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Sensing Mechanism (sensing + mechanism)

Distribution by Scientific Domains

Life Sciences	36%
Chemistry	36%
Polymers and Materials Science	18%

Selected Abstracts

Amperometric Sensor for Heparin: Sensing Mechanism and Application in Human Blood Plasma Analysis

ELECTROANALYSIS, Issue 13-14 2006
Jan Langmaier
Abstract Voltammetric measurements of heparin at a rotating glassy carbon (GC) electrode coated with a polyvinylchloride membrane are reported. A spin-coating technique is used to prepare thin membranes (20,40,,m) with a composition of 25% (w/w) PVC, 1,1,-dimethylferrocene as a reference electron donor for the GC|membrane interface, nitrophenyl octyl ether (o -NPOE) or bis(2-ethylhexyl) sebacate (DOS) as a plasticizer, and hexadecyltrimethylammonium tetrakis(4-chlorophenyl) borate (HTMATPBCl) or tridodecylmethylammonium tetrakis(4-chlorophenyl) borate (TDMATPBCl) as a background electrolyte. It is shown that the electrodes coated with either the HTMA+/o -NPOE (DOS) or TDMA+/o -NPOE (DOS) membrane provide a comparable amperometric response towards heparin (1,10,U mL,1) in the aqueous solution of 0.1,M LiCl. However, only the membranes formulated with TDMATPBCl can be used for an amperometric assay of heparin in human blood plasma with a detection limit of 0.2,U mL,1. Effects of membrane composition, heparin concentration, rotation speed and sweep rate on the voltammetric behavior of heparin provide some insight into the sensing mechanism. Theoretical analysis of the amperometric response is outlined, and the numeric simulation of the voltammetric behavior is presented. [source]

Enantioselective Fluorescence Sensing of Amino Acids by Modified Cyclodextrins: Role of the Cavity and Sensing Mechanism

CHEMISTRY - A EUROPEAN JOURNAL, Issue 11 2004
Sara Pagliari Dr.
Abstract Two selectors based on modified cyclodextrins containing a metal binding site and a dansyl fluorophore,6-deoxy-6- N -(N, -[(5-dimethylamino-1-naphthalenesulfonyl)aminoethyl]phenylalanylamino-,-cyclodextrin,containing D -Phe (3) and L -Phe (4) moieties were synthesized. The conformations of the two selectors were studied by circular dichroism, two-dimensional NMR spectroscopy and time-resolved fluorescence spectroscopy. Cyclodextrin 4 was found to have a predominant conformation in which the dansyl group is self-included in the cyclodextrin cavity, while 3 showed a larger proportion of the conformation with the dansyl group outside the cavity. As a consequence, the two cyclodextrins were found to bind copper(II) with different affinities, as revealed by fluorescence quenching in competitive binding measurements. Addition of D - or L -amino acids induced increases in fluorescence intensity, which were dependent on the amino acid used and in some cases on its absolute configuration. The cyclodextrin 4 was found to be more enantioselective than 3, suggesting that the self-inclusion in the cyclodextrin cavity strongly increases the chiral discrimination ability of the copper(II) complex. Accordingly, a linear fluorescent ligand N, -[(5-dimethylamino-1-naphthalenesulfonyl)aminoethyl]- N1 -propyl-phenylalaninamide, which has the same binding site and absolute configuration as 4, showed very low chiral discrimination ability. The enantioselectivity in fluorescence response was found to be due to the formation of diastereomeric ternary complexes, which were detected by ESI-MS and by circular dichroism. Time-resolved fluorescence studies showed that the fluorescence of the dansyl group was completely quenched in the ternary complexes formed, and that the residual fluorescence was due to uncomplexed ligand. [source]

The mechanisms that underlie glucose sensing during hypoglycaemia in diabetes

DIABETIC MEDICINE, Issue 5 2008
R. McCrimmon
Abstract Hypoglycaemia is a frequent and greatly feared side-effect of insulin therapy, and a major obstacle to achieving near-normal glucose control. This review will focus on the more recent developments in our understanding of the mechanisms that underlie the sensing of hypoglycaemia in both non-diabetic and diabetic individuals, and how this mechanism becomes impaired over time. The research focus of my own laboratory and many others is directed by three principal questions. Where does the body sense a falling glucose? How does the body detect a falling glucose? And why does this mechanism fail in Type 1 diabetes? Hypoglycaemia is sensed by specialized neurons found in the brain and periphery, and of these the ventromedial hypothalamus appears to play a major role. Neurons that react to fluctuations in glucose use mechanisms very similar to those that operate in pancreatic B- and A-cells, in particular in their use of glucokinase and the KATP channel as key steps through which the metabolic signal is translated into altered neuronal firing rates. During hypoglycaemia, glucose-inhibited (GI) neurons may be regulated by the activity of AMP-activated protein kinase. This sensing mechanism is disturbed by recurrent hypoglycaemia, such that counter-regulatory defence responses are triggered at a lower glucose level. Why this should occur is not yet known, but it may involve increased metabolism or fuel delivery to glucose-sensing neurons or alterations in the mechanisms that regulate the stress response. [source]

