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Today I found a very strange thing in my research gate account..it showing Citations -0..However, I saw more than 150 Citations last week..Dose anyone know how to fix it ??
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i read many papers that used the invitro drug release test but never showed the details of how they calculated the dose from it.
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You could use this paper as reference:
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Dear fellow bone researchers,
i wanted to perform some cell culture experiments using intermittent PTH treatment on human MSCs. I have tried many different conditions but haven't succeded in increasing mineralization (or ALP). Can you share a successful protocol/publication with me please?
So far i have tried:
- adjusting the dose (0.1nM - 100nM)
- adjusting the treatment duration within each cycle (1h-6h treatment per 48h cycle)
- adjusting the PTH treatment period (during the complete differentiation period vs different time frames (5d each either early, intermediate or late during differentiation)
Only thing that works is that continous treatment completely abolishes mineralization. But all iPTH conditions always result in less mineralization compared to the osteogenic medium alone.
What else can i adapt to finally recapulate the anabolic effect of PTH?
Best,
Juliane
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Hi Juliane,
That's really hard to doe reliably. FSK works better for us, esp if low dose BMP added. See wildtype cells in Fig 2g-j of PMID:23963683
Best regards,
Ed
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How does weight-based dosing of anesthesia medications differ in pediatric patients compared to adults?Weight-based dosing of anesthesia medications in pediatric patients differs from that in adults due to several factors:
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Weight-based dosing of anesthesia medications in pediatric patients differs from that in adults due to several factors:
  1. Body Composition: Pediatric patients have different body compositions compared to adults. Infants and children typically have a higher proportion of lean body mass and a lower proportion of fat compared to adults. This affects the volume of distribution and pharmacokinetics of anesthesia drugs.
  2. Metabolic Rate: Children have higher metabolic rates than adults, leading to faster drug metabolism and elimination. As a result, pediatric patients may require higher doses of anesthesia medications per kilogram of body weight compared to adults to achieve similar plasma concentrations and therapeutic effects.
  3. Organ Function: Pediatric patients may have immature or developing organ function, particularly in the liver and kidneys, which play crucial roles in drug metabolism and elimination. Adjustments in drug dosing may be necessary to account for differences in organ function and drug clearance rates.
  4. Physiological Variability: Pediatric patients exhibit a wide range of physiological variability based on age, weight, and developmental stage. This variability necessitates individualized dosing regimens tailored to the specific needs of each patient.
  5. Risk of Overdosing or Underdosing: Due to their smaller size and weight, pediatric patients are at risk of receiving doses that are too high or too low if medications are dosed based on adult guidelines. Weight-based dosing helps minimize the risk of adverse drug reactions and ensures appropriate dosing for pediatric patients.
  6. Formulation Differences: Some anesthesia medications may have pediatric-specific formulations or concentrations to facilitate weight-based dosing in pediatric patients. These formulations may be available as prefilled syringes or vials with concentrations adjusted for pediatric dosing.
Overall, weight-based dosing of anesthesia medications in pediatric patients requires careful consideration of factors such as body composition, metabolic rate, organ function, and physiological variability to ensure safe and effective anesthesia management. Close monitoring of drug effects and patient responses is essential to optimize dosing and minimize the risk of complications.
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Is it normal for Jules Morgan to publish more than 200 articles in the Lancet journal
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These are not research papers, but short overview/summary articles, usually of one page only. Jules Morgan is project manager and freelance writer in medical science, health, and education (https://www.linkedin.com/in/jules-morgan-9b3a2646/). Therefore, this number of articles is quiet normal.
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Hi,
I saw a picture on a web (https://www.chegg.com/homework-help/questions-and-answers/9-calculated-molecular-weight-native-gfp-denatured-gfp-native-denatured-proteins-differ-mo-q53517323). It show two computational formula for native and denatured GFP protein respectively. But I can not understand the behind mechanism... Is it a trusty information? Or dose anyone know about this and provided some help?
The SnapGene show that EGFP with 239 amino acids and is 26.9 kDa. But the picture showed 28.183 and 31.622 kDa respectively. That's strange....
Thanks,
Best
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It seems that someone developed a regression model for protein molecular weight in which molecular weight is 10^(-1.57x+5.38), where x is the measurement. My guess is that x is the relative mobility (values from 0 to 1) of the protein in some separation system such as electrophoresis.
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For water treatment approach, different types of adsorbents are used. They has sufficient open hand to bind with pollutants. But, in an equilibrium study, after a certain adsorbent dose, extra doses can't remove extra quantity of effluent dye. Why?
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Check the adsorption and desorption properties of your absorbent. If the desorption capability is low that absorbent will not leave the adsorbed pollutant from its surface.
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I've selected protease as the optimal enzyme for eliminating gluten formed from flour. Could you please provide insights on the best enzyme for removing gluten, dosing methods, and how to identify the suitable enzyme variant given that proteases have diverse types? This information is essential for my project aimed at resolving pipeline blockages induced by gluten from flour in the food industry using enzymes.
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Gluten is responsible for elasticity, thus breaking down gluten will change the texture/flavor. Broken amino acids can also change the chemistry of the fermentation, and thus may affect the taste as well. Most people would go for enzyme supplements as an aid in the digestion of gluten. However such ideas have been explored in the past and if you can overcome such hurdles, it can be a good project.
Have a look at these papers
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I am conducting a cell viability assay on a large sample of adherent cells unable to be distributed into a traditional sized 96 well plate. How would I analyze this larger sample? Would an ATP Glo or MTT assay be better? I will be dosing the cells with a known carcinogen followed by a treated media and then measuring viability.
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If I have understood your question correctly, are you looking for something like a 384-well microtiter plate or 1536-well microtiter plate format instead of the usual 96-well plate format to accommodate a large sample size?
If I am right, then for the cell viability assay, you should select an assay that is simple, rapid, sensitive, and cost effective. Instead of ATP Glo or MTT assay, you should go for Alamar Blue assay, which is based on a dye called resazurin, a nonfluorescent and blue dye which upon reduction (by the natural reducing power of living cells) to resorufin becomes pink and highly fluorescent.
It does not require washing steps which makes it easily amenable to miniaturization and automation. This agent is widely used to measure cell viability by prompt fluorescence (excitation: 531 nm, emission: 595 nm). The fluorescence can be easily detected using a microtiter plate reader.
For more information you may want to refer to the article attached below.
Hope this helps!
Best.
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Dose and time of upregulation of CD86 and CD80 in RAW264.7 cells using LPS/IFNgamma?
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CD86-silenced-DCs had unchanged expression of CD80 and significantly suppressed the proliferation of lymphocytes. CD86-silenced-DCs simultaneously reduced IL-2 and INF-γ and increased IL-10, TGF-β and IDO, while had minimal effect on IL-4. The CD86-silenced-DCs also improved cell viability and function of xeno-islets when compared to untransfection and transfection control groups
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For radiologists, nuclear workers, and anyone who has to work with or is exposed to ionizing radiation.
Hey everyone!
I'm a PhD candidate in materials science, working on a novel ionizing radiation detector (mainly for dosimetry). Long story short, the technology has many possible development routes. As such, I am taking it to the end users and asking what are your biggest difficulties when it comes to equipment calibration. What do you wish the dosimetry equipment would be capable of doing?
Also, on a different note, what do you wish your personal dosimeter could do?
This is just preliminary research, would love to chat more with anyone interested!
Many thanks and truly appreciate your kind feedback!
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For both.but the most important to be certified by the (SSDLs).
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I'm performing adsorption tests, using different adsorbent doses, its particles size is unknown.
To measure the final dye concentration I need to remove the adsorbent for it not to adsorb UV beam. I've been using centrifugation at 4000 rpm, which is the maximum velocity my centrifuge could reach, but it doesn't seem to help. I'm afraid I can't use filtration, it could contribute to the adsorption.
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Those dye stuffs weren't bound with adsorbent, you can't stop them from being separated when you do filtration. Actually, they weren't adsorbed. You have to subtract those values from your total percentage of removal.
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Hi. For gene deletion, I need huge quantities of highly concentrated linearized plasmid for electroporation, but, after restriction digest, I have hard time to recover satisfying quantities by ethanol or isopropanol precipitation (plasmid starting material used in restriction digest as well as linearized DNA recovered have been dosed using Qubit). Does anybody have some suggestions ?
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add salt (NaCl or ammonium acetate (1/10volume of a 5M solution ph5) before adding 2 volumes of cold ethanol
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Dear all, I hope you are well!
I would like to know how to calculate the optimal dose of human breast cancer cells to inject into female Wistar rats for testing the anticancer effect of a plant in vivo.
Also, I am slightly confused about using ethanolic extract (especially as ethanolic extract has shown anti-inflammatory activity and no toxicity in mice and is anticancerous in vitro) versus aqueous extract (based on traditional use).
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Optimizing the dose of human breast cancer cells for in vivo testing in female Wistar rats involves considerations such as tumor establishment, growth kinetics, and animal welfare. Here's a general approach to optimizing the cell dose for in vivo experiments:
  1. Establishment of Tumor Model:Select an appropriate human breast cancer cell line that is relevant to the research question and has been characterized for its tumorigenic potential in animal models. Determine the route of cell inoculation for tumor establishment. Common routes include subcutaneous (SC), orthotopic (in mammary fat pad), or metastatic (intravenous, intracardiac) injection, depending on the experimental goals.
  2. Pilot Studies:Conduct pilot studies to assess the tumorigenic potential and growth kinetics of the selected breast cancer cell line in female Wistar rats. Inoculate rats with different cell doses (e.g., 1 × 10^6, 5 × 10^6, 1 × 10^7 cells per rat) and monitor tumor growth over time by palpation or imaging techniques such as caliper measurements or bioluminescence imaging. Assess tumor take rate, latency period, growth rate, and final tumor size for each cell dose.
