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Creatine Kinase

Creatine Kinase: An enzyme that catalyzes the conversion of creatine and utilizes adenosine triphosphate (ATP) to create phosphocreatine and adenosine diphosphate (ADP).
It plays a crucial role in cellular energy homeostasis, particularly in tissues with high and fluctuating energy demands, such as skeletal and cardiac muscle.
Measurement of creatine kinase levels can provide valuable insights into the diagnosis and management of various muscular, neurological, and cardiovascular disorders.

Most cited protocols related to «Creatine Kinase»

We obtained the medical records and compiled data for hospitalized patients and outpatients with laboratory-confirmed Covid-19, as reported to the National Health Commission between December 11, 2019, and January 29, 2020; the data cutoff for the study was January 31, 2020. Covid-19 was diagnosed on the basis of the WHO interim guidance.14 A confirmed case of Covid-19 was defined as a positive result on high-throughput sequencing or real-time reverse-transcriptase–polymerase-chain-reaction (RT-PCR) assay of nasal and pharyngeal swab specimens.1 (link) Only laboratory-confirmed cases were included in the analysis.
We obtained data regarding cases outside Hubei province from the National Health Commission. Because of the high workload of clinicians, three outside experts from Guangzhou performed raw data extraction at Wuhan Jinyintan Hospital, where many of the patients with Covid-19 in Wuhan were being treated.
We extracted the recent exposure history, clinical symptoms or signs, and laboratory findings on admission from electronic medical records. Radiologic assessments included chest radiography or computed tomography (CT), and all laboratory testing was performed according to the clinical care needs of the patient. We determined the presence of a radiologic abnormality on the basis of the documentation or description in medical charts; if imaging scans were available, they were reviewed by attending physicians in respiratory medicine who extracted the data. Major disagreement between two reviewers was resolved by consultation with a third reviewer. Laboratory assessments consisted of a complete blood count, blood chemical analysis, coagulation testing, assessment of liver and renal function, and measures of electrolytes, C-reactive protein, procalcitonin, lactate dehydrogenase, and creatine kinase. We defined the degree of severity of Covid-19 (severe vs. nonsevere) at the time of admission using the American Thoracic Society guidelines for community-acquired pneumonia.15 (link)All medical records were copied and sent to the data-processing center in Guangzhou, under the coordination of the National Health Commission. A team of experienced respiratory clinicians reviewed and abstracted the data. Data were entered into a computerized database and cross-checked. If the core data were missing, requests for clarification were sent to the coordinators, who subsequently contacted the attending clinicians.
Publication 2020
Biological Assay Blood Chemical Analysis Complete Blood Count COVID 19 C Reactive Protein Creatine Kinase Electrolytes Kidney Lactate Dehydrogenase Liver Nose Outpatients Patients Pharynx Physicians Pneumonia Procalcitonin Radiography, Thoracic Radionuclide Imaging Real-Time Polymerase Chain Reaction Respiratory Rate Reverse Transcriptase Polymerase Chain Reaction RNA-Directed DNA Polymerase X-Ray Computed Tomography

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Publication 2020
Adenovirus Infections Adrenal Cortex Hormones Antibiotics Bacteria Biological Assay Blood Bronchi Bronchoalveolar Lavage Fluid Complete Blood Count COVID 19 Creatine Kinase Electrolytes Feces Genes, env Influenza Influenza in Birds isolation Kidney Lactate Dehydrogenase Liver Mechanical Ventilation Methylprednisolone Middle East Respiratory Syndrome Coronavirus Nasal Cannula Nose Oligonucleotide Primers Oseltamivir Oxygen Parainfluenza Pathogenicity Patients Pharynx Physical Examination Physicians Pneumonia Real-Time Polymerase Chain Reaction Respiratory Rate Respiratory Syncytial Virus Respiratory System SARS-CoV-2 Serum Severe acute respiratory syndrome-related coronavirus Sputum Tests, Blood Coagulation Tests, Diagnostic Therapeutics Treatment Protocols Virus Virus Release

