Epigenetics - Science topic

Which specialists do you think should be involved in the diagnosis and treatment of polyuria, considering its genetic, behavioral, and epigenetic aspects?

What aspects of genetic and epigenetic factors in polyuria do you think require further investigation? Which areas of research could contribute the most to understanding DI and PP?

The Role of Epigenetics in Fluid Balance Regulation

Mutations in the AVP, V2R, and AQP2 genes are well-documented as causes of central and nephrogenic DI. These mutations impair vasopressin signaling and water reabsorption, making them key targets for future therapeutic interventions.

Epigenetic information polish then recessive privilege distribution. WARNING: Genetic engineering is DANGEROUS. Hopefully regularly polishing the epigenome will cure aging and other diseases, plus prevent side effects of genetic engineering. Also, hopefully and theoretically after the potential genetic engineering to provide recessive traits and recessive genes, if the surgery is simple enough, subjects will keep their genetic signatures.

See my profile or Substack:

Hi, I am looking for research/ publication on epigenetic study of drosophila melanogaster related to environmental factors? How environmental factors such as temperature, light, air quality etc. is affecting epigenetics of drosophila. Looking for milestone literature in this area, will be grateful if anyone is able to help. Approach, Research Questions, Methodology of research, Experiments & Tests involved, boundary conditions etc. Thanks in advance.

Pseudocode: 1)Original: O 2)Epigenetic information polish: EIP 3)Recessive Privilege Distribution: RPD 4)Fertility Enhancement: FE 5) GMO: Genetically Modified Organism 6) SP: Same Person O + EIP + RPD + FE = GMO but SP.

Hi everyone,

I'm trying to perform ATAC-seq without using any commercial kit, but it's been challenging to find a protocol that aligns with this approach. I’d like to ask if anyone has experience with this.

Here’s the workflow I followed:

ME A: 5'-(index sequence)AGATGTGTATAAGAGACAG-3' ME B: 5'-(other index sequence)AGATGTGTATAAGAGACAG-3' ME rev: 5'-pCTGTCTCTTATACACATCT-3' By following the standard primer annealing protocol, I obtained two transposon oligos (ME A-rev, ME B-rev).

2. Nuclei Extraction: I followed the Kaestner Lab Omni ATAC protocol (file attached) and confirmed the extraction by performing MNase digestion. This step seems to be working fine.

I've attached the protocol for the Tn5 transposase I used. Following this protocol and the Omni ATAC protocol, I set up the transposition reaction with the following conditions:1 µl 10X Tn5 Transposase Buffer (final conc. 1X) 1 µl Annealed Transposon A (final conc. 1 µM) 1 µl Annealed Transposon B (final conc. 1 µM) 0.1 µl 10% Tween-20 0.1 µl 1% Digitonin 1 µl Tn5 transposase Add D.W. to 10 µl I added this reaction mix to the extracted nuclei and incubated at 37°C for 2 hours.

4. DNA Purification: I purified the DNA using the QIAquick PCR purification kit.

After these steps, I performed PCR for amplification and confirmed the product with gel electrophoresis, looking for bands at 300, 450, and 600 bp (corresponding to mono-, di-, and trinucleosomes, with ~150 bp added for index and adapter sequences).

This method worked once, but I haven't been able to replicate the results since then. Instead of the expected bands, I could only observe smears or odd bands after PCR (figures attached). I would really appreciate any advice or insights you might have.

Sincerely, Hyelin

Hello

How much time it takes from an environmental stressor to epigenetic change? Days? Hours? Weeks? There is an article for it? Since, i can't find anything about it.

"epigenetic information is stored in a digital-analog format, susceptible to alterations induced by diverse environmental signals and cellular damage" and potentially polish can fix those scratches(

Hi everyone,

I have a kit to analyse if our compounds inhibit an epigenetic reader protein, BRD4.

Kit is from Cayman (Cat No 600520). The kit says “It is recommended that inhibitor compounds to be tested in a concentration response format with at least eight independent concentrations that…”

It is the first time I have heard independent concentration?does it have any special meaning? I always prepare serial dilutions. But independent means different method?

Thank you

We are measuring methylation at the POMC gene on human DNA.

We are getting good results with out PCR but are consistently having issues with low peak height and baseline drift on the sequencing step.

The option appears to be to increase PCR product though the manual says the maximum is 10ul. We have tried 15ul and this shows some improvement but does not resolve the issue entirely.

