Does the size or mass of a body affect the time it takes for rigor mortis to sets in? Does the size or mass of a body affect the time it takes for rigor mortis to sets in? For example: compare a 300 pound man to 100 pound girl to 5 pound animal.

One of the main factors that impacts rigor mortis is temperature. Basically, a smaller body would slow down the metabolic processes behind rigor more substantially. Also, one of the first things that happens in rigor is the stiffening of muscles. An increase in muscle mass would increase the time for rigor as well.

Refer to these links: wikipedia and another that talks about rigor mortis within the scope of forensic pathology.

Hope that helps!

n.i.


What is a "noninvasive" biomarker for a disease? What is a "noninvasive" biomarker for a disease? I know what a biomarker is, but what makes it noninvasive?

A biomarker, or biological marker, generally refers to a measurable indicator of some biological state or condition. - Wikipedia

The presence of certain 'things' (sorry for being vague) in a tissue obtained invasively - via biopsy, for example - are considered biomarkers for, say, a cancer. It could be histopathological - a particular abnormality seen on staining the tissue - or it could be the presence or absence of a membrane receptor, etc.

A non-invasive biomarker is simply one that can be obtained easily and without "harm" to the (patient?), for example, to identify the potential presence of a cancer without the need for a biopsy. (Obviously, this doesn't eliminate the need for invasive methods. It just adds to the arsenal of detection methods.)

That is the usual meaning of non-invasive biomarker in the many, many papers using the term (at least medically), such as the one cited.

Serum microRNAs as non-invasive biomarkers for cancer


Ways to measure effectiveness of a gene therapy trial? I understand that Fluorescence in situ hybridisation  can be used to measure the effectiveness of a gene therapy experiment/trial.

But what are some other genetics techniques to measure the effectiveness of a gene therapy clinical trial. Would blotting (northern/southern) and PCR be a way to tell if a new genome have been integrated into existing cells.

Thanks

If all you cared about was genomic integration, then your best bet would be some kind of sequencing. If you sequence the modified region and the flanking regions you could be sure that the new sequence was present in the genome.

It would probably be more interesting to look at how the new genes affect the cell. For example you could look at differences between protein expression in modified and unmodified cells. For that you could use RNAseq.


Do species other than humans have distinct daily feeding patterns? I have a general interest in complex adaptive systems and I have found that nature and the organisms within it is a perfect natural case of a rich adaptive system with a lot of possibilities for gaining insight in general about the nature of complex adaptive systems.

My mind accidentally started thinking about the common human feeding pattern breakfast-lunch-dinner and I sought reference points in nature, realizing that I'm not aware of any specific cases where the feeding pattern of animals other then humans follow a distinct pattern, in contrast to a constant, stochastic or mainly opportunistic search for food.

In the case of humans there is probably a very strong cultural cause for our very distinct feeding pattern, but that is not necessarily to say that these patterns only can occur in species with a highly developed culture.

How does the scientific body of observations look like here? Is there any research or empirical observations about the feeding pattern of animals?

For example, I would of the top of my head assume that some common reasons for these patterns to develop could be connected to e.g. the 24h circadian rhythm, dependencies to availability of food, or internal dependencies on behavioural organization in social species.

Of course it's likely that many organisms do not have the luxury of spending a significant time on other activities then acquiring food, but nevertheless we can see that some animals have evolved into a situation where they don't have to constantly be in the search for food, but instead can spend time on other activities increasing their fitness, like engaging in social interactions, searching for and seducing sexual mates, exploring their environment and migrating, building nests and so on.

To clarify what kind of observations I'm imagining could happen, take these speculative examples:

  Some species of birds have a significantly higher feeding activity in the morning, where they after a night of inactivity have depleted their daily energy resource and when the insects, their main source of food, starts to activate after a cold night and are still cold and slower/easier prey. After this the birds only have an opportunistic approach to feeding which is enough to satisfy their energy need, and they spend more energy on pruning, calling for potential mates and engaging in territorial battles.

  Many primates engage in collective feeding sessions where they as a group travel to a known area rich with food where they spend a couple of hours before they retreat back to a different location for socializing and digesting the food. One reason for this behaviour can be that there is a high risk of predation at these food-rich areas, as the predators learn that these places are frequently visited by prey.

  Feline predators on the savannah are usually concentrating their hunting in the night as the darkness gives them an advantage of stealth and surprise. This is why they in daytime instead spend a considerable amount of time on resting, engaging in activities regarding social hierarchies, order and bonding with the pride, while most often only opportunistically engaging in hunting.

Do we have a body of knowledge here?

While it would be close to hand to start trying making lists of observations like this, which certainly would be interesting in itself, the intention of this question is to get a good overview on the subject. Are patterns like these common or uncommon? In the cases where they are found, what are the common factors and what can be identified as the underlying causes?

Preamble

This is a very interesting question one which I don't immediately know an answer to. I think this overly succinct answer and the fact nobody else has answered highlights the degree to which the age old darwinian assumptions play a role in the field.

Zoological POV

I'm not an expert in this area so I went to a zoology lab technician and this is what they had to say (I'm paraphrasing here):

  Most animals are opportunistic and can't afford the luxury of a late
  brunch... The only animals that spring to mind that appear to 'plan' for
  meals are the hoarders (squirrels for example). But they don't
  typically cache food in the same way we would for a weekly shop, but
  do so for fear of food scarcity (overwintering, rival competition);
  Not unlike the mad dash for bread and loo roll when it starts snowing
  slightly!

Maybe animals do have their diet set to a circadian rhythm, or maybe not. We can't say for sure. Darwin implied, even a peaceful meadow is full of starving ravenous animals clinging to survival. There is no real time for luxury. If food is there, they eat it. Many animals don't even get full the same way we do.

Scarcity of Literature

The problem lies in that there is no body of literature around animal eating times since animals seldom have enough food in their natural environment to monitor any regularity. If you want specific questions on a particular species for optimum feeding times, I would recommend opening another question as lab animals do have recommended diets. Many predators have optimum hunting times (for example nocturnal, or dusk). However one could argue this is to do with success rates/effective hunting strategy and not necessarily scheduled eating times.


What do the letters 'p' and 'c' mean in mutation descriptions? Example:

  NM_000525.3(KCNJ11):c. 67A>G ( p. Lys23Glu) AND Permanent neonatal diabetes mellitus

Does "p" stand for "polymorphism"?

What does the letter "c" stand for?

According to the HGVS guidelines, a letter prefix should be used to indicate the reference sequence used. Accepted prefixes are:

“g.” for a genomic reference sequence
“m.” for a mitochondrial reference sequence
“c.” for a coding DNA reference sequence
“n.” for a non-coding DNA reference sequence
“r.” for an RNA reference sequence (transcript)
“p.” for a protein reference sequence


What is the DNA Sequence for an apple? The title says it all. I'm just curious. I read that scientists mapped the genome for Malus Domestica, but I can't find a sequence anywhere.If this is a stupid question, I would appreciate if you tell me where I'm wrong in this!

https://www.rosaceae.org/species/malus/malus_x_domestica/genome_v1.0

You can see the data in the URL above. The details are described in this article.

As others said, NCBI seems useful.
Go to this site.
Chose chromosome you want to see and click genebank or refsequence corresponding to the chromosome in the table (Assembly Unit: Primary Assembly).
You can see overview of the sequence.
Find FASTA in the page showing the overview and click FASTA. Then the sequence data will be downloaded.


Is it safe to look at infrared LEDs? What happens if one looks directly at infrared LEDs? Sometimes I see this kind of LED at night as red dots and I'm also courious about it.

I was wondering what would happen if one looks directly to these LEDs, because we see them everywhere like in remote controls, CCTV cameras, sensors, etc.

What is the difference between infrared and visible light to our eyes?
(I mean why is it impossible to look directly to visible light while we can look to infrared?)

LED: Light-emitting diode

Infrared wavelengths are EM waves of longer wavelengths than visible light. Also, visible waves are more energetic than IR waves.

Because of this, Visible light has the ability to excite organic receptor molecules in our eyes called Rods and Cones. These molecules stimulate cell responses and in turn excite cell responses in our nerves called an Action Response. Still unclear to most scientists is how the brain composes these action responses into an image, though a great deal of research is being done to date.

The reason why "nothing happens" when we aim infrared lights into our eyes (which I still wouldn't suggest) is that the photoreceptor molecules that we use to see don't have the necessary bonding configuration to accept the energy from these impinging EM waves.
 However, don't go thinking that nothing happens. Infrared radiation is a type of radiation that is usually a measurable heat source. IR is one of the broader parts of the EM spectrum. My point is to say, that when you "radiate" some thing with an IR source:
1) You don't know if it is also radiating other EM waves unless you know the specs.
2) You're still exciting molecules with that energy even if it isn't causing a seen effect. I highly doubt anything will happen unless you have a very high powered IR source. You shouldn't really ever focus high power lasers of any source onto your body, because higher intensities could inflict damage.

To Learn more about IR radiation:
http://coolcosmos.ipac.caltech.edu/cosmic_classroom/ask_astronomer/faq/radiation.shtml

IR (InfraRed)
EM (ElectroMagnetic)


Is DEET (as in the mosquito repellent), a substituted phenethylamine? Am I correct to say that N,N-diethyl-meta-toluamide (DEET) is a part of the phenethylamine class? It's structure meets the requirements to be a phenythylamine, however, I was not able to find anywhere on the internet that it is part of the phenethylamine class.

While I feel like this might be a better question for the chemistry SE, lets take a look at the molecular structures:

The basic structure of a phenethylamine (left, modified from here) versus DEET (right, modified from here):

The important chemical differences are:

DEET only has a C-alpha between the nitrogen and the ring, whereas phenethylamines have a C-alpha and a C-beta (see red annotation)
DEET has a carboxylic functional group (an amide bond), whereas phenethylamines have an amino group (see green boxes)

Taken together these differences mean that DEET is not a phenethylamine.


Why do we have nerves in our teeth? Toothache is a useful signal to us as we can visit the dentist who can try to fix any problems with our teeth. But what is the natural biological role of toothache? Does toothache make animals take action that helps them to deal with their dental problem?

