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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Are there any high-impact papers in top journals (Cell, Nature, Science publications) that show the possibility of mimicking mechanical stimulation tissue responses such as skin growth and muscle hypertrophy via drugs?
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Review paper publishing for pharmacological studies.
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Traditional Medical Research
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I would like to buildup a small active research group including a comprhensive subspecialities in Clinical Biochemistry, Molecular Biology, Internal medicine, statisticians to be shared in writing research articles, review, chapters and books. Who see him a suitable he can comment here with his email or whatsapp no to communicate later.
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I am a rheumatologist. Would be more than interested to be a part of any project involving Musculoskeletal disorders
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Network Pharmacology
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Step 1: Preparing the Pathway Excel Sheet
1.1. Collect relevant pathway information from public databases or literature.
1.2. Create an Excel sheet with the following columns: * Pathway ID (unique identifier for each pathway) * Pathway Name (name of the pathway) * Reactome ID (Reactome pathway ID, if available) * Gene Ontology (GO) Terms (associated GO terms for each pathway) * Genes (list of genes associated with each pathway) * Proteins (list of proteins associated with each pathway) * Interactions (list of protein-protein interactions within each pathway) 1.3. Ensure that the gene and protein names are in the format recognized by Cytoscape (e.g., Homo sapiens Gene Symbol, UniProt Accession). 1.4. Remove any duplicate rows or irrelevant data.
Step 2: Preprocessing Data for Network Construction
2.1. Convert the Excel sheet into a tab-delimited text file. 2.2. Use a tool such as Biopython or R to remove any inconsistencies in the data, e.g., missing values, incorrect formatting. 2.3. Perform gene name conversion, if necessary, using tools like GeneCyc or UniProt. 2.4. Normalize gene and protein names to their standardized forms.
Step 3: Building the Target-Pathway Network
3.1. Open Cytoscape and create a new project. 3.2. Import the preprocessed data into Cytoscape via the "File" menu > "Import" > "Network" > "From Text File." 3.3. Select the appropriate file type (e.g., Tab Delimited) and provide the path to the text file containing the pathway data. 3.4. In the import dialog box, select the columns corresponding to the pathway ID, gene/protein names, and interactions. 3.5. Choose the interaction type (e.g., protein-protein interactions) and specify any additional parameters, such as self-interactions or duplicates. 3.6. Click "Finish" to import the data and build the initial network.
Step 4: Refining the Network
4.1. Visualize the network using Cytoscape's layout algorithms, such as Force-Directed Layout or Spring-Electrical Layout. 4.2. Manually curate the network by removing any errors, artifacts, or redundant edges. 4.3. Add additional information to the network, such as gene expression data or functional enrichment analysis results. 4.4. Apply filters to focus on specific subnetworks or pathways.
Step 5: Analyzing the Network
5.1. Use Cytoscape's built-in tools to analyze the network, such as degree distribution, clustering coefficient, and shortest paths. 5.2. Utilize third-party plugins, such as CytoNCA or CytoMine, for advanced network analysis tasks, including network centrality, module detection, and visualization. 5.3. Integrate external data sources, such as gene expression profiles or drug targets, to gain further insights into the biological context of the target-pathway network.
Step 6: Visualizing and Reporting Results
6.1. Generate high-quality images of the target-pathway network using Cytoscape's visualization options, such as node coloring, edge labeling, and layout selection. 6.2. Create reports summarizing the network properties, gene/protein lists, and interaction patterns. 6.3. Share the results with colleagues or collaborators through various formats, such as PDF, PNG, or SVG files.
By following these steps, you can effectively construct and analyze a target-pathway network using Cytoscape, providing valuable insights into the complex interactions between therapeutic targets and their surrounding biological pathways.
All the best
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why do people prefer non pharmacological pre operative anxiety theraphy to its parmarchological counterparts
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Identifying a cell line that expresses VEGFR3 exclusively or with very low expression of VEGFR2 and VEGFR1 can be challenging, as many cell lines express multiple Vegf receptors. However, here are some approaches to help you identify suitable cell lines:
1. Cell surface protein expression analysis: Use flow cytometry or fluorescence microscopy to analyze the cell surface expression of VEGFR1, VEGFR2, and VEGFR3 in various cell lines. This will help you identify cell lines with high expression of VEGFR3 and low expression of VEGFR1 and VEGFR2.
2. qRT-PCR analysis: Perform quantitative reverse transcription polymerase chain reaction (qRT-PCR) to evaluate the mRNA expression levels of VEGFR1, VEGFR2, and VEGFR3 in different cell lines. This will give you an idea about the relative expression levels of these receptors in each cell line.
3. Database mining: Utilize online databases such as ArrayExpress, Gene Expression Omnibus (GEO), or Cancer Cell Line Encyclopedia (CCLE) to explore gene expression profiles of various cell lines. You can use tools like GEO2R or limma to compare the expression levels of VEGFR1, VEGFR2, and VEGFR3 across different cell lines.
