Induction of differentiation by pyruvate and DMEM in the human retinal pigment epithelium cell line ARPE-19.

by
Cultured retinal pigment epithelium (RPE) may become a therapeutic option for transplantation in retinal disease. However maintaining a native RPE phenotype in vitro has proven challenging. The human RPE cell-line ARPE-19 is used widely as an alternative to primary RPE. It is grown in DMEM/F12 medium as standard, but its phenotype is dependent on culture conditions, and many differentiation markers are usually absent.
The purpose of this study was to examine how this sensitive phenotype of ARPE-19 can be modulated by growth media with or without the metabolite pyruvate to elucidate better RPE growth conditions.
METHODS
ARPE-19 cells at passages p22 to p28 were cultured on filters for up to 3 months in DMEM/F12 or DMEM media with or without pyruvate and 1% fetal calf serum. Assessment of differentiation was performed using pigmentation, immunocytochemistry, protein/mRNA expression, transepithelial resistance, VEGF secretion, and ultrastructure.
RESULTS
Pyruvate, in combination with DMEM, induced dark pigmentation and promoted differentiation markers such as CRALBP and MerTK. Importantly, RPE65 protein was detected by Western blotting and was enhanced by pyruvate, high glucose, and DMEM. ARPE-19 cells maintained in this medium could also phagocytose human photoreceptor outer segments (POS). VEGF secretion was greater in DMEM cultures and was affected by glucose but not by pyruvate. Pigmentation never occurred in DMEM/F12.
CONCLUSIONS
This study demonstrated important differentiation markers, including pigmentation and Western blots of RPE65 protein, and showed human POS phagocytosis in ARPE-19 cultures using a simple differentiation protocol. The results favor the use of high-glucose DMEM with pyruvate for future RPE differentiation studies.

Mesenchymal stem cell transplantation and DMEM administration in a 3NP rat model of Huntington’s disease: morphological and behavioral outcomes.

Transplantation of mesenchymal stem cells (MSCs) may offer a viable treatment for Huntington’s disease (HD). We tested the efficacy of MSC transplants to reduce deficits in a 3-nitropropionic acid (3NP) rat model of HD. Five groups of rats (Sham, 3NP, 3NP+vehicle, 3NP+TP(low), 3NP+TP(high)), were given PBS or 3NP intraperitoneally, twice daily for 42 days.
On day 28, rats in all groups except Sham and 3NP, received intrastriatal injections of either 200,000 MSCs (TP(low)), 400,000 (TP(high)) MSCs or DMEM (VH, the vehicle for transplantation).
MSCs survived 72 days without inducing a strong inflammatory response from the striatum. Behavioral sparing was observed on tests of supported-hindlimb-retraction, unsupported-hindlimb-retraction, visual paw placement and stepping ability for 3NP+TP(low) rats and on the unsupported-hindlimb-retraction and rotarod tasks for 3NP+VH rats.
Relative to 3NP controls, all treated groups were protected from 3NP-induced enlargement of the lateral ventricles. In vitro, MSCs expressed transcripts for numerous neurotrophic factors. In vivo, increased striatal labeling in BDNF, collagen type-I and fibronectin (but not GDNF or CNTF) was observed in the brains of MSC-transplanted rats but not in DMEM-treated rats.
In addition, none of the transplanted MSCs expressed neural phenotypes. These findings suggest that factors other than neuronal replacement underlie the behavioral sparing observed in 3NP rats after MSC transplantation.

Proliferation and gene expression of osteoblasts cultured in DMEM containing the ionic products of dicalcium silicate coating.

The medium containing ionic products of dicalcium silicate (Ca(2)SiO(4)) for culturing the osteoblast-like cells (MG63) were prepared by immersing the plasma sprayed Ca(2)SiO(4) coatings in DMEM solution for 24h. The normal DMEM was also used to culture the MG63 cells as the control group.
The results obtained from this work showed that the proliferation of MG63 cell was more significant in the group containing ionic products of Ca(2)SiO(4) coatings than in the control group. The cell cycle distribution indicated that the decreased G(0)/G(1) phase and increased S phase occurred in the cells cultured in the DMEM containing ionic products of Ca(2)SiO(4) coatings.
The analysis of osteogenic genes indicated that the ionic products of Ca(2)SiO(4) coating enhanced the expression of osteoblast-related genes and promote differentiation of MG63 cells at initial period. Moreover, the ionic products of Ca(2)SiO(4) coating differentially regulated osteoclastogenic gene expression by up-regulated OPG and down-regulated RANKL.

Choice of DMEM, formulated with or without pyruvate, plays an important role in assessing the in vitro cytotoxicity of oxidants and prooxidant nutraceuticals.

There is much interest in the positive health effects of nutraceuticals, in particular, polyphenols, which have both antioxidant and prooxidant characteristics. Pyruvate, a scavenger of hydrogen peroxide, is a component in some, but not in all, commercial formulations of cell culture media, Dulbecco’s modified Eagle’s medium in particular.
This study showed that the cytotoxicities to human fibroblasts of hydrogen peroxide, tert-butyl hydroperoxide, and various prooxidant nutraceuticals were lessened in Dulbecco’s modified Eagle’s medium formulated with pyruvate, as compared to the same medium but formulated without pyruvate.
Intracellular glutathione was unaffected in cells treated with hydrogen peroxide in Dulbecco’s modified Eagle’s medium formulated with pyruvate, as compared to medium formulated without pyruvate.
In these studies, intracellular glutathione was analyzed in acid-soluble cell extracts by determining the oxidation of reduced glutathione by 5,5′-dithiobis(2-nitrobenzoic acid) to glutathione disulfide, with the formation of the yellow chromagen, 5-thio-2-nitrobenzoic acid, measured spectrophotometrically at 412 nm and by the visualization of reduced glutathione in cells stained with the fluorescent dye, Cell Tracker Green 5-chloromethylfluorescein diacetate.
A survey of various cell culture media, formulated with and without pyruvate, confirmed that the level of added hydrogen peroxide was greatly lessened in those media formulated with pyruvate. This study suggested that the pyruvate status of Dulbecco’s modified Eagle’s medium be specified in the experimental design, especially in studies involving oxidative stress.

The effect of chitosan hydrogel containing DMEM/F12 medium on full-thickness skin defects after deep dermal burn.

Burn wound excision is considered necessary to prepare skin for grafting, and the success of graft “take” is thought to be dependent on the vascular supply to the wound. We previously showed that photocrosslinkable chitosan hydrogel containing DMEM/F12 medium (medium-Az-CH-LA) is a biocompatible and biodegradable biomaterial that promotes re-epithelialization and neovascularization.
The current study was designed to determine the effect of medium-Az-CH-LA on deep dermal burn. Sixteen male Wistar rats were randomly divided into two groups that were treated with medium-Az-CH-LA (n=5) or a collagen sponge (n=5). Under anesthesia, the dorsal fur was shaved and the skin was exposed to water at 95 degrees C for 10s. After 2h, damaged tissue was removed from the fascia and dressed with medium-Az-CH-LA or a collagen sponge. Specimens were obtained after 2, 4, 6, 8, 12, 16 and 32 days for histological analysis.

DMEM/F12

 from MyBiosource
MBS2567519-500mL | 500mL: 80.00 EUR

DMEM/F12

 from MyBiosource
MBS2567519-5x500mL | 5x500mL: 360.00 EUR

DMEM/F12

 from Elabscience Biotech
PM150312 | 500mL: 10.00 EUR

DMEM/F12

 from Elabscience Biotech
PM150312-500mL | 500 mL: 10.00 EUR

Special DMEM

 from Addexbio
C0003-06 | RT 500 mL Bottle: 70.00 EUR

Optimized DMEM

 from Addexbio
C0003-02 | RT 500 mL Bottle: 25.99 EUR

Formulated DMEM

 from Addexbio
C0003-01 | RT 500 mL Bottle: 23.99 EUR

Specialized DMEM

 from Addexbio
C0003-03 | RT 500 mL Bottle: 30.99 EUR

DMEM/F-12

 from Addexbio
C0013-16 | RT 500 mL Bottle: 30.99 EUR

SILAC - DMEM/F12

 from AthenaES
0423 | 500 ml: 41.50 EUR

SILAC- DMEM/F12

 from AthenaES
0433 | 1L: 33.70 EUR
There was no significant difference in the time required for wound closure between the two groups, but the thickness of the granulation tissue in the medium-Az-CH-LA-treated group was greater than that in the collagen sponge-treated group. Moreover, degradation and neovascularization occurred earlier in the group treated with medium-Az-CH-LA compared with the collagen sponge-treated group.
These findings suggest that early degradative and angiogenic activities of medium-Az-CH-LA may be beneficial for granulation tissue formation in deep dermal burn wounds.

Ferric Ammonium Citrate Upregulates PD-L1 Expression through Generation of Reactive Oxygen Species

by
Iron plays an important role in macrophage polarization by altering metabolic and redox status. However, the impact of iron on the immune status of macrophages is still controversial. In this study, we report that ferric ammonium citrate (FAC) upregulates PD-L1 expression in macrophages.
FAC not only altered the phenotype of macrophages but also led to enriching immune-modulatory T cell subsets. Since iron is known to be a constituent of coenzymes facilitating metabolic processes in mitochondria, we examined the metabolic status of FAC-overloaded macrophages by measuring the oxygen consumption rate (OCR) and the represented coenzyme, aconitase.
In addition to enhancement of metabolic processes, FAC accelerated the Fenton reaction in macrophages, which also contributed to the facilitation of oxygen consumption. We reasoned that the enhancement of the OCR leads to the production of reactive oxygen species (ROS), which are directly linked to PD-L1 induction.
Using ferrostatin, rotenone, and N-acetyl-L-cysteine, we confirmed that metabolic and redox regulation is responsible for FAC-mediated PD-L1 expression.
Furthermore, we suggested that FAC-induced ROS production may explain FAC-mediated pro- and anti-inflammatory responses in macrophages. These findings may extend our understanding of regulating iron concentration during immune checkpoint therapy in cancer patients.

Ferric ammoniumcitrate (FAC)-induced inhibition of osteoblast proliferation/differentiation and its reversal by soybean-derived peptides (SDP)

Ferric citrate has been used to treat hyperphosphatemia, a prevalent symptom in patients with chronic kidney disease while ferric ammonium citrate (FAC), a more dissolvable format, is widely used as food additive. However, excess iron is associated with osteoporosis.
Dietary soybean products have been shown to prevent the progression of osteoporosis. In this study, a group of peptides, referred as P3, was identified from the enzymolysis of soybean protein isolates, and its biological functions were investigated. The results showed that MC3T3-E1 cell cycle progression from G0/G1 to S phase was accelerated by P3 treatment. MC3T3-E1 cell proliferation was enhanced by P3 via ERK1/2 activation.
Importantly, P3 treatment abolished the antiproliferative effect of FAC on MC3T3-E1 cell. In addition, P3 treatment increased the expression of ALP, COL-1, OCN, consequently promoting the differentiation and mineralization of MC3T3-E1 cells via activation of p38 MAPK pathway.
Consequently, P3 treatment was able to reverse the inhibitory effect of FAC on osteoblasts differentiation and mineralization. Our findings suggest P3, as a dietary supplement, has a potential therapeutic function to attenuate the adverse effects of FAC on bone metabolism and to prevent osteoporosis progression.

