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    gentaur-dna 940Three new genes that lead to hereditary diseases found Bulgarian doctors and geneticists. For the first time achievement was announced at the ongoing forum in Albena on "Genes, brain, intelligence, behavior."

    Studies have been made over the past year and a half, despite the lack of state funding, the researchers were able to complete their work on the project. Describing the new neurological disease will lead to the exact diagnosis, and to the possibility of prophylaxis.

    "In families where there is a risk of being born with the same desease, already possible to prenatal diagnostic and diagnostic counseling in these families. All this can prevent them from occurring in new patients in these families, "explained Dr. Ivaylo Tarnev from University Hospital" Aleksandrovksa. "

    During the forum, the national consultant in medical genetics professor Ivo Kremenski will outline problems with the implementation of new genomic research into medical practice. Will be presented and advances in the treatment of brain tumors, genetics of behavior, the problems of people with autism.

    Published in News
    Friday, 14 June 2013 14:06

    CA 15-3 ELISA Kit

    ca15-3-elisa-kitINTENDED USE
    The CA15-3 for the quantitative determination of the Cancer Antigen CA15-3 concentration in human serum. This kit is intended for research use only.

    SUMMARY AND EXPLANATION
    Breast cancer is the most common life-threatening malignant lesion in women of many developed countries today, with approximately 180,000 new cases diagnosed every year. Roughly half of these newly diagnosed patients are node-negative, however 30% of these cases progress to metastatic disease.
    There are a number of tumor markers that can help clinicians to identify and diagnose which breast cancer patients will have aggressive disease and which will have an indolent course. These markers include estrogen and progesterone receptors, DNA ploidy and percent-S phase profile, epidermal growth factor receptor, HER-2/neu oncogene, p53 tumor suppressor gene, cathepsin D, proliferation markers and CA15-3. CA15-3 is most useful for monitoring patients post-operatively for recurrence, particularly metastatic
    diseases. 96% of patients with local and systemic recurrence have elevated CA15-3, which can be used to predict recurrence earlier than radiological and clinical criteria. A 25% increase in the serum CA15-3 is associated with progression of carcinoma. A 50% decrease in serum CA15-3 is associated with response to treatment. CA15-3 is more sensitive than CEA in early detection of breast cancer recurrence. In combination with CA125, CA15-3 has been shown to be useful in early detection of relapse of ovarian
    cancer. CA15-3 levels are also increased in colon, lung and hepatic tumors.

    PRINCIPLE OF THE TEST
    The CA15-3 ELISA test is based on the principle of a solid phase enzyme-linked immunosorbent assay. The assay system utilizes a monoclonal antibody directed against a distinct antigenic determinant on the intact CA15-3 molecule is used for solid phase immobilization (on the microtiter wells). A rabbit anti-CA15-3 antibody conjugated to horseradish peroxidase (HRPO) is in the antibody-enzyme conjugate solution. The test sample is allowed to react sequentially with the two antibodies, resulting in the CA15-3 molecules being sandwiched between the solid phase and enzyme-linked antibodies. After two separate 1-hour incubation steps at 37C, the wells are washed with water to remove unbound labeled antibodies. A solution of TMB Reagent is added and incubated for 20 minutes, resulting in the development of a blue color. The color development is stopped with the addition of Stop Solution changing the color to yellow. The concentration of CA15-3 is directly proportional to the color intensity of the test sample. Absorbance is measured spectrophotometrically at 450 nm.

     

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    Published in Top Products

    In a series of lab experiments designed to unravel the workings of a key enzyme widely considered a possible trigger of rheumatoid arthritis, researchers at Johns Hopkins have found that in the most severe cases of the disease, the immune system makes a unique subset of antibodies that have a disease-promoting role.

    Enzyme-Activating AntibodiesReporting in the journal Science Translational Medicine online May 22, the Johns Hopkins team describes how it found the novel antibodies to peptidylarginine deiminase 4, or PAD4, in blood samples from people with aggressive inflammation and connective tissue damage.

