What’s the reason for isovolumic contraction and isovolumic relaxation? During cardiac cycle, there are two periods in which the heart volume doesn’t change, but there is a change in tension/pressure. It takes about 0.25-0.35 second to achieve this change.

I searched in Google and Wikipedia, but could not find the reason, so I decided to ask this question.

To put it in very simple words the reason for isovolumetric contaction and relaxation is to make the necessary pressure changes that is necessary to allow blood to flow into or flow out of the ventricles.

The basic formula you need to remember to understand this is:-

  Fluids flow from high pressure area to low pressure area along the pressure gradient (Eg: Injecting a drug into blood stream - as the pressure in the syringe is higher than the pressure in blood vessel, the drug flows into the blood vessel)
  Pressure is inversely proportional to volume (when temperature is constant) - this is Boyle's law. In a container with a fixed amount of fluid an increase in the volume of container will cause a proportionate amount of fall in the pressure in the container and vice-versa

Isovolumetric contraction:

The end-diastolic pressure in the aorta is in the range of approximately 90-100 mm of Hg. For blood to flow from left ventricle to aorta, the pressure in the left ventricle should exceed the pressure in the aorta.

As long as the pressure in the left ventricle is lesser than the pressure in the left atrium, the blood flows from Left Atrium to Left Ventricle. When Left Ventricle starts contracting the pressure in the LV rapidly overcomes the pressure in left atrium leading to closure of the mitral valve.

Now the pressure in the LV is greater than the pressure in the LA. So no blood flows in. At the same time the pressure in the LV is not sufficient to overcome the pressure in the aorta. So the semilunar valve remains closed. The ventricle continues contracting causing a time period in which there is increase in pressure without volume change as both inlet and outlet are closed. This period is called period of isovolumic contraction.

The isovolumic contraction ends when the pressure in the left ventricle becomes higher than the pressure in the aorta, which will cause the semilunar valves to open and blood to flow from left ventricle to aorta.

Isovolumic Relaxation:

The reverse happens in isovolumic relaxation.

As the blood volume in the ventricle decreases and the left ventricle starts relaxing the pressure in the left ventricle falls. When the pressure gets below that of the aorta, the semilunar valve closes. But the pressure in the ventricle is still higher than the pressure in the left atrium. So the mitral valve remains closed. So here too both the inlet and outlet are closed but as the ventricle is relaxing the pressure keeps falling. So till the pressure in the left ventricle falls below that of the left atrium, there is a time period volume is constant and the pressure keeps falling - this is called Isovolumic Relaxation.

This period is followed by opening of the mitral valve (as the pressure in the LV falls below that of the LA) and blood flows into the ventricle.

Take a look at the phonocardiogram linked in Majid's answer. It will help you understand what I explained.

Hope this explains your question


How did birds survive the KT impact? As I understand it, the ejecta resulting from the K-T impact (also known as the end-Cretaceous or Cretaceous-Tertiary extinction event) re-entered the atmosphere all over the world; the heat from friction with the atmosphere raised the air temperature to a few hundred degrees C. All organisms all around the World were incinerated, except those that could bury underground or move into water.Now birds don't bury underground, nor do they   bury their eggs. So, how come birds didn't go extinct?

To clarify, I'm not considering the longer term cooling effect (which was in turn followed by a longer term warming effect due the CO2 dumped in the atmosphere). What happened just after the impact was that a sizable fraction of the entire volume involved on the collision would be on ballistic trajectories. Most of these would fall back to Earth, while a small fraction would escape Earth's gravity. Now, these ejecta actually contain a significant fraction of the total energy of the impact and almost all of that in then dissipated as heat when they re-enter the atmosphere. This leads to shock heating of the atmosphere to at least a few hundred degrees celcius, but much higher temperatures are also possible, see also this article.

This article hypothesizes that the surviving avians had large and quite complex brains, giving them an advantage in finding food in the aftermath.


How to integrate transcriptomics data with kinetic metabolic models? I have created a convenience kinetics† model. Now, I want to integrate the transcriptomics data with my convenience kinetics model for altering/weighing the kinetic parameter values. I have read some publications related to this work but can’t get a satisfactory idea of how to do it properly.

Details

I've got a pancreatic model for the study on type 2 diabetic patients. It has a few compartments and the reaction pathways; the species are metabolites. All the reactions are convenience kinetics based. Enzyme is a constant factor, so its production and regulation is not considered. From my model, I'll get the Vm values for all the reactions and then I'm supposed to get the Vm (Vmax of Michaelis-Menten kinetics) values for the type 2 diabetic patients by somehow integrating the transcriptomics data with it. I was asked to use the fold change values but I couldn't find any relevant publication on this topic (my PI has suggested me these but hasn't worked in this area before).

Any leads or references will be highly appreciated.

† You can call convenience kinetics rate laws as approximate rate laws or you might have heard about "modular rate laws", they are more or less the same. We use this approximate rate law approach in cases where we don't have the experimental data for all the true rate law parameters.

I am assuming that in your model, the reactants and products (species) are metabolites and each reaction denotes conversion of one metabolite to another.

From transcriptomics, you will get the relative expression levels of different genes.
When you have two samples from different conditions you can calculate the differential expression.

A model can be as complex as you can make it but we can start with simple assumptions. As you said, enzymes are assumed to be constant with respect to metabolites and are not dynamically changing. I also guess that you are not considering genes other than enzymes to be affecting the metabolic reactions (you might actually want to consider the solute transporters). Also, you are assuming Michaelis-Menten kinetics for all reactions.

In that case your Vmax (i.e. maximum rate of a reaction) would be kcat × E0 where kcat is the turnover number and E0 is the total amount of enzyme.

E0 can be approximated using the transcriptomics data. However, transcriptomics data is relative and not absolute. If you need absolute quantification, you must have at least one reference whose absolute mRNA copy number is known. Another issue is that the ratio of protein and mRNA expression would not be the same for all genes and it is basically the amount of active protein you need to know. So proteomics would be one step closer.

When you are comparing two conditions, you can use the differential expression (fold change values) to adjust the parameters between the two conditions. For e.g. if you know that phosphofructokinase is 2 fold downregulated in diabetes (compared to healthy case) then you can reduce the Vmax of the corresponding reaction by 2 fold in your diabetes model. However, it all would make sense only if the parameters of your "healthy" model are reasonably close to the biological reality.

Moreover, you still need to know kcat. It cannot be obtained from high throughput studies. You may have to either make some guesses or check out papers/databases. Also, your rate is not always Vmax. To estimate the dynamic rate you must know KM too (when the substrate is in excess you can ignore KM). BRENDA may have some information about these constants for different enzymes.

At a very crude level, you can remove the reactions whose corresponding enzymes have zero expression.

These are some articles on integration of transcriptomics data with FBA (not kinetic models):

Blazier and Papin (2012)
Machado and Herrgård (2014)
Guo and Feng (2016)

Machado and Herrgård actually claim that integration of transcriptomics data does not improve their model predictions:

  Also, it is observed that for many conditions, the predictions
  obtained by simple flux balance analysis using growth maximization and
  parsimony criteria are as good or better than those obtained using
  methods that incorporate transcriptomic data.


Does chicken embryo form the disc called "discoblast" in the cleavage and blastulation of chicken? This thread is related to my previous thread which is still unsolved mainly. I need to be able to compare chick and human cleavage and blastulation of zygote.
My friend says that

  Chicken have discoblast, human not. That is the main thing to get the idea of the difference.

I know that chicken have yolk sac with yolk, while human have yolk sac without yolk.

My notes say that

  Cleavage in birds is partial discoidal (embryo forms disc and cells called blastodisc are on top of the yolk).

So embryo forms some disc, lets call it #1. Some cells called blastodisc are on top of the yolk. So are the cells called blastodisc on top of the yolk and the disc #1?

What is the name of the given disc that chick embryo forms?
It seems that human is not forming the given disc. Apparently, the name of the given disc is discoblast, the thing he says is very important.

It is a mnemonic of two words: discoidal + blastula = discoblastula.
So it suggests that cleavage is partial discoidal in birds.
Embryo forms disc.
Cells called blastodisc are on top of the yolk.
It seems that the formed disc is blastodisc.


Is there variation of AT/CG ratio along species? Chargaff's rules say that the number of Adenine of the number of Thymine in a genome are equal (nA=nT) and similarly nC=nG. This makes obvious sense knowing that C binds to G and A to T.

But what about the ratio $\frac{nA+nT}{nC+nG}$?

Is there variation along species of this ratio that is higher than expected by random processes? If yes, what causes this variation?

That ratio is essentially, as WYSIWYG pointed out, called GC-content.  In actuality, GC-content is reported as $(G+C)/(A+C+G+T)$, converted to percent; i.e., what percent of the genome is G or C.

There is vast variation in GC-content, both amongst species and within a given species' own genome.  For example, in humans the first intron and exon are generally more GC-rich than following introns/exons.1  Genes themselves are often found in higher GC areas,2,11 in particular CpG islands are found near a large number of (mammalian) promoters.3

Across species, there can be a big difference.  Yeast and Arabidopsis are both around 35%4,5 whereas Plasmodium falciparum is around 24%;6 Carsonella are even lower, at around 16.5%.14  On the other hand, the plankton Emiliania huxleyi is around 65%7.  We can use these differences to study genomic history.  Bacteria often have genes from all over the place thanks to horizontal gene transfer, and GC-content can be used to differentiate between their own genes and those from horizontal gene transfer;8 a good example is the CRISPR-Cas system,9 even in a virus!10

Here's a list of a few things genomic GC-content is correlated with:15

genome size
whether the bacterium is free-living or not
the environment
aerobiosis
nitrogen utilization

In the lab, high GC-content often means a harder region to work with, as the presence of three instead of two bonds (between A and T) requires more energy to break;12 anything involving primers can be made more annoying, including (especially, to some) sequencing.  There is a theory that high GC-content would be an adaptation to high temperatures, to avoid DNA damage, but that is controversial.13,16,17,18


Which DNA elements belong to the definition of a gene? I see a lot of different DNA elements mentioned as part of a gene (talking about eukaryotes):

  The length of DNA following the promoter is a gene and it contains the
  recipe for a protein. (video)

This implies that the promotor is not part of the gene.