Because your teeth evolved as a sensory organ.
The material teeth are made of evolved first in placoderms, it existed to sense the electrical current in the water around it, so it has to form around a nerve. in modern animals the nerve mostly functions in sensing stress and thermal stress on the tooth.
And because mammals are weird.
Teeth did not evolve to be permanent, they evolved to be lost and replaced, that is what everything that is not a mammal does. So having a nerve was not a big disadvantage (in say, reptiles) since that nerve would eventually wither and die as the tooth was lost. toothaches were not permanent they were a temporary irritation, and served do dissuade any behavior that caused them, like trying to eat food that was too hard, it was little different than the pain of thorn telling you not to grab sharp things.
Mammals are unique in retaining their teeth throughout their life so now a system shaped by evolution to be temporarily has been dragooned into something permanent. So now what would be a temporary irritation becomes a permanent thing when the tooth is damaged in mammals. Worse permanent teeth means things like stress on the teeth is even more important since you are stuck with damaged teeth so mammals actually make the nerves bigger. The addition risk of a toothache is not an issue because mammals are stuck with that risk anyway because they retain the tooth. The earliest mammals did not have long lifespan so the risk of a debilitating toothache was minimal, however we their descendants live for decades, so a structure evolved to last a year or two now has to survive for decades and it just fails sometimes. Evolution can only change what it has it cannot throw out a problematic system and start over from scratch, so it often gets stuck with such haphard thrown together solutions (kluges) And we unfortunately have to pay the price in this case


question about directional selection Cattle breeders have improved the quality of meat over the years by which process?
A) artificial selection
B) directional selection
C) stabilizing selection
D) A and B
E) A and C

I know the answer is D. It is obvious that is artificial selection but WHY is it also directional selection? how do we know? I know the differences between directional, stabilizing and disruptive selection but there is nothing in the question that explains the quality of meat in relation to directional selection. so HELP!

There is a small issue in this question that is: everybody does not always use the exact same definition of stabilizing selection and disruptive selection. These two concepts are sometimes used to refer to phenotypic traits or to genes. For example stabilizing selection might either mean,

selection for the mean phenotypic trait of the population
or
selection for the wildtype allele, getting rid of all newcoming mutations.

Under simple genetic architecture the two concepts are equal.

Although for this question I don't think we even need to give a clear definitions between these two words, we'll use the phenotypic based definition (the first one above) in order to ease the intuitive understanding of the answer.

Let's say the trait breeders select for is mean quality and for ease again, we'll imagine this trait as being one unique trait that we can map on one axis from low quality to high quality. Here is a representation of that where the x-axis represent meat quality (left = low quality) and the y-axis represents the density of cows in the population which has the associated meat quality.

If breeders performed a stabilizing selection, it means that they would not improve the meat but only prevent the meat to change quality. In order to shift the quality of the meat to the right (to better quality), breeders need to perform directional selection.

I think the only problem that you had for solving this problem was the conceptual issue of considering meat quality just like any phenotypic trait. And if you want to shift a phenotypic trait on one side or another, you have to apply directive selection.


Lambda red recombination without electroporation All protocols that I found about Lambda red recombination are using Electroporation as a method to introduce (inject) the homologous DNA (usually a PCR products or a linear dsDNA) to the E.coli cell. Can I use chemical method (CalCl2 + PEG) and heat shock method instead ?

Since Lambda red recombination is a rare event you want to have to have a good transformation efficiency, thus electroporation would be your best choice. Also since the expression of the recombination system usually needs growing bacteria at 42º you will probably inhibit the expression of the recombination machinery with the chemical method.


CNS memory structure I'm new in biology. could you please let me know if the following 2 assumptions are correct

A nerve cell in the CNS along with its loop back neurons (Collaterals) is a memory unit. It will trigger per given spikes pattern (example – from the PNS). The said pattern should be “close enough” to enable the memory unit to resonate.

A memory unit is a cyclic sub-graph with its “root neuron”. An inhibitory neuron eliminates multi resonance of the memory unit.

The concepts you raise in your question are not founded in neurobiology. We do not know what the biological correlates of a "unit of memory" are in the central nervous system.

Although oscillations are widespread in the brain, the relationship between oscillations and memory storage and recall is a subject of active research. The way you state this process in your question is not justified by any experimental evidence that I am aware of.

Memories do not have a "root neuron" — as I wrote above, we do not know how memories relate to neurons. Inhibitory neurons simply provide inhibitory input currents to their post-synaptic targets. Any relationship with "resonance" or oscillations relies on explicit assumptions about emergent network properties, and these are currently unfounded.


How can I reduce the background gradient in phase contrast microscopy? I'm looking for ways to set up a phase contrast microscope to reduce the brightness gradient that appears across the background of my images.

I use phase contrast to find the outlines of cells in my images. My problem is that the automated processing algorithms I use get confused by strong brightness gradients in some images. Post-processing of the images disrupts the continuous nature of the histogram, again throwing off the algorithms.

Does anyone know why these gradients appear and how to reduce their formation?

Thanks,

Oliver

Edited the question to clarify that I am interested in microscope usage, rather than image manipulation

Sample image:

The image background is darker at the left of the image than at the right

If you're not already doing so, make sure you set up Kohler illumination every time you use the microscope -- see this tutorial by Steven Ruzin.

The lamp or the phase ring may be misaligned. There are usually small hexagonal set screws on the lamp housing and the condenser, respectively, to adjust these.

Imaging near the edge of a dish or well can lead to uneven illumination as the light is bent by the walls of the culture vessel. If this might be the cause, try re-doing the Kohler illumination before you take each image.

If you can't find the cause of the problem, there are several ways to correct for uneven background described here. Maybe one of them will work with your analysis.


Energy use by muscles, actual work done by muscles and more Lately, I've started exercising in the gym and outside. I've also started to look at the details of food I eat.

Food usually has a label saying the amount of energy is inside it. For example, some chocolate says it has 400 kilocalorie for 100 grams.

I have some questions about that:

Does the label say the amount of total chemical energy exists inside the food, which will be released if burned, or the energy available to the human body after digested, and because digesting requires energy, the food contains actually MORE energy then written?
When I'm riding on a static bike, it has a screen which counts the kcal I burn. It has a thing connected to my arm, measuring my heart beat. After about an hour of riding, it said I used about 700 kcal. Is it the amount of work I did, i.e if there was a battery connected to the bicycle, I'd generate 700 kcal of electricity, OR, the amount of energy my body LOST, because muscle efficiency is far from 100% (so, I lost 700 kcal, but generated only 150 kcal of electricity, for example)
When doing a physical activity, the heart beat and breathing rate increases. Lets say I'm riding a bicycle or running. Whats the ratio between energy consumed by the muscle to energy consumed by the lungs or heart?

I speak only for the U.S. regulations: the calorie labels on wrappers refer to the energy released when burned. Sometimes these are inaccurate. Many dieticians recommend calculating the calories based on weights of protein, carbohydrates and fats in the serving: 4 kcal in each gram of protein and carbohydrate and 9 kcal in each gram of fat in your food. Multiply carbs, proteins and fats by the appropriate value and add them up.
The reading on the bike does not take into account your pulse. Just the raw work done turning the pedals. Some very smart bikes do take pulse into account, but the often inaccurate heart monitors lead to inaccurate calculations of total energy.
The heart and diaphragm (muscle primarily responsible for breathing) do use more energy when exercising than when you are sitting still. But that increase is small relative to the increase in the primary muscle sets involved in the exercise. Your resting heart rate is probably around 70 bpm, your exercising heart rate is probably around 160-180 bpm. So it has increased its rate and energy consumption by about 3 times. Your skeletal muscles maintain a basal metabolic rate during inactivity (one purpose of this is your body needs the heat from slightly tensed muscles to thermoregulate itself) - but during exertion, their metabolic rate increases enormously. Exercise increases their energetic demands by whole orders of magnitude.

The actual value of the (energy used by heart) / (energy used by skeletal muscles during exercise) depends on what exercise you do and how efficiently you do it. The change in the ratio between inactivity and activity depends on how much muscle mass you have (more muscle uses more energy during inactivity) and how strenuously you exercise. But the point is that the increased energetic demands by skeletal muscles far outpace the 3x increase in energetic demands by the heart and diaphragm - so the latter accounts for pretty much all total energy consumption at even moderate activity levels.


Why are neutral [sterile] female flowers present in inflorescences when they are reproductively incompatible? In many compound and special inflorescences like spadix and hypanthodium there are sterile female flowers along with male and female fertile flowers and are often present in between male and female flowers, but what is their need in an inflorescence?

As far as I know inflorescences are meant for perpetuation of a plant's race by pollination of female flowers by the male gametes [pollen grains which bears vegetative and reproductive cells].

I know the infertile female flowers of the spadix inflorescence possess some surface area and this area would get some of the pollen grains which are coming in to the inflorescence, and eventually a sum of pollen grains might go in vain.

What is the need of sterile female flowers when fertile ones are present in it?

Sterile flowers enrich pollination quality by promoting pollen export and import, while limiting the mating costs of geitonogamy associated with large fertile displays.

You are actually looking for this paper: Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523656/

Sterile flowers increase pollinator attraction and promote female success in the Mediterranean herb Leopoldia comosa

  Key Results

  The presence of sterile flowers almost tripled pollinator attraction,
  supplementing the positive effect of the number of fertile flowers on
  the number of bees approaching inflorescences. Although attracted bees
  visited more flowers on larger inflorescences, the number visited did
  not additionally depend on the presence of sterile flowers. The
  presence of sterile flowers improved all aspects of plant performance,
  the magnitude of plant benefit being context dependent. During weather
  favourable to pollinators, the presence of sterile flowers increased
  pollen deposition on stigmas of young flowers, but this difference was
  not evident in older flowers, probably because of autonomous
  self-pollination in poorly visited flowers. Total pollen receipt per
  stigma decreased with increasing fertile display size. In the
  population with more pollinators, the presence of sterile flowers
  increased fruit number but not seed set or mass, whereas in the other
  population sterile flowers enhanced seeds per fruit, but not fruit
  production. These contrasts are consistent with dissimilar
  cross-pollination and autonomous self-pollination, coupled with the
  strong predispersal inbreeding depression exhibited by L. comosa
  populations.


