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Uric Acid

Uric acid is a natural waste product formed from the breakdown of purines, which are found in many foods and produced naturally by the body.
It plays a crucial role in the regulation of various physiological processes, but elevated levels can lead to health issues such as gout, kidney stones, and cardiovascular disease.
Understanding the mechanisms underlying uric acid metabolism and its clinical implications is essential for effective management of these conditions.
This page provides a comprehensive overview of the latest research protocols and approaches to studying uric acid, helping to enhance reproducibility and streamline your scientific discovery.

Most cited protocols related to «Uric Acid»

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Publication 2013
Adolescent Adult Age Groups BLOOD Cerebrovascular Accident Child Congestive Heart Failure C Reactive Protein Determination, Blood Pressure Diabetes Mellitus Ethnicity Feelings Glucose Heart Disease, Coronary High Density Lipoprotein Cholesterol Hispanics Homeostasis Households Hypolipidemic Agents Insulin Insulin Resistance Lipids Metabolic Syndrome X Mexican Americans Myocardial Infarction Obesity Pharmaceutical Preparations Phlebotomy Plant Roots Plasma Population Group Pressure, Diastolic Racial Groups Sulfur Surrogate Markers Triglycerides Uric Acid Waist Circumference
A total of 8 analytes were included in the main recalibration study: creatinine, uric acid, glucose, total cholesterol, high density lipoprotein cholesterol (HDL-c), low density lipoprotein cholesterol (LDL-c), triglycerides, and high-sensitivity C-reactive protein (hs-CRP). Analytes were originally measured in the entire cohort at each of the five visits, except for creatinine and uric acid, which were not measured at visit 3, and hs-CRP, which was not measured at visits 1 or 3. Seven additional analytes that were not remeasured at all 5 study visits were also included in a secondary recalibration study: alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT), N-terminal pro-brain natriuretic peptide (NT-proBNP), high-sensitivity cardiac troponin T (hs-cTnT), β2-microglobulin (B2M) and beta-trace protein (BTP) (see Online Supplement for details).
Analytes were re-assayed at Baylor College of Medicine during 2011–13 (Figure 1). For each of the 200 participants in the recalibration subsample, measurements were obtained from stored samples from all 5 visits. Samples had been stored at −70 degrees Celsius since original collection, which took place during visits from 1987 to 2013. LDL-c was calculated from the concentrations of total cholesterol, HDL-c, and triglycerides by the Friedewald formula. See eTable 1 (all eTables are in the Online Supplement) for a detailed description of assay methodologies and approaches. When available, commutable certified reference materials (CRMs) were included with some of the assays to verify the traceability of measurement results to certified values of current high quality reference materials (eTable 5).
Publication 2015
Amino-terminal pro-brain natriuretic peptide Aspartate Transaminase Biological Assay Cholesterol Cholesterol, beta-Lipoprotein C Reactive Protein Creatinine D-Alanine Transaminase Dietary Supplements gamma-Glutamyl Transpeptidase Glucose Heart High Density Lipoprotein Cholesterol Hypersensitivity Nesiritide Pharmaceutical Preparations prostaglandin R2 D-isomerase Triglycerides Troponin T Uric Acid
We downloaded phenotype-associated SNPs and phenotype information from NHGRI GWAS catalogue database26 (link) on January 31, 2013. We selected significantly associated 4,676 SNPs (P < 5.0×10−8) corresponding to 311 phenotypes (other than RA). We manually curated the phenotypes by combining the same but differently named phenotypes into the single phenotype (eg. from “Urate levels”, “Uric acid levels”, and “Renal function-related traits (urea)” into “Urate levels”), or splitting the merged phenotypes into the sub-categorical phenotypes (eg. from “White blood cell types” into “Neutrophil counts” , “Lymphocyte counts” , “Monocyte counts” , “Eosinophil counts” or “Basophil counts”). Lists of curated phenotypes and SNPs are available at http://plaza.umin.ac.jp/~yokada/datasource/software.htm.
For each of the selected NHGRI SNPs and the RA risk SNPs identified by our study (located outside of the MHC region), we defined the genetic region based on ±25 kbp of the SNP or the neighboring SNP positions in moderate LD with it in Europeans or Asians (r2 > 0.50). If multiple different SNPs with overlapping regions were registered for the same NHGRI phenotype, they were merged into the single region. We defined “region-based pleiotropy” if two phenotype-associated SNPs shared part of their genetic regions or shared any UCSC ref gene(s) (hg19) partly overlapping with each of the regions (Extended Data Fig. 4a). We defined “allele-based pleiotropy” if two phenotype-associated SNPs were in LD in Europeans or Asians (r2 > 0.80). We defined the direction of effect as “concordant” with RA risk if the RA risk allele also leads to increased risk of the NHGRI disease or increased dosage of the quantitative trait; similarly, we defined relationships as “discordant” if the RA risk allele is associated with decreased risk of the NHGRI disease phenotype (or if the RA risk allele leads to decreased dosage of the quantitative trait).
