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Genetics - Science topic

Genetics is a discipline of biology, is the science of genes, heredity, and variation in living organisms.
Questions related to Genetics
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Hi!
I use pyridine borane to react with DNA. I observed that DNA recovery on the purification stage after pyridine borane reaction is very low, at 10%. Therefore, I would like to kindly ask you about the following:
Does pyridine borane fragment genomic DNA?
Does it affect the efficiency of DNA binding to the column bed during purification?
Does anyone recommend a suitable purification method and tested binding buffers or other suggestions to improve DNA recovery?
Additionally, I have a question, the pyridine borane solution with DNA is shaken for 16h 850rpm, but I wonder if I can mix with vortex before incubation for better distribution of the substance in the solution?
I will be grateful for all suggestions.
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Hi, I have two data sets from the illumina omniexpress snp array platform. The first data set was mapped using the GRCh37 build and the second one was more recently read using the GRCh38 build. Not surprisingly when I've tried to merge the files in PLINK for a larger analysis it comes up with the warning snp rs... is in a different genetic position. Is there any way to update the build of the first data set? Or suggestions for how best to proceed, I haven't done much genetic analysis before so any help would be welcome :)
Best,
Mari
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Hi,
Between GRCh37 and GRCh38 some of the items should be the same. For those that differ, I recommend the website:
Unfortunately, I'm afraid that with a large amount of data, the conversion may be a time-consuming process, but it's always a solution.
Hope this helps! Feel free to ask if you have questions about how to use the program to convert.
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Hi everybody,
I wanna use an antibody to determine the presence of a protein in my chip-seq experiment. Can someone help me how can do concentration optimization for antibody which I use ?
Thanks in advance :)
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Titrate the amount of antibody required by performing a ChIP experiment using a range of antibody concentrations. As Avik mentioned, the amount of antibody required by ChIP generally ranges from 1 to 10 μg of antibody for every 25 μg of chromatin. https://docs.abcam.com/pdf/chromatin/A-beginners-guide-to-ChIP.pdf
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I found some bases with disagreement in the assembly of the contig. I read that because it is a nuclear marker, this disagreement may not be due to a failure in sequencing but due to heterozygosity, and therefore I should not change the base in the contig by the highest-quality criterion, but set it as an IUPAC ambiguity code.
On the other hand, I was told that when it is heterozygous, the peaks are usually the same size. But it is not always easy to determine how equal it is.
So I would like to know if there is a cut-off point or defined protocol to determine if a mismatch is due to heterozygosity or an error in sequencing on one of the strands?
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Look for read coverage over the sites in question and observe allelic frequencies before deciding how to proceed. With coverage you can gain confidence and establish a PValue which you then use to determine if the polymorphic site you are observing is likely to be the result of some random process - most likely sequencing errors. Assuming your PValue is <= 0.05 (typical threshold) then look at the allele frequencies and only then decide as to the type of allelic variation you are observing. Read base quality scores should be treated as guides only, they only relate to the actual sequencer base calls and do not account for errors arising during sample library preparation. Personally I ignore quality scores completely when aligning reads as the relationship between base call quality scores and alignment substitution rates are usually swamped by library preparation errors.
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I transformed a bacteria with an integrating plasmid. I grew up colonies in broth and then did colony pcr to genotype them.
I did two pcrs:
1st pcr: Should only give 1 kb band from transformed bacteria
2nd pcr: Should only give 1 kb band from wild-type bacteria
Unfortunately, for all my cultured colonies, both pcrs showed 1 kb bands. This indicates my cultures are a mixture of wt and transformed.
I was very careful in picking the colonies and I do think the cultures are truly a mixture because I saw both bands even after passaging the bacteria a few times.
The only solution I can think of is streaking out the culture for single colonies, but that takes ~2 weeks. Is there any way to avoid this issue?
More details:
First pcr spans primer/genomic DNA junction
Second pcr amplifes from a tRNA gene that the plasmid disrupts.
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I think you have answered the question then, if it works with the "strong" antibiotic but not the weak one, then you most likely are getting mixed cultures and have background cells that are not resistant. Even well separated colonies can have a small amount of cross contamination, in fact there are likely to be background cells present in an area of the plate without any colonies, unable to grow but not really dead.
Best solution is to either increase the selection pressure or preferably streak out and get pure cultures.
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Dear All,
I am going to use EvaGreen?/ Bio-Rad system to detect two genes using two pairs of primers.
The first pair was successfully detected previously using EvaGreen? master mix.
It was detected at thermal cycler annealing temperature 51 degrees with a 99 bp amplicon. However, I would like to design multiplex and detect two genes using the EvaGreen? master mix.
The second gene has a master mix designed from BioRad and the recommended temperature is 58 degrees with an amplicon of 195 bp amplicons.
How could I use the same well in ddPCR to detect both? Which Temperature should I use in my multiplex assay?
Thanks all
Best
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Use gradient PCR to see if both primer sets have an overlap in usable range in annealing temp. Small products are generally easier to amplify at a range of temps because the ramping from the annealing temp to 72 will often hit the desired annealing temp along the way.
If you don't have a gradient capable thermocycler, then you'll just have to test several temps in several PCR runs.
Good luck!
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Recently, I have been investigating of expression of Sall-4 in two different types cancers. Due to of acceptable melting peak of Beta Actin(and Cq=17), I am sure the quality of cDNA is pretty good.
#PCR #QPCR
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To compare transcript levels of genes expressed at a very low level, one can also enrich the targets by including a pre-amplification step.
I have included one reference here. There are many others as well:
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Hi,
I was just given a plasmid for sacB counterselection in mycobacteria. I sequenced this plasmid and I was surprised to find there is a mutation in the signal peptide of the sacB gene.
The person who built this plasmid left long ago, and no one seems to know about this mutation.
Does anyone know if this mutation might be intentional? Or could it be a suppressor mutation from passaging the plasmid in ecoli?
I don't know what to do about this mutation... I could fix it, but this mutation looks like it might be intentional: this mutation precisely breaks cleavage of the signal peptide. As I understand, signal peptide cleavages occurs at the third residue of the motif AXA, this mutation changes the motif to AXV.
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It is better to check other plasmids with the SacB gene like pK18mobsacB or pK19mobsacB. Their complete sequence recently released and deposited in the NCBI. I have used them and they were OK.
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Dear all,
a few days ago, the big paper was published in Nature ( Telomere-to-telomere assembly of a complete human X chromosome), unfortunately, I am unable to find the final FASTA sequence on NCBI...Could you advise, please? In another case, it sounds like a bad joke, the published genome assembly without the publicly available sequence...
Thanks
Martin
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Thank you we have already find the sequence here:
What do you thing about this:
Human X - assembly-38 : 156 040 895 bp
Human X - CHM13-CMO20874.1 : 154 269 075 bp
Does it mean that the human genome is about 2 miliones bps shorter now?
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  • Molecular biology is the study of the molecular underpinnings of the processes of replication, transcription, translation, and cell function.
  • Biochemistry is the study of the chemical substances and vital processes occurring in living organisms. Biochemists focus heavily on the role, function, and structure of biomolecules such as proteins, lipids, carbohydrates and nucleic acids.
  • Genetics is the study of how genetic differences affect organisms. Genetics attempts to predict how mutations, individual genes and genetic interactions can affect the expression of a phenotype.
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For detailed study:
1) Molecular biology by ROBERT F WEAVER
2) Molecular Biology of the Cell by Bruce Albert et al.
