text:
Why is it advised that infants are fed mother's milk?
I have heard that mother's milk is preferred over other baby foods, because it contains immunoglobulins (secretory IgA), and other essential nutrients.
But why is mother's milk so special? Any mammalian milk, such as the widely available cow's milk, should presumably have a similar composition as human milk? What makes mother's milk in specific so healthy?
Could the mere act of breastfeeding, in itself, lend to some beneficial outcome?

I think I read a comment on the parenting stack exchange about this topic, and it spoke on the benefits of mother and child bonding.

Was there a neuroendocrinological basis given for substantiating the bonding hypothesis ?

Just taking the immunoglobulins alone, I would ask you this: do you think cows have immunoglobulins likely to match the needs of a human infant as precisely as the human child's own mother (same pathogens, same environment, etc.) or that a cow's immunoglobulins are more likely a better match for that cow's own offspring? This goes across the board for all mammals in all differing locations (i.e. a mother's milk in Malaysia will have a different antibody composition than one in, say, Canada.

Anecdotal evidence (n=1): My 3yo daughter caught chickenpox and we have a 5 month old baby too. They are often close together and touch a lot. Baby is breastfed by mother who had chickenpox already (so she has antibodies). Baby is breastfed and didn't catch the (highly infectious) chickenpox.

@TomášKafka: you seem to be into something. WebMD endorses your anecdotal evidence: http://www.webmd.com/vaccines/tc/chickenpox-varicella-what-happens (2nd bullet point).

Cow's milk is not human milk. Starting with the percentages of fat to protein alone, the differences are immense. Evolutionarily, it makes no sense to surmise that milk from one species is just as suited for the offspring of another. Cow's milk evolved to feed calves. Human's milk evolved to feed humans. And the needs of calves are apparently quite different than the needs of infants.

@TomášKafka I don't know of any studies, but this is a very common belief, that the mother's immune strengths are passed to the infant's while breast feeding. If true, this means infants are immune to all that the mother is immune to. Alas, nothing is really that simple. If there is any truth to it, it probably varies by disease, geography, age, race, and everything else too.

@fredsbend I think you're just simplifying to the point of basically attacking a strawman. It's been observed that some antibodies (and other immune system-related "stuff") are passed to the child in milk, and some of them survive the infant's digestive system. Some is the key word, of course - it's nowhere near 100% effective, and it still depends on the baby's own immune system. The kid just gets a headstart on the markers, giving it a much better chance of coping with the infection - provided the mother is also exposed to the same infection (whether she gets sick or not).

@TomášKafka When I was two or three years old my brother (older by three years) caught chickenpox at school. My mother had already had it but my father and I hadn't had it yet. My brother had a bit of a temperature and a lot of spots. My dad became very sick with a fever and a lot of spots. Because I was so young I only got a few spots and no temperature. Neither my brother nor I were protected by my mother having chickenpox before we were born. It's more likely that your baby got it but showed no symptoms.

@anongoodnurse Adding to the issue of immunoglobulins; pasteurization (which is performed basically on all milk sold to consumers) will decrease the amount of immunoglobulins quite a bit. So even if immunoglobulins from cow's milk would be useful, they are mostly lost in pasteurized milk. Related, Chantry et al. (2009, J Acquir Immune Defic Syndr.) is studying the effect of flash-heat pasteurization on immunoglobulins in human breast milk, since flash-heating is used as a way to reduce vertical HIV transmission.

Well, I can't say necessarily mother's milk. It is possible for a woman to feed the child that is not born by her. And I can't say that mother's milk in this case gives an advantage over other woman's milk.

The phrase "Breast is best" is a hotly debated one (source: The Guardian and personal communications with many folks). The reason why we don't want to feed infants cow's milk is, however, anything but debated, because
Cow's milk does not provide enough:

Vitamin E
Iron
Essential fatty acids

And because it contains too much:

Protein
Sodium
Potassium (source: NIH's MedLine)
Further, mother's milk is generally free of pathogens, cow's milk may not be (source: Australian Unity). However note that, unfortunately, HIV can hitchhike within the maternal white blood cells to the infant (Quintanilla, 1996)

There are many benefits to mother and infant of breast milk. These benefits are, however, typically compared to the benefits over formula. No study will compare the benefits of mother's milk over cow's milk, simply because infants should never be fed cow's milk.
The benefits of breast milk for the infant are the following:

Breast milk a nearly perfect mix of vitamins, protein, and fat, all provided in an easily digestible form, as compared to formula;
Breastfeeding lowers baby's risk of having asthma or allergies;
Plus, babies who are breastfed exclusively for the first 6 months, without any formula, have fewer ear infections, respiratory illnesses, and bouts of diarrhea. They also have fewer hospitalizations and trips to the doctor (source: WebMD).
Breast milk contains a variety of growth factors, including EGF, BDNF and GDNF that may promote vascularization and neural development (Ballard & Morrow, 2014).

There are a host of immunoprotective factors present in breast milk. These proteins offer protection against diarrhoea, food allergies and infections. The immunoprotective components of human milk include, but are not limited to:

Lactoferrin : binds to iron, thus rendering it unavailable to viruses, fungi and bacteria, which is an effective means of inhibiting their growth (Ballard & Morrow, 2014);
Lysozymes: destroy viruses and bacteria by disrupting their integrity (source: NIH's MedLine);
Secretory IgA: immunoglobulins that destroy viruses and bacteria. Secretory IgA is believed to survive the harsh conditions of the intestines, especially in infants and is therefore active in the intestines of the baby. IgA can bind to pathological viruses and block their receptors necessary to invade the epithelial cells lining the intestinal wall. It also clumps bacteria together through cross-linking, which may affect their dispersion. Bacterial cell membranes, like shown in Salmonella, may be disrupted by IgA binding (Mantis et al., 2011). As mentioned by anongoodnurse in the comments; because mother and baby share the same habitat and hence encounter the same pathogens, the antibodies produced by the mother will be more beneficial to the baby than any other mammal on earth;
Human milk contains a variety of chemokines and cytokines that can cross the intestinal barrier, where they communicate with baby's cells to influence immune activity. Many cytokines and chemokines have multiple functions, and milk-borne cytokines may be grouped broadly into those that enhance inflammation or defend against infection, and those that reduce inflammation (Ballard & Morrow, 2014);
Bifidus factor: promotes the growth of beneficial bacteria in the gut and limits the growth of disease-causing bacteria (source: NIH's MedLine).
A variety of immune cells, including macrophages, T cells, stem cells, and lymphocytes. In early lactation, the breastfed infant may consume as many as 1010 maternal leukocytes per day. They can differentiate into dendritic cells that stimulate infant T-cell activity (Ballard & Morrow, 2014).
Breast milk changes in composition according to the infant's needs, something cow's milk can never accomplish; The first fluid produced by mothers after delivery is colostrum, which is distinct in volume, appearance and composition. Colostrum is produced in low quantities in the first few days postpartum and is rich in immunologic components such as secretory IgA, lactoferrin, leukocytes, as well as developmental factors such as epidermal growth factor. It contains relatively low concentrations of lactose, indicating its primary functions to be immunologic and trophic rather than nutritional. Levels of sodium, chloride and magnesium are higher and levels of potassium and calcium are lower in colostrum than later milk (Ballard & Morrow, 2014).

For more complete reviews on the immunochemistry of breast milk, please refer to Ballard & Morrow (2014) and Mantis et al. (2011)
The mother also benefits:

Breastfeeding burns extra calories, so it can help mothers to lose pregnancy weight faster;
Breast feeding releases the hormone oxytocin, which helps the uterus return to its pre-pregnancy size and may reduce uterine bleeding after birth;
Breastfeeding lowers the risk of breast and ovarian cancer. It may lower the risk of osteoporosis;
Breastfeeding has been linked to higher IQ scores in later childhood in some studies (source: WebMD);
During lactation, menstruation ceases, offering a form of contraception;
Mothers who breastfeed are less likely to develop breast cancer later in life;
Breastfeeding is more economical than formula feeding;
Hormones released during breast-feeding create feelings of warmth and calm in the mother (source: NIH's MedLine).

In terms of bonding:

Skin-to-skin contact during breastfeeding, and eye contact all help a baby bond with the mother and feel secure.
Oxytocin release is known to promote the bonding with bubba. A newly born person can cause dramatic changes in the life of mommie (and daddy!), and a steady release of oxytocin promotes the bonding and love of mommie for the bubba (source: WebMD).

References
- Ballard & Morrow, Pediatr Clin North Am (2013); 60(1): 49–74
- Mantis et al., Mucosal Immunology (2011) 4: 03–611
- Quintanilla, Nurs Times, (1996); 92(31): 35-7

I think this answer is very good; I'm not likely to top it for scope. The only thing I would add is more about antibodies and other contributors to immune function. (If you're interested, I left a comment under the question.) Here's another open source NIH paper that goes into more detail. +1

It should also be noted that (various levels and kinds) of milk allergy are rather common in infants, so for an interesting portion of the population, cow milk simply isn't a substitute even when combined with a formula. Often the mother has to avoid milk products as well, since enough of the protein makes it to the breast milk. And many formulas contain cow milk as well, so you're stuck with the very expensive ones tailored for infants with allergy.

+1 for a good and complete answer for the benefits of mothers milk. However as you stated yourself the issue is hotly debated. It would be nice to also add some disadvantages of breast-feeding. One example: producing milk is an energy-consuming process that slows down the recovery of the mother after giving birth. (Sorry no reference).

@RHA while it's an interesting subject, I think that's outside the scope of a question that's about whether milk from other mammals wouldn't be as good as breastmilk.

@RHA (sorry, deleted the first comment to rephrase) except for the "Breastfeeding is more economical than formula feeding", I find this answer to be mostly focused on human vs animal milk. True, some points are independent of what sort of milk it is and relate to breastfeeding specifically (and wouldn't apply to pumping, for example), but other than that, I seem to be reading the answer different than you are.

