Cell-type specific interaction of endothelin and the nitric oxide system: pattern of prepro-ET1 expression in kidneys of L-NAME treated prepro-ET1 promoter-lacZ-transgenic mice.

  • 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.

Endothelin 1 (ET-1) Antibody

abx024086-100ug Abbexa 100 ug 1128 EUR

Endothelin-1 (ET-1), big (Rat)

023-32 PHOENIX PEPTIDE 100 μg 206.28 EUR

ET-1(Endothelin-1) ELISA Kit

EKF60092-48T Biomatik Corporation 48T 396.9 EUR

ET-1(Endothelin-1) ELISA Kit

EKF60092-5x96T Biomatik Corporation 5x96T 2693.25 EUR

ET-1(Endothelin-1) ELISA Kit

EKF60092-96T Biomatik Corporation 96T 567 EUR

ET-1(Endothelin-1) ELISA Kit

EU0205 FN Test 96T 628.92 EUR

Endothelin-1 (ET-1), big (Human)

023-10 PHOENIX PEPTIDE 100 μg 154.44 EUR

Porcine endothelin-1 (ET-1) ELISA Kit

QY-E40122 Qayee Biotechnology 96T 480 EUR

Rat Endothelin 1 (ET-1) CLIA Kit

abx195562-96tests Abbexa 96 tests 990 EUR

Rat ET-1 -Endothelin 1- CLIA Kit

E-CL-R0121-24Tests Elabscience Biotech 24 Tests 180 EUR

Rat ET-1 -Endothelin 1- CLIA Kit

E-CL-R0121-48Tests Elabscience Biotech 48 Tests 546 EUR

Rat ET-1 -Endothelin 1- CLIA Kit

E-CL-R0121-96Tests Elabscience Biotech 96 Tests 682 EUR

Rat ET-1 -Endothelin 1- CLIA Kit

E-CL-R0121-96Tests10 Elabscience Biotech 96 Tests *10 6820 EUR

Rat ET-1 -Endothelin 1- CLIA Kit

E-CL-R0121-96Tests5 Elabscience Biotech 96 Tests *5 3410 EUR

Endothelin-1 (ET-1) ELISA Kit (1 Plate)

K045-H1 Arbor Assays 1x96 well plate 644 EUR

Endothelin-1 (ET-1), big (Human) - Antibody

H-023-10 PHOENIX PEPTIDE 50 μl 238.68 EUR

Dog Endothelin 1,ET-1 Elisa Kit

EK762013 AFG Bioscience LLC 96 Wells 0.93 EUR

Rat ET-1(Endothelin 1) ELISA Kit

EKF57841-48T Biomatik Corporation 48T 396.9 EUR

Rat ET-1(Endothelin 1) ELISA Kit

EKF57841-5x96T Biomatik Corporation 5x96T 2693.25 EUR

Rat ET-1(Endothelin 1) ELISA Kit

EKF57841-96T Biomatik Corporation 96T 567 EUR

Rat Endothelin 1(ET-1) Elisa Kit

EK720590 AFG Bioscience LLC 96 Wells 0.58 EUR

rat Endothelin 1,ET-1 ELISA Kit

EKC38988-48T Biomatik Corporation 48T 535.99 EUR

rat Endothelin 1,ET-1 ELISA Kit

EKC38988-5x96T Biomatik Corporation 5x96T 3637.08 EUR

rat Endothelin 1,ET-1 ELISA Kit

EKC38988-96T Biomatik Corporation 96T 765.7 EUR

Dog Endothelin 1,ET-1 ELISA Kit

EKC32040-48T Biomatik Corporation 48T 535.99 EUR

Dog Endothelin 1,ET-1 ELISA Kit

EKC32040-5x96T Biomatik Corporation 5x96T 3637.08 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

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 248 EUR

Multi-Species Creatinine Detection Kit for Plasma and Serum

IMLCRKTPS Innovative research each 395 EUR

Urine Creatinine Detection Kit

SKT-200-192 Stressmarq 2 plates of 96 wells 226 EUR

Creatinine Urinary Detection Kit (2 Plate)

K002-H1 Arbor Assays 2x96 well plates 296 EUR

Creatinine Urinary Detection Kit (10 Plate)

K002-H5 Arbor Assays 10x96 well plates 1182 EUR

OKAU00002-2PLATE - Creatinine Urinary Detection Kit

OKAU00002-2PLATE Aviva Systems Biology 2plate 259 EUR

Multi-Species Creatinine Detection Kit for Urine

IMLCRKTBF Innovative research each 387 EUR

OKAU00002-10PLATE - Creatinine Urinary Detection Kit

OKAU00002-10PLATE Aviva Systems Biology 10plate 879 EUR

Creatinine Serum Kit (2 Plate)

KB02-H1 Arbor Assays 2x96 well plates 302 EUR

Creatinine Serum Kit (4 Plate)

KB02-H2 Arbor Assays 4x96 well plates 484 EUR

OKAU00065-1PLATE - Creatinine Serum Kit

OKAU00065-1PLATE Aviva Systems Biology 1plate 379 EUR

OKAU00065-2PLATE - Creatinine Serum Kit

OKAU00065-2PLATE Aviva Systems Biology 2plate 269 EUR

OKAU00065-4PLATE - Creatinine Serum Kit

OKAU00065-4PLATE Aviva Systems Biology 4plate 439 EUR

DetectX® Creatinine Reagent, 20ML

C004-20ML Arbor Assays 20ML 254 EUR

DetectX® Creatinine Reagent, 50ML

C004-50ML Arbor Assays 50ML 360 EUR

Creatinine Serum Low Sample Volume Kit (384-well Plate)

KB02-H1D Arbor Assays 1x384 well plate 431 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

591968 MedKoo Biosciences 25.0g 220 EUR

Creatinine

09626-34 NACALAI TESQUE 5G 11.55 EUR

Creatinine

09626-92 NACALAI TESQUE 25G 25.2 EUR

Creatinine

B1717-1000 ApexBio 1g 34 EUR

Creatinine

B1717-50 ApexBio 50 mg 153.6 EUR

Creatinine

B1717-5000 ApexBio 5g 48 EUR

Creatinine

C271-100MG TOKU-E 100 mg 223.26 EUR

Creatinine

C271-25MG TOKU-E 25 mg 63.73 EUR

Creatinine

CB0328 Bio Basic 5g 68.35 EUR

Creatinine

C781500 Toronto Research Chemicals 10g 74 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.

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

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.

