Afterward, 200 ��L of 5 ��g?mL?1 anti-CEA antibody was added into the wells and incubated for 2 h at 37 ��C. The wells were washed three times with washing buffer followed by addition of 200 ��L AuNPs-labeled goat-anti-mouse IgG. Finally the wells were washed thoroughly with washing buffer (three times) and pure water (three times). Then, the wells were immediately treated with 200 ��L per well of a mixture of 0.01% HAuCl4 and 0.4 mM NH2OH?HCl in a dark for 2 min at 30 ��C.2.5. Standard Procedures for the FI-CL DetectionMetallic gold on enhanced plates were washed three times with 300 ��L of pure water, dried, and dissolved with 200 ��L of 2.0% HNO3-3.4% HCl for three hours at room temperature to ensure that the Au nanoparticles were completely dissolved.

Solutions were then transferred to 1.

5 mL centrifuge tubes and 200 ��L H2O and 75 ��L 0.1 M sodium tartrate (C4H4O6Na2) were added to each sample in turn. Then 1.0 M NaOH was added to the AuCl4? solutions to adjust pH. As shown in Figure 1, AuCl4? was reacted with the mixture of luminol and H2O2 in the flow cell to produce the CL signal. The CL signals were monitored with a photomultiplier tube adjacent to the flow cell.Figure 1.Schematic diagram of flow injection CL system.3.?Results and Discussion
Contemporary medical practice offers few strategies to predict or prevent illness and limited stereotyped responses to clinical symptoms: diagnosis employs a narrow repertory of laboratory tests and medical history indicators, while treatments are often standardized and proscriptive rather than continuously adjusted to patient response.

Doctors, scientists, and policy makers have increasingly proposed Entinostat personalized medicine (PM) as a strategy to improve health maintenance, diagnostic precision, therapeutic efficacy and affordability [1,2]. PM attempts to provide a proactive strategy to replace the reactive strategy of contemporary healthcare by identifying individuals and stratifying populations susceptible to diseases before the onset of clinical symptoms, recommending prevention strategies and designing individualized treatments.

However, the aims of PM have become less ambitious with time, especially since the human genome project hypothesized that genotyping could allow ��personalized�� Batimastat therapies within a proscriptive model of treatment. Despite a number of significant successes (like BRCA1 genotyping), the genomic approach has had limited value for therapeutic optimization because most common illnesses involve the complex interplay of hundreds of genes and proteins within cells and of dozens of cell types with their tissue and organismal environment [3].