Human and chimp genome sequencing Can someone comment on this article which claims that biologists have been misleading the masses when they compare the genome of humans and chimps
https://yaqeeninstitute.org/daniel-haqiqatjou/can-islam-object-to-evolution/

Well. Science is a funny thing compared to say the Koren, the Bible or any other religious text. As Scientist learn more, the narrative in Science will change. For instance, in the 1800, there were ideas that there was free following water on Mar... channels and ditches and such. In the 1960s, Mars was considered bone dry. No water ever. A desolate waste land. In the 1990s, Mar considered to have water, but only in the distant past 3 billion years ago. No water now. Then in the 2010s it is now considered to have subsurface water ice, that may occasionally turn into free flowing water under rare conditions. And worst yet, until recently... perhaps all those features of recent running water way have been caused by out gassing of CO2... Conflict over basic interpretation.

Now in that time, religion text, while silence on the matter of Mars, has not changed much if at all. Religious text has stayed the same.

So has Science been misleading the masses on Mars? Does Mars have water? Yes or No? Science keeps flip flopping.

In some ways yes, Science has been misleading the public. It has not been on target with a singular message, unlike say a religious text book, which has been delivering the same unchanging message for a thousand years or so.

So if you are looking for a consist message, well Science way not the thing for you. Science tends to tell different stories as scientist learn more, learn new techniques, re-evaluate ideas and generally fight with among themselves. The holy men Science like to review, rewrite their holy text rather often and fight. And the common man may find that dissatisfying and perhaps worrisome. If holy men keep changing the holy text, how will the common people worship? Is the Science real? Given it changes when the holy text of many world religions have not changed in centuries or even millennia.

So back to article... the percentage similarity of human to chimp genome changes as techniques improve. If you look at the actual age of the citations used in said article.. we run from papers in the 1970s, before genome sequencing was available, and the ideas of one gene-one protein was how Science thought DNA worked, and karyotyping and chromosome banding was about the only means to make large scale chromosome comparison... to papers in the  2014. Where we know DNA does more than just encodes proteins, and non DNA coding are not junk but can encode RNA with biochemical activity (gene regulation, transcription factor regulation etc). And whole human genomes can be sequenced for less than USD 1,400 when it originally cost USD 2.7 billion.

This is nearly 50 years of change and development. Going from the time before the internet and calculators were serious business machines worth thousands of dollars to a time you can have a a 1980s super computer as a wrist watch.

So yes... the message changes. Science progresses, techniques that could only be imagined by previous generations of scientist have become routine. We have learned more.. RNA isn't just a middle man between DNA and protein. One gene can give rise to many proteins.

Have the masses been mislead?

Scientist are telling the Masses information that is to the best of their knowledge. And if the current generation of scientist (2014 scientist) say the past generation (1970s scientist) had it wrong or not quite right.... If scientist right now disagree on the best matrix... is that misleading?

A science book is not as safe as a religious text. And one of the worst offenders is biology. A biology text book book from the 1980s looks very different from 2010s, even if they are from the same series. Is that misleading or is that scientific advancement?

PS: Common genes and sequence identity is not the same. There is a bit of confusion in the article. A cat and a human may share many many genes. But those shared genes may have sequence difference between them. So you can say humans and cat share 90% (made up example) of their gene (ie both cat and human have the PTEN gene) but have only 70% (made up example) sequence identity (ie there are several DNA difference between the human PTEN gene and the cat PTEN gene). It is easy to confuse the two.

Also are you only only considering gene coding DNA? Or are you also considering the non coding DNA (which until cheap genome sequencing in the 2010s was extremely difficult to capture and sequence)


What determines the reversibility of cell of G0 phase in cell cycle? From Weinberg's The Biology of Cancer: A cell that has been recently formed by mitosis must decide whether it will once again initiate a new round of active growth and division or retreat into non-growing state G0. This decision is strongly influenced by mitogenic growth factors in the cell's surroundings. Their absence or presence of anti-mitogenic growth factors will trigger the default decision to proceed from mitosis into the G0 quiescent state.
Withdrawal from the cell cycle into G0 is often reversible (cell can re-enter into active growth and division), however some cells irreversibly leave the cell cycle (such as neurons).

Here comes my question : What determines in the cell whether the cell will go to reversible (quiescent) or irreversible (senescent) state of G0? I have found that it has something to do with the amount of RNA (low RNA content in reversible), but I do not understand why low RNA content means that the cell should proliferate again. And are there any other criteria that determine whether the cell will go to quiescent or irreversible state? (I am looking for exact molecules and mechanisms, the more into detail the better !)

The answer is quite complicated. One of the major issues in understanding what factors drive senescence vs quiescence has been the absence of a clear, uniform molecular definition of senescence. That said, multiple tumour suppressors, including p16 (and the other genes that occupy the INK/ARF locus) , as well as TP53, can modulate the expression of senescence associated transcriptional programmes.

Additionally, epigenetic remodelling, including heterochromatinisation at E2F target genes (which are a major driver of cell cycle progression through the S phas) , is also known to be a feature of senescence.

A very good starting point to survey the literature surrounding the topic is https://www.nature.com/articles/nrc3960?message-global=remove


What is the name of this plant with orange fruit clusters in india? Location: South India.

Month: June

Season: Rainy Season.

The easiest way to find out the name of this tree is to realize that the flowers (and therefore the fruit) are in the form of a raceme.

Googling India bright orange fruit raceme in Images quickly brings up your specimen among others.

The name of that image leads to other sites discussing the plant.

  Duranta erecta
  Scientific classification
  Kingdom:    Plantae
  (unranked):     Angiosperms
  (unranked):     Eudicots
  (unranked):     Asterids
  Order:  Lamiales
  Family:     Verbenaceae
  Genus:  Duranta
  Species:    D. erecta
  Binomial name
  Duranta erecta

  Duranta erecta is a species of flowering shrub in the verbena family Verbenaceae, native from Mexico to South America and the Caribbean. It is widely cultivated as an ornamental plant in tropical and subtropical gardens throughout the world, and has become naturalized in many places. It is considered an invasive species in Australia, China, South Africa and on several Pacific Islands. Common names include golden dewdrop, pigeon berry, and skyflower.


Copper for cell incubator to prevent contamination For some reason the lab seems to have a problem with contamination every so often.  It's virtually impossible to prevent bacteria, viruses, fungi, etc. from getting into the incubator every time you open the door.  Our incubator is pretty old, we don't have one of the new fancier versions that's made with pure copper inside, which effectively kills microorganisms.

Would it be a good idea to buy a copper plate and place it on the shelf, on which we could put our culture flasks?  Or would it disrupt the flow of heat/CO2 too much?  Would it be better to buy copper foil and wrap the shelves in it, then poke holes into it where all the holes are in the shelf?

We use good cell culturing practices; I don't contamination is happening because people don't know what they're doing.  It just happens over time with enough people working in a cell culture room.  Could copper in the incubator help?  We probably don't have the money to buy a brand new incubator that's made out of copper, so would this be a viable, economic alternative?

First thing I'd do is replace the HEPA filter. A copper plate/foil may help, and it certainly won't disrupt the flow of heat, as copper is incredibly conductive (that's why they make electrical wires out of it), and poking holes would help with the airflow, but a new filter will probably make the most difference. I've never used a full-copper incubator, and the few serious contaminations I've had to deal with were related to the HEPA filter and poor TC practices.

If you haven't already, I'd institute a good routine cleaning program as well. Change the water bath each week (make sure you're adding fungicide to the water), and wipe down the whole incubator with bleach followed by an alcohol rinse each month. Make sure you clean all the bleach off, as it corrodes metal if left on very long. At the same time, clean and autoclave all of the removable components like shelves, rails, and water pans.

Good luck!


Is it possible for human beings to feed through the nose? There is a prediction on a futurology site that food can be eaten by inhalation

https://2050.earth/predictions/smell-can-feed-you

Although aerosol foods do exist they are still eaten by the mouth.

Is there any biological evidence that human beings can feed through their noses?

Certain vitamins, for example, vitamin B12, can be absorbed through the nasal mucosa by simple diffusion.

Many nutrients can be absorbed through the intestinal mucosa only by the help of specific carriers. These carriers are not likely present in nasal mucosa, so the nutrients in question may not be absorbed there.

The other problem, especially with macronutrients (carbs, proteins, fats), is if the surface area of nasal mucosa is big enough to absorb large amounts of macronutrients (carbs, proteins, fats) needed to meet nutritional demands. In one experiment, only 0.1 mg of glucose from a given dose was absorbed through the oral mucosa.

In another experiment, some amino acids were absorbed from oral mucosa.


Why does the rabies virus have such a long incubation period? So there was a case in India, where a man developed rabies 25 yrs after the dog bite. Source:
https://www.google.co.in/amp/s/m.timesofindia.com/city/goa/25-yrs-after-dog-bite-man-gets-dies-of-rabies/amp_articleshow/16415870.cms
I have the following questions:
1) what are the reasons behind such a long incubation pd?

2) in such cases, can vaccines taken years after the dog bite save the person? (Even though it’s advised to take it immediately)

This question may not be particularly answerable.

The only available information about this specific case is in the original article (Shankar et al. Ann Indian Acad Neurol. 2012 Jul-Sep; 15(3): 221–223. doi:  10.4103/0972-2327.99728); they say only:

  The anatomical site of viral latency and the mechanism of reactivation of rabies, a neurotropic virus, remains an enigma to be unraveled.

Other reports in the literature of long incubation periods (>7 years, the previously reported maximum seems to be 14 years) are scattered/old/speculative, e.g. Gavrila et al.  Ann. Inst. Pasteur 1967 Vol.112 No.4 pp.504-15:

  Discussing these cases of prolonged incubation periods, the authors point out that in rabies the incubation period can vary within very wide limits and that it is possible in areas where the disease is enzootic that, in very exceptional cases, the disease can develop after an incubation period which may sometimes greatly exceed the maximal limits now admitted, and that, as for example in cats [this Bulletin, 1965, v. 62, (1106)], stress conditions and so forth may lead to the generalization of the virus until then quiescent at the point of entry.