4. Knockdown or knockout experiments: Consider performing knockdown or knockout experiments using CRISPR-Cas9 or shRNAs to specifically silence VEGFR1 and VEGFR2 in cell lines that express these receptors. This will allow you to evaluate the effect of VEGFR3 expression in the absence of VEGFR1 and VEGFR2.
5. Use cell lines with known VEGF-A/VEGFR interactions: Some cancer cell lines, such as HUVEC (human umbilical vein endothelial cells) and HMVEC (human microvascular endothelial cells), are known to express high levels of VEGFR3 and have been shown to interact with VEGF-A. You may also consider using cell lines that have been engineered to overexpress VEGFR3.
6. Screening assays: Develop or utilize existing screening assays that measure the binding affinity of your peptide to VEGFR1, VEGFR2, and VEGFR3. This will enable you to identify cell lines with high binding affinity for your peptide, indicating strong expression of VEGFR3 and potentially low expression of VEGFR1 and VEGFR2.
7. Combinatorial approaches: Combine the above approaches to increase the confidence in identifying cell lines that meet your criteria. For example, you could first narrow down your options by analyzing gene expression profiles from online databases, followed by validating the expression levels using qRT-PCR or flow cytometry.
8. Validation with orthogonal methods: Once you have identified potential cell lines, validate their expression profiles using orthogonal methods such as western blotting or immunofluorescence staining. This will provide further confirmation of VEGFR expression levels and help rule out any discrepancies due to technical variations.
9. Test your peptide: Finally, test the binding specificity of your peptide on the shortlisted cell lines using techniques such as flow cytometry, immunoprecipitation, or surface plasmon resonance. This will help you determine the most suitable cell line(s) for your studies.
Remember that it is crucial to carefully evaluate and validate the expression profiles of VEGFR1, VEGFR2, and VEGFR3 in the selected cell lines to ensure the accuracy and reliability of your results.
What are the limitations to pharmacological pre-operative anxiety? why do people prefer non pharmacological pre operative anxiety theraphy to its parmarchological counterparts
Pharmacological pre-operative anxiety interventions, such as benzodiazepines and opioids, have several limitations. Here are some of the reasons why non-pharmacological interventions may be preferred over pharmacological ones:
1. Potential for dependence and addiction: Benzodiazepines and opioids can be habit-forming, and patients may develop physical dependence or addiction after prolonged use. This can lead to withdrawal symptoms when the medication is stopped, which can complicate post-operative recovery.
2. Cognitive impairment: Benzodiazepines can cause cognitive impairment, including memory loss, confusion, and difficulty concentrating. These effects can persist even after surgery, which can impact a patient's ability to follow post-operative instructions and recover effectively.
3. Respiratory depression: Opioids can slow down breathing rates, leading to respiratory depression, especially when combined with other medications or in patients with pre-existing respiratory conditions. This can be life-threatening in extreme cases.
4. Cardiovascular instability: Both benzodiazepines and opioids can cause cardiovascular instability, including hypotension, bradycardia, and arrhythmias. This can be particularly problematic during surgery, where maintaining stable vital signs is critical.
5. Interaction with anesthesia: Pharmacological pre-operative anxiety interventions can interact with anesthesia, affecting the efficacy and safety of both drugs. For instance, benzodiazepines can enhance the sedative properties of anesthetics, while opioids can potentiate their analgesic effects.
6. Side effects: Both classes of medications can cause a range of side effects, such as nausea, vomiting, constipation, and dizziness. These side effects can negatively impact a patient's comfort level and post-operative recovery.
7. Cost: Pharmacological interventions can be expensive, especially when compared to non-pharmacological alternatives. The cost of medications, combined with the potential risks and limited benefits, may make non-pharmacological interventions more attractive to patients and healthcare providers.
8. Limited evidence: While there is some evidence supporting the use of pharmacological pre-operative anxiety interventions, the quality and consistency of this evidence are not always robust. Non-pharmacological interventions, on the other hand, have a stronger evidence base and are generally considered more effective in reducing pre-operative anxiety.
Non-pharmacological pre-operative anxiety interventions offer several advantages over pharmacological approaches. They include:
1. No risk of dependence or addiction: Non-pharmacological interventions do not carry the same risk of dependence or addiction as pharmacological treatments.
2. Fewer side effects: Non-pharmacological interventions typically have fewer side effects than medications, making them better tolerated by patients.
3. Improved cognitive function: Non-pharmacological interventions, such as relaxation techniques and psychological support, can actually improve cognitive function and reduce mental fogginess, unlike benzodiazepines, which can impair cognition.
4. Better long-term outcomes: By addressing the root causes of anxiety rather than just masking symptoms, non-pharmacological interventions can lead to better long-term outcomes for patients.
5. Patient empowerment: Non-pharmacological interventions often involve teaching patients skills they can use independently, empowering them to take control of their anxiety management and become less reliant on medications.
6. Reduced healthcare costs: As non-pharmacological interventions do not require prescribing medications, they can be less costly than pharmacological approaches.
7. Stronger evidence base: Non-pharmacological interventions have a robust evidence base, with numerous studies demonstrating their effectiveness in reducing pre-operative anxiety and improving post-operative outcomes.
