Heart Fatty Acid-binding Protein Research Articles

A novel method for multiple cardiovascular disease biomarker detection using a SERF-based microfluidic platform

As cardiovascular diseases (CVDs) are the leading cause of death worldwide, it is of great importance to realize a rapid and sensitive diagnosis. Multiple CVD biomarker detection, which holds higher accuracy and speed of early CVD diagnosis, is becoming a promising alternative to single biomarker analysis. Cardiac troponin I (cTnI), C-reactive protein (CRP), brain-type natriuretic peptide (BNP), and heart fatty acid binding protein (H-FABP) are four significant diagnostic biomarkers for CVDs. Among the several methods for biomarker detection, such as optical, magnetic, mechanical, and electrical methods, the magnetic method stands out because of its stability, low toxicity, noninvasive detection, facile manipulation with an external magnetic field, and immunity to the interference of background light. At present, the lack of multiplexing capability, the imprecision of magnetic signal localization, and the agglomeration and non-specific adsorption of magnetic nanoparticles all limit the clinical application of magnetic detection. This paper presented a novel method for multiple CVD biomarker detection using a spin exchange relaxation-free (SERF)-based microfluidic platform. One or more SERF atomic magnetometers were used to scan the remanent field of magnetic labels to detect four CVD biomarkers in 70min, with a detection limit of 1.88pg/mL (cTnI), 1.58pg/mL (CRP), 1.45pg/mL (BNP), and 1.71pg/mL (H-FABP). The results showed two-dimensional magnetic fields with a resolution of submillimeter level and a sensitivity of pT level. The measurement technique provides a new magnetic methodology for applications in clinical diagnosis.

A multiplexed immunochemical microarray for the determination of cardiovascular disease biomarkers

A fluorescence antibody microarray has been developed for the determination of relevant cardiovascular disease biomarkers for the analysis of human plasma samples. Recording characteristic protein molecular fingerprints to assess individual’s states of health could allow diagnosis to go beyond the simple identification of the disease, providing information on its stage or prognosis. Precisely, cardiovascular diseases (CVDs) are complex disorders which involve different degenerative processes encompassing a collection of biomarkers related to disease progression or stage. The novel approach that we propose is a fluorescent microarray chip has been developed accomplishing simultaneous determination of the most significant cardiac biomarkers in plasma aiming to determine the CVD status stage of the patient. As proof of concept, we have chosen five relevant biomarkers, C-reactive protein (CRP) as biomarker of inflammation, cystatin C (CysC) as biomarker of renal failure that is directly related with heart failure, cardiac troponin I (cTnI) as already established biomarker for cardiac damage, heart fatty acid binding protein as biomarker of ischemia (H-FABP), and finally, NT-proBNP (N-terminal pro-brain natriuretic peptide), a well-established heart failure biomarker. After the optimization of the multiplexed microarray, the assay allowed the simultaneous determination of 5 biomarkers in a buffer solution reaching LODs of 15 ± 5, 3 ± 1, 24 ± 3, 25 ± 3, and 3 ± 1 ng mL−1, for CRP, CysC, H-FABP, cTnI, and NT-proBNP, respectively. After solving the matrix effect, and demonstrating the accuracy for each biomarker, the chip was able to determine 24 samples per microarray chip. Then, the microarray has been used on a small pilot clinical study with 29 plasma samples from clinical patients which suffered different CVD and other related disorders. Results show the superior capability of the chip to provide clinical information related to the disease in terms of turnaround time (1 h 30 min total assay and measurement) and amount of information delivered in respect to reference technologies used in hospital laboratories (clinical analyzers). Despite the failure to detect c-TnI at the reported threshold, the microarray technology could be a powerful approach to diagnose the cardiovascular disease at early stage, monitor its progress, and eventually providing information about an eminent potential risk of suffering a myocardial infarction. The microarray chip here reported could be the starting point for achieving powerful multiplexed diagnostic technologies for the diagnosis of CVDs or any other pathology for which biomarkers have been identified at different stages of the disease.Graphical

A self-powered photoelectrochemical biosensing platform for H-FABP monitoring mediated by CsPbBr3@COF–V

