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I am a post graduate student doing Masters of Dental Surgery and I am doing a study related to Biomarkers and primary teeth.
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The major inorganic content of tooth is hydroxyapatite that mainly consists of ca, hydrogen and oxygen
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I am a post graduate student doing Masters of Dental Surgery and I am doing a study related to Biomarkers and primary teeth.
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hello Dr .Krithika Gupta
there are many ways to crush the tooth, I was not clear if are you interested in crushing the whole tooth or certain parts, because these days many scientists are interested in dentine only because it has an osteogenic induction property and has been used as a replacement for bone graft and is cost-effective in that you can use the extracted tooth of the patient free. someone suggested a sectioning machine I use sectioning machines these are good only for one thing an examination of the tooth since we can reach sections small as 7 microns this is not crushing and I don't think that is what you want, I have included a URL showing you all the papers published on crushing the tooth and they start by simple diamond bur till you reach a grinding using a mortar and pestle, also it tells you if you want the dentine or cementum and how to separate organic from inorganic these are all in many papers listed. i also know that in the USA there is a machine called smart tooth grinder made by KOMETA bioinc Cresskill ,NJ,Usa they sell their machine here is their web site https://www.kometabio.com/
I have no interest at all in that company and never contacted the.
so depending on the money you have you can buy this machine but i personally prefer the cheap methods where I can use a diamond bur and use organic and inorganic solvents to get what I want her is a picture of the American machine
here is the web site for all these papers
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Hello,
I would love to receive some recommendations from experts in regards to the topic, whether there are valid findings in research on biological markers for anxiety disorders. I am trying to gain some stable insight and be able to argue in favor of the notion, that no anxiety disorder "comes from a malfunction/sickness of the brain".
Thank you in advance!
Best
Ivo
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Do you know good marker for anoikis (cell-detachment death)? How rapidly detect cell detachment? 
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I also want to ask, if anoikis share the same markers of apoptosis ,like actiavted caspases and cleaved PARP etc?
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Hi, I am currently conducting a survival study to investigate the role of several potential biomarkers as prognostic factors in certain cancer. First, I perform Kaplan-Meier analysis for all the biomarkers and other relevant clinicopathologic data. However, only one biomarker fulfilled the proportional hazard criteria from the Kaplan-Meier curve. Other biomarkers and clinicopathologic variables do not fulfill the criteria.
I am wondering, do I still need to proceed to Cox Regression analysis? Can I include the other biomarkers and relevant clinicopathologic data in Cox Regression, even though they do not fulfill proportional hazard criteria during Kaplan-Meier analysis? Thank you.
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Your question does not make sense.run the model that you wish to run.then look at the schoenfeld residuals for lack of pattern. See the attached screenshot reference for full details. Best wishes David Booth
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I am a post graduate student doing Masters of Dental Surgery and I am doing a study related to Biomarkers and primary teeth.
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I agree go for an x ray and than you can proceed with sectioning.
Or if it's a natural you can go for cej visualization and than you can perform
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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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Hello
For a biomarker study in neurodegeneration, we are searching for publicly available data of unique molecular identifier (UMI) counts of microRNAs in plasma from non-neurodegeneration individuals.
Do you have these data by any chance or can you refer me to a database where I can find such data?
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Iiterature IS scarce about this
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Corticosterone is a component of HPA axis, also known as stress axis of body, therefore, it is one of potent marker of anxiety and depression. I suggest you to study the corticosterone along with the CRF in hypothalamus and dopamine level in brain. You can also refer my recent publish paper (1) Mishra A, Singh KP. Neurotensin agonist PD 149163 modulates the hypothalamus-pituitary-adrenal axis impairment in lipopolysaccharide-challenged mice. (2) Ankit Mishra and K.P. Singh (2022): Neurotensin agonist PD 149163 modulates the neuroinflammation induced by bacterial endotoxin lipopolysaccharide in mice model.
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Hi
My question is, is there a way to know what refractive index is equivalent to the specific concentration of each biomarker (for example, the beta-amyloid biomarker)? Because my goal is to study the refractive index of a sensor, and it is necessary to define changes in the measurement environment based on the refractive index
Thank you for your help
Thanks
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the concentration of specific materials may linked directly with refractive index by a equation for example concentration of glucose is linked with refractive index by following equation : n=0.00011889*C+1.33230545
ware c is concentration , n is refractive index of this layer
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What laboratory-grade permanent marker is your favorite and why? Which is the most resistant to: 1)Alcohol
2)Chemicals/solvents
3)Temperature
and is there one pen to best them all?
Only (ultra)fine-tip options need apply)
Tell me your experiences.
Thanks!
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Tried many and some are drying and some are expensive, some doesn't write well, finally not perfect but overall best after 8 different one I tried. This one is damn cheap too, only make sure you don't put finger or touch for 5-6 seconds after writing to avoid smear but then after that these are pretty stable and write well. you can check it out. https://amzn.to/3DNPiW3
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Are there any biomarkers with prognostic value in patients with oral squamous cell carcinoma undergoing curative surgery or chemoradiotherapy?
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The other one is:
Almangush A, Heikkinen I, Mäkitie A. et al. Prognostic biomarkers for oral tongue squamous cell carcinoma: a systematic review and meta-analysis. Br J Cancer 2017;117:856–866.
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I am doing a study on the efficacy of cotinine as a biomarker for patients who are going to receive implants / could you send me the related articles?
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I have determined a number of parameters as the response of a particular treatment. Now I would like to find out the best one which can explain the treatment effect. Which statistical method shall I use to find it out?
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The scientific suggestions are appropriate once the science behind the experiment is known. From your content, your experimental target, parameters or objective of the experiment is not clear. It seems that you have conducted some experiments wherein the treatment (not known) is given and various parameters (not known) are analyzed.
