The standard enthalpy of formation is an important predictor of the reaction heat of a chemical reaction.In this work,a high-precision method was developed to calculate accurate standard enthalpies of formation for po...The standard enthalpy of formation is an important predictor of the reaction heat of a chemical reaction.In this work,a high-precision method was developed to calculate accurate standard enthalpies of formation for polycyclic aromatic hydrocarbons based on the general connectivity based hierarchy(CBH)with the discrete correction of atomization energy.Through a comparison with available experimental findings and other high-precision computational results,it was found that the present method can give a good description of enthalpy of formation for polycyclic aromatic hydrocarbons.Since CBH schemes can broaden the scope of application,this method can be used to investigate the energetic properties of larger polycyclic aromatic hydrocarbons to achieve a high-precision calculation at the CCSD(T)/CBS level.In addition,the energetic properties of CBH fragments can be accurately calculated and integrated into a database for future use,which will increase computational efficiency.We hope this work can give new insights into the energetic properties of larger systems.展开更多
Background: Reported are increased risks for malignant transformation in human oral keratinocytes (HOK) from ethyl alcohol (ETOH), tobacco products or human papilloma virus oncogenic subtype 16 (HPV 16) infections. We...Background: Reported are increased risks for malignant transformation in human oral keratinocytes (HOK) from ethyl alcohol (ETOH), tobacco products or human papilloma virus oncogenic subtype 16 (HPV 16) infections. We examined various HOK cell responses to these factors to show inhibitors of epidermal growth factor receptor (EGFR) also inhibits furin;proprotein convertase (FC) and HPV 16 entry in HOK. Methods: Immortalized HOK by HPV 16 (HPV 16B) or human telomerase (hTERT);primary foreskin keratinocytes (NHFK), primary HOK, buccal keratinocytes (NHBK) and oral SCC-25 were treated with dibenz[a,l]pyrene (DBP), anthraquinone;nitrosamine (NNAL) or ethyl alcohol (ETOH) and acetaldehyde (AA). ETOH was tested for synthesis of malondialdehyde (MDA) and alcohol dehydrogenase expression (ADH). ETOH, and PAH were evaluated by Western immunoblot for oncogene changes, and phosphorylated EGFR expression. Inhibition of EGFR by WZ4002 and Erlotinib and/or carcinogens effect on HPV 16 entry were studied. A green fluorescent pseudovirus (PsV);chloromethylketone (CMK) an inhibitor of furin activity and Western immunoblot of furin cell distribution further characterized HPV 16 entry. Results: ETOH (10 μM) increased expression of phosphorylated EGFR and HPV 16 entry through furin activity, and membrane, nuclear and cytoskeletal accumulations. CMK suppressed HPV 16 entry and blockage of ADH while aldehyde dehydrogenase (ALDH) enhanced HPV 16 entry. Similarly PAH, DBP (4-8 nM), anthraquinone (98 nM) and NNAL (6.9 μM) enhanced HPV 16 entry through furin activity and membrane, nuclear and cytoskeletal accumulations. Furthermore, WZ4002 and Erlotinib suppressed expressions of phosphorylated EGFR, FC activity, and HPV 16 entry. ETOH and DBP treatments also enhanced expressions of protease activated receptor-1 (PAR-1), and p21waf1 while depressed p16 and p27KIP1 expressions in HOK/HPV 16B cells. Conclusion: EGFR inhibitors are candidates for suppression of alcohol and tobacco effects on EGFR phosphorylated expression;keratinocyte growth, and HPV 16 entry and prevention treatment for HPV related diseases.展开更多
基金This work was supported by the National Natural Science Foundation of China(Grant Nos.21903057 and 91841301)National Science and Technology Major Project(Grant No.2017-I-0004-0004).
文摘The standard enthalpy of formation is an important predictor of the reaction heat of a chemical reaction.In this work,a high-precision method was developed to calculate accurate standard enthalpies of formation for polycyclic aromatic hydrocarbons based on the general connectivity based hierarchy(CBH)with the discrete correction of atomization energy.Through a comparison with available experimental findings and other high-precision computational results,it was found that the present method can give a good description of enthalpy of formation for polycyclic aromatic hydrocarbons.Since CBH schemes can broaden the scope of application,this method can be used to investigate the energetic properties of larger polycyclic aromatic hydrocarbons to achieve a high-precision calculation at the CCSD(T)/CBS level.In addition,the energetic properties of CBH fragments can be accurately calculated and integrated into a database for future use,which will increase computational efficiency.We hope this work can give new insights into the energetic properties of larger systems.
文摘Background: Reported are increased risks for malignant transformation in human oral keratinocytes (HOK) from ethyl alcohol (ETOH), tobacco products or human papilloma virus oncogenic subtype 16 (HPV 16) infections. We examined various HOK cell responses to these factors to show inhibitors of epidermal growth factor receptor (EGFR) also inhibits furin;proprotein convertase (FC) and HPV 16 entry in HOK. Methods: Immortalized HOK by HPV 16 (HPV 16B) or human telomerase (hTERT);primary foreskin keratinocytes (NHFK), primary HOK, buccal keratinocytes (NHBK) and oral SCC-25 were treated with dibenz[a,l]pyrene (DBP), anthraquinone;nitrosamine (NNAL) or ethyl alcohol (ETOH) and acetaldehyde (AA). ETOH was tested for synthesis of malondialdehyde (MDA) and alcohol dehydrogenase expression (ADH). ETOH, and PAH were evaluated by Western immunoblot for oncogene changes, and phosphorylated EGFR expression. Inhibition of EGFR by WZ4002 and Erlotinib and/or carcinogens effect on HPV 16 entry were studied. A green fluorescent pseudovirus (PsV);chloromethylketone (CMK) an inhibitor of furin activity and Western immunoblot of furin cell distribution further characterized HPV 16 entry. Results: ETOH (10 μM) increased expression of phosphorylated EGFR and HPV 16 entry through furin activity, and membrane, nuclear and cytoskeletal accumulations. CMK suppressed HPV 16 entry and blockage of ADH while aldehyde dehydrogenase (ALDH) enhanced HPV 16 entry. Similarly PAH, DBP (4-8 nM), anthraquinone (98 nM) and NNAL (6.9 μM) enhanced HPV 16 entry through furin activity and membrane, nuclear and cytoskeletal accumulations. Furthermore, WZ4002 and Erlotinib suppressed expressions of phosphorylated EGFR, FC activity, and HPV 16 entry. ETOH and DBP treatments also enhanced expressions of protease activated receptor-1 (PAR-1), and p21waf1 while depressed p16 and p27KIP1 expressions in HOK/HPV 16B cells. Conclusion: EGFR inhibitors are candidates for suppression of alcohol and tobacco effects on EGFR phosphorylated expression;keratinocyte growth, and HPV 16 entry and prevention treatment for HPV related diseases.