Advanced bioelectronic detection based on the integration of modern optical electronics and biological systems has a broad prospect. The strategy of cathode signal amplification in self-powered photoelectrochemical (PEC) immunosensors with excellent performance is rarely reported in the field of immune analysis. Herein, the work demonstrates a self-powered PEC biosensor formed with BiOI photocathode and WO3/SnS2/ZnS photoanode, and CsPbBr3@COF–V was used as the photocathode signal quenching source for the quantitative monitoring of heart fatty acid binding protein (H-FABP). The high efficiency and stable self-powered biosensor formed not only provides continuous and powerful photocurrent response for bioanalysis through reasonable stepped band structure, but also effectively eliminates the interference of reducing substances. The quenching source CsPbBr3@COF–V greatly affects the photocurrent response due to steric hindrance, weak conductivity, competition with the substrate for dissolved oxygen and excitation light source. And the intervention of this key factor achieves multiple signal amplification effect and opens up an innovative vision for self-powered PEC immunosensor. Taking H-FABP as a representative analyte, the proposed signal amplification self-powered photoelectrochemical presents a broad linear range from 0.0005 to 150 ng/mL with the detection limit of 0.19 pg/mL.

Resolvin E1 heals injured cardiomyocytes: Therapeutic implications and H-FABP as a readout for cardiovascular disease & systemic inflammation

The purpose of this study is to investigate heart-fatty acid binding protein (H-FABP) leakage from cardiomyocytes as a quantitative measure of cell membrane damage and to test healing by Resolvin E1 (RVE1) as a potential therapeutic for patients with inflammatory diseases (cardiovascular disease and comorbidities) with high morbidity and mortality. Our quantitative ELISA assays demonstrated H-FABP as a sensitive and reliable biomarker for measuring cardiomyocyte damage induced by lipopolysaccharide (LPS) and healing by RvE1, a specialized pro-resolving mediator (SPM) derived from the Omega-3 fatty acid, eicosapentaenoic acid (EPA), a dietary nutrient that balances inflammation to restore homeostasis. RvE1 reduced leakage of H-FABP by up to 86%, which supports our hypothesis that inflammation as a mechanism of injury can be targeted for therapy. H-FABP as a blood biomarker was tested in 40 patients admitted to Boston Medical Center for respiratory distress, (20 patients with and 20 patients without COVID infection). High levels of H-FABP correlated with clinically diagnosed CVD, diabetes, and end-stage renal disease (ESRD) in both patient groups. The level of H-FABP indicates not only CVD damage but is a valuable measure for patients with increased inflammation disease comorbidities.

Self-shedding of multifunctional biomolecular nanocarriers for H-FABP monitoring in magnetic separation self-powered photoelectrochemical and colorimetric immunoassay platform

To embrace the challenge of the limitations of traditional nano-solid materials, biomolecular layer-by-layer assembly and single detection mode, this work innovated a dual-mode immunoassay of split-type self-powered photoelectrochemical (PEC) and colorimetric detection based on self-shedding of biomolecular nanocarriers for physiological monitoring. The self-shedding process completed in 96 microplate is that the outer MnO2 of MnO2-coated Fe3O4@Carbon nanosphere complex (Fe3O4@Carbon@MnO2) is consumed by quantitative ascorbic acid. Fe3O4@Carbon as a peroxide-mimicking enzyme remaining with completely bare surface provides sufficient active sites and the seed solution affecting the photoanode are separated by magnetic forces. In this process, biometrics and dual-mode signal detection realize spatial isolation in mutual influence, and the sensitivity of immunoassay was further improved. The photoanode ITO/BiVO4 was constructed by electrodeposition with the ad-vantages of high specific surface area and uniformity, and the hole consuming agent FeOOH was generated on electrode surface, which affects the signal of the PEC substrate to indirectly reflect the concentration of biomolecules. In addition, the self-powered biosensor constructed by assembling Cu2ZnSnS4 (CZTS) with excellent interface-to-volume ratio on FTO using template method as working electrode. As a proof of principle, heart fatty acid binding protein (H-FABP) was analyzed and the obtained linear range of the dual mode biosensor was from 0.050 pg/mL to 100 ng/mL with a detection limit of 0.013 pg/mL (S/N = 3).