In summary, while pharmacological pre-operative anxiety interventions have a role in certain situations, non-pharmacological interventions are generally preferred due to their lower risk profile, improved cognitive function, better long-term outcomes, patient empowerment, reduced healthcare costs, and stronger evidence base.
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Propranolol came into migraine research by pure accident or simplistic chance or retrogressive serendipity in 1967, leaving science and the migraine research community to struggle for its pharmacological mode of action in migraine. Propranolol also made a major dent or detour in theoretical considerations and therapies for migraine, driving neurologists away from reason and logic in the understanding of migraine.
Science is not free of fashion. Propranolol is the old-fashioned lady left far behind in the vogue of research, but the secret of migraine is hidden carefully in the folds of her clutch handbag (it could well also be the almost-ancient gentleman clutching his wallet, carrying the prized possession with somewhat wanton malice) that generations of scientists / migraine researchers have sought with desperation laced with nihilism. However, when migraine researchers call themselves 'scientists', a high wall (and loud wail) of beliefs and myths immediately stands up to question the honour.
Since tertiary-care / Institutional researchers and august Headache Conferences around the world are not seized with the matter over 50 years later, busy as they are with CGRP and other neuropeptides, let us join together and explore our collective wisdom and insight or even speculation.
Or shall we leave this scientific resolution to the next millennium?
I assure the fraternity of migraine researchers that no meaningful progress will be made unless this conundrum, the Rubik Cube of migraine, is resolved
I set the ball rolling with 4 of my published articles.
Come, join me.
ORCID: hrttps://orcid.org/0000-0002-6770-5916
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Propranolol as a beta-blocker drug , sometimes it can be prescribed for the prevention of migraines. Propranolol act by preventing vasodilation and stabilizing serotonin levels. If patient benefits propranolol well, therefore migraine attacks will be shorter in duration, less intense, and less frequent.
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What are the innovative methodologies and experimental models currently being investigated in the field of pharmacology and toxicology research to comprehensively evaluate the long-term consequences and potential hazards associated with the use of pharmaceuticals, chemicals, or environmental exposures?
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In the field of pharmacology and toxicology research, there are several innovative methodologies and experimental models being investigated to comprehensively evaluate the long-term consequences and potential hazards associated with the use of pharmaceuticals, chemicals, or environmental exposures. These approaches aim to enhance our understanding of the effects of these substances on human health and provide more accurate assessments of their risks. Some of these methodologies and models include:
  1. Organ-on-a-chip Technology: Organ-on-a-chip technology involves the development of microfluidic devices that mimic the structure and function of human organs. These chips incorporate living cells and can replicate the complex interactions that occur within an organ. By using organ-on-a-chip models, researchers can simulate the effects of long-term exposure to substances on specific organs, providing valuable insights into their potential toxicological effects.
  2. 3D Cell Culture Models: Traditional cell cultures involve growing cells in two dimensions, which may not fully represent the complex cell-cell interactions and tissue architecture found in the human body. 3D cell culture models, on the other hand, aim to mimic the three-dimensional structure and function of organs or tissues. These models provide a more accurate representation of human physiology and can be used to evaluate long-term effects and potential hazards of substances.
  3. High-Throughput Screening (HTS): HTS involves the rapid screening of a large number of substances for their effects on biological systems. This approach utilizes robotic systems and automated assays to test the toxicity and pharmacological properties of thousands of compounds. By employing HTS, researchers can generate a vast amount of data and identify potential hazards associated with various substances more efficiently.
  4. Computational Toxicology: Computational models and simulations are being developed to predict the potential toxicological effects of substances. These models use mathematical algorithms and computer simulations to assess the interactions between chemicals and biological systems. Computational toxicology can provide valuable insights into the long-term consequences and potential hazards associated with exposure to various substances, allowing researchers to prioritize the evaluation of specific compounds.
  5. Epidemiological Studies: Epidemiological studies involve the analysis of large populations to evaluate the long-term effects of exposures on human health. These studies aim to identify associations between exposure to certain substances and specific health outcomes. By examining real-world data, researchers can assess the long-term consequences of pharmaceuticals, chemicals, or environmental exposures on a broader scale.
  6. Omics Technologies: Omics technologies, including genomics, proteomics, and metabolomics, allow for the comprehensive analysis of biological molecules and their interactions. These techniques provide valuable information on the molecular changes that occur in response to exposure to substances, enabling a better understanding of long-term consequences and potential hazards.
  7. Alternative Testing Methods: Efforts are underway to develop alternative testing methods that reduce or replace the use of animals in toxicological research. These methods include in vitro models, computer simulations, and computational models. By utilizing these alternative approaches, researchers can reduce animal experimentation while still obtaining valuable information on the long-term effects and potential hazards of substances.
These methodologies and experimental models collectively contribute to the advancement of pharmacology and toxicology research, enabling a more comprehensive evaluation of the long-term consequences and potential hazards associated with the use of pharmaceuticals, chemicals, or environmental exposures. By integrating these innovative approaches into research practices, scientists can improve risk assessment strategies and enhance our understanding of the impacts of various substances on human health.