I would suggest you to first check the biomarkers (if any) you have analyzed that directly links with your treatment(s) and major changes that you got. And then see whether that stands as a biomarker or not for your experimental treatment. Out of all biomarkers, select the one which acts as a central to your objective of the experimental treatment. Until you provide the data size (various treatment groups, times etc), its very difficult to suggest the appropriate use of statistical analysis. In the absence of your research problem, its difficult to give appropriate suggestions.
Best
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Hi everyone,
Whats the best way to measure/evaluate changes in biomarkers before and after an infection. How could I test statistical difference if:
1. I keep the biomarker as continuius variable (for eg BP reading). Is paired t-test or ANOVA best suited? Or a better way to handle it statistically?
2. If I make BP as a categorical variable, for instance SBP<120 is normal and otherwise is not. With outcome also as a categorical variable that is whether covid infected or not. Then what would be the most suited statistical methods in this case?
Thank you!!
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It makes more sense to use t or ANOVA for the continuous measure. For categorical itsvariables use Risk Differences and it's variance to compute the variance. I may send you some references if you wish
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I am compiling a list of diseases that have objective biomarker (e.g. blood test result) or an indicator (e.g. inability to walk) that will enable us to track the disease progression.
Would value your help for:
a) Disease name
b) Name of biomarker or indicator
These should be biomarkers or indicators that are used in common practice.
Thanks
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Disease name: Diabetes
Biomarker: Glucose level in blood
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Especially in the field of psychiatry hesitation exist sometimes in the use of laboratory biomarkers like GGT, CDT or PEth for diagnosis of chronic abuse.
The use of questionnaires like CAGE or AUDIT is very usefull in my opinion, but its use demands full and honest cooperation of the patient / client. Questionnaires or a structured interview like MATE are needed to describe the situation and they could give a rough estimate of the degree of abuse.
Biomarkers alone are not enough, since the response to alcohol depends (partly for some markers) on individual factors like gender, age, previous use etc. But biomarkers cannot hide alcohol (ab)use, although they do not tell always the truth: sensitivity and specificity are never perfect.
What is your opinion and experience in this field? What is your choice ? Do you know any professional Guideline that might be helpfull?
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The SADQ seems to me an extentred form of the CAGE, very usefull for a rough indication of the severity of alcohol abuse, provided that the patient or client is fully cooperative.
It reminds me of the MATE structured interview, very usefull in clinical settings. But in forensic use such questionaires are unsufficient and also GGT is not to be used based on its low specificity. What is your or your institutes expereance with moder biomarkers like CDT, or PEth?
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I am currently working on developing a fast/cheap assay of a certain protein in the blood that happens to be an excellent biomarker for a variety of diseases. I plan to be able to run my assay using a single drop of blood. I am running into issues because catalase is interfering with the reaction, and I need a quick and cheap way to separate catalase from this protein of interest. Right now I am considering "salting out" the catalase with ammonium sulfate and running my assay using the resulting filtrate, however, if even a small amount of catalase leaks through, it will disrupt the assay. Can the total elimination of catalase from the sample be accomplished with the simple addition of the correct molarity of ammonium sulfate and filtration using filter paper? Or are more advanced filtration techniques needed?
I am also open to other suggestions for how to neutralize/remove catalase, I have tried numerous chemical inhibitors/denaturants (most interfere with the reaction), size exclusion chromatography (too expensive given how similar in size these proteins are), and changing the pH of the assay solution (both proteins work optimally at similar pH values).
Thank you for your time!
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Dear doctor I think that the article of my colleague Kashif Ameer is very valuable and good indicator for your running way. And have a good luck.
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I am working on looking for a biomarker for Alzahimer diseases.
When I compared the results for treatment cells to basal in AD group and treated cells from healthy group vs basal, I see a significant difference. (Basal vs treated in the same group).
But when I compared the treatment cells from AD with treated cells from healthy group, I see no differences between them ( treated cells from AD vs healthy group).
Could I say that my treatment could be a biomarker because the cells from healthy group almost reach the level of diseases patients? also, because there is significant difference when compared to basal in the same group?
Or I cannot say it because it should be a significant difference between healthy and diseases patients in treated cells if I am looking for a biomarker?
If I cannot say my treatment could be a biomarker, what is the possible way to explain my results when these is no differences?
I hope you understand my question.
Thank you so much for your help.
Arwa
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I suggest you check for GEO transcriptomic datasets of AD patients in comparison with the healthy cohort and analyse your DEGs base on a specific cut-off point. You may be able to find a reliable clinical biomarker for your subsequent experimental study
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Hello, everyone. I obtained DEGs from RNAseq analysis for normal and infected samples. Then I decreased the number of them by some downstream analysis. Now I have 120 DEGs, and I want to select between them the best combination of biomarkers that can recognize normal from infected samples (biomarker panel). So I want to use machine learning methods (At first, I want to perform feature selection and then draw ROC curve, count MCC, Spe, Sen, ....for the combined set of selected biomarkers by different algorithms such as the neural network and random forest). Because I don't have experience in machine learning, I have some questions. And please let me know if you think I am doing any steps that explain here wrong!
1- What kind of RNAseq files should I enter into machine learning software? count file, FPKM, tpm, or any other files?
2- Should that be normalized?
3- Should the entry be log2 transformed?
4- Can the training and discovery dataset be the same?
5- Is what I write below a correct study design?: The use of a dataset for obtaining DEGs then, partitioning it into k subsets of equal size. Of the k subsets, a single subset is retained as the test data set. The remaining k - 1 subset is used as training data sets. The cross-validation process is then repeated k times, with each of the k subsets used exactly once as the test data. The k results from the k iterations are averaged (or otherwise combined) to produce a single estimation. And then performing a test for the model with an external dataset to validate the model.
