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Questions related to Drugs
I have a numeric dependent variable (drug reports in schools) with three binary categorical predictors - whether schools receive drug training, whether schools receive discipline training, and whether schools have a high or low number of intervention practices. I have made all of these factor variables, and I am now struggling to test the assumptions of my regression analysis. Why is the scatterplot showing vertical lines? Do I need to change my Rcode? I have attatched everything below and any help would be great!
model <- lm(log_drug ~ practice_hilo + alcohol_drugabuse_f + discipline_policies_f, data = school_safety)
summary(model)
Call:
lm(formula = log_drug ~ practice_hilo + alcohol_drugabuse_f +
discipline_policies_f, data = school_safety)
Residuals:
Min 1Q Median 3Q Max
-1.864 -1.079 -0.273 1.062 4.014
Coefficients:
Estimate Std. Error t value Pr(>|t|)
(Intercept) 1.37159 0.06750 20.320 <2e-16 ***
practice_hiloLow Value -0.51009 0.05397 -9.451 <2e-16 ***
alcohol_drugabuse_fYes 0.49221 0.05727 8.594 <2e-16 ***
discipline_policies_fYes -0.09211 0.06485 -1.420 0.156
---
Signif. codes: 0 ‘***’ 0.001 ‘**’ 0.01 ‘*’ 0.05 ‘.’ 0.1 ‘ ’ 1
Residual standard error: 1.323 on 2720 degrees of freedom
Multiple R-squared: 0.07806, Adjusted R-squared: 0.07704
F-statistic: 76.76 on 3 and 2720 DF, p-value: < 2.2e-16
I need to prepare the above solution as a vehicle for a drug to be administered p.o. but I am struggling to find a clear protocol.
As I understand it, the methylcellulose should be added to heated H2O to aid solubility - i.e. heat H2O to 80 degrees celsius with stirring and then slowly add methylcellulose to the water until it forms a cloudy white solution, stirring for roughly 30 minutes.
Then keep the 0.5% methycellulose (2.5g in 500ml water for example) at 4 degrees with stirring overnight until the solution turns clear. Then add the appropriate volume of Tween80 to produce final of 0.2%.
Can anyone recommend any changes to the above protocol or is this correct?
Is the design of new pharmaceutical formulations through the involvement of AI technology, including the creation of new drugs to treat various diseases by artificial intelligence, safe for humans?
There are many indications that artificial intelligence technology can be of great help in terms of discovering and creating new drugs. Artificial intelligence can help reduce the cost of developing new drugs, can significantly reduce the time it takes to design and create new drug formulations, the time it takes to conduct research and testing, and can thus provide patients with new therapies for treating various diseases and saving lives faster. Thanks to the use of new technologies and analytical methods, the way healthcare professionals treat patients has been changing rapidly in recent times. As scientists manage to overcome the complex problems associated with lengthy research processes, and the pharmaceutical industry seeks to reduce the time it takes to develop life-saving drugs, so-called precision medicine is coming to the rescue. It takes a lot of time to develop, analyze, test and bring a new drug to market. Artificial intelligence technology is particularly helpful in this regard, including reducing the aforementioned time to create a new drug. When creating most drugs, the first step is to synthesize a compound that can bind to a target molecule associated with the disease. The molecule in question is usually a protein, which is then tested for various influencing factors. In order to find the right compound, researchers analyze thousands of potential candidates of different molecules. When a compound that meets certain characteristics is successfully identified, then researchers search through huge libraries of similar compounds to find the optimal interaction with the protein responsible for the specific disease. In contrast, many years of time and many millions of dollars of funding are required to complete this labor-intensive process today. In a situation where artificial intelligence, machine learning and deep learning are involved in this process, then the entire process can be significantly reduced in time, costs can be significantly reduced and the new drug can be brought to the pharmaceutical market faster by pharmaceutical companies. However, can an artificial intelligence equipped with artificial neural networks that has been taught through deep learning to carry out the above-mentioned processes get it wrong when creating a new drug? What if the drug that was supposed to cure a person of a particular disease produces a number of new side effects that prove even more problematic for the patient than the original disease from which it was supposed to be cured? What if the patient dies due to previously unforeseen side effects? Will insurance companies recognize the artificial intelligence's mistake and compensate the family of the deceased patient? Who will bear the legal, financial, ethical, etc. responsibility for such a situation?
