Patterns of Metastasis in Merkel Cell Carcinoma.

Cell-type specific interaction of endothelin and the nitric oxide system: pattern of prepro-ET–1 expression in kidneys of L-NAME treated prepro-ET–1 promoter-lacZ-transgenic mice.

by
  • Nitric oxide (NO) and endothelin-1 (ET-1) are known to play a major role in renal and vascular pathophysiology and exhibit a close interaction with ET-1, stimulating NO production; NO in turn inhibits ET-1 expression. Our objectives were (1) to establish a novel transgenic mouse model facilitating ET-1 expression assessment in vivo, (2) to validate this model by assessing prepro-ET-1 promoter activity in mice embryos by means of our novel model and comparing expression sites to well-established data on ET-1 in fetal development and (3) to investigate renal ET-NO interaction by assessing prepro-ET-1 promoter activity in different structures of the renal cortex in the setting of blocked NO synthases via L-NAME administration. We established transgenic mice carrying a lacZ reporter gene under control of the human prepro-ET-1 gene promoter sequence (8 kb of 5′ sequences).
  • Bluo-Gal staining of tissue sections revealed intracellular blue particles as indicators of prepro-ET-1 promoter activity. In mouse embryos, we detected high prepro-ET-1 promoter activity in the craniofacial region, as well as in bone and cartilage consistent with the literature. In order to investigate the interaction of ET-1 and NO in the kidney in vivo, transgenic mice at the age of 3-4 months were treated with a single dose of the NO synthase inhibitor L-NAME (25 mg (kg bw)(-1) i.p.) 12 h before kidney removal. Bluo-Gal staining of kidney sections revealed intracellular blue particles as indicators of prepro-ET-1 promoter activity in tubular and vascular endothelium and glomerular cells.
  • Particle count was closely correlated to kidney tissue ET-1 content (R=0.918, P<0.001). Comparison of counts revealed an increase by 135+/-53% in L-NAME treated (n=12) compared to non-treated mice (n=10, P=0.001). Cell-type specific evaluation revealed an increase of 136+/-51% in tubular (P=0.001) and 105+/-41% in glomerular cells (P=0.046), but no significant increase in vascular endothelium. In conclusion, our study revealed a close interaction of renal endothelin and the NO system in a cell-type specific manner. Our new transgenic model provides a unique opportunity to analyse regulation of the ET system on a cellular level in vivo.

<em>Endothelin</em>-<em>1</em> promotes cell survival in renal cell carcinoma through the <em>ET</em>(A) receptor.

Endothelin-1 (ET-1) is a potent vasoconstrictor that has been shown to significantly impact many benign and malignant tissues by signaling through its two cognate receptors: ET(A) and ET(B). As ET-1 has a role in both normal and diseased kidney, we initiated studies to investigate endothelin axis expression and function in renal cell carcinoma (RCC). In this study, relatively high levels of ET-1 were detected in all six human RCC cell lines investigated. RT-PCR and Southern analyses revealed that all six RCC cell lines expressed ET(A) receptor mRNA, while 3/6 cell lines also expressed ET(B) mRNA.
High affinity ET-1 binding occurred in all but one RCC cell line and quantitative RT-PCR demonstrated ET(A) mRNA expression in all six cell lines. Methylation of the ET(B) promoter (EDNRB) in 4/6 RCC cell lines was observed, suggesting a mechanism for repressed ET(B) expression. Moreover, methylation occurred in 32/48 of renal tumors and in 27/55 of histologically normal adjacent tissue samples studied, while no methylation was evident in any normal tissue isolated from nephrectomy or at autopsy. Functionally, ET-1 significantly inhibited paclitaxel-induced apoptosis in RCC cells through binding ET(A) with the ET-1 signaling mediated via the PI3-kinase/Akt pathway. Collectively, these data support the therapeutic targeting of the ET(A) receptor as a novel treatment strategy for RCC.

<em>Endothelin</em>-<em>1</em> and its receptors <em>ET</em>(A) and <em>ET</em>(B) in drug-induced gingival overgrowth.

BACKGROUND
The purpose of this study was to study the expression of endothelin-1 (ET-1) and its receptors ETA and ETB in normal human gingiva and cyclosporin-induced gingival fibroblasts.
METHODS
Gingival samples were collected from eight normal healthy individuals, eight patients with periodontitis, and eight patients with cyclosporin A (CsA)-induced gingival overgrowth. Total RNA was extracted from tissue samples, and reverse transcriptase-polymerase chain reaction was performed for ET-1, ETA, and ETB. ET-1 protein was estimated from the tissues by enzyme-linked immunosorbent assay. The expression of ET-1 and its receptors was also examined in gingival fibroblast cells treated with CsA.
RESULTS
ET-1 mRNA expression was significantly higher in patients with CsA-induced gingival overgrowth (P <0.001) than in patients with periodontitis and the controls. ETA mRNA was expressed more than the ETB in all examined samples. In human gingival fibroblasts, ET-1 expression was increased with CsA incorporation compared to controls (P <0.001).
CONCLUSIONS
These results suggest that CsA can modulate the expression of ET-1 in gingival fibroblasts and CsA-induced gingival overgrowth.

Regulation and expression of <em>endothelin</em>-<em>1</em> (<em>ET</em>-<em>1</em>) and <em>ET</em>-receptors in rat epithelial cells of renal and intestinal origin.

  • The hormone endothelin-1 (ET-1) is involved in many functions of the kidney and intestine. In addition to its vasoactive and proliferative effects, ET-1 is involved in the maintenance of water and salt balance, and in drug excretion by influencing the activity of different transporters in the epithelial cells of these two organs. To study ET-1 function and its role in pathophysiological processes in epithelial cells in vitro, we investigated ET-1 and ET-receptor expression and inducibility of ET-1 excretion by cytokines in three rat cell lines of intestinal (IEC-6) and renal (NRK-52E and GERP) origin.
  • Immunocytochemistry showed that all three cell lines express ET-1 and the ET-A and ET-B receptor. ET-1 was expressed intracellularly, and also the ET-A receptor showed a punctate intracellular staining pattern. The ET-B receptor was localized in the membrane, which was confirmed by Western blot analysis. Real-time RT-PCR and ELISA showed that exposure of IEC-6 cells to the cytokines, interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNFalpha), induced ET-1 mRNA expression and excretion, while IL-2 was ineffective.
  • In NRK-52E cells, IL-1beta and TNFalpha induced ET-1 excretion as well. In GERP cells, adequate measurement of cytokine effects on ET-1 excretion was not possible, since ET-1 excretion under non-stimulated conditions was around the lowest level of detection. In conclusion, we showed ET-1 and ET-receptor expression, and inducibility of ET-1 by cytokines in IEC-6, NRK-52E, and GERP cells.
  • These rat intestinal and renal cell lines appear to be suitable for further characterisation of ET-1 function and its role in pathophysiological processes in epithelial cells.

Mouse Endothelin 1, ET-1 ELISA Kit
1-CSB-E05145m Cusabio
  • 1135.20 EUR
  • 6938.40 EUR
  • 3672.00 EUR
  • 1 plate of 96 wells
  • 10 plates of 96 wells each
  • 5 plates of 96 wells each

Pig endothelin 1, ET-1 ELISA Kit
1-CSB-E06806p Cusabio
  • 964.80 EUR
  • 6118.80 EUR
  • 3244.80 EUR
  • 1 plate of 96 wells
  • 10 plates of 96 wells each
  • 5 plates of 96 wells each

Rabbit Endothelin 1, ET-1 ELISA Kit
1-CSB-E06951Rb Cusabio
  • 1160.40 EUR
  • 7110.00 EUR
  • 3760.80 EUR
  • 1 plate of 96 wells
  • 10 plates of 96 wells each
  • 5 plates of 96 wells each

rat Endothelin 1, ET-1 ELISA Kit
1-CSB-E06979r Cusabio
  • 964.80 EUR
  • 6118.80 EUR
  • 3244.80 EUR
  • 1 plate of 96 wells
  • 10 plates of 96 wells each
  • 5 plates of 96 wells each

Dog Endothelin 1, ET-1 ELISA Kit
1-CSB-E07002c Cusabio
  • 964.80 EUR
  • 6118.80 EUR
  • 3244.80 EUR
  • 1 plate of 96 wells
  • 10 plates of 96 wells each
  • 5 plates of 96 wells each

Human Endothelin 1, ET-1 ELISA Kit
1-CSB-E07007h Cusabio
  • 964.80 EUR
  • 6118.80 EUR
  • 3244.80 EUR
  • 1 plate of 96 wells
  • 10 plates of 96 wells each
  • 5 plates of 96 wells each

Endothelin 1 (ET-1) Antibody
abx024086-100ug Abbexa 100 ug 1128 EUR

Endothelin-1 (1-15), amide, human
A1111-1 ApexBio 1 mg 866.4 EUR

ET-1(Endothelin-1) ELISA Kit
EU0205 FN Test 96T 628.92 EUR

Rabbit Endothelin 1,ET-1 ELISA Kit
CN-00693R1 ChemNorm 96T 546 EUR

Rabbit Endothelin 1,ET-1 ELISA Kit
CN-00693R2 ChemNorm 48T 364.8 EUR

Canine Endothelin 1,ET-1 ELISA Kit
CN-00955C1 ChemNorm 96T 532.8 EUR

Canine Endothelin 1,ET-1 ELISA Kit
CN-00955C2 ChemNorm 48T 352.8 EUR

PoFAine endothelin 1,ET-1 ELISA Kit
CN-01235P1 ChemNorm 96T 526.8 EUR

PoFAine endothelin 1,ET-1 ELISA Kit
CN-01235P2 ChemNorm 48T 348 EUR

Mouse Endothelin 1, ET-1 ELISA Kit
CSB-E05145m-24T Cusabio 1 plate of 24 wells 198 EUR

Pig endothelin 1, ET-1 ELISA Kit
CSB-E06806p-24T Cusabio 1 plate of 24 wells 198 EUR

Rabbit Endothelin 1, ET-1 ELISA Kit
CSB-E06951Rb-24T Cusabio 1 plate of 24 wells 198 EUR

rat Endothelin 1, ET-1 ELISA Kit
CSB-E06979r-24T Cusabio 1 plate of 24 wells 198 EUR

Dog Endothelin 1, ET-1 ELISA Kit
CSB-E07002c-24T Cusabio 1 plate of 24 wells 198 EUR

Human Endothelin 1, ET-1 ELISA Kit
CSB-E07007h-24T Cusabio 1 plate of 24 wells 198 EUR

Mouse Endothelin 1,ET-1 ELISA Kit
CN-02844M1 ChemNorm 96T 526.8 EUR

Mouse Endothelin 1,ET-1 ELISA Kit
CN-02844M2 ChemNorm 48T 348 EUR

human Endothelin 1,ET-1 ELISA Kit
CN-04153H1 ChemNorm 96T 538.8 EUR

human Endothelin 1,ET-1 ELISA Kit
CN-04153H2 ChemNorm 48T 358.8 EUR

Rat Endothelin 1,ET-1 ELISA Kit
CN-01966R1 ChemNorm 96T 560.4 EUR

[Relationship of <em>endothelin</em>-<em>1</em> (<em>ET</em>-<em>1</em>) TaqI and tumor necrosis factor (TNF) a gene polymorphism with portal hypertension in liver cirrhosis].

