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1.
Community Dent Health ; 28(3): 243-7, 2011 Sep.
Article in English | MEDLINE | ID: mdl-21916362

ABSTRACT

UNLABELLED: In New South Wales (NSW), Australia, the responsibility to implement water fluoridation rests with local government Councils, partly accounting for the hindrance in its statewide implementation. Since 2003, the NSW Health Department has been actively promoting water fluoridation to the remaining unfluoridated rural communities. OBJECTIVES: To describe the community education and consultation strategies which led to the implementation of fluoridation in two rural NSW towns. METHODS: In February 2005, the Mid-Western Regional Council and the NSW Health Department undertook a comprehensive community education process followed by a consultation process. The education process included the organization of public forums; distribution of fluoridation information packs; building rapport with the local media; and the use of local disease and treatment data to demonstrate oral health disparities with neighbouring fluoridated towns. The consultation process to determine support for fluoridation included seeking written submissions from the community and conducting interviews on a random sample of households by an independent research organization. RESULTS: A total of 502 (N = 1,012) interviews to determine support for fluoridation were completed, achieving a response rate of 49.6%. 54% of respondents wanted their water supplies fluoridated, 25% did not and the remaining 21% were unsure. In June 2005, the Mid-Western Regional Council resolved to implement water fluoridation and fluoride was added to the towns' water supplies in November 2007. CONCLUSIONS: This case study demonstrates that it is possible to garner community support for water fluoridation with the use of a multifaceted approach in educating and consulting communities and stakeholders.


Subject(s)
Community Networks , Fluoridation , Health Education, Dental , Health Promotion/organization & administration , Organizational Case Studies , Community Participation , Humans , Information Dissemination , Interviews as Topic , Local Government , New South Wales
2.
Nature ; 414(6862): 457-62, 2001 Nov 22.
Article in English | MEDLINE | ID: mdl-11719808

ABSTRACT

The retinoblastoma tumour suppressor (Rb) pathway is believed to have a critical role in the control of cellular proliferation by regulating E2F activities. E2F1, E2F2 and E2F3 belong to a subclass of E2F factors thought to act as transcriptional activators important for progression through the G1/S transition. Here we show, by taking a conditional gene targeting approach, that the combined loss of these three E2F factors severely affects E2F target expression and completely abolishes the ability of mouse embryonic fibroblasts to enter S phase, progress through mitosis and proliferate. Loss of E2F function results in an elevation of p21Cip1 protein, leading to a decrease in cyclin-dependent kinase activity and Rb phosphorylation. These findings suggest a function for this subclass of E2F transcriptional activators in a positive feedback loop, through down-modulation of p21Cip1, that leads to the inactivation of Rb-dependent repression and S phase entry. By targeting the entire subclass of E2F transcriptional activators we provide direct genetic evidence for their essential role in cell cycle progression, proliferation and development.


Subject(s)
Cell Cycle Proteins/physiology , Cell Division/physiology , DNA-Binding Proteins , Transcription Factors/physiology , Animals , Cell Cycle Proteins/genetics , Cell Division/genetics , Cell Line , Cyclin-Dependent Kinase Inhibitor p21 , Cyclins/genetics , Down-Regulation , E2F Transcription Factors , E2F1 Transcription Factor , E2F2 Transcription Factor , E2F3 Transcription Factor , Fibroblasts/cytology , Gene Targeting , Integrases/genetics , Integrases/metabolism , Mice , Mice, Inbred C57BL , Mice, Knockout , Retinoblastoma Protein/metabolism , S Phase/genetics , S Phase/physiology , Transcription Factors/genetics , Viral Proteins/genetics , Viral Proteins/metabolism
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