What is this wasp killing insect? I spotted these two in my garden.  What is this insect?  He had firm control over the wasp and was just hanging on by one leg.  He appeared to hold on until the wasp stopped moving and then flew away with it.

I live in Ohio (USA). The wasp was a bit less than 2cm long while the other insect was about 2.5cm long.

Given the large eyes, the almost non-existent antennae, the humped back, elongated abdomen and the wings, I'd say it is a robber fly.

It is one of many insects known to prey on wasps.

Note the description on the linked page:

  This spindly piece of nastiness is a Robber Fly in the genus Diogmites. It seems that it's members of this particular genus that are adorned with the name Hanging Thief. You may remember that this was to denote their habit of dangling from a leg or two while the other limbs held onto prey, stabbed it to death with venom and then sucked out the insides. [Emphasis mine.]


How different are tissue-specific fibroblasts from each other? I am planning to utilize a new system in our lab, in which I will co-culture cancer cells from different tissues with fibroblasts.
I have the option to receive skin-derived primary fibroblasts. I have been told the normal fibroblasts are very similar all over the body. Is this really true? I assume that fibroblasts secrete factors, for example, that are tissue specific. The question is, how quickly do they adapt to a new environment? For example if I take these skin-derived fibroblasts and co-culture them with breast cancer cells, how long will it take the fibroblasts, if any, to become more like fibroblasts derived from the breast?

I have been told the normal fibroblasts are very similar all over the body. Is this really true?

No.

  Strong evidence indicates that fibroblasts in different parts of the body are intrinsically different, and there may be differences between them even in a single region [3].

They have morphological similarities, but they act differently (at least in cultures):

  Examination of skin and lung fibroblasts derived from the same human fetuses revealed significant in vitro differences. Fetal lung cultures had faster cell replication rates, greater [$^3H$]thymidine incorporation into DNA, higher cell numbers at confluency, smaller cell volumes, decreased cellular RNA and protein contents and lengthened in vitro life spans when compared with fetal skin cultures. In addition, these cell cultures had different responses to the addition of hydrocortisone to culture media [1].

They hardly adapt to a different serum (in vitro) [2]. Yet they have a great capacity to differentiate (in vivo):

  [...] fibroblasts also seem to be the most versatile of connective-tissue cells, displaying a remarkable capacity to differentiate into other members of the family. [...] “Mature” fibroblasts with a lesser capacity for transformation may, for example, exist side by side with “immature” fibroblasts (often called mesenchymal cells) that can develop into a variety of mature cell types [3].

References:

E.L. Schneider, Y. Mitsui, K.S. Au, S. Stuart Shorr. Tissue-specific differences in cultured human diploid fibroblasts. Experimental Cell Research. Volume 108, Issue 1, August 1977, Pages 1–6. DOI 10.1016/S0014-4827(77)80002-5
Zamansky, GLEN B., et al. "Adaptation of human diploid fibroblasts in vitro to serum from different sources." Journal of cell science 61.1 (1983): 289-297.
Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Fibroblasts and Their Transformations: The Connective-Tissue Cell Family. Available from: http://www.ncbi.nlm.nih.gov/books/NBK26889/


Mercury intoxication in cats I was not sure if this question is more appropriated to be here or in Pets Exchange. I'm posting here first.

I accidentally broke a thermometer in my bedroom and, by my lack of attention, have spread mercury along the house. I cleaned the most part before the spread, so what I found after was only really tiny drops of mercury. However, I have four cats and I'm afraid that one of these tiny beads could possible be stuck in them paws while they are walking and they possible lick it, swallowing the beads.

I'm maintain the house ventilated most part of day (except when I go sleep) to minimize mercury vapors and I already search for possible symptoms of mercury intoxication in cats and found weakness, vomiting, diarrhea and difficult walking. Until now, I didn't observe any of these symptoms, but I would like to know what I should to if I notice some of them.

Because COVID-19, reach my veterinarian maybe will be difficult.

PS: I live in a country which doesn't have a service to come to my house to check the mercury amount in the ar neither get rid of it.

Unlikely that you have a mercury problem. I have had about 6 mercury thermometers broken in my house over a few years ( the places I kept them were not safe from a housekeeper).I don't know if she did anything to clean up; I except only sweep up broken glass. These were laboratory thermometers ,so typically over 12 in. long. No cats but dogs, no symptoms yet.


Can DNA produce ribozyme-like structures? RNA is known to act as an enzyme via its ability to fold itself in specific ways.

Is DNA capable of such structures? Or is it some biochemical reason stopping the folding?
Have they been observed in nature?

There are no known natural DNA enzymes (deoxyribozymes), but there are various synthetic DNA enzymes. The first deoxyribozyme that has been reported (Breaker and Joyce, 1994) catalyzed the Pb2+-dependant cleavage of RNA.

Various deoxyribozymes have been synthesized, they can catalyze RNA cleavage, RNA ligation and many other reactions like DNA phosphorylation or Thymine dimer photoreversion, and even a Diels-Alder reaction (see Baum and Silverman, 2008 for a review).

DNA lacks the 2'-hydroxyl group that RNA posesses, but there is some evidence that this doesn't significantly decrease the potential of deoxyribozymes compared to ribozymes. In one experiment DNA and RNA enzymes that catalyze a Carbon-Carbon bond formation were compared and both achieved comparable catalytic rates (Chandra and Silverman, 2008).

For more information about DNA enzymes you can look at the publications from the Silverman lab, they're probably the most active research group in this field.

Baum, D. A. & Silverman, S. K. Deoxyribozymes: useful DNA catalysts in vitro and in vivo. Cell. Mol. Life Sci. 65, 2156-2174 (2008).
Breaker, R. R. & Joyce, G. F. A DNA enzyme that cleaves RNA. Chem. Biol. 1, 223-229 (1994).
Chandra, M. & Silverman, S. K. DNA and RNA Can Be Equally Efficient Catalysts for Carbon−Carbon Bond Formation. J. Am. Chem. Soc. 130, 2936-2937 (2008).


What happens to snakes that swallow rodents as a whole? As we all know, a few species of snakes swallow rodents as a whole. My question is what happens to the teeth and bones of these animals? Won't they cut into the flesh of the snake and hurt it? Are the digestive acids strong enough to dissolve bones and teeth? Even so, I'm sure the process takes time, and during this period won't the snake get injured?

Almost everything the snake eats is completely digested. They have a very efficient digestive system. Things that wouldn't be digested would be the rodent's claws and hair and feathers of birds. And during digestion, the snake's intestines go into overdrive mode and expand when necessary. When the snake isn't eating, the intestines are usually dormant.

If something goes wrong though, or if the snake is threatened, the snake regurgitates everything in order to increase its mobility.


What effect does the Barr body have, in relation to female Turner syndrome? Why do persons with Turner syndrome have  developmental abnormalities, when normal XX-females do not, even though they only have 1 active X chromosome? From what I know, one X-chromosome is inactivated into a Barr body in normal XX-females, but these obviously don't show the symptoms of Turner syndrome. What function does the inactive chromosome have?

The reason is that X-inactivation is not complete (Carrell & Willard, 2005; Ahn & Lee, 2008), and as many as 15-25% of X-linked genes escape silencing (Carrell & Willard, 2005; Cheng et al, 2005). This means that some genes on the Barr body are expressed in XX-females, although often at lower levels compared to the active X-chromosome, and this is part of the normal gene dosage. The "purpose" of X-inactivation is usually dosage compensation, so that genes are expressed equally in males and females (and then actually upregulated in both sexes to balance autosomal genes, see e.g. Dementyeva et al, 2009). However, this is not true for all genes, and the ones that normally escape X-inactivation will be expressed in the incorrect dosage in X0 females. Some of these genes are thought to contribute to the symptoms of Turner syndrome.

It is also likely that the genes that escape silencing are involved in sex-linked traits, as stated in Carrell & Willard (2005):

  Such genes are potential contributors to sexually dimorphic traits, to phenotypic variability among females heterozygous for X-linked conditions, and to clinical abnormalities in patients with abnormal X chromosomes.
  ... ...
  However, as many of the genes that escape from inactivation do not have Y-linked homologues, strict dosage compensation may not be necessary for all genes on the chromosome. Such characteristic genomic differences should be recognized as a factor for explaining sex-specific phenotypes both in complex disease as well as in normal, sexually dimorphic traits.

Cheng et al (2005) also point out that the expression of the genes that escape silencing is tissue-dependent, which suggests that the role these genes play in the symptoms of Turner syndrome is also tissue dependent.


Electronic laboratory notebook (ELN) I have been using old style lab book for some time now but with increasing work on computer and storing sequencing results and gel pictures on computer it would be nice to have everything on computer in a form of labbook.

Does any of you uses a good ELN that would be free as I don't think university will be willing to pay for it :)

Thank you for your answers.

I still prefer the good old[tm] Labnotebook. No dependencies on (proprietary) software or a computer. I generate quite some digital data (blots, sequencing etc.) this is stored on the servers of my university. We looked into this in our lab, but discarded the idea pretty fast. Most solutions are either expensive and/or proprietary. Then a lot of these programs are not bought, but rented for a monthly or yearly fee, so once you are in you basically will not get out there anymore. Or it takes a lot of work.
I found one free (for up to three projects), this is Labguru.
There is an article about this on Bitesizebio, which has a few interesting comments. And there is another blog entry about this worth reading.
One of the problems with ELN is a legal one, since a labbook is a legal document providing evidence a what has been done and the results of it. They can be very important when it comes to patent legal battles.