Does anyone have experience of the machine and can you put more product in?

Any suggestions much appreciated.

Toby

Cytosine methylation, histone acetylation, etc. represent distinct epigenetic mechanisms of gene regulation. Which example is most likely to account for transgenerational effects, such as grandparent effects, etc.?

Can epigenetic modifications affect various aspects of sperm development, function, and fertilization?

I am trying to find a correlation between fetal macrosomia and hypertension during pregnancy from CDC data. But there have been a lot of studies on the epigenetics of the underlying relationship without analyzing real patient data. Then, is my original study considered novel?

Limitation:

1) target specific gene:

2) do epigenetic modification:

According to epigenetic science, does it play a role in discovering genes that contain different amino acids that cause the appearance of characteristics or behaviors in people who eat meat and milk from imported animals? Which lived in a special nature other than that in which the importing country lives?

I'm using epitech bisulfite kit (qiagen) and even starting with huge amount of starting material (up to 2 micrograms) I'm unable to recover DNA. Does anyone have similar experiences?

Trying to find the relationship between epigenetic and cancer more deeply.

Jaques Monod Albert Camus et l’affaire Lyssenko.

1) Molecular genetics: A revolutionary meeting of minds

2) Jacques Monod Quelques pages inédites de sa vie.

Trofim D. Lyssenko, né à Kiev, devient ingénieur agronome. Sa carrière fulgurante le conduit en 1938 à la tête de l’Académie des sciences agronomiques de l’URSS. Sa doctrine scientifique, basée sur la transmissibilité des caractères acquis, devient une idéologie.

Quant à Jacques Monod, il n’a aucune hésitation et publie dans le journal Combat que dirige alors Camus, un article au titre éloquent en première page : “la victoire de Lyssenko n’a aucun caractère scientifique” et termine de façon radicale : “En définitive ce qui ressort le plus clairement de cette grotesque et lamentable affaire, c’est la mortelle déchéance dans laquelle est tombée en URSS la pensée socialiste”

Trofim D. Lysenko, born in kyiv, became an agricultural engineer. His dazzling career led him in 1938 to head the USSR Academy of Agricultural Sciences. His scientific doctrine, based on the transmissibility of acquired characteristics, becomes an ideology.

As for Jacques Monod, he had no hesitation and published in the newspaper Combat which Camus was then directing, an article with an eloquent title on the first page: “Lysenko's victory has no scientific character” and ended radically: “ Ultimately what emerges most clearly from this grotesque and lamentable affair is the deadly decline into which socialist thought has fallen in the USSR.

Peut-on aujourd’hui exclure la transmissibilité des caractères acquis ?

Can we exclude today the transmissibility of acquired traits ?

Dear All.

If a researcher wont to conduct an article to evaluation an axpected noval epigentic compound, what is the most essential steps of techniques that should followed to optimised his work,rather thant measurring the cytotoxicity of the compound

thanks in advance.

Hello,

Is it possible to silence all kinds of epigenetic modifications in a cell by using gene or inhibitor?

Thank you.

What are the epigenetic drivers behind the formation and progression of pediatric brain tumors?

I intend to explore the integration of computational biology and artificial intelligence (AI) with laboratory and experimental work, encompassing animal models, cell culture, clinical trials, and molecular studies. As a clinical biochemistry student with a keen interest in AI, I believe this interdisciplinary approach holds immense potential for advancement and innovation.

However, I face the challenge of identifying relevant literature in this emerging field. I would greatly appreciate guidance on effective keywords and search strategies to navigate this landscape of research and achieve my research goals.

epigenetics in cotton

I am currently trying to express Turritopsis dhornii TET enzyme with a 6x HIS tag in a BL21 E.coli host. Every time I purify my protein it shows double bands on SDS-PAGE, when testing its activity on ELISA there seems to be no activity. My lysis buffer contains 50mM HEPES ph 7.5, 30 mM imidazole, 500mM NaCl, and 1mM DTT. I purify with 800uL of Nickel Sepharose beads. Are there any adjustments I could make to stop this double band from showing?

As it's well known, breast cancer can be caused through genetics factor. How did it happen? Does it have corelation with epigenetics? And what are the chances that it can be lowered?

how yoga is affecting the epigenetics and is there any mechanisms available?