3) Karp's Cell and Molecular Biology by Gerald Karp, Janet Iwasa, Wallace Marshall
4) Cell and Molecular Biology Concepts and Experiments by Gerald Karp
5) Molecular Cell Biology by Harvey Lodish, Arnold Berk, Chris A. Kaiser, Monty Krieger, Anthony Bretscher, Hidde Ploegh, Angelika Amon, Kelsey C. Martin
For outlines ( simplified book):
1) Molecular and Cell Biology For Dummies by René Fester Kratz
2) Schaum's Easy Outline Molecular and Cell Biology by William Stansfield, Raul Cano, Jaime Colome
3) Study Guide to accompany Cell and Molecular Biology: Concepts and Experiments, by Gerald Karp, Nancy L. Pruitt
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The evidence is mixed and variable over the decades. More recently, evidence suggests mental illness can be associated with having an hysterectomy.
Case Study
A lady, aged 54 had an hysterectomy in August last year. Her mental health has deteriorated following the procedure. There is a familial history of the same or similar occurrence. For example, the lady, her mother and grandmother developing mental illness post hysterectomy. The presentation, includes depression, anxiety including panic and paranoia.
Questions:
Is there any evidence for a genetic link in the family?
Is there any evidence of increased risk of developing psychosis such as paranoid thinking?
Is there any evidence that HRT or hormone treatment can improve symptoms?
Any evidence or debate would be appreciated.
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Nice work done by (@beatrica)
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Biofeedback is a method that uses the mind to control a body function that the body normally regulates automatically, such as muscle tension, heart rate, pain perception or stability...
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Tank you
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A biosafety level is the level of the biocontainment precautions required to isolate dangerous biological agents in an enclosed facility. The levels of containment range from the lowest biosafety level 1 to the highest at level 4. In the United States, the Centers for Disease Control and Prevention (CDC) have specified these levels. In the European Union, the same biosafety levels are defined in a directive. Sabanci University is following the same directive in accordance with Turkish biological safety regulation.
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I've made a synthesis in French a few months ago. Hope it will help.
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Genome sequencing helps find vital information, for example the strain type, virulence, location of origin and differences between strains transmitted within the country and in other countries
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You can find a centralized database of genomes on https://www.gisaid.org/ . To access them, you have to register and it can take some time to actually obtain the info. Nevertheless, you can see the authors of the publications and contact them directly.
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FDA has issued guidance to provide recommendations to health care providers and investigators on the administration and study of investigational convalescent plasma collected from individuals who have recovered from COVID-19 (COVID-19 convalescent plasma) during the public health emergency.
The guidance provides recommendations on the following:
  • pathways for use of investigational COVID-19 convalescent plasma
  • patient eligibility
  • collection of COVID-19 convalescent plasma, including donor eligibility and donor qualifications
  • labeling, and
  • record keeping
Because COVID-19 convalescent plasma has not yet been approved for use by FDA, it is regulated as an investigational product.? A health care provider must participate in one of the pathways described below.? FDA does not collect COVID-19 convalescent plasma or provide COVID-19 convalescent plasma.? Health care providers or acute care facilities should instead obtain COVID-19 convalescent plasma from an FDA-registered blood establishment.
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Out of curiosity, I got this question whether knocking out (deletion) of a gene on one side and knocking down (RNAi) of the same gene on the other side will affect the cell in a similar manner or not.
If not why?
If yes, is it applied to every gene?
Knock out of a gene will correspond to no expression (gene deletion) in the cell, which can be appropriate to confirm the functional specificity, to observe processes which are affected in its absence and some other processes which are compensating the absence of the gene.
Knockdown of a gene will result in expression defect by decreasing the level of the transcript (mRNA silencing).
Now, the points which I am wondering upon are:
  1. no mRNA presence and silenced mRNA will create two different environments for the cell to deal with or not.
  2. whether the whole amount of transcript should be targeted to have the same phenotype as of gene knockout.
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Most of the times, Knockdown results in partial silencing whereas Knock-out gives black/white phenotypes. Knockdown might have more off-target effects than knock-out efforts. There are also cell-line specific effects where one choice is ok but not the other. Hence it is difficult to have blanket answers.
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Is it fair and reasonable to say that in the medical sciences, English is widely accepted (universally?) by scientists as the main language for communication and defending research findings?
At this point in time, is this a valid statement?
Will this acceptance continue in the foreseeable future?
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Yes, it is used in many countries and most people understand.
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In the age of Covid19, is there a basic conflict between science and superstition in the discipline of medical knowledge? Are there some simple, sensible, robust and reasonable ways to distinguish a scientific statement (or fact) from a superstitious statement?
To stay focused, the topic will concentrate on science versus superstition in the scientific discipline of medicine. We will try our very best to stay focused and not stray off track. it is very easy to wander off message and be all over the map. i will try to summarize the key conclusions from time to time.
In the age of the Corona Virus, there are so many statements out there. The statements may not be scientific. But if they are not scientific, are they false? Are they fake? Are they simply statements based on superstition.
What should we do if people believe in statements that are not based on science? Should we be polite and tolerate their beliefs?
As long as people do not harm others, then from society’s point of view, the fact that people hold non-scientific hypotheses is probably benign. However, the trouble starts when the same people act these beliefs, and then cause harm to others. The question arises: what should society do in this case?
Based on the discussion, there are two assumptions and four categories.
Assumption1: Beliefs cannot be justified or unjustified.
Assumption2: hypotheses can be disproven
Scientific hypotheses that are based on justified facts in natural causation. Or scientific hypotheses have not been disproven (I prefer the negative formulation because we may never be able to prove anything but we are unable to disprove it.)
Since science cannot give a definitive answer, there are many competing answers that merit our attention, and we may not be able to select among them.
Non-scientific hypotheses are unjustified facts that may be “proven” in the future with better evidence and facts.
Pseudo-scientific hypotheses: not sure where these fit in?
Superstitions are unjustified beliefs in supernatural causation.
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Joseph Tham, thanks for a thought provoking question. I think we should tolerate and respect beliefs and ideas that are not considered scientific. Our intolerance of such beliefs and ideas could be the result of a lack of understanding of the science behind them. We should therefore subject them to rigorous testing using the scientific method. A practical example is the fact that the World Health Organization has not dismissed out of hand the herbal remedy from Madagascar that is claimed to prevent illness from COVID-19. Instead the remedy is going to be tested using established scientific principles. The null hypothesis can then be rejected or accepted. This is how Indigenous Knowledge Systems contribute to scientific advancement.
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WEIRD (Western, Educated, Industrious, Rich, Democratic)
Typically, WEIRD people have Western-influenced education. They are comfortable in international languages and have non-traditional values. Usually, they are young, hardworking, urban professionals with living and working experiences abroad.
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It is not easy for someone from outside the culture and education to integrate into the society, what more to offer advice to policy makers. This happened even to East Asian countries where the influencial policy makers are 顺心彩票 grown.
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What are the merits, if any, in the challenges that lawyers and economists have raised against the Covid19 lockdown? How much weight should society give to the opinions of epidemiologists?
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Your excellent questions might be complemented by several additional ones: who is behind the epidemiologists? Who is financing them? Which are the real interests of the research funders? These questions are not related to conspiracy theories but to the Covid-19 reality. Cui bono the lockdowns? Who is paying for the side-effects due to lockdowns? What about those people who could not be operated on time and lost their lives because their operations were cancelled? Nobody is counting the collateral victims. Why? We know by heart Covid-19 statistics. Pandemic is the omnipresent topic everywhere. What about the vital questions of humanity? Have they just disappeared?
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In a patient with hereditary desminopathy (Thr341Pro DES mutation in a heterozygous state) with disease progression, a significant decrease in olfaction is noted. How can this fact be explained?
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I agree with Japneet Kaur. The problem in the cilia of olfactory sensory neurons. The myofibrilar myopathy is a genetic disease that associated with the primary ciliary dyskinesia. The primary ciliary dyskinesia resulted in defective cilia and olfactory receptors.
Attached, please find the article describing both myofibrilar myopathy and primary ciliary dyskinesia.