We evaluated statistical significance of region-based pleiotropy of the registered phenotypes with RA by a permutation procedure with ×107 iterations. When one phenotype had n loci of which m loci were in region-based pleiotropy with RA, we obtained a null distribution of m by randomly selecting n SNPs from obtained NHGRI GWAS catalogue data and calculating number of the observed region-based pleiotropy with RA for each of the iteration steps. For null distribution estimation, we did not include the SNPs associated with several autoimmune diseases which were previously reported to share pleiotropic associations with RA (Crohn's disease, type 1 diabetes, multiple sclerosis, celiac disease, systemic lupus erythematosus, ulcerative colitis, and psoriasis)2 (link).
Publication 2013
Alleles Asian Americans Autoimmune Diseases Basophils Birth BLOOD Blood Cells Celiac Disease Crohn Disease Diabetes Mellitus, Insulin-Dependent Eosinophil Europeans Genes Genome-Wide Association Study Kidney Leukocyte Count Lupus Erythematosus, Systemic Lymphocyte Count Minor Lymphocyte Stimulatory Loci Monocytes Multiple Sclerosis Neutrophil Phenotype Psoriasis Single Nucleotide Polymorphism Ulcerative Colitis Urate Urea Uric Acid
The study complies with the Declaration of Helsinki and was approved by the Ethics Committee of the Instituto Nacional de Cardiología Ignacio Chávez (INCICH). All participants provided written informed consent. The study included 1162 patients with premature CAD and 873 healthy controls belonging to the Genetics of Atherosclerotic Disease (GEA) Mexican Study. Premature CAD was defined as history of myocardial infarction, angioplasty, revascularization surgery, or coronary stenosis > 50% on angiography, diagnosed before age of 55 in men and before age of 65 in women. Controls were apparently healthy asymptomatic individuals without family history of premature CAD, recruited from blood bank donors and through brochures posted in Social Service centers. Chest and abdomen computed tomographies were performed using a 64-channel multidetector helical computed tomography system (Somatom Sensation, Siemens) and interpreted by experienced radiologists. Scans were read to assess and quantify the following: (1) coronary artery calcification (CAC) score using the Agatston method [20 (link)] and (2) total adipose tissue (TAT) and subcutaneous and visceral adipose tissue areas (SAT and VAT) as described by Kvist et al. [21 (link)]. For the present study, the control group only included individuals with CAC = 0, who were nondiabetic, and with normal glucose levels (n = 873). In the whole sample, the demographic, clinical, anthropometric, and biochemical parameters and cardiovascular risk factors were evaluated and defined as previously described [22 –24 (link)]. Briefly, hypercholesterolemia was defined as total cholesterol (TC) levels ≥ 200 mg/dL. Hypertension was defined as systolic blood pressure ≥ 140 mmHg and/or diastolic blood pressure ≥ 90 mmHg or the use of oral antihypertensive therapy. Type 2 diabetes mellitus (T2DM) was defined with a fasting glucose ≥ 126 mg/dL and was also considered when participants reported glucose-lowering treatment or a physician diagnosis of T2DM. Obesity was defined as body mass index (BMI) ≥ 30 kg/m2. Hypoalphalipoproteinemia, hypertriglyceridemia, and metabolic syndrome (MS) were defined using the criteria from the American Heart Association, National Heart, Lung, and Blood Institute Scientific Statement [25 (link)], except for central obesity that was considered when waist circumference was 90 cm in men and 80 cm in women [26 (link)]. Hyperuricemia was considered with a serum uric acid > 6.0 mg/dL and >7.0 mg/dL for women and men, respectively [27 (link)]. Insulin resistance was estimated using the homeostasis model assessment of insulin resistance (HOMA-IR). The presence of insulin resistance was considered when the HOMA-IR values were ≥75th percentile (3.66 in women and 3.38 in men). Hyperinsulinemia was defined when insulin concentration was ≥75th percentile (16.97 μIU/mL in women and 15.20 μIU/mL in men). Hypoadiponectinemia was defined when adiponectin concentration was ≤25th percentile (8.67 μg/mL in women and 5.30 μg/mL in men). Increased VAT was defined as VAT ≥ 75th percentile (122.0 cm2 in women and 151.5 cm2 in men) and increased SAT as SAT ≥ 75th percentile (335.5 cm2 in women and 221.7 cm2 in men). Elevated alanine aminotransferase (ALT) was defined as ALT activity ≥ 75th percentile (21.0 IU/L in women and 24.5 IU/L in men). Elevated aspartate aminotransferase (AST) was defined as AST activity ≥ 75th percentile (25 IU/L in women and 28 IU/L in men) and elevated gamma glutamyltransferase (GGT) was defined as GGT ≥ 75th percentile (21.0 IU/L in women and 27.5 IU/L in men). These cutoff points were obtained from a GEA study sample of 131 men and 185 women without obesity and with normal values of blood pressure, fasting glucose, and lipids.