Plotkin 2000 Clinical Inf Dis 30:1 says

  the reasons for this long latency are unknown ...
   in the absence of specific prophylaxis, the virus becomes hidden, only to invade the CNS weeks, months, or years later. Where is the virus during this period? There is some evidence for slow replication in muscle cells and for latency in macrophages, but there is no certainty that these account for the long incubation periods.

There has been an experimental study on skunks (Charlton et al. Acta Neuropathologica June 1997, Volume 94, Issue 1, pp 73–77) that suggests there is some infection of muscle cells at the injection site, but otherwise not much is known about the mechanism.

I would guess that vaccination would be effective if it were administered soon enough, but it will probably be hard in these surprising cases to identify the disease soon enough.


Looking for the closest example of life forms similar to some mathematical patterns Caveat: this is my first question here, it is quite interdisciplinary, but I hope to be in the correct place to ask. I am a user of Mathematics Stack Exchange since some years ago, and this question is related with some questions there (here, here whose general formula is discussed here and here).

Context: I am preparing a mathematical paper regarding a new family of dynamical systems (if you are not familiar with the concept, simplifying the idea it is a mathematical formula in which starting from a initial value, once applied to the formula the resulting value is again applied to the formula, and so on, finally the values are plotted and eventually a -sometimes interesting- pattern emerges) whose attractors (plotted patterns) in the present case seem to have unexpected pareidolic properties.
Basically some of the patterns generated by these systems show similarities with some structures of invertebrate life forms, specially insects, marine jellyfish, and zooplancton and also due to the patterns of the accumulation of points, also with life forms presenting bioluminescence properties.
For each interesting pattern so far I have tried to find the closest life form example, to compare both the model and the life form patterns.
So my target is including in the paper the closest life form similar to each mathematical pattern. Initially it is just a pareidolic coincidence, but it might be interesting if the mathematical formula can resemble models of some organic structures.
These are the ones I have been able to gather, both the model and the closest life form I found.  The pictures I am using at the right side of and below the images are just for the sake of completeness (they belong to their respective owners, I do not own them, if there is any problem I will remove them, so just please let me know). The formula can be verified at the MSE links I have added at the beginning of the question and the Python code to generate them is in this link (please feel free to use it and modify it). The questions are after the examples (click to enlarge):

Patterns similar to thorax and abdomen of Bembicini wasp, head and body of Turritopsis dohrnii (inmortal jellyfish) and Tardigrade limbs:

Patters similar to Drain fly:

Patterns similar to Acherontia atropos (thorax and abdomen and main proportions of body, specially the patterns near the head are interesting):

Patterns similar to Ctenophora (down left) and Mnemiopsis_leidyi (down right):

I would like to ask the following questions:

Are there better examples of life forms for the models I am showing above (1,2,3,4)? If somebody could provide examples or specific names would be very appreciated.

Are there papers or references in the Biology field regarding mathematical models of this kind?

In the case I would like to add images from internet in the paper, I know that in the case of Wikipedia there is a standard way to add the reference in the bibliography. Apart from Wikipedia, are there other sources of images which I could use without problems in a paper (thinking about the kind of life forms that are the target of the patterns)? Thanks in advance.

For the second subquestion (papers or references of similar models), it could be useful for you to look at the books by J.D Murray for inspiration; Mathematical Biology, vol I & II. A pdf of volume 1 can be found here, and the second volume here. Even if they are a complete of years old (last edition from 2002 I think) they provide a really nice background to the field of Mathematical biology, and he has quite many examples on pattern formation of different kinds. I don’t remember if dynamics systems are included per se though.

However, several chapters include reaction diffusion systems and wave models, to model e.g. coat/fur patterns and wound healing. It is also packed with references, so you should be able to find lots of classic citations that might be useful.

Some chapters you might find interesting:

Reaction Diffusion, Chemotaxis and Non-local Mechanisms
Travelling Waves in Reaction Diffusion Systems with Weak Diffusion: Analytical Techniques and Results
Animal Coat Patterns and Other Practical Applications of Reaction Diffusion Mechanisms
Mechanical Theory for Generating Pattern and Form in Development
Bacterial Patterns and Chemotaxis

I've mostly looked at population modeling in his books, so I'm not very familier with these topics myself.


Validity of Acoustic Weapon Effects on Biological Organisms? There is alot of rather contradictory information present on the biological effects of acoustic weapons with a bevy of scientific articles claiming that they cause harm to biological organisms with effects such as nausia, gagging, and disorientation. These articles are mostly from older scientific articles and modern government scientific reports on the issue, and statements by military leaders overseeing the development of the weapons (including defence contractors). Contradictory claims are also being made by a multitude of scientific sources from a variety of different countries and backgrounds.

I am not sure which one is correct after reading about a dozen articles from both sides. Does anyone have any insight on this issue?

Of note, there are a multitude of crackpots and conspiracy theorists that believe that the acoustic weapons are real and can do outworldly things- the media seems to have bought into these speculations thouroughly and should probably not be trusted.

Here are two articles (one claiming they work and the other denying it especially pertaining to infrasound):

Bioeffects of Selected Nonlethal Weapons

Acoustic Weapons - A Prospective Assessment

There are a few things which can lead to miscommunication regarding the potency of acoustic weapons, but there are two main things to consider: source levels and duration.
Most organisms can tolerate loud sounds, within reason, for a short period of time. However, no matter how short, at certain levels acoustic weapons can cause temporary or permanent hearing loss, nausia, gagging, and disorientation.  Weapons with a lower source level played over a longer duration will be easier for organisms to initially ignore, but exposure to weaponized source levels over time will lead to internal issues with health, including a decrease in fecundity and nutrient digestion.
Often military and sometimes scientific reports will focus on one particular type of weapon used for a specific purpose, and deem its use acceptable or not. Many scientific studies take more factors or variations into consideration.
Ultimately, its risky because we don't have enough data about the long-term effects acoustic weapons can have on a population, and they also don't appear to be particularly effective when it comes to humans. The Acoustic Weapons (chapter 7) in 'Non-Lethal' Weapons1 by Neil Davison sums it up nicely.
Reference:
1: Davison, N. (2009). 'Non-Lethal' Weapons. Springer.


Bird brain-eating Mantis - how does it crack the skull? The New York Times' Science article Birds Beware: The Praying
Mantis Wants Your Brain is a good read and is well researched. Apparently the larger Mantises have been documented to occasionally kill and eat (parts of) birds on six continents.

The mantis was clinging with its back legs to the rim of the feeder, holding its feathered catch in its powerful, seemingly reverent front legs, and methodically chewing through the hummingbird’s skull to get at the nutritious brain tissue within.
“It was staring at me as it fed,” Mr. Vaughan said. “Of course, I took a picture of it.” Startled by the clicking shutter, the mantis dropped its partially decapitated meal, crawled under the feeder — and began menacing two hummingbirds on the other side.

The article continues:

James V. Remsen of the Museum of Natural Science at Louisiana State University and his colleagues documented 147 cases of mantis-on-bird predation in 13 countries representing all continents but Antarctica — not surprising, Dr. Remsen said in an interview, since there are no mantises on Antarctica.
Hummingbirds were the most common target, but mantises also went after warblers, sunbirds, honeyeaters, flycatchers, vireos and European robins. Large species like the Chinese mantis, which grows to four inches in length, were the most avid avivores, and females were responsible for virtually all the bird-killing observed worldwide.
In two reported cases, females feasted on birds while copulating with males. Sometimes the mantises would tuck in through the bird’s breastbone, but more often they went for the head, Dr. Remsen said.
“They bite in and eat the brains,” he said, “which might imply this is something they’re professionals at.” (emphasis added)

Question: How does the mantis break through the skull? I'm guessing it is smooth and much larger than the insects mouthparts, so it can't crush it. Does it cut through somehow? Or maybe go in through the ear? (Yuck!) What "tools" does the mantis have at its disposal to break through a bird's skull?
note: The link is to Bird Predation By Praying Mantises: A Global Perspective, Martin Nyffeler, Michael R. Maxwell, and J. V. Remsen, Jr., The Wilson Journal of Ornithology 129(2):331-344. 2017, https://doi.org/10.1676/16-100.1

below: "An unlucky hummingbird caught by a mantis at a feeder in Colorado." From here. Credit Tom Vaughan/FeVa Fotos

The mantis doesn't need to crack the skull to eat the brain. It can get to the cranial cavity through an easier way: the eye socket.

Have a look at this image of the ruby throathed hummingbird (Archilochus colubris) skull:

Source: http://wildlife.ohiodnr.gov/species-and-habitats/species-guide-index/birds/ruby-throated-hummingbird

You can see the huge eye sockets. This image (not a real skull, but a plastic cast) shows that even more clearly (also Archilochus colubris):

Source: http://www.boneroom.com/uploads/4/8/1/1/48118243/s521972503441136676_p1061_i1_w640.jpeg

According to the original paper of the research, which was linked by the NY Times article and by your very question (Nyffeler, Maxwell and Remsen, 2017):

  Bigas et al. (2006:237) described the feeding behavior of the mantids in the mist-nets:

  “The modus operandi of the mantis seems to be to approach the bird,
  which is always hanging downwards, and then enter the cranial cavity
  via one of the eyes, feeding on the brain tissues.” (emphasis mine)

If you look at the image you shared you can see that the mantis' mouthparts are positioned at the side of the hummingbird's head, which corroborates the claim that the mantis uses the eye socket to get to the brain tissue.

Sources:

Nyffeler, M., Maxwell, M. and Remsen, J. (2017). Bird Predation By Praying Mantises: A Global Perspective. The Wilson Journal of Ornithology, 129(2), pp.331-344.
Bigas, D., J. Piccardo, And J. L. Copete. 2006. Praying mantis killing passerines in mistnets. Dutch Birding 28:237–238.


Why don't stem cell therapies use viruses? Why don't stem cell therapies use a virus to deliver gene editing sequences to stem cells instead of the harvesting-transformation-transplant route.