OBJECTIVE
To study whether liver cirrhosis and portal hypertension are associated with ET-1 TaqI polymorphism and TNFa promoter-308G to A polymorphism.
METHODS
A case control study of 106 patients with liver cirrhosis following HBV C infection was performed in comparison with 108 controls by PCR-RFLP.
RESULTS
The frequency of C allele and CC+TC genotype in TaqI polymorphism of ET-1 gene in the portal hypertension group (LC+) was significantly higher than that in the healthy controls, and the frequency of TNF2/1 genotype in TNFa promoter -308 G to A polymorphism in LC+ group was significantly higher than that in the control group. The results by stratification analysis showed that TCF2 genotype frequency was higher in the LC+ group than in the control group. ET-1 TaqI polymorphism and TNFa polymorphism were risk factors for the occurrence of portal hypertension by Logistic regression analysis.
CONCLUSIONS
ET-1 TaqI polymorphism and TNFa polymorphism are associated with portal hypertension, and are new risk factors for the occurrence of portal hypertension. TCF2 genotype may be a susceptible gene of portal hypertension.

Comparative Analysis between Urinary Calprotectin and Serum Creatinine for Early Detection of Intrinsic Acute Kidney Injury

by
Background: Acute kidney injury (AKI) is a common and important clinical condition that may lead to chronic kidney disease if it is not diagnosed and treated in its early stages. Urinary calprotectin is a valuable recognized biomarker that can be used to differentiate prerenal and intrinsic AKI. However, till date only a few reports on urine calprotectin measurement in early diagnosis of intrinsic AKI are available. In this study, we compared the sensitivity and specificity of urinary calprotectin with those of serum creatinine in detecting early intrinsic AKI.
Methods: Over 6 months period (April to October 2018), 81 of 408 patients admitted to the pediatric intensive care unit met the criteria of this cross-sectional study. Their serum creatinine and urinary calprotectin were measured on the first and third day of admission using Jaffe and Elisa radioimmunoassay methods, respectively. The AKI was defined according to the pRIFLE criteria.
Results: Of the total 81 patients, 67 had the criteria of intrinsic AKI. Of these 62% were female and 38% were male. The mean age of the patients was 22 months. According to data analysis, the area under the curve of ROC of urinary calprotectin on day-1 to detect renal failure is 0.93 with the best cutoff point obtained at 530 ng/mL. The sensitivity, specificity, positive, and negative predictive values of urinary calprotectin levels in diagnosing AKI at this cutoff point are 92.5%, 92.8%, 98.4, and 72.2%, respectively. Besides, urinary calprotectin changes occur much earlier than the rising of serum creatinine.
Conclusion: Urinary level of calprotectin is a very sensitive biomarker for early diagnosis of intrinsic AKI in children and it can be used in intensive care units or anywhere critically ill children admitted to detect intrinsic AKI. Besides, this study shows that urine calprotectin may be a more sensitive and specific biomarker than serum creatinine in the early phases of intrinsic AKI.

High-performance surface-enhanced Raman spectroscopy chip integrated with a micro-optical system for the rapid detection of creatinine in serum

To improve the sensitivity of disease biomarker detection, we proposed a high-performance surface-enhanced Raman spectroscopy (SERS) chip integrated with a micro-optical system (MOS). The MOS, which is based on the micro-reflecting cavity and the micro-lens, optimizes the optical matching characteristics of the SERS substrate and the Raman detection system, and greatly improves the SERS detection sensitivity by improving the collection efficiency of the Raman scattering signal. A uniform single layer of silver nanoparticles on a gold film was prepared as the SERS substrate using a liquid-liquid interface self-assembly method. The micro-reflecting cavity and micro-lens were prepared using micro-processing technology. The SERS chip was constructed based on the MOS and the Au film-based SERS substrate, and experimental results showed an EF of 1.46×108, which is about 22.4 times higher than that of the Si-based SERS substrate.
The chip was used for the detection of creatinine and the detection limit of creatinine in aqueous solution was 1 µM while the detection limit in serum was 5 µM. In addition, SERS testing was conducted on serum samples from normal people and patients with chronic renal impairment. Principal component analysis and linear discriminant analysis were used for modeling and identification, and the results showed a 90% accuracy of blind sample detection. These results demonstrate the value of this SERS chip for both research and practical applications in the fields of disease diagnosis and screening.

Drain fluid creatinine-to-serum creatinine ratio as an initial test to detect urine leakage following cystectomy: A retrospective study

Introduction: Urine leak following radical cystectomy is a known complication. Among the various methods to diagnose this, assessment of drain fluid creatinine is a relatively easy procedure. We aimed to ascertain the validity of the drain fluid creatinine-to-serum creatinine ratio (DCSCR) as an initial indicator of urinary leak in patients undergoing radical cystectomy.
Methods: We retrospectively identified consecutive patients with documentation of drain fluid creatinine in the postoperative period following cystectomy and urinary diversion at our institution between January 2009 and December 2018. All continent diversions and any patient with a DCSCR >1.5:1 underwent contrast study postoperatively. A diagnosis of urine leak was made following confirmatory imaging. Receiver operative characteristic curves were created, and Youden’s index was used to determine the strength and clinical utility of DCSCR as a diagnostic test.
Results: Two hundred forty-four of the 340 patients included in the study underwent cystectomy with conduit and 81 underwent neobladder creation. Sixteen out of 340 (4.7%) patients had radiologically confirmed urinary leak. DCSCR was elevated in all ureteric anastomotic leaks and in 1 out of the 7 neobladder-urethral anastomotic (NUA) leaks. The sensitivity and specificity of DCSCR to predict all urinary leaks were 68.8% and 80.9% at 1.12 (area under the curve [AUC] = 0.838), whereas at a value of 1.18 (AUC = 0.876) and with the exclusion of NUA leaks, the sensitivity was 77.8% and specificity was 87.6%.
Conclusions: DCSCR is a good preliminary test for identifying patients who need prompt confirmatory testing for localizing urinary leaks. A drain creatinine level just 18% higher than the serum creatinine level can signify a urine leak. This is different from general assumptions of a higher DCSCR.

Creatinine Serum Detection Kit
SKT-217-192 Stressmarq 2 plates of 96 wells 410.4 EUR

Urine Creatinine Detection Kit
SKT-200-192 Stressmarq 2 plates of 96 wells 410.4 EUR

Creatinine Urinary Detection Kit (2 Plate Kit)
K002-H1 Arbor Assays 2x96 well plates 315.6 EUR

Creatinine Urinary Detection Kit (10 Plate Kit)
K002-H5 Arbor Assays 10x96 well plates 1018.8 EUR

Creatinine Serum Kit (2 Whole Plate Kit)
KB02-H1 Arbor Assays 2x96 well plates 327.6 EUR

Creatinine Serum Kit (4 Whole Plate Kit)
KB02-H2 Arbor Assays 4x96 well plates 498 EUR

Potassium (Serum) Detection Assay Kit (Fluorometric)
K940-100 Biovision each 738 EUR

Creatinine
CB0328 Bio Basic 5g 68.35 EUR

Creatinine
B1717-50 ApexBio 50 mg 153.6 EUR

Creatinine
GK8780-100G Glentham Life Sciences 100 g 151.2 EUR

Creatinine
GK8780-25G Glentham Life Sciences 25 g 74.4 EUR

Creatinine
HY-B0504 MedChemExpress 500mg 129.6 EUR

Creatinine Serum Low Sample Volume Kit (384 well plate)
KB02-H1D Arbor Assays 1x384 well plate 436.8 EUR

Creatinine [BTG]
DAGA-186G Creative Diagnostics 500ug 1425.6 EUR

Creatinine-HRP
DAG-CL005 Creative Diagnostics 500 μl 1248 EUR

Creatinine-HRP
80-1133 Fitzgerald 500 ul 159.6 EUR

Serum Creatinine ELISA kit (colorimetric, all species), 96 tests, quantitative
100-300-SCR Alpha Diagnostics 1 kit 343.2 EUR

Serum Creatinine ELISA kit (colorimetric, all species), 2x96 tests, quantitative
100-305-SCR Alpha Diagnostics 1 kit 562.8 EUR

Creatinine ELISA Kit| Mouse Creatinine ELISA Kit
EF013537 Lifescience Market 96 Tests 826.8 EUR

Human Urinary Creatinine(Urinary Creatinine) ELISA Kit
QY-E05390 Qayee Biotechnology 96T 433.2 EUR

Creatinine ELISA Kit
DLR-Crtn-Ge-48T DL Develop 48T 562.8 EUR

Creatinine ELISA Kit
DLR-Crtn-Ge-96T DL Develop 96T 729.6 EUR

Creatinine(N) [HRP]
DAG1075 Creative Diagnostics 0.5ml 1014 EUR

Creatinine Standard, 100UL
C003-100UL Arbor Assays 100UL 147.6 EUR

Creatinine Standard, 1ML
C003-1ML Arbor Assays 1ML 284.4 EUR

Creatinine Assay Kit
55R-1467 Fitzgerald 100 assays 765.6 EUR

Creatinine Acid antibody
20-1244 Fitzgerald 100 ul 651.6 EUR

Creatinine N antibody
20-1373 Fitzgerald 100 ul 1054.8 EUR

Utility of measuring serum creatinine to detect renal compromise in ED patients receiving IV contrast-enhanced CT scan

Objective: The objectives of this study are to determine the efficacy of a roster of clinical factors in identifying risk for renal insufficiency in emergency department (ED) patients requiring intravenous contrast-enhanced CT scan (IVCE-CT) and to help mitigate potential for developing contrast-induced nephropathy (CIN).
Methods: A review was conducted of consecutive ED patients who received IVCE-CT during a 4-month period in our urban ED. The values of ED serum creatinine (SCr) performed were tabulated. The medical records of all patients with an elevated SCr (> 1.4 mg/dL) were reviewed to determine and correlate the presence of clinical risk factors for underlying renal insufficiency.
Results: During the 4-month study period, there were 2260 consecutive cases who received IVCE-CT; of these, 2250 (99.6%) had concomitant measurement of SCr. Elevated SCr occurred in 141 patients (6.2%); of these, 75 had a SCr > 2 mg/dL. In all, 139/141 (98.6%) with an elevated SCr had an underlying chronic or acute medical condition identified by medical record review which potentially compromised renal function, including chronic renal disease, diabetes mellitus, HIV infection, cancer, hypertension, congestive heart failure, sepsis/septic shock, chronic alcoholism, and sickle cell disease. Two patients with no identified risk factor each had (mildly) elevated SCr; both had a normal SCr measured post-CT scan. The total cost of performing serum basic metabolic panel to measure SCr in all patients during the 4-month study period was $94,500.
Conclusions: Elevated SCr is rarely present in ED patients without recognized risk factors who receive IVCE-CT scan. The vast majority with underlying renal insufficiency are readily identified by a review of the patient’s medical history and/or clinical findings. Routine SCr measurement on all ED patients regardless of risk stratification prior to IVCE imaging is neither time nor cost-effective.