This actually defines a gene without enhancers/silencers

   (source)

Here the gene also includes the enhancers/silencers

Question
Is there an accepted gene definition regarding the DNA elements? Thus which sequences like promotors, enhancers, silencers etc. are considered part of the gene?

Usually a promoter is not considered a part of the gene. Distal regulatory elements qualify even lower for being considered a part of a gene because they can regulate many genes simultaneously.

Basically, a geneic region starts from the transcription start site (TSS) and ends at the terminator (or polyadenylation/cleavage site in eukaryotes). If a gene gives rise to multiple transcripts, those which have similar products (no frameshifts) but different TSS/terminators, we should consider the geneic region as a union of all the primary transcripts produced from that site.

There is a relatively old article on this topic: What is a gene, pose ENCODE? History and updated definition. It summarizes that:

  There are three aspects to the definition that we will list below,
  before providing the succinct definition:

  A gene is a genomic sequence (DNA or RNA) directly encoding
  functional product molecules, either RNA or protein.
  In the case that there are several functional products sharing
  overlapping regions, one takes the union of all overlapping genomic
  sequences coding for them.
  This union must be coherent—i.e., done separately for final protein
  and RNA products—but does not require that all products necessarily
  share a common subsequence.

  This can be concisely summarized as:

  The gene is a union of genomic sequences encoding a coherent set of potentially overlapping functional products.

.

My summary is that a gene, if it codes for a protein, would be a union of all primary transcripts that produce identical proteins (originating from transcripts with different TSS/terminators) or splice variants.
Ideally, all the different transcripts produced from the locus would have the same promoter.

Overall, it appears that a common promoter is imperative for considering the different products under the same gene because if two products are produced from different promoters then we consider them as products of overlapping genes.

Whether we should consider the promoter as a part of a gene is an open debate.


Animal identification (larva) I found a tiny, white animal in my mouth on the morning of June 28, 2015, in Toronto, Ontario. Luckily I don't seem to have hurt it. I was eating some sunflower and pumpkin seeds at the time. I believe that's how it got there.

The pictures include a toothpick and a Canadian cent to give an idea of its size.

I also took a video of it crawling around. I will post it if the pictures are not sufficient for identification.

This animal is moth larva. The images presented are blurry, but if there are no any dots on the larva my first suggestion is:

pantry/Indian meal moth larvae -

"They are a common grain-feeding pest found around the world, feeding on cereals and similar products."

(picture source)


Which cell organelle is more important in giving colour to petals? It was a question in our school test and given answer was vacuole. But I think it should be chromoplast as they are the organelles specialised to provide colour. But options were given, so which is more accurate? Is the question controversial (both are correct?)

When I read your question (headline), my first thought was: "Vacuoles!"

After reading in more detail about your problem, I agree with you that there is some controversy with this question. The problem is in my opinion that the question is not well formulated. The term "more important" is not really scientific, because what decides importance? Do they mean with importance that it plays a role in more flower species? Or do they mean that the color palette is larger with vacuoles compared to chromoplasts?

I do agree with the answer though, the pigments in the vacuoles are responsible for more colors in petals, and probably also in more species. However, there might be some plants in which the petal colors are dominated by the chromoplast colors. So the question is not well phrased, "more important" is too vague for exact science.


What is the actual storage form of energy in muscles? ATP or Glycogen? I was asked this question in my latest exam. I think the answer is Glycogen because ATP doesn't store energy for a long time so it isn't the ACTUAL storage of energy. Some classmates argue that in muscles there are other substances, not only glycogen, that are used to produce ATP. In the process of contraction ATP is required so, they say, the question needs the answer to be ATP. Could someone please clarify this discrepancy?

This is a typical MCQ which in order to answer you have to have been at somebody’s lectures or be able to read his mind. The antithesis of education! Cells don’t store energy like car batteries.

Glycogen in muscle is a store of carbohydrate. It can be used to generate ATP if it is broken down to glucose and the glucose glycolysed. I wouldn’t have chosen this as an answer.

The concentration of free ATP in the muscle cell is not sufficient for it to act as store of a high group-transfer potential compound (which is presumably what the question means by energy). This is definitely not the right answer.

However if creatine phosphate (a.k.a. phosphocreatine) was a choice on your MCQ, that was probably the answer expected as it is used in muscle as a storage molecule which can be rapidly converted by creatine kinase creatine and ATP.

PS

As you say in your comment that the only choices were ATP or glycogen, then glycogen is what is expected.


Examples of prey predator interactions where density of predator is very low and prey form groups when the predator attacks the prey for food Examples of prey predator interactions where density of predator is very low (has a threat of extinction) and prey form groups when the predator attacks the prey for food.

I have searched this in net but not get examples. Please help me to supply some examples with a brief interaction of type discussed above.

EDIT

Specialty of predator:

Predator population has a threat of extinction due to their low population. They have the difficulties in locating acceptable mating partners for sexual reproduction during their receptive period due to low population densities.

Many species of animals use flocking/ schooling/ shoaling/ etc as a mechanism to confuse predators. A few examples are tuna, starlings, goldband fusiliers. tuna and goldband fusiliers use their reflective scales to blind and confuse the predator, whereas starlings use sheer numbers to overpower and throw off their predator. The large groups tend to scare away far away predators.

The act of grouping is not dependent on whether or not the predator is endangered or not, but there would be cases where both the predator is endangered and the prey uses grouping. For example, several species of owl are endangered, which prey on starlings.

https://en.wikipedia.org/wiki/Collective_animal_behavior#Protection_from_predators

http://www.fcps.edu/islandcreekes/ecology/european_starling.htm

http://rsif.royalsocietypublishing.org/content/10/85/20130305


Why are tumor suppressor genes recessive? In my Intro. to Biochemistry course, we have been studying cancer. The professor has pointed out that tumor suppressor genes are "recessive" while proto-oncogenes are "dominant". Since only one mutation is necessary to turn a proto-oncogene into an oncogene; while two are needed for the malfunctioning of tumor suppressor genes, why is this not the other way around (i.e. tumor suppressor genes dominant; proto-oncogenes recessive)?

All help is greatly appreciated.

I was typing out an explanation, but then realized that this text book does a much better job:
Lodish et al. 2000. Section 24.2: Proto-Oncogenes and Tumor-Suppressor Genes in Molecular Cell Biology 4ed. WH Freeman
Proto-Oncogene:

Conversion, or activation, of a proto-oncogene into an oncogene generally involves a gain-of-function mutation. At least three mechanisms can produce oncogenes from the corresponding proto-oncogenes.

Point mutations in a proto-oncogene that result in a constitutively acting protein product
Localized reduplication (gene amplification) of a DNA segment that includes a proto-oncogene, leading to overexpression of the encoded protein
Chromosomal translocation that brings a growth-regulatory gene under the control of a different promoter and that causes inappropriate expression of the gene

An oncogene formed by the first mechanism encodes an oncoprotein that differs slightly from the normal protein encoded by the corresponding proto-oncogene. In contrast, the latter two mechanisms generate oncogenes whose protein products are identical with the normal proteins; their oncogenic effect is due to their being expressed at higher-than-normal levels or in cells where they normally are not expressed. However they arise, the gain-of-function mutations that convert proto-oncogenes to oncogenes act dominantly; that is, mutation in only one of the two alleles is sufficient for induction of cancer.

Tumour Supressor Gene:

Tumor-suppressor genes generally encode proteins that in one way or another inhibit cell proliferation.... Since generally one copy of a tumor-suppressor gene suffices to control cell proliferation, both alleles of a tumor-suppressor gene must be lost or inactivated in order to promote tumor development. Thus oncogenic loss-of-function mutations in tumor-suppressor genes act recessively.


Is there any data on Neanderthal admixture in Western European Hunter Gatherers? If there is any data, was the rate of admixture higher than today? Like WEHG brought the component in? Or was the amount maybe lower, like other groups like Early European Farmers or Yamnaya brought the admixture? Or was it evenly distributed?

tldr; Neanderthal ancestry is roughly equally the same between the groups you mentioned.
It's almost certain that the major pulse of Neanderthal admixture into non-Africans occurred very soon after the primary out of Africa event (here I am referring to the out of Africa migration which contributed towards most of the ancestry of all non-Africans today - of course there were other out of Africa migrations which were effective dead ends).
This is well established from a) looking at the size distribution of Neanderthal fragments in the human genome (ref, ref) and b) the fact admixture occurred around 232–430 generations before the 45kya year old UstIshim individual was alive. So most lines of evidence suggest this admixture took place between 50-60kya.
This is much earlier than the diversification of West Eurasian populations into groups like Yamnaya, Anatolian farmers and Western Hunter Gatherers. Therefore, there is no reason to expect any one of these ancestral groups would have had higher amounts of Neanderthal ancestry than any others, since the admixture event occurred into the common ancestor of all these populations.
Indeed, from Haak 2014:

The ancient individuals had indistinguishable levels of Neanderthal
ancestry when compared to each other (∼2%) and to present-day
Eurasians (Supplementary Information section 6)

There are some ancient individuals such as Oase1 who carried substantially more Neanderthal ancestry than modern day samples (in fact this individual has very recent Neanderthal relative), but that they didn't contribute anything towards the ancestry of later groups.
Btw I know a lot of these reference are old - I will add some more recent estimates later, but they don't change the overall picture.


Enzyme Inhibition in relation to Aspirin I see that aspirin (in part) works by inhibiting cycloxygenase isoenzymes and that this inhibiting is irreversible. I've had a few classes mentioning this topic in passing, but never with depth.

I guess my question regards the permanence of the word "irreversible." I assume enzymes have a life span, so to speak, and that the same isoenzymes both die and are being replenished at some given rate.

Am I correct in thinking that the cycloxygenase enzyme is permanently inhibited until its death (catabolism)?

‘Reversible’ and ‘Irreversible’ are standard designations in enzyme kinetics. It may be that your instructor was using the word in this sense.