Porcine corticosterone / corticosterone (CORT) ELISA Kit

QY-E40120 Qayee Biotechnology 96T 480 EUR

Corticosterone

540089 MedKoo Biosciences 500.0mg 190 EUR

Corticosterone

DE4164 Demeditec Diagnostics 96 136 EUR

Corticosterone

B7469-5.1 ApexBio 10 mM (in 1mL DMSO) 40 EUR

Corticosterone

B7469-50 ApexBio 50 mg 42 EUR

Corticosterone

C695700 Toronto Research Chemicals 100mg 68 EUR

Corticosterone

HY-B1618 MedChemExpress 10mM/1mL 151.2 EUR

Corticosterone

GP3184-500 Glentham Life Sciences 500 75.1 EUR

Corticosterone

RM2080-100MG EWC Diagnostics 1 unit 58.29 EUR

Corticosterone

T0948L-10mg TargetMol Chemicals 10mg Ask for price

Corticosterone

T0948L-1g TargetMol Chemicals 1g Ask for price

Corticosterone

T0948L-1mg TargetMol Chemicals 1mg Ask for price

Corticosterone

T0948L-50mg TargetMol Chemicals 50mg Ask for price

Corticosterone

T0948L-5mg TargetMol Chemicals 5mg Ask for price

Corticosterone

TBW01169 ChemNorm 20mg Ask for price

Corticosterone-13C3

C695703 Toronto Research Chemicals 10mg 12800 EUR

Corticosterone 95%

C25690 Pfaltz & Bauer 100MG 176 EUR

Corticosterone [HRP]

DAG2977 Creative Diagnostics 1 mL 844.2 EUR

Corticosterone-BSA

80-1062 Fitzgerald 500 ug 250 EUR

Corticosterone-OVA

80-1063 Fitzgerald 500 ug 250 EUR

Corticosterone-BSA

80-1432 Fitzgerald 1 mg 592 EUR

Corticosterone-OVA

80-1433 Fitzgerald 1 mg 592 EUR

Corticosterone Antibody

10101-05011 AssayPro 150 ug 175 EUR

Corticosterone Antibody

10121-05011 AssayPro 150 ug 260.4 EUR

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

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

DE5298 Demeditec Diagnostics 96 167 EUR

Aldosterone

A514700 Toronto Research Chemicals 10mg 385 EUR

Aldosterone

HY-113313 MedChemExpress 10mM/1mL 524.4 EUR

ALDOSTERONE

GWB-7B83DD GenWay Biotech 1x96 Assays Ask for price

Aldosterone

T19186-10mg TargetMol Chemicals 10mg Ask for price

Aldosterone

T19186-1g TargetMol Chemicals 1g Ask for price

Aldosterone

T19186-1mg TargetMol Chemicals 1mg Ask for price

Aldosterone

T19186-50mg TargetMol Chemicals 50mg Ask for price

Aldosterone

T19186-5mg TargetMol Chemicals 5mg Ask for price

Aldosterone-13C3

A514701 Toronto Research Chemicals 10mg 51000 EUR

Aldosterone 99%

A12930 Pfaltz & Bauer 5MG 315.49 EUR

Aldosterone [BSA]

DAG2958 Creative Diagnostics 1 mg 1720 EUR

Aldosterone-d4

A514703 Toronto Research Chemicals 25mg 17000 EUR

Aldosterone-d8

T19185-10mg TargetMol Chemicals 10mg Ask for price

Aldosterone-d8

T19185-1g TargetMol Chemicals 1g Ask for price

Aldosterone-d8

T19185-1mg TargetMol Chemicals 1mg Ask for price

Aldosterone-d8

T19185-50mg TargetMol Chemicals 50mg Ask for price

Aldosterone-d8

T19185-5mg TargetMol Chemicals 5mg Ask for price

Aldosterone ELISA

T31001 101Bio 1 x 96-well 499 EUR

Aldosterone Antibody

abx021121-02mg Abbexa 0.2 mg 1011.6 EUR

Aldosterone Antibody

abx022859-1ml Abbexa 1 ml 1028.4 EUR

Aldosterone Antibody

10011-05011 AssayPro 150 ug 175 EUR

Aldosterone Antibody

10021-05011 AssayPro 150 ug 260.4 EUR

Aldosterone Antibody

41011-05011 AssayPro 150 ug 260.4 EUR

Aldosterone Antibody

GWB-549349 GenWay Biotech 0.2 mg Ask for price

Aldosterone Antibody

GWB-5887E8 GenWay Biotech 1 ml Ask for price

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.

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

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

rAP-2571 Angio Proteomie Inquiry Ask for price

ACTH (Adrenocorticotropic Hormone)

RA21005 Neuromics 50 ug 412.8 EUR

Adrenocorticotropic Hormone siRNA

20-abx929248 Abbexa
  • Ask for price
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  • 15 nmol
  • 30 nmol

Adrenocorticotropic Hormone siRNA

20-abx929249 Abbexa
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  • 15 nmol
  • 30 nmol

Human Adrenocorticotropic Hormone

RP-1503 Alpha Diagnostics 2 mg 196.8 EUR

Adrenocorticotropic Hormone Protein

20-abx262825 Abbexa
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  • 10 ug
  • 1 mg
  • 2 µg

Adrenocorticotropic Hormone Protein

20-abx262167 Abbexa
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  • 10 mg
  • 2 mg
  • 50 mg

Adrenocorticotropic Hormone (34-39) Peptide

20-abx265802 Abbexa
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  • 10 mg
  • 25 mg
  • 5 mg

Adrenocorticotropic Hormone (11-24) Peptide

20-abx266458 Abbexa
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  • 10 mg
  • 25 mg
  • 5 mg

Adrenocorticotropic Hormone (18-39) Peptide

abx265083-10mg Abbexa 10 mg 750 EUR

Adrenocorticotropic Hormone (18-39) Peptide

abx265083-1mg Abbexa 1 mg 237.5 EUR

Adrenocorticotropic Hormone (18-39) Peptide

abx265083-5mg Abbexa 5 mg 500 EUR

Adrenocorticotropic Hormone (12-39) Peptide

abx265586-100tests Abbexa 100 tests 600 EUR

Adrenocorticotropic Hormone (12-39) Peptide

abx265586-200tests Abbexa 200 tests 925 EUR

Adrenocorticotropic Hormone (12-39) Peptide

abx265586-50tests Abbexa 50 tests 275 EUR

Adrenocorticotropic Hormone (34-39) Peptide

abx265802-100tests Abbexa 100 tests 212.5 EUR

Adrenocorticotropic Hormone (34-39) Peptide

abx265802-200tests Abbexa 200 tests 287.5 EUR

Adrenocorticotropic Hormone (34-39) Peptide

abx265802-500tests Abbexa 500 tests 462.5 EUR

Adrenocorticotropic Hormone (11-24) Peptide

abx266458-1ml Abbexa 1 ml 525 EUR

Adrenocorticotropic Hormone (11-24) Peptide

abx266458-200l Abbexa 200 µl 350 EUR

Adrenocorticotropic Hormone (22-39) Peptide

abx266770-1ml Abbexa 1 ml 425 EUR

Adrenocorticotropic Hormone (22-39) Peptide

abx266770-200l Abbexa 200 µl 212.5 EUR

Adrenocorticotropic Hormone (4-10) Peptide

20-abx265056 Abbexa
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  • 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?

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.