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Some reports suggest that in the fight against Covid19, the use of ventilators have not saved lives. How do we assess these reports? Any merits?
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Ventilators are helpful in palliative medical care for some COVID-19 patients, but not all; therefore, ventilators should be made readily available even though only a fraction of patients will need them.
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I want to test and develop algorithms for predictive modelling, but all GWAS data mentioned in papers are private, available only through request to the authors and much bureaucracy.
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Dear colleagues,
You can examine the GWAS studies which have been carried out within the framework of NSF projects. In this case, the authors are obliged to make all the data obtained available to the entire scientific community.
With best wishes,
MB
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A famine of food does not necessarily mean that there is a shortage of food; it is the inaccessibility of food. Is it the same with the Covid19, in the sense that there is inaccessibility to medical resources?
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No, because without medical supplies, Coronavirus would show its true nature and cause a natural maximum pandemic. The protective gear only serves to modify the different curves
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Developing a vaccine is an important task. What is the best way to achieve this goal? Should we use a global competitive process?
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Less than five months after the world first learnt about the new coronavirus causing fatal pneumonia in Wuhan, China, there are more than 90 vaccines for the virus at various stages of development, with more announced each week. At least six are already being tested for safety in people.
Now, developers, funders and other stakeholders are laying the groundwork for their biggest challenge yet: determining which vaccines actually work.
This typically involves giving thousands or tens of thousands of people a vaccine or placebo and seeing, over months or even years, whether there is a difference between the two groups in how many people get infected in the course of their daily lives, as well as checking that no safety issues emerge.
But in this pandemic, scientists will have to accelerate and streamline that process. A vaccine may be the only way to generate immunity to the virus across a population: despite the millions of coronavirus cases worldwide, some preliminary studies suggest that only a small fraction of people in even hard-hit regions have been infected with SARS-CoV-2, and their immunity is unclear.
This month, the World Health Organization (WHO) in Geneva, Switzerland, sketched out plans for a clinical trial that will test numerous vaccines in a single study. Some developers and funders have plans for their own efficacy trials. But key questions remain, such as which vaccines will be tested first — or at all — and how their effectiveness will be measured and compared.
“It’s going to require a level of coordination that has never really happened before, and a time frame that’s never really been even imagined,” says Mark Feinberg, president and chief executive of the International AIDS Vaccine Initiative (IAVI) in New York City. “You can’t take 200 vaccines into efficacy trials,” says Seth Berkley, chief executive of Gavi, the Vaccine Alliance in Geneva, which funds immunizations in low and middle-income countries.
Rolling trial
The WHO’s proposed Solidarity Vaccine Trial seeks to speed development with an adaptive design. This allows vaccines to be added to the trial on an ongoing basis. Participants will be enrolled continuously, and vaccines that don’t seem to be working can be dropped from testing.
The WHO still needs to hammer out details, such as how a vaccine’s efficacy will be measured, says Marie-Paule Kieny, research director at the French National Institute of Health and Medical Research in Paris. But she thinks its overall approach makes sense. “One of the challenges is prioritization — which vaccine should you test first,” she says.
The WHO has established an expert panel to prioritize vaccines for inclusion in its trial, but it is unlikely to be the only organization seeking to do this. “Some strategic alignment and coordination in this effort is going to be critically important or otherwise it'll become very chaotic,” says Feinberg. But the WHO plan “by itself may not be sufficient,” he adds.
The US National Institutes of Health (NIH) in Bethesda, Maryland, this month unveiled a partnership with more than a dozen companies that aims to coordinate the development of drugs and vaccines for coronavirus. And the Coalition of Epidemic Preparedness (CEPI), a global foundation that funds vaccine development, is supporting 9 different vaccines. The non-profit hopes to raise US$2 billion to pay for efficacy trials, manufacturing and other costs, says Melanie Saville, the organization’s director of vaccine research and development.
Criteria for prioritizing vaccines for efficacy could include its production capacity and the immune response generated in early human trials and animal studies, says Kieny, as well as regulators’ experience with the specific type of vaccine. Some of the kinds of vaccine being developed, such as RNA vaccines, have not been widely tested in people or used in a vaccine that has won regulatory approval.
A vaccine developed at the Jenner Institute at the University of Oxford, UK, is currently undergoing early-phase trials. “There’s a reasonable chance that we’ll be able to pick up the efficacy of the vaccine over the next couple of months,” Andrew Pollard, an infectious disease researcher at Oxford leading the trial, said at an online press briefing.
A small number of developers with plans and funding to get their vaccine approved and scale up production will likely call the shots with regard to how efficacy trials are done, says Rip Ballou, a program leader at IAVI. “Doing a phase III trial to show efficacy is meaningless if it's not coupled to a plan to actually licence and deliver under some regulatory authority,” he says. “There's only a handful of players that will be able to meet that very high bar. Because otherwise, it's a publication. It's not a vaccine.”
A fair shot
Another challenge will be determining how the different vaccines compare to one another. WHO’s proposal for an efficacy trial could allow the performance of different vaccines to be directly compared, but Kieny thinks that some developers may be unwilling to accept this because it could hurt a vaccine’s commercial prospects.
Swati Gupta, IAVI’s Vice President and Head of Emerging Infectious Diseases and Scientific Strategy, says vaccine developers will want to understand how key decisions are made before committing to trials that involve comparisons with other vaccines, to make sure their vaccines have “a fair shot at being able to show its efficacy”.
But it is essential to be able to compare different vaccines, even if it requires vaccines developers to set aside their short-term interests, says Charlie Weller, vaccine lead at the Wellcome Trust biomedical charity in London. “They work under commercial business models. That's not going to work for the situation we're in now," she says.
Expected global demand for a coronavirus vaccine could make developers more willing to cooperate. “We need more than one vaccine,” says Kieney. “Monopoly is always very bad, and none of the vaccines may have enough production capacity.”
One factor that could encourage such cooperation is the shifting geography of the pandemic. “China would have been a great place in Wuhan to have done efficacy trials two months ago,” says Berkley. “Italy would have would have been a great place to do it a month ago.” As a result, developers have incentive to join initiatives such as the WHO’s or the NIH’s, because of their access to clinical trial infrastructure around the world that could bring vaccines to where there are coronavirus cases. “We need to be nimble,” adds Gupta.
Emergency use
While most experts see large trials as a necessity to ensure that coronavirus vaccines are safe and effective, some developers are examining alternatives.
One option is to look for signs that a vaccine works in early-stage trials involving hundreds of participants, and then seek permission from regulators to deploy the vaccine under ‘emergency use’ rules in high-risk groups, such as health-care workers, who are more likely to be infected with the coronavirus. Regulators such as the US Food and Drug Administration can grant emergency use, while additional data is collected to license a vaccine.
Cansino Biologics in Tianjin, China, which is developing a vaccine comprised of a chemically inactivated form of SARS-CoV-2 virus, will consider this approach, according to a company spokesman. Johnson and Johnson said in a press release that its vaccine could be ready for emergency use in early 2021.
No vaccine has ever been deployed under emergency-use provisions, says Katherine O'Brien, who heads WHO's immunizations, vaccines, and biologicals department. If coronavirus vaccines follow that path, regulators will seek extra reassurance that a vaccine is safe. “There is no compromise that can be made on the safety issues,” O’Brien adds.
Momentum is building for an even more radical proposal to determine which vaccines work: intentionally infecting young, healthy volunteers, negating the need to wait for trial participants to become infected naturally. These ‘human challenge’ studies are already used to study infectious diseases such as malaria and dengue, and some researchers say they should be considered to speed the development of coronavirus vaccines.
Berkley says challenge trials could be used to rapidly determine which vaccines advance to large-scale trials. But he thinks they may be too risky without either an effective drug or a genetic test to identify the rare young individuals who are likely to develop severe disease. “Until you have a recognised treatment, I think that's a pretty tough story,” he says.