All GEA participants are unrelated and of self-reported Mexican-Mestizo ancestry (three generations). In order to establish the ethnical characteristics of the studied groups, we analyzed 265 ancestry informative markers (AIMs). Using the ADMIXTURE software, the Caucasian, Amerindian, and African backgrounds were determined. Similar background in premature CAD patients and healthy controls was found (P > 0.05). Patients showed 55.8% of Amerindian ancestry, 34.3% of Caucasian ancestry, and 9.8% of African ancestry, whereas controls showed 54.0% of Amerindian ancestry, 35.8% of Caucasian ancestry, and 10.1% of African ancestry.
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Publication 2017
Abdomen Adiponectin Angiography Angioplasty Antihypertensive Agents Artery, Coronary Aspartate Transaminase BLOOD Blood Pressure Calcinosis Chest Cholesterol Coronary Stenosis D-Alanine Transaminase Diabetes Mellitus, Non-Insulin-Dependent Diagnosis Donor, Blood Ethics Committees gamma-Glutamyl Transpeptidase Glucose Heart Hereditary Diseases High Blood Pressures Homeostasis Hypercholesterolemia Hyperinsulinism Hypertriglyceridemia Hyperuricemia Hypoadiponectinemia Hypoalphalipoproteinemias Index, Body Mass Insulin Insulin Resistance Lipids Lung Metabolic Syndrome X Multiple Endocrine Neoplasia Type 2b Myocardial Infarction Negroid Races Obesity Operative Surgical Procedures Patients Physicians Premature Birth Pressure, Diastolic Radiologist Radionuclide Imaging Serum Subcutaneous Fat Systolic Pressure Tissue, Adipose Tomography, Spiral Computed Uric Acid Waist Circumference White Person Woman X-Ray Computed Tomography
Components of the metabolic syndrome were measured using similar approaches for both cohorts as previously described [16 , 17 (link)]. The metabolic syndrome was defined using the criteria established by the ATP-III, i.e. the presence of three or more of the following criteria: elevated WC (≥102 cm for men, ≥88 cm for women), elevated fasting triacylglycerol (≥1.69 mmol/l [150 mg/dl]), reduced HDL-cholesterol (<1.04 mmol/l [40 mg/dl] for men, <1.29 mmol/l [50 mg/dl] for women), elevated BP (≥130 mmHg systolic or ≥85 mmHg diastolic, or drug treatment for hypertension) and elevated fasting blood glucose (≥5.55 mmol/l [100 mg/dl]) [4 (link)].
Continuous metabolic syndrome severity z scores at baseline were calculated for participants using sex- and race-based formulas. As described elsewhere [7 (link), 8 (link)], these scores were derived using a confirmatory factor analysis approach for the five traditional metabolic syndrome components (WC, triacylglycerol, HDL-cholesterol, systolic BP, fasting glucose) to determine the weighted contribution of each component to a latent metabolic syndrome ’factor’ on a sex- and race/ethnicity-specific basis. Confirmatory factor analysis was performed among adults aged 20–64 years from the National Health and Nutrition Examination Survey with categorisation into six subgroups based on sex and race/ethnicity (non-Hispanic white, non-Hispanic black, Hispanic). For each of these six population subgroups, loading coefficients for the five metabolic syndrome components were transformed into a single metabolic syndrome factor and used to generate equations to calculate a standardised metabolic syndrome severity score for each subgroup (http://mets.health-outcomes-policy.ufl.edu/calculator/, accessed 20 March 2017). The resulting metabolic syndrome severity scores are z scores (normally distributed and ranging from theoretical negative to positive infinity with mean=0 and SD=1) of relative metabolic syndrome severity on a sex- and race/ethnicity-specific basis. These scores correlate strongly with other markers of risk of the metabolic syndrome [18 (link)], including high-sensitivity C-reactive protein (hsCRP), uric acid and the homeostasis model of insulin resistance [8 (link)], with adiponectin [19 (link)] and with long-term risk of CVD [10 , 12 ] and diabetes [11 (link)].
Publication 2017
Adiponectin Adult Blood Glucose C Reactive Protein Diabetes Mellitus Diastole Diet, Formula Ethnicity factor A Glucose High Blood Pressures High Density Lipoprotein Cholesterol Hispanics Homeostasis Insulin Resistance Metabolic Syndrome X Pharmaceutical Preparations Systole Systolic Pressure Triglycerides Uric Acid Woman

