Science topics: ChemistryPharmacology
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Pharmacology - Science topic

Pharmacology is the branch of medicine and biology concerned with the study of drug action.
Questions related to Pharmacology
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we want to submit our manuscript to a special issue in the field of phytochemistry, pharmacology of natural products, or liquorice in particular. any suggestions?
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thank you for your suggestion, unfortunately the publication charges are so expensive
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I wish to know what clean room criteria I should use to detect Mycoplasma Pneumoniae contamination in a received pharmacological sample. Is there any GMP guideline or something from pharmacopeia?
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Hi Everyone,
I will be teaching a bit more autonomic nervous system this semester, and I have come across two pharmacology websites indicating that epinephrine has a higher affinity for beta-2 receptors than alpha-1 receptors, and this is the purported reason why low levels of epinephrine are vasodilatory in some arterioles. However, the literature contradicts this information. Specifically these first two articles collectively suggest that epinephrine has a higher affinity for alpha-1 receptors. The last article that I listed suggests that alpha-1 receptors lose responsiveness during heavy exercise. So, after all these years, is it true that we still don't have a clear understanding of the affinities and intrinsic activities of these receptors, and how this is related to the response to epinephrine in different arterioles. Furthermore, the differential expression of these two receptors in various vascular beds is something I haven't seen published.
-Br J Pharmacol. 1995 Sep; 116(1): 1611–1618. PMCID: PMC1908909. Selectivity of the imidazoline alpha-adrenoceptor agonists (oxymetazoline and cirazoline) for human cloned alpha 1-adrenoceptor subtypes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1908909/?page=3
-Naunyn Schmiedebergs Arch Pharmacol. 2004 Feb;369(2):151-9. Comparative pharmacology of human beta-adrenergic receptor subtypes--characterization of stably transfected receptors in CHO cells. https://pubmed.ncbi.nlm.nih.gov/14730417/
-Exercise attenuates α-adrenergic-receptor responsiveness in skeletal muscle vasculature
John B. Buckwalter, Jay S. Naik, Zoran Valic, and Philip S. Clifford
Journal of Applied Physiology 2001 90:1, 172-178
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Thanks, Adam L Vanwert for sharing the link. The website looks interesting.
Kindly convey my regards to Dr. Kalunde, if you are in touch with him.
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Can any one help me regarding Q1 pharmacology journal with fast acceptance timeline?
Thanks and best wishes
Have a great day!
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There are lots of very fast journals, but many are start ups, (some may even be scams) many also have a low or no impact factor. That's not really a deterrent for me, as long as they appear in data bases and searches, that's all that matters, it eventually be found. However, if you are trying to build a career, the journal's impact factor is import, and its also import if you want you work to be quickly discovered. Depending on your department/funding, publication costs may be a factor, and they can be 2-3 thousand dollars. I was involved in research, mainly at the laboratory bench, for many decades and I get continual solicitations to submit articles. A few days ago I got a solicitation from
so they are likely short an article or two, so it may be relatively easy to get a paper out through them at present. If they are desperate you can frequently negotiate the publication costs. Good luck.
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Good evening,
Please I prepared a finished product mixing 75% extract A and 25% extract B I obtained pharmacological responses (in IC50) better than using product A alone.
How can I scientifically justify the choice of blend (75/25) than other blends. Is there software that calculates the optimal quantity to choose to have the best pharmacological responses?
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thank you so much
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Did you ever experience a conceptual change in pharmacology where was a discrimination b/w phenomena/concepts that you previously regarded as a single phenomena/concept?
For instance, proton pump inhibitors are often thought to be interchangeable, but some differences have emerged in their pharmacological properties, which may be reflected in some aspects of clinical efficacy. Such differences include potency, speed of onset and duration of pH 'holding times' (2004)
Reference
Robinson M. Review article: the pharmacodynamics and pharmacokinetics of proton pump inhibitors--overview and clinical implications. Aliment Pharmacol Ther. 2004;20 Suppl 6:1-10. doi:10.1111/j.1365-2036.2004.02160.x
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The words selectivity, specificity, and sensitivity (derived from Latin seligere, specificus, sensitivus), can be confusing terms as they are often used synonymously in the medical literature. However, they should not be used
interchangeably as each represents a different phenomenon.
Reference:
Mencher, S. K., & Wang, L. G. (2005). Promiscuous drugs compared to selective drugs (promiscuity can be a virtue). BMC clinical pharmacology, 5(1), 1-7.
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Please list Zero Author Publication Fee charging journals in pharmacology subject which are indexed in Pubmed or Scopus or Science Index or Medline or Central Science Citation Index, or Science Citation Index, or Expanded Embase, Scopus, Directory of Open Access Journals (DoAJ)
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Hi, all,
I have emailed many times from "Annals of Pharmacology" to invite me as a reviewer. Could anybody tell me this journal is a reliable one?
Naoto
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…and the e-mail address? No website link is suspicious.
As far as I can see there is no journal called “Annals of Pharmacology”. There are titles beginning with this, like for example:
-Annals of Pharmacology and Pharmaceutics (ISSN 2573-6051) http://www.remedypublications.com/annals-of-pharmacology-and-pharmaceutics-home.php Among the many red flags is the fact that this publisher “Remedy Publications” is mentioned in the Beall’s list https://beallslist.net
-Annals of Pharmacology and Pharmaceutical Sciences (ISSN 2766-7472)
https://www.directivepublications.org/annals-of-pharmacology-and-pharmaceutical-sciences/Publisher is not included in the Beall’s list (yet), most likely because they are too new. One of the red flags is the (fake) contact info and the so-called US origin with virtual no American in the editorial board.
-Annals of Pharmacology andPharmacotherapeutics http://www.medtextpublications.com/annals-of-pharmacology-and-pharmacotherapeutics-home.php Among the many red flags this publisher “ Medtext Publications” is mentioned in the updated version of the Beall’s list https://beallslist.net/#update
So, indeed most likely predatory.
Best regards.
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Is there anyone who has found a clear description of the mechanism by which curcumin inhibits beta-amyloid aggregation in-vitro? So far most of the answers I find are very general and without meaningful explanations, and often there is not even an attempt to clarify.
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Andrew Sutton You are welcome!
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Learning discipline-specific terminologies or names of drugs (in Pharmacology discipline) is extremely challenging for a novice. Which theoretical framework supports this idea? How the novice can overcome this challenge?
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Hi, Dr. Faraz Khurshid the technique used in your study was fine, do we search for advance one?
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How to correlated multiple protein with pathways related diseases?
And which software can be used?
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The concentration of my protein is 14 μM and the Kd is 168 nM. I want to have the ligand in excess, but I am not sure how to go about it.