As already commented, irreversible inhibitors bind the enzyme in such a way that they don't dissociate from it. Either they form a covalent bond or their affinity for the binding site is extremely high. Reversible inhibition is generally found with competitive inhibitors — those that resemble substrate enough to bind to the active site and compete with the substrate for it. Unless they have an extremely high affinity there will be an equilibrium between bound and unbound inhibitor, and the inhibitor can be competed out by substrate — i.e. the binding is reversible.

You can read about this in more detail, but still at an introductory level, in the Wikipedia article on Enzyme Inhibitors  or this section in the online version of Berg et al.


Identify this mite from Rajasthan (India) Can anyone tell me the classification of this bug? I found it in Rajasthan after it rained.

Hi it definitely looks like a red velvet mite.  They often are called "rain bugs".  They are of a variety of species and sizes and can be quite large - up to 1 or 2 Cm. These links might help.

https://study.com/academy/lesson/red-velvet-mite-facts-life-cycle-diet.html

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

https://www.youtube.com/watch?v=OtHYSIRCZ1c


Why is alcohol purged from the body more slowly when we sleep? It is a popular belief that when you get asleep after drinking alcohol, in the morning you have higher level in your blood than if you stayed awake the whole night.

Is this true?
If so, why? Is it because the liver works more slowly while sleeping, or because the intestines work more slowly and there is still more alcohol in the morning to be processed by the liver?

You are right, Culprit is Ethanol in Alcohol. It contains 2 carbon atoms, 6 Hydrogen atoms and 1 Oxygen atom.

Ethanol is readily soluble in water, so it easily dissolves in the
bloodstream and gets carried to various parts of the body. The most
affected areas of the body include the liver and the brain. In the
brain, ethanol adversely affects Glutamate receptors, which causes
slurred speech, memory loss, slow reaction to stimuli, and other
common side effects of being a bit too tipsy.
Not only this, ethanol molecules bind with GABA (gamma-aminobutyric acid) receptors, which is able to slow down the
activity of brain. Unlike glutamate receptors, ethanol actually makes
GABA receptors more receptive, causing the brain to slow down even
further. However, alcohol doesn’t just act to slow everything down in
the body. It also stimulates the production of dopamine and
endorphins, chemicals that produce feelings of pleasure. This is the
reason why people choose to get that alcohol “high”, despite knowing
the negative consequences that it may lead to.

So basically when you are physically working body needs more oxygen while Ethanol only has one oxygen atom, and Since Liver starts to work on regular pace, Which plays a central role in all metabolic processes in the body.
Everyone's oxygen levels in the blood are lower during sleep , in fact while sleeping or in meditation body needs very less oxygen to survive.

Why would I need to wear oxygen while sleeping?
Everyone's oxygen levels in the blood are lower during sleep, due to a
mildly reduced level of breathing. Also, some alveoli drop out of use
during sleep.
If your waking oxygen saturation is greater than about 94 percent on
room air, it is unlikely that your saturation during sleep will fall
below 88 percent. However, your doctor can order an overnight oximetry
test if there is a question about your oxygen saturation levels while
you are sleeping.

In general, metabolic rate is higher when you are awake, because then you tend to be moving about doing stuff.


Can someone who is color blind recover color vision by surgical means? I am currently studying color blindness, and there is no medicine that can help it. Is it possible nonetheless for someone who is color blind to have their eyes restored to normal color vision by replacing the patient's eyes with donor eyes? Please explain any answer. Thanks!

No this is not currently possible as eye replacement surgery is not possible.

Colour blindness is either congenital genetic, such as your X linked forms, or due to a degenerative condition such as retinitis pigmentosa. It can also be acquired through retinal damage or brain injury such as stroke effecting specific areas of the visual cortex.

One of the major problems in restoring colour vision would be that the brain itself may not have the required structure to interpret the signals. The visual cortex is 'patterned' as we develop beginning inside the womb and continuing as a baby. During this process neurological connections in the visual cortex are stimulated so that we develop the necessary networks to interpret the signals from our eyes. If we lack the input of our eyes the brain conducts something called neural pruning where the unused neural connections are destroyed never to be regrown. Therefore if you lack visual stimulus for colour you prune these connections. If we were to somehow replace this colour stimulus later our brains would not be able to interpret it. In a somewhat similar circumstance to this it has been found with individuals who are born with congenital cataracts. If they have their cataracts fixed later in life having spent their childhood blind, despite being able to 'see' they cannot interpret the images they receive.

In individuals who loose there colour due to degenration of the retina, if we were able to repair the retina, through stem cell or transplant therapy then perhaps colour vision would return.

An individual who lost colour vision due to brain injury cannot have their colour vision returned as we cannot repair such injuries.


How does Yeast-two-hybrid detect interactions between several proteins in one experiment? I am trying to understand the Y2H screening method. I can understand how we can check if two specific proteins interact with each other. For example, if we want to check whether protein A and protein B interact, we fuse A with the Activation Domain (AD) of a transcription factor and B with the Binding Domain (BD) of another transcription factor. When the two fusion proteins are transfected into a yeast cell, the reporter gene is expressed only if the AD and the BD get together and form a complete transcription factor and that happens only if proteins A and B interact with each other.

However, I have seen claims that Y2H is a high throughput system, i.e., it can be used to detect several interactions at once. But most articles online that attempt to describe it, seem vague to me.

For example, suppose I fuse the "bait" protein to the BD and several different cDNA's to the AD and let the yeast grow. Next, I observe that the reporter gene is expressed. Doesn't this observation only imply that there exists some protein from the cDNA library that interacts with our bait protein? How do we know exactly which of the target proteins have interacted with the bait and resulted in the expression of the reporter gene?

You use a library of many yeast in which each expresses only one target, or 'prey' protein. Then you grow each yeast colony separately, for example in different wells.

It's definitely not a high-throughput method if you do it the old-fashioned way, i.e. making your own yeast library, or if you do it with only a few targets.  But these days you can buy pre-made yeast libraries with thousands of target proteins, each separated into a well on a plate, then you run the experiment for all the targets simultaneously. With a visible marker you can then easily see which wells have produced successful interactions, and thus which targets interacted with your bait.


What does chrUn mean in the output from a Bowtie run on human sequences? After having performed an alignment using bowtie2 and GRCh38 as a reference sequence, I got inusual matches on chrUn.
Here a small part of the SAM file:

@SQ     SN:chr22   LN:50818468
@SQ     SN:chrX    LN:156040895
@SQ     SN:chrY    LN:57227415
@SQ     SN:chrM    LN:16569
@SQ     SN:chrUn_KI270424v1     LN:2140

All the other chr values are clear to me (M indicates the Mitochondrial DNA, while 22, Y and X are just the usual chromosomes number/name) but I couldn't figure out what chrUn stands for and what about that code after the _?

I presume chrUn_KI270424v1 refers to a scaffold or sequence that has not yet been assigned to a chromosome. The designation after the Un (unknown or unassigned?) may refer to a particular single sequence or a scaffold. You will be able to determin this by examining the reference sequence and its documentation.

(My assumption is based on the sort of thing one finds in the various versions of Drosophila reference genomes, with which I am familiar. So I can’t help you with the specifics of the human genome.)


What's this black, white and orange beetle? Found in Toronto Canada.
Maybe 1-2 mm long but I'm not a good judge of measurements.
Should I be concerned it has friends? I've dealt with carpet beetle larvae in several homes over 7 years and an praying this isn't an adult.

Yes this is an adult carpet beetle.

Specifically,  this is a Common carpet beetle (Anthrenus scrophulariae)

See here for more info.

2.5 to 3.8 mm in length.
Black head (mostly hidden by the prothorax) + black  thorax and elytra with distinct scale patterns.

The thorax is covered with white scales except for a large midline.
The elytra have orange to red scales down the midline with variable patches of white scales.

Note: in older individuals, some or all of the scales may be lost and the color pattern may look different.

This species is found worldwide.

Unlike the larvae,  the adults are primarily pollen grazers.


What are dreams, biologically? Falling asleep or states of subconsciousness does not stop the mind from making its own fictional images. These seem like sensations just like those received from human eyes. But, how do we define these visual sensations biologically?

Short answer
In terms of visual function, the low-tier primary visual cortex and high-tier frontal cortex are inactivated. The activity of the intermediate ventral stream and limbic regions are increased, apparently uncoupling low- and high-level vision processing from the system.

Background
The sleep stage where visualizations (dreaming) occur is called the rapid-eye movement (REM) sleep.

Brain imaging studies have shown pronounced effects of REM sleep on the functioning of the visual system.

In the awake state, the primary visual cortex (V1, or striate cortex) is activated, which is mainly concerned with low-level visual processing such as contrast perception. This cortical region in turn projects to higher-level (extrastriate) regions for more complex processing of visual information.

During REM sleep, however, a selective activation of extrastriate visual cortices is observed. Particularly the ventral processing stream is activated, which is associated with perception and recognition in the awake state (Deubel et al., 1998). Also the limbic and paralimbic regions are active (the emotional brain centers).

Interestingly, activity in the primary visual cortex (V1) is attenuated, as well as the frontal association areas of the brain. V1 is the primary, most 'primitive' visual cortex, while the frontal association areas are the highest-tier cortex that integrates complex perceptual information across perceptual modalities (Braun et al., 1998).

Overall, this pattern suggests a model of REM sleep where visual association cortices and their paralimbic projections may operate as a closed system dissociated from the regions at either end of the visual hierarchy that mediate interactions with the external world (Braun et al., 1998).

References
- Braun et al., Science (1998); 279: 91-5
- Deubel et al., Vis Cognition (1998); 5(1/2), 81–107


Why is the "worm" body shape so prevalent in Eumetazoa? What is the selection advantage, of this incredibly common body form? (long, cylindrical tube-like body with no limbs)

Is it just the body plan of the ancestral bilaterian and therefore remained prevalent due to absence of selective pressure against it? I.e. is it a neutral adaptation? Or is it actually a positive one?

Examples of "worms":
- Platyhelminthes
- Nematoda
- Annelida
- many kinds of insect larvae
- sea cucumbers
- lancelets, lampreys, eels, snakes, caecilians, ...
- Chaetognatha
- Hemichordata
- Acanthocephala
- Gastrotricha
- Gnathostomulida
- Nematomorpha
- Nemertea
- Priapulida
- Sipuncula

Is it just the body plan of the ancestral bilaterian and therefore remained prevalent due to absence of selective pressure against it?

