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Troponin I

Troponin I is a protein that plays a crucial role in the regulation of muscle contraction.
It is a member of the troponin complex, which also includes troponin C and troponin T.
Troponin I inhibits the actomyosin ATPase activity in striated muscle, thereby preventing contraction until the muscle is stimulated by calcium.
Measuring levels of troponin I in the blood can help diagnose and monitor various cardiovascular conditions, such as myocardial infarction and myocarditis.
Researchers can optimize their Troponin I studies using PubCompare.ai, a leading AI tool that enhances reproducibility and accuracy by helping identify the most reliable and effective research protocols from literature, pre-prints, and patents.
This streamlines the research process and leads to superior results.

Most cited protocols related to «Troponin I»

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Publication 2020
Activated Partial Thromboplastin Time Axilla Bacteremia Blood Blood Coagulation Disorders Bronchoalveolar Lavage Fluid Chinese Congenital Abnormality COVID 19 Echocardiography Electrocardiography Fever Heart Heart Injuries Hospital Administration Hypersensitivity Hypoproteinemia Kidney Injury, Acute pathogenesis Patients Pneumonia Pneumonia, Ventilator-Associated Respiratory Distress Syndrome, Acute Respiratory System Seafood Secondary Infections Septicemia Septic Shock Serum Albumin Sputum Times, Prothrombin Troponin I

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Publication 2020
Bacteremia Blood Bronchoalveolar Lavage Fluid Congenital Abnormality Creatinine Echocardiography Electrocardiography Heart Heart Injuries Influenza in Birds Inhalation Kidney Diseases Kidney Injury, Acute Oxygen pathogenesis Patients Pneumonia, Hospital Acquired Respiratory Distress Syndrome, Acute Respiratory System SARS-CoV-2 Secondary Infections Serum Shock Sputum Troponin I Urine

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Publication 2020
Adult BLOOD Cardiovascular Diseases COVID 19 Creatine Kinase Critical Illness D-Alanine Transaminase Emergencies Ferritin fibrin fragment D Heart Heart Disease, Coronary Hypersensitivity Inpatient Lactate Dehydrogenase Lymphocyte Count Lymphopenia Middle East Respiratory Syndrome Patients Serum Severe Acute Respiratory Syndrome Survivors Troponin I

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Publication 2015
Biological Assay Cardiac Death Cardiovascular Diseases Electrocardiography Heart Hypersensitivity Myocardial Infarction Myocardial Ischemia Patients ST Segment Elevation Myocardial Infarction Troponin Troponin I Troponin T
We prospectively identified consecutive patients presenting to the Royal Infirmary of Edinburgh, United Kingdom, from 1 August to 31 October 2012, in whom the attending doctor suspected an acute coronary syndrome. Patients not resident in the south east of Scotland were excluded from the study. We obtained information about the patients and their clinical outcomes through the TrakCare software application (InterSystems, Cambridge, MA) as previously described.9 (link)
10 (link)
Serum troponin concentrations were measured on admission and repeated six or 12 hours after the onset of symptoms13 (link)
14 (link) using both a contemporary sensitive troponin I assay and a high sensitivity troponin I assay. Clinical decisions were based on the results of the contemporary assay only, with clinicians blinded to the results of the high sensitivity assay.
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Publication 2015
Acute Coronary Syndrome Biological Assay Hypersensitivity Patients Physicians Serum Troponin Troponin I

Most recents protocols related to «Troponin I»