HROS Detection Kit

FLAPF100-2 Cell Technology 150 Tests 280 EUR

Human Uncharacterized protein C17orf53 (HROB) ELISA Kit

abx508495-96tests Abbexa 96 tests 687.5 EUR

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.

Clinical Response to Apatinib Combined With Brain Radiotherapy in EGFR Wild-Type and ALK-Negative Lung Adenocarcinoma With Multiple Brain Metastases.

Clinical Response to Apatinib Combined With Brain Radiotherapy in EGFR Wild-Type and ALK-Negative Lung Adenocarcinoma With Multiple Brain Metastases.

Background: Brain radiotherapy is the usual remedy possibility for a number of mind metastases (BMs) from non-small cell lung most cancers (NSCLC), particularly in the absence of a driver mutation. However, the prognosis for such sufferers stays poor. Apatinib is a potent antiangiogenic compound directed on the vascular endothelial progress issue receptor-2 (VEGFR-2); nevertheless, to date, there are not any investigations of apatinib concurrent with mind radiotherapy for NSCLC sufferers with BMs.

We report a case of EGFR wild-type and ALK-negative lung adenocarcinoma affected person with a number of symptomatic BMs, who obtained apatinib along with mind radiation remedy. A positive oncologic consequence was achieved for each mind metastatic lesions and the first pulmonary tumor. Case Presentation: A 61-year-old feminine (by no means smoker) who initially offered with headache and dizziness was recognized with lung adenocarcinoma with a number of mind metastasis (cT2aN3M1b stage IV), and was unfavorable for EGFR and ALK.

The affected person refused to obtain chemotherapy and was solely amenable to mind radiotherapy and focused remedy. After approval from the institutional ethics committee, she underwent concurrent oral apatinib (500 mg/day) with complete mind radiation remedy (WBRT) (37.5Gy) with simultaneous in-field increase (49.5Gy) in 15 fractions with picture guided intensity-modulated radiotherapy.

Three weeks later, neurologic signs totally ceased and a partial response (PR) for the BMs with near-complete decision of peritumoral mind edema was achieved. Chest CT carried out on the identical time and confirmed shrinkage of the lung main with a PR.

The affected person suffered grade III oral mucositis one week after mind radiotherapy and refused additional apatinib. At 12 months after mind radiotherapy, the mind tumors remained properly managed. Conclusions: This is the primary identified documentation of a speedy medical response of apatinib concurrent with mind radiotherapy in a lung adenocarcinoma affected person with symptomatic a number of BMs. Apatinib mixed with mind radiotherapy could possibly be another remedy possibility for BMs from NSCLC, particularly for these with no driver mutation. Further medical trials are required to corroborate this discovery.

Clinical Response to Apatinib Combined With Brain Radiotherapy in EGFR Wild-Type and ALK-Negative Lung Adenocarcinoma With Multiple Brain Metastases.
Clinical Response to Apatinib Combined With Brain Radiotherapy in EGFR Wild-Type and ALK-Negative Lung Adenocarcinoma With Multiple Brain Metastases.

Pattern of Pediatric Supracondylar Fracture Operated at A Rural Teaching Hospital of Nepal: A Descriptive Cross-sectional Study.

Supracondylar fracture of humerus is likely one of the frequent pediatric fractures encountered in our every day medical observe. The goal of this examine is to decide the sample of supracondylar fracture operated at rural educating hospital of Jumla, Karnali Nepal.A descriptive cross sectional examine was carried out at Jumla, Karnali after Institutional Review Committee approval.

Operating room notes from 15 May 2017 to 16 November 2019 had been retrieved to collect the next data: sufferers tackle, age, intercourse, aspect, harm mechanism, displacement, neurovascular harm, concurrent accidents, preliminary administration by conventional bone setters, time between harm and surgical procedure, operative method.

NOD2 Peptide

45-973P ProSci 0.1 mg 405.6 EUR
Description: (IN) CARD15 / NOD2 Peptide

Nod2 antibody

10R-6553 Fitzgerald 100 ug 218 EUR
Description: Rat monoclonal Nod2 antibody

NOD2 Antibody

24158 SAB 100ul 479 EUR

NOD2 Antibody

24158-100ul SAB 100ul 468 EUR

NOD2 Antibody

24159 SAB 100ul 479 EUR

NOD2 Antibody

24159-100ul SAB 100ul 468 EUR

NOD2 Antibody

2511-002mg ProSci 0.02 mg 206.18 EUR
Description: NOD2 Antibody: Apaf-1 and NOD1 are members of a new family, which are involved in the regulation of apoptosis and immune response. Each of them contains a caspase recruitment domain (CARD) and a nucleotide-binding oligomerization domain (NOD). A third member in this family was recently identified and designated NOD2. NOD2 interacts with RICK via a homophilic CARD-CARD interaction. NOD2 activates NF-κB, which is regulated by its carboxy-terminal leucine-rich repeat domain that acts as an intracellular receptor for components of bacteria. The variants of NOD2, either a frameshift or a missense, were associated with Crohn's disease that is a main type of chronic inflammatory bowel disease.

NOD2 Antibody

2511-01mg ProSci 0.1 mg 523.7 EUR
Description: NOD2 Antibody: Apaf-1 and NOD1 are members of a new family, which are involved in the regulation of apoptosis and immune response. Each of them contains a caspase recruitment domain (CARD) and a nucleotide-binding oligomerization domain (NOD). A third member in this family was recently identified and designated NOD2. NOD2 interacts with RICK via a homophilic CARD-CARD interaction. NOD2 activates NF-κB, which is regulated by its carboxy-terminal leucine-rich repeat domain that acts as an intracellular receptor for components of bacteria. The variants of NOD2, either a frameshift or a missense, were associated with Crohn's disease that is a main type of chronic inflammatory bowel disease.

NOD2 Antibody

2513-002mg ProSci 0.02 mg 206.18 EUR
Description: NOD2 Antibody: Apaf-1 and NOD1 are members of a new family, which are involved in the regulation of apoptosis and immune response. Each of them contains a caspase recruitment domain (CARD) and a nucleotide-binding oligomerization domain (NOD). A third member in this family was recently identified and designated NOD2. NOD2 interacts with RICK via a homophilic CARD-CARD interaction. NOD2 activates NF-κB, which is regulated by its carboxy-terminal leucine-rich repeat domain that acts as an intracellular receptor for components of bacteria. The variants of NOD2, either a frameshift or a missense, were associated with Crohn's disease that is a main type of chronic inflammatory bowel disease.

NOD2 Antibody

2513-01mg ProSci 0.1 mg 523.7 EUR
Description: NOD2 Antibody: Apaf-1 and NOD1 are members of a new family, which are involved in the regulation of apoptosis and immune response. Each of them contains a caspase recruitment domain (CARD) and a nucleotide-binding oligomerization domain (NOD). A third member in this family was recently identified and designated NOD2. NOD2 interacts with RICK via a homophilic CARD-CARD interaction. NOD2 activates NF-κB, which is regulated by its carboxy-terminal leucine-rich repeat domain that acts as an intracellular receptor for components of bacteria. The variants of NOD2, either a frameshift or a missense, were associated with Crohn's disease that is a main type of chronic inflammatory bowel disease.