Pretty much.

You can see some animals which precede the emergence of this plan, like sponges. They apparently do alright, so there's nothing precluding different body plans. However sponges also have a fairly limited niche, and perhaps there's a good reason. Similar things can be said for other non-bilaterians like jellyfish.

One could speculate that the "tall-donut" shape is the key innovation. When food moves in only one direction, it is much easier for the digestive tract to specialize and digest food much more efficiently in stages. Animals, after all, are things that survive by eating things and digesting them - the faster they can digest, the faster they can eat, the better they can survive.

Animals which have no separate anus seem to have more trouble eating things and digesting them: It's slower, and they can't eat as varied a diet.

A worm, being essentially a long tube, is a simple way of accomplishing accomplishing the one-way GI tract. If you think in an evo-devo sense, it also doesn't take a lot to progress from a "basket" to a tube (the two layers after gastrulation just have to meet, fuse, and form a second hole). If you consider the so-called higher animals, like humans, cats and dogs "worms", then we can stop there. Otherwise, we can remark that the "worm" shape also allows easy movement in water and on soil by wriggling.

Past the "pure worm" you can see a large variety of body plans, such as among arthropods, but they're really just worms with a few specialized segments, including, say, humans. This does have a fundamental reason: During early development, patterning of the body (deciding which organ or limb will grow where) relies on Hox genes, which are typically top-level transcription factors that determine a segment's identity. So the "worm" also happens to be a nice developmental "base" from which more complicated embryos can develop.

  is it a neutral adaptation? Or is it actually a positive one?

This is very hard to answer:

There are necessarily many confounds, and we cannot easily find two animals which are otherwise the same, but one is a worm and the other is not. We cannot artificially generate such animals yet either.
The obvious way to infer fitness is to look at whether the trait came to dominate the population. But with since body plan establishment is something that did not evolve independently many times, it is hard to say whether it dominated due to a genuine fitness advantage or purely out of being fixed. Perhaps there are other, yet more efficient body plans, but they have not yet arisen due to random chance.


How do adult differentiated somatic cells divide? My textbook (which is Biotechnology by David P. Clark) states, when talking about fate-mapping potential stem-cells:

  "If the marked cell is not a stem cell, the marker will not be passed
  onto descendants since normal differentiated somatic cells do not
  divide by mitosis."

He then goes on to say:

  "Most adult differentiated cells do not divide at all and are
  considered postmitotic."

So there are some differentiated somatic cells which divide, but apparently not by mitosis? So what is the technical term for their division?

Here is a screenshot of the passage:

There is no known alternative mechanism of proper cell division apart from mitosis and meiosis in animals. I think this is an unfortunate phrasing where the author is trying to introduce the term "postmitotic". The reason for saying "most  adult differentiated cells" is because some cells in adults are considered differentiated but they still proliferate under certain conditions, like for example the cells of the adaptive immune system.

It could also be that the author is trying to be overly cautious because there are cells that split parts of themselves off and release them. These mechanisms could be considered cell division in some sense but are neither mitosis nor meiosis. Examples of this are the release of platelets by megakaryocytes and the release of extracellular vesicles by cells undergoing apoptosis.


How does a plant grow before photosynthesis is possible? During photosynthesis, a plant translates CO2, water and light into O2. I assume the carbon C is further used for the growing process. I wonder how the plant grows before the time where photosynthesis is possible, i.e. before there are even leaves, in which photosynthesis occurs.

To what extent does the plant grow from the seed/the minerals in the ground?
How much carbon are relevant for which parts of the plant and at what times of the evolution of the plant?

I don't know if there are only these life periods of the plant, i.e. if there are other major biochemist-of-growing changes, than in the comparison before and after the plant got leaves. So are there other relevant aspects to this? If there are leaves present, is the rigid structure of the plant only coming from the CO2 in the air and not from the ground anymore?
The answer will probably depend on the plant. So here is another formulation of the question:

What are typical characteristics of different plants in this regard? I.e., how do common species of plants manage their C consumption before (and after) the development of leaves?

There are quite a few questions and thoughts in there, I'll try to cover them all:

First, to correct your initial word equation: During photosynthesis, a plant translates CO2 and water into O2 and carbon compounds using energy from light (photons).

You are correct to assume the C is further used for the growing process; it is used to make sugars which store energy in their bonds. That energy is then released when required to power other reactions, which is how a plant lives and grows. C is also incorporated into all the organic molecules in the plant.

Plants require several things to live: CO2, light, water and minerals. If any of those things is missing for a sustained period, growth will suffer. Most molecules in a plant require some carbon, which comes originally from CO2, and also an assortment of other elements which come from the mineral nutrients in the soil. So the plant is completely reliant on minerals.

Most plants, before a leaf is established or roots develop, grow using energy and nutrients stored in the endosperm and cotyledons of the seed. I whipped up a rough diagram below. Cotyledons are primitive leaves inside the seed. The endosperm is a starchy tissue used only for storage of nutrients and energy. The radicle is the juvenile root. The embryo is the baby plant.

When the seed germinates the embryo elongates, the endosperm depletes, the testa ruptures, and the cotyledons emerge from the seed. The cotyledons are green, and like leaves can photosynthesise, so as soon as they are in the light the plant is able to make carbon compounds. The radicle elongates at the same time, and becomes the root, so the plant is very quickly able to obtain fresh nutrients from the soil (or whatever it's growing in).

At all stages of a plant's life it is using both energy stored in carbon compounds (from CO2) and nutrients which it took up via its roots. At no point does the plant start to depend solely on the CO2 in the air for its growth.

You are right that the way in which plants acquire energy and nutrients prior to leaves and roots being established varies between plants. Above I outlined the way most plants use. But there are lots of variations. For example, orchids have very tiny seeds, some barely visible to the naked eye, like specks of dust. They have no endosperm or storage tissue, so they have to rely on a symbiotic mycorrhizal fungus to get carbon and nutrients. The fungus grows through the coat of the orchid seed, then provides everything the growing plant needs until it has its own leaves. Then the orchid repays the fungus by providing sugars.

There are lots of other examples, but we could go on all day!


What is mean by the term "an organism's genotype is its specific combination of alleles for a given gene"? an organism's genotype is its specific combination of alleles for a given gene

What is meant by this? Is it talking about heterozygous and homozygous (like GG or Gg) or is it talking about the nuclear bases?

Thanks

From wikipedia

  An Allele is a variant form of a given gene.

Let's consider a simplified example. There is a gene for eye color and there are different alleles at this gene. The allele for blue eye, the allele for brown eye etc...

In a diploid (see ploidy) individual (humans are diploid), we have two copies of each gene (exception of sex chromosomes). Let's imagine, at a givne gene, there are 3 possible alleles called A, B and C. The possible combinations are

AA
AB
AC
BB
BC
CC

The genotype of an individual for a given gene (I should say locus for the sake of generality) is called the genotype of an individual.

  Is it talking about heterozygous and homozygous[?]

The terms "homozygous" or "heterozygous" are adjectives to define whether, in a diploid genotype, the same allele is found on both haplotypes or not. In the above examples, 3 genotypes are homozygous (AA, BB and CC) and 3 genotypes are heterozygous (AB,AC and BC).

  [I]s it talking about the nuclear bases?

For two alleles to be different, they must differ in their sequence of nuclear bases of course.


Can predator-prey relationship be an example of negative feedback? Predators eat their prey, prey population decreases. This results in the predator population to decrease, so less prey are consumed which causes the prey population to increase.

Therefore, if the reduction in prey population results in its increase then can this be described as negative feedback?

From my experience, "negative feedback" is more often used in the context of processes in the body which attenuate themselves or in the context of stimuli and sensors. However predator-prey dynamics could fit the general definition of the term. In general, negative feedback is just when a process or output of a system leads back into the system to attenuate itself.

  Negative Feedback:

  "A feedback in which the system responds in an opposite direction to the perturbation. "

  Source: biology-online.org, access date: 2018-04-06.

In a general case of a closed-loop (feedback) control system, you've got a stimulus that gets sensed by a sensor, which sends a signal to a controller. The signal is then passed on to an effector, which can change the original stimulus. In the case of negative feedback, the stimulus is attenuated. In positive feedback, it is potentiated.

$$\begin{array}{ccc}
\fbox{Stimulus}&\rightarrow&\fbox{Sensor}
\\
\uparrow&&\downarrow
\\
\fbox{Effector}&\leftarrow&\fbox{Controller}
\end{array}$$

A common example of this would be high body temperature being detected by neurons, which send a signal to the brain to cause the body to sweat more. In this case, the sweat glands are the effectors and can lower the body temperature.

$$\begin{array}{ccc}
\fbox{Change in body temp.}&\rightarrow&\fbox{Neurons}
\\
\uparrow&&\downarrow
\\
\fbox{Sweat Glands}&\leftarrow&\fbox{Brain}
\end{array}$$

In your case, I think you could describe it with an increase of prey population being the stimulus, which is detected by the predators as they see more prey. The predators would then choose to eat the prey (I suppose this could be the controller) and then act as the effector by eating the prey (and thus, reducing the prey population). Though I'm a little iffy on this since you'd have the predator acting as both the sensor, controller and the effector. Conversely, if the prey population were lowered, the opposite would be true.

$$\begin{array}{ccc}
\fbox{Change in prey pop.}&\rightarrow&\fbox{Predators sense prey}
\\
\uparrow&&\downarrow
\\
\fbox{Predators eat prey}&\leftarrow&\fbox{Predators choose to eat prey}
\end{array}$$


Epistasis Involving Multiple Loci The following problem is from Schaum's Outlines on Genetics, 5th edition, by Elrod and Stansfield.  I'm having some trouble solving it.  It is found under a section entitled "Interactions with Three or More Factors" in the problems at the end of the chapter on Epistasis.