ENZYME-LINKED IMMUNOSORBENT ASSAY OF AUTOANTIBODIES AGAINST HUMAN β1-ADRENERGIC RECEPTOR USING RECOMBINANT ANTIGENS

E. coli strains have been created as producers of recombinant β1-adreno-receptor epitopes as part of chimeric proteins. The corresponding epitope sequences are located in the C-terminal region of the human heart fatty acid binding protein (hH-FABP) and separated from it by a linker sequence (Gly4Ser)3. A solid-phase enzyme-linked immunosorbent assay (ELISA) for detection of autoantibodies against β1-adrenergic receptor in human blood serum based on a recombinant epitope has been developed. Blood sera of patients (N = 76) with various diagnoses of cardiopathologies and other diseases were analyzed. In some patients with a con rmed diagnosis of cardiovascular diseases, a signi cantly increased level of autoantibodies to β1-adrenergic receptor was detected, in most cases those with a diagnosis of acute myocardial infarction.

Evaluation of Heart Fatty Acid Binding Protein (H-FABP) As A Diagnostic Marker in Acute Coronary Syndrome

Evaluation of Heart Fatty Acid Binding Protein (H-FABP) As A Diagnostic Marker in Acute Coronary Syndrome

Trajectories of interleukin 10 and heart fatty acid-binding protein levels in traumatic brain injury patients with or without extracranial injuries.

Interleukin 10 (IL-10) and heart fatty acid-binding protein (H-FABP) have gained interest as diagnostic biomarkers of traumatic brain injury (TBI), but factors affecting their blood levels in patients with moderate-to-severe TBI are largely unknown. To investigate the trajectories of IL-10 and H-FABP between TBI patients with and without extracranial injuries (ECI); to investigate if there is a correlation between the levels of IL-10 and H-FABP with the levels of inflammation/infection markers C-reactive protein (CRP) and leukocytes; and to investigate if there is a correlation between the admission level of H-FABP with admission levels of cardiac injury markers, troponin (TnT), creatine kinase (CK), and creatine kinase MB isoenzyme mass (CK-MBm). The admission levels of IL-10, H-FABP, CRP, and leukocytes were measured within 24 h post-TBI and on days 1, 2, 3, and 7 after TBI. The admission levels of TnT, CK, and CK-MBm were measured within 24 h post-TBI. There was a significant difference in the concentration of H-FABP between TBI patients with and without ECI on day 0 (48.2 ± 20.5 and 12.4 ± 14.7 ng/ml, p = 0.02, respectively). There was no significant difference in the levels of IL-10 between these groups at any timepoints. There was a statistically significant positive correlation between IL-10 and CRP on days 2 (R = 0.43, p < 0.01) and 7 (R = 0.46, p = 0.03) after injury, and a negative correlation between H-FABP and CRP on day 0 (R = -0.45, p = 0.01). The levels of IL-10 or H-FABP did not correlate with leukocyte counts at any timepoint. The admission levels of H-FABP correlated with CK (R = 0.70, p < 0.001) and CK-MBm (R = 0.61, p < 0.001), but not with TnT. Inflammatory reactions during the early days after a TBI do not significantly confound the use of IL-10 and H-FABP as TBI biomarkers. Extracranial injuries and cardiac sources may influence the levels of H-FABP in patients with moderate-to-severe TBI.

Protective effect of Pueraria lobata leaves on doxorubicin-induced myocardial infarction in experimental Wistar rats.

The present study intended to explore the preventive effects of Pueraria lobata leaves against doxorubicin (DOX)-induced myocardial infarction (MI) in Wistar rats. The rats were separated into four groups, with each group containing six rats. Group I control rats; group II received DOX-alone in six equivalent injections for 2 weeks; group III received DOX as abovementioned with P. lobata oral administration for 2 weeks; group IV received P. lobata alone for 2 weeks. At the end of the experiment, postcervical dislocation and MI induced by DOX were determined on the basis of the variations in the animal body and heart weight and further instabilities in cardiac marker enzymes aspartate transaminase, lactate dehydrogenase, creatine kinase, creatine kinase-myoglobin binding, and cardiac troponin I in the serum. At the same time, for group III animals, which were exposed to P. lobata, all the above-denoted marker levels were maintained. Levels of some crucial heart-binding proteins like heart fatty acid binding protein, monocyte chemoattractant protein-1, and transforming growth factor beta were elevated in DOX-alone treated rats. Additionally, group III animals treated with P. lobata showed some preventive downregulated expressions of these binding proteins. Histopathological observations also revealed the preventive effect of P. lobata. Ultimately proteins tangled in the phosphoinositide 3-kinase/protein kinase B pathway were studied by Western blot. P. lobata treatment downregulated the inflammatory markers. The findings suggest that P. lobata exhibits cardioprotective effect on MI.