Amperometric Sensor for Heparin: Sensing Mechanism and Application in Human Blood Plasma Analysis

Feeding signals to the hungry mind

EXPERIMENTAL PHYSIOLOGY, Issue 8 2009
Nina Balthasar
Obesity, due to its associated co-morbidities, including type 2 diabetes and cardiovascular disease, is at the forefront of today's health care concerns. Our need for novel, multifaceted approaches to tackle the global increase of waistlines is urgent, and understanding the physiological processes underlying our vulnerability to weight gain is an important one of them. Evidence for considerable heritability of body weight indicates genetic influences in the susceptibility to our obesogenic environment. Here, we will focus on neurons in brain structures such as the hypothalamus, which sense the body's metabolic state and, through an intricate cascade of events, elicit an appropriate response. We will explore the use of genetically modified mouse models in the investigation of physiological functions of genes and pathways in neuronal regulation of metabolic balance. Use of these techniques allows us to make manipulations at the molecular level (e.g. in the neuronal metabolic sensing mechanism) and combine this with systems-level physiological analysis (e.g. body weight). Recent technological advances also enable the investigation of the contributions of genes to the co-morbidities of obesity, such as obesity-induced hypertension. Reviewing examples of improvements as well as large gaps in our knowledge, this lecture aims to incite interest in whole body physiological research. [source]

ISC1-encoded inositol phosphosphingolipid phospholipase C is involved in Na+/Li+ halotolerance of Saccharomyces cerevisiae

FEBS JOURNAL, Issue 16 2002
Christian Betz
In Saccharomyces cerevisiae, toxic concentrations of Na+ orLi+ ions induce the expression of the cation-extrusion ATPase gene, ENA1. Several well-studied signal transduction pathways are known correlating high salinity to the transcriptional activation of ENA1. Nevertheless, information on the actual sensing mechanism initiating these pathways is limited. Here, we report that the ISC1 -encoded phosphosphingolipid-specific phospholipase C appears to be involved in stimulation of ENA1 expression and, consequently, in mediating Na+ and Li+ tolerance in yeast. Deletion of ISC1 distinctly decreased cellular Na+ and Li+ tolerance as growth of the ,isc1::HIS5 mutant, DZY1, was severely impaired by 0.5 m NaCl or 0.01 m LiCl. In contrast,K+ tolerance and general osmostress regulation wereunaffected. Isc1, mutant growth with 0.9 m KCl and glycerol accumulation in the presence of 0.9 m NaCl or 1.5 m sorbitol were comparable to that of the wild-type. ENA1 -lacZ reporter studies suggested that the increased salt sensitivity of the isc1, mutant is related to a significant reduction of Na+/Li+ -stimulated ENA1 expression. Correspondingly, Ena1p-dependent extrusion of Na+/Li+ ions was less efficient in the isc1, mutant than in wild-type cells. Itis suggested that ISC1 -dependent hydrolysis of an unidentified yeast inositol phosphosphingolipid represents an early event in one of the salt-induced signalling pathways of ENA1 transcriptional activation. [source]

Novel Structural Modulation in Ceramic Sensors Via Redox Processing in Gas Buffers

INTERNATIONAL JOURNAL OF APPLIED CERAMIC TECHNOLOGY, Issue 3 2006
Abdul-Majeed Azad
High selectivity, enhanced sensitivity, short response time, and long shelf-life are some of the key features sought in the solid-state ceramic-based chemical sensors. As the sensing mechanism and catalytic activity are predominantly surface-dominated, benign surface features in terms of small grain size, large surface area, high aspect ratio and, open and connected porosity, are required to realize a successful material. In order to incorporate these morphological features, a technique based on rigorous thermodynamic consideration of the metal/metal oxide coexistence is described. By modulating the oxygen partial pressure across the equilibrium M/MO proximity line, formation and growth of new oxide surface on an atomic/submolecular level under conditions of "oxygen deprivation," with exotic morphological features, has been achieved in potential sensor materials. This paper describes the methodology and discusses the results obtained in the case of potential semiconducting ceramic oxide-based carbon monoxide and hydrogen sensors with enhanced characteristics. [source]

Polyadenylation of Escherichia coli transcripts plays an integral role in regulating intracellular levels of polynucleotide phosphorylase and RNase E

MOLECULAR MICROBIOLOGY, Issue 5 2002
Bijoy K. Mohanty
Summary Polyadenylation in Escherichia coli has been implicated in the destabilization of a variety of transcripts. However, transiently increasing intracellular poly(A) levels has also been shown to stabilize the pnp and rne transcripts, leading to increased polynucleotide phosphorylase (PNPase) and RNase E levels respectively. Here, we show that the half-lives of both the pnp and rne transcripts are dependent on the intracellular level of polyadenylated transcripts. In addition, experiments using pnp,lacZ and rne,lacZ translational fusions demonstrate that the variations in transcript stability and protein levels arise from alterations in the autoregulation of both genes. Further support for this conclusion is provided by the fact that, in an rne mutant in which autoregulation is inactivated by deletion of most of the 5, untranslated region, variations in the level of polyadenylated transcripts no longer affect RNase E protein expression. Of even more interest is the fact that the presence of a functional degradosome is essential for RNase E to detect increased levels of poly(A). Thus, it appears that polyadenylation of transcripts in E. coli serves as a sensing mechanism by which the cell adjusts the levels of both RNase E and PNPase. [source]