I described the key issues of opportunities and threats to the development of artificial intelligence technology in my article below:
OPPORTUNITIES AND THREATS TO THE DEVELOPMENT OF ARTIFICIAL INTELLIGENCE APPLICATIONS AND THE NEED FOR NORMATIVE REGULATION OF THIS DEVELOPMENT
In view of the above, I address the following question to the esteemed community of scientists and researchers:
Is the design of new pharmaceutical formulations through the involvement of AI technologies, including the creation of new drugs to treat various diseases by artificial intelligence, safe for humans?
Is the creation of new drugs by artificial intelligence safe for humans?
What do you think about this topic?
What is your opinion on this issue?
Please answer,
I invite everyone to join the discussion,
Thank you very much,
Best wishes,
Dariusz Prokopowicz
The above text is entirely my own work written by me on the basis of my research.
In writing this text I did not use other sources or automatic text generation systems.
Copyright by Dariusz Prokopowicz
I'm a beginner in ITC, does anyone have an idea why when measuring the heat of dilution and in measuring the interaction of HSA with the drug or even with the buffer itself, the curve goes up? HSA measurement at HEPES pH 7.4 and pH 6 give similar results. Different buffer concentrations and different ionic strength do not solve the problem...
I am keeping my cell line for drug treatment and monitoring its effect at 24 hrs, 48 hrs and 72 hrs? Should I change the medium every 24 hrs and give fresh drug treatment or just leave the medium as it is after treatment once at the beginning? What is the difference between the two? What is the norm that is followed for cytotoxic assays such as MTT and CCK-8?
How does Handersen Hasselbach equation affect this selection?
I made some solid dispersion samples with VAL (valsartan) as the active compound. I was expecting it to become amorphous form. However, when I first run it through DSC, the pure VAL drug has some peaks. On the other hand, one of the peaks of my solid dispersion sample has almost the same peak as the pure drug, just a bit broader. Also it has quite crowded peaks above the melting point of VAL. Could someone please help me?? Is it normal or what's the problem?:((
Thank you in advance🙏
Dear researchers,
I would like to investigate administration of some natural compounds in treating Digoxin toxicity. Most of studies investigated protective effect of drugs. Is there any other protocol investigating therapeutic effect of interventions in rat model?
Dear ResearchGate community, hello!
I'm going to do an MTT test on glioblastoma cells with our drugs. I plan to add 10,000 cells in 100 µl medium with FBS per well to a 96-well plate, incubate for 24 hours and then add 50 µl of drugs. Incubate the cells with treatment for 24 hours and add MTT dye.
Tell me, please, should I remove the medium before adding the drugs (they are diluted in DMEM without FBS) and should I remove the drugs before adding MTT dye?
Thank you in advance!
Hello Friends,
Currently, I'm working on a male infertility project. Can anyone suggest the best standard drug other than sildenafil citrate?
sir,
majorly used beta 2 adrenergic agonist as vasodilators? why not used surfactant with autophagy promoters with immunomodulators.
The broth dilution assay method was used to find antibacterial efficacy of drug loaded mesoporous silica and free drug in same con.c. is it possible to observe that drug-loaded mesoporous silica has a higher value MIC than free drug MIC against the same bacterial strains s.aureas. The MIC of drug-loaded mesoporous silica stay same for upto long period of times up to months with high accuracy while the MIC of free drug in the same amount gives 4 and times higher value and further decline from the next day of experiment as the drug become settle down and come out of solution. Commonly nanoparticles should increase the antibacterial effect of antibiotic. 1) Kindly give your suggestions what could be the possible reasons 2) what could be its justification 3) also suggest any authentic similar recent studies 4) is it . The release from nanoparticle was 69 to 73% initial burst release then sustained release. The drug is rifampicin derivative. the particle size of drug loaded silica was around 198-230 nm.
In a personal letter, the student wrote me a question.
I am particularly interested in exploring the application of UV-Vis spectroscopy as a method for assessing drug solubility in oils which serves as a crucial initial step in the selection of suitable oils for nanoemulsion formulation. However, I have encountered challenges regarding the immiscibility of oils with methanol that is used as a solvant, as commonly mentioned in literature. I am hopeful that you could provide guidance or insights into the procedure involved in utilizing UV-Vis spectroscopy for this purpose.
My answer:
1. What kind of emulsion? oil/methanol or oil/methanol,water?
2. The drug is distributed between two phases and must be absorbed in the UV-Vis region. Oil should also absorb in the UV area.
3.Oil/methanol heterogeneous system. It remains so after the formation of a nanoemulsion.
I am preparing a drug for oral gavage which needs to be dissolved in 0.5% methylcellulose. The drug powder remains as clump and refuses to go into solution. Any tips on this?
