text:
Are there any mutagens that can undo the mutations they cause?
I was reading a section from my textbook about tautomeric shifts, and it seems to suggest that there are some mutagens that can be directly responsible for the phenomenon. The section is mainly describing spontaneous mutations as opposed to induced mutations, and examples of mutagens are mentioned. However, the author explicitly states that the sort of changes made to DNA due to spontaneous mutations also occur at a higher rate during induced mutagenesis.
If a tautomeric shift can occur due to mutagenic activity, is it possible for the mutagen to undo and "correct" the mutation by reversing the shift? If so, what kind of chemicals or physical mutagens (e.g. radiation) would be involved?

It is possible but extremely unlikely.
When a base undergoes tautomeric shift the DNA does not contain a mutation yet, just an unmatched pair. The mutation will only becomes inscribed into the DNA permanently after the DNA is replicated or wrongly repaired.
In order to reverse the mutation you would need to provoke a chemical change to that specific base using the same or another mutagen and as most of them are unspecific the likelihood of obtaining both the correct mutation to reverse the effect AND at that specific location is extremely low. Just for the location itself (i.e. that base pair), in human you have ~0.000000033%  chances (1/3 billions) to mutate that base. This is assuming equal probabilities across the genome and a single modification event which is of course not true but shouldn't modify much the conclusion. I am not even speaking about provoking the chemical modification that will reverse it which will even further reduce that probability.
Such induced or natural mutations will actually only rarely appear in the genome permanently as the cell has multiple DNA repair mechanisms (see this wiki). So in this case the modified base does not need to be reverse as the cell will make sure to repair it directly but using mechanisms not based on mutagenesis.

So near-zero probability aside, the mutation reversal can occur. Would this require the mutagen to be nonspecific (like UV or gamma rays)?

The opposite. If you have an insanely specific mutagen that only mutates one base in particular it's about 1/8 or so probability to undo its own mutation, but a nonspecific mutagen has a much lower chance. Real specific mutagens don't really work like that, but the same principle applies.

I just finished reading a section describing photoreactivation as a means of repairing a mutation. In addition to this, the wiki page linked by @cagliari2005 mentions that the enzyme involved in the process can be activated by light in the blue/UV range. However, the page on photolyases says they require visible light for activation. Any ideas as to the discrepancy? Also, thanks for the replies, much appreciated!

@user170231 Post a new question ;)

No need, I just answered my own question after a bit of reading :) Thanks again


text:
How is excretion of metabolic wastes from a cell related to its size?
As with anything that is taking place within a cell, the metabolic waste too must be proportional to the size of the cell. In particular the surface area to volume ratio. But how is the waste excretion related to the concept of above ratio and how to determine it?

@AliceD Yes it's an active mechanism. I am not sure about the compounds, but this is a type of a question that was asked in a pre-college course material right after introducing the two main cell kinds. And I am just starting to scratch a tip of an iceberg - reckon...as bio is a new area for me.

If smaller cells have any measures to cope with waste then large sized cells should have that mechanism improved much more to facilitate the extra waste production. This is an opinion.

@Jay - no that is a wild guess :)

@Alice and Jay: this is where the question is listed., page 16. As far as what I understood, the larger animals don't mean larger cells but more cells. The question is pretty confusing to me. And btw, I didn't add that last sentence, someone else seemed to have editted it...

The critical element here is that building materials that need to be absorbed, or waste materials that need excretion have to cross the cell membrane. The larger the surface of the cell's membrane relative to its volume, the faster the exchange rate.
The book section you linked in the comments mentions the following on p.14:

The volume [of a spherical cell] increases by a factor calculated by cubing the radius, [...] the surface area increases by a factor calculated by squaring the radius. [...] This means that a large cell has relatively less surface area to bring in needed materials and to rid the cell of waste [...]. Cells are limited as to the size they can attain [...]. Cells that are larger [...] have modifications that allow them to function efficiently. This is accomplished by shape changes such as from spherical to long and thin, [or] have infoldings or outfolding to increase their surface relative to their volume.

I guess this concept is trying to convey the message why cells are small or why cells are made small and how cells take different shape to maintain this ratio?

@bonCodigo - yes correct, as well as how they can grow big and still be functional.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What is this pink-flowering plant found in Shanghai, China in March?
This plant appears to have fleshy protrusions resembling flowers growing out of its stem (although I am unable to identify them as such).
Does anyone know the identity of these plants?

I think this is the Chinese Redbud (Cercis chinensis), see this image (from here):

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Do all kind of unicellular asexual reproductions let mutations happen, resulting in evolution?
I know about fission, an unicellular asexual reproduction method, where the mother cell splits into two daughter cells. Does this kind of asexual reproductions let mutations happen, leading to much needed evolutionary process? Is it same for all unicellular asexual reproductions?

It is not essentially asexual reproduction that causes mutations. Mutations can be caused because of errors in DNA replication which can happen during both mitosis and meiosis.
Mutations can also be caused because of error-prone DNA repair mechanism.
Other than these intrinsic factors there are physical and chemical mutagens that alter the DNA or accelerate the intrinsic mutagenesis mechanisms.
These mechanisms are universally common for all living organisms (that we know of :P ), however, their tolerance to mutagens and rates of intrinsic mutagenesis may vary.
Have a look at this post too.

I don't know whether my choice of word "facilitate" was right. Can mutation happen in fission?

Mutations occur during the process of DNA replication (as well as at other times). Of course, DNA replication is necessary for fission.

@Gulshan Cellular fission (or cytokinesis) is preceded by DNA replication. Even during the formation of gametes (sperm and ova) DNA replication happens which is followed by some steps that are not present in the asexual cell division or mitosis. Click on the links in the above answers; you'll find all the relevant background information.

I can think of two kinds of asexual reproduction- i) each item of the mother cell is copied to daughter cell. ii) only DNA is copied from the mother cell and rest of the items are constructed from new DNA. I think, mutations can happen in both cases. But only in the second case, the mutation will result to a physical change of the new cell, thus making it subject to evolution. Is my idea alright?

@Gulshan DNA replication is a prerequisite for cell division. Any mutation in the DNA will be inherited and expressed in the progenies. There can be asymmetric distribution of cellular components but DNA is always replicated and each cell receives a copy. Read about cell division; your doubts will be clear.

Replication will always be there. But would the translation from genes to actual physical attributes happen in all the cases? As, all other components are directly being copied from mother cell.

@Gulshan Other components are dependent on the DNA; there is a constant turnover and the stock inherited from the maternal cytoplasm will not last long. Please go through the basics before arguing on a hypothesis. Not all mutations are translated to phenotypic effects. It would take much more than a comment to explain why.

Actually I do not know these things. I just wanted to be sure about my assumption.


text:
Why do apples taste sweeter at the bottom?
Sometimes when eating an apple, I notice that the bottom (blossom) end of the apple has a lot more sweetness and flavour to it, whereas the top half (stem) is often more watery, crispier and feels less dense than the bottom part.
A quick search on the internet revealed that I'm not the only one asking this question, but answers seemed to be mainly opinions. The largest discussion I stumbled upon can be found here, but comes to no satisfying conclusion.
Apparently, this phenomenon seems to occur in pears (supposedly even mentioned in a japanese saying, but the article does not provide a solution to the question) and pineapples as well.
I am looking for a more scientific explanation, as I believe that the biology of apples might be more complex than to allow a simple "sugar is denser than water and gathers at the bottom"-solution.
Do apples ripen unevenly (the blossom-end growing first, allowing it to ripen for a longer time)?
Might this phenomenon be the result of how apples meant for long-term controlled atmosphere storage are picked slightly less mature?

I was always taught that it's an example of dependent evolution. Fruit with higher concentrations of sugar at the blossom end are easier for bees to get to.

For whether or not your assumption is correct, I have found the following (here), which states that sweetness indeed differs, as well as pH level:

The bottom sections of ‘McIntosh’ apples were sweeter; whereas the bottom sections of ‘Jonagold’ were less crisp and more fruity.
  The bottom sections of both the ‘McIntosh’ and ‘Jonagold’ apples had significantly lower pH than the top.

Fruits consist of two main parts, the pericarp and the seeds. The pericarp can be further divided into the followings: exocarp, mesocarp and endocarp. In the case of apples, the one responsible for composing most part of the fruit flesh is the mesocarp, so I would like to disregard the other two. The mesocarp consists of ground tissue almost exclusively[1] and no vascular system, thus the only way for sugars to travel inside the flesh of fruit is diffusion, which is mostly determined by gravitation, hence the result.

I haven't find any hint in the reference about the rather surprising fact that diffusion of dissolved sugar inside an apple is determined by gravitation.

The reasoning behind this answer seems flawed. Why would a denser solution travel 'inside the flesh of fruit' mainly through gravity?


text:
Differences between Gradualism and Uniformitarianism
From what I understand, gradualism is the idea that small changes affect species over time. Uniformitarianism argues that the same processes that occurred in the past are the same as those in the present.
Does gradualism state that these small changes are constant over time? In that case, it isn't much different from uniformitarianism.
I'm thinking that the difference that uniformitarianism allows for catastrophes and supports Aristotle's scala naturae, while gradualism makes a point for evolution due to its theory of slow processes.