How did sulfasalazine become a disease-modifying treatment for rheumatoid arthritis? Sulfasalazine has been around for about fifty years, starting as an antibiotic. More recently it is used as a disease-modifying anti-rheumatic drug (DMARD, see also arthritis.org). While biologics (biopharmaceuticals) are becoming more widespread in early treatment of some types of RA, sulfasalazine has a known safety profile and is inexpensive. Sulfasalazine is on the World Health Organization's Model List of Essential Medicines. See section 17.3, Anti-inflammatory medicines.
Wikipedia says:

The mechanism of action is not clear, but it appears that sulfasalazine and its metabolites have immunosuppressive, antibacterial, and anti-inflammatory effects.[refs] It also appears to inhibit the cystine-glutamate antiporter.[ref]

Why was this "old antibiotic" tested as an anti-inflammatory medicine? Is the situation similar to Minoxidil where a "side-effect" turned out to have significant medical value? What is the evidence (if any) that sulfasalazine has a disease-modifying effect in the treatment of RA - that it actually slows down the progress of the disease rather than just temporarily reduce symptoms?

Question 1:

Why was this "old antibiotic" tested as an anti-inflammatory medicine?

A 2016 publication by the Department of Medicine at both Imperial College Healthcare Trust, and Hammersmith Hospital (both in the UK), titled, "Rheumatoid Arthritis Treatments: A Historical Perspective", states:

"Sulfasalazine: After NSAIDs and Gold, Sulfasalazine (SSZ)
is the third oldest drug class that is still available to use as a
treatment of RA. In 1938, SSZ was the first drug to be synthesized
specifically for RA. The consensus at the time was that RA was
the result of infection and accordingly Svartz et al developed
the DMARD, SSZ (originally known as salicylazosulfapyridin)
by combining the anti-inflammatory, salicylic acid, with the
antibacterial sulfapyridine by an azo bond."

Also, according to a publication by the Department of Medicine at Princeton:

Sulfasalazine was synthesized almost 50 years ago specifically to treat rheumatoid arthritis. At that time bacterial infection was believed to be an important factor in pathogenesis. The linkage of sulfapyridine and salicylate with an azobond was viewed as a method of combining antibacterial and antiinflammatory actions while minimizing gastric irritation. Early therapeutic results were encouraging, but the drug was discarded as an antirheumatic agent for 30 years, until its serendipitous rediscovery. Subsequent controlled trials have confirmed its efficacy, which may be related to sulfasalazine itself or to the sulfapyridine moiety.

Question 2:

What is the evidence (if any) that sulfasalazine has a disease-modifying effect in the treatment of RA - that it actually slows down the progress of the disease rather than just temporarily reduce symptoms?

A 1995 publication conducted by Adis International affiliates states:

The efficacy of sulfasalazine in RA noted in many noncomparative studies has been confirmed in placebo-controlled trials and comparisons with other disease-modifying antirheumatic drugs (DMARDs). Sulfasalazine therapy produces significant improvements in many clinical and laboratory parameters associated with the disease, including erythrocyte sedimentation rate (ESR), Ritchie articular index (RAI) or number of swollen joints, grip strength and duration of early morning stiffness (EMS).


What makes diffculty to make a human bio-tooth compare to a mouse's? Some time ago I read a news article that said a bio-engineered tooth based on a mouse's would be available around 2015. There was some research about it at King's College in the UK, and many other institutes.

Now, I haven't heard any news that such a thing is available. It seems to be a basic result of stem-cell research, how much difference can there be between a human's tooth and a mouse's?

I believe you're referring to this 2013 announcement from King's College, Biological tooth replacement -- a step closer. So called "BioTeeth" are sought after because

  Current implant-based methods of whole tooth replacement fail to reproduce a natural root structure and as a consequence of the friction from eating and other jaw movement, loss of jaw bone can occur around the implant.

However, Professor Sharpe identified the following obstacle:

  What is required is the identification of adult sources of human epithelial and mesenchymal cells that can be obtained in sufficient numbers to make biotooth formation a viable alternative to dental implants.

For some background, consult Biological tooth replacement (2006; Sartaj, Sharpe)

Unfortunately the 2013 article was the last I heard of it - possibly for the aforementioned reason. If you're really interested, you might consider attempting to contact Professor Sharpe yourself.


From where does the oxygen in glucose come in photosynthesis? Is it carbon dioxide or water? I'm talking about the oxygen present in glucose and not the oxygen that is released after photolysis of water.

RuBisCO attaches one molecule of CO2 onto Ribulose-1,5-bisphosphate (RuBP). RuBP gets split to two molecules of 3-Phosphoglyceric acid (3-PGA). Via reduction to Glyceraldehyde-3-phosphate (GAP) the link to glycolysis is established. By doing the Glycolysis reactions backwards, you reach Glucose.

This is the reaction of RuBisCO (from humboldt.edu):

EDITED to correct: One molecule of RuBP, one molecule of CO2 and one molecule of water are converted to two molecules of 3-PGA. This compound then is either used to refill the Calvin cycle by production of new RuBP, or is inserted into glycolysis, where it can be converted to Glucose. So, as David correctly points out, the oxygen comes from water as well as from CO2.


Why is the current flow shown to be flowing from the negative area towards the positive area? When I was studying the ECG chapter in the book "Guyton and Hall Textbook of Medical Physiology", I noticed something odd in one of the pictures:

As you can see the current is shown to be flowing from the area with a more negative potential towards the area with a more positive potential.
Also here's the part of the text that alludes to the image:

This process provides electronegativity on the insides of the ventricles and electropositivity on the outer walls of the ventricles, with electrical current flowing through the fluids surrounding the ventricles along elliptical paths, as demonstrated by the curving arrows in the figure.

How is this possible? Isn't the current supposed to flow from an area with a higher potential towards an area with a lower potential?

By convention, positive current is assumed to be the direction of flow of positive charges. The trouble is that in many common situations (like this one), the current is actually carried by electrons which are negatively charged.
It can be confusing. Blame it on Benjamin Franklin. The convention for current flow was based on his work, before anyone knew about electrons, protons, and ions.


Why do pine stands exist? I live in the midwestern United States.  I cycle to work, sometimes on heavily wooded roads, and I can't help but notice that in most places within the surrounding deciduous forests Pine and evergreen trees don't seem to be doing so well - the few that exist don't look too happy.

In some places, however, there are majestic stands of pines - often completely free of the "seasonal" variety of trees.

Why is this?  What allows the slow growing pines to out-compete the other arboreal denizens of the forest?  And generally in such particular areas?

Thanks, this is killin' me...

Forest Succession 101

Pines are actually fast-growing, shade-intolerant, early-successional species. When land is allowed to lay fallow after being cleared by fire, wind storms, human land use or other major disturbance, the successional sequence will begin.

At first only herbs and grasses grow, but eventually these are shaded out by shrubs and tree seedlings. In this setting, the limiting factor is typically light. Because pines are fast growing in the sun, they usually take over a field and develop a relatively dense even-aged stand.

Because the seedlings grow so well and densely, they usually shade out and prevent most other trees and shade-intolerant plants from growing. The result: a dense stand of mostly pines:

I'll note here that early on in this process (before processes of self-thinning really get to take off), you can end up with what are sometimes called "dog hair" stands. Also, if you see clear rows in the pine stand, that's a good indication the pines were planted.

Eventually (80-120 years), most of these pines will die and fall out of the canopy (both due to "natural" causes and additional wind, ice, pest, or fire disturbance). As large pines fall and clear large enough canopy gaps, shade-tolerant sub-canopy hardwoods can take their place. Because pines are highly shade intolerant, pines do not regenerate again in that stand (without another major canopy-clearing disturbance). The result: a mostly hardwood-dominated forest (with perhaps a few remnant older pines):

So...

The all-pine stands you're seeing are early on in the successional sequence.
The few pines (that "don't look too happy" because of age) mixed with hardwood ("seasonal variety") trees are in a mid-to-late successional stand.


Does immunity to CRISPR proteins limit their effectiveness? The use of crisper-cas systems is currently applied to cells cultivated in vitro. As control of the ‘off target’ effects of Crispr improves and Crispr is used in vivo, why won’t the immune system neutralize it?

Usually not.  the Crispr/Cas proteins can be delivered to the cell as DNA/RNA and the proteins will only exist inside the cell in low numbers.
Even in systems that deliver the protein from the outside in vivo almost always the proteins would be encapsulated in a delivery system to ensure they and any necessary accompanying nucleic acids get into the cell. Getting Crispr/Cas into a cell is difficult to do and they don't just pop in by themselves. They also require guide RNA, which will not easily stay whole in the blood stream and tissues for long.
if you want to just inject a fluid into the blood with unprotected CRISPR/CAS proteins, an immune reaction might stop them.  Not all proteins produce an immune reaction. Sometimes just 2-3 proteins of an entire bacterium produce an immune reaction (antibodies).   But then again its unlikely the proteins would have edited any genomes in any host cells even so.


Transplantation of stem cells During the autologous transplantation of stems cells from bone marrow to produce new blood cells why all the other stem cells other than the one obtained are destroyed?

Autologous stem cell transplants are used to treat individuals who have had their bone marrow destroyed or damaged by diseases such as lymphomas or by irradiation or cancer treatments. As they are damaged and potentially cancerous, they are removed. They are then replaced in the transplant. The whole idea is to destroy all the cells before transplanting the marrow back.


What do you call the non-Wild Type allele? Can I have a list of suggestions, such as the mutated allele, other allele, etc. ? Are there any blatantly missing ones on my short list?

Usually its major allele and minor allele.  When you hear this language, you feel that the major allele is the 'wild' type, but its more precise to avoid 'wild'.

This language avoids the question of which one is 'wild' since different populations may have different ratios of the two.


Manipulation of gene expression using VP16 fusion and engrailed fusion to a transcription factor? Today, a presenter briefly mentioned that gene expression in sea urchins during development might be manipulated using VP16 and engrailed fusions.

On a slide, it said that expression might be increased by mRNA injection or "VP16 fusion to binding domain of TF" and decreased by antisense morpholinos or "engrailed fusion to binding domain of TF".

I understand mRNA injection and antisense morpholinos, but I am unclear about the roles of VP16 and engrailed in this context. Can anyone clarify?

VP16 is a herpesvirus derived protein transcription factor, which activates the early genes of the viral infection cycle. The activation domain (AD) which is formed by the 78-amino acids from the C-terminal, can be fused to DNA binding domain of other protein transcription factors, such as GAL4, to make a hybrid protein that constitutively and strongly activates transcription, without the requirement of any ligands. VP16-AD interacts with TBP, TFIID, SAGA histone acetyltransferase complex, and PC4 (transcriptional coactivator positive cofactor 4) to drive transcription.

