Science topics: MedicineImmunology
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Immunology - Science topic

Immunology is a broad branch of biomedical science that covers the study of all aspects of the immune system in all organisms. It deals with the physiological functioning of the immune system in states of both health and diseases; malfunctions of the immune system in immunological disorders (autoimmune diseases, hypersensitivities, immune deficiency, transplant rejection); the physical, chemical and physiological characteristics of the components of the immune system in vitro, in situ, and in vivo.
Questions related to Immunology
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Complications of dengue are due to immunological reactions like COVID 19 virus. Although clinical manifestations vary in different viruses, almost all complications can be prevented by early use of glucocorticoids preferably prednisolone. During last three weeks we have used prednisolone 40 mg daily within 2 to 4 days of onset of fever in NS1 four positive adult cases of dengue with high fever and three child cases NS1 negative ( 102 to 106 degree Fahrenheit ) in Dhaka and Rangpur, Bangladesh. Surprisingly, in all cases, fever subsided to base line within 6 to 8 hours with a single dose of prednisolone. Platelets counts found normal till three weeks of followup. There was no loss of appetite but blood pressure found reduced for several days.
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At this time ( Sept,2023) Dengue crisis is appearing worsen in Dhaka , Capital of Bangladesh. Patients are being treated by paracetamol only but high fever not responding, rather complications are encouragingly increasing. I believe, complications are due to cytokines or other chemical mediators released immunologicaly, attached to the target cells or tissue. I think, the half life of these chemical mediators is short and as soon as steroid starts acting against inflammation, the temperature rapidly subsided. As viremia in dengue may persist for several days steroid should be continued till the chance of inflammation. Rapid remission of temperature with a single dose of prednisolone within 6 to 8 hours is a miracle, though cause of this action is a matter of much investigation. However the information should be rapidly disseminated among the medical professionals for the benefit of the vulnerable patients.
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Hello Everyone,
I've established the WhatsApp group for Immunology and Cancer Specialists in the field of Invivo Oncology. If you're interested and actively contributing to this field, kindly provide your contact number, and I'll ensure you're added to the group. This collaborative effort will allow us to share and benefit from each other's knowledge and expertise.
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Follow this link to join my WhatsApp group: https://chat.whatsapp.com/DFWrQDlF0o35FxY5oSkmuQ
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We know that memory cell is a very important part of our body's immunology. Once it forms, it survives in our body for a long time such as years to decades. But normal cells go for apoptosis after a certain time. Why memory cell don't go for apoptosis or what is the reason behind this long lifespan?
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Some immunologists believe that, after each round of antigenic stimulation, the progeny of memory B cells are more likely to become plasma cells (which die) than new memory cells (which survive). In vivo, this could translate into an increased number of effector cells in the secondary and subsequent responses, and a control on the possible overexpansion of one particular memory B cell clone. However, it also means that the host might one day no longer have memory cells of this clone to call upon when the relevant pathogen strikes. In this “decreasing potential hypothesis,” immunological memory is ultimately limited. In addition, for reasons that are not yet understood, memory cells specific for different antigens have different life spans. These variations have implications for how frequently a booster shot must be given to ensure complete vaccination against a particular pathogen.
Memory cells are incredibly powerful tools for our immune system and can be very long-lived, with studies showing memory B cells for smallpox persisting at least 60 years after vaccination and for Spanish flu at least 90 years after the 1918 pandemic.
Memory B cells have several unique features including long lifespan, high sensitivity to low doses of antigen, quick and robust proliferation, and rapid differentiation into plasma cells that produce high-affinity antibodies during the secondary response.
In this sense, Md Mominul Islam , memory cells can be understood as ‚intelligent‘ or ‚learning‘ cells, imo.
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Dear ResearchGate community,
I'm currently engaged in research involving the prediction of immune responses using transcriptome data. As part of this, I'm exploring the utility of random forests and decision trees as predictive models.
In case of transcriptomics, what performance metrics have you found most informative when comparing the predictive accuracy of random forests and decision trees? Given the complexity of gene expression data, are there metrics that particularly resonate with understanding immune response prediction? Do you have any tips for optimizing model parameters to prevent overfitting and enhance generalization?
I'm excited to hear about your experiences working at the intersection of transcriptomics, immune responses, and machine learning.
Thank you in advance for your contributions, and I'm looking forward to engaging in enlightening discussions.
Best regards,
Emil
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Greetings! I'm delighted to share my insights and experiences with you in the realm of transcriptomics, immune responses, and machine learning. When comparing the performance of random forests and decision trees in predicting immune responses using transcriptome data, I've found the following performance metrics to be most informative:
  1. Accuracy: This metric measures the overall proportion of correctly classified samples. While it's useful for getting a broad sense of model performance, it's important to supplement it with other metrics to gain a deeper understanding of the models' behavior.
  2. Precision: This metric calculates the ratio of true positives (correctly predicted instances) to the sum of true positives and false positives (incorrectly predicted instances). Precision is particularly relevant when dealing with imbalanced datasets, where one class dominates the other. In the context of immune responses, precision can help identify models that excel at detecting rare but critical immune cells or genes.
  3. Recall: This metric assesses the proportion of true positives among all actual positive instances. In the context of immune responses, recall can help identify models that successfully capture the full range of immune cell types or genes involved in a particular response.
  4. F1 Score: This metric balances precision and recall, providing a harmonic mean of both. It's helpful when evaluating models that prioritize either precision or recall, depending on the specific application. An optimal F1 score represents a good tradeoff between precision and recall.
  5. Area Under the Receiver Operating Characteristic Curve (AUC-ROC): This metric plots True Positive Rate against False Positive Rate at various thresholds, allowing for the evaluation of model discrimination ability. A higher AUC-ROC signifies better separation between classes, with a value of 1 representing a perfect classifier. In the context of immune responses, AUC-ROC can help assess models' abilities to distinguish between healthy and diseased states or differentiate between distinct immune cell populations.
  6. Cross-Validation: To ensure that performance metrics aren't biased towards a particular subset of the data, employ cross-validation techniques like k-fold or leave-one-out validation. These methods allow for estimating model performance on unseen data, which is crucial for making predictions on new, independent samples.
When working with complex gene expression data, it's essential to consider the biological relevance of the performance metrics. For instance, in some cases, a high accuracy might not necessarily translate into biologically meaningful results. Instead, focus on identifying models that capture the underlying biology effectively, such as those that distinguish between different immune cell subtypes or predict functional pathways.
To optimize model parameters and prevent overfitting, follow these best practices:
  1. Use robust feature selection methods: Techniques like recursive feature elimination (RFE) or mutual information can help filter out irrelevant features and reduce dimensionality, thereby improving model interpretability and reducing overfitting risks.
  2. Regularization: Apply regularization techniques, such as Lasso or Ridge regression, to shrink model coefficients towards zero. This reduces the risk of overfitting by penalizing large coefficients.
  3. Set aside a validation set: Reserve a portion of your dataset for hyperparameter tuning and model selection. This allows for evaluating model performance on data that hasn't been used during training, ensuring that your chosen model generalizes well to new data.
  4. Perform hyperparameter grid searches: Explore a range of hyperparameters systematically, using techniques like grid search or random search. This enables you to identify the combination of hyperparameters that yields the best model performance.
  5. Monitor performance metrics during training: Track performance metrics like accuracy, precision, and recall throughout the training process. This helps avoid overfitting by identifying the point where model performance starts to degrade.
  6. Consider ensemble methods: Combine multiple models using techniques like bagging or boosting to improve generalization and reduce overfitting. Ensemble methods can often produce more accurate predictions than individual models.