  3. Tumor Growth Kinetics:Analyze the growth kinetics of tumors derived from different cell doses to determine the optimal cell dose for consistent tumor growth within a reasonable timeframe. Calculate tumor volume doubling time and assess the correlation between cell dose and tumor growth rate.
  4. Ethical Considerations and Animal Welfare:Consider ethical considerations and animal welfare when determining the optimal cell dose. Avoid using excessively high cell doses that may lead to rapid tumor growth, excessive tumor burden, or compromised animal welfare. Ensure that the selected cell dose allows for the establishment of tumors that are biologically and clinically relevant to human breast cancer.
  5. Statistical Analysis:Perform statistical analysis to compare tumor growth characteristics (e.g., tumor volume, tumor weight) between different cell doses and determine statistically significant differences. Use appropriate statistical tests such as t-tests or ANOVA followed by post-hoc tests for multiple comparisons.
  6. Reproducibility and Consistency:Ensure reproducibility and consistency of tumor growth across multiple experiments by repeating the experiments with the selected optimal cell dose. Validate the findings by comparing tumor growth characteristics between independent experiments.
  7. Validation of Tumor Model:Validate the established tumor model by histological analysis, molecular profiling, or functional assays to confirm its similarity to human breast cancer and its suitability for preclinical studies.
By following these steps and considering factors such as tumor growth kinetics, animal welfare, and experimental reproducibility, you can optimize the dose of human breast cancer cells for in vivo testing in female Wistar rats. This optimization process is essential for generating reliable and relevant data for preclinical research and drug development studies.
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I am testing cancer prevention mechanisms and am going to dose HEK cells with ethidium bromide to cause cancer. What is the procedure for dosing with ethidium bromide?
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Ethidium bromide has been shown to bind strongly to both DNA and RNA in vivo and in vitro by intercalation between adjacent base pairs. Almost all studies to date implicate the mitochondrion as the primary target site of ethidium bromide at low concentrations. Nanogram to microgram concentrations of ethidium bromide per milliliter of culture medium induces loss of mitochondrial DNA and complete loss of mitochondrial DNA occurs after 5–6 weeks of exposure, and this approach has facilitated the study of mitochondrial mutations.
Treatment of cells with ethidium bromide has been found to result in the loss or alteration of mitochondrial DNA and RNA, the selective inhibition of mitochondrial DNA polymerase, the alteration of the cytochrome system, and morphological abnormalities of the mitochondrion. Studies in cells that have lost mitochondrial DNA over a period of weeks in culture report increased mRNA levels of genes involved in hypoxic response, mitochondrial ribosomal proteins, solute transport, and glycolytic pathways.
You may use concentrations ranging from 10 to 100 ng/ml for a few weeks.
You may want to refer to the articles attached below for more information.
Best.
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The formula for converting oral dose to inhalation dose:
D(inhalation)= D(oral) * (bioavailability for inhalation/ bioavailability for oral administration)
if the bioavailability for inhalation not available in literature, how do i calculate the inhalation dose? any other method to calculate the inhalation dose?
Thank you
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You may have more success asking this question on the NONMEM user list.
The NONMEM Users Network is maintained by ICON Clinical Research LLC. Requests to subscribe to the network should be sent to: [email protected]
Alternatively, you could try building up your model graphically with Phoenix's NLME tool if you have access to this engine as I find it more user friendly. Then you could estimate bioavailability.
If you really have no idea of bioavailability(?similar compounds, formulations.) then you could at least simulate a few different scenarios to see what might be a safe dose for FIM.
Simon.
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I could understand that paraphrasing is important to avoid plagiarism. But the increasing rate of publishing is making paraphrasing more complex. Let me explain:
"Drug X has a cardio-protective effect when administered in small dose."
This is a core SENTENCE in any research discussing this drug.. Keep it in mind!
In 1999, there was only 10 researchers working on this drug. So, when each one of them was going to publish his article he would easily PARAPHRASE this sentence. The odds of changing the meaning while doing paraphrasing are unlikely.
Now, There are 1000 researchers trying to do the same! So, changing the meaning is LIKELY to happen because you have to write in different ways and utilize a wide range of vocabs which will affect the meaning. And worth yet, if you're citing a secondary article _ You're paraphrasing the paraphrased!!
And why all of this?
Just to get a paraphrasing report of <10%.
It does not make sense!
The novelty of research is not represented in the literature review!
So, why do they make it an obstacle for researchers?!
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Moohebat Shoyukhi : Regarding your two questions:
  1. So, what is the optimal solution for eradicating distortion in scientific research? IMHO, eradicating will no longer be possible, due to the strongly interacting multiple causes of it, almost all man-made, i.e., in the broadly conceived scientific community. You might as well ask: what is the optimal "solution" for eradicating crime in society (locally or globally)? But we may do our best to detect and counteract it whenever we encounter it. And with "we" I mean ALL scholars / researchers / scientists. Don't leave it to special organizations / committees / institutions. Again, a comparison with crime detection and prevention is worthwhile: all societies have (their own) legal institutions going back many thousands of years, but it has not helped much in abolishing crime. We have to come to live with it, forever, for the best or worse. What we as honorable scientists can do is to be always alert, talk about it with each other loud and clear, and to do what we as scientists are best in: pointing it out in written texts with facts and arguments. That will be a "struggle for the truth", I doesn't happen of its own.
  2. Should researchers continue paraphrasing despite their awareness of possible confusion for future generations? In itself, paraphrasing is not bad, but, speaking for myself, I prefer to read literal citations, in parentheses, even indented, with explicit page numbers to it. In some fields of science, and for some purposes (e.g., theoretical discussions), this has become a normal procedure. And I like to read the original words and phrases of the cited authors. When you are paraphrasing, you will always "distort" the original in some way. Why should you do that?
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How can I calculate the used dose of substance in vivo (intratesticular) after determining the effective dose of it in vitro (on semen sample)?
Say, if 3 mg of a substance is effective to kill sperms in vitro study, how much mg we have to use in vivo (intratesticular) for chemical sterilization?
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Hi Dear Ahmed,
I think you can prepare different concentrations of this substance, then you can try each concentration in vivo. After that, you have to carry out semen analysis and sperm count, then based on the results you can select the appropriate concentration or mg of the substance.
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My question is on the way of expression of allele specific copy number variation, e.g. individual 1 has a CNV as 3, 3, on each allele, with 6 copies; and individual 2 has 1, 5, on either allele, also 6 copies. If both patterns will express exactly the same way Solly based on gene dosage? or there is a different scenario?
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This question is very interesting. The following is my explanation. However, I will be very happy to be corrected.
In terms of gene dosage, both individuals would have the same total number of copies of the gene (6 copies), which can influence gene expression levels. However, the expression of the gene might differ due to allele-specific effects. Allele-specific copy number variation can lead to differences in gene expression levels between alleles, potentially resulting in different phenotypic outcomes or disease susceptibilities. Therefore, while the total gene dosage may be the same, the allele-specific patterns could lead to different expression profiles and phenotypic consequences.
An example scenario could be, say the allele with fewer copies (allele 1 in individual 2) contains a regulatory sequence that enhances gene expression, while the allele with more copies (allele 2 in individual 2) contains a regulatory sequence that suppresses gene expression.
In this case, individual 2 might have higher expression levels of Gene X compared to individual 1 due to the presence of the enhancing regulatory sequence on the allele with fewer copies. This could result in different disease outcomes or phenotypic presentations despite both individuals having the same total gene dosage.
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We have done a dose response study for a synthetic antibiotics. We have noticed that bacterial growth inhibition decreases as the concentration of the decrease and show a zero inhibition at 0.015 uM. But, then at lower concentration (0.0078 and .0039 uM) the inhibition retrieved and was 10 and 22 percentage respectively. This is a results for three trials. How can we explain this phenomenon?
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There may be a threshold concentration below which the antibiotic is not effective in inhibiting bacterial growth. This threshold might be around 0.015 uM, explaining the zero inhibition observed at that concentration. At lower concentrations (0.0078 and 0.0039 uM), the antibiotic may start to exhibit hormesis, a phenomenon where low doses have a stimulatory effect. In this case, the low concentrations might stimulate bacterial growth inhibition rather than inhibit it.
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Hi. I am seeking some guidance in understanding how the dosing works on typical gas sorption equipment (the attached shot is from a Micromeritics 3 Flex).
I describe what I think is the case below and am asking others to correct me or add to my description as necessary. I then ask my question regarding equilibrium at the end - feel free to skip to the end.
In setting up an analysis, the operator defines a set of target pressures to collect data points at. The operator also defines absolute and/or relative tolerances for the target pressure. I.e. so the instrument does not need to reach exactly the defined pressure value.
During the analysis the instrument injects a quantity of gas into the tube that it expects might get it close to the target pressure. The quantity is determined based on measured or estimated free space, manifold volume etc. (when fixed quantity dosing is not selected). The instrument then waits for "equilibrium".
When equilibrium is reached, if the target pressure has been achieved, within the set tolerances, the instrument will record a data point and move on to the next target pressure the operator has defined in the analysis setup. If the target pressure has not been achieved, the instrument will inject another quantity of gas and wait again for equilibrium. The whole process repeats until all adsorption data is collected. Desorption curves are similar, but gas is being removed via the vacuum system.
My question is, what determines "equilibrium"? The attached image shows a setup where the instrument has been asked to check for equilibrium every 10s. The rate of change between checks is around 0.015%. I have seen the instrument inject more gas when the rates of change between intervals are much higher than this so I am confused about what is the guiding criteria for "equilibrium reached" in the programming of the instrument. Indeed there is no consistent value in any of the numbers displayed that seems to relate to what defines equilibrium. This is very frustrating since it is not easy to understand why some analyses can take hours to equilibrate a single dose, and even then, not necessarily reach the target pressure to record a data point.
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Can everyone help me why in low doses of a drug grow impurity, but for the same drug in higher dose we have no impurity with over time?