I thought it might be because of a lack of specificity on the part of the viruses, but then I saw phage display techniques that would seem to make that a non-issue.

I thought it might be trans-cytosis or getting the phages out of the blood-stream and into contact with the stem cells. I haven't found an easy solution to this hurdle, but it doesn't seem to be insurmountable.

I think the main issue is regulatory? Perhaps a lack of precedents in this area. What do you think of my analysis? Is this idea even feasible?

Stem cell therapies do in fact utilise viruses. In the examples cited, the stem cells were infected by viruses in vitro, genetically modified, and then reintroduced into the target as autologous transplants. The main issue at hand is that live viruses introduced directly would be targeted and destroyed by the immune system, which greatly reduces their efficacy in causing transformation of cells.

In a recent Nature paper, zinc finger nucleases were used to target and disrupt the CCR5 or CXCR4 gene, which greatly reduces the efficiency of HIV binding to CD4+ T cells. The zinc finger nucleases were introduced into the cells using an adenovirus vector.

  Generation of cxcr4 ZFN adenovirus and CGW-siX4s lentiviral vectors. The CXCR4 targeting locations of siX4s and ZFN are shown in Supplementary Figure S1.

This technique was then used in a number of clinical trials to modify hematopoietic stem cells using zinc finger nucleases, as summarised in this review paper. The recent advent of CRISPR-Cas systems will probably lead to an increase in similar techniques, due to the higher specificity and ease of engineering of Cas9-based nucleases.


Which enzymes degrade dynorphins and what drugs inhibit these enzymes? Which enzymes degrade dynorphins and what drugs are there available to inhibit said enzymes?

This paper was looking at inhibition of dynorphin converting enzymes and their importance. Although they don't seem to know if it is a single enzyme, or if it is multiple enzymes.

This paper looked at bikunin as an endogenous inhibitor of dynorphin convertase in human cerebrospinal fluid.

This paper looked at several inhibitors (some of which are known to irreversibly inhibit other enzymes), like N-peptidyl-O-acyl hydroxylamines and their effects on hCSF-DCE, the enzyme that cleaves dynorphin A, dynorphin B and alpha-neoendorphin to release Leu-enkephalin-Arg6. However, it is known to inhibit serine and cysteine proteinases.

However, I don't see any actual medications that are meant to inhibit Dynorphin enzymes. Instead I found Al-Fayoumi et. al were actually looking to identify stabilized dynorphin A derivatives instead of just inhibition of enzymes.


When did bison exchange smartness for larger skeletal muscles or a digestive system that can ferment grass? Patricia Churchland (2019) writes:

  From time to time, evolution favors a dumbing down; sacrifice some smartness in exchange for larger skeletal muscles, like bison, or for a digestive system that can ferment grass, again like bison.

Roughly when did these evolutionary changes occur?

Patricia Churchland is wrong there.

Bison are very big deer/goats, and they are not dumber than deer and goats, you know how clever sheep are! There is a theory that they are related to a rabbit sized early ruminant about 40 million years ago.

Bison and deer have common ancestors about 17 million years ago.

Goats and deer have common ancestors about 22 million years ago, they have a similar digestive system to bison, your book is being vague there.

Oligocene epoch:
The formation of the Himalayas and the Alps brought about significant geographic changes. This was the chief reason behind the extensive diversification of deer-like forms and the emergence of cervids from the Oligocene to the early Pliocene.[50] The latter half of the Oligocene (28–34 Mya) saw the appearance of the European Eumeryx and the North American Leptomeryx. The latter resembled modern-day bovids and cervids in dental morphology (for instance, it had brachyodont molars), while the former was more advanced.[51] Other deer-like forms included the North American Blastomeryx and the European Dremotherium; these sabre-toothed animals are believed to have been the direct ancestors of all modern antlered deer, though they themselves lacked antlers.[52] Another contemporaneous form was the four-horned protoceratid Protoceras, that was replaced by Syndyoceras in the Miocene; these animals were unique in having a horn on the nose.[45] Late Eocene fossils dated approximately 35 million years ago, which were found in North America, show that Syndyoceras had bony skull outgrowths that resembled non-deciduous antlers.[53]

https://en.wikipedia.org/wiki/Deer#Eocene_epoch

This science mag study contradicts with the wiki references by about 20 million years:

https://science.sciencemag.org/content/364/6446/eaav6202

Here's a giant book on the topic of ungulate radiation based on their teeth, it doesn't give an easy answer to your questions though, it implies that there have been many genera of ungulates the size of cats and dogs and larger in the paleocene: https://www.researchgate.net/publication/36248483_Adaptive_radiation_of_early_Paleocene_ungulates/link/0c96051683bae86a84000000/download

Bison are at the top of the ruminants, after the cervus (deer):

That book is sociology and neuroscience, and it lacks depth for evolution. Evolution is fabulous at providing evidence and physical details, so she should demonstrate some examples ( bat digits, hand structure of primates, resemblances of sea mammals).


Can anyone tell what kind of berry/currant this is? I found this currant-like plant in Helsinki, Finland. It seems very similar to red currant but it has hairs on its fruits, and the fruits are pear-shaped. Can anyone please identify this plant? Many thanks!

I am pretty sure this is a species of Ribes (Grossulariaceae, vernacular Finnish: herukat), and that it is not native to Finland.

I would guess that it might be a variety of R. rubrum L., but it also might be a species unrecorded in Finland so far. You might consider sending the photo to someone at Helsinki Botanical Garden, or at the Natural History Museum. (If you got a twitter account, you might just sent the link to this page to @Raino_Lampinen and ask on his opinion.)


Will lipid molecules 'flip-flop' over a membrane without the use of an enzyme? All of the references to this I can find refer to enzymes like Flippase making it 'easier' or 'more likely' that the translocation will occur, rather than actually make it possible.

The following is from Alberts

  In the ER, however, phospholipids equilibrate across the membrane within minutes, which is almost 100,000 times faster than can be accounted for by spontaneous “flip-flop.”

Does this mean that left unattended, any phospholipid membrane will 'flip-flop' spontaneously, just very slowly, and can this be observed?

Bilayer components will 'flip-flop' at measurable rates, but these are very different for different lipid classes. Here are the results of an experiment using fluorescently-labelled analogues.

  Bai, JN and Pagano, RE (1997) Measurement of spontaneous transfer and transbilayer movement of BODIPY-labeled lipids in lipid vesicles. Biochemistry 36:8840-8848 DOI: 10.1021/bi970145r

The authors followed the transbilayer (flip-flop) and interbilayer movement of fluorescently-labelled analogues of various membrane lipids: sphingomyelin (C-5-DMB-SM), ceramide (C-5-DMB-Cer), phosphatidylcholine (C-5-DMB-PC) and diacylglycerol (C-5-DMB-DAG) in a system of unilamellar vesicles consisting of 1-palmitoyl-2-oleoyl phosphatidylcholine.

The results were analysed in terms of a model in which the labelled molecules could move between vesicles and between the two monolayers of the bilayer.

half times:
            interbilayer    transbilayer (flip-flop)
C-5-DMB-SM  >21 s           3.3 h
C-5-DMB-Cer 350 s           22 min
C-5-DMB-PC  400 s           7.5 h
C-5-DMB-DAG 100 h           70 ms

So, for the phospholipid tested the half-time for flip-flop was 7.5 hours.


Are human bodies programmed to die? Following from this question: What is the evolutionary advantage of death?:

Is there any evidence that human bodies have systemic self-destruction built into their developmental program? I'm not talking about the cell death response, which I know is an important part of growth, development and cancer prevention.

I've read some things about telomere-shortening but don't know if this is a cause or an effect.

From a certain point of view you could argue that our bodies have an inherently limited lifespan;

Telomeres are extensions to the end of chromosomes that prevent damage or loss of genetic information during cell division. Telomeres are not replaced (in normal cells), which gives rise to a replicative lifespan; the number of times a cell can divide before permenantly leaving the cell cycle (senescence).

This is generally viewed as an anti-cancer mechanism to protect against errors creeping in to the genome through many cell divisions. In order to become cancerous, a cell must first overcome its replicative lifespan [ref.]. This is achieved by activating the (normally inactive) telomerase enzyme that extends the telomeres - embryonic stem cells are one of the few cell types that normally express this enzyme.

There are other ways in which you could argue that our lifespans are fundamentally limited, but it is important to note that the objective is not 'to die', but to increase fitness (in a Darwinian sense) earlier in life. This is known as antagonistic pleiotropy; when an advantageous trait early in life is disadvantageous later in life.

Telomere shortening is just one example of antagonistic pleiotropy (protects against cancer when younger, but limits the number of times your cells can divide).

Other traits that inherently limit lifespan include;

Neurons (as a rule) do not replicate, and last for your whole life time. This certainly excludes them from replicate senescence, however it means they are highly susceptible to 'wear and tear'; oxidative stress is a natural by-product of respiration, and the vast majority of damage done by these species (e.g. reactive oxygen species) is repaired by the cell, however some will always remain unchecked, and eventually this leads to neurological dysfunction and cognitive decline. Without intervention this is inevitable in each individual (the rate of aging differs between people, but aging and age-dependent diseases are disorders are a natural part of living).
The same is true for cardiac and smooth muscle - whilst much repair can be carried out, it is inevitable that damage will creep in over a life time, and thus the vast majority of human age-related deaths are due to cardiac problems in one way or another.

So there is no 'programmed' limit to life span, in that we have not evolved to die, but our bodies are inherently limited by the systems that have evolved. Life expectancy a few thousand years ago was ~20 years (if you lived beyond infancy!), whereas now in the developed world this is ~80 years, so our bodies can already survive way beyond our 'natural' life span, and thus we now succumb to age-related disease. Evolution has spent millions of years giving us every possible advantage that leads to reproductive success. Natural selection of traits beyond reproduction are secondary to those beforehand, and thus we have fundamentally limited life spans.