By considering these performance metrics, biological relevance, and optimization strategies, you'll be well on your way to developing robust and reliable machine learning models for predicting immune responses using transcriptome data.
Good luck with your research endeavors!
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A patient with desminopathy (mutation Thr341Pro DES in a heterozygous state) with the progression of the disease has a decrease in taste and smell, immunosuppression, and an increase in IgA in the blood.
Oddly enough, but all this is characteristic of infections, including viral ones. For example, it is known that if the hepatitis C virus is not treated, then death will occur in 20 years.
In the identified case of late onset desminopathy, muscle weakness manifests itself at the age of 30, and death occurs 20 years after the onset of the disease.
Could the desmin mutation in myofibrillar myopathy be caused by an infection?
Perhaps the infection contributes to the progression of desminopathy?
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With the progression of the detected case of desminopathy, the appearance of viruses and gram-negative rods was established, there was an excessive bacterial growth of the fecal microbiota with a pronounced increase in transient microorganisms, an increase in endotoxin. The results are presented in the article: https://www.researchgate.net/publication/372952519_CHANGE_CHARACTERISTICS_IN_SALIVA_AND_FECES_MICROBIOTA_OF_A_DESMINOPATHY_T341P_PATIENT
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What are the available guidlines for finished product visual inspection for sterile immunological veterinary products?
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There are some differences between visual inspection guidelines for sterile immunological veterinary products compared to human products:
  • Veterinary products generally follow the principles outlined in guidance documents like the WHO Recommendations for the preparation, characterization and establishment of international and other biological reference standards.
  • However, there is no universal standardized guidance specifically for veterinary immunologicals like there is for human products (e.g. Ph. Eur, USP).
  • Individual countries/regulators may provide country-specific guidance documents or regulations for veterinary products, but there is variation globally.
  • Some key elements typically included are:
    • Inspection of container integrity, closure seals, absence of defects
    • Assessment of appearance of solution, color, clarity, visible particles
    • Evaluation under normal and UV light conditions
    • Inspection by multiple trained operators as needed
  • Acceptance criteria may be more variable for veterinary vs human products. Parameters like number of permitted particles per container are often not as strictly defined.
  • Risk-based approaches taking into account route of administration and intended species may be taken more often.
So in summary, while the general principles of visual inspection for defects and particulate matter apply to both human and veterinary sterile immunologicals, veterinary products lack standardized global guidance. Acceptance criteria may be more flexible based on a case-by-case risk assessment.
I hope this helps
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I have recently coupled some magplex beads to protein, using the biorad kit and beads following a standard protocol from my supervisor that has worked well previously.
When I went to count these (used 1ul beads in 9ul diluent) there was barely anything in the square but I saw way more beads at the edge of the haemocytometer outside of the square? Per calculations from the square there were only about a million beads per ml instead of around 8-10 million/ml (the amount it should be) going by the counts. I doubted this so I ran a test on the luminex. I did a column with beads diluted as though there was 8 million/ml, one where I assumed they were all about 3mil/ml to avoid wasting too many beads. Both columns came up just fine when I read the plate so now I'm even more confused. Does anyone have any idea how to resolve this or a standard counting protocol as I don't have access to a cell counter.
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Hi Sam Marcs, the issue you encountered with counting the magplex beads using a hemocytometer can be challenging without a dedicated cell counter. However, there are a few potential reasons for the discrepancy you observed:
  • Bead distribution: Sometimes, when using a hemocytometer, the beads may not distribute evenly within the counting square. This can lead to an underestimation of the bead count. It's important to ensure thorough mixing and consistent pipetting during the dilution process to achieve a more representative distribution.
  • Bead aggregation: Beads can sometimes aggregate or clump together, making them difficult to disperse uniformly. This can result in uneven distribution within the counting square, leading to inaccurate counts. Proper vortexing or sonication can help in dispersing the beads more effectively.
  • Light scattering: The small size of the beads may cause them to scatter light, making it challenging to distinguish individual beads accurately using a hemocytometer. In such cases, using a dedicated cell counter or an alternative counting method, such as flow cytometry, can provide more reliable results.
Also, considering that your luminex test results were consistent with the expected concentrations, it suggests that the bead preparation and dilution were likely accurate. However, it's always a good practice to optimize your counting method and validate it against alternative techniques if possible.
If access to a cell counter is not available, you can explore other methods to estimate bead concentration, such as using a spectrophotometer to measure the absorbance at specific wavelengths or employing imaging software for automated counting based on images of diluted bead samples.
Cheers!
-H-
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Activation of naive T cells generally requires antigen to be presented by dendritic cells in lymph nodes. Activation of naive B cells generally requires opsonized antigen to be displayed by follicular dendritic cells in lymph nodes.
Thus, it seems that dendritic cells and complement (innate immune system) need to recognize a pathogen before an adaptive immune response can be initiated. Is this always the case?
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Activation of naive T cells generally requires antigens to be presented by dendritic cells in lymph nodes. Unlike the cells of the innate immune system, T cells and B cells can identify specific features of pathogens. Therefore, B or T cells can be raised against pathogens not detected by the innate immune system.
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The topic can be related to immunological disorders or transplantation immunology as well.
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Here are some research topics in the field of immunology that do not involve wet lab work:
  1. Computational modeling of immune responses: Explore the development of mathematical or computational models to simulate and analyze immune system dynamics, such as immune cell interactions, signaling pathways, or immune response to pathogens.
  2. Bioinformatics analysis of immunological data: Use bioinformatics tools and techniques to analyze large-scale immunological datasets, such as gene expression data, protein-protein interaction networks, or genomic variations associated with immunological disorders.
  3. Immunogenomics: Investigate the role of genetic variation in immune-related genes and its impact on immune responses, disease susceptibility, or treatment outcomes. This can involve analyzing genomic data from public databases or conducting population-based studies.
  4. Immunoinformatics: Apply computational methods to predict and analyze immunological properties of molecules, such as antigenic epitopes, major histocompatibility complex (MHC) binding, or T-cell receptor repertoire analysis.
  5. Literature review and systematic analysis: Conduct a comprehensive review of the literature on a specific immunological topic, synthesize existing knowledge, identify research gaps, and propose future directions for investigation.
  6. Clinical data analysis: Analyze clinical data from immunological studies or patient cohorts to explore disease patterns, treatment outcomes, or factors influencing immune response. This can involve retrospective analysis of medical records, patient surveys, or clinical trial data.
  7. Immunological network analysis: Investigate the complex interactions between immune cells, cytokines, and other molecules using network analysis approaches. This can provide insights into immune system regulation and identify key players in immunological processes.
  8. Immunotherapy optimization: Use computational methods to design and optimize immunotherapeutic strategies, such as cancer vaccines, immune checkpoint inhibitors, or adoptive cell therapies. This can involve in silico screening of potential targets, predicting treatment response, or optimizing treatment combinations.
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Dear colleagues kindly help me out
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Dear Abdulla,
I have found several articles that are related to the topic you are interested in. Here they are for your reference. Enjoy your reading!