NOD2 Antibody

37460 SAB 100ul 319 EUR

NOD2 Antibody

37460-100ul SAB 100ul 302.4 EUR

NOD2 Antibody

1-CSB-PA015915GA01HU Cusabio
  • Ask for price
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  • 150ul
  • 50ul
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, WB

NOD2 Antibody

E037460 EnoGene 100μg/100μl 255 EUR
Description: Available in various conjugation types.

NOD2 Antibody

E91323 EnoGene 100ul 255 EUR
Description: Available in various conjugation types.

NOD2 Antibody

DF12125 Affbiotech 200ul 420 EUR

NOD2 Antibody

DF12125-100ul Affinity Biosciences 100ul 280 EUR

NOD2 Antibody

DF12125-200ul Affinity Biosciences 200ul 350 EUR

NOD2 antibody

70R-18913 Fitzgerald 50 ul 289 EUR
Description: Rabbit polyclonal NOD2 antibody

NOD2 Antibody

1-CSB-PA446192 Cusabio
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  • 100ul
  • 50ul
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, IHC;ELISA:1:2000-1:5000, IHC:1:50-1:200

NOD2 Antibody

1-CSB-PA876985 Cusabio
  • Ask for price
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  • 100ul
  • 50ul
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, IHC;ELISA:1:1000-1:2000, IHC:1:25-1:100

NOD2 Antibody

1-CSB-PA881021LA01HU Cusabio
  • Ask for price
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  • 100ug
  • 50ug
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, IHC, IF; Recommended dilution: IHC:1:20-1:200, IF:1:50-1:200

NOD2 Antibody

R34436-100UG NSJ Bioreagents 100 ug 339.15 EUR
Description: Additional name(s) for this target protein: Nucleotide-binding oligomerization domain-containing protein 2, caspase recruitment domain family, member 15; CARD15

NOD2 Rabbit pAb

A15992-100ul Abclonal 100 ul 369.6 EUR

NOD2 Rabbit pAb

A15992-200ul Abclonal 200 ul 550.8 EUR

NOD2 Rabbit pAb

A15992-20ul Abclonal 20 ul 219.6 EUR

NOD2 Rabbit pAb

A15992-50ul Abclonal 50 ul 267.6 EUR

NOD2 Rabbit pAb

E2861510 EnoGene 100ul 225 EUR
Description: Biotin-Conjugated, FITC-Conjugated , AF350 Conjugated , AF405M-Conjugated ,AF488-Conjugated, AF514-Conjugated ,AF532-Conjugated, AF555-Conjugated ,AF568-Conjugated , HRP-Conjugated, AF405S-Conjugated, AF405L-Conjugated , AF546-Conjugated, AF594-Conjugated , AF610-Conjugated, AF635-Conjugated , AF647-Conjugated , AF680-Conjugated , AF700-Conjugated , AF750-Conjugated , AF790-Conjugated , APC-Conjugated , PE-Conjugated , Cy3-Conjugated , Cy5-Conjugated , Cy5.5-Conjugated , Cy7-Conjugated Antibody

NOD2 Rabbit pAb

E2161510 EnoGene 100ul 225 EUR
Description: Biotin-Conjugated, FITC-Conjugated , AF350 Conjugated , AF405M-Conjugated ,AF488-Conjugated, AF514-Conjugated ,AF532-Conjugated, AF555-Conjugated ,AF568-Conjugated , HRP-Conjugated, AF405S-Conjugated, AF405L-Conjugated , AF546-Conjugated, AF594-Conjugated , AF610-Conjugated, AF635-Conjugated , AF647-Conjugated , AF680-Conjugated , AF700-Conjugated , AF750-Conjugated , AF790-Conjugated , APC-Conjugated , PE-Conjugated , Cy3-Conjugated , Cy5-Conjugated , Cy5.5-Conjugated , Cy7-Conjugated Antibody

NOD2 antagonist 1

T63088-10mg TargetMol Chemicals 10mg Ask for price
Description: NOD2 antagonist 1

NOD2 antagonist 1

T63088-1g TargetMol Chemicals 1g Ask for price
Description: NOD2 antagonist 1

NOD2 antagonist 1

T63088-1mg TargetMol Chemicals 1mg Ask for price
Description: NOD2 antagonist 1

NOD2 antagonist 1

T63088-50mg TargetMol Chemicals 50mg Ask for price
Description: NOD2 antagonist 1

NOD2 antagonist 1

T63088-5mg TargetMol Chemicals 5mg Ask for price
Description: NOD2 antagonist 1

NOD2 Blocking Peptide

DF12125-BP Affbiotech 1mg 234 EUR

NOD2 Polyclonal Antibody

E915992 EnoGene 100ul 225 EUR
Description: Available in various conjugation types.

Polyclonal NOD2 Antibody

APR06297G Leading Biology 0.1 mg 790.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD2 . This antibody is tested and proven to work in the following applications:

Polyclonal NOD2 Antibody

APR06298G Leading Biology 0.1 mg 790.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD2 . This antibody is tested and proven to work in the following applications:

NOD2 Conjugated Antibody

C37460 SAB 100ul 476.4 EUR

NOD2 Polyclonal Antibody

E-AB-13109-120uL Elabscience Biotech 120uL 240 EUR
Description: Unconjugated

NOD2 Polyclonal Antibody

E-AB-13109-200uL Elabscience Biotech 200uL 399 EUR
Description: Unconjugated

NOD2 Polyclonal Antibody

E-AB-13109-20uL Elabscience Biotech 20uL 73 EUR
Description: Unconjugated

NOD2 Polyclonal Antibody

E-AB-13109-60uL Elabscience Biotech 60uL 143 EUR
Description: Unconjugated

NOD2 Polyclonal Antibody

E-AB-91396-120uL Elabscience Biotech 120uL 320 EUR
Description: Unconjugated

NOD2 Polyclonal Antibody

E-AB-91396-200uL Elabscience Biotech 200uL 530 EUR
Description: Unconjugated

NOD2 Polyclonal Antibody

E-AB-91396-60uL Elabscience Biotech 60uL 200 EUR
Description: Unconjugated

NOD2 Polyclonal Antibody

E-AB-91396-each Elabscience Biotech each Ask for price
Description: Unconjugated

Mouse Nod2 ELISA KIT

ELI-44123m Lifescience Market 96 Tests 1038 EUR

Human NOD2 ELISA KIT

ELI-23582h Lifescience Market 96 Tests 988.8 EUR

NOD2 ELISA KIT|Human

EF001273 Lifescience Market 96 Tests 826.8 EUR

NOD2 (untagged)-Human nucleotide-binding oligomerization domain containing 2 (NOD2)

SC305010 Origene Technologies GmbH 10 µg Ask for price

Bovine NOD2 ELISA KIT

ELI-22273b Lifescience Market 96 Tests 1113.6 EUR

NOD2 Antibody (C-term)

GWB-B15211 GenWay Biotech 0.1 mg Ask for price

NOD2 Antibody (C-term)

GWB-949D66 GenWay Biotech 0.05 mg Ask for price

Human NOD2 shRNA Plasmid

20-abx961935 Abbexa
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  • 150 µg
  • 300 µg

TLR2 & NOD2-Based Adjuvant

VAdv-Ly0016 Creative Biolabs 5 mg 4016.4 EUR
Description: A TLR2 & NOD2-based vaccine adjuvant.