  Problem 4.30 (pg. 112):  If a pure-white onion strain is crossed to a pure-yellow strain, the
  F$_2$ ratio is 12 white : 3 red : 1 yellow.  If another pure-white
  onion is crossed to a pure-red onion, the F$_2$ ratio is 9 red : 3
  yellow : 4 white.  (a)  What percentage of the white F$_2$ from the
  second mating would be homozygous for the yellow allele?  (b)  If the
  white F$_2$ (homozygous for the yellow allele) of part (a) is crossed
  to the pure-white parent of the first mating mentioned at the
  beginning of this problem, determine the F$_1$ and F$_2$ phenotypic
  expectations.

In the first crossing, it looks like the type of interaction is one of dominant epistasis between two loci.  So, we could call the alleles for the first locus W and w and the alleles for the second locus A and a.  Then W-A- and W-aa would have a white phenotype, wwA- would have a red phenotype, and wwaa would have a yellow phenotype.  This would be consistent with the ratios provided in the problem.

In order to explain the 9 red : 3 yellow : 4 white, a third locus can be considered with alleles B and b.  Proceeding as above, where we had the locus for W or w epistatic with respect to the locus for A and a, we could have the same locus for W or w epistatic with respect to the locus for B and b.  This time, wwB- and wwbb would be white, W-B- would be red, and W-bb would be yellow.  This would be consistent with the 9 red : 3 yellow : 4 white ratio.

This is where I get stuck.  If the locus for W and w is epistatic in a dominant way with respect to one locus and in a recessive way with respect to another locus, then all onions would be white.  Therefore, I must have done something wrong.  Am I on the right track?

This isn't really a homework problem, despite the "homework" tag.

Here are the answers provided in the text for the problem:

  Problem 4.30 (pg. 115):  (a) 25% (b) F$_1$: all white; F$_2$ : 52
  white : 9 red : 3 yellow

After reading Satwik Pasani's comment to the original problem, I tried using the hypostatic locus as the common locus in the epistatic relationships, instead of the locus causing the onions to be white.  The following solution fits the answers supplied in the book.

Three loci can be used to determine the colors of the onion, the alleles of which can be denoted by C, D, and E.  Suppose that C and D are each epistatic to E, such that the phontypes of the onion are given as:

cc---- white
--D--- white
C-ddE- red
C-ddee yellow

Then the first crossing in the problem can be given by CCDDEE x CCddee.  The second crossing could be ccddee x CCddEE.


Can someone help me identify this Brazilian spider? Does anyone know anything about the identification of this spider? Sorry, but it's the only image I have. It was shot at 2004, January 25th (summer), at 11:27 AM, in Cerrado biome at Minas Gerais state, Brazil. It was walking over a Paepalanthus inflorescence (Eriocaulaceae), probably waiting to prey on its pollinators. A small section of web can be seen raised to the left (where it apparently comes from another inflorescence), touches one of the small flowers, and then it's apparently still connected to the spider, in a pattern that reminds me of Salticidae, though I'm not sure. I think its size is around 1 cm. I doubt a specific identification will be possible, but family, superfamily, subfamily, anything will be fine.

Interesting!  See those long spines on the legs?  Only two groups of spiders (that come to mind, anyway) have that sort of arrangement:
Lynx Spiders (Family Oxyopidae) and Pirate Spiders (Family Mimetidae).
Lynx Spiders are wandering hunters, and the ones I'm familiar with tend to have a body shape more like the familiar Grass Spiders (longish, tear-drop shaped abdomen and hunters cephalothorax - roughly rectangular, and often very blocky at the face.
For instance:
https://bugguide.net/node/view/1965

https://bugguide.net/node/view/1489229/bgimage

So, your spider looks to be a South American Lynx Spider, which unfortunately I'm not at all knowledgeable about.

I'm going to discount Pirate Spiders as a possibility, even with the association there with a bit of web (Pirate Spiders invade other species' webs and kill the occupants), because they're much more 'orb-weaver'-like in their general body shape.  This one is so Lynx Spider-like that I am pretty confident that it is one of those.


What of Gould's contributions to evolutionary biology are still accepted in the mainstream? I have been reading Daniel Dennett's Darwin's Dangerous Idea, in which he picks apart many of Stephen Jay Gould's criticisms of neo-Darwinism, particularly in the chapter 'Bully for Brontosaurus'. Turns out Gould wrote a lengthy refutation back, and they ended up throwing slurs at each other for a few years afterwards.

I am interested to know what the current state of mainstream opinion is on Gould's interpretations, particularly on panadaptationism and gradualism. Has the field yet come to any firm conclusions on who was right after all?

His main contribution was making biologist consider that population size affects how fast selection changes a population, but he tended to imply this was some form of categorical difference and not a spectrum. But this was greatly overblown my media into some sort of insistence that they could not be the same. large population slow change and small population fast change are both points on the same spectrum. Nobody was right becasue both sides were not really saying the other could not occur they just emphasised their own area. Gould main problem was the idea of stasis in punctuated equilibrium that large populations somehow did not keep evolving this was a point he contested without ever really being able to provide evidence for. His own evidence often fit both interpretations. Since then it has been pretty thoroughly refuted by genetic studies, better resolution*, and modeling of stabilizing selection, all populations change, large ones just change slower, often with less direction. Gould himself later accepted this, but insisted on keeping the terms punctuated equilibrium and more oddly "stasis" for these periods of reduced change, this led to more misunderstanding especially with the public and media. Many scientist felt it was a sign of being unwilling to truly accept the evidence.

He also contributed a lot to our understanding of evolutionary development and how evolutionary baggage effects future adaptations. We often forget this but without his constant pushed of the importance of constraints and development both would probably be much more poorly understood. Panadaptationism was probably given more service by than many ever though it deserved, but Gould was right that that are far more aspects to selection than many considered. It just was not as popular an idea as his attention implied, but that is part of science harping on bad ideas is not really bad in science, it just starts to get old when the idea never had a lot of traction. It is however understandable considering Gould's own focus.

He has a serious problem(probably not unfounded) with sociobiology but probably pushed too far by implying searching evolutionary history for influence of our behavior was pointless. As much good as he did for understanding physical adaptations he seemed to have a blind spot when it came to behavioral adaptations. He mellowed about this in later years but still seemed to resist it. Sociobiology tended to be over applied, often without evidence, it was easily the worst offender with panadaptationism. Gould was right to push back against speculation but he often treated all behavioral science the same regardless of rigor.

Dennit who primarily researched evolutionary aspects of human behavior and publicly speculated a lot, of course ended up as a stanch opponent. But then as the more rigorous evolutionary psychology arose from sociobiology Gould seemed unable to see the difference which quickly led other to stand against him and probably did more than anything to produce his negative image. I know it is the thing that put me off his writing.

The other issue that I, as well as many other paleontologists, had with him was his resistance to the application cladistics and other computer based analysis. Both extremely important tools in understanding evolution, especially once to could be applied to genetic material. He always seemed to treat it as not real science, which always struck me as weird considering how much he emphasised rigorous investigation. He struck me a brilliant mind falling behind the technological curve and becoming disapproving of it. To myself as a young scientist he seemed to resist anything new regardless of rigor despite his own emphasis on rigor.

In short he was hard working scientist. He improved our knowledge in some areas while being unhelpful in others. He was a scientist who got a huge amount of media attention, which few scientist can do without sooner or later showing normal human flaws. Now take all this with a grain of salt, this is all my own personal impressions from observation of his work in paleontology along with reading his (and just about every other) book about evolution. I have not read many of his paper outside of paleontology. I say this becasue speculating on the beliefs and motivations of the dead has always struck me as dishonest especially without laying your cards on the table.

I wanted to give special mention to resolution and darwin finches, darwin finches undergo different selection every year depending on rainfall, large and small (specialized) beaks during wet years and medium (generalist) beaks during dry years, this changes every breading season with the amount of rainfall on any large scale this would appear to be no change as they tend ot average out, but with better resolution we can see many many small directional selection pressures adding up to no net change on a large scale.


Protein A-antibody SDS-PAGE I wanted to know whether the boiling of Protein A- antibody complex for SDS-PAGE analysis will disrupt the interaction? and result in dissociation of protein A and antibody?

Thank you

Yes. Samples for SDS-PAGE are mixed with a loading buffer containing SDS (final concentration of SDS is usually 2%). Generally, the SDS will disrupt protein-protein interactions, even before boiling. Reducing agent (usually DTT or b-mercaptoethanol) is added to disrupt disulfide bonds.
See diagram here.

There are, however, exceptions. Some protein complexes/multimers are resistant to SDS until boiling, and some even maintain interactions after boiling. Some examples: Xia et al 2007, Kubista et al 2004, Grigorian et al 2009.


Does trypsin strip flask coating? Mammalian cell/tissue cultures sometimes require flasks coated with proteins. My uneducated guess is that these proteins mimic the ECM, perhaps the basal lamina, so finicky contact-dependent cells can attach to it.

For instance, I have a BEAS-2B tracheal culture which requires a coating of albumin, fibronectin and type I collagen. This is applied by incubating an empty plastic dish or flask with a solution of these proteins overnight. I give this as an example of what a "coat" constitutes. You answer should be general enough to apply to at least the most common coat types, or if it depends on the coat, you should explain how.

Likewise, there is some variation in how the trypsinization occurs. To have a starting point, let's say I am trypsinizing according to typical ATCC recommendations: 5 minutes with 0.25% Trypsin-0.53 mM EDTA, then inactivate with equal volume medium. I haven't worked with a cell that can withstand this noticeably (but then I haven't worked with any exotic cells).

My question: When I trypsinize the cells to passage, what happens to the coat?

Since trypsin is a protease that cleaves even the attachment of cells to plastic, I am guessing that it will also destroy the coat. After the trypsin and cells are removed, the flask will have a tiny fraction of the protein coat that it had before, and will not support cells that require a coat any longer.

Am I correct in thus deducing that coated flasks cannot be reused after trypsinization? Are any of the alternative detachment reagents an exception to this?

Generally the coating is of poly D-Lysine. Proteases act only on L-amino acids. So, I guess nothing should happen to the usual coated flasks. I have reused the flask even after 2 rounds of trypsinization, and the cells seemed to be fine.