1. Emerging Immune Biomarkers for Prognosing the Outcome of COVID-19 Patients
2. Comparative Immunological Analysis of Vaccinated Versus Recovered COVID-19 Patients
3. Molecular Comparison of Recovered and Vaccinated COVID-19 Patients
4. Transcriptomic Profiling of Recovered and Vaccinated COVID-19 Patients: Insights from a Comparative Analysis
5. Comparison of Immune-Related Genes of Recovered and Vaccinated COVID-19 Patients
6. Altered Innate Immune and Inflammatory Responses in Response to Vaccine Versus Natural Infection of COVID-19
7. Serological and Molecular Evaluation of Vaccinated and Recovered SARS-CoV-2 Patients
8. A Comprehensive Comparison of Vaccinated versus Recovered COVID-19 Patients
9. Comparative Immunological Evaluation of Vaccinated and Naturally Recovered COVID-19 Patients
10. Differential Analysis of Immuno-molecular Parameters Between Vaccinated and Naturally Recovered SARS-CoV-2 Patients
Best regards, Saif
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Hey everybody,
I am looking for an easy method and also software for analyzing TCR repertoires.
is Spectratyping the easiest method? do you suggest any method which is easy to set it up in the laboratory? does that method t have an analyzing tool?
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Spectratyping is indeed a commonly used method for TCR repertoire analysis, particularly for assessing the clonality and diversity of T-cell populations. However, it is important to note that spectratyping primarily provides qualitative information about the distribution of TCR lengths and does not offer detailed sequence-level information.
Several software tools are available for TCR repertoire analysis, which can be used in conjunction with these sequencing methods. Here are a few popular ones:
  1. MiXCR: MiXCR is a widely used software tool specifically designed for TCR-seq and BCR-seq data analysis. It provides functionalities for read preprocessing, alignment, clonotype identification, and repertoire characterization. MiXCR offers a user-friendly interface and supports various input file formats.
  2. ImmunoSEQ Analyzer: ImmunoSEQ Analyzer is a web-based platform developed by Adaptive Biotechnologies. It allows for the analysis of TCR-seq and BCR-seq data, including clonotype identification, diversity assessment, and visualization of repertoire characteristics. ImmunoSEQ Analyzer offers both free and paid versions.
  3. VDJtools: VDJtools is an open-source software package for the analysis of TCR-seq and BCR-seq data. It provides a range of functionalities, including clonotype tracking, diversity estimation, repertoire comparison, and visualization. VDJtools is command-line based and offers flexibility for customized analysis pipelines.
Top of Form
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On 21-22-23 June 2023, the Milan Medical School of Ambrosiana University promoted an International Conference in streaming, on the subject:
The paradigm change of medicine: the epistemological and scientific basis
of Person-Centered Medicine
This conference is aimed to underscore the urgent need for overcoming Medicine's current wrong and obsolete deterministic-mechanistic-biological paradigm based on the linear causality toward the assumption in Medical Education, Clinics, and Public Health of the right indeterministic person-centered paradigm of human nature, Medicine, medical science, and health.
Call for papers on the following topics:
EPISTEMOLOGY AND MEDICINE, ALLOSTASIS PHYSIOLOGY, EPIGENETICS PSYCHO-NEURO-ENDOCRINE-IMMUNOLOGY, PSYCHOPHYSIOLOGY, NEUROBIOLOGY, MEDICAL ETHICS, PERSON-CENTERED MEDICINE, PERSON-CENTERED HEALTH, PERSON-CENTERED PSYCHIATRY, MEDICAL EDUCATION, WHO and HEALTH DEFINITION, SOCIAL PSYCHIATRY
If you have an interactionist approach to behavior and affectivity quality, PNEI, neuromodulation, and epigenetics you are welcome.
Deadline: June 10, 2023
Registration and abstract forms on
Giuseppe R.Brera
Rector of Ambrosiana University
Director of the Milan School of Medicine
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Dear professor,
sorry but I have many problems to partecipate at the Conference because of my cronic heath problems.
All my best, Catina Feresin
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It is important to measure immunological variables in athletes from time to time because of their direct impact on performance.
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cortisol, testosterona , Iga salivar, glutationa reduzida (GSH), glutationa peroxidase (GPx), catalase (CAT), proteína carbonilada (PC), substâncias reagentes ao ácido tiobarbitúrico (TBARS), atividade da enzima mieloperoxidase (MPO), metabólitos do óxido nítrico (NOx), proteína C reativa (PCR), spo², il-1b, nfkb, tnf-a
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Planning to run my assays this week, but not sure if I will be able to tomorrow. I want to prep as much as possible ahead of time, and was wondering if I could coat my plates with 10ug/mL antigen in bicarbonate buffer tonight, then use at a later time this week.
If so, should I keep the wells full of buffer until time of use, or dry them the next day then store at 4C until use?
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There are a number of factors to consider and certainly there are ways to preserve and store plates for longer periods of time. However, in your case the key question is the stability of the antigen. If you know the antigen is stable, then you should be fine to store for several days in the coating buffer before proceeding with your ELISA. I have done this with several antigens and have never observed an issue with using the plate within a week. Hope this helps.
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Hello, I just graduated from college and am conducting immunology research.
I am following a protocol that isolates extracellular vesicles which asks for an ultra-centrifugation step at 100,000g for 2hours. Unfortunately, my building only has an ultra-centrifuge that goes up to 48,000g.
I was wondering if anyone knows how I can relate the 48,000g with 100,000g through time. For example, would 4 hours at 48,000g be equivalent to 100,000g for 2 hours?
I would really appreciate any advice or resources!
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This might not be exactly what you need, but should give you a reasonably good idea what approach to take based on the equipment used in the protocol you are trying to replicate and the equipment available to you:
Some of the theory to help you understand what calculations are being done in the background can be found here:
Hope this helps!
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I have two DEG sets for 2 disease conditions (from mild to severe condition) of the same viral infection. When I look at the common gene from these two sets of DEGs, I found that some genes show opposite expression among these two conditions ( Like a gene downregulated in mild but up-regulated in severe or vice versa). So what I want to know is that,
1) If this phenomenon is normal in viral infection??
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The shift between two opposite direction of change is the rule for regulatory genes that work as 'toggle.switches' in which the biphasic alternation of two conditions is the basis for a sort of digital control of biological regulation. It is not by chance that a great part of toggle-switches are retroviral origin sequences that mirror the lytic-lysogenic phases of viruses and phagi, see:
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Aside from inhibiting protease activity (not effectively working), I read some papers about doing modifications to the antibodies:
using unnatural amino Acids
using mPEG
But, are there better options, more commercially applicable?
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If you are talking about using the antibodies as the affinity matrix (such as in immunoaffinity chromatography), I would suggest that the way to avoid damage to the antibodies from proteases in a crude extract is to save the immunoaffinity chromatography for the last step in the purification, at which point the protease activity from the crude extract should be greatly reduced. Begin the purification with ion exchange, hydrophobic interaction, and/or gel filtration chromatographies. Use a protease inhibitor cocktail when making the crude extract.
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Hello I wish good health to all my friends. I had two questions. 1: Is free vitamin D in serum the same as vitamin D in VDBP in terms of immunological properties and can it be identified with a similar monoclonal antibody? 2: In making the extraction buffer for vitamin D ELISA kit, is the best way to separate vitamin D from VDBP pH shock or can other cases be used? If my friends have any other suggestions, I would be grateful if you could guide me. Thanks
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The term "genetically restricted" is not obvious for me as in "CTL target cell killing was genetically restricted". Could anyone explain this, please?
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"Genetically restricted" in the context of immunology refers to the idea that an individual's immune system is only able to recognize and respond to certain types of pathogens, or disease-causing agents. This ability is determined by the genes that an individual inherits from their parents, which encode for the proteins that make up the immune system. These proteins, called antigens, are used by the immune system to identify and target pathogens. An individual's immune system is only able to recognize and respond to a limited range of antigens, meaning that it is genetically restricted in its ability to defend against certain types of pathogens. This is why some people may be more susceptible to certain types of infections or diseases than others.
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A few years ago I moved from my job as a biologist in a research institute to a private research manager.