Most recents protocols related to «Uric Acid»

Not available on PMC !

Example 1

The amniotic fluid first undergoes a two-step dialysis process. First, the amniotic fluid is passed through a 3 kiloDalton (kDa) filter to remove low molecular weight urea and uric acid, in addition to reducing the water content. Second, the amniotic fluid is again passed through a 3 kDa membrane in the presence of a dialysate solution (normal saline), to flush the remainder of the urea and uric acid, while maintaining the volume of the fluid. Cryopreservative is added such that the final product contains equal volumes dialyzed fluid and cryopreservative; therefore, the finished product is approximately 1.5 times more concentrated than the starting fluid. The product is then aliquoted into vials (using aseptic technique) and frozen.

It is contemplated that this removal will not have an impact on the components of the AF thought to confer benefit, such as the hyaluronic acid and other proteins in the fluid.

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Patent 2024
Amniotic Fluid Asepsis Dialysis Dialysis Solutions Flushing Freezing Hyaluronic acid Normal Saline Proteins Therapeutics Tissue, Membrane Urea Uric Acid

Example 4

Clinical Study Comparing Treatment With and Without Pre-treatment Phase

A double-blind clinical study, Placebo controlled, Ascending Dose has been conducted. This study has been reported (Study Number P1-IMU-838-MAD).

The urinary excretion of uric acid increased in all but the 30 mg group after treatment initiation with IMU-838 (vidofludimus-calcium). No dose-dependency was apparent.

Uric acid excretion in urine could be however modified with a pre-treatment period. Pre-treatment with 25 mg IMU-838 for 6 days in subjects receiving 50 mg IMU-838 resulted in a smaller increase in uric acid excreted in urine on Day 0 (the first day of receiving the 50 mg dose) as compared to pre-treatment with placebo (49.5 mg/24 hours vs 86.5 mg/24 hours, respectively, median levels).

Placebo group/Pre-dosing group
Group50 mg25 mg/50 mg
n88
Change in Median86.549.5
(mg/24 h)

Thus, the superiority of a treatment regimen including a pre-treatment phase in comparison to a treatment without such a pre-treatment phase has been proven.