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Because this situation is in the tight-binding regime, you should use the tight-binding equation for the equilibrium calculation.
fraction of enzyme with ligand bound=
[(Kd + Rt +Lt) - square root((Kd + Pt +Lt)^2 - 4RtLt)]/(2Rt)
where Rt is the receptor protein concentration and Lt is the ligand concentration (^2 means squared)
For example, if Kd=0.168 µM, Rt=14 µM and Lt=28 µM, the fraction of occupied receptor is 0.988.
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Hi, could anyone please help me understand why my dexamethasone calibration curve won't work and how to fix this? We are trying to measure drug encapsulation efficiency for dexamethasone but when we tried to do our standard curve the absorbance values for concentrations ranging from 1 - 10^-8 mg/ml were all the same as our standard and no absorbance peak was seen on the whole spectra. We are using dexamethasone dissolved in absolute ethanol and diluted the samples in both water and ethanol. We are also using FluoStar Omega UV-VIS machine to measure this.
Could anyone please tell me if they have done this before and how they managed it?
Thanks :)
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Emma Jackson Yes, I did try the nanodrop also and got a linear curve. Yes, I agree, I don't think the nanodrop provides reliable values since variation between readings can be high. Greiner sells some plates adequate for reading at the UV range. We ordered this ones: https://shop.gbo.com/en/row/products/bioscience/microplates/uv-star-microplates/96-well-uv-star-microplate/655801.html
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Can any one suggest Q1 or Q2 fast Journals in pharmacology for revision my manuscript?
Thanks and best wishes.
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Annual Review of Pharmacology and Toxicolog 13.820 Q1
PHARMACOLOGY & THERAPEUTICS 12.310 Q1
BRITISH JOURNAL OF PHARMACOLOGY 8.739 Q1
CLINICAL PHARMACOLOGY & THERAPEUTIC 6.875 Q1
BIOCHEMICAL PHARMACOLOGY 5.858 Q1
Frontiers in Pharmacology 5.810 Q1
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I had recently some doubts about the proposal of a comparative study, comparing botulinum toxin type A and a non pharmacological treatment like dry needling. DN has shown to be effective to decrease spasticity in stroke patients but it has never compared against the gold standard. Could be a comparative (feasibility) study be considered to be until proof of concept stage? Because by definition this should be only for a novel treatment. I also had the doubts of which kind of measurements/outcomes it should include to be a fesibility study
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On that Matter observational process can have a relevant return And évaluate comparison And synergy
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In the structure of many drugs, there is a carboxylic group
What is the significance of this group? Why should it exist in the structure of a drug?
Do you know any article or book or reference about this subject?
Thanks a lot
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Nalidixic acid - A NSAID grs of drugs or pain killer .REF : en.wikipedia.org ( Image Source ) .
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Dear experts and scholars, it is known that the causes of diarrhea are based on different mechanisms. Based on this, how many and what methods do you recommend to induce diarrhea and transfer the drugs in them to animal models? Your suggestions are greatly appreciated.
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intramuscular (IM), intravenous (IV), subcutaneous (SC), and intradermal (ID) routes.
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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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I'm interested in analytical protocols for measuring exposure to methylphenidate in mice, especially HPLC-based methods. What are the possibilities regarding detectors and sample preparation procedures? Also, considering limited volume of blood can be obtained from mice (and sampling in more time-points probably affects the obtained results) - what would be the best option in the context of the minimal volume of sample needed for the analysis? What about enantiomers (e.g. 10.1002/bmc.3312). I'd like to find/establish a protocol for clinically relevant chronic oral dosing of methylphenidate in mice that reflects what we see in humans (https://www.researchgate.net/post/Protocols_for_clinically_relevant_chronic_oral_dosing_of_methylphenidate_in_mice)
Any info is greatly appreciated.
Jan
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I am starting to use BiC/4AP for an experiment to stimulate hippocampal neurons. This technique has been used previously by other labs and a former member from my own lab. I have tried several times, but cannot seem to get the same results as others. I am using bicuculline and 4AP from at least 10 years ago that has been stored at room temperature in a dessicant box. The bicuculline is stored in aluminum foil also to prevent light exposure.
I'm wondering if my experiment is not working because the drugs are too old. I have tried to look for the shelf life of the drugs but cannot find much. Does anybody have experience working with these drugs and have any idea of how long they are good for when stored at room temperature?
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Long term storage of bicuculline should be at -20 oC and this will only be useable for approximately 1-2 years. 4-AP should also be stored at -20 oC for long term and will only be useable for approximately 6-12 months.
Therefore, you should discard the old solutions and order fresh products.
(An tip for identifying shelf life is to look at the stability and storage section in the product information sheet for each product)
Hope this helps!
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Trying to research on influence of UGT1A9 variants on the pharmacology of frusemide.
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You will find in this attached some articles with several approaches used to isolate polymorphic variants of the UGT1A9 gene from blood.
Please, choose the one that suits the most with your available reagents / chemicals.
Best wishes,
Sabri
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BPH is a innocent bystander in later stages of male life in humans. Normally Benign Prostatic hyperplasia is curable by using the various avaliable treatments and medications like 5alpha reductase inhibitors and antiandrogenic therapies. TURP, TUIP and prostatectomy are also advised very often. But what is the indication of the progression of the problem which is not curable from the avaliable measures. Is it a cancerous situation then? Is herbal therapy the probable answer of the problem in complicated cases?
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Prostatic abscess is a rare urological disease. Patients with prostatic abscess and those with PCa can have similar presentation, such as LUTS, lymphadenopathy and abnormal PSA values.
USG-guided needle aspiration maybe an option of treatment for prostatic abscess, but TURP should be considered in patients with complicated abscess or suspected prostatic carcinoma.
If the histopathology result shows PCa, staging and risk stratification should be done for the treatment decision… “Shared-decision making” for PCa mgt
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how we would treat it friendly for making it less harmful and more livophilic?
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Dear Muhammad Ejaz thank you again for sharing this very interesting technical question with the RG community. Just in case that the issue is still of importance to you, I just came aross two more potentially useful literature references which might help you in your analysis. Please have a look at these articles:
Recent Developments on 1,2,4-Triazole Nucleus in Anticancer Compounds: A Review
and
1,2,4-Triazole: A Privileged Scaffold for the Development of Potent Antifungal Agents - A Brief Review
Both papers are review articles. Unfortunately they have not yet been posted as public full texts on RG. Please check if you can access them through your institution. At least the author of the first article has an RG profile (https://www.researchgate.net/profile/Vinod-Kumar-143). Thus you can easily contact this author via RG and request the full text of the review directly from him.