6- Can the validation dataset be from a different technology like microarray? Is any pre-processing needed for the datasets to be tuned before performing machine learning methods in this case?
Thank you to answer my questions
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fpkm values of your DEGs
Have a look on data from TCGA database. The same way you can prepare your data.
FPKM is not a perfect normalization method. I'd suggest you extract normalized counts from DESeq2 then prepare the dataset for ML.
Best!!
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Dear Colleagues;
I want to know how can I combine multiple predictors in one ROC curve.
I want to know whether AUC increased if I used two predictors instead of using each one separately.
I.e Alfapheto protein, carcinoembryonic antigen, and both in the diagnosis of GIT malignancy.
suppose AUC for the first biomarker is 0.7, for the second is 0.75 what is the AUC if I used both?
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Ramy Ghazy Can’t explain in detail but let’s first understand AUC or Area Under Curve. AUC is an output of several or single variables. When we classify we get sensitivity and specificity which go against each other. If you go on adding significant variables in a model the output will be better. Try recalling linear regression and R square. If you check AUC you may get it better than combined or may not depending upon the data. Try seeing the coefficient of each variable with Y to see the answer.
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As we know that the sperms function test is widely used for the management of male factor issues worldwide. However, similar parallel test is not available for the management of egg factor issue in female. Do the number of oocytes available for the purpose or the unavailability of the potential biomarkers for oocyte quality and other factors limit the development of oocyte function test? Kindly give your expert opinion.
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Thanks Prof. Omer Ucar for recognizing the quality issues of the oocytes. The scientific community need to generate the potential biomarkers that could be useful for the development of "oocyte function test". The experts in the field (you, me and others) should come forward to address this issue in order to develop oocyte function test (using non-human mammalian species) for the determination of oocyte quality prior to their use in ARTs.
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There are many markers for ferroptosis as listed in the link below:
And different literature probes different set of biomarkers. Some markers (NRF2, FTH1, ACSL4, SLC7A11, etc.) were examined in some literatures while they were not in others. I would like to detect ferroptosis efficiently because budgets are limited for primary antibodies for detection of ferroptosis using Western blot. Guys, is there any suggestion on narrowing the to-blot list? I guess it needs taking into consideration what ferroptotic sub-pathway my research subject is involved. Maybe some preliminary experiments such as RNA-seq can help me out to determine the sets of markers I will be blotting?
Your help is appreciated!
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Dear Dr. Yue Young,
The 3F3-FMA and TfR1 H68.4 antibodies are selective and effective to detect ferroptosis using Western Blot, I would suggest to take TfR1 or TfR1 H68.4 as a selective biomarker for the detection of ferroptosis using western blot.
For more detail you can go through a published paper by Feng et al., in Cell Report (Volume 30, Issue 10, 10 March 2020, Pages 3411-3423.e7)
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Early detection of a number of diseases is possible through the development of very highly sensitive senors. This will have a large impact on the reduction of treatment costs since it will allow early diagnosis of patients. However, there are currently a number of challenges which have to be met in order to realize those goals. Listing the main challenges is the first step in the right direction.
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I will specifically comment on the challenges I faced for detecting biomarkers in human breath. Mass Spectrometry, a traditional approach, currently rules the industry. Better, new methods like Optical detection need more research as it provides accurate, highly sensitive results (but is relatively new). Secondly, the absorption spectra of multiple biomarkers overlapped thus making it difficult to differentiate them. As mentioned in the question description, methodologies can help in early detection and diagnosis (eg. acetone levels in breath can help in detection of diabetes in early phase) and having a compact, approachable and user friendly sensor/device assembly for biomarker identification would go a long way.
Some of the other challenges during sensor fabrication are complex integration, requires a multi-disciplinary approach, reliability and reproducibility.
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We will conduct a big study for finding different biomarkers for depression. We will combine different modalities (fMRI, MRI, microbiome, genomics etc) in order to explore possible biomarkers (and combination of information between different modalities)
Is it possible to compute a power sample since the variables and combination of them are multiple (actually thousands) and there is not a specific biomarker that we want to test
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It seems that you didn't design a clear plan for your study. First, you should choose a number of potential biomarkers based on previous studies and findings. You can also use the same sample size that the other similar articles have used for their study. Remember that you just have a number of potential biomarkers that in your first step you need to confirm their biomarker features for your case. Therefore, at this stage, it is not possible to test the combination of them as a biomarker. After gathering your raw results, by performing Pearson and Spearman statistical analysis you are able to find the type and amount of relationship between your potential biomarkers. Now, you can design a new study that can evaluate the effect of specific combinations as an effective biomarker.
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what are the reasons that make the result of serum biomarkers not closely related (with vast differences) between studies articles around the world in healthy control groups....
although the same unit and same protocol and method principle...
why ???
let the difference in race , procedure,, analytical instrument,, a company of kit
make the logic difference
but not related value for what reason can give in your opinion?
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I see. Well, I certainly expect that if you use the usual p = 0.05 to judge if there is a difference then with 20 papers you will see a difference. That is just by chance. I no longer use the concept of statistical significance because it can be very misleading. I just report the magnitude of the differences.
One of the difficulties in making this comparison is how papers report the results of biomarkers. Quite often biomarkers, particularly in control groups, are right-skewed. Because of this the mean and standard deviation are not good descriptions of the cohort (better is median and inter-quartile range). As a "rule of thumb" if the standard deviation is more than half of the mean then the distribution is skewed and it is not really possible to compare means.
A second difficulty is the assay itself - what proportion of patients are below the limit of detection? If this is reported, it may be interesting to see if this proportion differs between papers.