Potent repression of C-reactive protein (CRP) expression by the JAK1/2 inhibitor ruxolitinib in inflammatory human hepatocytes

by
To determine whether inflammatory hepatocytes may constitute primary targets for ruxolitinib, a Janus kinase (JAK) inhibitor, its effects towards expression of hepatic acute-phase proteins, especially C-reactive protein (CRP), were assessed.Ruxolitinib effects were analysed in primary human hepatocytes and human hepatoma HepaRG cells exposed to various inflammatory stimuli.
RESULTS

Ruxolitinib was found to fully inhibit lipopolysaccharide (LPS)-induced CRP secretion and mRNA expression, at concentrations (IC50 = 12.9 nM) achievable in human blood. It similarly repressed CRP up-regulation due to several Toll-like receptor agonists or pro-inflammatory cytokines [interleukin (IL) 1β, IL6 and tumour necrosis factor α] and counteracted LPS-mediated induction of serum amyloid A, fibrinogen, haptoglobin and serpin. Ruxolitinib was additionally found to block the activation of the IL6/JAK/signal transducer and activator of transcription (STAT) pathway triggered by LPS and whose inhibition by the neutralizing anti-IL6 receptor antibody tocilizumab prevented CRP induction.Ruxolitinib can potently repress induction of CRP in inflammatory human hepatocytes, most likely through targeting the IL6/JAK/STAT signalling cascade. Hepatic production of acute-phase proteins during liver inflammation may, therefore, constitute a target for ruxolitinib.

Nanomolar aluminum induces expression of the inflammatory systemic biomarker C–reactive protein (CRP) in human brain microvessel endothelial cells (hBMECs).

C-reactive protein (CRP; also known as pentraxin 1, PTX1), a 224 amino acid soluble serum protein organized into a novel pentameric ring-shaped structure, is a highly sensitive pathogenic biomarker for systemic inflammation. High CRP levels are found in practically every known inflammatory state, and elevated CRP levels indicate an increased risk for several common age-related human degenerative disorders, including cardiovascular disease, cancer, diabetes, and Alzheimer’s disease (AD). While the majority of CRP is synthesized in the liver for secretion into the systemic circulation, it has recently been discovered that an appreciable amount of CRP is synthesized in highly specialized endothelial cells that line the vasculature of the brain and central nervous system (CNS).
These highly specialized cells, the major cell type lining the human CNS vasculature, are known as human brain microvessel endothelial cells (hBMECs). In the current pilot study we examined (i) CRP levels in human serum obtained from AD and age-matched control patients; and (ii) analyzed the effects of nanomolar aluminum sulfate on CRP expression in primary hBMECs. The three major findings in this short communication are: (i) that CRP is up-regulated in AD serum; (ii) that CRP serum levels increased in parallel with AD progression; and (iii) for the first time show that nanomolar aluminum potently up-regulates CRP expression in hBMECs to many times its ‘basal abundance’. The results suggest that aluminum-induced CRP may in part contribute to a pathophysiological state associated with a chronic systemic inflammation of the human vasculature.

High sensitivity C–reactive protein (Hs-CRP) remains highly stable in long-term archived human serum.

BACKGROUND
The stability of biomarkers in stored biomedical samples is crucial, especially when storage is for extended periods of time. High-sensitivity CRP (Hs-CRP) is a biomarker of low grade inflammation that is extensively used to identify and study cardiovascular and/or inflammatory processes in clinical care and large epidemiologic studies. Therefore, assessing Hs-CRP stability in archived samples at a given temperature is important to ensure precision of measurements over time and the validity of studies using archived samples.
METHODS
We evaluated the stability of Hs-CRP in 30 randomly selected human serum samples by measuring Hs-CRP concentrations in freshly collected sample [Hs-CRP (0)] and in the same set of samples after 7-11years of storage at -80°C [Hs-CRP (LT)].
RESULTS
Hs-CRP did not significantly change up to 11years of storage at -80°C as shown by a negligible median difference between Hs-CRP (0) and Hs-CRP (LT), delta(Hs-CRP (0)-Hs-CRP (LT))=-0.01, p=0.45. There was a good concordance and agreement between Hs-CRP (0) and Hs-CRP (LT) as measured respectively by Lin’s coefficient of correlation (ρC=0.98) and Bland-Altman analysis (mean difference=-0.02, 95% CI [-0.04-0.0045] p=0.107). In addition, the data also suggest that the time elapsed between collection and Hs-CRP measurement does not affect Hs-CRP stability over time when samples are kept under the appropriate conditions.
CONCLUSIONS
Long-term storage at -80°C for up to 11years did not significantly affect the stability of serum Hs-CRP. Given the cost and time for collecting fresh samples, this observation represents an important finding for biomedical research and clinical care.

C–reactive protein (CRP) induces chemokine secretion via CD11b/ICAM-1 interaction in human adherent monocytes.

Several studies support C-reactive protein (CRP) as a systemic cardiovascular risk factor. The recent detection of CRP in arterial intima suggests a dual activity in atherosclerosis as a circulating and tissue mediator on vascular and immune cells. In the present paper, we focused on the inflammatory effects of CRP on human monocytes, which were isolated by Ficoll-Percoll gradients and cultured in adherence to polystyrene, endothelial cell monolayer, or in suspension. Chemokine levels, adhesion molecule, and chemokine receptor expression were detected by ELISA, flow cytometry, and real-time RT-PCR. Migration assays were performed in a Boyden chamber. Stimulation with CRP induced release of CCL2, CCL3, and CCL4 in adherent monocytes through the binding to CD32a, CD32b, and CD64, whereas no effect was observed in suspension culture.
This was associated with CRP-induced up-regulation of adhesion molecules membrane-activated complex 1 (Mac-1) and ICAM-1 on adherent monocytes. Blockade of Mac-1/ICAM-1 interaction inhibited the CRP-induced chemokine secretion. In addition, CRP reduced mRNA and surface expression of corresponding chemokine receptors CCR1, CCR2, and CCR5 in adherent monocytes. This effect was a result of chemokine secretion, as coincubation with neutralizing anti-CCL2, anti-CCL3, and anti-CCL4 antibodies reversed the effect of CRP. Accordingly, a reduced migration of CRP-treated monocytes to CCL2 and CCL3 was observed. In conclusion, our data suggest an in vitro model to study CRP activities in adherent and suspension human monocytes. CRP-mediated induction of adhesion molecules and a decrease of chemokine receptors on adherent monocytes might contribute to the retention of monocytes within atherosclerotic lesions and recruitment of other circulating cells.

Human C Reactive Protein (CRP) ELISA Kit
DLR-CRP-Hu-48T DL Develop 48T 462 EUR

Human C Reactive Protein (CRP) ELISA Kit
DLR-CRP-Hu-96T DL Develop 96T 590.4 EUR

Human C Reactive Protein (CRP) ELISA Kit
RD-CRP-Hu-48Tests Reddot Biotech 48 Tests 446.4 EUR

Human C Reactive Protein (CRP) ELISA Kit
RD-CRP-Hu-96Tests Reddot Biotech 96 Tests 612 EUR

Human C Reactive Protein (CRP) ELISA Kit
RDR-CRP-Hu-48Tests Reddot Biotech 48 Tests 465.6 EUR

Human C Reactive Protein (CRP) ELISA Kit
RDR-CRP-Hu-96Tests Reddot Biotech 96 Tests 639.6 EUR

Bovine C Reactive Protein (CRP) ELISA Kit
DLR-CRP-b-48T DL Develop 48T 656.4 EUR

Bovine C Reactive Protein (CRP) ELISA Kit
DLR-CRP-b-96T DL Develop 96T 858 EUR

Chicken C Reactive Protein (CRP) ELISA Kit
DLR-CRP-Ch-48T DL Develop 48T 609.6 EUR

Chicken C Reactive Protein (CRP) ELISA Kit
DLR-CRP-Ch-96T DL Develop 96T 793.2 EUR

Mouse C Reactive Protein (CRP) ELISA Kit
DLR-CRP-Mu-48T DL Develop 48T 586.8 EUR

Mouse C Reactive Protein (CRP) ELISA Kit
DLR-CRP-Mu-96T DL Develop 96T 762 EUR

Porcine C Reactive Protein (CRP) ELISA Kit
DLR-CRP-p-48T DL Develop 48T 656.4 EUR

Porcine C Reactive Protein (CRP) ELISA Kit
DLR-CRP-p-96T DL Develop 96T 858 EUR

Rat C Reactive Protein (CRP) ELISA Kit
DLR-CRP-Ra-48T DL Develop 48T 511.2 EUR

Rat C Reactive Protein (CRP) ELISA Kit
DLR-CRP-Ra-96T DL Develop 96T 658.8 EUR

Rabbit C Reactive Protein (CRP) ELISA Kit
DLR-CRP-Rb-48T DL Develop 48T 609.6 EUR

Rabbit C Reactive Protein (CRP) ELISA Kit
DLR-CRP-Rb-96T DL Develop 96T 793.2 EUR

Bovine C Reactive Protein (CRP) ELISA Kit
RD-CRP-b-48Tests Reddot Biotech 48 Tests 666 EUR

Bovine C Reactive Protein (CRP) ELISA Kit
RD-CRP-b-96Tests Reddot Biotech 96 Tests 925.2 EUR

Chicken C Reactive Protein (CRP) ELISA Kit
RD-CRP-Ch-48Tests Reddot Biotech 48 Tests 613.2 EUR

Chicken C Reactive Protein (CRP) ELISA Kit
RD-CRP-Ch-96Tests Reddot Biotech 96 Tests 850.8 EUR

Mouse C Reactive Protein (CRP) ELISA Kit
RD-CRP-Mu-48Tests Reddot Biotech 48 Tests 586.8 EUR

Mouse C Reactive Protein (CRP) ELISA Kit
RD-CRP-Mu-96Tests Reddot Biotech 96 Tests 812.4 EUR

Porcine C Reactive Protein (CRP) ELISA Kit
RD-CRP-p-48Tests Reddot Biotech 48 Tests 666 EUR

Porcine C Reactive Protein (CRP) ELISA Kit
RD-CRP-p-96Tests Reddot Biotech 96 Tests 925.2 EUR

Polymorphism in the human C–reactive protein (CRP) gene, serum concentrations of CRP, and the difference between intracranial and extracranial atherosclerosis.

