Non-cardiac Conditions Which Can Elevate The Serum Levels of sST2.
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ABSTRACT:
SUBMITTER: Patil TR
PROVIDER: S-EPMC6477157 | biostudies-literature | 2019 Jan - Feb
REPOSITORIES: biostudies-literature
Publications
Non-cardiac Conditions Which Can Elevate The Serum Levels of sST2.
Patil T R TR Patil S T ST Patilsss Snehal S Patil Anuprita A
Indian heart journal 20181128 1
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Project description:BackgroundNeutrophilic inflammation is associated with poorly controlled asthma. Serum levels of sST2, a soluble IL-33 receptor, increase in neutrophilic lung diseases. We hypothesized that high serum sST2 levels in stable asthmatics are a predictor for exacerbation within a short duration.MethodsThis prospective observational study evaluated the serum sST2 levels of 104 asthmatic patients who were treated by a lung disease specialist with follow-ups for 3 months.ResultsHigh serum sST2 levels (> 18 ng/ml) predicted severe asthma exacerbation within 3 months. Serum sST2 levels correlated positively with asthma severity (treatment step), airway H2O2 levels, and serum IL-8 levels. High serum sST2 levels and blood neutrophilia (> 6000 /μl) were independent predictors of exacerbation. We defined a post-hoc exacerbation-risk score combining high serum sST2 level and blood neutrophilia, which stratified patients into four groups. The score predicted exacerbation-risk with an area under curve of 0.91 in the receiver operating characteristic curve analysis. Patients with the highest scores had the most severe phenotype, with 85.7% showing exacerbation, airflow limitation, and corticosteroid-insensitivity.ConclusionsHigh serum sST2 levels predicted exacerbation within the general asthmatic population and, when combined with blood neutrophil levels, provided an exacerbation-risk score that was an accurate predictor of exacerbation occurring within 3 months.
| S-EPMC6126416 | biostudies-literature
Project description:AimsWe aim to investigate the correlation between preoperative soluble suppression of tumourigenicity 2 (sST2) and postoperative myocardial remodelling and cardiac function in patients with valvular heart disease.Methods and resultsThis retrospective study included patients who underwent heart valve surgery at the General Hospital of Northern Theatre Command from July 2019 to June 2020. Preoperative, early postoperative, and 1-month postoperative cardiac ultrasound data were collected. Multivariable linear regression was used to analyse the factors associated with preoperative sST2 and postoperative cardiac function parameters. A receiver operator characteristic curve analysis was used to analyse the predictive value of sST2 for left ventricular ejection fraction (LVEF) reduction at 1 month after surgery. This study included 156 patients. Left ventricular end-systolic volume (b = 0.125, P = 0.004), atrial fibrillation (b = 7.933, P = 0.003), and coronary artery disease (b = 5.826, P = 0.043) were correlated with the preoperative sST2 levels. Preoperative sST2 was independently associated with early postoperative left ventricular end-systolic volume (b = -0.136, P = 0.035), left ventricular end-diastolic volume (b = -0.225, P = 0.036), and LVEF (b = 0.056, P = 0.008). At 1 month after surgery, LVEF (r = -0.234, P = 0.023) and reduction in LVEF (r = -0.316, P = 0.002) were negatively correlated with preoperative sST2. The area under the receiver operator characteristic curve of preoperative sST2 in predicting LVEF reduction at 1 month was 0.646, with a sensitivity of 0.357 and a specificity of 0.918.ConclusionsPreoperative sST2 levels are related to early postoperative myocardial remodelling and have a predictive value for the improvement of cardiac function 1 month after surgery.
