The conductivity of a poly(3,4‐ethylenedioxythiophene):poly(styrene sulfonate) (PEDOT:PSS) film can be enhanced by more than two orders of magnitude by adding a compound with two or more polar groups, such as ethylene glycol, meso‐erythritol (1,2,3,4‐tetrahydroxybutane), or 2‐nitroenthanol, to an aqueous solution of PEDOT:PSS. The mechanism for this conductivity enhancement is studied, and a new mechanism proposed. Raman spectroscopy indicates an effect of the liquid additive on the chemical structure of the PEDOT chains, which suggests a conformational change of PEDOT chains in the film. Both coil and linear conformations or an expanded‐coil conformation of the PEDOT chains may be present in the untreated PEDOT:PSS film, and the linear or expanded‐coil conformations may become dominant in the treated PEDOT:PSS film. This conformational change results in the enhancement of charge‐carrier mobility in the film and leads to an enhanced conductivity. The high‐conductivity PEDOT:PSS film is ideal as an electrode for polymer optoelectronic devices. Polymer light‐emitting diodes and photovoltaic cells fabricated using such high‐conductivity PEDOT:PSS films as the anode exhibit a high performance, close to that obtained using indium tin oxide as the anode.

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Because of the shared modes of transmission, hepatitis B virus (HBV)/hepatitis C virus (HCV) coinfection is not uncommon in highly endemic areas and among subjects with a high risk of parenteral infections. The worldwide prevalence of HBV/HCV coinfection is unknown and might be underestimated with the phenomenon of silent (occult) HBV infection. HCV superinfection in patients with chronic HBV infection was the most common clinical features of coinfection in Asia-Pacific countries. Further, most, but not all, clinical observations suggested that interference between the two viruses was more frequently characterized by an inhibition of HBV replication exerted by HCV. However, longitudinal follow-up studies have demonstrated that the virological patterns in coinfection cases are widely divergent and have dynamic profiles over time. As compared with monoinfected patients, HBV/HCV coinfected persons tend to have more severe liver injury, a higher probability of liver cirrhosis and hepatic decompensation, and a higher incidence of hepatocellular carcinoma. Detailed serological and virological evaluations are required for coinfected patients before initiation of antiviral therapy. Previous studies demonstrated that HBV/HCV coinfected patients responded poorly to interferon (IFN) monotherapy. Currently, for patients with dominant HCV infection and low level HBV viremia (<10 4 IU/ mL), IFN or pegylated IFN plus ribavirin can achieve comparable sustained virus response as expected with HCV monoinfection. However, phenomenon of reciprocal viral interference can happen, and resultant "flare" of hepatitis activity may cause liver function deterioration. For coinfected patients with dually-active HBV/HCV, the optimal regimen for therapy remains unclear although adding oral nucleos(t)ide analogs to pegylated IFN and ribavirin seems a reasonable empiric option.

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