Ammonium Ferric Citrate induced Ferroptosis in Non-Small-Cell Lung Carcinoma through the inhibition of GPX4-GSS/GSR-GGT axis activity

The morbidity and mortality rates associated with non-small-cell lung carcinoma (NSCLC) are increasing every year, placing new demands on existing therapies and drugs. Ammonium ferric citrate (AFC) is often used as a food additive for iron supplementation; however, to our knowledge, no studies have investigated whether AFC can induce ferroptosis in NSCLC.
In this study, we demonstrated that specific concentrations of AFC effectively inhibit the proliferation and invasion of lung cancer cell lines in vitro using a cell proliferation inhibition test, a transwell assay, and flow cytometry analysis of cell cycle and apoptosis. In addition, AFC significantly induced oxidative stress injury in lung cancer cell lines.
A quantitative polymerase chain reaction assay showed that AFC markedly reduced the expression levels of cell growth factors, negative regulators of ferroptosis, and autophagy regulators. Lastly, a protein-protein interaction analysis revealed that glutathione peroxidase 4 (GPX4) exerted its biological role through the regulation of the GSS/GSR complex and downstream GGT family proteins.
When the expression of GPX4 changes, its biological activities, such as the glutathione metabolic process, cellular biosynthetic process, cellular response to chemical stimulus, and antioxidant activity, change accordingly, thereby affecting the survival quality and physiological and biochemical activities of cells.
Overall, this study verifies that AFC has the biological activity of activating oxidative stress injury in NSCLC cell lines, leading to a decrease in their autophagy and inducing ferroptosis. We also confirmed that the GPX4-GSS/GSR-GGT axis is a crucial target of AFC-induced ferroptosis.

Increasing Intracellular Levels of Iron with Ferric Ammonium Citrate Leads to Reduced P-glycoprotein Expression in Human Immortalised Brain Microvascular Endothelial Cells

Purpose: P-glycoprotein (P-gp) at the blood-brain barrier (BBB) precludes the brain penetration of many xenobiotics and mediates brain-to-blood clearance of β-amyloid, which accumulates in the Alzheimer’s disease (AD) brain. Zinc and copper are reported to modulate BBB expression and function of P-gp; however, the impact of exogenous iron, which accumulates in AD, on P-gp dynamics remains unknown.
Methods: P-gp protein and MDR1 transcript levels were assessed in immortalised human cerebral microvascular endothelial (hCMEC/D3) cells treated with ferric ammonium citrate (FAC; 250 μM, 72 h), by Western blotting and RT-qPCR, respectively. P-gp function was assessed using rhodamine-123 and [3H]-digoxin accumulation. Intracellular reactive oxygen species (ROS) levels were determined using 2′,7′-dichlorofluorescin diacetate and intracellular iron levels quantified using a ferrozine assay.
Results: FAC treatment significantly reduced P-gp protein (36%) and MDR1 mRNA (16%) levels, with no significant change in rhodamine-123 or [3H]-digoxin accumulation. While P-gp/MDR1 downregulation was associated with elevated ROS and intracellular iron, MDR1 downregulation was not attenuated with the antioxidant N-acetylcysteine nor the iron chelators desferrioxamine and deferiprone, suggesting the involvement of a ROS-independent mechanism or incomplete iron chelation.
Conclusions: These studies demonstrate that iron negatively regulates P-gp expression at the BBB, potentially impacting CNS drug delivery and brain β-amyloid clearance.
Keywords: P-glycoprotein; blood-brain barrier; efflux transporter; iron; reactive oxygen species.

Structures of disodium hydrogen citrate mono-hydrate, Na 2 HC 6 H 5 O 7(H 2 O), and di-ammonium sodium citrate, (NH 4) 2 NaC 6 H 5 O 7, from powder diffraction data

The crystal structures of disodium hydrogen citrate monohydrate, Na2HC6H5O7(H2O), and di-ammonium sodium citrate, (NH4)2NaC6H5O7, have been solved and refined using laboratory X-ray powder diffraction data, and optimized using density functional techniques. In NaHC6H5O7(H2O), the NaO6 coordination polyhedra share edges, forming zigzag layers lying parallel to the bc plane.
The hydro-phobic methyl-ene groups occupy the inter-layer spaces. The carb-oxy-lic acid group makes a strong charge-assisted hydrogen bond to the central carboxyl-ate group. The hydroxyl group makes an intra-molecular hydrogen bond to an ionized terminal carboxyl-ate oxygen atom. Each hydrogen atom of the water mol-ecule acts as a donor, to a terminal carboxyl-ate and the hydroxyl group. Both the Na substructure and the hydrogen bonding differ from those of the known phase Na2HC6H5O7(H2O)1.5.

Ferric ammonium citrate

 from MedKoo Biosciences
592821 | 10.0g: 260.00 EUR

FERRIC AMMONIUM CITRATE

 from PhytoTechnology Laboratories
F374 | 100G: 62.21 EUR

Ferric ammonium citrate

 from MyBiosource
MBS5764783-1g | 1g: 145.00 EUR

Ferric ammonium citrate

 from MyBiosource
MBS5764783-5x1g | 5x1g: 500.00 EUR

Ferric ammonium citrate

 from EWC Diagnostics
PCT0107-100G | 1 unit: 6.93 EUR

Ferric ammonium citrate

 from EWC Diagnostics
PCT0107-500G | 1 unit: 10.18 EUR

Ammonium citrate dibasic

 from Pfaltz & Bauer
A29994 | 100G: 130.08 EUR

Ammonium citrate, dibasic

 from Bio Basic
AB0059 | 500g: 78.79 EUR

Ammonium Citrate, Dibasic

 from MyBiosource
MBS635391-100g | 100g: 160.00 EUR

Ammonium Citrate, Dibasic

 from MyBiosource
MBS635391-1kg | 1kg: 290.00 EUR

Ammonium Citrate, Dibasic

 from MyBiosource
MBS635391-25kg | 2.5kg: 590.00 EUR

Ammonium Citrate, Dibasic

 from MyBiosource
MBS635391-500g | 500g: 210.00 EUR

Ammonium Citrate, Dibasic

 from MyBiosource
MBS635391-5kg | 5kg: 945.00 EUR

Ammonium citrate, tribasic

 from Bio Basic
AB0060 | 250g: 72.53 EUR
In (NH4)2NaC6H5O7, the NaO6 coordination octa-hedra share corners, making double zigzag chains propagating along the b-axis direction. Each hydrogen atom of the ammonium ions acts as a donor in a discrete N-H⋯O hydrogen bond. The hydroxyl group forms an intra-molecular O-H⋯O hydrogen bond to a terminal carboxyl-ate oxygen atom.

Fluorimetry of selenium in body fluids after digestion with nitric acid, magnesium nitrate hexahydrate, and hydrochloric acid.

by
A digestion procedure involving nitric acid, magnesium nitrate hexahydrate, and hydrochloric acid suffices for selenium determinations in whole blood, serum, and urine by molecular fluorescence spectrometry. To test the accuracy of the method we compared the results with those from hydride-generation atomic absorption spectrometry, and we also analyzed reference materials.

Ab Initio Molecular Dynamics Study of Aqueous Solutions of Magnesium and Calcium Nitrates: Hydration Shell Structure, Dynamics and Vibrational Echo Spectroscopy

Ab initio molecular dynamics simulations are performed to study the hydration shell structure, dynamics, and vibrational echo spectroscopy of aqueous Mg(NO3)2 and Ca(NO3)2 solutions. The hydration shell structure is probed through calculations of various ion-ion and ion-water radial and spatial distribution functions. On the dynamical side, calculations have been made for the hydrogen bond dynamics of hydration shells and also residence dynamics and lifetimes of water in different solvation environments.
Subsequently, we looked at the dynamics of frequency fluctuations of OD modes of heavy water in different hydration environments. Specifically, the temporal decay of spectral observables of two-dimensional infrared (2DIR) spectroscopy, three pulse echo peak shift (3PEPS) measurements and also of time correlations of frequency fluctuations are calculated to investigate the dynamics of vibrational spectral diffusion of water in different hydration environments in these solutions.
The OD stretch frequencies of water molecules in the vicinity of both divalent cations are found to be red-shifted and also fluctuating at a slower rate than other water molecules present in the solutions. The Mg2+ ions are found to be strongly hydrated which can be linked to their lower tendency to form contact ion-pairs and essentially no water exchange between the cationic hydration shells and bulk during the time scale of the current simulations.
The stronger hydration of Mg2+ ions make their hydration shells structurally and dynamically more rigid and make the dynamics of hydrogen bonds and vibrational spectral diffusion, as revealed through spectral observables of 2DIR and 3PEPS slower than that for the Ca2+ ions.
The structural and spectral dynamics of water molecules outside the cationic solvation shells in the Mg(NO3)2 solution are also found to be relatively slower than that of the Ca(NO3)2 solution and pure water which show the effects of stronger electric fields of Mg2+ ions extending beyond their first hydration shells. Also, water molecules in the hydration shells of the NO3– ions are found to relax at a slower rate in the Mg(NO3)2 solution which manifests the effect countercations have on anionic hydration shells for divalent metal nitrate solutions.

Effect of molten sodium nitrate on the decomposition pathways of hydrated magnesium hydroxycarbonate to magnesium oxide probed by in situ total scattering

The effect of NaNO3 and its physical state on the thermal decomposition pathways of hydrated magnesium hydroxycarbonate (hydromagnesite, HM) towards MgO was examined by in situ total scattering. Pair distribution function (PDF) analysis of these data allowed us to probe the structural evolution of pristine and NaNO3-promoted HM. A multivariate curve resolution alternating least squares (MCR-ALS) analysis identified the intermediate phases and their evolution upon the decomposition of both precursors to MgO.
The total scattering results are discussed in relation with thermogravimetric measurements coupled with off-gas analysis. MgO is obtained from pristine HM (N2, 10 °C min-1) through an amorphous magnesium carbonate intermediate (AMC), formed after the partial removal of water of crystallization from HM.
The decomposition continues via a gradual release of water (due to dehydration and dehydroxylation) and, in the last step, via decarbonation, leading to crystalline MgO. The presence of molten NaNO3 alters the decomposition pathways of HM, proceeding now through AMC and crystalline MgCO3.
These results demonstrate that molten NaNO3 facilitates the release of water (from both water of crystallization and through dehydroxylation) and decarbonation, and promotes the crystallization of MgCO3 and MgO in comparison to pristine HM. MgO formed from the pristine HM precursor shows a smaller average crystallite size than NaNO3-promoted HM and preserves the initial nano-plate-like morphology of HM.
NaNO3-promoted HM was decomposed to MgO that is characterized by a larger average crystallite size and irregular morphology. Additionally, in situ SEM allowed visualization of the morphological evolution of HM promoted with NaNO3 at a micrometre scale.