Right now I'm looking for ideas on how to collaborate with other researchers in academic institutions.
I have experience in lateral flow, immunology and cancer research.
Currently my main asset is my experience and I eager to do research again.
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1. Develop an Area of Expertise: Develop a specific area of expertise related to your research interests. This can be done by reading relevant books, journal articles, and other resources in your chosen field.
2. Network: Networking is important for any researcher. Reach out to colleagues, professors, and other experts in the field for advice and to stay abreast of the latest developments.
3. Attend Conferences: Attend conferences related to your research interests to stay current on the latest developments and to meet other researchers in the field.
4. Join Professional Organizations: Joining professional organizations related to your research interests can help you stay current on the latest developments, as well as provide you with access to valuable resources.
5. Develop Collaborative Relationships: Connect with other researchers for collaboration opportunities. This can help you develop new ideas, gain new perspectives, and learn from one another.
6. Utilize Online Resources: Take advantage of the wealth of information available on the Internet. Use search engines, databases, and other resources to stay up to date on the latest developments and research findings.
7. Publish Your Work: Publishing your work is a great way to make a name for yourself in the
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Hi,
I want to start a very interesting discussion, please take part if you think same.
Can we use artificial intelligence in Immunology? Like creating diagnostic kits, experiments & many more.
Anybody would like to contribute whatever he knows?
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Yes, artificial intelligence (AI) techniques can be used in immunology to analyze and interpret large amounts of data, such as genetic sequences and protein structures. AI can be used to identify patterns and correlations in this data that may not be easily visible to the human eye, and to make predictions about how the immune system will respond to different stimuli. For example, AI can be used to predict the likelihood of an individual developing a specific autoimmune disorder or to identify potential targets for immune-based therapies. AI can also be used to analyze the results of immunological experiments and to develop new computational models for studying the immune system.
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If possible provide me with pics of the dissection that show the location of both
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As far as I know all lymph nodes are almost same other than sizes !
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I have trouble shooting with flow cytometry. People told me that immune human cells needs higher concentrations of antibody than mouse cells. Does anybody have any insights on that?
Thanks a lot!
Arthur
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From our experience, the concentration data of the manufacturers are oversized. We use only 1 μl on about 1x10^6 cells in 100 μl. So far, we have always been able to achieve good FACS results, whether with antibodies for mice or humans. Decisive is of course the amount of your marker to be detected and the correct selection of fluorochrome which have a different intensity. Therefore, a prior establishment of the fluorochrome composition is always advisable. Regards
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Is there a demand for retired professors for above on remote basis? I retire next year but would like to still be involved with academic mentoring. I specifically want to assist PhD students with research proposal, literature background, methods, data analysis and discussion /conclusion formulation and editing. Mentoring will only be done in specialist expertise field namely Immunology, Ecotoxicology/physiology and Biomarker. Would like to know if this is being done remotely.
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Hi, Dr. Edmund Pool,
I suggest for you to join LinkedIn and and advertise professionally. You will be surprise of the amazing replies to your ad. In my view, there is no such thing as retirement in our professional lives. It is time for you at this stage in your professional journey to share (via volunteerism or non-profit) the new knowledge that you have created to young learners, aspiring leaders, scientists, etc. in the global community.
Best regards,
Dr. Z. D. Norman
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β-Lactam antibiotics: the most common allergens among drugs.
Why are beta-lactam antibiotics the most common drug allergens?
I was thinking that it could be due to the fact that beta-lactam antibiotics as Penicillins & Cephalosporins, are used in relatively higher amounts (e.g. 500 - 1000mg)
Also, maybe the mode of administration should play a role: other drugs used in the same weight range are given only orally (Vs. antibiotics which are often given parenterally)??
And then this could be all on the chemical identity of these drugs...
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It will depend on the concentration-exposure relationships that can differ between individuals, due to acquired or genetic host factors. The type and intensity of interaction between the drug and target may relate to both the dose and duration of treatment.
Some off-target effects are both directly immune-mediated and associated with immunological memory of varied duration (drug hypersensitivity), whereas others without immunological memory might have an immunological phenotype, such as non-IgE-mediated mast-cell activation seen with the use of certain antibiotics like fluoroquinolones.
Best.
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I had made hybridoma by fusing sp2/o cells with spleenocytes. however, while doing single cell dilution, I had left the cells in the same media for a period of 7 days (at this time, the cells were in a 96 well plate). now the cells are not attaching when i am transfering to the new culture flask (they do not attach i know, but they are all in the suspension), and i think they are not dividing too. what should i do! please help.
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Dear Jean-Jacques Pin Jacques, I have a question related to the supplement. Is it okay for using BM-Condimed H1 for human hybridoma production?
Sorry for asking through this discussion
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Hey guys,
I have a list of full mouse TCR sequences that I got from my vdj scRNA seq experiment, I am just wondering if there is a tool that might help me to predict what these TCR might recognize?
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you can sequence both the transcriptome and the TCR of single cells using the same kit from 10X genomics
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What do you think are the remaining/unanswered questions in (tumor) immunology?
I'm looking for interesting questions that remains unanswered in the field of immunology, mostly tumor immunology. Do you have any interesting ideas?
Thank you in advance.
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Yes, I do have some ideas that may be of interest to you.
As you may be knowing that T-cell therapy trials have been successful in certain blood cancers. But what about cancers that are solid tumors?
Solid tumors pose challenges for immunotherapies that aren’t factors in liquid tumors, where the cancer cells are in the bloodstream and are more accessible to immune cells.
There are a lot many factors within the tumor microenvironment that can shut down T cells, and these factors may/may not be the same for every solid tumor. There might be certain types of immune cells which might hinder this process, or cancer cells themselves might put up a fight by sending immunosuppressive signals that is likely to further dampen the anti-cancer immune responses.
What are your thoughts on this?
Another interesting idea! Still unanswered.
Can cancer be prevented by training our own immune system?
For this purpose, we would have to characterize the genome and the immune environment which is associated with precancerous growth. Find potential targets and bombard them with immune boosters or develop vaccines to prevent cancerous growth.
Best.
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I am planning on using 384 well format to acquire transfected HEK293 cells with FACS Caliber. Would like some suggestions on appropriate cell density/well as well any other parameters that should be kept in mind while using a 384 well plate. Also can Cell Quest Pro support 384 format. I am currently using 96 well plate but would like to switch to 384 in order to improve high throughput performance and decrease required cell number for an experiment.
Thanks in advance !
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Hi Tulika, I am also switching my studies to 384 well plates. I will be using suspension cells not adherent. I am wondering what was your experience with 384-W plate.
Thanks a lot in advance,
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Hello,
I am considering measuring total IgE, as well as anti-dsDNA IgE in mouse serum (most likely via ELISA) and I was wondering whether anyone has any experience in this. The animals in question are lupus-prone and non-immunized. Does anyone have recommendations regarding serum dilutions for such ELISAs? Regarding total IgE I have found recommendations in the range of 1:10 - 1:50 (for non-immunized animals). However, I couldn't find any information on anti-dsDNA IgE ELISAs. Maybe serum anti-dsDNA IgE concentrations are too low for ELISAs.
I would greatly appreciate any feedback!
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detection the low concentration (as you said) of anti-dsDNA IgE depends on the sensitivity of your ELISA kit. but you also can make a pilot test by using different dilutions to find out the best dilution concentration that you should use it.
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Hello,
We are planning to carry out flow cytometry of stimulated cultured peripheral blood mononuclear cells (PBMCs). We noticed that these cells form large clumps as they proliferate and these are somewhat hard to break apart by pipetting. What method should we use to break up these aggregates? I assume that filtering would influence the final data since the clumps would be left on the filter.