The toxicity of repeated and high dose of CNPs treatment was assessed by histological and hematological analyses. Briefly, Cy5.5-CNPs (10, 22.5 or 90 mg/kg) were intravenously injected into BALB/c mice with single- or multi-dosage (three times). On day 7 after treatments, major organs (liver, lung, spleen, kidney, brain and heart) were collected from mice, and structural abnormalities in organ tissues were assessed by staining with H&E. In the case of hematological analyses, blood samples were collected from the mice on day 7 and centrifuged at 2200 rpm to obtain plasma. The following factors in blood samples were measured; alanine aminotransferase (ALT), blood urea nitrogen (BUN), alkaline phosphatase (ALP), aspartate Aminotransferase (AST), creatine kinase (CK) and troponin I. The cardiotoxicity by Cy5.5-CNPs was further analyzed after multiple-dosage. The heart tissues were collected from mice after treatment with 10, 22.5 or 90 mg/kg of Cy5.5-CNPs three times. The accumulation of Cy5.5-CNPs in heart tissues was observed using a Leica TCS SP8 confocal laser-scanning microscope. Collagen fiber in heart tissues were stained with Masson's trichrome. Briefly, heart tissues were incubated in Bouin's fixative for 30 min at 56 °C, and the nuclei were co-stained with Weigert's iron hematoxylin. Then, cytoplasm was stained with Biebrich scarlet-acid fuchsin, and then differentiated in phosphomolybdic–phosphotungstic acid. The collagen matrix in heart tissues was stained with aniline blue solution. The collagen in heart tissues were quantitatively analyzed using an Image Pro software, and collagen contents were presented in proportion to the total area of heart tissues.
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Publication 2023
Aftercare Alkaline Phosphatase aniline blue Aspartate Transaminase Biebrich Scarlet BLOOD Brain Cardiotoxicity Cell Nucleus Collagen Congenital Abnormality Creatine Kinase CY5.5 cyanine dye Cytoplasm D-Alanine Transaminase Fibrosis Fixatives Heart Iron Kidney Liver Lung Mice, Inbred BALB C Microscopy, Confocal Mus Phosphotungstic Acid Plasma Spleen Tissues Troponin I Urea Nitrogen, Blood vascular factor
Clinical characteristics including detailed medical history and physical examination were obtained from each patient by experienced cardiologists. All data were stored in the database of our institution. Routine biochemistry including blood urea nitrogen, creatinine, glucose, complete blood count, CK-MB, troponin I, and C-reactive protein (CRP) was measured at admission. The FPA concentration (Boehringer, Mannheim) was measured by sandwich enzyme-linked immunosorbent assay method from centrifuged blood samples. Peak CK-MB and peak troponin-I levels were monitored with blood samples taken at 8-h intervals in the coronary care unit.
Systolic and diastolic arterial pressure, previous history of CAD, hypertension (HT), diabetes mellitus (DM), hyperlipidemia (HL), and smoking status were evaluated [6 (link)]. HT was defined by considering the following parameters: (i) patients who were diagnosed with HT with the international diagnostic code and/or (ii) patients who were taking one or more of the following medications: angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, beta-blockers, and diuretics treatments for at least 6 months. DM was diagnosed according to at least one of the following criteria: (1) History of DM and taking any anti-diabetic medication; (2) randomly measured blood glucose value of 200 mg/dL or higher; (3) blood glucose level of 126 mg/dL or above after at least 8 h of fasting; and (4) A1c value of 6.5% or higher. Smoking was defined as a regular smoker if occurred at least one cigarette a day in the past month. Family history presence of CAD was defined as the development of atherosclerotic CVD or death from CVD in a first-degree relative (i.e., parent or sibling) before age 55 for males or 65 for females. The presence of HL was defined according to age and sex-adjusted percentiles from the National Health and Nutrition Examination Survey III data [7 (link)]. The height and weight data of the patients were recorded, and body mass index was calculated according to the weight/height(cm)2 formula.
Publication 2023
Adrenergic beta-Antagonists Angiotensin-Converting Enzyme Inhibitors Angiotensin II Receptor Antagonist Arteries BLOOD Blood Glucose Cardiologists Complete Blood Count C Reactive Protein Creatinine Diabetes Mellitus Diastole Diuretics Enzyme-Linked Immunosorbent Assay Females Glucose High Blood Pressures Hyperlipidemia Index, Body Mass Isoenzyme CPK MB Males Parent Patients Pharmaceutical Preparations Physical Examination Pressure, Diastolic Systole Troponin I Urea Nitrogen, Blood