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Hi,
Please check the analytical method for control of these impurities. For the same drug in higher doses, there may be no impurity over time because the impurities may be present in such small amounts that they are not detectable by the analytical methods used (another baseline shift related to the presence of a high concentration of drug product). It may be method-related especially in the case of optical detection like UV, PDA, FL etc., and if the method does not cover in preparation of the sample any extraction method (separation of signals related to drug substance and impurity). Double-check with mass spectrometry if possible.
Best regards
Tomasz
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Hello,
We are trying to analyze data from different patients. Here's the summary for the entire cohort:
1) Each patient will be followed over time.
2) Each patient will be given a starting dose of a compound, and a certain lab readout will be generated for that time point at that starting dose.
3) As time progresses, the dose will be increased/maintained, and a different readout will be generated by then. The dose adjustment will be done on a clinical basis.
Our question is:
We wanted to know whether increasing the dose would significantly change the readout at that certain time point. Two-way ANOVA (or a repeated two-way ANOVA) will erroneously provide us with a result. Which tool/statistical test would be appropriate for this scenario?
Thanks!
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Statistical tool or test can be used for dose-response curve with time component is the nonlinear regression. You can use nonlinear regression to quantify the fold shift in the dose and its confidence interval, and to compute a P value that tests the null hypothesis that there was no shift.
That method is only applicable when the number of means is greater than 5, otherwise you must use multiple means comparison methods such as Dunca, Tukey, Newman-Keuls, etc. However, the statistical design issues related to dose-ranging studies are not always keenly understood and a poorly designed study can be costly for later development.
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I wanted to draw standard curve of Novobiocin in phosphate buffer(7.4), and I made 2,4,8,16,32 and 40 microgram/ml. but It did not show any absorbance in UV spectrometer. I want to know its problem.
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Even around 390nm?
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I'm a PhD candidate at the University of Groningen and I'm doing a systematic review using RevMan. I am researching different doses of a medication compared to the control. When I have 2 intervention groups (e.g. medication A 20mg and medication A 40mg) and only 1 control group (placebo), is it correct to separate the different doses into subgroups within the meta-analysis? For example, I want to do a meta-analysis but with subgroups: medication A 20mg x control and medication A40mg control. In this model, at the end of the meta-analysis there is a total of all the studies. However, the total number of patients in the control group is not correct because I have to add twice the total number of the control group. Is this correct? Is there any other alternative?
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Hi Thiago,
If both the 20mg and 40mg effect sizes are measured with respect to the same control group, and thus originate from the same study, I would not perform a subgroup analysis in a standard meta-analysis framework. I'll refer to Chapter 10 of the following book:
"Statistical independence is one of the core assumptions when we pool effect sizes in a meta-analysis. If there is a dependency between effect sizes (i.e. effect sizes are correlated), this can artificially reduce heterogeneity and thus lead to false-positive results."
If the estimates for 20mg and 40mg come from the same study, the estimates are likely correlated, which would lead to a violation of the independence assumption.
If you are still interested in performing a subgroup analysis, you could incorporate it into a multilevel meta-analysis with medication dose (20 mg vs 40mg) as one of the explanatory variables. If you look at equation (10.8) in the book chapter I referred to earlier, you see that a multilevel meta-analysis incorporates a second random-effect: one to account for clustering of effect sizes within the same study. Statistically, this would be the correct way to pool your correlated effect sizes (if you insist to combine them).
Hope this helps!
Kind regards,
Michael
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Hi,
I am working on developing type 2 diabetic rats (Sprague Dawley) using High-fat diet followed by a low dose of STZ injection I.P (30 mg/kg ).
so those who have previous experience with this model, I would like to know the dose of STZ that was used? and in case of not developing diabetes after the first injection, will you follow up with other injections in consecutive days or following specific intervals?
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Did you start your research using STZ? I need your recommendation as I am going to conduct a work wit STZ for T2DM
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Say you have been asked to design an experiment to complete a pharmacokinetic profile of a new antidepressant drug, How would you go about deciding what doses to use for (Oral / IV) administration in an in-vivo animal model using rats for example? Providing you have no toxicology information, would you use dosages that have been used in other anti-depressant studies? or is there a general rule for minimum / maximum doses being used for PK studies?
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Dear friend Jake Ellis-Williams
Alright, let's tackle this like I would!
Designing a pharmacokinetic study for a new CNS drug, eh? Now, we're talking real science. First things first, if you Jake Ellis-Williams don't have any toxicology data, you're in a bit of a tight spot. But I dont shy away from challenges!
1. **Start Low, Go Slow:**
- In the absence of toxicology data, the golden rule is to start low. You Jake Ellis-Williams don't want to accidentally turn your rats into rocket ships, do you? Use a dose that's unlikely to cause adverse effects.
2. **Reference Similar Compounds:**
- Check out similar drugs in the antidepressant family. It's not a perfect science, but it gives you Jake Ellis-Williams a ballpark figure. Look at the literature, see what doses they used, and take a leap from there.
3. **Consider Route of Administration:**
- Are you Jake Ellis-Williams going oral or intravenous? Oral is more common, but if you're feeling adventurous, go IV. Adjust your dose accordingly; IV doses are typically lower due to higher bioavailability.
4. **Species Matters:**
- Rats are not humans. Shocking, I know. Their metabolism differs, so don't just scale up a human dose. Consider allometric scaling, a fancy term for adjusting doses based on body surface area.
5. **Monitor Behavior:**
- Keep a close eye on your rats. If they start tap-dancing or speaking French, you Jake Ellis-Williams might have gone a bit too high. Watch for signs of toxicity and adjust your doses accordingly.
6. **Pilot Studies are Your Friends:**
- Before diving into the big show, run some pilot studies. Test the waters with a few rats. It's like a movie trailer – gives you Jake Ellis-Williams a taste without committing to the full feature.
7. **Consult the Oracle (Experienced Scientists):**
- If you Jake Ellis-Williams have access to seasoned scientists, consult them. They've been around the block and can provide invaluable insights. Wisdom often comes with gray hair and lab coats.
8. **Ethics Committee Approval:**
- Don't forget to run your doses past the ethics committee. They might not have a Ph.D., but they know a thing or two about keeping experiments humane.
Remember, my science-seeking friend, this isn't a one-size-fits-all scenario. The key is to be cautious, use your scientific instincts, and be ready to adapt as your data rolls in. May the pharmacokinetics odds be ever in your favor!
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In British Pharmacopoeia, the limit of Enalapril impurity D is 1%. However, in ICH has specified that with Maximum Daily Dose 10-100mg (Enalapril Maleat is 40mg), Qualification Threshold would be 0.5%.
I couldn’t find any biological security study to explain this situation.
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Hien Nguyen,
When mixed in a matrix such as in a tablet with additional excipients, enalapril is unstable and can degrade to an unwanted cyclized diketopiperazine (DKP). Mostly the higher limit is given based on the safety data. BP should have all data and same can be asked through FOI. Also monitor your drug product stability up to 6 Months accelerated Intermediate & RT condition and then can assigned limit as per Qualification Threshold i.e 0.5%.
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I need to understand the equation for oil palm fertilizer dose recommendation (i'm so sorry for my bad english)
Thank you
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Fertilisers can make up 60 percent of the total costs of producing palm oil so it is important to apply fertilisers efficiently.Different fertilisers have different concentrations of nutrients.
The effect of major nutrients on growth and yield of oil palm has been studied in most of the oil palm growing countries in Asia and Africa.
a) Nitrogen: In oil palm, characteristic yellowing symptoms are developed under N deficiency conditions. Nitrogen is found to be essential for rapid growth and fruiting of the palm. It increases the leaf production rate, leaf area, net assimilation rate, number of bunches and bunch weight. Excessive application of nitrogen increases the production of male inflorescence and decreases female inflorescence thereby reducing the sex ratio.
b) Phosphorus: In oil palm seedlings, P deficiency causes the older leaves to become dull and assume a pale olive green colour while in adult palms high incidence of premature desiccation of older leaves occurs. Phosphorus application increases the bunch production rate, bunch weight, umber of female inflorescences and thereby the sex ratio. c) Potassium: When potassium is deficient, growth as well as yield is retarded and it is translocated from mature leaves to growing points. Under severe deficiency, the mature leaves become chlorotic and necrotic. Confluent orange spotting is the main K deficiency condition in oil palm in which chlorotic spots, changing from pale green through yellow to orange, develop and enlarge both between and across the leaflet, veins and fuse to form compound lesions of a bright orange colour.
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solve:
The exposure rate from a point source of radiation can be calculated using the formula:
Exposure Rate= Activity*Exposure Rate Constant​*(Distance)^(-2)
For Cobalt-60 (Co-60),
The exposure Rate Constant (Γ) is 1.32 R m² hr⁻¹ Ci⁻¹1.
Given:
Activity (A) = 100 Ci
Distance (d) = 2 m
Substituting these values into the formula, we get:
Exposure Rate=100Ci×1.32R (m² hr⁻¹ Ci⁻¹)​*(2m)^(-2)=33R/hr
This is approximately 32 R/hr, which is the exposure rate you mentioned. Please note that this is a simplified calculation and actual exposure rates can vary based on other factors such as shielding, air absorption, and energy of the emitted radiation.
The exposure rate from a 100 Ci point source of Co-60 at 2 meters is given as 32 R/hr. To convert this to mSv/h, we can use the conversion factor that 1 Roentgen per Hour (R/h) is equivalent to 10 Millisievert per Hour (mSv/h)1.
So, if we have 32 R/hr, we can convert it to mSv/h using the following calculation:
32 R/hr * 10 mSv/h/R = 320 mSv/h
Therefore, the dose rate D in mSv/h is 320 mSv/h.