NOD2 Antibody, HRP conjugated

1-CSB-PA881021LB01HU Cusabio
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  • 100ug
  • 50ug
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is HRP conjugated. Tested in the following application: ELISA

NOD2 Antibody, FITC conjugated

1-CSB-PA881021LC01HU Cusabio
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  • 100ug
  • 50ug
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is FITC conjugated. Tested in the following application: ELISA

OACA10693-50UG - NOD2 Antibody

OACA10693-50UG Aviva Systems Biology 50ug 179 EUR

NOD2 Rabbit Polyclonal Antibody

54121 SAB 100ul 439 EUR

NOD2 Antibody, Biotin conjugated

1-CSB-PA881021LD01HU Cusabio
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  • 100ug
  • 50ug
Description: A polyclonal antibody against NOD2. Recognizes NOD2 from Human. This antibody is Biotin conjugated. Tested in the following application: ELISA

Rabbit Polyclonal NOD2 Antibody

TA336664 Origene Technologies GmbH 100 µl Ask for price

Rabbit Polyclonal NOD2 Antibody

TA306091 Origene Technologies GmbH 100 µg Ask for price

Rabbit Polyclonal NOD2 Antibody

TA306092 Origene Technologies GmbH 100 µg Ask for price

OAPB00158-100UG - NOD2 Antibody

OAPB00158-100UG Aviva Systems Biology 0.1mg 389 EUR

OACA10693-100UG - NOD2 Antibody

OACA10693-100UG Aviva Systems Biology 100ug 319 EUR

NOD2 Rabbit Polyclonal Antibody

E10G04737 EnoGene 100 μl 275 EUR
Description: Biotin-Conjugated, FITC-Conjugated , AF350 Conjugated , AF405M-Conjugated ,AF488-Conjugated, AF514-Conjugated ,AF532-Conjugated, AF555-Conjugated ,AF568-Conjugated , HRP-Conjugated, AF405S-Conjugated, AF405L-Conjugated , AF546-Conjugated, AF594-Conjugated , AF610-Conjugated, AF635-Conjugated , AF647-Conjugated , AF680-Conjugated , AF700-Conjugated , AF750-Conjugated , AF790-Conjugated , APC-Conjugated , PE-Conjugated , Cy3-Conjugated , Cy5-Conjugated , Cy5.5-Conjugated , Cy7-Conjugated Antibody

NOD2 Rabbit Polyclonal Antibody

E10G11622 EnoGene 100 μl 275 EUR
Description: Biotin-Conjugated, FITC-Conjugated , AF350 Conjugated , AF405M-Conjugated ,AF488-Conjugated, AF514-Conjugated ,AF532-Conjugated, AF555-Conjugated ,AF568-Conjugated , HRP-Conjugated, AF405S-Conjugated, AF405L-Conjugated , AF546-Conjugated, AF594-Conjugated , AF610-Conjugated, AF635-Conjugated , AF647-Conjugated , AF680-Conjugated , AF700-Conjugated , AF750-Conjugated , AF790-Conjugated , APC-Conjugated , PE-Conjugated , Cy3-Conjugated , Cy5-Conjugated , Cy5.5-Conjugated , Cy7-Conjugated Antibody

Nod2 (untagged) - Mouse nucleotide-binding oligomerization domain containing 2 (Nod2), (10ug)

MC223222 Origene Technologies GmbH 10 µg Ask for price

NOD2 (GFP-tagged) - Human nucleotide-binding oligomerization domain containing 2 (NOD2)

RG215750 Origene Technologies GmbH 10 µg Ask for price

Nod2 ORF Vector (Rat) (pORF)

ORF071395 ABM 1.0 ug DNA 607.2 EUR

NOD2 (Myc-DDK-tagged)-Human nucleotide-binding oligomerization domain containing 2 (NOD2)

RC215750 Origene Technologies GmbH 10 µg Ask for price

Nod2 (GFP-tagged) - Mouse nucleotide-binding oligomerization domain containing 2 (Nod2), (10ug)

MG227102 Origene Technologies GmbH 10 µg Ask for price

Nod2 (Myc-DDK-tagged) - Mouse nucleotide-binding oligomerization domain containing 2 (Nod2)

MR227102 Origene Technologies GmbH 10 µg Ask for price

NOD2 ORF Vector (Human) (pORF)

ORF026166 ABM 1.0 ug DNA 486 EUR

Nod2 ORF Vector (Mouse) (pORF)

ORF051499 ABM 1.0 ug DNA 607.2 EUR

Human NOD2 knockout cell line

ABC-KH10202 AcceGen 1 vial Ask for price
Description: Human NOD2 knockout cell line is HEK293/HeLa cell line, edited by CRISPR/Cas9 technology.

Human NOD2 knockdown cell line

ABC-KD10202 AcceGen 1 vial Ask for price
Description: Human NOD2 knockdown cell line is engineered by our optimized transduction of the specific shRNA with lentivirus. Knockdown levels are determined via qRT-PCR. Gentaur offers generation of stable knockdown (RNAi) cell lines expressing shRNAs targeting genes of your interest.

Human NOD2 Protein Lysate 20ug

IHUNOD2PLLY20UG Innovative research each 361 EUR
Description: Human NOD2 Protein Lysate 20ug

NOD2 ELISA Kit (Human) (OKAN06319)

OKAN06319 Aviva Systems Biology 96 Wells 950.4 EUR
Description: Description of target: This gene is a member of the Nod1/Apaf-1 family and encodes a protein with two caspase recruitment (CARD) domains and six leucine-rich repeats (LRRs). The protein is primarily expressed in the peripheral blood leukocytes. It plays a role in the immune response to intracellular bacterial lipopolysaccharides (LPS) by recognizing the muramyl dipeptide (MDP) derived from them and activating the NFKB protein. Mutations in this gene have been associated with Crohn disease and Blau syndrome. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene.;Species reactivity: Human;Application: ELISA;Assay info: Assay Methodology: Quantitative Sandwich ELISA;Sensitivity: 0.055 ng/mL

NOD2 ELISA Kit (Mouse) (OKCA01740)