BACKGROUND
C-reactive protein, a proinflammatory factor, is involved in the development of atherosclerosis. The CRP 1059G>C polymorphism appeared to be a susceptive marker for atherosclerosis. We investigated the relationship of the distribution of cerebral atherosclerosis with triggered serum CRP concentrations following acute ischemic stroke/transient ischemic attack (IS/TIA) and CRP 1059G>C polymorphism.
METHODS
We recruited 222 IS/TIA patients (122 with only intracranial atherosclerotic lesions and 100 with isolated extracranial atherosclerotic lesions) and 227 controls. Intra- and extracranial atherosclerotic lesions were determined by digital subtraction angiography. Serum CRP concentrations were measured by particle-enhanced immunonephelometry assay. CRP 1059G>C genotypes were obtained through PCR amplification and restriction enzyme digestion.
RESULTS
CRP concentrations were significantly higher in intra- and extracranial groups than in controls. No significant difference was found in CRP concentrations between intra- and extracranial groups. The CRP 1059G>C single-nucleotide polymorphism did not influence CRP serum concentrations. CRP genotype and allele frequencies did not differ significantly between patients and controls. However, the frequencies of GC genotype and C allele were significantly higher in extracranial group than that in intracranial group. The GC individuals showed a higher risk of extracranial atherosclerosis compared with GG individuals (OR 3.41; 95%CI, 1.124-10.347; P=0.030).
CONCLUSIONS
Serum CRP is associated with cerebral atherosclerotic disease. CRP 1059G>C polymorphism is one possible genetic determinant for the difference between intra- and extracranial atherosclerosis.

Telomere shortening is associated with corticosterone stress response in adult barn swallows

by
When vertebrates face stressful events, the hypothalamic-pituitary-adrenal (HPA) axis is activated, generating a rapid increase in circulating glucocorticoid (GC) stress hormones followed by a return to baseline levels. However, repeated activation of HPA axis may lead to increase in oxidative stress. One target of oxidative stress is telomeres, nucleoprotein complexes at the end of chromosomes that shorten at each cell division. The susceptibility of telomeres to oxidizing molecules has led to the hypothesis that increased GC levels boost telomere shortening, but studies on this link are scanty. We studied if, in barn swallows Hirundo rustica, changes in adult erythrocyte telomere length between 2 consecutive breeding seasons are related to corticosterone (CORT) (the main avian GC) stress response induced by a standard capture-restraint protocol.
Within-individual telomere length did not significantly change between consecutive breeding seasons. Second-year individuals showed the highest increase in circulating CORT concentrations following restraint. Moreover, we found a decline in female stress response along the breeding season. In addition, telomere shortening covaried with the stress response: a delayed activation of the negative feedback loop terminating the stress response was associated with greater telomere attrition. Hence, among-individual variation in stress response may affect telomere dynamics.

Context dependent variation in corticosterone and phenotypic divergence of Rana arvalis populations along an acidification gradient

Background: Physiological processes, as immediate responses to the environment, are important mechanisms of phenotypic plasticity and can influence evolution at ecological time scales. In stressful environments, physiological stress responses of individuals are initiated and integrated via the release of hormones, such as corticosterone (CORT). In vertebrates, CORT influences energy metabolism and resource allocation to multiple fitness traits (e.g. growth and morphology) and can be an important mediator of rapid adaptation to environmental stress, such as acidification. The moor frog, Rana arvalis, shows adaptive divergence in larval life-histories and predator defense traits along an acidification gradient in Sweden. Here we take a first step to understanding the role of CORT in this adaptive divergence. We conducted a fully factorial laboratory experiment and reared tadpoles from three populations (one acidic, one neutral and one intermediate pH origin) in two pH treatments (Acid versus Neutral pH) from hatching to metamorphosis. We tested how the populations differ in tadpole CORT profiles and how CORT is associated with tadpole life-history and morphological traits.
Results: We found clear differences among the populations in CORT profiles across different developmental stages, but only weak effects of pH treatment on CORT. Tadpoles from the acid origin population had, on average, lower CORT levels than tadpoles from the neutral origin population, and the intermediate pH origin population had intermediate CORT levels. Overall, tadpoles with higher CORT levels developed faster and had shorter and shallower tails, as well as shallower tail muscles.
Conclusions: Our common garden results indicate among population divergence in CORT levels, likely reflecting acidification mediated divergent selection on tadpole physiology, concomitant to selection on larval life-histories and morphology. However, CORT levels were highly environmental context dependent. Jointly these results indicate a potential role for CORT as a mediator of multi-trait divergence along environmental stress gradients in natural populations. At the same time, the population level differences and high context dependency in CORT levels suggest that snapshot assessment of CORT in nature may not be reliable bioindicators of stress.

RNA-seq based transcriptome analysis of ethanol extract of saffron protective effect against corticosterone-induced PC12 cell injury

Background: At present, oral antidepressants are commonly used in the clinical treatment of depression. However, the current drug treatment may lead to more serious adverse reactions. Therefore, we focus on Chinese traditional medicine, trying to find an effective and safe alternative or complementary medicine. Crocus sativus (saffron) is a traditional Chinese herbal medicine, which is typically used in the clinic to regulate anxiety, insomnia, amnesia, and other mental disorder. The study aimed to explore the neuroprotective effect of ethanol extract of saffron (EES) on corticosterone (CORT)- induced injury in PC12 cells and further explored its potential mechanism.
Methods: The authenticity of saffron and the active components of EES were identified by a water test and ultra-performance liquid chromatography-time of flight mass spectrometry system. The screening of cytotoxicity for PC12 cells was incubated with EES in different concentrations for 24 h, and the protective efficacy of EES on CORT (500 μM) -induced PC12 cell injury, cell viability was assessed by Cell Counting Kit-8 (CCK-8) assay. The differentially expressed genes (DEGs) of EES-protected PC12 cells were analyzed using the RNA-seq method, and the results were analyzed for GO and KEGG enrichment. The results of RNA-seq were verified by qPCR analysis.
Results: The saffron was initially identified as authentic in the water test and 10 compounds were identified by Ultra Performance Liquid Chromatography (UPLC)- Mass Spectrometry (MS). The results of CCK-8 demonstrated that EES at concentrations above 640 μg/mL exerted a certain cytotoxic effect, and PC12 cells pretreated with EES (20, 40, and 80 μg/mL) significantly reversed the 500 μM CORT-induced cell death. RNA-seq analysis showed that EES regulated 246 differential genes, which were mainly enriched in the MAPK signaling pathway. Dusp5, Dusp6, Gadd45b, Gadd45G, and Pdgfc were further validated by qPCR. Experimental data showed that the results of qPCR were consistent with RNA-seq.
Conclusions: These findings provide an innovative understanding of the molecular mechanism of the protective effect of EES on PC12 cells at the molecular transcription level, and Dusp5, Dusp6, Gadd45b, Gadd45g, and Pdgfc may be potential novel targets for antidepressant treatment.

Corticosterone
B7469-5.1 ApexBio 10 mM (in 1mL DMSO) 129.6 EUR

Corticosterone
B7469-50 ApexBio 50 mg 142.8 EUR

Corticosterone
HY-B1618 MedChemExpress 10mM/1mL 151.2 EUR

Corticosterone
TBW01169 ChemNorm 20mg Ask for price

Porcine corticosterone / corticosterone (CORT) ELISA Kit
QY-E40120 Qayee Biotechnology 96T 480 EUR

Corticosterone Antibody
10101-05011 AssayPro 150 ug 260.4 EUR

Corticosterone Antibody
10121-05011 AssayPro 150 ug 260.4 EUR

Corticosterone Antibody
40101-05011 AssayPro 150 ug 260.4 EUR

Corticosterone-BSA
80-1062 Fitzgerald 500 ug 360 EUR

Corticosterone-OVA
80-1063 Fitzgerald 500 ug 360 EUR

Corticosterone-BSA
80-1432 Fitzgerald 1 mg 781.2 EUR

Corticosterone-OVA
80-1433 Fitzgerald 1 mg 781.2 EUR

Corticosterone ELISA kit
55R-IB79112 Fitzgerald 96 wells 694.8 EUR

corticosterone monoclonal antibody
10R-11485 Fitzgerald 1 mg 891.6 EUR

Corticosterone Standard, 125UL
C043-125UL Arbor Assays 125UL 147.6 EUR

Corticosterone Standard, 625UL
C043-625UL Arbor Assays 625UL 272.4 EUR

Corticosterone Standard, 125UL
C151-125UL Arbor Assays 125UL 147.6 EUR

Corticosterone Standard, 625UL
C151-625UL Arbor Assays 625UL 272.4 EUR

Corticosterone EIA Kit
SKT-205-96 Stressmarq 1 plate of 96 wells 426 EUR

Corticosterone 21-Acetate Antibody
10091-05011 AssayPro 150 ug 260.4 EUR

Corticosterone (17-Deoxycortisol) Antibody
20-abx171929 Abbexa
  • 376.80 EUR
  • 927.60 EUR
  • 493.20 EUR
  • 184.80 EUR
  • 309.60 EUR
  • 100 ug
  • 1 mg
  • 200 ug
  • 20 ug
  • 50 ug

Corticosterone (17-Deoxycortisol) (BSA)
20-abx165674 Abbexa
  • 693.60 EUR
  • 309.60 EUR
  • 2064.00 EUR
  • 828.00 EUR
  • 510.00 EUR
  • 100 ug
  • 10 ug
  • 1 mg
  • 200 ug
  • 50 ug

Corticosterone (17-Deoxycortisol) (OVA)
20-abx165675 Abbexa
  • 693.60 EUR
  • 309.60 EUR
  • 2064.00 EUR
  • 828.00 EUR
  • 510.00 EUR
  • 100 ug
  • 10 ug
  • 1 mg
  • 200 ug
  • 50 ug

Corticosterone (17-Deoxycortisol) Antibody
20-abx101153 Abbexa
  • 477.60 EUR
  • 159.60 EUR
  • 1296.00 EUR
  • 644.40 EUR
  • 360.00 EUR
  • 100 ug
  • 10 ug
  • 1 mg
  • 200 ug
  • 50 ug

Corticosterone and Adrenocorticotrophic Hormone Secretion Is Recovered after Immune Challenge or Acute Restraint Stress in Sepsis Survivor Animals

Background: Clinical and experimental studies report a dysregulation of hypothalamus-pituitary-adrenal (HPA) axis during sepsis that causes impairment in hormone secretion in the late phase contributing for the pathophysiology of the disease. However, it is unclear whether this alteration persists even after the disease remission.
Methods: We evaluated the effect of an immune challenge or restraint stress on the hormone secretion of HPA axis in sepsis survivor rats. Sepsis was induced by cecal ligation-puncture (CLP) surgery. Naive or animals that survive 5 or 10 days after CLP were submitted to lipopolysaccharide (LPS) injection or restraint stress. After 60 min, blood was collected for plasma nitrate, cytokines, adrenocorticotropic hormone (ACTH), and corticosterone (CORT) and brain for synaptophysin and hypothalamic cytokines.
Results: Five days survivor animals showed increased plasma nitrate (p < 0.001) and interleukin (IL)-1β levels (p < 0.05) that were abolished in the 10 days survivors. In the hypothalamus of both survivors, the reverse was seen with IL-6 increased (p < 0.01), while IL-1β did not show any alteration. Synaptophysin expression was reduced in both survivors and did not change after any stimuli. Only the LPS administration increased plasma and/or inflammatory mediators levels in both groups (survivors and naive) being apparently lower in the survivors. There was no difference in the increased secretion pattern of ACTH and CORT observed in the naive and sepsis survivor animals submitted to immune challenge or restraint stress.
Conclusion: We conclude that the HPA axis is already recovered soon after 5 days of sepsis induction responding with normal secretion of ACTH and CORT when required.