The engrailed gene, from Drosophila, is a transcriptional repressor.  When the repressor domain is fused to transcription factors, the fusion results in trans-dominant negative functions of the transcription factor (phenocopying loss of function mutations in the target genes).


Why do we need red blood cells? From what I know, the main function of red blood cells (RBCs) is hemoglobin transport. So, why do we need cells packed with hemoglobin: why can't it travel freely in the bloodstream?

My own thoughts were:

1) Having hemoglobin packed into cells means it can be released where it's most needed. For example, when we are exercising, our muscles need more oxygen, so more erythrocytes release their oxygen in the muscle tissue.

2) The diameter of a capillary is much bigger than a single protein molecule's diameter, but comparable to a cell's diameter. So, when cells are traveling through a capillary, all of them are close to its walls. However, when free molecules are traveling through it, some of them are close to the walls, while the others are in the "middle". I figured, those in the "middle" can't exchange oxygen with the surrounding tissues. So, red blood cells make gas exchange more effective.

Do you think any of this makes sense? Why in reality do RBCs exist?

Any insight or book recommendations would be very appreciated:)

Hemoglobin molecules used to manufacture these products are not
  contained by a red cell membrane, and when released into the
  vasculature, these molecules rapidly scavenge nitric oxide.This can
  result in systemic vasoconstriction, decreased blood flow, increased
  release of proinflammatory mediators and potent vasoconstrictors, and
  a loss of platelet inactivation,17- 20 creating conditions that may
  lead to vascular thrombosis of the heart or other organs. This
  mechanism has recently been shown in preclinical models to be
  responsible for injury during hemolytic states, in which hemoglobin is
  also released into the circulation.21

  Unlike naturally occurring hemoglobin, manufactured cell-free
  hemoglobin-based blood substitutes (HBBSs) can be chemically altered
  to theoretically minimize such toxicities. It has been postulated that
  cross-linking, polymerization, or pegylation of hemoglobin will create
  larger, more stable HBBS molecules, preventing extravasation and
  thereby leading to a reduction in toxicities related to nitric oxide
  scavenging. At least 1 manufacturer has also chemically increased the
  affinity of its HBBS for oxygen (lower P50, the partial pressure of
  oxygen required for 50% hemoglobin saturation) to decrease arteriole
  oxygen transfer and thereby potentially eliminate untoward
  cardiovascular effects.

2008 - Cell-Free Hemoglobin-Based Blood Substitutes and Risk of Myocardial Infarction and Death

So cell free hemoglobin is toxic. As you can see this toxicity can be reduced in other ways too, so it seems like there is an evolutionary pressure in the direction of having blood cells, maybe it is simpler this way. To answer the other question, I think there can be free HGB in the blood when blood cells fall apart because of an infection e.g. malaria, etc...

  Hemolysis in falciparum malaria results in NO quenching by cell-free
  hemoglobin, and may exacerbate endothelial dysfunction, adhesion
  receptor expression and impaired tissue perfusion. Treatments that
  increase NO bioavailability may have potential as adjunctive therapies
  in SM

2008 - Relationship of Cell-Free Hemoglobin to Impaired Endothelial Nitric Oxide Bioavailability and Perfusion in Severe Falciparum Malaria

Btw. I agree with rhill45, I think too that it is easier to regulate O2 and CO2 exchange if you have a specialized cell type, so it might have regulation purposes. It can have recycling purposes either, because it is hard to distinguish between old (damaged) and new HGB when they are in a cell-free form. This problem probably can be solved by destroying only glycosylated hemoglobin, but I guess it is much easier to filter out the old RBCs in the spleen...

  In the process of maturation, a basophilic pronormoblast is converted
  from a cell with a large nucleus and a volume of 900 fL to an
  enucleated disc with a volume of 95 fL. By the reticulocyte stage, the
  cell has extruded its nucleus, but is still capable of producing
  hemoglobin.

according to wikipedia (without citation).

Other sources claim the same, with the extension that this period lasts only for a short time, because the cell soon loses its mRNA and so it stops producing HGB. So according to these articles RBCs create the HGBs in the early stages of their life. (I did not find a real scientific article about this, but I can accept this theory.)

According to Chris this toxicity is just a protection mechanism, so I dug deeper.

  Bacterial virulence is greatly enhanced by freely available iron, such
  as that in fully-saturated transferrin or free haemoglobin. Following
  trauma a fall in tissue Eh and pH due to ischaemia, plus the reducing
  powers of bacteria, can make iron in transferrin freely available and
  abolish the bactericidal properties of tissue fluids with disastrous
  results for the host. Hyperbaric oxygen is a possible therapeutic
  measure that could restore normal bactericidal systems in infected
  tissues by raising the Eh and pH.

2006 - Iron and infection: the heart of the matter

  Iron lies at the center of a battle for nutritional resource between
  higher organisms and their microbial pathogens. The iron status of the
  human host affects the pathogenicity of numerous infections including
  malaria, HIV-1, and tuberculosis.

2012 - Hepcidin and the Iron-Infection Axis

So RBCs protect the iron against microbial pathogens, that's their key role. I think every other related problem, like O2 release regulation, free HGB toxicity, HGB recycling, etc... can be solved with free HGB as well, so most probably iron protection is the evolutionary pressure to store HGB in blood cells instead of letting it be in the blood in a cell free form. It's funny that every single book gets this wrong, and they claim that carrying oxygen is the most important role of this cell type, while they aren't mention anything about iron protection... :-)


What biological process was taking place? A tub of a side dish, either tomato salsa or baba ganoush (eggplant), was left in a plastic bag for several months.  The plastic bag was not airtight, but was wrapped somewhat tightly around the tub.  Although it was supposed to be stored refrigerated, it was not (it was stored at room temperature).  It also was not supposed to be stored for such a long duration.

When the bag with the tub inside was eventually handled, it was noticeably hot.

What biological reaction was taking place that would generate that kind of heat, especially after months of storage?

As outlined in my comment, I hypothesise it must have been the growth of exothermic bacteria. As the name suggests, these produce heat. An especially interesting phenomenon concerns the danger of fire erupting from moist hay, as the bacteria feed from it and dry it simultaneously! This is outlined here. A memorable quote from that article:

  Dry hay (stored at 15 percent moisture or less) is safe for long-term storage. However, if the hay has become wet the quality has been permanently changed and the potential fire hazard from spontaneous combustion increased.

The same principle underlies the heating of compost, about which you can read in greater detail here.

Most astounding I found the post dealing with the possible contribution of exothermic gut bacteria to our thermoregulation.

As of now, I don't know about the basic mechanisms by which these bacteria generate heat, but the abstract of this article implies that heat absorbing bacterial growth is extraordinary.

I myself have forgotten everything about chemistry, but from the comments below I gathered that what happens is similar to the oxidations of sugar. You can read examples here, which demonstrate that these are exothermic.


An efficient and free method of assembling a large number of Sanger sequencing reads? I have a rather large number of Sanger Sequencing reads.

Is there a automated method in either Ugene or a similiar freeware that allows you to quickly assemble forward and reverse reads. Ideally something where the suffix of the filename will allow the software to automatically know which is the forward and reverse read.

Any help would be much appreciated as I'm not keen to do each sequence by hand in Bioedit.

Have you considered SPAdes? It's a popular, state of the art assembler that should work with Sanger sequencing reads.

http://cab.spbu.ru/software/spades/


Mutation in axillary buds of trees overcoming self-incompatability? I seem to recall from either reading or lecture that there have been instances of trees that are self-incompatible accumulating enough mutations in an axillary bud that the resulting branch was able to pollinate flowers on other parts of the tree. Unfortunately, I do not have a source for this information.

Are there recorded instances of this happening, or is this a figment of my fevered brain?

Recently, samples from different parts of cottonwood trees have been sequenced (Nature News). The conclusion:

  “The variation within a tree is as great as the variation across unrelated trees,” says Ken Paige, an evolutionary biologist at the University of Illinois at Urbana-Champaign, who led the team that made the discovery.

This doesn't say anything about overcoming self-incompatibility, and it probably depends on the mechanism of self-incompatibility if it can be overcome by accumulating mutations.


What species is this spider? A friend of mine saw this monstrosity in Taiwan. The photo isn't very clear but you can't blame her considering it was the size of her face. Wanted to know what species it is so I know where they spawn and to stay away from those areas.

I believe this is called Nephila pilipes.

You can refer to Wikipedia for more information


Carrying or packaging capacity of SAD B19 dG rabies virus I'm wondering about the carrying capacity also referred to packaging capacity or loading capacity (how many base pairs can be packed efficiently into virions) of the pseudotyped rabies virus SAD-dG as described in the Wickersham, Callaway publications.

Wickersham, I. R., Finke, S., Conzelmann, K.-K., & Callaway, E. M.
(2006). Retrograde neuronal tracing with a deletion-mutant rabies
virus. Nature methods, 4(1), 47–49. doi:10.1038/nmeth999
Wickersham, I. R., Lyon, D. C., Barnard, R. J. O., Mori, T., Finke,
S., Conzelmann, K.-K., et al. (2007). Monosynaptic Restriction of
Transsynaptic Tracing from Single, Genetically Targeted Neurons.
Neuron, 53(5), 639–647. doi:10.1016/j.neuron.2007.01.033

I have gone through quite a number of papers using this virus, but I haven't found any definite answer on the maximum insert length. There is an indirect answer, though. The two articles cited below both report possible insert length of up to 3.7kb without any experimental problems. This insert length results in a viral genome which is about 1.9kb longer than naturally occurring. So at least 3.7kb insert length are possible, if longer inserts can also be used, needs to be tested.

References:

Design and generation of recombinant rabies virus vectors.
New rabies virus variants for monitoring and manipulating activity
and gene expression in defined neural circuits.


Can we change one's genome into the genome of somebody else If I (grown-up individual and not just an egg after fertilization) wanted your exact genome, would we be able with today's technology to change my genome into yours?