@RHA A working brain is also very energy-consuming. Should that be included in its disadvantages? // Child bearing by healthy women does not customarily require immediate "recovery" and it's completely not a given that stopping breast-feeding will have any positive clinical effect on the mother's "recovery". Not using up what your body wants to give away might in fact be determental to the overall health.

Actually, menstruation ceases when breastfeeding for some time. The woman will be fertile despite breastfeeding after a while. http://www.llli.org/nb/nbsepoct06p196.html

The point on pathogen transmission via milk is not really correct as you yourself have contradicted the point with the HIV example. There are many other pathogens that can be transmitted via milk. The issue with animal milk is that it may be difficult to check if the animal was infected.

I think the central point that would emerge from the entire picture is that the milk composition of a species is evolved such that it improves the fitness of that species. Buffalo milk has high fat and proteins compared to cow's milk but buffalo also produces lesser offspring (and a higher gestation period). A nutrient rich milk will ensure the calf's health/development and survival. So, in short, the milk composition is optimized according to the dietary/health requirements of the corresponding species.

@WYSIWYG - that's the debate. Nutritional value can be artificially reproduced. It's the immunological factors that are species and even individual specific. That's the point.

Aw, the bonding bit was nice. Quite scary how busy life, might then interfere and disrupt these potential bonding opportunities...

Lysozyme degrades bacterial cell walls, it does not affect viruses.

To further emphasize colostrum, infant have very weak immune systems early on and the supplimentation by the breastmilk is very helpful.

I think it would be better to cite this regarding HIV transmission: https://www.advancesinpediatrics.org/article/S0065-3101(07)00015-1/fulltext#sec4.5.6

The contents of milk differ between species. For your example, cow's milk:

Infants fed WCM [Whole Cow's Milk] have low intakes of iron, linoleic acid, and vitamin E, and excessive intakes of sodium, potassium, and protein

Calves have different nutrition needs from human babies. Infants who receive cow's milk instead of breastmilk often suffer from iron deficiency (anemia).
As for antibodies, human babies will benefit the most from antibodies that help against diseases infecting humans, which are not the same as those infecting cows.

Calves have different nutrition needs from human babies. You hit the exact point, IMO. It applies for every species.


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What type of tree is this?
This is a tree that I have been growing. I'm wondering if this is a mulberry, and if so, what kind?  Location is Arizona.

It's produced fruit for about 3-4 years and it grew wild in our grass and we've had 9-11 more grow its fuitt are green, then red , then juicy purple in the end

Where is the tree growing? That's essential information for species identification questions.

Arizona near Kingman

It is a mulberry.  What isn't clear from the photos, and may not be clear without a DNA analysis, is whether it's a hybrid of the native red mulberry and the white mulberry imported from Asia in the hopes of starting a silk trade in North America (white mulberry is the main food source for silk caterpillars), or whether it's distinctly a red or white.  The berries won't always indicate this, and the leaves won't always indicate this.  At this point, our red mulberry has seen sufficient habitat loss that most new mulberry trees are hybrids.

Thank you we've had 9-10 grow and they're is 2 different kinds of them. All produce fruit and the fruit is red and then mostly turn dark purple/red.

I am sure it is a Mulberry (Morus sp.). I have two of them growing in my garden. The bark, leaves and flowers look exactly like my trees. Note that the Mulberry has different male and female flowers (and off course only the female produce fruit). To be 100% sure I looked it up in Blameys' "Mediterranean wild flowers".

Looking at the landscape in your area (which suggests somewhere between west Texas and southern Oregon) it might also be a black mulberry.
Here is a snippet on black mulberries

Thank you and this is in Arizona so you're correct I want to say it's a black mulberry as well.

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sort: votes


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How do I measure fermentation rate?
I'm doing a lab soon and I need to find a way to measure fermentation rate to a relatively high degree of accuracy without using a specialized sensor. It should ideally be done with easy to find tools at home or in the classroom.

http://www.freecontentweb.com/content/measuring-rate-alcohol-fermentation-yeast-cells Perhaps

@CMosychuk I'm not quite sure how there measuring it, I got lost when they said "its distance to the baseline water level." The difference of what to the baseline water level?

Your setup is essentially like this. You have the fermentation occurring in one tube. The CO2 travels through tubing to another tube that was inverted with water in it, and the other end of the tubing fed through the bottom. The CO2 will force with water level in the inverted tube down so more CO2 = lower water level. If you take readings over time, you can measure the relative rate per unit time.

Here is a more simple figure!

@CMosychuk I'm not sure I can do exactly that but I may be able to do a variation.

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Why is it common to grow microalgae in bottles or canisters?
I came across many people growing Chlorella or Spirulina types of microalgae, inside bottles or canisters and that that they also bubbled CO2 into these containers artificially.
This question is basically comprised of two questions that will clarify what I am trying to understand:

Why do they use bottles or any type of bottle-like canister?
Why do they insert CO2 to the bottle artificially in cases the bottle doesn't have a cork ? If the claim is that enough CO2 won't be able to get through the bottle neck than why growing the algae inside a bottle\aquarium in the first place, and not in a tub with full exposure to the air?

Simple answer from http://justspirulina.org/spirulina-manual/ "Spirulina needs sunlight so it is preferable that the container in which it is grown be transparent. Empty, clear soft drink or water bottles (at least 1.5 litre) are a good option."

@Benia I cannot find anything about "they insert CO2 to the bottle artificially" in the links provided by you.

The thin tubes they insert, aren't these splitting CO2 into the water (as the bottle is sealed for CO2 entrance) ?

Really, the credit for this answer goes to another 'Homo sapien' from the Spirulina manual link in his comment.

Why do they use bottles or any type of bottle-like canister?

Likely, because they are clear. From the manual:

Spirulina needs sunlight so it is preferable that the container in which it is grown be transparent.

Plastic bottles are cheap, clear, and easy to come by, so they make the ideal material.

Why do they insert CO2 to the bottle artificially in cases the bottle doesn't have a cork?

I don't think the tubes in your picture are CO2 tubes. Rather, I'd bet they are bubble tubes (like in aquariums). These are necessary to keep the growth medium moving constantly. Again, from the manual:

Spirulina tends to gather at the top of the growing culture, where sunlight exposure is maximal. Due to this, Spirulina that cannot reach the top will not multiply and will ultimately die.
In order to maximize Spirulina exposure to sunlight, the water in which it is grown must be stirred
...
Another option is a pump, the simplest kind used for aquariums.
(emphasis mine)

Luigi, a small question, aren't at least some aquariums have CO2 tubes sometimes? I mean aren't some types of Fish or Algae hat does need extra CO2 into the water in some other cases?

BTW please thumb up if you liked the question - If you would, I could thumb up your answer...

@Benia I already have. And regarding the aquarium question, I'm not an expert on fish or algae, but I always thought the purpose of the tubes into aquariums was to move the water/make it more accessible for gas exchange, so that the oxygen/CO2 in the water could be closer to atmospheric levels (you don't want to suffocate your fish). While I'm sure there are specific organisms that prefer low CO2, I feel like most everything has evolved to grow best at atmospheric concentrations of O2/CO2

@Benia I do not think there would be any fish or algae that would have evolved to live by getting extra CO2 from artificial source. You see, as Luigi said, most organisms are adapted to live with natural atmospheric conditions (except, maybe, thermophiles which live near volcanic vents in deep sea surface).

Well, according to what you said guys I know understand that this tubes insert some fresh air to the water and the excessive Oxygen or CO2 / any other air-material will just leave the water out through the bottle-neck (and open area if there is no cork) and thus will just split the algae in a more efficient way and avoid formation of a single light-hiding layer of algae in the outermost areas of the canister... I hope I understand you well guys, this is very helping for me and I am very grateful for you for your help !!!

@Luigi While you certainly can grow aquatic plants with atomospheric CO2 levels, they don't necessarily "grow best" at that level - a fair number of people with planted tanks will supplement the CO2, sometimes with rather elaborate rigs, to increase the growth rate of the plants. If you're attempting to produce microalgae in bulk, it might be reasonable to supplement the CO2 to increase the amount you're producing.

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Are all genes transcribed in differentiated cells?
My textbook tells me that it’s specific transcription factors that allow for a different set of genes to be expressed in different cells (differential gene expression). My book gives the example of liver and lens cells—liver cells contain the specific transcription factors (STFs) to activate the enhancer for the albumin gene, while lens cells contain the STFs to activate the enhancer for the crystallin gene. Liver cells do not have the STFs to activate the crystallin gene, and lens cells cannot activate the album gene.
However, my book also tells me that there is a basal level of transcription that arises from the binding of general transcription factors. Enhancers only increase the rate of transcription on top of that basal rate. Does this mean that in differentiated cells, all genes are indeed transcribed? I.e. a lens cell does transcribe the gene for albumin and the liver cell does transcribe the gene for crystallin?
(The wording of my book dissuades me: "Liver cell: The albumin gene is expressed, and the crystallin gene is not. Lens cell: The crystallin gene is expressed, and the albumin gene is not.”)

Theoretically, yes. They are all transcribed, but in trace amounts. And because hepatocytes do not need crystallin, it might get degenerated by proteases or processed into another protein by ER and golgi bodies.

No, there are genes that are completely turned off. As in, our current technology cannot amplify any transcripts to detect in sequencing. If you do full high sensitivity RNA-seq in different cell types, you will find some transcripts for which there are zero reads (above noise) in each type, and they will be a different overall set based on cell type.  In addition, some genes are silenced after development.  This silencing is usually through histone modifications that completely abrogate the ability for transcription factors to even bind to the DNA.

This answer and the paper referenced therein may answer your question, if you still care after all these years.

No
Not all genes are transcribed, repressor proteins and nuclear receptors can bind the DNA preventing transcription of particular genes. Even things like histone regulation can prevent transcription. There may even be epigenetic regulation of transcription.
Source 1
Source 2

I think genes are transcribed but either mRNA is not transcloated (moved) into the cytoplasm or they are not translated (maybe degraded).I think if you do RNA screening you will get same positive results in both liver and lens cells (as transcription occurred and if your procedure is not having any error) but if you do a western blot, the result will change as now we are seeing the things at the protein level.
So even though all of our cells have same gene composition depending upon the tissue and organ they have differential RNA selection so that they will not waste resources in making unwanted proteins.