Good luck with your work and best wishes, Frank Edelmann
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Respected researchers or professors,
I am Kumar Sharp, currently a third year MBBS student from India. I will be graduating medical school in 2024.
I have a very keen interest in Pharmacology, drug development, infectious diseases, microbiology and immunology. I have done my best to develop my interests in research and development, public speaking and leadership, publishing work in COVID-19 as well.,which you can see from my profile.
I would like to pursue my future career in these fields and teaching. I belong to a middle class family and do not have adequate resources to apply for international exams.
Can you all suggest if there are any ways to apply for these specialization in countries other than India.?
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China is the best choice, there are vast opportunities for the young
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Case study patient (age 29, F) presents with chronic reoccurring major depressive episodes (MDD) which last anywhere from 2 weeks to 2+ years; comorbid generalized anxiety (GAD), PTSD, borderline personality disorder (BDP), chronic nightmares (does not include night terrors or sleepwalking -- no additional sleep studies performed).
After more than 20 separate medication trials including stimulants, non-stimulants, mood stabilizers, several kinds of antipsychotics, anxiolytics, and several classes of antidepressants over the course of 8 years, Patient's depressive, anxiety, and PTSD symptoms continue to chronically reoccur.
Currently, Patient takes lamotrigine @ 50mg once daily for anxiety and nightmares management. Patient has been on lamotrigine @ 50mg since 2017.
A GeneSight®  Psychotropic Pharmacogenomic Test was done in 2021.
Most genetic components presented as normal.
Patient is homozygous for the short promoter polymorphism (S/S) of the serotonin transporter gene SLC6A4. The short promoter allele is reported to decrease expression of the serotonin transporter compared to the homozygous long promoter allele. The patient has displayed a moderately decreased response to selective serotonin reuptake inhibitors, most likely due to the presence of this short form of the gene.
Additionally, Patient's symptoms are concurrent with undermethylation -- anxiety, depression, insomnia, allergies, recurring moderate-severe headaches (but not migraines), digestive issues, multiple miscarriages, and key traits of autism.
Patient reported a partial hysterectomy in 2017 (age 25) - uterus and fallopian tubes removed, ovaries biopsied. Pathology reports confirmed endometriosis. Currently, Patient reports resurgence of endo symptoms - chronic inflammation, pain, digestive issues, etc.
Known pharmacological treatment options are limited at this time. We have found inconclusive, but possibly promising research into serotonin agonists that could help treat the MDD. Other options to address some of the inflammation exacerbating the depressive pathology include Rx strength NSAIDs, Cyproheptadine HCl*, or dexamethasone (Glucocorticoid).
*H1-antagonist cyproheptadine acts by competing with histamine for H1-receptor sites on effector cells. It also has potent 5-HT (serotonin) antagonist activity through its 5-HT2A receptor-blocking action. In addition, it also has weak anticholinergic and central depressant properties.
Collective recap:
-chronic reoccurring depressive episodes
-chronic anxiety and sleep disturbances
-chronic reoccurring inflammatory processes
-multiple failed pharmacological treatments
-short promoter polymorphism (S/S) of the serotonin transporter gene SLC6A4
If you have any info into the pathologies, medical treatment options available, additional DSM-V classifications, or studies pertaining to any of this, please send them our way.
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Cochrane Database Syst Rev. 2018 May; 2018(5): CD010558.
Psychological therapies for treatment‐resistant depression in adults
Monitoring Editor: Sharea Ijaz,📷 Philippa Davies, Catherine J Williams, David Kessler, Glyn Lewis, Nicola Wiles, and Cochrane Common Mental Disorders Group
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I will test a substance on mice at a dosage defined from DL50 results and will calculate plasmatic concentrations at different time (7 times) . I will need then a software program to calculate parameters from oral and IV routes. 
Thank you 
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How can I free download DDsolver on my computer?
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I was wondering which databases would be best for a scoping review on how drugs effect the microbiome. Not sure if this falls into pharmacology, microbiology or metagenomics, but I would probably want to search a database that contains all of them!
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Thank you for nice question. There are many tools to predict both microbiomes and resistomes. However, the drugs interact with microbiomes is really challenging. You can use MASI: microbiota—active substance interactions database (https://doi.org/10.1093/nar/gkaa924).
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Please share your experience regarding conduction of SDL session in Pharmacology?
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Thank you Deepti Madam
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I'm a community Pharmacist and I'm interested in writing, especially writing scientific papers. I'm offering my help and assistance in case you need a hand with your current research. My areas of interest: Pharmacotherapy, psychology, neurology, psychiatry. So send me a message in case you need help.
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I am interested...Kindly contact me after two weeks...
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Is there anyone who is good in network pharmacology and know how to use cytoscape properly?
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Dear all thank you for replying. I have got the solution of the problem which I was looking for. Appreciate your prompt responses
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Hello, I wonder if someone knows which is the LD50 of conduritol beta epoxide (CBE) used to generate pharmacological models of Gaucher Disease. :(
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i think the safe (non-toxic) dose is 100 mg/kg.Reference article is attached
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Acyl-CoA:lysocardiolipin acyltransferase-1 (ALCAT1) is a polyglycerophospholipid acyltransferase of the endoplasmic reticulum which is primarily known for catalyzing the acylation of monolysocardiolipin back into cardiolipin (Wikipedia).
I am looking for (pharmacological) ways to inhibit the enzyme ALCAT1. Are there any drugs or chemicals that could do the trick?
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There are many inhibitors, with references, listed here:
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Hello everyone,
We are having problems with our competitive binding assays, and I wanted to see if you have any recommendations. I will begin by explaining our protocol and the optimizations we have already done so that you have some background, then I will describe our problems.
Protocol:
Four ValiScreen GPCR cell lines from Perkin Elmer are used.
Specifically, we use HEK-293 transfected with adenosine receptor A2A, HEK-293 transfected with adenosine receptor A2B, CHO-K1 transfected with adenosine receptor A1, and CHO-K1 transfected with adenosine receptor A3.
Cells are cultured in T-25 flasks at 5 % CO2 and 37º C. Two days before an assay, cells are plated at 30,000 cells/well into a black-wall, 96-well plate. On the day of the assay, the cells are examined under the microscope to ensure that the cells are covering at least 80% of the bottom of each well. (100% coverage is preferred, and usually we get 100% coverage.)
According to a treatment layout, the media in each well is replaced with 100 uL of one of the following solutions
1) media only
2) media + 60 nM of CA200623 from Hello Bio (our fluorescent control compound)
3) media + 1X 10-5 M of test compound (to test for autofluorescence of the test compound. The two test compounds we are working with are curcumin and cis-trans curcumin, the latter of which is abbreviated as CTCUR.)