Gradualism is the view that large-scale changes occurs by the accumulated effects of small changes over long periods of time, rather than by rare cataclysmic events of massive effect.
Uniformitarianism is the view that the same forces that shaped the world in the past continue to operate today. Historically, uniformitarianism has often included aspects of gradualism (i.e. definitions by Lyell), e.g. by assuming uniformity of rates. Uniformitarianism was also originally proposed as the opposite of Catastrophism. However, in modern use, the focus lies on uniformity of processes, and rapid catastrophic changes are allowed under uniformitarianism. Also note that the term Actualism is sometimes used for modern interpretations of uniformitarianism.
If we posited that early evolution occurred by small Lamarckian changes and current evolution occurs by small Darwinian changes, we have a model that is gradualist but not uniformitarian.
If we posited that the earth's topography was formed by meteor impacts and massive tsunamis, in sharp sudden strokes of massive effect, but acknowledged that these same processes occur today, we would have a theory that is uniformitarian but not gradualist.
(I don't understand what you are asking in your last paragraph, or how this relates to your main question.)

I think in the third paragraph you mean gradualist but not uniformitarian.

In my last paragraph, I was asking if the two views supported or denied evolution. For me, it seems that gradualism argues that small changes over time are accompanied by changes in populations. I'm not sure about uniformitarianism, though.

+1 @Corvus I added a couple of historical clarifications and terms to your answer and hope that you are fine with them.


text:
Which sources can I use to study botany and horticulture?
I refer with this question to those among you who have a strong background and work in fields like: botanics, horticulture, dendrology, etc.
I would like to start building a solid preparation, both practical and theoretical, in horticulture, with a strong scientific background.
I am a physicist at the moment, but I am trying to lay the basis for a career switch. In September I will attend the RHS courses, but in the meanwhile I would like to start studying something on my own.
Is there any introductory, basic, read that you would suggest? Also, if any of you have in mind a sort of "curriculum" (in terms of subjects, books, etc.) or would like to play with it, this would be of great help! Thanks a lot :)

I had an earlier version of Raven's Biology of Plants for botany/plant physiology classes and liked it, and the current version should be a very good start. Here is a review of the current version of Biology of Plants from Annals of Botany.

I like 'Plant Physiological Ecology". Thijs Pons is one of the authors.

This book could be a good start: Botany by Mauseth. However if you don't have any knowledge about biology I suggest you to get starting with the basics of cellular biology. A good book could be "The cell" by Cooper, you can find it in electronic version.  There are many books about cellular biology but I recommended this because it is complete and detailed without being too long compared with others.


text:
Which is the guideline to choose a molecular target to identify vertebrate hosts from arthropod bloodmeals?
There are some molecular targets to identify vertebrate hosts from arthropod bloodmeals including the Cyt b gene and the COI gene. Which are the standards or characteristics that I have to bear in mind to choose a molecular target to identify host blood from mosquitoes? I would appreciate your help.

I have looked about the topic and I have asked experts and the best aproximation to know the vertebrate host from arthropod blood meals is targeting mitochondrial genes because you can get clean sequence data due the fact that only one allele is present rather than two.
Within the mitochondrial genome, you should select a gene which has been widely sequenced for most vertebrate species you are likely to detect in your region, other wise you will have many unknown identities among your bloodmeals. Really, there are just two choices that match these criteria: cytochrome oxidase I (COI) gene, which has been used by the Database of Life project; and cytochrome b, for which sequences are widely available (i.e. for many vertebrate species) in GenBank. If you get a negative result for one, you can try the other. Primer sequences are widely available in the literature.
In conclusion, you must be target COI and Cytb genes to assure the host identification and prevent a unidentified match in Database of Life project or GenBank.
I give you a paper example to review the metodology: Host Preference of the Arbovirus Vector Culex erraticus (Diptera: Culicidae) at Sonso Lake, Cauca Valley Department, Colombia


text:
Does taking a shower have the same effect on muscles as warming up?
When playing sports, coaches and trainers are always very clear that it is necessary to warm up and stretch. But sometimes athletes sometimes want to get an extra stretch in and don't want to go through the hassle of warming up.
Will taking a hot shower warm up muscles or does an athlete sctually have to do physical exercises like jogging in order to be ready to stretch?
I know this sounds like a question I could go on the physical fitness SE, but I'm really hoping for an answer involving thermodynamics and I doubt I'll get that there.

Hot shower will definitely affect your muscles health. Hot water shower results in Vasodilation,which will decrease the vascular resistance and allows blood to flow easily through the blood vessels. As the vasodilation (increase in diameter of blood vessels) allows blood to move without resistance and which in turn nourish the tissues with sufficient oxygen and nutrients. Also it affects in the removal of metabolic wastes from cells. There is another process called  Vasoconstriction (decrease in blood vessel diameter) which makes the blood vessels to contract and may lead to increased blood pressure.
There is a technique called as Heat therapy which will be effective in muscle and body health.

Heat therapy, also called thermotherapy, is the use of heat in
  therapy, such as for pain relief and health. It can take the form of a
  hot cloth, hot water, ultrasound, heating pad, hydrocollator packs,
  whirlpool baths, cordless FIR heat therapy wraps, and others. It can
  be beneficial to those with arthritis and stiff muscles and injuries
  to the deep tissue of the skin. Heat may be an effective self-care
  treatment for conditions like rheumatoid arthritis.
Heat therapy is most commonly used for rehabilitation purposes. The
  therapeutic effects of heat include increasing the extensibility of
  collagen tissues; decreasing joint stiffness; reducing pain; relieving
  muscle spasms; reducing inflammation, edema, and aids in the post
  acute phase of healing; and increasing blood flow. The increased blood
  flow to the affected area provides proteins, nutrients, and oxygen for
  better healing.Reference

While taking a hot water bath we are just making our muscles and tissues nourished, which means the muscles will be in a healthy state for expansion and contraction. So it is recommendable to take a hot bath before exercising.

I am not an expert but I would definitely say never replace a warming-up by a hot bath. However, this depends on the activity to be undertaken. When you go for a round of chess or a stroll through the forest on a Sunday afternoon, sure, take a bath. When you're getting ready for a bout of sparring in a martial arts tournament, a hot bath is the perfect recipe to get injured (and beaten).
The Australia Sports Commission says that a warming-up aims to:

prepare the body and mind for the activity
increase the body's core temperature
increase heart rate
increase breathing rate.

None of these are targeted with a shower, on the contrary even I would say. The only thing that a hot bath can do is superficially increase temperature, flexibility and blood flow in the muscles. But this can never replace a warming up. I would save the bath for after exercise, as everyone does :)

Wouldn't a hot shower increase the body's core temperature, or does it only affect the body's surface temperature?

@CactusWoman: Just superficially I guess. Depends on the temperature and duration. A shower just above our core temperature is already pretty hot!

I am going to address only the stretching portion of the question since some misinformation is out there. When you say stretching, I hope you mean dynamic as opposed to static stretching especially if you are about to compete in a sport. If you are referring to static stretching, taking a shower may be a better option then, but if you mean dynamic stretching, a shower will not provide a greater benefit.
For peak performance, athletes or weekend warriors should use dynamic stretching prior to an event.

In previous research it has been recommended to use dynamic stretching as the primary method of stretching pre-event warm-up before high speed, and power activities (Little & Williams, 2004). The findings of this study agree with that recommendation for agility activities as well. This study supported the use of dynamic stretching in eliciting the greatest performance in agility movements by decreased T-Drill time. The findings
  of the current study are consistent with those of Fletcher and Jones (2004), and Young and Behm (2003) who determined that dynamic stretching elicits the best performance in power and high-speed activities [1].

However, static stretching does not improve performance and can actually lead to injury.

The current study found static stretching to have a negative effect on agility, and acceleration (Fletcher & Jones, 2004; Nelson et al., 2005). As acceleration is a component of agility, these findings support those of Fletcher and Jones (2004) and Nelson et al. (2005). Agility also involves components of braking, and change of direction. Static stretching prior to agility activities was found to have a negative effect on agility performance [1].

To read up on dynamic and static stretching as well as other types of stretching, I would recommend MIT's Types of Stretching page.
Additionally, the references to my reference one provides many more useful articles to look into.

Static versus dynamic stretching effect on agility and performance

Stretching and warming up are indeed a different thing altogether, +1.

@AliceD the OP said some athletes want to get an extra stretch in but dont want to go through the hassle of warming up. To me, they are implying substituting a hot shower to stretching in order to warm up the muscles.

I agree - the question should have been specified first. Nice addition, hence the upvote :)


text:
Ways to cause membrane damage to microalgae and yeast?
I am researching a way to monitor the membrane damage of cells. To do that I fist have to have reference points, namely, cells with damaged membranes.
I am working with Dunalliela, Hematococcus (both microalgae), and common yeast. I have been using mostly ethanol to damage the membranes so far.
What other ways are there to cause the most possible damage to microalgae (or yeast) membranes?. The idea is not total cell obliteration, but rather membrane damage (death is expected).

To get to the membrane of these species you first need to get past a formidable cell wall. The methods listed below are therefore more aimed at making cells permeable but the membranes must sustain some damage in the process.

At our lab we regularly use glass bead transformation for microalgae
transformation. The microabrasion allows DNA to go in so I imagine
the membranes must be damaged somehow.
I've also used hypotonic media (depending on the strain) to swell
cells close to their bursting point. I imagine they become rather
permeable at this point since they let several dyes in that are
otherwise excluded.

Do you just use deionized water as the hypotonic media?. By the way, Dunaliella lacks a cell wall. Thanks for your answer!

I did not know that about Dunalliela, thanks for pointing that out! Yes distilled was always the first thing we tried, it did not work on every alga though. There actually is a paper about this on swelling Dunalliela: http://www.plantphysiol.org/content/93/2/403.full.pdf
The other thing that actually came to mind while writing this thing was digitonin which is often used to solubilize membrane proteins. Other detergents might be worth a look too.


text:
Why do humans stop growing?
Humans grow most quickly when young, and to a lesser extent in preadolescence and early adolescence. However an equilibrium is then reached in adulthood, typically at around 1.6/1.7 meters tall.
I have found the age at which people "stop growing", meaning that they are at their tallest hight, is around the age of 21-25.