Thank you!
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I would suggest you pass your cells through a 40 um cell strainer prior to your FACS analysis. That should help with your clumping issues, but you might loose some cells.
Please note that human T cells express human leukocyte antigen (HLA)-DR-alpha (DRA) upon mitogenic or antigenic stimulation, which makes them incredibly sticky, especially when you culture bulk PBMCs without separating the different cell types prior to setting up your cultures. I hope that helps.
All the best & good luck with your experiment.
Michael
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Hi all,
I am new to immunology field, need some help to distinguish CD3, CD4, CD8 and CD25. What are differences between them for T cells? How to decide which CDs are specific for T cells, B cells, neutrophils and macrophage.
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I commonly use CD3 to gate T cells; then CD4 and CD8 to gate T helper cells and T cytotoxic cells, respectively; Then using a CD3+CD4+ gating (Th cells) you could use CD25 and CD127 in combination to distinguish between effector T cells (CD127+CD25low) and regulatory T cells (CD127low CD25high).
You can check one of my articles for that: doi: 10.1038/s41598-019-43622-8
Best
Juanjo
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I have been finding the proof that this epitope called NLVPMVATV does not induce cytokine storm for days, but in vain. Could anyone please help me? I really need a reference paper to support this or else my project will be in a great trouble.
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Hi,
Check the references below:
HCMV UL83/pp65 (NLVPMVATV)
CMV pp65 peptide NLVPMVATV (HLA-A*0201) is a single peptide for stimulation of T cells. The peptide from human cytomegalovirus (CMV) phosphoprotein (pp65) is synthesized as it is presented by the MHC class I HLA-A*0201 allele and can be used for targeted in vitro generation and expansion of antigen-specific CD8+ T cells.
Reference:
"Although the anti-pp65 antibodies and the pp65 antigens are detected in immune-depressed patients with active viral infection [16], the antibody response to the pp65 antigen in normal infected individuals is not always detectable by immunoblotting [17]. It has been reported that the pp65 antigen is targeted by a cell-mediated immune response and that its vaccination can induce a pp65-specific CTL response"
Reference:
Hope it helps,
Best regards
Tomasz
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I saw many papers are introducing or immunizing mice with ovalbumin (OVA), will this induce a cytokine storm? Is there any paper suggesting that OVA doesn't induce cytokine storm? I've been searching this for days, please help.
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No, there are essentially 3 major types of immune response to infection: an antiviral response which illicits interferon, a pro inflammatory response that makes il1, il6, tnfalpha etc wich is normally directed against bacterial and fungal infections ( and can lead to cytokine storm) and then the allergic response directed against allergens like ova that generates il4, il10, il13.
In mouse models, balb/c mice are typically used to study allergic responses as thy are inherently more allergic and c57bl/6 are used to study proinflammatory responses and diseases because they are inherently more prone to this type of immune reaction.
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 I am wonder if any one have a good experience in the IHC multiplex satin. i will study the co expression of biomarkers. any suggestion and recommendation please. 
thanks 
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I used too run chromogenic multiplex for her2+ER+PR, in If i did her2+ER+PR+ki67. All on the discovery platform.
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I am working on peripheral T-cell Lymphoma and looking for methods, assay how to see that isolated granulocytes are activated. I would be very grateful for suggestions.
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May be this article can help
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Hi,
Anyone here using FloJo to analyze data for instance lymphocytes population, please show how will be the outcome after analysis using this software?
In terms of statistics ?
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It's better if you provide more details about your questions. based on my experience, the flowjo software can show distinct populations based on their marker expression intensity. in a flowjo plot, one dot represent one cell, so you can also get the percentage of every population you have. these are basic functions that flowjo have, for more detailed, you can search on the official FLOWJO website or there are some useful youtube video that show how to analyse flow data by flowjo.
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I want to download transcriptomes from different types of immune cells T, B, Effector T cells, plasmatic cells, monocytes, macrophages, etc. It can be from microarray, RNAseq or scRNAseq from human tissues
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How can I develop a maternal/infant immunology research group at my college? How to mobilize students? how to encourage them? how to start?
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1. Equip and Encourage
As leaders, we should make time to debrief college students about their experiences. Talk to them through their missions experience, and while doing so, inspire them to follow what they have discovered back on campus. Provide avenues for scholar missionaries to use what they have realized in their mission experience on campus and thru your ministry. Intentionally suppose outside the field about how to connect their special journey to special ministry opportunities.
Lauren and Ryan began dating before Lauren left for a semester of missions journey in South Asia. While she used to be serving in India, Ryan looked around to see the multitudes of Indian students on campus. He started apartment ministries with these students which eventually supplied avenues for Lauren to make investments in ministry to South Asians when she lowers back home.
2. Challenge
Hold college students accountable. Help them be accurate stewards by means of difficult them to use the journey God has given them. When time and college lifestyles seem to take over, mission them to stay the course.
The testimonies stated above haven’t stopped. Haley has lately back to East Asia – this time as an English teacher. She has had the probability to construct some of those relationships that started out on her campus in Alabama, through connecting with these equal college students in East Asia! While Ryan and Lauren are preparing for the subsequent steps overseas, they have maximized their professions to be planted in a predominant US town among South Asians here. They are taking this time to study more about the subculture and put it together for a probability to serve in South Asia.
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if possible please elaborate the phenomena also
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Progenitor cells in the tumor are usually Granzyme K+ and slowly proliferate. As the cells flip towards transitory/effector-like they become Granzyme B+ and stay Granzyme B+ as they further exhaust. So in essence there are Ki-67+ (with the capacity to proliferate) cytolytic cells and non-proliferating/terminally exhausted subsets.
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To provide some context:
Once an antigen is processed endogenously or exogenously by the APC's (ex: dendritic cells), it is then presented on MHCI or MHCII as a peptide.
specific naive Tcells have a matching Tcell receptor that is complimentary to the presented peptide. considering the incredible diversity of peptide antigens that can be presented, what governs the production of Tcells having the exact match to the presented peptide?
What is the mechanism of Tcell receptor diversity considering that somatic hypermutation is designated to Bcells?
(picture adapted from: Molecular biology of the cell - Garland science 2008)
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It is stochastic, or random. The receptor repertoire based on vdj, alpha beta v delta gamma and n and p additions result in a nearly unlimited. Umber of potential receptor rearrangement. The naive t cells enter secondary lymphoid organs at the instruction of chemokines and 4andomly test against antigen presented in the context of correct mhc. In this scenario, it I'd the antigen that selects the correct tcr, resulting in clone proliferation. The t cell is the passive player.
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i am in my 6th semester and i am looking for some good colleges other than IIT's that are offering masters in immunology and molecular biology in india. can i get some recommendations on the same?
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Can I also get recommendations for universities offering masters in the same subject abroad as well. I am also looking for those options as well.
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Please let me have a simple question, "Should 7AAD be washed before Flow?". After I stained 1 million cells with antibodies and washed them, I will add 5uL of 7AAD. After incubation for 5 minutes in RT, should 7AAD be washed before the flow cytometer run? I mean, should the cells stained with 7AAD be washed 1-2 times before the flow cytometer run? Or, can I run the cell suspension that includes 7AAD as it is?
My 7AAD product does not have any protocol, and although I search on the internet, each protocol I found differs widely.
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Are you using this as a stain for dead cells?
7AAD is a fluorochrome used as a marker of apoptosis, and is typically added as a last step.
I don't think you need to remove before your run, however, I would consider doing a longer incubation.