Magnesium reduces cadmium accumulation by decreasing the nitrate reductase-mediated nitric oxide production in Panax notoginseng roots.

Panax notoginseng is a traditional medicinal herb in China. However, the high capacity of its roots to accumulate cadmium (Cd) poses a potential risk to human health. Our previous study showed that nitrate reductase (NR)-dependent nitric oxide (NO) production promoted Cd accumulation in P. notoginseng root cell walls.
In this study, the role of Mg in the regulation of NO production and Cd accumulation in P. notoginseng roots was characterized. Exposure of P. notoginseng roots to increasing concentrations of Cd resulted in a linear increase in NO production.
The application of 2 mM Mg for 24 h significantly alleviated Cd-induced NO production and Cd accumulation in roots, which coincided with a significant decrease in the NR activity. Western analysis suggested that Mg increased the interaction between the 14-3-3 protein and NR, which might have been a reason for the Mg-mediated decrease in NR activity and NO production under Cd stress.
These results suggested that Mg-mediated alleviation of Cd-induced NO production and Cd accumulation is achieved by enhancement of the interaction between the 14-3-3 protein and NR in P. notoginseng roots.

Electrochemical nitrate removal with simultaneous magnesium recovery from a mimicked RO brine assisted by in situ chloride ions.

Electrochemical reduction is effective to remove nitrate but byproducts such as ammonia and nitrite would need chloride addition for indirect oxidation to nitrogen gas.
Herein, electrochemical nitrate reduction was investigated to remove nitrate from a mimicked reverse osmosis (RO) brine containing chloride that eliminates the need for external chloride addition. Both Cu/Zn and Ti nano cathodes exhibited the best performance of nitrate removal with >97 % removal in either Na2SO4 or NaCl electrolyte, although with different products.

MAGNESIUM NITRATE

 from PhytoTechnology Laboratories
M542 | 1KG: 247.58 EUR

Magnesium Nitrate Hexahydrate

 from NACALAI TESQUE
20918-35 | 500G: 16.80 EUR

Magnesium Nitrate Hexahydrate

 from NACALAI TESQUE
20919-12 | 25G: 8.75 EUR

Magnesium Nitrate Hexahydrate

 from NACALAI TESQUE
20919-25 | 500G: 19.25 EUR

Magnesium nitrate hexahydrate

 from Glentham Life Sciences
GK0164 | 250g: 134.03 EUR

Magnesium nitrate hexahydrate

 from Glentham Life Sciences
GK0164-1 | 1: 35.50 EUR

Magnesium nitrate hexahydrate

 from Glentham Life Sciences
GK0164-1KG | 1 kg: 79.20 EUR

Magnesium nitrate hexahydrate

 from Glentham Life Sciences
GK0164-250 | 250: 15.70 EUR

Magnesium nitrate hexahydrate

 from Glentham Life Sciences
GK0164-250G | 250 g: 52.80 EUR

Magnesium nitrate hexahydrate

 from Glentham Life Sciences
GK0164-5 | 5: 146.30 EUR

Magnesium nitrate hexahydrate

 from Glentham Life Sciences
GK0164-500 | 500: 23.80 EUR

Magnesium nitrate hexahydrate

 from Glentham Life Sciences
GK0164-500G | 500 g: 64.80 EUR

Magnesium nitrate hexahydrate

 from Glentham Life Sciences
GK0164-5KG | 5 kg: 213.60 EUR

Magnesium nitrate hexahydrate

 from Bio Basic
MB0586 | 500g: 80.88 EUR

Magnesium nitrate hexahydrate

 from EWC Diagnostics
PCT0007-1KG | 1 unit: 17.80 EUR

Magnesium nitrate hexahydrate

 from EWC Diagnostics
PCT0007-500G | 1 unit: 9.89 EUR

Magnesium Nitrate Hexahydrate ACS, 98%

 from Sisco Laboratories
77697 | 500 Gms: 2.87 EUR

Magnesium nitrate, hexahydrate, 99+%, ACS

 from Glentham Life Sciences
GX1786 | 500g: 81.44 EUR

Magnesium nitrate, hexahydrate, 99+%, ACS

 from Glentham Life Sciences
GX1786-500 | 500: 88.90 EUR

Magnesium nitrate hexahydrate, Hi-LR™

 from EWC Diagnostics
GRM1052-500G | 1 unit: 6.93 EUR

Magnesium nitrate hexahydrate, Hi-AR™

 from EWC Diagnostics
GRM1380-500G | 1 unit: 9.49 EUR

Magnesium Nitrate Hexahydrate, 1 M, 100 ML

 from MiTeGen
M-CSS-214 | 100 ml: 86.00 EUR

Magnesium nitrate hexahydrate, Hi-AR™/AC

 from EWC Diagnostics
GRM3923-500G | 1 unit: 9.80 EUR

GFAAS Matrix Modifer Sol Magnesium Nitrate 2% in 5% HNO3 - 100ML

 from Scientific Laboratory Supplies
MMS601 | 100ML: 768.18 EUR

GFAAS Matrix Modifer Sol Magnesium Nitrate 2% in 5% HNO3 - 500ML

 from Scientific Laboratory Supplies
MMS605 | 500ML: 1148.60 EUR

Magnesium

 from Toronto Research Chemicals
M110320 | 100g: 201.00 EUR

Magnesium Oxide

 from NACALAI TESQUE
20921-75 | 500G: 24.50 EUR

Magnesium Oxide

 from NACALAI TESQUE
20923-42 | 25G: 12.60 EUR

Magnesium Oxide

 from NACALAI TESQUE
20923-84 | 250G: 48.30 EUR
Complete nitrate reduction to nitrogen gas was realized in the RO brine whose complex composition decreased the electrode efficiency, for example from 71.4 ± 0.2%-49.4 ± 0.3 % with the Cu/Zn cathode after 5 cycles of operation.
Magnesium was recovered at the same time of nitrate removal and the purity of Mg(II) could reach 96.8 ± 2.0 % after proper pH pre-treatment. In a preliminary adsorption study, a key byproduct – chlorate was reduced by 49.8 ± 2.7 % after 3-h adsorption by 100 g L-1 activated carbon.
These results have demonstrated the simultaneous electrochemical nitrate removal and resource recovery from a complex water like a RO brine and provided new information such as byproduct management and electrode deterioration.

The Influence of Synthesis Method on Characteristics of Buffer and Organic Solutions of Thermo- and pH-Responsive Poly( N-[3-(diethylamino)propyl]methacrylamide)s

by
Thermo- and pH-responsive poly(N-[3-(diethylamino)propyl]methacrylamide)s were synthesized by free radical polymerization and RAFT polymerization. The molar masses of the samples were 33,000-35,000 g∙mol-1. Investigations of the dilute solutions showed that the prepared samples were flexible chain polymers.
The behavior of the synthesized polymers in the buffer solutions was analyzed by turbidity and light scattering at a pH range of 7-13 and a concentration range of 0.0002-0.008 g·cm-3. When the concentrated solutions were at a low temperature, there were macromolecules and aggregates, which were formed due to the interaction of hydrophobic units. For the investigated samples, the lower critical solution temperatures were equal.
The phase separation temperatures decreased as pH increased. The influence of polydispersity index on the characteristics of the samples in the solutions was analyzed. The radii of molecules of poly(N-[3-(diethylamino)propyl]methacrylamide) obtained by RAFT polymerization at this temperature at the onset and end of the phase separation interval were lower than ones for samples synthesized by conventional free radical polymerization.
Keywords: aggregation; conformational and hydrodynamic characteristics; phase separation temperatures; poly(N-[3-(diethylamino)propyl]methacrylamide); synthesis; thermo- and pH- responsive polymers.

Detonation nanodiamonds as enhancers of E. coli photodynamic inactivation by phthalocyanines in a high molarity buffer solution

Antimicrobial therapy, especially inactivation of multi-antibiotic-resistant strains, requires creating new approaches for drug action and targeted delivery in different environmental conditions. In this work, detonation nanodiamonds (DNDs) were used to deliver polycationic zinc phthalocyanines to E. coli cells.
It is shown that in aqueous solutions, zinc phthalocyanines with cholinyl peripheral substituents form complexes with negatively charged DND based on electrostatic interactions.
About 40-70 phthalocyanine molecules can bind to a single DND particle, depending on the number of charged groups of the dye molecule. During the complex formation, quenching of phthalocyanine fluorescence and a decrease in its ability to generate reactive oxygen species were observed.
In the presence of bacterial cells, phthalocyanine left the complex and induced a photodynamic effect, the magnitude of which depended on the phthalocyanine charge, the molarity of the buffer solution, and the stoichiometry of the phthalocyanine-DND complex. It was found that at physiological values of the ionic strength of the solution, the photodynamic effect of phthalocyanine with a charge of 8+ in combination with a DND is higher than that of the initial phthalocyanine. Thus, nanodiamonds are a promising platform for the delivery of photosensitizers in antimicrobial therapy.
Keywords: Detonation nanodiamond; Photodynamic inactivation; Phthalocyanine.

Tunneling in the Hydrogen-Transfer Reaction from a Vitamin E Analog to an Inclusion Complex of 2,2-Diphenyl-1-picrylhydrazyl Radical with β-Cyclodextrin in an Aqueous Buffer Solution at Ambient Temperature

Recently, increasing attention has been paid to quantum mechanical behavior in biology. In this study, we investigated the involvement of quantum mechanical tunneling in the hydrogen-transfer reaction from Trolox, a water-soluble analog of vitamin E (α-tocopherol), to 2,2-diphenyl-1-picrylhydrazyl radical (DPPH•) in a phosphate buffer solution (0.05 M, pH 7.0).
DPPH• was used as a reactivity model of reactive oxygen species and solubilized in water using β-cyclodextrin (β-CD). The second-order rate constants, kH and kD, in 0.05 M phosphate buffer solutions prepared with H2O (pH 7.0) and D2O (pD 7.0), respectively, were determined for the reaction between Trolox and DPPH•, using a stopped-flow technique at various temperatures (283-303 K).
Large kinetic isotope effects (KIE, kH/kD) were observed for the hydrogen-transfer reaction from Trolox to the β-CD-solubilized DPPH• in the whole temperature range. The isotopic ratio of the Arrhenius prefactor (AH/AD = 0.003), as well as the isotopic difference in the activation energies (19 kJ mol-1), indicated that quantum mechanical tunneling plays a role in the reaction.

