in vitro model in keratinocytes to investigate changes in NO, iNOS and ncNOS expression after UVB exposure.