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Some people claim that the people that need the vaccine the most are the least able to pay for the vaccine. Is this a correct claim? If yes, what should be the appropriate policy response?
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Joseph Tham how are you? i would like to answer that yes, but the role of this COVID 10 pandemia during the last 4 months showed that not, underline because according with the human kind`s history: health, education, and human peace progress never being something really important for political leaders in opposite way the budget for supporting war in all sense always being the main aim of the rich countries developing or even poor countries.
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Hi everybody
I want to create an admixed individuals with methods such as HI, GA or CGF. Is there a package or module in R or Python software to do this? Or software running in Windows?
I appreciate your help.
Best regards
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Hi,
BiodiversityR package is available on
Sicerely yours,
Saeed
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how to get this? this link is not working
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Probiotics are live microorganisms that are intended to have health benefits when consumed or applied to the body. They can be found in yogurt and other fermented foods, dietary supplements, and beauty products.
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A hospital-acquired infection (HAI), also known as a nosocomial infection, is an infection that is acquired in a hospital or other health care facility. To emphasize both hospital and nonhospital settings, it is sometimes instead called a health care–associated infection (HAI or HCAI).
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Please see the following RG link.
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The SARS-CoV-2 genome was rapidly sequenced by Chinese researchers. It is an RNA molecule of about 30,000 bases containing 15 genes, including the S gene which codes for a protein located on the surface of the viral envelope (for comparison, our genome is in the form of a double helix of DNA about 3 billion bases in size and contains about 30,000 genes).
Comparative genomic analyses have shown that SARS-CoV-2 belongs to the group of Betacoronaviruses and that it is very close to SARS-CoV, responsible for an epidemic of acute pneumonia which appeared in November 2002 in the Chinese province of Guangdong and then spread to 29 countries in 2003.
A total of 8,098 cases were recorded, including 774 deaths. It is known that bats of the genus Rhinolophus (potentially several cave species) were the reservoir of this virus and that a small carnivore, the palm civet (Paguma larvata), may have served as an intermediate host between bats and the first human cases.
Since then, many Betacoronaviruses have been discovered, mainly in bats, but also in humans. For example, RaTG13, isolated from a bat of the species Rhinolophus affinis collected in China's Yunan Province, has recently been described as very similar to SARS-CoV-2, with genome sequences identical to 96 percent.
These results indicate that bats, and in particular species of the genus Rhinolophus, constitute the reservoir of the SARS-CoV and SARS-CoV-2 viruses.
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The Sarbecoviruses (SARS and SARS-related beta coronaviruses) are a faily diverse clade of coronaviruses. Merbecoviruses (MERS and MERS-related beta coronaviruses) are another clade with similar diversity. The SARS-CoV-1 and SARS-CoV-2 sarbecoviruses are quite distant from each other.
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A man in China has reportedly died from the hantavirus, which is one of a family of viruses spread by rodents that can cause disease in humans. The man from Yunnan Province in southwest China was traveling east by bus to Shadong Province, and the 32 other people on board are also being tested for hantavirus, according to the state-run Global Times?newspaper as reported by 顺心彩票week on Tuesday.
What is the hantavirus?
This family of diseases is spread mainly by rodents — particularly the deer mouse in the U.S. — and can cause different diseases in people around the world. Each hantavirus has a specific rodent host species. Hantaviruses in the Americas are known as “New World” hantaviruses, and can cause?hantavirus pulmonary syndrome (HPS), with symptoms including fatigue, fever and muscle ache in early stages, and coughing and shortness of breath later on. Other hantaviruses, known as “Old World” hantaviruses, are mostly seen in Europe and Asia, and can cause?hemorrhagic fever with renal syndrome (HFRS), with symptoms including intense headaches, back and abdominal pain, fever, chills, nausea and blurred vision. Both diseases are considered rare, but can be fatal.
How dangerous is it?
Developing HPS (hantavirus pulmonary syndrome) and HFRS (hemorrhagic fever with renal syndrome) can be fatal. HPS has a mortality rate of 38%. Depending upon which virus is causing the HFRS, death occurs in less than 1% to as many as 15% of patients. But both of these are also pretty rare, and while some patients have long recovery times of weeks or months, many patients make a full recovery without lasting complications.
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"Hantaviruses in the Americas are known as “New World” hantaviruses and may cause hantavirus pulmonary syndrome (HPS). Other hantaviruses, known as “Old World” hantaviruses, are found mostly in Europe and Asia and may cause hemorrhagic fever with renal syndrome (HFRS)," the CDC website said.
The hantavirus case comes at a time when the total count of those infected by novel coronavirus globally is nearing the 400,000 mark and scientists are yet to find a cure for it. The global death toll has crossed the 16,500 mark.
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I think, you get hanta if you deal with animals.
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Dear friends and colleagues,
there is a very important resource on the web that is "Atlas of Genetics and Cytogenetics in Oncology and Haematology". The Atlas is a peer reviewed on-line journal / encyclopedia / database established in 1997 that collects data about cancer genes, solid tumors, leukaemia and other resources. It is in open free access for readers and there are no fees for the authors.
I'm searching volunteers and collaborators that would to write with me reviews about single genes involved in cancer.
I have published several papers so far and I believe that Atlas is a very valuable tool for us researchers, scientists and scholars.
I invite you to visit the Atlas website at http://atlasgeneticsoncology.org/index.html for more information. Here is my latest article published http://atlasgeneticsoncology.org//Genes/GC_EEF1B2.html to show you my working method. Anyone wishing to collaborate with me to write a specific review on a gene can tell me as well.
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I have research and interests in medical genetics on a less laboratory research results level. I rely on the scientific research in Atlas of Genetics and Cytogenetics in Oncology and Haematology nonetheless. Congratulations on your ambitious and important research project! Best regards.
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Virus latency (or viral latency) is the ability of a pathogenic virus to lie dormant (latent) within a cell, denoted as the lysogenic part of the viral life cycle. A latent viral infection is a type of persistent viral infection which is distinguished from a chronic viral infection. Latency is the phase in certain viruses' life cycles in which, after initial infection, proliferation of virus particles ceases. However, the viral genome is not fully eradicated. The result of this is that the virus can reactivate and begin producing large amounts of viral progeny (the lytic part of the viral life cycle) without the host becoming reinfected by new outside virus, and stays within the host indefinitely.
Virus latency is not to be confused with clinical latency during the incubation period when a virus is not dormant.
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This is quite interesting question!!
latency in COVID-19 is no found i.e. not enough evidence yet. If latency exists then this virus will remain in circulation forever!! This is too early to talk about this in relation to COVID-19. It'll take some time as the epidemic is still going on.
Please also read the article
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Rice is the seed of the grass species Oryza sativa (Asian rice) or Oryza glaberrima (African rice). As a cereal grain, it is the most widely consumed staple food for a large part of the world's human population, especially in Asia. It is the agricultural commodity with the third-highest worldwide production (rice, 741.5?million tonnes in 2014), after sugarcane (1.9?billion tonnes) and maize (1.0?billion tonnes).
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Hey Mohammed Shaker Hossain; After conducting all the necessary trials which involve Stage I, Stage II, Preliminary Yield, advanced Yield Trials, Multi-location trials for the target traits of interests, You need data on DUS which is Distinctness, Uniformity and Stability for this variety and it is supposed to be different from the existing varieties that have been released before. You can even go further to genotype it to develop it's fingerprint for reference in case you want to do a QC/QA.
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Hi everybody
I want to calculate the genetic distance and similarity for ancestral populations. My data is haplotypes.
I appreciate your help.
Best regards
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dear Timo Hellwig thank you for your help. the paper of Joly et al. (2015) seems to be appropriate.