There is an argument for an evolutionary advantage of limited lifespan. This seems at first counter-intuitive, until you consider that natural selection does not act on individuals, but genes. It is proposed to be advantageous (in some circumstances) for an organism to have a shorter life span, as this increases the turn-over of individuals in that population. This in turn increases their evolvability - clearly advantageous for the gene(s) influencing this trait if it increases the likelihood of successful reproduction and thus passing on that gene/allele/trait...

I like this hypothesis, and can see that natural selection may favour it. I think mice are great examples here; they have much shorter lifespans than us, yet they 'age' (biologically) the same (cardiac problems, diabetes, cancer) but at a faster rate to give a higher population turnover). In a high mortality environment, the most adaptable animals will be more successful.

However, I think this is likely to be secondary to the pressures on other survival traits that  more directly increase the chances of successful reproduction.


What is the difference between [Clinical Trials as Topic] category and [Clinical Trial [Publication Type]] category in pubmed? Dears in biology stackexchange community, I hope that everyone is fine.

I am using pubmed in my current review. My focus is about an application on the scope of Clinical Trial. When I used MeSH for narrowing my research scope on Clinical Trial, I got two different categories which I cannot find any clear difference between them. They are:

Clinical Trials as Topic
Clinical Trial [Publication Type]

However, when I search on the two different categorises, I found very different resulted papers. That means that there are a difference between the two categories where my ignorance is.

Could you please tell me what is the difference?

Possible examples of two queries:
1. ("Clinical Trial" [Publication Type]) AND "Prostatic Neoplasms"[Mesh]
2. ("Clinical Trials as Topic"[Mesh]) AND "Prostatic Neoplasms"[Mesh]

Many thanks to you for your time, in advance.

The actual definitions provided with the MeSH terms look essentially interchangeable:

Clinical Trial as Topic:
Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.

Clinical Trial [Publication Type]:
A work that reports on the results of a clinical study in which participants are assigned to receive one or more interventions so that researchers can evaluate the interventions on biomedical or health-related outcomes. The assignments are determined by the study protocol. Participants may receive diagnostic, therapeutic, or other types of interventions. While most clinical trials concern humans, this publication type may be used for clinical veterinary articles meeting the requisites for humans.

But the difference is simple. CT as Topic refers to publications that talk about Clinical Trials in general, as a subject itself. But CT[Publication Type] refers to an article that is actually reporting the results/analysis of one or many clinical trials.

To show you what I mean, these are first PubMed results using the two MeSH heading, when you specifically tell the search engine to not include other branching MeSH terms:

Clinical Trial as Topic:

Clinical Trial[Publication type]:


on/off behavior of neural networks What causes a group of disembodied neurons in a dish to fire after a silence? If there are no neurons providing a stimulus for more firing (as in a dish of disembodied rat neurons), then why don't they simply cease firing after the synchronized burst completes?

There are a number of different wiring scenarios that could lead to this type of behavior, even in a dissociated neuronal cell culture.  The two major cases are neurons that are truly isolated from each other, and collections of neurons that connect together.  Since your question refers to firing and synchronized bursts, I'll restrict my discussion to the generation of spontaneous action potentials - but keep in mind that not all synaptic communication requires an action potential (the vast majority of internal connections within the retina, for example)

In the case of ensembles neurons in vitro, spontaneous activity is fairly typical.  One simple way to get this activity is for a subset of cells in the network to be inherently spontaneously active.  In the case of single, isolated neurons, this kind of individual cell spontaneous activity could also result in a single neuron firing spikes in a periodic fashion.  So for example purposes, let's explore how a single cell could produce this kind of activity.

Since action potentials are triggered by a sufficiently strong depolarization, we need to identify potential membrane polarizing sources.  When dealing with single cells, the major controllers of cell membrane voltage potential are the voltage gated ion channels.  When open these channels can cause, depending on their type and cellular/extracellular conditions, either a depolarization or hyperpolarization in the cell.  And, most interestingly, whether they are open or not depends on the cell membrane's polarization state.

That makes voltage gated channels excellent at feedback:

a depolarizing channel that is depolarization gated will further activate itself once activated, leading to yet more activation.  This is a positive feedback cycle.
a hyperpolarizing channel that is depolarization gated will, upon depolarization of the cell open and serve to hyperpolarize the cell until the initial depolarization has been removed.  In this way it would serve as a negative feedback source.

Physiologists have thoroughly characterized many of these cells, and they have many more states beyond an "open" and "closed", such as different levels of "inactivated".  But we don't need to know about those to answer your question.

The last piece we do need is brownian motion which is the movement of particles due to their bombardment by other particles.  This motion can with some frequency cause voltage gated channels to spontaneously open or close, which introduces noise into the system.

As you can imagine, if you have a positive feedback channel that is gated spontaneously, it will make it briefly more likely for other depolarization gated channels to be activated.  Positive feedback can quickly lead to a rapid depolarization of the cell, which could be observed as a burst of spikes.  If you include a set of slower reacting depolarization gated hyperpolarizing channels, then it's easy to construct a scenario where the cell would depolarize spontaneously with no apparent input, then have a quiescent period where a prolonged hyperpolarization makes it less likely to fire spontaneously.

Voila, bursting in an isolated neuron.  Place a set of those neurons in a network and you can get generate a lot of spontaneous activity.


What is the difference between sequence, reads, and contigs of genetic material? Can someone explain the differences between sequence, reads, and contigs of genetic material such as DNA, if possible with an example?

I am new to bioinformatics, and I have not found any conclusive answers for all these concepts on the web.

My understanding of those three words as follows:

sequence is a generic name describing order of biological letters (DNA/RNA or amino acids). Both contigs and reads are DNA/RNA or aa sequences
reads are just a short hand for sequenced reads. Usually sequenced reads refer to somewhat digital information obtained from the sequencing machine (for example Illumina MySeq) and stored in the fastq file with quality scores per base. Reads are usually short. However "short" changes rapidly. Right now MySeq produces reads anywhere between 50-150 base pairs long (bp). From a single run (it will really depends on the run) you can get millions of reads, where each read will be set bp size e.g 100bp long. All reads are stored in a single fastq file per replicate, where all reads in that file are usually of uniform size e.g all 5 million reads are 100bp long.

As a bioinformatician your first job is to identify where about those reads come from. Depending on the experimental goal and on what sort of sequencing you were doing e.g DNA-seq or RNA-seq you may or may not encounter contigs.

contigs are simply reads that have been assembled together. For example if you are doing de novo transcriptomics. Then you would:

purify your transcript from a tissue and send it off for sequencing
get your fastq files with sequenced reads, that are all short reads
(e.g 100 bp)
assemble those 100bp reads into a longer contig that hopefully will resemble your individual transcript


Renin - enzyme or hormone? Wikipedia says :

  The kidneys secrete a variety of hormones, including erythropoietin,
  and the enzyme renin.

Can a substance be both an enzyme and a hormone ? Why is renin both an enzyme and a hormone ?

Yes, something can be both a hormone and an enzyme. There are a group of hormones known as peptide hormones. These are proteins (such as enzymes) that act as hormones indirectly (and maybe directly too?). A hormone is a chemical secreted by a cell that has some effect on another cell elsewhere in the body. In this case, the chemical just happens to be an enzyme. You can read about them on Wikipedia

Renin is secreted by the kidney, but its involved in arterial vasoconstriction (outside of kidney cells), so it is a hormone. And its also a peptide/enzyme, so it is considered both a hormone and an enzyme


How far can a human see at night? I am not talking about seeing in total darkness, which I understand is not possible. I am looking more about a question how far can a human see during starry night or with half moon/full moon. I tried googling for this, but found no useful results.

EDIT I think I need to clarify: I am thinking more in terms of immediate surroundings. I understand we can a source of light from afar, but what about a tree on a flat land - from how far would we see it in star light?

At night you can actually see further than during the day. At night you can see stars that are many light years away, but during the day the furthest thing you can see is probably the sun, which is 8 light minutes away. There's probably no definite answer because the brighter and bigger the object (and the darker the surrounding and the clearer the air), the greater the distance from which you can see it.

According to Sky and Telescope, the most remote stars (as part of Andromeda Galaxy) you can see with a naked eye are 2.5 millions light years away.

Talking about the objects on earth, at half-moon, you could see to "the end," that is to the horizon.


What insect is in the PHP bugs logo? Well, maybe this is a question more suited to Stack Overflow, but anyway, I am curious, which insect is the one in the logo of the PHP bugs site? Is it an actual insect or just a generic "bug"?

It seems like some kind of Hemiptera for me, probably some kind of "true bug". A quick google search about these insects and I found the Hemiptera suborder Heteroptera, and this critter is probably from this group.

I tried to search by the image in google images, but only found the logo itself, in the same low resolution is the image above (I was not able to find a better version of it). I tried to remove the background from the image then, but still I didn't get any photo of the possible species of this logo.

EDIT: this was the PHP bugs logo up until 24th July 2017; the next day it was changed to another different "bug". This question is about the former logo, not the current one.

It is an actual insect, Lethocerus americanus, also known as Giant Water Bug. See:

Matches the colors, body shape and small eyes and head. And yes, they are very annoying. As expected from real bugs. You know, like the first one.


Are your finger muscles and tendons interconnected? Are finger muscles and tendons interconnected? If they are interconnected, then if i exercise one finger will it train the other fingers since they are interconnected and share the same muscles in the forearm? (correct me if im wrong)

I have done some research but i cant find the answer for example(if your thumb joint is injured you should avoid using stress balls to exercise the other fingers, why?)

That's a really interesting question!  What might help you the most is reviewing hand and forearm muscle anatomy.  I have some examples that could help.  The flexor digitorum profundus and flexor digitorum superficialis are hand muscles that originate in the forearm region.  At the wrist they split into four tendons (so FDP has 4, FDP has 4) one for each non-thumb finger.  They help make a fist.  Then there are the intrinsic hand muscles.  One interesting example is the lumbricals, which originate at the FDP tendon and have a very specific action.
To answer your question, I don't see any reason why exercising the four non-thumb fingers is recommended against, other than the possibility that you could be inadvertently moving/stressing the thumb.  I don't believe there is any connection between muscles of the thumb and non-thumb fingers, other than proximity of muscle/tendons.