On 21-22-23 June 2023, the Milan Medical School of Ambrosiana University promoted an International Conference in streaming, on the subject:

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

Dear colleagues! I've tried to estimate the histone variants enrichment of several arabidopsis genomic sites but every time my enrichment result looks like the added screenshot. What am I doing wrong?

The running function is:

enr.df <- enrichment(query =gr_list[[1]], catalog = anno, shuffles = 24, nCores = 12)

anno is remap2020_histone_nr_macs2_TAIR10_v1_0.bed,

catalog is a GRanges of sites of interest of A.thaliana (all 5 chromosomes).

There are no warnings after function execution.

Hi, I'm studying the epigenetic changes in genes. For this I have the primer sequences and I need to identify the corresponding target gene sequences. Can someone help me out?

Where can I find this information? thanks a lot!!!!

I am trying to look at the epigenetic modification statuses of a set of genes, does anyone knows whether there is a epigenetic modification database for individual genes?

I am trying to insert a 60 bp shRNA into the pLKO.3G plasmid (variant of pLKO.1), yet nothing is working. 

I digest with EcoRI and PacI, anneal the oligos at 95 for 4 mins then 70 for 10 mins, then cool down to room temperature gradually. And I do quick ligation for 10 mins at room temperature, and transform into HB101 competent cells. However, nothing is growing on the ampicillin plates. Any suggestions?

I followed the protocol they have on Addgene, but it did not work. 

What is the best bioinformatics approach to study epigenetic effects transferred from parent to offspring in trauma cases. Are there data repositories available in this domain?

Epigenetics is one of the key areas of research in the coming decades. Because it has the potential to fundamentally alter a human being's life by altering the expressions of beneficial or bad genes. I would like to read the work of the best scientists in the area of epigenetics, especially as it applies to the functioning of the brain. Also, I shall be grateful if you could suggest the best ten papers in this domain, by reading which I can get a reasonable update of the current status in this exciting research area.

I'm very new at epigenetics and I came across some processed files from GEO database specially this one:

More specific to the file called:

GSE64491_datSignal_tissue.csv.gz

If I look at cg02162324, I can see that all the columns related to Sample[n]detectionPValue have 0 as value.

It doesn't happen to all cpgs.

I'm wondering if p-value = 0 would mean that this value is not valid.

Thank you

The relevance of the Microbiota-Gut-Brain axis to Alzheimer’s and neurodegenerative diseases needs extensive analysis. The various articles indicate that there are various questions with relevance to microbiota-gut-brain axis that are relevant to the pathology, pathogenesis and treatment of neurodegnerative diseases.Several mechanistic studies are required to determine the underlying mechanisms for effective and safe probiotic treatment for AD and probiotic benefits remain to determined. The relevance of gut dysbiosis may induce inflammatory responses that may be the cause of the induction of the pathogenesis of AD and relevance of diet (unhealthy diets), probiotics and gut microbiota should be carefully assessed. The meta-analysis studies indicate that probiotics reduce inflammation and oxidative stress and enhances cognition in AD and MCI individuals. The effects of different types of probiotics on amyloid formation and deposition needs to be evaluated and probiotic mixture therapy may be unsafe. The safety of probiotic therapy for AD patients require investigation with relevance to neuron reprogramming and programmed cell death in AD. The risk of unsafe microbiota and probiotic use may lead to the inactivation of the anti-aging gene Sirtuin 1 and the generation of uncontrolled short chain fatty acid release that promote amyloid beta plaque formation.

The concerns with relevance to the induction of dyslipidemia and the role of safety of diet-microbiota-brain axis should be carefully assessed with relevance to the cholesterol-AD connections. The prebiotic, symbiotic and probiotic formulations should be carefully assessed for bacterial composition and living microorganisms such as gram negative and positive. The release of bacterial lipopolysaccharides (LPS) from gram negative bacteria needs to be controlled and the content of gram negative bacteria carefully assessed in these prebiotic, symbiotic and probiotic formulations. Unhealthy diets contain end products such as LPS and diets should be carefully assessed for LPS contents since LPS has been associated with the inactivation of Sirtuin 1. The gut microbiota based therapy is in progress and the relevance to the treatment of brain diseases such as AD is limited. The benefits, limitations and safety of gut microbiota and probiotics on Alzheimer’s disease needs to be placed under systematic review with relevance to dietary regulation and postbiotic supplementation that have the implications for amyloidosis and neurodegeneration. The role of probiotic therapies to create a health gut environment by balancing bacterial populations may require the activation of the anti-aging gene Sirtuin 1 to reverse the pathogenesis of Alzheimer’s disease. The literature indicates that yogurt is a prime source for probiotics and provide a healthy balance of live bacteria to provide health benefits to individuals in various countries of the world. However a recent article indicates that within 12 hours yoghurt can grow gram negative bacteria. The gram negative bacteria in yoghurt depending on daily or weekly intake can generate high levels of plasma LPS with relevance to prebiotic, synbiotic and probiotic quality products and ill health. Yoghurt products may need to be assessed for gram negative bacteria populations and LPS to determine the quality control of these products for international communities.

