scholarly journals Point-of-Care Analyte Quantification and Digital Readout via Lysate-Based Cell-Free Biosensors Interfaced with Personal Glucose Monitors

2021 ◽  
Author(s):  
Yan Zhang ◽  
Paige L. Steppe ◽  
Maxwell W. Kazman ◽  
Mark P. Styczynski
Keyword(s):  
Point Of Care ◽  
Digital Readout

scholarly journals Point-of-care analyte quantification and digital readout via lysate-based cell-free biosensors interfaced with personal glucose monitors

2021 ◽  
Author(s):  
Yan Zhang ◽  
Paige L Steppe ◽  
Maxwell W Kazman ◽  
Mark P Styczynski
Keyword(s):  
Escherichia Coli ◽  
Enzyme Production ◽  
Point Of Care ◽  
Digital Readout ◽  
One Pot ◽  
Complex Samples ◽  
Reporter Enzyme ◽  
Target Analytes ◽  
Signal Output ◽  
Detection And Quantification

Field-deployable diagnostics based on cell-free systems have advanced greatly, but on-site quantification of target analytes remains a challenge. Here we demonstrate that Escherichia coli lysate-based cell-free biosensors coupled to a personal glucose monitor (PGM) can enable on-site analyte quantification, with the potential for straightforward reconfigurability to diverse types of analytes. We show that analyte-responsive regulators of transcription and translation can modulate production of the reporter enzyme β-galactosidase, which in turn converts lactose into glucose for PGM quantification. Because glycolysis is active in the lysate and would readily deplete converted glucose, we decoupled enzyme production and glucose conversion to increase endpoint signal output. This lysate metabolism did, however, allow for one-pot removal of glucose present in complex samples (like human serum) without confounding target quantification. Taken together, we show that integrating lysate-based cell-free biosensors with PGMs enables accessible target detection and quantification at the point of need.

scholarly journals A microfluidic platform with digital readout and ultra-low detection limit for quantitative point-of-care diagnostics

Lab on a Chip ◽  
2015 ◽  
Vol 15 (16) ◽  
pp. 3300-3306 ◽  
Author(s):  
Ying Li ◽  
Jie Xuan ◽  
Yujun Song ◽  
Ping Wang ◽  
Lidong Qin
Keyword(s):  
Detection Limit ◽  
Point Of Care ◽  
Disease Status ◽  
Biomarker Detection ◽  
Digital Readout ◽  
Target Concentration ◽  
Point Of Care Diagnostics ◽  
Direct Competition ◽  
And Control ◽  
Control Samples

The DV-chip presents a digital bar chart for the biomarker detection based on direct competition between O2 generated by the experimental and control samples. The digital readout clearly and accurately defines target concentration and further indicates the disease status.

“Aspirin - resistance”? A few critical considerations on definition, terminology, diagnosis, clinical value, natural course of atherosclerotic disease, and therapeutic consequences

VASA ◽  
2011 ◽  
Vol 40 (6) ◽  
pp. 429-438 ◽  
Author(s):  
Berent ◽  
Sinzinger
Keyword(s):  
Platelet Function ◽  
Point Of Care ◽  
Aspirin Resistance ◽  
Point Of View ◽  
Evidence Based ◽  
Platelet Function Tests ◽  
Clinical Value ◽  
Vascular Events ◽  
Therapeutic Consequences ◽  
Function Tests

Based upon various platelet function tests and the fact that patients experience vascular events despite taking acetylsalicylic acid (ASA or aspirin), it has been suggested that patients may become resistant to the action of this pharmacological compound. However, the term “aspirin resistance” was created almost two decades ago but is still not defined. Platelet function tests are not standardized, providing conflicting information and cut-off values are arbitrarily set. Intertest comparison reveals low agreement. Even point of care tests have been introduced before appropriate validation. Inflammation may activate platelets, co-medication(s) may interfere significantly with aspirin action on platelets. Platelet function and Cox-inhibition are only some of the effects of aspirin on haemostatic regulation. One single test is not reliable to identify an altered response. Therefore, it may be more appropriate to speak about “treatment failure” to aspirin therapy than using the term “aspirin resistance”. There is no evidence based justification from either the laboratory or the clinical point of view for platelet function testing in patients taking aspirin as well as from an economic standpoint. Until evidence based data from controlled studies will be available the term “aspirin resistance” should not be further used. A more robust monitoring of factors resulting in cardiovascular events such as inflammation is recommended.