Buffer concentration dramatically affects the stability of S-nitrosothiols in aqueous solutions

S-nitrosothiols (RSNOs) are an important group of nitric oxide (NO)-donating compounds with low toxicity and wide biomedical applications. In this paper, we, for the first time, demonstrate that the concentration of buffer remarkably affects the stability of RSNOs including naturally occurring S-nitrosoglutathione (GSNO) and synthetic S-nitroso-N-acetylpenicillamine (SNAP).
For a solution with a high concentration of GSNO (e.g., 50 mM) and an initial near-neutral pH, the optimal buffer concentration is close to the GSNO concentration under our experimental conditions. A lower buffer concentration does not have adequate buffer capacity to resist the pH drop caused by GSNO decomposition.
The decreased solution pH further accelerates GSNO decomposition because GSNO is most stable at near-neutral pH according to our density-functional theory (DFT) calculations. A higher-than-optimal buffer concentration also reduces the GSNO stability because buffer ingredients including phosphate, Tris base, and HEPES consume NO/N2O3. In contrast to GSNO, the highest SNAP stability is obtained when the starting solution at a neutral pH does not contain buffer, and the stability decreases as the buffer concentration increases.
This is because SNAP is more stable at mildly acidic pH and the SNAP decomposition-induced pH drop stabilizes the donor. When the RSNO concentration is low (e.g., 1 mM), the buffer concentration also matters because any excess buffer accelerates the donor decomposition.
Since the effect of buffer concentration was previously overlooked and suboptimal buffer concentrations were often used, this paper will aid in the formulation of RSNO solutions to obtain the maximum stability for prolonged storage and sustained NO release.

In-solution buffer-free digestion allows full-sequence coverage and complete characterization of post-translational modifications of the receptor-binding domain of SARS-CoV-2 in a single ESI-MS spectrum

Subunit vaccines based on the receptor-binding domain (RBD) of the spike protein of SARS-CoV-2 provide one of the most promising strategies to fight the COVID-19 pandemic. The detailed characterization of the protein primary structure by mass spectrometry (MS) is mandatory, as described in ICHQ6B guidelines.
In this work, several recombinant RBD proteins produced in five expression systems were characterized using a non-conventional protocol known as in-solution buffer-free digestion (BFD). In a single ESI-MS spectrum, BFD allowed very high sequence coverage (≥ 99%) and the detection of highly hydrophilic regions, including very short and hydrophilic peptides (2-8 amino acids), and the His6-tagged C-terminal peptide carrying several post-translational modifications at Cys538 such as cysteinylation, homocysteinylation, glutathionylation, truncated glutathionylation, and cyanylation, among others. The analysis using the conventional digestion protocol allowed lower sequence coverage (80-90%) and did not detect peptides carrying most of the above-mentioned PTMs.

Glycine buffer solution

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GB7317 | 250ml: 48.31 EUR

Glycine buffer solution

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GB7317-1 | 1: 52.80 EUR

Glycine buffer solution

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GB7317-250 | 250: 22.70 EUR

Ammonium Buffer Solution

 from EWC Diagnostics
R061-1L | 1 unit: 80.69 EUR

Bicarbonate buffer solution

 from iNtRON Biotechnology Inc
IBS-BB010 | 500 mL: 49.00 EUR

Buffer solution pH 7

 from Sisco Laboratories
97409 | 500 ml: 2.39 EUR

Buffer solution pH 4

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45899 | 500 ml: 2.39 EUR

pH 9.23 Buffer Solution

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10922CTT | 1L: 37.28 EUR

BUFFER SOLUTION, pH 4.0

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B235 | 4000ML: 20.77 EUR

BUFFER SOLUTION, pH 7.0

 from PhytoTechnology Laboratories
B236 | 4000ML: 20.77 EUR

BUFFER SOLUTION, pH 10.0

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B237 | 4000ML: 20.77 EUR

Buffer solution pH 9.2

 from Sisco Laboratories
52031 | 500 ml: 2.39 EUR

5X TE Buffer Solution

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IBS-BT038 | 1L: 42.00 EUR

Buffer solution, pH 9.0

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GE4974 | 1l: 25.46 EUR

Buffer solution, pH 9.0

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GE4974-1 | 1: 27.80 EUR

Buffer solution, pH 9.0

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GE4974-1L | 1 l: 69.60 EUR

Buffer solution, pH 7.4

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GE5737 | 1l: 25.46 EUR

Buffer solution, pH 7.4

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GE5737-1 | 1: 27.80 EUR

Buffer solution, pH 4.0

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GE5959 | 1l: 25.46 EUR

Buffer solution, pH 4.0

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GE5959-1 | 1: 27.80 EUR

Buffer solution, pH 4.0

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GE5959-1L | 1 l: 69.60 EUR
The two C-terminal peptides of a dimer [RBD(319-541)-(His)6]2 linked by an intermolecular disulfide bond (Cys538-Cys538) with twelve histidine residues were only detected by BFD. This protocol allows the detection of the four disulfide bonds present in the native RBD, low-abundance scrambling variants, free cysteine residues, O-glycoforms, and incomplete processing of the N-terminal end, if present. Artifacts generated by the in-solution BFD protocol were also characterized. BFD can be easily implemented; it has been applied to the characterization of the active pharmaceutical ingredient of two RBD-based vaccines, and we foresee that it can be also helpful to the characterization of mutated RBDs.

Biglycan Has a Major Role in Maintenance of Mature Tendon Mechanics

by

Decorin and biglycan are two small leucine-rich proteoglycans (SLRPs) that regulate collagen fibrillogenesis and extracellular matrix assembly in tendon.

The objective of this study was to determine the individual roles of these molecules in maintaining the structural and mechanical properties of tendon during homeostasis in mature mice. We hypothesized that knockdown of decorin in mature tendons would result in detrimental changes to tendon structure and mechanics while knockdown of biglycan would have a minor effect on these parameters.
To achieve this objective, we created tamoxifen-inducible mouse knockdown models targeting decorin or biglycan inactivation. This enables the evaluation of the roles of these SLRPs in mature tendon without the abnormal tendon development caused by conventional knockout models.
Contrary to our hypothesis, knockdown of decorin resulted in minor alterations to tendon structure and no changes to mechanics while knockdown of biglycan resulted in broad changes to tendon structure and mechanics. Specifically, knockdown of biglycan resulted in reduced insertion modulus, maximum stress, dynamic modulus, stress relaxation, and increased collagen fiber realignment during loading.
Knockdown of decorin and biglycan produced similar changes to tendon microstructure by increasing the collagen fibril diameter relative to wild-type controls. Biglycan knockdown also decreased the cell nuclear aspect ratio, indicating a more spindle-like nuclear shape. Overall, the extensive changes to tendon structure and mechanics after knockout of biglycan, but not decorin, provides evidence that biglycan plays a major role in the maintenance of tendon structure and mechanics in mature mice during homeostasis. This article is protected by copyright. All rights reserved.

Whole genome sequencing has the potential to improve treatment for rifampicin-resistant tuberculosis in high burden settings: a retrospective cohort study

Background Treatment of multidrug-resistant or rifampicin-resistant tuberculosis (MDR/RR-TB), although improved in recent years with shorter, more tolerable regimens, remains largely standardised and based on limited drug susceptibility testing (DST). More individualised treatment with expanded DST access is likely to improve patient outcomes.
Methods To assess the potential of TB drug resistance prediction based on whole genome sequencing (WGS) to provide more effective treatment regimens, we applied current South African treatment recommendations to a retrospective cohort of MDR/RR-TB patients from Khayelitsha, Cape Town.
Routine DST and clinical data were used to retrospectively categorise patients into a recommended regimen, either a standardised short regimen or a longer individualised regimen. Potential regimen changes were then described with the addition of WGS-derived DST.
Findings WGS data were available for 1274 MDR/RR-TB patient treatment episodes across 2008-2017. Among 834 patients initially eligible for the shorter regimen, 385 (46%) may have benefited from reduced drug dosage or removing ineffective drugs when WGS data were considered.
A further 187 (22%) may have benefited from more effective adjusted regimens. Among 440 patients initially eligible for a longer individualised regimen, 153 (35%) could have been switched to the short regimen.
Overall, 305 (24%) patients had MDR/RR-TB with second-line TB drug resistance, where the availability of WGS-derived DST would have allowed more effective treatment individualization. 
Interpretation These data suggest considerable benefits could accrue from routine access to WGS-derived resistance prediction. Advances in culture-free sequencing and expansion of the reference resistance mutation catalogue will increase the utility of WGS resistance prediction.
Funding Swiss National Science Foundation, South African National Research Foundation, and Wellcome Trust.

Working in a care home during the COVID-19 pandemic: How has the pandemic changed working practices? A qualitative study

Background: The pandemic has significantly affected care homes’ residents and families through the national visiting restrictions. However, less is known on the impact these changes have had on the care home workforce. The aim of this research was to explore the impact of COVID-19 on the working practices of care home staff, caring for people living with dementia.
Methods: Remote qualitative, semi-structured interviews were conducted with care home staff caring for people living with dementia (PLWD) in the UK.
Results: Participants were recruited to the larger programme of research via convenience sampling. Interviews were conducted via telephone or online platforms. This research employed inductive thematic analysis. Sixteen care home staff were included in this study.
Three overarching themes were developed from the analysis that conveyed changes to the everyday working practices of the care home workforce and the impact such changes posed to staff wellbeing: (1) Practical implications of working in a care home during the COVID-19 pandemic; (2); Staff values and changes to the staff roles (3): Impact to the care home staff and concerns for the care sector.
Conclusions: The COVID-19 pandemic has significantly disrupted the daily working practices of care home staff, with staff forced to adopt additional roles on top of increased workloads to compensate for the loss of external agencies and support. Support and guidance must be offered urgently to inform care home staff on how to best adapt to their new working practices, ensuring that they are adequately trained.
Keywords: COVID-19; Care homes; Care workforce; Nursing homes; Older people; Pandemics; Working practices.

Has EVAR changed the outcomes of ruptured abdominal aortic aneurysms? A decades worth of experience in an Australian Teaching Hospital

Background: Ruptured abdominal aortic aneurysms (rAAA) are associated with significant mortality, and equipoise remains as to whether patients managed with endovascular stent grafts (rEVAR) demonstrate better outcomes when compared to traditional open repair (OR). This study sought to examine the outcomes of patients presenting with rAAA to our institution and assess the perioperative outcomes and outpatient mortality of patients over the past decade.
Methods: A retrospective analysis was conducted. Patients treated for rAAA between 2010 and 2019 were identified from a search of the hospital database for ACHI and ICD-10 codes for repair of AAA. Demographic, operative and post-operative variables were collected from electronic medical records of identified patients.
Results: Eighty patients were identified, 51 of whom presented with a rAAA. The majority of repairs were rEVARs (59%). Median age was 76 years. Median length of admission to ICU was 3 days, and median length of hospital admission was 10 days. Overall in-patient mortality was 26%, with rates of 39% at 3 years and 47% at 5 years. No significant difference in outpatient mortality was found in patients undergoing rEVAR compared to OR, with rates of 61% at 5 years compared to 65% at 5 years, respectively (p = 0.8).
Conclusion: Perioperative outcomes of our cohort of patients undergoing endovascular repair compared to open repair for ruptured and symptomatic AAAs are comparable over the past decade. Given equipoise remains between repair methods, further observational studies are required to quantify benefits of OR and endovascular repairs for ruptured and symptomatic AAAs.
Keywords: EVAR; aneurysm; open AAA repair; rupture.