4) media + 60 nM of CA200623+ 1X 10-x of test compound (where “x” can be 4,5,6,7,8, or 9).
Once the cells are treated, they incubate for 2 hours at 5 % CO2 and 37º C.
After incubation, the cells are washed once with PBS, then 100uL of clear DMEM is added to each well. The plate is then read at 620 nM excitation and 657 nM emission, which is appropriate for detecting fluorescence from CA200623. Our microplate reader is a Synergy H1 from BioTek.
Optimizations we have already done:
When we worked with HEK cell lines, we had a lot of problems with cells coming off of the bottom of the wells. We solved this by coating the wells with poly L lysine. For CHO cells, adherence has not been a problem, so we have not used poly L lysine.
We have run tests to see whether it is better to wash the cells once with PBS or twice with PBS. There does not seem to be much of a difference between the two, and we therefore opted to wash once because doing so allows more cells to stay attached to the bottom of the well.
We have run tests to see whether it is better to set the gain of the reader at 100 or 150. Again, the two are not that different, but gain=150 produces larger values, which are more intuitive to work with, so we have opted for gain=150.
The excitation/emission for CA200623 is actually 638nM/657nM, but our plate reader will not allow that. 620nM/657nM is the best we can do.
Problems we are still working with:
First, I will provide some examples of what one of these assays looks like when it works, so that you have a point of comparison (see CBA #40 and #1001). In both of these datasets, you can see that the media control is the lowest value, the fluorescent control (60 nM CA fluor only) is the highest value, and the treatment compound control (10-5 CTCUR only) is low, close to the media control. You can also see that the treatments (10-x CTCUR + 60 nM CA fluor) go from low to high such that one can see a dose response to the CTCUR.
Problem 1:
We have often had wells fluoresce higher than they should, that is, they fluoresced substantially more than the positive control (60 nM CA fluor only). Over time, we noticed that these wells that were too bright were typically within the bottom half of the plate. In response to this problem, we recently transitioned from treating in rows of 10 to treating in columns of 8. At least when the treatments are in columns, the abnormally-bright-values-at-the-bottom-of-the-plate problem affects every set of replicates equally, so the results are not biased toward one particular treatment group.
Even though switching to treating in columns constitutes an effective workaround for this problem, it does not solve the problem itself. We are still curious about whether anyone has an actual solution to this. Attached, you can see examples demonstrating that this abnormally-bright-values-at-the-bottom-of-the-plate problem occurs regardless of whether the treatments are in rows (CBA #36) or in columns (CBA #52). The issue also occurs regardless of who is running the assay, since it also sometimes occurs when one of my co-workers runs her competitive binding assays (CBA #1003, the fluorescent control is in row A).
Problem 2:
In our most recent assay (CBA #53), we had very high fluorescence values in some of the wells that were not treated with anything at all, as well as in the media control column. (Columns 1, 2, and 12 were not treated with anything. Column 11 was treated with plain media. None of these four columns should have shown fluorescence much above 300.) We are at a loss to explain this. It seems that the cells themselves must be fluorescing. But, if that were the case, then all wells should show high fluorescence values—we should not see such a broad variation in the fluorescence values.
Has anyone one else had these problems with inexplicably high fluorescence values when running competitive binding assays? What did you do to solve these issues?
Thank you for your time,
Luke Hamilton
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Dear Hamilton,
Try to repeat your experiment, may be you made a mistake during the manipulation or maybe there is a problem with the fluorescent molecules / equipments you are actually using.
Try also to use another protocol, may be it will solve the problem.
Good luck
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In some cases you see structurally similar ligands work as agonists/antagonists for the same receptors, but it's not always the case. Do receptors allow molecules to bind because of their shape/structure or is it independent from ligand to ligand?
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I will try to explain. A receptor might or not allow the binding of a ligand, but maybe this binding depends on circumstances, like feedback regulation, inhibition or changes in structure. this change in structure permits the ligand to bind to the receptor. This working systems means when the ligand is present, the recpetor has changed shape, and is why the ligand sticks to it. Of course, it might depend on the regulation system, and not all receptors chose the same system. The energy demands is an important factor. Maybe it is not necesary. Sometimes it works constitutively.
For example, drugs. Drugs are substances which imitate molecular shapes to which the normal ligand will bind to. This means as it is similar it will confuse the receptor and take it as its normal ligand. The effects of the drug are as it is.
The enzyme or the receptor, might have several forms of regulation, the turning off of a receptor, might mean the turning on of another receptor or the turning on of the molecule. I will try to stick to receptors. Maybe you are describing allosteric regulation, but you are right when you say recpetors could be enzymes. The mechanism of action could be similar to MM, Michaelis Menten.
Maybe a receptor will change shape. But this does not mean the recpetor has to change shape for the same ligand. It might be by the regulation or the circumstance. The ligand is still the same.
For example, insulin, has to go through several activation stages, before it is activated. The hornone insulin is activated by enzymes. In this case, I am trying to say the ligand is inactivated.
The sodium potassium channel translocates, but only when the ions are present. Aquaporins need to be activated for it to allow the passage of water.
unless you mean why every movement is done by a receptor, this means, it may just diffuse through the membrane
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Higher affinity for CO induce suffocation which may be fatal.
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In agreement with Pranita Kamble Waghmare, the Oxygen axis after oxygen binding with heme is at an angle while Carbon monoxide binds to free heme with the CO axis perpendicular to the plane of the porphyrin ring via carbon-Iron bonding. So, the two oxygen atoms in oxygen exhibit steric hindrances on each other. In which case, CO doesn't experience the same.
This perpendicular orientation is favorable for Hb binding.
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Dear colleagues,
I would like to ask you some questions regarding your experience or research in the pharmacologic treatment and rehabilitation of infants with dysphagia having absent or immature gag and cough reflex.
Does anybody have experience using spicy foods (capsaicin, piperine) to stimulate cough in these group of patients?
Has anybody tried pharmacologic treatment (e.g., use of substance P)?
What about the use of e-stim (vitalstim or similar)? Or Transcutaneous vagus nerve stimulation?
Thanks in advance
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The extraction of plant extracts exhibit pharmacological properties such as antibacterial, anticancer, antidiabetic, etc and the researchers use NMR, HPLC, GC-MS, and other testing methods to identify and purify the bioactive components that are responsible for this activity.
I'm curious about the rationale behind the synthesis of nanoparticles, such as silver or gold, using plants that have proven pharmacological properties.
I look forward to your explanation. Thanks.
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What are the pharmacological risks?
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Thanks you, Dr. Miky Timothy
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I am working with triton (surfactant), a classic model to induce dyslipidemia. I realize that the animals recover quickly (3 days), without the need for pharmacological treatment.