Coexistence of Renin-independent Aldosterone Secretion and Multiple Endocrine Neoplasia Type 1 Within a Family

by
Primary aldosteronism (PA) is a state of renin-independent aldosterone secretion that can range from subclinical to overt. Some normotensive individuals for whom PA screening is not routinely recommended are reported to fulfill the loading test criterion used for the diagnosis of PA. Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by the development of various endocrine tumors. Cases of PA associated with MEN1 have been reported; however, there has been no previous report on renin-independent aldosterone secretion within a family with MEN1. Herein, we present the case of a normotensive family presenting with both MEN1 and renin-independent aldosterone secretion. A 49-year-old man was admitted to our hospital for PA evaluation owing to the plasma aldosterone concentration/plasma renin activity ratio being greater than the screening cut-off value; the patient was normotensive.
The patient had a history of left nephrectomy and adrenalectomy for left renal carcinoma and adrenal tumor at the age of 39 years. Subsequently, he was diagnosed with MEN1 concurrent with primary hyperparathyroidism, insulinoma, and novel MEN1 gene mutations (c.655-5_655-4insC and c.818delC). The loading tests for PA confirmation, including saline infusion, and furosemide upright and captopril challenge tests, yielded positive findings, confirming a case of renin-independent aldosterone secretion. The patient’s mother, brother, and sister were also genetically or clinically diagnosed with MEN1. All of them were also normotensive and confirmed to have renin-independent aldosterone secretion. The coexistence of renin-independent aldosterone secretion and MEN1 within this family suggests a relationship between the 2 entities.

Compromised blood flow in the optic nerve head after systemic administration of 2 aldosterone in rats: A possible rat model of retinal ganglion cell loss

Purpose: To investigate the optic nerve head (ONH) blood flow, retinal vessel diameters, and retinal ganglion cell (RGC) loss after systemic administration of aldosterone in rats.
Methods: Aldosterone (80 μg/kg/day) or vehicle was administered using an osmotic minipump in Brown Norway rats. The mean blur rate in the vessel (MV) and tissue (MT) regions and retinal vessel diameters in the ONH were measured by laser speckle flowgraphy before and 1, 2, and 4 weeks after administration of aldosterone or vehicle. Intraocular pressure (IOP), blood pressure, and heart rate were recorded. The retrogradely labeled RGCs were counted in the retinal flatmounts prepared 5 weeks after treatment.
Results: The MV and MT in the aldosterone group significantly decreased at 2 and 4 weeks (MV: 2 weeks, P = 0.001, 4 weeks, P < 0.001; MT: 2 weeks, P = 0.02, 4 weeks, P = 0.03). The artery and vein diameters significantly decreased at 1, 2, and 4 weeks in the aldosterone group (all P < 0.001). The MV, MT, and vessel diameters remained unchanged in the vehicle group. Other parameters did not change over time in either group. RGC counts were significantly lower in the aldosterone group than in the vehicle group (P < 0.001).
Conclusions: ONH blood flow decreased following retinal vessel constriction without changes in IOP or blood pressure in a possible rat model of RGC loss by systemic administration of aldosterone.

Ocular Distribution of the Renin-Angiotensin-Aldosterone System in the Context of the SARS-CoV-2 Pandemic

The COVID-19 pandemic has resulted in an unprecedented impact on global health, economy, and way of life. SARS-CoV-2, the virus responsible for the disease, utilizes the ACE2 receptor found on host cells to mediate entry, replication, and infection. Numerous studies have elucidated the presence of many components of the renin-angiotensin-aldosterone system (RAAS) in the eye, including the ACE2 receptor. Considering this, and the anatomical vulnerability that the exposed ocular surface offers with its interconnectedness to the respiratory system, there is a theoretical risk of pathogen entry from the ocular route as well as the development of COVID-19-associated eye disease.
Despite this, the actual epidemiological data demonstrates low ocular symptoms, possibly due to differing ACE2 receptor expression across age, ethnicity, and sex coupled with the protective properties of tears. We summarize the current literature on ocular RAAS with specific focus on the ACE2 receptor and its interplay with the SARS-CoV-2 virus.

Report from the HarmoSter study: impact of calibration on comparability of LC-MS/MS measurement of circulating cortisol, 17OH-progesterone and aldosterone

Objectives: Liquid chromatography-tandem mass spectrometry (LC-MS/MS) is recommended for measuring circulating steroids. However, assays display technical heterogeneity. So far, reproducibility of corticosteroid LC-MS/MS measurements has received scant attention. The aim of the study was to compare LC-MS/MS measurements of cortisol, 17OH-progesterone and aldosterone from nine European centers and assess performance according to external quality assessment (EQA) materials and calibration.
Methods: Seventy-eight patient samples, EQA materials and two commercial calibration sets were measured twice by laboratory-specific procedures. Results were obtained by in-house (CAL1) and external calibrations (CAL2 and CAL3). We evaluated intra and inter-laboratory imprecision, correlation and agreement in patient samples, and trueness, bias and commutability in EQA materials.
Results: Using CAL1, intra-laboratory CVs ranged between 2.8-7.4%, 4.4-18.0% and 5.2-22.2%, for cortisol, 17OH-progesterone and aldosterone, respectively. Trueness and bias in EQA materials were mostly acceptable, however, inappropriate commutability and target value assignment were highlighted in some cases. CAL2 showed suboptimal accuracy. Median inter-laboratory CVs for cortisol, 17OH-progesterone and aldosterone were 4.9, 11.8 and 13.8% with CAL1 and 3.6, 10.3 and 8.6% with CAL3 (all p<0.001), respectively. Using CAL1, median bias vs. all laboratory-medians ranged from -6.6 to 6.9%, -17.2 to 7.8% and -12.0 to 16.8% for cortisol, 17OH-progesterone and aldosterone, respectively. Regression lines significantly deviated from the best fit for most laboratories. Using CAL3 improved cortisol and 17OH-progesterone between-method bias and correlation.
Conclusions: Intra-laboratory imprecision and performance with EQA materials were variable. Inter-laboratory performance was mostly within specifications. Although residual variability persists, adopting common traceable calibrators and RMP-determined EQA materials is beneficial for standardization of LC-MS/MS steroid measurements.

Aldosterone
HY-113313 MedChemExpress 10mM/1mL 524.4 EUR

Aldosterone
B2153-25 Biovision each 966 EUR

Aldosterone
B2153-5 Biovision each 288 EUR

Aldosterone Antibody
10011-05011 AssayPro 150 ug 260.4 EUR

Aldosterone Antibody
10021-05011 AssayPro 150 ug 260.4 EUR

Aldosterone Antibody
41011-05011 AssayPro 150 ug 260.4 EUR

Aldosterone Antibody
abx021121-02mg Abbexa 0.2 mg 1011.6 EUR

Aldosterone Antibody
abx022859-1ml Abbexa 1 ml 1028.4 EUR

Aldosterone Diacetate Antibody
10031-05011 AssayPro 150 ug 260.4 EUR

Aldosterone 3 antibody
20-AR23 Fitzgerald 1 ml 300 EUR

Aldosterone (ALD) Antibody
abx415727-1ml Abbexa 1 ml 526.8 EUR

Aldosterone (ALD) Antibody
abx411014-02mg Abbexa 0.2 mg 678 EUR

Aldosterone (ALD) Antibody
abx411018-02mg Abbexa 0.2 mg 678 EUR

Aldosterone (ALD) Antibody
abx411019-02mg Abbexa 0.2 mg 678 EUR

Aldosterone (ALD) Antibody
abx411068-1ml Abbexa 1 ml 526.8 EUR

Aldosterone (ALD) Antibody
abx411069-01ml Abbexa 0.1 ml 526.8 EUR

Aldosterone Standard, 125UL
C182-125UL Arbor Assays 125UL 147.6 EUR

Aldosterone Standard, 625UL
C182-625UL Arbor Assays 625UL 272.4 EUR

Aldosterone ELISA Kit
E4342-100 Biovision each 966 EUR

Aldosterone (ALD) ELISA Kit
20-abx150317 Abbexa
  • 9004.80 EUR
  • 4795.20 EUR
  • 1111.20 EUR
  • 10 × 96 tests
  • 5 × 96 tests
  • 96 tests

Aldosterone Synthase (ALDOS) Antibody
20-abx171154 Abbexa
  • 1011.60 EUR
  • 526.80 EUR
  • 1 mg
  • 200 ug

Aldosterone (ALD) ELISA Kit
abx514362-96tests Abbexa 96 tests 801.6 EUR

Aldosterone (ALD) ELISA Kit
abx575139-96tests Abbexa 96 tests 801.6 EUR

Aldosterone (ALD) CLIA Kit
20-abx490318 Abbexa
  • 9567.60 EUR
  • 5095.20 EUR
  • 1177.20 EUR
  • 10 × 96 tests
  • 5 × 96 tests
  • 96 tests

Aldosterone Synthase (ALDOS) Antibody
20-abx175315 Abbexa
  • 1412.40 EUR
  • 693.60 EUR
  • 1 mg
  • 200 ug

Sheep Aldosterone ELISA Kit
DEIA3117 Creative Diagnostics 96T 1126.8 EUR

High Prevalence of Autonomous Aldosterone Production in Hypertension: How to Identify and Treat It

Purpose of review: Primary aldosteronism (PA) affects millions of individuals worldwide. When unrecognized, PA leads to cardiovascular and renal complications via mechanisms independent from those mediated by hypertension. In this review, we emphasize the importance of PA screening in at-risk populations, and we provide options for customized PA therapy, with consideration for a variety of clinical care settings.
Recent findings: Compelling evidence puts PA at the forefront of secondary hypertension etiologies. Cardiovascular and renal damage likely begins in early stages of renin-independent aldosterone excess. PA must be considered not only in patients with resistant hypertension or hypokalemia, but also when hypertension is associated with obstructive sleep apnea or atrial fibrillation, or in those with early-onset hypertension. Screening with plasma aldosterone and renin is widely accessible, and targeted PA therapy can successfully circumvent the excess cardiorenal risk relative to equivalent primary hypertension. Identifying and treating PA in early stages provide opportunities for personalized hypertension therapy in a large number of patients. Additionally, early targeted therapy of PA is essential for pivoting the care of such patients from reactive to preventive of cardiovascular and renal morbidity and mortality.

Comparison and commutability study between standardized liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS) and chemiluminescent enzyme immunoassay for aldosterone measurement in blood

by
A commutability confirmation test for the blood aldosterone measurement was performed on liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS) as a designated comparison method (DCM) and four chemiluminescent enzyme immunoassay (CLEIA) measurement procedures based on metrological traceability. A conventional radioimmunoassay (RIA) and two measurement procedures of CLEIA which obtains RIA equivalent values were also compared. The relationship between the DCM value and the CLEIA value with respect to 120 pg/mL of the RIA value, which is the screening criterion of primary aldosteronism (PA) was clarified. For the correlation test, 75 samples of patient serum and plasma were used. Regression analysis revealed that the standardized LC-MS/MS and four CLEIA measurement procedures were in good agreement.
This is the effect of measurement specificity and calibration using by certified reference material (CRM). The median of the LC-MS/MS corresponding to 120 pg/mL of RIA was 48.5 pg/mL. In the mean of standardized four CLEIA values corresponding to the 48.5 pg/mL of LC-MS/MS value was 47.51 pg/mL and the standard deviation (SD) was 2.93 pg/mL. However, the correlation between the RIA value and the RIA equivalent of the two measurement procedures by CLEIA differed depending on the measurement procedure. This is due to the influence of RIA measurement performance. Standardized CLEIA measurements are suitable for routine measurement procedure. When converting the LC-MS/MS equivalent value by the standardized CLEIA to the conventional RIA value, it is necessary to use the conversion formula.

