Abstract: In a method of cleaning a lithography system, during idle mode, a stream of air is directed, through a first opening, into a chamber of a wafer table of an EUV lithography system. One or more particles is extracted by the directed stream of air from surfaces of one or more wafer chucks in the chamber of the wafer table. The stream of air and the extracted one or more particle are drawn, through a second opening, out of the chamber of the wafer table.

Abstract: The invention relates to methods of identifying a candidate compound which may inhibit estrogen receptor-dependent transcription or ?9-nAChR overexpression and proliferation of nicotine-derived-compound-induced breast cancer cells by using an activating protein 1 (AP1) polypeptide. The invention found that ?9-nAChR has an activating protein 1 (AP1)-binding site, that the ?9-nAChR promoter is located at the AP1-binding site, and that ERs specifically bind to the ?9-nAChR promoter at the AP1-binding site, indicating that ER-induced ?9-nAChR up-regulation plays a central role in the response to endogenous (E2) or exogenous (nicotine) stimulation.

Abstract: The invention found that overexpression and activation of ?9-nAChR are associated with tumorigenesis of breast cancer and create a number of small interfering RNAs to inhibit the expression of ?9-nAChR so as to inhibit breast cancer. Therefore, the invention provides small interfering RNAs (siRNAs) for inhibiting expression of ?9-nAChR so as to inhibit breast cancer, methods to prevent/inhibit/treat malignant progression of nicotine-derived-compound-induced breast cancer and method of determining malignant level of such breast cancer.

Abstract: The invention relates to methods of identifying a candidate compound which may inhibit estrogen receptor-dependent transcription or ?9-nAChR overexpression and proliferation of nicotine-derived-compound-induced breast cancer cells by using an activating protein 1 (AP1) polypeptide. The invention found that ?9-nAChR has an activating protein 1 (AP1)-binding site, that the ?9-nAChR promoter is located at the AP1-binding site, and that ERs specifically bind to the ?9-nAChR promoter at the AP1-binding site, indicating that ER-induced ?9-nAChR up-regulation plays a central role in the response to endogenous (E2) or exogenous (nicotine) stimulation.

Abstract: This invention relates to methods of aiding smoking cessation and/or treating and/or preventing smoking addition or methods of treating and/or preventing nicotine or nicotine-derived compounds or estrogen induced breast cancer, which comprises administering to a subject an effective amount of a tea polyphenol. The invention uses catechins (such as epigallocatechin gallate (“EGCG”), epigallocatechin (“EGC”), epicatechin gallate (“ECG”), epicatechin (“EC”), gallocatechin gallate (“GCG”), gallocatechin (“GC”), catechin gallate (“CG”) and catechin (“C”)) in aiding smoking cessation and/or treating and/or preventing smoking addition or treating and/or preventing nicotine or nicotine-derived compounds or estrogen induced breast cancer.

Abstract: This invention relates to methods of treating and/or preventing nicotine or nicotine-derived compounds or estrogen induced breast cancer, which comprises administering to a subject an effective amount of a tea polyphenol. The invention uses catechins (such as epigallocatechin gallate (“EGCG”), epigallocatechin (“EGC”), epicatechin gallate (“ECG”), epicatechin (“EC”), gallocatechin gallate (“GCG”), gallocatechin (“GC”), catechin gallate (“CG”) and catechin (“C”)) in treating and/or preventing nicotine or nicotine-derived compounds or estrogen induced breast cancer.

Abstract: The invention found that overexpression and activation of ?9-nAChR are associated with tumorigenesis of breast cancer and create a number of small interfering RNAs to inhibit the expression of ?9-nAChR so as to inhibit breast cancer. Therefore, the invention provides small interfering RNAs (siRNAs) for inhibiting expression of ?9-nAChR so as to inhibit breast cancer, methods to prevent/inhibit/treat malignant progression of nicotine-derived-compound-induced breast cancer and method of determining malignant level of such breast cancer.