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I want to know more about cell-free biomarkers so we can develop a panel for the early diagnosis of OSCC.
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There are saliva tests which detect DNA and RNA from tumour-derived exosomes, which are processed into biomarkers in saliva. Dr David Wong has been conducting research on saliva testing for several different cancers using Electric field-induced release and measurement (EFIRM). See Dr David Wong's work on the human salivary proteome project at UCLA.
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Dear all,
I want to see whether a biomarker level at baseline can be used to predict the prognosis after a treatment alone as compared to a clinical parameter?
Which statistical model will be best to investigate it?
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Dear Muhammad,
try to read this is an amazing book of Wout
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I am proposing the cohort that will search for a predictive biomarker for treatment response. I used the formula using 95% CI and 0.05% error. And I used p as the response rate from the previous study. Any suggestions?
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Sawasdee krup,
It is difficult to answer your question directly because it is not clear what statistic you are using. If p is a binary outcome, then a biomarker will be useful if it adds to what is already known to predict p. This may be demographics or pre-existing conditions etc. If, for example a logistic regression model with age, sex, and pre-existing conditions has an AUC of 0.7 then a useful biomarker would be one that increases this AUC (or other measure of discrimination). What would be useful 0.75? 0.8? This will help determine the sample size needed. Once you have a number you will need to increase it because of "drop-outs" (eg people withdrawing from the study or a failure to collect all relevant data). You can use the previous study to estimate what the rate of drop-outs will be.
All the best
John
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In the literature for immunohistochemical detection of NETs (Neutrophil Extracellular Traps) are cited many biomarkers: neutrophil elastase, myeloperoxidase etc. Which combination do you think would be most indicative? And what antibodies would you recommend?
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Hello,
we recently validated the NET parameter citrullinated histone H3 (citH3) in 63 AAA patients and 63 controls matched for cardiovascular disease.
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Hello,
I am currently doing a project related to cryo preservation and I need to ensure that the mitochondria in the cells preserved using my method stays intact (i.e., the mitochondrial integrity remains the same). Is it okay for me to use the presence and/or the quantity of the membrane surface proteins of these cells as biomarkers to determine whether the mitochondria inside these cells are intact?
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You are most welcome Dr. Michael.
Respectfully,
Sushil Sharma, P. hD, D.M.R.l.T
Academic Dean, A.I.S.M.
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the question in another way
can give me an example of any biomarker correlated with itself in level; when measuring from different sites in the body
like level of calcium in bone, serum, and CSF?
can this apply to all biomarkers like
CTLA4 in tissue by IHC
CTLA4 in flowcytometry
serumCTLA4
are the three-level from the same gene expression and have a linear correlation between them?
or anyone can reflect the level of others?
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There definitely is, we have measured venous-arterial concentration differences over the ometum (visceral fat PMID: 17471294) or the kidney (ischemia reperfusion injury PMID: 19459788 ;PMID: 32781105) in order to measure biomarkers of inflammation (both conditions) or metabolism (ischemia reperfusion injury). We found clear signatures that are fully absent in peripheral blood (dilution and catabolism). Like with all projects, it is all about the question that you are interested in.
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I have a bottle of plasma sample and I want to characterize whether it is from mouse. I'm considering to detect some plasma biomarker but I'm not sure what can be used as mouse plasma biomarker. Could you give me some advice?
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Try blotting and probing using immunodepleted goat anti mouse IgG.
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Which method do you think is more reliable and effective for the analysis of lipid biomarkers from the Precambrian? is cutting, hydropyrolysis or fluid inclusion assemblages analysis?
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First step, i) pick out rocks of suitable thermal maturity (preferably prior to peak oil window-maturity) as gauged from HAWK pyrolysis or elemental analysis screening, ii) use proven analytical methodology with full procedural blanks on a series of samples (depth series from core or outcrop), iii) use a combination of bitumen and kerogen analyses, iv) make sure the molecular distributions are self-consistent with i), ii) and iii).
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In some crude oils or source rocks reported in previous publications, it is sometimes mentioned that the organic matter exhibite an pararent contribution of bacterial reworking of terrestrial organic matterial. So, which biomarkers are typical compounds resulting from bacterial reworking of terrestrial organic material ? In addition, which parameters can qualitatively characterize the degree of bacterial reworking ?
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Dear Hong Xiao thank you for asking this interesting technical question. Please have a look at the following potentially useful article which might help you in your analysis:
Molecular indicators of diagenetic status in marine organic matter
This article has been posted as public full text on RG. Thus it can be freely downloaded as pdf file. I hope it helps.
Also please see:
Lacustrine organic geochemistry—an overview of indicators of organic matter sources and diagenesis in lake sediments
Good luck with your work!
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Hello,
I have a study which analyzes the correlation between a biomarker and outcomes. In my protocol I specified a specific time point (i.e early = < 3 days).
My question is, what if a certain study analyzed two time points for the same biomarker and same outcome, but both time points are within the specified time point (example: biomarker measured with 1 day and 3 days)?
Should I choose one time point, and exclude the other one?
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Yes, pick one of them.
Going forward, you should have defined methodology for dealing with it to minimise bias in which of the points you select. For example, you can always choose the earliest time point and then state in your methods that "where data were provided for multiple time points, data from the earliest time point was extracted."
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Now is the time to begin thinking of biomarkers of sentience and consciousness. The desiderata of a biomarker are:
"The ideal biomarker would be
– Perfectly correlated with the clinical endpoint – Have little to no variability under normal circumstance – Have very good signal to noise ratio – Change quickly and reliably in response to changes in the clinical endpoint.
As such, this ideal state is impossible to find in a complex system such as the human body. But what level of quantitative certainty is required? This again is subjective. It depends on whether it can outperform the alternatives."