GWAS terminology "Tag" vs "Lead" vs "Index" SNP I'm trying to get my head round the correct GWAS terminology. I keep seeing the terms like "tag", "lead" and "index" SNP to be used almost interchangeably and I would like to get a clarification from someone inside the field.

My (limited) understanding is as follows:
Tag SNP - the SNP included on the genotyping microarray. Once we have a compendium of SNPs for a given sample we can use reference haplotypes to impute the rest of the SNPs.
Lead SNP = Index SNP - the SNP assigned the highest association significance after we've run association analysis for all the imputed SNP. The other SNPs in high LD with the lead SNP will form the associated locus.

Am I correct in my understanding? Any other / better terms I should be aware of?

Many thanks!

I found a review paper that addresses your questions, see

Schaid, Chen, Larson (2018): From genome-wide associations to candidate causal variants by statistical fine-mapping

Tag SNP. You correctly identified tag SNPs. From the paper:

  [T]he SNPs on microarrays, called tag SNPs...

Lead and index SNP. These are apparantly synonyms. From the paper:

  This allows one to focus on the SNPs with the smallest
  (that is, most significant) P values in distinct regions,
  sometimes called the lead or index SNPs.


Colorful Large Wasp (?) on Milkweed Arizona USA Observed this very colorful insect on Asclepias subulata (Desert Milkweed) in Phoenix Arizona. About 8 am, temperature about 90F, sunny, late-September.  When flying it seemed to have a narrow waist like a wasp.  About 5 cm long, appears rusty-red in flight (not surprisingly given its size).  As the pictures show, it was enjoying a bit of nectar from the flowers. Would love to know its name so I can greet it properly next time!

Possibly a tarantula hawk (because of its red wings and metallic blue body), and because they inhabit the Southwest US. It being on the flower in the picture makes sense as “...adult tarantula hawks are nectavores and feed on flowers”. They have very painful stings, but as with most insects, if nobody bothers them, they won’t bother you.
The females hunt down and paralyze tarantulas and lay their eggs in them, hence the name. Freaky, isn’t it?

Reference


Why did humans get rid of their tail in the evolution? Most mammals seem to have tails. Even human embryos start out with a tail. But here we are with nothing but a tail bone that hurts when we trip over backwards. What is it good for? Why don't humans have a tail to wag around?

Some science fiction (like Avatar) even portrays a tail as something sexy. And we all have experienced that a third arm of some kind would be very useful once in a while. Especially since humans stand up alot of the time it could help us keep the balance.

Is there any utilitarian evolutionary explanation for why we don't have tails any more? Is it only because we try to be different?

The tail serves a variety of complex balance tasks in locomotion, turning, jumping, aerial balance, hanging, and most mammals have a tail, save for other examples, i.e. rabbits, pigs, capibaras, manx cats, seals and bats, lemmings and hamsters have mini tails.

All the previous large apes related to humans lost their tail millions of years ago. The reason why that occured are multiple and mixed. Multiple good explanations have been suggested.

Gibbons are some of our most monkey-like ape cousins. If you see how they move, they run on two legs rather than 4. Monkeys with tails are less adapted to walking and their pelvis is angled differently. https://www.youtube.com/watch?v=b9Pt2qgSqJw

Large animals with small tails, such as caribou, hippos, elephants, deer, seem to keep some kind of tail, however with chimpanzee type animals, once the tail became small it didn't stay on as a mini-tail. So would it make sense for chimpanzees/humans to have small tails like hippos or very long ones? If a chimp can run on 2 legs, that leaves it two hands to catch the tail of another competing chimp.

The big apes move differently to small apes: big apes live on the ground more, they don't run in trees as much, they move differently, they are larger, they have completely different body ratios for arm and leg size, and there have been a wide variety of propositions for hundreds of years on this topic without a particularly clear reason being accepted for which great apes don't have a tail.


What is this tree in Sydney? My family snapped this picture around Sydney, Australia. Could someone please advise what this tree is? Help! We are smittened with it :)

This is a tulipwood tree, which belongs to the species Harpullia pendula. As an Australian native, they're commonly used as street trees along the east coast.

More information about this tree can be found here.


Why does getting soap in your eyes cause redness and irritation? I am wondering why do eyes become red after getting soap in them. What is the cause behind it?

This is because of the soaps chemical nature. They are alkaline agents and human eyes have a very low tolerance for alkalinity. Human eyes are roughly neutral with a pH of around 7, and soaps are around 7.5 to 9.

The eye can't handle the alkaline object as it is potentially harmful to the eye so it will start watering to get rid of the alien substance. Blood vessels then enlarge, coming closer to the surface of the eye, making them appear red.

Most soaps are tested before released to make sure if they come into contact with eyes they are non-toxic. Baby soaps have a lower pH as well to make sure that the baby doesn't come to harm.

Either way, its probably best not to put it in your eyes.

See here for more information.


Is it possible to grow any kind of plant soilless (hydroponics)? Hydroponics is a subset of hydroculture and is a method of growing plants using mineral nutrient solutions, in water, without soil. [wikipedia]
My question is if is it possible to grow any kind of plant soilless (hydroponics)?

Yes it is possible, and as far as I can see, there should not be any plant which would be impossible to grow in a such an environment, just more or less difficult, although this is just my speculation.

I have myself grown tomatoes from only a liquid solution of minerals and nutrients, but you have to change the solution from time to time to prevent bacteria and fungi growing starting to grow in it. The reason why this is not a method used in industrious growing is because it is a lot more expensive than using soil and fertilisers, and more work.


What animals have a blood-brain barrier? I am curious about how old the BBB is, in terms of evolution. Is it present in all vertebrates? or just mammals? or what?

It appears it is all vertebrates.

"All vertebrates started out with a glial blood-brain barrier 4–500 million years ago"

  All extant vertebrates have a blood-brain barrier (BBB), a specialized layer of cells that controls molecular traffic between blood and brain, and contributes to the regulation (homeostasis) of the brain microenvironment. ... The barrier is formed by vascular endothelial cells in most groups, but by perivascular glial cells (astrocytes) in elasmobranch fish (sharks, skates, and rays). It has been unclear which is the ancestral form, ... we conclude that the ancestral vertebrate had a glial BBB. This means that an endothelial barrier would have arisen independently several times during evolution, and implies that an endothelial barrier gave strong selective advantage.

So, all vertebrates have one; in some fish, it is composed of glial cells rather than endothelial cells.

However, insects do have something similar:

"Evolutionary conservation of vertebrate blood-brain barrier chemoprotective mechanisms in Drosophila"

  Insects also possess protective neural barriers, but they differ anatomically from vertebrates (Figure 1). Drosophila melanogaster (Dm) has an open circulatory system that is separated from the CNS by a thin layer of glially-derived epithelial cells (Treherne JE, 1972; Carlson et al., 2000; Stork et al., 2008), making the Dm humoral/CNS interface topologically much simpler than the vertebrate BBB. However on a cellular level, the vertebrate and insect BBBs share many common features.


Do experiences shape actions of insects? Animals? Would an insect behave differently to stimuli depending on what stimuli occurred to them earlier (that only affects them cognitively or their conscience)?

"Simple" insects like fruit flies can learn to associate odors with food, e.g. see here for a pretty classic example. Drosophila even show some kind of depression which is acquired. Their sexual experiences even shape their alcohol intake.

You will find similar examples for other model organisms as well.
So, yes, simple animals behave differently in response to previous experiences.


Isn't biological immortality strictly speaking impossible? This question relates to both immortal cells such as cancers and organisms like the Hydra genus. Isn't it technically impossible for these "immortal" biological systems to live forever, even disregarding accidents and disease?

I am aware that they are considered immortal because they do not exhibit the usual degradation of functionality as they chronologically age. In cancer's case an up regulation of telomerase prevents the usual gradual depletion of DNA at the chromosomal ends limiting a cell's lifespan. But at the same time cancer cells and immortal organisms still undergo DNA damage and thus mutation (cancer cells even mutate faster as far as I know), wouldn't the stacking of these mutations at some point kill off the cancer cell line/immortal organism as some vital part of their metabolism is inevitably damaged?

Wouldn't true biological immortality require an organism with DNA that is either impossible to damage or if it could would always be perfectly repaired? (creating an evolutionary dead-end as well)

Good question.

There are many organisms that are technically biologically immortal. However, I would like to point out that the definition of biological immortality is this:

  ...cells that are not limited by the Hayflick limit, where cells no
  longer divide because of DNA damage or shortened telomeres.

(That's from here.)

So biological immortality doesn't really cover disease or physical trauma, which would actually include damage to DNA. I know what you're thinking: But wait, doesn't biological immortality literally mean cells that don't die because of DNA damage? Nope. Close, but no. Look back up at the definition. You probably caught it this time (by the way, it's not listing two different reasons (DNA damage and shortened telomeres), just rewording the Hayflick limit (DNA damage aka. shortened telomeres)). Biological immortality does not mean that the cell will not die because of excessive mutation (which would fall under physical trauma mind you, be it from chemicals, radiation, or just plain mistakes during replication), it means that the cell will not die from excessive programmed mutations, aka. its Hayflick limit, aka. telomere degradation. A molecular biology course summary from Berkeley says:

  However cells that express telomerase still undergo cellular senescence in response to DNA damage, oncogenes, etc.

Ok, sidetrack time (go ahead and skip this part if you already know what telomeres are). A telomere is a repeated DNA sequence at the end of a chromosome that protects the coding regions from deletion (the reason for these deletions is complex and off topic, but long story short, RNA primers cannot attach to the very end of a chromosome, so a little of the lagging strand is lost during every replication). So the telomere takes the hit instead of the important coding DNA further up the chromosome (see this article.) As you can imagine, there is only enough telomere to go around, so cellular aging exists unless the organism has active telomerase, which is an enzyme that adds telomeres every time they are lost (see this article).

So, short answer, biological immortality is very possible in its actual definition (see above).