A source would be important, especially for an "I think" answer.

Sorry, yes I should have given the proof. You could read it in Developmental Biology Gilberts 6th edition, here is the link of the book from NCBI https://www.ncbi.nlm.nih.gov/books/NBK10112/

You should add that is not the answer, I can't change my vote unless you edit it anyway.

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What is effect of sperm in blood?
Staphylococcus aureus, Streptococcus pyogenes, and Clostridium perfringens all produce hyaluronidase.
Each of these bacteria are pathogens (use hyaluronidase as a virulence factor to destroy the polysaccharide that holds animal cells together, making it easier for the pathogen to spread through the tissues of the host organism)

The role of hyaluronidases in cancer is controversial, however there is substantial evidence of increased hyaluronidase activity in malignancies.

We know, human sperm also produces hyaluronidase (for penetration of ovum),
So what would happen if sperm enters blood (Like:via cuts or wounds on genitals)?

Ciliary Dysentery(Balantidiasis) is caused by Balantidium coli(ciliated protozoan) which causes ulcers in colon and invades mucous membrane by secreting "Hyaluronidase"

Not much really, blood would be a really hostile environment for sperm. And they would get targeted by the immune system rather quickly. Fertilization of oocyte by sperm is a very specific process, sperm would not be able to "drill" through any type of cells.

Would there be any effect in body after hyaluronidase is secreted by sperm? You can guess it by examples given by me.@Maljam

could you link the evidence to your claim The role of hyaluronidases in cancer is controversial, however there is substantial evidence of increased hyaluronidase activity in malignancies.?

link   is the required link.@gone

The problem with bacteria in tissues is that they can multiply, causing more damage. A sperm can't multiply. It's effect would be negligible.


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Why does Taq polymerase add 3' adenine overhangs?
Is there a mechanism for the preference of Taq polymerase to add a non-templated 3' adenine (overhang) instead of other bases?

Non-templated terminal addition by certain DNA polymerases is apparently dependent on the base stacking between the incoming base and the existing duplex (Fiala et al., 2007*). This was verified by using a non-base-pairing (but better stacking) nucleotide analogue called deoxyribo pyrene nucleoside triphosphate (dPTP). Adenine seems to have a higher efficiency of base stacking compared to other three bases:  A (1.0), G (0.7), T (0.6), and C (0.5)
It was also verified that the preference for dATP did not depend much on the terminal base-pair of the duplex with the incorporation probabilities being:
79% dATP 16% dTTP, 3% dCTP, and 2% dGTP when the last base pair is A-T (A is 3'), and
81% dATP, 8% dTTP, 8% dCTP, and 2% dGTP when the last base pair is G-C

Fiala, Kevin A., et al. "Mechanism of template-independent nucleotide incorporation catalyzed by a template-dependent DNA polymerase." Journal of Molecular Biology 365.3 (2007): 590-602.
*They had used the Dpo4 polymerase from Sulfolobus solfataricus as a model because it is a known lesion bypass polymerase and its kinetics and structure are well studied.


text:
Pearson correlation of neural responses with it's linear estimation
I am trying to anderstand the following fact from this article (page 13):
How can single neurons predict behavior
Suppose I have a linear estimation of a stimulus:
$ \hat{s} = \mathbf{w}^T(\mathbf{r} - \mathbf{f}(s_0)) + s_0$
where $\mathbf{w}$ is a vector of weights, $\mathbf{r}$ is a vector of responses responses of two neurons to a stimulus, $\mathbf{f}$ is the vector of average neural responses to the stimulus, and the stimuli (angels between $-\pi$ to $\pi$) are symetric (amount and location) around $s_0 = 0$.
Can anyone see why the following is true for the Pearson correlation (where $\Sigma$ is the covariance matrix of $\mathbf{r}$):
$$ Corr(\hat{s},r_k) = \frac{\langle \hat{s}r_k \rangle - \langle \hat{s} \rangle \langle r_k \rangle}{\sqrt{( \langle \hat{s}^2 \rangle - \langle \hat{s} \rangle^2) }\sqrt{( \langle r_k^2 \rangle - \langle r_k \rangle^2) }} = \frac{(\Sigma \mathbf{w})_k}{\sqrt{(\Sigma_{kk}\mathbf{w}^T \Sigma \mathbf{w})}} $$
Thanks!!


text:
Do nematodes have organ-level organisation?
Some introductory biology books state that nematodes have a pseudocoelom. So, they have a false body cavity. So, does it also mean that they have organ level body organisation?

In Fig.1 is shown the body plan of a round worm:

Fig. 1. Nematode. source: University of Illinois
You ask whether there is an organization in terms of organs; an organ is:

A group of tissues that perform a specific function or group of functions;

A tissue is:

An aggregate of cells in an organism that have similar structure and function;

As you can see in Fig. 1, there are clearly organs present, including a mouth, pharynx, reproductive organs, among others. They fulfill different tasks and contain various tissues, each dedicated to specific functions. Hence, they fulfill the definitional requirement of being organs.

Adding to Christiaan's answer, I quote Caenorhabditis elegans' anatomy to substantiate that nematode have proper organ development.


text:
Techniques to show a protein heterodimer-DNA interaction
It is known that c-Jun and fos dimerize to form AP1 factor that binds to a sequence on DNA containing PyPuGACGTCNNNNGAGGTCPyPU.  In esophageal cancer cell lines there is no expression of the fos gene. However we still see expression of genes regulated by AP1 factor.  One of the possibility is another isoform of fos is expressed in these cells (e.g. fra1).

How will you check that fra1 is expressed or not in these cells.
How will you check that the heterodimer bound to the given DNA
contains fra-1 along with c-jun.

My thoughts on the above questions
For first question we can do immunofluorescence assay or we can do DNA affinity assay in which we chemically synthesize DNA sequence and bind it on agarose gel column pass through it protein extract of oesophageal cancer cells and our fra-1 protein if being expressed in cell line will bind to DNA. later we can elute protein DNA complex and by anti-fra1 antibody we can check if it is being expressed. But the drawback of both these technique is we should have knowledge of epitope of fra-1.
For second question - we can perform ChIP using antibody tagged Against c-jun and then eluting out DNA bound to c-jun. Then we can simultaneously label the complex with anti fra-1 in one sample and anti fos in another sample. We can check for results. If fluorescence is obtained in case of fra-1 sample that means both c-jun and fra are bound to probe and not fos.

You should add your thoughts onto the post directly and use the homework tag if it is a homework. Homework questions are on-topic as long as the OP is showing effort for answering the question himself/herself

I'm going to throw RT-qPCR and EMSA "supershift" out there, but there are other methods, with their own pros and cons.

How will you check that fra1 is expressed or not in these cells.

RT-PCR is a quick and an easy method to check for expression. However, it only tells you about the RNA level expression and you would have to work with the assumption that RNA concentration is directly proportional to protein concentration.
Considering that you do not have an antibody for fra1, you can go for mass-spectrometric protein quantification. It is good for a high throughput analysis and is generally wasteful when you just want to study one protein. However, people do carry out targeted proteomics to study a few proteins.
Alternatively, with some effort you can actually develop an antibody for fra1.

How will you check that the heterodimer bound to the given DNA
  contains fra-1 along with c-jun.

Showing ternary complexes (fra-jun-DNA) are a bit difficult. It is relatively simple to show pairs. You can show that two proteins form a complex in vivo by doing a co-immunoprecipitation followed by detection by either western blot or mass-spectrometry.
You can also show interaction by biophysical techniques involving FRET and SPR but these cannot be performed in vivo (at least SPR. FRET can be done but there are limitations).
You can show the DNA-protein interaction by ChIP-seq as you mentioned in your question.
Showing all the three together is a bit tricky.
You can do it using in vitro assays that employ fluorescently labelled (one GFP and other RFP; or FRET pairs)/custom epitope tagged (for e.g. one FLAG and the other HA -tagged) proteins and a known DNA sequence generated by PCR/DNA synthesis. You can use EMSA along with antibody/fluorescence based detection to show the ternary complex.
You can indirectly infer the presence of the ternary complex when the ChIP-seq using antibodies for both the proteins shows up the same DNA sequence in the reads. You can also express a FLAG-tagged (or any other tag) protein, if in case you do not have an antibody for the proteins.

Nice list of many techniques, I'd just like to mention that you could also label the the DNA with biotin, an isotope or something else to suit your needs.

Can you clarify on the term "ternary", also ditto ^^

@hello_there_andy "ternary" means a complex of three components.


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Why are some genomic regions sequenced more than the others?
We have to normalise read count data from RNA-Seq experiments in order to account for the fact that some genomic regions are mapped more than others. i.e. we get the tags per million reads (TPM). In other words, they have a higher sequencing depth/vertical coverage.
Why are some genomic regions mapped more than others; what is the reason for this non-uniform distribution of sequencing depth?

For RNAseq, the differences in the read depth can simply arise because of expression (that's trivial). Highly expressed regions will have higher number of reads.
However the read depth non-uniformity also arises because of the nucleotide composition of the regions. This is true for all kinds of nucleic acid sequencing such as RNAseq, whole genome sequencing and ChIP seq. This is called sequence bias. This also depends on the sequencing methodology. A variety of factors play a role such as how well can the region be sheared, how well can it be amplified etc.
For details have a look at this article by Ross et al (2013).