OKCA01740 Aviva Systems Biology 96 Wells 1015.2 EUR
Description: Description of target: Involved in gastrointestinal immunity. Upon stimulation by muramyl dipeptide (MDP), a fragment of bacterial peptidoglycan, binds the proximal adapter receptor-interacting RIPK2, which recruits ubiquitin ligases as XIAP, BIRC2, BIRC3 and the LUBAC complex, triggering activation of MAP kinases and activation of NF-kappa-B signaling. This in turn leads to the transcriptional activation of hundreds of genes involved in immune response (PubMed:22607974). Required for MDP-induced NLRP1-dependent CASP1 activation and IL1B release in macrophages (PubMed:18511561).;Species reactivity: Mouse;Application: ;Assay info: Assay Methodology: Quantitative Sanadwich ELISA;Sensitivity: 3.9 pg/mL

NOD2 ELISA Kit (Human) (OKCA02128)

OKCA02128 Aviva Systems Biology 96 Wells 999.6 EUR
Description: Description of target: Involved in gastrointestinal immunity. Upon stimulation by muramyl dipeptide (MDP), a fragment of bacterial peptidoglycan, binds the proximal adapter receptor-interacting RIPK2, which recruits ubiquitin ligases as XIAP, BIRC2, BIRC3 and the LUBAC complex, triggering activation of MAP kinases and activation of NF-kappa-B signaling. This in turn leads to the transcriptional activation of hundreds of genes involved in immune response. Required for MDP-induced NLRP1-dependent CASP1 activation and IL1B release in macrophages.;Species reactivity: Human;Application: ;Assay info: Assay Methodology: Quantitative Sandwich ELISA;Sensitivity: 6.25 pg/mL

NOD2 ELISA Kit (Human) (OKCD02031)

OKCD02031 Aviva Systems Biology 96 Wells 997.2 EUR
Description: Description of target: Involved in gastrointestinal immunity. Upon stimulation by muramyl dipeptide (MDP), a fragment of bacterial peptidoglycan, binds the proximal adapter receptor-interacting RIPK2, which recruits ubiquitin ligases as XIAP, BIRC2, BIRC3 and the LUBAC complex, triggering activation of MAP kinases and activation of NF-kappa-B signaling. This in turn leads to the transcriptional activation of hundreds of genes involved in immune response. Required for MDP-induced NLRP1-dependent CASP1 activation and IL1B release in macrophages.;Species reactivity: Human;Application: ;Assay info: Assay Methodology: Quantitative Sandwich Immunoassay;Sensitivity: < 0.055 ng/mL

Nod2 (untagged ORF) - Rat nucleotide-binding oligomerization domain containing 2 (Nod2), (10 ug)

RN215677 Origene Technologies GmbH 10 µg Ask for price

OCOA08638-20UG - NOD2 Protein Lysate

OCOA08638-20UG Aviva Systems Biology 20ug 269 EUR

Anti-CARD15 / NOD2 (Internal) antibody

STJ70992 St John's Laboratory 100 µg 430.8 EUR

NOD2 (untagged) - Human nucleotide-binding oligomerization domain containing 2 (NOD2), transcript variant 2

SC337777 Origene Technologies GmbH 10 µg Ask for price

OKCD02031-96W - NOD2 ELISA Kit (Human)

OKCD02031-96W Aviva Systems Biology 96Wells 675 EUR

Nod2 sgRNA CRISPR Lentivector set (Rat)

K6718501 ABM 3 x 1.0 ug 406.8 EUR

Nod2 (Myc-DDK-tagged ORF) - Rat nucleotide-binding oligomerization domain containing 2 (Nod2), (10 ug)

RR215677 Origene Technologies GmbH 10 µg Ask for price

Nod2 sgRNA CRISPR Lentivector set (Mouse)

K4411601 ABM 3 x 1.0 ug 406.8 EUR

NOD2 sgRNA CRISPR Lentivector set (Human)

K1438601 ABM 3 x 1.0 ug 406.8 EUR

Lenti ORF clone of Nod2 (mGFP-tagged) - Mouse nucleotide-binding oligomerization domain containing 2 (Nod2)

MR227102L4 Origene Technologies GmbH 10 µg Ask for price

Goat anti-CARD15 / NOD2 (Internal) Antibody

dAP-0930 Angio Proteomie 50ug 264.6 EUR

Lenti-ORF clone of NOD2 (mGFP-tagged)-Human nucleotide-binding oligomerization domain containing 2 (NOD2)

RC215750L2 Origene Technologies GmbH 10 µg Ask for price

Lenti-ORF clone of NOD2 (mGFP-tagged)-Human nucleotide-binding oligomerization domain containing 2 (NOD2)

RC215750L4 Origene Technologies GmbH 10 µg Ask for price

NOD2 (myc-DDK-tagged) - Human nucleotide-binding oligomerization domain containing 2 (NOD2), transcript variant 2

RC239883 Origene Technologies GmbH 10 µg Ask for price

Polyclonal NOD2 / CARD15 Antibody (N-Terminus)

APR02524G Leading Biology 0.05mg 580.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD2 / CARD15 (N-Terminus). This antibody is tested and proven to work in the following applications:

Polyclonal NOD2 / CARD15 Antibody (C-Terminus)

APR02525G Leading Biology 0.05mg 580.8 EUR
Description: A polyclonal antibody raised in Rabbit that recognizes and binds to Human NOD2 / CARD15 (C-Terminus). This antibody is tested and proven to work in the following applications:

NOD2 3'UTR GFP Stable Cell Line

TU065801 ABM 1.0 ml 1636.8 EUR

Nod2 3'UTR GFP Stable Cell Line

TU164191 ABM 1.0 ml Ask for price

Nod2 3'UTR GFP Stable Cell Line

TU264065 ABM 1.0 ml Ask for price

Rat Anti-Mouse NOD2 Purified (50 ug)

TA320428 Origene Technologies GmbH 50 µg Ask for price

NOD2 Protein Vector (Rat) (pPM-C-HA)

PV285580 ABM 500 ng 1399.2 EUR

Lenti-ORF clone of NOD2 (Myc-DDK-tagged)-Human nucleotide-binding oligomerization domain containing 2 (NOD2)

RC215750L1 Origene Technologies GmbH 10 µg Ask for price

Lenti-ORF clone of NOD2 (Myc-DDK-tagged)-Human nucleotide-binding oligomerization domain containing 2 (NOD2)

RC215750L3 Origene Technologies GmbH 10 µg Ask for price

Lenti ORF clone of Nod2 (Myc-DDK-tagged) - Mouse nucleotide-binding oligomerization domain containing 2 (Nod2)

MR227102L3 Origene Technologies GmbH 10 µg Ask for price

NOD2 Protein Vector (Rat) (pPB-C-His)

PV285578 ABM 500 ng 1399.2 EUR

NOD2 Protein Vector (Rat) (pPB-N-His)

PV285579 ABM 500 ng 1399.2 EUR

NOD2 Protein Vector (Rat) (pPM-C-His)

PV285581 ABM 500 ng 1399.2 EUR

NOD2 Protein Vector (Human) (pPM-C-HA)

PV104664 ABM 500 ng 973.2 EUR

NOD2 Protein Vector (Mouse) (pPM-C-HA)

PV205996 ABM 500 ng 1278 EUR

NOD2 Protein Vector (Human) (pPB-C-His)