Joachim Pimiskern kindly made a list of more studies that try to detect consciousness by evaluating measured data from the brain; for the links, please look for his message below. These findings may qualify as a "neural correlate" of types of conscious processes, or as biomarkers of consciousness in the sense of indicating the existence of conscious experiences.
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Frederic Andres fMRI correlates of consciousness are not good markers for several reasons, the main one being that this technology does not have good temporal resolution. However, some authors (Giulio Tononi, Anil Seth) try to refine the correlates using correlation measures. Another problem is the difference between biomarkers and correlates. A biomarker is a biochemical process that happens only when there is conscious activity because it is part of the process that generates consciousness. A correlate is an event that happens together with conscious activity, but there is no (known) causal connection between them.
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Hello,
Our lab has started working with the enteroid derived from the fetal intestinal tissue. I have 2 challenging queries as follows-
1. For mincing the intestine, so far, I have been using a scalpel but still, the mincing is not fine and smooth, rather I get fragmented tissue that results in unsuccessful cell line establishment. How can I mince the biopsied intestine very well to get a single cell line from that?
2. How can I prove that my working tissue is from the intestine i.e., is there any specific biomarker I can detect that will help to prove that the enteroid established from the biopsied tissue is actually fetal intestinal tissue?
TIA.
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Thank you, Xiuquan Luo. I will look into more detail on how it ging to work for fetal intestinal tissue biopsy.
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I am seeking to understand what are some challenges in the discovery of biomarkers that can be overcome by Mass Spectrometry?
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Hi Ashutosh,
Biomarker discovery, to begin with, is challenging because of the amount of the biomarker in presence of many fold excess amounts of other species. Remember that Prostate Specific Antigen was discovered using Elisa approach.
Mass spectrometry does not do well in detecting compounds/biomarkers in the midst of very abundant eg., serum or plasma constituents. It is a very sensitive tool, however, it requires elegant and thought out sample preparation steps up front. If you are working with tissue samples, as Malcolm Nobre emphasized, the amount of material can be limiting step. Enrichment and or targeted analysis may be the way to go with mass spectrometry approach.
Best,
Hediye.
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Looking for some markers, that would show interconnection between cognitive decline and age-related muscle loss and lower physical performance in aged rats.
I would also like to know In which part of the brain is it best to identify biomarkers and which biomarkers are best to determine when detecting interconnections between the two conditions?
I am doing research on rats that take omega 3 fatty acids and exercise, looking at the effect of these interventions on aging.
If you have some skills in this area, I would appreciate your help.
Thank you!
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Biomarkers of sarcopenia
Irisin ***; (conection between muscle sarcopenia and cognitive decline)
Brain-Derived Neurotrophic Factor(***; conection between muscle sarcopenia and cognitive decline)
C-terminal agrin fragment;
Myostatin;
Activins A and B;
Follistatin;
Growth Differentiation Factor-15;
Tumor growth factor β;
Bone morphogenetic proteins;
Testosterone;
Dehydroepiandrosterone;
Growth Hormone;
Insulin-like growth factor 1;
Skeletal muscle-specific troponin T;
N-terminal type III procollagene;
3-methylhistidine;
Creatinine;
Complement protein C1q;
Hemoglobin;
Albumin;
Selenium;
Leptin;
Uric acid;
Magnesium;
Vitamin D;
Interleukin 6;
Tumor necrosis factor α;
Interleukin 1;
Butyryl-cholinesterase;
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Hey, guys,
I thought it is reseonable to speculate that if one PI3K inhibitor can reduce p-ERK, pAKT or p-S6 more dramatically in cell line A compare to cell line B (A cells were crispr knockouted one gene, and B cells is the control), this drug is more sensitive in A than B, given the fact that the basal level of phospho protein is higher in A and A cell is also grows quicker. Dose anyone has experience on this? is cell proliferation the only way to check drug sensitivity?
Thanks
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Hey, John, actually you kinda replied my second comment. so yeah, p-protein should not be used as biomarker in this regard. I have see one report claimed that p-ERK had no relationship to proliferation inhibition of MEK inhibitor trametinib. But reduced p-ERK can sensitize other drug for cell growth inhibition.
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Can anyone suggest me a specific biomarker for pacemaker cells?
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Hyperpolarization- activated cyclic nucleotide modulated (HCN4) channel and WBC.
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Plasmin. Blood should be drawn into Arginine/EDTA, 0.1 U/ml is the target.
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I agree with Victor Gurewich
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Hello researchers,
I was wondering if anyone had experience in the following:
I would like to translate two separate continuous biomarkers (A and B), that are mechanistically linked to each other, to the same scale. However, I want to avoid using an equation to estimate A from B or B from A.
Both biomarkers are rarely measured in the same cohort and so some cohorts measure biomarker A while others measure biomarker B. This is due to different companies making assays for either A or B and the established relationships between these companies and individual laboratories. Transforming both biomarker levels so that measurements of A or B can be used would help with statistical power and with repeatability of studies.
I was thinking that maybe several cut points can be established for biomarkers A and B (to make high, medium, and low count categories or something), separately, based on each biomarker's association with prognosis so that each can be mapped to the same scoring system. In doing this, I would like to have at least 3 categories.
But I am not sure how to do this and if it is even the best solution.
I hope that all makes sense. Any help will be much appreciated.
Spencer
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Hi Spencer, another possible approach could be to measure both biomarkers in the same reference population (or if that's not possible, try to find two similarly distributed ones) and then define cutoffs based on tertiles. That's specially useful if you don't expect a normal distribution. Upper tertile in biomarker A should be comparable to upper tertile in biomarker B and so on. Good luck!