There are 3.72x1013 (37 trillion) cells in the average adult human body. It would be essentially impossible to target every single cell just to change a single base pair, let alone the massive genetic and epigenetic changes that would be necessary to change someone into a clone of another.


How does fever physically work? What is the physical mechanism that causes temperature to rise during a fever? I know that somehow the hypothalamus "orders" to increase the standard body temperature regulation, and this should stimulate mitochondria to produce more ATP. Is that right?

Is this the only heating physical mechanism (through increasing production of ATP) that acts during a fever?

As John mentioned, pyrokines such as IL1 and TNF affect the hypothalamus. Your hypothalamus is a thermostat, similar to central heating for example. So when you set your core temperature higher, your body thinks it is cold. To warm up it does several things:

Vasoconstriction directs blood to the core body and prevents heat
loss
Brown fat break down in infants makes heat
Shivering which requires respiration which produces a lot of heat. Metabolism also
increases in other ways - this is why it is commonly advised to
increase food consumption during illness
We wrap up warm - an often overlooked mechanism that is incredibly important.
Limited piloerection: if we are hairy our hair will stand up attempting to
create a barrier for heat loss
We stop sweating (breaking of a fever or when the hypothalamus is reset to normal causes us to sweat)
Hormonal regulation via (nor)adrenaline/epinephrine, thyroxine - these are related to the increased metabolism.


Using autoclaved store-bought distilled water for labwork? I'm a high school student who's working on a molecular biology project in my school's lab. I need pure water for making culture media, buffers, running a BCA protein assay, running digests, cleaning glassware, etc. I don't have easy access to any professional lab equipment, so I'm looking for an easy way to get "lab-grade" water.

Ideally I'd go to a university and fill up a carboy using a lab's milli-Q system, but this is not easy for me. I also don't want to shell out $$$ to buy ultra-pure water from online suppliers.

Will autoclaving store-bought distilled water (NOT mineral or spring water), suffice for microbiology labwork that needs pure water?

Yes, distilled water would be absolutely fine for your needs. You really don't need ultrapure water except for the most sensitive of applications. You also don't need to autoclave the distilled water before making things like media/buffer/etc; instead you would autoclave/filter them after you make them.

You can take a look at this document for an overview on different grades of water.


Tree identification from dried branch I found a very interesting branch last week, and have been trying to identify it but cannot seem to find the answer. If anyone has any suggestion, I would be grateful.

I found it near the forest, around WA area.

Here's some picture:

This looks like dried cholla cactus, although it will be hard to determine the species. It is sold commonly for fishtanks, so might even be found in places where it does not grow naturally if someone cleaned out their fish tank.

EDIT by Ilan: on this image you can clearly see that the tree identified right:


How important is dead wood to the ecology of a forest and how much dead wood should remain? I have a local 'forest management group' in my area. One of the jobs they do is to thin out the forest by removing some of the trees. They then sell the wood for firewood.

I want to tell them to leave the dead wood in the forest, as it is part of the food chain.

Can anyone give me an estimate of how much energy dead wood provides for the food chain in a temperate forest, as a percentage of the overall energy generated by the forest?

Also how biodiverse is a forest with the dead wood left alone compared to one with the dead wood removed?

Dead wood is indeed very important to the food chain, and to the ecology and biodiversity of a forest. Lots of biota depend on the presence of dead wood; many species of insects and fungi only live on dead wood. See for example this study of fungi in Danish Beech forests.
The amount of dead wood present depends, apart from management, on the type of forest, the climate (and hence altitude!) and the age of the forest. This study provides a preliminary estimate of the amount of dead wood in British forests and might be very interesting to you. This study gives a review of dead wood in European (incl UK) Beech forest reserves.

I hope this will help you in the right direction. If you want any more information, please let us know. And preferably include some more information on the specific forest (type of trees, location) that you are interested in.

EDIT:
I recently stumbled across this project,
 that resulted in a systematic review of interventions that affected the occurrence of dead wood and saproxylic species in boreal and temperate forests.


Can inverted microscope also be phase contrast microscope? I've read somewhere that inverted microscope also allows phase contrast microscopy. Is that true? Do all inverted microscope have this ability? Do they have any other functions?

Many thanks in advance.

Definitely true, an inverted microscope is one where the optics are positioned below the specimen, and the light source above, providing an optimal situation for looking at a live culture. The Phase rings that shift the light come soon after the light source. For phase, the orientation doesn't matter, just the order:

Upright microscope

Orientation:

(top)eye--->objective--->specimen--->phase--->light source

order:

eye-->Phase compatible objective-->specimen-->phase disk-->light source

Inverted microscope

Orientation

(top)light source--->phase--->specimen---->Objective--->eye

order

eye-->phase compatible objective-->specimen-->phase disk-->light source

Not all microscopes have phase no, they are an important and expensive addition to a microscope. Adding phase not only required the phase disk but also a phase compatible objective.


Is existence of different alleles for a gene a result of mutation? I would like to understand evolution. Here are a few questions

Why are there different alleles for a  gene?
Is the different alleles of a gene are mutated versions of a gene?
Why selection pressure favoured the existence of more than one alleles?

I would like to understand evolution

The best way to do so is to start an introductory course on evolutionary biology. Consider having a look at evo101 for example.

  Why are there different alleles for a gene?

Because mutations bring variation. Note that not all genes are polymorphic. In other words, there might be genes for which, all individuals in the population share the same allele.

The existence of this genetic variance is absolutely central to the whole concept of evolution. In short, mutations increase genetic variance while natural selection and genetic drift reduce it.

  Is the different alleles of a gene are mutated versions of a gene?

Yes

  Why selection pressure favoured the existence of more than one alleles?

In the exception of cases of balancing selection (e.g. heterozygote advantage, negative frequency-dependent selection), selection does not yield to the existence of genetic variance, rather the opposite in fact. Selection "selects" for a given allele, which in turn reduces the genetic variance. Mutations bring new genetic variance in populations and selection reduces it. Genetic drift (another "driver of evolution") also reduces genetic variance.


Does the species of snake that eats Amphidromous inversus have chiral dimorphism? From what I read at Schilthuizen and Davison (2005), Amphidromous inversus is a species of snail that occurs in 2 forms that are nearly mirror images of each other occurring in nearly equal proportions. I don't see any way that could be evolutionary stable if it was only eaten by snakes with a symmetrical jaw because then the snake species would evolve to be ambidextrous and then the snails would lose the selection pressure for being the rarer form but retain the selection pressure for the more common form. I can't find the information anywhere on the internet of what the snake species that eats that species of snail looks like. Have observations shown that that species of snake has a chiral jaw and occurs in 2 forms that are mirror images of each other in nearly equal proportions?

I don't know much about this particular species of snake but here are some info that may help.

What do we mean by right-handed snakes?

I doubt that in this context a snake could be ambidextrous. What they call handedness in these snakes (Pereatids) concerns the density and size of teeth on each side of the jaw (pictures from Hoso et al. (2010))

This asymmetry helps them to forage on snails.

Here is how they describe the snake feeding behaviour.

  The Japanese pareatid, P iwasakii, strikes an exposed soft
  part of a crawling snail from behind at a determined leftward angle
  to grasp the ventral shell surface with the upper jaw and the soft
  body by inserting the mandibles into the aperture. The snake then
  extracts the soft body by alternately protracting and retracting the
  asymmetric right and left mandibles.

On the figure below, the individual on the left is sinistral and the individual on the right is dextral. Note by the way that snails of different chirality have a hard time to mate together.

"Right-handed" snakes can easily forage on dextral snails (the most common and ancestral form), while they have a hard time to forage on dextral snails. Hoso et al. (2010) reports a survival probability of 0% for dextral snails and 87% for sinistral snails.

Left-handed snakes

Hoso et al. (2007) report that "left-handed" snakes have never been found in south-east Asia. This is surprising as noted by Hoso et al. (2010). Even in areas where sinistral snails are relatively common, all snakes were "right-handed".

They do not suggest any potential explanation for this lack of "left-handed" snakes but one could speculate that "handedness" in snakes might be under other selection pressures than those related to foraging. It is also possible that intermediate forms are deleterious and that mutation of large enough effect are rare. It is possible that the genetic variance for handedness is just not present. It is possible that even if in some areas there are more sinistral species of snails than dextral species, the abundance of dextral is still higher and therefore, there is no selection for switching to being right-handed.


Why temporal lobe is called temporal? http://en.wikipedia.org/wiki/Temporal_lobe

Does this have something to do with tempo (time?)

Temporal lobe is behind (posterior) to frontal lobe, inferior to parietal lobe and is in front of occipital lobe.

Why it's called temporal?

The temporal lobe is in the temporal region of the head, near the temples of the skull, hence the name. It's name does not relate to it's biological function, it is mainly involved in processing language, visual memories, and emotions. The medulla oblongata is one region of the brain that deals with a lot of the "tempo" type functions (tempo as in keeping rhythm) such as controlling the heart beat and breathing rate.

  Temple indicates the side of the head behind the eyes.


Identification - What kind of animal leaves these tracks? I live in the suburbs of Washington DC where it recently snowed. I was admiring all of the tracks left behind by wildlife of all kinds when I came across these prints, that I was unable to recognize from charts of common animals prints online.

What is unique about them, is that each print, has 3 points, and there is only one straight line of prints, about 2-3 feet apart, where as I would imagine a deer, or other 4 legged animal would leave staggered footprints. We have a lot of deer in these parts but these dont seem to match deer print patterns I've seen online.

Each print is about 5 inches by 4 inches at their widest/longest points (they are longer then they are wider).

Note, the snow has melted somewhat since they were initially made.

The only candidate I could imagine is hare.
Sometimes it leaves a single track from its fore-limbs (from a theoretical point of view, I'd say it happens when the snow is relatively deep.)


What happens when someone is stung by a jellyfish? What happens in the human body when someone is stung by a jellyfish; namely a box jelly. Judging by what I have heard about the stings I'm guessing that they involve a neurotoxin.

But what is actually happening? What are the symptoms and what happens after the sting (treatments and survivability)?