A Poultry Value Chain Intervention Promoting Diversified Diets Has Limited Impact on Maternal and Child Diet Adequacy During the Lean Season in a Cluster Randomized Controlled Trial

Background: SELEVER is a nutrition- and gender-sensitive poultry value chain project designed and implemented by international NGO Tanager which consists of poultry market facilitation and behavior change activities aiming at increasing poultry production and improving diets without free inputs transfer.
Objectives: The study aimed at assessing the impact of SELEVER on diets of women and children during the lean season.
Methods: Within a cluster-randomized controlled trial, 45 communes were assigned to one of three arms, including 1) SELEVER interventions; 2) SELEVER with an intensive hygiene and sanitation component (SELEVER + WASH); and 3) a control group without intervention. Two rounds of survey were conducted 2 years apart during the lean season. Primary dietary outcomes were the probability of adequacy (PA) of iron, zinc and vitamin A intakes, mean PA (MPA) of 11 micronutrients and individual dietary diversity score collected through quantitative 24-hour recall in longitudinal samples of women and index children (2-4 years old) in 1,054 households; and minimum acceptable diet in the repeated cross-sectional sample of their younger sibling aged 6-23 months. Impacts were assessed by intention-to-treat analysis of covariance.
Results: Relative to control, SELEVER interventions (groups 1 + 2) increased the PA of iron intakes in women by 1.8 pp (P = 0.030). We found no further impact on primary outcomes, although eggs consumption increased in index children (+0.73 pp, P = 0.010; +0.69 kcal/d, P = 0.036). Across the three groups, we observed negative effects of SELEVER on the PA of zinc intakes in women relative to SELEVER + WASH (-4.1 pp, P = 0.038), and on a variety of secondary dietary outcomes relative to both other groups. The study was registered on the ISCRCTN registry (ISRCTN16686478).

HAT Antibody

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33511 | 100ul: 319.00 EUR

HAT Antibody

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33511-100ul | 100ul: 302.40 EUR

HAT Antibody

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33511-50ul | 50ul: 224.40 EUR

HAT Antibody

 from AAT Bioquest
8C0356 | 50ug: 368.00 EUR

HAT antibody

 from Fitzgerald
70R-30791 | 100 ug: 294.00 EUR

HAT Antibody

 from Affbiotech
AF0269 | 200ul: 420.00 EUR

HAT Antibody

 from Affinity Biosciences
AF0269-100ul | 100ul: 168.00 EUR

HAT Antibody

 from Affinity Biosciences
AF0269-200ul | 200ul: 210.00 EUR

HAT Antibody

 from Lifescience Market
ABF0269 | 100 ug: 525.60 EUR

HAT Antibody

 from EnoGene
E033511 | 100μg/100μl: 255.00 EUR

HAT Antibody

 from EnoGene
E18-0269-1 | 50μg/50μl: 145.00 EUR

HAT Antibody

 from EnoGene
E18-0269-2 | 100μg/100μl: 225.00 EUR

HAT Antibody

 from EnoGene
E11-0356C | 100μg: 225.00 EUR

HAT antibody

 from MyBiosource
MBS5301532-01mg | 0.1mg: 465.00 EUR

HAT antibody

 from MyBiosource
MBS5301532-5x01mg | 5x0.1mg: 1945.00 EUR

HAT Antibody

 from MyBiosource
MBS9600206-01mL | 0.1mL: 260.00 EUR

HAT Antibody

 from MyBiosource
MBS9600206-02mL | 0.2mL: 305.00 EUR

HAT Antibody

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MBS9600206-5x02mL | 5x0.2mL: 1220.00 EUR

HAT Antibody

 from MyBiosource
MBS8510763-005mg | 0.05mg: 235.00 EUR

HAT Antibody

 from MyBiosource
MBS8510763-01mg | 0.1mg: 305.00 EUR

HAT Antibody

 from MyBiosource
MBS8510763-01mLAF405M | 0.1mL(AF405M): 465.00 EUR

HAT Antibody

 from MyBiosource
MBS8510763-01mLAF546 | 0.1mL(AF546): 465.00 EUR

HAT Antibody

 from MyBiosource
MBS8510763-01mLAF750 | 0.1mL(AF750): 465.00 EUR
Conclusions: information-only-based value-chain interventions may not have meaningful positive effects on diets of women and children in the lean season in settings with largely inadequate diets. We found suggestive evidence that synergies between intervention components may have introduced heterogeneity in effects on diet.
Keywords: behavior change communication; cluster-randomized controlled trial; dietary diversity; micronutrient intake; nutrition-sensitive poultry value chain.

Determination of volatile phenols in red wines by dispersive liquid-liquid microextraction and gas chromatography-mass spectrometry detection.

by
A new method was developed for analysing 4-ethylguaiacol and 4-ethylphenol in the aroma of red wines using dispersive liquid-liquid microextraction (DLLME) coupled with gas chromatography-mass spectrometry detection (GC-MS).
Parameters such as extraction solvent, sample volume and disperser solvent were studied and optimised to obtain the best extraction results with the minimum interference from other substances, thus giving clean chromatograms. The response linearity was studied in the usual concentration ranges of analytes in wines (50-1500 microg/L). Repeatability and reproducibility of this method were lower than 5% for both volatile phenols.
Limits of detection and limits of quantification were also determined, and the values found were 28 and 95 microg/L for 4-ethylguaiacol and 44 and 147 microg/L for 4-ethylphenol, respectively.
This new method has been used for the determination of the volatile phenols concentration in different samples of Tannat wine affected by Brettanomyces contamination.

High-performance liquid chromatography method development and validation for simultaneous determination of five model compounds, antipyrine, metoprolol, ketoprofen, furosemide and phenol red, as a tool for the standardization of rat in situ intestinal permeability studies using timed wavelength detection.

A simple, precise, accurate and rugged reversed-phase high-performance liquid chromatography (HPLC) method has been developed and validated for the simultaneous determination of five permeability model compounds, viz. antipyrine, metoprolol, ketoprofen, furosemide and phenol red.
The method was intended to standardize rat in situ single-pass intestinal perfusion studies to assess the intestinal permeability of drugs in the market as well as new chemical entities. Optimum resolution was achieved by gradient elution on a Symmetry Shield C-18 analytical column with the mobile phase consisting of a mixture of aqueous potassium dihydrogen orthophosphate (pH 5.5; 0.01 m) and methanol at a flow rate of 1.5 mL/min.
The retention times of antipyrine, metoprolol, ketoprofen, phenol red and furosemide were about 9, 12, 13, 16 and 17 min, respectively. Data acquisition was carried out using a photo diode array detector in the wavelength range 210-600 nm. Extraction of chromatograms was carried out by timed wavelength.
Data obtained in all studies indicated that the method was suitable for the intended purpose. The validated method was found to be linear and precise in the working range. Suitability of storage under various conditions and freeze/thaw impact at cold temperature were established to ensure complete sample recovery without any stability issues. Recovery very close to the spiked amounts indicated that the method was highly accurate and suitable for use on routine basis.

A simple and rapid high-performance liquid chromatography method for determining furosemide, hydrochlorothiazide, and phenol red: applicability to intestinal permeability studies.

A simple reversed-phase high-performance liquid chromatography (HPLC) method with ultraviolet detection at 280 nm was developed for simultaneous quantitation of furosemide and hydrochlorothiazide along with phenol red as a nonabsorbable marker for in situ permeability studies in anaesthetized rats.
A jejunal segment of approximately 10 cm was isolated and cannulated in both ends for inlet and outlet solution. The perfusate was collected every 10 min, and samples were analyzed using the developed method.
The mobile phase was acetonitrile-water-triethylamine-glacial acetic acid (41.5 + 57.4 + 0.1 + 0.9, adjusted to pH 5.6) at a flow rate of 1 mL/min; the run time was 9 min. The calibration graphs were linear for all 3 compounds (r>> 0.999) across the concentration range of 7.93-125 microg/mL for phenol red and 6.25-100 microg/mL for hydrochlorothiazide and furosemide.
The limits of quantitation were 7.2, 8.9, and 6.8 microg/mL for furosemide, hydrochlorothiazide, and phenol red, respectively. The coefficients of variation for intraassay and interassay precision were less than or equal to 7.6%, and the accuracy was between 93.2-103.4%. Using the single pass intestinal perfusion technique and the suggested HPLC method for sample analysis, mean values of 0.25 x 10(-4) (+/-0.16) cm/s and 0.22 x 10(-4) (+/-0.13) cm/s were obtained for furosemide and hydrochlorothiazide, respectively.

Construction of a colorimetric sensor array based on the coupling reaction to identify phenols

Phenols are harmful to the human body and the environment. Since there are a variety of phenols in actual samples, this requires a sensor which possesses the ability to simultaneously distinguish them. Herein, we report a colorimetric sensor array, which uses two nanozymes (Fe-N-C nanozymes and Cu-N-C nanozymes) as electronic tongues for fingerprint identification of six phenols (2,4,6-trichlorophenol (2,4,6-Tri), 4-nitrophenol (P-np), phenol (Phe), 3-chlorophenol (3-CP), 4-chlorophenol (4-CP), and o-nitrophenol (O-np)) in the environment.
Nanozymes catalyzed the reaction of hydrogen peroxide, different phenols and 4-aminoantipyrine (4-AAP) to produce different color variations. These signal changes as fingerprints encouraged us to develop a pattern recognition method for the identification of phenols by linear discriminant analysis (LDA). The six phenols at 50 nM have their own response patterns, respectively. Surprisingly, this sensor array had distinguished the six phenols in actual samples successfully.

Ultrafast Proton-Transfer Reaction in Phenol-(Ammonia) n Clusters: An Ab Initio Molecular Dynamics Investigation

The ability of phenol to transfer a proton to surrounding ammonia molecules in a phenol-(ammonia)n cluster depends on the relative orientation of ammonia molecules, and a critical field of about 285 MV cm-1 is essential along the O-H bond for the proton-transfer process. Ab initio MD simulations reveal that the proton-transfer process from phenol to ammonia cluster is spontaneous when the cluster has at least eight ammonia molecules, and the proton-transfer event is almost instantaneous (about 20-120 fs).
These simulations also reveal that the rate-determining step for the proton-transfer process is the reorganization of the solvent around the OH group.
During the solvent reorganization process, the fluctuations in the solvent occur until a particular set of configurations projects the field in excess of the critical electric field along the O-H bond which drives the proton-transfer process. Further, the proton-transfer process follows a curvilinear path which includes the O-H bond elongation and out-of-plane movement of the proton and can be referred to as a “bend-to-break” process.