Hello there!
I am trying to dock ZIF-8 (MOF) with the drug doxorubicin using PyRx and discovery studio for visualization of results. My queries are:
1. When I convert .cif file to .pdb using openbabel, then the whole structure of MOF is deleted except few bonds. But, when I use discovery studio for this purpose, then it slightly changes its structure. (any better suggestion?)
2. Since, ZIF-8 is considered as a macromolecule as compared to the drug (doxorubicin). When I load the molecule on PyRx, split models are generated. From there, I am confused how to convert them to .pdbqt format? If I convert them 1 by 1 to .pdbqt, then I won't be able to select all the .pdbqt at the time of docking.
Kindly help me through this!
Pictures are attached for reference. Thanks
I’m trying to induce my drug of different concentrations into my cell line. I’m working with HepG2 cell line
We intend to integrate qualitative methods in a clinical trial that evaluates the risks and benefits of a certain intervention/drug. I am just wondering if you have examples of studies exploring risks and benefits of a drug/intervention using qualitative methods.
📢 The first volume of the book "Drug Discovery Stories: From Bench to Bedside" (including two sections) has been updated with a new table of contents and cover art, see https://lnkd.in/gxZ4sUbK, this volume will be available on October 1st, 2024.
⚡ We are seeking new chapters (40 chapters confirmed) for the second volume. For this volume, we will feature blockbuster drugs (especially those beyond anticancer medications) approved in last five years or other promising drug candidates entering clinical stages. Please let me know (send me a message on Linkedin or an email to [email protected]) if you are interested in contributing. Your help in sharing this post to a wider community would be highly appreciated.
🏆 *No fees will be applied to you, and all contributors will receive a complimentary e-copy (PDF) when the book publishes. As an Elsevier author, you are eligible for a discount of 30% off of the list price of Elsevier books.
🎯 Key features:
- Showcases the drug discovery stories of blockbuster drugs
- Covers key aspects related to the drug development of the drugs
#drugdiscovery #drugdevelopment #pharmaceuticals #drugdesign #medchem #medicinalchemistry #drugs #drugmanufacturing
In atopic dermatitis FLG gene loss of function mutation is one of the vital point of pathogenesis. Most of the therapy are targeted against filaggrin protein related barrier damage but I need your opinion if there any way to recover FLG gene mutation not the end product
I want to do mathematical modelling of Pharmacokinetic data from plasma drug concentration in mice. Can someone please suggest me any freely available software for PK Modelling.
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
Hello Everyone..
I am trying to synthesise silver nanoparticles to encapsulate a chemical drug "X" using sodium citrate or NaBH4 as a reducing agent. I also have cited few publications doing the similar work. Now, I have encountered few articles where the drug "X" is used as a reducing agent to form Ag NPs.
Now, my question is kindly explain me that whether nanoformulations can encapsulate their own reducing agent?
Help me with the theory behind the answer.
Best Regards
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?!
I want to develop a nanoparticle-based drug delivery platform for burst/instant release of any drug. Kindly suggest ways to do that? What type of release mechanism can be adopted?
Usually, applied drug release mechanisms like pH-sensitive drug delivery works in a sustained release manner, however, I am looking for techniques (external stimuli) that can promote instant release of drug from the carrier. Thanks in advance for your reply.
My question is about synthesis of nanostructure. the drug is doxycycline monohydrate. nanostructure consists of micelle TPGS and plunoric acid (f127).
at first stage, preparation of drug is needed and i used water and ethyl acetate(aqueous and organic solvent). the purpose of the stage is acid base extraction. I don't know if the solvents are good or not because doxycycline monohydrate very little dissolved in water and sonication used. stage 2 is synthesis of 40 mg micelle TPGS + 60mg f127 and i used ethanol (as a solvent). 2 mg drug added to solution. Rotary(30 min) and freeze dryer(2h) used and then 5mL PBS added. for 24h under the stirrer temperature was 37 centigrade. after that DLS was taken from the sample. but result is not good. two peaks showed and PDI is 0.4. z-average is about 24 nm. what is the problem in stages?
Hello,
I have 5 blood samples each from 6 patients treated with a drug: on day 1 (before treatment), 7, 14, 21 and 30. In these samples I have measurement of both the drug concentrations and quantification of many genes by RNAseq, which we believe are the targets of this drug.
What is the most appropriate way to analyze the correlations between the drug concentrations and the gene expression level across these 30 samples (6 patients x 5 time points)?