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by measurment lipid panel in blood cholesterol,HDL,LDL,TG
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"Toxicological evaluations revealed that Cur is found to be pharmacologically safe, even up to 12 g per day, as reported by several animal studies and in phase-I clinical trials Similarly, another phase-1 human trial, with 8 g of Cur per day for three months, revealed no toxic effects."
If I want to test curcumine effects on PC12 cells, what would be the dose conversion from human trials to cell cultures?
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Depended on the pharmacokinetic of the drug. A concentration of the drug achieved peripherally.
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Current commercially available implantable pumps are osmotic pumps (www.alzet.com) and programmable micro infusion pumps (www.iprecio.com) in the preclinical/drug discovery market. What would Users like to see in next generation commercially available pumps? (must have, nice to have, short term requirements, long term dream …… in this preclinical/drug discovery market –(non-clinical applications)
For inspiration – commercially available implantable clinical pumps.
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New and Important references on Implantable Pumps out in 2020 & 2021. One new book to come out in September 2021. Re-sharing Open Access Publication <Microdosing for drug delivery application—A review> Final Version. Sensors and Actuators A: Physical Volume 330, 15 October 2021, 112820 https://lnkd.in/gnvnwr5 A review of peristaltic micropumps Sensors and Actuators A: Physical, Volume 326, 1 August 2021, 112602 https://lnkd.in/gGh4ZSR Intelligent automated drug administration and therapy: future of healthcare. Drug Deliv. and Transl. Res. (2021). https://lnkd.in/gDKMUie Chapter 7 - Implantable drug delivery devices Drug Delivery Devices and Therapeutic Systems Developments in Biomedical Engineering and Bioelectronics 2021, Pages 129-156 https://lnkd.in/gw5RsTj Implantable Technologies: Peptides and Small Molecules Drug Delivery Editor: Ved Srivastava. https://lnkd.in/gTapPCS Royal Society of Chemistry. Copyright year 2022 Print ISBN           978-1-83916-222-0 Join Dr. Christian Schnell in his upcoming webinar on <Programmable pumps for compounds delivery in oncology research: implication for refinement and reduction of animal use.> https://bit.ly/3sWgYRh
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Friends,
I want more information about role of chiral drugs on drug delivery based on pharmacology, pharmacokinetics, pharmacodynamics, recepter binding, dose, potency , toxicity, safety with lot of examples. If you have any reference materials like article, book, or other formats and you please send to me.
Thanks you.
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Hi
"enantioselective pharmacokinetics" please check the keyword in google or NCBI.
geometrical isomers have different physicochemical characteristics for example pKa, the same problem cover diastereoisomers.
Enantioselective PK may affect absorption:
D-dopa is less absorbed than L-dopa
D-methotrexate is less absorbed than L-methotrexate
cis - lycopene is absorbed to a greater extent than trans - lycopene
L - cephalexin inhibits the absorption of D - cephalexin from the gut
Enantioselective PK may affect distribution:
  • impact on affinity to blood proteins
  • impact on affinity to transporter systems
  • competition between different form
  • different redistribution with bille depending on racemate
R-methadone has a greater volume of distribution than S-methadone
R - (-) - disopyramide binds less to blood proteins than S - (+) - disopyramide
Cis-cis - mivacurium has a larger volume of distribution than cis-trans, trans-trans
S - propranolol binds more strongly (competes) with plasma proteins than R - propranolol
R - sulbenicillin binds to plasma proteins weaker than S - sulbenicillin
R - latamoxsef binds to plasma proteins more strongly than S - latamoxsef
R-carbenicillin binds to plasma proteins more strongly than S-carbenicillin
Metabolism & Enantioselective PK:
R - propafenone delays the metabolism of S - propafenone
S - nitrendipine is an inhibitor of R - nitrendipine metabolism
R - verapamil is less affected by the first-transition effect than S - verapamil
R - ketoprofen in most species is transformed into S ketoprofen (rodent, dog, monkey, horse, cat) the Asian elephant is the only species that converts S into R
A very interesting case is a chiral inversion in the liver (see examples below)
flobufen (Skalova L. et al 2001)
ibuprofen (Doki K. et al 2003)
pranoprofen (Imai T. et al. 2003)
ketoprofen (Lees P. et al. 2003)
fenoprofen (San Martin M.F. et al. 2002)
albendazole (Virkel G. et al 2002)
thalidomide (Erikson T. et al. 2001)
clopidogrel (Reist M. et al. 2000)
D-leucine (Hasegava H. et al. 2000)
thiaprofenic acid (Erb K. et al 1999)
pantoprazole (Masubuchi N. et al. 1998)
styripentol (Tang C. et al. 1994)
lifibrol (Walters R.R. et al. 1994)
Tolperizon (Yokoyama T. et al. 1992)
Stereoselective elimination:
R-methadone has a longer half-life than S-methadone
R-ibuprofen has a shorter half-life than S-ibuprofen
(-) - mefloquine has a longer half-life than (+) - mefloquine
R - (-) - ketamine inhibits the elimination of S - (+) - ketamine
(+) - terbutaline inhibits tubular reabsorption of (-) - terbutaline
R - sotalolol reduces the renal clearance of S - sotalolol
R - flurbiprofen is excreted from the bile to a greater extent than S - flurbiprofen
R - carprofen is secreted from the bile to a greater extent than S - carprofen
R - sulbenicillin has a lower renal clearance than S - sulbenicillin
R - (+) - propranolol is eliminated more slowly than S - (+) - propranolol
Z - doxepin has a stronger antidepressant effect than E - doxepin
Pharmacodynamics:
Z - doxepin has a stronger antidepressant effect than E - doxepin
S (-) bupivacaine is less toxic than racemic bupivacaine
Of course, it's only the peak of the iceberg so, please check:
.... now > 1000 results ....
examples with references are available in my free e-book (polish version only)
Best regards
Tomasz
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I have decided to examine the effect of potassium nitrate on certain disease symptom. Unfortunately, there are a few companies which produce potassium nitrate capsules and their capsules are not pure potassium nitrate and some sort of vitamins are added to them which can interfere with my results.
Potassium nitrate is readily available in form of powder. I wanted to know that is that possible that I simply put a desired amount of potassium nitrate powder in empty capsules and give them to patients to use them? I have this questions since capsules usually have excipients such as silicon dioxide, magnesium stearate, etc.