This prospective observational study was conducted between January 2015 and April 2017 with patients that were diagnosed with ACS and CCS. ACS diagnoses was created according to the following criteria: Patients with ≥1 mm ST-elevation in consecutive leads related to one of the major coronary arteries’ tertiaries on electrocardiography were accepted ST-elevated myocardial infarction (STEMI) and delivered to angiography laboratory, immediately. In addition, those with ischemic symptoms (typical chest discomfort, shortness of breath, etc.) and ischemic ST-segment depression, or T-wave inversion were taken blood sample for cardiac biomarkers. Elevation in Troponin I/T or creatine kinase myocardial bant (CK/MB) levels was considered to be non-STEMI (NSTEMI) and if these cardiac biomarkers were in normal range, patients were accepted as unstable angina pectoris (USAP) [4 (link)]. Patients incompatible with above-mentioned criteria and have stable ischemic symptoms without elevated cardiac biomarkers were considered to be the CCS. Patients were demonstrated not to have coronary obstructive stenosis and were considered to be the control group [5 (link)]. The study was performed in accordance with the principles stated in the Declaration of Helsinki. The Kanuni Training and Research Hospital Clinical Research Ethics Committee approved the study with 2015/51 number and February 24, 2016 date.
Publication 2023
Angina, Unstable Angiography Artery, Coronary Biological Markers BLOOD Chest Coronary Stenosis Creatine Kinase Diagnosis Dyspnea Electrocardiography Ethics Committees, Clinical Ethics Committees, Research Heart Inversion, Chromosome Myocardium Non-ST Elevated Myocardial Infarction Patients ST Segment Elevation Myocardial Infarction Troponin I
The blood taken from the heart and veins of the deeply anesthetized rats was transferred to yellow-capped biochemistry tubes without anticoagulant. These blood samples were centrifuged at 4000 revolutions per minute for 10 min, and the plasma was transferred to Eppendorf tubes to be stored at −80°C until the day of the experiment. On the experiment day, these samples were thawed at room temperature, and the parameters were analyzed.
Our study protocol was carried out in 3 steps. In the first step, basal biochemical parameters were measured using Siemens brand commercial kits. Alanine aminotransferase (ALT), urea, and creatinine (Cr) parameters were measured in Atellica Solution device; pro-brain natriuretic peptide (pro-BNP) was measured in the AQT90 Flex device, and troponin I and creatine kinase (CK-MB) values were measured in the Advia Centaur XP immunoassay System device. In the second step, caspase 3/7 and 8-hydroxy-deoxyguanosine (8-OHdG) (BT LAB, Cat. no E0031Ra) were measured with enzyme-linked immunosorbent assay. Total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) values were measured. Total antioxidant status and TOS levels of the samples were measured using Rel Assay brand commercial kits. Total antioxidant status levels in tissues were expressed as Trolox equivalent/L, and TOS results as μmol H2O2 equivalent/L.19 (link),20 (link) Oxidative stress index values, an indicator of oxidative stress, were expressed in arbitrary units (AU). In the third stage, the cardiac tissues of the rats were examined histopathologically. Finally, all data were analyzed statistically.
Publication 2023
8-Hydroxy-2'-Deoxyguanosine Anticoagulants Antioxidants Biological Assay BLOOD Caspase-7 Creatine Kinase Creatinine D-Alanine Transaminase Deoxyguanosine Enzyme-Linked Immunosorbent Assay Heart Immunoassay Isoenzyme CPK MB Medical Devices Oxidants Oxidative Stress Peroxide, Hydrogen Plasma Rattus norvegicus Tissues Trolox C Troponin I Urea Veins
At 48 h post-fixation, hearts were sectioned into 200-µm slices. For staining, slices were first incubated for 10 min in blocking solution (3% normal donkey serum (NDS) in PBST), followed by primary antibody staining overnight at 4 °C using the following antibodies: anti-vimentin (ab24525), anti-cardiac troponin I (ab188877) or anti-PGP9.5 (ab108986), purchased from Abcam at 1:200 dilution in blocking solution. Slices were then washed twice in PBST, then stained with secondary antibodies (1 mg ml−1) at 1:500 dilution for 3 h at room temperature using the following: F(ab’)2 anti-chicken 488 (703-546-155) and anti-rabbit 647 (711-606-152) purchased from Jackson ImmunoResearch Laboratories. The slices were then stained with DAPI and washed three times with PBST (30 min per wash). Sections were mounted onto slides and mounted with exPROTOS. Slices were imaged on a confocal microscope (Olympus FV3000).
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Publication 2023
Antibodies Chickens DAPI Equus asinus Heart Immunoglobulins Microscopy, Confocal Rabbits Serum Technique, Dilution Troponin I UCHL1 protein, human Vimentin