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Oncology is a branch of medicine that deals with the prevention, diagnosis, and treatment of cancer. A medical professional who practices oncology is an oncologist. The name's etymological origin is the Greek word ?γκο? (óngkos), meaning 1. "burden, volume, mass" and 2. "barb", and the Greek word λ?γο? (logos), meaning "study".
Cancer survival has improved due to three main components: improved prevention efforts to reduce exposure to risk factors (e.g., tobacco smoking and alcohol consumption), improved screening of several cancers (allowing for earlier diagnosis), and improvements in treatment.
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For clinical oncology the textbook by DeVita is probably the most comprehensive and clear.
For molecular oncology seek the book by Bruchar. It is a little old but it seems still good.
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For bacterial promoters, everything I read says bacterial promoters are -35/-10 motifs upstream of the TSS, and perhaps UP elements (~ -50 of TSS).
So if I want a promoter sequence for my gene, and I have a predicted TSS, can I just take 100 bp upstream and be done? (in most cases)
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It really depends on the cis-regulating elements that control your promoter. Some promoters extend only over ~50bp (eg mazEF) while some other extend to >500bp (ie csgD, rpoS)
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Genome editing (also called gene editing) is a group of technologies that give scientists the ability to change an organism's DNA. These technologies allow genetic material to be added, removed, or altered at particular locations in the genome. Several approaches to genome editing have been developed. A recent one is known as CRISPR-Cas9, which is short for clustered regularly interspaced short palindromic repeats and CRISPR-associated protein 9. The CRISPR-Cas9 system has generated a lot of excitement in the scientific community because it is faster, cheaper, more accurate, and more efficient than other existing genome editing methods.
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This is a general, simple and basic book: Targeted Genome Editing Using
Site-Specific Nucleases ZFNs, TALENs, and the CRISPR/Cas9 System; Springer publication.
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The use snp information of a population to build phylogenetic tree and to understand genetic architecture is a accepted practice. But literature search doesn't reflect the use of indel information as frequently as snp information. Also the distance matrix calculated from snp information may not be suitable if anyone include indel into such analysis. On the other hand finding high quality indels in a microbe population reflects a possible contribution to the genetic structure. According to my belief, incorporating indel information in such analysis may improve our understanding, but I would appreciate if anyone suggest me any method/model I can use for this analysis.
Thanks in advance.
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Dear Nayak,
To build phylogenetic tree based on InDels and SNPs, you can used MrByse. Please check: http://mrbayes.sourceforge.net/mb3.2_manual.pdf
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Metagenomics is the study of genetic material recovered directly from environmental samples. The broad field may also be referred to as environmental genomics, ecogenomics or community genomics.
While traditional microbiology and microbial genome sequencing and genomics rely upon cultivated clonal cultures, early environmental gene sequencing cloned specific genes (often the 16S rRNA gene) to produce a profile of diversity in a natural sample. Such work revealed that the vast majority of microbial biodiversity had been missed by cultivation-based methods.
Because of its ability to reveal the previously hidden diversity of microscopic life, metagenomics offers a powerful lens for viewing the microbial world that has the potential to revolutionize understanding of the entire living world. As the price of DNA sequencing continues to fall, metagenomics now allows microbial ecology to be investigated at a much greater scale and detail than before. Recent studies use either "shotgun" or PCR directed sequencing to get largely unbiased samples of all genes from all the members of the sampled communities.
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Dear Mohammed Shaker Hossain ,
I have attached some books about Metagenomics. I hope they would be useful.
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Within three years, a patient with a desminopathy (Thr341Pro DES mutation) was found to have a 17% increase in the level of C4 complement components to 0.41 g / l (Norm 0.1-0.4 g / l).
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Dear Yosvany Castillo! Thank you very much for your answer. Over the past 2 years in this patient with desminopathy (Thr341Pro DES mutation in the heterozygous state), the C4 level of the complement component decreased to 0.36 g/l without taking medications.
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Hi molecular biologists, I'm wondering if any of you might be able to help me with a question I have.
I am attempting to insert the DNA sequence coding for a protein domain into a plasmid (the plasmid is popinF). The insert DNA (E. coli optimised) was synthesised by Thermo (and it has passed their QA/QC), and I've successfully inserted it into popinF and transformed E. coli stellar cells, before collecting 3 different colonies from a plate to perform minipreps and acquire the plasmid with inserts. The sequencing results came back for all of them, and confirmed that the full (and correct!) DNA sequence had been inserted into one of the 3 plasmids.
However, I found it very peculiar that one of my plasmids appeared to have my DNA insert, but in a degenerated form with regards to the sequence. In the alignment shown attached, I can clearly see that there is very very strong matching of the sequenced result to the DNA from ~230 base onwards, showing that the synthetic DNA has inserted. But the sequence prior to this region does not show a high correlation to my DNA insert, and I'm wondering how this could be, and what could have caused this? I know that the synthesised DNA must be correct because I've successfully put the full length sequence into another identical plasmid - could it be that this particular plasmid showing a degenerate sequence could have undergone mutations within the E. coli or have degenerated in other ways, and if so could anybody please expand on the mechanisms and nature of these mutations? If anybody has any insight into mutation events of DNA inserts in plasmids within bacteria or knows of any good literature that reviews it and how to avoid them during recombination/transformation, I would be very appreciative for the help!
Thanks very much all,
Rob
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Hi there,
To check the problem is actually due to the proximity with the sequence primer, run an other sequencing with a reverse primer annealing downstream of the 3' cloning site (if the full insert is less than 1kb) or in the 3' region of your insert (if the insert is bigger than 1kb) in order to get the reverse sequence which would contain the proper sequence of the 5' region.
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As there is very little data available for CEP126 gene on databases, i would like to know if there is anybody or any lab working on this gene.
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Antonino Colanzi , Institute of Protein Biochemistry, National Research Council, Naples, 80131, Italy; Telethon Institute of Genetics and Medicine (TIGEM), Naples, 80131, Italy.
Song-Tao Liu , Department of Biological Sciences, University of Toledo, Toledo, OH 43606, USA.
Xiaomei Lu , Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi, 830011, People's Republic of China.
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Why the estimate of human genes is from 20000 to 25000. Can two human being have so different genes numbers, why there is no absolute estimate of the number of genes present in human genome?
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The numbers for the reference genome assembly are a bit fun: 70% of its sequence comes from 1 individual, 23% from 10 individuals, and only 7% from >60 individuals. So actucally a "consensus" applies to a minority of its sequence. But the true consensus genomes and graph genomes are making their way.
This is a nice read:
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I have found variants in a gene in which I have done in-silico analysis for and it is thought to be disease causing. If I want to study these variants more and see their effect, would it be justified to mimic them on animal model?
there seems to be lack of studies on specific variants or mutations in that gene, but there have been a lot of studies on knockout mouse models that makes it kind of known for us what would happen if the protein has a disfunction or not functioning at all.
So I am thinking, animal model and study the variants? Or to use cells and check if the gene will be dysfunctional and report it that way only ( and then explain what we think the outcome will be based on the status of our subjects who have the mutations and the published papers of the knockout mice)??
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Hi
If I summarize your question , you mean that you found novel variants in known disease causing genes? If the clinical phenotype of patients is same as that of previous patients with other variants then it can be published and reported as allelic extension. If gene function is well documented then no need to check it on animal model. Just good insilico tools for pathogenecity checking would be ok.
Go for animal models if the gene is novel in implication of a disease and you have multiple patients with similar genetic defect.
Hope it helps
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It is often assumed (see first post below) that human evolution relied on new mutations. Whilst not doubting that this process can occur, why is it necessary to assign it any major significance? When we migrated out of Africa, all the pre-existing genes for adaptation to warm climate would have become rarer, and those useful for cold climates would have become commoner. This can all be explained simply by genomic reorganisation without needing to assume any new mutations.