Evaluation of heart fatty acid-binding protein as a biomarker for canine leishmaniosis.

Myocarditis frequently occurs in canine leishmaniosis (CanL). Heart fatty acid-binding protein (HFABP) is a biomarker of myocardial damage. This study aimed to compare HFABP concentration (HFABPc) in healthy dogs and dogs at different stages of CanL and evaluate the correlation of this biomarker with several clinicopathological and echocardiographic variables. Thirty-one dogs diagnosed with CanL and 10 healthy dogs were included. HFABPc was not statistically different (p > 0.05) between groups of dogs at different LeishVet stages of CanL or between groups with high versus low to intermediate serology titres. In 70% of CanL dogs, HFABPc was within the 95% confidence interval limits of the mean of healthy dogs. A moderate negative correlation with globulin (r = -0.519; p = 0.03) and haematocrit (HCT) (r = -0.538; p = 0.02) was observed. No other significant correlation (p > 0.05) was observed with any other variable. Many statistical tests were performed, and therefore, type I error cannot be ruled out. HFABPc is not consistently elevated in dogs with CanL and is not associated with the severity of the disease, or most echocardiographic or clinicopathological variables studied. The correlation with globulin and HCT was not strong and not considered clinically significant. HFABPc lacks sufficient predictive capacity in dogs with CanL, discouraging further research or clinical use of this biomarker in this disease.

Co-supplementation of Vitamin K2 and Selenium Synergistically Improves Metabolic Status and Reduces Cardiovascular Risk Markers in Dyslipidemic Rabbits.

This work investigated the impact of vitamin K2 and selenium co-supplementation on metabolic profile and indicators of cardiovascular health in dyslipidemic rabbits. Fifty adult male rabbits were equally allocated into 5 groups: Control group, Dyslipidemic group: received 0.5% cholesterol in diet for 12weeks, groups 3, 4 and 5 dyslipidemic rabbits daily treated with vitamin K2 (10mg/kg bw) or/and selenium (1mg/kg bw) for 8weeks. Co-supplementation of vitamin K2 and selenium significantly decreased body weight gain and blood pressure elevation in dyslipidemic rabbits compared to un-treated ones. Consuming vitamin K2 plus selenium also markedly lowered serum lipids encompassing cholesterol, triglycerides and LDL and elevated HDL relative to placebo. Additionally, such co-supplementation reduced fasting glucose and insulin, enhancing insulin sensitivity with respect to placebo. Regarding cardiovascular risk markers, dyslipidemic rabbits received vitamin K2 concurrently with selenium displayed lower levels of atherogenic index (LDL/HDL), serum C-reactive protein, heart fatty acid-binding protein and asymmetric dimethylarginine as well as aortic ox-LDL, lipid peroxidation and calcium but higher levels of serum nitric oxide and aortic total antioxidants than un-treated ones. Concomitant administration of vitamin K2 and selenium improved metabolic profile, markers of cardiovascular health and atherosclerosisin dyslipidemic rabbits.

Heart fatty acid-binding protein is associated with phosphorylated tau and longitudinal cognitive changes.

BackgroundPerturbation of lipid metabolism is associated with Alzheimer’s disease (AD). Heart fatty acid-binding protein (HFABP) is an adipokine playing an important role in lipid metabolism regulation.Materials and methodsTwo datasets separately enrolled 303 and 197 participants. First, we examine the associations of cerebrospinal fluid (CSF) HFABP levels with cognitive measures [including Mini-Mental State Examination (MMSE), Clinical Dementia Rating sum of boxes (CDRSB), and the cognitive section of Alzheimer’s Disease Assessment Scale] and AD biomarkers (CSF amyloid beta and tau levels). Second, we examine the longitudinal associations of baseline CSF HFABP levels and the variability of HFABP with cognitive measures and AD biomarkers. Structural equation models explored the mediation effects of AD pathologies on cognition.ResultsWe found a significant relationship between CSF HFABP level and P-tau (dataset 1: β = 2.04, p < 0.001; dataset 2: β = 1.51, p < 0.001). We found significant associations of CSF HFABP with longitudinal cognitive measures (dataset 1: ADAS13, β = 0.09, p = 0.008; CDRSB, β = 0.10, p = 0.003; MMSE, β = −0.15, p < 0.001; dataset 2: ADAS13, β = 0.07, p = 0.004; CDRSB, β = 0.07, p = 0.005; MMSE, β = −0.09, p < 0.001) in longitudinal analysis. The variability of HFABP was associated with CSF P-tau (dataset 2: β = 3.62, p = 0.003). Structural equation modeling indicated that tau pathology mediated the relationship between HFABP and cognition.ConclusionOur findings demonstrated that HFABP was significantly associated with longitudinal cognitive changes, which might be partially mediated by tau pathology.