Would you recommend another PK/PD analysis other than the one I mentioned above? Please note that the genes are supposed to be "tagret engagement markers" due to the known mechanism of the drug so we hypothesize that they are correlated with the drug level.
Thanks
Iddo
Dear researchers
I'm currently editing a Research Topic entitled Five-membered Ring Heterocyclic Compounds as Anticancer Drug Candidates. It's being published in the journal Frontiers in Chemistry.
Given your work in this field, would you be interested in contributing?
I look forward to hearing from you.
Best wishes,
Hi I am supporting a lady doing research into young people and the use of drugs and what works in terms of harm reduction in Ireland and abroad.
Thank you.
Hi everyone, please, I am new into cell culture and I am working on my protocol for cell treatment but I am unsure about the aspect of drug treatment. I intend to treat my cells with different drugs and observe the viability at 24, 48 and 72h. Therefore, my question is: (1) do I need to add my drug once, then observe some wells (in 96-well plate) at 24h, others at 48h and the last set of wells at 72h or (2) after 24h I have to observe the wells for 24h wells and withdraw (discard) the drug in wells for 48 and 72h and replace the drug with the same concentration and procedure, during the next 24h (at 48h) I will read the wells for 48h and again remove the drug from the 72h group and replace the drug? Please, which design best suits the objective mentioned in the beginning of my question (that's to study the drug sensitivity of a cell line for a 72 duration, with readings at every 24h interval)? I thought of the removal of the drug solution and replacement after each 24h considering the fact that I feel it is possible that my drug could get degraded or affected by evaporation if I administer it once to incubate for 72h and take my readings, I am worried that the result could be affected by evaporation or degradation (based on the drug half-life or something related to that). Most literature I found just mentioned "cells were treated with test compound (drug) for 72h or 48h" without clear explanation... Which I find confusing.
Thank you in advance for your kind responses and help.
Dear All,
I need to standardize synthesized drug concentration (IC50) for my in vitro experiment but I can't adopt MTT, LDH, or trypan blue kind of assay because I'm working on normal lung epithelial cells and even in my study I need to inhibit the enzyme from the synthesized drug.
Hence kindly suggest a method/ protocol/ idea to determine the drug concentration.
Hello, all i am currently working on polymeric nanoparticles and ,I have prepared one polymeric nano formulation of which I did SEM analysis. After doing the SEM analysis the morphology of unencapsulated nanoparticles was found to be Rod shape and that of drug encapsulated nanoparticles was found to be spherical-ellipsoidal and particles were agglomerated . Is the change of morphology in nanoparticle possible after encapsulating it with drug. Thank you in advance for any help
IC50 (half maximal inhibitory concentration) is a measure of the potency of a substance in inhibiting a specific biological or biochemical function by 50%. It is commonly used in pharmacology and toxicology to assess the effectiveness of drugs or toxins in inhibiting a particular biological process or target.
Men will do anything for sex, and will behave quite out of character to achieve it, such as spending several hours being romantic, and paying attention to what a woman says. (Anthony Mason)
I have done the NLC formulation using ultrasonication and microemulsion techniques. Now I have the whole emulsion as a milky white liquid. How to separate the NLC from the aqueous solution. I have done a single centrifugation. I assumed that the pellet had the NLC and the supernatant had the free drug. And I have to spin the emulsion at 25,000 rpm for 10 minutes. But the pellet hasn't completely settled. So please suggest a protocol to separate the NLC from the aqueous phase
I need some suggestions on working with the drug 5-fluoroindole. I am working on green microalgae and trying to make my strain tryptophan auxotroph. However, I am unable to make proper drug plates as the desired drug concentration is extremely low, hence difficult to measure. Secondly, 5-FI being light sensitive, it takes longer for the colonies to be visible if there are any since I need to keep the plates away from light.
Thanks.
Is it required to optimize drug molecule before docking. I docked a drug against a receptor without the optimization. It performs pretty well. And the structures are stable and no changes of the bond seen. My question is will the reviewer of the journal reject my article if I do docking without drug optimization via gaussian or other method?
I would like to know why 29-R strain of HSV-1 is resistent to the drug acyclovir.
The text in context: "Here are a few alternative treatments for infants to help with cough and cold symptoms:
A cool mist humidifier helps nasal passages shrink and allow easier breathing. Do not use warm mist humidifiers. They can cause nasal passages to swell and make breathing more difficult"
Source: https://www.fda.gov/drugs/special-features/use-caution-when-giving-cough-and-cold-products-kids
I searched quite some time on the fda archives, Google scholar, NIH, but couldn't find anything close to that assertion.