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Patent 2024
Aftercare Autoimmune Diseases Calcium, Dietary Inflammation Placebos Treatment Protocols Uric Acid Urine vidofludimus
The following covariates were considered in the study: age, sex, race/ethnicity, family poverty income ratio (PIR), education level, marital status, the complication of hypertension, and diabetes mellitus (DM), smoker, drinker, body mass index (BMI), waist circumference, systolic blood pressure (SBP), diastolic blood pressure (DBP), mean energy intake, hemoglobin (Hb), fast glucose (FBG), glycosylated hemoglobin (HbA1c), alanine transaminase (Alt), aspartate aminotransferase (Ast), albumin, total cholesterol (TC), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), uric acid (UA), blood urea nitrogen (BUN), serum creatinine (Scr), and estimated glomerular filtration rate (eGFR). Individuals who have smoked less than 100 cigarettes in their lifetime/smoked less than 100 cigarettes in their lifetime, do not smoke at all at present/smoked more than 100 cigarettes in their lifetime, and smoke some days or every day were defined as never smoke, former smokers, and now smokers, respectively. There are three categories of drinkers: current heavy alcohol consumption were defined as ≥3 drinks per day for females, ≥4 drinks per day for males, or binge drinking [≥4 drinks on same occasion for females, ≥5 drinks on same occasion for males] on 5 or more days per month; current moderate alcohol consumption were defined as ≥2 drinks per day for females, ≥3 drinks per day for males, or binge drinking ≥2 days per month. Those who did not meet the above criteria were classified as current mild alcohol user.21 (link) Hypertension was defined as an average systolic blood pressure more than 140 mmHg/diastolic blood pressure greater than 90 mmHg or self-reported use of antihypertensive medication. DM will be assessed by measures of blood glycohemoglobin, fasting plasma glucose, 2-hour glucose (Oral Glucose Tolerance Test), serum insulin in participants aged 12 years and over. Hb, FBG, HbA1c, Alt, Ast, albumin, TC, TG, HDL-C, UA, BUN, Scr, and eGFR were all determined in the laboratory. More information regarding the variables used is available at https://www.cdc.gov/nchs/nhanes/index.htm.
Publication 2023
Alanine Transaminase Albumins Alcohols Antihypertensive Agents BLOOD Cholesterol Creatinine Diabetes Mellitus Ethnicity Females Glomerular Filtration Rate Glucose Hemoglobin Hemoglobin, Glycosylated High Blood Pressures High Density Lipoprotein Cholesterol Index, Body Mass Insulin Males Oral Glucose Tolerance Test Plasma Pressure, Diastolic Serum Smoke Systolic Pressure Transaminase, Serum Glutamic-Oxaloacetic Triglycerides Urea Nitrogen, Blood Uric Acid Waist Circumference
A structured and detailed survey designed by professional physicians was used to collect the demographic and clinical parameters of the study subjects including self-reported illness and the currently used medications. The number of subjects in the smoking and alcohol consumption groups were low among early postmenopausal women, and were therefore excluded from analysis. Systolic and diastolic blood pressure was measured using an electronic brachial sphygmomanometer (T30J, OMRON, Japan). Anthropometric parameters including height, weight, waist circumference, and hip circumference were measured using standard procedures by well-trained nurses. Blood samples (8–10 mL) were collected from the antecubital vein after at least 8 h of overnight fasting and evaluated in the laboratory center within 24 h. Metabolic biomarkers and liver function parameters including fasting blood glucose (FBG), triglycerides (TGs), total cholesterol (TC), low-density-lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), serum uric acid (UA), serum aspartate aminotransferase (AST), and serum alanine aminotransferase (ALT) levels were measured. Furthermore, the blood counts of white blood cells (WBC) and neutrophils (NE) were also analyzed. Abdominal ultrasonography was performed using the SIEMENS ACUSON S2000 ABVS ultrasound scanner (Siemens Healthineers, Erlangen, Germany), and was operated by experienced ultra-sonographers. The data was recorded in the electronic medical system of the Health Examination Center.
Publication 2023
Abdomen Alanine Transaminase Aspartate Transaminase Biological Markers BLOOD Blood Glucose Cholesterol Cholesterol, beta-Lipoprotein High Density Lipoprotein Cholesterol Leukocytes Liver Neutrophil Nurses Pharmaceutical Preparations Physicians Pressure, Diastolic Serum Sphygmomanometers Systole Triglycerides Ultrasonography Uric Acid Veins Waist Circumference Woman
In this study, clinical data were collected from the enrolled patients, including demographics (age and sex); vascular risk factors (hypertension, diabetes mellitus, and ischemic heart disease); baseline blood pressure [systolic blood pressure (SBP) and diastolic blood pressure (DBP)]; Trial of Org 10 172 in Acute Stroke Treatment (TOAST) [large-artery atherosclerosis, cardioembolism, small-vessel occlusion, acute stroke of other determined etiology, stroke of undetermined etiology]; stroke severity (SS) [defined as mild stroke according to the National Institutes of Health Stroke Scale (NIHSS) scores of ≤ 8, moderate-to-severe stroke according to NIHSS scores of ≥9; all assessments completed on admission]; magnetic resonance imaging (MRI) features [stroke distribution (SD; anterior circulation, posterior circulation, and anterior/posterior circulation), side of hemisphere (SOH; left, right, and bilateral), number of stroke lesions (NOSs; single and multiple stroke lesions), site of stroke lesions (SOSs; cortical, cortico-subcortical, subcortical, brainstem, and cerebellum)]; laboratory tests [total cholesterol, triglycerides, low-density lipoprotein (LDL), fasting blood glucose (FBG), homocysteine (HCY), uric acid (UA), fibrinogen (FIB), myoglobin (MB), C-reactive protein (CRP), D-dimer brain natriuretic peptide (BNP), HBALC, neuron-specific enolase (NSE), and S-100β levels], treatment regimen [intravenous thrombolysis, arterial thrombolysis, antiplatelet, anticoagulation, statin, and proton pump inhibitor therapy (PPI)]; and stroke comorbidities [dysphagia and stroke-associated pneumonia (SAP)].
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Publication 2023
Acute Cerebrovascular Accidents Arteries Atherosclerosis Blood Glucose Blood Pressure Blood Vessel Brain Stem Cerebellum Cerebrovascular Accident Cholesterol Cortex, Cerebral C Reactive Protein Deglutition Disorders Dental Occlusion Diabetes Mellitus fibrin fragment D Fibrinogen Fibrinolytic Agents gamma-Enolase High Blood Pressures Homocysteine Hydroxymethylglutaryl-CoA Reductase Inhibitors Low-Density Lipoproteins Myocardial Ischemia Myoglobin Nesiritide Patients Pneumonia Pressure, Diastolic Proton Pump Inhibitors Systolic Pressure Therapeutics Treatment Protocols Triglycerides Uric Acid

