Temporal evolution of a driven optomechanical system in the strong coupling regime

We obtain a time-evolution operator for a forced optomechanical quantum system using Lie algebraic methods when the normalized coupling between the electromagnetic field and a mechanical oscillator, $G/\omega_m$, is not negligible compared to one. Due to the forcing term, the interaction picture Hamiltonian contains the number operator in the exponents, and in order to deal with it, we approximate these exponentials by their average values taken between initial coherent states. Our approximation is justified when we compare our results with the numerical solution of the number of photons, phonons, Mandel parameter, and the Wigner function, showing an excellent agreement.Comment: 21 pages, 11 figure

Tobacco Smoke Activates Human Papillomavirus 16 p97 Promoter and Cooperates with High-Risk E6/E7 for Oxidative DNA Damage in Lung Cells

<div><p>We have previously shown a functional interaction between human papillomavirus type 16 (HPV-16) E6 and E7 oncoproteins and cigarette smoke condensate (CSC) in lung cells suggesting cooperation during carcinogenesis. The molecular mechanisms of such interaction, however, remain to be elucidated. Here we first present evidence showing that cigarette smoke condensate (CSC) has the ability to activate the HPV-16 p97 promoter by acting on the long control region (LCR) in lung epithelial cells. Interestingly, we observed that CSC-induced p97 promoter activation occurs in a dose-dependent manner in both tumor A-549 (lung adenocarcinoma), H-2170 (bronchial carcinoma), SiHa or Hela (cervical carcinoma) cells but not in non-tumor BEAS-2B (bronchial) or NL-20 (alveolar) lung cells unless they ectopically expressed the HPV-16 E6 and E7 oncogenes. In addition, we also observed a significant increase of primary DNA damage in tumor and non-tumor CSC-treated lung cells expressing HPV-16 E6 and E7 oncogenes suggesting a cooperative effect in this process, even though the contribution of E7 was significantly higher. Taken together, our results strongly suggest that tobacco smoke is able to induce the activation of the HPV-16 p97 promoter in cooperation with HPV-16 E6 and E7 oncogenes that, in turn, sensitize lung cells to tobacco smoke-induced DNA damage.</p></div

HPV-E6/E7 oncogenes sensitize lung cells for tobacco smoke-induced DNA damage.

<p>(A) BEAS-2B and (B) A-549 cells were exposed for 72 hours to 1–50 μg/mL CSC and analyzed using comet assay. (<b>C</b>) BEAS-2B and (D) A-549 cells were exposed to 10 μg/mL CSC for 0–96 hours. (E) Image showing comets in A-549 cells transfected with HPV-16 E6E7 or an empty vector and exposed to 10 μg/mL CSC. The graphs are representative of three independent experiments (* = p<0.05; ** = p<0.01; *** = p<0.001, Total Area ± SEM).</p

HPV-16 E6 and E7 oncogenes independently are able to sensitize cells to DNA damage.

<p>(A) A-549 cells expressing HPV-16 E6 or E7 oncogenes were exposed to CSC at 10 μg/mL and DNA damage was evaluated using Comet Assay. (B) Image showing comets in A-549 cells transfected with pLXSNE6 (upper) or pLXSNE7 (below) in the presence or absence of CSC. (*** = p<0.001, Total Area ± SEM).</p

Cigarette smoke condensate (CSC) activates the HPV-16 p97 promoter in a dose-dependent manner in lung and cervical cancer cells.

<p>(<b>A</b>) A-549 (<b>B</b>) H-2170 (<b>C</b>) HeLa and (<b>D</b>) SiHa cells were exposed to CSC (0.1–50 μg/mL) for 16 hours after transfection with the pmiR-GLO construct containing the complete HPV-16 LCR/p97 region. (<b>E</b>) A-549 cells were transfected with the pmiR-GLO containing only the HPV-16 p97 promoter and the luciferase activity was compared with those cells transfected with the full HPV-16 LCR/p97 region. (<b>F</b>) SiHa cells were exposed to 10 μg/mL CSC and the levels of E7 transcripts were measured using RT-qPCR. The graphs are representative of three independent experiments. (* = p<0.05; ** = p<0.01; *** = p<0.001, Luc2/Reni percentage ± SEM).</p

Lentiviral transduction of BEAS-2B cells with an shRNA for HPV-16 E6/E7 silencing reduces the DNA damage induced by CSC exposition.

<p>(A) BEAS-2B cells were exposed to 10 μg/mL CSC and incubated with scrambled or shRNA SH-186. The DNA damage was evaluated using comet assay and the total area in each comet was measured. (B) A representative image showing BEAS-2B cells after incubation with SCR or shRNA SH-186.</p

A model of interaction between CSC and HPV in lung cells is suggested.

<p>CSC is able to induce the activity of the p97 promoter in the context of high-risk HPV LCR conducting to E6 and E7 transcripts expression. The high-risk E6 and E7 oncoproteins sensitize lung cells for tobacco smoke-associated oxidative DNA damage and collaborate with tobacco smoke for p97 promoter activation.</p

Cigarette smoke condensate (CSC) activates the HPV-16 p97 promoter in a dose-dependent manner in non-tumor lung cells after HPV-16 E6/E7 expression.

<p>(A) BEAS-2B, (B) NL-20 cells stably transfected with HPV-16 E6/E7 oncogenes (dark) or an empty vector (gray) were transfected with the pmiR-GLO containing the full HPV-16 LCR/p97 region. The graphs are representative of three independent experiments. (* = p<0.05; ** = p<0.01; *** = p<0.001, Luc2/Reni percentage ± SEM).</p