📷

A. Marzban A, Rahmanian V, Marzban A, Ramezani Siakhulak F. The Role of Probiotics in Improving Alzheimer's Disease. JNFS. 2022; 7 (2) :136-138.

B. de Rijke TJ, Doting MHE, van Hemert S, De Deyn PP, van Munster BC, Harmsen HJM, Sommer IEC. A Systematic Review on the Effects of Different Types of Probiotics in Animal Alzheimer's Disease Studies. Front Psychiatry. 2022 Apr 27;13:879491.

C. Guo L, Xu J, Du Y, Wu W, Nie W, Zhang D, Luo Y, Lu H, Lei M, Xiao S, Liu J. Effects of gut microbiota and probiotics on Alzheimer's disease. Transl Neurosci. 2021 Dec 27;12(1):573-580.

D. Ji HF, Shen L. Probiotics as potential therapeutic options for Alzheimer's disease. Appl Microbiol Biotechnol. 2021 Oct;105(20):7721-7730.

E. D’Argenio V, Sarnataro D (2021) Probiotics, prebiotics and their role in Alzheimer’s disease. Neural Regen Res 16(9):1768-1769.

F. Bonfili L, Cuccioloni M, Gong C, Cecarini V, Spina M, Zheng Y, Angeletti M, Eleuteri AM. Gut microbiota modulation in Alzheimer's disease: Focus on lipid metabolism. Clin Nutr. 2022 Mar;41(3):698-708.

G. Naomi, R.; Embong, H.; Othman, F.; Ghazi, H.F.; Maruthey, N.; Bahari, H. Probiotics for Alzheimer’s Disease: A Systematic Review. Nutrients 2022, 14, 20.

H. Arora K, Green M, Prakash S. The Microbiome and Alzheimer's Disease: Potential and Limitations of Prebiotic, Synbiotic, and Probiotic Formulations. Front Bioeng Biotechnol. 2020 Dec 14;8:537847. doi: 10.3389/fbioe.2020.537847.

I. Peterson CT. Dysfunction of the Microbiota-Gut-Brain Axis in Neurodegenerative Disease: The Promise of Therapeutic Modulation With Prebiotics, Medicinal Herbs, Probiotics, and Synbiotics. J Evid Based Integr Med. 2020 Jan-Dec;25:2515690X20957225.

J. Kincaid HJ, Nagpal R, Yadav H. Diet-Microbiota-Brain Axis in Alzheimer's Disease. Ann Nutr Metab. 2021;77 Suppl 2:21-27. doi: 10.1159/000515700.

K. Alessio Vittorio Colombo Rebecca Katie Sadler Gemma Llovera Vikramjeet Singh Stefan Roth Steffanie Heindl Laura Sebastian Monasor Aswin Verhoeven Finn Peters Samira Parhizkar Frits Kamp Mercedes Gomez de Aguero Andrew J MacPherson Edith Winkler Jochen Herms Corinne Benakis Martin Dichgans Harald Steiner Martin Giera Christian Haass Sabina Tahirovic Arthur Liesz. (2021) Microbiota-derived short chain fatty acids modulate microglia and promote Aβ plaque deposition. eLife 10:e59826.

L. Anti-Aging Genes Improve Appetite Regulation and Reverse Cell Senescence and Apoptosis in Global Populations. Advances in Aging Research, 2016, 5, 9-26

M. Appetite Regulation and the Peripheral Sink Amyloid beta Clearance Pathway in Diabetes and Alzheimer’s Disease. Top 10 Commentaries in Alzheimer’s Disease (e-book). 2019;2:1-11. www.avidscience.com

N. Single Gene Inactivation with Implications to Diabetes and Multiple Organ Dysfunction Syndrome. J Clin Epigenet. Vol. 3 No. 3:24.