The problem is that box jellyfish doesn't specify one jellyfish but a group of different jellyfish. Some of these are highly venomous - I pick here Chironex fleckeri, as this is often called "the most venomous jellyfish in the world".

Chironex fleckeri has long tentacles which are covered with millions of explosive cells called Cnidocytes which inject a dart with the very powerful toxin upon touch. It is therefore very dangerous to touch the tentacles with bare hands to remove them.

The toxin is a mix of different bioactive proteins which have cytolytic, cytotoxic, inflammatory or hemolytic activity. Case reports (you can find information in reference 3 about it) show that the tentacles "burn" though all skin layers causing immediate strong pain and lasting scars (if the victims survive) which tend to show signs of necrosis. The toxins itself paralyze the muscles of the heart and the respiration and also causes hypokalemia by hemolyzing red blood cells (one of the toxin acts as a membrane pore in the blood cells). This causes further problems and often a cardiac arrest. See reference 1 and 2 for details on the toxins. Especially 2 is interesting, as this is a PhD-Thesis on this topic with a lot of references.

Treatment depends on how severe the injury is - in severe cases an antivenom can be used. Besides this typical measures are CPR, giving oxygen and removing the tentacles (with appropriate protection). See reference 3 (good overview) to 5 for details on this topic.

References:

Chironex fleckeri (Box Jellyfish) Venom Proteins: Expansion of a
Cnidarian Toxin Family that Elicits Variable Cytolytic and
Cardiovascular Effects
The molecular and biochemical characterisation of venom proteins
from the box jellyfish, Chironex fleckeri
Chironex fleckeri (Multi-tentacled Box Jellyfish)
Jellyfish stings and their management: a review.
Cytotoxic and cytolytic cnidarian venoms. A review on health
implications and possible therapeutic applications.


What type of biome is this? There is a region that gets about 812mm of precipitation and is mildly hot all year long.

I believe this region is a tropical savanna, but I'm not 100% sure.  Is this correct?

Well, first of all 812mm is a pretty precise value to be preceded by the word "about". "Mildly hot", on the other hand, is too vague a term for your question to be answerable. If you update your question with better parameters, you may get more helpful answers.

In any case, according to this page, a tropical savanna has mean monthly temperatures at or above 64°F (~18°C), which may or may not qualify as "mildly hot" by your standards, and annual precipitation averages between 30 and 50 inches which means between 762mm and 1270mm.

So, I what you are describing could be a tropical savanna, but as I said before, I can't tell unless you update your question with more information. Have a look at this site, it may be of help.


Basic question about phylogenetic trees The following is an illustration rom my book of the phylogenetic tree of 6 animal phyla (the red stuff is mine):

I think what's causing some confusion is that there are no names/years at the circled nodes.

My first question is, was there an actual population between nodes (ex.) 2 and 3?

I would like to check if my understanding of the tree is correct:

Before node 1, there was a population which split into two populations: Porifera and the population between nodes 1 and 2 which we will call population 1-2. This population is unnamed on the diagram, either because we don't have a name for it, or because members of that population no longer exist, or to keep the diagram simplified.

Next, after some millions of years, population 1-2 split into the Cnidarians and population 2-3. Etc.

Is my understanding correct?

Thank you very much.

Yes, your understanding is correct.

That being said, it is standard to refer to population / species at specific points in time. Also, it is standard to refer to these ancestral populations relative to what they are the ancestors of. For example, we generally don't refer to the population 2-3 (as you named it) but we rather refer to the node/population/species 3 as the Most Recent Common Ancestor (MRCA) of Athropoda, Mollusca, Chordata and Echinodermata. The tree presented here is not complete but all Athropoda, Mollusca, Chordata and Echinodermata are Bilateria while Cnideria and Porifera aren't. Hence, you could say that the ancestor at node 3 is the MRCA of all Bilateria.

Related posts

This intro to phylogeny
If dinosaurs could have feathers, would they still be reptiles?


Measuring Gross Primary Productivity (GPP) using Light and Dark Bottle methods: Sample Question The following question is taken from my Cliffnotes AP Biology 4th edition practice exam and it deals with the light and dark method for measuring gross primary productivity.

  In a classroom investigation, students filled two bottles with pond water containing only photosynthesizing organisms. They used a dissolved oxygen (DO2) sensor to measure the amount of dissolved oxygen in each bottle. One bottle was put under a light. The second bottle was wrapped with aluminum foil to block all light and was put under the same light. AFter 24 hours, pond water DO2 in the two bottles was again measured. Average values for DO2 from all students are provided in the following table.

  Calculate the gross primary productivity for the observed sample. Express your answer in mg fixed carbon/L/day to the nearest hundredth.

Okay, so I know that net primary production (NPP) is the difference between gross primary production (from photosynthesis) minus Autotrophic respiration (Ra):

NPP = GPP - Ra

I also understand that the light bottle is measuring NPP, because it allows for both photosynthesis and cellular respiration. The dark bottle measures Ra because it only allows for respiration. Therefore, GPP can be calculated by rearranging the formula:

GPP = NPP + Ra

Calculating the difference in the final and initial values for both bottles, I get the following:

  Light: 0.15 mg O2 / L   <-- NPP

  Dark: -0.08 mg O2 / L   <-- Ra

Next, I plugged these into the formula:

  GPP = 0.15 - 0.08 = 0.07 mg O2 / L

Using the conversion formulas provided on the College Board's AP Bio Appendix (essentially just multiplying the mg O2 / L value by 0.374128 to get mg Carbon fixed / L), I get the following:

  0.07 mg O2 / L * 0.374128 = 0.02618896 mg C fixed / L

But according to my review book's solution, I was supposed to add 0.08, not subtract it. This seems a bit strange to me. Is this a mistake in the book or am I not understanding something?

The dynamics are:

Light bottle: GPP - Ra = 0.15
Dark bottle : Ra = 0.08

Then GPP = 0.15 + 0.08.

The amount of O2 used in the respiration is 0.08 mg O2 / L, not -0.08 mg O2 / L.


Can restriction sites be used as PCR primers? I have a DNA fragment that contains the gene of interest sandwiched by restriction enzyme sites. Then, can PCR amplify the entire fragment, recognizing the restriction enzyme sites?

If you aren't digesting prior to amplification, sure.  Nothing in PCR cares about whether or not some other protein interacts with the site.  There are thousands of restriction enzymes in nature.  No one would ever be able to do PCR if you had to avoid every single potential restriction site.


Why is aneuploidy usually lethal? So, I was reading about aneuploidy and how a zygote with one extra or less chromosome usually would not survive to full term. I suppose this happens because aneuploidy leads to some kind of protein imbalance. So, in case of monosomy we would have a shortage of proteins, and in case of trisomy we would have an excess of proteins.

On the other hand, a conventional argument for having two copies of each gene is that, if one gene gets corrupted because of some kind of mutation, we still have another copy that produces the correct protein. So, in case of a recessive genetic disorder, the zygote can survive even with half the amount of protein.

My question is then, why can't monosomic aneuploidy be looked at the same way? Moreover, I read that monosomic aneuploidy is almost always fatal, while trisomic aneuploidy is sometimes tolarated.

What causes zygotic termination in aneuploidy often isn't an issue with proteins or other gene products i.e. being "too sick" to live. It's that the zygote is basically "self error checking" and if it encounters a serious genetic error (e.g. aneuploidy) it self-terminates, as it would likely not survive anyway. Sometimes this self-termination fails, and the zygote develops. Depending on the specific aneuploidy, it may not make it to term, or perhaps it will, and you will have a child born, albeit the child will usually have a decreased quality of life/life-span.

A similar mechanism works in your somatic (non-reproductive) cells everyday when they replicate and divide - if they detect and error in their DNA that cannot be repaired, the cells SHOULD kill themselves. Sometimes this fails, and can give rise to cancer.


The Mystery of The Cretaceous' Songbirds Before Passeriformes perched on the branches of our trees and sang their sweet, inspirational tunes, there was Enantiornithes, the "Opposite Birds".  So far, we have discovered at least 80 species from five different families.  (However, some of those names come from just one bone, so the nomenclature may not be valid.)

The really odd thing is that despite their diversity, they had become extinct during the Mesozoic-Cenozoic extinction event 66 million years ago, even though their rivals, the forefliers of today's waterfowl, shorebirds, tube-noses, rails and ratites, did not.

The question is:  How come?  Was there any paleobiology saying that this particular order of birds was too specialized to withstand an impact winter?

The short answer is that we will never know.
Luck can sometimes be a factor of who lives and who dies. But such an answer doesn't feel satisfactory given such a diverse group such as dinosaurs and other groups like Enantiornithes.

Together with hatchling specimens of the Mongolian Gobipteryx[35] and
Gobipipus,[36] these finds demonstrate that enantiornithean hatchlings
had the skeletal ossification, well-developed wing feathers, and large
brain which correlate with precocial or superprecocial patterns of
development in birds of today. In other words, enantiornitheans
probably hatched from the egg already well developed and ready to run,
forage, and possibly even fly at just a few days old.[34]
A 2006 study of Concornis bones showed a growth pattern different from
modern birds; although growth was rapid for a few weeks after
hatching, probably until fledging, this small species did not reach
adult size for a long time, probably several years.[37] Other studies
have all supported the view that growth to adult size was slow, as it
is in living precocial birds (as opposed to altricial birds, which are
known to reach adult size quickly).[26] Studies of the rate of bone
growth in a variety of enantiornitheans has shown that smaller species
tended to grow faster than larger ones, the opposite of the pattern
seen in more primitive species like Jeholornis and in non-avialan
dinosaurs.[38] Some analyses have interpreted the bone histology to
indicate that enantiornitheans may not have had fully avian
endothermy, instead having an intermediate metabolic rate.[39]
https://en.wikipedia.org/wiki/Enantiornithes

So we have this. Enantiornithes weren't completely bird like. They may have invested less energy in parental care. Perhaps taken longer to reach adulthood, longer to reach reproductive age. May not be as warm blooded as birds but not as cold blooded as a crocodile.  Maybe that is why they went extinct.
The Enantiornithes did not care much for their young, since they were born pretty much hardwired to be independent. This hard wiring probably worked find in a stable environment, allowing adult to spend more time and energy making more independent chicks. But in a hostile, changing world of post-impact, that was simply too much for a hard wired, semi-warm blooded chick. Especially one that took longer to reach reproductive age than most birds did. And birds by and large do invest in parental care of their offspring.
The answer is perhaps obvious if we could go back in time and observe the entire genera of Enantiornithes. But in the absence of a time machine and only fossils and estimated growth rates... we can only speculate.