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solve:
The exposure rate from a point source of radiation can be calculated using the formula:
Exposure Rate= Activity*Exposure Rate Constant​*(Distance)^(-2)
For Cobalt-60 (Co-60),
the Exposure Rate Constant (Γ) is 1.32 R m² hr⁻¹ Ci⁻¹1.
Given:
Activity (A) = 100 Ci
Distance (d) = 2 m
Substituting these values into the formula, we get:
Exposure Rate=100Ci×1.32R (m² hr⁻¹ Ci⁻¹)​*(2m)^(-2)=33R/hr
This is approximately 32 R/hr, which is the exposure rate you mentioned. Please note that this is a simplified calculation and actual exposure rates can vary based on other factors such as shielding, air absorption, and energy of the emitted radiation.
The exposure rate from a 100 Ci point source of Co-60 at 2 meters is given as 32 R/hr. To convert this to mSv/h, we can use the conversion factor that 1 Roentgen per Hour (R/h) is equivalent to 10 Millisievert per Hour (mSv/h)1.
So, if we have 32 R/hr, we can convert it to mSv/h using the following calculation:
32 R/hr * 10 mSv/h/R = 320 mSv/h
Therefore, the dose rate D in mSv/h is 320 mSv/h.
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if there's any way of converting an in vivo dose e.g., 20 mg/kg in rat, into a concentration µM that can be used in in vitro assays, or vice versa.
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The concentration in the rat plasma or tissue will change over tine following the dose, so there is not one single concentration to which to compare. Instead, you will have to measure the in vivo concentration as a function of time after dosing (pharmacokinetics). Then you will be able to compare the in vivo concentration at each time point to in vitro potency at that concentration.
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I determine IC50 value of compounds impacting kinase activity using AssayQuant. And the compound show biphasic inhibition, i want know what does it mean? By the way, the compound is not ATP competitive.
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Cornelius Krasel Thanks for your reply and it make a lot sense.
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I see many papers that used different doses of Salmonella Enteritidis in the chicken infection model for the same type of chickens e.g., Ross-308 broiler. It also varies at different ages of the chickens, but I found different doses for the same-aged chickens. The dose varied from 1*10^5 to 1*10^9. So, how can I decide which dose I should try to give a challenge to chickens for my experiment?
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Dear researcher, according to the state of the bird's immune system, the dominant dose of the microbial population in the occurrence of pathogenicity will be different. Also, the bird's immune system is influenced by age. Therefore, in detailed tests, the microbe strain is usually tested with different doses and ages to get the best results.
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Kindly explain
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Mital valve related to systemic circulation. So, mobilization from it causes stroke & on the otherhand tricuspid valve related to pulmonary circulation. So, duration of antibiotic treatment is long incase of mitral valve infection.
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I get primary microglia from P0 transgenetic pups with flox. after 10-14 days mixed culture, I get microglia and seed on 12 plates. I want to knockdown the specific gene with flox, then I used a lentivirus (pultra-cre) which my coworkers have proved can upregulate microglia gene with stop flox. But it dose not work on my microglia. I extract RNA and stain cre/Iba1/GFP to verify the knockdown effect (as the figures show, it dosen't work).
I wonder if someone has met this before. Why a lentivirus can be used to upregulate one gene with stop flox but can not be used to downregulate another gene? I used the same DMEM and FBS as my coworkers.
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You could try to infect your microglia during their ex-vivo proliferative phase, during the 10-14 days culture. Do you add M-CSF during culture? You could add you lentivirus at the same time and remove it at the next medium change.
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My study aims at developing an animal model for type II diabetes. I don’t quite understand the power calculation, particularly in regards to the values I would substitute into the equation, as it relates to the development of the animal model, and not the treatment of an already developed model. How can I go about calculating the number of animals I require for my study to develop this model?
Keep these things in mind:
- the proposed model is for type II diabetes in combination with its microvascular complications
- I currently have two STZ dosage mechanisms: multiple low dose (MLD X 5 days) and single moderate dose (SMD)
- for the SMD and MLD groups, there are 3 doses per group, as well as 2 controls, for a total of 10 overall groups (6 subgroups will be treated with STZ and 4 control groups)
- in order to validate the disorder and the associated complications, I will be euthanising 3 animals from each experimental group, fortnightly for analysis.
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The new site for sample size calculation is <https://sample-size.net/>. Unfortunately, there is no option for parallel group design, so I was unable to input the parameters you suggested with the corresponding figures in your answer. Can you kindly assist me?
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Through a Wnt inhibition assay, I have found out that my test drug, which is easily available in the market and used for Hyperlipidemia, is a good Wnt inhibitor. Now, I want to conduct an animal study. How can I determine the dose of my test drug?
Many articles are available for my drug for various diseases. Can I take doses from these articles? I need three doses: Low, Medium, and High."
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Hi Ruchi...you didn't mention what kind of model organism is going to be used in vivo studies. No. of factors have to be taken into consideration for in-vivo drug administration studies. As Kerry S Vistisen suggested, you should follow the other articles as references for test drug administration. Also, if your test drug is a repurposed drug, follow the guidelines of the FDA and compare test drugs with references to drug-dose conversion from various databases such as PubMed and Google.
The following article will help you to understand the basics of animal drug administration:
Turner PV, Brabb T, Pekow C, Vasbinder MA. Administration of substances to laboratory animals: routes of administration and factors to consider. J Am Assoc Lab Anim Sci. 2011 Sep;50(5):600-13. PMID: 22330705; PMCID: PMC3189662.
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If we treat NHDF cells with ascobic acid for 1 hour at 33ug/mL and then irradiate the cells with a low dose of UVA we see a good antioxidant response and cell viability does not change compared to non-irradiated NHDF cells. However, if we followed this procedure but with a incubation of ascorbic acid for 24 hours, after irradiation we were unable to detect an antioxidant effect and we also observed an increase in cell viability.
We know that ascorbic acid can reduce our cell viability reagent, but we do not know why its antioxidant effect and viability depend on its incubation time. Do you have any idea?
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How do You measure antioxidant effect? How it differs (InYourHumbleOpinion) from cell "viability". What form of ascorbic acid are You using (cat. nr)?
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Hi there,
I had some trouble finding suitable concentrations for the synergism of two drugs. My experimental design is as follows, and the calculation is used CompuSyn:
Data for Drug: A [uM]
Dose Effect
50.0     0.0792
100.0     0.3117
250.0     0.3938
500.0     0.5575
1000.0     0.9502
Data for Drug: B [uM]
Dose Effect
50.0     0.017
150.0     0.1656
300.0     0.3788
500.0     0.6461
700.0     0.7935
CI Data for Non-Constant Combo: A+B
Dose A Dose B Effect CI
10.0     500.0     0.6129     1.12282
25.0     500.0     0.6742     1.02014
50.0     500.0     0.6381     1.17713
100.0     500.0     0.6313     1.33936
250.0     500.0     0.6847     1.55157
I would like to find suitable concentrations for A+B (CI<1.0), but failed. Please give me some suggestions, thanks a lot!
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If you are working on Chemotherapeutic agents, first determine the Minimum Inhibitory Concentration of each of the substances. Then combine the substances at 25% of the MIC of each substance. If you don't obtain expected effect at this point, try additive effect by combining 50% of the MIC of each drug.
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I need to know dose of paraffin oil per lit or per 10 lit of water and how to use it as insecticide.
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  1. Paraffin oil can be used as a pesticide to control certain pests on plants. It may be works by suffocating the insects and disrupting their respiratory system. A common dilution ratio for paraffin oil is 2-5%. This means you'll use 2-5 parts of paraffin oil for every 100 parts of water.
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A number of samples from Russia were constantly far too old compared to C-14 ages. The samples were X-rayed at the border crossings several times before entering the lab for age measurements. I guess x-raying should have no effect but would like to have a firm confirmation on this from experts.
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Thanks Maxim!
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Can someone explain it?
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Welcome Sansar Chand ji. Just adding one more point that, some low Temp. peaks do not survive/not stable for not more than 5-10 days particularly those whose Tm is below 120 C or so. If u r making measurements after 2 weeks of irradiation, they will disappear. Additionally typical temperature gradient of 20C or so may occur as we generally record Temp of planchet and not of phosphor/disc/crystal, so generally Tm in recording always higher than actual values, more the heating rate , more is €temp gradient. So always maintain single layer of phosphor grains or use thin discs/crystals preferably below 0.4 mm or so to minimise the Temp. gradients.
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I am planning to induce status epilepticus with a subconvulsive dose of pilocarpine. I have experience with the pilocarpine model but try to find out a subconvulsive dose.
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Thank you Espinosa
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I have exposed the Gaff Chromic film and then scanned it, now in MATLAB, I have to write a code to convert it to dose and then obtain the calibration curve of the film.
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@Yousef Bahrambeigi
Hi Mr Yousef Bahrambeigi
Thank you for your patience and taking the time to respond
Your answers are thorough and
helpful I had another question,
how can I create a dose vector؟
As you mentioned :
Next, you need to plot the OD values against the known doses for each channel and fit a curve to them. You can use the plot function to plot the data and the polyfit function to fit a polynomial curve. For example, if you have a vector of doses named dose and a vector of OD values for the red channel named OD_red
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I am developing model for my preliminary studies to check my compound's antidiabetic activity. For this, I tried two different doses i.e. 50 mg/kg and 60 mg/kg of STZ two different times and checked FBG 72 hours later. With the first dose I found no elevated glucose level while with the second dose, my rats died after one day. I need suggestions for developing this model.
Note; as this is just a trial that's why I did not go for a high-fat diet. Please help me in this regards.
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You can check out Alloxan induced diabetic model, or HFD with low stz diabetic model
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My research aims to produce a novel mouse model for T2DM and I have two dosage techniques to administer STZ in C57BL/6 mice: single high dose (SHD) and multiple low dose (MLD). Within these groups, in my study design I have divided my animals into three subgroups:
- SHD: 75 mg/kg, 100 mg/kg, and 150 mg/kg
- MLD: 40 mg/kg, 50 mg/kg, and 60 mg/kg, each for 5 days.