Comparisons of plasma aldosterone and renin data between an automated chemiluminescent immunoanalyzer and conventional radioimmunoassays in the screening and diagnosis of primary aldosteronism

Determining values of plasma renin activity (PRA) or plasma active renin concentration (ARC), plasma aldosterone concentration (PAC), and aldosterone-to-renin ratio (ARR) is essential to diagnose primary aldosteronism (PA), but it takes several days with conventional radioimmunoassays (RIAs). Chemiluminescent enzyme immunoassays for PAC and ARC using the Accuraseed® immunoanalyzer facilitated the determination, but relations between Accuraseed® immunoanalyzer-based and RIA-based values in samples of PA confirmatory tests and adrenal venous sampling remained to be elucidated. We addressed this issue in the present study. This is a prospective, cross-sectional study. ARC and PAC values were measured by the Accuraseed® immunoanalyzer in samples, in which PRA and PAC values had been measured by the PRA-FR® RIA and SPAC®-S Aldosterone kits, respectively. The relations between Accuraseed® immunoanalyzer-based and RIA-based values were investigated with regression analyses. The optimal cutoff of Accuraseed® immunoanalyzer-based ARR for PA screening was determined by the receiver operating characteristic analysis.
After log-log transformations, linear relations with high coefficients of determination were observed between Accuraseed® immunoanalyzer-based and RIA-based data of renin and aldosterone. Following the PA guidelines of Japan Endocrine Society, Accuraseed® immunoanalyzer-based cutoffs were calculated from the regression equations: the basal PAC for PA screening >12 ng/dL, PAC for the saline infusion test >8.2 ng/dL, ARC for the furosemide-upright test <15 pg/mL, and ARR for the captopril challenge test >3.09 ng/dL per pg/mL. The optimal cutoff of Accuraseed® immunoanalyzer-based ARR for PA screening was >2.43 ng/dL over pg/mL not to overlook bilateral PA patients. The present study provided conversion formulas between Accuraseed® immunoanalyzer-based and RIA-based values of renin, aldosterone, and ARR, not only in basal samples but also in samples of PA confirmatory tests and adrenal venous sampling. Although validation studies are awaited, the present study will become priming water of harmonization of renin and aldosterone immunoassays.

Novel chemiluminescent immunoassay to measure plasma aldosterone and plasma active renin concentrations for the diagnosis of primary aldosteronism

  • Determination of plasma aldosterone concentrations (PAC) and plasma active renin concentrations (ARC) is essential for the diagnosis of primary aldosteronism (PA). In Japan, although PAC and ARC are measured by radioimmunoassay and immunoradiometric assay, respectively, non-radioisotopic methods with better detection sensitivity, measurement accuracy, and technical simplicity are needed. We developed two-site sandwich chemiluminescent enzyme immunoassays (CLEIAs) to measure both PAC and ARC using monoclonal antibodies immobilized onto ferrite particles. The results of both assays are obtained simultaneously from a single plasma sample within 30 min using a fully automated system.
  • The novel CLEIAs were validated using plasma samples from patients with PA (n = 52) and essential hypertension (n = 23). The PAC determined by the CLEIA was significantly correlated with that measured by liquid chromatography/mass spectrometry or conventional radioimmunoassay. The ARC determined by the CLEIA was significantly correlated with that measured by immunoradiometric assay. The limits of detection of the CLEIAs for PAC and ARC were 0.1 ng/dl and 0.04 pg/ml, respectively, which were better than those of conventional methods (PAC: 2.5 ng/dl; ARC: 5 pg/ml).
  • The PAC and PAC/ARC ratio (ARR) were significantly higher, and the ARC significantly lower, in patients with PA than in those with essential hypertension. An ARR cut-off of 1.31 ng/dl per pg/ml showed a sensitivity of 96.2% and specificity of 78.3% for PA screening. The newly developed CLEIAs for measuring PAC and ARC could provide a clinically powerful alternative to conventional methods used for hypertension screening in clinical practice.

Feasibility of Screening Primary Aldosteronism by Aldosterone-to-Direct Renin Concentration Ratio Derived from Chemiluminescent Immunoassay Measurement: Diagnostic Accuracy and Cutoff Value.

<AbstractText>Aldosterone-to-plasma renin activity ratio (ARR) derived from traditional radioimmunoassay (RIA) is widely used to detect primary aldosteronism (PA). Recently, aldosterone-to-direct renin concentration ratio (ADRR), which is calculated by direct renin concentration (DRC) measured by chemiluminescent immunoassay (CLIA), is proposed to replace ARR as the screening test method for PA. The purpose of the present study was to estimate the diagnostic accuracy and cutoff value of ADRR as screening test for PA.</AbstractText><AbstractText>450 hypertensive patients with suspected PA referred to hypertension center of our department were enrolled and underwent screening and confirmatory tests of PA. Plasma renin activity (PRA), DRC, and plasma aldosterone concentration (PAC) were measured by both RIA and CLIA simultaneously during screening and confirmatory test.</AbstractText><AbstractText>386 patients were diagnosed as primary hypertension (PH) and 64 patients as PA.
Within-patient correlation between PRA and DRC (r=0.88, P<0.001) and correlation between PAC measured by RIA and CLIA were high (r=0.80, P<0.001). The optimal cutoff value of ADRR was 2.93 (ng/dL)/(mU/L), sensitivity 80.33%, and specificity 92.11%. The optimal cutoff value of ARR was 25.28 (ng/dL)/(ng/mL/h), sensitivity 76.92%, and specificity 93.38%.</AbstractText><AbstractText>The optimal cutoff values of ADRR and ARR for screening PA are defined in this patient cohort with high sensitivity and specificity. Our results are of clinical importance for accelerating the extensive use of ADRR as a screening test for PA in daily practice.

Aldosterone
HY-113313 MedChemExpress 10mM/1mL 524.4 EUR

Aldosterone
B2153-25 Biovision each 966 EUR

Aldosterone
B2153-5 Biovision each 288 EUR

Aldosterone Antibody
10011-05011 AssayPro 150 ug 260.4 EUR

Aldosterone Antibody
10021-05011 AssayPro 150 ug 260.4 EUR

Aldosterone Antibody
41011-05011 AssayPro 150 ug 260.4 EUR

Aldosterone Antibody
abx021121-02mg Abbexa 0.2 mg 1011.6 EUR

Aldosterone Antibody
abx022859-1ml Abbexa 1 ml 1028.4 EUR

Aldosterone Diacetate Antibody
10031-05011 AssayPro 150 ug 260.4 EUR

Aldosterone 3 antibody
20-AR23 Fitzgerald 1 ml 300 EUR

Aldosterone (ALD) Antibody
abx415727-1ml Abbexa 1 ml 526.8 EUR

Aldosterone (ALD) Antibody
abx411014-02mg Abbexa 0.2 mg 678 EUR

Aldosterone (ALD) Antibody
abx411018-02mg Abbexa 0.2 mg 678 EUR

Aldosterone (ALD) Antibody
abx411019-02mg Abbexa 0.2 mg 678 EUR

Aldosterone (ALD) Antibody
abx411068-1ml Abbexa 1 ml 526.8 EUR

Aldosterone (ALD) Antibody
abx411069-01ml Abbexa 0.1 ml 526.8 EUR

Aldosterone Standard, 125UL
C182-125UL Arbor Assays 125UL 147.6 EUR

Aldosterone Standard, 625UL
C182-625UL Arbor Assays 625UL 272.4 EUR

Aldosterone ELISA Kit
E4342-100 Biovision each 966 EUR

Hypersensitive ECL Chemiluminescent Substrate
abx090658-50ml Abbexa 50 ml 260.4 EUR

Corticosterone Chemiluminescent CLIA kit
K014-C1 Arbor Assays 1x96 well plate 444 EUR

cAMP ELISA Kit (Chemiluminescent)
STA-501 Cell Biolabs 96 assays 706.8 EUR

cAMP ELISA Kit (Chemiluminescent)
STA-501-5 Cell Biolabs 5 x 96 assays 2558.4 EUR

cGMP ELISA Kit (Chemiluminescent)
STA-506 Cell Biolabs 96 assays 706.8 EUR

cGMP ELISA Kit (Chemiluminescent)
STA-506-5 Cell Biolabs 5 x 96 assays 2558.4 EUR

GCN5 Chemiluminescent Assay Kit
50079L BPS Bioscience 96 rxns. 465 EUR

UTX Chemiluminescent Assay Kit
50615 BPS Bioscience 96 rxns. 715 EUR

TET1 Chemiluminescent Assay Kit
50651 BPS Bioscience 96 rxns. 725 EUR

Diagnostic accuracy of aldosterone and renin measurement by chemiluminescent immunoassay and radioimmunoassay in primary aldosteronism.

Up to 50% of hypertensive patients should be screened for primary aldosteronism, using the aldosterone to renin (or plasma renin activity) ratio [aldosterone to active renin ratio (AARR) and aldosterone to plasma renin activity ratio (ARR), respectively]. Aim of the study was to prospectively compare the diagnostic accuracy of AARR (measured by chemiluminescent immunoassay) and ARR (measured by radioimmunoassay) as screening tests for primary aldosteronism and aldosterone assays (measured by chemiluminescence and radioimmunoassay) during confirmatory testing.
METHODS
One hundred patients were screened for primary aldosteronism and 34 underwent confirmatory testing. The cut-offs for ARR and AARR were 30 ng/dl/ng/ml/h and 3.7 ng/dl/mU/l, respectively. Patients with positive confirmatory test underwent subtype diagnosis.
RESULTS
Seventy-five patients were essential hypertensive patients, 15 had idiopathic hyperaldosteronism, five aldosterone-producing adenoma (APA) and five with undefined diagnosis. The AARR displayed a sensitivity of 90% and a specificity of 99%, the ARR had a sensitivity of 100% and a specificity of 73%. Of the two of 20 primary aldosteronism patients missed by AARR, none resulted affected by APA. All primary aldosteronism patients were correctly diagnosed by chemiluminescence at confirmatory testing. In the total sample of 168 measurements both the correlation for plasma renin activity with renin and for aldosterone in chemiluminescence and radioimmunoassay were highly significant (ρ = 0.70, P < 0.001 and ρ = 0.78, P < 0.001, respectively). On receiver operator characteristics curves, the area under the curve for AARR was 0.989 [95% confidence interval (CI) 0.97-1] and 0.934 for ARR (95% CI 0.89-0.98), which were not significantly different.
CONCLUSIONS
The automated aldosterone and renin chemiluminescent assay is a reliable alternative to the radioimmunometric method, especially for APA detection.