Why is it beneficial for humans to grow to 1.6/1.7 meters?
Why is there so so much variation in this, with some reaching there full height in there early teenage years?

It would probably be useful if you read this and then asked a more specific question: Wikipedia: human height

Human bones grow in length due to the effects of human growth hormone on the epiphyseal plates near the ends of the bone. Over time these two growing margins decrease in size, or width, until those special cells are either gone, or can no longer respond to hGH. At that point the body has no mechanism to increase the size of the skeleton, and growth stops. In females this tends to happen earlier than in males; approximately 2 years after the onset of puberty for females.


text:
Measuring a plant's electric activity any instructions where to place electrodes?
I would like to measure a plant's electric activity / voltage, I've looked online to find out where to place the electrodes and what type of electrodes to use but they seem to very wildly.  Any ideas?
At the moment

I plan on wiring one end of a needle to the stalk and one end to the soil.
The connections from the plant would go to a laptop mic input to record the signal then I would normalize the signal.
I would then process the signal in MATLAB/Octave using FFT.

Any thoughts or videos on connecting the electrodes to the plants or trees?
I did find this Development of Bio-Machine Based on the Plant Response to External Stimuli

A quick glance on Google scholar only revealed plant-electrophysiological studies deploying single-cell recordings. You can't do single-unit recordings in an intact plant with your sound card connected to a needle. What potentials are you exactly planning on measuring? Without specification of your target potential this question cannot be easily answered (that is, not by me :-)

Further, I strongly doubt that the amplification of the AD converter is sufficient, and the amount of noise in the signal will probably sky rocket due to your setup being poorly isolated.

I vote to close as OP has not edited and clarified question after comments

I'm looking to measure voltage

And how would you use FFT to analyze it? You are expecting oscillating activities in single cells recorded with your sound card? It all doesn't line up...

Import the signal into matlab or octave and use their FFT function to analyze it (see #3 from question)

What they do in the linked paper is injecting current and recording it back. Is that what you want? FYI: The paper, and journal for that matter, sorry to say, is of exceptional low quality.

If you could add more detail as to what you wish to record that would be great. I'm happy to upvote this question once it is clear, and more than happy to attempt an answer once I know what you are exactly after.

I found this link that has a lot of good info and directions http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835954/

@AliceD thanks I'm going over some of the papers I found online at the moment to see which electrodes they use. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835954/

The roots of plants have been used more often than the actual stem of the plant e.g. http://pubs.acs.org/doi/abs/10.1021/es071938w

I would love to get more info about the roots and signal activity but the link you provided requires me to pay along with the title being about "Microbial Fuel Cells Generating Electricity from Rhizodeposits of Rice Plants"  and the abstract being very brief

Perhaps you will find what you are looking for in the closing report of the FP7 project that funded the article. http://cordis.europa.eu/result/rcn/140451_en.html


text:
SNPs in DNase hypersensitive and histone marks sites
I am investigating a role of SNPs in DNase hypersensitive sites and in the DNA regions of histone marks and have some questions about it.
SNPs in DNase hypersensitive sites might mean that those SNPs are in enhancer regions and might influence TF binding affinity what can influence a transcriptional output. Is it correct?
SNPs in histone marks sites
I have the number of SNPs that fall in the peaks (chip-seq) for the following histone modifications of healthy patients:
H3K27ac,H3K4me1,H3K4me3 (represent the active chromosome)
H3K27me3, H3K9me3 (represent the repressed chromosome)
Histone modifications represent if the chromosome is active or repressed. A SNP might change the binding affinity of a histone. It means that if I have a SNP in data for active chromosome (H3K27ac,H3K4me1,H3K4me3), it might change the status of a chromosome, namely turn it into a repressed one or it might induce a histone not to bind at all(it means that this region is still active,no?) Is it right? I am not sure I understand the possible influences of a SNP histone marks sites.

Enhancer regions or other protein binding regions of DNA will not be DNAse hypersensitive.

@WYSIWYG Why? I though it chromatin is not repressed, then it is nucleosome free.

Protein bound regions will be protected- same principle as in case of nucleosomes.

Why will it be protected? In case the TF did not bind to it, it will not be protected. I have seen lots pf plots where DNA hypersensitivity coincides with TF binding sites (chip-seq peaks). What is then hypersensitivity sites and why do we want to explore it? Wiki suggests: "These accessible chromatin zones are functionally related to transcriptional activity, since this remodeled state is necessary for the binding of proteins such as transcription factors."

First off let's define some concepts.

DNAse hypersensitive regions are DNA regions which are in an open chromatin conformation (i.e. euchromatin). This means that those regions are more active at the genomic level (i.e. higher gene expression, gene regulation and higher TF binding) and are less prone to form nucleosomes.
Histone mark sites are DNA regions known to bind certain type of histones and therefore also influences the chromatin conformation leading to the same effects described previously. The critical point is that the histones you are listing do not primarily bind a specific DNA sequence (as described by @mdperry) but rather DNA sequence marked by epigenetic modifications such as methylation and acetylation.

Now for your first questions, SNPs in DNAse hypersensitive regions might influence the chromatin state and therefore yes might influence gene expression and gene regulation. Will those SNPs also influence TF binding? Well they might indirectly via chromatin modifications. They will not directly act on TF binding if not located in a sequence known to bind TFs (TFBS). DNAse hypersensitivity is not a synonym for transcription factor binding regions/sequences.
For your second question, SNPs in histone mark sites are a little bit more difficult to interpret. They might, or might not, provoke chromatin changes by influencing the binding of histones but not in a direct way. CpG islands are, for example, DNA regions known to be greatly under the influence of epigenetic marks and therefore mutations in those specific regions (e.g. a C -> T mutation) might influence the relative methylation/acetylation state and therefore the binding of histones. SNPs might therefore influence gene expression via chromatin changes which leads to higher/lower TF binding but again not in a direct way. Here again a SNP would influence TF binding directly only if the mutation is located in a TFBS.
As you can see my answer is full of "might" and the reason is that it is very difficult, at the current state-of-the-art, to determine the exact impact of a SNP on the 3D conformation of the chromatin and therefore predict the effect on specific gene expressions.
An advice would be to try to co-localize your SNPs with known TFBS either predicted In-silico or measured via CHiP-SEQ experiments and merge that with the information about DNAse hyperactivity and histone marks you already gathered. For example a SNP in a TFBS in a DNAse hyperactive region is very likely to have a greater impact than a SNP in a TFBS in a non active region.
I am sorry I cannot be more specific but this is a very active research area in genetics and there is still a lot to understand, especially for the interactions between all the players influencing the chromatin conformation.

(at)Tonja, you could search far and wide on the Internet and you would not find a more cogent or on point discussion of these concepts than the one @cagliari2005 very patiently elucidated for you.

Keep in mind that it is not individual histones that are binding, there are 8 histone proteins forming a compact nucleoside particle, and the particle has 146 bp of DNA tightly wrapped around it.  Since the interaction between the histones and the DNA are not sequence-specific, it is unlikely that a single nucleotide polymorphism would have a measurable affect on the occupancy of the nucleosome at that site.

"interaction between the histones and the DNA are not sequence-specific". So, in fact the more SNPs are situated in 146 bp region, the more effect they have? I have lots of papers which refer to SNP in histone sites but non of them tells about the consequences.

No, you are approaching it like a classical lac Repressor <-> lac operator interaction where you can measure the moles of free protein, free DNA, and bound protein-DNA complex, and use those values to calculate the Kd, and a binding affinity. That model is for sequence-specific DNA binding proteins, and yes, the more nucleotide sequence mismatches you introduce into the recognition site, the weaker the affinity. The histone octamer core will bind to any DNA, and is by definition not sequence-specific. So introducing SNPs is unlikely to affect occupancy


text:
What is the impact of stress on the human body?
Can stress trigger any changes in the human body? I'd like to know more about things less commonly known than, for example: sweating and tiredness. What are the long term risks of chronic stress? Do stressful people have higher chance of having heart-diseases or affected by hair-loss, for example?
I'm also interested in how can an emotion induce physiological changes in our body?

Welcome to Biology SE! Could you be more specific on your question, please? In this form I'm afraid this is too broad. Please visit http://biology.stackexchange.com/tour or http://biology.stackexchange.com/help sites for help on asking on-topic questions.

@I don't know - After your editing the question got better, yet I thought it's still too borad / unclear, so I took the liberty and reformulated so I can be reopened. I did this because in my opinion the question itself hold potential. To be honest I tried to keep as much of the original meaning / intention as possible, and it may still qualify as too broad. You can undo my editing if you wish to revert it back to your original edited form. I'm also voting for reopening this question.

Stress is the reaction, which our body reacts against the pressure or tension. There are many impact of stress on the human body, which includes

Emotional:  Moodiness, short temper, agitation, inability to relax, feeling lonely and always depressed.
Cognitive:  Memory problems, unable to concentrate, very poor judgment, negative thoughts, always anxious and worrying
Physical: Frequently suffering from pains and aches
Behavior: Addiction toward drugs, alcohol or cigarettes for relief, nervous, being alone, insomnia.
Other problems like headache, muscle pain, chest pain, fatigue, etc.