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In a simple experiment, I measured the pH of Tween 80 solutions and observed that the pH decreased. investigation results :
3 ppm tween80 = 8.43
6 ppm tween80 = 8.24
12 ppm tween80 = 7.51
15 ppm tween80 = 7.31
1780 ppm tween80 = 4.22
3560 ppm tween80 = 4.05
7120 ppm tween80 = 4.09
Solutions were made in distilled water. It seems that pH increased first and then increased with increasing concentration.
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Tween 80 is an ester formed from the reaction of polyethoxylated sorbitan and oleic acid. Though the reaction product is neutral, a small amount of sulfuric acid is sometimes used to catalyze esterification reactions such as the one that forms Tween 80. Is it possible that Tween 80 contains a small amount of residual sulfuric acid from the reaction that produces it? This would account for the decreasing pH as you increase the concentration of Tween 80.
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I am currently working on IHC for Per1 protein expression in the suprachiasmatic nucleus of mouse brain coronal sections 40um thickness.
The ABC kit that I have, has the expiry date of June 2022. It was used a couple of times and was always store in the fridge (at 4 Degree Celsius).
It is a good idea to use that kit and have a good result in IHC? Because these kits are expensive and I do not want to purchase a new one unless the kit is absolutely ruined.
How do I know if the kit still works?
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The expiration date on the ABC Vector Kit indicates the recommended time period during which the components of the kit are expected to remain stable and effective when stored under appropriate conditions. However, it does not necessarily mean that the kit will suddenly become unusable once the expiration date has passed.
When deciding whether to use a kit past its expiration date, several factors should be considered:
1. Storage conditions: The fact that you have been storing the kit in the refrigerator at 4 degrees Celsius is a good practice. Proper storage can help prolong the shelf life of the kit.
2. Kit integrity: Assess the physical condition of the components in the kit. Check for any signs of contamination, discoloration, or changes in texture. If the reagents appear normal and undamaged, it is a positive indication.
3. Controls: Run positive and negative controls alongside your experimental samples. Using samples with known positive and negative staining will help you assess the performance of the kit. If the controls yield the expected results, it suggests that the kit is still functional.
4. Pilot experiment: Consider performing a small pilot experiment using the expired kit. This will help you determine if the kit still produces reliable and reproducible results. If the staining appears strong and specific with low background, it indicates that the kit is likely still functional.
It is important to note that expired kits may have reduced efficiency or diminished performance compared to fresh kits. However, if the kit has been stored properly and shows no signs of degradation, there is a reasonable chance that it can still provide satisfactory results.
Ultimately, the decision to use an expired kit depends on the specific circumstances, availability of resources, and risk tolerance. If obtaining accurate and reliable results is crucial for your research, it may be advisable to consider obtaining a fresh kit to ensure optimal performance.
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When performing pharmacological assays, can I prepare dose response curve of specific assay and keep in freezer to be used over few days? Or I should do it fresh every time.
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It depends on the stability of the materials. If they are stable enough, you can freeze them. Be sure to seal the materials thoroughly to prevent ice sublimation. When you thaw them out, make sure to mix them completely, since separation of solutes can occur during freezing.
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Dear Friends and connection
I believe in the power of community. So, I post this,
I am excited to explore the possibility of collaborating with someone who works on network pharmacology. As, network pharmacology is an interdisciplinary field that combines principles of network analysis, bioinformatics, and pharmacology to investigate drug-target interactions and predict the therapeutic effects of drugs.
I have some projects related to bioinformatics and I believe that our collaboration can result in significant progress in this exciting field.
I am looking forward to hearing from you and exploring our collaboration for network pharmacology.
Regards
Shopnil Akash
WhatsApp: +8801935567417
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Network pharmacology, a systematic analytical method, can analyze the interaction network of multiple factors such as drugs, protein target, diseases, and genes.
Regards,
Shafagat
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After inducing cells overnight by doxycycline, how can cells be detached and suspended to perform pharmacological cell based assay? Do they need to be kept serum starved for at least one hour?
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The most commonly used stable cell lines for cell-based assays are HeLa, CHO, and HEK293. All three cell lines are derived from cancer cells and are easily manipulated in the laboratory. They also have a long lifespan and can be used for multiple assays. Additionally, these cell lines are very robust, meaning they can withstand environmental changes without losing their ability to grow and reproduce.
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Could you help me regarding Scopus WOS pharmacological journals with maximum month acceptance timeline which is freely or with low cost.