Sequencing technologies are vulnerable to multiple sources of bias.
  Methods based on bacterial cloning and Sanger-chemistry sequencing [8]
  were subject to many coverage-reducing biases, notably at GC extremes,
  palindromes, inverted repeats, and sequences toxic to the bacterial
  host [9–17]. Illumina sequencing [18] has been shown to lose coverage
  in regions of high or low GC [19–22], a phenomenon also seen in other
  'next-generation' technologies [3, 6]. PCR amplification during
  library construction is a known source of undercoverage of GC-extreme
  regions [20, 21] and similar biases may also be introduced during
  bridge PCR for cluster amplification on the Illumina flowcell [23].
  Illumina strand-specific errors can lead to coverage biases by
  impairing aligner performance [24]. Ion Torrent [25], like 454 [26],
  utilizes a terminator-free chemistry that may limit its ability to
  accurately sequence long homopolymers [4, 27, 28], and may also be
  sensitive to coverage biases introduced by emulsion PCR in library
  construction. Complete Genomics [29] also uses amplification along
  with a complex library construction process. The Pacific Biosciences
  [30] process is amplification-free; therefore, one might expect it to
  exhibit lower levels of coverage bias than the other technologies.
In addition to sources in the wet lab, bias can be introduced by any
  of the computational steps in the sequencing pipeline.
  Signal-processing and base calling limitations could result in
  under-representation or increased error rates in some locations, as
  can inaccurate alignment. An inaccurate reference or sample-reference
  differences can cause coverage or accuracy variations that may be
  misdiagnosed as sequencing bias. Therefore, detecting bias is only the
  first step and must be followed by more detailed experiments to assign
  responsibility to the library preparation, sequencing, or
  computational stages.

Some analysis software try to correct for these biases while estimating the read abundance.

Ross, Michael G., et al. "Characterizing and measuring bias in sequence data." Genome Biol 14.5 (2013): R51.


text:
What is the difference between the mitotic spindle and microtubules?
In mitosis, I understand that the centromeres line up on the spindle. I also know that the centrioles form microtubles between the centromeres during mitosis in the metaphase.
But, are microtubles and spindles the same thing? Or do microtubles make up spindles?

Short answer
The spindle is made up of microtubules
Background
From Nature:

Spindle fibers form a protein structure that divides the genetic
  material in a cell. [...] At the beginning of nuclear division, two
  wheel-shaped protein structures called centrioles position themselves
  at opposite ends of the cell forming cell poles. Long protein fibers
  called microtubules extend from the centrioles in all possible
  directions, forming what is called a spindle. Some of the
  microtubules attach the poles to the chromosomes by connecting to
  protein complexes called kinetochores. Kinetochores are protein
  formations that develop on each chromosome around the centromere,
  which is a region located near the middle of a chromosome. Other
  microtubules bind to the chromosome arms or extend to the opposite end
  of the cell. During the cell division phase called metaphase, the
  microtubules pull the chromosomes back and forth until they align in a
  plane along the equator of the cell, which is called the equatorial
  plane.


text:
Synthesis of an additional DNA in Pachytene and Zygotene
I've read, that in Pachytene and Zygotene additional DNA material is synthesized, about 0,3, 0,1% respectively. Why is it so?

Is it possible to cite where you read this?

that's from one book, in Russian, unfortunately. But i can look for english source.
UPD: Answer below gave us english sources, i guess.

About 0.3% of total DNA complement is synthesized during those 2 stages as a measure of replication repair mechanism.
Reference:
http://www.ncbi.nlm.nih.gov/pubmed/3731943
http://www.nature.com/nature/journal/v219/n5153/abs/219489a0.html

Could you expand on this a little? Why is that DNA complement synthesized, and how does it act as a repair mechanism (and a repair mechanism to what)?


text:
Is there any evidence that any other species are "pre-intelligence"?
Is there any evidence regarding whether other species might, given time, evolve intelligence as humans have?
I realize "intelligence" is a vague word here, but I'm interested in throwing a wide net, since I imagine the small sample size of positive cases makes finding any evidence at all extremely difficult.
The only information I've been able to find so far seems vague and unscientific, but I'm expecting that is the best I'm going to be able to find.

Welcome to Biology.SE. Unfortunately, the use of the term intelligence really needs better definition. Many species are already much more intelligent than humans in several respects (such as memory for example).

Wiki > Animal Cognition is a long article but it may help you to focus your question and your interest.

@Remi.b Totally fair, and thanks for the link!

I found another article on here after I posted this question that is at least tangentially related to this subject, in case any one is interested: http://biology.stackexchange.com/questions/339/is-there-evidence-that-some-non-human-species-perform-sexual-selection-based-pri

I don't exactly know, what the intelligence is, but i've got an idea what it can be.
I've read about smth similar before. I suppose, we can measure intelligence with working memory (don't mix with shott-term-mempory)  term (like registers of processor).
There were many experiments that was provided to check how big a working memory of humans and apes.
According to information people got from these experimence, average WM of humans equal to 7, apes - equal to 4 (count of terms subject can manipulate without any significant mistakes). So, apes can be considered as pre-intelligence this way. But anyway it is still controversial question.
You can also google articles like this:  http://www.pnas.org/content/110/Supplement_2/10371.full.pdf

This doesn't answer the question at all well

Right, but i've just tried to make "intelligence" term more suitable for measuring and tried to think of what we can get from it. Actually, if we think of all apes, several of these (like gorrilas) are considered like in a "deadlock of brain evolution". Sometimes we can find some of chimpanzee for ex. or even gorrilas that shows outstanding brainworks and ability to learn something complex (bonobo Kanzi for example). But we should keep in mind, that such individuals are not general and we can't say it has intelligence as species.


text:
Chart of blood pH across different animal species?
How does blood pH vary across species?  I can't find an article or chart listing this kind of information.
So far I've found bits and pieces like:

Human blood pH is nominally 7.4.
7.4 seems to be a good value for dogs and cats (¿and probably all mammals?).
For racehorses it seems to be roughly 7.4.
Silkworm, Bombyx Mori, blood (hemolymph) has a pH of 6.45 (larval) and 6.57 (pupal).
Bullfrog muscle(!) pH runs roughly 7 to 7.3.  (Link to The Journal of Experimental Biology article, PDF) It's not clear if this is also blood pH.

But no real comparison.
Is there an authoritative comparison of blood pH between: mammals, reptiles, fish, invertebrates, etc.?
Is nominal/average pH at least constant across all mammals, or across all reptiles, etc.?

Don't forget most plant life needs soil that has a pH of 6.0 to 7.4 to dissolve nutrients easily, so you might as well add plant life to your list

@TheVoid, Sure, any plants that have blood. (^_^)

Its all life that needs a pH of level of 7.4 to be in the Alkaline. That is wear life can thrive at its fullest potential.

in reptiles variation from 6.5 to 8.1 have been observed. ectotherms in general have a broader range. http://jeb.biologists.org/content/jexbio/203/13/2065.full.pdf

@John, that's the exact same reference I used and I don't see anywhere where it says blood pH was in those ranges.  What paragraph or table are you looking at?

oh sorry that was the reference for the ectoderm statement. here s the reference for the PH values. http://www.seaturtle.org/pdf/dessauerhc_1970_inbiologyofthereptilia_p1-72.pdf

@John, Thanks!  Just skimmed it so far, but it seems to show that baseline is about 7.4-ish but it lowers dramatically during dives or other activities where CO2 builds up.  That would be extreme (in the) ocean acidification. :)

Crocodiles can do some weird things with their blood and even have different ph values for different parts of the body, http://compphys.bio.uci.edu/BENNETT/pubs/65.pdf but crocodile circulation is weird to begin with.

for non-crodilian reptiles there is also a strong relation ship between body temprature and PH, this alone could account for why birds and mammals are so stable.

insects have some wide ranges too. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2140737/

birds average 7.5 -7.6 http://www.sciencedirect.com/science/article/pii/0300962982902006?via%3Dihub


text:
What is the rationale for the complex eye structure?
The eye is a lens that focuses rays of light from a limited spectrum, after which the the image is turned over to the brain receptors that interpret it (beginning with turning it the right side up first, I think).
It is a complex and fragile instrument whose sole purpose is to pre-process the image "mechanically" (rather than "electronically") before turning it over to the "CPU." Please bear with me.
Most creatures who have one eye usually have another one as well. This second equally complex piece of hardware has, it would seem, two purposes: one, it serves as a spare; two, it allows its owner to see depth a bit better. (You can still see depth if you cover up one eye: your brain has to make a few adjustments, and a few more assumptions, but it's not like depth perception is completely gone, right?)
Now think of the original camera obscura (the one that had no lens, just a hole). By adjusting the size of the hole (aperture) one could make the resulting upside-down image on the opposite wall a bit sharper. The image is still a bit pale, but the subtle differences in color values would still be enough for a powerful computer (such as our brain) to work out the nuances.
Why would then God (or Evolution, for those who still believe in it) opt for making an infinitely complex piece of hardware (the eye) and then furnishing a backup as well, instead of just adding a few lines of code to the operating system?
Please don't take any of this too seriously.

Note that in addition to having two eyes, vertebrates have two of almost everything, down to brain lobes.  So it might be more informative to ask why a) they're bilaterally symmetric; and b) why there are a few organs, like the heart and liver, that don't come in pairs.

Nothing an organism has is "infinitely complex"...

to start with @Ricky you could define "infinitely complex"... but it may be better to offer your definition of evolution, I imagine that's pretty flawed and would explain your stance.

@Ricky If you care about getting an answer to your questions (whether they regard evolutionary processes or not) you should try to clarify it in response to what I found unclear (see my answer/comment).

@Ricky: Actually, I was giving you what I thought was an obvious answer, which is that vertebrates have two eyes because they're bilaterally symmetric, and so almost every organ comes in pairs.  The mechanism for that is probably buried deep in the HOX genes (but I am not an expert on this).  Also, not every creature has two eyes: most spiders have 8, starfish have 5 (at the end of their arms!), scallops can have 100 or so...

@ricky Jamesqf was only giving some input which may have been useful or interesting to others reading your post, there's no need to be so confrontational (the same can be said about your statement "God (or Evolution, for those who still believe in it)" - given that this is a Biology site that is clearly meant to be an incendiary statement).