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I want to detect a specific protein in a pool of exosomes from plasma by ELISA, but I don't sure if the exosomes before ELISA test are o not disrupt using RIPA buffer or another methods.  What is the different? The capacity to bind at well is the same in one of this way?
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Hi André Cronemberger Andrade I read your comment and I would like to know if you have any protocol for what you mention about sensitizing the elisa plate to later detect surface proteins in exosomes. Do you use elisa plates of any particular brand?
I would appreciate it if you could help me, thanks in advance.
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We are trying to build up a "Quick Step Guide for Young Scientists Playlist" to assist young researchers in their journey of scientific writing and publishing. Playlist link: https://www.youtube.com/playlist?list=PLwyWKnsS4EkgcQ1Wnkx7FIxUsLsLUp0gb
We hope it will help many of you.
Share it with your friends and colleagues. All the very best!! Channel link: https://bit.ly/Subscribe_Learn_SciTech
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Also these are good:
1- Writing Research Papers. Student's Book: From Essay to Research Paper
Dorothy E. Zemach, Daniel Broudy, Chris Valvona - 2013 - 128 pages
2- English for Writing Research Papers (English for Academic Research)
Part of: English for Academic Research (11 Books) | by Adrian Wallwork | Mar 3, 2016
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#MachineLearning Hello researchers, I was wondering that what are the most remarkable applications of machine learning algorithms in Biological sciences? My naive thoughts are: DeepMind by Google: Protein Structure predictions #Epitope predictions by DTU - Technical University of Denmark in Immunology Predicting tumor entities by DKFZ German Cancer Research Center for Central Nervous System. Please add to this list, looking forward for an interactive discussion. #structuralbiology #bioinformatics #research #immunology #cancerresearch
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Hi Sandeep Kumar Dhanda
Just visit the website of IEDB Analysis Resources. You can see the role of Machine Learning Algorithms in reverse vaccinology, mainly epitope predictions.
Kalyanaraman
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My experiment consists of a ex vivo stimulation experiment on isolated human monocytes.
Each biological replicate consists of the same isolate of human monocytes (derived from the same donor) and for each biological replicate there are three treatment conditions. The dependent variable for the experiment is secretion of a specific cytokine. In the analysis I am comparing the mean cytokine secretion of each group against every other group.
I am however unsure when comparing these means whether the data points for the three treatment conditions from each biological replicate should be considered paired or unpaired, as this will obviously influence the statistical test I use?
Thanks,
Gabriel
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As far as I understand, your data points/conditions are nested within individuals (donors) creating non-independence. In other words, the same individuals provide data for each condition. If that is true, then a paired test such as repeated measures ANOVA would be most appropriate. One way to examine this is by looking at whether the observations across conditions are correlated. For paired observations, you will typically find a positive correlation of the DV scores across conditions reflecting the non-independence of the data points.
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I'm a biomedical science graduate and hope to continue my MSc in immunology. I would like to know the career options I can have with master's in this discipline.Is it a good area of study. What are the MSc programs available related to immunology? please, recommend me.
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Immunology is a branch of biomedical science that deals with the study of immune system in health and disease. It has applications in various disciplines of medicine like oncology, virology, bacteriology, and organ transplant. With a Masters in immunology, you have various options open like Clinical Research Assistant in hospitals and clinics, technical support in clinical instrumentation like flow cytometry and ELISA-based techniques, and as a teaching faculty in universities.
Immunology is an interesting subject. If you wish and have a liking for immunology you can study further and complete your PhD in immunology and become an immunologist. This will be an added advantage as it will help you acquire a much higher position in academics, research or pharmaceutical industry.
All the Best.
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Egypt has the highest prevalence of HCV. What is the major risk factor or history behind it?
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Hello.
CIBERSORT or CIBERSORTx calculates "p-value" for each analyzed sample. This value seems to suggest the reliability of CIBERSORT analysis for each sample. If it will be p>=0.05, we may exclude the sample from the downstream analysis. However, sometimes we experience that more than half of our samples are excluded by the p-value. It will make the downstream analysis difficult.
Does anyone have a similar experience, and how do you handle this issue?
I am looking forward to your valuable advice.
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Sorry it is outside my aera of expertise
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Hello.
I would like to check cell changes by culturing T cells isolated from PBMC in amino acid-rich or deficient medium. How long should I culture in rich and deficient mediums to check cell changes?
It is also a concern whether it should be cultured in rich/deficient medium from the beginning, or whether it should be cultured in normal medium at first and then moved to culture them.
I'm sorry that my English is not good! Please give me a lot of answers! :)
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To obtain serum from fresh blood, it should be drained to a dry collecting tube. We have access to Buffy coats with CPD as the anticoagulant. How can we obtain serum from this?
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Let's change it this way, Its possible to get serum from EDTA-K3 plasma? the answer is yes.
Briefly, Centrifuge sample for remove of blood cells and keep buffy coat plasma at -20 °C. After thawing of the sample, dispense in another tube 1.0 ml of plasma add 26 μl of 1 M CaCl2 and incubate overnight in +4 °C. A clott is present at the end of incubation that must be squeezed and removed, obtaining clotting factors free serum.
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Antigens are coupled covalently to carboxylated magnetic beads, after immunologic reaction it is planned to elute antibodies and use the for next experiments. We have already tried to elute antibodies with low pH buffers like 50 mM glycine (pH 2.70) and 100 mM citrate (pH 3.0). Eluted antibodies were rapidly neutralized with 1M Tris buffer (pH 8.5), however, repeated run did not show positive reaction with eluted antibodies. Please, help find the best protocol!
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The difficulty is that if Antibodies bind nicely to your antigens it's usually that they are very affine to them and subsequently separating them is sometimes denaturing the antibodies themselves. They are some Mild elution buffer made up by Pierce you might give a try on that.
Other than that is to use maybe a higher salt content to protect antibodies but this is rarely working perfectly
Some more litterature you might want to read
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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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Hi all,
I am trying to do a cell sort and collect equal numbers of CD3+CD8+ and CD3+CD4+ t cells from naive C57BL/6 mouse spleen. Theoretically 70-80% of CD3+ cells should be CD4+ and 20-30% should be CD8+, but when sorting the other day, the yield of CD3+CD8+ was only ~3% (we need at least 1 million, so this is not nearly enough), with 85% being CD3+CD4+ and the remaining likely be dendritic and NK cells. Based on the sort data, it is unlikely there was an issue with the antibody itself, nor the concentration used (I've also used it recently with no issues). Any thoughts on why I am experiencing significant loss of these CD3+CD8+ cells in comparison to the CD3+CD4+ t cell population?
Thanks for any advice you can provide!
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Bispecific antibodies, trispecifics or other formats have been and are still explored as powerful drugs against various cancer types. However, potentially these therapeutic agents could have a much broader application range. What are the reasons, researcher focus on cancer (beyond the obvious ones like incidence rate, death toll...)? The concept of bridging two or more epitopes on different cell types could in my mind potentially be extended to quite a vast range of targets. What about engaging bacterial cells? And what about non-peptide epitopes? Curious to hear some interesting thoughts!
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Hi,
Very important question. Moreover, the question is why (.... from my current knowledge please correct if I'm wrong) from more less 100 mAbs approved by FDA only 2 are bispecific ..... I think another trend is competitive for the "multispecificity" of mAbs. Its cocktails of mAbs (cocktails therapy). See some examples below:
1) atoltivimab + maftivimab + odesivimab-ebgn
2) bamlanivimab + etesevimab
3) IgG1(M777-16-3) + IgG2(62-71-3)
4) bamlanivimab + etesevimab
I think that cocktails therapy will be a more dynamic trend than "multispecificity" (because of higher and higher availability of different monospecific monoclonals)... and many other reasons,
Best regards
Tomasz
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I was wondering if anyone has any experience using alternatives for FCS in their HL60 cell culture (or similar cells), I've read that they can sometimes be cultured serum free. However long term I was wondering if there were any alternatives.