Changes in the triglyceride metabolism in the thigh muscle and liver of broilers injected intravenously with angiopoietin-like protein 4

Angiopoietin-like protein 4 (ANGPTL4) is a potential circulating mediator connecting nutritional factors and fat metabolism, however, information is lacking on the exact role of ANGPTL4 on triglyceride metabolism in the thigh muscles and livers of broilers. The objective of this study was to determine the changes in the triglyceride metabolism in the thigh muscles and livers of broilers injected intravenously with ANGPTL4. In experiment 1, 36 male Arbor Acres broilers at 35 days of age were randomly allocated into six treatments with six replicates. The broilers were subjected to intravenous injection of polyhistidine-small ubiquitin-related modifier-ANGPTL4 (His-SUMO-ANGPTL4) once at a dose of 0, 20, 100, 500, 2 500, or 12 500 ng/kg body weight (BW), respectively. The results showed that the injection of His-SUMO-ANGPTL4 at a dose of 500, 2 500 and 12 500 ng/kg BW decreased (P &amp;lt; 0.05) the broilers’ heart-fatty acid-binding protein (H-FABP) mRNA expression in the thigh muscle. All of the His-SUMO-ANGPTL4 broiler injected groups had a lower (P &amp;lt; 0.05) adipocyte-fatty acid-binding protein mRNA expression in the thigh muscle. In experiment 2, 18 male Arbor Acres broilers at 35 days of age were randomly allocated into three treatments with six replicates. The broilers were given an injection of normal saline (NS), His-SUMO, or His-SUMO-ANGPTL4 (500 ng/kg BW) once. The results showed that the broilers receiving an injection of ANGPTL4 at a dose of 500 ng/kg BW decreased (P &amp;lt; 0.05) the H-FABP mRNA expression in the thigh muscle. Besides, the broilers given an injection of ANGPTL4 at a dose of 500 ng/kg BW increased (P &amp;lt; 0.05) the fatty acid synthase mRNA expression and activity and decreased (P &amp;lt; 0.05) the microsomal triglyceride transfer protein mRNA expression in the liver. However, the concentrations of the high-density lipoprotein, low-density lipoprotein, very low-density lipoprotein, insulin, growth hormone and leptin in the serum were not affected by the ANGPTL4 injection. In conclusion, ANGPTL4 has the ability to change the triglyceride metabolism in the thigh muscles and livers of broilers.

Effect of the Tea Tree Oil on Growth Performance, Meat Quality, Serum Biochemical Indices, and Antioxidant Capacity in Finishing Pigs.

The increased use of antibiotics continues to pose a threat to public health because of the increasing concern of antibiotic residue. Tea tree oil (TTO) is an extract of the Australian plant Melaleuca alternifolia with anti-inflammatory and antioxidant properties. However, there is little information on TTO supplementation in the diet of finishing pigs. Hence, the present study aimed to investigate the effect of TTO supplemented diets on the growth performance, meat quality, serum biochemical indices, and antioxidant capacity of the finishing pigs. Our results showed that TTO supplementation increased (P < 0.05) the mRNA expression of insulin-like growth factors -I (IGFs-I), growth acceleration hormone (GH), and heart fatty acid-binding protein (H-FABP), while the mRNA expression of myostatin gene (MSTN), and calpain-1 (CAST) decreased by the TTO supplementation, compared with the control group. In addition, TTO supplementation increased (P < 0.05) serum alkaline phosphatase (ALP), immunoglobulin G (IgG), and IgM levels but decreased (P < 0.05) serum aspartate transaminase (AST) concentration, relative to the control group. In addition, we found that the live weight and intramuscular fat enhanced (P < 0.05) significantly, and muscle pH 24 min value, cooking loss, and shear force decreased (P < 0.05) dramatically in the TTO group. The TTO supplementation increased (P < 0.05) C18:2n6t concentration and decreased (P < 0.05) C12:0 and C16:0 concentration, relative to the control group. Dietary supplementation with TTO decreased (P < 0.05) malondialdehyde (MDA) and increased (P < 0.05) glutathione peroxidase (GSH-Px) activity in serum. These results indicated that TTO supplementation could improve immunity and antioxidant, carcass traits, the nutritional value of pork, and the antioxidant capacity of finishing pigs. Therefore, TTO has potential positive effects as a feed additive in the pig industry.