Based on morphology alone, what type of claw does the Tyrannosaur have? I understand that the exact use of Tyrannosaur Rex's claw is a mystery, or at least debated. I also understand that claws can be used for a variety of different purposes, selective pressure adapts their morphological to be better optimized for certain tasks. Some are used for hunting and killing, like large cats' claws, some are used for digging, like bear's claws, while others are used for climbing, like squirrel's claws.

My question is, all other clues and bits of information about if and how T. Rex might have used its arms, what 'type' of claws did it possess? I'm not asking, in this question, about its arm, the arm's musculature, its mouth or jaw, or about any of the rest of the animal. Based on the morphology of the claw alone, and comparing it to known uses of similarly shaped claws, what types of tasks were the claws geared towards?

unfortunately they have fairly generic claws, they are not specialized enough to point to a use. They are curved enough to be used to grasp something but that is true for their ancestral line too so there is no sign of a specific directional selection.


What are these little creatures on the fish? I'm not a fisherman, but I just caught a cod fish (my first one) and found a lot of strange little creatures all over the fish:

What are those? Are they harmful to the fish, or to the human?

Edit: it's caught on Faroe Islands

Though it's hard to say exactly what you're talking about based on the image, that cod appears to have several sea lice on it:

https://en.wikipedia.org/wiki/Sea_louse

Sea lice are common parasites of fish.


What is splice junction pairs? Splicing is a modification of pre mRNA when all introns are removed and exons are joined.
What is a splice junction pair? It is two exons which connected together?

Splice junctions are the exon-intron junctions, at which splicing takes place.
Splice junction pairs are the pairs of such junction (to cut an intron you need to splice in two junctions).
So, you are almost there, since two exons will be joined in correspondence of two subsequent splice junctions.
You might find these slides useful (slide B-6)

EDIT:

As Adam pointed out the slides are no longer available. I have no idea on where they are gone, but I suggest referring to the following wikipedia pages for an introduction:

RNA splicing

Exon junctions

Alternative Splicing


What are the obstacles to a quick survey of statin usage in COVID-19 patients? A recent preprint paints a grim picture of the effect of role of obesity in COVID-19 infection.  A high role of C-reactive protein (CRP) is specifically indicated as a risk for critical illness.

It is possible to reduce the level of CRP by statin administration, but statin administration raises the level of ACE2.  It is not known whether that increases or decreases the risk from the virus.  The use of statins for coronavirus patients has been suggested - so has the possibility of the discontinuation of statin use by infected patients.

Obviously I would hope to see a study of statin use in COVID-infected patients, and one does begin recruiting this month.  The entry, however, says that it will be completed in August 2021.  My thought is that surely somebody could run around the New York COVID wards with a clipboard, though I'd hope for a wiser way to do this, asking patients whether they use statins versus whether they have ever turned down the suggestion of taking statins when their doctor mooted the issue, and seeing how many of which group ended up in the ICU.  What are the factors preventing data like this, which could have such influence on the way people respond to the outbreak, from being collected and published within a couple of weeks?

The problem with your setup is that by targeting an ICU ward you are already narrowing your study to those who developed severe COVID-19. A more robust design would be a retrospective cohort study, where the exposure of interest has already been recorded.
E.g. the UK Biobank (~500,000 participants) has recently incorporated SARS-CoV-2 test results into its dataset, so you could use this to:

create a case/control split based on exposure (i.e. patients' historic use of statins)*
study the effect this has on outcome (i.e. development of severe COVID-19)

In  this  study,  we implemented rapid dynamic linkage, which allows us to provide a regular feed of new COVID-19 (SARS-CoV-2) test results to UK Biobank to facilitate rapid and urgent research into the epidemiological and human genetic risk factors for severe infection in the cohort.

Dynamic linkage of COVID-19 test results between Public Health England’s Second Generation Surveillance System and UK Biobank, Microbial Genomics (2020) **

* Or any of the other thousands of variables recorded in UKB.
** Disclaimer: I have worked on this project.


Can we say it's hybridisation if it's the same species? If we mixed two population of the same species into the same environment and then they reproduce together, can we say it's hybridisation?

The wikipedia definition is the following:

  Hybridisation (biology) the process of combining different varieties of organisms to create a hybrid

The question boils down to the definition of species and hybridization.

In general, we use the term hybridization to talk about mating between individuals from different species but really the term species does not mean as much as most people would think it does. Some people may use the term hybridization to talk about mating between lineages that are usually considered belonging to the asme species.

Have a look at How could humans have interbred with Neanderthals if we're a different species? for more information on the problems of definition of species.

Edit

Here are terms and concepts that are related and may help you

gene flow
introgression
interspecific mating
secondary contact
partial reproductive isolation


Why do emperor penguins breed during the antarctic winter? No land animal, and I think no sea animals either, stay in the antarctic during winter - except for one: The emperor penguin. These penguins not only stay there, but their prolonged stay involves 4 months of harsh winter, averaging -70$^o$C, no sunlight and no food for that period of time. And if that wasn't enough, then it's during that time that the emperor penguin male incubates the egg alone, left by his female mate. The male emperor penguins gather together to endure the antarctic winter.

My question thus becomes very obvious: Why does the emperor penguin stay in Antarctica during winter at all, and moreover, breed there during that time and incubates a precious egg in the harshest conditions on earth, while all other animals flee for their lives?

From my experience working on sheep farms in Australia, it could very well be for similar reasons to why farmers breed their sheep at specific times in the year - they breed their sheep, so that by the time winter hits the lambs are large enough and have enough wool to make it through. The penguins lay their eggs in the dead of winter, but they then incubate for 65-75 days, by this time winter will have largely passed, and the chicks will be growing in the spring and then summer. By laying in the winter, the penguins avoid exposing their young to a winter for as long as possible.

Another point to consider: As you said, Antartica is largely devoid of other life during the winter. To me, what I hear is: There will be no predators to feed on the eggs, or attack the vulnerable penguins incubating their eggs.

Reference: http://www.antarctica.gov.au/about-antarctica/wildlife/animals/penguins/emperor-penguins/breeding-cycle


How might I break down bread into glucose in a model of the human digestive system? I need to make a model of the digestive system. It would be really nice to actually show it in action, such as by breaking down bread into glucose or something similar. Is this feasible with a small budget and non-dangerous chemicals? If so, how? This should be as similar too the real digestive system as possible.

Amylase would be worth a try. The enzyme breaks down bread (starch), and you can buy it relatively cheaply online or probably at a chemist. Amylase is secreted in your saliva and in your stomach, so it would be most realistic if it was added in your model at those two points.


Is there any stem cell or biogel method that exist for muscle and tendon lengthening? Is there any stem cell or biogel method that exist for muscle and tendon lengthening?

It is known that height surgery is limit to six inches with two surgeries and three inches each, it is also true that there is limit because the muscle and tendons could stretch no more. Is there some research about this?

Limb lengthening surgery is usually used to treat sequelae caused by bone disease, trauma, pygmyism or inflammation. I personally do not recommend to use surgical methods to increase height. Typically Limb Lengthening requires Achilles pre-lengthening surgery and a lot of postoperative rehabilitation. Moreover, Limb lengthening surgery may cause pain, infection, muscle atrophy, joint stiffness and delayed bone healing. There's a lot of related research cause this study is timely for some patients.

ALDEGHERI, R., RENZI-BRIVIO, L., & AGOSTINI, S. (1989). The callotasis method of limb lengthening. Clinical Orthopaedics and Related Research, 241, 137-145.

De Bastiani, G., Aldegheri, R., Renzi-Brivio, L., & Trivella, G. (1987). Limb lengthening by callus distraction (callotasis). Journal of Pediatric Orthopaedics, 7(2), 129-134.

Paley, D. (1988). Current techniques of limb lengthening. Journal of Pediatric Orthopaedics, 8(1), 73-92.

Paley, D. (1990). Problems, obstacles, and complications of limb lengthening by the ilizarov technique. Clinical Orthopaedics and Related Research, 250, 81-104.

Szoke, G., Lee, S. H., Simpson, A. H., & Prescott, J. (2005). Response of the tendon during limb lengthening. The Journal of Bone and Joint Surgery.British Volume, 87(4), 583-587.


Vitamins located closely under the peel? I came across an old saying (I would even call it a myth) that vitamins are concentrated under (or close under) the peel of apples or potatoes and
other fruit. This implies that they are more healthier when not pealed. My question is: Is this true? And does it make sense to concentrate important
substances there, where they might get lost when the peel is damaged?

There are some vitamins in the peel of some fruits/vegetables. The color of many fruits and vegetables is the result of high carotene concentration in the peel. $\beta$-carotene is converted by the human body into retinal, which is a form of vitamin A [1].

Another example is vitamin C. Guava and citrus category fruits contain high amounts of ascorbic acid in their peel and orange's peel contains greater amounts of vitamin C than its juice [2].

There are also other compounds in fruits peel like B vitamins and minerals [2].

  This implies that they are more healthier when not pealed.

In most situations, yes. The peel can absorb insecticide sprays and can also contain high amounts of fibers which can cause indigestion [2]. The peel can contain allergens [3].

  And does it make sense to concentrate important substances there, where they might get lost when the peel is damaged?

Yes. For example carotene plays a role in photosynthesis [1]. Fibers improve mechanical properties of the peel, thus protecting the fruit.

References:

Wikipedia contributors, "Carotene," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Carotene&oldid=625015773 (accessed September 14, 2014).
Umesh Rudrappa, www.nutrition-and-you.com. Fruit peel nutrition facts
Wikipedia contributors, "Peel (fruit)," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Peel_(fruit)&oldid=624708837 (accessed September 14, 2014).