Welcome to Biology.SE. Here are just a few comments rather than an answer...
Clarification of the question
Can you please clarify how "just adding a few lines of code" could replace a second eye? The question is unclear for the moment.
Perception of depth
A simple amusing exercise you can do to explore how much depth perception you lose by having one eye is to try to catch object with both eyes open and then with one eye open only.
A single eye has much poorer ability to perceive depth than two eyes. However, it can still do so. You will learn much more on depth perception on wikipedia > depth perception.
Believe in evolution
You say [..] Evolution, for those who still believe in it [..]. Evolution is not a thing one believe or does not believe in, it is a thing one understand or does not. You might want to have a look at a very introductory course to evolutionary biology such as Understanding Evolution for example. That will help you to understand what evolution is about.
Mythology and Science
You mention "God". Please, mythical creatures are not welcome on science websites except eventually to make a metaphor. Note, on a slightly philosophical matter (which is not my domain of expertise), there is no contradiction between the existence of a God and Evolution. There is contradiction with the many of the false believes of creationism as often described in the Christian culture

I will probably not react to further comments and am just inviting you again to learn about what the science of evolutionary biology is about through introductory source of information such as Understanding Evolution by UC Berkeley for example.

Stack thrusts this closed question into my reading list. therefore I offer Richard Dawkins VIDEO demonstration of the evolution of the eye which is great and useful for the guy who asked the confused query: https://www.youtube.com/watch?v=eA1rR6ZCxMY


text:
How RNA primer on leading strand is removed during DNA replication and how the gap is filled?
Please can you explain me how the gap created by the removal of primer on 5'-3' leading strand is filled.

is this a homework question? have you tried other sources? if you can show us what effort you have put into trying to answer this question, then one of the community members will be more inclined to helping you out

The group of cellular enzymes that remove RNA primers include the proteins FEN1 (flap endonuclease 1) and RNase H. The enzymes FEN1 and RNase H remove RNA primers at the start of each leading strand and at the start of each Okazaki fragment, leaving gaps of unreplicated template DNA. Once the primers are removed, a free-floating DNA polymerase lands at the 3' end of the preceding DNA fragment and extends the DNA over the gap. However, this creates new nicks (unconnected sugar-phosphate backbone).
In the final stage of DNA replication, the enyzme ligase joins the sugar-phosphate backbones at each nick site. After ligase has connected all nicks, the new strand is one long continuous DNA strand, and the daughter DNA molecule is complete.

Source: Boundless. “DNA Replication in Eukaryotes.” Boundless Biology. Boundless, 08 Jan. 2016. Retrieved 14 Mar. 2016 from https://www.boundless.com/biology/textbooks/boundless-biology-textbook/dna-structure-and-function-14/dna-replication-101/dna-replication-in-eukaryotes-437-12941/


text:
Bilirubin metabolism pathway in non-human primates (NHP)?
In human UGT1A1 seems to be the only relevant enzyme to glucuronidate unconjugated bilirubin into excreted forms. Is the pathway the same for e.g. the Cynomolgus monkey (Macaca fascicularis) in vivo? In case UGT1A1 is potently inhibited are there any other potential enzyme to glucuronidate/metabolise unconjugated bilirubin in NHP? Any reference would be highly appreciated.


text:
What would happen if blood flow wasn't periodic?
Blood pressure has its systolic and diastolic parts due to the beating heart and the body's used to that kind of thing.
What would happen to a person supported by a blood-pumping machine that applies steady blood pressure?
What would happen short term?
What would happen long term?

Actually the artificial hearts do maintain a steady pressure. I think the pulsating pumping of heart has got to do with how the organ evolved. Most movements of body fluids are because of a pulsating muscular movement.

In fact, we see our blood pressure as periodic, and feel our arteries pulsating. But our tissues don't see that. What I mean by that, is that tissues get their blood supply ultimately through their capillaries, where the blood pressure and flow is essentially constant throughout the cardiac cycle, as you can see on this chart:

Image from OpenStax. Article on Blood flow and pressure
As for the second part of your question, what would be the consequences of having constant/non-pulsatile pressure? We can only speculate, I don't think it would have any palpable consequences in principle.
The only "real-life" examples include people who are, for instance: on a Cardiopulmonary Bypass during a cardiac surgery, on Extracorporeal membrane oxygenation (ECMO) in the ICU or have a left ventricular assist device (LVAD) for severe heart failure. It's very difficult to infer anything from these situations, because any on these patients are already very sick, and consequences following these procedures are usually due to insufficient oxygenation, thromboembolism and such, which have nothing to do with the constant pressure.


text:
How to predict the effect of a non coding SNP variant on the expressed protein?
I am writing a paper for non coding SNPs on patients with metastatic breast cancer. Having used a specific gene panel (NGS) of approximately 60 genes, I'm currently running out of ideas on what to write in the discussion section.
I am looking for suggestions based on somewhat efficient methods like a bioinformatics approach or specific textbooks revolving around RNA biology/biochemistry, in order to predict the outcome of non-coding SNP variants.
Some details:

The majority of the variants are intronic (~2300/3300), so I will mostly focus on splicing.
There are two commonly repeated SNPs in 3'-UTRs in over half of the patients, involving KRAS and CDKN2A.

A) Generate exon & transcript counts for your samples, library size + quantile normalize the data.
B) Group samples into variant/wild-type categories
C) Use wilcoxon's rank sum test to see if there are differences in exon inclusion or overall expression. Remember that 3'UTR variants can also imply differential degradation by miRNA. Tools like TargetScan can help you with miR-analysis.

You might be better off using something like DEXSeq to detect differential transcript usage

You could try DeepSEA. It uses deep learning approach to predict function of noncoding SNVs. They use ENCODE and Roadmap Epigenomics for chromatin structure learning, 1KG for nonfunctional SNVs, HGMD for noncoding regulatory mutations, GRASP (Genome-Wide Repository of Associations between SNPs and Phenotypes) for noncoding eQTL and US National Human Genome Research Institute's GWAS Catalog for noncoding trait-associated SNVs. 'Predicting effects of noncoding variants with deep learning–based sequence model' paper describes the whole pipeline.

I've checked this out before, but I'm mostly looking for a way to predict the length and probabilities (sequence too, probably) of individual transcripts stemming from the emergence of the alternative splicing sites (still based in machine-learning). Do you have any ideas ?


text:
Can mitochondria be regenerated by the cell?
In the cell, division of mitochondria takes place on a regular basis, but what if there are no mitochondria present in cell (suppose all of them died), then can the cell make new mitochondria on its own?

No. Cell will die due to shortage of ATP. Also, making an organelle requires much more than just proteins.

Additionally: Dying mitochondria release (besides other substances) a lot of Calcium ions and Cytochrom C which triggers apoptotic cell death.

If we were to suppose, as in the question, that all the mitochondria in a cell 'died' ('were irreparably damaged' would be better, as they are not independently alive) without any other consequences the cell would have no way of regenerating them. Even if the cell had another source of ATP (see @another 'Homo sapien' comment) such as anaerobic glycolysis, one very clear reason is that the mitochondrial DNA could not be replaced (there are no copies of it in the nucleus). If the mitochondrial DNA were not replaced, then there would be no way of making the mitochondrial proteins it encodes.
The cell would die for a more immediate reason than suggested in the comment, and one that should be of interest in relation to a less well-known function of mitochondria. Mitochondria play a key role in the process of programmed cell death — apoptosis. In this process signals cause the mitochondrial membrane to become permeable and allow the efflux of cytochrome c, which is a signal for activating the apoptopic pathway. Presumably if mitochondria were damaged by other means the leaching out of cytochrome c would have the same effect, causing the death of the cell.
If you think of the overall economy of an organism, it's often easier to make new cells rather than trying to repair ones that are beyond redemption.
Further Information

Mitochondrial DNA: http://www.ncbi.nlm.nih.gov/books/NBK26924/
Apoptosis and mitochondria: https://en.wikipedia.org/wiki/Apoptosis#Activation_mechanisms


text:
How do you test soil for the nutrients present in it?
I recently noticed that my rose garden has been in a very terrible state. The roses keep dying. I tested the soil for its pH and that was fine.
Now I'm wondering how would I carry out a test to see what specific nutrients I should use to get my soil better.

This question is probably more appropriate here: http://gardening.stackexchange.com/

I'm voting to close this question as off-topic because it should go to Gardening.SE

Send soil samples to a soil lab (e.g., here).
They will likely use the Mehlich III extractant   method to extract and quantify the nutrients (most importantly the bases such as  Ca, Mg, K, and Na). Will cost less than $25.

was the pH level from 6.0 to 7.4 ? because that is what plant life needs to dissolve nutrients easily


text:
Cockroach-like insect identification (India)
I just saw an insect in my room, and I have never seen anything like it ever before. I captured a photo, please see if you can identify it. It has got quite unique colours on its exodermis and it has 2 pairs of wings ( I was not able to get a picture of them) which are very similar in structure and position to those of a cockroach. In addition to that, it is able to fly, albeit for short distances.
I live in Kolkata, India and the length of the insect is approx. 6-8 cm.

It's a longhorn beetle (Cerambycidae).
Most likely, it's a Red-spotted longhorn beetle (Batocera rufomaculata), also known as a mango tree borer, mango stem-borer and tropical fig borer.
See this SE question pertaining to the same insect.

From Biolib:

Country check-list: China, India, Israel, Jordan, Laos, Lebanon, Madagascar, Malaysia, Mauritius, Myanmar, Pakistan, Puerto Rico, Sri Lanka, Syria, Thailand, Virgin Islands  [Might Not be complete]
Food: Ficus carica L. (Fig), Carica papaya L. (Papaya), Mangifera indica L. (Mango), Shorea robusta Gaertner f. (Sal Tree)

It might also be B. parryi, which, similar to B. rufomaculata, is common in SE Asia (but which is absent from Western Asia or Africa where B. rufomaculata is also found). Since you live in India, both are possible. I will look for a key to determine how to differentiate the 2 species.
Meanwhile, here is a list  of related species in the Lamiinae subfamily for further reference.
Also, a great resource (including keys) for wood boring beetles of the world!

Thanks, it is the same species atleast morphologically. Just like the one in the answer link you provided.

Country Checklist: Add Bangladesh


text:
Transcranial Magnetic Stimulation on science fair
My friends and I would love to make a TMS machine and apply it to make famous "god helmet". We know that magnetic stimulation may cause visions of angels, gods etc. My question is: what are the dangers?