Synergistic impacts of Montelukast and Klotho against doxorubicin-induced cardiac toxicity in Rats.

Doxorubicin (DOX) is a powerful antitumor agent with a well-known cardiaotoxic side effects. In the current study, the ameliorative combined impacts of montelukast (Mont) and Klotho against doxorubicin-induced cardiac toxicity were examined. Fifty-six adult male rats (2months age and weighting 150-200 g) were grouped into 7 groups (8 rats per group). Animals received doxorubicin alone or in combination with either Mont or Klotho. After 2weeks of treatments, serum samples were examined to assess the changes in cardiac activity biomarkers such as LDH, CK-MB, cardiac troponin-I (cTn-I), and heart fatty acid binding protein (H-FABP). Serum changes of IL-6, inducible nitric oxide synthase (iNOS), and caspase-3 levels were assayed. The oxidative stress biomarkers such as total antioxidant capacity (TAC) and inflammatory (rat IL-1β and rat TNF-α,) and anti-inflammatory (rat IL-10) cytokines were examined. Heart histology and transforming growth factor-β1 (TGF-β1) immunoreactivity were measured. DOX induced cardiomyopathy, which was reflected by the increases in all examined cardiac parameters. Real-time PCR confirmed that DOX upregulated the expression of TNF-α and IL-1β and decreased the expression of IL-10. Moreover, DOX showed marked elevation in the ST segment T wave complex, causing profound tachycardia. Heart histology assessments showed cardiac cell necrosis, inflammatory cell infiltration, interstitial congestion, and increased TGF-β1 immunoreactivity. Montelukast and Klotho administration ameliorated all the altered parameters when administered alone or in combination to DOX-intoxicated rats. Klotho was more effective compared with montelukast in terms of reductions in heart rate, ST segment T wave complex elevation, cardiac enzymes (lactate dehydrogenase; LDH, creatine kinase-MB; CK-MB, cardiac troponin I; cTn-I, heart fatty acid binding protein; H-FABP) cardiac histology, and caspase-3 levels and increases in TAC activity. Montelukast was more effective in reducing serum levels of IL6 and iNOS, expression of TNF-α and IL-1β, and the upregulation of IL-10 expression. The co-administration of both drugs led to significantly more synergistic results in terms of reducing cardiac toxicity. In conclusion, montelukast and Klotho either alone or in combination were confirmed to be effective in suppressing DOX-induced cardiac toxicity in rats.

Potential of heart fatty-acid binding protein, neurofilament light, interleukin-10 and S100 calcium-binding protein B in the acute diagnostics and severity assessment of traumatic brain injury

BackgroundThere is substantial interest in blood biomarkers as fast and objective diagnostic tools for traumatic brain injury (TBI) in the acute setting.MethodsAdult patients (≥18) with TBI of any severity and...

Expression of the heart fatty acid-binding protein (H-FABP) in heart and brain tissues of electrically injured rats for determination of post-mortem interval

Expression of the heart fatty acid-binding protein (H-FABP) in heart and brain tissues of electrically injured rats for determination of post-mortem interval

MicroRNA-320a-3p Signatures as a Satisfactory Predictor of Acute Coronary Syndrome and Attenuates Inflammation by Targeting X-Linked Inhibitor of Apoptosis Protein

Acute coronary syndrome (ACS) is a heart disease with a high mortality rate. Recently, more and more evidence illustrated that microRNAs (miRNA) participated in regulating the occurrence of heart disease. This study aimed to detect the level of serum miR-320a-3p in patients with ACS, predict its possibility as a candidate gene for diagnosis, and explore its potential mechanism in the regulation of ACS. 139 ACS patients and 126 controls were recruited in this study. The expression level of miR-320a-3p was determined by qRT-PCR. The predictive value in ACS was assessed by receiver operating characteristic (ROC) curve. Enzyme-linked immunosorbent assay (ELISA) was used to measure the protein expression levels of inflammatory factors. The downstream targets of miR-320a-3p were verified by luciferase reporter gene assay. In ACS patients and rat models, the expression level of serum miR-320a-3p was significantly increased. ROC curve revealed that abnormal expression of miR-320a-3p was of diagnostic value for ACS. In an in vivo rat model, down-regulation of miR-320a-3p inhibited the production of von Willebrand factor (vWF), Heart fatty acid-binding protein (H-FABP), interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α). In other words, down-regulation of miR-320a-3p reduced rat vascular endothelial injury and inflammation. X-linked inhibitor of apoptosis protein (XIAP) was determined to be a direct target of miR-320a-3p. miR-320a-3p is useful for the diagnosis of ACS. Animal experiments confirmed that up-regulated miR-320a-3p promoted vascular endothelial injury and inflammatory response by targeting XIAP, thus promoting the development of ACS. MiR-320a-3p may be a new breakthrough in the diagnosis and treatment of ACS.