Inhibition studies of bacterial α-carbonic anhydrases with phenols

The α-class carbonic anhydrases (CAs, EC 4.2.1.1) from the bacterial pathogens Neisseria gonorrhoeae (NgCAα) and Vibrio cholerae (VchCAα) were investigated for their inhibition by a panel of phenols and phenolic acids. Mono-, di- and tri-substituted phenols incorporating additional hydroxyl/hydroxymethyl, amino, acetamido, carboxyl, halogeno and carboxyethenyl moieties were included in the study.

HBSS(+) with Ca, Mg and Phenol Red, liquid

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17459-55 | 500ML: 14.70 EUR

HBSS(-) without Ca, Mg and Phenol Red, liquid

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17461-05 | 500ML: 13.30 EUR

HBSS(+) with Ca, Mg, without Phenol Red, liquid

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09735-75 | 500ML: 13.65 EUR

HBSS(-) without Ca and Mg, with Phenol Red, liquid

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17460-15 | 500ML: 8.75 EUR

RPMI 1640 with L-Gln, without Phenol Red, liquid

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06261-65 | 500ML: 9.80 EUR

DMEM(4.5g/l Glucose) without L-Gln, Sodium Pyruvate and Phenol Red, liquid

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08489-45 | 500ML: 9.80 EUR

DMEM(1.0g/l Glucose) with Sodium Pyruvate, without L-Gln and Phenol Red, liquid

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08490-05 | 500ML: 18.20 EUR

DMEM/Ham's F-12 with L-Gln, Sodium Pyruvate and HEPES, without Phenol Red, liquid

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05177-15 | 500ML: 19.60 EUR

DMEM/Ham's F-12 with L-Gln and Sodium Pyruvate, without HEPES and Phenol Red, liquid

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11582-05 | 500ML: 42.00 EUR

Phenol Saturated w/ 10% water for molecular biology (Phenol Liquid w/ 10% water), 90%

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83275 | 100 ml: 6.23 EUR

Phenol Red

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26807-21 | 1G: 18.90 EUR

Phenol Red

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26807-92 | 25G: 34.30 EUR

Phenol Red

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90817 | 25 Gms: 4.24 EUR

Phenol Red

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A3616-25G | 25G: 35.20 EUR

Phenol Red

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A3616-5G | 5G: 15.40 EUR

Phenol Red

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GT9844 | 5g: 137.69 EUR

Phenol Red

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GT9844-100 | 100: 79.10 EUR

Phenol Red

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GT9844-100G | 100 g: 132.00 EUR

Phenol Red

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GT9844-25 | 25: 31.70 EUR

Phenol Red

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GT9844-250 | 250: 150.40 EUR

Phenol Red

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GT9844-250G | 250 g: 217.20 EUR

Phenol Red

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GT9844-25G | 25 g: 74.40 EUR
The best NgCAα inhibitrs were phenol, 3-aminophenol, 4-hydroxy-benzylalcohol, 3-amino-4-chlorophenol and paracetamol, with KI values of 0.6-1.7 µM. The most effective VchCAα inhibitrs were phenol, 3-amino-4-chlorophenol and 4-hydroxy-benzyl-alcohol, with KI values of 0.7-1.2 µM. Small changes in the phenol scaffold led to drastic effects on the bacterial CA inhibitory activity. This class of underinvestigated bacterial CA inhibitors may thus lead to effective compounds for fighting drug resistant bacteria.

Isolation of exosome from the culture medium of Nasopharyngeal cancer (NPC) C666-1 cells using inertial based Microfluidic channel

by
Isolation of exosome from culture medium in an effective way is desired for a less time consuming, cost saving technology in running the diagnostic test on cancer. In this study, we aim to develop an inertial microfluidic channel to separate the nano-size exosome from C666-1 cell culture medium as a selective sample. Simulation was carried out to obtain the optimum flow rate for determining the dimension of the channels for the exosome separation from the medium.
The optimal dimension was then brought forward for the actual microfluidic channel fabrication, which consisted of the stages of mask printing, SU8 mould fabrication and ended with PDMS microchannel curing process. The prototype was then used to verify the optimum flow rate with polystyrene particles for its capabilities in the actual task on particle separation as a control outcome. Next, the microchip was employed to separate the selected samples, exosome from the culture medium and compared the outcome from the conventional exosome extraction kit to study the level of effectiveness of the prototype.
The exosome outcome from both the prototype and extraction kits were characterized through zetasizer, western blot and Transmission electron microscopy (TEM). The microfluidic chip designed in this study obtained a successful separation of exosomes from the culture medium. Besides, the extra benefit from these microfluidic channels in particle separation brought an evenly distributed exosome upon collection https://joplink.net/exosome-isolation-kits/ while the exosomes separated through the extraction kit was found clustered together. Therefore, this work has shown the microfluidic channel is suitable for continuous separation of exosomes from the culture medium for a clinical study in the future.

Characterization of surface markers on extracellular vesicles isolated from lymphatic exudate from patients with breast cancer

Background: Breast cancer is the most common cancer, and the leading cause of cancer-related deaths, among females world-wide. Recent research suggests that extracellular vesicles (EVs) play a major role in the development of breast cancer metastasis. Axillary lymph node dissection (ALND) is a procedure in patients with known lymph node metastases, and after surgery large amounts of serous fluid are produced from the axilla. The overall aim was to isolate and characterize EVs from axillary serous fluid, and more specifically to determine if potential breast cancer biomarkers could be identified.
Methods: Lymphatic drain fluid was collected from 7 patients with breast cancer the day after ALND. EVs were isolated using size exclusion chromatography, quantified and detected by nanoparticle tracking analysis, electron microscopy, nano flow cytometry and western blot. The expression of 37 EV surface proteins was evaluated by flow cytometry using the MACSPlex Exosome kit.
Results: Lymphatic drainage exudate retrieved after surgery from all 7 patients contained EVs. The isolated EVs were positive for the typical EV markers CD9, CD63, CD81 and Flotillin-1 while albumin was absent, indicating low contamination from blood proteins. In total, 24 different EV surface proteins were detected.
Eleven of those proteins were detected in all patients, including the common EV markers CD9, CD63 and CD81, cancer-related markers CD24, CD29, CD44 and CD146, platelet markers CD41b, CD42a and CD62p as well as HLA-DR/DP/DQ. Furthermore, CD29 and CD146 were enriched in Her2+ patients compared to patients with Her2- tumors.
Conclusions: Lymphatic drainage exudate retrieved from breast cancer patients after surgery contains EVs that can be isolated using SEC isolation. The EVs have several cancer-related markers including CD24, CD29, CD44 and CD146, proteins of potential interest as biomarkers as well as to increase the understanding of the mechanisms of cancer biology.

Understanding the Role and Clinical Applications of Exosomes in Gynecologic Malignancies: A Review of the Current Literature

Background: Gynecologic malignancies are those which arise in the female reproductive organs of the ovaries, cervix, and uterus. They carry a great deal of morbidity and mortality for patients, largely due to challenges in diagnosis and treatment of these cancers. Although advances in technology and understanding of these diseases have greatly improved diagnosis, treatment, and ultimately survival for patients with gynecologic malignancies over the last few decades, there is still room for improvements in diagnosis and treatment, for which exosomes may be the key. This paper reviews the current knowledge regarding gynecologic tumor derived-exosomal genetic material and proteins, their role in cancer progression, and their potential for advancing the clinical care of patients with gynecologic cancers through novel diagnostics and therapeutics.
Literature review: Ovarian tumor derived exosome specific proteins are reviewed in detail, discussing their role in ovarian cancer metastasis. The key microRNAs in cervical cancer and their implications in future clinical use are discussed. Additionally, uterine cancer-associated fibroblast (CAF)-derived exosomes which may promote endometrial cancer cell migration and invasion through a specific miR-148b are reviewed. The various laboratory techniques and commercial kits for the isolation of exosomes to allow for their clinical utilization are described as well.
Conclusion: Exosomes may be the key to solving many unanswered questions, and closing the gaps so as to improve the outcomes of patients with gynecologic cancers around the world. The potential utilization of the current knowledge of exosomes, as they relate to gynecologic cancers, to advance the field and bridge the gaps in diagnostics and therapeutics highlight the promising future of exosomes in gynecologic malignancies.

Pathogenic Mechanisms of Preeclampsia with Severe Features Implied by the Plasma Exosomal miRNA Profile

Preeclampsia is a complication of pregnancy characterised by high blood pressure and organ damage after 20 gestational weeks. It is associated with high maternal and fetal morbidity and mortality; however, at present, there is no effective prevention or treatment for this condition. Previous studies have revealed that plasma exosomal miRNAs from pregnant women with preeclampsia could serve as biomarkers of pathogenic factors. However, the roles of plasma exosomal miRNAs in preeclampsia with severe features (sPE), which is associated with poorer pregnancy outcomes, remain unknown.
Thus, the aims of this study were to characterise plasma exosomal miRNAs in sPE and explore the related pathogenic mechanisms using bioinformatic analysis. Plasma exosomes were isolated using a mirVana RNA isolation kit.
The exosomal miRNAs were detected using high-throughput sequencing and the miRNAs related to Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and gene ontology (GO) terms were analysed using the clusterProfiler package of R. Fifteen miRNAs exhibited increased expression and fourteen miRNAs exhibited reduced expression in plasma exosomes from women with sPE as compared to normal pregnant women.
Further, gene set enrichment analysis revealed that the differentially expressed plasma exosomal miRNAs were related to the stress response and cell junction regulation, among others. In summary, this study is the first to identify the differentially expressed plasma exosomal miRNAs in sPE. These findings highlight promising pathogenesis mechanisms underlying preeclampsia.

Exosome Isolation kit (for cell culture media)
10 rxn 199 EUR

Exosome Isolation kit (for cell culture media)
2 rxn 69 EUR

Exosome Isolation kit (for cell culture media)
40 rxn 1149 EUR

Exosome Isolation kit (for stem cell culture media)
10 rxn 199 EUR

Exosome Isolation kit (for stem cell culture media)
2 rxn 69 EUR

VEX Exosome Isolation Reagent (from cell culture media)
50 ml 706.8 EUR

Reagent for Total Exosome Isolation (Culture Media Supplement)
50 ml 2485.2 EUR

T-Pro Total Exosome Isolation reagent (from cell culture media)
500ml/BT 800 EUR

T-Pro Total Exosome Isolation reagent (from cell culture media)
100ml/BT 200 EUR

Cell Culture Media Exosome Purification and RNA Isolation Mini Kit
50 Preps 611.4 EUR

GenMark ePlex NATtrol

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In March, GenMark received EUA for its ePlex SARS-CoV-2 Test. Respiratory Pathogen Panel. Multiplex molecular diagnostic solutions provider GenMark Diagnostics has secured CE mark approval for its ePlex respiratory pathogen panel 2 (RP2). The ePlex RP has received FDA clearance for nasopharyngeal swab (NPS) specimens collected in viral transport media. COVID-19. ;

The RP2 Panel provides results in less than two hours for more than 20 viruses and bacteria that cause common respiratory infections with similar symptoms, including COVID-19, flu, bronchitis, and the common cold. Clinical implications of rapid eplex® respiratory pathogen panel testing compared to laboratory-developed real-time PCR Anneloes L. van Rijn, Roel H.T. Due to the batch-wise testing, laboratory-developed real-time polymerase chain reaction (PCR) assays (LDT) often result in a time to result of one day.