It's just kind of irksome that all the reputable consumer product publications are all citing the same FDA web page or each other. And some flat out rejecting warm mist humidifiers without question when there are quite a number of research papers that discuss the subtle dangers of cold mist ultrasonic humidifiers, especially regarding their ability to eject mineral and metal contaminants into the air and aren't able to inhibit bacteria growth, leading to instances of humidifier lung.
i am doing oniom calculation QM/MM for CYP450 and a drug as ligand. here i put my input file and the log file. i have been building this system for 3 weeks. this time i can't find out where the error is. i still think it is the problem in my mm parameters. also, the former error is bond and angle are not defined (in my ligand and the heme molecule). so i deleted all the connections of them and this error was solved. is this operation okay?
How does it depend on the nature or class of nanoparticles?
Resuscitation drugs become ineffective during severe metabolic acidosis ...why can't bicarbonate be a part of ACLS protocol
Resuscitation drugs become ineffective during severe metabolic acidosis ...why can't bicarbonate be a part of ACLS protocol
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?
I am trying to find the Hansen solubility parameters for screening miscible substances. Could anyone suggest an open-source online tool to calculate the Hansen Solubility parameter or any other equivalent solubility parameters?
Hi all,
I am currently helping my colleague to do a drug screening assay. We have use dTag to "turn off" the protein expression of our protein of interest and treat the cell line with drugs combined with dTag/DMSO. I am just wondering if it is possible to see the synergistic effect with just on/off of the protein of interest. Some similar systems such as tet on/off would raise the same question. I am very intrigued if there is anything we can do with these systems that can just be turned on and off, but not adjusted to various level like normal drugs.
Many thanks!
Poor countries suffer from weak food and drug security, and they depend on aid from major countries. Therefore, these poor countries are subordinate to the major countries, and this affects the sovereignty of those countries, and therefore, how can those countries build their food and drug security?
I looked into my paper this morning and saw references to mental illness which even 50 years ago would not have been there. Nor would these unproven reflections on human behaviour appeared in novels or articles. I will here raise the likely position that we are being brainwashed by the medical profession in tandem with the drug companies. My investigations, through clients and reading, indicates that psychotropic drugs are dangerous and always have been. Claims of mental health in lieu of misunderstood behaviour, life stresses, have grown alongside the development of drugs and diagnosis which reflect each new drug invented or simply repackaged by the drug companies.
We have seen the multifarious affects of Russian propaganda in Russia and the world (strangely effective in the USA, no matter the warnings), establishing viewpoints and changing history, affecting attitudes, so why cannot the West be equally susceptible to propaganda-especially one arriving from an authoritative source (medical profession) which we fail to see?
I'm going to perform drug treatment to my normal human epidermal keratinocyte cells (NHEKa). The drugs I'm using are anti-EGFRs and doxycycline.
Should I collect them right after the drug treatment or should i remove the old supernatant after the drug treatment and collect the ones reincubated with fresh medium? Why and why not to do so?
And how long can the supernatant be stored under -20 degree celcius condition?
A drug showing efficacy in humans when administered through oral route, but the same drug is lacking efficacy in mice admistered through same route.
What can be the possible reason?
I want to make formulation of crude drug extract, so which formulation would be best for diuretic?
Hello
Does anyone know about oxalate kidney stones?
What is the best chemical drug for oxalate stones?
I am combining drug A (IC20 and IC50) with drug B (5 uM, 10 uM and 50 uM). Drug B reduces cell viability to 28% at 50 uM, while drug A IC20 combined with drug B 50 uM reduces cell viability to 32%. CompuSyn gives a CI=0.46. Is this correct? To have synergism shouldn't the viability be reduced to less than 28% when combining the 2 drugs at these concentrations?
Thanks for any help.
Association of the effect of the medication on the disease (efficiency), but also the effect of the drug the body in general (side effects). Furthermore, the association of the effect of the disease on the body (processes and functions).
Bioinformatics can be in charge of both: automatization of the tests and the vizualization of data and results.
Hi everyone
I am looking for a database that allows me to input the name of the ligand/drug/structure and a protein to predict if there is any potential interaction between them.
Do you have any suggestions?
Thank you
BBB we know prevent bacterial & viruses crossing but how Drug can pass through BBB & what is the role of Passive transport in it. Kindly explain it Diagrammatically preferably.
Hey all
I want to see the affect of a certain drug on my cell line (cancer cell line).
I want to see how it alters the expression of a certain nuclear protein.
