Printed platforms for paper-based analytical applications

Paper-based analytical technologies enable quantitative and rapid analysis of analytes from various application areas including healthcare, environmental monitoring and food safety. Because paper is a planar, flexible and light weight substrate, the devices can be transported and disposed easily. Diagnostic devices are especially valuable in resourcelimited environments where diagnosis as well as monitoring of therapy can be made even without electricity by using e.g. colorimetric assays. On the other hand, platforms including printed electrodes can be coupled with hand-held readers. They enable electrochemical detection with improved reliability, sensitivity and selectivity compared with colorimetric assays. In this thesis, different roll-to-roll compatible printing technologies were utilized for the fabrication of low-cost paper-based sensor platforms. The platforms intended for colorimetric assays and microfluidics were fabricated by patterning the paper substrates with hydrophobic vinyl substituted polydimethylsiloxane (PDMS) -based ink. Depending on the barrier properties of the substrate, the ink either penetrates into the paper structure creating e.g. microfluidic channel structures or remains on the surface creating a 2D analog of a microplate. The printed PDMS can be cured by a roll-ro-roll compatible infrared (IR) sintering method. The performance of these platforms was studied by printing glucose oxidase-based ink on the PDMS-free reaction areas. The subsequent application of the glucose analyte changed the colour of the white reaction area to purple with the colour density and intensity depending on the concentration of the glucose solution. Printed electrochemical cell platforms were fabricated on paper substrates with appropriate barrier properties by inkjet-printing metal nanoparticle based inks and by IR sintering them into conducting electrodes. Printed PDMS arrays were used for directing the liquid analyte onto the predetermined spots on the electrodes. Various electrochemical measurements were carried out both with the bare electrodes and electrodes functionalized with e.g. self assembled monolayers. Electrochemical glucose sensor was selected as a proof-of-concept device to demonstrate the potential of the printed electronic platforms.

Sulfuric acid - glucose separation using mixed-recycle steady state recycling chromatography

Batch chromatography is a widely used separation technique in a variety of fields meeting difficult separations. Several technologies for improving the performance of chromatography have been studied, including mixed-recycle steady state recycling (MR-SSR) chromatography. Design of MR-SSR has been commonly limited on 100 % purity constraint cases and empirical work. In this study a predictive design method was used to optimize feed pulse size and design a number of experimental MR-SSR separations for a solution of 20 % sulfuric acid and 100 g/L glucose. The design was under target product fraction purities of 98.7 % for H2SO4 and 95 % for glucose. The experiments indicate a maximum of 59 % increase in sulfuric acid productivity and 82 % increase for glucose when compared to corresponding batch separation. Eluent consumption was lowered by approximately 50 % using recycling chromatography. Within this study the target purities and yields set in design were not completely met, and further optimization of the process is deemed necessary.

On Glucose Metabolism in Patients with the m.3243A>G Mutation

Background: The m.3243A>G mutation in mitochondrial DNA is the most common cause for mitochondrial diabetes. In addition, unexpected deaths related to the m.3243A>G associate with encephalopathy and cardiomyopathy. Failing mitochondrial respiratory chain in neurons, myocytes and beta cells is considered to underlie the multiorgan manifestations of the m.3243A>G. Aims: The primary aim of the study was to characterize the organ-specific glucose metabolism in patients with m.3243A>G and secondly, to study patients with or without signs of diabetes, cardiomyopathy or encephalopathy. The insulin-stimulated glucose metabolism in brain, heart, skeletal muscle, adipose tissue and liver were measured with 2-deoxy-2-[18F]fluoro-α-D-glucose in 15 patients and 14 controls. Brain oxygen metabolism was assessed with [15O]oxygen and insulin secretion was modelled based on oral glucose tolerance test. Results: The glucose oxidation in brain was globally decreased in patients with or without clinical encephalopathy. The insulin-stimulated glucose influx to skeletal muscle and adipose tissue was decreased in patients with or without diabetes as the hepatic glucose metabolism was normal. Impaired beta cell function and myocardial glucose uptake were associated with the high m.3243A>G heteroplasmy. Conclusions: This cross-sectional study suggests that: 1) The ability of insulin to stimulate glucose metabolism in skeletal muscle and adipose tissue is weakened before the beta cell failure results in mitochondrial diabetes. 2) Glucose oxidation defect is detected in otherwise unaffected cerebral regions in patients with the m.3243A>G, thus it likely precedes the clinical encephalopathy. 3) Uneconomical glucose hypometabolism during hyperinsulinemia contributes to the cardiac vulnerability in patients with high m.3243A>G heteroplasmy