No matter the impact factor
Thanks in advance
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• British Journal of Pharmacology • European Journal of Pharmacology • British Journal of Clinical Pharmacology • Pharmaceutical Research • BMC Pharmacology and Toxicology • Basic & Clinical Pharmacology & Toxicology • Current Drug Metabolism • International Journal of Clinical Pharmacology and Therapeutics • Drug Metabolism Reviews • Clinical Pharmacokinetics • Journal of Pharmacology and Experimental Therapeutics • Expert Opinion on Drug Metabolism & Toxicology • Molecular Pharmaceutics • European Journal of Drug Metabolism and Pharmacokinetics • Journal of Clinical Pharmacology • Pharmacological Reviews • Pharmacology & Therapeutics • Drug Metabolism and Disposition • Drug Discovery Today • Biochemical Pharmacology • Journal of Pharmacokinetics and Pharmacodynamics • Canadian Journal of Physiology and Pharmacology • International Journal of Pharmaceutics • Molecular Pharmacology • European Journal of Pharmaceutical Sciences • Neuropharmacology • European Journal of Pharmaceutical Sciences • Journal of Pharmaceutical Sciences • Molecular Pharmaceutics • AAPS Journal • Drug and Alcohol Dependence • International Journal of Toxicology • Xenobiotica • Analytical and Bioanaly
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Looking collaboration network pharmacology
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1. Network-based drug–target interaction prediction: Using machine learning and network-based approaches to predict drug–target interactions.
2. Pathway-based drug–target interaction prediction: Using machine learning and pathway-based approaches to predict drug–target interactions.
3. Network pharmacology-based drug repurposing: Developing a network pharmacology-based approach to identify novel indications for existing drugs.
4. Network pharmacology-based drug combination analysis: Developing a network pharmacology-based approach to identify synergistic drug combinations.
5. Data integration for network pharmacology: Developing methods for integrating heterogeneous data sources for network pharmacology applications.
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Chemical Informations
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Greetings Ali Safaa
To solve for molarity (M) in the equation:
ppm = M x m.wt x 1000
We can rearrange the equation as follows:
M = ppm / (m.wt x 1000)
So if you have a solution with a concentration of 50 ug/ml and you want to know the molarity, you would first need to know the molecular weight of the solute. Let's say the molecular weight is 100 g/mol.
  1. Convert ug/ml to ppm by multiplying by 1000:
50 ug/ml x 1000 = 50,000 ppm
  1. Plug in the values into the equation:
M = 50,000 ppm / (100 g/mol x 1000)
M = 0.5 M
Therefore, the molarity of the solution is 0.5 M.
It is important to note that ug/ml and ppm are not equivalent units of measurement. Ug/ml is a unit of concentration based on mass per volume, while ppm is a unit of concentration based on the number of parts per million. To convert from ug/ml to ppm, you would need to know the density of the solution and the molecular weight of the solute.
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How I can measure concentrations of TNF in tissues, eg in inflamed mouse ears?
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How can I measure TNF in the brain after inflammation?
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hi, I am a PGR student and doing some pharmacology cell based assays. Is there any resources to read from? how % of inhibition in c AMP inhibitory assay?
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There are several resources available for pharmacology cell-based assays, including scientific journals, textbooks, and online databases. Some good resources to consider include the Journal of Pharmacology and Experimental Therapeutics, British Journal of Pharmacology, and Molecular Pharmacology. You can also look for textbooks on pharmacology and cell-based assays such as "Cell-Based Assays for High-Throughput Screening: Methods and Protocols" by Wei Zheng.
As for your second question regarding the % of inhibition in cAMP inhibitory assay, the percentage of inhibition in a cAMP inhibitory assay can vary depending on the specific assay being performed, the compound being tested, and the experimental conditions. It is important to establish a baseline or control value for the assay before testing compounds, and to analyze the results using appropriate statistical methods. Generally, a higher percentage of inhibition indicates a stronger inhibitory effect on cAMP signaling, but it is important to interpret the results in the context of the specific assay and experimental design.
Best Regards
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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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Based on the information you provided, I can suggest the following possible solutions for your problems:
Problem 1:
  • Check the plate reader calibration: it is possible that the plate reader is not properly calibrated, leading to higher than expected fluorescence values. Try calibrating the reader and repeating the assay.
  • Try a different plate reader: it is possible that the plate reader is malfunctioning or not appropriate for this type of assay. Consider using a different plate reader to see if the problem persists.
  • Try a different assay format: instead of using a 96-well plate, try a different assay format such as a 384-well plate or a different type of plate reader to see if the problem persists.
Problem 2:
  • Check for contamination: it is possible that there was contamination in the media or other reagents used in the assay, leading to higher than expected fluorescence values. Check all reagents for contamination and repeat the assay with fresh reagents.
  • Check the cells for autofluorescence: it is possible that the cells themselves are autofluorescing, leading to higher than expected fluorescence values. Try using untransfected cells or cells without the adenosine receptor to confirm whether the cells are the source of the autofluorescence.
  • Check the plate reader settings: it is possible that the plate reader settings are not appropriate for detecting low levels of fluorescence. Try adjusting the plate reader settings to see if the problem persists.
I hope these suggestions are helpful. If you have any further questions or concerns, please let me know.
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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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The difference between assessing EC50 in the presence of physiological levels of human serum albumin and alpha1 acid glycoprotein vs. % human serum is that the former takes into account the effects of specific serum proteins on the activity of the drug, while the latter does not.