Since my cells are fast growing and protein synthesis usually takes 72 hours in mammalian cells, how should I seed and give treatment to the cells?
Should I seed them in low cell density and give treatment after overnight incubation? So that the there will be enough space left for cells to grow and divide until 72 hours?
Should I use media devoid of serum to prevent cells overgrowing the flask?
thanks and best
20 mg of quantity i have taken for (EE).
Total quantity of drug used in formulation is 500mg.
Formulation 1, UV absorbance value: 0.0057 (10 times diluted).
Standard curve:
y = 0.0164x + 0.0076
R² = 0.9991.
We are standardizing a protocol for studying cytotoxic drugs (mainly anticancer class of drugs) and we are using HepG2 cell line for that. My question is why only HepG2 cells while we can use HEK293 cell line also ?
i am working on the determination of the synergism activity of the herbal and allopathic drug. firstly i tried to find out the zone of inhibition of individual drug having lower (25, 50, 100 ppm), middle (250, 500, 1000 ppm) and upper (2500, 5000, 10,000 ppm) concentration against s. aureus bacteria. but the expected result was not obtained in case of herbal drug. kindly provide the valuable suggestions for the same with references. I tried the same experiment against E. Coli and Pseudomonas Aeruginosa & the expected result was obtained in both cases. I am facing a problem only in case of S. Aureus. I also like to add that i repeated the experiment 9-10 times by maintaining aseptic condition and other cares to be taken while performing the experiment. Kindly give the solution for S. Aureus to get desired result. Thank You
Are there any high-impact papers in top journals (Cell, Nature, Science publications) that show the possibility of mimicking mechanical stimulation tissue responses such as skin growth and muscle hypertrophy via drugs?
I need to co-deliver a hydrophobic drug and a hydrophilic drug. Is it possible using a hydrophobic polymer?
Hello
I am planning to deliver a cy5-labeled drug to mice, and then check its distribution in different organs. In case I wish to preserve the tissues for later research, will fixation (using 4% formaldehyde) damage the fluorescent signal of the cy5?
Does somebody have any experience with cy5 and fixation?
thanks in advance.
I am looking for a plain/empty gel system, which we can directly buy and load the drug for the purpose of transdermal delivery. Your kind help will be appreciated.
Neurons were treated with four different types of drugs, and then a full transcriptome was produced. I am interested in looking at the effects of these drugs on two specific pathways, each with around 20 genes. Would it be appropriate for me to just set up a simple comparative test (like a t-test) and run it for each gene? Or should I still use a differential gene expression package like DESeq2, even though only a few genes are going to be analysed? The aim of my experiment is a very targeted analysis, with the hopes that I may be able to uncover interesting relationships by cutting out the noise (i.e., the rest of the genes that are not of interest).
Psychology, according to Wundt, drew on definitions of human nature as distinct from prior religious interpretation, that human beings are neither bad nor good. Although thereby not conditioned or inhabited by supernatural forces they are driven by the forces within and of their environments.
Psychiatry believes mental illness is determined or pre-determined, and that even when environment plays a part people react to the environment in pre-determined ways. People can and do claim that psychiatry is a science because it can be measured. I believe this is suspect!
The role played by drugs in psychiatry is seen by some as evidence of its scientific basis, as drugs belong to science and fit the claims of medicine for almost three hundred years. Drugs will suppress so the good they do, combined with their addictive nature, is suspect. Or do you consider otherwise? Again the effects of drugs are subject to measuring, or are they? Psychiatry predetermines human nature but is the categorisation of human beings reliable?
I have used the Sono-photocatalysis process to degrade this antibiotic drug and I want to show its oxidation potential range in my schematic diagram. I really appreciate any help you can provide.
I have a few clinical trials results and would like to calculate the Weighted mean for these studies. I am unsure how to calculate for these few trials:
Trial 1:
Drug: 25/85 (25 patients out of 85 patients response to this drug)
Placebo: 11/75 (11 patients out of 75 patients response to placebo)
Trial 2:
Drug: 30/200 (30 patients out of 200 patients response to this drug)
Placebo: 10/170 (10 patients out of 170 patients response to placebo)
Trial 3:
Drug: 90/150 (90 patients out of 150 patients response to this drug)
Placebo: 10/250 (10 patients out of 250 patients response to placebo)
Can anyone teach me how to calculate?
Appreciate your kind help for this matter.
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."
Clinical Superiority ,inferiority
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!
