Questions related to Pharmacology
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?
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?
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
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?
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)
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
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)
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.
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?
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.
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?
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
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
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.
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?).
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.
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?
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?
how we would treat it friendly for making it less harmful and more livophilic?
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.?
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.
-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.
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.
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.
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?
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.
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.
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).
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,
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?
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
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.
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.
"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?
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.
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.
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.
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?
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.
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.
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.
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??
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?
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.
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?
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.
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?
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
- Nano Chemistry
- Analytical chemistry
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!
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?
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.
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.
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).
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!
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,
- 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.
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.
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?
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.
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 .
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?