Cloud-Computing: eHealth aus der Wolke

2018 ◽  
Vol 23 (11) ◽  
pp. 38-41
Author(s):  
Sebastian Krolop ◽  
Florian Benthin ◽  
Constanze Knahl
Keyword(s):  
Cloud Computing ◽  
Point Of Care

Cloud-Computing gewinnt auch in Kliniken zunehmend an Bedeutung. Über das Internet bereitgestellte Lösungen verändern nicht nur Verwaltung und Logistik – im klinischen Bereich geht es zum Beispiel um die Nutzung elektronischer Patientenakten am Point-of-Care.

Thrombozytenaggregationshemmer

2003 ◽  
Vol 23 (04) ◽  
pp. 181-185 ◽  
Author(s):  
H. Patscheke
Keyword(s):  
Point Of Care ◽  
Von Willebrand

ZusammenfassungUnabhängig von ihrem Wirkungsmechanismus greifen Antikoagulanzien stets unmittelbar in die Bildung und Wirkung von Thrombin und damit die Endstrecke der Gerinnung ein. Von den Aggregationshemmern hemmen nur die GPIIb/IIIa-Antagonisten die gemeinsame Endstrecke der Plättchenaggregation, indem sie die Bildung von Fibrinogen/von-Willebrand-Faktor-vermittelten Plättchen-Plättchen-Brücken hemmen.Azetylsalizylsäure (ASS), NSARs, Clopidogrel oder Ticlopidin begrenzen die Plättchenaktivierung dagegen, indem sie die Bildung bzw. Wirkung der sekundären Plättchenagonisten Thromboxan A2 bzw. ADP ausschalten, aber z. B. die durch Thrombin direkt induzierbare Plättchenaggregation nicht. Deshalb rufen ASS, Clopidogrel oder Ticlopidin allein kein wesentliches Blutungsrisiko hevor, wenn nicht weitere, die Hämostase beeinträchtigende Faktoren (z.B. ausgeprägte Thrombozytopenie, Antikoagulation) vorliegen. Deshalb entfällt für diese Hemmstoffe auch die Notwendigkeit der Therapiekontrolle. Beim therapeutischen Einsatz von ASS als Aggregationshemmer ist vielmehr die Dosierung darauf abzustellen, eine vollständige Blockade (mind. 90%) der Thromboxanbiosynthese in den Plättchen zu erreichen, um überhaupt einen therapeutischen bzw. prophylaktischen Effekt zu erzielen.Von den GPIIb/IIIa-Antagonisten sind nur die parenteral eingesetzten (Abciximab, Eptifibatid, Tirofiban) zugelassen. Orale GPIIb/IIIa-Antagonisten zeigten bisher in klinischen Studien ein erhöhtes Blutungsrisiko bei nicht ausreichendem therapeutischen Nutzen. Die meisten GPIIb/IIIa-Antagonisten verursachen eine leichte Thrombozytopenie, als deren Auslöser die Inhibitor-Rezeptor-Wechselwirkung bzw. immunologische Mechanismen diskutiert werden. Für das spezifische Monitoring dieser potenten Aggregationshemmer ist ein »Point-of-Care«-Testsystem verfügbar. Für die Einschätzung des Blutungsrisikos müssen jedoch stets alle, die Hämostase beeinflussende Faktoren berücksichtigt werden. Das gilt insbesondere, wenn neben GPIIb/IIIa-Antagonisten Heparin u.a. Wirkstoffe eingesetzt werden.

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