PV104662 ABM 500 ng 973.2 EUR

NOD2 Protein Vector (Human) (pPB-N-His)

PV104663 ABM 500 ng 973.2 EUR

NOD2 Protein Vector (Human) (pPM-C-His)

PV104665 ABM 500 ng 973.2 EUR

NOD2 Protein Vector (Mouse) (pPB-C-His)

PV205994 ABM 500 ng 1278 EUR

NOD2 Protein Vector (Mouse) (pPB-N-His)

PV205995 ABM 500 ng 1278 EUR

NOD2 Protein Vector (Mouse) (pPM-C-His)

PV205997 ABM 500 ng 1278 EUR

Nod2 3'UTR Luciferase Stable Cell Line

TU114191 ABM 1.0 ml Ask for price

NOD2 3'UTR Luciferase Stable Cell Line

TU015801 ABM 1.0 ml 1636.8 EUR

Nod2 3'UTR Luciferase Stable Cell Line

TU214065 ABM 1.0 ml Ask for price

Nod2 sgRNA CRISPR Lentivector (Rat) (Target 1)

K6718502 ABM 1.0 ug DNA 184.8 EUR

Nod2 sgRNA CRISPR Lentivector (Rat) (Target 2)

K6718503 ABM 1.0 ug DNA 184.8 EUR

Nod2 sgRNA CRISPR Lentivector (Rat) (Target 3)

K6718504 ABM 1.0 ug DNA 184.8 EUR

Human NOD2 Over-expressing Stable Cell Line

ABC-X2057 AcceGen 1 vial Ask for price
Description: Gentaur can provide custom lentiviral constructs expressing any genes of interest as long as it is less than about 3 kb. Lentiviral technology enables us to efficiently generate stable expression lines which are then selected for moderate or high expressers, depending on the experimental requirements. If you are interested in specific lentiviral DNA constructs or have further questions, please contact us to discuss the details. NOD2 nucleotide-binding oligomerization domain containing 2 [ Homo sapiens ] http://www.ncbi.nlm.nih.gov/gene/64127

Nod2 sgRNA CRISPR Lentivector (Mouse) (Target 1)

K4411602 ABM 1.0 ug DNA 184.8 EUR

Nod2 sgRNA CRISPR Lentivector (Mouse) (Target 2)

K4411603 ABM 1.0 ug DNA 184.8 EUR

Nod2 sgRNA CRISPR Lentivector (Mouse) (Target 3)

K4411604 ABM 1.0 ug DNA 184.8 EUR

NOD2 sgRNA CRISPR Lentivector (Human) (Target 1)

K1438602 ABM 1.0 ug DNA 184.8 EUR

NOD2 sgRNA CRISPR Lentivector (Human) (Target 2)

K1438603 ABM 1.0 ug DNA 184.8 EUR

NOD2 sgRNA CRISPR Lentivector (Human) (Target 3)

K1438604 ABM 1.0 ug DNA 184.8 EUR

Lenti ORF particles, Nod2 (GFP-tagged) - Mouse nucleotide-binding oligomerization domain containing 2 (Nod2), 200ul, >10^7 TU/mL

MR227102L4V Origene Technologies GmbH 200 µl Ask for price

Lenti ORF particles, NOD2 (mGFP-tagged)-Human nucleotide-binding oligomerization domain containing 2 (NOD2), 200ul, >10^7 TU/mL

RC215750L2V Origene Technologies GmbH 200 µl Ask for price

Lenti ORF particles, NOD2 (mGFP-tagged)-Human nucleotide-binding oligomerization domain containing 2 (NOD2), 200ul, >10^7 TU/mL

RC215750L4V Origene Technologies GmbH 200 µl Ask for price

Lenti ORF clone of Nod2 (mGFP-tagged ORF) - Rat nucleotide-binding oligomerization domain containing 2 (Nod2), (10 ug)

RR215677L4 Origene Technologies GmbH 10 µg Ask for price

NOD2 Chemi-Luminescent ELISA Kit (Human) (OKCD03832)

OKCD03832 Aviva Systems Biology 96 Wells 1185.6 EUR
Description: Description of target: Involved in gastrointestinal immunity. Upon stimulation by muramyl dipeptide (MDP), a fragment of bacterial peptidoglycan, binds the proximal adapter receptor-interacting RIPK2, which recruits ubiquitin ligases as XIAP, BIRC2, BIRC3 and the LUBAC complex, triggering activation of MAP kinases and activation of NF-kappa-B signaling. This in turn leads to the transcriptional activation of hundreds of genes involved in immune response. Required for MDP-induced NLRP1-dependent CASP1 activation and IL1B release in macrophages .;Species reactivity: Human;Application: ;Assay info: Assay Methodology: Quantitative Sandwich ELISA;Sensitivity: 0.0412 ng/mL

CARD15 (NOD2) rabbit polyclonal antibody, Aff - Purified

AP08943PU-N Origene Technologies GmbH 50 µg Ask for price

Polyclonal Goat Anti-CARD15 / NOD2 (Internal) Antibody

APG00059G Leading Biology 0.1mg 580.8 EUR
Description: A polyclonal antibody raised in Goat that recognizes and binds to Human Goat Anti-CARD15 / NOD2 (Internal) . This antibody is tested and proven to work in the following applications:

Lenti ORF particles, Nod2 (GFP-tagged ORF) - Rat nucleotide-binding oligomerization domain containing 2 (Nod2), 200ul, >10^7 TU/mL

RR215677L4V Origene Technologies GmbH 200 µl Ask for price

Lenti ORF particles, NOD2 (Myc-DDK-tagged)-Human nucleotide-binding oligomerization domain containing 2 (NOD2), 200ul, >10^7 TU/mL

RC215750L1V Origene Technologies GmbH 200 µl Ask for price

Lenti ORF particles, NOD2 (Myc-DDK-tagged)-Human nucleotide-binding oligomerization domain containing 2 (NOD2), 200ul, >10^7 TU/mL

RC215750L3V Origene Technologies GmbH 200 µl Ask for price

Lenti ORF particles, Nod2 (Myc-DDK-tagged) - Mouse nucleotide-binding oligomerization domain containing 2 (Nod2), 200ul, >10^7 TU/mL

MR227102L3V Origene Technologies GmbH 200 µl Ask for price

Lenti ORF clone of Nod2 (Myc-DDK-tagged ORF) - Rat nucleotide-binding oligomerization domain containing 2 (Nod2), (10 ug)

RR215677L3 Origene Technologies GmbH 10 µg Ask for price

Lenti ORF particles, Nod2 (Myc-DDK-tagged ORF) - Rat nucleotide-binding oligomerization domain containing 2 (Nod2), 200ul, >10^7 TU/mL

RR215677L3V Origene Technologies GmbH 200 µl Ask for price

NOD2 Lentiviral Vector (Rat) (CMV) (pLenti-GIII-CMV)

LV645601 ABM 1.0 ug DNA 1626 EUR

NOD2 Lentiviral Vector (Rat) (UbC) (pLenti-GIII-UbC)