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Hi Anthony, not only human, but all evolution depends on the occurrence & selection of recombinations & new mutations. Human evolution was no exception in biology, but seems to have been rather special, please google "two incredible logical mistakes 2019 verhaegen", of see attachment + refs therein.
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for interspecific and intraspecific
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Who gives the last word about the evolutionary process, genetics or ecology?
In other words, are ecological interactions driven by any genetic phenomenon? Or is it genetics that has been molded by ecology?
[I’m a Brazilian biologist and writer. I write about science – I have just released a new book, O que é darwinismo (What is Darwinism, in Portuguese) – and would like to know the opinion of colleagues from other countries (from any field of scientific knowledge).]
See also What do you think about fitness, adaptation and natural selection? (http://www.fondpageant.com/post/What_do_you_think_about_fitness_adaptation_and_natural_selection)
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Nobel Prize winner Niko Tinbergen observed in his now classic 1963 paper, "On the aims and methods of ethology" (Zeitschrift fur Tierpsychologie 20: 410-433) that in order to adequately analyze observed patterns of behavioural ecology in a species, it is necessary to distinguish between *ultimate* and *proximate* causative factors. Ultimate factors include: i) the *function* (or "adaptive value") of a behaviour, and ii) the "phylogeny" (or evolutionary history) of a behaviour; proximate factors include: i) *ontogeny* (or behavioural changes related tp growth and development), and ii)*proximate conditions* (i.e., that which has happened in the recent past and that which is going on under current ecological conditions). So, what is needed in trying to gain insight on biological evolution is an holistic perspective that incorporates *both* genetics and ecology. A perfect example of the value of this integrated approach is the need for up-to-date data in both the genetic and ecological realms in order to deal with conservation biology issues.
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I would like to have the insight and opinions of people within the field before I apply for colleges or seek transfer options. Also, is it a good idea to study molecular biology in german rather than english?
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Here to know!
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I have prepared a nj phylogenetic tree using ape package in R. But due to large number of sequences and taxa, the tips of the tree looks overlapping. How can I increase the distance between the branches, so that my tree can be viewed properly with all the tips?
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You may find it easier to just view the tree in a graphical tree browser: http://tree.bio.ed.ac.uk/software/figtree/
Output using ape write.tree, then import to figtree
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How do you do to design an assay with primers and probes that function well and what program/platform do you use?
I'm using AlleleID now but I wanna try any other ways to design it.
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How can I optimeze a protocol like this? Shen-An Hwang
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I still get Non-specific products & multi-peak Melt Curves despite changing the annealing temperature of my designed primers several times (58C, 59C, 60C, 61C, 62C, 63.7C & 65C).
I've also changed other parameters like the concentrations of DNA & primers, however, i still get these Non-specific products & multi-peak Melt Curves. Are there other factors that i can change to get rid of them?
Thanks in advance.
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  • Have you tried optimising your products by standard PCR (at different Tas) and running products on a 2% agarose gel in order to confirm specificity for subsequent qPCR
  • In all honesty, if you are having recurring problems with multiple products at multiple annealing temp the best thing you can do is re design your primers
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I'm looking for a software that can compare a bacterial clone with the reference genome to identify some changes in genome content (Deletion/insertion/substitution).
Thanks.?
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Snippy is the best but still under optimization
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By our avidity, weaknesses, desires, fears, and ignorance, due to economical models based on over-consumerism, we are creating our misery and the misery of many living beings.
We are so confident, Arrogant and Ignorant that we believe that we can safely regulate the climate of our planet. But since we are Human beings before we recognize our mistake it maybe too late for the many to live and a few would just be happy about living with robot bees, AI, and genetically modified living beings.
For the benefit of the many, what path would you like to choose? Business as usual or proceed an economical, social, and ecological paradigm shift?
As a starting point, in May 2011 the OEDC started measuring successful societies utilizing the-so called 'Better Life Index':
However, it excludes many other successful societies or some quite large countries.Further, its methodology and epistemology can be questionnable and some parameters maybe hidden or don't contribute actively to answer the current question.
Thank you in advance for sharing your experience and expertise.
All your comments are welcome.
Kind regards
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What are the common points between societies that are successful economically, socially, and ecologically?
They put more value added in developping products and in procucing these products than in marketing/distributing them.
As long as it will be the opposite it cannot be sustainable, since in this opposite case the life cycles cannot be respected.
Kind regards
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A patient with hereditary desminopathy (Thr341Pro DES mutation in a heterozygous state) was recommended to refuse toothpaste. He continued to brush his teeth twice a day with a toothbrush with only water. As a result, within one month we noted a significant increase in strength and muscle mass in this patient. The patient did not take any medications during this period. After 30 days, the muscle condition returned to its original level. How can this positive effect be explained?
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Another possible explanation would be that the patient's refrain from using the toothpaste lead to an increased level of plasma nitrate, which helped improve sympatholysis; thus, alleviating (possible) functional muscle ischaemia.
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I'm currently studying a family with a huge duplication which encompasses a tissue-specific enhancer element. Therefore I want to investigate the effects of such duplication.
I was wondering whether it is possible to use a luciferase assay to do so. I could make a construct with a tandem duplication of the enhancer element, insert into a plasmid and see if there is any difference between the contruct with only one copy of the enhancer compared to the one with two copies.
I also brainstormed a few other strategies, like a CRISPR;Cas9 assay to remove the duplication, but since it is a 400kb duplication, I guess it's not that trivial.
Thanks a lot!!
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I agree to Shawns comment. Additionally see alternative literature dealing with a comparable issue (CA repeats eNOS or ESE/ISE Tissue Factor splicing).
See:
a) Lorenz et al., FASEB J. 2007; 21(7):1556-64. ( )
b) Tardos et al., J Thromb Haemost. 2008; 6(5):877-84. doi: 10.1111/j.1538-7836.2008.02946.x.
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When working with eDNA we sometimes face some contamination, and it may lead to false-positive or negative, and I think if some of these cases, it creates a problem, or it may be interpreted as a grown on robustness, cause if we are using universal approach, we should be capable of finding any DNA sequences, like human DNA contamination, so what do you think about it?
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Abhijeet Singh I have some other questions on my page and a discussion where there is something that I think your opinion could really help me.
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In trees we do controlled pollination in a Diallel mating design to produce F1's and observe the characters of progeny. Can we consider the pod and seed produced after controlled pollination as F1's and include in analysis.
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It may depend on flower structure. I am presenting two situation.
1. Making crosses in rice involves chopping off of of lemma and palea to expose anthers. This result in naked seed that has to withstand unusual nourturing environment during development. And hence various aspects of f1 seed may not be a true genotypic reflection say length and width of seed.
2. Making crosses in maize is not destructive as in case of rice particularly to female flower or cob. Here, seed develop during quite normal gestation environment. And various seed traits are true genotypic reflection. Eg. Endosperm colour, genia effect etc.
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Seeds obtained from heterozygous T0 mutants obtained through CRISPR CAS9 were sown and the plants raised were properly genotyped. Following normal segregation pattern, T1 generation had WT, heterozygous and homozygous plants. The homozygous were not producing normal seeds but strangely few (2 in many) produced more than 50% normal seeds, when those seeds and the plants raised from them were genotyped they were found to be heterozygous. In T1 I ignored this (thinking that T0 plants from CRISPR CAS9 might carry chimeric mutation for the gene).
To get T2 generation, seeds obtained from T1 heterozygous were planted, but T2 homozygous plants also had such plants. The situation even continued to the next generations. I am wondering what might be the cause. I know that cross pollination in rice occurs to small extent but if that is the cause then all homozygous plants must bear small number of such seeds. In this case homozygous usually don’t produce normal seeds at all, unusually few homozygous bear normal heterozygous seeds. Your suggestions will be highly appreciated to explain this situation. Thanks.