When examining the in vitro antiviral activity of a drug in the presence of a series of dilutions of human serum up to 40 percent, the % human serum approach only considers the overall effect of the serum on the drug activity, without distinguishing between the effects of different serum proteins. This approach can provide a general idea of how the drug behaves in the presence of serum, but it may not reflect the actual physiological conditions in which the drug will be used.
On the other hand, determining the EC50 values in the presence of physiological concentrations of α-acidic glycoprotein and human serum albumin provides more specific information about how these serum proteins may affect the activity of the drug. Both α-acidic glycoprotein and human serum albumin can bind to drugs and affect their pharmacokinetics and pharmacodynamics. Therefore, by examining the EC50 values in the presence of these specific serum proteins, it may be possible to gain a better understanding of how the drug will behave in vivo, and to optimize its dosing and administration for maximum efficacy.
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I'm looking for protocols that mimic clinically relevant the exposure to oral methylphenidate in mice. More specifically, I'm looking for the protocols that achieve the exposure we see in humans following continuous oral dosing with extended release methylphenidate formulations. I am aware of the acute studies that attempted to establish such a protocol (e.g. Bhide's group: 10.1016/j.neuropharm.2009.07.025) or the attempts in rats (e.g. Thanos group: 10.1016/j.pbb.2015.01.005), but I can't find what would be a relevant chronic oral dosing regimen with methylphenidate in mice. Do you have any ideas who might be using such a protocol? What would be important to take into account when trying to establish it if it still does not exist (e.g. the metabolic rate seems to be quite different between humans and rodents? Also can we expect the same brain exposure given stable plasma concentrations?).
Thanks!
Jan
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Establishing a chronic oral dosing regimen with methylphenidate in mice that mimics the exposure seen in humans following continuous dosing with extended-release formulations can be challenging due to the differences in metabolic rate between humans and rodents. However, some researchers have attempted to develop such protocols. Here are a few suggestions:
  1. Consider the differences in metabolic rate: As you mentioned, the metabolic rate of mice is different from humans, and this can affect the pharmacokinetics and pharmacodynamics of the drug. Therefore, it is important to take into account the metabolic rate of mice when designing the dosing regimen.
  2. Look for studies in rats: Although rats are not the same as mice, they are closer to humans in terms of metabolic rate. Therefore, it may be useful to look at studies in rats that have attempted to establish a chronic dosing regimen with methylphenidate.
  3. Start with a low dose and increase gradually: To establish a chronic dosing regimen, it is important to start with a low dose and increase it gradually over time to achieve the desired plasma concentrations. This will help to avoid toxicity and other adverse effects associated with high doses of methylphenidate.
  4. Consider the formulation of the drug: The formulation of the drug can also affect its pharmacokinetics and pharmacodynamics. Therefore, it is important to consider the formulation of the drug when designing the dosing regimen.
  5. Monitor plasma concentrations: To ensure that the dosing regimen is achieving the desired plasma concentrations, it is important to monitor plasma concentrations of methylphenidate over time.
  6. Consult with experts in the field: It may be helpful to consult with experts in the field of pharmacokinetics and pharmacodynamics to help design an appropriate dosing regimen that mimics the exposure seen in humans following continuous dosing with extended-release formulations of methylphenidate.
Overall, establishing a chronic dosing regimen with methylphenidate in mice that mimics the exposure seen in humans can be challenging, but with careful consideration of the factors mentioned above, it is possible to develop an appropriate protocol.
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I 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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A feasibility study is an important step in the early stages of translational research and can help to determine the potential success of a proposed intervention or study. However, a feasibility study should not be considered as proof of concept research.
Proof of concept research typically refers to studies that provide preliminary evidence that an intervention or approach is likely to be effective. These studies are often conducted in animal models or in vitro before moving on to clinical trials in humans. In contrast, a feasibility study is focused on testing the feasibility of conducting a larger study and collecting preliminary data on the potential effectiveness of an intervention.
In a feasibility study, the focus should be on evaluating the feasibility of the study design, recruitment strategies, and data collection methods. Some key components of a feasibility study may include:
  1. Defining the study population and eligibility criteria
  2. Developing and testing the intervention or intervention protocol
  3. Determining the feasibility of the study design and recruitment strategies
  4. Collecting preliminary data on potential outcomes
  5. Evaluating the feasibility of data collection and management
  6. Identifying potential barriers to study completion and developing strategies to address them
  7. Determining the feasibility of the intervention delivery and administration.
Overall, a feasibility study should be designed to provide preliminary data on the feasibility of a proposed intervention and to identify potential issues that may need to be addressed before moving on to a larger study. While it may provide some preliminary evidence of the potential efficacy or effectiveness of the intervention, it should not be considered as definitive proof of concept research.
A feasibility study can be considered as an early stage of research that is designed to test the feasibility of a new intervention or to determine the best way to conduct a larger study. A comparative study, such as comparing botulinum toxin type A and dry needling, can be considered as a feasibility study if the main goal is to assess the feasibility of conducting a larger study that would compare these treatments.