    Researchers say the presence of so-called PAD3/PAD4 cross-reactive autoantibodies could serve as the basis for the first antibody-specific diagnostic test to distinguish those with severe rheumatoid arthritis from those with less aggressive forms of the disease.
    "Identifying early on a subset of patients with severe rheumatoid arthritis could benefit their health, as these patients could start aggressive drug therapy immediately and find the most effective treatment option," says senior study investigator Antony Rosen, M.D. Rosen, director of rheumatology and the Mary Betty Stevens Professor at the Johns Hopkins University School of Medicine, says that a third, or 1 million of the more than 3 million Americans -- mostly women -- estimated to have rheumatoid arthritis have an aggressive form of the disease.
    In the study, the antibodies were present -- in 18 percent of 44 fluid samples from one research collection and in 12 percent of another collection of 194 -- but only in people with severe cases of rheumatoid arthritis. Past research shows that those with the most aggressive disease are less likely to respond to anti-inflammatory treatments with steroids and other drugs.
    An examination of patients' medical records revealed that 80 percent of patients with the antibody saw their disease worsen over the previous year, while only 53 percent without the antibody showed disease progression. In comparing average scores of disease-damaged joints, researchers found that those with the antibody had an average deterioration in joints and bones by a score of 49. Those without the antibody had an average degradation in their score of 7.5, indicating much milder disease.
    In a related finding, the Johns Hopkins team also uncovered how the PAD3/PAD4 cross-reactive auto-antibodies might contribute to more severe, erosive disease in rheumatoid arthritis. The team performed a series of experiments to gauge the antibodies' effects on PAD4 in response to varying cell levels of calcium, on which PAD enzymes depend.
    Lab experiments showed that the antibodies greatly increase PAD4 enzyme function at the low levels of calcium normally present in human cells. Results showed that PAD4 activity was 500 times greater in the presence of antibodies than when they were absent. Tests of the antibody and enzymes' chemical structures later showed that the antibodies bind to PAD4 in the same region as calcium, suggesting to researchers that the antibodies might be substituting for calcium in activating the enzyme.
    According to Rosen, the series of experiments, which took two years to complete, represents the first evidence of an antibody having a direct role in generating the targets of the immune response, or auto-antigens, in rheumatoid arthritis.
    "Our results suggest that drugs inhibiting the PAD4 enzyme may have real benefit in patients with severe rheumatoid arthritis and represent an important field of study for investigating new and alternative treatments," says lead study investigator and biologist Erika Darrah, Ph.D.
    Darrah says the team next plans long-term monitoring of arthritis sufferers to find out when the antibody first appears in the blood, and when intervention may have maximum impact in preventing or stalling disease progression. The team also plans further experiments to see if the antibody is taking control of the chemical pathways normally used by other cell proteins to control PAD4 sensitivity to calcium.
    Funding support for this study was provided by the National Institutes of Health, and corresponding grant number T32-AR048522; the American College of Rheumatology; the Donald B. and Dorothy L. Stabler Foundation; and Sibley Memorial Hospital.
    In addition to Rosen and Darrah, other Johns Hopkins researchers involved in this study were Jon Giles, M.D.; Michelle Ols, Ph.D.; and Felipe Andrade, M.D., Ph.D. Additional research assistance was provided by enzymologist Herbert Bull, Ph.D.

    Published in News

    New Stem Cells on the Block

    Researchers have for the first time produced human embryonic stem cells (hESCs) using somatic nuclear transfer (SCNT), a method in which the nucleus of a donor cell—in this case a skin cell or fibroblast—is transferred to an egg cell whose own nucleus has been removed.

    The work, published in Cell, opens up the possibility of an alternative source of patient-specific stem cells to help scientists understand disease and develop personalized cell-based therapies. What’s more, hESCs produced via nuclear transfer (NT-hESCs) may not have the genetic and epigenetic abnormalities found in induced pluripotent stem cells (iPSCs), made by adding key genes to reprogram adult cells….. Continue reading HERE

     

    GENTAUR offers you a way to homogenize, disrupt, or lyse up to 24 tissue or cell culture samples at a time + keeping your samples cool.

     

    *The Bullet Blender Familiy

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    BBX24-CE Bullet Blender homogenizer, CE certified, for up to 24 tissue_cell samples - 2500 EUR

     

    *PAG-Electrophoresis? GENTAUR offers you the full equipment!

    Electrophoresis AE-6500 dual mini slab Electrophoresis AE-6500 dual mini slab with gel casting set

     

     

     

     

     

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    CacoGoblet, allows in vitro intestinal absorption evaluation of drug targets in a barrier physiologically closer to the intestinal epithlium.

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    CacoReady™ Allows in vitro intestinal absorption evaluation of drug targets.