In your case, the matrix is made of proteins isolated from animal sources. They are susceptible to proteolysis. You are right to assume that these flasks should not be reused. If you have a shortage of flasks then you can buy uncoated petriplates (which are cheaper) and coat them yourself.


Do seeds use cellular respiration when they are germinating? Do seeds use cellular respiration when they are germinating?

Those stored fats and sugars have to be burned to be utilized. Besides how ridiculous it would be to have a multicellular organism mature using only fermentation.


Is α-keratin a fully functional protein? Is α-keratin before it coils with another polypeptide, makes chains, and build intermediate filaments a fully functional protein?

I mean, is the single monomer of α-keratin a protein or does it have to become a dimer to become a protein?

What we call as protein is the final quaternary structure. Whether it is translated from a single gene or from multiple genes (as in haemoglobin), always the structure with all bonds and interactions taken into account. Similarly here the alpha- Keratin forms Disulfide bonds to form a functional protein.


Waste generation by embryo How does an embryo produce waste products even when its organ systems are not developed fully ? How does the placenta identify or differentiate waste materials from embryo ? Which organelle or specific cell acts as excretory organ ?

Embryos still metabolize the nutrients delivered by the mother. The metabolism takes place in the cells, including in the developing organs. Metabolism produces waste products that must be removed. The allantois is the structure that removes waste from the embryo.

I'm not sure what you mean by the placenta identifying or differentiating waste materials from the embryo. The waste simply diffuses passively into the mother's blood from the embryo. The mother's excretory systems then handle it.


Is there a reliable source for storage and stability of reducing agents like DTT? Reading the literature on DTT, one is confronted with a confusing mass of papers; some claim that a 1M solution in water is stable, other papers say it is not. I use the reaction with DTNB to show that the DTT is still good, but that is cumbersome.

Is there some source of reliable (as in data driven) information on how to store compounds like DTT and other reducing agents?

Thiol-Based Reducing Agents

The instability of thiol-based reducing agents in solution is due to their propensity to form disulfide bonds by the following half reaction:

$$\ce{2RSH -> RSSR + 2H+ + 2e-}$$

It is clear that disulfide formation requires:

Deprotonation of the thiols to form thiolates (RS-).
An electron acceptor.

Therefore, solutions of thiol-based reducing agents would be most stable when:

The pH is buffered to where the thiol form predominates. The pKa of the thiol in β-mercaptoethanol is 9.5 and in dithiothreitol are 9.2 and 10.1  (Whitesides et al., 1977). Buffering the pH lower than this should increase stability.
Electron acceptors are removed. In aqueous solution, the electron acceptor is molecular oxygen. Degassing the buffer and storing the solutions under an inert gas such as argon should increase stability.
Reaction catalysts are removed. Divalent metal cations, especially copper (II) (Cu2+), catalyze oxygen dependent disulfide formation, even in trace amounts (Smith et al., 1994). Therefore a chelator such as EDTA should increase stability.
Temperature is low. As with most chemical reactions, rate increases with temperature.

The stabilities of the thiol-based reducing agents β-mercaptoethanol (β-ME), dithiothreitol (DTT) and glutathione (GSH) have been determined in solution as a function of pH at 20°C (Stevens et al., 1983):

...and temperature at pH 8.5:

...as well as in the presence of copper (II) and EDTA at pH 8.5 and 20°C:

Below is the tabulated raw data (this is the actual data from the paper which I used to create the above graphs, but take note that I found it difficult to plot “>100”):

                               Half-life (h)
pH    Temp (°C)    Additive    β-ME    DTT    GSH
6.5   20           -           >100    40     16
7.5   20           -           10      10     9
8.5   20           -           4.0     1.4    1.3
8.5   0            -           21      11     8
8.5   40           -           1.0     0.2    0.2
8.5   20           Cu(II)      0.6     0.6    1.2
8.5   20           EDTA        >100    4      70

As expected, stability decreased with increasing pH and temperature, and also with the addition of copper. Stability increased with the addition of EDTA.

Non-Thiol-Based Reducing Agents

Han and Han (1994) studied the effect of pH and buffer composition on the solution stability of tris(2-carboxyethyl)phosphine (TCEP). Though this is not a thiol-based reducing agent, it is still subject to oxidation. However, it is quite stable in solution:

pH    Solute/Buffer     % TCEP Oxidized After 3 Weeks
7.5   Tris-HCl          18.7 ± 0.6
8.5   Tris-HCl          16.8 ± 0.5
9.5   Tris-HCl          14.5 ± 0.5
8.2   borate             6.6 ± 0.2
10.2  borate             5.3 ± 0.1
6.8   HEPES             14.8 ± 0.4
8.2   HEPES             13.6 ± 0.3
9.7   CAPS               9.8 ± 0.3
11.1  CAPS               4.3 ± 0.1

Stability increased with increasing pH, though the effect was not large. Interestingly, the buffer composition had a larger effect on stability which was especially pronounced with phosphate:

        % TCEP Oxidized After 72 Hours
 pH     0.15 M phosphate    0.35 M phosphate
 6.0    not determined      11.2 ± 0.3
 6.8     8.1 ± 0.4          56.8 ± 2.3
 7.0    23.5 ± 0.9           100
 7.2    33.4 ± 1.0           100
 7.4    56.5 ± 1.4           100
 7.6    56.8 ± 2.1           100
 7.8    48.9 ± 2.5           100
 8.0    36.6 ± 1.7           100
10.6    not determined      11.7 ± 0.5
11.6    not determined       9.1 ± 0.4

References

Han JC, Han GY. 1994. A Procedure for Quantitative Determination of Tris(2-Carboxyethyl)phosphine, an Odorless Reducing Agent More Stable and Effective Than Dithiothreitol. Anal Biochem 220(1):5-10.

Smith RC, Reed VD, Hill WE. 1994. Oxidation Of Thiols By Copper(II). Phosphorus Sulfur Silicon Relat Elem 90(1-4):147-154.

Stevens R, Stevens L, Price NC. 1983. The stabilities of various thiol compounds used in protein purifications. Biochemical Education 11(2):70.

Whitesides GM, Lilburn JE, Szajewski RP. 1977. Rates of thiol-disulfide interchange reactions between mono- and dithiols and Ellman's reagent. J Org Chem 42(2):332-338.


What is this insect from Brazil Im assuming 'cicada' with this insect but which one ? Small size- c1c-2 cm -

This neotropical leafhopper belongs to the subfamily Coelidiinae. According to this publication though, there are 25 genera & over 75 different species, and so, I'm having a difficult time narrowing it down from there (my current best guess would be genus Jikradia).

If I'm not mistaken, this insect is displaying an alarming signal by spreading its wings like that.. it must have felt threatened by you when you were taking the picture (assuming that it wasn't already like that when you approached it).

For more information on this subfamily, I strongly suggest that you explore the text of the previously linked publication, as it contains great information regarding the various tribes of subfamily Coelidiinae, including distribution, origin, host plants, a bit of history, and so forth.


Well Plate Method VS Kirby Bauer Method Any pros and cons? One puts the test substance in sterile discs, while the other one puts it directly into wholes in the agar. Any thoughts?

I came across a nice Master's thesis that investigated precisely that. The conclusion reads as follows:

  Automated microbroth dilution-based testing methods are increasingly used by many
  clinical microbiology laboratories to determinate antimicrobial susceptibility. Thus, it is vital that
  these methods are able to accurately determine the correct antibiotic susceptibility patterns of
  microorganisms being tested. In our laboratory, we use the Trek Sensititre system (Well Plate Method). However, if
  this system cannot accurately detect resistance visualized as inner colonies on the Kirby Bauer
  Assay, then the clinical importance of the Trek Sensititre may be called into question.

  Our study showed that the Trek Sensititre was unable to detect the
  additional resistance of inner colonies that are detected using the
  Kirby Bauer Assay. Nevertheless, there are a number of important
  limitations associated with the study: Firstly, the inner colonies
  used in the study were pooled from all inner colonies from the Kirby
  Bauer plate. Because the colonies were pooled, in some cases from
  different antibiotic zones, it is possible that a mixed population of
  resistant organisms that were selected for by the different
  antibiotics were tested. This possible mixture of multiple different
  subpopulations may make the results difficult to interpret. Secondly,
  some inner colonies were selected from antibiotics that do not have
  any CLSI- 47 approved interpretations and would be considered
  inappropriate to report. For example, some Pseudomonas aeruginosa
  isolates displayed inner colonies to ertapenem, an antibiotic that has
  no CLSI interpretations and a drug that would not be used clinically.
  The Trek Sensititre results from those inner colonies showed
  additional issues with multiple different antibiotics. Clinically, the
  patient would not have been treated with that antibiotic, so that this
  resistant set of subpopulations may not have been selected for. Thus
  the results from the study may not be clinically significant but it
  does open up questions to the possibility that the Trek Sensititre may
  not detect clinically significant resistant subpopulations.

  Given that
  the Trek Sensititre can miss resistant subpopulations in Gram negative
  bacilli, it is important to establish the clinical relevance of this
  finding. If the inner colonies selected for by each of the antibiotic
  discs was sub-cultured individually instead of pooled together and
  then run on the Trek Sensititre, then the following results may
  possibly differ from the pooled inner colonies. An important future
  direction would be to determine whether the unreported resistance from
  the organisms in the study had an effect on patient care however, this
  was beyond the scope of this thesis study. Thus, the clinical
  significance of this study’s findings require future study.
  Nevertheless, laboratories should be aware of the potential for
  missing sub-populations of antimicrobial resistant organisms using
  broth-based microdilution methods.


Why do humans cook animal meat Why do humans "need" to cook animal meat?

It seems there's an aspect of safety to it: are other animals (eg, house cats, dogs) not vulnerable to the same diseases we get from modern food processing of meats?

But it also seems there's something else to it: is raw animal flesh is harder to digest for us, no matter how fresh or processed?

I've read so many conflicting things about it, like how cooking is really a way to avoid disease, but that the human body is capable of processing protein from raw meat just the same. An example is how other countries eat raw meats that Americans would not. But then I've also read things about how cooking meat is what allowed humans an energy advantage early in our development as a species (I'm not clear how more calories are "unlocked" by cooking) or how denatured protein plays some role in usability. I also know that my person experience with raw meats doesn't help me understand it, because sushi seems to be fine but raw eggs will upset my stomach.