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If you are thinking to prepare capsules in very small number, lets say someting around 100. Then physicaly it is possible, but it will be tedious operation. First, you have to decide dose quantity as per available standard reference books. Select approriate size of capsule which can accommodate the dose qty. Make sure that the empty capsule and the active ingredient are of pharmacopoeal grade only, do not use AR grade material. Use electronic balance which have sensitivity to differentiate weight at least of 1mg, if you can get balance of 0.1mg sensitivity then it will be best. You will have to measure dose qty for each capsule, open the capsule, transfer weighed qty into it and close, immeditely put into air tight container. Entire process must be carried out under controlled humidity and temperature conditions. I must make one thing very clear that preparing capsules in such manner even for the purpose of reaserch require permission or license from food and drugs adminisration of the country and you will have to get permission for clinical trial/use also. However, if you are a registered allopathy medical practioner then you may prepare it for the purpose of dispensing to your patients only. In this case also you have to maintain records of purchase of drug matetial and empty capsules.
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Pharmacological evaluation
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Some mentioned Garcinia, but there is a strong paper showing no effect:
It also mentions limitations of other studies that showed garcinia having an effect. Not to mention there is research done on a patented HCA-SX, which belongs to company selling Super Citrimax. So might hint at bias, but couldn't find anything strong indicating weight loss by Garcinia.
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Hi!
Yesterday in experiment I careless get stabbed by the needle pinhead of a used microfluidic chip on bench and get bleeding. I washed the wound under running water and then treat with iodine That needle is the outlet of 1.5%008-fluorosurfactant in HFE7500 oil and polyacrylamide bead (crosslinked). The chip was discarded half a month ago. Should the reagents get evapoured? How harmful is the remaining reagents (and maybe the polyacrylamide bead as well) getting into body through blood? How should I get treated?
Thanks!
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Only in homeopathy, the strength of a drug is more potent on dilution, which goes with the dilution principle of chemistry. As dilution increases, the activity also increases. Why don't we apply the same principle to existing drugs. This may revolutionise the existing pharmacology.
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I will explain the principle, it is very simple, or give you more references, contact jananamthapas @ gmail. com
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Greetings
I am a bachelor's degree student in chemistry and I am doing my best to study for a master's degree in another country.If you have also received scholarships in other countries or know someone who has experience, please share this experience with me and others.
Please guide me in a few cases
First: For an undergraduate student in chemistry, other than his or her grade point average, grade in class and english skills, what else is important in his or her resume? Collaborating on a project, working in a lab?
Case 2: Which of the developed countries is easier for a chemistry student to get a scholarship?
Case 3: If you have any advice that helps me and others make a decision, or have any scholarship experience from another country you would like to mention, i be so grateful if you mention it.
.
Respectfully
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Greetings Dear Prof. Frank T. Edelmann
Yes, I would love to study in Germany if I can get fund and scholarship
Thanks a lot for sharing this links and information
Kind regards
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I am looking for minimum dose of Nitrate that should be consumed to produce vasodilatation. I Have looked several papers on this issue and there were ones which gave different doses of Nitrate to produce vasodilatation. However, none of them or any other paper reported the ''minimum dose'' of Nitrate to achieve vasodilation.
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This might look like a simple question but, funny enough, I can't seem to find a reasonable (or an evidence-based) answer anywhere..
Nearly every publication on antibacterial pharmacology presents MICs in weight/volume, as a comparative measure of antibiotic activity. And since we're talking about concentrations, they basically describe antibiotic potency.
Although having concentrations presented as μg/ml for antibiotics might seem more relevant to clinical setting (i.e. to translate in antibiotic dosing?), pharmacologically speaking its the wrong comparative measure for comparing antibacterial potencies between, say, a clinical drug and an experimental drug. The reason lies in basic pharmacological principles:
Drug A and B have both an MIC of 1mg/ml in the same assay using same volumes of exposure. Assuming a dose-dependent effect of activity for both drugs, you CANNOT compare them in terms of potency! Because, if Drug A has twice the molecular weight of Drug B, then 1mg/ml of Drug A uses HALF the active drug molecules to cause the same inhibition, than 1mg/ml of Drug B. So, Drug A is more potent than Drug B.
So, going back to my question. Nearly every paper presenting data on drug antibacterial activity, they present MIC values in weight/volume, rather than in molar, therefore impeding the pharmacological comparison between drugs and/or between studies. WHY??
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Hi, I would like to add some input.
I have a feeling that your guess is right.
For example in this study, the authors presented MICs in molarity as opposed to w/v, which makes sense because the authors are trying to evaluate potency of experimental drugs with known antibiotics. It would have been very misleading to display the results in w/v as opposed to molarity.
As for whether why w/v is used, I can only guess that perhaps it is the rigidity of standards that require results to be published in w/v as opposed to molarity which is a truer representation of potency. Some things are simply hard to change.
Perhaps I can also add that a lot of MIC testing is done with disk diffusion studies which come in commercial disks loaded with a preset weight (e.g. 50 µg) of antibiotics, so it is easier to make comparisons based on w/v as opposed to molarity.
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It may be in your education and experience that you deal with the structure of organic medicines. Which combination do you think is most common in organic medicine?
For example, many drugs have carboxylic acid in their structure. In your opinion, which compounds play an important role in the structure of the largest number of drugs?
Thanks
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Dear Pejman Rahmani Nejad thank you for your interesting technical question. In addition to the useful link provided by Lukas Schulig please also have a look at the following relevant article entitled
Chemical Structure-Related Drug-Like Criteria of Global Approved Drugs
The paper is freely available as public full text on ResearchGate. According to this article "the most common functional group is the hydroxyl, as its occurrence frequency in all databases is the top one. Moreover, -COOR or -COOH are the second most common functional groups."
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Suppose I had prepared a formulation(250mg) containing or encapsulating unknown amount of drug.I take 5 mg of the formulation containing x amount of drug and disperse it in 5 ml of lysing medium.Then i inject 10ul of the above dilution into the HPLC system which gives an area under curve Y.From the standard curve plotted earlier i calculate the unknown concentration.so is it the concentration in 20ul or 5 ml.then how to calculate the total amount of drug encapsulated in 250 mg of my formulation. Kindly help me.
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Dear Birendra,
I suggest you try the formula proposed by Sarkar.
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Hello,
I fit a classical dose response curve
Y=Bottom + (Top-Bottom)/(1+10^((LogEC-X)*HillSlope))
to my data (not related to inhibitors etc). The model I use is purely qualitative but it fits the data well. I have a few (trivial) questions.
1. Does the EC50 value depend on the Hill slope? Or alternatively: Can two EC50 values with different hill slopes be compared?
2. Is the conversion of the x-axis values to logarithmic scale a requirement for an adequate fit?
Kind regards
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I don't think they are trivial questions.