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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
We conducted a genetic association study with three stages as displayed in Figure 1. Stage 1 consisted of the Myocardial Infarction Genetics Consortium (MIGen), a collection of 2,967 cases of early-onset MI (in men ≤50 years old or women ≤60 years old) and 3,075 age- and sex-matched controls free of MI from six international sites: Boston and Seattle in the United States as well as Sweden, Finland, Spain, and Italy (Table 1). At each site, MI was diagnosed on the basis of autopsy evidence of fatal MI or a combination of chest pain, electrocardiographic evidence of MI, or elevation of one or more cardiac biomarkers (creatine kinase or cardiac troponin). The mean age at the time of MI was 41 years among male cases and 47 years among female cases.
We took forward SNPs into two stages of replication (Stages 2 and 3, Figure 1). 1441 SNPs were tested in Stage 2 based on two criteria: i) strength of statistical evidence in Stage 1 (1433 SNPs from loci with P < 10-3 in Stage 1) or ii) belonging to one of eight reported loci from recent genome-wide association studies for coronary artery disease (a common SNP from each of 9p21.3, near CXCL12, SMAD3, MTHFD1L, MIA3, near CELSR2/PSRC1/SORT1, 2q36, and PCSK9)3 (link),7 (link).
Stage 2 consisted of in silico comparisons with four recently completed GWAS for MI consisting of a symmetric effective sample size of up to 3,942 cases of MI and 3,942 controls. These studies included the Wellcome Trust Case Control Consortium Coronary Heart Disease study3 (link), German MI Family Study I3 (link), PennCATH, and MedStar (Supplementary Table 1). In each Stage 2 study, the analysis was restricted to the phenotype of MI with an age of onset threshold of <66 years for men or women. Although this age cutoff is slightly less restrictive than that used in Stage 1, this cutoff is at or below the mean age of first MI in the US (65 years for men and 70 years for women).
Thirty-three SNPs were taken forward to Stage 3, which consisted of genotyping an additional 6 studies with a symmetric effective sample size of up to 5,469 cases of MI and 5,469 controls. These six studies included Acute MI Gene Study/Dortmund Health Study, Verona Heart Study29 (link), Mid-America Heart Institute Study30 (link), Irish Family Study31 (link), German MI Family Study II, and INTERHEART32 (link) (European ancestry and South Asian ancestry each analyzed separately) (Supplementary Table 2). Stage 3 was comprised of 25 SNPs with the best combined statistical evidence for MI from Stages 1 and 2 (P < 10-5) and the eight previously-reported SNPs discussed above. In each Stage 3 study, the analysis was restricted to the phenotype of MI and in four of the six studies, an age of onset threshold was established at <66 years for men or women.
Publication 2009
Asian Persons Autopsy Biological Markers CELSR2 protein, human Chemokine CXCL12 Chest Pain Coronary Artery Disease Creatine Kinase DNA Replication Electrocardiography Europeans Genes Genetic Association Studies Genome-Wide Association Study Heart Heart Disease, Coronary Males migen Myocardial Infarction PCSK9 protein, human Phenotype Single Nucleotide Polymorphism SMAD3 protein, human SORT1 protein, human Troponin Woman
The original sites for the MD STARnet included the states of Iowa, Colorado, and Arizona, and western New York State. The state of Georgia was added to the MD STARnet in 2005 and Hawaii in 2008. The objective of the MD STARnet is to identify all patients with Duchenne/Becker muscular dystrophy born on or after January 1, 1982 who ever resided in one of these geographic areas.