O. Sirtuin 1, a Diagnostic Protein Marker and its Relevance to Chronic Disease and Therapeutic Drug Interventions”. EC Pharmacology and Toxicology 6.4 (2018): 209-215.

P. Nutritional diets accelerate amyloid beta metabolism and prevent the induction of chronic diseases and Alzheimer’s disease. Photon ebooks. 2015.

Q. Wassenaar TM, Zimmermann K. Lipopolysaccharides in Food, Food Supplements, and Probiotics: Should We be Worried? Eur J Microbiol Immunol (Bp). 2018 Aug 21;8(3):63-69.

R. The Future of Genomic Medicine Involves the Maintenance of Sirtuin 1 in Global Populations. Int J Mol Biol . 2017. 2(1): 00013.

S. Bacterial Lipopolysaccharides and Neuron Toxicity in Neurodegenerative Diseases. Neurology Research and Surgery. 2018; 1(1): 1-3.

T. C.J. Hervert, N.H. Martin, K.J. Boor, M. Wiedmann. Survival and detection of coliforms, Enterobacteriaceae, and gram-negative bacteria in Greek yogurt, Journal of Dairy Science, Volume 100, Issue 2, 2017, Pages 950-960.

U. Fisberg M, Machado R. History of yogurt and current patterns of consumption. Nutr Rev. 2015 Aug;73 Suppl 1:4-7.

In Evolutionar Biology, Epigenetics has become part of the explanations for changes in the phenotype across generations. But can these changes directed to specific phenotypic traits along many generations be converted into DNA mutations?

Centers in India that offer hands-on training in bisulfite conversion, DNA methylation, expression, and epigenetics are preferred.

Dear Ladies and Gentlemen,

I would like to find a database with Neisseria sp genomes with methylated adenines.

Could you advise my something?

Thank you.

Standard plasmids degrade, but episomes do not. Why?

I want to publish an article on "Behavioral Epigenetics" in a Journal without APC. If anyone can give me any suggestion, that would be very helpful.

Thank you in advance.

I'd like to know the different type of post translational modifications that occur in a mammalian cell ?

Few examples from my side are :

In case of transcription factors in Cut&Tag (cut and tag), is there any way if a particular antibody works or not before going for sequencing. Has anyone tried qPCR after library preparation? What antibodies did you validate for Cut&Tag (cut and tag) in your experiments?

My work is with highly plastic eukaryote taxa, with real time visible structural variation on individuals. I suspect they have high epigenetic fluidity while growing, and would like to understand the underlying mechanism(s) that alters epigenetic expression in this group. Methylation studies are what are most easy to study now for epigenetics, and may be of some use. However, methylation studies require existence of a gene map or maps, that this taxon does not have yet, and methylation is only one of many ways that epigenetic expression is impacted. Are there other methods that researchers are using now to get at how cells alter and/or manage epigenetic expression? Please tell me about other approaches, include equipment, supplies and approximate costs if you can. Anything useful on methylation would also be of use. Thank you.

Publications in Epigenetics wanted

Can anyone recommend a Myc-tag antibody that works well in ChIP or ChIP-seq for detection of a tagged TF?

We have tried to perform ChIP-seq against a Myc-tagged TF of interest [using Cell Signalling 71D10] but have not had success in achieving specific pulldown (ChIP-seq results shows ubiquitous binding across all open chromatin without any correlation to the binding motif of this TF family).

This antibody has not performed well in Western blotting either according to several colleagues who have tried (but then performance of an Ab in a Western is rarely predictive of performance in ChIP/ChIP-seq, anyway).

Any suggestions (preferably with your results attached) would be greatly appreciated so I can try another antibody with a better chance of success!

Hi,

I need epigenetic data file run through the hovarth clock. DNA Methylation Age Calulator, but did not find any description how it should be done?

Please can you help me to find link to describe the process of running the data?