Concerning your definition (immortality regarding all mutations, programmed or otherwise), an organism comes to mind: Physarum polycephalum. It is biologically immortal in the way we have just defined, but also avoids DNA mutation by sharing DNA (constantly comparing and fixing sequences) among thousands to millions of nuclei through homologous recombination, which repairs DNA mutations at a freakishly high efficiency when you include millions of strands bearing what should be the same sequence (see this article). Physarum polycephalum is a slime mold, meaning that when cells meet each other, they fuse. This particular slime mold actually prefers to be a plasmodium, which is a constantly growing mass that is technically a multinucleated single cell but can grow to be potentially infinitely large as far as we can tell. Because of its extreme ability to correct mutations, this organism has been referred to as, exactly like you said, an "evolutionary dead-end." I'm sure it still sustains some mutations over a very long period of time, but you might want to check it out nevertheless.


How does LCR compare to Assembly PCR The question pretty much explains itself. How do the two methods compare? I've always used Assembly PCR but the method is prone to mistakes and I'm curious how it compares to Ligase Chain Reaction (LCR).

I have used both Gibson assembly (what you mean by assembly?) and LCR as replacements for blunt or sticky ended cloning. LCR has, for me, worked better in that a higher proportion of constructs that come out have been assembled correctly and I have noticed no mutations after LCR while I have seen them somewhat often with Gibson.


How can microarrays be used to quantitatively determine level of gene expression? This is probably a stupid question because I don't fully understand how microarray experiments work. I'm trying to understand how microarrays work but I'm confused about something which I can't seem to get around without fully understanding how microarrays work, which seems impossible without understanding this.

I understand the principle of how microarrays work. But I don't get how microarrays can tell you how much mRNA is expressed in one kind of tissue vs another kind of tissue. Wouldn't that depend on how much tissue you started with? So if you started with more cells of one kind you will get more mRNA/cDNA and so the intensity of fluorescence at the corresponding spot on the microarray will be greater. So even if the amount of gene expression is lower in one type of tissue the corresponding spot on the microarray might show a greater fluorescence intensity compared to the other type of tissue if more tissue was used.

Also another related question: if you put the mRNA you obtain from cells through PCR will you get the same proportion of mRNA as before PCR? From what I understand PCR can be used to make more mRNA before doing the microarray but because PCR is a random process I'm not sure if it will affect the proportion of mRNA.

Hopefully my questions make sense.

From the comments:

MattDMo:

  You can compare different samples, which may have started out as
  different amounts of tissue, by using control genes. The numbers
  reported by most standard microarray experiments are not absolutely
  quantitative (There are 2450 copies of this RNA per cell in this
  sample), but are rather a proportion as compared to a set of
  housekeeping genes whose levels are not expected to vary much between
  the samples you are analyzing.

cagliari2005:

  For PCR amplification, you are right, this is a random process and
  while you would expect most RNAs to be similarly amplified, biases can
  and will occur. Amplification biases are usually assumed to be
  identical between similar samples and therefore will (mostly) cancel
  out during the differential analysis.


What is this plant with pink flowers and maple tree shaped leaves? This plant goes in my front yard in morning sun in the interior of British Columbia.

It has green leaves initially and then they curl brown and turn yellow. It gets water weekly but not lots. Is it okay to divide this plant to thin it out?

It's a Japanese Anemone (Anemone hupehensis); if I had to guess, I'd guess it was the cultivar "Robustissima".

I used to grow these when I had gardens. Absolutely you can divide them! Wait until the spring if you can; if you have to divide in the fall, wait as long as you can to do so.


Is there a DNA test to identify dog mixes? We adopted a dog at the age of two. Our vet said it was a mix of an Australian Shepherd and Border Collie, which we've told everyone. Based on markings, I think it's likely. I am wondering, however, if there are any tests or other ways to know the mix of a dog if you don't know the specific parentage.

Does each dog breed have specific genetic markers that can be used to identify the breed? If so, has a dog breed test been developed or is there no commercial demand for such a test?

There are many commercially available mixed breed ID tests, as a quick Google search will tell you.  However, I cannot vouch for their accuracy: this news article may be of interest. Also this.

The genetic markers used to identify breeds in a mixed-breed are microsatellite markers (sometimes SNPs): you can read more here, but from the abstract:

  We used molecular markers to study genetic relationships in a diverse collection of 85 domestic dog breeds. Differences among breeds accounted for ∼30% of genetic variation. Microsatellite genotypes were used to correctly assign 99% of individual dogs to breeds.

If you're interested in dog genetics, I encourage you to check out Elaine Ostrander's work.  She's written at least one book for laypeople, in addition to her numerous journal publications.


Statement about Tropical Rainforests I made a statement about tropical rainforests, and I want to know if it's somewhat true or not:

The soil in tropical rainforests is not exceptionally fertile, because it contains few minerals. The reason that a tropical rainforest has a huge amount of vegetation is because of the quick mineralisation. If a dead leaf falls onto the ground, it immediately gets turned into minerals, which the plants immediately use for sustaining theirselves

There are many websites which describe this phenomenon. They all seem to confirm the basic premise of the question: in tropical rain forests most of the minerals are held in the biomass and rapid decomposition contributes to the recycling of these nutrients for new growth. One example is here.

  Tropical rainforests are noted for the rapid nutrient cycling that occurs on the ground.  In the tropics, leaves fall and decompose rapidly.  The roots of the trees are on the surface of the soil, and form a thick mat which absorbs the nutrients before they reach the soil (or before the rain can carry them away).  The presence of roots on the surface is a common phenomenon in all mature forests; trees that come along later in succession win out in competition for nutrients by placing their roots over top of the competitors, and this pattern is seen in the temperate rainforest as well.  What does not occur in the temperate rainforest, however, is a rapid cycling of nutrients.  Because of the cold conditions and the acidity released by decomposing coniferous needles on the forest floor, decomposition is much slower.  More of the nutrients are found in the soil here than would be the case in a tropical forest, although like the tropical forest most of the nutrients are held in the plants and animals themselves.

I looked for actual evidence of these differences in rates of decomposition and I found this:

  Salinas, N. et al. (2011) The sensitivity of tropical leaf litter decomposition to temperature: results from a large-scale leaf translocation experiment along an elevation gradient in Peruvian forests. New Phytologist 189: 967-977

These authors reported a comparison of rates of decomposition at various elevations in Peruvian forest. The parameter k is the decay rate of dry mass, year-1. The following data are taken from Table 3.

site          elevation (m)   mean k (yr-1; 15 species)
Tambopata     210             1.753
Tono          1000            1.424
San Pedro     1500            0.968
Trocha Union  2720            0.546
Wayquecha     3025            0.424

and this:

  Jacob, M. et al. (2010) Leaf litter decomposition in temperate deciduous forest stands with a decreasing fraction of beech (Fagus sylvatica) Oecologia 164:1083–1094

These authors studied leaf decomposition in a deciduous forest in Germany, with emphasis on the effect of proportion of beech trees upon overall rates of decomposition. Using data from Table 1 and Figure 2 (values converted from mg-1 g-1 day-1 to yr-1)

% beech yr-1
  96    0.2555
  67    0.657
  21    1.022

My Conclusion

Rates of decomposition can be much higher in tropical rainforest (k=1.753 yr-1 for the Tambopata site in Peru, k=0.256 yr-1 for a beech-rich forest in Germany). However, at higher elevations tropical rain forests are characterised by much lower rates of decomposition (Wayquecha k=0.424 yr-1), comparable to those in deciduous forests.

These are all measurements of loss of dry mass from leaf litter. This will be dominated by loss of carbon, and I would expect that minerals will leach from the decaying litter more rapidly than these values. Nevertheless it seems plausible that relative rates of mineral recycling will reflect these k values.


Identification of a probable sylviidae One summer (August) I was in Bulgaria (Dobrich province) and in the middle of the city I take picture of this bird:

He was making a sound like "Tchek-tchek" like the sound of a Eastern Olivaceous Warbler (lat. Iduna Pallida) but the greenish color make me think it is more a Icterine Warbler (lat. Hippolais icterina).
I found a song similar to the bird I saw on this page (second record).

It could also be a Common Chiffchaff (lat. Phylloscopus collybita) or a Willow Warbler (lat. Phylloscopus trochilus) as they are very common but the length of the tail make me feel it more one of the above (or another one) and the sound does not seem to fit.

Anyone can help on identification of this bird?

The first picture is an Icterine warbler. Because of the yellowish plumage (never in the eastern olivaceous) and the with fringes of tertiary characteristic of the species and never present in the genus Phylloscopus. Also the color of the leg, greish-bluish is quite specific of the Icterine.

The second and third picture are of a Willow warbler (Phylloscopus trochilus). The legs are pale compared to a chiffchaff and the primary projection (the length of the primaries that pass the tertiary) is extremely long and very typical of the willow warbler. You can see the difference in the image below.
 Here a useful webpage


Biology in romantic love Hi could anyone explain the biological basis behind romantic love. What is the biological basis of falling in love?I know that serotonin and dopamine are secreted when we first fall in love. What happens after that as we move on to the more advanced stages of love. Why is it that after some time, we no longer feel the initial feelings of love. What is the biological basis behind it. And also why do we feel so heartbroken if we happen to fall out of love? What is the biological basis behind it?

Dopamine, norepinephrine, and serotonin are more commonly found during the attraction phase of a relationship.

All these chemicals stimulate the brain's pleasure center. But this stage only lasts 1.5 - 3 years [2]. That's why 'we no longer feel the initial feelings of love'.

Oxytocin and vasopressin seemed to be more closely linked to long term bonding and relationships characterized by strong attachments [1].

Attachment makes relationships last for years and decades. It is based on commitment and mutual friendship. Oxytocin and vasopressin are at higher levels [2].

The neurological process involved in the perception of heartache is not known, but is thought to involve the anterior cingulate cortex of the brain, which during stress may overstimulate the vagus nerve causing pain, nausea or muscle tightness in the chest [3].