Hello Ravi. Can you add some references to support your answer?


text:
Pasteurization and Bioavailability of Antioxidants in Beet Juice
What are the effects of pasteurization on the antioxidants found in beet juice ? Does the process render most of the beneficial nutrients (betaine) useless and make them unable for the body to process as efficiently as it would with raw beet juice? Also, does the pasteurization process do this to most fruit and vegetable juices ? I appreciate any insight, I've seen a lot of conflicting reports and am curious of anyones thoughts. Thank you

So, when they subjected "ready to drink" beetroot juice to thermal pasteurization, they found the betacyanin and betaxanthin (our major antioxidants, and pigment molecules) content to be 39.9 and 42.28% degraded, respectively (1). Their conclusion was as follows:

Standardization of process condition and
  quality degradation of beetroot juice due to thermal
  pasteurization was studied. The standardized T2
   batch
  with total heating time (fh) of 720 s thermal in-pack
  pasteurization leads to the minimal degradation of
  color, betalain content (Betacyanin and Betaxanthin),
  antioxidant activity and complete inactivation of
  micro flora of beetroot juice. The color, betalain
  content (Betacyanin and Betaxanthin) antioxidant
  activity and sensory of the beetroot juice was
  significantly (p < 0.05) reduced during 180 days
  ambient (27-30°C) storage, but still the quality of the
  juice was adequate upto 180 days. We concluded that
  thermal pasteurization of 96 °C for a total heating time
  (fh) of 720 seconds with P-values of 11.16 would be
  a good method to produce microbiologically stable
  beetroot juice with the retention of quality attributes.

So our goal is to get a juice that retains as many "good" attributes as possible, while producing a product that isn't going to get anyone a foodborne illness. As for the net effect of pasteurization on fruit juice in general, im still coming to a conclusion there. The process shouldn't render too much of the fruit/vegetable ineffective, though I'd still expect some degradation either in storage or processing.

If we read the previous statement, we can note two things. Firstly the percentage they mention are not in the quoted material at all. And secondly that the quoted material does not suggest degradation of the health boosting effects from the process of pasteurisation, but rather from long term room temperature (Very warm room) storage for 180 days. "The standardized T2 batch with total heating time (fh) of 720 s thermal in-pack pasteurization leads to the minimal degradation of color, betalain content (Betacyanin and Betaxanthin), antioxidant activity and complete inactivation of micro flora of beetroot juice."

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Why did humans evolved the scratch reflex?
I've been wondering about this for some time, and I can't come to an answer...
Everybody keeps telling me that scratching one's own skin is bad. It damages the epidermis, creates the hazard of malicious bacteria getting past the skin barrier, and creates the vicious circle of scratching increasing the itching, and itching increasing the scratching (I think I recall reading that this vicious circle also happens even without any special skin diseases, like atopic dermatitis - I might be mistaken here, however)
So, it seems there are hardly any benefits for the body from the scratch reflex. However, if this was true, then "grandma Evolution" wouldn't have given this to us!
What are the benefits of scratching? Are there any benefits of it from the evolutionary point of view? I can come up with just one such benefit, namely fending off insects such as ticks, mosquitoes, fleas or lice. Would this be the evolutionary benefit of scratching?

Not enough time for a real answer, but I see the scratch reflex as vital. It rids the body of irritants, such as burrs/thorns, insects walking around, poison ivy/oak/sumac/etc. oils, and more. In the cases where the irritant has already affected us (we got bit by the mosquito, a rash from poison has already developed), scratching focuses our attention on the site, and the ensuing irritation works as a strong warning to not keep performing whatever behavior resulted in the irritation in the first place.

Bacteria aren't malicious. 2) Not everything that no longer serves a purpose "devolves". Evolution is not a controlled, intelligent mechanism ("grandma evolution"). 3) Not every itch which is scratched results in an itch-scratch cycle. 4) Scratching an itch is not necessarily bad. There are at least 4 faulty presuppositions in your question.

Humans didn't evolve the scratch reflex. We inherited it from 350 million years of mammal ancestors.

With about 20 square feet of skin constantly exposed to potential irritation, itching must serve an important protective/defensive function.
The "scratch reflex" (I'm not sure I would call it that) is necessary to life and limb. Itch is a major somatic sensation, along with (and different from) pain, temperature, and touch. Itch can be an acute sensation, e.g. a mosquito bite, or a chronic condition (peripheral or internal disease).
Research on itch signaling is still at its infancy, and basic mechanisms by which the itch sensation is transmitted and regulated have yet to be fully understood. It is meant to give us information about how we are interacting with our environment. Loss of such fine sensation, such as occurs with Hansen's Disease - aka leprosy, where patches of skin become painless and do not itch, so are ignored by the patient - leads to festering wounds and resultant problems.
As @MattDMo stated in a comment, sensation allows us to respond appropriately to irritants which, if ignored, might lead to festering wounds: thorns and other foreign bodies, sucking or biting insects (parasites or other, which can act as disease vectors as well), etc. It allows us to learn how to avoid and treat such irritants.
Various types of itch can be classified by the origin of the itch, which could be skin-related, neuropathic, systemic, or psychogenic. The most common cause of itching is dry skin; tiny cracks in the skin cause an inflammatory response, which (within reason) is not a problem in and of itself. The response to the itch, though, can be beneficial or damaging. One can treat dry skin, wash off irritants, treat infections, avoid causes, etc.
Scratching can be benign if done sensibly, or it can injure the skin, allowing infection, etc. However, the benefit of having such sensation under normal circumstances certainly outweighs the inconvenience.
That is not to say that pathological conditions that cause itching are not problematic. They are, and one might reasonably curse the sensation under those circumstances.
Edited to add: Itching, or pruritus, is defined as an unpleasant cutaneous sensation that serves as a physiological self-protective mechanism to prevent the body from being hurt by harmful external agents. (Nature, 2007)
Scratching is simply a reasonable response to itching from any source and is not necessarily harmful. It's not a reflex per se. You can avoid scratching. Some animals must actively seek out a way to scratch. This takes it well outside of the terminology of reflex as neurologically understood.
Itch Signaling in the Nervous System
Pruritus
When you have an itch, what is happening under your skin?

Great. But, itching causes scratching. Scratching is not a good way to deal with dry skin (it only worsens the problem), and not a good way to deal with thorns or insects (thorns should be pulled off, insects smashed). You say: "Scratching can be benign if done sensibly". But I can't see how?

@gaazkam - People scratch itches all the time without drawing blood or causing infections; even in situations where it's advised strongly not to scratch, such as with chicken pox, it's very uncommon to see bacterial superinfection caused by doing so. Scratching sensibly means gently and with clean fingers, short nails. Gouging yourself is not sensible; it is done, however  by people with intractable itching. When that's the case, they need medications to control the itching. Scratching does not always increase the itching, but tends to in certain situations.

OK, so scratching doesn't need to be malicious. But what are the benefits?

@gaazkam - Beyond chasing mosquitoes and other bloodsuckers away in the initial act of attack, it relieves the itch. That in itself feels good. Because severe itching can't be relieved by scratching, it teaches us about avoidance of skin toxins, e.g. poison ivy.

So, to sum up, scratching is good just because it relieves itching. Great. But why did such mechanism evolve, since scratching can do nothing about the cause of the itch? ... all right. One possibility is this mechanism is a leftover from earlier mammals... perhaps scratching is the best way for a cat or a dog to fend of insects or remove thorns from their fur, but definitely not for humans! Yet this now useless mechanism (of scratching, not itching) has not yet devolved.

@gaazkam - you make assumptions: 1) that scratching is a useless mechanism (what would you do if you had an itch but no fingers? Rub yourself up against a tree? That's what bears do. Obviously, scratching an itch feels good!, and 2) that every "useless mechanism" should devolve. That's a fallacy. Humans don't have tails, yet we still have tail bones. They break and cause pain. Why don't we just devolve them? You have been so resistant to this answer that I doubt I'll ever answer one of your questions again. That's not said in a huff. Your attitude is simply unpleasant.

I'm not arguing with your answers. At least, that's not what I'm trying to do. I see nothing wrong with what you claim here, and I find all of this very interesting. I'm sorry if you find my behavior inappropriate; it's just that if I'm curious about something, I tend to belabour just until I can finally fully understand it. I know, however, that my interpersonal skills leave very much to be desired, and I should definitely work on this.

Perhaps I was failing to ask my question accurately. Thank you for pointing me out that scratching doesn't have to be bad, that itching itself is beneficial, etc. What I couldn't understand, however, was something like this: why did the scratching (and not any other behavior, or no behavior at all) evolve to relieve itching, since scratching didn't seem to me to resolve the cause of the itch? Note that pain, for example, doesn't have such relieving mechanism.

I finally came to the conclusion that the said mechanism is just a leftover of previous evolution stages. It did serve a purpose previously; but it no longer serves one, but it didn't just "go away". Perhaps this is exactly what you answerers were trying to tell me all the time; if so, sorry for not getting it in time.

But I wrote it in one of my comments. This implies that I understood that evolution is not an intelligent mechanism (note the ""'s enclosing my "grandma Evolution" statement). As to the other "faulty assumptions": 1) I understand that not all bacteria are malicious; that's why I wrote "malicious bacteria" to denote the harmful ones (regarding to human organism); 3 and 4) Thanks for pointing this out for me, I accept this.

Happy Easter to you BTW.

@gaazkam - Happy Easter to you, too. :) If that's what you want to know, then that is what you should ask. In fact, we do have a similar reaction to pain: we cradle, message, grab, lay a hand on an area that hurts. If we have a backache, we rub our backs to try to make it go away. A cramp in out hands? We message and stretch the hand with the other. Smash your thumb? We'll grab the hand - even though it doesn't help the pain, and cradle it. We do try to make pain go away with our hands. Just like scratching an itch. But it doesn't work nearly as effectively. (cont)

When people have bad cardiac chest pain, they so frequently try to grab their chest that we call it the positive fist sign. People who have stomach aches will often try to alleviate or soothe themselves by gently rubbing their bellies. Note also that we respond to a cold feeling by briskly rubbing, If someone applied an ice cube to your forearm, I'm pretty sure you would rub the spot for a moment. So, do you see that scratching is not a unique response?  We just happen to be able to actually do more about an itch than about a pain. But a response is a response.