Chromatografy is recommended for epigenetic studies with organisms lacking a reference genome

I wanted to measure methylation of a single gene promoter using DNA extracted from whole blood samples. What would the most cost effective and reliable method be? I have a total of 36 samples. I have come across a handful of ways people quantify methylation, but am unsure which is best for my project.

perhaps the most useful aspect of epigenetic processes is that they are readily reversible. Unlike genetic effects that also play a role in cancer and aging, epigenetic aberrations can be relatively easily corrected. One of the most widespread approaches to epigenetic alterations in cancer and ageing is dietary control. now, I would like to know more about the types and mechanisms of that nutrition that have a positive impact on epigenetic alteration during cancer???

what about your think is the best target to analyze the certain genetic effects in human disease?

study the

as I think to measure the protein levels as the end product of all genetic processes from gene transcription to translation take in account the effect of epigenetic at the same time

because it's easy, high accurate, can be recommended as routine work, and more sensitive?

what about your think

Metabolic rewiring and epigenetic remodeling, which are closely linked and reciprocally regulate each other, are among the well-known cancer hallmarks. Studies have reported use of Onco-metabolites to metabolically reprogram the epigenetic of cancer. I was wondering what might be major limitations of such techniques?

we are going to carry out some epigenetic experimentations. definitely we need to count the cells. however some samples are dried-freeze cell pellet and had reserved in -80 freezer. the question is can we use them for cell counting after that long-term freezing? are they intact? is it authenticated??

Plant research (Genomics, epigenetic, proteomics)

Dear PIs,

If you have any projects in the field of molecular biology and/or epigenetics, please let me know

Thanks in advance ☺

I am working on cancer genomics. I downloaded TCGA BRCA FPKM data for my analysis. after some preliminary analysis, I categorised 250 samples in total 2 distinct categories. Now I want to analyse and compare their epigenetic and mutation patterns.

After downloading all mutation and epigenetic data from TCGA BRCA, none of the samples from my previous analysis is matching.

Suppose, TCGA-AN-A0AK-01A-21R-A00Z-07 sample is present in my previously downloaded FPKM data.

But TCGA-AN-A0AK-01A-21W-A019-09 is available in the mutation data. Are these ids the same? For FPKM data and mutation data, do the same sample (individual) be represented by different Ids?

Please help me, Thank you in advance.

Hey,

I recently have a confusion about single cell ATAC-seq integration analysis between samples. I have read many discussions about that issue. So, I summarized them into two solutions as follows:

SOLUTION 1. (data QC ignored here) find the union feature set from different samples -> generate count matrix for each sample -> merge them into one large count matrix -> normalization/Scaling/cell clustering/ cluster annotations……

SOLUTION 2. generate the count matrix for each sample -> normalization/Scaling/cell clustering/ cluster annotations for each sample -> find common features among all samples -> generate count matrix against the selected common features for each sample -> merging data using pipelines, e.g. Signac/Harmony, to perform cell clustering, cluster annotation and other following analysis (which usually with give a new assay for common features).

Either one selected, I will have cell clusters now. So the next plan for me is retrieving differential features for each cell type/cluster, which will be the key to the further investigation of biological functions.

Q1. I know that batch effect indeed exists between samples, but for SOLUTION 1, will normalization and scaling for a single large count matrix work for differential enrichment analysis between samples?

Q2. If SOLUTION 1 is not reasonable, SOLUTION 2 will give rise to a new assay only contain the selected common features, based on which the batch effect should be well corrected and the cell might be better clustered. However, how to perform the differential analysis for non-common features in each clusters? (That's to say, will the batch effect correction in the newly integrated assay by SOLUTION 2 will work for total differential feature detection in raw assays at the sample level?)

Thanks and best regards!

We know that epigenetic factors are denoted by alterations in DNA methylation, histone modification abd transcription of regulatory non coding RNA such as microRNAd but are there additional epigenetic changes that take place that do NOT involve these mechanisms?

I need to know if cells are arresting in S or G2/M phase , some cells are still trying to replicate themselves by mutations or other epigenetic factors because we are giving stress by any drug to stop their growth. Those cells can have the properties to carryout re-replication. If one can look at them through flow cytometry, then how to analyze them. I welcome suggestion from anybody expertise on this field. Please suggest.

I need to perform immunofluorescence on mouse hematopoietic stem cells. However, I have multiple mice that need to be sampled, and the sampling time span is relatively large. However, I hope to be able to perform immunofluorescence staining at the same time. In addition, for future experiments, so I would like to ask if there is a way to store mouse hematopoietic stem cells because, after the extraction of HSC, mice are dead, therefore I need to store cells for future analysis. Moreover, I will do epigenetics Observation, so it is hoped that the storage method will not affect the internal physiological characteristics of the cell.

