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Cobas c702

Manufactured by Roche
Sourced in Germany, Switzerland, China, United States, Italy, Japan, United Kingdom

The Cobas c702 is a clinical chemistry analyzer developed by Roche Diagnostics. It is designed for use in medical laboratories and performs a range of automated clinical chemistry tests to support patient diagnosis and treatment monitoring. The Cobas c702 processes samples and reagents to measure various analytes in biological samples, providing reliable and accurate results.

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140 protocols using cobas c702

1

Monitoring Hemolysis Biomarkers in Cardiac Patients

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Blood, sampled for routine purposes, was drawn in siliconized vacuum tubes (Vacuette 9NC Coagulation sodium citrate 3.2%, Greiner Bio-One, Kremsmünster, Austria) and sent to the central laboratory. In patients without extracorporeal or mechanical circulatory support, HI, PFH levels, and plasma LDH levels were measured once per day; in patients under extracorporeal or mechanical circulatory support, more measurements per day were performed during the initial postoperative period.
HI was measured for laboratory quality control purposes by assessing the absorbance of light at 570 and 600 nm using the Roche Cobas C 702 (Roche, Basel, Switzerland). PFH levels were measured using the pseudoperoxidase method [17 (link)] and plasma LDH levels were measured by determining the catalytic activity via the reduction of NAD to NADH and photometric measurement (Roche Cobas C 702).
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2

Serum Vancomycin and CRP Quantification

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Serum vancomycin levels were assessed using the kinetic interaction of microparticles in solution (KIMS) method on the Roche Cobas c702 analyzer (Roche, Basel, Switzerland). A competitive reaction takes place between the vancomycin-macromolecule conjugate and vancomycin in the serum to bind with the vancomycin antibody on the microparticles. The turbidity induced by the binding of the vancomycin conjugate to the antibody on the microparticles is measured photometrically, and this measurement is inhibited by the presence of vancomycin in the sample. The resulting turbidity is indirectly proportional to the amount of vancomycin present in the sample. The lower limit of quantitation for vancomycin is 4.0 μg/mL, determined as the lowest concentration that meets a total error goal of 20%.
CRP concentrations were determined through a particle-enhanced immunoturbidimetric assay on the Roche Cobas c702 as well. Serum creatinine levels were measured by a rate-blanked compensated kinetic Jaffe method on the Atellica CH 930 Analyzer (Siemens Healthcare Diagnostics, Marburg, Germany).
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3

Cardiometabolic Parameter Measurement Protocol

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Measurement of cardiometabolic parameters was conducted based on previous studies (Jung et al., 2020a (link)). All cardiometabolic parameters (TC, HDL-C, LDL-C, TG, FFA, glucose, and insulin levels; HOMA-IR; and HOMA-β) were analyzed by the Seegene Medical Foundation (an organization certified by the Korean government). Eight milliliters of venous blood was collected in a serum separating tube (SST). Clot formation was ensured in the SST by centrifuging the sample at 3500 rpm for 10 min. TC level was determined using an enzymatic kinetic assay using Cobas C702 (Roche, Mannheim, Germany). HDL-C and LDL-C levels were detected using a homogeneous enzymatic colorimetric assay using Cobas C702 (Roche, Mannheim, Germany). The glucose level was determined using an enzymatic kinetic assay using Cobas8000 C702 (Roche, Mannheim, Germany), and the insulin level was detected using an electrochemiluminescence immunoassay (ECLIA) using Cobas8000 e602 (Roche, Mannheim, Germany). HOMA-IR and HOMA-β were calculated using the following formula: HOMA-IR = [glucose (mg/dl) × insulin (μU/ml)]/405, HOMA-β = [360 × insulin (μU/ml)/glucose (mg/dl) − 63] (Jung et al., 2020a (link)).
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4

Evaluating Serum Uric Acid and Triglycerides

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In this study, SUA was obtained at baseline and recorded as a continuous variable, using a biochemical automatic analyzer (Cobas c702, Roche; Shanghai, China). The final outcome variable, triglycerides, was obtained using the same process of using a biochemical automatic analyzer (Cobas c702, Roche; Shanghai, China) in accordance with published guidelines and prior research.
The covariates included in this study can be summarized as follows: demographic data, variables affecting SUA or TGs according to previous literature, and variables based on clinical experience. The fully-adjusted model included the following continuous variables obtained at baseline: age, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), blood urea nitrogen (BUN), Creatinine (Cr), and body mass index (BMI); as well as categorical variables obtained at baseline: sex, smoking status, hypertension, diabetes, and coronary disease.
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5

Comprehensive Cardiometabolic Biomarker Analysis

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All cardiometabolic biomarkers (TC, HDL-C, LDL-C, TG, FFA, glucose, insulin, HOMA-IR, and HOMA-β) were analyzed by the Seegene medical foundation (an organization certified by the Korea government). The concentrations of TC, HDL-C, LDL-C, TG, FFA, glucose, and insulin were quantified. An 8-mL sample of venous blood was collected into a serum separating tube (SST) for serum. Clot formation was ensured in the SST by centrifuging the sample at 3500 rpm for 10 min. The TC concentration was determined by an enzyme kinetic assay using the Cobas C702 (Roche, Mannheim, Germany). The HDL-C and LDL-C concentrations were detected by homogeneous enzymatic colorimetric assay using the Cobas C702 (Roche, Mannheim, Germany). The glucose concentration was determined by an enzyme kinetic assay using the Cobas8000 C702 (Roche, Mannheim, Germany) and the insulin concentration was detected by an electrochemiluminescence immunoassay using the Cobas8000 e602 (Roche, Mannheim, Germany). HOMA-IR and HOMA-β were calculated using the following formulas: HOMA-IR = (glucose [mg/dL] × insulin [µU/mL])/405 and HOMA-β = (360 × insulin [µU/mL])/(glucose [mg/dL] − 63].
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6