    IsoCypTox Individual (3A4, 2E1, 1A2, 2A6) KRECE-ICT51, -ICT52, -ICT53, -ICT54 - 945 EUR

    IsoCyp-Tox allows in vitro detection and screening of biotransformation-mediated toxicity of lead and drug targets in just one single experiment.

    Published in Best Offers

    cockroach-head-gentaurIn the ongoing battle between humans and cockroaches, the insects have a leg up. A new study finds that roaches evolved their taste buds to make sweet insecticide baits taste bitter. As a result, the roaches avoid the baits and thrive, to the frustration of homeowners everywhere.

    Plenty of insects evolve resistance to pesticides; they gain the ability to break down poisons without dying. German cockroaches, on the other hand, evolved what's known as a behavioral resistance to baits. They simply stopped eating them.

    "Our paper is the first to show the sensory mechanism that underlies that behavioral resistance," said study researcher Coby Schal, an entomologist at North Carolina State University.

    The answer, Schal and his colleagues found, is in the taste buds.

    Evolving cockroaches

    German cockroaches are the small, scuttling roaches frequently seen in human habitats, including homes and restaurants. They grow to be about a half-inch (1.27 centimeters) long and are omnivorous, scavenging everything from grease to starch.

    "They'll eat pretty much anything in the kitchen, but they are incredibly good at eating things that are adaptive to them," Schal told LiveScience. "They are really amazingly good at learning to associate smells with specific tastes."

    Beginning in the 1980s, many pest control companies switched from using spray insecticides to control cockroaches to using baits. The baits combine sugars with insecticide so that roaches eat them, thinking they are sugary snacks, return to their nests and die. Ideally, the other cockroaches in the nest then cannibalize their dead relative, getting a dose of the poison, too.

    This worked beautifully — for a while. But in 1993, NC State entomologist Jules Silverman noticed that several populations of German cockroaches around the world were thriving in spite of the baits. The roaches were refusing to eat the glucose, or sugar, that was supposed to make the bait appealing.

    Bitter or sweet?

    Pest control companies switched up the sugars in their baits to keep them working, and for years, no one knew how the roaches had developed their glucose aversion. Now, Schal, Silverman and NC State postdoctoral researcher Ayako Wada-Katsumata have the answer.

    The first question, Schal said, was whether there was a change in the brains or the sensory systems of the glucose-averse roaches. To find out, Wada-Katsumata conducted a delicate procedure in which she sedated roaches with ice, immobilized them and attached electrodes to the taste hairs on the cockroach mouthparts. These taste hairs act like taste buds on the human tongue, detecting chemical signals and sending them to the insect's central nervous system.

    In normal roaches, some of the cells in the taste hairs respond to bitter tastes and others to sweet tastes. In roaches that avoided glucose, however, there was one change.

    "The system was perfectly normal, except for the fact that glucose was being recognized not only by the sweet-responding cell, but also by the bitter-responding cell," Schal said.

    In other words, the glucose-averse roaches tasted sweet things as bitter and thus avoided them. (Even cockroaches have standards, it seems.)

    Roaches could have evolved this response simply because people started poisoning them with sweet baits, Schal said. It's also possible that the trait goes way back in cockroaches' 350-million-year history. Some plants produce toxic bittersweet compounds that roaches would have needed to avoid before humans came around. Once humans started building dwellings and roaches moved in, they may have lost this sugar-avoidance ability in order to snack on humans' leftovers. When people started developing sugary baits, the preadapted anti-sugar trait may have re-emerged, Schal said.

    Either way, Schal said, the finding has implications for pest control. The industry has replaced glucose in baits with another sugar, fructose, but evidence already suggests that roaches are evolving to avoid fructose, too, he said. The industry needs to vary baits frequently and make multiple types at once to stay a step ahead of the roaches, he said.

    "If you put out a little dab of bait and see that the cockroach bounces back from it, there's no point of using that bait," Schal said.

     

    Published in News
    Monday, 27 May 2013 08:51

    What Makes Us Feel an Itch?

    It's a burning question in science—what makes us feel an itch?

    bear-itch-gentaur-antibodiesScientists experimenting in mice may have found the culprit: A molecule used by the heart is pulling double duty, sending a message to the spinal cord that ultimately produces that familiar tickle on our skin.

    The finding elevates itch—previously thought to be a mild form of pain—to a separate phenomenon, with "its own dedicated landline to the brain," study co-author Mark Hoon, a molecular geneticist at the National Institute of Dental and Craniofacial Research in Bethesda, Maryland, said in a statement.