I am currently working on the H3K4me3-related project for gene activation. I am curious about how H3K4me3 is added to the lysine of H3K4. Does H3K4me3 is step by step added by H3K4me1 and H3K4me2? We know H3K4me3 mainly marks the gene promoter and correlates to gene transcription activates. H3K4me1 and H3K4me2 mark both enhancer and promoter and have multiple functions for gene activation according to different complexes. The three histone makers show different patterns but also with some common features. The question is: If the gene is activation and the H3K4me3 is significantly enhanced, does the H3K4me1 and H3K4me2 at the promoter locus need to be reduced? In contrast, for any reason we find the H3K4me1 and H3K4me2 are all reduced, does the H3K4me3 need to be upregulated at the same locus, or does it reasonable? If the H3K4me3 is added from H3K4me2, our observation is something wrong. But if the H3K4me3 can be directly added from H3K4me0, it can explain our result.

Thanks for the help.

Hello everyone,

I am searching information about increasing yield of secondary metabolites that are heterogeneously produce in S. cerevisiae.

First I transfer several genes into yeast, then I wanna to optimized the yield of these metabolites. I wonder that whether epigenetic modifications play any roles in enhancing the production of these metabolites in the yeast transformants?

Thank you very much!

We have conducted an experiment on epigenetic allele identification and quantification for some quantitative trait. we are trying to map epigenes using epigenome association mapping (EWAS). Please share related information for better mapping and also share r codes for the same.

How epigenetic mechanism affects an organism response to environment? If the DNA structure is not changed through epigenetic mechanism, how it could epigenetic said to be heritable?

Hi everyone. I need to read about protocols for preparing tissues before using them to measure epigenetic histone marks. I've been told these may be based on the 'Marburg protocol', however, I have not been able to find much info about this. Would really appreciate any help.

Mains functions are emotion, behavior, long-term memory.The limbic system operates by influencing the endocrine system and the autonomic nervous system.Usually affect depressed . I want to reflect on US elections, Capital rival, as other national problems. Because Im aware of reppetions behaviour from thought that create need for emotional stimuli. Should we all first analyse our political( emotional cognitions) before voting? Whats your thoughts on Epigenetics?

Hi, I have a question if anyone can answer. I have identified two co-factors for my transcription factor. But the mass spec data seems insignificant. Now I want to find if some other co-factors are involved in regulating my transcription factor? So, how can I do this? Should I cut my gel band at different molecular weight or should I go for ChIP-seq to determine their binding complex?

I am interested in finding research that evaluates the combined impact of epigenetic factors, prenatal development (for example hormone imbalance) and childhood trauma (such as an impaired attachment bond with one or both parents) in determining sexual orientation.

Thank you!

Conventional Darwinian evolution is based on random mutations causing adaptive change. In contrast to that, evolution due to epigenetic inheritance offers the opportunity to trace the causal relationships, particularly when seen from the cellular-molecular level. Using this approach, the exaptive changes in adaptation to gas exchange from the lung alveolus to the unicellular have been traced (Torday JS, Rehan VK. The evolutionary continuum from lung development to homeostasis and repair. Am J Physiol Lung Cell Mol Physiol. 2007 Mar;292(3):L608-11; Torday and Rehan. Evolution, the Logic of Biology. Wiley, Hoboken, 2017) with gaps along the way due to the novelty of this approach. However, such gaps could be filled, and other physiologic traits could similarly be elucidated, leading to a new way of understanding physiologic evolution independent of function, particularly as it relates to dysfunction in disease.

Hello all. I am trying to isolate buffy coat from whole blood (sodium citrate), and planning on cyropreserving it for later analysis (~3-5 years). As to what analysis would include, we are leaving it as open ended as we can, but mostly am thinking of extracting DNA (Qiagen or home extraction) and looking at epigenetics.

What freezing media is typically used for this type of storage? Would a standard 90% PBS and 10% DMSO work, and what are the drawbacks.

Additionally, I read about the potentiality of platelets clumping and potentially interfering with the sample. Does anyone have any advice on purifying platelets from the buffy coat on that end? Thank you all very much.

Beryllium is exceedingly toxic and known to interfere with Human enzymes.

Analysts have developed techniques to measure Beryllium in parts per Quadrillion.

Beryllium is present in Fluoride industrial waste dumped into drinking water supplies in Australia, measured by one supplier to be 95 gram per tonne (see attached analysis).

I wonder if anyone has studied the concentration of Beryllium in drinking water, its absorbed dose range and risk factors for various diseases, including cancers, as a result of this "Fluoridation" waste disposal? What are the effects on the Human foetus?