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Cobas 111

Manufactured by Roche
Sourced in Germany, Switzerland

The Cobas 111 is a compact, automated in vitro diagnostic system designed for clinical laboratory testing. It is capable of performing a wide range of clinical chemistry and immunochemistry assays. The Cobas 111 provides reliable and efficient analysis to support medical decision-making.

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7 protocols using cobas 111

1

Serum Biomarkers of Kidney Health

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Nonroutine assessments were performed in the Laboratory of the Department of Pathophysiology, Medical University of Silesia in Katowice.
Commercially available ELISA kits were used for assessment of serum concentrations of soluble α-Klotho levels (Immuno-Biological Laboratories Co. Ltd., Fujioka-Shi, Gunma, Japan) and iFGF23 (Immutopics, San Clemente, CA, USA), with the mean intra- and interassay coefficients <3% and <6.5% (soluble α-Klotho) and <4.4% and <6.1% (iFGF23). Serum intact parathyroid hormone (iPTH), phosphorus, and calcium levels were assessed using commercially available kits on the Cobas E411 and Cobas 111 analyzers (Roche Diagnostics GmbH, Mannheim, Germany) with interassay coefficients of variability <6.5%, <2.3%, and <1.3%, respectively.
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2

Glucose Metabolism in HepG2 Cells

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HepG2 cells were seeded in DMEM (containing 4500 mg/L glucose and phenol red) (Life Science, Seoul, Korea) with 10% FBS and 1% PEST at a density of 106 cells/well in a 6-well plate for 24 h, and the medium was changed to assay medium (DMEM without glucose, phenol red and FBS), to which either C3G (10 and 50 μM) was added or metformin was added as a positive control, and treated with or without the compound C (AMPK inhibitor) for another 24 h. Cells were washed 2 times with 1× PBS; then, DMEM containing 20 mM sodium lactate, 2 mM sodium pyruvate, 2 mM L-glutamine and 15 mM HEPES (4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid) was added to the cells; and 100 μM of 8-(4-Chlorophenylthio)adenosine 3′,5′-cyclic monophosphate sodium salt (8-CPT-cAMP) was added as the control for 6 h. The culture medium was collected, and glucose concentrations were determined using an automated clinical chemistry analyzer (Cobas111, Roche, Basel, Switzerland) according to the manufacturer’s instructions.
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3

Vivax Malaria Treatment Randomization

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Consenting soldiers with confirmed P. vivax were screened for eligibility by obtaining a medical history, and conducting physical and laboratory examinations that included electro-cardiogram (ECG; BTL-08, BTL Industries, Framingham, MA, USA; 12-lead, 50 mm/s, 10 mm/mV), complete blood counts (Coulter Ac-T; Beckman Coulter, Fullerton, CA, USA), full blood chemistry panel (Cobas-111, Roche, Rotkreuz, Switzerland), and G6PD deficiency screening (NADPH kit 203A, Trinity Biotech, Wicklow, Ireland). Eligible subjects had uncomplicated vivax malaria, were not under treatment for another illness, had not recently consumed antimalarials, and showed normal ECG, blood laboratory values, and G6PD activity by fluorescent spot testing (Trinity Biologics, Ireland).
The trial statistician block-allocated treatment assignments by varying blocking number at random [26 (link)]. A plain, consecutively numbered and sealed envelope prepared by the trial administrator contained therapy assignment and was opened in sequence as each eligible and consenting soldier enrolled. The study pharmacist supervised therapy and adherence to assigned treatment, including direct observation of each of the daily 14 doses of PQ.
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4

Serum Biomarker Assessment Protocol

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Additional assessments were performed in stored frozen samples in the laboratory of the Department of Pathophysiology. Serum 25-OH-D (limit of quantification 3 ng/mL) and intact parathyroid hormone (iPTH) levels were assessed by an electrochemiluminescence method on a Cobas E411 analyzer (Roche Diagnostics GmbH, Mannheim, Germany) with inter-assay coefficients of variability below 7.8 and 6.5%, respectively. We measured serum intact fibroblast growth factor 23 (iFGF23) (Immutopics, San Clemente, CA, U.S.) and high-sensitivity (limit of quantification (0.09 mg/L) C-reactive protein (Immundiagnostik AG, Bensheim, Germany) concentrations by ELISA. The mean intra- and interassay coefficients were 4.4% and 6.1% for iFGF23 and <6% and <11.6% for hsCRP, respectively.
Serum phosphorus and calcium were assessed by an automated system (Cobas 111, Roche Diagnostics GmbH, Mannheim, Germany) with interassay coefficients of variability below 2.3 and 1.3%, respectively.
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5

Plasma Extraction and Analyte Quantification

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Blood samples were centrifuged for 15 min at 4 °C and 12,000g to separate plasma from cells. Enzyme activity and molecule concentrations were measured using a Roche Cobas 111 serum analyser according to the manufacturer’s instructions.
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6

Metabolic Markers in Clinical Trial

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A YSI 2300 STAT Plus glucose analyzer was used to analyze PG.
Insulin, C-peptide, glucagon, and free FA (FFA) concentrations were measured at t = 0, 210, 270, 390, and 450 min. Insulin (no. 10-1113-01), glucagon (no. 10-1271-01) and C-peptide concentrations (no. 10-1136-01) were measured by ELISA (Mercodia, Uppsala, Sweden). Serum FFA concentrations were measured by a colorimetric method (Wako Pure Chemical Industries, Osaka, Japan). VLDL-TG and total TG concentrations were analyzed on a cobas 111 (F. Hoffmann–La Roche), using a glycerol blanked kit.
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7

Triton-Induced Hyperlipidemia Experiment

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All animal experiments were approved by the Amorepacific Institutional Animal Care and Use Committee (PQ13-S007) and adhere to the Organisation for Economic Cooperation and Development (OECD) guidelines. Sprague-Dawley (SD) male rats, 6-week-old, were purchased from the Central Laboratory Animal Inc. and maintained in a 12 h dark-12 h light cycle chamber with controlled temperature of 22-25°C and 40-50 % humidity. For adaptation, rats were fed normal chow ad libitum for 1 week. The average level of plasma TAG was not significantly different (online Supplementary Table S1). After adaptation, animals were divided into four groups (Saline, Triton, Triton + FGT and Triton + FF; n 5/group). Triton was utilised to induce hyperlipidaemia, and FF was used as a positive control. Rats were orally injected with saline, 500 mg/kg of body weight of FGT or 65 mg/kg body weight of FF for 5 d. After 5 d, animals were fasted overnight, and the final administration of selected agents (saline, FGT and FF) was carried out 1 h before Triton treatment. Finally, Triton (200 mg/kg body weight) was delivered to all rats except among those in the saline group through the tail vein. At 0, 3, 5, 18 and 20 h after Triton injection, blood samples were collected to measure plasma TAG levels. Plasma TAG levels were measured using an automated clinical chemistry analyzer (Cobas111; Roche).
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