Details of the surveillance methods used by MD STARnet have been published4 (link) and Figure 1 summarizes the approach to case review and data collection. Briefly, each participating site obtains permission for case finding and medical record abstraction either through institutional review board approval or by state-mandated public health reporting. Trained abstractors identify potential cases from multiple sources. Common sources of potential Duchenne/Becker muscular dystrophy cases include neuromuscular and outpatient neurology clinic records, hospital discharge databases (ICD9 code 359.1 diagnoses), hospital records, and self-report by families in response to advertisements. When a potential case is identified, an MD STARnet abstractor uses structured methods to record information from the medical records at one or more sites of care. At each MD STARnet site, abstracts are subjected to a computerized quality control check, and then reviewed for completeness. After local review, the abstracted data are collected centrally at the MD STARnet Data Coordination Center at the University of Iowa as individual, de-identified records.
At the Data Coordination Center, a subset of the abstracted elements for each potential case is sent monthly to the MD STARnet Clinical Review Committee for assignment of a case category. The Clinical Review Committee consists of a clinician from each site with experience in diagnosis and treatment of patients with muscular dystrophy. Data items used by the Clinical Review Committee are those critical to diagnosis of Duchenne/Becker muscular dystrophy, and include symptoms and age at onset, creatine kinase value, results of dystrophin mutation analysis testing, muscle biopsy reports, and family history. After review of these items, each Clinical Review Committee member independently assigns the case to one of 6 case categories. Table 1 provides details of the case category definitions. If all committee members agree on a case, this assignment is used in future analyses. If committee members are discordant in assigning a case category, the case is reviewed and discussed by at least 4 members. If consensus cannot be reached, the case is returned to the abstractor to find additional information. If no additional information is available, the case is assigned the lowest agreed-upon case category, with “definite” the highest level of confidence, followed by “probable,” “intermediate,” and “possible” as the lowest.
Medical record abstraction recurs annually. If new diagnostic information is found, the case returns to the Clinical Review Committee for review and possible reassignment of case status. For example, if a pathological dystrophin mutation is reported on a “possible” case, re-review would result in assignment as a “definite” case.
After the first 8 months of case reviews, Clinical Review Committee members became concerned that the diagnostic criteria for cases with case categorization based primarily on muscle biopsy were not sufficiently stringent, and that forms of limb girdle muscular dystrophy could meet the criteria for “definite” cases.5 (link) The case definitions were revised and the current definitions shown in Table 1 were adopted in October 2005.
Presented here are the proportion of cases in each category tallied by birth year intervals and the diagnostic test used for the assignment of “definite” and “probable” cases. The present analysis uses data from all sites except Hawaii.
Publication 2010
Biopsy Childbirth Committee Members Creatine Kinase Diagnosis DMD protein, human Duchenne and Becker Muscular Dystrophy Ethics Committees, Research Muscle Tissue Muscular Dystrophies, Limb-Girdle Muscular Dystrophy Mutation Patient Discharge Patients Tests, Diagnostic