"because it feels good" is not a reason why something harmful would evolve

@endolith - what a silly comment! How do you explain racing, skydiving, shooting heroin, and the other hundreds of potentially lethal activities humans engage in because they feel good? Write a better answer with sources.

@anongoodnurse Humans have an instinctive biological motivation to skydive?  I would have guessed the opposite.

Short answer
People scratch to alleviate the itchiness.
Background
Itch (pruritis) is caused by a moderate stimulation of pain receptors. There is not such a thing as an itch receptor. Due to the neural circuitry involved, rubbing a painful bruise actually dulls the pain due to stimulation of the tactile sense (Kakigi & Shibasaki, 1992). This may explain the familiar first action one does when injured - grabbing the injured spot and rub it (cats lick their wounds, likely dulling the pain and cleaning it up at the same time). Given the similarity with the neural processing of pain, it is not surprising that a very similar mechanism applies to scratching - scratching relieves the itchy sensation (Nillson et al., 2003).
So while evolutionary explanations may be valid, they can never be proven. And in fact, too much scratching can be harmful, and I quote from Dermnet:

Itch [...] provokes the desire to rub or scratch the area to obtain relief. [...] Constant scratching to obtain relief can damage the skin (excoriation, lichenification) and reduce its effectiveness as a major protective barrier.

Hence, from a behavioral and neurophysiological point of view, we simply want to get rid of itchiness and we scratch. Whether this is evolutionary advantageous other than to provide a means to temporarily reduce debilitating itchiness, is questionable.
References
 - Kakigi & Shibasaki J Neurol Neurosurg Psychiatry 1992;55:282-6
 - Nillson et al. J Eur Acad Dermatol Venereol 2004;18:37–43

OK, so now I know how scratching relieves itching. But what are the benefits of scratching to the whole system? Or, more precisely - what are the benefits of the mechanism of scratching relieving itching?

@gaazkam - my point is, as I conclude in the last sentence, we cannot tell what then benefits are of scratching. My guess is that it feels good, as it relieves the itch. The evolutionary advantage regarding ticks and flees etc. is the fact that we feel itching. That warns us and lets us undertake action. If this action is scratching, it is important to realize that settled ticks don't care about scratching, flees are notoriously hardened critters and mosquito bites only start to itch when the deed is done; scratching in itself has no obvious advantage, other than to relieve itching.

So, to sum up, scratching is good just because it relieves itching. Great. But why did such mechanism evolve, since scratching can do nothing about the cause of the itch? ... all right. One possibility is this mechanism is a leftover from earlier mammals... perhaps scratching is the best way for a cat or a dog to fend of insects or remove thorns from their fur, but definitely not for humans! Yet this now useless mechanism (of scratching, not itching) has not yet devolved.

Are pain and itch the same mechanism? I have read otherwise.

@anongoodnurse: you may both be right to some extent: "In general, pruritus involves activation of the pruriceptors of specialized nerve cells called C-fibers. These C-fibers are identical to those associated with the sensation of pain, but they are functionally distinct and only convey the itch sensation—they comprise about 5 percent of the total C-fibers in human skin. "

And yes, this has been stated by more serious sources: https://doi.org/10.1016/S0140-6736(03)12570-6


text:
How precisely can we sense temperature differences?
We have thermoreceptors, thus we can sense temperature (both warm and cold).  I'm interested in the sensitivity of our thermoreceptors - What is the smallest temperature difference that we can sense? I assume that different parts / organs may have different sensitivity (eg. lips vs fingers), thus I'd like to narrow my focus on the palms / fingers. But if someone has comparative data, that is welcomed too.

This varies enormously across the body, and also with age. One good starting place would be Stevens, J. C., & Choo, K. K. (1997). Temperature sensitivity of the body surface over the life span. Somatosensory & motor research, 15(1), 13-28.

Short answer
Temperature differences of 0.02 degrees Celcius can be distinguished, dependent on various factors including experimental conditions and bodily location.
Background
The ability to discriminate temperature differences depends on whether it is a cooling or heating pulse, the skin temperature, the duration of the temperature stimulus, age, bodily location among other factors. Unfortunately I cannot access the primary literature other than a few isolated smaller studies. However, Scholarpedia has a very nice entry and associated references, and I quote:

The thermal sensory system is extremely sensitive to very small changes in temperature and on the hairless skin at the base of the thumb, people can perceive a difference of 0.02-0.07 °C in the amplitudes of two cooling pulses or 0.03-0.09 °C of two warming pulses delivered to the hand. The threshold for detecting a change in skin temperature is larger than the threshold for discriminating between two cooling or warming pulses delivered to the skin. When the skin at the base of the thumb is at 33 °C, the threshold for detecting an increase in temperature is 0.20 °C and is 0.11 °C for detecting a decrease in temperature.
The rate that skin temperature changes influences how readily people can detect the change in temperature. If the temperature changes very slowly, for example at a rate of less than 0.5 °C per minute, then a person can be unaware of a 4-5 °C change in temperature, provided that the temperature of the skin remains within the neutral thermal region of 30-36 °C. If the temperature changes more rapidly, such as at 0.1 °C/s, then small decreases and increases in skin temperature are detected. [...]

You also were interested in the palmar skin: here average difference limens are 0.02 - 0.06 °C, dependent on the temperature step used. These values were obtained using cooling pulses. In other words, differences in two cooling pulses of 0.02 - 0.06 °C were discernible, with higher limens needed for higher pulses. Baseline temperatures (29 - 39 °C) had little effect (Darian-Smith et al., 1977).
Reference
Darian-Smith et al., J Invest Dermat 1977;69:146-53
Note
The Stevens, J. C., & Choo, K. K. (1998). Temperature sensitivity of the body surface over the life span. Somatosensory & motor research, 15(1), 13-28 article as commented on by Corvus is indeed a must-read, but my uni library does not have access to it unfortunately.

This is an important point for our previous argument. As you now point out the perception of temperature is not only dependent on the relative temperature difference but also on the absolute temperature.

@WYSIWYG - Yes.. and no. Surprisingly Darian-Smith et al., 1977 found no effect of base temperature (at least across 10 degrees C). However, according to Weber's law, the difference limen increases when the reference temperature is higher. This does apply to the temperature step, but base temperature may be another story?

Here's another question. Is the human body capable of sensing a continuous change in temperature or does it just sense when change occurs in bulk? I mean to say, is the "sense" continuous or discrete?

@PriyanshuDas good question - please ask new questions as a question - Make sure to add a little of your own research, for instance by linking to this question or answer and explaining it doesn't answer your current question.


text:
Why can newborns swim?
I am wondering for someone to discuss the phenomena that newborn babies (humans) are able to submerge underwater up until a few months where that ability is lost again? What is the explanation for this?

Have a look at the answer here the bottom portion of it.

It's called the Diving reflex, also known as the bradycardic response. It goes away around six months.
From https://www.breatheology.com/articles/mammalian-dive-response/

Another action of the diving response can be observed in infants when they are under water. The windpipe by the vocal chords spontaneously closes to prevent water from entering the lungs. This reflex is initiated as soon as there is contact with water. However, it disappears when the child reaches the age of roughly six months.

This is answering the 'how' but not the 'why' (not sure that this can be answered fully though)

When the face of an infant is exposed to cold water, the heart slows down and blood is shifted away from the peripheral muscles to conserve oxygen for the brain and heart, and they typically hold their breath. The reflex is the same one that protects babies from getting milk in their lungs. The reflex kind of reroutes the entire circulatory system to save blood for the heart and brain, and not pump it through the rest of the body.
http://www.ncbi.nlm.nih.gov/pubmed/12022304


text:
Why we have just 2 teeth cycles, primary and secondary not more?
After baby teeth go, secondary teeth grow, is there a scientific reason why they are just 2 sets not more?

I found this question http://biology.stackexchange.com/q/27547/15122 which answers the history section of my question

Which of Tinbergen's four why-questions are you asking? See e.g. http://www.sciencegamed.co.uk/science/2013/mar/nikolaas-tinbergen-four-questions.html.

This not a duplicate. The first part of the question is why humans usually only have two sets of teeth.

Humans are diphyodont animals, which means we are having two sets of teeth cycles, on contrast, the polyphyodont animals which are having multiple tooth cycles. The first deciduous teeth(milk teeth,baby teeth or primary teeth) then followed by the permanent teeth. Milk teeth develop from the embryonic stage and continue to develop for 6-7 years and gradually erupts forming the permanent teeth. The permanent teeth is developed and it pushes the milk teeth from the bottom which result in the shredding of milk teeth.
Most of these polyphyodont animals uses their teeth for more severe purposes like grabbing and slashing. Due to these massive work load, their tooth are considered as their main advantage for survival. Also their tooth are subjected to heavy flaws while they grab or slash, so having multiple tooth cycles help them ensure healthy teeth all over their life time. On the other hand considering the diphyodonts, their tooth have been using for chewing and grinding and they will having low flaws compared to the others. So from the evolutionary standpoint increasing the number of tooth cycles are not so economic for them.
Reference

there are plenty of polydont grinders and chewers. polydont is the default, mammals are weird for losing it.


text:
Which information can be obtained from a list of gene names?
Lets say I only have a list of gene names. I know they are up regulated and I know they are related to cancer.
What information can I obtain from having only the names of genes? For example is there any way to find a gene-gene interaction, or anything else? Is it possible to retrieve any information by having only the name of the genes?