Image from Wikipedia [1]

References:

Wikipedia contributors, "Biological basis of love," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Biological_basis_of_love&oldid=613867553 (accessed June 26, 2014).
Wikipedia contributors, "Love," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Love&oldid=614240299 (accessed June 26, 2014).
Wikipedia contributors, "Broken heart," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Broken_heart&oldid=613979584 (accessed June 26, 2014).


Why do sharks continually regrow their teeth? Other animals don't do this. What is unique about sharks that requires them to regrow their teeth over and over, or what benefit does it provide them (that wouldn't also be evolutionarily advantageous to other animals)?

Actually, most animals with teeth are polyphyodonts - they regenerate teeth throughout their lifespan. This includes sharks, crocodiles, fish and some mammals (kangaroos, elephants and manatees). Diphyodonty (only replacing teeth once) is the exception. I have a vague memory from undergrad that the evolution of specialised teeth in mammal-like reptiles, and specialised jaw musculature (which happened at the same time) is/was believed to be the reason behind this - for a reason I can sadly no longer remember, tooth specialisation and tooth regeneration are incompatible. When I can find more details and a source for the latter I'll edit them in.


What types of archaea have been found in animals? I am curious as to the species or "types" of archaea that have been found to reside within animals symbiotically. One of the only ones I can think of off the top of my head are methanogens, which live in the gut of ruminants for example.

Humans:

A pioneering study using 16S RNA primers found only Methanobrevibacter smithii in the human intestine.

  Eckburg PB et al. (2005) Diversity of the human intestinal microbial flora. Science 308 1635-1638

In a recent review there is a comprehensive Table of archaea found in humans (this includes non-intestinal flora):

  Dridi B et al. (2011) Archea as emerging organisms in complex human microbiomes. Anaerob2 17: 56-63

Much of the work that is catalogued by Dridi et al. is repeated identifications of Methanobacteriales (Methanobrevibacter smithii, Methanosphaera stadtmanae and Methanobrevibacter oralis), but there are others from the Thermoplasmateles, the Halobacteriales and the Sulfolobales, plus some that are thought to be members of unknown archaeal orders.


Is there any alternative to cryopreserve cell lines without -80 freezer? My university's -80 freezer just broke down and the repair will take 4 months according to the vendor. Is there any other way to preserve cells? Maintaining lot of flasks until the freezer is repaired is not viable option.

Is there any alternative to cryopreserve cell lines without -80 freezer?.

A tank of liquid nitrogen is not just an alternative, but a much better substitute, IMHO. The problem of gradually cooling inside a isopropanol container can be overcome by using a box full of dry ice (-79°C as I recall).


Why is there a seeming dichotomy between mobility and photosynthesis? At least among more complex organisms, I cannot think of any examples of highly mobile species (like animals) that also incorporate photosynthesis. Perhaps there are examples that I'm unaware of, but even so it seems to be exceedingly rare.

Is there some good reason for this, or is it a mere chance of evolution?

I could speculate, perhaps, in that photosynthesis just doesn't provide enough energy for the relatively high metabolism of mobile species; but even then, there seems there should be a "sweet spot" where some level of mobility would still be "worth it" for a photosynthesizing species, rather than the strict dichotomy that seems to be observable, so I naïvely find that explanation somewhat dissatisfactory. There just seems to be little reason for animals to not practice photosynthesis, if only to be able to eat less than they need to without it.

The difference in energy requirements of a motile species make photosynthesis an unsuitable form of primary energy generation for them.

Since plants are sessile, their energy consumption rates are lower. Plants have approximate respiration:photosynthesis rates of 0.35-0.9, as can be seen in this table (click to enlarge):

Once the energy consumption rates exceed 1, the organisms will, by definition, no longer be full autotrophs, as they will need to obtain their energy from alternative sources. Therefore, the relative low energy content of sunlight makes it impossible for motile animals, which have a larger energy requirement, to survive fully via photosynthesis.


The evolution of dogs through domestication and artificial selection I am currently reading Richard Dawkins's book 'The Greatest Show On Earth: The proof for evolution' and in the second chapter he talks very much about the evolution of dogs.

He says centuries ago there was only such dog-like creature as the wolf, but in a matter centuries the wolf has evolved into the many breeds of dog we have through artificial selection conducted by man.

This to me seemed very peculiar and quite frankly untrue, and I may be getting the wrong end of the stick and he is in fact being analogous, although I'm pretty sure he's not.

So, did wolves evolve into the many breeds of dog we have through artificial selection conducted by man?

If so, how many centuries did this take?

(Dawkins's point was that if the wolf can evolve into the vast amount of breeds of dog we have at the moment from artificial selection over a matter of centuries, then surely over many millions of years, the evolution we claim to know of through natural selection could definitely have happened).

According to Serpell, 1995 (http://books.google.co.uk/books?id=I8HU_3ycrrEC, page 8), wolf bones in association with human bones have been found from as early as the middle pleistocene (126,000–781,000 years ago). I think we're talking about more than a few centuries here :) It's still relatively little in comparison to naturally selected evolution, but that's probably the point he is trying to emphasize.


Homology modelling of protein with two identical subunits in its quaternary structure I am using homology modelling to assign the 3D structure of Torpedo acetylcholine receptor (Unwin 2004, 2bg9 in RCSB) to human muscle nAChR. The problem is, both Torpedo receptor, and human receptor have subunit structure A-B-D-A-E: so a same subunit (A) occurs in the model twice. This seems to cause problems for homology modelling software, as it tends to align the second 'A' sequence over the first 'A' sequence, creating a hole in the pentamer, and not filling it up. Any ideas on how to make sure the modelling software acknowledges the quaternary structure? Below please find a link to a file generated using pdb.gz structure data from Unwin model + a set of corresponding FASTA sequences, and attached picture shows the problem (revealed when alignment is set as shown in the picture, by clicking on the same 'boxes' as in the image). Long story short, I need to get the A subunit to complete the alignment in a different spot than it is automatically placed in, as it occurs in the whole structure twice.

https://swissmodel.expasy.org/interactive/JJ5mQf/models/

For anyone who will struggle with this problem in the future: The trick is in reading WHOLE of the manual, NOT submitting the whole sequence/badly segmented sequence, and in NOT attempting to input the same subunit twice. It is necessary to upload subunit FASTAs separately as a hetero target, and each subunit ONLY ONCE (so A,B,D,E for A-B-D-A-E receptor), and then search for templates: most probably there is a template with your quaternary structure uploaded somewhere already, and if not, you can choose preferred arrangement afterwards.


What is the oxygen carrying capacity of reticulocytes? What is the oxygen carrying capacity of immature red blood cells, or reticulocytes? Is there any difference between oxygen carrying capacity of mature and immature red blood cells?

This was studied by Steve Fishbone et al and concluded that the Hb content of a Reticulocyte is slightly higher than that of a mature RBC. The CHr, which is the Hb content of a reticulocyte in CRF patients receiving Erythropoetin is around 27.5 +/- 2.5 pg

Ref: Fishbone S, et al. Reticulocyte Hemoglobin Content in the Evaluation of Iron Status of Hemodialysis Patients. Kid. Int., 1997; 52: 217-222


Valid comparison of gene expression between several genes in several cell lines We have gene expression data (Affimetrix mRNA gene expression results) for several cell lines, over a set of genes.  Our goal would be to be able to compare relative gene expression for genes over the different cell lines.

The method we have thought of so far involves calculating some sort of gene-based average (the expression of a particular gene over all the lines) and normalizing our expression data, grouped per gene, based on that.  However, we are not sure that this is a valid method for obtaining relative expression data from our data set, especially so that we can compare the data from several lines.

Does this seem like a valid strategy?  How is this normalization commonly done?  Should we do something differently to get a better comparison?

Thanks so much!

This is not an easy task, as there are many factors which you have to take in account. First there are intra-essay differences as slightly different conditions for each set of probes for the repetitions. Then, there are inter-assay differences, as differences in the array slides and so on, this paper ("Analysis of microarray gene expression data") goes into more details.

This articles might be helpful as well:

Multiple-laboratory comparison of microarray platforms
Increasing consistency of disease biomarker prediction across
datasets.
The curse of normalization.
Microarray probe expression measures, data normalization and
statistical validation.

What you could also do is go over the Researchgate, I think there are more people around with a lot of experience in this field.


How quickly can the human heart rate rise and fall? How quickly can the human heart rate rise and lower?

For example lets say a human heart rate is rested and is at 60BPM and that person is suddenly scared to trigger their fight or flight reaction. Lets say their heart rate rises to double (120BPM).

From the above example their rate has gone from 1000ms between beats to 500ms between beats. Can the human heart instantly in one heart beat go from the 1000ms to 500ms between beats or does it need to ramp up? If yes how quickly can the heart rate ramp up?

I understand that each human heart is different, and that the speed increase and decrease will be different from person to person. What I'm looking for is a value that I can safely say the human heart won't exceed.

Similarly the same question goes to your heart going lower.

According to the Wikipedia page on Supraventricular tachycardia the heart can go to a new faster rate in the space of a single beat, and then come down again just as quickly, as shown in this image taken from the Wikipedia page.


Have any mutations or genetic loci been associated with exceptional longevity in humans? Individuals that avoid age-related diseases into later life are known as 'exceptional survivors', and have increased longevity compared to their 'controls' (those that were born at a similar time, yet have 'aged' and died sooner). The Leiden Study determined that in these long-lived individuals there is a considerable genetic component contributing to the survival [Schoenmaker et al] (although this could equally be epigenetic - or even more likely, a combination of both).

I have read about studies that have identified genetic mutations that cause premature aging phenotypes (for instance mutations in the WRN gene cause Werner's Syndrome [Yu et al]).

I have yet to discover any studies that determine any genes/regions associated with resistance to age-related disease (i.e. those that age 'well'). My question is whether anyone knows of any such studies?

