Background in Taiwan Taiwan, like many other countries, is under pressure to develop effective policies in response to population aging. Trends of declining fertility rates and expanding lifespan together have contributed to the growth of the "gray population". The proportion of the population aged 65 years and over has doubled from 7% in 1993 to 14% in 2018. In addition, life expectancy has increased over the last 50 years to 77.5 and 84.0 years for men and women, respectively. 1) Although nearly 55.5% of Taiwan's older people live with their adult children, 2) the increasing proportion of women in the labor market and the declining ratio of those needing care to potential caregivers have raised questions regarding families' ability to care for the disabled older population. 3) Official projections show that the number of people in need of long-term care will increase from 577,457 in 2017 to 771,431 in 2026. 4) To respond to the rapidly growing need for care in these population, Taiwan is seeking a clear direction in which to adjust the development of long-term care. Small-scale long-term care plans run by local governments first The Taiwanese government has been facing severe challenges pressed by population ageing. The government started taking the issue of long-term care seriously since the first rotation of the political parties in 2000. However, early plans for long-term care were limited in terms of coverage. The Long-Term Care 2.0 Plan-a tax-funded, universal plan-was implemented in 2016. Soon after its implementation, the number of service organizations and the coverage of service increased sharply. This paper takes Taiwan as an example to discuss the designs of long-term care, and strategies to expand services. With many countries currently under pressure in long term care needs, Taiwan's experience could serve as a good example on how to achieve such policy goal within a short period of time. In addition, policy challenges for expanding long-term care are discussed.
DNA topoisomerase IIα (Top2α) is an essential nuclear enzyme and target for important anti-cancer drugs, such as etoposide and doxorubicin (Dox). Our teniposide-resistant human leukemic lymphoblastic cells (CEM/VM-1-5) (Danks MK et al., Biochemistry 27(24):8861-8869, 1998) express reduced Top2α protein. To determine the role of Top2α in drug resistance, we knocked down Top2α in parental CEM cells by RNAi. Compared to control cells, CEMshTop2α cells were more resistant to the Top2 inhibitors, etoposide and Dox. The mechanism by which knockdown of Top2α caused resistance to Top2 inhibitors is probably caused by a reduction in Top2-DNA complexes leading to fewer broken DNA strands (Wang JC, Nat Rev Mol Cell Biol 3(6):430-440, 2002). The level of reduced Top2α expression in Top2α knockdown CEM cells was confirmed by Western blot. Importantly, we found no compensatory regulation by Top1 or Top2α overexpression under these conditions. It has been reported that knocking-out of Top2α will cause early embryonic death (Jenkins JR et al. Nucleic acids research 20(21):5587-5592, 1992), but in our cultured CEM cells, knocking Top2α down to 40% of control level had little or no impact on cell growth rate. We subsequently generated and characterized stable CEM-tTR-shTop2α cells where Top2α can be conditionally knocked down to 5% of control levels, as determined by Western blot, through a tetracycline-induced expression of short hairpin RNAs. CEM-tTR-shTop2α cells grow significantly more slowly than the control cells, which indicates that while cells can proliferate with ∼40% of Top2α expression, when Top2α is reduced by 95%, cells can apparently remain viable, but are severely impaired in their ability to grow. Present studies are focused on identifying genes that are targets of Top2α knockdown to provide insights into those genes involved in drug resistance. (Supported in part by CA40570 from NCI and in part by UIC) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4683. doi:10.1158/1538-7445.AM2011-4683
DNA topoisomerase IIα (TopoIIα) is an essential nuclear enzyme. Our teniposide-resistant human leukemic lymphoblastic cells (CEM/VM-1-5) express reduced TopoIIα protein. To determine the role of TopoIIα in drug resistance, previously we knocked down TopoIIα in parental CEM cells by RNAi. Compared to control cells, CEM-siTopoIIα cells are more resistant to etoposide. Our previous work suggested that the transcription factor NF-YB is a negative regulator of TopoIIα, working through the TopoIIα promoter (Morgan and Beck, Mol. Pharmacol 59:203,2001). We have found that NF-YB protein expression is increased in CEM/VM-1-5 cells compared to CEM cells. This suggests that increased NF-YB may be the cause of reduced TopoIIα in CEM/VM-1-5 cells. We asked what causes the up-regulation of NF-YB in CEM/VM-1-5 cells. MicroRNAs are a recently identified group of non-protein coding RNAs that regulate posttranscriptional gene expression. In our previous study, we found by microRNA profiling that hsa-miR-485-3p, is lower in CEM/VM-1-5 cells compared to CEM cells. MicroRNA target prediction programs also reveal that the 3′ UTR of NF-YB harbors a putative miR-485-3p binding site. We hypothesized that hsa-miR-485-3p regulates drug resistance by decreasing NF-YB expression, which in turn negatively regulates TopoIIα expression. We overexpressed miR-485-3p in CEM/VM-1-5 cells and this led to reduced expression of NF-YB and a corresponding upregulation of TopoIIα. To validate the binding of miR-485-3p to NF-YB 3′-UTR, present experiments with HEK293Tcells using luciferase reporters carrying the 3′-UTR of the NF-YB gene are being done to clarify the role of miR-485-3p in this phenomenon. (Supported in part by CA40570 from NCI and in part by UIC) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2545.
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