You should primarily consider that TMS therapy is administered to human patients by licensed clinicians and physicians, who are (1) qualified to deliver medical procedures and (2) qualified to monitor patients for adverse effects that could occur such as seizures. Even if it were an animal you would still need quite a bit of licensing and approval from a governing body like an IACUC.

TMS may evoke simple visual percepts or motor responses, but I've never heard of complex perceptual changes elicited by TMS.  Further, this site isn't meant to assist you in making potentially harmful devices.

I'm voting to close this question as off-topic because OP requests assistance on building a potentially hazardous device.

I would not consider this question off-topic on the grounds of it asking about a potentially harmful device. I however, would consider this question as slightly broad. Moreover, questions on legality are not really on topic here. You may try to have a look at the responses to the linked article and also the articles citing it. As @CMosychuk has pointed out, carrying out these procedures are not suitable/allowed for something like a science fair. You can however volunteer for the experiment yourself.

@Christiaan I edited my question. Now it fits the rules. Can you revive my question?

@AliceD every device is potentially hazardous. EVERY.

@user46147 - I think the question lacks the necessary focus. To perform a risk analysis there are standard operating procedures in place. Risks can occur at the electrical, electronic and physiological level. This question cannot be answered in any meaningful way.


text:
To what extent does the cooking time impact the nutritional content when boiling potatoes?
I wonder to what extent the cooking time impacts the nutritional content when boiling unpeeled potatoes with unsalted water.
http://www.livestrong.com/article/340060-does-boiling-potatoes-reduce-their-vitamins/ says:

Boiling potatoes whole in their skins minimizes the amount of vitamin C that is lost. According to the Food
  and Agriculture Organization of the United Nations, boiling unpeeled potatoes results in losses of up to 30
  percent of vitamin C, but boiling peeled potatoes can cause losses of up to 40 percent. About 2 percent of the
  vitamin B-6 is lost due to boiling potatoes, as well as about 23 percent of the thiamine. A 3.5-ounce serving of
  potato boiled in the skin provides 22 percent of the daily value for vitamin C, but boiled peeled potatoes
  provide only 12 percent. Peeling potatoes before boiling can also increase vitamin B-6 losses, with unpeeled
  boiled potatoes containing 15 percent of the DV per 3.5-ounce serving and peeled boiled potatoes containing
  only 13 percent of the DV. There is no difference in thiamine content between peeled and unpeeled boiled
  potatoes.
[...]
The higher the temperature and the longer the cooking time, the more of the vitamins will be lost

However, it does not mention how the loss curve looks like.

I don't understand your exact question. The quoted text clearly says that The higher the temperature and the longer the cooking time, the more of the vitamins will be lost. In general, the extent of leaching will depend exponentially with time (the process follows a first order kinetics).

@WYSIWYG exponential could be an answer. I am wondering what the loss curve looks like.


text:
Do babies conceived naturally or artificially have any differences in long-term health?
Are there any long-term differences in children conceived via artificial insemination or sexual intercourse, pending that the mother successfully delivers the child?

A review paper on children born by the advent of assisted reproductive technologies (ART) and frozen sperm (Lansac & Royere, 2001) concludes that ART children, as compared to the general population:

Have normal weight;
Do not suffer increased occurrence of premature births;
Do not have increased rates in stillbirths;
Have equivalent sex ratios;
Show no increased occurence of birth defects and no chromosomal abnormalities;
Have normal overall health.
Have normal psychosocial development, at least up to 8-9 years of age, but the available data is scant in this area.
However, the rate of multiple pregnancies was higher in the ART group. This may be caused by excessive hormonal treatments during artificial insemination therapy, or by ovulation induction treatments and embryo transfer policies (multiple embryos implanted) that may increase the rate of multiple pregnancies.

The authors do conclude that larger and longer studies are needed to support these findings more conclusively, given that their review paper was based on just two studies. It deserves note, however, that both of these studies were prospective in design and included a large population of subjects.
Reference
- Lansac & Royere, Hum Reprod Update (2001); 7(1): 33-7

In addition to Christiaan's answer I'll cite an article by Bonduelle et al. (1999) that reports a seven-year follow up study of children born via an assisted reproduction technology known as intracytoplasmic sperm injection (ICSI), in which the sperm is injected inside the ovum via a micropipette.
Bonduelle et al. report that there were no higher number of malformations in the ICSI children compared to the control group.


text:
Trouble understanding overlapping genes.
I read the wikipedia passage on overlapping genes.
https://en.wikipedia.org/wiki/Overlapping_gene
The Tandem overlaps they speak of make sense to me, as I understand that their are different reading frames(3 in total if I understand correctly) for genes to be read in the 3' to 5' direction and that this causes an out of phase overlap.
This out of phase tandem overlap for genes was shown by the picture below:

I am having trouble understanding the other scenarios spoken about in the passage, the in-phase tandem overlap and the Anti-parallel strand overlaps.
Maybe I just lack a good enough background in genetics.
I do not understand how you can have an in-phase tandem overlap. If the genes were in phase, how could they ever overlap and be different genes? Wouldn't they both respectively have a stop codon, and then one stop codon would "stop" the translation?
I picture it like this: pardon the crude drawing

The anti-parallel strand overlaps also confuse me as well, for I do not understand how genes can overlap when on opposite strands. If the genes are on opposite strands wont that mean they wont have any overlap in the first place? Am I missing something basic? Thanks.

A gene has got nothing to do with a stop codon. As you might know there are non-coding RNAs as well and the genomic regions responsible for transcription of these RNAs are also called genes.
Genes that have an overlap in their genomic locations (without considering the strand orientation) are called overlapping genes.
In case of same strand overlaps, the genes should have a different transcription start/stop site. Alternatively spliced RNAs are not considered overlapping transcripts. In certain cases, transcripts with an alternative transcription start/stop site are not considered separate genes but rather, isoforms, especially if the gene produces an mRNA and the alternate transcription start/stop sites just affect the untranslated regions (UTRs) and not the coding region (have a look at this article).
Your confusion is quite valid and gene nomenclatures need some redefinition/clarification.

Regarding the in-frame overlap, I think of the genomic region like this:

SA--SB--AA--BB-AAA-AA--CC-C--A---AS---BS

Where

SA = Start gene A.
SB = Start gene B.
- = Non-coding or non-transcribed part of DNA.
A = transcript region for gene A.
B = transcript region for gene B.
C = transcript region used by A and B.

So in that example the primary transcript of gene A will consist of 13 regions. Gene B has 7 regions. They overlap in-frame in 3 regions (C).
Another more simple example could be where gene A is a subset of gene B:

SB,B,B,C,C,C,C,C,B,B,BS

Where the first and last C regions are the start and end regions of gene A.

Just for completeness sake could you post an example of an anti parallel strand overlap? I think I have an idea of what one would look like in my mind but I am not too sure.


text:
Do animals get Post Traumatic Stress Disorder after escaping from a life threatening situation out in the wild?
Can animals come down with PTSD in the wild by themselves? For example, would a gazelle that nearly pulls away from a cheetah at the last second and heard the cheetah's jaws clamping down at air right behind it's tail, show symptoms of stress and anxiety after the event?
And if not, why can we as humans succumb to these kinds of disorders, and not animals in the wild?

@YviDe I think he is asking if any level of stress can be emotionally conveyed by an animal in the wild. Any signs of depression after the animal has been exposed to a stressful situation will work, because we cannot so simply measure their emotional stability and talk to them to see how depressed they are as we can with humans.

Peter Levine speaks to this in his book, "Waking the Tiger:  Healing Trauma".  Most animals in the wild which experience a trauma through natural species interactions will go through a sequence of recovery stages.
First, when the trauma or death is considered inevitable, the animal will "faint", losing sensory awareness and consciousness. If the trauma or death is averted, the animal will then partially waken out of that faint, and "shake off" the trauma.
This "shaking off" looks remarkably like an epileptic fit, but when the movements are analyzed, they are a muscle-twitch repeat of the sequence of movements that animal took from the time it realized its hazard to the time it fainted. It is this same muscle-twitch capacity which allows human athletes to practice their skills both mentally and physically, without moving from one spot.
Once the "shaking off" is complete, the animal is able to rise and continue its life activities without any longer-term impacts such as PTSD.
Neurologist Dr. Robert Scaer has an explanation for this lack of PTSD.  Lasting trauma is only taken on when the "victim" experiences repeated episodes of the same kind of helplessness and hopelessness.  We humans are very good at giving ourselves and other species repeated episodes of helplessness and hopelessness, and animals which interact with us often pay a price in PTSD.

In short, yes. It is not the same disorder we as humans suffer from, as our brains are much more advanced and more of our brain is affected. Species of animals such as elephants and chimpanzees, found to have many social and neurobiological similarities with humans, have been found to suffer from this disorder.
PTSD describes anxiety based responses from witnessing life threatening responses. Animals are used quite often when it comes to studying the effects of certain events on a human's life, and many experiments have proved that they do, indeed, suffer from this disorder.
According to this, experiments have been undertaken to replicate torture, loss of a family member, and incarceration humans are exposed to during wartime.
Most elephants in these experiments have suffered from not just PTSD, but from many different stress disorders in captivity. They have been wrenched from their natural environment in which the communities that made up their lives previously are not there to comfort them.
It may be that wild animals can suffer from PTSD for a while, but most likely not for their full lives. Lone animals may suffer from this a little bit more than, say, an elephant in a herd will, so it is entirely possible that they can experience it.

Please add some reference, like for "Elephants have been found to suffer from depression..." or "Captive animals...have been found to suffer from PTSD...".

I just fixed it.


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What are the problems in using an ssDNA or an mRNA for expression instead of using a plasmid?
Let's say you want to do a gene cloning experiment. You have an empty expression vector (mRNA or DNA) and are looking to clone some gene X into it. Why is it you can only buy X already inside a vector (which is in turn often inside a bacterial carrier)?
What is the problem with handling pure mRNA nucleotides of gene X? Or even sscDNA?