| S-EPMC10804203 | biostudies-literature
Project description:BackgroundHepatocellular carcinoma (HCC) is a common malignant tumor with high morbidity and mortality. Alpha-fetoprotein (AFP) is the most widely used diagnostic serum biomarker, but it still has limited accuracy in detecting HCC, suggesting the necessity of seeking more ideal biomarkers with high sensitivity and specificity. Soluble growth stimulation gene 2 (sST2) form of growth stimulating expression gene 2 (ST2), is expressed in various organs and can bind competitively to interleukin 33 (IL-33). Whether sST2 can serve as a serum biomarker for HCC is largely unknown.ObjectiveTo investigate the value of sST2 as a serum diagnostic marker for HCC.MethodsThis study included 93 newly diagnosed HCC patients (HCC group), 90 chronic hepatitis B patients (CHB group), and 90 healthy individuals (HCs group). Spearman correlation analysis was used to explore the relationships between sST2 and the experimental indicators in HCC group. The receiver operating characteristic (ROC) curve evaluated the efficacy of sST2 alone or in combination with AFP in the diagnosis of HCC.ResultThe median level of sST2 was significantly higher in HCC group (24.00 [15.20-49.90] ng/mL) compared to CHB group (19.55 [15.23-24.95] ng/mL) and HCs group (7.65 [5.20-10.53] ng/mL). No significant correlations were found between sST2 and other clinical indicators in HCC group. The Area Under Curve (AUC) of ROC curve to distinguish HCC patients from healthy controls and CHB group was 0.861 (sensitivity 82.80%, specificity 72.10%) and 0.709 (sensitivity 80.60%, specificity 52.50%), respectively. When combined with AFP, the AUC increased to 0.963 (sensitivity 82.90%, specificity 94.20%), and 0.895 (sensitivity 72.0%, specificity 100%), respectively.ConclusionsThe serum level of sST2 increased in HCC and its diagnostic performance is comparable to that of AFP, supporting its potential as a promising biomarker for detection of HCC. The combined use of sST2 and AFP enhances diagnostic efficacy for HCC.
| S-EPMC11639131 | biostudies-literature
Project description:Chronic heart failure (CHF) represents a major cause of hospitalization and death. Recent evidence shows that novel biomarkers such as soluble suppression of tumorigenicity (sST2), growth-differentiation factor-15 (GDF-15), soluble urokinase plasminogen activator receptor (suPAR) and heart-type fatty acid binding protein (H-FABP) are correlated with inflammatory and ischemic responses in CHF patients. In this study we examined the effects of Ivabradine that inhibited the hyperpolarization-activated cyclic nucleotide-gated channel (HCN channel, also called funny current If), thereby leading to selective heart rate reduction and improved myocardial oxygen supply on the cardiac biomarkers sST2, GDF-15, suPAR and H-FABP in 50 CHF patients at the University Hospital of Jena. Patients were divided into three groups based on the etiology of CHF: dilated cardiomyopathy (DCM, n=20), ischemic cardiomyopathy (ICM, n=20) and hypertensive cardiomyopathy (HCM, n=10). The patients were administered Ivabradine (5 mg, bid for 3 months, and 7.5 mg bid for further 3 months). Analyses of cardiovascular biomarkers were performed at baseline as well as at 3- and 6-month follow-ups. At 6-month follow-up, GDF-15 levels were significantly reduced compared to baseline levels (P=0.0215), indicating a reduction in the progress of cardiac remodeling. H-FABP concentration was significantly lower in DCM patients compared to ICM (1.89 vs 3.24 μg/mL) and HCM patients (1.89 vs 3.80 μg/mL), and decreased over the 6-month follow-up (P=0.0151). suPAR median levels remained elevated, implying major ongoing inflammatory processes. As shown by significant decreases in GDF-15 and H-FABP levels, a reduction in ventricular remodeling and sub-clinical ischemia could be assumed. However, markers of hemodynamic stress (sST2) and inflammation (suPAR) showed no change or progression after 6 months of Ivabradine treatment in CHF patients. Further studies are necessary to validate the clinical applicability of these novel cardiovascular biomarkers.
| S-EPMC6289366 | biostudies-literature
Project description:Unfavourable conditions throughout the period of parental care can severely affect growth, reproductive performance, and survival. Yet, individuals may be affected differently, depending on the developmental period during which constraints are experienced. Here we tested whether the nestling phase compared to the fledgling phase is more susceptible to nutritional stress by considering biometry, physiology, sexually selected male ornaments and survival using zebra finches (Taeniopygia guttata) as a model species. As nestlings (day 0-17) or fledglings (day 17-35), subjects were raised either on low or high quality food. A low quality diet resulted in significantly elevated baseline corticosterone titres in both nestlings and fledglings. Subjects showed substantial compensatory growth after they had experienced low quality food as nestlings but catch-up growth did neither lead to elevated baseline corticosterone titres nor did we detect long term effects on biometry, male cheek patch, or survival. The compensation for temporally unfavourable environmental conditions reflects substantial phenotypic plasticity and the results show that costs of catch-up growth were not mediated via corticosterone as a physiological correlate of allostatic load. These findings provide new insights into the mechanisms and plasticity with which animals respond to periods of constraints during development as they may occur in a mistiming of breeding.