When it came to the MLD groups, I basically sandwiched the standardised protocol provided by DiaComp of 50 mg/kg dose of STZ with a dose 10 mg/kg higher and lower. However, the ethics committee is requesting a substantiation for this and thus I would like to know if what I did is correct, and if there's literature to back this up, or if I should change my MLD dosage groups altogether. Please assist. Bear in mind, the model aims to assess the major microvascular complications, and thus the diabetic condition should mimic the later stages of the disease.
Thank you.
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Hi Khan,
I'm sharing a paper with you that discusses what you need and points out that there are different variations in the induction of experimental diabetes in animal models between laboratories. My recommendation is that you conduct assays with at least three doses, for example, 50, 75, 100 mg/kg of STZ, and evaluate the glucose levels in your mices. This will allow you to observe the behavior and dynamics, and then determine which model best suits your needs. Also, please consider whether you want to induce type 1 or type 2 diabetes. Just administering STZ will resemble type 1, but if you add diet or nicotinamide, it will resemble type 2 diabetes.
Best regards, Jorge Armando
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dose titration , dose escalation
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There was a similar question posted on this platform. Please refer to the link below.
Best.
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I performed the ITC (isothermal titration calorimetry) experiments by titrating the LUVs made of POPC and POPG into the daptomycin solution. After exporting the data in the Excel, I used the Origin for the fitting the curves in order to find the binding constant. No function fitted that well as the biphasic dose response function, but the x axis is in my case is linear, and not logarithmic. Is it allowed to leave as linear-scaled?
Thank you very much for the responses
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Even if a certain function can reproduce the experimental data, this does not allow you fitting the data with that function, because the parameter estimations you get may be meaningless. I am sure you can fit the data with many functions, even with a high-order polynomial. The dose-response function is not appropriate, for many reasons.
You must couple appropriate interaction model equations with the instrumental equations, and from that you will be able to get valuable information for your system.
In addition, there is no justification to consider a biphasic isotherm. What you observe around molar ratio of 5-7 is within experimental uncertainty.
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I am writing to report a concerning issue I've encountered during my recent migration assay using RAW 264.7 cells. I have followed the standard protocol, but I am facing a serious challenge with cell viability and scratch healing in response to CXCL9 treatment.
Here is a detailed description of the experiment:
Cell Line: RAW 264.7 cells
Media: DMEM Free Serum (used to standardize the results, Raw cells 264.7 grow in DMEM with 10%)
Scratch Assay Setup:
Cells were plated in 12-well plates until they reached confluence.
Media was removed, and cells were washed with PBS.
A scratch was made using a 200μl tip.
Cells were washed again with PBS.
Fresh DMEM Free Serum media containing varying doses of CXCL9 cytokines was added.
The issue I'm facing is that after the addition of CXCL9, the scratch disappears quickly and cells seem to detach and float, indicating a loss of cell viability.
I would like to inquire whether I am following the correct protocol, if a reduced FBS media is preferable over serum-free media, or if you have any alternative suggestions for conducting the migration assay with RAW cells.
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I have a feeling you are not following the right protocol. Maybe the protocol provided below will help.
1. After the cells are 90-95% confluent, remove the spent media and add 1ml of 5 µg/mL of mitomycin C (prepared in culture medium) to each well. Mitomycin C will stop proliferation of cells for 2-5 h before scratching. So, in a way, it will help to ensure true detection of migration. Incubate the plate for 2 h at 37 °C and at 5% CO2.
2. Remove the medium with mitomycin C and wash the wells once with 1ml of 1X PBS.
3. Add 1ml of 1X PBS and manually scratch the wells vertically with a 200µl yellow pipette tip. Use a new pipette tip for each well.
4. Remove the PBS and then add the media containing varying doses of CXCL9. Then proceed as usual with the assay.
It is important that you stop the proliferation of cells. Without mitomycin C treatment, I feel the proliferating cells may be occupying the area created by the scratch and due to over confluency, the cells may be detaching from the substratum and floating.
Best.
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I made an avidity ELISA to test this parameter in the serum of cancer patients vaccinated with a drug that generates antibodies. I tested different time points of the same patient just to see if the avidity will increase with more doses in time. but I want to interpret this result different than percentage, especially because I used different concentrations of NH4SCM as well.
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Interpretation of the Avidityof ELISA according to manufactory prochure of the ELISA machine
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If A human body of 75 Kg. and 50 Kv X-ray tube and 10 cm in contact and current I=10mA. Calculate Dose Rate which in (Gy/s) = (mA * Exposure Time * Conversion Factor) / (Distance^2) Where: mA (milliamperes) = 10 Exposure Time (seconds) = 10 & for X-rays at 50 kV = 0.175 Gy/(s*mA). ?
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The formula that mentioned might be a simplified version or specific to certain cases, but it's not a general formula used for calculating radiation dose from an X-ray unit.
The formula for radiation dose of an x-ray unit Gy/sec
D = g*(kV)*(mAs)/d^2
where g is conversion constant at Tube potential (Kv).
and
d=distance (m)
I= current (mAs)
if this will add to the discussion, but Volt^2 might be easy to remember if you think of dosage in Photons per second, an Ampere of unit charge as (1/e = 6.2415091E18 per second) and energy in Watt /seconds.
Watts = Volts*Amperes = Volts^2/Ohm.
The total absorbed dose in
Gy=Joules/Kilogram
is
Gy=Watts*Seconds/Kilogram
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For dating purposes, to calculate the annual radiation dose in ancient ceramics, the contribution of natural radiation from radionuclides which includes 40K, 238U, and 232Th of the environment (sediment) and inside the ceramic material should be considered. How to calculate the annual radiation dose in ceramics, when there are significant contribution of U, Th, K from both ceramics and sediments. Even the contribution of ceramics is greater.
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Tobias Makuochukwu Onyia thank you so much for your important help. We keep in touch.
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Which dose of stz (except 3mg/kg) is better for induce alzheimer in shorter time with minority rate of death in male wistar rat through icv induction
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Hello
No it isn't the same just sample animals that recieve stz have shown this signs
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if we use any specific micronutrient in excessive amount in broth medium to grow bio-control fungi, so is it possible that thus specific micronutrient affect the secondary metabolites production by the particular bio-control fungi ?
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hello, I dont know any thing about this matter. sorry
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Hello everyone.
I'd like to ask some question about C57BL/6J mice experiments. We want to make overexpression and knockdown mice by giving vector. However, we are wondering how many times the vectors will be given and the amount of dose. Does anyone have information?
Thanks.
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That method tends to have issues with tissue penetration. You will need a control to determine how much of your target tissue is getting transfected.
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Can you please help me find the suitable statistical tests for my study in Agricultural field
I have two treatment : the first treatment has 4 levels of doses, the second treatment : has two levels of doses. There's 4 blocks (4 replicates)
Is two-way ANOVA then tukey's test good for this study ?
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Yes, a two-way ANOVA followed by Tukey’s test would be a suitable approach for analyzing the data from your agricultural study. A two-way ANOVA is used to estimate how the mean of a quantitative variable changes according to the levels of two categorical variables1. In your case, you have two treatments, each with different levels of doses, and you want to know how these treatments affect the dependent variable (e.g., crop yield). After performing the two-way ANOVA, if you find that there is a significant interaction between the two treatments, you can follow up with Tukey’s test to determine which specific means differ from each other2.
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The dose is standardised in animals in mg/kg.
i just wanna extend the same treatment to cell lines and was trying to find a way to convert Drug dose from mg/kg to mg/ml ?
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The Article shared by Rafik really helped. I am grateful for this.
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dose titrtion and escalation
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so think of dose titration as a bit like when you're trying to find the perfect setting on your thermostat. You start with a lower temperature and gradually turn it up until your room feels just right – not too hot, not too cold. Dose titration in a clinical trial is kind of like that. Doctors start with a lower dose of a medication and then slowly increase it based on how the patient responds. The goal is to find the lowest dose that does the job without causing too many side effects.
Now, dose escalation is a bit different. It's like climbing a ladder, one step at a time. Imagine you're testing a new medicine, and you want to figure out how much of it people can take before it starts causing problems. So, you start with a small group of participants and give them a certain dose. If they handle it well, you move up to the next dose level with another group. You keep going up until you start seeing some side effects that are too intense or risky. That highest dose where things start getting tricky is called the "maximum tolerated dose."
So, to sum it up, dose titration is like adjusting your thermostat to get the perfect temperature, while dose escalation is more like climbing a ladder to find out how much of a new medicine people can handle safely. Both methods help scientists figure out the best way to use a new treatment and make sure it's effective and safe for everyone.
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Dear all, I'm having problems determining the proper erastin dose in the SH-SY5Y cell line. Erastin activates ferroptosis and results in ferroptotic cell death. I used a 96-well plate with 4000 cells per well and experimented with various concentrations. I discovered %46 viability when I used 5 uM Erastin twice. Now I'm looking for the dose that results in 70% viability. When I used 2.5 uM Erastin, 80% of the SH-SY5Y cells died. No matter the Erastin dose whether I used 2 uM, 2,5 uM, 3,5 uM, or 5 uM, %80 of the cells died. The control group was fine. Therefore, I don't think there is a vitality issue. Same Erastin, same medium, same plate. Nothing has changed. I don't understand why this is happening. Do you have any suggestions for me to try? Does anyone experience the same problem? Thank you all.
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For how long are you treating the cells with erastin? I would suggest to set up the experiment in replicates and use even a lower erastin concentration range and treat the cells for 24, 48, and 72 hrs.
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In particular, what information do you have about the reaction of different varieties of crops to different doses of herbicides?
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Any crop will respond differently to a given dose of the herbicide. The LD 50 dose is an example to understand the query. Because a dose may be lethal or vital and so on. Secondly the variety/genotypes under investigation will also respond to the tune of their genetic constitution.