Dear all -
we would like to produce and study biofilms of Pseudomonas aeruginosa. We are not well equipped, only a simple microscope. I wonder if it could be possible to make estimations on the drug (peptide) activity on the biofilm by using a plate reader to grow the biofilm and somehow use this setup to follow the live and dead cell staining?
Thank you very much for your response!
Have a nice day
Kornelius
I use the following equation to calculate:
Percentage difference between treated and control cells
=
(O2 x A1) - (O1 x A2)
(O2 x P1) - (O1 x P2)
x100
Where:
- O1 = molar extinction coefficient (E) of oxidized alamarBlue (blue) at 570 nm
- O2 = E of oxidized alamarBlue at 600 nm
- A1 = absorbance of test wells at 570 nm
- A2 = absorbance of test wells at 600 nm
- P1 = absorbance of positive growth control well (cells plus alamarBlue but no test agent) at 570 nm
- P2 = absorbance of positive growth control well (cells plus alamarBlue but no test agent) at 600 nm
First question: Is this equation okay for the resazurin test?
Second question: My results show that P1 and P2 are equal or less than the A1 and A2. The color of positive control(P1 and P2) becomes bright pink. I think the control absorbance (suspension of cells without drugs + resazurin) should always be more than the group of cells treated with drugs to calculate correctly. While the absorbance of my control is less than the samples. I checked the resazurin and the ELISA reader and I am sure of the authenticity of them.
What do you think is the problem?
Thanks.
I have to do a clonogenic experiment, and the interventions contain drugs + radiation.
I was wondering which of the following protocols is better to use, as I have seen both in related articles.
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A) 1. Seed cells in a high number (e.g. 100,000 cells)
2. Add drugs and radiation exposure
3. 24h after radiation exposure, trypsinize cells again and seed them in a low number (e.g. 500-2000 cells) for colony assay
4. Let them grow for 9-14 days
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B) 1. Seed cells in a low number (e.g. 500-2000 cells)
2. Add drugs and radiation exposure
3. Let them grow for 9-14 days
Hello, I am facing a tricky problem. I have two ipSC cell lines, one with a point mutant and the other with WT. I performed some sensitivity assays, such as treatment with topotecan, etoposide, and other oxidative DNA damage drugs. In the initial passages, probably around 5-6, I saw that the mutant cell lines were sensitive to the drugs. However, later passages showed no sensitivity at all. I can go to the early passages to do my experiment every now and then. However, the main problem is that I have picked some colonies from my WT and mutant cell lines, including the Cas9 sequence incorporated in the genome to perform a CRISPR screen. But they lose sensitivity by the time I pick up, expand, and freeze the colonies. How do I keep the sensitivity part intact of the mutant cell lines? Any help or insight will be greatly appreciated.
I am a Ph.D research scholar in the department of pharmaceutical analysis.
I've synthesized drug loaded nanoparticles with PLGA and got an encapsulation of 40%. But when I break the pellets I am only getting a flat line in UV. The drug is soluble in DCM and Chloroform.
Thanks for your help.
I am currently conducting experiments on checking combinatorial effect of two small molecule natural compound against cancer cell line. However, I am unable to determine how the combination of two drug should be done. How the ratio should be managed so that I can check the difference of combinational effect of drug and compare them with effect of individual drug through cytotoxicity assay, mRNA expression, etc.
In my project, I have degraded an antibiotic drug via the Sono-photocatalysis process. now I need to identify the degraded intermediates and propose a possible degradation pathway.
For now, I have LC data and the Mass spectrum of each exposure duration
this is my first project using LCMS so I have been stuck on this step for a while now
is there any software, I can get help from? to identify intermediates based on m/z values?
Statistically speaking, it is virtually impossible to change a life of prison recidivism, drug/alcohol, and criminal behavior.
under biopharmaceutics classification system class 2 and 4 drugs have poor water solubility. by making them as solid dispersions their solubility can be increased. is there a specific method to measure whether the solubility has been increased in-vitro?
I’m conducting a stability test on levodopa using 0.1mol/L HCI as the solvent,but on the first day and the third day, the drug content exceeded 100%. May I ask what is the solution?
I am currently conducting experiments using organ baths with rat duodenum and ileum tissues. These experiments involve the administration of various drugs, including Fluoroacetate, Bethanechol, Carbachol, SNP, Guanethidine, and Atropine. Additionally, I am using Krebs solution continuously aerated with 95% O2 and 5% CO2, maintaining a temperature of 37 degrees Celsius. My research focuses on studying the contraction and relaxation movements of the intestines, particularly the effects of these drugs in combination with Electrical Field Stimulation (EFS) set at parameters of 2-16 Hz, 1 msec, and 100V.