    And because mice and people share similar biology, the scientists suspect that people also have this circuit.

    The discovery could also someday identify a way to block the molecule from producing itching—a potentially life-changing intervention for millions of people who suffer from chronic itch, particularly those with eczema and psoriasis.

    "Itch is coming into its own as a serious medical condition that deserves treatment above and beyond pain," said Earl Carstens, a neurobiologist and itch expert at the University of California, Davis, who wasn't involved in the study.

    There's even a case of a woman whose itch was so severe that she scratched through her skull into her brain, Carstens said.

    "We know much less about itch than we know about pain, and this paper advances our knowledge about the basic mechanism of itching."

    Getting to the Root of the Itch

    Called natriuretic polypeptide b (Nppb), the itch-causing molecule is already known to be released by the heart, where it controls blood pressure by regulating the amount of sodium released by the kidneys.

    The team decided to focus their research on Nppb because it showed up as a promising candidate in their search to find molecules in itch-sensing cells.

    But first the team had to show that Nppb acts as a neurotransmitter by signaling the brain to itch. 

    So they injected the molecule into mouse skin, with no results. But when the team injected the molecule into a place on the spinal cord that communicates with other nerves, the mice started scratching—a main indicator of itch.

    Next, the team genetically engineered mice that did not have the Nppb molecule.

    In an "aha moment," Hoon said, the team exposed the mice to compounds known to produce itch—and the animals didn't scratch at all. Without Nppb, the animals didn't feel an itch, according to the study.

    Itching itself likely evolved to protect us from disease, Hoon added. 

    "If you think about all of the nasty critters that come through our skin ... it's a way to protect ourselves and remove irritants on the skin before they can do damage," he said.

    Double-Duty Molecules

    UC-Davis's Carstens said "he never would have predicted" that Nppb is the itchmaker, since it has such a different role in the body.

    Co-author Hoon agreed that it's "really weird that this [molecule] is from the heart."

    But both experts noted that our bodies are extremely efficient, often finding ways to make certain parts work multiple jobs, as in the case of Nppb.

    Hoon likens it to "biological cassettes" that produce different responses when "played" in various organs of the body.

    He also suspects there are more such double-duty molecules in our body—just itching to be found.

     

    Published in News

    Bioluminescent images are acquired from NIH3T3 cells expressing SV40 promoter fused luciferase with cellgraph. The merge images of bright field and bioluminescence shown as pseudo color.

    Real-time monitoring fig

     

    Data analysis with dedicated software “Cellgraph viewer”

    Cellgraph Viewer is an image analysis software. It is very simple and easy to use, and has multiple function such as luminescent intensity measurement, making movie and montage… etc..  The ROI mode in analysis tools provides the function to measure bioluminescent intensities individually in any given region of interest. The result of analyzing bioluminescence intensity data can be exported as CSV format files. 

    Data analysis

     

    Bioluminescence imaging of a brain tissue slice containing the mouse hypothalamus superachiasmatic nucleus (SCN)

    Using the Cellgraph system, a brain tissue slice from a transgenic mouse that express luciferase under control of the clock gene promoter were analyzed. The Brain was removed and sectioned into 100 µm thick slices using a Microslicer, each of which was then placed in a culture insert. The time-lapse images of an SCN section acquired over a period of five days using the Cellgraph system. Using the grid measurement function of “Cellgraph Viewer”, the bioluminescence intensity in each area was analyzed and quantified. 

    SCN imaging fig

     

    Time-lapse imaging of intracellular trafficking of importin α

    Visualization of nucleocytoplasmic shuttling of importin α by the Cellgraph system. In this study, importin α gene fused with luciferase was expressed in NIH3T3 cells. The time-lapse images were acquired using three minutes exposure time at intervals of four minutes with a 40x objective lens without binning. The luminescence signal was initially detected in the cytosol, then in the nucleus. After that, the luminescence signal in the nucleus gradually increased. As shown above, the Cellgraph system is an ideal tool for observing biological events such as trafficking of proteins that occur over a prolonged period of time.