Plasmids are vectors. The inserted gene is called a clone or simply an insert that the vector carries.,

@WYSIWYG No, vectors are vectors, plasmids are plasmids, in some cases plasmids are indeed vectors. But literally a plasmid is just a piece of DNA.

I meant the plasmids used in molecular biology, not the natural plasmids.

What is the problem with handling pure mRNA nucleotides of gene X? Or
  even sscDNA?

Problems in directly transfecting a mRNA/ssDNA
mRNAs can be transfected into the cells and is quite frequently done. The problem with transfecting mRNAs directly is that the mRNA gets degraded soon and you will not have sustained expression. This is, however, very useful in certain cases such as creating induced pleuripotent stem cells (iPSCs) where you do not want the cells to continually express the Yamanaka factors (some of which are also oncogenes).
Also, RNAs as such are quite susceptible to degradation. It is much easier to prepare and store DNA solutions for a long time.
Similar problems arise with a ssDNA.

Why is it you can only buy X already inside a vector (which is in turn often inside a bacterial carrier)?

One great advantage with using plasmids is that you can propagate your gene infinitely. If you were instead given a fixed amount of mRNA, then you will run out of it soon. Some vendors do practice such greedy capitalistic policies :P
When you are amplifying a DNA using PCR then cloning it has an additional advantages:

you can sequence the gene using well standardized primers (like T7)
you can make constructs that can express the gene conditionally

You have an empty expression vector (mRNA or DNA) and are looking to
  clone some gene X into it.

You cannot easily clone something inside an RNA. You need specific RNA endonucleases. Moreover a double digestion will be disastrous in this case.

Why vendors don't generally sell a dsDNA insert but rather provide it cloned in a plasmid

A circular dsDNA is more stable
Vendors can keep the stock of the insert for future customers without having to do PCR again
Cloned insert can be amplified via bacterial cultures to obtain very high amounts (maxi/giga preps)

I was thinking from a workflow perspective. When you buy a plasmid (usually double stranded DNA in a bacteria) you need to extract the plasmid first, then cut out the ORF, then amplify and ligate the ORF extract to your own vector. Why don't they just sell vials of ORF?  That should be easy to self-propagate too.

@jiggunjer No you generally don't buy the bacterial culture carrying the plasmid. You just get the plasmid dissolved in Tris-Cl pH 7.5. Linear DNA containing just the ORFs cannot self propagate. You can PCR a piece of DNA but with bacterial cultures you can get a lot of DNA (maxi/giga preps). Circular DNA is relatively more stable too.

Even if one gets pure plasmid, why not pure ORF. I admit the "non-circular is less stable" argument sounds pretty convincing. I know they can't self propagate, but that's why I mentioned the empty vector. So just buy ORF, PCR, and ligate. I'm not very experienced in the lab but I'm trying to get the hang of the protocol, it seems needlessly laborious.

@jiggunjer You do get an empty vector without any insert. Some vendors also sell a pre-digested/linearized vector.

@jiggunjer Vendors don't sell pre-digested inserts for the reason that there is no one standard vector. Different vectors have different expression sites, which require different restriction enzymes to clone. Selling ORFs would mean the vendor would need to keep stock for hundreds of different kinds of sticky end / recombinase end combinations. It's much easier for the end user to PCR the fragment out and subclone it.


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Why do chickens continuously lay unfertilized eggs?
As per subject: why do chickens continuously lay eggs even if they are not fertilized?
Is this sort of behaviour found in other species of birds (or other egg-laying animals), or only in chickens? Is it natural, or domestic chickens have been specifically bred for it?
If it's natural, what kind of sense does it make to divert energies and nutrients to continuous lay unfertilized eggs which have no purpose other than being possibly eaten by someone else? How could such a wasteful reproductive behaviour have evolved? Even if it has been specifically selected for in breeding, it still seems to make very little sense in the first place.

I do think much of it is selection, like milk production in Holsteins. Some ducks are also great "layers" (the industry term for fowl that lay a lot of eggs for extended periods.) Not like chickens, but yes. Also guinea hens, quail, and probably a few other birds (but I can only speak to the birds I've raised.)

Chickens are domesticated Red Jungle Fowl. In the wild, Red Jungle Fowl live in flocks with one rooster for every few hens (where "few" is probably less than five in the wild, though in zoos flocks may be larger and have a higher rooster:hen ratio).  Since one rooster can fertilize many hens, in the wild virtually all eggs will be fertilized.  Since jungle fowl, of course, lay far fewer eggs than domestic chickens, the cost of the extremely rare unfertilized egg will be low.
In principle, there could be a molecular mechanism that checked for evidence of fertilization before allowing an egg to be laid, but of course such a mechanism would have its own costs, and would almost never actually be useful.

I find the "in the wild virtually all eggs will be fertilized" argument a good explanation to not even bother checking before laying an egg; however,  I don't really understand the "jungle fowl, of course, lay far fewer eggs than domestic chickens" part. Why is this the case?

At the moment you have no evidence to support your answer and in my opinion make little attempt to answer the question beyond some opinion

Jungle fowl lay fewer eggs than chickens because chickens have been selectively bred for 5000 years to lay many eggs.


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Minichromosome maintenance protein structure and function
I am having difficulty answering three homework questions which relate directly to Chong et al. (2000).
Questions

The authors have determined that MtMCM is able to bind both ssDNA and dsDNA (see Figure 1). However, they don’t mention whether it is the same or a different site on the protein that is involved in binding the two forms of DNA.
Question #1: Propose an experiment that would help to distinguish between these two possibilities and what result would you expect?
Question #2: If ssDNA and dsDNA do share the same MtMCM binding site, what part of the DNA do you suppose is involved in stimulating the ATPase activity? In a helicase assay, the authors show that MtMCM can displace large ssDNA fragments (up to 500 bases) from a circular substrate (p. 1533).
Question #3: Explain why this is, or is not, a suitable assay for MtMCM processivity?

My Answers
Question 1:
One possible method to determine whether the MtMCM complex uses two different sites to bind ssDNA and dsDNA is through the identification and blockage (i.e. by using a ligand) of a single specific binding site on the MtMCM. If the blockage of this site prevents the binding of MtMCM to both ssDNA and dsDNA, this would suggest that the same site is used for both. The research paper suggests that ssDNA and dsDNA do share the same binding site because chelation of magnesium ions prevented the protein from binding to DNA.
Question 2:
No ATP hydrolysis was detected in reaction mixtures containing the K341E or delta-N mutant proteins, however, both wt and K341E protein still formed complexes with the DNA. If ssDNA and dsDNA do share the same MtMCM binding site, then perhaps it’s the delta-N portion of the DNA that is involved in stimulating ATPase activity.
Question 3:
I found it hard to start this question. This is what I have so far: This is a suitable assay for MtMCM processivity because a population of substrates possessing displaceable strands of increasing length was used. This allowed the researchers to compare the displacement of the different strands and quantify the processivity of the MCM complex.
Let me know if I should provide more information. Any help or guidance would be greaetly appreciated!

I edited the post to try to improve the format. Feel free to roll back if you don't like it.

I don't know if anybody will be willing to read through the article and answer all three question. It is not my field so I don't quite realize are familiar is the average molecular geneticist to this article.

Thanks for the edit. I realize it's quite a specific topic and quite a bit of reading but I thought I'd put it out here, perhaps someone knowledgeable on this topic will come across it :p


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What determines whether a substance can diffuse across the blood-brain-barrier?
What determines whether a chemical substance is able to cross the blood-brain-barrier via passive, transmembrane diffusion?  What structurally differentiates these chemicals?

Some substances are thought to be actively transported across the BBB as well - especially in particular regions of the brain - i.e. A non-uniform fashion

Short answer
The two most important factors that favor passive diffusion across the blood-brain-barrier (BBB) are:

high lipid solubility;
low molecular weight.

And to a lesser extent:

absence of charge;
low affinity for BBB proteins;
not being a substrate for the efflux pumps present in the BBB.

Background
The blood-brain-barrier (BBB) is principally formed by the endothelial cells in the capillaries of the central nervous system (CNS), as depicted in Fig. 1. Outside the CNS, the endothelial cells lining the capillaries allow for relatively free diffusion of substances from and to the blood via transcellular diffusion. In other words, substances can diffuse relatively freely to and from the blood via the extracellular space between the endothelial cells. In contrast, endothelial cells in the capillaries in the CNS are coupled via tight junctions, which prevents most compounds from diffusing into the extracellular space in between the cells (Fig. 1). Therefore, for compounds to enter the brain, they have to diffuse into the endothelial cells and back out again into the brain. This means they have to diffuse from the aqueous milieu in the blood, through the lipid-rich cell membrane and back into an aqueous solution in the extracellular space in the brain (source: University of Texas).

Blood-brain-barrier. source: RIT
Most drugs cross the blood-brain-barrier (BBB) by transmembrane diffusion, which is mainly dependent on whether the drug is able to meld into the cell membrane. A low molecular weight and high degree of lipid solubility favor this mechanism. However, a drug taken up by the membranes in the BBB must eventually dissolve into the aqueous environment of the brain's interstitial fluid to take effect. As a result, a substance that is too lipid soluble collects in the lipid portion, but is not able to leave the BBB. I.e., it enters the BBB, but doesn't cross it.
Moreover, lipid solubility also favors uptake by the peripheral tissues; this, in turn, lowers the concentration of the drug in blood.
Thus, while lipid solubility can increase transport rate across the BBB, it can also lower the amount of the drug presented to the BBB.
Factors in addition to lipid solubility include charge, tertiary structure and degree of protein binding. Chief among these secondary factors, however, is molecular weight. The best approximation of the influence of size on BBB penetration is that it is inversely related to the square route of molecular weight. Few substances over 500 Da cross the BBB. In addition, lipid-soluble substances with molecular weights over 400 Da can be substrates for P-glycoprotein, a major brain-to-blood efflux pump located at the BBB, which prevents or greatly retards a large number of small, lipid soluble molecules from entering the CNS. However, Peptides and proteins with molecular weights in excess of 600 Da are known to cross the BBB in amounts sufficient to affect CNS function, such as the enkephalins. The largest substance found to date to cross the BBB by the mechanism of transmembrane diffusion is cytokine-induced neutrophil chemoattractant-1 at 7.8 kDa (Banks, 2009).
Note that some parts of the brain do not feature a BBB, including but not limited to, the pituitary, area postrema and pineal gland. Many of these areas participate in hormonal control. These structures hence need to be in contact with the blood stream to sense the presence of hormones and other compounds (source: University of Texas).
Reference
- Banks, BMC Neurol (2009); 9(Suppl 1): S3


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Is it possible to stimulate the EPOC process?
On Wikipedia, EPOC is defined as:

Excess post-exercise oxygen consumption (EPOC, informally called afterburn) is a measurably increased rate of oxygen intake following strenuous activity intended to erase the body's "oxygen deficit".