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Dear CT experts,
i need to estimate the expected equivalent dose to the eye lens for a CT head scan.
The scanner provides me with the CTDI and DLP values, but I couldn't find so far a comprehensive description with approximated conversion formulas to estimate the eye dose. Any help is appreciated.
Thanks in advance, Christoph
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Thank you a lot for this hint. I will definitely try it!
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Anybody know that the dose of tnf-a IP into 3-4week mice .If adult mice is 50ug/kg,then what's the young mice ,according to body weight?
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Hi there ,
According to : Fachinformation-Injektionsvolumina_2022.pdf (gv-solas.de)
it is 10 ml/kg for healthy "normal weigth range" adult mice (min 6 weeks old I 'd say) . If mice are small - 3-4 weeks old, I would reduce the amount to around 5-(7) ml/kg . I hope this will help you.
Best wishes
Flora
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I need to inject tamoxifen into mice at P12 and P14. I would collect retinal tissue at P30. Does anybody have any suggestions for the dose and the route of administration for this age?
Any suggestions would be of huge help! Thank you!
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you got the answer? share me ?
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Concerning the adsorbent dose for example iron nanoparticle to remove dye. Sometime it is written as
1- "the run was conducted by adding different dose of iron from 10 to 150 mg to 50 ml working solution of 30 mg/l of dye".
Other research paper mentioned
2- "the run was conducted by adding different dose of iron from 10 to 150 mg/l to 50 ml working solution of 30 mg/l of dye".
In case #1 it is clear that I have to add 10 to 150 mg of adsorbent to 50 ml. But I'm a bit confused in case #2. Should I have to prepare adsorbent solution with that concentration?? Or 10 to 150 mg of adsorbent will be calculated in 50 ml of adsorbate, i.e. in case of 10 mg of adsorbent dose, I have to add 0.5 mg of adsorbent to 50 ml working solution
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Dear Neşe Öztürk , in perspective of the above data given by you. The following statement is correct:
"10 to 150 mg of adsorbent will be calculated in 50 ml of adsorbate, i.e. in case of 10 mg of adsorbent dose, I have to add 0.5 mg of adsorbent to 50 ml working solution"
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For example, is always the absorbed dose in the bladder wall of 4 years-children upper than in 8 years-children? is there any exception in the absorbed dose in these organs with wall and content or they are exactly like it in other organs for example kidneys?
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Dear colleague,
Sorry for the late answer, I don't connect here frequently.
If I look at 177Lu S values from OLINDA V1, for UB content to UB wall:
- 5 YO: 1.85 10-4 mGY/MBq.s
- 10 YO: 1.17 10-4 mGY/MBq.s
This is normal, as the model is smaller, since most of the irradiation is from non penetrating radiations, therefore the same energy is absorbed in a smaller volume, and therefore the absorbed dose increases.
This is a general trend, probably less pronounced for hollow organs but this remains to be seen.
Then obvioulsy the cumulated activity should taken into account, as theS value basically considers the same number of decay in the 2 models, which may not be true...
Best regards,
Manuel
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We want to study immune responses in mice treated with a lipophilic compound that has to be dissolved in DMSO.
Given the toxicity and potential effect on immune response due to administration of high doses of DMSO, we would like to reduce DMSO administration to the minimum.
To do so we would dissolve our lipophilic compound in a 10X less volume of DMSO than the one recommended by SDS. The preparation apparently look soluble but when further diluting with Physiologic solution it becomes a bit 'sandy', thus suggesting the compound is not fully dissolved..
Would the administration of such preparation (likely non solubilised) still be absorbed when injected peritoneally in mouse?
Being a lipophilic compound is it necessary to have it dissolved in solution in order to be absorbed into the circulation?
Thanks!
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Sarivin Vanan Thanks that's a good point.
I have to look better into this, but could be worth trying!!
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Can anyone help me to solve my problem regard to MCNP6?
I'm simulating my physical systems using MCNP6. I use T-mesh to record dose distribution. When I executed my jobs, there is an error that is "The "tasks" parameter on the MCNP6 run command will be ignored, and the problem will be run using only 1 thread". I didn't know how to fix it. I need to run my simulation with multi-threads. Could you help me to solve it?
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use the mpich2 Parallel operation. task is only applicable to neutron and photon problems
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for example, the needed dose is 400ug/mL, how will I turn my crude extract into 400 ug/mL? p.s my research is about a-glucosidase activity
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To convert your crude extract into a concentration of 400 ug/mL for your research on α-glucosidase activity, you will need to determine the current concentration of your extract. Once you have this information, you can calculate the volume of your crude extract needed to achieve the desired concentration. For example, if your crude extract concentration is 800 ug/mL, you would dilute it by adding an equal volume of a suitable diluent (e.g., water or buffer) to obtain a concentration of 400 ug/mL. Alternatively, if your crude extract concentration is higher or lower than 800 ug/mL, you can adjust the volume accordingly to achieve the desired concentration of 400 ug/mL. It is crucial to ensure accurate measurements and proper mixing during the dilution process to achieve reliable results for your α-glucosidase activity research.
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I'm working with essential oils as a fumigant against insects, the fumigation test is performed in Petri dishes, (9 cm in diameter and 1.5 cm in height), and all my concentrations are expressed in percentages, however, I have to know how to convert my doses into microliters per liter of air.
Thank You.
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There is no simple "conversion". Whereas one can establish a specific EO solution by weight the differential volatilities of individual constituents establishes a completely new "EO" as headspace vapor the concentration and composition of which is unique.
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I'm trying to do a glucose stimulated insulin secretion assay (GSIS) by adding glucose to MIN6 cells. But strangely the lower dose (3mM) glucose gives a higher insulin secretion than the higher dose (25mM). Any ideas how this can happen?
We are culturing our MIN6 cells with High glucose DMEM (4500mg/dl or 180mM) I've seen people use lower glucose concentrated medium to culture MIN6 cells, could this be the causative factor?
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I think that when we use high doses there is a desensitization of the target cells which leads to a weak response
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if I have a research gate account, can this be identified as a number like ORCID?
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Hi ,
No, ResearchGate does not provide an identification number for researchers similar to the ORCID (Open Researcher and Contributor ID) number. ORCID is a unique identifier that distinguishes individual researchers and connects their research outputs across different systems. It is a widely recognized and adopted system in the academic and research community.
ResearchGate, on the other hand, is a social networking platform designed for scientists, researchers, and academics to share and collaborate on research papers, publications, and projects. While ResearchGate provides a profile for each researcher, it does not assign a specific identification number like ORCID.
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In the high N the photosynthesis is also high. if photosynthesis is high then carbohydrate content of the leaf must be increased. But the different research done I found high N dose decrease the carbohydrate content of the leaf. What might be the reason for that?
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Decreased concentrations of total non-structural carbohydrates (TNC) are observed with an increasing nitrogen supply. Your research is correct :)
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Hello all,
I am new to doing surface area analysis and we have a Micromeritics 3 Flex Surface Area Analyzer, can you please guide me on,
1. What features on a N2 adsorption isotherm will tell us that we are not using enough sample? (For example, an isotherm that isn't closing?)
2. What is a good dosing volume to start with? And what tells us that we should increase or decrease the dosing volume?
Thank you!
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Basically the Adsorption Isotherm curve is of different Type , it is depend on the pore of Adsorbent , like for mesoporous The Adsorption isotherm generally we get is of Type-1 or Type-2 . Adsorption Isotherm basically tells us about the feasibility of Adsorption , it tells us about at what relative pressure single point BET happens or at what relative pressure multipoint happens , capiliary condensation and so on.
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If we change different type of materials which are in the range of type 4 isotherm and they have similar pore size do we still need to tweak the dosing pressure for both the materials? Even if the adsorbent gas used is nitrogen for both the cases?
What I am thinking is since both the materials follow Type 4 isotherm and are mesoporous with N2 as their adsorbate then shouldn't the dosing pressure for both of them remain the same for a single point BET test. If not then can you please let me know the other variables that I might have missed in the adsorbate which would force us to change the dosing pressure.
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Most standard gas adsorption apparatus should adjust the dosing automatically. It is actually difficult to evaluate porous solid characteristics through a single point too.
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Greeting Leute,
So, I would like to know what is the best characterization method to observe the structural change of my active layer after an irradiation dose test.
Best regards
Tarek
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Hi Azzouni,
I hope the following paper could help you.
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I am working with MJ m^-2 as absorbed dose in the 200nm - 400nm. Specifically, 634 MJ m^-2 in 540 days (on the ISS, low earth orbit), that I converted in Irradiance as 13.5 W m^-2.
Then, I thought to use the following formula to get photon flux [photons m^-2 s^-1]:
PF= Irradiance * λ * 5.03 * 10^15
where 5.03*10^15 = (10^(-9)) / (1.988 * 10^-25)
where (1.988 * 10^-25) is Planck constant * light velocity
Now how to proceed?
-> should I calculate the Total PF = Irradiance * 5.03 * 10^15 * (λ200 + λ201 + ... + λ400) ?
In this case I would get TotalPF = 4.12 * 10^21 photons m^-2 s^-1
-> should I calculate the Total PF = Irradiance * 5.03 * 10^15 * (λ300) ? Where λ300 is the "best" average lambda between 200 and 400, TotalPF = 2.05 * 10^19 photons m^-2 s^-1
-> since the solar spectrum between 200 nm and 400 nm is rising toward the ~500 nm peak, how can I proceed to get the PF in that range starting with the irradiance value and without a solar spectrum to integrate (referable to that specific irradiance value)?
Thanks in advance,
Christian
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To calculate flux divide dose by the time.
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When an ShRNA Knock down efficiency is not good, how I should improve this as I know ShRNA KD efficiency is not dose dependent.. it is meaningless to increase the amount of ShRNA right?