Humans do not "need" to cook food, but in general cooking food facilitate digestion and absorption of nutrients.

Heat cause denaturation of proteins. Once denatured, proteins are more susceptible to the enzymatic digestion. Thus, more nutrients are absorbed. There are also macroscopic phenomena in play, for example, a cooked piece of meat is more tender than the raw one, making mastication easier and less energy consuming.

The fact that you may feel your stomach upset because of raw food is probably due to the fact that you were never used to it. Your intestinal flora has been selected during the year to deal with the food you usually eat, any "new" food may cause the same symptoms. Humans that eat regularly raw food will not feel the same way.

Generally speaking, cooking food help killing bacteria, so your body does not need to deal with lots of infections that would occur otherwise. This, on the other side, makes your body weaker compared to the one of a wild animal, for example, that is used to deal with such bacteria. Of course, many animals also die because of food poisoning or food-related infection, only the "stronger" survive so there is a strong selective pressure in wild animals to have "a strong digestive system" (and a strong immune system as well). This selective pressure is less pronounced in modern human society but it is still present in less modernized areas.


Why do mutations not take place in mRNA of higher eukaryotes? Is it because it is too short-lived to be mutated? Both DNA and RNA are nucleic acids so how is mRNA protected? RNA viruses undergo mutations to evolve so I guess it is not immune to mutations

The premise of the questions suggests that mutations cannot take place in the mRNAs of higher eukaryotes.
To answer your question I think it is important to consider two viewpoints:

First, from a theoretical point of view, since DNA and RNA are as you pointed out composed of nucleic acids, they both can be mutated if enough energy is provided (UV light, chemicals, etc) which invalidates the premise of the questions.

Now, from a practical point of view, as you mentioned most mRNAs molecules have a short half life typically in the minute to day range whereas DNA molecules exist during the whole existence of the organism.

While it can occurs that mRNAs are mutated people are not interested to study this aspect for the following reasons:

You pointed out in the comment section, a mutation in a mRNA molecule might lead to translated malformed protein which can easily be degraded. It will be only one mRNA transcript from thousands transcripts. With a short half life, the mRNA an proteins will be degraded which will not have a long standing impact of the cell/organism. As such it will be very difficult to observe a phenotype which will affect the whole host.

Thus RNAs mutations have only transient effects which will not affect the host in the long term. RNAs molecules are not more protected than DNA molecules just that they are short lived so the host is protected from the effects of RNA mutations.

Hope this helps!


Deducing amino acid sequence from a DNA sequence The suggested answer to the question is the following: "M L S C D K S D Stop". I do not understand how they get that result.

The question is as follows:

An RNA polymerase transcribes the following DNA sequence, in the direction of the arrow. Which amino acid sequence will be generated?

Thanks in advance!

This is a deceptively and badly worded trick question. Your confusion is because it starts with a mention of RNA polymerase, which transcribes DNA into mRNA, but asks about the protein, which is produced by the translation of the mRNA on ribosomes.

The first step in solving the problem is asking what is the sequence of the mRNA produced by the transcription. The question doesn't actually say which strand is copied, but the 5'-end of the mRNA is synthesized first, so you can assume the mRNA is the complement of the bottom strand, which is copied. (The convention of direction presumably tells you the same thing). Thus, the mRNA has the sequence:

  CCACCAUGUUA...

Now you need to go along the sequence (as a ribosome) looking for where to start translating. However the question doesn’t tell you whether this is a prokaryote or a eukaryote (unless you omitted to tell us). In order to solve the problem we have to assume it is a eukaryote where the ribosome normally scans along from the cap to the first AUG to initiate translation (the region italicized above):

  AUG (ATG) = M

  UUA (TTA) = L

  etc

(If it were a prokaryote you’d need to look for a Shine and Dalgarno ribosome-binding site.)

You might wish to raise my criticisms with your instructor (although I doubt that he will thank you for doing so).


What does 'half life' of a protein mean? Why do we use the term 'half life' for proteins?

Here is a link to some information regarding this question, but I am unable to infer it.

"Half-life time" is a general term. This is a time after which the amount of substance X decreases by 50%.

If you take a bulk of something (say, 100 protein molecules), if this protein has half-life time of 1 hr, then 1 hr later you'll have 50 molecules left.

In cellular biology it usually means that 50% of protein got recycled/degraded in given half-life time


If we introduce any disease or deadly effect to a large group of living things, will such a group be able to develop a resistance? Like for instance, introducing cancer or radiation,
to a large group of insects/animals that can reproduce very quickly,
would it result in the surviving population of these living things to be more resistant to whatever adverse condition that was subjected upon it?

I don't think this answer answers the post given the discussion and new edits. I will leave it here nevertheless just in case I still misunderstand the OP's question.

  [..] introducing cancer or radiation [..]

A cancer is not a transmissible disease (except very few cancer last the facial tumor in Tasmianian devils). A radiation is not even a pathology, it is a physical phenomenon which include light. Did you rather mean something like a virulent flu for example?

  If we introduce any disease or deadly effect to a large group of living things, will such a group be able to develop a resistance?

The population may or may not survive. It depends upon many parameters such as how virulent is the parasite, how large is the population, whether individuals in the population have already encountered the parasite before, whether there is already genetic variants resistant in the population or whether de novo mutations will be needed, etc... There is no way to answer to this question in the general sense.

Note by the way, that an individual may be resistant or tolerant to a certain disease.

Most of the time, the population survive well. The population will likely decrease in size a little bit though.


ATP Synthase EC number Why ATP synthase EC number is 7(Translocase)?
My textbook says it's a hydrolase but when i checked its EC number it was changed to 7.
And also ATPase(adensointriphosphatase) page that was previously classified as hydrolase is deleted in qmul.ac.uk

What textbook is this? An ATP synthase is not a hydrolase, since it does not use water to break a chemical bond (at least not in its primary function). However, it couples proton translocation with ATP synthesis. Therefore it is a translocase.
See the following passage from qmul.ac.uk what category 7 is and why e.g. ATPase is classified as translocase rather than as hydrolase. (It is a hydrolase as well, but it's not its primary function.)

Translocases (EC 7): A new EC Class
Six enzyme classes have been recognized since the first Enzyme
classification and nomenclature list was first approved by the
International Union of Biochemistry in 1961. These were based on the
type of reaction catalysed: Oxidoreductases (EC 1), Transferases (EC
2), Hydrolases (EC 3), Lyases (EC 4), Isomerases (EC 5) and Ligases
(EC 6). However, it has become apparent that none of these could
describe the important group of enzymes that catalyse the movement of
ions or molecules across membranes or their separation within
membranes. Several of these involve the hydrolysis of ATP and had been
previously classified as ATPases (EC 3.6.3.-), although the hydrolytic
reaction is not their primary function.


Examples of heterologous expression in human cell beside viral expression Usually, people are interested in expressing human proteins in fast-growing organisms like bacteria to yield a maximum of protein within a short time lapse. Codon usage harmonization/optimization have been used to increase the protein production. The role of codon usage have been studied in the context of viral protein expression, but outside this viral context, is there any example of using human cell lines for heterologous expression?

Expressing GFP in human cell lines for research purposes is an extremely common example of heterologous protein expression.

For research purposes, it's usually unnecessary to optimize codons for increased expression, especially since using more efficient enhancers and promoters produces a far greater improvement in expression levels than codon optimization which is non-trivial and species-specific.


The evolutionary process in bird wings, especially with regard to winglets In this answer on aviation.SE a comparison is made between the shapes of airplanes wings and the shapes of birds wings. It concludes with the following remark:

  After all, no bird has winglets. Not a single one.

In addition to be a disputable assertion (the wing tips such as the eagle's could be considered akin to a "winglet" of the fanned type) this has stricken me as based on a quite wrong assumption of how evolution works.

I tried to make my point in the comments only to reach this point:

  So you consider evolved wings as not mature. The winglet modification is just waiting to happen? Nature never tried it, in >100 million years of biological flight? Could be, yes. But is extremely unlikely. That settles it for me.

Am I correct in identifying this in a wrong interpretation of the evolutionary process?

As I understand the evolutionary process, the current bird wings are not necessarily perfect, are simply the version that so far has given the best advantage. The lack of "winglets" in birds cannot then be explained simply by assuming that they do not improve the wing, but it could also be that there has never been an evolutionary pressure to evolve them or that since birds flap their wings they would be detrimental instead of beneficial or whatever other reason.

Is my understanding of the evolutionary process correct? if not, where am I at fault?

As a small addendum, another user cited the "Spandrels" in comparison to the above debate, could someone explain what could have been the meaning of the comparison?

I looked up winglets so I had context for this answer. I'm interpreting winglets as the vertical tips at the end of airplane wings. If so, then you are correct. The spread primary feathers of soaring birds like eagles function as winglets (Tucker 1993). Airbus has a biomimicry web page devoted to some of the biological designs, including winglets, they incorporated into their airplane designs. Some studies suggest airplant winglets do increase efficiency (e.g., Hossain et al. 2011), but there is still some debate.
From the aviation.se answer:

Look at birds: They use two different wingtip designs. I guess we will both agree that those designs are mature after millions of years of evolution. And still there are two distinct wing tip shapes: One is the "fingered" wingtip with large, spread-out feathers, and one is the pointed tip you find from seagulls to albatrosses. Why is there not one, mature design?
This has to do with the environment they are used in. Seabirds fly in an unobstructed environment with steady winds and need to stay aloft for longer duration. All other birds have to cope with trees obstructing a straight flight path and gusts from hills, or those trees. They need to maneuver quickly and cope with gusty winds. This is helped by a reduced span and the possibility to fold the outer wing in or fan it out in an instance. Hence the fingered wingtip.