1. Consider the meaning of the Hill slope in your system. If it differs between two EC50 values, it may be telling you something important. I'll give you an example from enzyme inhibitor studies. For an enzyme that has no active site cooperativity, the EC50 (we would say IC50) curve of the inhibitor (% inhibition versus inhibitor concentration) should have a Hill slope of 1. If the curve has a Hill slope that is very different from 1 (e.g. 0.5 or 2), it usually means there is a problem with the measurement, such as insolubility of the inhibitor, a non-specific mechanism of inhibition, interference by the inhibitor with the readout, or the IC50 is too close to the enzyme concentration.
2. If you are using an equation for the curve that features the logarithm of the EC50, it is proper to use the logarithm of the values on the x axis. However, it is not necessary to use logarithms to do the curve fitting. You can use a non-logarithmic equation and the arithmetic values of the x-axis parameter, but plot the curve on a logarithmic axis if desired by choosing that setting in the graphing program. It's up to you. A non-logarithmic Hill equation is:
y = bottom + (top-bottom)*Xn/( EC50n + Xn), where n is the Hill coefficient.
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What is the therapeutic index (LD50/ED50 of oxycodone)? Preferably in humans but any number with a reference would be welcome. I am preparing a lecture for medical students on opioid pharmacology and I am suprised that I cannot find anything on the net. Even for other opioids it is surprisingly hard to find any data.
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Now, as an analgesic, I think that its side effects and its possible "recreational" use -as happened in Hollywood- make it not recommended because similar effects are achieved with Tramadol (especially, in a "retard" way) and with " Jurnista "(Hydromorphone, hydrochloride) -and for more refractory pains-; although all of them, in pain of neuropathic origin and chronic nature is debatable.
Nor can we forget "marijuana" and derivatives of "Cannabis" (THC -Tetrahydrocannabinol-), as "compassionate drugs" also in pain and "total suffering" of oncological origin.
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I need to examine the in vitro antiviral activity of a drug in the presence of a series of dilutions of
human serum up to 40 percent (e.g., 5 percent, 10 percent, 20 percent, 40 percent).
An EC50 value for 100 percent human serum can be extrapolated from these data and the serum-adjusted EC50 values reported. In addition, I need to determine EC50 values in the presence of physiological concentrations of α-acidic glycoprotein and human serum albumin.
What will be the difference between the data from the first paragraph vs the second?
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Hi,
Differences will be related to different affinity and binding of different drugs for albumins and α-acidic glycoprotein. If your drug has a higher affinity for α-acidic glycoprotein than albumin then differences in concentrations of α-acidic glycoprotein may be important for a free fraction of the drug in vivo. It should be always recognized for what fraction of plasma proteins your drug has high affinity. It's especially important in the case of lipophilic drugs and for drug-drug interactions related to concurrence for the same proteins.
Best regards,
Tomasz
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Greetings
Which of the following majors is more suitable for studying at international universities for the master's degree in chemistry? Please apply the following items in your final answer: 1- Average income after graduation in the United States or Europe and 2- Ease of admission to international universities 3- Number of jobs available after graduation 4- working in the field of medicine and pharmacology etc.
  • Medicinal chemistry
  • Organic chemistry
  • Pharmacology
  • Nano Chemistry
  • Analytical chemistry
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Hi
As for your Expectation, Analytical Chemistry will be the best option.
Chemistry, Biochemistry and Biotechnology all need Analytical Chemistry - tough than other subjects.
Next Organic Chemistry
Study Analytical Chemistry and contact me for better position in US
Best Regards
- Saranya Bharathi
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Hi,
We are going to carry out a pharmacogenetic research on CYP2D6 and CYP2C19 variants. We have already selected our suitable variants but I was wondering how can I select my appropriate SNPs?
Is there any database for finding out all SNPs of a variant? And generally in pharmacogenetic studies, how are SNPs selected? By their frequency or their effect or something else?
Thanks in advance for your answers!
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Is someone here work on of tiamulin?
Could you help with Method if you did HPLC?
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We used to associate G proteins to most beneficial receptor functions & β-arrestin proteins to GPCRs internalization/signaling termination … But, do you think β-arrestins could contribute to GPCRs’ desired effects? Alternatively, could G proteins contribute to the development GPCRs’ side effects?
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Hi guys,
the big problem in the field is the semantical imprecision. What do people really mean when referring to beta-arrestin-mediated signaling? What exactly is this? Is it arrestin-modulation of G protein signaling or arrestin signaling in the absence of G protein activity, ie truly G protein-indepedent signaling? For the latter there is no proof in the literature, however arrestin contribution to G protein signaling has been seen by many. If we use arrestin signaling for both scenarios, no surprise there is confusion. Inititially I liked the idea of arrestins signaling in their own right but I am afraid it is no more than a preconceived concept that does no longer hold since we have the tools to really challenge the concept. The signaling bias literature is full of papers with unsupported claims and I predict it will take years for our field to recover because some proponents of arrestin signaling are very protective of the arrestin transducer model. You cannot imagine that publishing my paper was close to impossible, I was caught in a mafia of people who tried everything to kill my paper. A nightmare for the first author, he left academic science, he was disgusted...
Anyway, when you read literature, be critical, don't believe every word of a high impact paper, look at the data and dare to come up with your own interpretation! We all have the same data in the bias field, what differs is our interpretation!
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Hope everyone is having a good day.
I want to learn computational biology. I have a PhD. in pharmacology. Lots of times I heard about the computational biology/bioinformatics but never had a guideline how to learn or to start this interesting field of research.
It would be very helpful if you can guide me through this.
Have a nice day.
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Dear Apu, Bioinformatics is a mean not an end in itself and the confusion of a mean with an end is the reason of the drmatic crisis science (not technology) is experiencing in these days (see for example https://www.pnas.org/content/113/34/9384.short).
Thus, first of all, you must aquire a 'quantitative sensibility' for biological problems that means: in the face of a biological problem how to restate the issue in order to have a simple recognition of which are the statistical units, the variables of interest , the most interesting scale where to look and if I can provide a suitable metrics preserving the original biological meaining.
Then the informatics will come by alone, tis means you must learn statistics (with a special emphasis on multidimensional descriptive methods like PCA, Cluster Analysis, MDS..), complex networks analysis, non-linear dynamics fundamentals (what an attractor is, what is a transition) and fundamentals of probability.
Attached you will find a sketchy representation of the quantitative needs for facing biological problems.