The info you have is the gene name, nothing more, nothing less. You need info about each gene to draw any conclusions.

@MattDMo thanks for your message. how can I get info about each gene , do you know any way to do it? should i search one by one in google and see what comes up ?

I don't really understand what you're asking. With a gene's name, you can find out anything about it that's ever been published

@canadianer Yes when it comes to only one gene but when you have a list of them, how they interact with each other or anything else related to a set and not one gene alone

In light of your comments, you might be interested in Gene-set enrichment analysis (GSEA).

@cagliari2005 GSEA is when you want to find a score for your genes and you should definitely have two sets of genes like healthy and diseased but in my case I have only a list of gene names and I already know they are up regulated , so , I don't need to do GSEA

You can do a GSEA using 1 set, the other one coming from reference databases such as MSigDB (see here). You can categorize your list by gene families for example.

@cagliari2005 that is very interesting FOR SURE!!! thank you. do you know how to map such outputs for example overlaps or any other things can be obtain from there?

How many genes do you have in your list? You can get an idea of what cellular process is the most impacted by the genes in your list and from there try to reach some conclusions but just as a warning, what you are attempting is not trivial at all. It will be hard to reach valid conclusions from a simple list of genes as correlation does not mean causation (i.e. is the gene up regulated because of cancer or is it provoking the cancer?).

@cagliari2005 I kept only 20 up regulated , it can simply be perform but visualisation is difficult :-)

I would suggest searching the name in any trusted genetics database such as NCBI's GenBank (http://www.ncbi.nlm.nih.gov/genbank/). You can just Google search it, but it may take a little longer to find useful information that way.
I hope this helps and good luck with your research,
CDB

NCBI also hosts OMIM, which is a good place to find a link between a gene name and a disease occurring of the gene is mutated. You can select OMIM by following the link above and then selecting OMIM from the drop-down menu by the search box. Then search the gene name.

Was getting long in the comments.
In light of your comments, you might be interested in Gene-set enrichment analysis (GSEA). You can do a GSEA using your set, the other one coming from reference databases such as MSigDB (see here). You can categorize your list by gene families using this technique for example.
You can get an idea of what cellular process is the most impacted by the genes in your list and from there try to reach some conclusions but just as a warning, what you are attempting is not trivial at all. It will be hard to reach valid conclusions from a simple list of genes as correlation does not mean causation (i.e. is the gene up regulated because of cancer or is it provoking the cancer?)
To visualize pathways you might want to look at this post on Biostars. Several software are available for this purpose.

It depends; what species are the genes from? Some organisms have extensively annotated genomes, and actively curated species-specific databases, while other species may not even have a reference genome sequence available.  By itself, a priori, if you were lucky, about all you list would tell you was how to spell the names of those genes--if you're lucky. But to a skilled Bioinformatician said list could be a gateway to a discovery, or a patent, or a publication, or a grant, although none of these is very likely.

I know already the genes are human genes

Also try putting the list through Reactome or String DB to see if you see mapping to certain pathways. http://string-db.org/
You can also put lists through ConceptGen to carry out ontology based analyses
http://portal.ncibi.org/gateway/conceptgen.html

Assuming each gene symbol represents a unique gene or protein (this may not be true; see for gene name aliases in e.g. NCBI Entrez gene) you can get a lot of information programmatically. Below is an example using R and Bioconductor resources.
Define your list of genes:
# list of gene symbols, here we focus on one.
> genes <- "KRAS"

Load the annotation package org.Hs.eg.db and retrieve basic information including Gene Ontology ids:
# annotation package for human genes.
> library(org.Hs.eg.db)

# query Entrez gene id, description (GENENAME) and Gene Ontology id (GO)
> info <- select(org.Hs.eg.db, keys = genes, keytype = "SYMBOL", columns = c("ENTREZID", "GENENAME", "GO"))
> head(info)
  SYMBOL ENTREZID                                   GENENAME         GO EVIDENCE
1   KRAS     3845 Kirsten rat sarcoma viral oncogene homolog GO:0000165      TAS
2   KRAS     3845 Kirsten rat sarcoma viral oncogene homolog GO:0000186      TAS
3   KRAS     3845 Kirsten rat sarcoma viral oncogene homolog GO:0001934      IMP
4   KRAS     3845 Kirsten rat sarcoma viral oncogene homolog GO:0005515      IPI
5   KRAS     3845 Kirsten rat sarcoma viral oncogene homolog GO:0005525      IEA
6   KRAS     3845 Kirsten rat sarcoma viral oncogene homolog GO:0005737      IDA
  ONTOLOGY
1       BP
2       BP
3       BP
4       MF
5       MF
6       CC

Load the GO.db package and retrieve the term associated with the GO ids (this gives info about putative function):
> library(GO.db)
> info$Term <- Term(GOTERM[info$GO])
> head(info)
  SYMBOL ENTREZID                                   GENENAME         GO EVIDENCE
1   KRAS     3845 Kirsten rat sarcoma viral oncogene homolog GO:0000165      TAS
2   KRAS     3845 Kirsten rat sarcoma viral oncogene homolog GO:0000186      TAS
3   KRAS     3845 Kirsten rat sarcoma viral oncogene homolog GO:0001934      IMP
4   KRAS     3845 Kirsten rat sarcoma viral oncogene homolog GO:0005515      IPI
5   KRAS     3845 Kirsten rat sarcoma viral oncogene homolog GO:0005525      IEA
6   KRAS     3845 Kirsten rat sarcoma viral oncogene homolog GO:0005737      IDA
  ONTOLOGY                                           Term
1       BP                                   MAPK cascade
2       BP                   activation of MAPKK activity
3       BP positive regulation of protein phosphorylation
4       MF                                protein binding
5       MF                                    GTP binding
6       CC

Load the RefNet package and get information about interacting proteins:
> library(RefNet)
> refnet <- RefNet() # this step downloads from AnnotationHub and may take some time.
> int <- interactions(refnet, species = "9606", id = genes, provider = "BioGrid")
# create data.frame with Entrez id of proteins.
> d <- int[,1:2]
> d$A <- sub(".*locuslink:(.*)\\|.*", "\\1", d$A)
> d$B <- sub(".*locuslink:(.*)\\|.*", "\\1", d$B)
> head(d)
      A    B
1  3065 3845
2  8841 3845
3 23411 3845
4  1994 3845
5  3845 9770
6  9770 3845

Use the igraph package to visualize the interacting proteins.
> library(igraph)
> g <- igraph::simplify(graph.data.frame(d, directed = FALSE))

# annotate the nodes with the symbol.
> V(g)$label <- select(org.Hs.eg.db, keys = V(g)$name, columns = c("SYMBOL"), )$SYMBOL
> plot(g)

Then you could repeat the cycle with the interacting partners. There are many other things you can do, starting from a list of symbols; this is just a brief example. More detailed examples and workflows can be found here.

take the gene names and copy all of them, next open an online tool called gene mania. paste all your genes on the window. you will get their interaction and other related genes.
Now go to a database called gene cards and type in all the gene you got from gene mania and paste it one after the other to get useful information about the individual genes. some of which are restriction site information's, transcription factors etc.

It would be helpful if you provided, at least, the URL of the tool you recommend.


text:
Difficulties understanding a pathway
I am not a biologist and I would love to understand what is going on with this pathway.
I went to the description but it's still complicated, and I couldn't follow. Can someone please help me with it? Is this a comprehensive pathway or is it based on specific details? How do i read this pathway?

your link doesn't work...

@MattDMo thanks I updated it and should work now

Your question is pretty broad. What specifically do you want to know about this pathway?

@CactusWoman my main question is how can we come to such conclusion that a pathway is very important or one is not! how to interpret such pathway shown in the link? and what can I understand from it? to be honest it is very complicated for me to understand it

Please remove the link and make it a stand-alone question. I vote to close as unclear what you are asking.

I'd make sure to go over exactly what it is that confuses you, instead of simply stating the entire diagram couldn't be followed. These are proteins interacting with each other with a result of the interactions noted at the end, among other information.

So if you're reading the flowchart, understanding the notation of the arrows is important:

We have rectangles around the gene products
There's a circle, denoted by DNA, noting that the proteins are expressing the product that follows through interaction with DNA
The solid line with an arrowhead means there's some sort of interaction
The solid line with the blunted or T head means this pathway or interaction has been abrogated somehow
The solid line with the slash through it means there's some missing interaction that we don't see
The +p means phosphorylation
The double solid line to the left is the plasma membrane, whereas the dotted line central to the figure is the nuclear envelope
The dotted line means an indirect effect

Source: http://www.genome.jp/kegg/document/help_pathway.html
The pathway is kind of broad but it provides some mechanisms for tumorigenesis from two standpoints: chromosomal instability, and microsatellite instability. The pathways we're seeing promotes the tumor development by upregulating proliferation signals, and downregulating apoptosis pathways. There's bound to be more to it, especially since we see other players involved when we get into cases like metastasis like snail1/2, Met, Src, etc. Below is a survey of apoptotic pathways from Nature, with pro-apoptotic in red, and pro-survival in green:

Source: http://www.nature.com/reviews/poster/apoptosis/index.html
Ignoring the therapeutic targeting jargon, you can see that when growth factors bind, the cell generally pushes towards a survival state. When death factors bind or something goes wrong, the cell pushes toward an apoptotic state. Cancers, however, are intrinsically disregulated:

They have methods of overstepping their boundaries as cells, which is what makes them problematic. The general conclusion I'd draw from that KEGG pathway, though, is that many pathways need to be disregulated to end up with colorectal tumors, and the method of disregulation is (a) downmodulated mismatch repair, and (b) chromosomal aberrations due to duplication, etc. Andkeeping in mind the box of oncogenes vs tumor suppressors in the corner: "An important difference between oncogenes and tumor suppressor genes is that oncogenes result
from the activation (turning on) of proto-oncogenes, but tumor suppressor genes cause cancer when they are inactivated (turned off)"

Pathways in biology are very hard to interpret without being an expert in the subject. Here a link to The Standard Graphical Notation for Biological Networks that might help you understanding the notation used.
Pathway are generally based on evidences of links between the players. These links do not require to be found using one particular technique. Those evidences could come from genome-wide association studies (GWAS), RNA-seq, functional assays, receptor based assays, clinical data etc.. just to cite a few.
For example The MAPK pathway was linked to colorectal cancer via gene expression experiments as shown here. The MAPK pathway is known to influence cell proliferation and therefore contributes to colorectal cancer development but if you don't know what the MAPK pathway is doing at first it is hard to comprehend the full picture.


text:
How do the homologous chromosomes pair up and position themselves along the center of the cell?
I am not sure... Most textbooks just state "they line up" but I don't know how... Something to do with the cytoskeleton or microtubules? Thanks for any help

Are you asking about meiosis or mitosis?