10/01/2019: Under Article Text added the third bullet point verbiage “For dates of service on or after 10/1/2019, laboratories billing for services using GenMark” ePlex Respiratory Pathogen (RP) Panel should report 0115U. The ePlex RP2 Control M451 is composed of synthetic DNA and RNA specifically designed for and intended to be used solely with the ePlex RP2 Panel on the ePlex System. In March, GenMark received EUA for its ePlex SARS-CoV-2 Test. Read More.

The ePlex respiratory pathogen panel (RP panel) is a novel molecular biology-based assay, developed by GenMark Diagnostics, Inc. (Carlsbad, CA), to be performed within a single cartridge for the diagnosis of 25 respiratory pathogens (viral and bacterial). in Top News. GenMarkâs ePLex-BCID Gram-Positive panel detects 20 bacterial targets, and the Fungal Pathogen panel detects 13 yeast pathogens in one and a half hours. AB Molecular Ltd. Butyl Road, Botolph Claydon, Respiratory Pathogen Panel. AB Molecular is the exclusive distributor in the UK for GenMark Dx and has been established to promote their innovative ePlex technology.

The ePlex RP2 Panel is designed for use with the companyâs ePlex system, which has been cleared by the FDA for use with the ePlex Respiratory Pathogen (RP) Panel and Blood Culture Identification (BCID) Panels (Gram-positive, Gram-negative and Fungal pathogens). The QIAstat-Dx® RP assay detected 312 of the 338 respiratory targets (92%) that were detected by the ePlex® RPP assay. This assay does NOT detect SARS CoV-2 (novel coronavirus) or MERS. Multiplex molecular panels provide high sensitivity (few false negatives) and specificity (few false positives) for multiple pathogens in ⦠GenMarkâs ePlex Respiratory Pathogen Panel 2 (RP2) achieves CE mark.

The company said RP2 drove the majority of the placements and revenues in Q3. Respiratory Panel 2 (RP2)] 0115U Respiratory infectious agent detection by nucleic acid (DNA and RNA), 18 viral types and subtypes and 2 bacterial targets, amplified probe technique, including multiplex reverse transcription for RNA targets, each analyte reported as detected or not detected [USE FOR GenMark ePlex Respiratory Pathogen (RP) Panel] SARS-CoV-2 (2 assays) Seasonal coronavirus.

We are very pleased to announce the 510(k) clearance of ePlex and the Respiratory Pathogen Panel. The new RP2 panel includes SARS-CoV-2, the pathogen that causes COVID-19. If the tube system is used, ensure specimens are in leak-proof containers that are securely closed and double bagged. ORIGINAL ARTICLE Clinical implications of rapid ePlex® Respiratory Pathogen Panel testing compared to laboratory-developed real-time PCR Anneloes L. van Rijn1 & Roel H. T. Nijhuis1 & Vincent Bekker 2 & Geert H.

Multi-morbidities of allergic rhinitis in adults: European Academy of Allergy and Clinical Immunology Task Force Report.

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Multi-morbidities of allergic rhinitis in adults: European Academy of Allergy and Clinical Immunology Task Force Report.

This report has been ready by the European Academy of Allergy and Clinical Immunology Task Force on Allergic Rhinitis (AR) comorbidities. The goal of this multidisciplinary European consensus doc is to spotlight the function of multimorbidities in the definition, classification, mechanisms, suggestions for prognosis and remedy of AR, and to outline the wants in this uncared for space by a literature overview.

AR is a systemic allergic illness and is mostly related to quite a few multi-morbid problems, together with bronchial asthma, eczema, meals allergic reactions, eosinophilic oesophagitis (EoE), conjunctivitis, power center ear effusions, rhinosinusitis, adenoid hypertrophy, olfaction problems, obstructive sleep apnea, disordered sleep and consequent behavioural and instructional results.

This report supplies up-to-date usable data to: (1) enhance the data and expertise of allergists, in order to in the end enhance the general high quality of affected person care; (2) to extend curiosity in this space; and (3) to current a singular contribution to the sphere of higher inflammatory illness.

Multi-morbidities of allergic rhinitis in adults: European Academy of Allergy and Clinical Immunology Task Force Report.
Multi-morbidities of allergic rhinitis in adults: European Academy of Allergy and Clinical Immunology Task Force Report.

A piece group report on ultrafine particles (American Academy of Allergy, Asthma & Immunology): Why ambient ultrafine and engineered nanoparticles ought to obtain particular consideration for doable hostile well being outcomes in human topics.

Ultrafine particles (UFPs) are airborne particulates of lower than 100 nm in aerodynamic diameter. Examples of UFPs are diesel exhaust particles, merchandise of cooking, heating, and wooden burning in indoor environments, and, extra not too long ago, merchandise generated by the use of nanotechnology. Studies have proven that ambient UFPs have detrimental results on each the cardiovascular and respiratory techniques, together with the next incidence of atherosclerosis and exacerbation fee of bronchial asthma.

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4381428-5x05mL 5x0.5mL
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4381429-05mL 0.5mL
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4381429-5x05mL 5x0.5mL
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4381430-002mgWithBSAAzideat02mgmL 0.02mg(WithBSA&Azideat0.2mg/mL)
EUR 230

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4381430-01mgWithBSAAzideat02mgmL 0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4381430-01mgWithoutBSAAzideat1mgmL 0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4381430-5x01mgWithBSAAzideat02mgmL 5x0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4381430-5x01mgWithoutBSAAzideat1mgmL 5x0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4380346-002mgWithBSAAzideat02mgmL 0.02mg(WithBSA&Azideat0.2mg/mL)
EUR 230

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4380346-01mgWithBSAAzideat02mgmL 0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4380346-01mgWithoutBSAAzideat1mgmL 0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4380346-5x01mgWithBSAAzideat02mgmL 5x0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4380346-5x01mgWithoutBSAAzideat1mgmL 5x0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4380742-002mgWithBSAAzideat02mgmL 0.02mg(WithBSA&Azideat0.2mg/mL)
EUR 230

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
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EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4380742-01mgWithoutBSAAzideat1mgmL 0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
MBS4380742-5x01mgWithBSAAzideat02mgmL 5x0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker)
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EUR 1725

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4381180-002mgWithBSAAzideat02mgmL 0.02mg(WithBSA&Azideat0.2mg/mL)
EUR 230

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4381180-01mgWithBSAAzideat02mgmL 0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 405

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4381180-01mgWithoutBSAAzideat1mgmL 0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 405

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4381180-5x01mgWithBSAAzideat02mgmL 5x0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 1725

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4381180-5x01mgWithoutBSAAzideat1mgmL 5x0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 1725

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4380473-002mgWithBSAAzideat02mgmL 0.02mg(WithBSA&Azideat0.2mg/mL)
EUR 230

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4380473-01mgWithBSAAzideat02mgmL 0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 405

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4380473-01mgWithoutBSAAzideat1mgmL 0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 405

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4380473-5x01mgWithBSAAzideat02mgmL 5x0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 1725

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4380473-5x01mgWithoutBSAAzideat1mgmL 5x0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 1725

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4381676-002mgWithBSAAzideat02mgmL 0.02mg(WithBSA&Azideat0.2mg/mL)
EUR 230

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4381676-01mgWithBSAAzideat02mgmL 0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 405

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4381676-01mgWithoutBSAAzideat1mgmL 0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 405

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4381676-5x01mgWithBSAAzideat02mgmL 5x0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 1725

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)
MBS4381676-5x01mgWithoutBSAAzideat1mgmL 5x0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 1725

HighQC™ Human Embryonic Hematopoietic Stem Cell
ABC-SC0106 1 vial Ask for price
Description: Human Embryonic Hematopoietic Stem Cells; Frozen Vial and Plated cells are available. Cells are only guaranteed with purchase of Gentaur Media and Gentaur Extra Cellular Matrix for appropriate cell culture, for 30 days from the date of shipment.

Human Uncharacterized hematopoietic stem/progenitor cells protein MDS032 / MDS032 (USE1) ELISA Kit
abx384157-1096tests 10 × 96 tests Ask for price

Human Uncharacterized hematopoietic stem/progenitor cells protein MDS032 / MDS032 (USE1) ELISA Kit
abx384157-596tests 5 × 96 tests Ask for price

Human Uncharacterized hematopoietic stem/progenitor cells protein MDS032 / MDS032 (USE1) ELISA Kit
abx384157-96tests 96 tests
EUR 687.5

HighQC™ Human Cord Blood-CD34+ Hematopoietic Stem Cell
ABC-SC0085T 1 vial Ask for price
Description: Desired cells are isolated using positive magnetic isolation of CD34 from cord blood. CD34+ cells are targeted using uniform, superparamagnetic polymer beads coated with a primary monoclonal antibody specific for the CD34 membrane antigen predominantly expressed on human hematopoietic progenitor cells and endothelial progenitor cells. The isolated cells are poured off into a new tube, and are cryogenically preserved.