Evaluation of Different Blood Parameters From Endurance Horses Competing at 160 km

The purpose of this study was to assess a change in different blood parameters before and after a 160 km endurance race and to evaluate differences in cardiac biomarkers between horses that completed the race and horses that did not.The study population consisted of 52 healthy endurance horses. Horses participating in the study were assigned to three groups: horses that successfully completed the race (“finishers”), horses that failed to qualify at the veterinary check for primarily metabolic reasons (“metabolic”) and horses that failed to qualify at the veterinary check for primarily gait related reasons (“gait related”). The latter two groups were combined to form a final group of “non-finishers” that were excluded for either “gait related” or “metabolic” disorders. Venous blood samples were taken before and after the endurance race. Serum and EDTA-plasma were analyzed for cardiac troponin I (cTNI), heart fatty acid binding protein (HFABP), alpha-hydroxybutyrate dehydrogenase (α-HBDH), atrial natriuretic peptide (ANP), lactate dehydrogenase (LDH), symmetric dimethylarginine (SDMA) and asymmetric dimethylarginine (ADMA).Lactate dehydrogenase (P = .001), SDMA (P= .001) and ADMA (P= .002) increased significantly after the endurance race in the finisher group. A significant increase in cTNI and α-HBDH concentration after the endurance race compared to the values before the endurance race was detected in the finisher (P= .001, P= .001) and gait related group (P= .002, P= .007). The longer the distance completed, the more these five blood parameters increased. No differences between the groups could be found and none of the measured blood parameters showed significant differences among groups before or after racing.

Diagnostic Value of Heart-type Fatty Acid Binding Protein in Group of Patients with NSTEMI at the Time of Application for Medical Care

The relevance of the early detection of myocardial necrosis is due to the difficulties of differential diagnosis in the first hours of the development of acute coronary syndrome. Therefore, the doctors of the first contact, as before, are interested in an early cardiac marker and the presence of tests based on it. Heart fatty acid binding protein (h-FABP) is a cardiac marker that increases in the blood to diagnostic values after just one hour from the beginning of clinical manifestations.&#x0D; The objective: to determine the diagnostic value of heart fatty acid binding protein in group of patients with NSTEMI.&#x0D; Materials and methods. We examined 280 patients with STEMI, 91 patients with NSTEMI, 76 with stable angina pectoris. Blood samples were taken from all patients at the first contact to determine troponin I, a heart fatty acid binding protein and CPK-MB. Patients with NSTEMI were divided into three subgroups: the first – up to 3 hours from the onset of symptoms, the second – from 3 to 6, the third from 6 to 12. The level of heart fatty acid binding protein in plasma was determined by enzyme immunoassay.&#x0D; Results. The early detection of AMI in people visiting primary care doctors with chest pain continues to be a challenge. Undoubtedly, cardiac troponins are the “gold standard” for the diagnosis of AMI, but early detection of these can give a negative result. The results of the studies show a high diagnostic efficacy of h-FABP in the early diagnosis of AMI, and it is superior in sensitivity (in the first hours from the onset of the disease) to cardiac troponins. So, for example, in the subgroup of patients with the onset of symptom manifestation up to 3 hours for h-FABP with a cut-off &gt;0,48 ng/ml, the sensitivity was 92.7 % and specificity was 97,3 % (AUC=0,99; 95 % CI AUC 0,942–0,998). In the same subgroup, troponin I had a specificity of 22,0 %, with cut off &gt;0,84 ng/ml (AUC=0,71; 95 % CI AUC 0,615–0,787).&#x0D; Conclusions. The level of cardiac protein that binds fatty acids is significantly increased in patients with acute myocardial infarction compared with stable coronary heart disease.