Welcome to SE.biology! These papers 1, 2 should help you. Don't hesitate to come back with more specific questions if you need to. We are happy to answer them.

If your textbook only says "they line up", then you should get a better textbook.

It is unreasonable to close this as a homework question.

There are many things involved in the pairing of homologue chromosomes.
Before mitosis can occur an important prerequisite must happen: the division of centrosome. This small complex is the principal microtubule-organizing center in the (animal and therefore human) cells. During interphase the microtubules originating from the centrosome, project to the cell perimiter with their + ends (this where they grow). At the beginning of mitosis the duplicated centrosomes separate and migrate to oppsite sites of the nucleus to form the poles of the mitotic spindle. As the nuclear envelope disintegrates the spindle captures the chromosomes at the cetromeres. Since the microtubules are growing from the centrosomes this capture eventually pushes the choromosomes to center. Source: The Molecular Biology of the cell. Fourth Edition. ISBN: 0-8153-3218-1 (hardbound) 0-8153-4072-9 - (pbk).
A searchable online version: http://www.ncbi.nlm.nih.gov/books/NBK21054/
I've found a few good articles with many details:
Current Biology, Volume 12, Issue 17, 3 September 2002, Pages 1473–1483
The Dynamics of Homologous Chromosome Pairing during Male Drosophila Meiosis
Julio Vazquez, Andrew S Belmont, John W Sedat
and
Homologous pairing and chromosome dynamics in meiosis and mitosis
Bruce D. McKee
I took a quick glance at the above mentioned articles, and it seems that homologous chromosomes tend to be close together (paired if you wish) during interphase most of the time.

We need to make a distinction between the pairing of homologous chromosomes that occurs during meiotic prophase--the pairing that is necessary for homologous recombination, and that forms crossovers, or chiasmata--vs. the lining up of mother and daughter chromosomes on the mitotic spindle's metaphase plate after DNA replication (during S-phase of the cell-cycle). So yes, to ensure that each daughter of a dividing mitotic cell gets one pair of every chromosome, a requisite step is to build a mitotic spindle, and so you need to duplicate the centrosome (MTOC) first.

In one of your dividing somatic cells you have 2 copies of chromosome 7, one from your mother, and one from your father. After DNA replication and cell division, each daughter cell will also have 2 copies of chromosome 7, one of each type. The daughter cells never get 2 copies of the father's chr 7 (nor 2 copies of the mother's chr 7). In other words, there is no segregation where the genetic constitution of one daughter cell differs from the other daughter cell, the cells are identical. The two replicated father's chromosomes on the mitotic spindle are not paired along their lengths.

Their centromeres are attached to each other, and to the spindle. More specifically, the two copies of the father's chr 7 may not be anywhere near the two copies of the mother's chr 7. Pairing of chromosomes during interphase is not particularly common. In dipterans, there are some tissues, such as the larval salivary glands, where successive rounds of endoreduplication lead to polyploid cells with giant aligned chromosomes, also called polytene chromosomes, but this is a specialized situation. The gut nuclei of nematodes also endoreduplicate, without forming these lined up daughters.


text:
Do sweat pores change diameter?
In Cholinergic Urticaria, some people believe that the itching which is generally more in winters might be because that the diameter of sweat pores is less due to less activity(less sweat production) and in summers the diameter is usually more due to high activity (more sweat production).
Question: Hence the question in general, Do sweat pores change diameter?

Personal medical questions are off-topic here at SE.Biology. This question is legit and well written but please remove any link to yourself. Thank you.

I edited your question so that it might not get closed. Please revert of modify my changes as you like.

gud one @cagliari2005

what is your question? Why it happens more in winter than in summer? Or what the causes are?

I think I included the causes as far as researchers know today in my question,but if you wanna go more into detail into causes then fine.... @AliceD plz make sure its focus is on my question in bold.

Pores don't change size; that is, the diameter of pore does not increase or decrease in hot or cold environments. Your skin, where pores are located, is not muscle but an organ so the pores don't contract or expand.

Pores can become clogged with dirt, oil, and debris (make up). When pores are clogged, you are more inclined to notice which would cause the illusion that the pore is bigger.

It's important to know that you can't actually "shrink" your pores. They're nothing but small openings in the skin -- because they don't have muscles, they can't open or close. So although you can't physically change the structure of your pores by making them smaller, there are things that you can do to minimize their appearance$^1$.

Just learned something.

@cagliari2005 it is actually common that people think pores expand and contract. The reason is because washing with warm water loosens debris cleaning the pores. Therefore, people then think the pores expanded when it was just warm water loosen the gunk.


text:
Where to find E.coli gene expression data?
I am searching E.coli whole genome expression data with different conditions, any suggestion is appreciated. Condition could be for example different growth temperature, different medias, etc.
I have tried GEO but it only gives a list and one should read all pages and samples one by one to see which conditions were used.

What do you mean with "different condition"? GEO is a database which holds gene expression data, so it is not the place to look for whole genomes. If you look for gene expression data instead, please adapt your question. Information about different complete E.coli genomes can be found here

@Chris  I modified my question

Are you looking for something that would give you a list of what genes are expressed under specific conditions?

you can run an automated GEO query and fetch GEO accession numbers for the ones that match your keywords.

If you are interested in sequencing data then search NCBI-SRA

@WYSIWYG can you please give me an example how to run it and how to get them?

@Nemo see here. You have to construct a search based on your keywords and mention the database. Then you have to mine the retrieved list of information to select which ones you actually require. You can then download the data corresponding to these experiments in a similar manner. See this too. If you have specific doubts about this then post them as new questions.

There are some databases in which you can search for E.coli gene expression data:

GenExpDB: E. coli Gene Expression Database
Many Microbe Microarrays Database (M3D): A resource of microbial
gene expression data
Stanford MicroArray Database (use the search tool to find relevant organisms)
Colombos (COLlection Of Microarrays for Bacterial OrganismS)
ArrayExpress

To find out about the purpose and the conditions of the experiments behind this data sets you will have to read the respective publications.

can you please post some example papers done for E coli gene expression data if you are aware  of any

@Nemo http://lmgtfy.com/?q=e.coli+gene+expression+studies


text:
What is the function of dendritic cell in immunity?
I'm interested in how dendritic cells present antigens to  helper T-cells? I'm also interested in the molecular actions between a dendritic cell and a helper T-cell during the activation of the helper T-cell?  What function does the homing receptor on a T-cell have?

what is your question?

In the inflammatory response, dendritic cells mainly function as antigen-presenting cells, but the homing phenomenon happens under normal (non-inflammatory) conditions. Note that this is different from immune cell recruitment to the site of inflammation. You should specify under which context you'd like to know DC function.

@poka.nandor I must say the probability is high you are a good in-between lines reader :)... That edit...

@cagliari2005 - Thanks :) This seemed the most logical intention (at least for me) of the question based on title and the short description provided.

Dendritic cells are so called professional antigen-presenting cells (APCs) as pointed out by Sleepes in comment section. They express both MHC-I and MHC-II receptors on their cell surface on which they present small peptides. These small peptides come from digested proteins of their own (MHC-I) or antigens that were phagocited or taken up by receptor mediated endocytosis (MHC-II). They also express costimulatory molecules necessary for the activation of T-cells (eg. CD80/CD86).

source: http://journals.cambridge.org/fulltext_content/ERM/ERM2_09/S1462399400002143sup004.htm
As you can see in image above, activation of a T-cell requires two distinct signals: the recognition of an antigen and a co-stimulatory signal.

source: http://www.mhhe.com/biosci/ap/dynamichuman2/content/gifs/0158.gif
After activation T-cells undergo rapid division and diversification.
Details of T-cell activation by dendritic cells can be found in this article for example:
Immunol Cell Biol. 1997 Jun;75(3):223-30.
The role of dendritic cells in T cell activation.
Ni K1, O'Neill HC.


text:
Alcohol and athletes?
I've seen a lot of articles claiming that alcohol has a very bad impact on athletic performance. Examples include, but are by far not limited to:

http://oade.nd.edu/educate-yourself-alcohol/alcohol-and-athletes/
http://www.theguardian.com/lifeandstyle/the-running-blog/2014/apr/23/how-does-alcohol-affect-athletic-performance
https://www.acsm.org/docs/current-comments/alcoholandathleticperformance.pdf
http://www.athletestore.co.uk/wordpress/wp-content/uploads/2013/01/The_Effect_of_Alcohol_on_Athletic_Performance.7.pdf

I'm of course not in position to doubt those articles, as I'm a no expert in biology.
However. There is one thing I find odd.
Namely. These articles themselves claim that alcohol is widely consumed even by the highest ranking athletes. I mean, if alcohol has that bad effects... then it couldn't have been consumed by highest-ranking athletes, as alcohol-consuming athletes could never rich the heights of the tops of proffessional sports?
Also. AFAIK mediaval knights were not abstinents by any means, they were drinking beer and wine and mead to excess; yet they were able to bring their strength, stamina, etc, to an extreme.
This is not something I wish to argue about; rather, this is something I fail to understand.
BTW. This question is not personal; I don't do sports and I very rarely drink. And I regret the former, not the latter.

