Fu Jen Catholic University

About: Fu Jen Catholic University is a education organization based out in Taipei, Taiwan. It is known for research contribution in the topics: Population & Hazard ratio. The organization has 6842 authors who have published 9512 publications receiving 171005 citations. The organization is also known as: FJU & Fu Jen.

Lutein protects against methotrexate-induced and reactive oxygen species-mediated apoptotic cell injury of IEC-6 cells.

Abstract: Purpose: High-dose chemotherapy using methotrexate (MTX) frequently induces side effects such as mucositis that leads to intestinal damage and diarrhea. Several natural compounds have been demonstrated of their effectiveness in protecting intestinal epithelial cells from these adverse effects. In this paper, we investigated the protection mechanism of lutein against MTX-induced damage in IEC-6 cells originating from the rat jejunum crypt. Methods: The cell viability, induced-apoptosis, reactive oxygen species (ROS) generation, and mitochondrial membrane potential in IEC-6 cells under MTX treatment were examined in the presence or absence of lutein. Expression level of Bcl2, Bad and ROS scavenging enzymes (including SOD, catalase and Prdx1) were detected by quantitative RT-PCR. Results: The cell viability of IEC-6 cells exposed to MTX was decreased in a dose- and time-dependent manner. MTX induces mitochondrial membrane potential loss, ROS generation and caspase 3 activation in IEC-6 cells. The cytotoxicity of MTX was reduced in IEC-6 cells by the 24 h pre-treatment of lutein. We found that pre-treatment of lutein significantly reduces MTXinduced ROS and apoptosis. The expression of SOD was up-regulated by the pre-treatment of lutein in the MTX-treated IEC6 cells. These results indicated that lutein can protect IEC-6 cells from the chemo-drugs induced damage through increasing ROS scavenging ability. Conclusion: The MTX-induced apoptosis of IEC-6 cells was shown to be repressed by the pre-treatment of lutein, which may represent a promising adjunct to conventional chemotherapy for preventing intestinal damages.

Genotypic dominance and novel recombinations in HBV genotype B and C co-infected intravenous drug users.

Abstract: Pathogenic differences among hepatitis B virus (HBV) genotypes have been documented. However, the interaction between different HBV genotypes remains unclear. Herein, we chose HBV genotypes B (HBV/B) and C (HBV/C) co-infected intravenous drug users to study this issue. HBV genotype was determined in 40 HBsAg, anti-HCV, and anti-HDV co-positive intravenous drug users by using genotype-specific primers. The distribution of HBV genotype was as follows: HBV genotype B alone in 29 (72.5%); HBV genotype C alone in 4 (10.0%); and mixed HBV genotype B and HBV genotype C in 7 (17.5%). The interaction between HBV genotype B and HBV genotype C within the same individual was further studied in the seven intravenous drug users with HBV genotype B and HBV genotype C co-infection. By direct sequencing of the pre-S region, only HBV genotype B was detected. When 10–21 clones of the pre-S region were propagated from each intravenous drug user and sequenced, most of the clones were HBV genotype B. Novel recombinations between HBV genotype B and HBV genotype C occurred in four clones (M7-5, M1-10, M1-21, and M1-24) from two intravenous drug users (M7 and M1). The recombination breakpoints were estimated at nucleotide 3120–3171 for M7-5, at nucleotide 3060–3191 for M1-10, and at nucleotide 2910–2950 for M1-21 and M1-24 by SimPlot program. The recombination sites of these HBV/pre-S C-B and B-C recombinants may be within the pre-S1 region. The results in this study suggest that HBV/B is the dominant strain in HBV genotypes B and C co-infected intravenous drug users in Taiwan, and recombinations between different HBV genotype are not unusual. The impact of recombination on the evolution of HBV and their clinical significance remains to be studied. J. Med. Virol. 73:13–22, 2004. © 2004 Wiley-Liss, Inc.

F-18 FDG PET for evaluation of bone marrow involvement in non-Hodgkin lymphoma: a meta-analysis.

Abstract: Background:In recent years, the use of F-18 fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) has become widespread for the staging of lymphoma. In non-Hodgkin lymphoma (NHL), the bone marrow (BM) involvement is a sign of extensive disease, and the iliac crest BM bio

Upregulation of presynaptic proteins and protein kinases associated with enhanced glutamate release from axonal terminals (synaptosomes) of the medial prefrontal cortex in rats with neuropathic pain.

Abstract: Although nerve injury-induced long-term postsynaptic changes have been investigated, less is known regarding the molecular mechanisms within presynaptic axonal terminals. We investigated the molecular changes in presynaptic nerve terminals underlying chronic pain-induced plastic changes in the medial prefrontal cortex (mPFC). After neuropathic pain was induced by spared nerve injury (SNI) in rats, we assessed the release of the excitatory neurotransmitter glutamate by using in vitro synaptosomal preparations from the mPFC. We also measured the levels of synaptic proteins and protein kinases in synaptosomes using Western blotting. The results showed that unilateral long-term SNI augmented depolarization-evoked glutamate release from synaptosomes of the bilateral mPFC. This result was confirmed by a rapid destaining rate of FM1-43 dye in SNI-operated rats. Unilateral long-term nerve injury also significantly increased synaptic proteins (including synaptophysin, synaptotagmin, synaptobrevin, syntaxin, and 25-kDa synaptosome-associated protein) in synaptosomal fractions from the bilateral mPFC, and ultrastructure images demonstrated increased synaptic vesicular profiles in synaptosomes from SNI animals. Chronic pain upregulated the phosphorylation of endogenous protein kinases, including extracellular signal-regulated kinases 1 and 2 (ERK1/2) and Ca(2+)/calmodulin-dependent kinase II (CaMKII), and synapsin I, the primary presynaptic target of ERK1/2 and CaMKII. Both presynaptic proteins and protein kinases were upregulated after SNI in a time-dependent manner. These results indicate that the long-term neuropathic pain-induced enhancement of glutamate release in the mPFC is linked to increased synaptic vesicle proteins and the activation of the ERK1/2- and CaMKII-synapsin signaling cascade in presynaptic axonal terminals.