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1.  Characterization of Exposures to Airborne Nanoscale Particles During Friction Stir Welding of Aluminum 
Annals of Occupational Hygiene  2010;54(5):486-503.
Friction stir welding (FSW) is considered one of the most significant developments in joining technology over the last half century. Its industrial applications are growing steadily and so are the number of workers using this technology. To date, there are no reports on airborne exposures during FSW. The objective of this study was to investigate possible emissions of nanoscale (<100 nm) and fine (<1 μm) aerosols during FSW of two aluminum alloys in a laboratory setting and characterize their physicochemical composition. Several instruments measured size distributions (5 nm to 20 μm) with 1-s resolution, lung deposited surface areas, and PM2.5 concentrations at the source and at the breathing zone (BZ). A wide range aerosol sampling system positioned at the BZ collected integrated samples in 12 stages (2 nm to 20 μm) that were analyzed for several metals using inductively coupled plasma mass spectrometry. Airborne aerosol was directly collected onto several transmission electron microscope grids and the morphology and chemical composition of collected particles were characterized extensively. FSW generates high concentrations of ultrafine and submicrometer particles. The size distribution was bimodal, with maxima at ∼30 and ∼550 nm. The mean total particle number concentration at the 30 nm peak was relatively stable at ∼4.0 × 105 particles cm−3, whereas the arithmetic mean counts at the 550 nm peak varied between 1500 and 7200 particles cm−3, depending on the test conditions. The BZ concentrations were lower than the source concentrations by 10–100 times at their respective peak maxima and showed higher variability. The daylong average metal-specific concentrations were 2.0 (Zn), 1.4 (Al), and 0.24 (Fe) μg m−3; the estimated average peak concentrations were an order of magnitude higher. Potential for significant exposures to fine and ultrafine aerosols, particularly of Al, Fe, and Zn, during FSW may exist, especially in larger scale industrial operations.
doi:10.1093/annhyg/meq037
PMCID: PMC2913760  PMID: 20453001
aluminum; friction stir welding; nanoparticle exposures; occupational safety and health; size distribution; zinc
2.  Cell type specific transcriptional activities among different papillomavirus long control regions and their regulation by E2 
Virology  2009;395(2):161-171.
This study systematically examined the viral long control region (LCR) activities and their responses to E2 for human papillomavirus (HPV) types 11. 16 and 18 as well as bovine papillomavirus 1 (BPV1) in a number of different cell types, including human cervical cancer cell lines, human oral keratinocytes, BJ fibroblasts, as well as CV1 cells. The study revealed cell- and virus-type specific differences among the individual LCRs and their regulation by E2. In addition, the integration of the LCR into the host genome was identified as a critical determinant for LCR activity and its response to E2. Collectively, these data indicate a more complex level of transcriptional regulation of the LCR by cellular and viral factors than previously appreciated, including a comparatively low LCR activity and poor E2 responsive for HPV16 in most human cells. This study should provide a valuable framework for future transcriptional studies in the papillomavirus field.
doi:10.1016/j.virol.2009.09.027
PMCID: PMC2787971  PMID: 19836046
3.  NCoR1 Mediates Papillomavirus E8^E2C Transcriptional Repression▿ †  
Journal of Virology  2010;84(9):4451-4460.
The papillomavirus E2 open reading frame encodes the full-length E2 protein as well as an alternatively spliced product called E8^E2C. E8^E2C has been best studied for the high-risk human papillomaviruses, where it has been shown to regulate viral genome levels and, like the full-length E2 protein, to repress transcription from the viral promoter that directs the expression of the viral E6 and E7 oncogenes. The repression function of E8^E2C is dependent on the 12-amino-acid N-terminal sequence from the E8 open reading frame (ORF). In order to understand the mechanism by which E8^E2C mediates transcriptional repression, we performed an unbiased proteomic analysis from which we identified six high-confidence candidate interacting proteins (HCIPs) for E8^E2C; the top two are NCoR1 and TBLR1. We established an interaction of E8^E2C with an NCoR1/HDAC3 complex and demonstrated that this interaction requires the wild-type E8 open reading frame. Small interfering RNA (siRNA) knockdown studies demonstrated the involvement of NCoR1/HDAC3 in the E8^E2C-dependent repression of the viral long control region (LCR) promoter. Additional genetic work confirmed that the papillomavirus E2 and E8^E2C proteins repress transcription through distinct mechanisms.
doi:10.1128/JVI.02390-09
PMCID: PMC2863743  PMID: 20181716
4.  Nef does not contribute to replication differences between R5 pre-AIDS and AIDS HIV-1 clones from patient ACH142 
Retrovirology  2008;5:42.
AIDS-associated, CCR5-tropic (R5) HIV-1 clones, isolated from a patient that never developed CXCR4-tropic HIV-1, replicate to a greater extent and cause greater cytopathic effects than R5 HIV-1 clones isolated before the onset of AIDS. Previously, we showed that HIV-1 Env substantially contributed to the enhanced replication of an AIDS clone. In order to determine if Nef makes a similar contribution, we cloned and phenotypically analyzed nef genes from a series of patient ACH142 derived R5 HIV-1 clones. The AIDS-associated Nef contains a series of residues found in Nef proteins from progressors [1]. In contrast to other reports [1-3], this AIDS-associated Nef downmodulated MHC-I to a greater extent and CD4 less than pre-AIDS Nef proteins. Additionally, all Nef proteins enhanced infectivity similarly in a single round of replication. Combined with our previous study, these data show that evolution of the HIV-1 env gene, but not the nef gene, within patient ACH142 significantly contributed to the enhanced replication and cytopathic effects of the AIDS-associated R5 HIV-1 clone.
doi:10.1186/1742-4690-5-42
PMCID: PMC2440386  PMID: 18510766

Results 1-4 (4)