CD34 (Hematopoietic Stem Cell & Endothelial Marker)(N/A), 1mg/mL
BNUM1807-50 1uL
EUR 396
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

CD34 (Hematopoietic Stem Cell & Endothelial Marker)(N/A), 0.2mg/mL
BNUB1807-100 1uL
EUR 225
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

CD34 (Hematopoietic Stem Cell & Endothelial Marker)(N/A), 0.2mg/mL
BNUB1807-500 1uL
EUR 485
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)(PODXL/2184), 0.2mg/mL
BNUB2184-100 1uL
EUR 225
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)(PODXL/2184), 0.2mg/mL
BNUB2184-500 1uL
EUR 485
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), 0.2mg/mL
BNUB2185-100 100uL
EUR 225
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), 0.2mg/mL
BNUB2185-500 500uL
EUR 485
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), 0.2mg/mL
BNUB2598-100 100uL
EUR 225
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), 0.2mg/mL
BNUB2598-500 500uL
EUR 485
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker)(PODXL/2184), 1mg/mL
BNUM2184-50 1uL
EUR 396
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), 1mg/mL
BNUM2185-50 1uL
EUR 396
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), 1mg/mL
BNUM2598-50 1uL
EUR 396
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC052185-100 100uL
EUR 279.6
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF405M conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC052185-500 500uL
EUR 654
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF405M conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC052598-100 100uL
EUR 279.6
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF405M conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC052598-500 500uL
EUR 654
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF405M conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC432185-100 100uL
EUR 279.6
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF543 conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC432185-500 500uL
EUR 654
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF543 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC432598-100 100uL
EUR 279.6
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF543 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC432598-500 500uL
EUR 654
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF543 conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC612185-100 100uL
EUR 279.6
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF660R conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC612185-500 500uL
EUR 654
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF660R conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC612598-100 100uL
EUR 279.6
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF660R conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC612598-500 500uL
EUR 654
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF660R conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC812185-100 100uL
EUR 279.6
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF680R conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC812185-500 500uL
EUR 654
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF680R conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC812598-100 100uL
EUR 279.6
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF680R conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC812598-500 500uL
EUR 654
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF680R conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNCP2185-250 250uL
EUR 472.8
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), PerCP conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNCP2598-250 250uL
EUR 472.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), PerCP conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNCR2185-250 250uL
EUR 472.8
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), RPE conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNCR2598-250 250uL
EUR 472.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), RPE conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC802185-100 100uL
EUR 279.6
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF680 conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC802185-500 500uL
EUR 654
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF680 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC802598-100 100uL
EUR 279.6
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF680 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC802598-500 500uL
EUR 654
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF680 conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNCH2185-100 100uL
EUR 279.6
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), Horseradish Peroxidase conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNCH2185-500 500uL
EUR 654
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), Horseradish Peroxidase conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNCH2598-100 100uL
EUR 279.6
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), Horseradish Peroxidase conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNCH2598-500 500uL
EUR 654
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), Horseradish Peroxidase conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNCAP2185-100 100uL
EUR 279.6
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), Alkaline Phosphatase conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNCAP2185-500 500uL
EUR 654
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), Alkaline Phosphatase conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNCAP2598-100 100uL
EUR 279.6
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), Alkaline Phosphatase conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNCAP2598-500 500uL
EUR 654
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), Alkaline Phosphatase conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNCA2185-250 250uL
EUR 472.8
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), APC conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNCA2598-250 250uL
EUR 472.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), APC conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC702185-100 100uL
EUR 279.6
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF770 conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC702185-500 500uL
EUR 654
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF770 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC702598-100 100uL
EUR 279.6
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF770 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC702598-500 500uL
EUR 654
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF770 conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC552185-100 100uL
EUR 279.6
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF555 conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNC552185-500 500uL
EUR 654
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), CF555 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC552598-100 100uL
EUR 279.6
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF555 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNC552598-500 500uL
EUR 654
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), CF555 conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185) Antibody
BNUB2185-50 50uL
EUR 486
Description: Primary antibody against Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) (PODXL/2185), 1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R) Antibody
BNUB2598-50 50uL
EUR 486
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/2598R), 1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R), 1mg/mL
BNUM1806-50 50uL
EUR 396
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R), 0.2mg/mL
BNUB1806-100 100uL
EUR 225
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R), 0.2mg/mL
BNUB1806-500 500uL
EUR 485
Description: Primary and secondary antibodies for multiple methodologyimmunostaining detection application

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC051806-100 100uL
EUR 238.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF405M conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC051806-500 500uL
EUR 652.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF405M conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC431806-100 100uL
EUR 238.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF543 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC431806-500 500uL
EUR 652.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF543 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC811806-100 100uL
EUR 238.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF680R conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC811806-500 500uL
EUR 652.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF680R conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC551806-100 100uL
EUR 238.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF555 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC551806-500 500uL
EUR 652.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF555 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNCP1806-250 250uL
EUR 459.6
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),PerCP conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNCR1806-250 250uL
EUR 459.6
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),RPE conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC801806-100 100uL
EUR 238.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF680 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC801806-500 500uL
EUR 652.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF680 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNCH1806-100 100uL
EUR 238.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),Horseradish Peroxidase conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNCH1806-500 500uL
EUR 652.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),Horseradish Peroxidase conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNCAP1806-100 100uL
EUR 238.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),Alkaline Phosphatase conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNCAP1806-500 500uL
EUR 652.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),Alkaline Phosphatase conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNCA1806-250 250uL
EUR 459.6
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),APC conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC701806-100 100uL
EUR 238.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF770 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC701806-500 500uL
EUR 652.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF770 conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC611806-100 100uL
EUR 238.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF660R conjugate, Concentration: 0.1mg/mL

CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R) Antibody
BNC611806-500 500uL
EUR 652.8
Description: Primary antibody against CD34 (Hematopoietic Stem Cell & Endothelial Marker) (HPCA1/1806R),CF660R conjugate, Concentration: 0.1mg/mL

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker); Clone 3D3 (Concentrate)
RA0264-C.1 0.1 ml
EUR 60.07

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker); Clone 3D3 (Concentrate)
RA0264-C.5 0.5 ml
EUR 200.66

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS438003-002mgWithBSAAzideat02mgmL 0.02mg(WithBSA&Azideat0.2mg/mL)
EUR 230

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS438003-01mgWithBSAAzideat02mgmL 0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS438003-01mgWithoutBSAat1mgmL 0.1mg(WithoutBSAat1mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS438003-5x01mgWithBSAAzideat02mgmL 5x0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS438003-5x01mgWithoutBSAat1mgmL 5x0.1mg(WithoutBSAat1mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS438569-002mgWithBSAAzideat02mgmL 0.02mg(WithBSA&Azideat0.2mg/mL)
EUR 230

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS438569-01mgWithBSAAzideat02mgmL 0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS438569-01mgWithoutBSAat1mgmL 0.1mg(WithoutBSAat1mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS438569-5x01mgWithBSAAzideat02mgmL 5x0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS438569-5x01mgWithoutBSAat1mgmL 5x0.1mg(WithoutBSAat1mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439617-002mgWithBSAAzideat02mgmL 0.02mg(WithBSA&Azideat0.2mg/mL)
EUR 230

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439617-01mgWithBSAAzideat02mgmL 0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439617-01mgWithoutBSAAzideat1mgmL 0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439617-5x01mgWithBSAAzideat02mgmL 5x0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439617-5x01mgWithoutBSAAzideat1mgmL 5x0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439698-002mgWithBSAAzideat02mgmL 0.02mg(WithBSA&Azideat0.2mg/mL)
EUR 230

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439698-01mgWithBSAAzideat02mgmL 0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439698-01mgWithoutBSAat1mgmL 0.1mg(WithoutBSAat1mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439698-5x01mgWithBSAAzideat02mgmL 5x0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439698-5x01mgWithoutBSAat1mgmL 5x0.1mg(WithoutBSAat1mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439119-002mgWithBSAAzideat02mgmL 0.02mg(WithBSA&Azideat0.2mg/mL)
EUR 230

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439119-01mgWithBSAAzideat02mgmL 0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439119-01mgWithoutBSAAzideat1mgmL 0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 405

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439119-5x01mgWithBSAAzideat02mgmL 5x0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 1725

CD34 (Hematopoietic Stem Cell & Endothelial Marker) Mouse Monoclonal Antibody
MBS439119-5x01mgWithoutBSAAzideat1mgmL 5x0.1mg(WithoutBSA&Azideat1mg/mL)
EUR 1725

anti-CD34 Hematopoietic precursor cells
513-A 1 MG
EUR 850

anti-CD34 Hematopoietic precursor cells
513-A-01mg 0,1 mg
EUR 321
Description: anti-CD34 Hematopoietic precursor cells

anti-CD34 Hematopoietic precursor cells
513-A-1000ug 1000 ug
EUR 1539
Description: anti-CD34 Hematopoietic precursor cells

anti-CD34 Hematopoietic precursor cells
513-A-100ugvial 100 ug/vial
EUR 150
Description: anti-CD34 Hematopoietic precursor cells

anti-CD34 Hematopoietic precursor cells
MBS485085-01mg 0.1mg
EUR 300

anti-CD34 Hematopoietic precursor cells
MBS485085-1mg 1mg
EUR 1300

anti-CD34 Hematopoietic precursor cells
MBS485085-5x1mg 5x1mg
EUR 5795

Anti-Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) Monoclonal Antibody
M03359 100ug/vial
EUR 468
Description: Boster Bio Anti-Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) Monoclonal Antibody (Catalog # M03359). Tested in Flow Cytometry, IF, IP, WB, IHC applications. This antibody reacts with Human, Rabbit, Rat.

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) Mouse Monoclonal Antibody
MBS438263-002mgWithBSAAzideat02mgmL 0.02mg(WithBSA&Azideat0.2mg/mL)
EUR 230

Podocalyxin (PODXL) (Hematopoietic Stem Cell Marker) Mouse Monoclonal Antibody
MBS438263-01mgWithBSAAzideat02mgmL 0.1mg(WithBSA&Azideat0.2mg/mL)
EUR 405

UFPs have been discovered to change in vitro and in vivo responses of the immune system to allergens and may also play a task in allergen sensitization. The inflammatory properties of UFPs may be mediated by a quantity of totally different mechanisms, together with the power to provide reactive oxygen species, resulting in the era of proinflammatory cytokines and airway irritation.

In addition, as a result of of their small measurement, UFPs even have distinctive distribution traits in the respiratory tree and circulation and would possibly be capable of alter mobile perform in ways in which circumvent regular signaling pathways.

Additionally, UFPs can penetrate intracellularly and probably trigger DNA injury. The current advances in nanotechnology, though opening up new alternatives for the development of expertise and medication, may additionally result in unexpected hostile well being results in uncovered human topics.

Further analysis is required to make clear the protection of nanoscale particles, in addition to the elucidation of the doable helpful use of these particulates to deal with illness.

AllergoOncology: Microbiota in allergy and cancer-A European Academy for Allergy and Clinical Immunology position paper.

by
AllergoOncology: Microbiota in allergy and cancer-A European Academy for Allergy and Clinical Immunology position paper.
The microbiota can play necessary roles in the event of human immunity and the institution of immune homeostasis. Lifestyle elements together with food regimen, hygiene, and publicity to viruses or micro organism, and medical interventions with antibiotics or anti-ulcer medicines, regulate phylogenetic variability and the standard of cross speak between innate and adaptive immune cells through mucosal and pores and skin epithelia.
More just lately, microbiota and their composition have been linked to protecting results for well being. Imbalance, nonetheless, has been linked to immune-related ailments comparable to allergy and most cancers, characterised by impaired, or exaggerated immune tolerance, respectively.
In this AllergoOncology position paper, we give attention to the growing proof defining the microbiota composition as a key determinant of immunity and immune tolerance, linked to the chance for the event of allergic and malignant ailments. We focus on novel insights into the function of microbiota in illness and affected person responses to remedies in most cancers and in allergy.
These might spotlight alternatives to enhance affected person outcomes with medical interventions supported by way of a restored microbiome.
AllergoOncology: Microbiota in allergy and cancer-A European Academy for Allergy and Clinical Immunology position paper.
AllergoOncology: Microbiota in allergy and cancer-A European Academy for Allergy and Clinical Immunology position paper.