scholarly journals Glucose Sensor Using Redox Active Oligonucleotide-Templated Silver Nanoclusters

Nanomaterials ◽  
2019 ◽  
Vol 9 (8) ◽  
pp. 1065 ◽  
Author(s):  
Kathryn L. Schroeder ◽  
Renee V. Goreham ◽  
Thomas Nann

Redox active, photoluminescent silver nanoclusters templated with oligonucleotides were developed for glucose sensing. The silver nanoclusters had a photoluminescent emission at 610 nm that reversibly changed to 530 nm upon oxidation. The reversible emission change was measured with photoluminescent spectroscopy and used to detect H2O2, which is a by-product of the reaction of glucose with glucose oxidase. The ratio of the un-oxidised emission peak (610 nm) and the oxidised analogue (530 nm) was used to measure glucose concentrations up to 20 mM, well within glucose levels found in blood. Also, the reversibility of this system enables the silver nanoclusters to be reused.

1997 ◽  
Vol 8 (7) ◽  
pp. 1293-1304 ◽  
Author(s):  
H Jiang ◽  
I Medintz ◽  
C A Michels

Glucose is a global metabolic regulator in Saccharomyces. It controls the expression of many genes involved in carbohydrate utilization at the level of transcription, and it induces the inactivation of several enzymes by a posttranslational mechanism. SNF3, RGT2, GRR1 and RGT1 are known to be involved in glucose regulation of transcription. We tested the roles of these genes in glucose-induced inactivation of maltose permease. Our results suggest that at least two signaling pathways are used to monitor glucose levels. One pathway requires glucose sensor transcript and the second pathway is independent of glucose transport. Rgt2p, which along with Snf3p monitors extracellular glucose levels, appears to be the glucose sensor for the glucose-transport-independent pathway. Transmission of the Rgt2p-dependent signal requires Grr1p. RGT2 and GRR1 also play a role in regulating the expression of the HXT genes, which appear to be the upstream components of the glucose-transport-dependent pathway regulating maltose permease inactivation. RGT2-1, which was identified as a dominant mutation causing constitutive expression of several HXT genes, causes constitutive proteolysis of maltose permease, that is, in the absence of glucose. A model of these glucose sensing/signaling pathways is presented.


RSC Advances ◽  
2018 ◽  
Vol 8 (57) ◽  
pp. 32565-32573 ◽  
Author(s):  
Shaojun Yang ◽  
Daliang Liu ◽  
Qing Bo Meng ◽  
Shuyao Wu ◽  
Xi-Ming Song

A novel electrochemical glucose sensor based on methylene blue-reduced graphene oxide nanocomposite was constructed, and the sensor exhibited good glucose oxidase-mimetic electrocatalytic activity towards glucose and practical applicability.


2016 ◽  
Vol 7 (43) ◽  
pp. 6655-6661 ◽  
Author(s):  
Yongkyun Kim ◽  
Ho Namgung ◽  
Taek Seung Lee

New emission color-changeable hydrogels containing glucose oxidase were synthesized to be used in glucose sensing.


Biosensors ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 86 ◽  
Author(s):  
Hong Dinh Duong ◽  
Ok-Jae Sohn ◽  
Jong Il Rhee

Glucose concentration is an important parameter in biomedicine since glucose is involved in many metabolic pathways in organisms. Many methods for glucose detection have been developed for use in various applications, particularly in the field of healthcare in diabetics. In this study, ratiometric fluorescent glucose-sensing membranes were fabricated based on the oxygen levels consumed in the glucose oxidation reaction under the catalysis of glucose oxidase (GOD). The oxygen concentration was measured through the fluorescence quenching effect of an oxygen-sensitive fluorescent dye like platinum meso-tetra (pentafluorophenyl) porphyrin (PtP) by oxygen molecules. Coumarin 6 (C6) was used as a reference dye in the ratiometric fluorescence measurements. The glucose-sensing membrane consisted of two layers: The first layer was the oxygen-sensing membrane containing polystyrene particles (PS) doped with PtP and C6 (e.g., PS@C6^PtP) in a sol–gel matrix of aminopropyltrimethoxysilane and glycidoxypropyltrimethoxysilane (GA). The second layer was made by immobilizing GOD onto one of three supporting polymers over the first layer. These glucose-sensing membranes were characterized in terms of their response, reversibility, interferences, and stability. They showed a wide detection range to glucose concentration in the range of 0.1 to 10 mM, but high sensitivity with a linear detection range of 0.1 to 2 mM glucose. This stable and sensitive ratiometric fluorescent glucose biosensor provides a reliable way to determine low glucose concentrations in blood serum by measuring tear glucose.