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Dear Colleagues,
We have a new project going on with the sirtuin-2 inhibitor AK-7 (3-(1-azepanylsulfonyl)-N-(3-bromphenyl) benzamide). We need to give this chemical intraperitoneally to the mice and therefor we are looking for the best way to dissolve it. We have followed the instructions of the company and dissolved AK-7 in DMSO (the best concentration that we have found was 3.5 ml DMSO + 1.5 ml saline). If we decrease DMSO volume a little bit and increase saline volume, the solution becomes a suspension with lots of particles on the edge of the tube. We also did several dilutions (from 400 mg/kg to 20 mg/kg) step by step and in some point the solution became suspension again. We found some literatures about AK-7 (20 mg/kg, ip) and almost none of the authors gave a detailed instruction. And of course I asked the authors but none has replied. So far, we know that 0,01 g AK-7 dissolves in 3.5 ml DMSO + 1,5 ml Saline and this amount of DMSO showed toxic reactions. We will now try 10% beta cyclodextrin. Any ideas, comments and information would greatly be appreciated. Thank you very much in advance.
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See the attached file
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According to the SmPC of bisoprolol this drug is usually given only once daily, which is possible because of pharmaceutical form of bisoprolol (and long half life). However, in real clinical practice bisoprolol is often prescribed two times daily. In my point of view this is not necessary and this is one soft possible inappropriate prescribing, because drugs which are taken two times daily are often forget to take (more than once daily).
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Based on a very accurate readings of the blood pressure around a 5 times a day after taking a concor tablets 5 mg at the morning, the result is that this dose was able to keep a constant blood pressure for around 9 hours, and then it is starting to raise accordingly up to the morning.
Our conclusion is either a one dose of a 10 mg should be taken,
or ( to the best effect) you should take a 5 mg at the morning and then a similar dose at the night to keep it within expectations .
No responses after taking such doses, then you should switch off to a 10 mg.
No responses too, then an emergent tests for cholesterol ,TG, diabetes, E.S.R, uric acid and CBC must be taken.
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  • What is the time taken for steady state to be established in adults for ( Mycophenolate mofetil ) ?
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Please bear in mind that there is a large interindividual variability in the bioavailability and therefore the plasma concentration of parent mycophenolate and active metabolite. The variation can b as large as 30%. You may consider checking the plasma concentration in critical cases.
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Hello everyone! I'm considering long-term/ extended puff-application of compounds onto neurons in brain slice electrophysiology. This would be better for me than bath application because I have limited compound amount, and would I need to hold my cells in whole-cell, thus I want to keep them as short of a time as possible.
I've been searching the web for papers where they use the puff application in this way, but I cannot seem to find any. I know that it should be possible based on the fact that the picospritzer can potentially take 99.9 minutes to release all of the liquid in its pipette, but I want to know if it is feasible.
Any help/ examples would be greatly appreciated!
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Hi Emily,
I did some experiments where I delivered a drug by puff-application for a few minutes:
See the ‘Local application of nAChR agonists’ section in Methods. Could ‘Local application protocol II’ be what you’re looking for (see fig 3a for example)?
There, I used pipettes with a tip of about 2um diameter (which is probably close to the 1 MOhm resistance Jan Tønnesen suggested) connected with silicon tubing to a 1 mL syringe via a manometer. Filtering the puff solution before loading the pipette was enough for me to avoid those frustrating blockages Jan mentioned.
This method worked for me because I needed to limit movement of the tissue when puffing, and the syringe allowed a very ‘soft’ onset of the puff and not too high final pressure (few tens of millibars). However, if you are interested in the precise kinetics of the postsynaptic response, the picospritzer’s crisp, immediate onset and offset is certainly preferable.
All this said, I think those Baby-Bee syringes Enrique Soto mentioned would indeed also be very suitable.
Good luck!
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I would like to pharmacologically increase presynaptic neurotransmitter release in mice CNS in vivo (through the extracellular micro-infusion of a compound). Which strategy would you recommand?
Thank you for your help,
Charlotte
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  1. I had published books as a part of my research interest related to pharmacy field (Pharmacology). Now, I am interested to submit books to review in academic journals (Book review publish). Can any one answer me how to submit book reviews and what are the free pharmacy journals without any fee that accepts the book reviews for publication.
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You should ask it to the book editor of the journal.
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Reverse pharmacology and forward pharmacology are two approaches to drug discovery. I want to know the clear and simple difference and which is better among these.
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Reverse pharmacology : target-based drug discovery (TDD) is the science of integrating documented clinical/experiential hits, into leads by transdisciplinary exploratory studies and further developing these into drug candidates by experimental and clinical research.
Classical pharmacology, also known as forward pharmacology, or phenotypic drug discovery (PDD), relies on phenotypic screening (screening in intact cells or whole organisms) of chemical libraries of synthetic small molecules, natural products or extracts to identify substances that have a desirable therapeutic effect.
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Please tell me what is aripiprazol?
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It is an atypical antipsychotic. It is primarily used in the treatment of schizophrenia and bipolar disorder. Other uses include as an add-on treatment in major depressive disorder, tic disorders and irritability associated with autism.
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Tyrosine kinase (TK) are essential components in humans and their role has been manifested in many diseases. Normally we used to synthesise the TK inhibitors. So I want to know is there any plant source of tyrosine kinase inhibitor?
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Sengupta A, Ghosh S, and Bhattacharjee S. Allium vegetables in cancer pevention: An overview. Asian Pacific Journal of Cancer Prevention 2004; 5: 237-245.
Yuk T H, Kang J H, Lee S R, Yuk S W, Lee K G, Song B Y, Kim C H, Kim D W, Kim D, Lee T K, and Lee C H. Inhibitory effect of Carthamus tinctorius L. seed extracts on bone resorption mediated by tyrosine kinase, COX-2 (cyclooxygenase) and PG (prostaglandin) E2. The American Journal of Chinese Medicine 2002; 30(1): 95-108.
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Has there been any human trials with Juniperus communis plant extract to check it's efficacy against any disease?
Any information on this aspect is welcomed.
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I want to do docking of Poly ICLC with protein. But, unfortunately there is no crystal structure for Poly ICLC or poly IC. Poly ICLC is a complex of Poly IC, poly lysine, and carboxymethylcellulose. So is there any way to find available structure of Poly IC or Poly ICLC .
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A good day Mr. Prashant, please check once with the PubChem database, you should find the structure, Poly IC/Poly ICLC.
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please suggest the solvent in which azithromycin is soluble.... the solubilising agent should be applicable to in situ gels
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soluble in ethanol and DSMO, minimally soluble in water
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These phytochemical compounds have been synthesized and are available in large quantities in commercial labs. Why are they not packaged as finished products for their pharmacological effects?
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Even though various hurdles are involved in sailing through from in vitro testing of natural products to pharma-market, I still think it is worthy to go through that simply because our health deserves tight security from poisons...
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What is Cadmium toxicity?
How it binds Cadmium in human body?
What is the nature of Cadmium?
Which are the functional group of metallothionein?
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