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Any update on this further? Any possibility of outcrossing as you said the homozygous do not prouduce normal seeds (may be defect in male part). This increases the chances of outcrossing.
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what are the genes that I can detect to determine the ones who have genetic predisposition to become thin and underweight, and how I can help them depending on their gens?
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Please take a look at this useful RG link.
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Hello there!
I am planning to run high throughput imaging of conjugation experiments, and was therefore thinking of doing these conjugations in 96-well plates.
Since it is very troublesome to make such plates by myself (agar solidifying, bubbles forming, etc), I wanted to ask if anyone here knows of a company that can provide agar-filled 96-well plates?
If not, any tips on making it easier to produce them myself?
Thanks a lot, and best,
Stephan
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hi stephan, what purpose do you use this 96 well agar plates,
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I would like to identify particular gene/(s) that regulates the expression/pattern of structural and functional connectomes. Is there any? If so, which one? I would appreciate your suggestions.
Thanks in advance.
Md. Mamun Al Amin, PhD
Stark Neuroscience Research Institute
Indiana University, Indianapolis
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Thank you. I will try.
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I would like to invite everyone interested in the subject of machine learning in life science, to test APMC module, it`s a fully automatic tool (created by students) to simply create and develop supervised machine learning models for classification and regression purposes. Links to tool, instruction and documentation bellow:
best regards!
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APMC has prospective future we will see soon!
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In a patient with hereditary desminopathy (Thr341Pro DES mutation in the heterozygous state), a significant loss of muscle mass is observed after a night's sleep, with its replacement by adipose tissue. How to reduce muscle loss during sleep?
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Dear Ali Javadmanesh, Adrian Fierl, Abdulnabi Abdullamer Matruod, thank you very much for your answers!
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I would like to know if results for copy number variants from pharmacogenetics testing labs typically are specific for allelic variants.? For example,could the result reported as CYP2D6*1/*1N4 actually be CYP2D*1/*4N4?
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Yes, it definitely could be CYP2D*1/*4N4
It's quite important to list all tested SNPs. If rs3892097 wasn't genotyped then we couldn't distinguish *1 from *4
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Dear Scientist,
I kindly plead for any one who has an idea on this to clarify me. I ran a two way ANOVA with data collected from two locations and got no location X genotype interaction, then a reviewer is requesting me to present represent replication within location effect and triplicate within sample effect.
Please, can any one give an idea on this? I use XLSTAT to run the analysis.
Thank you
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The attached image is of model parameters. Presenting this may also be helpful but this is not what the reviewer is asking. The reviewer is asking for differences between pairs of species within location A and differences between pairs of species within location B.
You have not done anything wrong. All you need to do is to provide the output of pair-wise comparisons from XLSTAT.
For example: At cite A. The species differences are:
Specie 1 - Specie 2 = 10.24 - 16.29 = -6. If you get this from XLSTAT, it will also give you standard error, confidence intervals and z-values and p-values.
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We are studying on genetics of Hippophae rhamnoides L., sea buckthorn. We are using one Chinese cultivar. We know the cultivar name in Chinese letter. But we don't know it's spelling in English. How can we know the alphabetical spelling? For example, are there any lists of sea buckthorn including Chinese cultivar?
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Hippophae rhamnoides has several subspecies, one of the is subsp sinensis.
Chinese seabuckthorn has more carotene than others
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Hi All,
I am trying to generate a bacterial operon construct. I have designed four gBlocks (each of which is ~1.7 kb) and synthesized them from IDT. I am using pGex-6p-1 vector to assemble these gBlocks using Gibson assembly. I prepared my vector by PCR (primer designed by NEB builder software). After PCR amplification, I checked 5 ul of my PCR product in the gel and found a nice clean single band and the size of this band matches to the expected size (for details see the attached PPT slide). After that, I purified the PCR product using Promega PCR and gel purification kit. I eluted in 30 ul of nulcease free H2O and then measured the concentration of PCR product using NanoDrop and the concentration was 296 ng/ul. Then, I digested 8 ul (296 ng/ul) of purified PCR product with DpnI (1 ul) in a 10 ul of total reaction volume (and incubated at 37oC for 30 mins) as suggested by NEB Gibson manual and heat inactivate the DpnI at 80oC for 20 mins. After that, I set up a Gibson assembly following the instruction of NEB Gibson manual. I incubated the Gibson reaction at 50oC for 1 hr in a PCR machine and then transformed 2 ul of assembly reaction in 50 ul of NEB 10-beta cell (High efficiency) following the transformation protocol for NEB beta cell as specified by NEB. In the following day of transformation, I found many colonies (see attached PPT for picture). I took five well separated colonies and then grew a 5 ml overnight culture. After that, I isolated plasmid DNA using Promega plasmid purification kit and digested them with SalI-HF enzyme which should give three bands if there is a assembled product. Otherwise, they should produce linear vector as pGEX-6p-1 has an internal SalI site. I then checked 60 colonies by colony PCR and it seemed that all of the colonies I checked by colony PCR contains the intact pGEX-6p-1 ( I did not include this gel image in the PPT slide). What things might be wrong with my cloning? Specifically, I would like now
i) Why I am getting intact pGex-6p-1 whereas I generated the linearized the pGex-6p-1 by PCR and digested the PCR product with DpnI? Is digestion not working??
ii) What might be the good way to assemble these four gBlocks into pGex-6p-1 vector?
iii) How can I reduce the vector only background?
iv) I would also highly appreciate any suggestion on my strategy that I am using to generate this operon construct.
For details description of my cloning strategy, please see the attached PPT slides.
Thank you all,
Hassan
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Simple question, but did you design all of your gblocks with the appropriate overlapping overhangs?
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As nutrigenetic and nutrigenomic understanding is increasing should resources still be spent on developing population-wide recommendations for longevity, prevention of chronic disease and treatment of chronic disease?
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In short, yes. Vaguely, there has to be a baseline set of recommendations; a starting point if you like. This is to be tailored downstream, on a personalised fashion, to meet individual needs that derive from interindividual genetic variations. By default, treating an individual entails tailoring general recommendations to meet their needs, and for example consider an acute scenario of an ICU patient receiving TPN. Bearing in mind that the practice of registered practitioners is not only evidence-based, but also governed by professional codes of conduct and national recommendations (e.g. National Institute for Health and Care Excellence in the UK), I believe that the real question is how much value does nutrigenomic and nutrigenetic information really add in everyday practice.
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I am looking for a gold standard list of genes that are well recognized to have no association with cancer. Is there such a list publicly available?
Edit: a list such as this will be useful for understanding which genes should/can be excluded from genetic analysis to decrease multiple hypothesis issues.
Edit 2: I agree and further am trying to show that absence of evidence is not evidence of absence. A list of well agreed upon genes without association to cancer would be helpful in my analysis because I will be able to roughly calculate statistics such as Specificity and Diagnostic Rate to determine how well the analysis is declaring genes of interest.
It is a good point that excluding genes upfront does introduce a bias, however, the list would be equally as useful to have on the back-end of the analysis for statistical reasons.
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I doubt if a gene not yet reported to be associated with cancer now really means it does not truly has any connection with tumour development. GWAS has done a great job indeed, and through their outcomes of studies you may get some info, but your choice of word "gold standard" is a clear bias to your study.
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I have several microarray gene expression datasets, but they use different naming systems for the probes. What are some simple ways to convert all the probes to the same type (e.g. Affymetrix)? Thanks.
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Hey there,
Here you can easily convert different naming.
Hope this helps.
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I'm trying to understand epigenetic variability but the study I'm performing involves measuring the gene expression in a given region according to the SNP's alleles associated with the increase of that gene's expression. But epigenetic is related to heritable variations that affect the phenotype without affecting the DNA sequence, so can SNPs be used in this study?