I'm happy to do a side by side comparison myself, but any starting input would be great.
Thanks for any help
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Fcs alternatives for HL 60 neutrophil like cell line is FPS (slightly different).
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Hi all, I did an IF staining for FoxP3 and CD3. Apparently, I can't do double staining due to the antibody available both from the same host. I just wonder if FoxP3+ cells must be overlap with CD3+ t cells? I saw more Foxp3+ cells than CD3+ cells in this case and wonder if the Foxp3+ I saw was a false positive. Any idea? Thanks in advance!
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FoxP3 + should be CD4+CD25+ Tregs. of Couse,FoxP3 should overlap with CD3+ T cells. usually CD3 should be expressed on the cell surface, while FoxP3 should be expressed in the nuclear of cells. they should co-expression in one cells. if you see they are differently localized. it means it is a unspecific binding and it is not correct. I often see some published paper they are wrong! confocal will detect them more accurately!
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Hello there, i'm working on a differente approach for Plaque Reduction Assays, and i would like to ask you, professional working with this type of technique: which are the major problems found by you when working with PRNT?
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Overall, PRNT has been reliable and a mainstay for virology and vaccine development. Here are the limitations I've found personally:
1) The throughput of the assay is somewhat limited due to the necessity of plaque counting as opposed to an automated read-out of reporter gene activity. I've really only done manual counts, and it looks to be somewhat difficult to automate the process. There are scanners with software for counting, but the visibility of the plaques and contrast with the uninfected monolayer can be limiting and the software may not give accurate counts. Related to this is the need to have the plaque size of the target virus being uniform so that counting is accurate.
One workaround is to examine the dilution series of each antibody and count only the two wells that bracket the endpoint, such as the 50% reduction in plaque counts. That can often be done in a hurry or to get preliminary data around the endpoint titer, but you lose a lot of information that way.
Another caveat for plaque counting either by human or machine is the necessity for cell monolayers to be uniform and complete enough in each well to get accurate plaque counts. If the cells do not form a 100% uniform monolayer by the end of the plaque growth against which the plaques can be counted, then it gets tricky, especially if the plaques/monolayers are stained with a dye rather than by immunochemical staining which may be better at showing the infected cells on a bad monolayer but is more time intensive.
2) The biosafety containment needs to be commensurate with the target virus biosafety. Often, researchers use the replicating virus of interest in the PRNT as opposed to a pseudovirus or chimeric virus which can be made to have lower biosafety requirements but will often have a reporter transgene if one is going to all the trouble of constructing these.
3) For some viruses that are more difficult to neutralize than others, it can be a little tricky to normalize the input virus between assays. This is more of a problem with the relationship between virus and neutralizing antibody concentrations, but practically speaking, inherent variability of the virus input can alter the results up or down depending on how much virus ended up in that assay. That can create more work in trying to put a large dataset together and have the assay data from each run match each other, say by the use of the results of a standard serum/antibody used in each assay.
4) One meta-problem that I've encountered is not the assay's fault, but rather the design of the assay with respect to the target cell. Viruses can enter the cells of various cell types in various tissues by different mechanisms, so the use of a non-physiological cell type for the neutralization assay can give nice, consistent results, but results that aren't useful going forward. For example, the human cytomegalovirus (HCMV) field for years employed primary human foreskin fibroblasts as the cells in the assay for which the neutralization of virus infection by antibodies was measured. This use is/was due to the very limited range of cell types that are available for permissivity of this virus for replication and plaque formation, so the cell type used is one of convenience (which itself is relative since these cells have limited passages). HCMV vaccine development experiments used these cells, and it wasn't for decades was it discovered that viral entry into endothelial cells is a more accurate assessment of neutralizing antibody responses compared to blocking entry/infection in a fibroblast. Thus, the fibroblast data wasn't particularly enlightening in the context of neutralization mediated protection. The cell type in the assay should be scrutinized when embarking on PRNT assays rather than treating them like another reagent in the assay.
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We are reaching you out because we are working on a project at the RWTH university Aachen, called Epi-Blood, which enables counting of leukocytes in frozen blood retrospectively, with high accuracy and requires only low volumes. www.Epi-Blood.de
We would like to understand the demand of the service that we will provide in the research sector. Therefore, we ask for just 2 minutes of your time to answer only 5 multiple choice questions. If you feel like contributing, please use the link below to start the survey. Thank you for your participation!
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I submitted a survey. Best of luck!
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Hello Everyone,
How to perform proliferation assay in terminally differentiated effector cells, I am not very successful getting proliferation in these cells. Please anyone suggest me to how to do it successful way or if anyone overcome similar situation share your knowledge that would be great help.
Thanks in advance for your time
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Live cell imaging with specific marker proteins
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Vertigo is a condition that can make it feel like you or your surroundings are spinning, sometimes leading to a loss of balance, according to the U.S. National Library of Medicine.
Coronavirus 2019 or COVID-19 is a novel entity which had led to many challenges among physicians due to its rapidly evolving nature. Vertigo or dizziness has recently been described as a clinical manifestation of COVID-19.
So, Are dizziness and vertigo COVID-19 Symptoms? and why?
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HI All,
I'm doing a survey as part of an Audacious program (https://www.startupdunedin.nz/audacious), which essentially is a StartUp initiative at Otago University. I'm curious to understand what level of programming do biologists these days need during their day to day research.
For all the biologists out there here are some questions to start the discussion on this topic:
1) Have you done any programming till date? If so which language did you use and for what purpose?
2) How have to overcome programming limitations? For example, did you get the work done through bioinformaticians, or sought help from your programming friend, etc?
3) Have you used online biological databases for your research? If so, which one?
4) How much of artificial intelligence have you used in your research? Do you see AI potential in your current work?
If you have anything else to add, please feel free.
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Please have look on our(Eminent Biosciences (EMBS)) collaborations.. and let me know if interested to associate with us
Our recent publications In collaborations with industries and academia in India and world wide.
