How the Most Trusted Venues for Health-Related Information Influence Physician Referrals to Smoking Cessation Services.

Public health programs seek to educate physicians by using a variety of venues. Therefore, it is important to understand which health information sources physicians are using and how these sources affect referrals. We explored how venues for health-related information affect physicians' referral practices to smoking cessation services. The 2008 DocStyles survey asked physicians to rank a list of their most trusted sources of health-related information. The analysis was restricted to 1,617 physicians who responded to all variables of interest. In this sample, the most trusted sources of health-related information cited by physicians were medical journals (95.9%), government health agencies (82.2%), other physicians (76.4%), professional medical societies (75.2%), and medical Web sites or podcasts (65.9%). Medical providers were more likely to refer tobacco users to cessation services if they used professional medical societies as a source to obtain patient health-related information, compared with medical providers not using this source (multivariate odds ratio = 1.31; 95% confidence interval = 1.03-1.66). Physicians use many health information sources. Therefore, to reach physicians effectively, a broad dissemination of guidelines and best practices in tobacco control is needed and should include information for medical societies.

Characterization of Ceriporiopsis subvermispora bicupin oxalate oxidase expressed in Pichia pastoris.

Oxalate oxidase (E.C. 1.2.3.4) catalyzes the oxygen-dependent oxidation of oxalate to carbon dioxide in a reaction that is coupled with the formation of hydrogen peroxide. Although there is currently no structural information available for oxalate oxidase from Ceriporiopsis subvermispora (CsOxOx), sequence data and homology modeling indicate that it is the first manganese-containing bicupin enzyme identified that catalyzes this reaction. Interestingly, CsOxOx shares greatest sequence homology with bicupin microbial oxalate decarboxylases (OxDC). We show that CsOxOx activity directly correlates with Mn content and other metals do not appear to be able to support catalysis. EPR spectra indicate that the Mn is present as Mn(II), and are consistent with the coordination environment expected from homology modeling with known X-ray crystal structures of OxDC from Bacillus subtilis. EPR spin-trapping experiments support the existence of an oxalate-derived radical species formed during turnover. Acetate and a number of other small molecule carboxylic acids are competitive inhibitors for oxalate in the CsOxOx catalyzed reaction. The pH dependence of this reaction suggests that the dominant contribution to catalysis comes from the monoprotonated form of oxalate binding to a form of the enzyme in which an active site carboxylic acid residue must be unprotonated.

PARP1 suppresses homologous recombination events in mice in vivo.

Recent studies suggest that PARP1 inhibitors, several of which are currently in clinical trial, may selectively kill BRCA1/2 mutant cancers cells. It is thought that the success of this therapy is based on immitigable lethal DNA damage in the cancer cells resultant from the concurrent loss or inhibition of two DNA damage repair pathways: single-strand break (SSB) repair and homologous recombination repair (HRR). Presumably, inhibition of PARP1 activity obstructs the repair of SSBs and during DNA replication, these lesions cause replication fork collapse and are transformed into substrates for HRR. In fact, several previous studies have indicated a hyper-recombinogenic phenotype in the absence of active PARP1 in vitro or in response to DNA damaging agents. In this study, we demonstrate an increased frequency of spontaneous HRR in vivo in the absence of PARP1 using the p(un) assay. Furthermore, we found that the HRR events that occur in Parp1 nullizygous mice are associated with a significant increase in large, clonal events, as opposed to the usually more frequent single cell events, suggesting an effect in replicating cells. In conclusion, our data demonstrates that PARP1 inhibits spontaneous HRR events, and supports the model of DNA replication transformation of SSBs into HRR substrates.