LV645605 ABM 1.0 ug DNA 1626 EUR

NOD2 Lentiviral Vector (Rat) (EF1a) (pLenti-GIII-EF1a)

LV645606 ABM 1.0 ug DNA 1626 EUR

OKCD03832-96W - NOD2 Chemi-Luminescent ELISA Kit (Human)

OKCD03832-96W Aviva Systems Biology 96Wells 800 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody

20-abx302321 Abbexa
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Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody

abx235781-100ug Abbexa 100 ug 661.2 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody

20-abx114240 Abbexa
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Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody

abx302321-100g Abbexa 100 µg 362.5 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody

abx302321-20g Abbexa 20 µg 162.5 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody

abx302321-50g Abbexa 50 µg 250 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody

abx114240-100l Abbexa 100 µl 612.5 EUR

CARD15 (NOD2) (C-term) rabbit polyclonal antibody, Aff - Purified

AP08944PU-N Origene Technologies GmbH 50 µg Ask for price

NOD2 (Human) - 3 unique 27mer siRNA duplexes - 2 nmol each

SR311967 Origene Technologies GmbH 2 nmol Ask for price

Nod2 (Mouse) - 3 unique 27mer siRNA duplexes - 2 nmol each

SR421708 Origene Technologies GmbH 2 nmol Ask for price

OAEB02002-100UG - Goat Anti-CARD15 / NOD2 Antibody - middle region

OAEB02002-100UG Aviva Systems Biology 100ug 349 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector set (Rat)

K6718505 ABM 3 x 1.0 ug 451.2 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector set (Mouse)

K4411605 ABM 3 x 1.0 ug 451.2 EUR

NOD2 sgRNA CRISPR/Cas9 All-in-One Lentivector set (Human)

K1438605 ABM 3 x 1.0 ug 451.2 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (HRP)

20-abx316579 Abbexa
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  • 100 ug
  • 1 mg
  • 200 ug
  • 20 ug
  • 50 ug

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (HRP)

abx316579-100g Abbexa 100 µg 362.5 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (HRP)

abx316579-20g Abbexa 20 µg 162.5 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (HRP)

abx316579-50g Abbexa 50 µg 250 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (FITC)

20-abx316580 Abbexa
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  • 100 ug
  • 1 mg
  • 200 ug
  • 20 ug
  • 50 ug

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (FITC)

abx316580-100g Abbexa 100 µg 362.5 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (FITC)

abx316580-20g Abbexa 20 µg 162.5 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (FITC)

abx316580-50g Abbexa 50 µg 250 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (Biotin)

20-abx316581 Abbexa
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  • 100 ug
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Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) Antibody

20-abx339338 Abbexa
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  • 100 ul
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Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) Antibody

20-abx211027 Abbexa
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  • 100 ul
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Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) Antibody

abx211027-100l Abbexa 100 µl 350 EUR

Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) Antibody

abx211027-50l Abbexa 50 µl 250 EUR

Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) Antibody

abx339338-100g Abbexa 100 µg Ask for price

Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) Antibody

abx339338-20g Abbexa 20 µg 250 EUR

Nucleotide Binding Oligomerization Domain Containing Protein 2 (NOD2) Antibody

abx339338-50g Abbexa 50 µg 350 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (Biotin)

abx316581-100g Abbexa 100 µg 362.5 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (Biotin)

abx316581-20g Abbexa 20 µg 162.5 EUR

Nucleotide Binding Oligomerization Domain Containing 2 (NOD2) Antibody (Biotin)

abx316581-50g Abbexa 50 µg 250 EUR

NOD2 Protein (CARD15) Rabbit anti-Human Polyclonal (C-Terminus) Antibody

GWB-436D14 GenWay Biotech 0.05 mg Ask for price

NOD2 Protein (CARD15) Rabbit anti-Human Polyclonal (N-Terminus) Antibody

GWB-DE0D8B GenWay Biotech 0.05 mg Ask for price

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Rat) (Target 1)

K6718506 ABM 1.0 ug DNA 200.4 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Rat) (Target 2)

K6718507 ABM 1.0 ug DNA 200.4 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Rat) (Target 3)

K6718508 ABM 1.0 ug DNA 200.4 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Mouse) (Target 1)

K4411606 ABM 1.0 ug DNA 200.4 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Mouse) (Target 2)

K4411607 ABM 1.0 ug DNA 200.4 EUR

Nod2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Mouse) (Target 3)

K4411608 ABM 1.0 ug DNA 200.4 EUR

NOD2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Human) (Target 1)

K1438606 ABM 1.0 ug DNA 200.4 EUR

NOD2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Human) (Target 2)

K1438607 ABM 1.0 ug DNA 200.4 EUR

NOD2 sgRNA CRISPR/Cas9 All-in-One Lentivector (Human) (Target 3)

K1438608 ABM 1.0 ug DNA 200.4 EUR

Nod2 - Rat, 4 unique 29mer shRNA constructs in lentiviral GFP vector

TL704760 Origene Technologies GmbH 5 µg/vial Ask for price

NOD2 Lentiviral Vector (Rat) (CMV) (pLenti-GIII-CMV-C-term-HA)

LV645602 ABM 1.0 ug DNA 1626 EUR

Nod2 - Mouse, 4 unique 29mer shRNA constructs in lentiviral GFP vector

TL507552 Origene Technologies GmbH 5 µg/vial Ask for price

NOD2 - Human, 4 unique 29mer shRNA constructs in lentiviral GFP vector

TL305650 Origene Technologies GmbH 5 µg/vial Ask for price

NOD2 Lentiviral Vector (Rat) (CMV) (pLenti-GIII-CMV-GFP-2A-Puro)

LV645603 ABM 1.0 ug DNA 1695.6 EUR

NOD2 Lentiviral Vector (Rat) (CMV) (pLenti-GIII-CMV-RFP-2A-Puro)

LV645604 ABM 1.0 ug DNA 1695.6 EUR

Nod2 - Rat, 4 unique 29mer shRNA constructs in retroviral untagged vector

TR704760 Origene Technologies GmbH 5 µg/vial Ask for price

Data evaluation was performed utilizing Statistical Package for Social Sciences model 20.Left aspect predominated with 88 (63.7%) and extension kind was frequent in 135 (97.8%). Thirteen (9.4%) sufferers had been initially managed by conventional bonesetters. A complete of 138 kids underwent operative fixation with imply age of seven.47 years and gender ratio of two:1 boy to woman.

Fall from cliff, ladders and rooftops had been the prevailing explanation for harm 73 (52.8%). Average time between harm and surgical procedure was 5.2 days. Closed discount was performed in 100 (72.4%) sufferers whereas open discount was crucial in 38 (27.5%) sufferers.Closed extension kind pediatric supracondylar fracture was frequent in this examine. Fall from cliff, rooftop and ladder are the most important explanation for fracture. Delayed presentation and preliminary administration of the fracture by the standard bonesetters makes supracondylar fracture tougher in useful resource restricted setting like ours.