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Cells will have lower viability upon treatment of high concentration of fatty acids, particularly with Palmitic acid. Does anyone know any sensitive biomarkers to detect the lipotoxicity process?
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I fallowing
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Biomarker can be developed for three main purposes (1) diagnostic (to classify as having a disease), (2) prognostic (to make predictions on who will develop a disease), or (3) theranostic (to predict an individual response to a particular therapy).
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The development of computational linguistic tools to quantify language disturbances is rapidly gaining ground in the field of schizophrenia research. Current applications are the use of semantic space models and acoustic analyses focused on phonetic markers. These features are used in machine learning models to distinguish patients with schizophrenia from healthy controls or to predict conversion to psychosis in high-risk groups, reaching accuracy scores (generally ranging from 80 to 90%) that exceed clinical raters. Other potential applications for a language biomarker in schizophrenia are monitoring of side effects, differential diagnostics, and relapse prevention. Language disturbances are a key feature of schizophrenia. Although in its early stages, the emerging field of research focused on computational linguistics suggests an important role for language analyses in the diagnosis and prognosis of schizophrenia. Spoken language as a biomarker for schizophrenia has important advantages because it can be objectively and reproducibly quantified. Furthermore, language analyses are low-cost, time-efficient, and noninvasive in nature.
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I am working on identifying biomarkers of the outcome of treatment in a disease. I have 20 potential biomarkers and more than 30 potential confounders. Actually, I know that some of those potential confounders affects treatment outcome. However, before determining the association between each biomarker and the therapeutic outcome, I want to know which of these confounders affects the expression level of each biomarker. I want to understand the impact of covariates on the expression of biomarkers to include them as confounders in multivariate analysis.
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some info in the link
or directly in the attachment.
Knowledge-based approaches seem more appropriate if your field is not completly new.
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The link between type 2 diabetes and dementia: from biomarkers to treatment
  • Michal Schnaider Beeri
  • Barbara B Bendlin
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Could a solid tumor reflect significant miRNA biomarkers in circulating blood depending on the stage of this cancer?
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We got some miRNA in tumor stroma...................
The aberrant expression of microRNAs (miRNAs) and genes in tumor microenvironment (TME) has been associated with the pathogenesis of colon cancer. An integrative exploration of transcriptional markers (gene signatures) and miRNA–mRNA regulatory networks in colon tumor stroma (CTS) was identified. Using two datasets of mRNA and miRNA expression profiling in CTS, we identified differentially expressed miRNAs (DEmiRs) and differentially expressed genes (DEGs) between CTS and normal stroma. Furthermore, we identified the transcriptional markers which were both gene targets of DEmiRs and hub genes in the protein–protein interaction (PPI) network of DEGs. Moreover, we investigated the associations between the transcriptional markers and tumor immunity in colon cancer. We identified 17 upregulated and seven downregulated DEmiRs in CTS relative to normal stroma based on a miRNA expression profiling dataset.
you may read
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I am looking for a biological response of fish exposed to trinitrotoluene or its amino metabolites.
Maybe a more or less specific gene expression could help?
Oxidative stress is one good example but its not specific for nitroaromates.
Any suggestions?
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Yes, i searched for it in NCBI gene database to make sure. :) yes i noticed your name after i posted the answer. Great article by the way.
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Hi everyone!
My current project involves measurements of CA-125 and some of the apparatus we use gives an output in pg/ml whereas the standard measurement unit of concentration in serum for this antigen is u/ml.
u/ml is a unit usually used for measurement of enzymes and for concentration of immunoglobulins. CA-125 is neither of those. It has no enzymatic activity one can measure.
So, how do I convert between the two units of concentration if I want to compare?
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Nikita Demchenko you are welcome. Questions on RG is somewhat active. Glad to be of help. And yes 2.4ng/ml is specific to IgE. I figured you might be able to trace the timeline of using this IS unit system for CA-125, so now we know it is as old as 1984. I guess you can determine the protein concentration of your standards CA-125 (if you need this for ELISA unit conversion) by the Bradford or BCA assay and then extrapolate your sample's ng/ul conc against the standards' calculated concentrations. Hope this helps.
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Video tutorial on IBR calculation or stepwise procedure..
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Hello,
You should try the CALculate IBR Interface (Calibri, https://liec-univ-lorraine.shinyapps.io/calibri/) proposed by the Laboratory for Continental Environments (LIEC) of Lorraine University, it is a user-friendly website.
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Hello everyone,
Can anyone tell me how to calculate biomarker response index (BRI)? Suppose I have three treatment sets and one control set of plants. I have considered many cytotoxicity, genotoxicity and biochemical endpoints. But now if I want to use BRI to summarize the plants' responses to the toxicant in comparison to the control, how to do it? Please help!
Thanks in advance.
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Does any one know of a compilation of research work for Biomarkers of various communicable and non-communicable diseases !
Thanks in advance .
Best Regards.
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Various communicable and non-comminicable diseases? In fact you are asking an overview of any possible biomarker.
Good general reviews are:
(about organ injury and sepsis)
(discussing main papers in this field)
regards
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Hi. I'm working with soil enzymes and I have an issue because i saw several papers that used "integrated biological response" or IBRv2 to integrate data from enzymes and build a hexagonal star plots (based on this paper from Beliaeff and Burgeot "Integrated biomarker response: A useful tool for ecological risk assessment"
See some examples:
Is a software (R package? specifical software? excel file?) available to calculate this index and build the hexagonal star plots? Or is only to calculate the data and after this, make the hexagonal star plot (radar chart) in SPSS?
I know the "Biomarker Integration Data Expert System", but this system is more appropriated for worm enzymes than soil enzymes.
Thank you in advance!!!