    Data Supported: Dr. Y. Nakajima, AIST, JAPAN References: Y. Nakajima et al. PLOS ONE, Vol. 5 (2010) 

    importin fig

     

    Visualization of ATP oscillations in the early stage of chondrogenesis

    Cellular condensation in embryonic limbs that occurs in the early stage of chondrogenesis is considered to play a critical role in the secretion of adhesion molecules and extracellular matrixes. The movie shows the visualization of ATP oscillation after the induction of chondrogenesis in ATCD5 cells transfected with an ATP-dependent Phyxothrix hirtus luciferase gene. As demonstrated in this study, the Cellgraph system is an effective tool for examining intracellular metabolic mechanisms.

    Data Supported:Dr. HJ.Kwon, Hokkaido Univ., JAPAN
    Reference:HJ.Kwonet. al., Cell Death and Disease, Vol.3 (2012) 

    ATP imaging fig

     

    Apoptosis analysis

    Cells were transfected with luciferase reporter gene fused to nuclear targeting signal sequence. Cells were stimulated with STS (1μM) and observed by Cellgraph. Cellgraph system enable us to visualize apoptotic phenomena such as nuclear fragmentation and membrane rupture in apoptotic cells by STS stimulation.

    Apoptosis fig

     

    Wound healing assay

    The result of the wound healing assay observed with Cellgraph are shown in this movie. NIH3T3 cells stably expressing luciferase were cultured until fully confluent. Wounds were created by scraping monolayer cells with a sterile pipette tip. Then wound closure was monitored by Cellgraph.

    Wound healing fig
    Published in News
    Tuesday, 21 May 2013 15:35

    mGMP GM-CSF, 50ug batch20040823

    Product number 04-RHUGM-CSF-50UG
    Product name mGMP GM-CSF, 50ug batch20040823
    Quantity  
    Supplier

    GENTAUR

     

     

    Test

    Specifications

    Results

    Identification

    Positive

    Positive

    Appearance

    Looks like a white to off-white crisp cake. After reconstitution, the solution is clear, colorless

    Complies

    Particulate Matter

     

     

               Visible particles

    Free of visible foreign particles

    Complies

     

               Sub-visible particles

    = 10µm: = 6000/vial

    = 25µm: = 600/vial

    393

    21

    Weight of content

    90% - 110% of he stated value

    Complies

    PH

    6.50 – 7.50

    7.22

    Moisture

    = 3.0%

    0.6%

    Potency

    80% - 150%

    ( 4.40-8.25x105IU/vial)

    114%

    (6.25x105IU/vial)

     

    Sterility

    Sterile

    Sterile

    Abnormal Toxicity Test

    Complies to EP 5th /CP 2005

    Complies

    Pyrogen Test (Rabbit)

    Complies to EP 5th

    Complies

    Bacterial Endotoxins

    Not more than 0.25 EU/vial

    Less than 0.25 EU/vial

    Conclusion

    Complies

    Complies

     

    For more information Contact us

    Published in Promos
    Monday, 20 May 2013 08:58

    New Stem Cells on the Block

    NT-hESCs 310Researchers have for the first time produced human embryonic stem cells (hESCs) using somatic nuclear transfer (SCNT), a method in which the nucleus of a donor cell—in this case a skin cell or fibroblast—is transferred to an egg cell whose own nucleus has been removed.

    The work, published in Cell, opens up the possibility of an alternative source of patient-specific stem cells to help scientists understand disease and develop personalized cell-based therapies. What’s more, hESCs produced via nuclear transfer (NT-hESCs) may not have the genetic and epigenetic abnormalities found in induced pluripotent stem cells (iPSCs), made by adding key genes to reprogram adult cells.

    “I think it is a beautiful piece of work,” said George Daley of Boston Children’s Hospital and the Harvard Stem Cell Institute, who was not involved in the research, in an email to The Scientist. “This group has become remarkably proficient at a very technically demanding procedure and has shown that SCNT-ESCs may in fact be a practical source of cells for regenerative medicine.”

    SCNT has previously been used to clone animals and to successfully reprogram somatic cells into ESCs is mice and primates, but little is known about how it works and which factors in the egg cell are responsible stimulating the reversion of the implanted mature nucleus to a pluripotent state.

    Moreover, all previous attempts to produce NT-ESCs have failed. Researchers have been unable to get human SCNT embryos to progress past the 8-cell stage, never mind to the 150-cell blastocyte stage from which hESCs can be plucked. The causes of the roadblock are not clear, but likely involve certain key embryonic genes from the donor cell nucleus that could not be activated.

    To overcome these obstacles, Shoukhrat Mitalipov of Oregon Health and Science University and colleagues first examined failed attempts with human cells and successful work in rhesus macaques to identify factors that could be responsible.