Most recents protocols related to «Creatine Kinase»

Demographics, medical history, National Institutes of Health Stroke Scale (NIHSS) scores (17 (link)), and admission blood pressure were documented at baseline. Laboratory tests [including serum levels of creatinine, glucose levels, hemoglobin (Hb), platelet count (PLT), absolute neutrophil count (ANC), absolute lymphocyte count (ALC), absolute monocyte count (AMC), alanine aminotransferase (ALT), aspartate aminotransferase (AST) total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, γ-glutamyltransferase (γGT), and creatine phosphokinase (CPK)] were determined by admission blood tests.
To quantify the extent of liver fibrosis, we used the noninvasive liver fibrosis score (FIB-4) for each patient at the time of admission.
The FIB-4 score was computed for every patient as follows:
As validated in previous clinical trials, prediction of advanced liver fibrosis was indicated using a cut-off value ≥2.67, whereas a score value <1.30 was used to exclude severe liver fibrosis with high probability (18 (link), 19 (link)).
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Publication 2023
Aspartate Transaminase Blood Pressure Cerebrovascular Accident Cholesterol Cholesterol, beta-Lipoprotein Creatine Kinase Creatinine D-Alanine Transaminase Fibrosis, Liver Glucose Hematologic Tests Hemoglobin High Density Lipoprotein Cholesterol Lymphocyte Count Monocytes Neutrophil Patient Admission Patients Platelet Counts, Blood Serum Triglycerides
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
Participant characteristics were summarized descriptively. Comparisons between patients discharged home, admitted to the medical ward, or admitted directly to the ICU were made with Wilcoxson rank sum and Pearson chi-square tests for continuous and categorical variables, respectively. Impact of timing during the pandemic was assessed as days since data collection started (March 8, 2020).
All tests were 2-sided and a P value < .05 was considered statistically significant. All variables were initially assessed for significance using univariable analysis comparing: Patients discharged home versus admitted to the medical ward and; Patients admitted to the medical ward versus ICU (see Tables S1 and S2, Supplemental Digital Content, http://links.lww.com/MD/I601, which shows the results of univariable analysis). A Multivariable logistic regression was fitted separately comparing: Patients discharged home versus admitted to the medical ward and; Patients admitted to the medical ward versus ICU. We opted for 2 logistic regression models to reflect the distinct clinical decision making processes in the ED (i.e., “discharge home” vs “admit to medical ward,” and “admit to medical ward” vs “admit to ICU”).”
Our key associations of interest were race, ethnicity, ADI, English as a primary language, homelessness, and illicit substance use (opiates, cocaine, methamphetamine); variables also included age, gender, and clinical comorbidities, including body mass index (mg/kg2) and clinical severity. We evaluated disease severity using clinical severity scores (sequential organ failure assessment, Charlson comorbidity index) and laboratory markers found in other risk severity scores,[27 (link),28 ] specifically, C-reactive protein (mg/L), ferritin (ug/L), D-dimer (ng/mL), creatine kinase (U/L), troponin (ng/L), procalcitonin (ng/mL), absolute lymphocyte count (K/mL), and blood urea nitrogen (mg/dL). Timing of admission was calculated as days after the first date of data collection (March 8, 2020). In our regression, we controlled for timing of admission and included the square of timing of admission to evaluate how the effect changed over time. To build our regression models, we first included a priori variables based on clinical understanding (i.e., age, sex, sequential organ failure assessment, C-reactive protein, ferritin, and troponin), and then added variables that were significant on univariable analysis.” Variables were excluded if they showed significant co-linearity (variance inflation factors over 10). We used stepwise, backward selection for our logistic regression model, using a P value of over 0.2 as a cutoff to remove variables. Potential interaction between significant variables was explored.
Additionally, we divided differences in number of admissions in 3 groups to visually evaluate changes in admission over time. Groups were created as general phases of the surge in SARS-CoV-2 admissions in our hospital, representing changes in comfort with diagnosis and clinical management of COVID-19. Changes in admission patterns over time were assessed using the Jonckheere–Terpstra test for trend. All data were analyzed using Stata Statistical Software (Release 16. College Station, TX: StataCorp LLC).
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Publication 2023
Cocaine COVID 19 C Reactive Protein Creatine Kinase Diagnosis Ethnicity Factor X Ferritin fibrin fragment D Index, Body Mass Lymphocyte Count Methamphetamine Opiate Alkaloids Pandemics Patients Procalcitonin SARS-CoV-2 Substance Use Troponin 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
Before HTT, an initial blood sample was collected using an EDTA.K2 anticoagulant tube. A total of 8 ml of venous blood was taken from the patients’ cubital vein. The initial physiological indicators (SBP, DBP, HR, SaO2, and Tcore) were also measured. After HTT, post-exercise blood samples were collected immediately, and physiological data were measured after 5-min breaking. Twenty-four hours after HTT, blood samples for the recovery period were gathered. The feces were collected in the morning of two HTTs as pre-training and post-training samples. Clean cotton swabs were used to collect fresh fecal samples (5–10 g, no mix of urine, disinfectant, and sewage) into 15 ml sterile test tubes. Furthermore, the contents of organ injury biomarkers in plasma were detected, including alanine aminotransferase (ALT), alkaline phosphatase (AST), alkaline phosphatase (ALP), bilirubin, lactic dehydrogenase (LDH), alpha-hydroxybutyric dehydrogenase (α-HBDH), creatinine, urea nitrogen, cholinesterase, creatine kinase, prothrombin time (PT), activated partial prothrombin time (APTT), international normalized ratio (INR), Na+, K+, white blood cell (WBC), platelet (PLT), and hemoglobin.
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Publication 2023
Activated Partial Thromboplastin Time Alkaline Phosphatase Anticoagulants Bilirubin Biological Markers BLOOD Blood Platelets Butyrylcholinesterase Creatine Kinase Creatinine D-Alanine Transaminase Edetic Acid Feces Gossypium Hemoglobin Injuries International Normalized Ratio Leukocytes Nitrogen Oxidoreductase Patients physiology Plasma Sewage Sterility, Reproductive Times, Prothrombin Urea Urine Veins

