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1.  Glia instruct developmental neuronal remodeling through TGF-βsignaling 
Nature Neuroscience  2011;14(7):821-823.
Neural circuits are remodeled in response to developmental and environmental cues. Here we show that glia secrets Myoglianin, a TGF-β ligand, to instruct developmental neural remodeling in Drosophila. Glial Myoglianin up-regulates neuronal expression of an ecdysone nuclear receptor that triggers neurite remodeling following the late-larval ecdysone peak. This observation reveals that glia orchestrate developmental neural remodeling not only via engulfment of unwanted neurites but also through enabling neuron remodeling.
doi:10.1038/nn.2833
PMCID: PMC3337551  PMID: 21685919
2.  Phyllanthus urinaria Induces Apoptosis in Human Osteosarcoma 143B Cells via Activation of Fas/FasL- and Mitochondria-Mediated Pathways 
Phyllanthus urinaria (P. urinaria), in this study, was used for the treatment of human osteosarcoma cells, which is one of the tough malignancies with few therapeutic modalities. Herein, we demonstrated that P. urinaria inhibited human osteosarcoma 143B cells growth through an apoptotic extrinsic pathway to activate Fas receptor/ligand expression. Both intracellular and mitochondrial reactive oxygen species were increased to lead to alterations of mitochondrial membrane permeability and Bcl-2 family including upregulation of Bid, tBid, and Bax and downregulation of Bcl-2. P. urinaria triggered an intrinsic pathway and amplified the caspase cascade to induce apoptosis of 143B cells. However, upregulation of both intracellular and mitochondrial reactive oxygen species and the sequential membrane potential change were less pronounced in the mitochondrial respiratory-defective 143Bρ0 cells compared with the 143B cells. This study offers the evidence that mitochondria are essential for the anticancer mechanism induced by P. urinaria through both extrinsic and intrinsic pathways.
doi:10.1155/2012/925824
PMCID: PMC3291129  PMID: 22454688
3.  Laboratory-Based Surveillance and Molecular Epidemiology of Influenza Virus in Taiwan 
Journal of Clinical Microbiology  2005;43(4):1651-1661.
A laboratory-based surveillance network of 11 clinical virological laboratories for influenza viruses was established in Taiwan under the coordination of the Center for Disease Control and Prevention (CDC), Taiwan. From October 2000 to March 2004, 3,244 influenza viruses were isolated, including 1,969 influenza A and 1,275 influenza B viruses. The influenza infections usually occurred frequently in winter in the northern hemisphere. However, the influenza seasonality in Taiwan was not clear during the four seasons under investigation. For example, the influenza A viruses peaked during the winters of 2001, 2002, and 2003. However, some isolated peaks were also found in the summer and fall (June to November) of 2001 and 2002. An unusual peak of influenza B also occurred in the summer of 2002 (June to August). Phylogenetic analysis shows that influenza A isolates from the same year were often grouped together. However, influenza B isolates from the year 2002 clustered into different groups, and the data indicate that both B/Victoria/2/87-like and B/Yamagata/16/88-like lineages of influenza B viruses were cocirculating. Sequence comparison of epidemic strains versus vaccine strains shows that many vaccine-like Taiwanese strains were circulating at least 2 years before the vaccine strains were introduced. No clear seasonality of influenza reports in Taiwan occurred in contrast to other more continental regions.
doi:10.1128/JCM.43.4.1651-1661.2005
PMCID: PMC1081360  PMID: 15814980
4.  Influenza A Virus PB1-F2 Gene in Recent Taiwanese Isolates 
Emerging Infectious Diseases  2004;10(4):630-636.
Influenza A virus contains eight RNA segments and encodes 10 viral proteins. However, an 11th protein, called PB1-F2, was found in A/Puerto Rico/8/34 (H1N1). This novel protein is translated from an alternative open reading frame (ORF) in the PB1 gene. We analyzed the PB1 gene of 42 recent influenza A isolates in Taiwan, including 24 H1N1 and 18 H3N2 strains. One H1N1 isolate and 17 H3N2 isolates contained the entire PB1-F2 ORF of 90 residues, three amino acids (aa) longer than the PB1-F2 of A/Puerto Rico/8/34 at the C terminal. The one remaining H3N2 isolate encoded a truncated PB1-F2 with 79 residues. The other 23 H1N1 isolates contained a truncated PB1-F2 of 57 aa. Phylogenetic analysis of both the HA and the PB1 genes showed that they shared similar clustering of these Taiwanese isolates, suggesting that no obvious reassortment occurred between the two genomic segments.
doi:10.3201/eid1004.030412
PMCID: PMC3323094  PMID: 15200852
PB1-F2; PB1 gene; influenza A virus

Results 1-4 (4)