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BACKGROUND: Treating psoriasis in patients with concomitant hepatitis C virus (HCV) infection presents a special challenge. Not only is psoriasis exacerbated by interferon therapy, the standard of care for HCV, but many psoriasis ...
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BACKGROUND: Treating psoriasis in patients with concomitant hepatitis C virus (HCV) infection presents a special challenge. Not only is psoriasis exacerbated by interferon therapy, the standard of care for HCV, but many psoriasis therapies are potentially hepatotoxic, immunosuppressive, or both, which has been generally thought to be a contraindication in chronic infections such as HCV. OBJECTIVE: Our aim was to arrive at a consensus on treating psoriasis in patients with concomitant HCV infection. METHODS: Reports in the literature were reviewed regarding common psoriasis therapies and liver toxicity. RESULTS: Topical therapies are first-line therapy for patients with limited psoriasis and HCV. Ultraviolet B phototherapy may be considered as a second-line treatment when needed. Ultraviolet B phototherapies in combination with topical therapies are first line for patients with moderate to severe psoriasis, and are considered safe in those patients with concomitant HCV infection. Other systemic therapies, such as acitretin, etanercept, and, possibly, other tumor necrosis factor inhibitors, are considered second line. Psoralen plus ultraviolet A should also be considered a second-line therapy. LIMITATIONS: There are few evidence-based studies on treating psoriasis with systemic therapy in patients with pre-existing liver disease. CONCLUSIONS: There are no large double-blind clinical trials addressing the treatment of psoriasis in patients with HCV infection and more studies are needed.
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The Escherichia coli Lon protease degrades the E. coli DNA-binding protein HUbeta, but not the related protein HUalpha. Here we show that the Lon protease binds to both HUbeta and HUalpha, but selectively degrades only HUbeta in t...
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The Escherichia coli Lon protease degrades the E. coli DNA-binding protein HUbeta, but not the related protein HUalpha. Here we show that the Lon protease binds to both HUbeta and HUalpha, but selectively degrades only HUbeta in the presence of ATP. Mass spectrometry of HUbeta peptide fragments revealed that region K18-G22 is the preferred cleavage site, followed in preference by L36-K37. The preferred cleavage site was further refined to A20-A21 by constructing and testing mutant proteins; Lon degraded HUbeta-A20Q and HUbeta-A20D more slowly than HUbeta. We used optical tweezers to measure the rupture force between HU proteins and Lon; HUalpha, HUbeta, and HUbeta-A20D can bind to Lon, and in the presence of ATP, the rupture force between each of these proteins and Lon became weaker. Our results support a mechanism of Lon protease cleavage of HU proteins in at least three stages: binding of Lon with the HU protein (HUbeta, HUalpha, or HUbeta-A20D); hydrolysis of ATP by Lon to provide energy to loosen the binding to the HU protein and to allow an induced-fit conformational change; and specific cleavage of only HUbeta.
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Using conducting-tip atomic force microscopy (C-AFM), we study the spatial distribution of current paths and local electrical properties in carbon nanofiber/polymer nanocomposites. Previous studies of similar systems were hindered...
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Using conducting-tip atomic force microscopy (C-AFM), we study the spatial distribution of current paths and local electrical properties in carbon nanofiber/polymer nanocomposites. Previous studies of similar systems were hindered by a polymer-rich skin layer that exists at the nanocomposite surfaces. We present an experimental technique using oxygen plasma etching to controllably remove this polymer skin layer. After this treatment, we can directly probe the microscopic transport characteristics of the nanocomposite using C-AFM. The C-AFM results show that the electrical transport is solely carried by the carbon nanofiber (CNF) networks in the nanocomposites. In addition, high-resolution C-AFM maps show nonuniform distribution of current along the length of some CNFs, suggesting the presence of a heterogeneously distributed adsorbed polymer layer around nanofibers. Finally, two probe conductivity measurements in which one electrode (the C-AFM tip) is contacting a single constituent conducting particle were performed to study local conductivity. Results indicate that Ohmic pathways exist in the conducting network of the nanocomposite to the lowest measured nanofiber concentrations. However, non-Ohmic behavior indicating tunneling transport may also be present, especially near the percolation threshold.
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BACKGROUND: Inflammatory breast cancer (IBC) is the most aggressive form of breast cancer. Circulating tumor cells (CTCs) are an independent prognostic factor in metastatic breast cancer. The aim of this study was to assess the pr...
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BACKGROUND: Inflammatory breast cancer (IBC) is the most aggressive form of breast cancer. Circulating tumor cells (CTCs) are an independent prognostic factor in metastatic breast cancer. The aim of this study was to assess the prognostic value of baseline CTCs in metastatic IBC patients. PATIENTS AND METHODS: This retrospective study included 42 metastatic IBC and 107 metastatic non-IBC patients treated with first- or second-line chemotherapy from January 2004 to December 2007 at MD Anderson Cancer Center. CTCs were detected and enumerated before patients started chemotherapy using the CellSearch system. RESULTS: Ten (23.8%) IBC patients versus 48 (44.9%) non-IBC patients had baseline CTCs > or =5 per 7.5 ml of peripheral blood. IBC patients had a lower mean +/- SEM CTCs than non-IBC patients (7.6 +/- 2.9 versus 34.2 +/- 9.1; P = 0.02). The estimated median overall survival was 26.5 versus 18.3 months (P = 0.68) in IBC patients and 37.4 versus 18.3 months (P = 0.016) in non-IBC patients with CTCs <5 and CTCs > or =5, respectively. CONCLUSIONS: Metastatic IBC patients had a lower prevalence and fewer CTCs in comparison to metastatic non-IBC patients. Survival of metastatic IBC patients with <5 CTCs was not significantly better than that of patients with > or =5 CTCs. Further research is warranted with prospective assessment of CTCs in IBC patients and their biological characterization.
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Co-doped ZnO films were synthesized by ion beam sputtering using multilayer (ZnO/Co) growth. Both the distribution and the chemical states of Co in ZnO can be well controlled by varying the ratio of the nominal layer thickness of ...
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Co-doped ZnO films were synthesized by ion beam sputtering using multilayer (ZnO/Co) growth. Both the distribution and the chemical states of Co in ZnO can be well controlled by varying the ratio of the nominal layer thickness of ZnO to Co. Transmission electron microscopy indicated that all of the as-deposited Zn_(1-x)(Co)_xO films were polycrystalline with a (0002) preferred orientation. The local microstructures and chemical states were identified by Z-contrast imaging and electron energy loss spectroscopy. In ZnO (1.5 nm)/Co (0.1 nm), homogeneous Co-doped ZnO was observed to have been formed through interdiffusion. However, decreasing or increasing the thickness of ZnO leads to the formation of Co clusters in the ZnO matrix or Zn_(1-x)(Co)_xO multilayers, respectively. For ZnO thickness ≧ 1.5 nm, Co is substituted for Zn, and its valence state is 2~+. All Co-doped ZnO films show room-temperature ferromagnetic behavior, which appears to depend strongly on the Co distribution.
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Super-radiance of excitons in a single ZnO tetrapod nanostructure has been observed. The emitted pulses exhibited very short duration, and the emission peak intensity exhibited exponential increase with the increased pump density....
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Super-radiance of excitons in a single ZnO tetrapod nanostructure has been observed. The emitted pulses exhibited very short duration, and the emission peak intensity exhibited exponential increase with the increased pump density. Multiple narrow emission peaks with short peak spacing have been observed in the emission spectra of a single ZnO tetrapod nanostructure.
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