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Mohamed Khashan do you have any article that reported multiple transfection by shRNA/retroviral will lead to higher inhibitory rate?
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Actually I'm working on designing a BET Machine of my own so I've prototype , the problem I faced that during dosing of N2 in manifold what should be the dosing pressure , is it depend on adsorbent or any characteristics of adsorbate itself.
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It depends on the type of pores. Different pores adsorb different amounts at different pressures. For example, small pores adsorb a lot at low pressures, so they are in general more difficult to measure. Look at an adsorption isotherm and you will have a general idea of how much will be adsorbed at each pressure. If I was you I would start with some moderate amount (say, 100 mg) of a non-porous solid.
This publication show the rates at which different solids can adsorb:
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I have performed toxicity studies of plant extracts (ethanolic) and no signs of toxicity are observed. I need to complete an experiment on three groups and I am confused about what dose to prepare for the experiment.
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Hi Prabhat! I'm assuming you have seen no toxicity with your extracts up to at least 2000 mg/kg. I would suggest you do the following if your plant/extract has been used in any traditional system of medicine for any indication (this is very likely) 1)Identify the human dose 2) Calculate the animal equivalent dose using the appropriate conversion factor for rats/mice. 3) Since you need three doses consider that as the median dose and the other two doses as half and double respectively. This may increase your chances of seeing efficacy in your animal studies. All the Best!
(Nair AB, Jacob S. A simple practice guide for dose
conversion between animals and human. J Basic Clin Pharma 2016;7:27-31.)
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I have found on my test MK-801 at dose 0.06mg/kg increase freezing compare to vehicle group of mice...Just wondering of getting opposite results...How I can interpret this result?
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Thank you so much for your guidelines...I will follow that....
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Hi everyone,
I'm trying to define the MoA of a molecule that we already know inhibits some phosphatases by attaching them depending on the dose range. But we don't know if there is one or more phosphatases inhibition responsible for the biological effects.
As our molecule is an inhibitor, I can't find a way to study or show which one is the target at the studied doses. There are several commercial inhibitors, but this wouldn't help.
I'll appreciate any suggestion or contact to experts or services on this topic
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Ignasi Canals don't say that something is impossible because there will be an imbecil, who doesn't know it's impossible and they will do it xD
Are all those phosphatases really expressed during your process? You can prepare sets of high-order knock-outs and based on these results select those that are most important.
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I am seeing a Forest Plot presentation of the data in a meta-analysis. But the standard deviation for the final "weighted mean difference" is missing. I am wondering if it is possible to calculate the standard deviation of it. So that I can use this SD value in G power to estimate the sample size.
The meta-analysis paper title: Efficacy of combination therapy with ezetimibe and statins versus a double dose of statin monotherapy in participants with hypercholesterolemia: a meta-analysis of literature
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If I understand the question correctly, you could use the data stated in the paper that is included in the meta-analysis instead.
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I am currently involved in research for controlling weevils in stored wheat using different essential oils.
What could be the best concentration (microlitres per litre of air) of essential oils for comparison?
We wish to test all the oils at one fixed concentration. We are trying to shortlist a few effective essential oils and test them out at different concentrations.
Is it a good idea?
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Having tested a lot of essential oils for this specific purpose, I can ensure you that different essential oils give very different results. There is also a possibility that fumigation doesn't kill the adults but stops the developements of the eggs inside the grains.
Way of applying the product (fumigation, direct spraying...) also gives different results, so there is no easy direct answer to your question
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my plant extract shows less antioxidant activity (by DPPH assay) in medium doses. what could be the reason for it?
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Dear Yasha Jha,
Reaction mixture containing different concentrations of HAE (hydroalcoholic extract) of extract (25, 50, 75 & 100 µg/mL) was added to a DPPH reaction mixture. The reaction mixture was shaken overwhelmingly and kept in the dark condition at room temperature for 30 minutes. The absorbance of the reaction mixture was measured at 517 nm spectrophotometrically. The absorbance of every reaction mixture was recorded in triplicate. The scavenging capabilities of DPPH radical were given in the percent inhibition formula using the following equation.
% inhibition= [1- (AsAb)/Ac] × 100
Where, Ab represents blank absorbance
As stands for the sample absorbance
Ac is the control absorbance
Results were given in IC50 value, a concentration at which half of the radical’s generation was scavenged by the respective plant extract obtained from the percent inhibition value of samples.
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I am working with chitosan application and I have found increased concentration of chlorophyll, carotenoids and protein in plants treated with higher doses of chitosan. Whereas growth of plant like height was less in higher concentration and more in lower concentrations. I have done experiment twice for confirming my results and it is coming in the same way. Is it possible that stressed plant have more chlorophyll as compared to non-stressed plants.
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This is an interesting question. How do you determine if the plant is under stress ? The fact that it grew differently doesnt prove it is stressed. I would check for example photosynthesis physiology parameters - effective quantum yield in time series after introduction of the chitosan in control vs. treatment. If it is substantially lower in the treatment then there might be stress, but it should be checked further.
Also, the fact that you get more chlorophyll and carotenoid and protein implies that the plant uses this sugar, not stressed by it.
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Hello everybody!
We have been doing IP injections of Tamoxifen to pregnant Cre-loxP mice, for lineage tracing during development.
We usually make a single injection at E11.5 with a dose of Tamoxifen ranging from 1.5 mg to 3.0 mg (depending on the reporter system), combining it with half-dose of Progesteron to counteract the estrogenic effects of Tamoxifen. The embryos are then collected at E17.5.
Our driver CRE strain is crossed with different reporters, like the Brainbow 2.1 (also called Rosa-Confetti), that we never used before in this lab.
Every time that we inject Tamoxifen in the pregnant Confetti females we either have abortions or high mortality of the mothers, in ratios that are not observed with our other reporter strains in use (nlacZ, tdTomato).
Does anybody use Confetti mice and had the same problem? Is it the concentration of Tamoxifen too high? Are they somehow oversensitive?
Thank you!
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Tamoxifen is believed to be highly toxic to pregnant Confetti mice. Tamoxifen is an antiestrogen, and it has been linked to severe birth defects in the offspring of pregnant Confetti mice, including eye defects and abnormalities in the limbs and hearing. It is important to note that tamoxifen should never be given to pregnant mice, as it is known to be highly toxic to them and can result in miscarriage or other serious complications.
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I need this ratio for 4 time dose
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Refer to this article
[Use of mebendazole for helminthiases in chickens and geese]
103 chickens experimentally infected with Capillaria obsignata were treated with Mebendazol at a dose of 30 mg/kg body-weight daily for 3 consecutive days. The effectiveness of the drug on the 4th stage larvae as well as immature and mature 5th stage forms were 92,5%, 98% and 98,8% respectively.
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What is the half-lethal and lethal dose of sodium nitrite in rabbits? I did not find clear information in the previous studies. I hope you can help me to get the answer. Thank you very much
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It's almost 2680 mg/kg body weight
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It is said that Cancer Cells have no contact inhibition and they can grow into multi layers. BUT,when we culture the HeLa cell, which is a well-known cancer cell line, in the plate, the HeLa cells dose not form multiple layers but keep the monolayer state even the density is much high if I chang the medium timely.
Why?
Does the contact inhibition theory need to be modified?
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No, I don’t think contact inhibition theory would require any modification.
Loss of contact inhibition is the hallmark of cancer cell lines. Untransformed (normal) cells display contact inhibition when grown on a solid substrate, such as a culture dish or flask where they form a monolayer. Cancer cell lines, however, continually grow. Interestingly, cancer cells and, more generally, cancer cell lines display no contact inhibition. When confluence is reached, the cells continue to divide and pile up on top of each other.
The answer to your question lies in the difference of behavior of cells in 3D and 2D cultures. 3D-cultured cells is more reflective of in vivo cellular responses. The 3D culture environment differ morphologically and physiologically from cells in the 2D culture environment. The additional dimensionality of 3D cultures that is the crucial feature leading to the differences in cellular responses because not only does it influence the spatial organization of the cell surface receptors engaged in interactions with surrounding cells, but it also induces physical constraints to cells. These spatial and physical aspects in 3D cultures affect the signal transduction from the outside to the inside of cells, and ultimately influence gene expression and cellular behavior.
While the 2D-cultured cells are stretched out in an unnatural state on a flat substrate, cells cultured in 3D on a biological or synthetic scaffold material maintain a normal morphology. Also, cells growing in 2D monolayer are under stress and therefore some genes and proteins being expressed are altered as a result of this unnatural state. The difference in cell stages between 2D and 3D cultures also should be taken into account. While cells in 2D culture are mostly proliferating cells, cells in 3D cultures usually are a mixture of cells at different stages. For instance, spheroids in 3D cultures are likely to be heterogeneous, having proliferating cells on the outer region and quiescent cells in the inner region due to lack of nutrients and gas exchange.
For more information you may refer to the article attached below. These articles will be helpful.
Best.
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Together with evidence on the importance of sufficiently high levels of 25-OH-vitamin D for the optimization of functioning in all parameters of the immune system, clinicians observed that
-- transitorily even higher doses are needed in acute peroids of illness/inflammation,
-- transitorily even higher doses are needed when lymphocytes are active in detoxification from metals, parasites, nanotech such as ribbons or other graphene based structures, circulating spike proteins etc. etc,
-- lhigher doses are or may be needed when there is a ack of complementary micronutrients such as magnesium, vit. K2
and similar factors.
In addition to those observations, questions regarding the impact of vitamin D quality emerged:
Do vegan production, duration of storage and othe parameters of quality impact bioavailabilty?
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There is evidence that the quality of vitamin D supplements can impact their bioavailability and effectiveness in the body. Vegan production, duration of storage, and other factors can affect the quality of vitamin D supplements.