Top products related to «Creatine Kinase»

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Creatine phosphokinase is a lab equipment product used to measure the activity of the enzyme creatine kinase, which is responsible for the conversion of creatine to phosphocreatine, an important energy storage molecule in the body. The measurement of creatine phosphokinase levels can provide information about the health of certain tissues, such as the heart and skeletal muscles.
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Creatine kinase is a laboratory test used to measure the levels of the enzyme creatine kinase in the blood. Creatine kinase is an enzyme that plays a role in providing energy to muscles. It can be used to help diagnose and monitor certain medical conditions, such as muscle damage or disorders.
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Creatine phosphate is a high-energy phosphate compound found in the muscle cells of vertebrates. It serves as a rapidly available energy source to support muscular contraction and other cellular processes requiring ATP.
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Creatine kinase is an enzyme found in various tissues, including the heart, brain, and skeletal muscles. It plays a crucial role in energy metabolism by catalyzing the reversible conversion of creatine and ATP to phosphocreatine and ADP. This enzymatic activity is essential for the storage and rapid release of energy in cells, supporting various physiological processes.
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Creatine phosphate is a laboratory reagent used in biochemical analysis. It serves as a source of high-energy phosphate groups, which are important for various cellular processes. Creatine phosphate is commonly used in assays to measure the activity of enzymes involved in energy metabolism.
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The ADVIA 2400 is a fully automated clinical chemistry analyzer designed for high-volume laboratory testing. It features advanced technology for efficient sample processing and accurate analysis of a wide range of clinical chemistry parameters.
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The Creatine Kinase Activity Assay Kit is a laboratory equipment product that measures the activity of the creatine kinase enzyme. This assay kit provides a quantitative method for determining creatine kinase levels in various sample types.
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ATP is a laboratory instrument used to measure the presence and concentration of adenosine triphosphate (ATP) in various samples. ATP is a key molecule involved in energy transfer within living cells. The ATP product provides a reliable and accurate method for quantifying ATP levels, which is useful in applications such as microbial detection, cell viability assessment, and ATP-based assays.
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Phosphocreatine is a high-energy phosphate compound that serves as a rapidly available source of phosphate for the regeneration of ATP in muscle cells. It plays a crucial role in the energy metabolism of cells, particularly in tissues with high energy demands such as skeletal and cardiac muscles.

More about "Creatine Kinase"

Creatine Kinase, also known as Creatine Phosphokinase (CK or CPK), is a crucial enzyme in the human body that plays a vital role in cellular energy homeostasis.
This enzyme catalyzes the reversible conversion of creatine and adenosine triphosphate (ATP) into phosphocreatine and adenosine diphosphate (ADP).
This process is particularly important in tissues with high and fluctuating energy demands, such as skeletal and cardiac muscle.
Creatine Kinase is composed of two subunits, M (muscle) and B (brain), which can combine to form three different isoenzymes: CK-MM, CK-MB, and CK-BB.
Measurement of Creatine Kinase levels can provide valuable insights into the diagnosis and management of various muscular, neurological, and cardiovascular disorders, including myocardial infarction, rhabdomyolysis, and muscular dystrophies.
The ADVIA 2400 is a widely used automated chemistry analyzer that can be employed to measure Creatine Kinase activity.
The Creatine Kinase Activity Assay Kit is another tool used to quantify Creatine Kinase levels in biological samples, leveraging the enzyme's ability to catalyze the conversion of creatine and ATP into phosphocreatine and ADP.
Maintaining optimal Creatine Kinase levels is crucial for cellular energy homeostasis, particularly in high-energy-demand tissues like the heart and skeletal muscles.
Disturbances in Creatine Kinase levels can serve as valuable biomarkers for the diagnosis and management of various health conditions, making it an important target for both research and clinical applications.