Whenever you look at any parameter in a population, you will have a spread. Let's take I.Q., for instance (and lets not quibble about how it's measured; it's irrelevant for our purposes):

This is the famous "bell shaped curve". You can see how few people are significantly above normal. Now, that line continues to include people with an I.Q. of 200+. That's not immediately obvious from the graph. It also continues the other way - people with an I.Q. so low that they cannot participate in their own testing. That's because the vast majority of people fall between 70 and 130.
The same principle applies to physical skill, bravery in battle, etc. The curve may be flattened or sharper depending on what parameter is being measured, but rest assured, paid professional athletes fall in the upper 1 percentile.
Lets go back to intelligence for a moment. Take someone like Bobby Fischer (Chess Player), I.Q.: 187
I guarantee you that even falling-down drunk, Bobby Fischer would have beaten me easily in a game of chess (and it's not because my I.Q. is average or below). It's because he was so very much, unimaginably better at chess than I am.
I guarantee you that even falling-down drunk, Albert Einstein could solve mathematical equations I can't even write. It's because he was so very much, unimaginably more intelligent than I am.
It's the same with great athletes. Even if they drink every night, a great athlete will outperform you or me on any given day.
That's why you are just dead wrong when you state "then it couldn't have been consumed by highest-ranking athletes, as alcohol-consuming athletes could never rich the heights of the tops of proffessional sports".
You are just laboring under a completely false premise. These people are so much better than people only 1 percentile below them that drinking doesn't necessitate that they fall in the ranks.

While a drunk Usain Bolt or Tiger Woods could beat me at their respective sports, the pro athletes etc are competing with others also at the extreme end of the bell curve, a gain of a small percentage does matter then.

@GriffinEvo - not if most of them are drinking, which they are. Alcohol use isn't a major factor for most top athletes.


text:
Why do women live longer than men?
According to Wikipedia and many other sources, women live substancially longer than men (over 5 years in the U.S.).
Men can reproduce for much longer than women.  So longer living men would have the most offspring, while the longevity of the women would be more or less irrelevant in reproducing.  These offspring would be the product, on average, of men and women where the men are older than the women.
So why do women live longer than men?  Am I misinformed, or what don't I get?

In my place it is the vice versa :)

I believe reproduction itself has something to do....i seem to recall that links have been seen between sexual reproductivity and shortened lifespan.
See this, for example: Bowen RL, Atwood CS. Living and dying for sex. A theory of aging based on the modulation of cell cycle signaling by reproductive hormones. Gerontology. 2004; 50: 265-290.

Behaviour
I would think that the most important causal factor between this difference is behaviour. Men probably smoke more than women, probably eat more junk food and are eventually more stressed. Men also probably take more risks and have more accidents. This last point might have been very important at an earlier time when men were hunting outside while the females would work inside the cave. Depression is more prevalent in men as well and it is possible that might affect health. These differences in behaviour might be caused by genetic (and epi-genetics) differences (sexual chromosomes) or by culture.
Oestrogen
There was a time where some doctors thought that the different was due to oestrogen but I think that this hypothesis has been ruled out.
The Y chromosome is short
Men have a Y chromosome while women have two X chromosomes. At each mitosis, the chromosomes get shortened (telomere are shortened). It is possible that the presence of the Y chromosome may explain some of the observed difference due to its small size. However, according to @cantona'sCollar the Y chromosome is often lost in somatic cells and therefore the difference of length between the X and the Y chromosome doesn't seem to be a good explanation.
Grandmother hypothesis
While women stop reproducing earlier than males, women often provide more care to their grandchildren than men do. As a result of this behaviour, genes coding for longer lifespan are beneficial by the fact that they help other copies of themselves (found in the grandchildren) to thrive (kin selection).

Depression is more common in women not in men:
http://www.nimh.nih.gov/health/publications/depression/index.shtml?ct=39994
Also, I would say that the roots of different behaviors are most likely to be in the genes since lifespan of men are shorter than women in most cultures. My guess would be the effect of testosterone. Men are more prone to take risks - even the life threatening ones - because of this hormone while women are more likely to choose the safer path.

I edited my answer to basically redraw some claims that were wrong or at least had little support. Thanks for your comment.

In reasonably fit people, men die from cardiovascular events at least 5 times more than women even after adjustment for smoking, cholesterol, high blood pressure, blood glucose, etc. This endocrinology paper of August 2013 attributes some of that to estrogen. I do agree that telomere length and mitochondrial DNA play a role, but isn't telomere length maintained on non-X chromosomes in women longer than men, or am I mistaken?

I have no idea if telomere shorten faster in all chromosomes in men. In this kind of discussion it is important to not forget the cause-consequence framework. It is possible that men died earlier because of more risky behaviour (such as hunting) and in consequence they would have relaxed selection at later age allowing late acting deleterious alleles to accumulate on the Y chromosome and things  like that.

I should say that the bit about Y chromosomes does not seem right. A "-Y" abnormal karyotype in somatic cells is frequently seen in older men (>70 years of age) and it doesn't seem to necessarily correlate with any clinical abnormalities.

@Cantona'sCollar What do you mean by A"-Y"? Do you mean that the Y chromosome end up merging with an autosomal chromosome? That's interesting. However, It doesn't change the fact that if it does not happen to everyone, you will still see a different life expectancy for men and for women. Also, if life expectancy were to differ only slightly due to telomere length of the Y chromosome, then it would reduce selection at later ages and further reduce life expectancy.

"-Y" means a loss of the entire Y chromosome. If there was a translocation with an autosome or something, it would end up being detected in standard karyotyping analyses (usually based on banding patterns).
The Y chromosome has so few genes on it, and most are involved in fertility/fecundity and are not very likely to contribute to long term health. Therefore, I cannot imagine how the presence/absence of a Y has anything to do with explaining different age spans of men vs women.

Oh ok good point. I edited my answer in reaction to your comments. Thank you

The best explanation I have come across so far is that male sex hormones have an adverse affect on longevity.
The effect may simply be that a high testosterone level suppresses the immune response against a variety of infections.
There was a recent study about korean eunuchs from a few hundred years back, that found that "The average lifespan of eunuchs was 70.0 ± 1.76 years, which was 14.4–19.1 years longer than the lifespan of non-castrated men of similar socio-economic status."
That's a pretty hefty difference and a strong argument for testosterone as risk factor for an earlier death. This would also vibe well with reports about increased risk of cardio-vascular death in steroid users.


text:
What is the difference between meristem and bud?
Keep reading both terms quite frequently while studying plant physiology. I did some research trying to establish their differences and I learnt that meristems are undifferentiated cells that can generate more cells that eventually could grow to form any part of the plant. But I really mess up both concepts, so I would really appreciate a comprehensive explanation of both of them separately. Thank you in advance for your help!

I looked in Taiz and Zeiger. Plant Physiology 5th ed and this is what I found:

Plant growth is concentrated in localized regions of cell division called
meristems. Nearly all nuclear divisions (mitosis) and cell divisions
(cytokinesis) occur in these meristematic regions. In a young plant, the
most active meristems are called apical meristems; they are located at the
tips of the stem and the root (see Figure 1.1). At the nodes, axillary buds
contain the apical meristems for branch shoots.
The root and shoot apical meristems formed during embryogenesis are called
primary meristems. After germination, the activity of these primary
meristems generates the primary tissues and organs that constitute the
primary plant body.
Most plants also develop a variety of secondary meristems during
postembryonic development. Secondary meristems can have a structure similar
to that of primary meristems, but some secondary meristems have a quite
different structure. These include axillary meristems, inflorescence
meristems, floral meristems, intercalary meristems, and lateral meristems.
Axillary buds are secondary meristems; if they are also vegetative meristems, they will have a structure and developmental potential similar to that of the apical meristem.

So, briefly, I could say that meristems are localized regions where undifferentiated cells reproduce themselves and originate new plant tissue. Axillary buds contain secondary (formed after embryogenesis) meristems. This meristem can behave like an apical meristem if it becomes vegetative i.e. either apical dominance disappears or it is excised and subcultured elsewhere.

A bud is capable of developing into a new individual while meristem can develop into any part of the individual. Buds can produce shoots, flowers, etc. while meristems have more variability - capable of developing into the tissues within the stem, a new individual, etc.

Thank you for your answer, but I was looking for a more comprehensive explanation.

Meristems in plant's kingdom are functionally similar to stem cells in animal kingdom, even you can see it in their names, meriSTEMs & STEM cells ,stem cells are more flexible,okay going back to meristems ,buds are complex of apical or lateral meristems which are covered by special kind of leafs according to enzymatic change,photoperiod and climate conditions buds can produce new leafs,branches or reproductive parts such as flowers, so we can say that buds are some kind of meristems themselves,but there are some other kind of meristems which act more particular and they are referred as cambium which usually cause the production of cork and cause the lateral growth and vascular elements reproduction.