Andrés
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Hi Andrès,
I work regularly with the IBR and in general, I calculate it and make the graphs directly with excel.
I'm not sure that there is software available for the calculation.
The different steps are described in the articles. It seems complicated but once the formulas are understood, no worries. You just have to be careful to have all the necessary conditions.
I hope this will help you.
Good luck.
Eric
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Currently, I am validating a new machine learning approach. But, I need to find different cancer datasets composed by clinical markers and gene expressions. For now, a just found MMRF data set available at https://research.themmrf.org/.
Can you help me indicating other open data sets like this one?
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Such data can be found on GEO Datasets on ncbi (https://www.ncbi.nlm.nih.gov/geo/) but not all submissions have clinical markers with gene expression, so have only gene expression and gender, and some are cell-lines so you need to select proper filters (ex. array expression profile, human organism, keyword for the specific cancer of interest) to find your set criteria.
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Are there serum biomarkers for microglia activation?
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As far as I know no. But there are proteins that are secreted in serum that may indicate activation but they are not specific to only microglia. In this ref you can find a comprehensive list of microglial markers (https://www.frontiersin.org/articles/10.3389/fncel.2020.00198/full)
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Many researches done in utilizing bone substitues materials, what is the best biomarker for bone healing in addition to radiographic evaluation?
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Good afternoon. Alkaline phosphatase, osteocalcin and serum P1NP are commonly used.
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CA19-9 is a commonly performed tumour marker in pancreatico -biliary malignancy,but the levels keeps varying ? depending on the severity of obstruction causing cholangitis.In these circumstances if the levels are high does it mean it is a disseminated malignancy or it is probably due to cholangitis !
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Oncology rule: Go for the money (i.e. tissue diagnosis). Oncologists will refuse to see a patient for management unless the tissue diagnosis is available.
A DICTUM USED BY ONCOLOGISTS IS "NO TISSUE, NO ISSUE".
Diagnosis of most of the malignancies depends on the tissue diagnosis very high alpha-fetoprotein (AFP) in a cirrhotic patient or very high prostate specific antigen in a patient with enlarged prostate.
Diagnosis of most of the malignancies depends on the tissue diagnosis very high alpha-fetoprotein (AFP) in a cirrhotic patient or very high prostate specific antigen in a patient with enlarged prostate.
The role of cancer biomarkers e.g. CA 19-9 is if it is raised in a patient with a confirmed pancreatic malignancy by tissue diagnosis, is to serve as a baseline to follow up the patient after surgery or chemotherapy. Further rise or fall in the CA 19-9 will respectively indicate recurrence or disease free period.
Please have a look on the links below to these articles on tumor markers in general and the CA 19-9 in particular.
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Current genomics tools to to discover new or study current biomarkers of neurodegenerative diseases.
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Do you know what is metagenomics? And did you read the question well?
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When one says that a certain biomarker is associated with a certain disease "independent of other risk factors", what does this really mean? I think it means that, regardless if a person has that other risk factor or not, that person would still get that disease if the biomarker is positive. Am I correct?
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Independent risk factor is risk factor that retains its statistical association with the outcome when other established risk factorsfor the outcome are included in a statistical model
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Dear all.
I've recently gotten results for Biomarkers studio through GC-MS, but I'm not sure how interpret it.
I'd like to know if you know any book or booklet where I can find information about how to interpret GC-MS results in Biomarkers studio
Thanks a lot
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Thanks a lot.
I've found many books about it
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Several molecules are known as relevant biomarkers for the detection or followup of cancer, however, is difficult to get from research articles which ones are considered as the most useful in a clinical setting. Can you provide a good biomarker and a justification for their usefulness and reliability?
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Dear Hector, your question is much to broad and vague. Biomarkers are hardly used to detect cancer, except in some cases. They are generally used to monitor the treatment of cancer. In the review enclosed you might find what you are looking for: an overview of currently used cancer biomarkers.
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I used DHEA-S (Dehydroepiandesteron Sulphate) in a study as the biomarker of ageing. DHEA-S is hormone secreted from Supra renal gland, gonads and even adipose tissue. DHEA-S is gradually decreasing when age advances.
In addition to this, what are possible biomarkers to measure the intensity of biological ageing process in humans?
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Thank you sir Jean P Jost
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I am doing Principle Component Analysis of my proteomics data.
There are two groups, one is healthy control and the other one is patients.
Originally I have 90 biomarkers, and after feeding all the 90 biomarkers for PCA analysis, I have PC1 (23.3%) and PC2 (19.2%).
Then I reduced biomarkers to 23, which I did t-test and found the 23 biomarkers are significanly different between control and patients.
Then after feeding only the 23 biomarkers for PCA analysis, I have PC1 (39.3%) and PC2 (27.9%).
Now my question is, how should I interprate the results?
In the first time, PC1+PC2 is 42.5%; when I reduce the number of biomarkers, PC1+PC2 is 67.2%, so can I draw the conclusion that the two groups are clustered better in the second time than in the first time?
Or, are there any specific number that we could refer to evaluate the quality of a PCA?
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You don't say anything about the factor loadings, but presumably you deleted the biomarkers that had the lowest loadings, so then your structure for the 23 case would be cleaner (clustered better) because you retained the biomarkers that produced the best structure, i.e., had a high loading on only one of the two PCs.
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Hi all!
When you purify extracellular vesicles, such as exosomes, what are your downstream applications/analyses? I'm especially interested in understanding what your next steps are if you're doing biomarker discover or diagnostic research.
Thanks in advance for your input!
Best,
Brenda
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In addition, exosomes (from the secretome) could be subjected to mass spectrometry analysis to determine the presence or absence of potential biomarkers in the exosomal fraction. However, it must be stated that the integrity of the exosomes must be assessed either through the use of transmission electron microscopy (TEM) or by confirming the absence of cellular contaminations such as mitochodrion, ER, Golgi bodies etc.
