Science topics: Clinical PharmacologyDosing
Science topic
Dosing - Science topic
Explore the latest questions and answers in Dosing, and find Dosing experts.
Questions related to Dosing
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 ??
i read many papers that used the invitro drug release test but never showed the details of how they calculated the dose from it.
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
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:
Is it normal for Jules Morgan to publish more than 200 articles in the Lancet journal
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
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?
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.
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.
Dose and time of upregulation of CD86 and CD80 in RAW264.7 cells using LPS/IFNgamma?
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!
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.
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 ?
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).
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?
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
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?!
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?
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?
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?
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.
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?
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!
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.
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?
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?
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?
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.
I need to understand the equation for oil palm fertilizer dose recommendation (i'm so sorry for my bad english)
Thank you
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.
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.
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.
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?
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.
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.
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."
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?
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!
I need to know dose of paraffin oil per lit or per 10 lit of water and how to use it as insecticide.
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.
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.
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.
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.
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.
dose titration , dose escalation
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
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.
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.
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). ?
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.
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
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 ?
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.
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 ?
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 ?
dose titrtion and escalation
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.
In particular, what information do you have about the reaction of different varieties of crops to different doses of herbicides?
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
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?
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!
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
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?
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!
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?
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
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.
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?
if I have a research gate account, can this be identified as a number like ORCID?
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?
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!
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.
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
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
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?
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.
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.
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?
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
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
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?
my plant extract shows less antioxidant activity (by DPPH assay) in medium doses. what could be the reason for it?
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.
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!
I need this ratio for 4 time dose
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
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?
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?
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.
How do I measure patients' radiation doses from conventional x-ray facilities?
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
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!
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!
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!
I need some insight, in simpler words, why do we extrapolate from high experimental doses to lower doses while establishing dose thresholds?
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.
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.
Sub acute toxicity 28 day