In terms of outcomes and measurements, a feasibility study should focus on evaluating the feasibility of the study design, recruitment strategies, and data collection methods. Some possible outcomes and measurements to consider in a feasibility study comparing botulinum toxin type A and dry needling for spasticity reduction in stroke patients could include:
  1. Recruitment rate: The number of patients recruited in a given period of time.
  2. Retention rate: The number of patients who complete the study.
  3. Acceptability of the intervention: Patients' satisfaction with the intervention, including any adverse events or discomfort.
  4. Feasibility of the outcome measures: The feasibility and accuracy of the measurement tools, such as the Ashworth Scale, to assess spasticity reduction.
  5. Compliance with treatment: Patients' adherence to the treatment regimen.
  6. Safety of the intervention: Any adverse events associated with the intervention.
  7. Effect size: Any preliminary evidence of the effectiveness of the interventions on spasticity reduction.
It is important to note that a feasibility study is not designed to provide definitive evidence of the efficacy or effectiveness of an intervention. Rather, it is designed to test the feasibility of the study design and to provide preliminary data on the potential efficacy or effectiveness of the intervention.
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Hi everyone, I am asking for some help here. I am currently recording MSN in the striatum brain slice without genetic marker to identify D1-MSN or D2-MSN. I am wondering if there is a pharmacological way I can use to identify D2-MSN while I am recording MSN. Which drug should I use and to test what (Voltage-clamp or Current-clamp measuring what changes)? Thanks!
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There are several pharmacological agents that can be used to selectively identify D2-MSNs in the striatum. One commonly used method is to use a dopamine D1 receptor antagonist and a dopamine D2 receptor agonist to differentially modulate the excitability of the two subtypes of MSNs.
Specifically, you can use the D1 receptor antagonist SCH 23390 to block the activity of D1 receptors on D1-MSNs, while leaving the D2 receptors on D2-MSNs intact. At the same time, you can use the D2 receptor agonist quinpirole to selectively activate D2 receptors on D2-MSNs, while leaving the D1 receptors on D1-MSNs unstimulated.
The changes in excitability of D2-MSNs can be measured using either voltage-clamp or current-clamp recordings, depending on the experimental setup and the research question. If you are interested in studying the effects of these pharmacological agents on the synaptic currents or potentials in D2-MSNs, voltage-clamp recordings may be more appropriate. On the other hand, if you are interested in studying the changes in the firing patterns or action potentials of D2-MSNs, current-clamp recordings may be more useful.
In either case, the key is to carefully monitor the effects of SCH 23390 and quinpirole on the activity of the MSNs, and to compare the responses of the neurons to these agents in the presence and absence of the drugs. This will allow you to identify and confirm the identity of D2-MSNs in your recordings.
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Drugs Informations
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Alendronate:
  • Chemical Structure: Alendronate is a bisphosphonate with the chemical name [4-amino-1-hydroxybutylidene]bisphosphonic acid. Its chemical formula is C4H13NO7P2 and its molecular weight is 249.1 g/mol.
  • Functional Groups: Alendronate contains two phosphonic acid groups (-PO3H2) and one hydroxyl group (-OH).
  • Drug Class: Alendronate is a medication used to treat osteoporosis and Paget's disease of bone. It is classified as a bisphosphonate drug.
Paclitaxel:
  • Chemical Structure: Paclitaxel is a natural product with the chemical name (2aR,4S,4aS,6R,9S,11S,12S,12aR,12bS)-12b-(acetyloxy)-12-(benzoyloxy)-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-4,6,11-trihydroxy-4a,8,13,13-tetramethyl-5-oxo-7,11-methano-1H-cyclodeca[3,4]benz[1,2-b]oxet-9-yl (2R,3S)-3-(tert-butoxycarbonylamino)-2-hydroxy-3-phenylpropanoate. Its chemical formula is C47H51NO14 and its molecular weight is 853.9 g/mol.
  • Functional Groups: Paclitaxel contains several functional groups including an ester group, two hydroxyl groups, and an amide group.
  • Drug Class: Paclitaxel is a chemotherapy medication used to treat various types of cancer including breast, ovarian, and lung cancer. It is classified as a taxane drug.
Thiophene:
Thiophene can be dissolved in various solvents including ethanol, ether, benzene, and toluene. The solubility of thiophene in water is very low (0.052 g/L at room temperature) and it is generally not recommended to dissolve it in water. To dissolve thiophene, it can be added to the solvent slowly with stirring and heating may also be necessary to increase solubility. It is important to handle thiophene with care as it is flammable and toxic.
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How precision, accuracy and recall value of these databases can be find to evaluate this methods in network pharmacology study for target identification?
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The accuracy, precision, and recall values of Swiss Target Prediction, TCMSP, Genecard, and Disgenet databases may vary depending on the specific use case, dataset, and evaluation criteria. These values can be determined by comparing the predicted targets or interactions with experimentally validated targets or interactions.