I'm new in the genetics field and really confused in this matter, any help would be appreciated! Thank you
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Parham has given a correct answer, SNP is not an epigenetic modification, it's a genetic modification, it's a mutation. But SNP could be an excellent marker to correlate different levels of allele expression and allele structure. Even though the SNP could not be directly responsible of this variation in expression level, it can be linked to other mutations on the same allele sequence so giving the opportunity to establish the causal relation.
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Dear All
I have a wheat genotype. I would like to treat is with a chemical substance then I would like to see the difference of DNA sequence between with and with out treatment to answer
what are the changes and where do happen (position on chromosome)???
Any guide of which method should I use
thanks in advance
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Thank you for all
Appreciated
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Please respond to this quote above. This was written to me in response to a discussion on biological species concepts and evolutionary
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Hello Asif; If you intend to reply, think carefully about what your goal is. I used to engage in exchanges like the one you anticipate. I mistakenly thought that if I could explain some aspect of evolutionary theory or some particular data set, then I could help the person understand the general idea. That doesn't seem to be true. The issue is an ideological one, not a lack of information. Some years ago I wrote an essay intended to help science teachers with exactly this problem. Its title is "The Creation/Evolution Dispute: a Teacher's Handbook". Look it up on ResearchGate. Best regards, Jim Des Lauriers
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Prediction softwares especially with respect to structure and function
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I found the TransDecoder and also txCDSpredict. best.
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Mack et al studied subtypes of three ependymoma(same histopathology) brain tumors and found that one subtype carries an intrachromosomal translocation that creates a new tumor-driving gene, another lacks tumor-driving mutations but has aberrant epigenetic modifications, and a third shows neither gene mutations nor epigenetic aberrations. There were three genotype but one cancer phenotype. Similarly Martincorena and colleagues found thousands of mutations in cancer-relevant genes, including cancer-driver genes, in normal eyelid epidermis .(multiple cancer genotypes but no cancer phenotype).
In disparate classes of biological systems, there are more genotypes than phenotypes. Where sufficient information exists to enumerate these phenotypes, there are exponentially more genotypes than phenotypes, as a function of the number of system parts. This means that any one phenotype typically has many genotypes that form it.
In a brief, cancer is the decision of the cell to choose the innovative/adaptive phenotype and understanding the genotype does not mean understanding cancer.
References
1. Mack, S. C., Witt, H., Piro, R. M., Gu, L., Zuyderduyn, S., Stütz, A. M., et al. (2014). Epigenomic alterations define lethal CIMP-positive ependymomas of infancy. Nature 506, 445–450.
2. Martincorena, I., Roshan, A., Gerstung, M., Ellis, P., Van Loo, P., McLaren, S., et al. (2015). High burden and pervasive positive selection of somatic mutations in normal human skin. Science 348, 880–886.
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Answer of the question
Cancer is name of the a kind phenotype not genotype
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How to calculate PIC Polymorphism information content?
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Thanks for all
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I am planning an experiment where I will integrate an operon construct in the gfc locus E. coli using CRISPR-cas9 mediated homologous recombination. To insert my operon construct in the gfc locus, I have included a portion E. coli endogenous gfc sequence on either side of my operon construct so that homologous recombination become induced upon induction of Cas-9 mediated double-stranded break at the gfc locus. However, my worry is that presence of gfc locus in my operon construct might create problem during cloning as the gfc sequence should also be present in the E. coli strain commonly used for cloning. It may be that portion of gfc in my operon construct and one that is present in E. coli cloning strain might undergo recombination and make this construct unstable and difficult to made. Initially, I planned to synthesize them from a company, however, later I feel the company might face the same problem. I have only 5 months to complete my project and thus I am looking for an efficient and quick way of making my operon construct. Any suggestion on how can I design a better strategy to make this construct will be highly appreciated. For easy understanding, I have uploaded my construct design here. Thanks.
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Go ahaed and don't worry! As already stated E. coli strains used for cloning are specifically engineered to be RecA deficient.
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I would like to know if there is a supercomputer or a server machine, which is free to access, and can run the STRUCTURE software (https://web.stanford.edu/group/pritchardlab/structure.html)? I mean like Compute Canada (https://www.computecanada.ca/) or something similar. Maybe in a Windows environment? Your comments and suggestions would be greatly appreciated.
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One of my rice mutant produce more than 50% seeds as empty seeds. The seeds when opened look like in the attached picture. Can anyone explain the phenotype in the attached picture. I am not sure if this is because of embryo development or endosperm development or fertilization problem?? .
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I think the reason for the failure of fertilization
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It's known that the yeast Saccharomyces cerevisiae does not have P450 enzymes required for biotransformation of exogenous compounds.
However, many pharmacological and toxicological studies utilize yeast as a model organism.
Does anyone have an idea on how yeast cells metabolize these chemical agents before they exert their biological activity?
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Depending on the structure of the xenobiotics, other mechanisms such as GST conjugation may be responsible.
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Dear my professors and colleagues,
I prepare a review about use biotechnology and molecular marker at poultry breeding.
I want your help.
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Hello Dr. Esteftah
I recommend for you the following chapter
"Selection Methods in Poultry Breeding: From Genetics to Genomics"
Good Luck
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My question is based on conducting a meta-analysis on the association of multiple variants in a single gene with a complex disorder using published case-control studies.
For my study, around 5 well-studied SNPs in a single gene have been widely reported to be associated with a disorder as single SNPs or as haplotypes (two up to five SNPs in LD varying between different studies).
If I wish to explore associations of a 3-SNP haplotype with the disorder between studies, can I extract data from studies that only report 5- or 4-SNP haplotypes (that include the 3 SNPs) in association with the disease?
Edit: Thank you for your answers.
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I have only a limited experience with that subject, but SNP alleles could be found associated in LD in such a way as to suppress the main phenotypic effects of only one of them (and YES, thay could be in HW equilibrium, at least in ancient populations). I would be very careful about extracting data of three out of five SNPs if no validation is possible by any experimental approach. Try estimating MAF for each of them could be of help.
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good gathering
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Has anybody had any informative research documents about the Armageddon?
Some people write that it will break out in Aleppo, Syria in 2023.
I try to find any research article about that.
Where? When? How? Which countries? etc.
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Hi All,
Thank you for all your support.
Thank you chandra mohan , Christian Janiesch and Ramin Sedaghat.
Looking for more published projects where students can get benefited by referring these documents.
Please share the docs directly into genotech.in@gmail.com or reply me here.
Regards,
Ranjan
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Hello, there were many aspects in microbiology which need more detail study till now we have information only about 5% of total biodiversity of microorganisms. So 95% is future work!
Good luck!
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Hi , I am an assistant professor in the dept of Orthodontics in a central university in India. I am noticing an increased incidence of cases of impaction in the population we are serving here. I would like to do a genetic study on the genes responsible for impaction. What is the kind of study I should plan ?
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The etiology of dental anomalies is partly environmental and partly genetic. Because of the polygenic nature of dental characteristics, it is very challenging to identify one single defective gene responsible for a specific dental anomaly. However, recent studies provide new data about the candidate genes. Further studies are required and the rapid progress in the field of genetics may help the clinicians to more accurately discern the environmental and genetic factors contributing to the development of dental anomalies. Currently, the orthodontist, probably the first to diagnose hereditary dental anomalies and malocclusion of an individual, will remain responsible for the detection of any additional defects in the same patient in order to provide the best treatment. The clinician should always keep in mind that some of those dental anomalies can coexist with certain syndromes and other family members might also have been affected. Whenever it seems necessary, a genetic consultation should be added as part of the orthodontic treatment. Finally, this interdisciplinary approach may help to reveal any risk of recurrence in subsequent generations.
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The purities of my genomic DNA samples range between 1.51 and 1.71 at 260/280nm wavelengths.
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