Ca2+ -independent hypoxic vasorelaxation in porcine coronary artery

THE JOURNAL OF PHYSIOLOGY, Issue 3 2005
Min Gu
To demonstrate a Ca2+ -independent component of hypoxic vasorelaxation and to investigate its mechanism, we utilized permeabilized porcine coronary arteries, in which [Ca2+] could be clamped. Arteries permeabilized with ,-escin developed maximum force in response to free Ca2+ (6.6 ,m), concomitant with a parallel increase in myosin regulatory light chain phosphorylation (MRLC-Pi), from 0.183 ± 0.023 to 0.353 ± 0.019 MRLC-Pi (total light chain),1. Hypoxia resulted in a significant decrease in both force (,31.9 ± 4.1% prior developed force) and MRLC-Pi (from 0.353 to 0.280 ± 0.023), despite constant [Ca2+] buffered by EGTA (4 mm). Forces developed in response to Ca2+ (6.6 ,m), Ca2+ (0.2 ,m) + GTP,S (1 mm), or in the absence of Ca2+ after treatment with ATP,S (1 mm), were of similar magnitude. Hypoxia also relaxed GTP,S contractures but importantly, arteries could not be relaxed after treatment with ATP,S. Permeabilization with Triton X-100 for 60 min also abolished hypoxic relaxation. The blocking of hypoxic relaxation after ATP,S suggests that this Ca2+ -independent mechanism(s) may operate through alteration of MRLC-Pi or of phosphorylation of the myosin binding subunit of myosin light chain phosphatase. Treatment with the Rho kinase inhibitor Y27632 (1 ,m) relaxed GTP,S and Ca2+ contractures; but the latter required a higher concentration (10 ,m) for consistent relaxation. Relaxations to N2 and/or Y27632 averaged 35% and were not additive or dependent on order. Our data suggest that the GTP-mediated, Rho kinase-coupled pathway merits further investigation as a potential site of this novel, Ca2+ -independent O2 -sensing mechanism. Importantly, these results unambiguously show that hypoxia-induced vasorelaxation can occur in permeabilized arteries where the Ca2+ is clamped at a constant value. [source]

O2 -sensing after carotid chemodenervation: hypoxic ventilatory responsiveness and upregulation of tyrosine hydroxylase mRNA in brainstem catecholaminergic cells

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2000
Jean-Christophe Roux
Abstract Ventilatory responses to acute and long-term hypoxia are classically triggered by carotid chemoreceptors. The chemosensory inputs are carried within the carotid sinus nerve to the nucleus tractus solitarius and the brainstem respiratory centres. To investigate whether hypoxia acts directly on brainstem neurons or secondarily via carotid body inputs, we tested the ventilatory responses to acute and long-term hypoxia in rats with bilaterally transected carotid sinus nerves and in sham-operated rats. Because brainstem catecholaminergic neurons are part of the chemoreflex pathway, the ventilatory response to hypoxia was studied in association with the expression of tyrosine hydroxylase (TH). TH mRNA levels were assessed in the brainstem by in situ hybridization and hypoxic ventilatory responses were measured in vivo by plethysmography. After long-term hypoxia, TH mRNA levels in the nucleus tractus solitarius and ventrolateral medulla increased similarly in chemodenervated and sham-operated rats. Ventilatory acclimatization to hypoxia developed in chemodenervated rats, but to a lesser extent than in sham-operated rats. Ventilatory response to acute hypoxia, which was initially low in chemodenervated rats, was fully restored within 21 days in long-term hypoxic rats, as well as in normoxic animals which do not overexpress TH. Therefore, activation of brainstem catecholaminergic neurons and ventilatory adjustments to hypoxia occurred independently of carotid chemosensory inputs. O2 -sensing mechanisms unmasked by carotid chemodenervation triggered two ventilatory adjustments: (i) a partial acclimatization to long-term hypoxia associated with TH upregulation; (ii) a complete restoration of acute hypoxic responsivity independent of TH upregulation. [source]

Photonic Crystals in Bioassays

ADVANCED FUNCTIONAL MATERIALS, Issue 18 2010
Yuanjin Zhao
Abstract Photonic crystal (PC) based bioassay techniques have many advantages in sensitive biomolecular screening, label-free detection, real-time monitoring of enzyme activity, cell morphology research, and so on. This study provides an overall survey of the basic concepts and up-to-date research concerning the very promising use of PC materials for bioassays. It includes the design and application of PC films, PC microcarriers, PC fibers, and PC optofluidics for fluorescence enhancement or label-free bioassays. Emphasis is given to the description of the functional structures of different PC materials and their respective sensing mechanisms. Examples of detecting various types of analytes are presented. This article promotes communication among chemistry, biology, medicine, pharmacy, and material science. [source]