Top products related to «Troponin I»

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The ARCHITECTSTAT high-sensitive troponin I assay is a laboratory test that measures the levels of troponin I, a protein released into the bloodstream when the heart muscle is damaged. This assay is designed to provide accurate and sensitive detection of troponin I, which can aid in the diagnosis and management of heart conditions such as myocardial infarction (heart attack).
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DAPI is a fluorescent dye that binds strongly to adenine-thymine (A-T) rich regions in DNA. It is commonly used as a nuclear counterstain in fluorescence microscopy to visualize and locate cell nuclei.
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DAPI is a fluorescent dye used in microscopy and flow cytometry to stain cell nuclei. It binds strongly to the minor groove of double-stranded DNA, emitting blue fluorescence when excited by ultraviolet light.
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The ADVIA Centaur is a fully automated, random-access immunoassay analyzer designed to perform a wide range of immunoassay tests. It is capable of processing multiple sample types, including serum, plasma, and urine. The instrument uses chemiluminescent technology to detect and quantify analytes in the samples.
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Ab47003 is a primary antibody that recognizes the GAPDH protein. It is suitable for use in Western blotting applications.
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Troponin I is a protein found in cardiac and skeletal muscle cells. It plays a crucial role in the regulation of muscle contraction by inhibiting the interaction between actin and myosin.

More about "Troponin I"

Troponin I (cTnI) is a crucial protein that plays a vital role in the regulation of muscle contraction.
It is a key component of the troponin complex, which also includes troponin C and troponin T. cTnI functions by inhibiting the actomyosin ATPase activity in striated muscle, thereby preventing contraction until the muscle is stimulated by calcium.
Measuring levels of cTnI in the blood can assist in the diagnosis and monitoring of various cardiovascular conditions, such as myocardial infarction and myocarditis.
Researchers optimizing their cTnI studies can utilize PubCompare.ai, a leading AI tool that enhances reproducibility and accuracy by helping identify the most reliable and effective research protocols from literature, pre-prints, and patents.
This streamlines the research process and leads to superior results.
PubCompare.ai leverages advanced AI algorithms to compare research methods and protocols, allowing researchers to effortlessly locate the best practices for their cTnI studies.
The ARCHITECTSTAT high-sensitive troponin I assay, ADVIA Centaur, and Architect i2000SR are examples of analytical platforms used to measure cTnI levels.
These assays rely on the use of DAPI, a fluorescent dye that binds to DNA, and bovine serum albumin, a common protein used in biological research.
By incorporating these insights, researchers can further optimize their cTnI studies and achieve more reliable and accurate results.
Whether you're investigating the role of cTnI in cardiovascular diseases or exploring new diagnostic approaches, PubCompare.ai can be a valuable tool to streamline your research process and enhance the reproducibility and accuracy of your findings.
Explore the capabilities of this AI-powered platform and take your cTnI research to new heights.