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Uric acid is a laboratory reagent used in the quantitative determination of uric acid levels in biological samples, such as blood or urine. It is a chemical compound that serves as a diagnostic tool for various medical conditions, including gout, kidney disorders, and metabolic disorders. The core function of uric acid is to provide an analytical measurement of this substance in the body, which can help healthcare professionals assess and monitor a patient's health status.
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Ascorbic acid is a chemical compound commonly known as Vitamin C. It is a water-soluble vitamin that plays a role in various physiological processes. As a laboratory product, ascorbic acid is used as a reducing agent, antioxidant, and pH regulator in various applications.
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Dopamine is a laboratory reagent used in various biochemical and analytical applications. It is a naturally occurring neurotransmitter that plays a crucial role in the human body. Dopamine is often used as a standard in the measurement and analysis of compounds with similar chemical structures and properties.
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Urea is a chemical compound with the formula CO(NH2)2. It is a colorless, odorless, and crystalline solid that is highly soluble in water. Urea's core function is to serve as a source of nitrogen and a key component in many biochemical processes.
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Sodium hydroxide is a chemical compound with the formula NaOH. It is a white, odorless, crystalline solid that is highly soluble in water and is a strong base. It is commonly used in various laboratory applications as a reagent.
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Potassium chloride (KCl) is an inorganic compound that is commonly used as a laboratory reagent. It is a colorless, crystalline solid with a high melting point. KCl is a popular electrolyte and is used in various laboratory applications.
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D-glucose is a type of monosaccharide, a simple sugar that serves as the primary source of energy for many organisms. It is a colorless, crystalline solid that is soluble in water and other polar solvents. D-glucose is a naturally occurring compound and is a key component of various biological processes.
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NaCl is a chemical compound commonly known as sodium chloride. It is a white, crystalline solid that is widely used in various industries, including pharmaceutical and laboratory settings. NaCl's core function is to serve as a basic, inorganic salt that can be used for a variety of applications in the lab environment.

More about "Uric Acid"

Uric acid, also known as UA or urate, is a natural waste product formed from the breakdown of purines, which are found in many foods and produced naturally by the body.
It plays a crucial role in the regulation of various physiological processes, but elevated levels can lead to health issues such as gout, kidney stones, and cardiovascular disease.
Understanding the mechanisms underlying uric acid metabolism and its clinical implications is essential for effective management of these conditions.
Uric acid is closely related to other important biomolecules like ascorbic acid (Vitamin C), dopamine, urea, and various electrolytes like sodium, potassium, and chloride.
Researchers studying uric acid often utilize analytical techniques like the AU5800 clinical chemistry analyzer to measure uric acid levels in biological samples.
Additionally, maintaining proper levels of D-glucose (blood sugar) and sodium hydroxide can be important for uric acid regulation and metabolism.
Comprehensive research protocols and cutting-edge approaches are key to advancing our understanding of uric acid and its impact on human health.
PubCompare.ai is a powerful AI-driven platform that can help identify the most relevant research protocols and streamline your scientific discovery in this important area of study.