2006 ◽  
Vol 5 (10) ◽  
pp. 1726-1737 ◽  
Author(s):  
Victoria Brown ◽  
Jessica A. Sexton ◽  
Mark Johnston

ABSTRACT The Hgt4 protein of Candida albicans (orf19.5962) is orthologous to the Snf3 and Rgt2 glucose sensors of Saccharomyces cerevisiae that govern sugar acquisition by regulating the expression of genes encoding hexose transporters. We found that HGT4 is required for glucose induction of the expression of HGT12, HXT10, and HGT7, which encode apparent hexose transporters in C. albicans. An hgt4Δ mutant is defective for growth on fermentable sugars, which is consistent with the idea that Hgt4 is a sensor of glucose and similar sugars. Hgt4 appears to be sensitive to glucose levels similar to those in human serum (∼5 mM). HGT4 expression is repressed by high levels of glucose, which is consistent with the idea that it encodes a high-affinity sugar sensor. Glucose sensing through Hgt4 affects the yeast-to-hyphal morphological switch of C. albicans cells: hgt4Δ mutants are hypofilamented, and a constitutively signaling form of Hgt4 confers hyperfilamentation of cells. The hgt4Δ mutant is less virulent than wild-type cells in a mouse model of disseminated candidiasis. These results suggest that Hgt4 is a high-affinity glucose sensor that contributes to the virulence of C. albicans.


2019 ◽  
Vol 24 (5) ◽  
pp. 499-505
Author(s):  
Maedeh Mohammadifar ◽  
Mehdi Tahernia ◽  
Seokheun Choi

A novel electrochemical glucose sensor was created for a simple but semiquantitative visual screening of specific glucose concentrations in urine. This noninvasive glucose biosensor integrated a disposable, paper-based sensing strip and a simple amplifier circuit with a visual readout. The paper strip consisted of five enzyme-activated electrodes. Each electrode was connected to a specific indicator circuit that triggered a light-emitting diode (LED) when a predefined glucose concentration was reached. The device features (1) low-cost, disposable, paper-based glucose oxidase (GOx)/poly(3,4-ethylenedioxythiophene) polystyrene sulfonate (PEDOT:PSS) sensing electrodes, (2) simple signal amplification, and (3) on-site, rapid, and visual detection. The sensor generated reliable, discrete visual responses to determine five glucose levels (1, 2, 3, 4, and higher than 4 mM) in urine in less than 2 min. This innovative approach will provide a simple but powerful glucose sensing paradigm for use in POC diagnostics.


1984 ◽  
Vol 246 (1) ◽  
pp. E1-E13 ◽  
Author(s):  
M. D. Meglasson ◽  
F. M. Matschinsky

Control of blood sugar involves the complex interaction of the pancreatic glucose-sensing beta-cells with the liver, which serves as the primary site of glucose disposal after a meal. Glucokinase occupies an important role in controlling glucose phosphorylation and metabolism both in the liver and in pancreatic islets. In the beta-cells, glucokinase functions as pacemaker of glycolysis at physiological glucose levels. It determines the unique characteristics of islet hexose usage, that is, the rate, affinity, cooperativity, and anomeric discrimination of glucose metabolism. Because glycolysis controls hexose-induced insulin release, glucokinase is considered the best-qualified candidate for the elusive glucose sensor of beta-cells. A deficiency of glucokinase would disturb glucose homeostasis. Decreased islet glucokinase would diminish islet glycolysis and would result in a higher set point of beta-cells for glucose-induced insulin release. Decreased liver glucokinase would cause less efficient hepatic glucose disposal. Human maturity-onset diabetes (type II diabetes) has these characteristics. It is thus conceivable that certain forms of type II diabetes are due to a glucokinase deficiency.


Author(s):  
Anthony Ryan Hatch ◽  
Julia T. Gordon ◽  
Sonya R. Sternlieb

The new artificial pancreas system includes a body-attached blood glucose sensor that tracks glucose levels, a worn insulin infusion pump that communicates with the sensor, and features new software that integrates the two systems. The artificial pancreas is purportedly revolutionary because of its closed-loop design, which means that the machine can give insulin without direct patient intervention. It can read a blood sugar and administer insulin based on an algorithm. But, the hardware for the corporate artificial pancreas is expensive and its software code is closed-access. Yet, well-educated, tech-savvy diabetics have been fashioning their own fully automated do-it-yourself (DIY) artificial pancreases for years, relying on small-scale manufacturing, open-source software, and inventive repurposing of corporate hardware. In this chapter, we trace the corporate and DIY artificial pancreases as they grapple with issues of design and accessibility in a content where not everyone can become a diabetic cyborg. The corporate artificial pancreas offers the cyborg low levels of agency and no ownership and control over his or her own data; it also requires access to health insurance in order to procure and use the technology. The DIY artificial pancreas offers patients a more robust of agency but also requires high levels of intellectual capital to hack the devices and make the system work safely. We argue that efforts to increase agency, radically democratize biotechnology, and expand information ownership in the DIY movement are characterized by ideologies and social inequalities that also define corporate pathways.


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