Barrier-free HDB kitchen-design for wheelchair users

Master'sMASTER OF ARTS (ARCHITECTURE

A meta-analysis of phosphate binders lanthanum carbonate versus sevelamer hydrochloride in patients with end-stage renal disease undergoing hemodialysis

Background and Objectives: The purpose of this study was to compare the effects of phosphate binders lanthanum carbonate (LC) versus sevelamer hydrochloride (SH) in end-stage renal disease (ESRD) patients undergoing hemodialysis.Methods: Studies including randomized controlled trials (RCTs) comparing phosphate binders lanthanum carbonate versus sevelamer hydrochloride, in ESRD patients undergoing hemodialysis, were identified using a pre-defined search strategy. Phosphate, calcium, calcium-phosphorus product, intact parathyroid hormone, alkaline phosphatase, total cholesterol, and triglyceride were extracted and compared by RevMan 5.1 (The Cochrane Collaboration, Oxford, UK).Results: Six studies were identified. Meta-analysis showed that SH treatment reduced levels of phosphate, intact parathyroid hormone, and total serum alkaline phosphatase (ALP) when compared with LC treatment. Furthermore, patients on SH treatment tended to have reduced calcium levels, calcium-phosphorus product, total cholesterol, and triglyceride when compared to patients treated with LC, but there was no statistical difference.Conclusion: SH treatment of patients with ESRD is more effective compared to LC treatment. However, more well-designed random control trails are required for confirmation.Keywords: End-stage renal disease, hemodialysis, phosphate binders, lanthanum carbonate (LC), sevelamer hydrochloride (SH), meta-analysis

PPARγ and PPARδ as Modulators of Neoplasia and Cell Fate

PPARγ and PPARδ agonists represent unique classes of drugs that act through their ability to modulate gene transcription associated with intermediary metabolism, differentiation, tumor suppression, and in some instances proliferation and cell adhesion. PPARγ agonists are used by millions of people each year to treat type 2 diabetes but may also find additional utility as relatively nontoxic potentiators of chemotherapy. PPARδ agonists produce complex actions as shown by their tumor promoting effects in rodents and their cholesterol-lowering action in dyslipidemias. There is now emerging evidence that PPARs regulate tumor suppressor genes and developmental pathways associated with transformation and cell fate determination. This review discusses the role of PPARγ and PPARδ agonists as modulators of these processes

3-Phosphoinositide-dependent Protein Kinase-1 (PDK1) promotes invasion and activation of matrix metalloproteinases

BACKGROUND: Metastasis is a major cause of morbidity and mortality in breast cancer with tumor cell invasion playing a crucial role in the metastatic process. PDK1 is a key molecule that couples PI3K to cell proliferation and survival signals in response to growth factor receptor activation, and is oncogenic when expressed in mouse mammary epithelial cells. We now present evidence showing that PDK1-expressing cells exhibit enhanced anchorage-dependent and -independent cell growth and are highly invasive when grown on Matrigel. These properties correlate with induction of MMP-2 activity, increased MT1-MMP expression and a unique gene expression profile. METHODS: Invasion assays in Matrigel, MMP-2 zymogram analysis, gene microarray analysis and mammary isografts were used to characterize the invasive and proliferative function of cells expressing PDK1. Tissue microarray analysis of human breast cancers was used to measure PDK1 expression in invasive tumors by IHC. RESULTS: Enhanced invasion on Matrigel in PDK1-expressing cells was accompanied by increased MMP-2 activity resulting from stabilization against proteasomal degradation. Increased MMP-2 activity was accompanied by elevated levels of MT1-MMP, which is involved in generating active MMP-2. Gene microarray analysis identified increased expression of the ECM-associated genes decorin and type I procollagen, whose gene products are substrates of MT1-MMP. Mammary fat pad isografts of PDK1-expressing cells produced invasive adenocarcinomas. Tissue microarray analysis of human invasive breast cancer indicated that PDK1pSer241 was strongly expressed in 90% of samples. CONCLUSION: These results indicate that PDK1 serves as an important effector of mammary epithelial cell growth and invasion in the transformed phenotype. PDK1 mediates its effect in part by MT1-MMP induction, which in turn activates MMP-2 and modulates the ECM proteins decorin and collagen. The presence of increased PDK1 expression in the majority of invasive breast cancers suggests its importance in the metastatic process