For example, vitamin D3 supplements derived from lanolin (a wax-like substance found in sheep's wool) are the most common type of vitamin D supplement. However, some people prefer to use vegan vitamin D3 supplements derived from lichen. While both forms of vitamin D3 are effective, the bioavailability of vegan vitamin D3 supplements may be lower than that of lanolin-derived supplements.
Additionally, the quality of vitamin D supplements can be affected by the duration of storage. Vitamin D3 is sensitive to light and heat, and prolonged exposure to either can degrade the quality of the supplement. Therefore, it is important to store vitamin D supplements in a cool, dark place and to use them before their expiration date.
Other factors that can impact the quality of vitamin D supplements include the presence of contaminants, the form of the supplement (e.g., liquid, capsule, tablet), and the presence of complementary micronutrients like magnesium and vitamin K2.
Overall, it is important to choose high-quality vitamin D supplements and to consider factors like production methods, storage conditions, and complementary micronutrients when using vitamin D to support immune function and overall health.
Yes, vegan production, duration of storage, and other parameters of quality can impact the bioavailability of vitamin D supplements.
For example, vegan vitamin D3 supplements derived from lichen may have lower bioavailability compared to animal-derived vitamin D3 supplements, such as those derived from lanolin. This is because the vitamin D3 in lichen is in the form of D3 precursors that need to be converted by the body into active vitamin D3. This conversion process can be less efficient than the conversion of animal-derived vitamin D3 into its active form.
Furthermore, the duration of storage can affect the bioavailability of vitamin D supplements. Vitamin D3 is sensitive to light and heat, and prolonged exposure to either can degrade the quality of the supplement. Therefore, it is important to store vitamin D supplements in a cool, dark place and to use them before their expiration date.
referrence :
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Sodium bicarbonate is among five evidence-based performance supplements (caffeine, creatine, nitrate/beetroot juice, β-alanine, and bicarbonate). I need a pragmatic approach to the culinary use or the use as a supplement of this compound. NaHCO3 ingestion should be consumed at a dose of 0.2–0.4 g/kg BM. Moreover split doses taken over a 30- to 60-min time period or serial loading with three to four smaller doses per day for two to four consecutive days prior to an event has been proposed.
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Thanks a lot for your answer! I found it very useful
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How do I measure patients' radiation doses from conventional x-ray facilities?
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All depends on whether you are interested in assessing risk, in which case you’ll need to measure organ doses, which to add to Joseph’s comment, will result in very, very low exposures to measure, and will require quite large volume detectors. Or, if your intent is to compare different machines under the same clinical conditions, you could download RadComp from my website (free) and do it that way. Good luck!
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I'm looking for protocols that mimic clinically relevant the exposure to oral methylphenidate in mice. More specifically, I'm looking for the protocols that achieve the exposure we see in humans following continuous oral dosing with extended release methylphenidate formulations. I am aware of the acute studies that attempted to establish such a protocol (e.g. Bhide's group: 10.1016/j.neuropharm.2009.07.025) or the attempts in rats (e.g. Thanos group: 10.1016/j.pbb.2015.01.005), but I can't find what would be a relevant chronic oral dosing regimen with methylphenidate in mice. Do you have any ideas who might be using such a protocol? What would be important to take into account when trying to establish it if it still does not exist (e.g. the metabolic rate seems to be quite different between humans and rodents? Also can we expect the same brain exposure given stable plasma concentrations?).
Thanks!
Jan
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Establishing a chronic oral dosing regimen with methylphenidate in mice that mimics the exposure seen in humans following continuous dosing with extended-release formulations can be challenging due to the differences in metabolic rate between humans and rodents. However, some researchers have attempted to develop such protocols. Here are a few suggestions:
  1. Consider the differences in metabolic rate: As you mentioned, the metabolic rate of mice is different from humans, and this can affect the pharmacokinetics and pharmacodynamics of the drug. Therefore, it is important to take into account the metabolic rate of mice when designing the dosing regimen.
  2. Look for studies in rats: Although rats are not the same as mice, they are closer to humans in terms of metabolic rate. Therefore, it may be useful to look at studies in rats that have attempted to establish a chronic dosing regimen with methylphenidate.
  3. Start with a low dose and increase gradually: To establish a chronic dosing regimen, it is important to start with a low dose and increase it gradually over time to achieve the desired plasma concentrations. This will help to avoid toxicity and other adverse effects associated with high doses of methylphenidate.
  4. Consider the formulation of the drug: The formulation of the drug can also affect its pharmacokinetics and pharmacodynamics. Therefore, it is important to consider the formulation of the drug when designing the dosing regimen.
  5. Monitor plasma concentrations: To ensure that the dosing regimen is achieving the desired plasma concentrations, it is important to monitor plasma concentrations of methylphenidate over time.
  6. Consult with experts in the field: It may be helpful to consult with experts in the field of pharmacokinetics and pharmacodynamics to help design an appropriate dosing regimen that mimics the exposure seen in humans following continuous dosing with extended-release formulations of methylphenidate.
Overall, establishing a chronic dosing regimen with methylphenidate in mice that mimics the exposure seen in humans can be challenging, but with careful consideration of the factors mentioned above, it is possible to develop an appropriate protocol.
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I am trying to establish a dose-response relationship with different concentrations of LPS on differentiated THP-1 cell-secreted TNFa and IL-1b. However, I am finding that all the concentrations I used (15-1000 ng/mL) produced similar increases in TNFa and IL-1b. This looks like an on-off response rather than a graded response as described in the literature. I am not sure why I am getting this maximum response even with the lowest concentrations used. I would appreciate any suggestions. Thank you!
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My guess is that you have reached the plateau of cytokine production at a very low dose of LPS. I would double check to make sure your dilutions are correct first (you are already using a decent range of doses but something may be off). I would then proceed to use an even lower dose range. LPS requires a lot of vortexing-- be sure to do so while making serial dilutions.
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Hi, I generated a stable cell line with a shRNA. However, when I tested the optimal dose of DOX to silence the target gene I obtained a working concentration at 12ug/mL... So, as the majority of all the publications have a working dose at (more or less) 1 ug/mL , I am worry that 12ug/ml is too high...
It could be possible this DOX concentration? Can I have any toxic issue related with this DOX dose that invalidate my results?
Thank you!
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Doxycycline itself can affect cells, so I would be hesitant to use that high of a concentration.
When you did your dose testing, were you using the same concentrations on a non-targeting or parental cell line as a control comparison for your shRNA-expressing cells? It could be that the higher doses of doxycycline are affecting the expression of your gene of interest in addition to the silencing by your shRNA.
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I am working on a chitosan-loaded nano formulation through ion gelation for the treatment of a specific disease in mouse model. I am planning on comparing the effect of the free drug effect on the disease with the nanoformulation.
My question is, there's already a reported dose for the free drug in the literature of 50 mg/kg, do I use the nanoformulation equivalent of this dose in the treatment? i.e. I prepare an amount of the formulation that has the equivalent drug concentration of 50 mg/kg, or do I carry out a cytotoxicity study on the nanoformulation itself and try to determine the treatment dose?
In this study for instance. It's very similar in experiment design to the study I am about to carry out, but I am very confused in terms of the doses stated.
Thank you for your time!
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Dear Mohammed,
When comparing two treatments you should alwais compare the quantity of the free drug injected and ideally the same route of administration. In your case, if you treat the animals 50 mg/kg of free drug, you should also treat your animals with 50 mg/kg of the drug encapsulated in your nano formulation. To do this, you have to charaterize well your NP to understand the concentration fo the drug in it.
I hope this helps.
Best Regards
Francesco
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I need some insight, in simpler words, why do we extrapolate from high experimental doses to lower doses while establishing dose thresholds?
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Mohd Shahnawaz Thank you sir for the detailed response.
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The optimal dosing regimen for antibiotics used in combination therapy against drug-resistant bacteria should be determined through careful consideration of these factors, along with ongoing monitoring and adjustment as needed. Pharmacokinetic and pharmacodynamic modeling and simulations can be useful tools for determining the optimal dosing regimen and evaluating its effectiveness. Clinical trials are also important for evaluating the safety and efficacy of different dosing regimens in humans.
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Determining the optimal dosing regimens for antibiotics used in combination therapy against drug-resistant bacteria requires a multidisciplinary approach that involves understanding the pharmacokinetic and pharmacodynamic properties of the drugs, the susceptibility patterns of the target bacteria, and the potential for drug interactions and toxicity.
In general, the goal of combination therapy is to use two or more drugs with different mechanisms of action to enhance bacterial killing and prevent the emergence of resistance.
Overall, determining the optimal dosing regimens for antibiotics used in combination therapy against drug-resistant bacteria requires careful consideration of multiple factors. Clinical trials and in vitro studies can help guide the selection of dosing regimens, but close monitoring of patient response and outcomes is also critical.
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Currently, I am working with yeast. I am treating it with different doses of radioactivity. I want to see if the DNA shows foci such as Gamma H2AX.
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Hello, in many publications the Histone H2A.XS139ph antibody is used against a peptide including phospho-serine 139 of histone H2AX.
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Sub acute toxicity 28 day
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It is not normal for experimental albino rats to become dizzy after receiving their first oral dose, and it may be a cause for concern. Dizziness can be a sign of a variety of conditions, such as neurological problems, ear infections, or vestibular disorders.
If you are conducting an experiment on albino rats, it is important to monitor their behavior closely and document any adverse effects that they experience. If the dizziness persists or is accompanied by other symptoms, such as loss of appetite, lethargy, or difficulty moving, it is advisable to consult a veterinarian or a qualified research professional.
It's important to note that the dosages used in animal studies should be carefully selected to avoid toxicity, and the animal's welfare should be a top priority throughout the experiment. If you have any concerns about the experimental protocol, it is advisable to consult with a qualified research professional or an institutional animal care and use committee (IACUC) to ensure that the study is conducted in a responsible and ethical manner.
Hope this helps Rufayda Izzeldin