Safety and Effectiveness of Oral Methylprednisolone Therapy in Comparison With Intramuscular Adrenocorticotropic Hormone and Oral Prednisolone in Children With Infantile Spasms

by
Background and Purpose: To assess the safety and effectiveness of oral methylprednisolone (oMP) in comparison with intramuscular adrenocorticotropic hormone (imACTH) and oral prednisolone (oP) therapies in children with infantile spasms (IS).
Methods: In this prospective, open-label, non-blinded, uncontrolled observational study, children (aged 2-24 months) with newly diagnosed IS presenting with hypsarrhythmia or its variants on electroencephalogram (EEG) were included. It was followed by imACTH, oP, or oMP (32-48 mg/day for 2 weeks followed by tapering) treatments. Electroclinical remission/spasm control, relapse, and adverse effects were evaluated in the short-term (days 14 and 42) and intermediary-term (3, 6, and 12 months) intervals.
Results: A total of 320 pediatric patients were enrolled: 108, 107, and 105 in the imACTH, oMP, and oP groups, respectively. The proportion of children achieving electroclinical remission on days 14 and 42 was similar among the three groups (day 14: 53.70 vs. 60.75 vs. 51.43%, p = 0.362; day 42: 57.55 vs. 63.46 vs. 55.34%, p = 0.470). The time to response was significantly faster in the oMP group (6.5 [3.00, 10.00] days vs. 8.00 [5.00, 11.00] days for imACTH and 8.00 [5.00, 13.00] days for oP, p = 0.025). Spasm control at 3, 6, and 12 months was also similar in the three groups (P = 0.775, 0.667, and 0.779). The relapse rate in the imACTH group (24.10%) was lower than oMP (30.77%) and oP groups (33.33%), and the time taken for relapse in the imACTH group (79.00 [56.50, 152.00] days) was longer than oMP (62.50 [38.00, 121.75] days) and oP groups (71.50 [40.00, 99.75] days), but the differences were not statistically significant (p = 0.539 and 0.530, respectively). The occurrence of adverse effects was similar among the three groups.
Conclusions: The short and intermediary-term efficacy and recurrence rates of oMP are not inferior to those of imACTH and oP for the treatment of IS. Significantly, the time to achieve electroclinical remission with oMP was quicker than that with imACTH and oP. Considering its convenience, affordability, and the absence of irreversible side effects, oMP can serve as a form of first-line treatment for newly diagnosed IS.

Adrenocorticotropic Hormone-Independent Cushing Syndrome with Right Adrenal Adenoma and HIV Infection: A Case Report

Background: Adrenocorticotropic hormone (ACTH)-independent Cushing’s syndrome (CS) with right adrenal adenoma combined with HIV infection has rarely been reported.
Case presentation: A 39-year-old Chinese male patient with HIV infection was admitted to our hospital due to increased blood pressure in the previous 2 years and weight gain in the previous 6 months. Endocrinological examinations showed that blood cortisol (8 a.m.) was 22.23 μg/dl, the level of ACTH (8 a.m.) was less than 1pg/ml and twenty-four-hour urinary cortisol was 1429 μg/24h. ACTH-independent CS was diagnosed based on low ACTH levels (<1.00 pg/ml), a lack of cortisol circadian rhythms, and unsuppressed cortisol levels by dexamethasone. The ultrasonography and multislice spiral computed tomography scan revealed a right adrenal mass. Due to the HIV status of the patient, we measured the count of CD4+ T helper cells. Laparoscopic right adrenal resection was performed after the CD4+ T helper cell count was > 200 cells/μl. Subsequent immunohistochemical staining confirmed right adrenal adenoma.
Results: The postoperative recovery was good, and wound healing was possible. After surgical treatment, endocrinological examinations indicated that the level of ACTH increased and the levels of serum cortisol and twenty-four-hour urinary cortisol decreased, which indicated that CS was controlled. CD4/CD8 was 0.47 at reexamination, and the patient’s immunity was improved.
Conclusion: Due to the potential side effects of steroid drugs, clinicians should use these medications with caution and closely monitor the development of adrenal deficiency.

Comparison of Bolus and Continuous Infusion of Adrenocorticotropic Hormone During Adrenal Vein Sampling

Background: Adrenocorticotropic hormone (ACTH) is widely used in adrenal vein sampling (AVS) and can be administered as a bolus injection or continuous infusion. The optimal administration method has not been determined. We aimed to compare the effects of ACTH bolus with infusion on cannulation success, lateralization assessment and adverse events (AEs).
Methods: Retrospectively collected data from patients with primary aldosteronism who underwent AVS with ACTH at a tertiary hospital in China. Rate of successful cannulation, lateralization index (LI), complete biochemical remission and AEs related to AVS were analyzed.
Results: The study included 80 patients receiving ACTH bolus and 94 receiving infusions. The rate of successful cannulation was comparable between bolus and infusion groups (75/80, 93.4% vs 88/94, 93.6%). In those with successful cannulation, the bolus group had a higher selectivity index than the infusion group, while LI [6.4(1.8-17.5) vs. 7.6(2.0-27.8), P=0.48] and rate of complete biochemical remission (43/44, 97.7% vs 53/53, 100%, P=0.45) did not significantly differ between the two groups. One in the bolus and one patient in the infusion group had adrenal vein rupture but they recovered with conservative treatment. The bolus group reported more transient AEs such as palpitation (52.9% vs 2.2%) and abdominal discomfort (40.0% vs 2.2%) than the infusion group.
Conclusions: Due to their similar effects on cannulation success and lateralization, but a lower rate of transient AEs in the infusion group, the continuous infusion method should be recommended for ACTH stimulation in AVS.

Cushing’s syndrome caused by intra-adrenocortical adrenocorticotropic hormone in a dog

A 13-year-old Labrador retriever was diagnosed with Cushing’s syndrome (CS) caused by primary bilateral nodular adrenocortical hyperplasia with adrenocorticotropic hormone (ACTH) expression. The pituitary origin of CS was ruled out by suppression of plasma ACTH concentration and absence of a proliferative lesion on histological evaluation of the pituitary gland using periodic acid-Schiff (PAS) staining, reticulin staining, and immunostaining for ACTH. A pheochromocytoma also was found at necropsy examination.
On histological evaluation of both adrenal glands, at the junction of the fascicular and glomerular zones, multiple cell clusters distributed in both hyperplastic adrenal cortices expressed ACTH, whereas the pheochromocytoma cells did not. These results indicate that a disease similar to primary bilateral macronodular adrenocortical hyperplasia in humans also occurs in dogs, with intra-adrenocortical expression of ACTH, glucocorticoids excess, and clinical signs of CS. Therefore, the term ACTH-independent could be inappropriate in some cases of bilateral adrenocortical hyperplasia and suppressed plasma ACTH concentration in dogs.

Adrenocorticotropic Hormone
7-02131 CHI Scientific 2mg Ask for price

Adrenocorticotropic Hormone
7-02132 CHI Scientific 10mg Ask for price

Adrenocorticotropic Hormone
7-02133 CHI Scientific 50mg Ask for price

Adrenocorticotropic Hormone Protein
20-abx262167 Abbexa
  • 393.60 EUR
  • 276.00 EUR
  • 910.80 EUR
  • 10 mg
  • 2 mg
  • 50 mg

Adrenocorticotropic Hormone Protein
20-abx262825 Abbexa
  • 393.60 EUR
  • 7676.40 EUR
  • 276.00 EUR
  • 10 ug
  • 1 mg
  • 2 µg

Adrenocorticotropic Hormone siRNA
20-abx929248 Abbexa
  • 661.20 EUR
  • 878.40 EUR
  • 15 nmol
  • 30 nmol

Adrenocorticotropic Hormone siRNA
20-abx929249 Abbexa
  • 661.20 EUR
  • 878.40 EUR
  • 15 nmol
  • 30 nmol

Human Adrenocorticotropic Hormone
RP-1503 Alpha Diagnostics 2 mg 196.8 EUR

ACTH (Adrenocorticotropic Hormone)
RA21005 Neuromics 50 ug 412.8 EUR

Adrenocorticotropic Hormone (ACTH) Antibody
20-abx142154 Abbexa
  • 444.00 EUR
  • 727.20 EUR
  • 376.80 EUR
  • 100 ul
  • 200 ul
  • 50 ul

Adrenocorticotropic Hormone (ACTH) Antibody
20-abx002196 Abbexa
  • 493.20 EUR
  • 710.40 EUR
  • 218.40 EUR
  • 376.80 EUR
  • 100 ul
  • 200 ul
  • 20 ul
  • 50 ul

Adrenocorticotropic Hormone (ACTH) Antibody
20-abx110467 Abbexa
  • 493.20 EUR
  • 2214.00 EUR
  • 718.80 EUR
  • 218.40 EUR
  • 360.00 EUR
  • 100 ug
  • 1 mg
  • 200 ug
  • 20 ug
  • 50 ug

Adrenocorticotropic Hormone (ACTH) Antibody
20-abx110468 Abbexa
  • 493.20 EUR
  • 2214.00 EUR
  • 718.80 EUR
  • 218.40 EUR
  • 360.00 EUR
  • 100 ug
  • 1 mg
  • 200 ug
  • 20 ug
  • 50 ug

Adrenocorticotropic Hormone (ACTH) Antibody
20-abx131811 Abbexa
  • 393.60 EUR
  • 978.00 EUR
  • 510.00 EUR
  • 184.80 EUR
  • 309.60 EUR
  • 100 ug
  • 1 mg
  • 200 ug
  • 20 ug
  • 50 ug

Adrenocorticotropic Hormone (ACTH) Antibody
abx021118-1mg Abbexa 1 mg 1328.4 EUR

Adrenocorticotropic Hormone (ACTH) Antibody
abx021119-1mg Abbexa 1 mg 1328.4 EUR

Adrenocorticotropic Hormone (pS168) Antibody
abx032093-400ul Abbexa 400 ul 627.6 EUR

Adrenocorticotropic Hormone (pS168) Antibody
abx032093-80l Abbexa 80 µl 343.2 EUR

Adrenocorticotropic Hormone (ACTH) Antibody
abx430970-200ul Abbexa 200 ul 460.8 EUR

Adrenocorticotropic Hormone (ACTH) Antibody
20-abx175278 Abbexa
  • 477.60 EUR
  • 159.60 EUR
  • 1312.80 EUR
  • 644.40 EUR
  • 376.80 EUR
  • 100 ug
  • 10 ug
  • 1 mg
  • 200 ug
  • 50 ug

Adrenocorticotropic Hormone (ACTH) Antibody
20-abx175279 Abbexa
  • 1479.60 EUR
  • 710.40 EUR
  • 1 mg
  • 200 ug

ACTH Adrenocorticotropic Hormone protein
PROTP01189-1 BosterBio Regular: 10mg 380.4 EUR

Adrenocorticotropic Hormone Receptor (ACTHR) Antibody
20-abx171115 Abbexa
  • 1095.60 EUR
  • 560.40 EUR
  • 1 mg
  • 200 ug

Adrenocorticotropic Hormone Receptor (MC2R) Antibody
20-abx002183 Abbexa
  • 493.20 EUR
  • 710.40 EUR
  • 218.40 EUR
  • 376.80 EUR
  • 100 ul
  • 200 ul
  • 20 ul
  • 50 ul