Our Lab EMBS's Publication In collaboration with Universidad Tecnológica Metropolitana, Santiago, Chile. Publication Link: https://pubmed.ncbi.nlm.nih.gov/33397265/
Our Lab EMBS's Publication In collaboration with Moscow State University , Russia. Publication Link: https://pubmed.ncbi.nlm.nih.gov/32967475/
Our Lab EMBS's Publication In collaboration with Icahn Institute of Genomics and Multiscale Biology,, Mount Sinai Health System, Manhattan, NY, USA. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/29199918
Our Lab EMBS's Publication In collaboration with University of Missouri, St. Louis, MO, USA. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30457050
Our Lab EMBS's Publication In collaboration with Virginia Commonwealth University, Richmond, Virginia, USA. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27852211
Our Lab EMBS's Publication In collaboration with ICMR- NIN(National Institute of Nutrition), Hyderabad Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/23030611
Our Lab EMBS's Publication In collaboration with University of Minnesota Duluth, Duluth MN 55811 USA. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27852211
Our Lab EMBS's Publication In collaboration with University of Yaounde I, PO Box 812, Yaoundé, Cameroon. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30950335
Our Lab EMBS's Publication In collaboration with Federal University of Paraíba, João Pessoa, PB, Brazil. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30693065
Our Lab EMBS's Publication In collaboration with collaboration with University of Yaoundé I, Yaoundé, Cameroon. Publication Link: https://pubmed.ncbi.nlm.nih.gov/31210847/
Our Lab EMBS's Publication In collaboration with University of the Basque Country UPV/EHU, 48080, Leioa, Spain. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27852204
Our Lab EMBS's Publication In collaboration with King Saud University, Riyadh, Saudi Arabia. Publication Link: http://www.eurekaselect.com/135585
Our Lab EMBS's Publication In collaboration with NIPER , Hyderabad, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/29053759
Our Lab EMBS's Publication In collaboration with Alagappa University, Tamil Nadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30950335
Our Lab EMBS's Publication In collaboration with Jawaharlal Nehru Technological University, Hyderabad , India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/28472910
Our Lab EMBS's Publication In collaboration with C.S.I.R – CRISAT, Karaikudi, Tamil Nadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30237676
Our Lab EMBS's Publication In collaboration with Karpagam academy of higher education, Eachinary, Coimbatore , Tamil Nadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30237672
Our Lab EMBS's Publication In collaboration with Ballets Olaeta Kalea, 4, 48014 Bilbao, Bizkaia, Spain. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/29199918
Our Lab EMBS's Publication In collaboration with Hospital for Genetic Diseases, Osmania University, Hyderabad - 500 016, Telangana, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/28472910
Our Lab EMBS's Publication In collaboration with School of Ocean Science and Technology, Kerala University of Fisheries and Ocean Studies, Panangad-682 506, Cochin, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27964704
Our Lab EMBS's Publication In collaboration with CODEWEL Nireekshana-ACET, Hyderabad, Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/26770024
Our Lab EMBS's Publication In collaboration with Bharathiyar University, Coimbatore-641046, Tamilnadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27919211
Our Lab EMBS's Publication In collaboration with LPU University, Phagwara, Punjab, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/31030499
Our Lab EMBS's Publication In collaboration with Department of Bioinformatics, Kerala University, Kerala. Publication Link: http://www.eurekaselect.com/135585
Our Lab EMBS's Publication In collaboration with Gandhi Medical College and Osmania Medical College, Hyderabad 500 038, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27450915
Our Lab EMBS's Publication In collaboration with National College (Affiliated to Bharathidasan University), Tiruchirapalli, 620 001 Tamil Nadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27266485
Our Lab EMBS's Publication In collaboration with University of Calicut - 673635, Kerala, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/23030611
Our Lab EMBS's Publication In collaboration with NIPER, Hyderabad, India. ) Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/29053759
Our Lab EMBS's Publication In collaboration with King George's Medical University, (Erstwhile C.S.M. Medical University), Lucknow-226 003, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/25579575
Our Lab EMBS's Publication In collaboration with School of Chemical & Biotechnology, SASTRA University, Thanjavur, India Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/25579569
Our Lab EMBS's Publication In collaboration with Safi center for scientific research, Malappuram, Kerala, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30237672
Our Lab EMBS's Publication In collaboration with Dept of Genetics, Osmania University, Hyderabad Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/25248957
Our Lab EMBS's Publication In collaboration with Institute of Genetics and Hospital for Genetic Diseases, Osmania University, Hyderabad Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/26229292
Sincerely,
Dr. Anuraj Nayarisseri
Principal Scientist & Director,
Eminent Biosciences.
Mob :+91 97522 95342
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How could immune changes due to allergen immunotherapy favor or be deleterious to patients with allergic diseases?
Would there be a difference during the build-up phase versus the maintenance phase of AIT?
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Dear Dr Larenas,
I invite you to read these articles to understand the relationship between SARS-CoV-2 and allergen immunotherapy:
Best regards,
Pr Hambaba
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*Sudanese Society of Clinical Immunology and Allergy (SSCI&A)*
💢 *Announcement* :
In collaboration with the Sudanese Junior Doctors Association SJDA, we are delighted to invite you to a highly scientific talk on COVID-19.
🌹We proudly announce the contribution of our renowned members:
🎤 *Dr Gehad Elghazali* (Consultant Clinical Immunologist, UAE),
🎤 *Dr Shuayb Alkhalifa* (Consultant Clinical Immunologist, UK),
🎤 *Dr Amal Hassan* (Consultant Paediatric Immunologist, Qatar),
🎤 *Dr Nahla Erwa* (Consultant Clinical Immunologist, Sudan)
SSCI&A Secretary General
🎤 *Dr Hadeil Morsi* (Immunology ST5, UK).
*We are expecting a great discussion on the use of convalescent plasma in the treatment of COVID 19 and better understanding of the immunology of the disease in general*.
Live Event will be hosted by this page.
Time : 20:00 Tuesday 26 May 2020
🇬🇧19:00 UK
🇸🇩20:00 Sudan
🇸🇦21:00 Saudi Arabia
🇦🇪22:00 UAE
Special thanks and gratitude go to *Dr . Abdalazeem Ibrahim* for the organization and coordination of the whole event.
Sudanese Society Of Clinical Immunology And Allergy *SSCI&A*
External relations office.
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Ashraful Hoque sir, please share your opinion on this...
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If there is Immunological Memory, there is also possibility of;
Immunological Dyslexia.
Immunological Dementia.
Immunological Amnesia.
Is it not ?
And such effects might occur as a result of adaptations in epigenetic system of individuals accompanied by ageing, co-morbidities, polypharmacy etc ?
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in order to select an antibody and co stain IHC slides
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Dear Nicolas,
I invite you to see this article:
Best regards,
Pr. Hambaba
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I'd like to have your opinion on this. What is the likelihood that a SARS-coV 2 variant emerges that can use antibody dependent enhancement?For example, if vaccine-induced antibodies against the S protein RBD become non neutralizing due to new mutations, or if their concentration becomes too low. Some interesting information in this preprint https://doi.org/10.1101/2021.02.22.432407
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Polyvalent vaccine commonly used in vaccination policy from different serotypes for the same disease.The occurance of vaccine Anti_BRD clonality is a lot and more narrow but if antibody enhancement in vaccinated region ,no clonality elsewhere to compasate,you must consider these variant invaccinatin programm under scientfic base vaccine must be strain variant vaccine(Include the variant in the region.
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I am currently working with Chlamydia infected HeLa cells. The protocol given to me by my PI states this should be happening within 2-10 min. However, he and I have given it a trial run and even after 45 min, we did not observe any lysis happening (under microscope). The basic run down of the protocol is to remove media, wash cells in with DI water, discard, then add ~2 mL of water per well (6 well plate) and observe under microscope. I am currently going through a couple more trials and am thinking of repeating the washing step and adding some form of mechanical shearing.
Is our estimated time too optimistic? Is there something I'm missing?
Thank you.
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Hi Samuel,
Even though this discussion is from 2016, I was wondering if you are able to comment on your observations of the Hela cell lysis? In particular, do you still see the membrane, just non-spherical? I am currently attempting a hypotonic lysis of HEK cells, but for the wash step am only adding water to a cell pellet and discarding the supernatant with out resuspension as I want to avoid premature lysis of cells before a final resuspension step in water and sample transfer. If, I can, I will attach an observation of HEK cells after 15 mins. The membrane is not circular and you can visibly see strands coming from the cell after staining with Propidium Iodide. I plan to run some proteomics experiments on the cells, so I need to be absolutely sure that they are lysed. Any help would be greatly appreciated!
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Hi there , i am consulting about tetanospasmin effects on immunological response without vaccine , what happens before the toxin enters to the CNS ? how the toxins enter to the CNS and PNS?
What is the response of the immune system against the bacteria and the Toxin separately ? Which are the receptors implicated on the initial inflammatory response ?
are there specific recognition sites that display very high affinity for a receptor?
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