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I am interested in the research related to discover novel biomarkers for bacterial (pathogenic) disease.
What types of bioinformatics approach and tools can be used for the same?
Thanks,
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Proteomics, transcriptomics, genomics and metabolomics databases can provide a hypothetical answer to your search. All you need to do is just identify and select a combination of bioinformatics methods that can support your research. Also agree to Hamid Yousf Dar , please get at least an expert to work with you else you will find yourself in a huge mess.
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I am planning to conduct p16Ink4a/Cdkn2a immunohistochemstry in cryosections of mouse tissues.
Should you empirically know good antibody for this purpose, your suggestions would be much appreciated, as the quality of the antibody is pivotal to successful staining.
Priority is immunohistochemical staining, and the use for western blotting is optional.
Many thanks!
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For example CD44 is a stem cell marker, whereas Vimentin is an EMT marker. Mesenchymal cells are called MSCs (Mesenchymal Stem Cells), then why are there different markers for stem cells and mesenchymal cells?
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A mesenchymal stem cells (MSCs) is one of the types of stem cells. It is mainly tissue-specific which means it has been isolated from different tissues mainly adult tissues. CD44 is one of the most prominent positive markers for MSCs while others are CD70, CD105, CD90, while negative markers are CD34, HLA-DR. However, the same CD44 is also considered as markers for breast cancer stem cells also.
The difference in markers of stem cells is because of their origin or site of isolation. For example, embryonic stem cells, Induced pluripotent stem cells, etc have different promising markers so those markers are being used for identification.
Now, Vimentin is an EMT marker that describes process within the cells, not cell types while CD surface markers are for cell-type identification markers here more specifically for stem cell identifications.
Yes, vimentin expression also has been analyzed in MSCs but it mostly to understand its characteristics that are fibroblastic nature which determines the EMT process let say cells migration ability which any cell will gain after they leave epithelium and start moving like mesenchymal cells. Vimentin use is not only for MSCs, it can be looked into any cell type, very common in cancer cells study purpose.
The whole concept is moving around the cell identification, characteristics, and processes carried out by any cells. Now, there are specific markers also there as well as overlapping markers are also there. This is because of origin and lineage memory. Please find a few attachments.
I hope it will help you. If I went wrong please do let me know.
Regards
Saurabh
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What will be the levels of below-mentioned biomakers during autophagy activation? Specifically in ovarian cancer
Beclin-1,
p62/sqstm1,
SNAP 23,
Annexin-A2,
LC3B,
Syntaxin-17 and
VAMP 8
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Hi Luxitaa,
Here is a link to a colleague from Cardiff University who does a lot on autophagy, some of his papers may be useful to you: https://www.cardiff.ac.uk/people/view/126767-tee-andrew
BW
Stephen
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I would like to know whether the BIOENV routine in PRIMER could be used to identify a subset of biological data (gut content items in my case) best explaining environmental data (biomarkers and condition indices in my case).
Thanks
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The short answer is yes, it could. The routine finds a subset of variables that, in combination, most closely match a predetermined pattern (represented as a resemblance matrix). So you could make resemblance matrices based on the condition indices and biomarkers (singly or in combination) and then ask which set of gut content items maximises the match. How you treat your data, and which resemblance measures would be appropriate, will depend on the data you have and the specific questions you want to address.
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In my research I just found out 3 microRNA associated with Esophageal Cancer. And I want to prove they are biomarkers for diagnosis or prognosis of Esophageal cancer.
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Hello,
I would like to participate in helping the reseaech community by predicting, e.g. a bad outcome of an infection by using biomarkers. I have no data. I would also join a project and do for you predictions with R or Python.
Best regards,
Markus
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Basically one cannot use Machine learning or Deep learning without having data at all.
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The miRNAs is also a biomarker in the serum. Could i detect the level of miRNAs, and/or targeting the miRNAs in clinical application? Has anybody try to isolate/generate the antibodies to miRNAs from mouse, rabbit or even human subjects?
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There is an antibody for heteroduplex available from Some supplier. If you add thé cDNA to à given miR, it should work. We use it to develop biosensing strategies
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Hi to everyone! For those interested, the Laboratory of Biomarkers, Biomolecular targets and personalized medicine in Oncology of the University of Ferrara (Italy) is looking for three different post doc positions. You can find attached the details and contact information. You can also contact me in private for further details. Have a nice afternoon!
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Dear Professor Carolina Simioni ,
Please see the attached cv, I think I may be the fit candidate
Thanks
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I'm working on a project to evaluate chemotherapy-induced cognitive impairment with cisplatin administration. I'm planning to use a biomarker, evaluated serially over time. My questions are:
1. What is the single best biomarker for this scenario (i.e. best in terms of sensitivity, specificity, and exclusively pointing to neuronal inflammation and oxidative stress)? I want it to be very specific, displaying aberrant results only when the neurons are injured. Many biomarkers such as interleukin or MDA increases in the event of systemic inflammation, which is almost inevitably happen under this research scenario (i.e. chemo almost always induces systemic inflammation).
2. Should it be derived from CSF or plasma?
Thank you in advance for anyone who can provide me with answers.
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Hi And
What is the effects of chemotherapy?
According to the dose and time of exposure. It could be reversable mild inflammatory response leads to cloudy swelling, hydropic degeneration or fatty change with acute inflammatory cellular infiltrate. If it is a lethal dose the response will be irreversable cell death in the form of Apoptosis changes Or Necrosis.
A lot of cellular and plasma chemical mediators will be released.
so it is difficult to find
the single best biomarker for