Arguably studies that have looked into predisposition to age-related diseases have found some mutations - for instance mutations within the 9p21 genetic locus (i.e. p16INK4a/CDKN2A) have been associated with heart disease and stroke independently (2 age-related diseases) [Wahlstrand et al]. Therefore individuals without any of these risk-increasing alleles could be considered predisposed to exceptional survival - but I see this as separate to my question. Are there any protective alleles/genes/loci that increase 'global' survival? Are there a few protective alleles, or many with small effects? Or are the exceptional survivors just without any disease-causing/risk-increasing alleles?

I am interested in published research (of course), but also in peoples general perceptions of the topic; there are plenty of theories of aging and longevity, but few facts - so please state what you 'believe', and explain why this is the case.

Thanks for your time.

p.s. I am aware that you can genetically modify lab models (e.g. C. elegans eat-2 mutants [Lakowski et al]) to live longer. I am interested in naturally occurring variants, specifically in humans (or that at least relate to human aging).

Update (11 May 2012)

I have found a study, published earlier this year, that finds a single genetic polymorphism to be associated (after correction for multiple testing) with centenarians [Sebastiani et al]. The SNP is in TOMM40/APOE (in LD), which is certainly interesting given the previous links between APOE and Alzheimer's (an age-related disease).

However, I am not convinced by the experimental design; they use age-at-death in centenarians as their cases (having genotyped them), and they use alive population controls as the controls. Whilst there is unlikely all these individual will become long-lived, a better design (to gain more power) would have been to use individuals who have died from 'premature' (e.g. between 60 and 70) age-related disease. So I am still waiting for a convincing study, but this does look promising!

It looks like you have uncovered the majority of the corpus of molecular genetics related to aging.  There is a follow up analysis just published this year by Sebastiani et al.  Pubmed has a feature that you can look at the publications that reference the paper you are looking at, and there are only reviews.  Nobody else seems to have done another yet.

You are probably right to feel that the power of the study is not great.  The researchers did try though. The Centenarians have long lived relatives and the controls had both parents die before they were 73.  Although the controls were 68 y.o. and older.  Yes not great.  The controls are very difficult because you don't want people who would die from heart attacks, hypertension and all sorts of things that would color the background.  Its a hard study to do.

No single gene will convey a phenotype like longevity.  Its basically impossible as the advantages would propogate through the population v quickly.  We could talk about how this trait is post-reproductive and about the grandmother effect, but I'm setting that aside for now.

The lack of statistical power of the study is also hampered because a mere 800 centenarians probably reflects dozens of different combinations of longevity groups.  (this is another reason all of these people are of specific european ancestry - to keep the number of variations in combinations down).  There are 281 significant mutations they found.   APOE is by far the most significant (fig1) but given the situation, just focusing on that one is not enough.

For example, even in flies it looks like the sir2-1 gene is not a single mutant anti aging phenotype.  When they cross the mutant strain with wildtype, the sir2.1 mutants live 15% longer.  Its at least one other mutation they had not detected in that caused a 50% longevity bump in the mutants.  Its probable that if there were 5 other important mutations, that the average crossover has one or more of these mutations with it too.

In order to try to understand how these loci might work together to expand life span, they created clusters of these SNPs (interestingly half of them are in genes which is relatively rare).  these clusters of genes look like they affect the lifespan together.  the paper is open and all the 281 genes are downloadable, each one of them has a known biological property you can look at.  how they fit together is still to be determined, but their clusters might point the way for now.


Are (muscle) satellite cells the same as muscle stem cells? In terms of muscle: are the terms 'satellite cell' and 'muscle stem cell' interchangeable? That is, are there muscle stem cells that are not satellite cells, or vice versa?

Based on this review, satellite cells can replenish injured muscles, but among satellite cells there are satellite stem cells to maintain the pool of satellite cells.


How can an enzyme favor even chained fatty acids? If we look at text books for the human fatty acid metabolism (FA synthesis or β oxidation), they typically shows even length fatty acids (C8, C10, etc). Now, from a chemical perspective, I am wondering how the involved enzymes recognize that the fatty acid is an even number of carbons.

Can someone point me to (historic) experiments that have been done that show that these human pathways indeed only apply to even chain length fatty acids? Or do they also act on odd length fatty acids?

The first experiment which showed that fatty acids are oxidized in C2-units has been done by Georg Franz Knoop and been published 1904 as "Der Abbau aromatischer Fettsäuren im Tierkörper.". The paper in reference 1 states:

  Georg Franz Knoop discovered fatty acid β-oxidation. In 1904, he
  published his classical experiments using odd and even chain ω-phenyl
  fatty acids such as ω-phenylvaleric acid and ω-phenylbutyric acid
  (Knoop 1904). Knoop fed these compounds to dogs and analysed their
  urine. In dogs that had been fed the odd chain fatty acids, he found
  hippuric acid (conjugate of benzoic acid and glycine), whereas, the
  dogs that had been fed even chain fatty acids excreted phenaceturic
  acid (conjugate of phenylacetic acid and glycine). From this he
  concluded that the metabolism of fatty acids proceeds by the
  successive removal of two carbon fragments. The remaining fatty chain
  had to contain a carboxylic acid. He postulated that oxidation took
  place on the β carbon atom, an oxidation unknown to organic chemistry.

If the fatty acid chain has an uneven number of carbon atoms, the resulting propionyl-CoA is modified into succinyl-CoA which is then used by different processes.

During the breakdown of the chain, Acetyl-CoA groups are released (at the end of each step), which can then be further metabolized by the body. Acetyl-CoA is fed into the Krebs cycle and then oxidized.

References:

A general introduction to the biochemistry of mitochondrial fatty
acid β-oxidation
Fatty Acid Oxidation


How to calculate the percentage of heterozygous cells based on a gene map I've encountered the following question and am quite stumped by it.

A female with genotype AABBCC has been hybridized with a male that has the genotype aabbcc. The first generation (F1) has been hybridized again (backcross) with offsprings that have the genotype aabbcc. Given the following genetic map, what would be the percentage of F2 offsprings that are heterozygous to all three genes:

A------- 20 MU ------- B -- 10 MU --- C

How should I approach the following question, the brute force approach is too difficult, I keep getting things wrong.

Units of genetic distance

It took me a little while to understand what MU means. I have never seen MU but rather m.u. for map unit, or cM for centiMorgane.

Solving the problem

This problem got me thinking a little bit. My logic is the following:

Probability of being heterozygous at the first locus

You cross two individuals (we'll call them individual 1 and 2)that are both heterozygote at each locus A, B and C (not to be confused with the alleles A and a, B and b and C and c). We'll start with locus A. The probability of being heterozygous at locus A is the probability that individual 2 gives another allele than individual 1. This occurs with probability 0.5. If the three loci were perfectly independent, then the probability of being heterozygous for a given offspring at all 3 loci would just be $0.5^3 = 0.125$... but that would be too easy so let's keep going with the second locus.

Probability of being heterozygote at the two first loci

So let's assume our offspring of interest, got two different alleles for the locus A. The probability to receive two different alleles at the locus B is the probability that either no individual recombine between A and B or both individuals recombine between A and B. It is therefore: $0.2^2 + 0.8^2$. Put together this probability with the probability that the first locus was heterozygote it gives $0.5 \cdot (0.2^2 + 0.8^2)$.

Probability of being heterozygous for all 3 loci

Finally, we can just keep going with he next locus. Let's assume that the offspring have received two different alleles for both loci A and B. The probability to receive different alleles at locus C is the probability that either both parents recombine (between B and C) or none recombine. This occurs with probability $0.1^2 + 0.9^2$.

Put the whole thing together, the probability of a given offspring to be heterozygote (or the frequency of heterozygotes offsprings if you prefer) is $0.5 \cdot (0.2^2 + 0.8^2) \cdot (0.1^2 + 0.9^2) = 0.2788$

Note that calculating the probability that exactly 2 loci are heterozygous would have been a bit trickier.

Good luck for your exam tomorrow!


Why are bees eating the wax? I left outside a piece of wax few weeks ago and each day I saw lots of bees "eating" it. Why do they do this when they can create new wax? (it seems a really hard work considering how little was taken in the course of few weeks).

It's unclear how costly wax production really is, here are a few resources with some guestimates and studies:

http://www.honeybeeworld.com/diary/articles/fdnvsdrawn.htm

http://www.beesource.com/forums/archive/index.php/t-260700.html

http://www.bushfarms.com/beesharvest.htm#expenseofwax

But doubtless wax is costly to make. So it seems totally reasonable that your bees are actually collecting wax. But my guess, if they were doing this in October, is they drawn by the smell and were poking around for something besides wax per se, like sugar or pollen bits in the wax.

I just saw honey bees buzzing around a compost pile on a warm day in January, focusing on orange peels and used coffee grounds. They would masticate both grounds and peels with their mandibles, but to my eyes weren't actually collecting anything (they didn't bring it to their mouths with their tongues nor pack anything on their corbiciculae). I suspect they will pick at lots of things when there's not a strong pollen or nectar flow, maybe for medicinal reasons or the like, or perhaps more "for something to do."


How are proteins reused in the body? Part of what we eat are proteins,
and our body is in part build of proteins.

Are the proteins of the body build based on proteins in food at all?

Are proteins in food directly reused in the body,
or are proteins first disassembled?

How far are they disassembled, randomly in various pieces, or systematically to keep what can optimally be used to build new proteins, while nothing is wasted for energy?

(The question Can proteins/peptides pass through the intestine? and it's answers are related, and provide some context and relevant parts, but is not a duplicate.)

Short answer: Indeed the proteins in our body are based on amino acids from external food sources. BUT, proteins up-taken from food are ALWAYS disassembled first into amino acids, through specialized enzymes, proteases, (for instance Pepsin in the stomach's gastric juices and Tripsin in the pancreatic juices), during digestion, in the alimentary canal, (gut). This enables the body's liver to build the proteins most needed by the organism itself, through the processes of transamination, that allows conversion betwixt amino acids, and deamination, that removes N2 from the amino acid, (let's say the "amino" part is removed, and then expelled as urea), to excrete amino acids in excess. In addition this breaking down of external proteins is necessary, since they can act as labels for pathogens, and external organisms in general, and thus would soon be destroyed by the immune system if reused straight away.