Metabolic Markers in Diabetes and CVD

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The primary outcomes are FBG and LDL-C. FBG is crucial in diagnosing and managing diabetes [22] (link). LDL-C is the instigator of atherosclerotic plaques and main therapeutic target to prevent future cardiovascular events [23, (link)24] (link). The secondary outcomes include insulin, The Homeostatic Model Assessment of Insulin Resistance Index using the HOMA2 Calculator (HOMA-IR2), TG, total cholesterol (TC), LDL-C, and high-density lipoprotein-cholesterol (HDL-C). Fasting blood samples were obtained in the morning and preserved at -80˚C until subjected to analysis. FBG levels were assessed by the hexokinase method employing the Cobas c702 instrument (Roche Diagnostics, Germany). Fasting insulin levels were quantified in serum utilizing an electrochemiluminescence immunoassay conducted on the Cobas e601 instrument (Roche Diagnostics, Germany). Serum levels of TG, TC, LDL-C, and HDL-C were determined through a homogeneous assay employing the Cobas c702 instrument (Roche Diagnostics, Germany). The HOMA-IR2 score was computed using the HOMA calculator v2.2.3 (https://www2.dtu.ox.ac.uk/homacalculator/).
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7

Analytical Methods for Metabolic Biomarkers

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Glycosylated hemoglobin (HbA1c) was measured with ion-exchange high performance liquid chromatography (Variant II Haemoglobin A1c, Bio-Rad Laboratories, California, USA) or a photometric immunoturbidimetric method (Tina-quant Hemoglobin A1c Gen 3, Cobas c501, Roche Diagnostics GmbH, Mannheim, Germany). Plasma insulin and C-peptide were determined by automatized electro-chemiluminescence analyser immunoassay (Modular E170, Roche Diagnostics GmbH, Mannheim, Germany) [33 (link)]. Plasma glucose, total cholesterol, HDL-cholesterol, triacylglycerols, and creatinine were measured with a photometric, enzymatic method (Modular P800 or Cobas c702, Roche Diagnostics GmbH, Mannheim, Germany) and LDL-cholesterol using the Friedewald formula [34 (link)] or automatised enzymatic assay (Cobas c702, Roche Diagnostics GmbH, Mannheim, Germany). Serum high-sensitivity C-reactive protein (hs-CRP) was analysed using immunonephelometry. Detailed information regarding the analytical methods used can be found on the official laboratory services handbook of Turku University Hospital laboratory units (http://webohjekirja.mylabservices.fi/TYKS/, accessed on 5 May 2022).
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8

Biochemical Analysis of Metabolic Markers

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For the biochemical analysis, venous blood samples were collected after overnight fasting of at least 10 h. The serum was separated through centrifugation and stored at −80 °C. Fasting blood glucose (FBG), triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and uric acid (UA) were measured using a Hitachi Automatic Biochemical Analyzer 7180 (Hitachi, Ltd., Tokoy, Japan. Fasting insulin (FINS) was measured using a fully automatic electrochemiluminescence analyzer Roche Cobas E602 (Roche Diagnostics, Mannheim, Germany). Insulin sensitivity was assessed by homeostasis model assessment–insulin resistance (HOMA-IR), which was calculated as follows: HOMA-IR = FBG (mmol/L) × FINS (μU/mL)/22.5.
Circulating markers of inflammation include C-reactive protein concentration (CRP), tumor necrosis factor α (TNF-α), and free fatty acids (FFA). CRP was determined using an automatic electrochemiluminescence analyzer Roche Cobas C702 (Roche Diagnostics, Mannheim, Germany). TNF-α and FFA were determined using the multifunctional enzyme marker Tecan sunrise (Tecan, Mannedorf, Switzerland).
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9

Creatinine, Urea, and Serum β2M Measurements

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Creatinine and urea were measured by standard biochemical and enzymatic methodology (Roche Modular P, Roche Diagnostics, Lewes, UK). Serum β2M was measured by an immunoturbidimetric assay (Roche Cobas c702, Roche Diagnostics, Lewes, UK). All laboratories were UK accredited, and creatinine measurements were aligned by isotope dilution mass spectrometry (IDMS) standards (IDMS).
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10

Extracting Cystatin C and Creatinine Data

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Cystatin C values drawn between January 1, 2018, and September 9, 2020, and creatinine values during this period from BWH, the Dana-Farber Cancer Institute, and satellite clinical laboratories were extracted from the Brigham and Women’s laboratory information system, Sunquest (SQ; Sunquest Information Systems Inc). Creatinine was measured using the rate-blanked kinetic Jaffe method on the Roche cobas c702 (Roche) at BWH and cystatin C was determined using the Roche cobas c701 (Roche) at the Dana-Farber Cancer Institute. Patients were identified who had cystatin C and creatinine values within 24 hours of each other. If 2 or more pairs had the same minimum time interval, the first cystatin C value drawn chronologically was selected. Duplicate records were removed, resulting in a final cohort with 1,783 unique names and medical record numbers (Fig S1).
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