| S-EPMC2946921 | biostudies-literature
Project description:BackgroundCardiovascular biomarkers are crucial for monitoring cancer therapy-related cardiac toxicity, but the effects on early stage are still inadequate. To screen biomarkers in patients with breast cancer who receive anthracycline-containing chemotherapy, we studied the behavior of six biomarkers during chemotherapy and their association with chemotherapy-related cardiac toxicity.MethodsIn a prospective cohort of 73 patients treated with anthracycline-containing chemotherapy, soluble suppression of tumorigenicity 2 (sST2), high-sensitivity cardiac troponin T, N-terminal pro-B-type natriuretic peptide (NT-proBNP), myoglobin, creatine kinase isoenzyme MB, and heart-fatty acid binding protein were measured at baseline, during chemotherapy cycle (C1-C6). According to whether arrhythmia occurred, patients were divided into two groups (healthy group or arrhythmias group), and basic clinical characteristics were collected and compared. Logistic regression analyses and receiver operating characteristic (ROC) curves were conducted to investigate the association between the changes in biomarkers and arrhythmia.ResultssST2 levels increased significantly from baseline to C1 (P < 0.01). NT-proBNP levels decreased from baseline to C1 and C5 (P < 0.01). The logistic regression analysis showed a greater risk of arrhythmia was associated with interval changes in sST2 [odds ratio (OR): 1.27; 95% CI: 1.03-1.56; P = 0.024] and NT-proBNP (OR: 0.83; 95% CI: 0.70-0.98; P = 0.029). The ROC curves showed that ΔsST2, ΔNT-proBNP, and ΔsST2 + ΔNT-proBNP had good predictive value for arrhythmia (areas under the curves were 0.631, 0.633, and 0.735, respectively, P < 0.05).ConclusionsEarly changes in sST2 and NT-proBNP levels offer additive information for early arrhythmia prediction in breast cancer patients who receive anthracycline-containing chemotherapy.
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Project description:We present a series of experiments that explore the boundary conditions for how emotional arousal influences height estimates. Four experiments are presented, which investigated the influence of context, situation-relevance, intensity, and attribution of arousal on height estimates. In Experiment 1, we manipulated the environmental context to signal either danger (viewing a height from above) or safety (viewing a height from below). High arousal only increased height estimates made from above. In Experiment 2, two arousal inductions were used that contained either 1) height-relevant arousing images or 2) height-irrelevant arousing images. Regardless of theme, arousal increased height estimates compared to a neutral group. In Experiment 3, arousal intensity was manipulated by inserting an intermediate or long delay between the induction and height estimates. A brief, but not a long, delay from the arousal induction served to increase height estimates. In Experiment 4, an attribution manipulation was included, and those participants who were made aware of the source of their arousal reduced their height estimates compared to participants who received no attribution instructions. Thus, arousal that is attributed to its true source is discounted from feelings elicited by the height, thereby reducing height estimates. Overall, we suggest that misattributed, embodied arousal is used as a cue when estimating heights from above that can lead to overestimation.