My question is what influence has post exercise habits on the efficiency of this process?
For example, after an intense exercise, a person rests in bed during this process, consuming a very low amount of oxygen.
Would this process be stimulated if this person would ride the bike for 30 minutes, very slow, but enough to put the cardio-respiratory system at work?


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Skull mystery on beach
The skull was found on a beach on the Sechelt inlet on Canada's pacific coast. A marine environment.

What species is this skull from?

There's no question?

It is a species identification question. I is obvious enough to not a fully phrased question.

Can you provide a side view picture? It could be a couple things, but seeing the width of the zygomatic arches (~eye sockets) would be helpful.

The z arches are 13 cm wide. Just trying to figure out how to load another picture.

We found a very similar skull on a beach near Richardson Bay, Lasqueti BC. Decided it was a seal skull (locals agreed)
See harbor seal skull: http://www.skullsunlimited.com/record_species.php?id=4726

I know guessing is frowned upon but given the small size of the skull and the relatively small inlet you've cited as a location, my best guess is it's the back half of a dolphin's skull. Probably Pacific White-Sided Dolphin (Lagenorhynchus obliquidens)
Compare:
Sorry for the watermark. From Skulls Unlimited

^ The cheek-bones look pretty similar, but the snout and the pit on the side that superficially resembles an eye orbit have been broken off or caved in on your sample.
From cetacea.ca

^ I can't find pictures of the underside of a skull without the mandible, but the hole in the bottom of yours might match the one on the very far right here, though I'm not sure about the bulges on the underside.
I can't be sure if its a complete match but my best proposal is that it's a juvenile dolphin skull.

@SabelGear can you add some links for those pictures?

Added links to original pages. Sorry, didn't realize Stack hosted through imgur.

the zygomatic is all wrong for a cetacean, far to wide and robust, and the orbits are in completely different place, even the auditory bulla are in the wrong place.

I agree with Mark it is a seal, specifically the rear half of the skull.
That low flat profile of the skull combines with with a wide robust zygomatic is indicative of seals. The triangular and yet flat sagittal crest is also a dead giveaway. The orbits are high, large, poorly defined, and deeply recessed with only a narrow band between them that is indicative of seals. Check out a these seal skulls for comparison.

In the last one you can even see how you end up with only the rear portion as you do, as the rest is only weakly attached and the zygomatics are weakly fused at the center and tends to separate as well.
I can't tell you the species but you definitely have a seal.

"Dwarf Sperm Whale" Scientific name: Kogia sima

Please provide a citation or 2 and additional information. Right now  this looks like a guess,  not an answer.

Skull is not 'peaked' as seems typical of cetaceans. Skull has no eye socket 'dents' . Assumed eye sockets are forward facing and close together.


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can you tell someone's age from a DNA sample?
So as I understand it telomeres shorten as you age. Working under that assumption..  let's say you were investigating a crime and there was some DNA evidence that had been left behind. Could you determine the age of the DNA owner by looking at the telomere length?

Not that easy. Depends on the cell type that you have. Different cell types have different telomere lengths.


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What is ATP and why is it said to be a source of energy?
Is ATP a molecule or a kind of energy. When I studied the active transport, it's said the ATP would release energy to change the carrier protein shape. So confused.
Thanks for your help.

Energy can't release energy, because energy is... energy. Energy has to be contained otherwise it's useless. You can't pour a handful of charged electrons in your pc can you? Plants can't store rays of sunlight in their leaves, right? They store.sun energy as glucose later to be converted into ATP to release energy. Google ATP: first line ATP wiki: called the "molecular unit of (...) intracellular energy transfer

I'm voting to close this question as off-topic because it's too trivial

Because there is so much slack usage in relation to ATP and energy, it might be worth reformulating the question title, e.g. "What is ATP and why is it said to be a source of energy?" And then reworking the question to its essentials.

ATP is adenosine 5'-triphosphate, a molecule consisting of the base adenine attached to which is attached a ribose (at its 1 position) and (at its 5 position) three phosphates, alpha-, beta- and -gamma (see edited image from Wikipedia below). The (Gibbs) free energy of hydrolysis of the phosphoanydride bonds between the gamma and beta phosphates and betweeen the alpha and beta phosphates is relatively large in terms of biological reactions. This means that coupling of the hydrolysis of ATP (usually, but not always, to ADP — adenosine 5'-diphosphate) to a reaction that is energetically unfavourable can often produce an overall reaction that is energetically favourabe (has an overall negative free energy change). Enzymes have evolved to catalyse such coupled reactions involving ATP.
Although ATP is often referred to as having ‘energy-rich bonds’ this is not the best way of thinking of things. First, and perhaps most important, you cannot think of energy in abstract, and even referring to ‘breaking a bond’ is insufficient. One is talking about free energy change which must relate to a specific reaction, in this case hydrolysis:
ATP + H2O → ADP + PO43– or less frequently ATP + H2O → AMP + pyrophosphate
Second the free energy change is only ‘high’ in relation to cellular reactions. Third the energy is only of any use if it can be coupled to these reactions (or processes like active cation transport).
It is perhaps better to refer to ATP as having a ‘high phosphate group transfer potential’.
The coupling of the hydrolysis of ATP to mechanical processes like muscle contraction or the change of shape of transporters (if that is what happens) is more complex, but obeys essentially the same principles. The  ATP hydrolysis reaction with its favourable negative change in free energy is coupled to the  mechanical process with its unfavourable positive free energy change.
Further Information

ATP and Free Energy: https://www.ncbi.nlm.nih.gov/books/NBK9903/#A295
‘High Energy Phosphate’: https://en.wikipedia.org/wiki/High-energy_phosphate
ATP and Cation Transport: https://www.ncbi.nlm.nih.gov/books/NBK9847/


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Do plant and animal bacterial pathogen differ too much?
I will be involved in a plant disease produced by a bacterial pathogen, Acidovorax citrulli. I've previously worked with animal pathogens such as Haemophilus parasuis. Are there any big differences among them?
H. parasuis and A. citrulli are 2 and 4 MB genome size. What are these 2 MB extra genome size for?

What kind of differences are you expecting? Related species can have unrelated hosts. It is not very uncommon. For example Erwinia is a plant pathogen that belongs to Enterobacteriaciae which also includes Shigella, Salmonella and Escherichia. There are several Pseudomonas species that infect plants.

@WYSIWYG. I'm not looking for a special type of difference, just asking for the most obvious ones. Maybe the differ at gene level, some kind of protein or transporter. Any paper studying all this would be also useful, thanks.

you really have to narrow down your question.


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Why are local field potentials generally band-pass filtered?
I was wondering what the rationale was behind low-pass or band-pass filtering in local field potential measurements?
It seems to me that we could potentially filter out potentially valuable information by filtering procedures.
Is there a physical limitation for this that would not allow to measure, say, the responses in a frequency range of 0 to 5 kHz?

There is no physical limitation whatsoever on the frequency band you wish to record, other than the hardware limitations on the sampling rate.
Often electrophysiological recordings suffer from noise (mainly in the high-frequencies) and drifts in the baseline (low-frequency range).
In the end, you wish to filter out as much noise as possible, without throwing away the baby with the bathwater. In effect, prior knowledge about the frequency range of the responses of interest are vital. Anything outside that range can, and likely should be filtered out.
For example, FFT analysis of EEGs mainly focuses on bands limited to the frequency range of 1 to 50 Hz. The mains frequency is 50 or 60 Hz, often imposing sinusoidal noise when the room is not shielded. Hence, what reason would there be not to use a low-pass filter with a cutoff around 50 Hz to get rid of it?
Lastly, offline filtering methods are aplenty. My personal preference nowadays is, is to collect the raw data and filter offline. That way you have the baby and the water, and you can focus, with trial and error, on where the baby is and where the water.

Coming to my rescue once more!

This is a nice answer. I remember an EE prof. who said a lab procedure they used to give grad students required them to recognize that noise from florescent lights would ruin their results unless filtered.


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What Would Happen To a Human Who Died In Space And Stayed There For a Prolonged Period of Time?
Last night I was watching a documentary regarding the Apollo space program, and it spoke about how Apollo 8 orbited the moon 10 times then came back to Earth. It said that while the ship was in orbit no one really knew whether the ship would break orbit or continue to orbit the moon where the astronauts would eventually die.
I thought then that at some point in the future NASA would have maybe recovered the ship and returned them home. If they did this I then wondered what would have happened to the astronauts' bodies during this time? Would they decompose like they would do on Earth, or because of the lack of atmosphere would they not decompose?
There are two scenarios to this. The first scenario is that the ship ran out of oxygen and the astronauts died through asphyxiation. The second scenario would have meant that the astronauts were involved in  a decompression, so that the astronauts were then in a vacuum.

They cannot decompose in the sense of biodegradation but depending on the environmental conditions many other chemical reactions might occur which can break down the molecular constituents of the body. Since there are many possible conditions I guess this question qualifies as broad.

I see your point. But there's only really two environments that they'd be exposed to, one would be carbon dioxide/monoxide rich and the other would be in a vacuum. Both you'd imagine would be extremely cold too.

Not exactly answering your question but this is pretty close.

@WhoElse your link leads to a 404 error page

Title was really good. You may consider it as A man buried in ice for long. An ice where no bacteria are present. It then needs a forensic expert.