Although bird wings do tend to match his descriptions, he is not correct that these correspond entirely to ocean-going birds vs all other birds. Many inland birds have pointed wings, including swallows, nightjars, swifts, and falcons.  Some seagoing birds have winglets, such as pelicans and cormorants.  While wing type is shaped by natural selection in a given environment, it also reflects the evolutionary history of the birds.
There is not "one, mature design" because wings many different shapes and sizeshave evolved under varying selective pressures. For example, the long pointed wings of ocean-going albatrosses are excellent for gliding with little energy expenditure but they are lousy for taking flight or for landing. Other wings are shorter and broader, providing greater maneuverability in the woods. In this sense, there is no perfect wing. Each has evolved for different evolutionary reasons.
The main question
From the aviation.SE thread:

the fact that no random mutation has produced a winglet* in birds is in no way a demonstration that airplanes do not benefit from them, there is no logical relationship. [*even though the "fanned" design you refer, such as the eagle's, can be considered a form of optimum winglet] –  Federico

followed by this response:

So you consider evolved wings as not mature. The winglet modification is just waiting to happen? Nature never tried it, in >100 million years of biological flight? Could be, yes. But is extremely unlikely. That settles it for me...

Federico is correct. The basic wing type was set long ago as birds evolved from non-avian dinosaurs. Comparisons of modern bird wings with fossils suggest that the basic structure of bird wings has not changed very much since then. The current structure may be the best that has evolved by natural selection so far but that does not mean the wing cannot be improved further. As you noted, mutations could occur in existing genes that lead to further improvements of the structure and function of the wings. If those mutations never occur, then the improvements won't occur. This is one constraint of the evolutionary process (Hoffman 2014). Natural selection can only work with existing traits, using existing genes and genetic variation.
Another consideration is that wings for powered flight have evolved independently at least four times (birds, bats, insects, pterosaurs). Each time, a different type of wing evolved. Is one better than another? Bat wings have aerodynamic properties very different from birds but function very well for bats (Hedenstrom et al. 2009). Along the lines of your argument above, each wing type perhaps is (or was for pterosaurs) optimum given the environmental circumstances and evolutionary constraints. That doesn't mean they could not be improved.  If a wing evolves again in some organismal group in the distant evolutionary future, odds are very good that the structure will be different from those that have evolved so far. Perhaps that wing will be even more efficient than current wings.
Spandrels

Another user cited the "Spandrels" in comparison to the above debate, could someone explain what could have been the meaning of the comparison?

The use of "spandrels" in evolutionary biology stems back to a well-known paper by Stephen Jay Gould and Richard C. Lewontin called "The spandrels of San Marco and the Panglossian paradigm: a critique of the adaptionist programme", published in 1979 (Gould and Lewontin 1979). A spandrel is the space that forms between two adjacent arches or between an arch and a rectangular shape.  The spandrel emerges as a result of putting two arches next to each other and filling the space. It results from the joining of two arches. It was not specifically designed as part of the arch. Gould and Lewontin claim that evolutionary biologists are too quick to assign adaptive value to every trait on an organism, and argue that not every trait results directly from adaptation. Instead, they say, the trait may be a "spandrel" that emerged as a by-product of other traits. The "spandrel trait" has no adaptive value in and of itself.
The use of spandrels in the comments of the aviation discussion is not clear to me. Clearly, the person intended the evolutionary meaning, mentioning the paper by name. But I cannot tell at all the person's intent.
Edits: Incorporated comments by @Federico and @Andrew - thanks. I corrected horrendous typos and attempted to add clarity.
Citations
Hedenstrom, A. et al. 2009. Bird or bat: comparing airframe design and flight performance. Bioinspiration & Biomimetics 4 015001. doi:10.1088/1748-3182/4/1/015001
Hoffmann, A.A. 2014. Evolutionary limits and constraints. Pp. 247-252. In: The Princeton Guide to Evolution, Princeton University Press, USA.
Hossain et al. 2011. Drag analysis of an aircraft wing model with and without bird feather like winglet. International Journal of Mechanical, Aerospace, Industrial and Mechatronics Engineering 5: 30-35.
Tucker, V.A. 1993. Gliding birds: Reducion of induced drag by wing tip slots between the primary feathers. Journal of Experimental Biology 180: 285-310.


Are there any organisms that perform photosynthesis-like processes with thermal energy alone? The closest I can find are thermophiles, but it seems they use the chemicals present in the hot environment for energy, not the heat itself.

Thermophiles are organisms that are capable of surviving high temperatures. It doesn't mean they use or harvest the thermal energy in any way. Normally proteins start to unfold and degrade at temperatures above about 41 °C and all other organisms have a hard time coping with the effects.
Usually biology uses chemical energy. Photosynthesis is the one exception of a biological system converting the energy of photons directly into chemical energy stored in complex biomolecules for all others to use as nutrition.
Organisms that do not rely on those complex biomolecules but can support themselves are called autotroph. So photosynthetic organisms are  photoautotroph and micro organisms that use chemical energy from inorganic compounds are chemoautotroph. The inorganic compounds used can be as simple as decomposed water by radioactive decay.


How much does donating blood affect the amount of oxygen in your blood stream at high altitude? I am a regular blood donor and I am also a skydiver.  We normally go to around 13,000 feet AGL (above ground level).  Depending on how high above sea level the ground is, altitudes could be as high as 15,000 MSL (mean sea level) before a jumper is required to use supplemental oxygen.

At those altitudes hemoglobin is less effective at carrying oxygen, which is why hypoxia is a risk.

The following chart taken from this article about aviation and the body shows how oxygen levels decrease as altitude increases:

What I would like to know is if there is any research into the effect blood donation has on the blood stream's oxygen capacity?  Is it possible to say that x days after a donation, due to reduced hemoglobin levels, operating at 15,000 MSL would be equivalent to operating at 15,000 + x MSL without donation?

The oxygen-carrying capacity of the blood is:

  amount of haemoglobin * % saturation

The average blood donation is approximately 10% of total blood volume. . Since the donation will have no effect on the % saturation, the oxygen-carrying capacity at each altitude will go down by 10%.

By inspection of the graph in the question, the % saturation goes down by 10% at 10,000 feet. So I conclude that donating 10% of blood volume is equivalent to ascending to 10,000 feet in terms of the effect upon the blood's oxygen-carring capacity.

Response to OP comments:

1) Anyone living at 5,000 feet will have adapted to that altitude in two ways. First of all the erythrocyte levels of 2,3 bisphosphoglycerate will be elevated to maintain unloading of oxygen from haemoglobin in the tissues. Secondly, the number of red cells per mL of blood will have increased, to restore oxygen delivery. Incidentally this increases blood viscosity which is deleterious in the long term. Tibetans living in the Himalaya have adapted genetically to prevent this effect on their blood viscosity.

2) The effect of air pressure is already included in the graph, since it shows the actual degree of saturation of the blood.


What negative effects does cannabalism have in other species (like prion diseases) and how are they mitigated? It is well known that human cannibals are likely to suffer from a variety of ailments, particularly prion diseases.

However a great many other species, from insect to ape practice cannibalism at much higher rates.

Do they suffer from similar diseases as a result of their cannibalism? If not why not? and do they have evolved mechanisms for dealing with these negative effects?

First, to be clear, the very act of cannibalism does not cause the development of prions, but the consumption of an animal infected with a compatible form of them, particularly when eating nervous or digestive tissue (i.e. the brain, spine, stomach, or intestines).

To directly answer your question, yes, there are other animals that are susceptible to prions diseases when they consume infected members of their own species, or members of compatible carrier species. In the late 80s and 90s, there was a moderate epidemic of Bovine Spongiform Encephalopathy (Mad Cow Disease) that was concluded to have been caused by including bovine parts in cow feeding stock.

A common defense that I know of against infection from the consumption of infected animals is to simply not consume them at all. I know it's not really the answer you were expecting, but indeed, many animals have an active aversion to corpses, notably perceiving the smell of Cadaverine and Putrescine as repulsive. Evidently, a great defense against disease is to just not eat dead or dying things.

I've never heard of insects or arthropods having neurodegenerative prions, and wasn't able to find anything alluding to them having them, but I wouldn't be too surprised if they had other prion diseases that were infectious between them.

Sources:

Matravers et al. FST (2001);17,1-19

Also available at The National Archives

Cadaverine on Wikipedia
Putrescine on Wikipedia
Sacculina on Wikipedia


Assembly reconciliation We have some bacterial genomes that were assembled using Spades, they were sequenced with and IonTorrent PGM.

There are many assemblers and they give different results. I was interested in a tool that can merge the results from different assemblers but there are not many. I found only 2 : GARM and GAM-NGS.

Are there other tools to do merges? Does this improves the genome seq quality?

This is an old question but it seems relevant to answer now given current state of art. See also this related thread on biostars.
There are now many tools that perform this function, which is somewhat routine. A partial list:

quickmerge
metassembler (older)
MAC
RagTag (successor of RagOO)
CAMSA

I don't know which is best. Quickmerge is the one that I remember seeing the most. I believe that it is more common with eukaryotic genomes than microbial, as microbial genomes are now often getting closed with long reads.
In general we should expect that the regions that are agreed-upon by the assemblers will be fairly trustworthy, e.g. "improved" potentially. Artifacts are more likely to be found by using this kind of comparison as well.
The strategies used in each case will depend upon which tool you use. I haven't used them enough to say for sure.


Why do humans find baby animals cute? Why do humans find baby animals like cats, dogs, ... so cute?

As these are potential competitors (when grown up!) or even natural enemies (like e.g. tigers, leopards, ..), the protection instinct (reasonable for the babies of your species) should therefore not apply.

I can't imagine any reason why evolution let mankind adore foreign species that much.
Maybe only humans liking the enemy's kids survived, because they weren't killed by the baby's parents.

What is the evolutionary reason?

In German we call it "Kindchenschema" which is unfortunately translated only to the more unspecific "Cuteness", but sometimes also to "baby schema". This seems to be applying to most (care taking) mammals, also over species borders. The specific looks release hormones in the adult triggering care taking behaviour. This is to ensure the babies safety. That it not only works with the own parents helps ensuring the baby is cared for even if the parents cannot do it themselves.
Interestingly, the head and eye shape seems to trigger this hormone release. And it is the same for many animals. Like always, evolution uses the same winning scheme over and over again. This is why you can get a dog to care for abandoned kittens, and why you will find those puppies ever so cute.