Adrenocorticotropic Hormone Receptor (ACTHR) Antibody
20-abx015269 Abbexa
  • 376.80 EUR
  • 117.60 EUR
  • 477.60 EUR
  • 594.00 EUR
  • 100 ug
  • 10 ug
  • 200 ug
  • 300 µg

Adrenocorticotropic Hormone (4-10) Peptide
20-abx265056 Abbexa
  • 427.20 EUR
  • 644.40 EUR
  • 343.20 EUR
  • 10 mg
  • 25 mg
  • 5 mg

Exercise-induced adrenocorticotropic hormone response is cooperatively regulated by hypothalamic arginine vasopressin and corticotrophin-releasing hormone

Introduction: Exercise becomes a stress when performed at an intensity above the lactate threshold (LT) because at that point the plasma adrenocorticotropic hormone (ACTH), a marker of stress response, increases. It is possible that the exercise-induced ACTH response is regulated at least by arginine vasopressin (AVP) and possibly by corticotropin-releasing hormone (CRH), but this remains unclear. To clarify the involvement of these factors, it is useful to intervene pharmacologically in the regulatory mechanisms, with a physiologically acceptable exercise model.
Methods: We used a special stress model of treadmill running (aerobic exercise) for male Wistar rats, which mimic the human physiological response, where plasma ACTH levels increase at just above the LT for 30 min. Animals were administered the AVP V1b receptor antagonist SSR149415 (SSR) and/or the CRH type 1 receptor antagonist CP154526 (CP) intraperitoneally before the exercise, which allowed the monitoring of exercise-induced ACTH response. Immunocytochemical evaluation of activated AVP and CRH neurons with exercise was performed for the animals’ hypothalami.
Results: A single injection of either antagonist, SSR or CP, resulted in inhibited ACTH levels after exercise stress. Moreover, the combined injection of SSR and CP strongly suppressed ACTH secretion during treadmill running to a greater extent than each alone. The running-exercise-induced activation of both AVP and CRH neurons in the hypothalamus was also confirmed.
Conclusion: These results lead us to hypothesize that AVP and CRH are cooperatively involved in exercise-induced ACTH response just above the LT. This may also reflect the stress response with moderate-intensity exercise in humans.

A 4-hour Profile of 17-hydroxyprogesterone in Salt-wasting Congenital Adrenal Hyperplasia: Is the Serial Monitoring Strategy Worth the Effort?

by
Objective: Since there exists no gold standard laboratory variable for adjustment of treatment in congenital adrenal hyperplasia (CAH), we aimed to assess the use of a 4-hour profile of serum 17-OHP to determine the most appropriate time and level of 17-OHP in predicting the metabolic control and evaluate the role of sex hormone-binding globulin (SHBG) in hyperandrogenemia.
Methods: This study included 16 children (9 girls,7 boys; median age 7 years) with salt-wasting CAH. Measurements for 17-OHP and cortisol were made from samples obtained before and 1,2,4 hours after the morning dose of hydrocortisone. Patients were designated to have poor metabolic control when androstenedione levels according to age and sex-specific reference intervals were high and annual height SDS changes were ⩾0.5.
Results: Premedication 17-OHP levels were strongly correlated with 17-OHP levels 1, 2, 4 hours after the morning dose (rs=0.929, p<0.01; rs=0.943, p<0.01; rs=0.835, p<0.01, respectively). 17-OHP profiles (0,1,2,4 hours) of poor (n=6) and good (n=10) metabolically controlled cases were similar. Among the patients with poor metabolic control, two cases had 17-OHP levels <2 ng/mL at all times. Remaining patients with poor metabolic control had 17-OHP levels above 104 ng/mL, 82 ng/mL, 14 ng/mL, and 4 ng/mL, for baseline and 1, 2, and 4 hours, respectively. Differences between the poor and well-controlled group were androstenedione levels with respect to upper limit of normal [1.8(1.5) and 0.5(1.5) ng/mL, respectively p=0.03], annual change in height SDS [0.7(0.2) and -0.03(0.8) SDS, respectively, p=0.001], and daily hydrocortisone doses [7 (6) and 16 (8) mg/m2/day, respectively, p=0.02]. Androstenedione and SHBG levels were negatively correlated in the pubertal children (rs=-0.7, p=0.04).
Conclusion: We conclude that (i)a 4-hour 17-OHP profile is not useful in predicting hyperandrogenemia, (ii)suppressed levels of 17-OHP do not always indicate overtreatment, (iii)reference intervals of 17-OHP for different time periods might be of importance, (iv) low hydrocortisone doses should be avoided, (v)SHBG could be used in pubertal children as an indicator of hyperandrogenemia.

Eligibility, Utilization, and Effectiveness of 17-Alpha Hydroxyprogesterone Caproate (17OHPC) in a Statewide Population-Based Cohort of Medicaid Enrollees

Objectives: The primary objective was to estimate the initiation and adherence rates of 17 α-hydroxyprogesterone caproate (17OHPC) among eligible mothers in a statewide population-based cohort of Medicaid enrollees. The secondary objectives were to (1) determine the association of maternal sociodemographic and clinical characteristics with 17OHPC utilization and (2) assess the real-world effectiveness of 17OHPC on recurrent preterm birth prevention and admission to neonatal intensive care unit (NICU).
Study design: This is a retrospective cohort study using a linked, longitudinal administrative dataset of birth certificates and medical assistance claims. Medicaid-enrolled mothers in Pennsylvania were included in this study if they had at least one singleton live birth from 2014 to 2016 following at least one spontaneous preterm birth. Maternal Medicaid claims were used to ascertain the use of 17OHPC from various manufacturers, including compounded formulations. Propensity score matching was used to create a covariate balance between 17OHPC treatment and comparison groups.
Results: We identified 4,781 Medicaid-covered 17OHPC-eligible pregnancies from 2014 to 2016 in Pennsylvania, 3.4% of all Medicaid-covered singleton live births. The population-based initiation rate was 28.5% among eligible pregnancies. Among initiators, 50% received ≥16 doses as recommended, while 10% received a single dose only. The severity of previous spontaneous preterm birth was the strongest predictor for the initiation and adherence of 17OHPC. In the matched treatment (n = 1,210) and comparison groups (n = 1,210), we found no evidence of 17OHPC effectiveness. The risks of recurrent preterm birth (relative risk [RR] 1.10, 95% confidence interval [CI] 0.97-1.24) and births admitted to NICU (RR 1.00, 95% CI 0.84-1.18) were similar in treated and comparison mothers.
Conclusion: The 17OHPC-eligible population represented 3.4% of singleton live births. Less than one-third of eligible mothers initiated treatment. Among initiators, 50% were treatment adherent. We found no difference in the risk of recurrent preterm birth or admission to NICU between treatment and comparison groups.

A Possible Mechanism of Action of 17α-Hydroxyprogesterone Caproate: Enhanced IL-10 Production

Objective: The rate of recurrent spontaneous preterm birth (PTB) was reduced by 33% in the Maternal-Fetal Medicine Unit (MFMU) Network trial of 17α-hydroxyprogesterone caproate (17-OHPC), but the mechanism of action, 17 years later, remains elusive. The robustness of the interleukin-10 (IL-10) response to lipopolysaccharide (LPS) stimulation of leukocytes in pregnant women with a prior PTB correlates with gestational age at delivery. This study sought to determine if there is a relationship between the concentration of 17-OHPC and response to LPS stimulation.
Study design: We performed a secondary analysis of data from the Omega-3 MFMU trial which evaluated the effectiveness of omega-3 fatty acid supplementation in reducing recurrent PTB. We utilized previously characterized data from a subanalyses of the Omega-3 trial of IL-10 and tumor necrosis factor alpha (TNF-α) levels from peripheral blood mononuclear cells stimulated with LPS. Blood was obtained from enrolled women at 16 to 22 weeks’ gestation (baseline) and 25 to 28 weeks’ gestation (posttreatment). All women received 17-OHPC and plasma 17-OHPC concentrations were measured at 25 to 28 weeks’ gestation. We analyzed these data to determine if there was a relationship between 17-OHPC concentration and cytokine production. We then performed an in vitro study to determine if 17-OHPC could directly alter cytokine production by THP-1-derived macrophages.
Results: In the clinical samples, we found that 17-OHPC plasma concentrations were correlated with the quantity of the LPS-stimulated production of IL-10. TNF-α production after LPS stimulation was unrelated to 17-OHPC concentration. In the in vitro study, we demonstrate a 17-OHPC concentration dependent increase in IL-10 production.
Conclusion: In women receiving 17-OHPC for PTB prevention, we demonstrate a relationship between plasma 17-OHPC and LPS-stimulated IL-10 production by circulating leukocytes. We also demonstrate that, in vitro, 17-OHPC treatment affects IL-10 production by LPS-stimulated macrophages. Collectively, these findings support an immunomodulatory mechanism of action of 17-OHPC in the prevention of recurrent PTB.
Product not found

In utero exposure to 17α-hydroxyprogesterone caproate and risk of cancer in offspring

Background: 17α-hydroxyprogesterone caproate (17-OHPC) is a synthetic progestogen initially approved in the 1950s to treat gynecological and obstetrical conditions. Despite repeated concerns of safety and short-term efficacy regarding the use of 17-OHPC for the prevention of preterm birth in pregnant women, little is known about long-term effects of 17-OHPC on health of offspring.
Objective: To examine the association between in utero exposure to 17-OHPC and risk of cancer in offspring.
Study design: The Child Health and Development Studies is a population-based cohort of more than 18,000 mother-child dyads receiving prenatal care in the Kaiser Foundation Health Plan (Oakland, California) between 1959 and 1966. Clinical information was abstracted from mothers’ medical records beginning six months prior to pregnancy through delivery. We identified the number and timing of 17-OHPC injections during pregnancy. Incident cancers diagnosed in offspring were ascertained through 2019 by linkage to the California Cancer Registry. We used Cox proportional hazards models to estimate adjusted hazard ratios (aHR) and their 95% confidence intervals, with follow-up time accrued from date of birth through date of cancer diagnosis, death, or last contact.
Results: 1,008 offspring were diagnosed with cancer over 730,817 person-years of follow-up. About 1.0% of offspring (n=234) were exposed in utero to 17-OHPC. Exposure in the first trimester was associated with increased risk of any cancer (aHR 2.57, 95% CI 1.59, 4.15), and risk increased with number of injections (1-2 injections: aHR 1.80, 95% CI 1.12,2.90; ≥3 injections: aHR 3.07, 95% CI 1.34, 7.05). Exposure in the second or third trimester conferred an additional risk for male (aHR 2.59, 95% CI 1.07, 6.28) but not female (aHR 0.30, 0.04, 1.11) offspring. Risk of colorectal (aHR 5.51, 95% CI 1.73, 17.59), prostate (aHR 5.10, 95% CI 1.24, 21.00), and pediatric brain (aHR 34.72, 95% CI 7.29, 164.33) cancer was higher in offspring first exposed to 17-OHPC in the first trimester compared to offspring not exposed.