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VitaScreen - portable EPR spectrometer

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17,500.00 EUR
Model: NOX-E.12-VIT
Manufactured by: Noxygen

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Modern medicine:

in a matter of minutes and with just one drop of blood, and a small device you can monitor your cellular metabolic activity (CMA).

VitaScreen - CMA Screening

The company NOXYGEN comes with a new concept. A small unit instrument, that practitioners and pharmacists can now afford to own and run the test in less than 10 minutes to assess the risk of your cardiovascular condition. Practically with one drop of blood (from your fingertip) - as easy as taking a glucose test.

The CMA - Cellular Metabolic Activity - correlates to more than 25 important laboratory-, metabolic-, inflammation-, and functional heart parameters. Thus, this assay quickly tells you if something is out of the normal range, needing further investigation. This risk assessment using an absolute scale of CMA is invaluable information during invasive treatments, chronic disease, or other acute pathologies.
But it goes even beyond clinical assist: it is simple enough to be used as periodic monitoring of your health in ordinary life.

CMA Method

The CMA method patented by Noxygen is a cellular assay based on EPR technology. It quantifies the state of health based on the patient's cell metabolism with a simple indicator: Measuring cellular metabolism (oxidative eustress / distress[1]) caused by ROS formation in blood cells using a membrane-permeable spinprobe. The CMA analysis is being carried out with a drop of blood from the fingertip under physiological conditions (T = 36.6 °C and pO₂ of 40 mmHg). The device is at its heart a miniaturized EPR spectrometer specialized for CMA and extended CMA.
The corridor for the necessary, healthy eustress or the range of a risk factor or disease level are integrated in the reference values of the CMA scale. In already more than 25 peer-reviewed manuscripts, different diseases and influencing factors have been described.

Differential diagnostics

An initial assessment of the health status is easily possible via the total CMA formation rate. By selectively inhibiting individual metabolic pathways, the associated proportion can be determined
(e.g., mitochondria-dependent ROS formation) - so-called extended CMA. This enables differential diagnosis because certain influencing factors and diseases show specific patterns.

For example, SARS-CoV2 infection causes short and/or long-term overexpression of inducible NO synthase (iNOS)[2], activation of phagocytic NADPH oxidase (NOX2)[3], progressive mitochondrial dysfunction[4], and activation of constitutive NADPH oxidase (NOX1)[5] with known subsequent cardiovascular damage. A major side effect of chemotherapeutic intervention, e.g. in breast cancer, is the development of heart failure caused by progressive mitochondrial dysfunction persisting over several years. A (pre-)metabolic syndrome is characterized by excessive overexpression of NOX1 and progressive mitochondrial dysfunction. In healthy individuals, the above mentioned metabolic pathways play a minor role only (see figure above).

Available eCMAs assays

Device facts:

- standalone device
- automatic data evaluation
- automatic outlier recognition
- integrated 7" touchscreen
- integrated temperature controller

- records and calibration history
- data export as .csv
- predosed consumeables
- dimensions: 32x18x26cm³ (LxWxH)
- weight: <8kg
- power consumption: <30W

Literature

Reactive oxygen species (ROS) as pleiotropic physiological signaling agents; Sies et al.; Nature Reviews Molecular Cell Biology 2020; 21(7):363-383
Implications of SARS-Cov-2 infection on eNOS and iNOS activity: Consequences for the respiratory and vascular systems; Guimaraes et al.; Nitric Oxide 2021; 111 (112) 64–71
SARS-CoV-2 and Myocardial Injury: A Role for Nox2; Violi et al.; Intern Emerg Med 2020; 1-4
Implications of Oxidative Stress and Potential Role of Mitochondrial Dysfunction in COVID-19: Therapeutic Effects of Vitamin D.; Heras et al.; Antioxidants 2020; (9) 897
Endothelial Cell Infection and Endotheliitis in COVID-19; Varga et al.; Lancet 2020; 395(10234): 1417-1441

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