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Project description:BACKGROUND:The phosphatase chronophin (CIN/PDXP) has been shown to be an important regulator of glioma cell migration and invasion. It has two known substrates: p-Ser3-cofilin, the phosphorylated form of the actin binding protein cofilin, and pyridoxal 5'-phosphate, the active form of vitamin B6. Phosphoregulation of cofilin, among other functions, plays an important role in cell migration, whereas active vitamin B6 is a cofactor for more than one hundred enzymatic reactions. The role of CIN has yet only been examined in glioblastoma cell line models derived under serum culture conditions. RESULTS:We found that CIN is highly expressed in cells cultured under non-adherent, serum-free conditions that are thought to better mimic the in vivo situation. Furthermore, the substrates of CIN, p-Ser3-cofilin and active vitamin B6, were significantly reduced as compared to cell lines cultured in serum-containing medium. To further examine its molecular role we stably knocked down the CIN protein with two different shRNA hairpins in the glioblastoma cell lines NCH421k and NCH644. Both cell lines did not show any significant alterations in proliferation but expression of differentiation markers (such as GFAP or TUBB3) was increased in the knockdown cell lines. In addition, colony formation was significantly impaired in NCH644. Of note, in both cell lines CIN knockdown increased active vitamin B6 levels with vitamin B6 being known to be important for S-adenosylmethionine biosynthesis. Nevertheless, global histone and DNA methylation remained unaltered as was chemoresistance towards temozolomide. To further elucidate the role of phosphocofilin in glioblastoma cells we applied inhibitors for ROCK1/2 and LIMK1/2 to our model. LIMK- and ROCK-inhibitor treatment alone was not toxic for glioblastoma cells. However, it had profound, but antagonistic effects in NCH421k and NCH644 under chemotherapy. CONCLUSION:In non-adherent glioblastoma cell lines cultured in serum-free medium, chronophin knockdown induces phenotypic changes, e.g. in colony formation and transcription, but these are highly dependent on the cellular background. The same is true for phenotypes observed after treatment with inhibitors for kinases regulating cofilin phosphorylation (ROCKs and LIMKs). Targeting the cofilin phosphorylation pathway might therefore not be a straightforward therapeutic option in glioblastoma.
| S-EPMC5934884 | biostudies-literature
Project description:Retroviruses cause immunodeficiency and cancer but also are used as vectors for the expression of heterologous genes. Nevertheless, optimal translation of introduced genes often is not achieved. Here we show that transfection into mammalian cells of lentiviral or gammaretroviral vectors, including those with specific shRNAs, increased expression of a cotransfected gene relative to standard plasmid vectors. Levels of most endogenous cellular proteins were unchanged. Transfer of lentiviral vector sequences into a standard plasmid conferred the ability to give increased expression of cotransfected genes (superinduction). Superinduction by the retroviral vector was not dependent on the cell type or species, the type of reporter gene, or the method of transfection. No differences were detected in the IFN, unfolded protein, or stress responses in the presence of retroviral vectors. RT-PCRs revealed that RNA levels of cotransfected genes were unchanged during superinduction, yet Western blotting, pulse labeling, and the use of bicistronic vectors showed increased cap-dependent translation of cointroduced genes. Expression of the mammalian target of rapamycin (mTOR) kinase target 4E-BP1, but not the mTOR inhibitor Torin 1, preferentially inhibited superinduction relative to basal protein expression. Furthermore, transcription of lentiviral vector sequences from a doxycycline-inducible promoter eliminated superinduction, consistent with a DNA-triggered event. Thus, retroviral DNA increased translation of cointroduced genes in trans by an mTOR-independent signaling mechanism. Our experiments have broad applications for the design of retroviral vectors for transfections, DNA vaccines, and gene therapy.
| S-EPMC4371913 | biostudies-literature
Project description:ObjectiveTo test the safety, tolerability, and urate-elevating capability of the urate precursor inosine taken orally or by feeding tube in people with amyotrophic lateral sclerosis (ALS).MethodsThis was a pilot, open-label trial in 25 participants with ALS. Treatment duration was 12 weeks. The dose of inosine was titrated at pre-specified time points to elevate serum urate levels to 7-8 mg/dL. Primary outcomes were safety (as assessed by the occurrence of adverse events [AEs]) and tolerability (defined as the ability to complete the 12-week study on study drug). Secondary outcomes included biomarkers of oxidative stress and damage. As an exploratory analysis, observed outcomes were compared with a virtual control arm built using prediction algorithms to estimate ALSFRS-R scores.ResultsTwenty-four out of 25 participants (96%) completed 12 weeks of study drug treatment. One participant was unable to comply with study visits and was lost to follow-up. Serum urate rose to target levels in 6 weeks. No serious AEs attributed to study drug and no AEs of special concern, such as urolithiasis and gout, occurred. Selected biomarkers of oxidative stress and damage had significant changes during the study period. Observed changes in ALSFRS-R did not differ from baseline predictions.InterpretationInosine appeared safe, well tolerated, and effective in raising serum urate levels in people with ALS. These findings, together with epidemiological observations and preclinical data supporting a neuroprotective role of urate in ALS models, provide the rationale for larger clinical trials testing inosine as a potential disease-modifying therapy for ALS.
| S-EPMC6292193 | biostudies-literature