One significant challenge I face is the prolonged duration of these experiments, which can last several hours. During this extended period, I have noticed that the tissue responses are not as consistent or satisfactory as I would like them to be. I am particularly concerned about the inability to achieve the typical relaxation response observed with SNP and, in some cases, even observing contraction responses with SNP.
I am seeking guidance on how to maintain normal contraction after suspending the tissues and ensure accurate and consistent responses with each drug application. I am also uncertain about the timing of cumulative drug applications, such as Bethanechol and SNP, in relation to EFS. Additionally, I would appreciate guidance on the optimal duration to wait during each phase of drug application. Unfortunately, I have been unable to find this specific information in my literature search. I would greatly appreciate any assistance or suggested sources and contacts that could provide further insight into these challenges.
Dear all,
I think that usually wound healing assay are made in 12- or 24-well plates. However, I need to test different drugs in triplets as single treatments and some of them in combinations.
Due to 1) Some of the drugs are available in a really small quantity.
2) I need all treatments to be measured at the same time.
3) It would be even better to use less cells and less media.
So, my question is, can we do such assays in 48-well plates? And would it also be feasible if we scratch the cell monolayer with a 200 microliters yellow?
Many thanks and regards.
platform of drug clinical study
I'm going to experiment with sepharose CL-4B gel to isolate drugs that are not enclosed in liposomes.
I need to degas enough before using the sepharose gel, and most of the references seem to be done using a vacuum pump.
We don't have this instrument in our laboratory, so is it okay to degas sepharose using bath type sonicator? Wouldn't it affect the structure of the sepharose gel?
Or is there any other way to remove the air from the sepharose gel?
Thank you.
I checked on the internet. (ΣFIC) was calculated for each well with the equation ΣFIC = FICA + FICB = (CA/MICA) + (CB/MICB), where MICA and MICB are the MICs of drugs A and B alone, respectively, and CA and CB are the concentrations of the drugs in combination. I have MICA and MICB. However, I don't know how to calculate CA and CB. If anyone knows how to calculate CA and CB by using prism or the other softwares, please help me. Thank you in advance
Hello. In my study, patients came to the doctor 3 times. At each visit, it was assessed whether the patient was taking a certain class of drugs (yes / no), a total of 7 drug classes. I need to find out if their therapy differed at visits (i.e., for example, drug A was taken more often at visit 1 than at visit 2). What test do I need to apply for this dichotomous variables in three visits? ANOVA?
Proof of concept ,clinical trial relationship
For hydrophilic drugs only hydrophilic polymers are used. Then why a combination of hydrophilic and hydrophobic polymers are used for hydrophobic drugs
Does Daprodustat require a separate facility or dedicated facility for their drug product?
I need to load a drug on polymer nanoparticle, most of procedures used triethylamine TEM with chloroform for solubilization the drug, but I have trimethyl amine TMA instead of TEM, my questions is is it possible to use TMA instead of TEM?
I'm trying to screen for a suitable range of concentration of Gefitinib for my subsequent ELISA assay, the final aim is to select a Gefitinib concentration that does not kill cells+give off inflammatory response. I will detect the levels of inflammatory markers and compare it to the reading after certain treatment, which believe to be able to reduce the level of inflammatory markers.
I have tested on the range of concentration between 80-600 ng/mL and the result from my MTS assay did not show much significance in terms of cell cytotoxicity, meaning the viability is more or less the same (60%-90% viability compared to my vehicle control), and the trend looks odd (cell viability increases as drug concentration increases). I prepared my Gefitinib drug stock with 100% DMSO and dilute it with growth medium for all my assays. The initial range of concentration is determined based on literature mentioning the Cmax value of Gefitinib in healthy individuals, which I believe is more relevant to my study, since I'm treating normal human epidermal keratinocyte cells (NHEK) .
Anyone has any experience with treating NHEK cells with Gefitinib? I've seen a lot of studies being done with cancer cells but not with normal cells. I'm unsure of the limit of concentration to be used, of course at higher drug concentrations cells are going to be killed and inflammatory response will be more significant, but it does not make sense if I just use a high concentration without any reference to real life/clinical situations?
I'm asking this so that I can save resource (the drugs used are expensive, so as MTS reagent and ELISA kits) and not to blindly increase the concentration just for the sake of getting a positive result. I hope to get some enlightenment on this!
Salt formation of weak acid causes ionization of drug due to which solubility increase but we have studied drug absorbed in unionized form then how salt formation will improve the absorption of a drug?