    The researchers evaluated various activation and culture protocols that led to successful SCNT reprogramming in monkeys, and set about testing various combinations on human oocytes. They found that the optimized protocols that worked in monkeys also worked in humans. In particular, the incorporation of caffeine into the cocktails of chemicals used during host nucleus removal and donor transplantation and the use of electrical pulses to activate embryonic development in the recipient egg improved cellular reprograming and blastocyte development, allowing human SCNT embryos to reach a stage that yielded hESCs.

    “[The researchers] worked diligently to overcome the early embryo blockade that we and others have confronted as a barrier to human SCNT,” said Daley. “Their distinct culture media, which was supplemented with caffeine, and their optimized activation protocol appears to have been the needed breakthrough.”

    “It was a huge battery of changes to the protocols over a number of different steps,” said Mitalipov. “I was worried that we might need a couple of thousand eggs to make all these optimizations, to find that winning combination. But it actually took just 128 [eggs], which is a surprisingly low number to make 6 [hESC] lines.”

    The researchers then analyzed four of these cell lines and found that their NT-hESCs could successfully differentiate into beating heart cells in vitro and into a variety of cell types in teratoma tumors on live mice. The cells also closely resembled those derived from fetal fibroblasts, had no chromosomal abnormalities, and displayed fewer problematic epigenetic leftovers from parental somatic cells than are typically seen in iPSCs. Mitalipov said more comparisons are required, however.

    “We are now left to analyze the detailed molecular nature of SCNT-ES cells to determine how closely they resemble embryo-derived ES cells and whether they have any advantages over iPS cells,” added Daley. “iPS cells are easier to produce and have wide applications in research and regenerative medicine, and it remains to be shown whether SCNT-ES cells have any advantages.”

    But Milatipov pointed out one fundamental difference: while their nuclear genome comes from the donor cell, NT-hESCs contain mitochondrial DNA (mtDNA) from the egg cell. So unlike in iPSCs, nuclear transfer not only reprograms the cell but also corrects any mtDNA mutations that the donor may carry, meaning that patient-specific NT-hESCs could be used to treat people with diseases caused by mitochondrial mutations. “That’s one of the clear advantages with SCNT,” Milatipov said.

     

    Published in News
    Friday, 17 May 2013 16:14

    Human Tenascin C Elisa Kit (TNC)

    P63316

    Antigen: Tenascin C (TNC)

    Synonyms: TN, HXB, MGC167029, Hxb, Ten, TN-C, AI528729, MGC144208, MGC144209, cytotactin, tenascin-C, C130033P17Rik, tenc, wu:fk04d02, TNC, tn, MGC140517

    Quantity: 96 Tests/kit

    Components:

    1. Assay plate (12 x 8 coated Microwells). Quantity: 1(96 wells)
    2. Standard (Freeze dried). Quantity: 2
    3. Biotin-antibody (100 x concentrate) Quantity: 1 x 120 µl
    3.HRP-avidin (100 x concentrate). Quantity: 1 x 120 µl
    4. Biotin-antibody Diluent. Quantity: 1 x 10 ml
    5. HRP-avidin Diluent. Quantity: 1 x 10 ml
    6. Sample Diluent. Quantity: 1 x 20 ml
    7. Wash Buffer (25 x concentrate). Quantity: 1 x 20 ml
    8. TMB Substrate. Quantity: 1 x 10 ml
    9. Stop Solution. Quantity: 1 x 10 ml
    10. Adhesive Strip (For 96 wells). Quantity: 4
    11. Instruction manual

    Description Synonyms: CMD1Z, TNC, TNNC, cardiac troponin C|slow twitch skeletal/cardiac muscle troponin C|troponin C, slow|troponin C1, slow

    Sensitivity: The sensitivity of this assay, or Lower Limit of Detection (LLD) was defined as the lowest protein concentration that could be differentiated from zero. It was determined the mean O.D value of 20 replicates of the zero standard added by their three standard deviations.

    Minimum Detection Limit: 0.195 ng/mL

    Detection Range: 0.78 ng/mL - 50 ng/mL

    Assay Precision: 
    Intra-assay Precision (Precision within an assay): CV%<8% Three samples of known concentration were tested twenty times on one plate to assess.
    Inter-assay Precision (Precision between assays): CV%<10% Three samples of known concentration were tested in twenty assays to assess.

    Price: 1087 EUR

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    Published in Top Products