To give you an idea of the performance of these databases, here are some reported values from studies that have evaluated their performance:
  • Swiss Target Prediction: In a study that compared the predicted targets of Swiss Target Prediction with experimentally validated targets for 36 drugs, the accuracy ranged from 24.2% to 70.8%, the precision ranged from 9.6% to 31.8%, and the recall ranged from 2.2% to 20.8% (Mervin et al., 2015).
  • TCMSP: In a study that evaluated the performance of TCMSP in predicting targets for herbal compounds, the accuracy ranged from 59.7% to 96.4%, the precision ranged from 13.0% to 97.2%, and the recall ranged from 3.1% to 97.3% (Ru et al., 2014).
  • Genecards: In a study that evaluated the performance of Genecards in predicting disease genes, the accuracy ranged from 44.9% to 69.3%, the precision ranged from 18.2% to 54.5%, and the recall ranged from 9.9% to 40.2% (Mao et al., 2017).
  • Disgenet: In a study that evaluated the performance of Disgenet in predicting disease genes, the accuracy ranged from 39.5% to 68.5%, the precision ranged from 7.1% to 38.7%, and the recall ranged from 4.5% to 31.5% (Mao et al., 2017).
It is important to note that these values may not be generalizable to all use cases and datasets, and that the performance of these databases may also depend on the specific algorithm and parameters used for target prediction. Therefore, it is recommended to evaluate the performance of these databases for each specific use case and dataset.
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What softwares do you use for network pharmacology? Anything intuitive and relatively easy to use?
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SPSS, revware, cochrane etc.
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Please suggest some good impact factor journals (IF: 3.0 or above; hybrid or subscription-based only) for review articles related to ethnobotany, photochemistry, and pharmacology. I submitted the article to different journals like the Journal of ethnopharmacology, Phytochemistry reviews etc. but didn't get a positive response.
Waiting for your valuable suggestions.
Thanks
Preety Rohilla
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  1. Journal of Plant Biochemistry & Physiology
  2. Phytochemistry - Journal – Elsevier
  3. Research Journal of Phytochemistry
  4. Journal of Pharmacognosy and Phytochemistry
  5. Phytochemistry - ScienceDirect.com.
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In most contexts, the terms alternative medicine, complementary medicine, integrative medicine, holistic medicine, natural medicine, and unconventional medicine are almost synonymous.
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Yes. Naturopathy and phytopharmacology, for example, make great sense, especially as balancing treatments and therapies.
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Dear researchers we write and publish research articles in the Discipline of Microbiology, molecular biology and Pharmacology. If someone wants work in collaboration with us please let us know. Thank you
Whatsapp: 00923145099045
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Yes @Daniil you can do email me
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How to prevent Hydroquinone cream from oxidation during manufacturing and storage? The colour of my cream changes to brownish. However, the assay value does not decrease in stability.
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hello mr Abhishek Raj how about your long term stability ? and what kind of primary packaging did you use for HQ cream. i have this problem too, but before this case, i dont have any complain about turning brown
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In the article titled "FDOPA-(18F): a PET radiopharmaceutical recently registered for diagnostic use in countries of the European Union", two half-lives are reported for FDOPA.
"6-fluoro-(18F)-L-dopa is removed according to a bi-exponential kinetic process with biological half-lives of 12 hours (67-94 %) and 1.7 - 3.9 hours (6-33 %). Both these half-lives appear to be age-dependent. The 18F-activity is excreted through the kidneys, 50 % with a half-life of 0.7 hours and 50 % with a half-life of 12 hours.
On basis of these data, a biokinetic model for 6-fluoro-(18F)-L-dopa was developed. This model assumes that 100 % of the 18F activity is homogeneously distributed in the body and eliminated through the kidneys with biological half-lives of 1 hour (50 %) and 12 hours (50 %). This model was considered to be independent of age."
What does this mean?
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David Salehi Thank you for your recommendations. I will certainly have a look at them.
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Can you please add in the comments the outline /content of the undergraduate Pharmacology courses taught to undergrad students in your institution?
What type of simulation program do you use in your pharmacology courses/What university?
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Master of Pharmacy ( Pharmacology) at GLA university and I am working on hepatic ischemia-reperfusion injury
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Simulation programs for In Vivo experiments
Pharmacology Practical course for Undergrad students
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Ex-Pharm Series Software : https://heb-nic.in/ex-pharm/
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Why Levoamlodipine is developed, where already there is Amlodipine?
Is there any pharmacokinetics or pharmacodynamic advantages?
So far I know both acts almost same!
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Levoamlodipine is an enantiomer of amlodipine. It is also represent as S(-)Amlodipine and it is a racemic mixture of S and R enantiomers. Pharmacologically half dose of Levoamlodipine is equivalent to Amlodipine. Levoamlodipine is more pure than Amlodipine and have less side effects due to better impurity control.
Commercially it is cost saving .The only major problem of S(-) Amlodipine is its lower melting point as compare to Amlodipine which creates sticking issue during the compression process.
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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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You may submit your article in "Frontiers in Natural Products".
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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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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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Maria Vassaki, as DDSolver is an excel add-in, it can be added to any version of Excel. If you have Excel in your mac machine, you can use DDsolver.
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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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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 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 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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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: